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INTERNAL MEDICINE

Cardiology
Inspection
-tall and long arms Marfans with aortic dissection and aortic insufficiency
-cyanosis or clubbing congenital heart disease or pulmonary disease
-Xanthomas lipid disorders and premature atherosclerosis
-Osler's nodes (painful) , aneways lesions (painless), petechiae infecti!e endocarditis
"#
-normal is $-% (diurese to &'cm in ()*)
-ele!ated in + or , !entricular dysfunction-
-pericardial tamponade (with no y depressions) and constricti!e pericarditis (large y dep)
-ele!ated in cor pulmonale (right heart failure)
-ele!ated in ."( syndrome (d/t lung cancer and bloc0age of the ."()
-1-wa!e atrial contraction (missing in atrial fib)
-large a wa!es caused by
-tricuspid stenosis
-+")
-pulmonary hypertension
-pulmonary stenosis
-cannon 1 wa!es due to 2rd degree )3
-(-wa!e tricuspid !al!e closure from !entricular contraction
-X-descent artrial rela4ation
-"-wa!e atrial filling before opening of the tricuspid !al!e
-5-descent opening of the tricuspid !al!e and blood going from atria to !entricles
-s6uare root sign (6uic0 and large y-descent) 7 constricti!e pericarditis
-absent y-descent (cardiac tamponade)
84amination of the 1rterial #ulse
-9ardus slow rate of upstro0e
-#ar!us diminished amplitude
-1ortic stenosis : tardus and par!us (slow rate and diminished)
-,ow output, cardiomyopathy : par!us
-1ortic regurgitation or 1" fistulae : bounding pulse
-,eft "entricular dysfunction : #ulsus alternans
-I).. ()O(M) : 3isfirens pulse
-1ortic (orarctation : +adial femoral delay
-Obstructi!e disease : auscultation bruits
-carotid bruits (cerebral !ascular disease)
-abdominal bruits (renal artery stenosis) hypertension
84amination of the 1pical Impulse
-;
th
I(. at the mid cla!icular line
-cardiomyopathy : diffuse and wea0 impulse
-,") or aortic stenosis : sustained cardiac impulse
-M+ : hyperdynamic
-M. : locali<ed and tapping
)eart .ounds
.= (M= and 9=) .> (1> and #>) .2 .?
Mitral then tricuspid closure 1ortic then #ulmonic closure "ol load on the left !ent #ressure o!erload
,oud
-M., high )+, low #+ int
,oud
-systemic or pulmonic )9@
1+, M+, dilated myopathy +epresents atrial 0ic0
-not seen in atrial fib
.oft
-(alcified !al!e, high #+ int
.oft
-(alcified !al!e
1., )9@, hyper myopathy
ischemia
#hysiological .plitting
-increased in ins
-decreased in e4p
Aide .plitting
-delayed pul closure
-#., M+, +333
*i4ed .plitting
-too much shunt to ha!e
much of a difference
-1.B, +ight "ent *ailure
#arado4ical .plitting
-delayed aortic closure
-1., 9+, ,333
.ystolic murmurs
-eCection murmurs
-high pitched, cresendo-decresendo, faint and locali<ed, upper left sternal border
-systolic murmurs of 1. or #. (midsystolic)
-systolic murmurs of M+ or 9+ (holosystolic)
-systolic murmurs of ".B (holosystolic)
Biastolic murmurs
-1ortic or pulmonic regurgitation
-Mitral or 9ricuspid .tenosis
-(an be combination of the two (i-e- D1ustin *lint murmur : 1+ E M.)
(ardiac Maneu!ers
-Inspiration increases all right sided murmurs (9+, #., #+)
-"alsal!a maneu!er
-inhibits !enous return to the heart (small heart)
-all cardiac murmurs will decrease e4cept for
=) I)..
>) Mitral and 9ricuspid "al!e #rolapse with regurgitation
-)and Frip -increases 9#+ and will reduce murmur of 1. and I).. but increase M+
-.6uatting 7increases "+ increase in ." causing a decrease in 9#+
-should increase all murmurs e4cept for
=) I)..
>) Mitral and 9ricuspid "al!e #rolapse with regurgitation
-.upine upright : decrease in "+ decrease in ." increase in 9#+
-should decrease all murmurs e4cept for
=) I)..
>) Mitral and 9ricuspid "al!e #rolapse with regurgitation
"al!ular )eart Bisease
SYSTOLIC murmurs DIASTOLIC murmurs
Aortic Stenosis
(1G.8.
-congenital bicuspid !al!e and in +)B (but usually mitral)
#19)O#)5.IO,OF5
-pressure o!erload ," hypertrophy O> cons
-systolic function is preser!ed until late
-diastolic dysfunction (need atrial 0ic0 to get blood in !ent)
-atrial arrhythmia (a fib) is poorly tolerated
#OO+ (,I@I(1, .5M#9OM. (with life e4pectancy)
-1ngina (& ; years) 7 e!en w/o (1BH d/t coronary arteries
-.yncope (& 2 years) 7 w/ e4ertion
-()* (& > years) 7 worst life e4pectancy w/o surgery
#BX
-pulsus tardus, .> impaired motion of the !al!e
-parado4ical splitting of .> and a .? is present
-midsystolic murmur that transmits to the carotids
B4 (diagnosis)
-8IF ,")
-8()O measures pressure grad across !al!e (area)
-(19) measure grad and concurrent (1B
94 : @O@8 e4cept .4 (surgery)
.4
-balloon !a!uloplasty usually only temporary
-!al!e replacement
biological wears out but no need for anticoagulation
-gi!en in elderly
mechanical last longer but re6uires anticoagulation
-gi!en in young
Aortic Regurgitation
(1G.8.
-+)B, I8, syphilis(from aortitis), aortic dissection, Marfans
.,8, 1n0ylosing .pondylitis
#19)O#)5.IO,OF5
-reguritant flow during diastole ,"8 and !olume o!erload
-." is maintained by ,"*#
- in systemic diastolic blood pressure pulse pressure
(,I@I(1, *819G+8.
-," failure d/t !olume o!erload
-syncope d/t diastolic arterial pressure
-angina d/t coronary artery flow (during diastole)
#BX
-apical impulse down and to the left
-high pitched blowing diastolic murmur at ,.3
-1ustin *lint murmurJ low pitched diastolic rumble
d/t !ibrations of the reguritant flow against M"
-increase pulse pressure
(orrigar pulse 7 rapid rise followed by a rapid fall
#istol-shot 7 femoral pulses
Buro<ie< sign 7 diastolic bruit o!er the femoral artery
Be Mussets sign 7 bobbing motion of the head
Kuinc0es pulse 7 blushing and blanching of nail bed
B4
-8IFE(X+E8()O
-BO##,8+ will show regurgitant flow
-(19) regurgitant !olume can be calculated
94
-loop diuretics to reduce afterload and reguritant !olume
.4
-when left !entricular decompensation begins to occur
Mitral Regurgitation
(1G.8. (+heumatic )eart Bisease, Mitral "al!e #rolapse, Infecti!e
8ndocarditis)
-+)B, M"#, I8, Bilated "entricle or
#apillary Muscle (temp ischemia, MI rupture)
#19)O#)5.IO,OF5
-pumping into the atrium as well as the aorta
-,1 pressure and (O
-B,O,#@) (dyspnea, orthopnea, and #@)) d/t bac0wards flow
#BX (physical e4am)
-hyperdynamic apical impulse shifted to the left
-holosystolic murmur that radiates to the a4illa
-widely split .> and .2 present
B4
-8IF enlargement of the ,1 and ,"
-(X+ enlargement of the ,1 and !ascular congestion
-8()O may demonstrate ruptured chordae or M"#
use for superimposed endocarditis
-(19) right heart cath re!eals DrL or c!-wa!es in the ,1
94
-!asodilators to reduce afterload for forward flow
-loop diuretics to reduce pulmonary congestion
-digo4in to control !entricular rates and contractility
-1nticoagulants in atrial fib to stop emboli<ation
.4
-for patients with progressi!e atrial enlargement
-done before irre!ersible left !entricular dysfunction
Mitral Stenosis
*819G+8.
->M years after +heumatic )eart Bisease (2M y/o patients)
-,1 pressure and pulmonary pressure
.5M#9OM.
-B,O,#@) (dyspnea, orthopnea, and #@))
-hemoptysis (rarely)
-1trial *ib complicates the matter (no atrial 0ic0)
-,"* causes +"* systemic 1@B pul emboli
#BX
-.= and O. (the earlier the O. the more se!ere the M.)
-low pitched rumbling diastolic murmur
-#> d/t pulmonary )9@ right !entricular lift
B4
-8IF enlargement of the +" and ,1, atrial fib,
-(X+ straight right border, double density on left d/t ,1)
pulmonary !eins are dilated in the upper lobes
-8()O reduced mitral area and thic0ening of the !al!e
-BO##,8+ shows se!erity of stenosis
-(19) to show se!erity of pul )9@, other !al!es, (1B
94
-Biuretics (loops) for congestion
-Bigo4in or (a
EE
channel bloc0er for the !ent rate in 1*
-1nticoagulants in 1* to stop emboli<ation
.4
-if no calcification or regurgitation commissurotomy
or balloon !al!uloplasty
-otherwise !al!e replacement (before pul )9@ occurs)
Mitral "al!e #rolapse
*819G+8.
-;N of adults (usually in young women)
-redundancy and elongation of the chordae of the mitral !al!e
-sudden tensing produces the mid-systolic clic0
-abnormal closure of !al!e produces the murmur of mitral regurgitation
(,I@I(1, *I@BI@F.
-most asymptomatic of the !al!ular disorders
-atypical chest pain tachyarrhythmia
-I8 (prophyla4is before .4 if they ha!e regurgitation will pre!ent this)
7 not needed if only clic0 is present
-murmurs are accentuated by rising from the supine position (smaller ,")
-mid-systolic clic0 at ape4 followed by a blowing late systolic murmur
B4
-8()O redundancy of the chordae
-BO##,8+ detects regurgitation
94
-o!erall prognosis is e4cellent with rare complications
-most patients dont re6uire therapy
-antibiotic prophyla4is for patients with mitral regurgitation only
-palpitation or other tachyarrhythmic symptoms are treated with -bloc0ers
+heumatic *e!er
F8@8+1, *819G+8.
-childhood and adolescence with group 1 -hemolytic .treptococcus (F13).)
(,I@I(1, *819G+8.
-immediate symptoms of fe!er, carditis, and migratory polyarthritis, Subcutanious @odules
8rythema Marginatum (e!anescent serpigenous rash) (comes and goes), Tragic (arditis
subcutaneous nodules of bony prominence O+8M8M38+ 9)8 O@8. (+I98+I1P Resol!ing (horea
-later findings are chorea Erythema Marginatum
(1+BI9I. Polyarthritis
-affects pericardium, myocardium, and endocardium
-may lead to acute !al!ular insufficiency, heart failure, arrhythmias
-most cases ha!e no clinical e!idence of the initial carditis
,O@F 98+M
-may be recurrent
-essential to continue prophyla4is against F13). after an attac0 of 1+*
-monthly ben<athine penicillin until age =%
-antibiotic prophyla4is before in!asi!e dental or surgical procedures for life
(1+BI1( (19)8+9IQ19IO@
Right .ided )eart (atheteri<ation (.wan Fan<) Let .ided )eart (atheteri<ation
9echni6ue
-+1+"#1 (balloon inflated to wedge)
-wedged catheter bloc0s blood flow
-measures pressures downstream in the ,1 (#(A#)
pea0s at =% mm)gH can ma0e a starling cur!e for ,"
9echni6ue
-cath is passed from brachial or femoral artery
-dye inCection allows e!aluation of aortic and mitral !al!es
-procedure for angiography and !entriculogram
Indications
-1ssessment of ,"B*# (in ,"* patients)
-patients with heart, lung, and 0idney disease
-measurement of cardiac output
-measurement of +" pressures and assess of pul )9@
-assessment of ,+ shunts and measure O> step up
Indications
-1ssessment for 1ortic Bissection
-"entriculogram
-Imaging of the coronary arteries and inter!ention in MI
such as angioplasty, balloon plasty, stents
(omplications
-wedged balloon may cause pulmonary infarct
despite bronchial circulation
-pul artery perforation, thrombus, infection (.taph)
-!entricular ectopy since cath is in +"
-+333 (dont do procedure if ,333 is present already)
(omplications
-!ascular damage at insertion
-dye anaphyla4is or 1+I (acute renal failure from dye)
-arterial thromboembolism
-aortic dissection
-MI, stro0e and death
)5#8+98@.IO@
-affects >MN of the population (higher in 1frican 1mericans)
-affects $MN of those greater than $M
#19)O#)5.IO,OF5
-increased e4tracellular fluid !olume
-renal dysfunction
-!asoconstriction w/ 9#+
-(O
O+F1@ B1M1F8 (no symptoms until end organ damage)
-cerebral hemorrhage
-,"), ()*
-aortic dissection or aneurysm
-retinopathy
#+IM1+5 )5#8+98@.IO@
-accounts for RMN of cases
-no identifiable causes
-presents between 2M-;M years of age w/ family history and an increasing blood pressure
.8(O@B1+5 )5#8+98@.IO@
-tends to be younger and ha!e more se!ere ele!ation with possibility of curingS
Renal !ascular Disease
-*ibromuscular dysplasia
young women
headache and retinopathy
-1thersclerosis of +enal 1-
older men
renal perfusionrenin
.e!ere )9@
.e!ere +etinopathy
+enal 1rtery 3ruit (+1.)
B4 +enal nuclear per scan
Bigital sub angiography
+esponds to 1(8 inh-
.amp of !en renin le!els
94 (orrect 1rtery .tenosis
*MBpercutanious angio
+1..4 re!asculari<e
Estrogen Induced "TN
-O(# pillH stop
Primary Aldosteronism
-retention of @a
E
-I
E
metabolic 1l0alosis
-aldosterone renin
-adenoma or hyperplasia
B4
-(9E adrenal !enous sam
.4
-ta0e out the mass
Pheochromocytoma
-stimulates receptors
-episodic )9@
-headache and nausea
-urinary !anylmandelic acid
-locali<ed tumor on (9
-#reoperati!e 94
+ bloc0ers
.4 : is choice
Cushing#s Syndrome
-84cess (ortisol
-(ushings .yndrome .igns
- >? urine cortisol
"y$erthyroidism
-increased pulse pressure
Coractation o the Aorta
-#ulsus tardus and par!us
-3# in arms and legs
-systolic murmur heard
between scapulae
-.4 is curati!e
Drugs
-steroids (aldosterone effects)
-sympathomimetics (decon)
-cocaine (young 8+ !isit)
9)8+1#5 *O+ )5#8+98@.IO@
@O@ #)1+M1(O,OFI(
-weight reduction, alcohol reduction, aerobic e4ercise, @a
E
reduction
9hia<ide Biuretics 1ntisympathetic 1gents "asodilators 1(8 inhibitors
+educes 8( fluid !olume
s Flucose, (a
EE
, G1, lipid
I
E
- use I
E
sparing
-use ,oops when in ()*
8ither or bloc0ers
bloc0ers for )9@ E (1B
-bad effect on lipids
-good for reduction of B#
B# : O> cons : )+43#
-cardioselecti!e
bloc0ers
-inhibit !asoconstriction
(a
EE
channel bloc0ers
-!asodilatation w/ (1B
)ydrala<ine
-9#+
-.,8 li0e syndrome
-salt and water retention
Mino4idil
-9#+
-salt and water retention
#re!ent 19-II formation
-I
E
-no cholesterolemia
-no glucose
-prolongs sur!i!al in
patients w/ ()*
.election of 1ntihypertensi!e Medication
-11 patients often respond to Biuretics and (a
EE
channel bloc0ers
--bloc0ers are contraindicated in high lipids and (O#B
-1(8 inhibitors increase sur!i!al in ()*
-need to use diuretics in direct !asodilators
M1,IF@1@9 )5#8+98@.IO@
*819G+8.
-se!ere )9@ and end organ damage occurring o!er )OG+.
-end organ damage results in
,"*, (@. changes, headache, !isual disturbances, M., retinopathy, papilledema, stro0e, acute renal failure
-goal of treatment is to lower blood pressure w/o cutting off circulation to !ital organs
-usually ha!e atherosclerosis
B+GF 9)8+1#5
-nitroprusside the arterial !asodilator (nitroglycerin is !enous more than arterial)
-administer by continuous infusion (may cause sudden hypotension so must be on a unit and be monitored)
-metaboli<ed to cyanide and thiocyanate (metabolic acidosis) so be careful (94 : with methemoglobin)
Ischemic "eart Disease %Coronary Artery Disease&
.table 1ngina 0now what it ta0es to get pain (problem of demand)
Gnstable 1ngina at rest, or less e4ertion, new onset angina
.ilent Ischemia dont feel it (diabetics)
MI, )*, arrhythmias sudden death
+I.I *1(9O+.
-old, male, female after menopause, serum cholesterol, smo0ing, )9@, diabetes, family history, O(#, obesity
-males o!er ?;, females o!er ;;H male family members under ;; female family members under $;
#BX
-can ha!e a perfectly normal e4am during ischemic episode
-)9@, .?,
-e!aluate for complications of ischemia
-dys0inetic cardiac ape4 (no longer functioning)
-cardiac enlargement in repeated attac0s
-"B
-.2 (!ery ominous finding and shows global ischemia)
-murmur of papillary muscle dysfunction of mitral regurgitation
-e!idence of arrhythmias (irregular pulses and cannon 1 wa!es)
-e!aluation for other possible causes of chest discomfort
@O@ I@"1.I"8 98.9I@F
-8IF must be done first
-84ercise stress testing (3ayesian #robability) use on ?? year old male with atypical chest pain
-+adionuclide stress testing -use on >> y/oH can show portion of the heart with problem
-#harmacoligic stress testing 7use Bipyramiol (causes !asoconstriction) Bobutamine (causes contractility)
I@"1.I"8 98.9I@FJ (1+BI1( (19)898+IQ19IO@
-permits e!aluation of left !entricular function
-measurement of hemodynamic parameters
-selecti!e !isuali<ation of the coronary arteries
-indications
=) se!ere (1B
>) E stress test
2) failed medical management
?) false negati!e stress test
;) ergomo!ine may be administered to pro!o0e coronary spasm ie- #rin<metals angina
-produces !asoconstriction and reproduces pain
1ngina #ectoris
-Intermittent tightness substernallyH ,a!ines .ign : epigastric area
-Biaphoresis, palpitations, .O3, +ad to ,8, nec0, or CawH 9ypical episodes last at least se!eral minutes
-Bifferential Biagnosis 1ortic .tenosis (also I)..), #ericarditis (pleuritic), 1ortic Bissection (tearing sensation)
esophageal disease, #GB, biliary disease, M. disease (costochondritis) pressing on chest
pleurisy, pulmonary infarction, pneumothora4
'nsta(le Angina Prin)metal#s Angina Silent Ischemia
+est angina or new onset 1ngina at rest w/ .9 (1B w/o chest pain
Intermediate sit between chronic
stable and acute MI
B/t !asospasm, +aynauds syndrome 94
-nitrates and (a
EE
channel bloc0ers
8IF shows .9
9 wa!e in!ersion
Must distinguish from non K-wa!e MI
94
-nitrates and (a
EE
channel bloc0ers
-BO@9 G.8 -bloc0ers
,ong term prognosis is uncertain
94
-rule out MI
-I" nitroglycerin to relie!e pain
-aspirin and anti-platelet for thrombus
-cath- *or patients who dont stabili<e
9+819M8@9 O#9IO@. *O+ (1B
*irst treat underlying cause if there is one
-anemia gi!e *e
-hyperthyroidism treat
-hypo4ia O>
Initial therapy is sublingual nitroglycerin #+@ (only gi!e once a day and ha!e brea0 period to pre!ent toleri<ation)
,ong acting nitrates (a
EE
channel bloc0ers -bloc0ers are added se6uentially if symptoms continue
-nitrates relie!e angina by !enodilation which cardiac wall tension
-(a
EE
channel bloc0ers relie!e angina by afterload, )+, and contractility
-"erapamil )+ and contractility (dont use with ,"* (failure) or bradycardia)
-Biltia<em a mi4 of the two
-@ifedipine no appreciable )+ or contractility (OI to use in ,"* or bradycardia)
--bloc0ers relie!e angina by )+, 3#, and contractility (most effecti!e for double product ()+43#)
-useful in e4ercise induced ischemia
-dont use in bronchial spasm or bradycardia
-should be titrated to )+ &'M (if not then add -bloc0ers until below 'M)
-Biuretics and 1(8 inhibitors
-useful in those with left !entricular dysfunction by reducing wall tension and O> demand
-aspirin reduces ris0 for first non-fatal myocardial infarction in men
-(13F (coronary artery bypass graft) 7 I* M8B. BO@9 AO+I
-I@BI(198B *O+ 9)8 *O,,OAI@FJ
-=) left main coronary disease (not ,1B and ,(X)
->) triple !essel disease (+(1, ,1B, ,(X) 1@B 8* &;MN
-2) patency rate is better with internal mammary artery than with saphenous !ein graft
-1ngioplasty
-o!erall success rate of %M-RMN but with restenosis of 2MN
-I@BI(198B *O+ 9)8 *O,,OAI@FJ
-=) single or two !essel disease whose angina is poorly controlled with medication
M5O(1+BI1, I@*1+(9IO@
-occurs when myocardial blood flow is interrupted for a duration sufficient to cause tissue necrosis
-usually atherosclerosis E thrombotic coronary occlusion
-early therapeutic strategies focus on reestablishing blood supply through reperfusion
(,I@I(1, #+8.8@919IO@-persistent anginal pain that lasts for more than =M-=; minutes (similar to angina pectoris)
#BX
-search for possible complications of myocardial infarction (heart failure and arrhythmias)
-91()5(1+BI1 from pump failure, an4iety, pericarditis
-3+1B5(1+BI1 inferior wall ischemia (+(1) or increased !agal tone
-"B right or bi!entricular failure
-I++8FG,1+ )81+9 3819. arrhythmias
-.2 significant left !entricular dysfunction
-@8A 1#I(1, .5.9O,I( MG+MG+ papillary muscle dysfunction
-#8+I(1+BI1, *+I(9IO@ +G3 more than >? hours after ischemia or pericarditis
"istory E*+ changes Cardiac isoen)yme measurements
-prolonged angina of T=; minutes 1) .9 (in specific leads)
>) K-wa!e
2) @ormali<ation of .9
?) 9-wa!e in!ersion
(#I-M3 starts at $
pea0s at =>->? (may stay up)
ends at '>-R$
1.9 or ,B) then begins
Biagnostic BifficultyJ
-#rior MI
-,333 (non infarct K-wa!es)
-#acema0er
(#I-M3 est the si<e of the infarct
(#I-M3 pea0s around => (early)
-when reperfusion was successful
(#I-M3 ele!ated when in persistent
post-infarct ischemia ((19) pat)
94
-stabili<e patients 3#
-relie!e pain by administering morphine sulfate
-assess hemodynamics ("#)
-determine eligibility of patient for thrombolysis (see contraindications)
9)+OM3O,59I( 9)8+1#5
-gi!e lidocaine first to pre!ent reperfusion arrhythmia
-must be administered within = hour of the onset of symptoms (doesnt wor0 after $ hours)
-patency in ';N and hemorrhagic stro0e in =N
-(ontraindicated with
-bleeding disorder, recent stro0e, uncontrolled hypertension, recent surgery, #GB, diabetic retinopathy
-heparin and aspirin are also used to reduce re-occlusion rates
-dont use heparin and strepto0inase together howe!er
-typical patient to use on isJ )4 of chest pain, ongoing for >M minutes, .9 in > contiguous leads
M1@1F8M8@9 O* 1++)59)MI1.
