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Disease & Patho/Mech Clinical S/S Dx/ Tests/Labs Tx Notes

Def
Platelet or Petechiae For PLT fx: Other findings
Vessel Mucosal NEVER order in plt dysfx:
disorder: bleeding bleeding time test -Menorrhagia,
Bleeding from sf 1. PFA (plt fx hematuria
scratches analysis) -Bleeding
Epistaxis (MC from tooth
S/S) 2. Plt aggregation extraction
Easy bruising study sites
-GI &
intracranial
blding
Coagulatio Inherited defect: Deep 1. aPTT: Factor
n disorder: deficiency affecting hematomas Intrinsic pthwy + inhibitors:
single clotting Hemarthroses common pthwy (XII, 1. Ab (esp w/
factor Delayed XI, IX, VIII) FVIII)
bleeding 2. meds:
Acquired defects: 2. PT: heparin
affect multiple Coaguation Extrinsic pthwy 3. non-specific
coagulation factors; defect: (VII)/common Ab: lupus
due to decreased a) Lrg post- - INR: standardized anticoagulant
synthesis (ex-Vit K traumatic PT results (not clinically
defic) ecchymoses or significant)
or shortened half hematomas 3. Thrombin time:
life (ex- DIC) b) Prolonged - tests conversion of
(may see bleeding after fibrinogen to fibrin
prolonged PT & laceration or - do w/ elevated PTT
PTT) any surgical (rule out
prodceure dysfibrogenemia)
XLR: factors VIII & c) Bleeding into
IX GI & urinary 4. Mixing studies:
tracts -do w/ nml PT, abn
all others: d) PTT
autosomal & hemarthroses - distinguish betw
recessive, except e) factor deficiency &
vWF = AD retroperitoneal inhibitor
& deep muscle -PTT resolves w/ add
bleeding plasma = factor
deficiency; no
ex) pt who change = inhibitor
oozes blood for
days post
dental
procedure
Disease & Patho/Mech Clinical S/S Dx/ Tests/Labs Tx Notes
Def
Activated abn fV w/ (m) that recurrent nml: PTT w/ APC --> Coumadin MCC of
Protein C alters specific venous PTT should increase; for hereditary
Thrombophillia

Resistance cleavage site for thrombosis & In APCR: no preventio thrombophilia


(Factor V Protein C --> fV not thromboembolis increase in PTT n (5% of
Leiden) inactivated m when APC added caucaisans)
-DNA probe for Genetic
htz: 7x inc risk Leiden variant of fV counselin 60% of
thrombus, g hereditary TE:
htz + OCP: 35x, fV Leiden
hmo: 80x Compressi Prothrombin
Anti-ppl Ab on
auto IgG, IgM or IgA usually asympto PTT (artifact of lab Prevent polymor.Ab
Anti-ppl
syndrome vs. coag Ps that w/ anomalies in testing) stockings a/w
PE: (m) Protein
SLE = C,
(APS) bind ppl (beta2- lab data -paradoxcial b/c -LMWH S,
Anti-
GP1, prothrombin, would expect Antithrombin
1st, then Cardiolipin Ab
apoH) recurrent clotting deficiency shift to III
("lupus
venous & vs. tendency Coumadin anticoagulant)
sometimes arterial TE @ (INR ≥ 3) ; causes false
Thrombophillia

associated w/ SLE, young age: fetal Anti-Cardiolipin Ab positive


AI dz (RA), or meds loss w/ infarct levels -no OCPs syphillis test
Prothrombi G-->A (m) at 3'UTR placenta, PE,
(Pronestyl/procaina PC 2nd MCC of
n 20210A of prothrombin
mide) MI, stroke, low possibly: ANA, anti- hereditary
transition gene --> elevated plts ssDNA, Coombs thrombophilia
prothrombin levels, (2-3% of
increase venous population)
Methylene results
thrombiin moderate PT: nml PTT: nml decrease
tetrahydrof increase in homocyst
olate homocysteine eine w/
reductase levels, a/w both suppleme
(m): arterial & venous nt folate,
thrombus vitamins
Acute ITP: -homocysteine
Plt AutoAb (IgG) vs. Abrupt onset 1- PC:  B12 & B6
Self-
Immune inactivates
GpIIB-IIIa proteins
(TII HS 3 wks after a BT:  limited;
Thrombo- C&S
rxn) viral infection. PT & PTT: nml usu
cytopenic -target for phago at Present with resolves
sorders: Thrombocytopenia

