Pembahasan TO1 Reguler PDF

Pasien , 48 tahun
Sulit BAK
Kaki bengkak
Mual muntah
Riwayat kencing batu
Kadar ureum 115, kreatinin 5,8, glukosa 168
Jenis Pemeriksaan
Nilai Normal
Deskripsi
Blood Urea Nitrogen

(BUN)
7-25 mg/dL
Urea dihasilkan dari metabolisme

protein, difiltrasi di glomerulus.
Jika GFR urea direabsorbsi ,
kembali ke aliran darah
Kreatinin
0,6-1,5 mg/dL
Produk pemecahan keatinin fosfat

dari otot rangka
Glukosa sewaktu
65-110 mg/dL
Chronic renal failure

Elevated concentration of urea
nitrogen
Bacteria produce urease to disintegrate
urea high-concentration nitrogen
Stimulate gastrointestinal mucous
membrane
Nausea & vomiting
Laki-laki dewasa mudah merasa lemas. Sulit

tidur, nyeri sendi dan otot selama 5 minggu
yang lalu. Nafsu makan baik tetapi merasa BB
.
PF : TB 155 cm dan BB 39 kg (IMT = 16,2
Underweight). Luka-luka kecil yang
menggaung yang pada awalnya terlihat seperti
jerawat.
Lab : CD4 575
http://www.microbiologybytes.com
, 40 tahun
Kuning seluruh tubuh sejak 2 minggu yll
BAB dempul
Bilirubin direk , bilirubin indirek normal
Bilirubin direk = conjugated bilirubin

Bilirubin indirek = unconjugated bilirubin
Destruction of RBC
Heme phagocytosed
by macrophage
Globin degraded into
amino acid
Oxidation of heme
molecule
catalyzed by
microsomal enzyme
heme oxygenase
Biliverdin, iron, CO
Reduction of
biliverdin by
cytosolic enzyme
biliverdin reductase
Conjugated bilirubin
(water soluble)
Excreted from the

liver into the biliary
& cystic ducts, as
part of bile
Conjugated with
glucuronic acid,
catalyzed by the
enzyme UDPglucuronyl
transferase
Intestinal bacteria
convert it into
urobilinogen
Bound to serum
albumin, travels to
the liver
Unconjugated
bilirubin
Reabsorbed by the
intestinal cells
transported to the
kidney passed out
in the urine as
urobilin
Oxidized to
stercobilin
passed out in the
feces
Wikipedia
Color Atlas of Pathophysiology
Wikipedia
, 35 thn
Kuning 4 hari yang lalu, mual, muntah, lemas
Riwayat menggunakan suntik narkotika
PF hepatomegali
SGOT : 100, SGPT : 350, alkali fosfatase 720,
bilirubin total : 8, bilirubin direct 6
, 39 tahun
Riwayat peminum alkohol
PF: tampak tidur lelap, kurus, spider nevi (+)
di dinding perut, terdapat bercak darah pada
bibir dan bau amandel, ransang nyeri (-)
Lab : ammonia darah meningkat

www. wikimed.com
, 61 tahun
Perdarahan sejak 2 jam yll setelah cabut gigi
Penderita jantung koroner dengan konsumsi
aspirin 100mg selama beberapa tahun
Aspirin has an
antiplatelet effect by
inhibiting the
production
of thromboxane,
which under normal
circumstances
binds platelet molec
ules together to
create a patch over
damaged walls of
blood vessels
Hemostasis (hemo=blood; sta=remain)

the stoppage of bleeding, which is vitally
important when blood vessels are damaged.
is
Following an injury to blood vessels several

actions may help prevent blood loss, including:
Formation of a clot
Injured blood vessel

releases ADP, which
attracts platelets (PLT)
PLT comming in contact
with exposed collagen
release: serotonin,
ADP, TXA2, which
accelerate
vasoconstriction and
causes PLT to swell and
become more sticky
, 40 tahun
Badan lemas, tidak nafsu makan, demam(-)
Lab : WBC: 4000 gr/dl, Hb: 8 gr/dl, Ht 34% MCV: 114
fl. Gambaran darah tepi: netrofil hipersegmen,
makroovalosit
Anemias are defined based on cell size (MCV) and

amount of Hgb (MCH).
MCV less than lower limit of normal: microcytic
anemia
MCV within normal range: normocytic anemia
MCV greater than upper limit of normal: macrocytic
anemia
MCH less than lower limit of normal: hypochromic
anemia
MCH within normal range: normochromic anemia
MCH greater than upper limit of normal:
hyperchromic anemia
Pernicious
anemia (megaloblastic
anemia due to vitamin
B12 deficiency)
Disturbance of
proliferation and
differentiation of stem
cells
ANEMIA
Impaired RBC
production
Increased RBC
destruction (hemolytic
anemias)
Disturbance of
proliferation and
maturation
of erythroblast
Anemia of folic acid

deficiency (megaloblastic
anemia)
Anemia of prematurity
(premature infants at 2
to 6 weeks of age)
Iron deficiency anemia

(deficiency of heme
synthesis)
Intrinsic
Thalassemia(deficiency
of globin synthesis)
Extrinsic
Congenital
dyserythropoietic
anemias
Blood loss
Anemia of renal failure
Fluid overload
Anemia (of macrocytic

classification) that results
from inhibition of DNA
synthesis in red blood cell
production
Pathopgenesis
Folate and vitamin B12

deficienciesdefective RNA
and DNA syntheses
continuing cell growth without
division
Erythrogenic precursorslarger
than mature red blood cells
(RBCs)
http://emedicine.medscape.com/article/
http://en.wikipedia.org/wiki/Megaloblastic_anemia
Laboratorium Findings:
Decreased red blood cell
(RBC) count and hemoglobin
levels[
MCV >95 fl
Increased MCH
Normal MCHC, 3236 g/dL
Decreased Reticulocyte count
destruction of fragile and
abnormal megaloblastic
erythroid precursor
Blood smear:
hypersegmented neutrophils
macroovalocytes macrocytes
with oval shape RBC
Anisocytosis (increased
variation in RBC size) and
poikilocytosis (abnormally
shaped RBCs).
an X-linked recessive hereditary disease

characterised by abnormally low levels of
glucose-6-phosphate dehydrogenase
Blood smear: Heinz body in RBC
http://www.diseaseaday.com/wpcontent/uploads/2009/05/g6pddeficiencyprocess.png
http://en.wikipedia.org/wiki/Gluco
se-6-
, 16 tahun
Sesak napas saat beraktivitas sejak 3 bulan yll
PF: Auskultasi P2 mengeras, opening snap saat
diastolik dengan nada rendah pada apikalis,
hepatomegali (-)
Opening Snap
High-frequency early diastolic sound
(occurs 50-100 msec after A2)
associated with mitral stenosis; sound
due to abrupt deceleration of mitral
leaflets sound with associated murmur
Loud P2 (pulmonic) component

of the (S2) pulmonary
hypertension secondary to severe
mitral stenosis
An opening snap heard after the
A2 (aortic) component of the (S2)
correlates to the forceful
opening of the mitral valve
The mitral valve opens when
the pressure in the left atrium
is greater than the pressure in
the left ventricle
This happens in ventricular
diastole (after closure of the
aortic valve), when the
pressure in the ventricle
precipitously drops
Pathophysiology of
Mitral Stenosis
The sounds waves

responsible for heart
sounds are generated by
vibrations induced by:
valve closure,
abnormal valve opening,
vibrations in the
ventricular chambers,
tensing of the chordae
tendineae,
turbulent or abnormal
blood flow across valves
or between cardiac
chambers
closure of the
mitral and
tricuspid
valves at the
beginning
of isovolumetr
ic ventricular
contraction
When audible,
occurs early
inventricular
filling
may represent
tensing of the
chordae
tendineae and
the AV ring,
which is the
connective
tissue
supporting the
S1
S2
S3
S4
closure of the
aortic and
pulmonic
valves at the
beginning
of isovolumetr
ic ventricular
relaxation
When audible,
is caused by
vibration of
the ventricular
wall
during atrial
contraction.
Usually
associated
with a
stiffened
ventricle.
Murmur:
Abnormal
movement
of blood
across
valves and
between
cardiac
chambers
Divided
into:
-ventricular
contraction
(systole)
-ventricular
filling
(diastole)
Pasien 59 thn
Sesak napas, riwayat hipertensi dengan BP
150/90
PF : distensi vena leher, krepitasi pada kedua
basal paru, dan edema pada extremitas
Symptoms of heart failure
Diastole process by which

the heart returns to its relaxed
state
the cardiac muscle is perfused.
Diastolic dysfunction
the heart is able to meet the
bodys metabolic needs,at
a higher filling pressure
Transmission of higher enddiastolic pressure to the
pulmonary circulation
pulmonary congestion
dyspnea right-sided
heart failure.
http://www.aafp.org/afp/2006/0301/afp20060301p841-f1.gif
Nyeri kepala hilang timbul selama 1 minggu,

mual muntah, riwayat hipertensi selama 10
tahun
PF : TD 180/110, GDS 375 dan proteinuria +1
, 25 thn
Luka robek di kaki akibat kecelakaan suntik
lidocaine 1% infiltrasi untuk anestesi luka
robeknya 5menit kemudian tjd gatal2 pada
ekstremitas, muka flushing, kepala melayang
dan sulit bernafas
PF : BP 80/40, HR 84x/menit, RR 32x/menit,
suhu 37 c, auskultasi : stridor wheezing
Vasodilatation
mucosaoedema
Oedem
larynx
Stridor
Brochospasm
Wheezing
Keluhan 1 jam yang lalu nyeri dada seperti

ditindih beban berat
EKG irama sinus , ST Elevasi V1-V4, denyut
jantung 72x/menit, peningkatan enzim jantung
serial
http://ceaccp.oxfordjournals.or
g/content/4/6/175.full
Left coronary artery

mensuplai area:
Anterior LV
The bulk of the
interventricular septum
(anterior two thirds)
The apex
Lateral and posterior LV
walls
Right coronary artery

mensuplai area:
Right ventricle (RV)