-prophylactic lidocaine is contro!ersial but is gi!en before thrombolytic therapy to pre!ent rep arr-
-=
st
degree heart bloc0 (#+ TM->sec) rarely re6uires therapy
->
nd
degree heart bloc0 Mobit< I
-ischemia abo!e the 1" node
-inferior wall MI (+(1) 7 leads II, III, a"*
-rarely progresses to complete heart bloc0
-#+ gets progressi!ely longer with occasional loss of K+.
-no pacema0er needed
->
nd
degree heart bloc0 Mobit< II
-ischemia below the 1" node
-anterior wall MI (,1B) 7 leads "> and "2
-often progresses to complete heart bloc0
-#+ remains the same with occasional loss of the K+.
-pacema0er is needed
#1(8 M1I8+ +8(OMM8@B19IO@.
-in!ol!ement of ,333 and +333 (escape rhythm is slow w/ wide K+. comple4)
-alternating 333 li0e +333 then ,333 then +333
-333 with 1" bloc0
-+333 with left anterior fascicular or left posterior fascicular bloc0
(OM#,I(19IO@.
#ost-infarct ischemia
-persistent pain for >? hours after
-more common in non-K-wa!e MI
-94 : nitroglycerin and heparin
-consider cardiac (19)
#ump *ailure (.hoc0 if ?MN or more)
-significant MI E prior infarction
-)+ (bad if persistent)
-may actually be d/t stunning
this is only transient ischemia
-.wan-Fan< cath to det ,"8B#
Myocardial +upture
-occurs at the >
nd
to the ;
th
day
-shoc0, 8MB, tamponade !ia 8()O
-papillary muscle !-wa!e on (19)
-".B ,+ shunting (O> step up)
-94 : .4 immediately
#ericarditis
-occurs on the >
nd
to 2
rd
day
-pleurtic pain not angina
-pericardial rub, )+, #+, global.9
-94 : aspirin and @.1IB.
-dont gi!e thrombolytics (rupture)
-Bresslers .yndrome is >-$ wee0s
fe!er,pericarditis,pleuritis94:@.1IB.
,eft "entricular Mural 9hrombus
-formed by dys0inesia
-usually ant MI E apical dys0inesia
or apical aneurysm
-B4 : 8()O
-94 : anticoagulants (emboli<ation)
+ight "entricular Infarction
-inferior wall MI (+(1)
-hypotension, "B, clear lung fields
-.9 in "= and "> (right precordial)
-94 : fluids not dobutamine or digo4in
.8(O@B1+5 #+8"8@9IO@
-bloc0ers -reccurent MI
-careful in (O#B
Biltia<em -non K-wa!e
-not for ()*
9#1 or
strepto0inase w/
aspirin
- mortality and recurrent MI
-dont use heparin w/ strepto0inase
+I.I .9+19I*I(19IO@
-systolic function is assessed with 8()O or radionuclide studies (MGF1)
-%MN diastolic dysfunction
-;;N normal or diastolic dysfunction
->MN systolic dysfunction
-e4ercise testing stratifies patients w/ inducible ischemia
-this is done with a subma4imal stress test
-do this before sending home
-high ris0 patients should be considered for coronary (19)
38*O+8 .8@BI@F )OM8
=) nuclear 8* assessment
2) -bloc0ers if 8* T?;N
2) diltia<em if non K-wa!e
?) 1spirin if no contraindication
;) .ubma4imal stress test
(O@F8.9I"8 )81+9 *1I,G+8
-inability to pump sufficiently to supply tissues with ade6uate O>
89IO,OF5
(ontractility
-ischemia and MI
-cardiomyopathy ((higas Bisease)
-"al!ular heart disease
!al!ular stenosispressure o!erload
!al!ular regurg!olume o!erload
1fterload
-from 9#+ and from )9@
#reload
-causes pulmonary !ascular cong-
-BO#@) (dyspnea, orthopnea,
#aro4ysmal nocturnal dyspnea)
.IF@. 1@B .5M#9OM.
-signs and symptoms may be due to right sided or left sided congestion (lung or body)
-right sided failure is due to
=) left sided failure
>) (O#B (right sided pressure o!erload)
-bac0ward congestion problems
-BO#@), nocturia, peripheral edema
-anore4ia d/t splanchnic congestion
-signs -)+, rales, "B, cardiomegaly, ascites, hepatic congestion (hepatoCugular reflu4)
BI1F@O.9I( 98.9. (B4)
8IF
-? chamber enlargement
-ischemia
-effects from medication
digitalis .9 (dig effect)
diuretics I
E
G-wa!es
(X+
-cardiomegaly
-cephali<ation of flow (up)
-Ierley 3 ,ines
septal lines d/t interst edema
-pleural effusion (transudate)
&;MN of serum protein
-pulmonary edema
8()O
-assesses function
-si<e of chambers
-!al!ular disease
-pericardial disease
+adionuclide "entriculography
-MGF1 (multigated ac6uistion)
-assessment of 8*
-8* in patients w/ diastolic dys
not as acurate if M+ (atrium loss)
-assesses wall abnormalities
9)8+1#5
-identify treatable etiologies ((1B, "al!ular, non compliance (@a
E
), thyroto4icosis, anemia, thiamin def-)
-thiamine deficiency causes 3eri 3eri )eart Bisease (high output failure) 7 re!ersible
-also causes Aerni0es Iorsa0offs .yndrome
-also causes intranuclear opthalplegia
-common cause of altered mental status in the 8+ (gi!e coc0tail of 9hiamine, B;M, and @arcan)
-remember to gi!e thiamine before glucose B+I# because glucose will suc0 up thiamine
-treat high preload and afterload loop diuretics (furosemide) 7 reduces symptoms not mortality
-treat contractility digo4in, -agonists li0e dobutamine and dopamine, amrinone if bad
-BIFOXI@ 7 (only indicated for 8* & ?MN) 7 not shown to decrease mortality)
-inhibits @a
E
/I
E
19#ase
-e4creted by the 0idney (must reduce dose in renal insufficiency
-drug interactions with 6uinidine, theophylline, !erapamil (all digo4in le!els)
-BIFOXI@ 9OXI(I95
-narrow theraputic window and to4icity is possible in this window
-happens in I
E
, elderly, and renal failure (for which diuretics would be gi!en)
-causes anore4ia, nausea, !omiting and !isual disturbance (#ainterJ "an Fooh effect)
-8IF
-#"(s are common
-.9 (dig effect)
-#19 with !arying heart bloc0 (in different parts of the 8IF) 7 classic
-history of 1* that is now Dregulari<edL at a rate of ?;-$M bpm 7 classic
-=) dig gi!en o!er a period of time w/o complications
->) !erapamil is gi!en for some reason ( digo4in le!els)
-2) you get 1" nodal escape rhythm (non sinus 7 no p-wa!e)
-94 : readCust I
E
le!el and use Big antibodies
-if I
E
is high insulin w/ glucose, (a
EE
carbonate to stabili<e
-@esiritide (I" med used in drip form for acute decompensated ()*
-I" form of natrietic peptide
-supposedly better diuresis and shorter hospital stay (not shown to decrease mortality)
-9he following are medications that "A!E been shown to decrease mortality in ()*J
,ACE inhi(itors %lisinopril, enalapril, captopril) and AR-S (losartan, irbesartan)
-must be careful of hyper0alemia, acute renal insufficiency, and angioedema (rare)
-start early in the coarse of an e4acerbation (i-e- when the patient is D.etL)
-better to start captopril first since it has shorter half life and can titrate up faster
,,(loc/ers (only metoprolol and car!edilol)
-must be careful to start !ery low dose and titrate up or else could e4acerbate ()*
-must be careful of hyper0alemia, bronchospasm (especially in (O#B, asthma)
-start after e4acerbation is treated (i-e- when the patient is Ddry0)
,S$ironolactone
-must be careful of hyper0alemia, and acute renal insufficiency
CARDIOMYOPAT"Y
Bilated (ardiomyopathy ((OMMO@) )ypertrophic (ardiomyopathy +estriciti!e (ardiomyopathy
-Most commonly from ischema
-bi!entricular failure
-()* with 8* in the >Ms
-U= : ischemia
-alcoholism, infections (co4sa0ie)
-idiopathic, post partum
-systemic or pulmonary emboli
-atrial and !entricular arrhythmias
-enlargement causes M+ and 9+
-summation gallop .2 and .?
-restriction of !entricular filling
-obstruction to outflow
-!entricular hypertrophy (sym or asym)
(1G.8.
-amyloidosis (#rotein)
-hemochromatosis (*e)
-still !entricle and pre!ent filling
-normal cardiac si<e and function
-8*
I)..
-asymmetrical hypertrophy
-bisfriens pulse
.ystolic function is OI
Biastolic function is impaired
,198 *I@BI@F.
-atrial arrhythmias and 1" bloc0
8IF changes
-non specific changes (.9 and 9)
-,") may be present
Increase murmur
-!olume depletion
-nitrates
94 : d/t diastolic dysfunction
-(a
EE
channel bloc0ers
(X+
-? chamber enlargement
-pulmonary !ascular congestion
+ising from s6uating
1,(O)O,I( (1+BIOM5O#19)5
-alcohol acutely ," function
)oliday )eart .yndrome (re!ersible)
1trial *ib
-(ong cardiomyopathy ta0es ;-=My
not 3eri 3eri (9## defE hyperd circ-)
.5M#9OM.
-chest pain indistinguisable from
angina
-e4ertion syncope (I)..)
-arrhythmias
-sudden death
1(G98 M5O(1+BI9I.
-from !iral infection
-.1 (hagas )eart Bisease 9-cru<i
-most resol!e spontaneously
94
--bloc0ers, (a
EE
channel bloc0ers
rela4ation outflow obstruction
-may re6uire .4 on the septum
#8+I#1+9GM (1+BIOM5O#19)5
-2 months after deli!ery 7 re!ersible
-no e!idence of infection
-autoimmune mechanism
#8+(1+BI1, BI.81.8
1cute #ericarditis (ardiac 9amponade (onstricti!e #ericarditis
(auses
-!iral, bacterial, fungal, 93
-neoplastic (melanoma)
-drug related (causing .,8-li0e)
procainamide, hydrala<ine, isonia<id
-collagen !ascular diseases
.,8, scleroderma, +1
- penetrating inCury, aortic dissection
-radiation from )odg0ins 94
-Gremia, MI (dresslers .yndrome)
-)ypothyroidism (weight change)
#athophysiology
-pressure from fluid
-more li0ely is accumulates fast
-compression at +1 +"
e6uali<ation of pressures
-no y,descents on 1!P
-," filling, .", (O gradually
-compression of all 4 chambers and
equalization of all diastolic pressures
@ormal heart in non ( (a
EE
pericard-
-compression of all 4 chambers and
equalization of all diastolic pressures
-restriction of diastolic filling
-no effusion, and no large heart
-caused by a chronic pericarditis
,s2uare root y,.a3es on 1!P
#athophysiology
-rigid shell around the heart
-!entricle 0noc0s against pericardium
-Iussmauls .ign "# w/ ins
(linical *eatures
-pleuritic chest pain
-pericardial rub in sys and diastole
-less pain when leaning forward
B4
-pulsus parado4us T=M mm)g w/ ins
-8()O immediately
B4
-normal heart si<e w/ pericardial (a
EE
-8()O e4cludes tamponade etcV
-(9 measures the thic0ness of (a
EE
8IF findings
-)+, .9 in all leads, #+
.4
-pericardiocentesis immediately
.4
-stripping of the (a
EE
for the cure
#ericardial 8ffusion
-more to do with speed of effusion
-may be asymptomatic if slow
-distant heart sounds
-no friction rub
-8IF shows !oltage and alternating
electrical patterns d/t floating
-8()O is the definiti!e test
(1+BI1( 1++)59)MI1.
.inus 9achycardia
-stress, ischemia,
.", infection, fe!er,
dehydration, 9?
-94:underlying cause
#aro4ysmal 1trial
9achycardia
-can feel )+ (>MM)
-narrow K+.
-94:carotid massage
!alsal!a maneu!er
di!ing refle4
!erapamil, -bloc0er
digo4in
1trial *lutter
-some 1" node bloc0
-if >J= bloc0
reg )+ of =;M
-hidden p-wa!es
-94:carotid massage
!alsal!a maneu!er
di!ing refle4
drugs may slow sinus
rate so that =;M >MM
1trial *ibrillation
-Irregularly irregular
-underlying cause
hypo4ia, #8,
pericarditis, 9?
ischemia, M"#
-94 underlying cause
slow )+
!erapamil, diltia<em
digo4in, esmolol
cardio!ersion
medical or electrical
digo4in 6uinidine,
procainamide
1nticoagulate
If T = wee0
Multifocal 1trial
9achycardia
-multiple #-wa!es
different atrial parts
-patients w/ (O#B
-94 : correct (O#B
dont treat heart
1" Cunctional
1rrhythmias
-pic0s up when sinus
node slows
-usually at ?;-$M
-protecti!e mech-
-no 94 needed
1" node reentrant tachycardia
-causes paro4ysmal super!entricular
-onset sudden with =J= conduction
->MM bps
-seen with absence of structural heart disease
-94 carotid sinus massage or "alsal!a
!erapamil, -bloc0er, digo4in, adenosine
gi!e cardio!ersion if hemodyamic unstable
#re-e4citation syndrome
-abnormal conduction between 1 and "
-1" node is bypassed (shorter #+)
-A#A from 8bsteins 1nomaly
-ass w/ #19 (down accessory limb E up 1")
-94 : bloc0 both the accessory and 1" node
#"(s
-K+. is wider than -=> sec
-bigeminyJ K+.-#"(-K+.-#"(
-trigeminyJ K+.-K+.-#"(-K+.-K+.-#"(
-2 #"(s in a row : !entricular tachycardia
-caused by tobacco, caffeine, alcohol, etc-
-if asymptomatic w/o heart disease 7 no 94
"9
-T2 #"( in a rowH sustained T2M sec
-9ornado de #ointes:Dtwisting around baselineL
caused by long K9 -(a
EE
, 6unidine, procaine
-K+. T-=? sec, 1" diss ((annon 1 wa!es)
-!entricular rate : >MM
-cause most cases of sudden death
-if after MI : poor prognostic sign
-gi!e electric cardio!ersion if hemodyanmic
if low 3# gi!e the paddles (high !oltage)
-correct underlying hypo4ia, I
E
, ischemia
-I" lidocaine for peri-infarct "9
-chronic treatment with class I antiarrythmics
6uinidine and procainamide
" flutter
,ife 9hreatening
-sine wa!e (>MM-2MM)
" *ibillation
-chaotic baseline
-no organi<ed K+.
1"9+IO"8@9+I(G,1+ 3,O(I ()81+9 3,O(I)
=
st
degree heart bloc0 >
nd
degree heart bloc0 (omplete )eart 3loc0
-Belay of TM->M sec at the 1" node
-normal # wa!es and K+. comple4es
Ty$e I
-4enc/e(ach
-progressi!e #+ prolongation
-non conducted #-wa!e
-more benign
-inferior wall MI (+(1)
-bloc0 at the 1" node
-asymptomatic
Ty$e II
-sudden failure of # wa!e to conduct
-Bisease below the 1" node
-fre6uently causes syncope
-occurs with anterior wall MI (,1B)
-re6uires a $acema/er
@o conduction reaches the !entricle
-cannon 1 wa!es
"entricular escape in )I. bundle
-narrow K+. and rate of ;M
-congenital
9rifascicular bloc0 results in a slower
escape rate and wide K+.
-ac6uired
3oth types re6uire $acema/er
Inectious Disease
Immuni)ations
-d9 gi!en e!ery =M years
-d9 gi!en e!ery ; years if fresh wound found
-#olio !irus gi!en for all non-immune adults (immigrants)
-MM li!e !irus should be gi!en if there is no pre!ious history of these illnesses or !accinations
-+ubella must be screened for in child-bearing age women
Must gi!e )epatitis 3 inJ
-homose4ual men, I" drug users, prostitutes, hemophiliacs, health care wor0ers
8lderly and chronically ill (cardiac or pulmonary disease)
-pneumococcal !accine, and October influen<a !accination
1splenic patients (motorcycle accidents or sic0le cell disease)
-pneumococcal !accine
-meningococcal !accine
S$eciic Ris/ 5actors or Inection
BI13898.
-ischemic foot and lower leg ulcers associated with osteomyelitis (small bones) and charcot Coint
-G9I due to bladder hypomotility (urosepsis due to stasis)
-!aginal yeast infections d/t increased sugar
-silent cholecystitis 7 if asymptomatic gall stones dont remo!e gall bladder
-soft tissue ischemia and gangrene (perirectal abscess)
-metronida<ole (anaerobes) and clindamycin (for .taph)
-murcormycosis paranasal sinus infection found in BI1
-see air fluid le!els and can ascend into the brain (deadly !ery 6uic0ly) 7 must ha!e low inde4 of suspicion
1,(O)O,I(. (homeless)
-aspiration pneumonia d/t altered consciousness and organisms in the mouth
-anaerobic lung infections
-lung abscess (ca!itary lesions)
-fatal empyema 7 pleural space thoracentesis
-93 cough 1*3 stain
-F(-) bacterial pneumonias (lobar Ilebsiella)
-.pontanious 3acterial #eritonits
-suspect in any alcoholic with ascites and fe!er
-B4 : >;M #M@s !ia paracentesis
-94 : 2
rd
generation cephalosporin for F(-) ((eftria4one)
-alcoholic hepatitis mimics acute cholecystitis (Murphys .ign)
-1.9/1,9 T >
I" Brug Gsers (.hooters)
-ris0 of infection not related to drug inCected but in unsterile techni6ue
-bacterial endocarditis (shooter with fe!er)
-need 2 3(4 to +/OH would also need transesophageal echocardiogram (988) to +/O
-9ricuspid "al!e regurgitation (#ulmonary 8mboli)
-S.Aureus 7 tends to attac0 the tricuspid !al!e
-patients at ris0 for multiple pulmonary and systemic emboli
-cellulitis at area of inCection (Ds0in poppersL)
-infectious arthritis (S. Aureus) 7 use (ephale4in
-amyloidosis in patients who are chronic Ds0in-poppersL
-!iral hepatitis 3, (, B,
-)I" (low inde4 of suspicion)
)OMO.8XG1, M8@
-)I" and related infections (transmitted se4ually) penis to proctitis
-DFay bowel syndromeL with Chlamydia Trachomatis, Treponema pallidum, Entamoeba histolytica, )#", )."
#+O.9)89I( B8"I(8.
-.taph 1ureus, .taph 8pidermidis
-greatest ris0 with heart !al!es
-prophylactic antibiotics re6uired before dental wor0, endoscopy, or surgery
-in-dwelling I" catheters is dependent on the line insertion and line manipulation
-usually happens in I(G and patients with fe!er and rigor
F+1@G,O(5O9O#8@I1
-usually d/t endogenous flora (8- coli, #- 1eruginosa, (- 1lbicans)
-if febrile treat with antibiotics as it can be rapidly fatal
-if longer than = wee0 antifungals li0e 1mphotericin 3 -gi!e meperidine for the drug reaction
(O+9I(O.98+IOB 1@B O9)8+ I19+OF8@I( IMMG@O.G##+8..IO@
-defect in cellular immunity
-fungal, mycobacterial, (M" are all li0ely
-may ha!e A3( in absence of infection d/t steroids demargination
-may ha!e A3( in absence of infection d/t a<athioprine (need to titrate to correct le!els)
@O.O(OMI1, I@*8(9IO@.
-thin0 of M+.1 (Methicillin +esistant .taph 1ureus), #seudomonas, and "+8 ("ancomycin +esistant 8nterococcus)
-ris0 of prophylactic antibiotics, multiple instrumentation, and lac0 of hand washing
8@BO(1+BI9I.
-infection of the !al!es usually but also the endocardial surfaces
-+is0 *actors
-pre!iously damaged !al!e
-+heumatic *e!er
-M"# AI9) regurgitation
-pre!iously infected !al!es
-I" drug users and I" catheters
-.pecific Organisms
-S- Aureus normal !al!es, I" drug users, in-dwelling catheters,
-S- Viridans pre!iously damaged !al!es, subacute endocarditis, dental wor0
-Enterococcus ecalis after obstetric procedures, older men with FG procedures (9G#), I" drugs
-S- Epidermitis #rosthetic !al!es (along with .- 1ureus)
-)1(8I (!aemophilus, Actinobacillus, Cardiobacterium, Ei"enella, #in$ella) all F(-) bacteria
-endocarditis with large !egetations, emboli, and need for !al!e replacement, hard to culture
(linical *eatures
-consider in any pt with fe!er and heart murmur
-peripheral embolic disease +oth .pots, Oslers nodes, aneways lesions, *GO
-subacute endocarditis fe!er, weight loss, malaise, and anemia or chronic disease
-septic emboli may in!ol!e spleen, 0idney (infarct or immune-comple4 glomerulonephritis OproteinuriaP)
brain (stro0e), pulmonary emboli (I" drugs from the tricuspid !al!e)
Biagnosis
-need three sets of cultures from multiple sites (if dont get it then try )1(8I)
-8()O (988)
9herapy
-antibiotics for ?-$ wee0s
-need to B4 M+.1 (only sensiti!e to !ancomycin)
-indications for surgery
-if you cant get a negati!e culture (serial blood cultures)
-fungal endocarditis
-recurrent emboli (spleen, toes, brain, etcV)
-()* from !al!ular problems
#rophyla4is
-B8@91, #+O(8BG+8.
(amo4icillin) 2g ---- = hour -----#+O(8BG+8 ----- $ hours -------=-;g
(erythromycin) =g ---- = hour -----#+O(8BG+8 ----- $ hours ------- ;MM mg
-FI and FG #+O(8BG+8.
(ampicillin and gentamicin)
(!ancomycin)
OSTEOMYELITIS
-infections by =) adCacent infection >) direct infection 2) hematogenous spread
=) .- 1ureus
>) 1naerobes
2) .almonella (in sic0le cell patients d/t autosplenectomy)
?) #seudomonas
-Immunocompromised patients F(-) osteomyelitis
-most common site is the tibia
-93 s0eletal tuberculosis
-adCacent arthritis often occurs
(,I@I(1, *819G+8.
-usually at site of pre!ious trauma
-local pain and swelling
-with BM seen with !ascular insufficiency and often occurs in toes or small bones
BI1F@O.I.
-if hematogenous, A3(, and E blood cultures
-if chronic osteomyelitis 8.+ but no fe!er and normal A3( 7 re6uire debridement
-definiti!e B4 is bone biopsy but not done in diabetics (M+I instead)
-X-rays periosteal ele!ations and lytic changes
-+adionuclear scans will not distinguish well soft tissue infection from osteomyelitis
9+819M8@9
-treat cases empirically for .- 1ureus for $ wee0s and wait for bone biopsy culture
-chronic osteomyelitis re6uires debridement
!ASC'LAR IN5ECTIONS
*819G+8.
-common cause of hospital-ac6uired fe!ers by S. Epidermidis or S Aureus
-infections is usually e!ident at site of insertion
-treat with remo!al of the catheter or treat with antibiotics alone if no significant soft tissue infection
-fungal infections re6uire remo!al of catheter - always
-if central line has been in for a wee0 ta0e it out
"1.(G,1+ F+1*9 I@*8(9IO@.
-diagnosis is made with consistently positi!e blood cultures
-mycotic aneurysm may de!elop away from focus of infection
-treatment in!ol!es remo!al of the graft
(8@9+1, @8+"OG. .5.98M ((@.) I@*8(9IO@.