Purpura spleen epistaxis, easy Meas anti-platelet spontaneo


bruising, Abs usly w/in 6
Most common petechiae (esp mos
cause at lower body) no need for BM bx
thrombocytopenia (but would show Glucocorti
in children 2-6 NO increased coids if
years of age lymphadenopat megakaryocytes) severe
hy or
splenomegaly
Plt Blding Disorders: Thrombocytopenia

Disease & Patho/Mech Clinical S/S Dx/ Tests/Labs Tx Notes


Def
Chronic ITP IgG antibodies Insidious onset PC:  Complications
directed against -Petechiae, esp BT:  Splenecto : intracranial
GpIIb-IIIa receptors at dependent PT & PTT: nml my (if &
at plts (type II HS) areas severe; subarachnoid
-may blend Plt Ab test: req 2-3 spleen = hemorrhages
Most common ->ecchymoses wks for result major site
cause of -Oft hx of easy of phago
thrombocytopenia bruising, BM: nml/inc removal)
in adults nosebleeds, megakaryocytes
blding gums (response to low plt
Most common in count)
women (3:1) 20-40 May present w/ -would NOT get BM
years of age melena, bx
hematuria,
Heparin menorrhagia
Type 1: (most)- due Type 1: see PB: lrg platelets in Type II: Complications
Induced to direct plt thrombocytopen PB = signs of inc plt Discontinu : possible limb
Thrombocytopenia

Thrombo- aggregating effect NO ia immediately destruction e therapy loss due to


cytopenia of heparin splenomegaly
after start tx; & switch clots at large
(HIT) or l.node
little clinical to non- arteries; PE
Type II: = AI enlargement
consequence heparin from DVT
Ab vs. heparin-PF4 anticoagul (serious!)
cmplx; binding Type II: see 5- ant
activat platelets --> 14 days after
thrombosis, even start tx;
w/ low plts
Disease & Patho/Mech Clinical S/S Dx/ Tests/Labs Tx Notes
Def
HIV One of MC
Associated hematologic
Thrombo- manifestations of
cytopenia HIV infxn
- due to both
decreased
Plt Blding Disorders: Thrombocytopenia

production &
increased b/d

CD4 & CXCR4 (R &


co-R) present on
megakaryocytes -
allows infxn w/ HIV
--> infected cells
undergo apoptosis
= dec plt
HUS production
Most often caused Primarily occurs Plasma
(Hemolytic by endothelial in kids exchange
Uremic B Cell dysfx
damage dueintoHIV: <10 years old
Syndrome) also may prod
Shiga-like toxin of (& elderly) (steroids)
autoAbs
O157:H7vs. plts =
serotype
 b/d
of E. coli A few days after
episode of
bloody diarrhea,
see:

Clinical Triad:
Thrombocytope
nia
MAHA
Renal failure
Disease & Patho/Mech Clinical S/S Dx/ Tests/Labs Tx Notes
Def
TTP Acquired or genetic Clinical pentad: PC  *Plasma Enhanced by
(Thromboti deficiency in vWF- Fever BT:  exchange other factors
Plt Blding Disorders: Thrombocytopenia