The posterior third of the
interventricular septum
The inferior wall
(diaphragmatic surface) of
the left ventricle (LV)
A portion of the posterior
wall of the LV (by means
of the posterior
descending branch)
http://acutemed.co.uk/diseases/ACS+%28Acute+Coronary+Syndrome%29
, 68 tahun
Sesak nafas + batuk sejak 3 minggu, dahak
kental kuning sampai kecoklatan. Riwayat
batuk darah disangkal. Perokok berat sejak
usia 17th
PF : hemithorax cembung dan perkusi
hipersonor di kedua lapang paru
Obstructive lung disease reduced ventilation the ratio of the

duration of expiration to that of inspiration is increased
obstructed expiration distends the alveolar ductules (centrilobular
emphysema), lung recoil decreases (compliance increases) and the
midposition of breathing is shifted toward inspiration (barrel
chest) raises the functional residual capacity
Asma sudah 10 tahun

PF : RR 32x/ menit, FN 110x/ menit
GINA Report 2011
MANAGEMENT
IN STABLE
CONDITION
Pathophysiology of
Asthma
Algorithm
of Asthma
Diagnosis
http://www.eguidelines.co.uk
Devices
Flow Rate
(L/min
Oxygen
Concentratio
n
Description
Nasal Cannula
15
2844%
Rebreathing
Mask/Simple
Oxygen Mask
6-10
35-60%
-First third of exhaled gases mix

with reservoir
-Exhaled gases from upper airway
are oxygen rich
Non Rebreathing
Mask
10-12
95%
Two valves added to prevents:

-Entrainment of room air during
inspiration
-Retention of exhaled gases
during expiration
Venturi Mask
4-8
25-60%
Ventilator
can be set
21-100%
GINA report 2011
, 40 th
Letih lemah sejak 2 bulan yll, saat ini terapi TB,
mengeluh bb turun, dibawah siku warna kulit
tampak menjadi hitam
PF : TD 80/50, nadi 72, tidak ada penyakit
jantung
Adrenal tuberculosis is a manifestation of

disseminated disease presenting rarely as adrenal
insufficiency
Addison's disease results from progressive
destruction of the adrenals, which must involve
>90% of the glands before adrenal insufficiency
appears
The adrenal is a frequent site for chronic
granulomatous diseases, predominantly
tuberculosis(70%-90% cases), but also
histoplasmosis, coccidioidomycosis, and
cryptococcosis
Effects and
Symptoms of
Adrenocortical
Hormone
Deficiency
, 25 tahun
Kenaikan BB 10 kg dalam dua bulan. asupan
makan tidak banyak bertambah meski cepat
lapar.
Riwayat alergi makanan membeli sendiri
obat alergi atau jamu-jamuan.
PF:TB 158 cm, BB 65 kg (IMT = 26
Overweight),
TD 140/90 mmHg Hipertensi, FN
80x/menit, RR 18 x/menit dan suhu 36,5 C
Cushing's syndrome
(hyperadrenocorticalism/hypercortisolism)
s the clinical condition resulting from chronic exposure

to excessive circulating levels of glucocorticoids
The most common cause: excess ACTH secretion from

the anterior pituitary gland (Cushing's disease).
Silbernagl S, et al. Color atlas of pathophysiology. Thieme; 2000.

McPhee SJ, et al. Pathophysiology of disease: an introduction to clinical
medicine. 5th ed. McGraw-Hill; 2006.
, 20 th
Gaduh gelisah sejak 2 jam yll. Riwayat DM (+)
obat suntikan sejak 3 bulan yll, 2 hari ini
menghentikan obat.
PF TB 155cm, BB 45kg, apatis, RR 32x/menit,
tensi 90/60 mmHg, nadi 110x/menit, nafas
kussmaul, lidah kering, turgor kulit menurun
Acute Effect of Diabetes

Mellitus
(Diabetic Ketoacidosis)
, 30 tahun
Dada berdebar-debar sejak 1 minggu yll,
gelisah, sulit tidur, mudah lelah, dan diare
PF : TD 130/80 mmHg, HR 120x/mnt, RR
24x/mnt, mata exopthalmus, pembesara
kelenjar tiroid difus, akral hangat
Laboratorium: peningkatan T3 dan T4, TSH
rendah
, 35 tahun
Pasca tiroidektomi sering mengalami kaku dan
kejang

19. Disorder of
Calcium Metabolism

Wanita, 30 tahun
Nyeri dan bengkak pada sendi
metakarpophalang dan interfalang kedua
tangan, dan bengkak pada sendi lutut.
Dirasakan saat bangun pagi
LED 184 mm(), kadar urat serum 6,2 mg/dl
Rheumatoid Arthritis
Definition:
Chronic inflammatory
Autoimmune disorder, that affect the joints and may cause
systemic manifestation
Reumatoid
Arthritis
a score of 6 fulfilling the requirements for RA
, 25 tahun
Penurunan kesadaran 2 jam yll, riwayat
demam hilang timbul, demam tinggi,
menggigil dan keringat dingin
PF: TD 100/70 mmHg, S 38,5oC, kulit tampak
pucat, konjungtiva anemis.
Lab : ditemukan plasmodium sausage shape
Possible cause:
Binding of
parasitized red
cells in cerebral
capillaries
permeability of
the blood brain
barrier
Excessive
induction
ofcytokines
http://www.microbiol.unimelb.edu.au
, 17 tahun
Demam sejak 4 hari yang lalu disertai nyeri
kepala, mual, nyeri otot dan sendi.
PF : TSS, TD 120/80 mmHg, Suhu 38,3C, Nadi
98x/menit. Konjungtiva pucat (-). Thoraks: BJ
I-II normal, vesikuler. Abdomen : nyeri tekan
epigastrium (+). Ext : petechiae pada lengan
atas kanan dan kiri.
Lab: Hb 12 g/dL, hematokrit 36%, Leukosit
4700, Trombosit 98000
Dengue Infection: Classification
A.
B.
C.
D.
E.
Airway
Establish patent airway
Breathing
Assess and ensure adequate oxygenation and ventilation
Circulation
Level of consciousness
Control hemorrhage
Skin color and temperature
Restore volume
Pulse rate and character
Reassess parameters
Disability
Baseline neurologic evaluation
GCS scoring
Pupillary response
Environment
Completely undress the patient
ATLS
optimized by optima
optimized by optima
Componet:
A. History :
Allergic Medication Past illness Last
meals Event
B. Physical exam : head to toe

C. Every orrifice examination
D. Complete Neurological examination
E. Special diagnostic tests
F. Re-evaluation
optimized by optima
1.
2.
3.
An incised wound that is clean and sutured closed is

said to heal by primary intention.
Often, because of bacterial contamination or tissue loss,
a wound will be left open to heal by granulation tissue
formation and contraction; this constitutes healing by
secondary intention.
Delayed primary closure, or healing by tertiary
intention, represents a combination of the first two,
consisting of the placement of sutures, allowing the
wound to stay open for a few days, and the subsequent
closure of the sutures
8th ed Schwartz's Principles of Surgery
optimized by optima
8th ed Schwartz's
Principles of Surgery
optimized by optima
optimized by optima
25. Shock
Definition
A physiologic state
characterized by
Inadequate tissue
perfusion
Clinically manifested
by
Hemodynamic
disturbances
Organ dysfunction
optimized by optima
optimized by optima
Hemorrhagic Shock
Parameter
II
III
IV
Blood loss (ml)
<750
7501500
15002000
>2000
Blood loss (%)
<15%
1530%
3040%
>40%
Pulse rate
(beats/min)
<100
>100
>120
>140
Blood pressure
Normal
Normal
Decreased
Decreased
Respiratory rate
(bpm)
1420
2030
3040
>35
>30
2030
515
Negligible
Normal
Anxious
Confused
Lethargic
Urine output
(ml/hour)
CNS symptoms
Crit Care. 2004; 8(5): 373381.
optimized by optima
optimized by optima
optimized by optima
optimized by optima
Occurs when pleural space fills with blood

Usually occurs due to lacerated blood vessel in
thorax
As blood increases, it puts pressure on heart
and other vessels in chest cavity
Each Lung can hold 1.5 liters of blood
optimized by optima
Hemothorax
optimized by optima
Hemothorax
optimized by optima
Hemothorax
May put pressure on the heart

optimized by optima
Where does the blood come

from.
Lots of blood vessels

optimized by optima
Anxiety/Restlessness
Tachypnea
Signs of Shock
Frothy, Bloody Sputum
Diminished Breath Sounds on Affected
Side
Tachycardia
Flat Neck Veins
optimized by optima
ABCs with c-spine

control as indicated
Secure Airway assist
ventilation if necessary
General Shock Care due
to Blood loss
Consider Left Lateral
Recumbent position if
not contraindicated
RAPID TRANSPORT
Contact Hospital and
ALS Unit as soon as
possible
optimized by optima
Monitor Cardiac Rhythm