-ACTERIAL MENI+ITIS
-adolescents and young adults Dcollege studentsL %. &enin$iditis
-petechial rash and possible Aaterhouse-*riderichsen syndrome (adrenal insufficiency)
-adults S. pneumoniae
-asplenic patients, sic0le cell (pre!ented by pneumo!a4 !accine)
-immunocomprmised patients 'isteria monocyto$enes
-usually on chemotherapy
-pneumonia or otitis media !. (nfluenzae or S. )neumoniae
-epidemic forms or recent contact %. menin$itidis
-should recei!e +ifampin prophyla4is
(,I@I(1, *819G+8.
-fe!er, headache, stiff nec0, photophobia
-immediate ,# (A3(, #M@, protein, glucose)
9)8+1#5
-gi!e early antibiotics pending cultures (MG.9 FI"8 M8@I@FI9I( BO.8.)
-if no organism on gram stain
-1mpicillin (to co!er ,isteria) and +ocephin (to co!er e!erything else)
ASEPTIC MENIN+ITIS
-!iral disease
-A3( (mild), normal #M@., normal protein, normal glucose
-always as0 if antibiotics ha!e been pre!iously used 7 as it may be partially treated bacterial meningitis
C"RONIC MENIN+ITIS
-in the absence of immunosupression (most common cause) the common causes areJ
-93 usually seen other signs of 93 and (@ in!ol!ement
-malignancy ,3F-M( are the most common metastatic cancers
-.arcoidosis e4trapulmonary manifestations and 3ells #alsy
-(ryptococcus India In0 and more common in 1IB.
ENCEP"ALITIS
-usually caused by !iruses and get M. and sei<ures
-(.* may be normal or similar to aseptic meningitis
BI1F@O.I.
-measure antibody titers to !iruses
-)." is diagnosed with brain biopsy (temporal lobe) and culture
-must treat empirically before neurologic decompensation
9)8+1#5
-high dose of acyclo!ir for patients with herpes simple4 encephalitis
-must rule out other re!ersible causesJ =) 9o4oplasmosis, Brug into4ication, (@. lupus (94 : steroids)
INTRACRANIAL A-SCESS
-most come from sinus and ear infections from .- #neumococcus or 1naerobic organisms
-less commonly hematogenous spread
-diagnosis with (9 or M+I
-treatment with high doses of penicillin and metronida<ole which can penetrate 333
-do not do ,# because of herniation
SE6'ALLY TRANSMITTED DISEASES
"ERPES
-bilateral inguinal adenopathy and systemic manifestations
-initially !esicles preceded by !iremia
-patient may ha!e prior history of similar lesions
-treatment with acyclo!ir hastens reco!ery and recurrence rates are reduced if used as maintenance
SYP"ILIS
-incubation is 2-RM days (e4posure to primary symptoms)
-#rimary .yphilis diagnosis is made by Bar0field e4amination
-.econdary .yphilis is >-% wee0s after chancre
-rash, condylomata, alopecia
-serological testing is possible and organisms are in the blood
-*91-13. is most specific but is positi!e for life (always positi!e in spite of treatment)
-"B+, may be negati!e in 2MN of patient (can trac0 result and will turn negati!e with treatment)
-*alse positi!es in .,8 li0e syndromes (1)1)
-,atent .tage (early) is still serology positi!e
-,atent .tage after = year are late
-9ertiary .yphilis in!ol!es
-ascending aorta causing 1+ and 11
-hepatitis
-neurosyphilis 7 dementia, 9abes Borsalis, *eet slapping - no proprioception
-@eurosyphilis
-diagnosis by (.* (mononuclear cells and protein)
-(.* "B+, is only ;MN sensiti!e
-!ascular syphilis stro0e
-9abes Borsalis sensory and autonomic (painful) 7 no proprioception
-(hronic progressi!e dementia
-9reatment
-81+,5 .5#)I,I. (primary, secondary, latent (early)) >-? million G of ben<athine penicillin IM 67
-,198 .5#)I,I. (tertiary) >-? million G of ben<athine penicillin IM 68 (for 2 wee0s)
-@8G+O.5#)I,I. >? million G penicillin I" daily or t.o .ee/s
Lym$hogranuloma 3enereum %L+!&
-Chlamydia trachomatis (,=-,2)
-tender unilateral adenopathy
-*rei s0in test and stelate granulomas (pus)
-intracellular and $ainless swelling
-bilateral groo3e sign
-lymphedema of penis and !ul!a
Calymmatobacterium donovani
-Bono!an bodies in the scrapings of the ulcer
-no giant lymph nodes
-dermal lymph obstruction
Chancroid
-!aemophilus ducreyi
-genital ulcers and tender nodes
-painful unilateral but not systemically ill
-male frenulum and female !ul!a
'RET"RITIS
-discharge and dysuria
-GU vs NGU (Chlamydia)
-gram stain of urethral discharge is 0ey diagnostic test
-F(-) intracelluar diplococci indicates gonococcal infection
-#M@s w/o organisms shows (- trachomatis or *reaplasma *treticum
-9reatment
-Fonorrhea ceftria4one IM 97 : must also treat or chlamydia
-(hlamydia do4ycycline for ; days
-need to treat se4ual partners WWWW
!A+INAL DISC"AR+E
9+I()OMO@I1.
-green/gray copious watery discharge (p) is high) 7 strawberry cer!i4
-wet mount re!ealing motile, flagellated trichomonas 7 reproduces by fission
-94 : Metronida<ole 97
(1@BIB1, "1FI@I9I.
-thic0, white, and cottage-cheese (p) is low) 7 budding yeast with pseudohyphe
-topical anti-fungal agent gi!en as a suppository (flucona<ole)
"1FI@O.I.
-+ardinella ,a$inosis, &ycoplasma !ominis, 1naerobes
-!aginal p) is generally ;-' p) (high)
-fishy odor after adding IO) to !aginal secretions
-homogenous adherent white or gray !aginal discharge
-clue cells : ragged epithelial cells coated with bacteria
-94 : Metronida<ole 9 7 .ee/
+ONORR"EA
-causes urethritis, cer!icitis, pharyngitis, may also ha!e sore throat (Xoral se4)
-asymptomatic carrier state is common and is responsible for re-infection
-rectal cultures should be ta0en to +/O Fay 3owel .yndrome
-B4 is with gram stain and 9M culture
-94
-Fonorrhea ceftria4one IM 97 : must also treat or chlamydia
-(hlamydia do4ycycline for ; days
BI..8MI@198B FO@O(O((8MI1
-menstruating women
-bacteremic phase complicated by tenosyno!itis (tendon sheath), s0in lesions (purpura), and polyarthralgias
-non bacteremic phase presents with monoarticular arthritis of 0nee, wrist, or an0le
-94 : (eftria4one I" for ; days
TO6IC S"OC* SYNDROME
-pt is ill with high fe!er, hypotension, des6uamating rash, multiple organ system in!ol!ement
-FI tract 7 !omiting and diarrhea
-se!ere myalgias
-hyperemia of mucosal membranes
-abnormal ,*9s
-thrombocytopenia (low platelets)
-(@. manifestations and disorientation w/o focal neuro signs
-d/t .taph 1ureus TO6IN associated with women using tampons (organisms in tampon @O9 body)
"I!
-neurotropic and neurologic dysfunctions are common
-8,I.1 screening
-Aestern 3lot (onfirmatory
-8,I.1 p>? antigen (not antibody)
-#(+ !iral genome (need to do to diagnose infants up to > years of age)
#BX -low-grade fe!er, facial seborrhea, ,1B, splenomegaly, thrush, "-Q infections
(,I@I(1, *819G+8. 7 asymptomatic, persistent fe!ers and chills, night sweats, fatigue, anore4ia, depression
.#8(I*I( *819G+8.
*8"8+
-most common complaint
-3(4 for bacteria, fungus, M1(, (M"
-if ,1B and organomegaly -T lymphoma
Bysphagia
-(andida esophagitis 94 : flu or 0etocona<ole
-)." esophagitis 94 : acyclo!ir
-(M" esophagitis 94 : gangcyclo!ir
-Idiopathic )I" ulcers 94 : prednisone
(+5#9O(O((1, M8@I@FI9I.
-headache with meningeal signs
-antigen and India in0
,1B
-biopsy if especially enlarged or single node
-M1(, 93, 9o4oplasmosis, and )istoplasmosis
Biarrhea
-small-bowel infectionhigh !olume watery
cryptosporidium, microsporidium, giardia,
8ntamoeba histolytica, .almonella, .higella
-colonic infectionsbloody fre6uent, tenesmus
(M"
-proctitis Dgay bowel syndromeL
B8M8@9I1
-depression and apathy
-neurological e4am is unremar0able
- infection, paraparesis, incontinence, demen
-(9 re!eals diffuse atrophy
.II@ ,8.IO@.
-pruritus and folliculitis
-Iaposis .arcoma (usually homose4ual)
not in I" drug users
chemotherapy may be effecti!e
-cryptococcus and histoplasma cause
necrotic ulcers or papules
)81B1()8 1@B .8IQG+8.
-to4oplasma is the most common cause
(9 shows ring-enhancing lesions
94 : pyrimethamine and sulfadia<ine (life)
3,I@B@8..
-(M" retinitis 94 : gangcyclo!ir
-#(# cotton wool spots in the retina
-(andidiasis and 9o4oplasmosis
B5.#@81
-#(# is the most common setting
presents as constitutional
fe!er, night sweats, progressi!e cough
(X+ shows diffuse infiltrates
(yst or tropho<oites in sputum
94 : septra, or pentamidine
-O9)8+ (1G.8. .G() 1.
-93, M1(, cryptococcus, histoplasma, (occidi
encapsulated bacteria (.- #neumo, )emoph)
d/t bad 3-cells as well
pul lymphoma and Iaposis sarcoma
O9)8+ (@. ,8.IO@.
-(@. lymphoma
-#M, ,( 7!irus and ."-?M
-)." temporal lobe
-(M" biopsy and (a
EE
peri!entrically
-mycobacterial or fungal brain abscesses
non ring enhancement
-cryptococcal meningitis
)8M19O,OFI( 13@O+M1,I9I8.
-I9#
-anemia of chronic disease
-lymphocytopenia
-polyclonal gammopathy
9)8+1#5
-below ;MM 1Q9
-below >MM .8#9+1 (89<.ee/) for #(# prophyla4is
-!accination with pneumococcal, influen<a and hepatitis !accine
-ris0 for re-infection for 93 and syphilis
I@OA (B? counts and the appropriate drugs to add for prophyla4is
"EMATOLO+Y
)emostatis
-#9 and #99 (0now factors)
-factor ' has the shortest half life and therefore #9 will show up first as being abnormal
-use #9 to monitor (oumadin
-use #99 to monitor )eparin
-all factors are made in the li!er e4cept "III (endothelium)
#latelet problem
-petechiae, purpura, ecchymosis
-test by using platelets and 39
(oagulation
-deep tissue bleeding, hemarthroses
-test by using the #9 and #99
#,198,89 BI.O+B8+.
#roblems with the numbers
-normal platelet count is >;M,MMM
-bleeding usually with platelets &>M,MMM
-spontaneous bleeding with platelets &=M,MMM (intracranial bleeding)
-scarcity of platelets on a blood smearS
-marrow failure d/t leu0emia (leu0oeryroblastemia Y myleopthysis),
aplastic anemia, myelofibrosis (myelodysplastic syndromes)
chemotherapy syndromes and ethanol, 3=> and folate deficiency (B@1)
#roblems with .plenic .e6uestration
-usually counts of ?M-=MM,MMM (no bleeding) 7 hypersplensim and splenomegaly
-low A3(
-splenectomy not usually necessary
#roblems with destruction
I9# 99# )G.
*ine e4cept for petechiae and purpura
,abs are all normal e4cept for platelets
3M shows increased platelets
1ssociated with
-mono, .,8, )odg0ins, and (,,
-also )I", pregnancy, 6uinidine, sulfa, gold
-.,8 drugs (hydrali<ine, procainamide) histone
9reatment
-I"Ig steroids, !incristine, splenectomy
loo0 for accessory spleens,
ne!er gi!e platelets
)G. E *8"8+ and (@.
9hromobocytopenia
M1)1 (micro-angiopathic hemolytic anemia)
.ei<ures, coma
1rteriolar plugging in the 0idney
*e!er
9reatment
-plasma e4change
,ow platelets E
)emolysis d/t !eroto4in (O=;'J)')E
Gremia
1ssociated with bloody diarrhea
@o fe!er or neurological signs
#roblems with function (abnormal bleeding times) 7 39
=) 1spirin
>) @.1IB.
2) "AB
?) Gremia (0idney failure)
(O1FG,19IO@ BI.O+B8+.
)8MO#)I,I1 1 (factor "IIIJc) "A* (factor "IIIJag)
-X-lin0ed usually males
-soft tissue and point bleedings, (@. bleedings with minor trauma
-spontaneous hematuria ureteral colic (blood clots in the ureter)
-#99 and "IIIJc but normal "A*
-9reatment : "III replacement (need to measure)
watch out for )(" and )I" (common but less now d/t e4pensi!e form)
watch out for antibodies to the factor (the factor will not rise on trans-
Its OI to ha!e .4 7 Cust 0eep trac0 of the le!els
-"A* stabili<es factor "III, aggregation, adhesion
-mucous membrane bleeding, prolonged bleeding from gums
-menorrhagia
-#99, 39, "II, "A*, abnormal aggregation with riscocetin
-9reatment
cryo##9 with "III and "A*
BB1"#
8strogens and O(# increase "A*
1c6uired (oagulation Bisorders
"it I ,i!er Bisease BI( ,upus 1nticoag-
>,',R,=M,.,(
-need to eat but also bacteria ma0es
-poor inta0e, fat malabsorption,
-antibiotics can 0ill bacteria
-e!erything low e4cept for factor
"III
-#9 is the first sign
-wide spread acti!ation
-depletion of the factors
-fibrinolysis *.#
#9, #99, 39
-*ibrinogen
-M1)1 schistocytes
(1G.8.J
-sepsis, dead fetus, eclampsia
-99#, )G., M1)1, M2 1M,
-94 : heparin only for M2 1M,
-doesnt ha!e to be .,8
-many patients don ha!e .,8
-#99 in !itro
:actually hypercoaguable
-seen in miscarriages in >
nd
tri
ANEMIAS
"y$ochromic anemias
*e Beficiency .ideroblastic 1nemia of (hronic Bisease
(1G.8.
-imbalance between diet and needs
-usually due to menstrual or FI bleed
-achlorhydria (reduced absorption)
seen in pernicious anemia or omepra<ole
-hospital phlebotomy
,13 *I@BI@F.
-first becomes microcytic then hypochromic
-+BA, M(", ferritin but if chronic disease
-N sat but 9I3(
-gold standard is 3M with iron stores
#russian 3lue .tain
9+819M8@9 is with *e.O?
-reticulocytes in = wee0
-)gb in 2 wee0s
-*e often causes constipation and blac0 stools
also peptobismol turns your stool blac0
-#ro4 distil : *e
EE
, (a
EE
, *olate, "it 3=>
-defect in heme synthesis
-e4cess *e in the mitochondria
-more absorption of *e in the pro4imal gut
hemochromatosis results
-seen with I@), ethanol, #,# def,
-94 : #,# (!it 3$)
-cant use the *e
-diminished response to 8# from the 0idney
-*e, 9I3(, ferritin, M(", retics
-dont gi!e 8# or *e but treat underlying
disease
Macrocytic anemias
9hree different mechanisms
=) 1ccelerated erythropoesis (reticulocytes ma0e the M(" bigger)
>) Increased membrane si<e (li!er disease and large target cells)
2) Befecti!e B@1 synthesis (folate or !it 3=> deficiency) 7 megaloblastic (pancytoplastic) anemia
Megaloblastic 1nemia
-megaloblastic anemias
-+3(s are large and o!al
-hypersegmented polys (; or $ lobes)
-pancytopenia (affects all of your cells)
"it 3=> deficiency *olate deficiency
"it b=> binds factor + in sali!a I* made in stomach pancreatic
en<yme clea!es + factor in intestines allowing I* to bind
3acteria also consume 3=> so that may be a cause of deficiency
1bsorption occurs in the terminal ileum
.()I,,I@F 98.9
I* (O++8(9. AI9)J 9)8@ 9)8 B8*8(9 I.J
I* pernicious anemia or gastrectomy
#ancreatic en<ymes pancreatic insufficiency
1ntibiotics bacterial o!ergrowth or blind loop
Bi!erticulitis
#8+@I(IOG. 1@8MI1
-most common cause of !it 3=> deficiency anemia
-se!ere atrophic gastritis
-antibodies to parietal cells or I*
-associated with )ashimotos Fra!es, BM, 1ddisons and !itiligo
-9hymomas
-increased ris0 of gastric cancer Y carcinoid d/t low acid and high gastrin
-(ommon in alcoholics (dietary deficiency rare)
-celiac sprue
-impaired folate metabolism d/t drugs, 89O), methotre4ate,
pyrimethamine, septra, sulfasala<ine, phenobarbital, and phynetoin
-also caused by increased demand d/t pregnancy
Ma0e sure that you dont get in the Dfolate trapL by treating a !it b=>
deficiency with only folate because youll correct the anemia but miss the
neurological symptoms-
"emolytic anemias
+3( membrane defects 8n<yme defects (F$#B def) )emolytic 1nemias
)..
-mild hemolytic anemia, Caundiced
-spelomegaly and (iliru(in gallstones
-osmotic fragility
-94 : splenectomy
1canthocytosis
-=MN of 11 males
-sulfa, 6uinine, furantoin, sepsis, hepatitis
-)ein< bodies are trapped in the spleen
-B4 : 6uantifiying the F$#B acti!ity
may be normal after hemolysis episode
A1+M
-positi!e direct (oombs test
-IgF or ( Z 2=-= (
-.,8, lymphoma, (,, or drugs
(O,B
-cold agglutinins Z ? (
In vit B12 you see in addition
-neurological symmetric myelopathy and neuropathy
-early paresthesias, late ataxia
-cerebral and psychiatric manifestations (dont x !ith folate)
-spur cells with li!er dis or abetalipoproteinemia
-steatorrhea or retinitis pigmentosa
.tomatocytosis
-+3(s with a slit 7 seen in 89)1@O, 13G.8
-re!ersible
-IgM
-mycoplasma or mono
B+GF induced
-)apten 7 penicillin (binds membrane)
-3ystander 7 6uinidine, sulfa, phenothia<ines
-1lpha-methydopa 7 (modifies membrane)
"emoglo(ino$athies
.ic0le (ell Bisease 9halassemias
-usually due to intra!ascular sic0eling, !ascular thrombosis, infection
-leg ulcers, chronic hematuria, renal papillary necrosis
-functional asplenia
-priapism impotence
-pigmented gallstones (billirubin (a
EE
radio opa6ue stones)
cholesterol stones are radio lucent
-bone infarcts aseptic necrosis of femoral heads
-osteomyelitis salmonella common (need bone scan)
-pulmonary infarct cor pulmonale (right heart failure)
-drug addictions because most need to be put on narcotics
1(G98 .I(I,8 (+I.I.
-acute pain and fe!er (chest syndrome) 7 gi!e fluids not diuretics
-abdominal pain mimics the acute abdomen
along with BM and also prone to cholecystitis
-need to +/O infection while treating symptomatically
-if infected with 3=R aplastic crisis
monitor reticulocyte count and may need +3( transfusion
-most common is thalassemia minor
beta
-normal life e4pectancy in Mediterranean, .outhern 8urope, 1frica
-high )gb1>, low M(", high +3(, mild reticocytosis
"EMATOLI+IC MALI+NANCIES
@on )odg0ins ,ymphoma )odg0ins ,ymphoma
-Frading is the primary diagnosis and prognosis
-low grade slow grower but no cure
-high grade fast grower but cure

Lym$ho(lastic lym$homa
-meningeal and testicular in!ol!ement
-most are 9-cell and resemble 91,,
Adult T,cell lym$homa
-?M,MMM A3(
-)9,"-= ()9,"-> is for )airy cell and )9,"-2 is really )I")
-hypercalcemia
-lytic bone lesions
-s0in infiltration
-usually seen in (aribbean and apan
Small cell non,clea3ed , -ur/itt#s
-common in 8astern 1frica
-e4tranodal in!ol!ement
-83" infection with c-myc t(%,=?)
-3-symptoms : fe!er, night sweats, weight loss
or can be asymptomatic (1)
-pain in lymph nodes after 89O) ingestion
-#el 8bstein fe!er
high fe!er for > wee0s at a time at night separated by no fe!er
.91FI@F (MO+8 IM#O+91@9 9)1@ F+1B8)
-= : single node or local site
-> : more than one node on the same side of the diaphragm
-2 : in!ol!ement on both sides of the diaphragm
-? : diffuse
B4 : +. cells in the lymph nodes
#19)O,OFI( 95#8. (F+1B8)
-lymphocyte depletion (worst)
-mi4ed cellularity
-lymphocyte predominance
-nodular sclerosis (38.9)
AO+I-G#
-chec0 history for 3-symptoms (worse prognosis)
-#BX lymph nodes, li!er, spleen, bone tenderness
-,13. 7 (3(, ,*9s, renal failure, 9*9s, 3M biopsy
-IM1FI@F 7 (X+, abdominal (9, lymphangiography (shows si<e of
lymphs in the abdomen), gallium scan (malignant nodes light up),
e4ploratory laparotomy (if youre not sure of spleen in!ol!ement and you
need the correct stage)
9+819M8@9
I and II radiation only (may consider chemo if II with b-symptoms)
III and I" radiation and chemotherapy (MO## and 13"B)
AC'TE LE'*EMIAS
-uncontrolled proliferation of a malignant clone of hematopoietic cells
-dont respond to normal regulatory growth factors
-the abnormal clone may suppress the growth and differentiation of normal hematopoietic cells
-problems d/t
=) anemia
>) low platelets
2) low A3(
-9herapy for treatment for 1(G98 ,8GI8MI1.
Induction #rophyla4is (onsolidation Maintenance +elapse
-need complete remission
-!incristine
-prednisone
-Bo4irubricin
Intrathecal Methotre4ate Induction drugs needed to
0eep consolidation during
remission
"incristine, prednisone,
methotre4ate, $-M#
+einduction followed by
3M transplant
ALL
-fatigue, pallor, bruising, petechiae, bleeding, fe!ers, inf-
-bone pain d/t e4panding bone marrow mass
-I(# d/t leu0emic infiltration of the meninges (31B)
-diffuse lymphadenopathy and hepatosplenomegaly
,13 "1,G8.
-RMN ha!e A3(
-hypocellular marrow with lymphoblasts
-normal cells greatly reduced
(8,, M1+I8+.
-most are 31,, and e4press (1,,1 and 9d9
-91,, is the worst prognosis
AML
-increases with age
-1ssociated with .weets Bisease
-can occur after chemotherapy or myelodysplastic syn
-myelopero4idase E
-M2 7 acute promyelocytic leu0emia
BI( treated with heparin
t(=;,=') associated with M2
chemo with all trans retinoic acid (!it 1)
-M; 7 acute monocytic leu0emia
s0in or gum infiltration with leu0emic cells
CLL
-hypogammaglobulinemia
-.91F8.