c Thrombo- metalloprotease Thrombocytope (removes that damage


cytopenic "ADAMS13" in endo nia PB: shistocytes & autoAbs & endothelial
Purpura) cells --> multimers Renal failure helmet cells provides cells (e.g.,
of vWF accum -> CNS deficits functional ticlopidine,
promote plt MAHA w/ ADAMS13) clopidogrel,
activation & schistocytes & cyclosporine,
aggregation helmet cells oral
contraceptive
Excess plt (+)ation Occurs in adult s;
-> plt derived females hypertension,
hyaline postpartum)
microaggregates in
microvasc Mortality rate:
10-20%
Microthrombi -->
MAHA + organ TTP/HUS:
dysfx, platelet
w/ consumption of consumption
Bernard- plts = to
AR; due thrombocytopen PC: decreased + hemolytic
B.S. = Binding
thrombocytopenia
Soulier Dz defective plt ia BT: increased anemia w/
Site issue
adhesion to giant plts PFA: abn (increased shistocytes
Platelet Bleeding disorderss: Abn Quality/Fxn

subendo matrix lifelong closure time) +


bleeding PAggTest: abn thrombocytop
Inherited defect in problem enia
protien GpIb(-IX
cmplx) = defective
Glanzmann plt
AR,plug formation
defective plt lifelong PC: nml G = Grouping,
's (and aggregation)
aggregation bleeding BT: increased Gathering
thrombasth problem PFA: increased problem
enia Inherited PltAggTest: abn
defect/absence of nml plt count
Storage defective
GpIIb-IIIa rls of Numerous,
pool certain mediators varies w/ dz
disorders of plt aggregation, (beyond our
such as ADP & scope)
TXA2
Platelet Bleeding disorde

Disease & Patho/Mech Clinical S/S Dx/ Tests/Labs Tx Notes


Def
Acquired Aspirin: irreversible Herbal: Uremia:
defects in inhibitor of COX Ginseng, Ginko, acquired defect in
plt fx: NSAIDS: reversible Ginger, Garlic: plt adhesion,
inhib interact w/ secretion &
warfarin & aggregation -->
inhibit plts PC: nml BT: 
Von AD (most; TIII = plt and coag PT:
Lab nml aPTT:innml
findings Type Desmopre Type O blood:
Willebrand' AR) defect (but I: ssin 25% less vWF
s Dz (vWD) clinical features BT:  (& PFA) acetate, vs. other
Quantitative primarily of plt PC: nml OCPs in blood types
defect=  vWF: defect) PT: nml women
Hemorrhagic Diatheses: Clotting Factor Abnormalities