Establish Large Bore IV preferably 2 and draw
blood samples
Airway management to include Intubation
Rapid Transport
If Development of Hemo/Pneumothorax
needle decompression may be indicated
optimized by optima
Opening in lung tissue

that leaks air into
chest cavity
Blunt trauma is main
cause
May be spontaneous
Usually self correcting
optimized by optima
S/S :
Chest Pain
Dyspnea
Tachypnea
Decreased Breath
Sounds on Affected
Side
Th/
ABCs with C-spine
control
Airway Assistance as
needed
If not contraindicated
transport in semi-sitting
position
Provide supportive care
Contact Hospital and/or
ALS unit as soon as
possible
optimized by optima
Opening in chest
cavity that allows air
to enter pleural
cavity
Causes the lung to
collapse due to
increased pressure
in pleural cavity
Can be life
threatening and can
deteriorate rapidly
optimized by optima
optimized by optima
Inhale
Exhale
optimized by optima
Inhale
Exhale
optimized by optima
Inhale
Inhale
optimized by optima
S/S :
Dyspnea
Sudden sharp pain
Subcutaneous
Emphysema
Decreased lung sounds
on affected side
Red Bubbles on
Exhalation from wound
(Sucking chest wound)
Th/ :
ABCs with c-spine control
as indicated
High Flow oxygen
Listen for decreased breath
sounds on affected side
Apply occlusive dressing
to wound
Notify Hospital and ALS
unit as soon as possible
optimized by optima
Occlusive Dressing
optimized by optima
Air builds in pleural

space with no where
for the air to escape
Results in collapse of
lung on affected side
that results in
pressure on
mediastium,the other
lung, and great
vessels
optimized by optima
Each time we inhale,

the lung collapses further.
There is no place for the air
to escape..
Each time we inhale,

the lung collapses further. There
is no place for the air to
escape..
The trachea is
pushed to
the good side
Heart is being
compressed
optimized by optima
Anxiety/Restlessness
Severe Dyspnea
Absent Breath sounds
on affected side
Tachypnea
Tachycardia
Poor Color
Accessory Muscle Use

JVD
Narrowing Pulse
Pressures
Hypotension
Tracheal Deviation
(late if seen at all)
optimized by optima
ABCs with c-spine as indicated

Needle Decompression of Affected Side
High Flow oxygen including BVM
Treat for S/S of Shock
Notify Hospital and ALS unit as soon as
possible
If Open Pneumothorax and occlusive dressing
present BURP occlusive dressing
optimized by optima
Locate 2-3 Intercostal space midclavicular line

Cleanse area using aseptic technique
Insert catheter ( 14g or larger) at least 3 in
length over the top of the 3rd rib( nerve, artery,
vein lie along bottom of rib)
Remove Stylette and listen for rush of air
Place Flutter valve over catheter
Reassess for Improvement
optimized by optima
optimized by optima
Urinary tract stone disease

Signs:
Flank pain
Irritative voiding symptom
Nausea
microscopic hematuria
Urinary crystals of
calcium oxalate, uric acid,
or cystine may
occasionally be found
upon urinalysis
Diagnosis: IVP
optimized by optima
optimized by optima
DEFINITIONS
PATHOPHYSIOLOGY
Congenital megacolon
the absence of
myenteric and
submucosal ganglion
cells in the distal
alimentary tract
decreased motility in
the affected bowel
segment
optimized by optima
Results from the absence

of parasympathetic
ganglion cells in the
myenteric and
submucosal plexus of the
rectum and/or colon.
These ganglion cells arrive
in the proximal colon by 8
weeks of gestational age
and in the rectum by 12
weeks of gestational age.
Arrest in migration leads
to an aganglionic segment.
FREQUENCY
PREDILECTION
approximately 1 per 5000

Classical HD (75% of
live births.
cases): Rectosegmoid
Sex: 4 times more common
Long segment HD (20% of
in males than females.
cases)
Age:
Total colonic
Nearly all children with
aganglionosis (3-12% of
Hirschsprung disease are
cases)
diagnosed during the first
rare variants include the
2 years of life.
following:
one half are diagnosed
before they are aged 1
Total intestinal
year.
aganglionosis
Minority not recognized
Ultra-short-segment HD
until later in childhood or
(involving the distal
adulthood.
rectum below the pelvic
Mortality/Morbidity:
floor and the anus)
The overall mortality of
Hirschsprung
enterocolitis is 25-30%,.optimized by optima
Rontgen :
Plain abdominal radiography
Newborns :
Failure to pass meconium
within the first 48 hours of
life
Abdominal distension
that is relieved by rectal
stimulation or enemas
Vomiting
Neonatal enterocolitis
Symptoms in older children
and adults include the
following:
Severe constipation
Abdominal distension
Bilious vomiting
Failure to thrive
Contrast enema
Dilated bowel
Air-fluid levels.
Empty rectum
Transition zone
Abnormal, irregular contractions
of aganglionic segment
Delayed evacuation of barium
Biopsy :
absence of ganglion cells

hypertrophy and hyperplasia
of nerve fibers,
optimized by optima
Abdominal distension, explosive diarrhea,

vomiting, fever, lethargy, rectal bleeding, or
shock
The risk is greatest:
before HD is diagnosed
after the definitive pull-through operation.
children with Down syndrome
optimized by optima
HIRSCHSPRUNG
DISEASE
HD-ASSOSCIATED
ENTEROCOLITIS
surgical removal or
bypass of the
aganglionic bowel,
rehydration,
intravenous
antibiotics and
colonic irrigations.
optimized by optima
Peritonitis
Infection, or rarely some other type of
inflammation, of the peritoneum.
Peritoneum is a membrane that covers
the surface of both the organs that lie in
the abdominal cavity and the inner
surface of the abdominal cavity itself.
optimized by optima
Early or diffuse infection results in localized or

generalized peritonitis.
Late and localized infections produces an intraabdominal abscess.
optimized by optima
Primary: Caused by the

spread of an infection from
the blood & lymph nodes to
the peritoneum. Very rare <
1%
Usually occurs in people

who have an accumulation
of fluid in their abdomens
(ascites).
The fluid that accumulates
creates a good environment
for the growth of bacteria.
optimized by optima
Secondary: Caused by the

entry of bacteria or enzymes
into the peritoneum from the
gastrointestinal or biliary tract.
This can be caused due to an
ulcer eating its way through
stomach wall or intestine
when there is a rupture of the
appendix or a ruptured
diverticulum.
Also, it can occur due to an
intestine to burst or injury to
an internal organ which bleeds
into the internal cavity.
Swelling & tenderness

in the abdomen
Fever & Chills
Loss of Appetite
Nausea & Vomiting
Increased breathing &
Heart Rates
Shallow Breaths
Low BP
Limited Urine
Production
Inability to pass gas or
feces
Exam :
The usual sounds made
by the active intestine
and heard during
examination with a
stethoscope will be
absent, because the
intestine usually stops
functioning.
The abdom may be
rigid and boardlike
Accumulations of fluid
will be notable in
primary due to ascites.
optimized by optima
Lab :
Blood Test
Samples of fluid from
the abdomen
CT Scan
Chest X-rays
Peritoneal lavage.
th/
optimized by optima
Hospitalization is
common.
Surgery is often
necessary to remove the
source of infection.
Antibiotics are
prescribed to control the
infection & intravenous
therapy (IV) is used to
restore hydration.
Stomach/duodenum Perforation
Presentation :
abdominal pain
Pain on palpation
Release pain
rigidity
peritonism, shock
Air under diaphragm
on X-ray
Treatment
antibiotics,
resuscitate
repair
optimized by optima
optimized by optima
The most commonly injured organs

Spleen
Liver
Retroperitoneum
small bowel
kidneys
Bladder
Colorectum
Diaphragm
pancreas
optimized by optima
Cardiogenic shock - a major component of the

the mortality associated with cardiovascular
disease (the #1 cause of U.S. deaths)
Hypovolemic shock - the major contributor to
early mortality from trauma (the #1 cause of
death in those < 45 years of age)
Septic shock - the most common cause of death
in American ICUs (the 13th leading cause of
death overall in US)
optimized by optima
Kumar and Parrillo (1995) - The state in which

profound and widespread reduction of effective
tissue perfusion leads first to reversible, and
then if prolonged, to irreversible cellular
injury.
optimized by optima
Hypovolemic shock - due to decreased circulating blood volume in

relation to the total vascular capacity and characterized by a reduction
of diastolic filling pressures
Cardiogenic shock - due to cardiac pump failure related to loss of
myocardial contractility/functional myocardium or structural/
mechanical failure of the cardiac anatomy an characterized by
elevations of diastolic filling pressures and volumes
Extra-cardiac obstructive shock - due to obstruction to flow in the
cardiovascular circuit and characterized by either impairment of
diastolic filling or excessive afterload
Distributive shock - caused by loss of vasomotor control resulting in
arteriolar/venular dilatation and characterized (after fluid
resuscitation) by increased cardiac output and decreased SVR
optimized by optima
Hemorrhagic
Trauma
Gastrointestinal
Retroperitoneal
Fluid depletion
(nonhemorrhagic)
External fluid loss
Dehydration
Vomiting
Diarrhea
Polyuria
optimized by optima
Interstitial fluid
redistribution
Thermal injury
Trauma
Anaphylaxis
Increased vascular
capacitance
(venodilatation)
Sepsis
Anaphylaxis
Toxins/drugs
Myopathic
Blunt Cardiac Injury
(trauma)
Myocarditis
Cardiomyopathy
Post-ischemic myocardial
stunning
Septic myocardial
depression
optimized by optima
Pharmacologic : Calcium
channel blockers
Mechanical
Valvular failure (stenotic
or regurgitant)
Hypertropic
cardiomyopathy
Ventricular septal defect
Arrhythmic
Bradycardia
Tachycardia
Impaired diastolic filling

(decreased ventricular preload)
Direct venous obstruction
(vena cava)
intrathoracic obstructive
tumors
Increased intrathoracic
pressure
Tension pneumothorax
Mechanical ventilation
(with excessive pressure or
volume depletion)
Asthma
Decreased cardiac compliance
Constrictive pericarditis
Cardiac tamponade
optimized by optima
Impaired systolic contraction

(increased ventricular afterload)
Right ventricle
Pulmonary embolus
(massive)
Acute pulmonary
hypertension
Left ventricle
embolus
Aortic dissection
Septic (bacterial, fungal, viral, rickettsial)