M : lymphocytosis
= : lymphocytosis E big nodes
> : lymphocytosis E big spleen or li!er
2 : lymphocytosis E anemia
? : lymphocytosis E low platelets (bleeding is worse)
-usually =M-=; years sur!i!al unless late >-? years
-rarely 9-cell (worse)
-death usually due to infection
94 : 8arly stages 7 not necessary
,ate stages 7 chlorambucil and prednisone
If Cust spleens or lymph nodes radiate
If !ery high A3( leu0opharesis (hyper!iscosity)
CML
-entire spectrum of #M@s from blasts to mature
-peripheral smear loo0s li0e a 3M aspirate
-#hiladelphia (hromosome t(R,>>) c-abl
-,ow 1l0aline #hosphatase
-gradual increase in A3( massi!e splenomegaly
-terminal phase is blast crisis (sur!i!al $ months)
94 : oral hydro4yurea or bisulfan
IM interferon

)airy cell leu0emia
-3-cells with hairy cell proCections
-can ha!e huge spleens (Cust li0e (M,)
-usually slow progression
-9artrate +esistant 1cid #hosphatase
94 : pentostatin, interferon, and cladribine
Chronic Myelo$rolierati3e Disorders
#olycythemia !era
-uncontrolled proliferation of red blood cells precursors
(.econdary polycythemia)
-increase in +3(s d/t hypo4emia or other stimulus
-itching
-usually ;M-'M y/o, hyper!iscosity or thrombotic tendencies
-hepatosplenomegaly is !ery common
-B4 : must +/O hypo4emia, will ha!e high +3( and A3(, ele3ated -7= %decreased in =
nd
$oly&
PLASMA CELL DISORDERS
Multi$le Myeloma
-monoclonal cells produce M-protein (hea!y and light chain)
-most common is F and 1
-light chain is +
-late age of onset of 'M years old
-suppression of normal plasma cells fewer normal immunoglobulins (more infections)
)I and .#
-bone destruction common due to O1*, I,-=, 9)*
-lytic lesions common in s0ull, lower bac0, pel!is, rib cage (also presents as osteopenia)
-hypercalcemia especially with bone destruction
-renal insufficiency (amyloid or obstructed ureters)
-hyper!iscosity syndrome (confusion, !isual impairment, purpura)
Biagnosis
-serum and urine .#8# (electrophoresis) and I#8# (to figure out the type of Ig)
-s0eletal X-ray sur!ey
-bone marrow has T>MN plasma cells
#rognosis
-> microglobulin is a mar0er of total myeloma
-low > and younger patients ha!e best prognosis
-worst prognosis : older, high >, high ,B), low platelets
9reatment
-if symptomatic melphalan and prednisone
-bone pain management effecti!e chemotherapy
radiation if sharply locali<ed pain or pending fracture
mobili<e patient
positi!e (a
EE
balance
biphosphonates to inhibit bone resorption
Plasmacytoma
-locali<ed collection of monoclonal plasma cells (usually younger patients)
-can occur in bone or e4tramedullary (usually in upper airways) 7 dont cause bone destruction
or cause renal failure
-after surgical e4cision, monoclonal protein should disappear from blood and urine
"ea3y,chain disease
--component of the immunoglobulin hea!y chain
-infiltrates small bowel and causes malabsorption
4aldenstrom#s macroglo(ulinemia
-older men with IgM (big .#8# spi0e IgM)
-hyper!iscosity occurs which responds to plasmapheresis
-binds to platelets and clotting factors epista4is, gingi!al bleeding
-binds to peripheral ner!es peripheral neuropathy
Primary amyloidosis
-neoplasm 7 monoclonal
-light-chain immunoglobulin
-deposits in tongue macroglossia (difficulty swallowing)
-stain positi!e with (ongo +ed
-amyloid is multisystemicH in!ol!es heart, intestines(malabsorption), li!er, 0idney, ner!ous system
M+'S
-persistent monoclonal gammopathy
-low serum le!els of the M-protein
-spi0e on .#8# (may not be a malignancy)
-bone marrow plasma cells &=MN
-asymptomatic
-=/2 of patients progress to multiple mywloma within =M years
+I MEDICINE
ESOP"A+'S
@ormal
-upper =/2 is striated (can be effected in muscular dystrophies)
-lower >/2 is smooth muscle
-stratified s6uamous epithelium 7 all o!er
-G8. pre!ents FI reflu4 from entering pharyn4 and respiratory tree
-3ody of the esophagus is peristalsis
-,8. has .M inner!ated by !agus ner!e
-contracted at rest, rela4es with swallow
-most important defense against gastroesophageal reflu4 (F8+)
-oropharyngeal phase of swallowing 7 function of multiple striated muscles
-=) difficulty initiating swallow (close nasopharyn4, close trachea, mo!es to bac0 of throat)
->) nasopharyngeal regurgitation
-2) pulmonary aspiration (older age gets asthma and recent aspiration pneumonias)
-nursing home, (@. problems (stro0e), myasthenia
-?) food pooling in the oropharyn4
(,1..I( MO9I,I95 BI.O+B8+. O* 9)8 8.O#)1FG.
1chalasia
-absent peristalsis, high pressure of the ,8., incomplete rela4ation with swallow
-dysphagia to both li6uids and solids (motility problem)
-problems with swallowing li6uids in the beginning 7 lunch on the pillow in the morning
-(obstruction has problems swallowing large things first then small things)
-X-ray dilated esophagus with Dbirds bea0L and air fluid le!els
-B4 : is confirmed by manometrically
-94 : pneumatic dilation or surgical myotomy or 3O9OX (nitrates dont wor0)
-ris0 of perforation
.cleroderma (from (+8.9)
-reduced peristalsis and reduced ,8. resting pressure all due to fibrosis
-symptoms 7 dysphagia and terrible reflu4 symptoms ("8+5 31B)
-late symptoms bay be due to peptic strictures (they also appear as birds bea0)
-late scleroderma (obstruction) loo0s li0e 1chalasia on X-ray (differentiate using )E#)
@on cardiac chest pain
-5OG MG.9 +/O ()8.9 #1I@
-may be secondary to diffuse spasm in esophagus (cor0 screw on 3a swallow)
-94 : nitrates in the lower >/2
-F8+B is the most common cause of non cardiac chest pain
-3ernstein test is pouring down acid into the esophagus
-9ensilon test (8drophonium) shows if theres a spasm (motility)
F8+B
-reduced ,8. pressure (most important) 7 anticholinergic drugs increase reflu4
-also reflu4 of caustic material ()> bloc0ers stop), reduced esophageal peristalsis, low
esophageal bicarb/salt, delayed gastric emptying
-symptoms may be esophageal or e4tra-esophageal
-esophageal heartburn, dysphagia, odynophagia
-e4traesophageal hoarseness, whee<ing, aspiration anaerobes
-B4 7 suggested by history, X-rays show normal but may show ulcers or strictures
-endoscopy may be normal but may show esophagitis, ulcers, 3arretts and
strictures, and allows biopsy
->?-hour p) monitor is definiti!e proof that acid reflu4 is causing the symptoms
-do this if there is a non-classical history (Fold .tandard)
-3ernstein test during manometry testing
-+ole of )iatus )ernia
-loss of the diaphragmatic pinch and reser!oir of relu4ate within chest
-sliding hiatus hernia causes more prone to reflu4
-get it with aging
-94
-lifestyle modifications (ele!ate 38B, lose weight (large intraabdominal pressure),
no 89O), no snac0s, certain drugs, fat, chocolate, peppermint
-drug therapy
-antacids
-alginic acid (coats the esophagus)
-sucrafalte (coats the stomach)
-)> bloc0ers
-##I
-pro0inetic agents (metaclopramide 7dopa antagonist)
(cisapride 7 1() agonist)
-both increase ,8. and increase pro0inetc mo!ements
.4 : reduce hiatal hernia and perform fundoplication
-complications of F8+B
-peptic stricture 7 gradual progression of obstructi!e type of dysphagia
-solids more than li6uids (not li0e achalasia)
-3arretts esophagus 7 transformation from s6uamous to columnar
-premalignant and needs sur!eillance (biopsies) adenocarcinoma
8sophageal (ancer
-most are late and incurable
-+is0 factors for .6uamous (ell (1
-achalasia
-lye stricture 7 suicidal when young and dran0 poison
-89O)
-#lummer-!inson syndrome: *e def, upper esophageal web, s6uamous (1
-head and nec0 (1 #9)rp
-+is0 factors for 1deno(1
-3arretts 8sophagus (lower =/2)
-B4
-progressi!e obstructi!e symptoms
-post-prandial cough : 9racheobronchial fistula
-barium swallow (=/> apple core lesion with rough and ratty edge)
-endoscopy with biopsy is the ne4t step
-.taging
-tumor is usually local but can spread to the aorta and tracheal tree (98 fistula)
-(9 scan can diagnose
-endoscopic G.
-9reatment
-.4 if it is caught early
-palliation 7 laser .4, radiation therapy and chemotherapy if it is caught late
1IB. and the esophagus
-patients ha!e odynophagia and dysphagia
-if you see oral thrush then you must treat for esophageal candidiasis
-94 : 0etocona<ole (not if on )> bloc0ers) and flucona<ole
-(M" 94 : ganciclo!ir
-)." 94 : acyclo!ir
-)I" (idiopathic )I" ulcer) prednisone (not usually what you want to do but it wor0s)
+I@F., 9I(., 1@B 981+.
-.chat<0i ring (.tea0house syndrome)
-mucosal web or ring in the lower esophagus
-may cause intermittent dysphagia
-located at the F-8 Cunction
-sudden dysphagia on eating
-nice and smooth folds
-#lummer-"inson syndrome
-G8. web causing dysphagia
-associated with *e deficiency anemia
-s6uamous cell (1
-Qen0ers di!erticulum
-classic symptom is post prandial cough and gurgling
-di!erticulum is in the pro4imal esophagus and food may be e4pelled by pressing on
the throat
-Mallory-Aeiss tear (usually from 89O))
-mucosal laceration 7 superficial 7 heals spontaneously
-may cause upper FI bleeding
-classic symptom is retching first followed by hematemesis
-3oerhaa!es syndrome
-perforation of the esophagus caused by forceful !omiting or forceful endoscopy
-3a swallow shows e4tra!agation of 3a into the medistinum
-mortality is high e!en with .4
-Bo gastrograph and call .4
.9OM1()
-.timuli
-Fastrin from antral F cells
-)istamine from the body of the stomach
-1cetylcholine
-)
E
/I
E
19#ase which is bloc0ed by ,osartin and ##I
-Inhibitory *actors
-#rostaglandins (misoprostol 7 but causes uterine contractions)
-..9
-#rotecti!e factors
-mucus and )(O2
-
secretion
-prostaglandin synthesis
-+ole of inCurious factors
-@.1IB. and 1.1 and 89O) (they cause disruption of the protecti!e barrier)
-cigarettes
-)- #ylori
-not an in!asi!e organism but li!es in the surface of the stomach
-presence in gastritis, g#GB and d#GB, and cancer
-eradication may lead to cure and eliminate recurrence
-94 : P#I, Ampicillin, Clarithromycin
-3i can also be used but can turn the stools blac0 (confounder in case of gastritis)
#8#9I( G,(8+
-pain relie!ed after eating and reappears >-2 hours after (also nocturnal pain that awa0ens)
-bleeding and obstruction from repeated ulcers and peptic strictures
-perforation which can be seen as free air under the diaphragm
-B4 : endoscopy w/ e4tras to control hematemesis
-94 : antacids (not as effecti!e)
sucralfate 7 binds to the ulcer only when the p) is low
)> bloc0ers 7 most common but watch for cimetidine which causes gynecomastia
Omepra<ole 7 only gi!e after meals and it increases gastrin
#rostaglandin (misoprostol) 7 increases cramps and diarrhea and abortion
"agotomy
Must treat )- #ylori to eradicate the disease (B
4
with serum 1b test)
-Qollinger-8llison syndrome
-se!ere recurrent ulcers with or without diarrhea
(neuroendocrine inacti!ation of en<ymes)
-high gastrin but other things can cause high gastrin
-Omepra<ole
-+enal *ailure
-#ernicious 1nemia
-+etained antrum syndrome
-.ecretin stimulation test (usually secretin inhibits acid production by lowering gastrin)
-in the case of Q-8 syndrome is increases it
-@on ulcer causes of dyspepsia
-drugs, pregnancy, F8 reflu4, delayed gastric emptying, gastroduodenitis, I3., biliary
pancreatic distress, mesenteric ischemia (disparity in symptoms)
-anore4ia is loss of wanting to eat
-early satiety is filling up early
F1.9+I( MO9I,I95 BI.O+B8+.
-Fastroparesis 7 slow gastric emptying
-early satiety, bloating, distention, pain
-caused by narcotics and low 9?, BM, low (a
EE
, low Mg
EE
-B4 : gastric emptying scan (if there is nuclear material in stomach after > hours)
-you must e4clude mechanical causes such as ulcer and cancer (gastric or
pancreatic)
-Medical 94
-metaclopromide (anti dopamine) 7 get #ar0insonian .yndrome
-(isapride (pro 1()) 7 best (now off G. mar0et)
-8rythromycin (binds motilin receptors) 7 best when used in BM
MALA-SORPTION : surace o the intestine
-diarrhea, weight loss, 1B8I deficiency (night blindness, osteoporosis, bleeding)
-edema due to loss of protein
-tetany due to loss in (a
EE
(*I() and !it B
-3=> deficiency (if the loss is lower down)
,13.
-anemia (*e, folate, 3=>)
-low cholesterol and carotene
-low (a
EE
, Mg
EE
, 1lbumin, folate, 3=>, high #9
-8"1,G19IO@
-Kualitati!e fecal fat (using sudan red stain to detect fat in stool)
-Kuantitati!e fecal fat ('> hours collection of stool
-B-4ylose test 7 is no absorption must be a problem with absorption unlessV-
-gastroporesis, ascites, renal failure (if measuring in the urine)
-small bowel X-ray and biospy (if these are normal then do thisV--)
-measures of pancreatic function
-.chilling test (remember that pancreas clea!es the + factor bound to the 3=>)
-3enteromide test 7 measures pancreatic en<ymes
-#131-OOOOOOOO is eaten and pancreatic en<ymes clea!e bond
-#131 is free to get absorbed and to be e4creted into the urine to be detected
(8,I1( .#+G8
-sensiti!ity to gluten (gliaden) 7 wheat barley, +ye
-biopsy is also used in other diseases li0e !iral gastroenteritis (but 6uic0ly comes bac0)
-also seen in tropical sprueS
-lesion is usually seen in the pro4imal .I (low in *I()
-)oneymoon period is seen but the disease is life long (some childhood history)
-1ssociated with dermatitis herpetiformis (loo0s li0e !esicles of bullae)
-If patient doesnt respond to therapyJ
-=) most common reason is @O@ (OM#,I1@(8
->) A+O@F BI1F@O.I.
-2) .G#8+IM#O.8B ,5M#)OM1 O+ G,(8+19I"8 8G@OI,8I9I.
-?) +8*+1(9O+5 .#+G8 (9+5 .98+OIB.)
-ulcerati!e CeCunoilieitis shows symptoms of weight loss and inflammation
-increased incidence of gastric cancers, intestinal lymphomas, and ulcerati!e CeCunoileitis
-B4 : re6uires biospy, gluten remo!al and rebiospy
9+O#I(1, .#+G8
-(aribbean, India, northern coast of south 1merica
-biospy may be identical but the lesion is more lower down
-responds to folate and broad spectrum antibiotics (celiac wont respond to these agents)
I@*8(9IOG. 89IO,OF5
-Fiardia 7 troho<oites in lumen and on mucosa
-upper FI symptoms (malabsorption syndrome)
-stool tests unreliable 7 need duodenal aspirate
-national par0s, middle east, +ussia, Me4ico
-(occidiosis (1IB.) 7 cocci on the tips of the !illi
-cryptosporidia, Isospora, microsporidia
M1,BIF8.9IO@ 7 bad intraluminal phase
-they ha!e a normal B-Xylose
-post-gastrectomy and 3ilroth II (gastroCeCunostomy) 7 stomach bypasses duodenum
-no pancreatic en<ymes no bile salts 7 dumping syndrome
-no *I( (folate, Iron, (alcium)
-bile salt deficiency 7 no more micelles but B-Xylose is normal
-pancreatic insufficiency 7 bloc0ed pancreas
-bacterial o!ergrowth competes for 3=> and bile acids (brea0s them down)
-this causes maldigestion (no fat digestion)
3ilroth II
-poor timing and mi4ing of food and en<ymes
-rapid emptying into the small bowel
-loss of absorpti!e area for *I( (folate iron calcium)
3acterial O!ergrowth
-causes maldigestion by deconCugating bile salts
-uses up 3=>
-bacterial o!ergrowth is caused by
-hypomotility (BM, scleroderma, pseudo-obstruction)
-blind loop due to surgery or fistula
-small bowel di!erticuli
-partial small bowel obstruction (adhesions, (rohns disease)
-diagnosed by breath tests (none ideal), schilling test, small bowel aspirate colony counts
-treatment 7 empiric trial antibiotics (cipro) 7 if it gets better, you ha!e B4
BI1++)81
9ra!elers Biarrhea Biarrhea in 1IB.J @on-infectiousH non-malabsorpti!e
8nteroto4igenic 8- coli (M" .ecretory
-watery, no blood -bloody colitis (in!asi!e)
-need biopsy to B4
-persists with fasting and no gap
->(@aEI) : stool Osm
3i is prophyla4is @eoplasms
-lymphoma
-Iaposis sarcoma (FI too)
(auses
-Fastrinoma 7 strong ulcer history
-"I#oma 7 watery diarrhea
1ntibiotics for prophyla4is (maybe) 1IB. enteropathy
-watery diarrhea 7 diffuse
-..9 7 BM gallstones 7 stops gallstones
-Medullary (1 of thyroid 7 hypocalcemia
94 :loperamide (imodium)
94 : 9M#/.MX or (ipro
#roto<oan 7 watery
-cryptosporidium
-isospora belli
-microsporidium
-giardia
-entaboeba histolytica
-(arcinoid 7 flushing, whee<ing, 9+, #.