Type I: 70-80%, PTT:  vWD: AD, MC


mild dz a) Epistaxis & Factor VIII - hereditary
Type III: AR, near spontaneous (enzymatic):  desamino- coag disorder
absent, severe dz bleeding from vWF Ag:  D-arginine (1% of
mucous mbs; vWF:Rcof plt vasopressi population)
Qualitative defect petechiae aggreg: negative n
(= nml lvls) b) Excessive Electrophoresis: (DDAVP): vWD
Type II: 10-20%; bleeding from nml mutimeric increases associations:
mild-mod blding wounds pattern vWF lvls MVP, Marfan
IIA: 75% of TII c) Menorrhagia synd,
- dx w/ heavy 1) Ristocetin -fVIII w/ angiodysplasi
vWF Fxns: menses in post- cofactor platelet vWF a
*1. Bridge betw pubertal female aggregation (if DDAVP
collagen and (vWF:Rcof): ineffective vWD: plt &
Gpb1= plt - often = measure of vWF ) coag dz
adhesion unnoticed until function; Ristocetin
(dz = dec plt plug episode of = tetracycline AB; in vWD:
formation) hemostatic binds to plts & (+)s pregnancy PTT, BT
stress (dental vWF Rs (Gpb1) --> : monitor VIII:c, vWF
*2. Carrier P for procedure, leads to plt fVIII levels BT, despite
factor VIII surgery) aggregation if vWF (will nml PC
(dz = is avail to form increase
coagulopathy) - clinical bridges betw plts in preg) Rx vWD:
- t1/2 fVIII w/ vWF: presentation - degree of desmopressin
12 hrs varies widely & aggregation = acetate, OCP
-t1/2 fVIII w/out: 2 many diff measure of vWF
hrs mutations can activity
cause
Produced at endo 2) vWF antigen:
cells & detects amount of
megakaryocytes vWF
(plts)
3) Multimer studies:
electrophoresis to
Disease & Patho/Mech Clinical S/S Dx/ Tests/Labs Tx Notes
Def
Causes of easy bruising Prolonged PT and Acquired
deficiency: PTT prolonged PT
1. Decreased syn of & aPTT: prob
Vit K by colonic @ final
bacteria common
-newborns req VitK pthwy, Vit K
supplement betw Ps, meds
days 2-5 (coumadin),
2. Decreased reabs liver dz
at SI (w/ fat
malabsorption dz)
3. Dec activation of
Vit K by epoxide
reductase @ liver
- Warfarin inhibits
reductase
-Cirrhosis = dec
(+)ation vit K & syn
VitK factors
Disease & Patho/Mech Clinical S/S Dx/ Tests/Labs Tx Notes
Def
Hemophilia XLR PC: nml rx as MC hereditary
A (Factor (m) in factor VIII a) Easy bruising PT: nml needed dz assoc w/
VIII & massive PTT: prolonged life
deficiency) Extrinsic pthwy hemorrhage PFA: nml 1) FFP threatening
defect--> after trauma or (contains bleeding
decreased operative F8)
generation of procedures 30% new (m)-
thrombin: b) 2) no fam hx
a) unable to form "spontaneous" Cryopreci (m)s same as
Hemorrhagic Diatheses: Clotting Factor Abnormalities

stable clot in hem in trauma- pitate beta thal


response to injury prone areas (subset of
b) inappropriate c) hemarthroses FFP)
fibrinolysis - w/ recurrent
(thrombin nmlly blding into jt, 3)
regulates) causes crippling Recombin
deformity ant fVIII ($
Level of activity (destroys $$)
correlates w/ dz articular
severity: cartilage) 4)
6-50% active: mild d) deep muscle experimen
dz hemorrhage tal gene
2-5%: moderate; therapy w/
<1%: severe - tendency to adeno v.
bleed at joints,
VIII = essential muscles & CNS 5) stim
cofactor of IX, req fibrin clot
to (+) X petechieae formation
characteristicall w/
y absent extrinsic
pthwy…
Hemophilia XLR Indistinguishabl PT: nml Infusions FIX present
B Variable clinical e from FVIII PTT: prolonged of
- many but non-
(Christmas severity defic, but usu recombina
hemophili fxional in 15%
Dz, Factor less severe dx of Christmas dz nt acsFIX
IX is only possible by contracte
deficiency) assay of factor d HIV from
levels repeated
transfusio
Factor XI Autosomal Indistinguishabl Check for if VIII & IX
ns
defic e from FVIII are nml
Disease & Patho/Mech Clinical S/S Dx/ Tests/Labs Tx Notes
Def
DIC Mech: Variable; PT: prolonged Remove TNF- DIC in
1. Widespread common PTT: prolonged or tx sepsis
deposition of fibrin patterns: PC: decreased cause -induces
microthrombi @ 1) Fibrinogen: expression of
microvasc --> Microangiopathi decreased TF
ischemia of O2 c hemolytic D dimer: increased -reduces
sens tissues & anemia expression of
microangiopathic 2) dyspnea, thrombomodu
hemolytic anemia cyanosis, resp lin
(as RBCs squeeze failure --> pro-
thru narrowed 3) convulsions coagulation
vessels) & coma - increases
2. Use up plts, 4) oliguria & expression of
factors + (+) ARF adhesion
Disseminated Intravascular Coagulation