Toxic shock syndrome
Anaphylactic, anaphylactoid
Neurogenic (spinal shock)
Endocrinologic
Adrenal crisis
Thyroid storm
Toxic (e.g., nitroprusside, bretylium)
optimized by optima
optimized by optima
Brachial systolic blood pressure: <110mmHg

Sinus tachycardia: >90 beats/min
Respiratory rate: <7 or >29 breaths/min
Urine Output: <0.5cc/kg/hr
Metabolic acidemia: [HCO3]<31mEq/L or base
deficit>3mEq/L
K 51-70yr:
Hypoxemia: 0-50yr: <90mmHg;
<80mmHg; >71yo<70mmHg;l
Cutaneous vasoconstriction
k
vs.j
vasodilation.
Mental Changes: anxiousness, agitation,

indifference, lethargy, obtundation
Etiology of shock example
CVP CO
SVR
VO2 sat
low
high
low
high low
high
low
preload
hypovolemi low
c
contractility
cardiogenic
afterload
distributive
optimized by optima
ETIOLOGY
OF SHOCK
EXAMPLE
AFTERLOAD
DISTRIBUTIVE
CVP
CO
SVR
VO2 SAT
Hyperdynamic Septic
Low/High
High
Low
High
Hypodynamic
Septic
Low/High
Low
High
Low/High
Neurogenic
Low
Low
Low
Low
Anaphylactic
Low
Low
Low
Low
optimized by optima
Decreased preload->small ventricular end-diastolic

volumes -> inadequate cardiac generation of pressure
and flow
Causes:
bleeding: trauma, GI bleeding, ruptured aneurysms,
hemorrhagic pancreatitis
protracted vomiting or diarrhea

adrenal insufficiency; diabetes insipidus
Dehydration
third spacing: intestinal obstruction, pancreatitis,

cirrhosis
Signs & Symptoms: Hypotension, Tachycardia, MS

change, Oliguria, Deminished Pulses.
Markers: monitor UOP,CVP, BP, HR, Hct, MS, CO, lactic
acid and PCWP
Treatment: ABCs, IVF (crystalloid), Trasfusion Stem
ongoing Blood Loss
optimized by optima
Mechanism: release of inflammatory mediators leading to
1. Disruption of the microvascular endothelium

2. Cutaneous arteriolar dilation and sequestration of blood in
cutaneous venules and small veins
Causes:
1. Anaphylaxis, drug, toxin reactions
2. Trauma: crush injuries, major fractures, major burns.
3. infection/sepsis: G(-/+ ) speticemia, pneumonia,
peritonitis, meningitis, cholangitis, pyelonephritis,
necrotic tissue, pancreatitis, wet gangrene, toxic shock
syndrome, etc.
Signs: Early warm w/ vasodilation, often adequate urine

output, febrile, tachypneic.
Late-- vasoconstriction, hypotension, oliguria,
altered mental status.
Monitor/findings: Earlyhyperglycemia, respiratory
alkylosis, hemoconcentration,
WBC typically normal or low.
Late Leukocytosis, lactic acidosis
Very Late Disseminated Intravascular
Coagulation & Multi-Organ
System Failure.
Tx : ABCs, IVF, Blood cx, ABX, Drainage (ie abscess)
pressors.
optimized by optima
Mechanism: Intrinsic abnormality of heart -> inability to

deliver blood into the vasculature with adequate power
Causes:
1. Cardiomyopathies: myocardial ischemia, myocardial infarction,
cardiomyopathy, myocardiditis, myocardial contusion
2. Mechanical: cardiac valvular insufficiency, papillary muscle
rupture, septal defects, aortic stenosis
3. Arrythmias: bradyarrythmias (heart block), tachyarrythmias
(atrial fibrillation, atrial flutter, ventricular fibrillation)
4. Obstructive disorders: PE, tension peneumothorax, pericardial
tamponade, constrictive pericaditis, severe pulmonary
hypertension
Characterized by high preload (CVP) with low CO

Signs/SXS: Dyspnea, rales, loud P2 gallop, low BP,
oliguria
Monitor/findings: CXR pulm venous congestion,
elevated CVP, Low CO.
Tx: CHF diuretics & vasodilators +/- pressors.
LV failure pressors, decrease afterload,
intraaortic ballon pump &
ventricular assist device.
optimized by optima
Mechanism: Loss of autonomic

innervation of the cardiovascular system
(arterioles, venules, small veins, including
the heart)
Causes:
1. Spinal cord injury
2. Regional anesthesia
3. Drugs
4. Neurological disorders
Characterized by loss of vascular tone &

reflexes.
Signs: Hypotension, Bradycardia,
Accompanying Neurological deficits.
Monitor/findings: hemodynamic instability,
test bulbo-carvernous reflex
Tx: IVF, vasoactive medications if refractory
optimized by optima
optimized by optima
It is a fracture of the proximal

1/3rd of the Ulna with
dislocation of head of radius
anteriorly. Posteriorly or
laterally
Head of Radius dislocates
same direction as fracture
It requires ORIF or it will
redisplace
optimized by optima
optimized by optima
It is a fracture of distal
Radius and dislocation of
inferior Radio- Ulnar joint
Like Montegia fracture if
treated conservatively it
will redisplace
This fracture appeared in
acceptable position after
reduction and POP
optimized by optima
optimized by optima
Most common fracture in Osteoporotic

bones
Extra-Articular : 1 inch of distal Radius
Results from a fall on dorsi flexed wrist
Typical deformity : Dinner Fork
Deformity is : Impaction, dorsal
displacement and angulation, radial
displacement and angulation and
avulsion of ulnar styloid process
optimized by optima
optimized by optima
optimized by optima
optimized by optima
optimized by optima
Almost the opposite of Colles fracture

Much less common compared to colles
Results from a fall on palmer flexed wrist
Typical deformity : Garden Spade
Management is conservative : MUA and Above
Elbow POP
optimized by optima
The progressive
degeneration of a disc,
or traumatic event,
can lead to a failure of
the annulus to
adequately contain the
nucleus pulposus
This is known as
herniated nucleus
pulposus (HNP) or a
herniated disc
Symptoms
Back pain
Leg pain
Dysthesias
Anesthesias
Varying degrees
Disc bulge
Mild symptoms
Usually go away with
nonoperative treatment
Rarely an indication
for surgery
Extrusion (herniation)
Moderate/severe
symptoms
Nonoperative treatment
Diagnosis
Magnetic resonance
imaging (MRI)/patient
exam
Nonoperative Care
Initial bed rest

Nonsteroidal antiinflammatory (NSAID)
medication
Physical therapy
Exercise/walking
Steroid injections
Surgical care
Failure of nonoperative
treatment
Minimum of 6 weeks in
duration
Can be months
Discectomy
Removal of the
herniated
portion of the disc
Usually through a small
incision
High success rate
Cauda Equina
Syndrome
Caused by a central disc

herniation
Symptoms include
bilateral leg pain, loss of
perianal sensation,
paralysis of the bladder,
and weakness of the anal
sphincter
Surgical intervention in
these cases is urgent
Gradation of
spondylolisthesis
Meyerdings Scale
Grade 1 = up to 25%
Grade 2 = up to 50%
Grade 3 = up to 75%
Grade 4 = up to 100%
Grade 5 >100%
(complete dislocation,
spondyloloptosis)
Symptoms
Low back pain

With or without buttock or
thigh pain
Pain aggravated by standing

or walking
Pain relieved by lying down
Concomitant spinal stenosis,
with or without leg pain,
may be present
Other possible symptoms
Tired legs, dysthesias,

anesthesias
Partial pain relief by leaning
forward or sitting
Diagnosis
Plain radiographs
CT, in some cases with
leg symptoms
Nonoperative Care
Rest
NSAID medication
Physical therapy
Steroid injections
Surgical care
Failure of nonoperative
treatment
Decompression and
fusion
Instrumented
Posterior approach
With interbody fusion
Spondylolysis
Also known as pars defect

Also known as pars
fracture
With or without
spondylolisthesis
A fracture or defect in the
vertebra, usually in the
posterior elementsmost
frequently in the pars
interarticularis
Symptoms
Low back pain/stiffness

Forward bending
increases pain
Symptoms get worse
with activity
May include a stenotic
component resulting in
leg symptoms
Seen most often in
athletes
Gymnasts at risk
Caused by repeated strain
Diagnosis
Plain oblique radiographs

CT, in some cases
Nonoperative care
Limit athletic activities

Physical therapy
Most fractures heal
without other medical
intervention
Surgical care
Failure of nonoperative treatment

Posterior fusion
Instrumented
May require decompression
optimized by optima
injuries to the
abdomen, pelvis
and genitalia are
generally caused
by accidents
involving high
kinetic energy
and acceleration
or deceleration
forces
abdominal injuries can be

either open or closed
open injuries are caused
by sharp or high velocity
objects that create an
opening between the
peritoneal cavity and the
outside of the body
closed injuries are caused

by compression trauma
associated with
deceleration forces and
include:
contusions
ruptures
lacerations
shear injuries
The type of injury will depend on whether the organ injured is

solid or hollow.
hollow organs include:

stomach
intestines
gallbladder
bladder
solid organs
include:
liver
spleen
kidneys
HOLLOW ORGAN INJURIES
when hollow organs

rupture, their highly
irritating and infectious
contents spill into the
peritoneal cavity,
producing a painful
inflammatory reaction
called peritonitis
SOLID ORGAN INJURIES
damage to solid organs

such as the liver can cause
severe internal bleeding
blood in the peritoneal
cavity causes peritonitis
when patients injure solid
organs, the symptoms of
shock may overshadow
those from peritonitis
abdominal injuries can

be obvious, such as an
open wound, or subtle,
such as a blow to the
flank that initially
causes little pain, but
damages the liver or
spleen
suspect abdominal
internal injury in any
patient who has a
penetrating abdominal
wound or has suffered
compression trauma to
the abdomen
Largest organ in abdominal

cavity
Right upper quadrant
Injured from trauma to:
Eighth through twelfth
ribs on right side of body
Upper central part of
abdomen
Suspect liver injury when:
Steering wheel injury
Lap belt injury
Epigastric trauma
After injury, blood and bile

leak into peritoneal cavity
Shock
Peritoneal irritation
Management:
Resuscitation
Laparotomy and repair or
resection.
Avulsion of pedicle is fatal
Upper left quadrant