-,a4ati!e abuse with phenolphthalein
can turn urine pin0 on O) addition
-Flucagonoma
Biarrhea
Bermititis 7 pellagra-li0e rash
Biabetes Mellitus 7 d/t low insulin
.hould be good in >? hours 3acterial
-M1( 7 gall 7 bladder too
-.almonella 7 bradycardia
-.higella 7 bloody
-(ampylobacter 7 most common
-(lostridium difficile
-bacterial o!ergrowth 73=>
Osmotic
-ceases with fasting (e4cept with la4ati!e)
-disaccharidase deficiency
lactose intolerance 7 most common
-Mg containing antacids (not 1l or (a)
-Motility
hypothyroidism, BM, I3. (bacterial grow)
I3. most common reasons for !isit
-Brugs
colchicine, dig, 6uinidine, theophylline
I@*,1MM19O+5 3OA8, BI.81.8
Crohn#s Disease 'lcerati3e Colitis
9ransmural and in ileum and colon Glcerated mucosa, bloody diarrhea
Franulomas with perianal disease, fistulas, and abscess (ontinuous symmetric fashion, !ariables portions of colon
.0ip lesions 5oung people, if in old thin0 ischemic colitis (pain)
Ileitis may loo0 li0e 1##5H colitis symptoms (an mimic infectious colitis
Obstructi!e symptoms d/t fibrosis, and inflammation 1ll new cases should ha!e stool studies to +/O infection
*istuli<ing disease 7 bladder, s0in, !agina, psoas muscle
(limp), and intraabdominal abscesses
Increased ris0 after long-standing inflammation
,ong )4 of diarrhea w/o bleeding should thin0 of other B4
84traintestinal manifestations (same as (G() E
-malabsorption
-bile-salt deficiency after ileal resection
-more absorption of o4alate since less bile salts ((a
EE
)
-nephrolithiasis, hydronephrosis, hydroureter, gallstones
which are cholesterol stones
84traintestinal manifestations related to bowel acti!ity
-#eripheral arthritis
-8rythema nodosum
-#yoderma gangrenosum (may need to ta0e out colon)
-8piscleritis, conCuncti!itis
9reatment
-colitis same as for G( with increased antibiotics (cipro)
-ileitisH mesalamineEMetronida<ole-sulfa not abs until colon
perianal disease 7 metronida<ole
-$M# and 1<ithioprine for those who are on steroids
84traintestinal manifestations not related to bowel acti!ity
-1n0ylosing spondylitis and sacroileitis (),1-3>')
-u!eitis (photophobia and blindness)
-sclerosing cholangitis (inflammation of bile duct)
.urgical 9herapy
-failure of medical therapy
-obstruction, abscess, cancer, perforation, post op
-;MN get post-op recurrences
(ancer ris0
-duration of disease T=M
-e4tent of disease (only proctosignoiditis not at ris0)
-sur!eillance with colonoscopy and biopsy for dysplasia
need to do annually H if seen colectomy
9reatment
-Bistal disease topical with mesalamine or steroids
oral with mesalamine or sulfasala<ine
-84tensi!e disease steroids with sulfa or mesalamine
cant stay on for too long so use $M# and 1<ithioprine
-9o4ic Megacolon subtotal colectomy is not responsi!e
(lostridium difficile
-antibiotics li0e ceph, amp, and clinda
-can happen months after use or days after use
-nosocomial spread (hospital is the source)
-clinical presentation diarrhea, fe!er (may be solitary), abdominal tenderness, A3(
-may get to4ic megacolon
-diagnosis (-difficile to4in 3 assay
fle4ible signoidoscopy with pseudomembranes
-treatment 7 #O/I" metronida<ole or #O !ancomycin (not absorable)
-relapses in =M->MN of cases 7 Cust use metronida<ole again
-relapse is not from resistance but from spores left behind
.higella
-classic presentation is dysentery
-to4ic patient, bloody diarrhea, many fecal A3(s
-in!asi!e colitis intensi!e inflammatory
(ampylobacter
-can be bloody
-most common cause of bacterial diarrhea
-symptoms !ary from mild diarrhea to colitis closely mimic0ing (G(
-leads to Fuillain-3arre syndome (ascending paralysis) in some cases
5ersinia enterocoliticae
-typically ileitis or ileocolitis may mimic G( or (rohns disease (1#5)
-diagnosis with serology or stool culture
1mebiasis 7 8ntameoba histolytica
-homose4ual men and tra!lers diarrhea
-can cause ileocolitis loo0s li0e (G( and crohns disease
-ameoboma can cause mass effect (loo0s li0e a cancer) 7 inflammatory cells
-diagnosis is by stool (4, biopsy, serology
+adiation colitis
-can happen after radiation (anywhere from months to >M years)
-greater incidence with prior abdominal surgery
-lesion is secondary to ischemia 7 small blood !essels
-may be small or large bowel (colitis or illeus)
"1.(G,1+ BI.81.8. O* 9)8 3OA8,
1ngiodysplasia (!ascular ectasias)(1" malformations)
-usually lower FI bleeding in elderly
-usually cecal (right sided) but can occur anywhere
-B4 and 94 with endoscopeH should not use 3a enema
-other maCor cause is di!erticulosis
-may be associated with aortic stenosis
-thin0 of Osler-Aeber-+endu if nose-bleeds or other telangectasias
-another name for it is )ereditary )emorrhagic 9elangectasias
-gastric arterio-!enous malformations common in chronic renal failure (better with estrogen)
1bdominal 1ngina
-implies ischemia in > of 2 !essels ((eliac, .M1, IM1)
-rare to ha!e the celiac in!ol!ed
-postprandial pain and sitophobia (fear of eating), and weight loss
-B4 is not with endoscope but with angiogram
-94 : re!asculari<ation
Mesenteric Ischemia (can 0ill patients)
-.M1 ischemia (duodenum splenic fle4ure
-usually due to low flow of blood (()*, hypotension, or digitalis)
-can also be due to embolus in 1*
-pain out of proportion to e4am (pain and agony but abdomen is soft)
-,13. ,actic 1cidosis high I
E
and high A3(
-abd X-ray finger printing (submucosal hemorrhage) get angiogram for early B4
Iscehmic colitis
-IM. ischemia
-usually due to low flow with small !essel disease (dont get angiogram)
-can occur up to ? days post op 111 repair (get IM. damage)
-usually in the elderly but if in young suspect =) O(# if female >) cocaine use
-usually presents in the splenic fle4ure and rectosigmoid colon (watershed)
-all the way from painless bleeding to bloody diarrhea
-ne!er in!ol!es the entire colon
BI"8+9I(G,1+ BI.81.8
#ainful di!erticulosis
-spasm and muscular hypertrophy (due to low fiber in the diet)
Bi!erticular bleeding
-3ris0 bleeding (3+3+#)
-Gsually self limited
-treatment is a high fiber diet and antispasmotic
-if bleeding masse!ely do angiogram if find, resect portion of bowel
Bi!erticulitis
-usually in the lower left 6uadrant (loo0s li0e an 1##5)
-d/t a micro or macro perforation
-can also present as fistulas (the three things that can present as fistulas are)J
=) di!erticulitis
>) (rohns disease
2) (ancer
-94 : antibiotics for 8-(oli and anaerobes : (efota4ime
F1.9+OI@98.9I@1, 3,88BI@F
Initial Management
-stabili<e the patient with transfusions (orthostatis : =MN, shoc0 : >;N of blood !olume)
-monitor !ital signs
-establish secure I" access
Is it upper or lowerX
Gpper FI bleeding (abo!e ligament of treit<) ,ower FI bleeding (abo!e liagment of treit<)
)ematemesis Maroon .tools
Melena (blac0 and tarry) (only blac0 : 3i or *e)
-increased 3G@/creatinine ratio (?M/=)
+arely melena type stool with slow right-sided
colonic bleed
)ematoche<ia (3+3#+)
Fuaiac-positi!e stool
'$$er +I (leeding
Glcers
-bris0 or slow
-painless bleeding with history of smo0ing and bleeds
-esophageal, gastric, or duodenal
Fastritis
-usually slow and common after @.1IB. and aspirin
-thin0 of in an arthritis patient
8sophageal !arices
-e!idence of portal hypertension
-usually bris0 bleeding
-can be fatal in up to ?MN
Mallory-Aeiss tear
-!ariable bleeding usually after history of !omiting or retching (mucosal laceration)
-retching w/o blood and then w/ blood
(ancer
-bleeding is an unusual presentation 7 but if large enough and ulcerated
-if there is bleeding then thin0 of leiomyosarcoma or leiomyoma (benign)
-pain and weight loss
Management
-need to stabili<e the patient
-endoscopy with control of bleeding
-cautery
-inCection (alcohol and epinphrine)
-sclerotherapy if !enous 7 inCect the !eins directly
-..9 (octriotide) and nitroglycerin 7 to counteract other systemic effects on heart E preload
-.engota0en-3la0emore tube for !ariceal bleeders
-> balloons(stomach and esophagus), pressure stops bleeding
-complications are perforation and ischemia
-9I#. : hepatic artery 7 portal !ein shunt
-Medical 9reatment ()> bleeders) do not stop bleeding
Lo.er +I (leeding
)emorrhoidal 7 3+3#+ is the most common cause
Bi!erticular bleed 7 usually arterial and bris0
1" malformations 7 usually bris0
-!ariable rate of bleeding, usually in the elderly, aortic stenosis, renal failure
(olon polyps or cancer 7 usually occult bleeding *e deficiency
Ischemic (olitis 7 bleeding with diarrhea no bleeding w/o diarrhea (anything)
-usually associated with other atherosclerotic diseases
-also seen in women on O(#
-also seen in young people on cocaine
LI!ER AND -ILIARY TRACT DISORDERS
Acute "e$atitis
)epatitis 1
-incubation is 2 wee0s
-fecal oral transmission
-ne!er is chronic
-associated with mollus0s
-only I" needle stic0 can infect if patient has acute hepatitis 1
-B4 : )1" IgM (!irus shed in the stool early, )1" IgM is the only mar0er we ha!e, not IgF)
-(ourse is cholestatic or hepatocellular (1,9) or asymptomatic
-=N can die in fulminant, ne!er chronic
-if e4posed, must gi!e IgF (immuni<e human immunoglobulin)
)epatitis 3
-B@1 !irus that re6uires re!erse transcriptase
-perinatal (asian), parenteral, se4ual transmission (easiest to transmit this way)
-incubation is 2 months
-Biagnosis : )bs1g (?->M wee0s) 7 if persistent, shows chronic infection
-if you ha!e the antibody immune from )ep 3
-;N dont get 1b and get fulminant disease or become asymptomatic
)bc1b 7 IgM (>M wee0s) 7 window period
)be1g 7 if ele!ated means infecti!ity, if antibody is ele!ated means not
-If you are e4posed you must recei!e !accine and )3IF
-If you are immuni<ed against )ep 3 you will ha!e anti-)bs1g but not anti-)bc1g
-serum sic0ness li0e symptoms (arthritis, rash, glomerulonephritis -which gradually resol!es)
-may become hepatoma (li!er cancer)
)epatitis (
-#ost-transfusion hepatitis
-B4 is not anti-)(" in the first few months since it ta0es se!eral months to serocon!ert
-;MN get chronic hepatitis and >MN get cirrhosis
-get cryoglobinemia and glomerulonephritis
)epatitis B
->
nd
easiest to transmit se4ually
-obligate co-infection with hepatitis 3 is needed
-either simultaneous or superinfection with chronic carrier
-suspect in chronic 3 carrier who has been pre!iously silent who now has symptoms
-more se!ere course
-more pre!alent in I" drugs abusers, hemophiliacs
)epatitis 8
-8pidemic in 1sia and India and Me4ico
-fecal7oral transmission
-usually self-limited, not chronic
-fulminant disease in pregnancy
*G,MI@1@9 )8#19I9I.
-hepatic failure within % wee0s of onset of illness
-encephalopathy and increased #9
-massi!e hepatic necrosis, !iral hepatitis, li!er necrosis, Ailsons Bisease, +eyes, shoc0,
-acute fatty li!er of pregnancy, ischemic li!er necrosis
-(omplications
-cerebral edema (low albumin) and hypoglycemia (low glucose)
-9reatment : li!er transplant
B+GF I@BG(8B ,I"8+ BI.81.8
71cute hepatitis
-I@), and methlydopa (antihypertensi!e)
-(holestasis (increased bilirubin)
-chlorproma<ine (used in schi<ophrenia)
-erythromycin
-estrogens (also 3ud (hiari .yndrome and )epatic 1denomas)
*atty ,i!er
-steroids, 89O), tetracycline, amiodarone
*ibrosis
-methotre4ate (may need to stop drug)
-used for +1, psoriasis, (hemotherapy
1cetaminophen
-most popular drug to o!erdose on in 8ngland
-dose related and can be se!ere and fatal (usually se!eral days after ta0ing them)
-mediated by the #-?;M system
-se!ere to4icity associated with low dose and 89O)SSSS (usually seen with hango!er)
-1.9 or 1,9 seen in the ;,MMM 7 =M,MMM range
-treatment is acetylcysteine (ta0e o!er for the F.) which is being used up)
1,(O)O,I( ,I"8+ BI.81.8
-alcoholic hepatitis
-fe!er, tachycardia, Caundice, and +GK symptoms
-dont confuse with cholecystitis (alcoholic pt, may die in .4)
-,13 : 1.9/1,9 : >
-treatment is steroids if Caundiced or ele!ated #9 or encephalopathy
*1995 ,I"8+
-common cause of asymptomatic ,*9 abnormalities (in fat people)
-re!ersed by weight loss
-rarely goes to hepatitis or cirrhosis (uncommon usually benign)
MI(+O"8.I(G,1+ *19
-+eyes syndrome
-1cute *atty li!er of pregnancy
-tetracycline, !alproic acid, and 89O)
M1(+O"8.I(G,1+ *19
-89O)
-BM II
-malnutrition
-obesity
-CeCunoileal bypass
-9#@ (classic)
-Brugs
()+O@I( )8#19I9I.
)epatitis 3
-persistence of ,*9 for longer than $ months
-can go to cirrhosis and hepatoma
-9reatment is -I*@ (for ? months) and is successful in =/2 and patients
)epatitis (
-fre6uently progresses to chronic li!er disease
-94 : I*@ (peg) for $ months (2 million G .K 9IA) (genotype = less responsi!e)
-?MN respond and then dont need further treatment
->MN respond and continue to need I*@
-decompensated cirrhosis li!er transplant
1utoimmune DlupoidL hepatitis
-not associated with lupus
-seen in younger women (may appear (ushingoid e!en if not on steroids)
-associated with other autoimmune diseases such as thyroid and .Cogrens
-94 : steroids and a<athioprine (if you cant get them off steroids)
IN"ERITED LI!ER DISEASE
Ailsons Bisease
-suspect whene!er you ha!e hepatitis with hemolytic anemia (retic of >;N)
-low ceruloplasmin, high serum and urine (u
-(u 6uantitati!e determination is on biopsy (gold standard)
-hepatic presentation can be anywhere from asymptomatic to fulminant hepatic failure
-other symptoms neuropsychiatric (#ar0insonian, )emolysis, *anconis, +91,
Iayser-*leischer ring in Bescemets membrane
-94 7 B-penicillamine (chelation)
-Qn, triene (chelation), transplantation cures underlying disease
-beware of 3M suppression, nephrotic syndrome, arthralgias
)emochromotosis
-screening is easily achie!ed with ferritin T>;M or N *e sat T ;MN
-done in li!er disease, BM II, heart disease, Impotence, and first degree relati!es
-clinical features
-li!er disease with increased ris0 of hepatoma
-bron<e diabetes
-arthopathy
-restricti!e cardiomyopathy
-bron<e s0in
-impotence (due to pituitary dysfunction) 7 hard heart only
-94 : phlebotomy before organ failure
= 7 antitrypsin deficiency (1+)
-normal : #iMM and abnormal : #iQQ
-precocious emphysema, neonatal hepatitis, chronic hepatitis in adults
-cirrhosis and hepatoma
-B4 : measure = 7 antitrypsin le!els (if low determine phenotype)
-94 : treatment of the complications if necessary
-hepatoma sur!eillance (1*#)
-li!er transplant for end-stage li!er disease (they do well after)
(ystic *ibrosis
-(*9+ on (h' is dysfunctioning
-basis for sweat test (ele!ated (l in the sweat)
-chronic respiratory tract infections
-cirrhosis, biliary tract strictures and gall stones
-pancreatic e4ocrine insufficiency malabsorption and failure to thri!e in children
-meconium ileus in newborns
-can get !aricele hemorrhage
APPROAC" TO T"E PATIENT 4IT" 1A'NDICE
-hyperbilirubinemia
-unconCugated
-hemolysis
-upta0e of conCugation defect (Filberts .yndrome) [ >-? in ele!ation
-conCugated
-intrahepatic (medical)
-e4trahepatic (surgical)
MODALITIES 5OR "EPATIC DISEASES
G.
-need good operator
-good for gall stones
(19 scan
-better anatomy !isuali<ation
-not operator dependent
,I"8+ F1,, .(1@
-function of li!er, gall bladder, and biliary tree
-scan follows bile flow
-,I"8+ F1,, 3,1BB8+ 9+88
-when gall bladder doesnt light up : cholecystitis
8+(#
-most direct to see the bile duct
-used for problems in the common bile duct
-see normal smooth walls
,I"8+ 3IO#.5
-usually not needed if other modalities are used correctly
C"OLESTATIC DISEASES
#rimary .clerosing (holangitis (#.()
-obstruction of the intra and e4tra hepatic bile ducts
-associated with I3B (G(T(rohns
-cholestasis, Caundice, pruritus (due to bile salts)
-superimposed episodes of bacterial cholangitis (pain, fe!er, nausea)
-increased ris0 of cholangiocarcinoma
-B4 : 8+(# shows strictured ducts and antibodies to p1@(1
-94 : ursodeo4ycholic acid and methotre4ateX
-endoscopic dilatation or stenting of the dominant stricture
-transplantation (but beware of cholangiocarcinoma)
#rimary 3iliary (irrhosis (#3()
-=M4 more females (and younger in life) also ha!e - 1nti Mitochondrial 1ntibody
-cholestasis (either ha!e increased 1l0#hos, FF9#, or bilirubin O+ pruritis (d/t bile salts)
-can be anywhere from normal to cholestatic (4anthelasma, osteoporosis, 1B8I deficiency)
-B4 : 8+(# (if normal, you need a li!er biopsy)
-94 : ursodeo4ycholic acidX, cholchicineX, cyclosporineX
-definiti!e treatment is transplant
LI!ER DISEASES O5 PRE+NANCY
Associated .ith Preeclam$sia Not associated .ith $reeclam$sia
)8,,# (hemolysis, ele!ated ,*9, low #latelets) )yperemesis gra!idarium (first trimester)
-mild ele!ation of 1.9 and 1,9
)epatic infarction and rupture
-se!ere pain, shoc0, and hemoperitoneum
3enign cholestatis of pregnancy (any trimester)
-intense pruritus
-94 : supplement !it I and other !itamins
1cute *atty li!er of pregnancy
-B4 : biopsy
9reatment for all of the abo!e is deli!ery of fetusS
!ASC'LAR DISORDERS O5 T"E LI!ER
3udd-(hiari syndrome
-hepatic !enous outflow obstruction
-B4 : G. doppler or !enography
-clinical associations
-p-!era (myeloproliferati!e disorders)
-thrombotic disorders
-O(#s
-tumors (hypercoagulability of malignancy)
-trauma
-94 : medical : treat the underlying disorder
-.4 : decompress shunt .4 earlyH transplantation late
)epatic !eno-occulsi!e disease
-non thrombotic occlusion of intrahepatic !eins
-presents li0e a 3udd (hiari
-clinical associations
-3M transplantation
-chemotherapy
-$-M#
-1Q1
-thioguanine
-3ush 9ea
-presentation
-hepatomegaly
-pain, Caundice and ascites
(irculatory failure
-()* in the presence of right sided failure
-clinical presentation : hepatomegaly, +GK tenderness, Caundice
-B4 : dilated hepatic !eins on G. (doesnt need biopsy)
.hoc0 ,i!er
-*ollows a hypotensi!e episode and may occur days later
-9ransminases and !ery high due to the ischemic e!ent
-treatment is supporti!e
PORTAL "YPERTENSION
8sophagogastric !arices
-portal pressure must be abo!e => mm)g
-the ris0 factors for bleeding are si<e and endoscopic criteria (need to scope them)
-94 : propanolol will stop a first bleed and rebleeds
-..9 and nitroglycerin (decreases inflow to portal system while 0eeping flow to heart
-controls acti!e bleeding with high rebleeding rate
-8ndoscopic sclerotherapy
-ineffecti!e pre!ention of a first bleed
-highly effecti!e in aborting acti!e bleeding
-complications : esophageal ulcers, stricture, bacteremia, and .3#
-3anding 7 has reduced complications (no .3#)
-#ortal (a!al shunt
-not used prophylatically
-as effecti!e as sclerotherapy but more e4pensi!e
-chief ad!erse effects is encephalopathy E complicates future li!er transplant
1scites
-if T>;M #M@s : .3#
-culture in bedside blood culture bottles
-.11F (serum albumin/ascitic gradient) T =-=
-94 : diuresis and >g @a diet
-large !olume paracentesis (but not too much or else third spacing and hypotension)
-albumin infusion if no peripheral edema
-perito!enous shuntH ad!erse effects : BI(, infection, thrombosis
SPONTANIO'S -ACTERIAL PERITONITIS
-if see a low grade fe!er you must tap
-low protein ascites at high ris0 (thin0 that protein is actually Ig that protects)
-B4 : T>;M #M@s
-E.coli and enteric F(-) organisms
-if more than one bug, thin0 of perforation or other secondary type
-94 : (eftota4ime for ' days
-repeat paracentesis to monitor therapy
-a!oid aminoglycosides (since such low renal perfusion anyway)
"EPATORENAL SYNDROME
-a<otemia, oliguria, urine @a
E
&=Mm86/l (Cust li0e prerenal a<otemia)
-must distinguish from hepatorenal syndrome by hydrating the patient
-if still DprerenalL, then hepatorenal
-##9 factors
-aminoglycosides
-@.1IB.
-!olume loss (diuretics, paracentesis, e4cess lactulose)
-0idney wont get better until the li!er does
-0idneys are OI when li!er transplant
-0idneys transplanted into another body with good li!er wor0 OI
PORTOSYSTEMIC ENCEP"ALOPAT"Y
-##9 factors : infection (.3#), hypo0alemia or al0alosis, (stimulates @)2 production),
-a<otemia (iatrogenic) or FI bleed d/t 3G@ or sedati!es li0e ben<odia<epines
-9reatment
-correct e4acerbating factors from abo!e
-restriction of animal protein (low protein diet)
-lactulose (osmotic la4ati!e that causes @)2 @)?
E
)
-must be careful not to cause prerenal syndrome (hepatorenal syndrome)
-neomycin (non absorbable antibiotic that eliminates bacteria producing @)2)
-*luma<enil (inhibits the endogenous ben<odia<epines)
"EPATOMA
-presents as abdominal mass or pain or decompensation of pre!ious cirrhosis
-B4 : ele!ated 1*#, G. or (9, li!er biopsy
-.creen high ris0 patient ()ep 3 E ( and =-antitrypsin def) with 1*# and G.
-94 : must find early for .4 (especially if fibrolamellar type) 7 better prognosis
if found late only hope is transplantation and (1 recurrence may occur (low sur)
-ris0 factors (cirrhosis, hep 3 E (, hemochromotosis, alcohol, aflato4ins, p;2 mutation)
LI!ER A-SCESS
#5OF8@I( (bacteria) 1M83I( (parasitic)
-most commonly from the biliary tract cholangitis
-portal !ein (pylephlebitis) 7 appendicitis, di!erticulitis,
(rohns disease
-hematogenous 7 endocarditis
-contiguous 7cholecystitis
-penetrating trauma 7 stab wounds
1cute febrile illness
Gsually 5oung hispanic population
Gsually not amebic dysentery uncommon
Organisms
-8-coli, 8nterococci, 1naerobes
B4 : serology by Dancho!y-sauceL aspiration
9reatment
-antibiotics and drainage
94 : metronida<ole (BO8.@9 +8KGI+8 B+1I@1F8)
LI!ER TRANSPLANTATION
-gi!en in
-end-stage chronic li!er disease when post-necrotic, #3(, #.(, 89O)
-fulminant hepatic failure when to4in-related or !iral (or else they will die soon)
-@O9 FI"8@ I@
-)I"E (low prognosis d/t immunosuppression)
-Malignancy outside the li!er (low prognosis d/t immunosuppression)
-acti!e infection (low prognosis d/t immunosuppression)
-acti!e alcoholism (if not less than $ months)
-ad!anced cardiopulmonary disease (cant be with any .4)
-G.G1,,5 @O9 FI"8@ I@
-ad!anced age, stage I" coma, ad!anced renal failure, portal !ein thrombosis,
-prior shunt .4, hepatoma or cholangiocarcinoma (may ha!e spread)
-chronic hepatitis 3 7 new li!er will get infected but can be treated with I*@
-complications
-post op bleeds, hepatic artery or portal !ein thrombosis, biliary tract lea0s, strictures
-infections (!iral, bacterial, fungal)
-reCection (acute or chronic)
-9reatment #rednisone, 1<ithioprine, (yclosporine
+ALLSTONES
-if stuc0 in the gall bladder asymptomatic or dyspepsia (non-specific)
-if in cystic duct only and then lea!es biliary colic
B4 : )istory and G.
-if in cystic duct only and stays acute cholecystitis (gall bladder inflammation)
-fe!er, A3(, pain (Murphys .ign)
B4 : )IB1 (nuclear scan) which shows flow bloc0ed in the cystic duct
-if in common bile duct and stays cholangitis ((harcots triad : pain, fe!er, Caundice)
B4 : 8+(# with dilated common bile duct
-if in lower common bile duct gallstone pancreatitis
B4 : 8+(#, (9
-9reatment
-dissol!e the gallstone with ursodeo4ycholic acid (GB(1)
-;MN effecti!e with much recurrence
-useful for only small cholesterol stones (radio lucent
-to4icity minimal
-lithotrypsy (sound wa!es) in combination with GB(1
-cholecystectomy (lap !s routine) 7 this is the choice method
-*actors associated with stone formation
-decreased bile salts cause increase in cholesterol
-stones result from e4cess cholesterol secretion
-pronucleation factors present in stone-formers
-gallbladder hypomotility (9#@, fasting, pregnancy) 7 stasis crystali<ation
-8pidemiology and natural history
-women T men (more progesterone) related to pregnancy
-increases with age
-'MN of patients are asymptomatic (prophylactic cholecystectomy @O9 ad!ised)
-3iliary .ludge and acalculosis cholecystitis
-sludge probable precursor to stones
-sludge fre6uent in 9#@ patients, post-op, prolonged 9#@, and 1IB. ((M" etc-)
PANCREATIC DISORDERS
1(G98 #1@(+819I9I. ()+O@I( #1@(+819I9I. #1@(+819I( (1@(8+
RMN from 89O) and Fallstones
-high (a
EE
, high trigly (normal amy)
-trauma, infections (co4sac0ie,
mumps, hepatitis, (M" etcV-)
-Brugs (see ne4t bo4)
RMN from 89O) @O9 F1,,.9O@8.
-cystic fibrosis (thic0 discharge)
-tumor, stricture, trauma
-pancreas di!isum
drained through minor papilla
(hronic pancreatitis
(igarettes
89O)
(affeine
*urosemide, 1<ithioprine, .ulfa,
9hia<ide, "alproate, 8strogen,
9etracycline, #entamidine, Bdi
#1I@, #1I@, #1I@ (demerol addict)
-e4ocrine insufficiency steatorrhea
-endocrine insufficiency BM type I
1bdominal pain to bac0 that 0eeps
patient up at night
1nore4ia, weight loss, Caundice
#ost prandial bac0 radiating pain aundice 7 O3. in common duct Fastric outlet obs, new onset BM
8pigastric tenderness
#eritoneal signs
Frey-9urner sign/(ullen sign
-ruptured ectopics
#ulmonary findings
-pleural findings li0e 1+B.
(alcification in 2MN of cases on X-ray
.ecretin stimulation test
Measure output !ia @F tube
Ahen stimulated with secretin
,ow : chronic pancreatitis
8+(# shows beading and dilation
B4
-G. and (9
if you see mets you can stop
if you see local in!ol!e then 8+(#
-8ndoscopic G.J assess resectability
nodes between stomach and pan
1mylase (not specific)
-seen in mumps (sali!ary glands)
-tuboo!arian process
-macroamylasemia
9reatment 7 for pain
-#1I@ (O@9+O, (no alcohol)
-narcotics (beware of addiction)
-celiac a4is bloc0
-(a =R-R
-angiogram before .4
,ipase
-far more specific for pan disease
-#uestow procedure
long pancreatectomy
+1@.O@. (2 or more : bad prog)
1ge (;;) pO> ($M)
A3( (=$,MMM) *luid se6 ($,)
Flucose (>MM) 3ase deficit
,B) (2;M) 3G@ (;)
1.9 (>;M) )ct (=M)
((a
EE
)
9reatment 7 for malabsorption
-medium chain triglycerides
-pancreatic en<yme supplements
also treats pain by (-) feedbac0 inh-
-gastric acid secretion suppression
)> bloc0er
94 : surgical cure is only ;-=MN
#alliati!e pruritus, cholangitis
3y doing 8+(#/stent and
(holedochoCeCunostomy if lesion in
distill common bile duct
Fastric duodenal obstruction
Bo gastroCeCunostomy -allows eating
1bdominal X-ray
-sentinel loop or colon-cutoff (illeus)
-loss of psoas shadow
-non specific ileus (most common)
#ain control
@arcotic infusionsH celiac a4is bloc0
G.