plasminogen = 5) sudden or molec at endo


hem diathesis progressive cells = inc
circulatory WBC bind and
2 Major Etiologies: failure & shock rls ROS
1) Rls of tissue
factor or Acute DIC (a/w (Lipid A at LPS
thromboplastic obstetric comp stimulates rls
substances into & major of TNF & IL-1)
circulation trauma):
- obstetric tissue dominated by AdenoCA:
-massive trauma, bleeding mucus rlsed
extensive surgery, diathesis can directly
severe burns activate factor
-cplasmic granules Chronic DIC X
in acute (a/w cancer):
promyelocytic thrombotic Plasmin: b/d
leukemia complications fibrin and
- mucus rlsed from factors V &
adenoCA (MC = Microthrombi VIII
lung, panc, colon, most often at:
stomach) brain> heart> Fibrin
lungs> degredation
2)Widesprd injury kidneys> products:
to endo cells adrenals> inhibit plt agg,
-injury that exposes spleen> liver fibrin
sub-endo collagen polymerizatio
- sepsis (direct Kidneys: n & thrombin
injury & TNF) microinfarcts,
-immune bilat cortical
complexes (SLE) necrosis
-extreme temps
(as RBCs squeeze failure --> pro-
thru narrowed 3) convulsions coagulation
vessels) & coma - increases
2. Use up plts, 4) oliguria & expression of
factors + (+) ARF adhesion
Disseminated Intravascular Coagulation
plasminogen = 5) sudden or molec at endo
Disease & Patho/Mech
hem diathesis Clinical S/S
progressive Dx/ Tests/Labs Tx Notes
cells = inc
Def circulatory WBC bind and
2 Major Etiologies: failure & shock rls ROS
1) Rls of tissue
factor or Acute DIC (a/w (Lipid A at LPS
thromboplastic obstetric comp stimulates rls
substances into & major of TNF & IL-1)
circulation trauma):
- obstetric tissue dominated by AdenoCA:
-massive trauma, bleeding mucus rlsed
extensive surgery, diathesis can directly
severe burns activate factor
-cplasmic granules Chronic DIC X
in acute (a/w cancer):
promyelocytic thrombotic Plasmin: b/d
leukemia complications fibrin and
- mucus rlsed from factors V &
adenoCA (MC = Microthrombi VIII
lung, panc, colon, most often at:
stomach) brain> heart> Fibrin
lungs> degredation
2)Widesprd injury kidneys> products:
to endo cells adrenals> inhibit plt agg,
-injury that exposes spleen> liver fibrin
sub-endo collagen polymerizatio
- sepsis (direct Kidneys: n & thrombin
injury & TNF) microinfarcts,
-immune bilat cortical
complexes (SLE) necrosis
-extreme temps
Thymic absence/ severe Tetany Thymus &
(burns, heat stroke) Lung: hyaline
Aplasia, lack of T cells & (hypocalcemia) parathyroids fail to
-microorganisms mbs
Hypoplasia: cell-mediated Recurrent develop-->
(meningococci, (reminiscent of
DiGeorge immunity viral/fungal decreased T cells,
rickettsiae) ARDS)
synd a/w failed develop infxns decreased PTH,
of parathyroids (T-cell decreased Ca
MC due to: Adrenals: fibrin
22q11 deletion: deficiency) -absent thymic
obstetric thrombi cause
failure to develop Congenital shadow on CXR
complicaitons massive hem in
3rd & 4th heart & great
(50%), malignant Waterhous-
pharyngeal vessel defects
neoplasms (33%), Freid synd
Thymus

pouches
sepsis, major
trauma Sheehan
postpartum
pituitary
necrosis
Disease & Patho/Mech Clinical S/S Dx/ Tests/Labs Tx Notes
Def
Thymus