Rich blood supply
Slightly protected by organs
surrounding it and by lower
rib cage
Most commonly injured
organ from blunt trauma
Associated intraabdominal
injuries common
Suspect splenic injury in:
Motor vehicle crashes
Falls or sports injuries
involving was an impact to
the lower left chest, flank,
or upper left abdomen
Kehrs sign
Left upper quadrant pain
radiates to left shoulder
Common complaint with
splenic injury
Management :
Resuscitation.
Laparotomy (repair,
partial excision or
splenectomy)
Observation in hospital
for patients with subcapsular haematoma
Not commonly injured by blunt trauma

Protected location in abdomen
Penetrating trauma may cause gastric transection or
laceration
Signs of peritonitis from leakage of gastric contents
Diagnosis confirmed during surgery
Unless nasogastric drainage returns blood
BLEEDING
PERFORATION
Presentation :
abdominal pain
rigidity
peritonism, shock
Air under diaphragm on
X-ray
Treatment
Presentation :
Haematemesis +/Melaena
Severity
Increased PR>90
Fall BP<100
Antibiotics
resuscitate
repair
Treatment :
optimized by optima
transfusion
inject DU
Accounts for 5% of all acute surgical admissions

Patients are often extremely ill requiring prompt
assessment, resuscitation and intensive monitoring
Obstructive ileus
A mechanical blockage arising from a structural abnormality
that presents a physical barrier to the progression of gut
contents.
Paralytic Ileus
is a paralytic or functional variety of obstruction
Obstruction is: Partial or complete
Simple or strangulated
8L of isotonic fluid received by the small intestines (saliva,

stomach, duodenum, pancreas and hepatobiliary )
7L absorbed
2L enter the large intestine and 200 ml excreted in the faeces
Air in the bowel results from swallowed air ( O2 & N2) and bacterial
fermentation in the colon ( H2, Methane & CO2),
600 ml of flatus is released
Enteric bacteria consist of coliforms, anaerobes and strep.faecalis.
Normal intestinal mucosa has a significant immune role
Distension results from gas and/ or fluid and can exert hydrostatic
pressure.
In case of BO Bacterial overgrowth can be rapid
If mucosal barrier is breached it may result in translocation of bacteria and
toxins resulting in bactaeremia, septaecemia and toxaemia.
Obstruction results in:

1.
2.
3.
4.
5.
6.
7.
8.
Initial overcoming of the obstruction by increased paristalsis

Increased intraluminal pressure by fluid and gas
Vomiting
sequestration of fluid into the lumen from the surrounding
circulation
Lymphatic and venous congestion resulting in oedematous tissues
Factors 3,4,5 result in hypovolaemia and electrolyte imbalance
Further: localised anoxia, mucosal depletion necrosis and perforation
and peritonitis.
Bacterial over growth with translocation of bacteria and its toxins
causing bacteraemia and septicaemia.
Decompress with NGT

Replace lost fluid
Correct electrolyte abnormalities
Recognise strangulation and perforation
Systemic antibiotics.
The Universal Features

Colicky abdominal pain, vomiting, constipation (absolute), abdominal
distension.
Complete HX ( PMH, PSH, ROS, Medication, FH, SH)
High
Pain is rapid
Distal small bowel
Pain: central and

colicky
Vomitus is feculunt
Vomiting copious and
contains bile jejunal
Distension is severe
content
Visible peristalsis
May continue to pass
Abdominal distension is
flatus and feacus before
limited or localized
absolute constipation
Rapid dehydration
Colonic
Preexisting change in
bowel habit
Colicky in the lower
abdomin
Vomiting is late
Distension prominent
Cecum ? distended
Persistent pain may be a sign of strangulation

Relative and absolute constipation
Luminal
Mural
F. Body
Neoplasms
Bezoars
lipoma
Gall stone
polyps
Food Particles
leiyomayoma
A. lumbricoides hematoma
lymphoma
carcinoid
carinoma
secondary Tumors
Crohns
TB
Stricture
Intussusception
Congenital
Extraluminal
Postoperative
adhesions
Congenital
adhesions
Hernia
Volvulus
General
Vital signs:
P, BP, RR, T, Sat
dehydration
Anaemia, jaundice,
LN
Assessment of
vomitus if possible
Full lung and heart
examination
Abdominal
Abdominal
distension and its
pattern
Hernial orifices
Visible peristalsis
Cecal distension
Tenderness, guarding
and rebound
Organomegaly
Bowel sounds
High pitched
Absent
Rectal examination
Others
Systemic examination
If deemed necessary.
CNS
Vascular
Gynaecological
muscuoloskeltal
Resuscitate:
Air way (O2 60-100%)

Insert 2 lines if necessary
IVF : Crytloids at least 120 ml/h. (determined by estimated fluid
loss and cardiac function). Add K+ at 1mmmol/kg
Draw blood for lab investigations

Inform a senior member in the team.
NPO.
Decompress with Naso-gastric tube and secure in position
Insert a urinary catheter (hourly urinary measurements) and
start a fluid input / output chart
Intravenous antibiotics (no clear evidence)
If concerns exist about fluid overloading a central line should be
inserted
Follow-up lab results and correction of electrolyte imbalance
The patient should be nursed in intermediate care
Rectal tubes should only be used in Sigmoid volvulus.
Immediate intervention:
Evidence of strangulation (hernia.etc)
Signs of peritonitis resulting from perforation
or ischemia
Associated with the following conditions:
Postoperative and bowel resection
Intraperitoneal infection or inflammation
Ischemia
Extra-abdominal: Chest infection, Myocardia

infarction
Endocrine: hypothyroidism, diabetes
Spinal and pelvic fractures
Retro-peritoneal haematoma
Metabolic abnormalities:
Hypokalaemia
Hyponatremia
Uraemia
Hypomagnesemia
Bed ridden
Drug induced: morphine, tricyclic antidepressants
Clinical features
Is there an under lying cause?
Is the abdomen distended but tenderness is not marked.
Is the bowel sounds diffusely hypoactive.

Radiological features:
Is the bowel diffusely distended
Is there gas in the rectum
Are further investigasions (CT or Gastrografin studies)

helpful in showing an obstruction.
Does the patient improve on conservative measures
Potential complications
Fluid and Electrolyte loss Hypovolemia
Hypothermia, Infection, Acidosis
catecholamine release, vasoconstriction
Renal or hepatic failure
Formation of eschar
Complications of circumferential burn
An important step in
management is to
determine depth and
extent of damage to
determine where and
how the patient should
be treated
Depth Classification
Superficial
Partial thickness
Full thickness
Thermal burn
Skin injury
Inhalation injury
Chemical burn
Skin injury
Inhalation injury
Mucous membrane
injury
Electrical burn
Lightning
Radiation burn
1st degree (Superficial burn)
Involves the epidermis

Characterized by reddening
Tenderness and Pain
Increased warmth
Edema may occur, but no
blistering
Burn blanches under
pressure
Example - sunburn
Usually heal in ~ 7 days
2nd degree
Damage extends through the
epidermis and involves the
dermis.
Not enough to interfere with
regeneration of the epithelium
Moist, shiny appearance
Salmon pink to red color
Painful
Does not have to blister to be
2nd degree
Usually heal in ~7-21 days
3rd degree
Both epidermis and dermis are
destroyed with burning into SC fat
Thick, dry appearance
Pearly gray or charred black color
Painless - nerve endings are
destroyed
Pain is due to intermixing of 2nd
degree
May be minor bleeding
Cannot heal and require grafting
Often it is not possible to predict the exact

depth of a burn in the acute phase. Some 2nd
degree burns will convert to 3rd when infection
sets in. When in doubt call it 3rd degree.
Rule of Nines
Adult
Palm Rule
Rule of Nines
Peds
For each yr over 1 yoa,
subtract 1% from head

and add equally to
legs
Palm Rule
Raynaud phenomenon is a
vasospastic disease of the
digital arteries; occurs in
susceptible people when
exposed to cool temperatures
or during emotional stress.
Symptoms:
numbness,
paresthesias, or
Pain
Vasospasm of digital arteries

obliterates the lumen
Inhibited blood flow triphasic
color response
fingers blanch to a distinct white as
blood flow is interrupted
cyanosis, related to local accumulation
of desaturated hemoglobin
Raynaud's syndrome is used

to encompass both the
primary & secondary
ruddy color as blood flow resumes
conditions causing Raynaud
Lilly LS. Pathophysiology of heart disease. 5th ed. Lipincott William &
phenomenon.
Wilkins; 2011.
Raynaud disease:
Raynaud phenomenon:
may appear as a component of

Predominantly woman ages 20other conditions.
40
Causes:
Mechanism:
connective tissue diseases
(scleroderma & SLE)
sympathetic discharge in
arterial occlusive disorders.
response to cold,
carpal tunnel syndrome,
vascular sensitivity to
thermal or vibration injury.
adrenergic stimuli, or
In patients with connective tissue
vasoconstrictor stimuli
diseases/arterial occlusive disease:
(serotonin, thromboxane, &
the digital vascular lumen is
largely obliterated by sclerosis or
endothelin)
inflammation lower
Treatment:
avoiding cold environments, dressing in intraluminal pressure & greater
susceptibility to sympathetically
warm clothes, & wearing insulated
mediated vasoconstriction.
gloves or footwear.
Preventing vasospasm with CCB or
alpha blocker.
Lilly LS. Pathophysiology of heart disease. 5th ed. Lipincott William & Wilkins;
2011.
Anterior Urethral
Trauma
Position : Distal from
urogenital diagphram
Etiology :
Clinical Signs :
Straddle Injury
Instrumentation
Blood from urethral meatus