-bile duct e!aluation 94 : 8+(#
-not so good for the pancreas
(9 scan
-most useful imaging study
-dem phlegmon (swollen gland)
-pseudocyst and abscess (en<ymes)
Management
-@#O and @F suction (rest pancreas)
-I" hydration (need to a!oid (+*)
-pain meds (M.)
-remo!e the stone
-if gallstone pancreatitis suspected
8+(# E sphincterotomy and stone
84traction
84trapancreatic complications
-en<ymes destroy al!eoli (1a grad)
-pleural effusions (high in amylase)
-1+B. 7 non cardiogenic edema
-hypocalcemia, hypomagnesemia
-a<otemia d/t third spacing
,ocal (omplications
-phlegmon 7 swollen pancreas
-pancreatic abscess (=w-T$m) drain
-#seudocyst (watch if & $ wee0s old)
can bleed, obstruct, infected, lea0
NE'ROLO+Y
Bementia
-1lert and Oriented
-progressi!e mental disorder that impairs abstract thought, memory, and Cudgement
-must first rule out re!ersible causes of dementiaS
-depression (pseudodementia) 7 patients doesnt feel li0e answering 6uestions
-normal pressure hydrocephalus
-hypothyroidism
-!it 3=> deficiency
-thiamine deficiency (usually in hospitali<ed patients)
-1l<heimers subtype
-most common cause of chronic dementia in the G.
-occurs with age and associated with (h >= and 1po 8 gene
-trouble with anomia, abstract thought and Cudgement
-patients are alert and e4hibit progressi!e memory loss and cogniti!e decline
-also e4hibit paranoia
-B4 : (9 shows !entricular enlargement and increased sulci
-88F is usually normal but done to +/O other diseases (M1B (OA.)
-increased !oltage : metabolic disturbance
-normal : 1l<heimers
-94 : important to treat medical depression with non anti 1() antidepressants
-also treat agitation, and insomnia usually with haloperidol
-#ic0s Bisease (similar to 1l<heimers)
-seep temporal lobe and language dysfunction (usually unilateral)
Belirium
-wa4ing and waning
-may be disoriented and usually re!ersible and treatable
-caused by infections, drug induced, and withdrawal symptoms
-appears agitated
@ormal pressure hydrocephalus
-cogniti!e impairment (dementia)
-urinary incontinence
-gait disturbance (broad based gait) 7 magnetic gait
-(9 scan re!eals !entricular enlargement but normal sulci
-94 : need to ma0e diagnosis early because can treat with "# shunt
-often they impro!e after an ,#
)81B1()8
@onneurologic causes
-sinus infection (frontal is more life threatening)
-glaucoma (especially if unilateral) 7 get sinus series or (9 of head
-oral infections
-9M disease
-(-spine problems (pain reflected to one side of head (occipital neuralgia) ((>E(2))
#otentially fatal causes
-Intracranial mass
-de!elops slowly and progressi!ely worsens and 0eeps the patient up at night
-signs of increased I(# li0e @/" etc-
-.ubarachnoid hemorrhage
-sudden onset Dworst headache of my lifeL
-M+I is of no help here must use (9 (if that is negati!e then use ,#)
-(9 will show white around the brain
-if diagnosis is still in doubt then use cerebral angiogram
-sometimes see sentinel bleed little bleed w/o (9 findings
-94 : neuro .4
-(a
EE
channel bloc0er li0e nimodipine pre!ents !asospasm and hemistro0es
Migraine 9ension (luster
##9 factors
#ost stress, no sleep, O(#, menses
(affeine withdrawal, M.F, tyramine
3and li0e around the head
Often associated with stress
Occipital E (er!ical muscles : tender
MenTTAomen
#eriorbital pain in clusters o!er wee0s
Gnilateral
(lassic : aura, scomata, pulsatile,=s
photophobia, @/"
94 : (outalbital/caffine/1spirin) 1ss w/ lacrimation, conCuncti!itis
@asal congestion
(ommon :w/o aura, photophobia,@/" @e!er bilateral
Maybe hemiplegia and hemisensory 94 1borti!e:.umatriptan, 8rgos or O>
#rophylatic : ,i, .teroid, (a
EE
bloc0
94 : 1borti!e : .umatriptan E 8rgos
#rophylatic : -bloc0ers E 9(1s
Methysergide causes retreoperitoneal
fibrosis
.umatriptan : ;-)9=B agonist 8rgos may cause ergotism
-cut of circulation to the brain
9emporal 1rteritis
-unilateral headache in the temporal or occipital area in patient o!er ;M
-associated with blindness d/t cut off circulation, Caw claudication, and constitutional sym
-weight loss and low grade fe!er
-;MN associated with #olymyalgia rheumatica
-8.+ T ?M
-B4 : temporal artery biopsy (ma0e sure not BM or osteoporosis)
-steroid treatment is effecti!e as well (also for #olymyalgia rheumatica)
#seudotumor cerebri
-benign intracranial hypertension
-maCor ris0 factors are
=) #regnancy
>) O(#
2) .,8
-usually see papilledema and headache with !isual disturbances
-neurological e4amination is otherwise normal
-(9 or M+I re!eal no cause of increased intracranial pressure
-howe!er the ,# opening pressure is high
-94 -steroids or diuretics may be effecti!e (1ceta<olamide)
-repeated lumbar punctures effecti!e in reducing the pressure and symptoms
-if !isual symptoms are present lumboperitoneal shunt to sa!e !ision
9rigeminal @euralgia (9ic Bouloureu4)
-se!ere facial pain with a lancinating 6uality
-only seen in one branch of the trigeminal ner!e
-facial sensation intact but pain is triggered by touch
-associated with M.
-94 : carbama<epine, baclofen, gabapentin or .4 on inferior ner!e leads in #O@.
STRO*E
Bisease of the (entral @er!ous .ystem
-ischemic cardiac emboli, large artery disease, small artery disease, other disorders
-hemorrhagic subarachnoid hemorrhagic, intraparenchymal bleeds
(ardiac 8mbolic .tro0e
-most common cause is 1trial *ib
-also caused by recent MI with a0inetic segment
-also by alcoholic cardiomyopathy or any other cause of dilatation
-prosthetic heart !al!es
-endocarditis
-left atrial my4oma
-B4 : patient with cardiac ris0 factor with sudden onset of neurological findings
suspect in patients with multiple distributions (corte4 and brain stem simultaneously)
suspect in patients with other e!idence of systemic emboli
-94 : If small embolic infarction get a (9
-if no blood seen I" heparin
If large embolic stro0e no I" heparin until >-' days (dont want hemorrhagic infarct)
-oral anticoagulation is continued to reduce ris0 of additional embolic stro0e
-target I@+ : >->-;
-endocarditis patients ha!e mycotic aneurysms (dont use anticoagulants either)
-dont anticoagulate if obtunded of comatose
,arge 1rtery Bisease ((arotid 1rteries)
-carotid bruit (not transmitted murmur)
-if asymptomatic E $MN occluded endarterectomy !s- antiplatelet therapy
-if complete stro0e no role for anticoagulation since nothing to be gained (dead)
-if incomplete stro0e use anticoagulation
-9+1@.I8@9 I.()8MI( 1991(I. (neurological deficit &>? hours)
-ischemia from the carotid or !ertebrobasilar system
-(1+O9IB DamaurosisL unilateral blindness and contralateral wea0ness E sens
-window shades coming down
-"8+983+O31.I,1+ transient blindness, ata4ia, !ertigo, diplopia
-cant operate on the !ertebrobasilar system
-B4 : (9 : hypointensity M+I 9= : hypointensity and 9> : hyperintensity
-duple4 e4amination or M+ angiography for the e4tracranial carotid artery
-9ranscranial Boppler studies for intracranial arterial perfusion
-for M(1 and basilar (cant operate on these either)
-FO,B .91@B1+B is angiography but can get renal failure from dye
-echocardiogram to assess for !al!ular lesions and thrombi
-94 : if symptomatic e4tracranial disease with T'MN stenosis of internal carotid artery
-do carotid endarterectomy
if lesser obstruction treat with aspirin or ticlopidine or #a!le4
if cresendo 9I1s or stuttering 9I1s use anticoagulation with heparin warfarin
-I.()8MI( I@*1+(9IO@ .8(O@B1+5 9O ,1+F8 1+98+5 BI.81.8
-if significant function reco!ery with T'MN stenosis carotid endarterectomy
-if stro0e caused by intracranial artery anticoagulants or antiplatelet therapy
.mall !essel disease
-deep in the hemispheres called lacunae
-due to microhyalini<ation from U= BM and U> )9@
-94 : controlling BM and )9@ and use of antiplatelet therapies (aspirin) or ticlopidine
to reduce subse6uent ischemia
.ystemic and hematological causes of ischemia
-)bs, #- !era, myeloma, hypercoagulable states (protein ( and . deficiency)
such as lupus anticoagulant and anticardiolipin and low 19-III, O(#, !asculitis
(auses of deterioration after an ischemic stro0e
-progressi!e occlusion of additional !essels
-to aggressi!e therapy to reduce 3# causes reduced perfusion pressure
-inade6uate anticoagulation therapy
-con!ersion of a bland infarct into a hemorrhagic infarct
-de!elopment of cerebral edema with large stro0es
.tro0e in the young patient
-hypercoagulable states, 1ntiphospholipid antibody syndrome, protein ( or . deficiency
-cardiogenic emboli (mitral !al!e prolapse)
-!asculitis (such as lupus)
-)I" associated disease
-cocaine use in young patients
.ubdural and 8pidural hemorrhages
-usually caused by trauma
-(9 or M+I to B4
-94 : .4 : within ? hours (use I" manitol infusion)
.ubarachnoid hemorrhage
-usually caused by ruptured berry aneurysm (1dult poly cystic disease) or 1" malformation
-also caused by coagulopathy, head trauma, and mycotic aneurysm
-sudden onset of !ery se!ere headache (worst in their life)
-altered le!el of consciousness is a !ery ominous sign
-B4 : (9 scan w/o contrast usually re!eals subarachnoid blood
,# gi!es +3(s
1ngiography will confirm the B4 and locali<e the site of the bleed
-94 : .4 early to stop rebleeding
: (a
EE
bloc0ers to reduce !asospasm and stro0e
: a!oid dehydration and hypotension that would cause !asospasm
Intraparenchymal bleeds
-caused by chronic hypertension
-also caused by coagulopathy (BI(), aneurysm, 1" malformation
-may also be caused by cocaine
-94 : lowering I(# and resection of cerebellum threatening hematoma
SEI>'RES
(lassification
-generali<ed : loss of consciousness
-con!ulsi!e : tonic-clonic motor acti!ity
-sei<ure is often followed by post-ictal state
1bsence sei<ures
-alteration in consciousness with blin0ing and focal myoclonic Cer0s (but can carry on)
-88F shows spi0es and 2 )< wa!es
.imple partial sei<ures
-no change in le!el of consciousness
-isolated clonic-tonic acti!ity or altered sensory perception
-may spread by ac0sonian march (starts on face and marches down same side of body)
(omple4 partial sei<ures
-aura (smell or music heard) change in consciousness for se!eral minutes
.tatus 8pilepticus
-sei<ure acti!ity lasting T2Mminutes
-medical emergency
-hypo4ia, aspiration, rhabdomyolysis ((#I 7 renal failure), and trauma
-noncon!ulsi!e status epilepticus will result in delirious patient with a fluctuating M.
-88F is diagnostic
-94 :establish unobstructed airway and ade6uate O>
:gi!e thiamine and glucose
:dia<epam or lora<epam (short acting)
:I" phenytoin or phenobarbital for possible arrhythmias, resp dep, and hypotension
Other causes of sei<ures
-idiopathic
-stro0e and other !ascular disease (!asculitis)
-.,8, infection, pre!ious trauma, mass lesions, eclampsia (94 : Mg
EE
), theophylline,
lidocaine, cocaine, barbiturate withdrawal, alcohol withdrawal,
ben<odia<epine withdrawal, noncompliance with antisei<ure meds, narcotic antag,
electrolyte disorders
Biagnostic e!aluation of patient with sei<ures
-+/O metabolic abnormalities @a
E
, glucose, (a
EE
, Mg
EE
, uremia, hepatic encephalopathy
-history to determine the abo!e conditions
-(9 or M+I to detect structural lesions
-88F
Management of sei<ures
-correct underlying metabolic abnormalities
-+/O other possibilities
-antisei<ure medication may not be necessary (if only one sei<ure or withdrawal)
-94 : !alproic acid or ethosu4imide (1bsence sei<ures)
: phenytoin, phenobarbital, !alproic acid, carbama<epine (grand mal, com partial)
- !alproic acid and carbama<epine is only #O inta0e
: see abo!e for status epilepticus
Ongoing Management
-ability to dri!e, wor0 en!ironment, recreational en!ironment, education of family
MO!EMENT DISORDERS
#ar0insons Bisease
-degeneration of the substantia nigra
-brady0inesia, rigidity (cog wheel), resting tremor, mas0ed facies, postural instability
-cogniti!e impairment and gradual dementia in ;MN of patients (especially if low 1())
-94 : le!odopa and carbidopa (sinemet)
: anti1() (ben<tropine) good for tremor 7 may ma0e the patient more confused
: .elegiline (M1O3 inhibitor) 7 slows the clinical progression
: pergolide or bromocriptine are post-synaptic dopamine agonists
: amantadine
: all the abo!e can cause confusion and hypotension
: doctors see the on/off phenomena of good bad symptoms
3enign (essential, senile, intention) 9remor
-usually familial
-in!ol!es the hands and impairs fine mo!ement when mo!ing
-94 : -bloc0er or primadone is choice treatment
@8G+O,8#9I(.J
Lo. Potency Medium Potency "igh Potency
(hlorproma<ine (2MM) ,o4apine (2M) 9rifluopera<ine (=;)
9hiorida<ine (2MM) ?@@ A (lind )alperidol (;)
*luphena<ine (;)
side eects (early in treatment)
-anti histamine
sleepiness
-anti 1()
dry mouth, constipation etc-
-anti alpha=
orthostatic hypotension
side eects (late in treatment)
-n euroleptic malignant syn-
!ary rapid and !ery fatal
due to big bloc0 of dopamine
rigidity, high fe!er, (#I,
confusion, delirium, coma
sto$ the treatmentBBBBBBBBBBBB
T9 A (romocri$tine < dantrolene
-e ndocrine changes
increased prolactin, impotence
-. eight gain
e4cept for molindone (loss)
-tardi!e dys0inesia
in!oluntary non-rhythmic musc
.rithing o tongue and ace
after 2 months -T permanent
>MN-;MN common
side eects
in the middle
side eects (late in treat-)
-neuroleptic malignant syn-
-endocrine changes
-weight gain
-tardi!e dys0inesia
side eects (early in treatment)
-high 8#.
PB, dystonia, a0athisa
(restlessness)
-94 : anti 1()
side eects (late in treatment)
-neuroleptic malignant syn-
-endocrine changes
-weight gain
-tardi!e dys0inesia
female, 8#., age, mood
s.itch to clo)a$ine %SDA&
DEMYELINATIN+ DISEASES
Multiple .clerosis ((@.) Fuillan-3arre syndrome (#@.)
B4 : history, (@. demyelination (white and gray)
Multiple clinical remission and relapses
Bemyelination of #@. motor neurons
Immunologic w/ demyelination of (@. white matter
-e4tended period of time with se!eral white matter pathways
(aused by !iral syndrome, )ep 1, or mononucleosis
Or recent .4
(linical *eatures
-optic neuritis (I@O), bladder dysfunction, ata4ia, tremor
-all this but better in 2 days
(linical *eatures
-sudden or gradual ,8 wea0ness in!ol!ing other organs
-big worry is the respiratory paralysis
-arefle4ia and fasciculations
B4
-M+ best to see white matter lesions
-(.* re!els IgF and oligoclonal bandsE myelin basic protein
-somatosensory, !isual, and brainstem audition e!o0ed
potentials demonstrate white matter disease (timed)
B4
-(.* has normal cell count but ele!ated protein
-slow ner!e conduction
-intubate if lung !olume is too low
-also can get cardiac arrhthymia d/t autonomic dys-
94
-if acute episode steroids
-reduces fre6uency of relapses and se!erity -I*@
-for optic neuritis I" methylprednisalone
-reduces fatigue amantadine
-reduces spasticity baclofen (F1313 agonist or dia<epam
94
-I"Ig or plasmapheresis
DISORDERS O5 T"E NE'ROM'SC'LAR 1'NCTION
Myasthenia Fra!is 8aton-,ambert Myasthenic Bisease
1nti-receptor antibodies 1ssociated with small cell lung cancer
Bouble !ision, swallowing, spea0ing, wea0ness, fatigue .ymptoms of wea0ness and impaired autonomic function
>;N ha!e thymoma $MN ha!e thymic hyperplasia +epetiti!e ner!e stimulation causes increase in strength
8!aluation
-9insilon test 7 causes impro!ement
-repetiti!e ner!e stimulation causes wea0ness
-(9 or M+I may demonstrate resectable thymoma
(3lac0 Aidow .pider 9o4in causes more (a
EE
release
Ocular Myasthenia (subtype)
-only of the eye
-still 9insilon E and 8MF E and antibiody E
94 : steroids (although sometimes ma0es it worse)
: pyridostigmine 7 longer acting than 9insilon
: .4 : for thymic hyperplasia
TO6IC AND META-OLIC DISORDERS
"itamin 3=> deficiency
-demyelination and a4onal degeneration
-peripheral ner!es and spinal cord (#@. and (@.) combined system degeneration
-no !ibratory and position (dorsal columns)
-sensory peripheral neuropathy
-impaired gait
-cogniti!e impairment
-B4 : megaloblastic anemia, macrocytosis
-can ha!e psychiatry problem first without the anemia
-low !it 3=> le!el
-94 : !it 3=> IM
Aernic0es encephalopathy
-thiamine deficiency
-glucose w/o thiamine
-stomach stapling and problems with transport
-nystagmus and ocular palsies
-Iorsa0offs psychosis inability to form new memories and learn psychosis
-also confabulates (entity can be seen alone)
+ecreational drug to4icity
-@arcotics (hypo!entilation, pinpoint pupils, low consciousness
-94 : nalo4one
-wean with methadone or else you get
-you get withdrawal symptoms of */"abdominal pain and goose bumps
-(ocaine
-norepinephrine e4cess
-!asculitis of the brain
-fe!ers, hypertension, tachycardia, MI, arrhythmias, stro0e, abdominal ischemia
-#(#
-wildly combati!e
-acute to4icity delirium, ata4ia, nystagmus, agitation, sei<ures,
psychosis schi<ophrenia
:94 : @F drainage and conser!ati!e management
RESPIRATORY DISORDERS
#ulmonary *unction 9ests (#*9s)
-lung !olumesJ 9,( : +" E "(
-Obstructi!e Biseases high +" low "(
-+estricti!e Biseases low +" low "( and low 9,(
-*8"= forced e4piratory !olume in the =
st
second
-can ha!e abo!e M-%, and still be allowed to go to .4 (normal is ;,)
-low in both obstructi!e and restricti!e diseases
-*8"=/*"(
-&M-'M in obstructi!e diseases
-can be TM-'M in restricti!e diseases
-Biffusion capacity (B,(O)
-if low : disrupted al!eolar-capillary surface (large 1-a gradient)
-abnormal in emphysema and interstitial fibrosis with destruction of the parenchyma
-1rterial 3lood Fas
-hypo!entilation : p(O>T?;
-hyper!entilation : p(O>&2;
-acute respiratory change is =M mm)g [ -M% p)
-chronic respiratory change is =M mm)g [ -M2 p)
-1aBO> (al!eolar 7 arterial difference)
-it is a measure of gas e4change
-normal : =M mm)g and elderly is ma4 >M mm)g
-: O#IO> 7 =->(#(O>)P 7 pO>
-on room air #IO> is usually =;M mm)g O>=N of '$M 7 ?' (water !apor)P
1.9)M1
-re!ersible increased resistance to airflow d/t airway narrowing
-d/t to bronchospasm and inflammation
-9riggering factors
-irritants, pollutants (occupational), e4ercise, cold air, dry air
-upper and lower respiratory tract infections
-F8 reflu4
-(linical features of cough, whee<ing, and dyspnea
-#hysical findings are only during the e4acerbation
-tachypnea
-inspiratory whee<ing (worse)
-e4piratory whee<ing
-use of accessory muscles
-pulsus parado4us
-parado4ical mo!ement of the abdomen (should go out on inspiration but it goes in)
-Biagnosis
-low pea0 flow e4piratory rate
-*8"=, *"(, *8"=/*"( during e4acerbation
-lung !olumes are normal or increased
-diffusion capacity is normal or increased
-can impro!e flow rates with bronchodilators
-can e4acerbate the flow with methacholine or histamine (methacholine challenge)
-mild eosinophilia (not as high as in the #I8)
-(X+ hyperinflation, mucus plugging, and atelectasis
-13F hypocapnia, mild hypo4emia, (if normal (O> 8M8+F8@(5)
-94 :anti-inflammatory drugs
-inhaled steroids (for long term management) then long acting beta-agonist
-complications of oral thrush and chronic cough
-oral steroids (for acute management)
-complications of (ushings if long term
-coromolyn 7 pre!ents mast cell degranulation (only prophyla4is)
:bronchodilators
-much o!er used and the reason for poor control of asthma today
-can get as MBI or M@
-anticholinergics 7 atropine and ipratropium
-must ha!e proper techni6ue in using the drug (metered dose and spacer)
-aminophylline preparations (narrow therapeutic window)
-not used as much d/t cardiac arrhthymias
-stimulates !entilating dri!e
:management of an acute attac0
-> agonist E steroids inhalers E ipratropium
-oral steroids
-aminophylline nor epinephrine is @O9 helpful in the control of an acute attac0
:management of chronic asthma
-inhaled steroids for maintenance and inhaled > agonist for symptoms
-add ipratropium
-use aminophylline with nocturnal brea0-through
-short course or oral steroids if bad attac0s as an out-patient
-1llergic bronchopulmonary aspergillosis (13#1)
-this is episodic asthma with non-in!asi!e aspergillosis immune reaction
-transient migratory pulmonary infiltrates
-eosinophilia and high serum Ig8 to aspergillus
-grows well in house, dust, air conduits, decaying !egetation
-B4 : upper lobe infiltrates
: atelectasis due to inspissated mucus
: ##BE
: Ig8 antibodies to aspergillus and high IgF
-94 : clear mucus plugs are cleared by chest #9
: treat inflammation with steroids
: since not in!asi!e systemic antifungals are @O9 indicated
(O#B ((hronic Obstructi!e #ulmonary Bisease) - cant get air outS
8mphysema 3ronchitis 3ronchial 1sthma 3ronchiectasis
abnormal $ermanent
enlargement of the air
spaces distal to the
terminal bronchial
accomplished by
destruction of their walls
acinus and blood !essel
destruction
persistent cough
sputum production-2 months
two consecuti!e years
usually seen w/ emphysema
=) airway inflammation
>) Re3ersi(le Obstruction
2)airwayhyperresponsi!ness
triggered by
=) dust,fumes or allergens
>) !iral infections
1llergic (atopic)
-9ype I (Ig8)
@onallergic (non reagenic)
-un0nown - infections
abnormal $ermanent
dilation of bronchi and
bronchioles d/t repeated
infections
CYSTIC FI!"SIS
-most common cause
-chronic purulent cough
-clubbing
-(X+:air-fluid le!els (tram)
thic0ened bronchi
9obacco smo0ing and age
(RMN)
-loss of !asculature
-destruction of blood !essels
-"/K ratio
#athogenesis
=) chronic irritation
-hypersecretion of mucous
>) microbiological infection
-maintains the condition
Mechanism (+8"8+.I3,8)
-inflammatory disease
-mast cell
!asodilation Y
bronchoconstriction
-late response cyto0ines
-endothelium sloughing
-airways obstructed
#athogenesis
-becomes irre!ersible
=) obstruction persists
>) added infection
-wea0ens bronchial wall
-endobronchial obliteration
atelectasis distal to obl
bronchiectasis
alpha-= antitrypsin (=N)
deficiency
.6uamous Metaplasia
-plugging w/ deadspace
-+-T , shunting
81+,5 +8.#O@.8
-minutes
-histamine (!aso and bronc)
Morphology
-seen in the lower lobes
(entriacinar 8mphysema
((entrilobular)
-cigarettes and u$$er lo(e
-no4ious particles
-pro4imal resp- bronchiole
Morphology
-mucinous secretions in
airway
-large mucous gland to
total ratio (+eid Inde4)
,198 +8.#O@.8
-hours
-endothelial cells adhesion
-cyto0ines
-inflammation
-sloughing of cells (mucous)
(linical Manifestations
-,O9. O* .#G9GM
-purulent
-disease is historical e4cept
in cystic fibrosis
#anacinar 8mphysema
(#anlobular)
-alpha-= #I deficiency
-lo.er lo(es
-all of the resp- bronchiole
Morphology
-Frossly : mucous plugs
-micro : eosinophils
hypertrophy of bronchial
wall musc and submucosal
mucous glands,thic0 3M
94 : treat infection
-)I, .#, .1, #seud, 1naer
-bronchodilators
-mucolytics (ases) and O>
-postural drainage
-.4 : resection of region
#araseptal 8mphysema
(Bistal 1cinar)
-distal acinus
-under pleura
-cause of SC $neumothora9
in young people e4ercising
#athogenesis (theory)
-protease-antiprotease bal-
-smo0ingJ
recruit #M@s and elastase
inact of alpha-=-19
.lowing of forced e4piration
(auses of death
-respiratory acidosis
-massi!e pneumothora4
-+)* %.< (ronchitis&
(OM#1+I@F 3G9 1,A15. .88@ 9OF89)8+
)yperinflationH small heart #rom !essels, large heart
#in0 #uffer 3lue 3loater
early se!ere dyspnea mild late dyspnea
*8"=
*8"=/*"(
9,(
+"/9,(
8mphysema has B,(O
#olycythemia is d/t hypo4ia
(ompensated respiratory acidosis (chronic)
=Mmm)g (O> : M-M2 p)
(X+ showsJ
-hyperinflation with bullae
-flat diaphragms
-reduction in !ascular mar0ings
9+819M8@9J
-smo0ing cessation
-antibiotic co!erage for )I, .#, and M(19
-if re!ersible : > agonists, ipratropium, aminophylline
-if can demonstrate effecti!e #*9 : steroids
-if not than must stop due to ris0 of infection
-supplemental O> if #O> &;; IMPRO!ES S'R!I!AL
-low flow O> or else will decrease hypo4ic dri!e
-correct to $M mm)g or RMN sat
rare cor pulmonale common cor pulmonaleJ
-plugging-Thypo4emia-T
spasm-Tthic0ened walls-T
pulmonary hypertension
(5.9I( *I3+O.I.