Thymic a/w myasthenia


hyperplasia gravis
AI: Ab vs. AchR @
Thymomas NMJbenign or
malignant
a/w pure red cell
aplasia
Mediastinal 4 Ts:
tumors Thymomas
Teratomas
Terrible Lymphoma
Thyroid
Small 1. Vascular 2. Platelet phase: 3. Coagulation 4. Fibrinolytic phase:
vessel phase: a. adhesion phase: a. Plasmin cleaves
hemostas a. transient vC b. Plt rls rxn a. fibrinogen insoluble fibrin monomers
is response b. FVII locally c. Plt syn & rls TXA2 bound GpIIb/IIIa holding plts together
to injury (+) by TF d. Temporary plt plug converted to
c. exposed stops blding fibrin by
collagen (+)s thrombin
Primary 1. Adhesion:
FXII 2. Secretion: 3. Aggregation:
b. forms stable Ticlopidine, clopidogrel, Plt surface ppl
Hemostas Platelet binds a) alpha granules: plt-plt
plt plugadherence abciximab: interfere with ("Plt factor 3"-
is: subendo secrete fibrinogen (FI), via fibrinogen GpIIb-IIIa receptor function PF3): substrate
-formation collagen via fibronectin (FXIII), FV, bridge betw plt required for
of plt plug Gp1b binding FVIII, & vWF GpIIb/IIIa Rs Important platelet storage clot formation
w/ vessel vWF b) dense bodies: w/ proteins: ADP, vWF,
injury -ADP: helps plts adhere fibrinogen PF4: heparin
to endothelium (makes = temporary plt neutralizing
vWF: syn at sticky) plug: only held Platelet function: stabilizes factor, w/in
Wiebel-Palade -Ca: binding agent for by fibrinogen (no intercellular adherens alpha granules
bodies in endo Vit K dependent factors fibrin) junctions in venular
cells c) TXA2 generation via endothelial cells (plt dysfx-
COX --> vC & plt > RBC leakage -->
vWF binds VIII aggreg. peticheae)
and prevents d) conformational
degredation; change --> more ppl PDGF: stimulates sm m cell
decreased exposed at plt surface hyperplasia, important in
vWF= pathogeneisis of
decreased VIII atherosclerosis
Secondar Extrinsic Intrinsic system: XII, XI, Final common Extrinsic system: factor VII Vitamin K-
y system: IX, VIII pthwy: - eval w/ PT dependent
hemostas factor VII X, V, II, I factors:
is: (+) X via form cmplx: (II- thrombin) Intrinsic system: factors procoagulants
formation - activated by IXa, VIIIa, Ca2+, PF3 (I- fibrinogen) XII, XI, IX, VIII II, VII, IX, X;
of fibrin tissue factor (plt ppl) - eval w/ PTT anticoagulants
clot (thromboplastin (+) thrombin via protein C and
, FIII) -contact imp for (+) of form cmplx: Factor XIIa: activates the S
pthwy in lab; in real Xa, Va, Ca2+, kininogen system
(+) X via cmplx: life, likely activated by: PF3 Vitamin K:
VIIa + tissue TF-VIIa (extrinsic) --> Final common pathway: liver activated
factor (+) IX factors X, V, II, I by epoxide
Thrombin cleaves reductase; γ-
IXa + VIIIa ((+) by IIa) fibrinogen to Factor XIII: cross-links carboxylates
--> (+)X fibrin & activates insoluble fibrin monomers factors -->
FXIII able to bind Ca
& plt ppl (PF3)
Factor XII (Hageman FXIII: polymerizes
factor) links fibrinolytic & cross links Calcium: binds
system, coagulation fibrin monomer = γ-carboxylated
system, complement solid fibrin plug vitamin K-
system & kinin system dependent
Anti- PGI2 Aspirin/NSAIDs: Plavix: acts at note: factors
platelet (prostacyclin), XIIa (+)ated
inhibit by of
formation GpIIb/IIIa Rs to factors at serum: II, VII, IX,
mechanis NO: exposed subendo
TXA2 inhibit X
ms -vD & inhibit collagen, HMWK, & aggregation Barium sulfate plasma: I, V,
aggregation contact factors VIII, XIII
- secreted by
nml (serum - supranate formed
endothelium after centrifuge sol'n
containing clot; lacks
factors consumed in clot)
Anti- Anti-thrombin Thrombomodulin: note: Thrombin How to keep clotting
coagulatio III: 1. modulates thrombin fxs: localized?
n -(+) by heparin- 2. activates Protein C (pro-fibrin)
like molecule 1) locally When swept away from
- inactivates II (+) Protein C augments fibrin injury site, thrombin
(thrombin), Xa inactivates deposition via inactivated by
& IXa FV & FVIII (+)ation of thrombomodulin which also
- estrogen (birth intrinsic pthwy leads to (+) of Protein C
control) inhibits -APC inhibs V & VIII
= pro-coagulant 2) augments -other factors removed at
factors that liver
inhibit fibrinolysis
Fibrinolytic Activation of Control of Fibrinolysis: Plasmin b/d Alteplase & reteplase =
system plasminogen 1. alpha2 plasmin fibrin, produces recombinant tPA
(b/d of by: inhibitor (binds and fibrin split
fibrin by -tPA inhibits plasmin) producs (A, B, D) other activators of
plasmin) -Urokinase-like plasminogen: factor XIIa,
PA 2. plasminogen D split products Streptokinase, Anistreplase
(urokinase from activator inhibitor = "D dimers" =
human urine) (inhibits tPA) cross linked fibrin Aminocaproic acid: inbibits
monomers plasminogen