Hematom, perineal pain
Urinary retenstion
Radiology : urethrogram
Therapy :
Sistostomy
immediate repair
Tanagho EA, et al. Smiths general urology. 17th ed. McGraw-Hill; 2008.
Posterior Urethral
Trauma
Etiology
Clinical Symptoms
Radiology
Therapy
Pelvic bone fracture

Blood from meatus
Urinary retention
Pain, hematom on pubic region
Pelvic Photo
Urethrogram
Sistostomy
Repair 3-4 days later.
Tanagho EA, et al. Smiths general urology. 17th ed. McGraw-Hill; 2008.
Etiology of cardiac
tamponade:
neoplastic, postviral, &

uremic pericarditis.
Acute hemorrhage into

pericardium:
blunt/penetrating chest
trauma,
rupture of the left
ventricular free wall
following MI,
dissecting aortic
aneurysm
Thorax expansion during

inspiration
Intrathoracic pressure become

more negative
Facilitates venous return &

right ventricle filling
Increase in RV size
diminishes LV filling
LV stroke volume & systolic

blood pressure decline slightly
In cardiac tamponade, the

normal situation (left diagram) is
exaggerated because both
ventricles share a reduced, fixed
volume as a result of external
compression by the tense
pericardial fluid.
Pulsus paradoxus may also be
manifested by other conditions in
which inspiration is exaggerated,
including severe asthma &
COPD.
McPhee SJ, et al. Pathophysiology of disease. 5th ed. McGraw-Hill; 2006.

Silbernagl S. Color atlas of pathophysiology. 1st ed. Thieme; 2000.
Lilly LS. Pathophysiology of heart disease. 5th ed. Lipincott William & Wilkins; 2011.
Management:
ABCs with c-spine
control as indicated
High Flow oxygen
Cardiac Monitor
Large Bore IV access
Rapid Transport
What patient needs is
pericardiocentesis
Pericardiosentesis
Using aseptic technique,

Insert at least 3 needle at the
angle of the Xiphoid Cartilage
at the 7th rib
Advance needle at 45 degree

towards the clavicle while
aspirating syringe till blood
return is seen
Continue to Aspirate till

syringe is full then discard
blood and attempt again till
signs of no more blood
Closely monitor patient due

to small about of blood
aspirated can cause a rapid
change in blood pressure
A condition in which
increased pressure
within a limited space
compromises the
circulation and function
of the tissues within
that space.
Elevated tissue
pressure within a
closed fascial space
Reduces tissue
perfusion - ischemia
Results in cell death necrosis
True Orthopaedic Emergency

optimized by optima
Compartment Size
tight dressing; Bandage/Cast
localised external pressure; lying on limb
Closure of fascial defects
Compartment Content
Bleeding; Fx, vas inj, bleeding disorders
Capillary Permeability;
Ischemia / Trauma / Burns / Exercise / Snake Bite /
Drug Injection / IVF
optimized by optima
optimized by optima
optimized by optima
Fractures-closed and
open
Blunt trauma
Temp vascular
occlusion
Cast/dressing
Closure of fascial
defects
Burns/electrical
optimized by optima
Exertional states
IV/A-lines
Intraosseous
IV(infant)
Snake bite
Arterial injury
Pain out of proportion

Palpably tense compartment
Pain with passive stretch
Paresthesia/hypoesthesia
Paralysis
Pulselessness/pallor
optimized by optima
Pain and the aggravation of pain by passive

stretching of the muscles in the
compartment in question are the most
sensitive (and generally the only) clinical
finding before the onset of ischemic
dysfunction in the nerves and muscles.
Whitesides AAOS 1996

optimized by optima
Pain most important. Especially pain out of

proportion to the injury (child becoming
more and more restless /needing more
analgesia)
Most reliable signs are pain on passive
stretching and pain on palpation of the
involved compartment
Other features like pallor, pulselessness,
paralysis, paraesthesia etc. appear very late
and we should not wait for these things.
Willis &Rorabeck OCNA 1990
optimized by optima
Infusion
manometer
saline
3-way stopcock
(Whitesides, CORR
1975)
16 - 18 ga.
Needle
(5-19 mm Hg
higher)
transducer
monitor
Catheter
wick
slit wick
Arterial line
Stryker device
Side port needle
optimized by optima
Remove cast or dressing

Place at level of heart
(DO NOT ELEVATE to optimize
perfusion)
Alert OR and Anesthesia
Bedside procedure
Medical treatment
optimized by optima
Fasciotomy
Casts and tight

bandages
remove
or
loosen any
constricting
bandages
All compartments !!!

optimized by optima
Bayi perempuan (neonatus), kuning

Lahir cukup bulan, APGAR 5/8
Ibu B Rh-, ayah O Rh+
Hb 15, bilirubin total 8, golongan darah O
Tidak terkonjugasi:
Bilirubin indirek
Tidak larut dalam air
Berikatan dengan albumin
untuk transport
Komponen bebas larut
dalam lemak
Komponen bebas bersifat
toksik untuk otak
Terkonjugasi:
Bilirubin direk
Larut dalam air
Tidak larut dalam lemak
Tidak toksik untuk otak
Secara umum penyebabnya:
Meningkatnya produksi bilirubin akibat hemolisis

Kurangnya albumin sebagai alat transport
Penurunan uptake oleh hati
Penurunan konjugasi bilirubin oleh hati
Penurunan ekskresi bilirubin
Peningkatan sirkulasi enterohepatik
Setiap penyakit yang menyebabkan hemolisis yang

berlebihan atau gangguan pada metabolisme/ekskresi
bilirubin biasanya akan menyebabkan ikterus
Ikterus fisiologis:
Ikterus non fisiologis:
Awitan terjadi setelah 24 jam

Memuncak dalam 3-5 hari, menurun dalam 7 hari (pada NCB)
Ikterus fisiologis berlebihan ketika bilirubin serum puncak
adalah 7-15 mg/dl pada NCB
Awitan terjadi sebelum usia 24 jam
Tingkat kenaikan > 0,5 mg/dl/jam
Tingkat cutoff > 15 mg/dl pada NCB
Ikterus bertahan > 8 hari pada NCB, > 14 hari pada NKB
Tanda penyakit lain
Gangguan obstruktif menyebabkan hiperbilirubinemia

direk. Ditandai bilirubin direk > 2 mg/dl. Penyabab:
kolestasis, atresia bilier, kista duktus koledokus.
20
18
16
14
12
10
8
6
4
2
0
fisiologis
non- fisiologis
hari 1 hari 2 hari 3 hari 4 hari 5 hari 6 hari 7
Ikterus yang berkembang cepat pada hari ke-1
Kemungkinan besar: inkompatibilitas ABO, Rh, penyakit

hemolitik, atau sferositosis. Penyebab lebih jarang: infeksi
kongenital, defisiensi G6PD
Ikterus yang berkembang cepat setelah usia 48 jam
Kemungkinan besar: infeksi, defisiensi G6PD. Penyebab lebih

jarang: inkompatibilitas ABO, Rh, sferositosis.
Daerah tubuh Kadar bilirubin (mg/dl)

Muka
Dada/punggung
Perut dan paha
Tangan dan kaki
Telapal tangan/kaki
4 -8
5 -12
8 -16
11-18
>15
Penyakit
Keterangan
Inkompatibilitas
ABO
Adanya aglutinin ibu yang bersirkulasi di darah anak

terhadap aglutinogen ABO anak.
Inkompatibilitas Rh
Adanya antibodi ibu yang bersirkulasi di darah anak

terhadap antigen Rh anak. Jarang pada anak pertama.
Hematoma darah
ekstravaskuler
Akibat proses persalinan.
Defisiensi G6PD
Penyakit terkait kromosom X. Enzim G6PD berfungsi

untuk melindungi eritrosit dari kerusakan oksidatif.
Sferositosis herediter
Terdapat defek protein membran yang menyebabkan

instabilitas eksoskeleton eritrosit
Polisitemia
Peningkatan pembentukan eritrosit yang menyebabkan

peningkatan destruksi eritrosit
Bayi usia 2 hari

BAB berdarah, muntah darah, petekie
Persalinan ditolong dukun
Stadium
Characteristic
Early HDN
Occurs within 2 days and not more than 5 days of life.

Baby born of mother who has been on certain drugs:
anticonvulsant, antituberculous drug, antibiotics, VK
antagonist anticoagulant.
Classic HDN
Occurs during 2 to 7 day of life when the prothrombin

complex
is low. It was found in babies who do not received VKP or
VK supplemented.
Vit K deficiency
Occurs within 2 days and not more than 5 days of life.