-most common genetic lethal disease in (aucasians
-impaired mucociliary clearance
-meconium ileus
-maldigestion and failure to thri!e
-recurrent pulmonary infection result in bronchiectasis
-B4 : sweat test (more than %M)
: airflow obstruction
: same as emphysema *8"=, *8"=/*"(, 9,(, +"/9,(
: (X+ shows bronchiectic changes (cysts, bullae and tram trac0 signs)
-pulmonary complications
-clubbing, hemoptysis, pneumothora4 (se!ere chest pain with low breath sounds)
-pulmonary hypertension with corpulmonale
-recurrent sinusitis and nasal $oly$s
-other organ in!ol!ement
-pancreatic insufficiency fat maldigestion, *99
-meconium ileus
-biliary cirrhosis
-reproducti!e complications
-a<oospermia
-secondary amenorrhea (no eggs)
-thic0 cer!ical mucus
-males ha!e no fertility
-females ha!e decreased fertility
31(98+I1, #@8GMO@I1
-acute onset with rigor, chills, pleuritic chest pain, and fe!er
-lobar consolidation with bronchial breath sounds, whispered pectorilo6uy
-!ocal fremitus and dullness to percussion
-can ha!e e4tension to the pleura pleural effusion
-lower lobes can refer pain to the upper abdomen
-B4 : high A3( with more #M@s (low A3( is a bad prognostic sign)
: 13F with respiratory al0alosis and 1a gradient hypo4ia lactic acidosis
-respiratory acidosis is also a bad prognostic sign
: .putum Fram .tain
-good if lots of A3(s and no epithelials
-=M-=; #M@s on )#*
-if diagnostic culture (e4- FramE cocci in pairs : pneumococcus)
: (X+ shows infiltrates, lobar consolidation, ca!itation, effusions
-8tiology
-(ommunity 1c6uired .#, )I, .1W
-)ospitali<ed or neutropenic patient #seud
-1lcoholic I#, 1naer
-Biabetics F(-) and .1 (more se!ere pneumonia)
-splenectomy, sic0le cell, MM, (,, encapsulated organisms
-I" drug user .1
-con!alescent phase of !iral influen<a .1 and .#
-(* #seud, )I, and .1
-Iartageners syndrome (de4trocardia, situs in!ersus) recurrent pneumonia
195#I(1, #@8GMO@I1
-usually constitutional symptoms of fe!er, malaise, headache, pharyngitis,- FI upset
-non-producti!e cough
-+1+8J lobar consolidation or pleural in!ol!ement
-usually mild leu0ocytosis with lymphocytes esp with !iral pneumonia
-interstitial
-Mycoplasma pneumonia
-young adults with fe!er malaise, cory<a, pharyngitis, non-producti!e cough
-(ullous or hemorrhagic myringitis
-'MN of patient ha!e cold agglutins (hemolysis)
-erythema multiforme
-interstitial infiltrate
-94 : erythromycin or tetracycline
-,egionella
-air conditioning ducts and water cooling systems
-more li0ely to affect (O#B patients
-constitutional symptoms of high e3er, confusion, +I sym$toms, ele3ated L5Ts
-non-producti!e cough, low @a
E
and low #O?
2-
-B4 : B*1 (direct fluorescent antibody
: serocon!ersion re6uires % wee0s
: culture on special media (*e and cysteine)
-94 : high dose of I" erythromycin or other macrolide
-"iral #neumonia
-influen<a, adeno!irus, +.", parainfluen<a
-outbrea0s in late winter early spring
-epidemic patter
-army barrac0s are associated with adeno!irus
-(X+ bilateral diffuse interstitial infiltrates
1@18+O3I(-(1"I91+5 #@8GMO@I1 .5@B+OM8
-patient with predisposition for aspiration
-89O), dysphagia, altered M., sei<ure in history
-poor dentition, peridontal disease
-(X+ shows air fluid le!els (pus : abscess)
-,ung 1bscess due to necrosis
-caused by 91@I.#
-93, 1naerboes, @ocardia, Ilebsiella, .taph, #seudomonas)
-most common in alcoholics with putrid smelling sputum
-may present as subacute illness with few wee0s of weight loss, anemia, etc-
-94 : anaerobic co!erage (metronida<ole) for $-% wee0s
-(omplication is spread to pleura empyema and re6uires surgical drainage
O##O+9G@I.9I( #@8GMO@I1
-@eutropenia .1, 1erobic F(-) bacteria, (andida, Mucor, 1spergillus (in!asi!e)
-)umoral immunodeficiency MM, (,,, splenectomy, )I" (encapsulated etiology)
-(ellular-Mediated Immunodeficiency )I" pneumocystis, !iral , fungal, mycobacterial
9G38+(G,O.I.
-1*3, spread by inhalation of infected droplets
-;N d/t primary infection lower lobes
-R;N d/t secondary infection upper lobes (reacti!ation)
-may also in!ol!e 0idney, long bones, !ertebral column, lymph nodes, meninges
-pulmonary reacti!ation characteri<ed by infiltrates, ca!ities, and caseating necrosis
-#+IM1+5 mid to lower lobes with unilateral hilar adenopathy
-B4 : tissue biopsy and culture (ta0es se!eral wee0s)
-#,8G+I.5 with 8**G.IO@ e4udate
-=;N are 1*3 E
-?MN are positi!e culture (ta0es se!eral wee0s)
-best yield is by pleural biopsy or with adenosine deaminase le!el in fluid
-.8(O@B1+5 months to years after primary
-upper lobes and other organs
-physical e4am is !ariable
-may get pulmonary infiltrates in all lung fields
-IMMG@O(OM#+OMI.8B #19I8@9. ()I")
-fre6uently atypical presentation li0e Cust wasting
-multiresistant organisms d/t to low compliance with drugs
-must consider 93 in the differential of all infiltrates in )I"E patients along with #(#
-B4 : ##BE measuring the induration (must also do control study)
: sputum 1*# stains (only specific not sensiti!e)
: ( E . (ta0es wee0s)
-94 : I@) E +ip for R months
: I@) E +ip E #Q1 for > months I@) E +ip for ? months
: if drug resistant add ethambutol
-1*3 and cultures should be negati!e after 2 months
-#rophyla4is (I@) for $-=> months)
-+8F1+B,8.. O* 1F8 with PPDD and
-close contacts
-newly con!erted
-abnormal (X+ who ha!ent recei!ed prior therapy
-G@B8+ 2; with PPDD and (if e!erything else normal including normal (X+)
-O"8+ 2; with PPDD and
-BM, 3 cell malignancy, 8.+B, chronic steroids, )I"E silicosis
-Brug resistance
-must ha!e patient on at least two non-resistant drugs
-most are resistant to streptomycin and I@)
-usually ac6uired with poor compliance and use of a single drug
-Brug 9o4icity
-+ifampin : interferes with O(#, theophylline, and anti )I" drugs (low le!els)
-I)@ : hepatitis and raises dilantin le!els
-#Q1 7 hyperuricemia
-8thambutol 7 optic neuritis
O((G#19IO@1, ,G@F BI.81.8.
Silicosis As(estosis
Mining, sandblasting, 6uarrying and tunneling #rogressi!e pulmonary fibrosis with dyspnea, pleuritic chest pain
Obstructi!e and +estricti!e Impairments (X+ pleural pla6ues, thic0ening and ha<y infiltrates
(X+ symmetric rounded opacities in u$$er lung +estricti!e pattern on the #*9s *erruginous bodies
Ahorls or collagen and polari<ed light -ronchogenic Carcinoma more than Mesothelioma
MI.(8,,1@8OG. I@98+.9I9I1, 1@B 1,"8O,1+-*I,,I@F ,G@F BI.81.8.
Foodpastures syndrome
-diffuse al!eolar hemorrhage and glomerulonephritis
-Ig deposition along al!eoli and F3M (anti-F3M)
-symptoms of hemoptysis, cough, dyspnea, hematuria, renal insufficiency
-(X+ bilateral, symmetric, al!eolar-filling infiltrates
-94 : steroids and cyclophosphamide
: cytoto4ic drugs washout globulin
: plasmapheresis
#I8 syndromes
-pulmonary infiltrates of eosinophils (much) and peripheral eosinophilia
-(X+ photographic negati!e of pulmonary edema (fluffy infiltrate peripherally)
-94 : prompt response to steroids (prednisone)
1l!eolar proteinosis
-al!eolar filling with an acellular, lipoproteinaceous surfactant li0e material
-symptoms of dyspnea, producti!e cough, fe!er, weight loss
-B4 : (X+ shows perihilar distribution of al!eolar infiltrates
: 31, is diagnostic with tremendous amounts of fluids
-94 : whole lung la!age under general anesthesia
+adiation induced lung disease
-pneumonitis with T2,;MM rads
-symptoms occur $-=> wee0s after completion of radio therapy (for any cause)
-fibrosis can occur years after completion of radio therapy
-(X+ 7 infiltrates limited to radiation port
-94 : steroids can by used to pneumonitis but not for fibrosis
B+GF I@BG(8B ,G@F BI.81.8
-(ancer chemotherapy methotre4ate and belomycin (fibrosis)
-(ardiac Meds 1minodarone (pneumonitis with bilateral interstitial or al!eolar pattern)
beta bloc0ers (bronchoconstriction)
1(8 inhibitors non producti!e cough
hydrala<ine, procainamide, 6uinidine (pleurisy from lupus)
-1nti-inflammatory aspirin (bronchospasm, nasal polyps, rhinitis)
gold and penicillamine (hypersensiti!ity pneumonitis)
steroids (increased ris0 of infection) dont gi!e if 93 suspected
-Illicit Brugs o!erdose of heroine (noncardiogenic pulmonary edema)
talc (cut with drugs causes interstitial lung disease li0e asbestos)
septic emboli from right sided endocarditis (tricuspid !al!e most common)
.1+(OIBO.I.
-multisystem with noncaseating granulomas in affected organs
-pulmonary in!ol!ement in TRMN of sarcoid patients
-.tage M : normal
-.tage = : hilar lymphadenopathy
-.tage > : hilar lymphadenopathy and parenchymal infiltrates
-.tage 2 : NO hilar lymphadenopathy and parenchymal infiltrates
-.tage ? : ad!anced fibrosis and bullae
-no hilar in!ol!ement is badS
-e4trapulmonary features
-lymphadenopathy (hepatosplenomegaly)
-s0in
-erythema nodosum (li0e in (rohns Bisease)
-lupus pernio (blue-purple lesion of the face and fingers)
-eye
-u!eitis
-.Cogrens syndrome (no lacrimation)
-ner!ous system
-3ells #alsy
-Myocardium (conduction disturbances causing bradycardia)
-)ypercalcemia d/t !it B production
-nephrocalcinosis
-nephrolithiasis
-B4 : (X+ : perihilar calcified nodules
: noncaseating granulomas (histologically must see before steroids)
: negati!e fungal and tissue studies (must +/O infections)
: ##B-li0e test for sarcoid : I!im test
-94 : steroids for se!ere lung in!ol!ement
: steroids for e4trapulmonary in!ol!ement
-ocular disease (u!eitis), hypercalcemia, cardiac arrhythmia, neurological (in
addition to 3ells #alsy), arthritis, disfiguring s0in lesions
F+1@G,OM19OG. "1.(G,I9I.
Aegeners granulomatosis
-necroti<ing granulomatous !asculitis of upper and lower respiratory tract and glomeruli
-G+I nasal and sinus symptoms
-,ungs cough hemoptysis, dyspnea
-(X+ multiple, nodular, infiltrates
-,13. ele!ated anti (-1@(1 (cytoplasmic anti-neutrophilic cytoplasm antibodies)
-p stands for perinuclear
-94 : steroids and cyclophosphamide
(hurg-.trauss syndrome (#I8)
-allergic angiitis and granulomatosis
-asthma, allergic rhinitis
-associated with the use of .ingular
-eosinophillic !asculitis (s0in lesions, peripheral neuropathy, (@. !asculitis)
-myocardial and pericardial disease
-,13 peripheral eosinophilia (#I8 syndrome)
high 8.+ (!asculitis)
high Ig8
-(X+ : fleeting pulmonary infiltrates
-94 : steroids and other immunosuppressants
BI.81.8. O* 9)8 #,8G+1
-fluid can accumulate between the spaces of the wall
-fluid pleural effusion
-infected fluid empyema
-air pneumothora4
-blood hemothora4 (if T;MN of )ct of the blood)
-pleural effusions
-low breath sounds, dullness, low tactile fremitus, friction rub
-pleuritic chest pain, dyspnea, cough
-(X+ blunting of the costophrenic angle (need 2MM cc)
free flowing fluid seen in lateral decubitus position (if not loculated)
need G. or (9 if the fluid is loculated (poc0et)
-9horacentesis
-cell count and diff
-chemistries (,B) E protein E glucose E amylase E p)) 7 e4udate !s- transudate
-(4 : bacteria, 93, fungi
-stains 7 gram, 1*3, and fungal
-cytology need a lot of fluid
-8XGB198.
-must ha!e at least one factor
-=) fluid protein is T;MN of serum
->) fluid ,B) T$MN of serum
-2) fluid ,B) is T >/2 of upper limit of normal
-pulmonary embolism more than =MM,MMM +3(s
-93
-more than =MM,MMM +3(s
-glucose & $M and protein is T ;
-p) & '-M
-hemothora4 more than =MM,MMM +3(s
-parapneumonic effusion (fluid ne4t to pneumonia)
-glucose & $M
-p) & '-M
-malignancy
-glucose & $M
-positi!e cytology in ?M-RMN of patients
-lung, breast, stomach, lymphoma, mesothelioma
-94 : may re6uire sclerosis (pleurodesis) to close up pleural space by fibrosis
-rheumatoid arthritis
-glucose & 2M (for non infectious reasons)
-+* (IgM)
-.,8 1@1
-pancreatitis high amylase
-esophageal rupture (3ore-)aa!e)
-high amylase
-p) & '-M
-empyema
-fran0 pus in the pleural space (.4 needed to drain !ia chest tube)
-also consider chest tube (complicated effusion) if
-p) & '-M, glucose & ;M or organisms are seen in stain
-(hest 9ube is recommended
-9+1@.GB198.
-either reduced oncotic pressure or increased hydrostatic pressure
-()*, cirrhosis, nephrosis, my4edema or hypothyroidism (low I and slow flow)
-chec0 a 9.) le!el
-#@8GMO9)O+1X
-air in the pleural space
-sudden dyspnea and pleuritic chest pain
-diminished breath sounds and tympani to percussion
-(X+ hyperinflation seen best when in e4piration
-spontaneous pneumothora4
-iatrogenic in chest tube, central line, li!er biopsy, and barotrauma
-idiopathic is usually seen in tall thin males
-also occur in (O#B, asthma, and bullous emphysema
-tension pneumothora4
-can ha!e cardiac arrest while still ha!ing a good 8IF good (8MB)
-air trapped in pleura and compress intrathoracic structures (heart, !essels)
-loss of breath sounds on affected side with tracheal shift
-94 : chest tube placement
-small asymptomatic pneumothora4 can be treated conser!ati!ely
-*IO>N and */G (X+
#G,MO@1+5 9)+OM3O83O,I.M (#8)
-blood clot lodged within the pulmonary circulation
-most originate from deep !enous thromboses (B"9) from legs or pel!is (>MN - cal!es)
-=MN may be fatal
-pul resistance rises, high pulmonary artery pressure, and increased +" afterload
-ris0 factors
-immobili<ation, pel!ic/leg surgery, pancreatic cancer (9rousseaus syndrome)
-obesity, ()* (!ascular stasis), O(#, hypercoagulable conditions
-dyspnea, pleuritic chest pain, hemoptysis (pleural infarct), +" afterload, loud #>, +" hea!e
-loo0 signs of B"9 (if positi!e then probably #8)
-;MN of patients will ha!e no signs suggesti!e of #8
-B4 : history and physical
: (X+ is usually normal but can show regional oligemia, opacity (infarct), or effusion
: 8IF shows .=K292 (s wa!e in lead I, K wa!e in lead III, and in!erted 9 in lead III)
: 13F =
st
respiratory al0alosis and hypocapnia
-can ha!e !arying hypo4emia
-increased 1a gradient
: "/K scanJ if high probability see segmental perfusion defect with normal !entilation
-if pneumonia usually Cust a !entilation problem and not a perfusion one
-the uni6ue thing about #8 is that only the flow is upset
: pulmonary angiography is the gold standard
-used when the "/K scan is not high probability or indeterminate
: !enogram or non-in!asi!e testing for lower e4tremity B"9
-used when contraindication to pulmonary angiography
: (9 #ulmonary 1ngiogram will show if there is a clot- If it is negati!e, can safely
withhold anticoagulation
B88# "8I@ 9)OM3O.I. (B"9)
-leg pain, tenderness, warmth, redness, palpable cord (!ein)
-)omans sign pain in calf with dorsifle4ion of the foot
-physical e4am is !ery insensiti!e and should not relied upon
-B4 : !enogram is the gold standard (but too in!asi!e)
: duple4 sonography is most used but only ;MN sens in the cal!es
: impedance plethysmography (I#F) but only ;MN sens in the cal!es
:
=>;
I-fibrinogen is the best for calf-!ein thrombosis (use with I#F)
-94 : I" heparin for ; days with >-2 o!erlap with warfarin for 2-$ months
-longer duration if other complications such as recurrent emboli or
-lupus, protein (E. deficiency or pancreatic cancer
: inferior !ena ca!a interruption if anticoagulation contraindicated or #8 while 94
-greenfield filter is one used
)5#8+(O1FG,13,8 .9198.
-usually ha!e strong family history, recurrent thromboembolism, early age, unusual sites
-upper arms and a4illa is not a usual place to ha!e clots
-usually ha!e difficulty anticoagulating
-19-III deficiency is the most common inherited defect
-re6uires life-long anticoagulation if thrombosis occurs
-#rotein ( and . deficiency
-,upus anticoagulant (high #99) - antiphospholipid antibody (miscarriages in >
nd
trimester)
-malignancy (9rousseaus syndrome in pancreatic cancer)
-BI( (M1)1)
-myeloproliferati!e syndromes li0e polycythemia !era (too many +3(s)
1@9I(O1FG,19IO@
-heparin
-enhances 19-III acti!ity, follow with #99, .K or I", antidote : protamine sulfate
-thrombocytopenia is an important side effect
-Aarfarin (coumadin)
-inhibit >,',R,=M, ( E . and follow with #9 (I@+)
-s0in necrosis is a complication
-beware of drug interactions
-6uic0 antidote is **#
-longer acting antidote is !it I
-9hrombolytic therapy
-stimulates fibrinolysis, has high bleeding ris0
-use only with life-threatening #8 (not ordinary)
@O@-9)+OM3O9I( #G,MO@1+5 8M3O,I
-septic right sided endocarditis in I" drug users and infected catheters
-malignant emboli of tumor cells (seeding)
-fat after long bone fractures and usually seen in the white matter
-petechiae and confusion
-amniotic fluid during childbirth or early post-partum
-the fluid is obstructi!e and thromboplastic
1##+O1() 9O 9)8 #19I8@9 AI9) )8MO#95.I.