Thrombosi Perfect storm Endothelial injury: Hypercoag state: Venous stasis:


s: of: -turbulent flow at -genetic: APCR, nml small amount of
1. Endothelial arterial bifurcation, increased spontaneous factor
injury area of plaque, cig homocysteine, activation doesn't get
2. Abn blood smoke --> arterial increased diluted and swept away by
flow (stasis) thrombi prothrombin blood flow
3. -form just upstream of
Hypercoagulabl valves, propogate in
Nonthromb Small
e states Platelet count, direction of flow
ocytopenic hemorrhages bleeding time, PT
purpuras: (peticheae & & PTT:
purpura) at skin ALL normal
or mucous mbs,
esp the gingiva

Infxn: Henoch-Schonlein Scurvy, Ehlers- Hereditary hemorrhagic Perivascular


Meningococcem purpura: Danlos, Cushing's telangiectasia (Osler amyloidosis:
ia, septicemia, systemic HS dz, dz: weaken Weber Rendu) weakens
endocarditis, unknown cause; vessel walls AD; dilated, tortuous vessel walls =
rickettsial dz; Purpuric rash, colicky vessels w/ thin walls, bleeding; MC
vasculitis & DIC abd pain, readily bleed --> MC under seen w/
polyarthralgia, acute mucous mbs of nose amyloid light
Drugs: IC HS GN (epistaxis), tongue, mouth, chain
Deficiency alcoholism
vasculitis - all due to IC prolonged PT and eyes, through GI tract amyloidosis
Vit K deposition PTT (b/c factors
dependent invovled in both
proteins pthwys)
Tx of DVT w/ PE: O2 + Unfractionated heparin, Heparin: meas Heparin: advantage =
cardiac & pulm to INR at 2-2.5 PTT reversible w/ protamine
support + - LMWH: does not affect
heparin PTT (dose based on pt Coumadin: meas Coumadin:
w/out: heparin weight) PT reverse w/ vit K but takes
-protamine doesn't fully 6-8hrs
reverse LMWH (both PT & PTT Proteins C & S also drop
-gradually wean from prolonged in both -CAN clot on coumadin,
heparin, place on drugs, but since especially at beginning of
Coumadin (INR: betw 2- fVII rebounds tx!! Proteins C & S drop 1st
3) fast, use PT to = hypercoagulable in pts
-APS: tx pt to INR > 3 follow coumadin) who are deficient in Protein
(only case where tx to C (htz included)
INR >3!) -also poss skin necrosis