Definite etiology inducing VKP is found in association
with bleeding: malabsorption of VK ie gut resection,
biliary atresia, severe liver disease-induced intrahepatic
biliary obstruction.
Late HDN /
APCD
Acquired bleeding disorder in the 2 week to 6 month age

infant caused by reduced vitamin K dependent clotting
factor (II, VII, IX, X) with a high incidence of intracranial
Anak perempuan, usia 2 tahun, pucat, rewel,

nafsu makan berkurang
Gizi kurang, anemia, atrofi papila lidah, tidak
ada hepatosplenomegali & limfadenopati
Hb 6,2; leukosit 8.000; Ht 19,5%; tro 350.000;
MCV 62; MCH 21; MCHC 28
Parameter
Kadar normal
Satuan
Hb
6 bln - 2 thn: 10,5-13,5

2-6 thn: 11-14,7
6-12 thn: 11,5-15,5
12-18 thn: 13-16 (L); 12-16 (P)
g/dL
Ht
2 thn: 33-42
Leukosit
2 thn: 6000-17.500
/L
Trombosit
150.000-400.000
/L
MCV
2 thn: 70-86
fL
MCH
2 thn: 23-31
pg/sel
MCHC
2 thn: 30-36
%Hb/sel
Hipokrom: MCH normal

Mikrositik: MCV normal
Hiperkrom: MCH normal

Makrositik: MCV normal
Penyakit (tambahan)
Hereditary, Lipid
disorders,
splenectomy
Hb C disease, post
splenectomy
Myeloid
metaplasia
Uremia, following
heparin injection,
def pyruvate
kinase
Thalassemia,
anemia
megaloblastic, iron
deficiency
Stage
Iron Depletion
I
Iron Deficiency
II
IDA
III
Serum Iron
Normal
Hb
Normal
Normal
MCV, MCH
MCHC
Iron Store
(Ferritin)
Penyebab:
Peningkatan kebutuhan (pemakaian Fe , infeksi berulang)

Perdarahan kronik
Asupan diet kurang
Malabsorpsi
Kurangnya cadangan besi (prematur, gemelli, anemia pada ibu hamil)
Bayi perempuan, usia 4 bulan, perdarahan

Riwayat keluarga +
Hb 11,2; leukosit 7.500; trombosit 300.000; BT
2; PT 12; aPTT 70
Didiagnosis hemofilia A
PT
aPTT
Tekanan di dalam Jantung
Congenital
HD
Acyanotic
With volume
load:
With pressure
load:
- ASD
- Valve stenosis
- VSD
- PDA
- Coarctation of
aorta
Cyanotic
With
pulmonary blood
flow:
With
pulmonary blood
flow:
- ToF
- Atresia
pulmonal
- Transposition
of the great
vessels
- Atresia
tricuspid
- Truncus
arteriosus
- Valve
regurgitation
1. Nelsons textbook of pediatrics. 18th ed.

2. Pathophysiology of heart disease. 5t ed.
With volume load
Clinical Findings
The most common: left to right

shunting
e.g. ASD, VSD, PDA
Blood back into the lungs
compliance & work of breathing
Fluid leaks into the interstitial space

& alveoly
Pulmonary edema, tachypnea, chest

retraction, wheezing
Heart rate & stroke volume
High level of ventricular output ->

sympathetic nervous system
If left untreated, volume load will

increase pulmonary vascular resistance
Oxygen consumption -> sweating,

irritability, FTT
Remodelling: dilatation & hypertrophy
Eventually leads to Eisenmenger

Syndrome
With pressure load
Clinical Findings
Obstruction to normal blood

flow: pulmonic stenosis, aortic
stenosis, coarctation of aorta.
Hypertrophy & dilatation of

ventricular wall
Dilatation happened in the later

stage
Defect location determine

the symptoms
Severe pulmonic stenosis in

newborn right-sided HF
(hepatomegaly, peripheral
edema)
Severe aortic stenosis leftsided (pulmonary edema, poor

perfusion) & right-sided HF
Cyanotic lesions with pulmonary blood flow must include both:

an obstruction to pulmonary blood flow & a shunt from R to L
Common lesions:
Tricuspid atresia, ToF, single ventricle with pulmonary stenosis
The degree of cyanosis depends on:
the degree of obstruction to pulmonary blood flow
If the obstruction is mild:
Cyanosis may be absent at rest
These patient may have hypercyanotic spells during condition of stress
If the obstruction is severe:
Pulmonary blood flow may be dependent on patency of the ductus arteriosus.
When the ductus closes hypoxemia & shock
Cyanotic lesions with pulmonary blood flow is not

associated with obstruction to pulmonary blood flow
Cyanosis is caused by:

Abnormal ventricular-arterial
connections:
- TGA
Total mixing of systemic venous

& pulmonary venous within the
heart:
- Common atrium or ventricle
- Total anomolous pulmonary
venous return
- Truncus arteriosus
Flow across VSD
Pansystolic murmur & thrill

over left lower sternum.
Over flow across mitral valve
If defect is large 3rd heart sound

& mid diastolic rumble at the apex.
LA, LV, RV volume

overload
High systolic pressure &

high flow to the lungs
pulmonary hypertension
ECG: Left ventricular hypertrophy

or biventricular hypertrophy,
peaked/notched P wave
Ro: gross cardiomegaly
Dyspnea, feeding difficulties, poor
growth, profuse perspiration,
pneumonia, heart failure.
Duskiness during crying or infection
Ph/: increased of 2nd heart sound
cardiomegaly with
prominence of
both ventricles,
the left atrium, &
the pulmonary artery.
pulmonary vascular
marking
The degree of L-to-R shunting is dependent on:

- the size of the defect,
- the relative compliance of the R and L ventricles, &
- the relative vascular resistance in the pulmonary & systemic circulations
Infant has thick & less compliant RV minimal symptoms

As children grow older: subtle failure to thrive, fatigue, dyspneu on
effort, recurrent respiratory tract infection
Overflow in the right

side of heart
Enlargement of the RA & RV

Dilatation of the pulmonary artery
The LA may be enlarged
Pulmonary vascular resistance may begin to increase in adulthood

reversal of the shunt & cyanosis
Ro:
Increased flow into right

side of the heart & lungs
- enlargement of RV, RA, &

pulmonary artery
- increased vasvular marking
Constant increased of
ventricular diastolic volume
Wide, fixed 2nd heart sound

splitting
Increased flow across tricuspid

valve
Mid-diastolic murmur at the

lower left sternal border
Increased flow across

pulmonary valve
Thrill & systolic ejection murmur,

best heard at left middle & upper
sternal border
Flow across the septal defect doesnt produce murmur because the pressure
gap between LA & RA is not significant
size of the main

pulmonary artery
size of the right atrium
size of the right ventricle
(seen best on the lateral
view as soft tissue filling in
the lower & middle
retrosternal space).

2. Essentials of Radiology. 2nd ed.
Etiology:
Salmonella typhosa
Clinical features:
Step ladder fever in

the first week, the
persist
Abdominal pain
Diarrhea/constipati
on
Headache
Coated tongue
Hepatosplenomegal
y
Rose spot
Harrisons principles of internal medicine.
Infection through the

mucosa or wounded skin
Proliferate in the
bloodstream or
extracellularly within organ
Disseminate
hematogenously to all
organs
Multiplication can cause:

Hepatitis, jaundice, & hemorrhage in the liver
Uremia & bacteriuria in the kidney
Aseptic meningitis in CSF & conjunctival or scleral hemorrhage in the aqueous humor
Muscle tenderness in the muscles
Harrisons principles of internal medicine. 18th ed.
Sodium functions:
fluid balance (the major
factor in extracellular
osmolality)
nerve impulse
generation &
transmission
(neuromuscular
function).
Lauralee S. Human physiology. From cells to system.
Many symptoms of
hyponatremia are associated
with the hypotonic hydration.
The most common symptoms:
Headache
Nausea
Disorientation
Tiredness
Muscle cramps
Johnson JY. Fluids and Electrolytes demystified. 2008
Natrium concentration is influenced by the balance of

natrium & water in the body.
Harrisons principles of internal medicine. 18th ed.
Hypernatremia
Fluid moves out of the cells
Cell dehydration with shrinkage
Dry tissues dry mucous

membrane, loss of turgor, & thirst
Hypernatremia can
affect brain cells and
cause neurologic
damage, resulting in
Confusion
Paralysis of the
muscles of the
lungs
Coma
Even death
Burtis Ca et al. Tietz textbook of clinical chemistry &

molecular diagnostic. 4th ed.2008
K has important role in resting membrane potential & action

potentials.
The level of K influences cell depolarization
the movement of the resting potential closer to the threshold

more excitability & hyperpolarization
decreased resting membrane potential to a point far away
from the threshold less excitability.
The most critical aspect of K, it affects:
Cardiac rate, rhythm, and contractility

Muscle tissue function, including skeletal muscle and muscles of
the diaphragm, which are required for breathing
Nerve cells, which affect brain cells and tissue
Regulation of many other body organs (intestinal motility)
Hypokalemia
Disorientation
Confusion
Discomfort of muscles
Muscle weakness
Ileus paralytic
Paralysis of the
muscles of the lung,
resulting in death
Hyperkalemia
Rapid heart beat
(fibrillation)
Skin tingling
Numbness
Weakness
Flaccid paralysis
Seizure:
a paroxysmal event
due to abnormal
excessive or
synchronous neuronal
activity in the brain.
Epilepsy:
a condition in which a
person has recurrent
seizures due to a
chronic, underlying
process.
Most seizures in
children are provoked
by somatic disorders
originating outside the
brain:
high fever,
infection,
syncope,
head trauma,
hypoxia,
toxins, or
cardiac arrhythmias.
A simple febrile convulsion

usually associated with a core temperature that increases rapidly to
39C.
Generalized & tonic-clonic in nature,
lasts a few seconds <15 min,
followed by a brief postictal period of drowsiness, &
occurs only once in 24 hr.
Complex febrile convulsion
duration is >15 min,
repeated convulsions occur within 24 hr, or
when focal seizure activity or focal findings are present during the
postictal period
If any doubt exists about the possibility of meningitis, a lumbar puncture
is indicated, especially if seizures are complex or sensorium remains
clouded after a short postictal period.
Poliomyelitis:
90-95% of all infection remain

asymptomatic
5-10% abortive type:
Fever
Headache, sore throat
Limb pain, lethargy
GI disturbance
1-2% major poliomyelitis:
Meningitis syndrome
Flaccid paresis with asymmetrical
proximal weakness & areflexia,

mainly in lower limbs
Paresthesia without sensory loss or
autonomic dysfunction
Muscle atrophy
Color atlas of neurology
314
316
Delayed immune response to infection

with
group
A
beta
hemolytic
streptococci.
After a latent period of 1-3 weeks
antibody
induced
immunological
damage occur to heart valves ,joints,
subcutaneous tissue & basal ganglia of
brain
Jones Criteria (Revised) for Guidance in the