-must e4clude bronchitis and FI bleeding (most common)
-(X+ findings
-93 apical ca!ity
-cancer central mass
-pneumonia consolidation and increased contrast
-Food pastures syndrome diffuse al!eolar filling
-bronchiectasis bullae tram trac0s
-pulmonary embolism pleural infarct
-94 : patient may die from asphy4iation and therefore must protect airway
: position bleeding side down
: use rigid bronchoscopy as it allow better suction
: angiography may locate site of bleeding
: codeine to limit the amount of cough and trauma
,G@F (1@(8+
-leading cause of cancer deaths in both men and women
-o!erall ; year sur!i!al is less than =M years
-first and second hand smo0e has been shown to gi!e increased ris0
-asbestos e4posure and synergistic with tobacco as lung cancer ris0 (multiplicati!e)
-cough, hemoptysis, chest pain, weight loss, anore4ia, fe!er
-bronchial obstruction post-obstructi!e pneumonia
-compression of the ."( ele!ated !enous pressure in nec0, arms and face
-malignant pericardial effusion cardiac tamponade
-esophageal compression dysphagia
-recurrent laryngeal ner!e damage hoarseness
-)orners syndrome (miosis, ptosis, anhidrosis)
-#ancoast tumor damage to brachial ple4us wea0ness and parathesia in ulnar arm
-seen with apical tumors
-two types of cancer
Non,small cell Small Cell %oat cell& %small (lue cell&
I@ F8@8+1,J
-only hope is for .4 e4cision
-for non .4 need palliation (radio therapy)
-@O .G+"I"1, 38@8*I9 AI9) ()8MO
.6uamous
-slow growing and may achie!e a large si<e
->/2 are hilarH =/2 are peripheral
-#9)rp secretion
-usually hilar or perihilar
-early mets to the bone, li!er, and brain
-secretes 1B), and 1(9)
)9@, hyper0alemia, hyperglycemia, pro4imal wea0ness
)igh 1M cortisol which does not suppress with de4amethasone
-8aton-,ambert syndrome (antibodies against (a
EE
channel)
muscles increase in strength after use from wea0ness
decreased B9+ and autonomic dysfunction
hypercalcemia (or from bone mets) -.taging
without chemo : 2 month sur!i!al 9)8+8 I. 1 .G+"I"1, 38@8*I9
with chemo : =% month sur!i!al but o!erall is &;N for ; year
1denocarcinoma
-peripheral nodules
-occurs in non smo0ers
-may arise as a scar carcinoma
,arge cell
-peripheral masses
-may ca!itate
-all type of cancer show hypertrophic pulmonary osteoarthropathy
-clubbing, polyarthritis, and periosits (shunting)
-B4 : bronchoscopy or needle-biopsy (can use sputum cytology but not as reliable)
1##+O1() 9O 9)8 #19I8@9 AI9) .O,I91+5 #G,MO@1+5 @OBG,8
-single nodule in the lung parenchyma & $-M cm
-must determine whether or not malignant
38@IF@ M1,IF@1@9
-younger
-no growth in > years (with old (X+)
-small si<e (&= cm)
-pattern of (a
EE
dense central, multiple punctate, laminated pattern
popcorn suggests hamartoma
-smooth margins
-older
-smo0ing history
-large si<e (T2 cm)
-pattern of (a
EE
eccentric calcification
-irregular margins
-wor0 up
-(9 can assess for e!erything abo!e as well as chec0 for masses in mediastinum
-bronchoscopy only if the mass is central in location
-percutanious needle biopsy used in granulomas or hamartomas
-cannot be used to +/O a malignant diagnosis
-mini-thoracotomy 7 can +/O (1 7 but usually finds other places where (1 is
+8.#I+19O+5 9)8+1#5 98()@IKG8.
-supplemental O>
-for patients with pO> & ;; mm)g on room air at rest
-dont suppress hypo4ic dri!e (only to RMN sat and $M mm)g)
-high concentrations of O> cause O> to4icity and parenchymal damage
-mechanical !entilationJ indications
-apnea or inade6uate al!eolar !entilation
-se!ere hypo4emia despite O> supplementation (large 1-a gradient)
-airway protection (from a tumor in the laryn4)
1BG,9 +8.#I+19O+5 BI.9+8.. .5@B+OM8 (1+B.)
-non cardiogenic pulmonary edema (damage to membranes) stiff lungs
-se!ere hypo4emia (pO> less than $M mm)g on *IO> T $M) (large 1-a gradient)
-(X+ shows bilateral pulmonary infiltrates
-normal or low pulmonary artery pressure (not due to flow bac0 OcardiogenicP)
-mortality is ;MN and usually due to MO* (multiorgan failure)
-causes
-sepsis syndrome, o!erwhelming pneumonia, BI(, maCor trauma, multiple
transfusions, pancreatitis (phospholipase damaging al!eoli), drowning
-94 : treat underlying cause
: O> (but if theres intrapulmonic shunting this will limit effecti!eness)
: #88# increases lung !olumes and allows lower *IO>
: ris0 is low cardiac output (due to compression) and barotrauma (pneumothora4)
:the only thing that has shown benefit is low tidal !olumes ($ml/0g)
M'SC'LOS*ELETAL E CONNECTI!E T'SSIE DISORDERS
O.98O1+9)+I9I.
-wear and tear arthritis (degenerati!e Coint disease)
-represents deterioration of articular cartilage and underlying bone
-pain that worsens with acti!ity and is relie!ed with rest
-morning stiffness (shorter) and less than +heumatoid 1rthritis (which is =-> hours)
-tenderness may be present in in!ol!ed Coints, with erythema and flare-ups
-howe!er they are usually cool (not inflammatory and not hot)
-pain with motion in the larger Coints and crepitus
-Coint enlargement and deformity occur
-)eberdens nodes (BI#)
-3ouchards nodes (#I#)
-B4
-no 8.+, low A3(, no crystals
-X-rays show space narrowing, osteophytes, increased bone density
-94
-weight loss and Coint rest, Coint supports, e4ercise, application of heating pads or ice
-drugsJ @.1IB. and aspirin
-causes FI bleeding, renal, and confusion (morbidity)
-pretreat with misoprostol (#F8>)
steroids are not to be used in osteoarthritis
intra-articular steroids may be of temporary !alue in a flare-up
repeated inCection should be a!oided
-.4 : may be necessary to restore function and reduce pain
: allows a total Coint replacement of the 0nee or hip
FOG9
-RMN of high uric acid can ha!e no gout
-high gout causes urate deposition in articular as well as e4tra-articular areas
-only =MN of hyperuricemic patients de!elop gout
-gout has serum urate le!el greater than ' mg/dl
-O"8+#+OBG(8+. O* G+I( 1(IB (=MN)
-e4crete more than ';M mg uric acid per day
-primary o!erproduction (purine pathway en<ymatic disorders)
-secondary o!erproduction (increased cell-turn o!er)
-malignancies, chemotherapy, chronic hemolysis, alcohol use (saturnine)
-anything that has large cells being 0illed
-must pretreat w/ allopurinol
-G@B8+8X(+898+. O* G+I( 1(IB (RMN)
-e4crete less than 'MMM mg of uric acid per day
-most common cause is drugs
-diuretics, alcohol, low-dose aspirin
-also due to renal insufficiency
-1(G98 FOG95 1991(I
-middle-aged or elderly men
-typical attac0 is of a monoarticular lower e4tremity arthritis
-most common podagra (sudden painful swelling of the first M9# Coint)
-may e4tend into the soft tissues
-attac0 usually subsides within se!eral days
-prolonged hyperuricema predisposes to the de!elopment of microtophi
-small crystal aggregates in cartilage and syno!ial membrane
-microtophi release crystals into the Coint space
-the urate crystals trigger the inflammatory cascade and cause the crystals to be
ingested by neutrophils
-neutrophils are damaged and release en<ymes into the syno!ial fluid producing
additional inflammation
-B4 : serum uric acid may be normal during an acute attac0
: urate crystals in syno!ial fluid
: needle shaped and negati!ely birefringent in polari<ed light
: syno!ial fluid A3( is ele!ated but not septic
-94 : @.1IB. in high doses and then tapered (unless FI bleeder)
: (olchicine usually I" (#O associated with @ and ")
: intraarticular corticosteroid inCections (not in acute)
: a!oid drugs that affect uric acid le!els since it may prolong attac0 -allopurinol
and niacin and )(9Q
-()+O@I( 9O#)1(8OG. FOG9
-tophus : urate crystal mass en!eloped by inflammatory cells and fibrosis
-pinnae of the ear, e4tensor surfaces of arms, 1chilles tendon and olecranon bursa
-ta0e years to de!elop and may cause erosion of cartilage and subchondral bone
-crystals can be aspirated from the tophi
-B4 : mobile, firm, yellow or cream-colored and can s6uee<e chal0 out of it
: appear on X-ray as punched out erosions of the subchondral bone
-remember #3-I9, (I9, are lytic as well as 3)
: crystals can be aspirated from the tophi
-94 : control hyperuricemia
: if undere4creter (RMN) probenicid (ma0e sure no renal stones)
: if o!er producer (=MN) allopurinol (wor0s with 0idney problems)
-urate crystals are =MN of 0idney stones and are radiolucent
: can also use colchicine (inhibits #M@ chemota4is)
#.8GBOFOG9
-calcium pyrophosphate dihydrate deposition disease ((##B)
-)yperparathyroidism >
nd
to hyperphosphatemia
-)emochromotosis
-)ypothyroidism
-Onchronosis
-Ailsons Bisease
-hits the 0nee swelling, pain, and stiffness
-can ha!e pseudorheumatoid arthritis (minority)
-most ha!e pseudoosteoid arthritis (;MN)
-B4 : wea0ly positi!e birefringent rhomboid crystals in polari<ed light
: ele!ated A3( but less so than in gout
: X-ray chondrocalcinosis of articular cartilage or osteoarthritic changes
-94 : @.1IB.
: inCection of intra-articular steroids
: fre6uency of attac0s reduced by colchicine (inhibits #M@s)
+)8GM19OIB 1+9)+I9I. (+1)
-polyarticular symmetrical arthritis and e4tra-articular manifestations occur
-+* present (IgM) 7 polyclonal
-if seropositi!e : more se!ere disease with more e4tra-articular features
-symmetrical Coint in!ol!ement with sparing of the of the BI# Coints
-most common Coint are #I#, M(#, and wrist Coints
-tendons and ligaments may be inflamed causing carpal tunnel syndrome
-also causing rotator cuff tendinitis, and ligament in!ol!ement at the atlantoa4ial Coint
-8X9+1-1+9I(G,1+ M1@I*8.919IO@.
-found in seropositi!e disease
-rheumatoid nodules (most common) found in areas of trauma
-ocular in!ol!ement
-.Cogrens syndrome, scleritis, episcleritis (dep e4tra-intestinal man- in (G()
-s0in nodules, pericarditis
-pleural effusions (with !ery low glucose O&2MP), interstitial fibrosis and lung nodules
-restricti!e disease (*8"/*"( is normal or increased)
-anemia of chronic disease (low 9I3( and low *e) 7 normocytic or microcytic
-*eltys syndrome : +1 E splenomegaly and neutropenia
-amyloidosis nephrotic syndrome hypercholestermia
-!asculitis in!ol!ing the s0in and ner!es
-history
-chronic inflammatory polyarthritis
-prolonged morning stiffness (se!eral hours 7 6uantitated)
-weight loss, anore4ia, and malaise
-pain in the in!ol!ed Coints typically worse in the morning
-physical e4amination
-sparing of the BI# and in!ol!ement of the wrists, M(# and #I#
-rheumatoid nodules o!er the e4tensor surfaces especially near the olecranon
-laboratory features
-anemia of chronic disease, leu0ocytosis, thrombocytosis (poormans 8.+)
-rheumatoid factor in appro4imately $M-%MN of patients
-syno!ial fluid with A3( of ;,MMM->M,MMM (if =;M,MMM thin0 infection)
-X-ray
-soft tissue swelling
-osteopenia around in!ol!ed Coints
-erosions and Coint space narrowing is a !ery common feature
-94 : rest of the Coint and e4ercise of the muscles around the Coint
: #9 and O9
: @.1IB. for inflammation and pain (but renal, FI, and mental problems)
: corticosteroids (systemically or intra-articular)
: second-line agents ha!e no analgesic effect and may re6uire wee0s
-methotre4ate watch out for dose related hepatic fibrosis
-hypersensiti!ity pneumonitis
-chloro6uine antimalarial (optic disturbance)
-B-penicillamine 7 also effecti!e in Ailsons Bisease
-side effects of lupus li0e, nephrotic syndrome, rashes
-Fold renal problems, diarrhea, and colitis
-BM1+B. 7 +emicade (newest therapy) - e4pensi!e
-e!aluating the response to therapy
-reduction in constitutional symptoms, morning stiffness, U of Coints, .+,
-chronic disease anemia, and reduction of thrombocytosis
-.4 : total hip replacements may be necessary to relie!e pain or restore function in
se!erely damaged Coints
: syno!ectomy may be necessary to decrease the inflammatory response in areas
that are refractory to drug treatment
.#O@B5,O1+9)+O#19)I8. (peripheral and a4ial Coints)
-sacroiliitis (Coint) and spondylitis (spine) 7 I@B8#8@B8@9 O* 1(9I"8 3OA8, BI.81.8
-),1-3>' associated
-peripheral arthritis
-inflammatory changes of tendon and fascial insertions enthesopathy (seen in +1 also)
-anterior u!eitis (+1 has episcleritis)
-usual onset in young adult males
-associated with human adult males
1n0ylosing .pondylitis +eiters .yndrome #soriatic 1rthritis 8nteropathic 1rthritis
-not related to bowl disease
in (G(
also #.( and u!eitis
-chronic low bac0 pain
-stiffness in sacroiliac area
-low spinal mobility
-no peripheral in!ol!ement
e4cept for shoulder E hip
-wal0s stiffly (bamboo)
>-? wee0s after diarrheal
illness or !enereal e4p
-mucopurulent urethral dis-
-conCuncti!itis
-acute arthritis (0neesEfeet)
-enthesopathy of 1chilles
se!ere heel pain
-incomplete presentation
-self-limited disease
38)(898. BI.81.8
-genital ulcers
-oral ulcers
-eye findings and arthritis
-BI# Coint in!ol!ement
-psoriatic changes present
-nail pitting
-slowly progressi!e
can be destructi!e
#eripheral symmetric arth-
-dependent on bowel dis-
I@*8(9IOG. 1+9)+I9I.
3acterial 1rthritis ,ymes Bisease
Causes %(ut you don#t need a (ad Foint&
-pre!ious Coint damage, I" drug abuse
-repeated septicemia, prosthetic Coints (.taph)
-immunosuppression from chemotherapy
-sic0le cell disease encapsulated
-bacteremia .trep #
Inectious agents %/neeG .ristG an/les&
-Fonococcus 7 most common in se4ually acti!e
-@on-gonococcal organisms
.1 or .8 in I" drug users and prosthetic Coints
F13).
F(-) enteric organisms in elderly or immunocompromised
8-coli seen in urosepsis
-bacteria !ia blood stream and direct inoculation
Multisystemic illness
-s0in, Coints, neurological, cardiac system
E$idemiology
-maCor !ector is the spirochete -orrelia bur$dorferi
-transmitted by the l4odes deer tic0
-only =/2 0now that they ha!e been bitten
Stage 7
-tic0 bite 2 days 7 2 wee0s of---
-erythema migrans in >/2 and ,1B
Stage =
-cardiac conduction and myocarditis
-headache, fatigue, 3ells #alsy, radiculopathies
Stage 8
-1rthritis in the 0nee (asymmetric)
+onococcal arthritis
-periarthritis7dermatitis syndrome
migratory polyarthralgias w/ fe!er, tenosyno!itisEdermatitis
this is the part that co!ers the tendon
s0in changes are maculopapular or !esicular and gradually
become !esiculopustular
-get acute mono- or oligoarthritis w/ purulent Coint effusions
-se4ually-acti!e adult w/ arthritis w/o crystals : gono arthritis
-cultures should be ta0en from pharyn4, urethrea, rectum
Diagnosis
-fluid get Fram stain, ( E ., A3( and diff w/ T;M,MMM
-A3( T ;M,MMMH RMN are #M@s
Treatment
-treat all unless no se4ual contact or crystals
-ceftria4one I" and then after cefuro4ime #O
-.taph treated by nafcillin I"H .trep treated by penicillin (I")
-enterococcal arthritis treated with ampicillin and gentamicin
-daily drainage, open .4 drainage if hip Coint or atheroscopic
-(@.J fatigue, tremor, chronic, encephalomyelitis, ata4ia
-depression
Diagnosis
-difficult to isolate the -orrelia bur$dorferi
-use serological testing (IgM in .tage >)
T9
-8arly Bisease amo4icillin, do4ycycline, erythromycin
-(@. ceftria4one or high dose penicillin I"
.5.98MI( ,G#G. 8+59)8M19O.G. (.,8)
-chronic immune disorder
-circulating immune comple4 and antibodies lead to tissue damage and dysfunction
-blac0 female
-low (2 and (? le!els
Bermatological
-butterfly, malar rash
-discoid lesions (coin)
-mucous membrane
ulceration (oralEgenital)
as seen in 3echets
-alopecia (not areata)
-digital !asculitis
-photosensiti!ity
-+aynauds phenomenon
-.Cogrens syndrome
@er!ous system
(@.
-depression, psychosis
-cogniti!e abnormality
-sei<ures (by steroids too)
-94 : w/ steroids
#@.
-neuropathies
-mononeuritis multiple4
loss of .EM in a ner!e
#ulmonary
-=/2 ha!e pleuritis
-restricti!e changes
-pul )9@ from pul !ascul-
+" hea!e E #>
(ardiac
-pericarditis E effusions
-myocarditis
arrhythmiasEconduction
-no ()*
-coronary artery !asculitis
seen in women with (1B
-premature ath-- w/ steroid
-,ibman .ac0s
from phospholipid 1ntib
causes emboli etc----
+enal
-!ery common
-+3(, A3( or casts
shows glomerulonephritis
-high 3G@ and creatinine
-anti dsB@1 and low (
-glomerulonephritis
common mesangial
worst diffuse proliferati!e
94 : steroids
FI
-@/" and abdominal pain
-mesenteric ischemia
infarction and perforation
-pancreatitis from B< or 94
-gastritis from @.1IB
Musculos0eletal
-arthralgias
-symmetric arthritis
-tendon la4ity
-erosi!e Coint disease
-muscle wea0ness (pro4)
)ematological
-anemia d/t chronic d<
-hemolytic anemia
-low #M@. (*eltys)
-I9# and high 8.+
-lupus anticoagulant
second trimester abort
.erological
-false E "B+,
-*91-13. can be used
but this type is always E
Immunological
-low (2 and (?
also in post-strep glom-
-hyper 3-cell
high Ig
-1@1, anti dsB@1, .m
-anti-histone
procainamide, 6unidine
hydral<ine, penicillamine
-anti +o and ,a
photosensiti!ity
Malar rash
Discoid rash
Serositis 7 pleuritis or pericarditis
Oral ulcers
Arthritis (nonerosi!e)
Photosensiti!ity
Neurological disorder (sei<ures or psychosis)
"ematologic disorder 7 hemolytic anemia, leu0openia, lymphopenia, or thrombocytopenia
Antinuclear antibody
Immunological disorder (positi!e ,8), anti B@1, anti .m, false E "B+,
Renal disorder 7 persistent proteinuria or the presence of cellular casts
94
-sunscreen for photosensiti!ity
-@.1IB. for serositis, Coint complaints, fe!er
-problems in the 0idneys, M. and FI bleeding
-antimalarial drugs for arthritis and s0in findings
-chloro6uine or hydro4ychloro6uine
-.teroids
-topical preparations for s0in abnormalities
-systemic steroids for arthritis, serositis, se!ere hemolysis, thrombocytompenia,
pneumonitis, (@. or peripheral ner!ous system inflammation, cardiac or s0eletal
muscle in!ol!ement, renal disease, !asculitis
-se!ere lupus in!ol!ement is often treated with pulse steroids in!ol!ing I" doses
-pulse steroids for patients with se!ere renal (@., cardiopulmonary or blood abnormalities
-cytoto4ic therapy
-a<athioprine and cyclophosphamide are used to treat se!ere cases
-especially in renal disease
-also used in patients refractory to steroids
.(,8+OB8+M1 (anti .(,-'M 1ntibody)
-connecti!e tissue disease characteri<ed by fibrosis of the s0in and multiple organs
-Multisystemic in!ol!ement
-heart, lung, 0idneys, FI tract
.0in FI ,ung (ardiac Iidney
-all patients
-begins with hands
-+aynauds in all
whitebluered
-9elangiectasias
-s0in ulcers
(infarctions)
-hypomotility
-,8. impaired
-se!ere reflu4
-gastroparesis
early satiety
-too much bacteria
malabsorption
low !itamin le!els
94 : ciproflo4icin
#ul fibrosis and )9@
-produces I,B
-progressi!e BO8
-restricti!e lung
-94 : transplant
-interstitial
myocardial disease
-(1B from fibrosis
females
-arrhythmias in fibrose
heart bloc0
(risis occur in
uncontrolled )9@
94 : 1(8 inhibitors
.een with M1)1
-shistocytes
-+3( damage in !es-
May get (+*
(+8.9 syndrome (anti centromere 1ntibody)
-milder form of disease
Biffuse *orm
-more aggressi!e form the disease
-anti scl-'M antibodies and antinucleolar antibodies
9+819M8@9
-+aynauds (a
EE
channel bloc0ers
-8sophageal disease antireflu4 medication (##I)
-3acterial o!ergrowth broad-spectrum antibiotics
-+enal Bisease 1(8 inhibitors
,1+F8 "8..8, "1.(G,I9I.
9a0ayasus arteritis (*emale 1sians &?M years)
-granulomas of the aortic arch in young 1sians
-upper e4tremity claudication, angina, congesti!e heart failure from aortic in!ol!ement
-dissects bac0 to the aortic arch
-arterial bruits may be heard
-blood pressure differences may be elicited between the two arms
-94 : steroids
9emporal 1rteritis (Male (aucasians T;M years)
-patients o!er ;M
-;MN ha!e polymyalgia rheumatica (problems climbing stairs)
-pro4imal muscle wea0ness
-ele!ated 8.+
-symptoms from ischemia of !essels in the carotid artery region
-headache, !isual disturbance, and Caw claudication
-patients may ha!e tenderness o!er the temporal artery distribution
-B4 : biopsy
-94 : high dose steroids to pre!ent blindness
I@*,1MM19O+5 MG.(,8 BI.81.8
-polymyositis and dermatomyositis (s0in findings)
-inflammatory muscle disease and pro4imal muscle wea0ness
-ele!ated (#I and aldolase
-biopsy re!eals a myopathic dysfunction
-rash of dermatomyositis 7red patches, causes heliotrope rash, digital nodules
-associated with malignancy and seen in up to one-6uarter of patients-
-,G@F, 3+81.9, FI
O.98O#O+O.I.
-decrease in bone !olume increased ris0 of fractures
-normally declines after 2; years
-(a
EE
deficiency predisposes to inade6uate bone !olume
-bone loss is accelerated when estrogen le!els decline in women
-alcoholics are at increased ris0
-fractures and pain from prior fracture
-pain usually re!eals a diminished bone density
-need =/2 loss of bone before bone loss
-bone absorptiometry is a more sensiti!e method to assess bone density
-#O.9M8@O#1G.1, O.98O#O+O.I.
-affects women in the first =; years after menopause
-!ertebral fractures are most common
-usually trabeculae bone
-94 : estrogen but effects of
-endometrial cancer, uterine bleeding, fluid retention, )9@, gallbladder (stasis)
-good effects of high )B, and low ,B, and low (1B
-.8@I,8 O.98O#O+O.I.
-affects both men and women
-loss of both trabeculae and cortical bone
-fractures of the hip (cortical bone)
-fractures of the !ertebral column (trabecular bone)
-.8(O@B1+5 O.98O#O+O.I.
-steroid therapy
-malabsorption (low !it B)
-prolonged immobili<ation
-94 : in general
-(a
EE
inta0e should be at least =;MM/day
-(alcitonin inhibits osteoclast acti!ity and therefore reduces the rate of bone loss
-8tidronate also inhibits osteoclast acti!ity
FOOB ,G(IS

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