Diagnosis of Rheumatic Fever*
Major Manifestation
Carditis
Polyarthritis
Chorea
Erythema Marginatum
Subcutaneous Nodules
Minor
Manifestations
Clinical
Previous
rheumatic
fever or
rheumatic
heart disease
Arthralgia
Fever
Laboratory
Acute phase
reactants:
Erythrocyte
sedimentation
rate,
C-reactive
protein,
leukocytosis
Prolonged PR interval
Supporting Evidence
of Streptococal Infection
Increased Titer of AntiStreptococcal Antibodies ASO
(anti-streptolysin O),
others
Positive Throat Culture
for Group A Streptococcus
Recent Scarlet Fever
*The presence of two major criteria, or of one major and two minor criteria,
indicates a high probability of acute rheumatic fever, if supported by evidence of
Group A streptococcal nfection.
Recommendations of the American Heart Association
Pre-eruptive Stage
demam
Catarrhal Symptoms dimulai dari
kavitas nasal (rhinitis)
konjungtiva (konjungtivitis)
orofaring bronkus (bronkhitis)
Respiratory Symptoms muncul
awalnya seperti common cold -->
batuk
Eruptive Stage/Stage of Skin Rashes
Exanthem sign Erupsi di kulit
Maculopapular Rashes appears
2-7 days after onset
With high fever increases
steadily
Anorexia and irritability are
disturbing particularly at the
height of the fever
Diarrhea, pruritis, lethargy and
occipital lymphadenopathy
Stage of Convalescence
Rashes menghilang sama dengan
urutan munculnya (muka lalu ke
tubuh bag bawah) membekas
kecoklatan
Demam akan perlahan menghilang
saat erupsi di tangan dan kaki
memudar
Paramyxovirus
At risk:
Preschool age children unvaccinated

School age children in whom vaccine failed
Season: late winter/spring

Incubation: 8-12 days
Infectious: 1-2 days before prodrome to 4 days
after onset of rash
Prodrome
Day 7-11 after exposure

Fever, cough, coryza, conjunctivitis
Enanthem
Kopliks spots appear 2 days before rash and lasts 2

days into rash
Otitis Media
Bronchopneumonia
Encephalitis
Pericarditis
Subacute sclerosing panencephalitis late
sequellae due to persistent infection of the
CNS
Togavirus
At risk: Unvaccinated adolescents
Season: late winter/early spring
Incubation: 14-21 days
Infectious period: 5-7 days before rash to 3 to
5 days after rash
Asymptomatic infection in up to 50%

Prodrome
Children: absent to mild

Adolescent & adult: fever, malaise, sore throat,
nausea, anorexia, painful occipital LAD
Enanthem
Forschheimers spots petechiae on the hard

palate
Arthralgias/arthritis in older patients

Peripheral neuritis, encephalitis,
thrombocytopenic purpura (rare)
Congenital rubella syndrome
Infection during first trimester

IUGR, eye findings, deafness, cardiac defects,
anemia, thrombcytopenia, skin nodules
Exanthem Subitum
Human Herpes Virus 6 (and 7)
At risk: 6-36 months (peak 6-7 months)
Season: sporadic
Incubation: 9 days
Infectious period:
Virus is intermittently shed into saliva throughout life;

asymptomatic persistent infection
High fever for 3-4 days

Abrupt defervescence with appearance of rash
Associated seizures likely due to infection of
the meninges by the virus
1.
2.
3.
KEP : mild, moderate, severe

KEP severe :
Kwashiorkor: protein deficiency
Marasmus: energy deficiency
Marasmic/ Kwashiorkor: combination of
chronic energy deficiency and chronic or acute
protein deficiency
Protein
Serum Albumin
Tekanan osmotik koloid serum
Edema
Carbohydrate
Fat analysis
+ Protein analysis
Subcutaneous Fat
Muscle wasting
NEFROTIK SINDROM
Osmotic
Secretoric
Inflammatoy
Altered motility
IN THE SMALL INTESTINE

Ingestion of non-absorbable solutes
Fluid entry into the small bowel

Intraluminal solutions become iso-osmotic with the plasma
Intraluminal Na+ concentration drop below 80 ml osmol
Steep lumen to plasma gradient
IN THE COLON
Carbohydrate
Non metabolizable substrates
Metabolized by Bacteria
Na+ and H2O
Short Chain fatty acids
may be absorbed by colon
(Organic anions)
Quadrupling the Osmolality
A linear relation between

ingested osmotic load &
stool water output
Short-Chain Fatty Acids

(Organic Anions)
Promote more fluid in the colon
Obligate retention of inorganic cations
Further increasing the osmotic load
More fluid in the colon
Exogenous
Osmotic Laxatives
Antacids containing MgO or Mg(OH)2
Dietetic foods, candies and elixirs
Drugs e.g.:
Colchicine
Cholestyramine
Endogenous
Congenital
Specific Malabsorptive Disorders e.g Disaccharidase

deficiencies
Generalized Malabsorptive Diseases e.g
Abetalipoproteinemia
Pancreatic insufficiency e.g cystic fibrosis
Acquired
Specific Malabsorptive Diseases

Generalized Malabsorptive Diseases
Pancreatic insufficiency
Celiac disease
Infections
Electrolyte transport diarrhea
The intestine is able to
Secret
Absorb
Fluids & electrolytes
Secretion originates in the crypts

Absorption is mainly a villous function
Intracellular cyclic-AMP & -GMP
are a corner stone in initiating Intestinal secretion
Neurotransmitters
Hormones
Bacterial Enterotoxins
Cathartics
Stimulate receptors on the enterochromaffin cells

stimulate
Cyclic AMP Cyclic GMP
Ca ions
stimulate
Cl-, H2O and CHO3
Secretion by the enterocytes
Exogenous
Stimulant Laxatives e.g. Anthraquinones, senna
Medications
Diuretics
Asthma medication
Eye drops
Bladder stimulants
Cardiac drug
Prostaglandins
Toxins
Metals
Organophosphorous
Seafood toxins
Bacterial toxins
Luminal or invading
Viruses
Bacteria
Protozoa
Helminths
Immunological mechanisms
Complement
T-lymphocytes
Proteases
Oxidants
Minimal or severe inflammation

Enterocyte damage or death
Malabsorption and secretion
Colonization - Adherence - Invasion

by microorganisms
IL-8
Activation of RESIDENT
Recruitment OF NEW
PHAGOCYTES
Complex Organism
e.g. worms
Bacterium
Complex Organism
Mast cell activation by cross linking of IgE & IgG Receptors
Direct stimulation of Enterocytes & Enteric nervous system
Smooth muscle cells
Explosive release of
Histamine
Adenosine
Prostaglandins
Intestinal secretion
Smooth muscle contraction
Not unlike
Bronchial Asthma
Inflammatory Diarrhea
BACTERIUM
Release of Chemotactic substances in the lumen
Neutrophils cross the epithelium
Release of mediators
Prostaglandins
Leukotrines
Platelet activating factor
Hydrogen peroxide
Intestinal secretion
Smooth muscle contraction
Inflammatory Diarrhea
Of Any Mechanism
Damage to absorbing epithelium
Repopulation of damaged absorptive surface:
By immature cells with poor absorptive capacity
Malabsorption of ions and nutrients
Release of inflammatory mediators from cells

in the lamina propria
Stimulate secretion from the
Remaining crypts
Immature villous surface cells
Adequate absorption requires

Adequate and long enough exposure to
intestinal epithelium
Accelerated Transit time

Decreased absorption
Large fluid load to the colon
Disordered motility is
Colonic irritability
The cause of diarrhea
Diarrhea
OR
Diminished peristalsis
An effect of diarrhea
Bacterial overgrowth
Secretory diarrhea
IBS-D
Functional Diarrhea
Diabetic neuropathy
Scleroderma
Thyrotoxicosis
http://www.metrohealth.org/documents/patient%20services/neonatology/
Transition%20to%20Extra%20uterine%20Life.pdf
BEFORE BIRTH
No Gas exchange in lungs
Lungs receive little blood flow (23%
cardiac output)
Lungs produce fluid 100cc/kg of
baby/day
Lungs fluid filled
AFTER BIRTH
All Gas exchange in lungs
Lungs receive 100% cardiac output
Lungs produce minimal fluid
Lungs must clear 250 ml fluid
http://www.chop.edu/export/system/galleries/images/hospital/conditions/the-neonatal-intensive-care-unitnicu-125889.gif
Judith S. Mercer, Rebecca L.

Skovgaard. Neonatal Transitional
Physiology:
A New Paradigm. 2002
Deprivation of oxygen to a newborn infant that

lasts long enough during the birth process to
cause physical harm, usually to the brain
Etiology:
Intrauterine hypoxia
Infant respiratory distress syndrome
Transient tachypnea of the newborn
Meconium aspiration syndrome
Pleural disease (Pneumothorax,
Pneumomediastinum)
Bronchopulmonary dysplasia
http://en.wikipedia.org/wiki/Perinatal_asphyxia
Hyaline Membrane Disease (Respiratory Distress

Syndrome). Nelson Textbook of Pediatrics
Etiology:
Surfactant deficiency
(decreased production and
secretion)
Surfactant
Necessary for the lung alveoli
to overcome surface tension
and remain open
The major constituents
dipalmitoyl
phosphatidylcholine
(lecithin)
Phosphatidylglycerol
apoproteins (surfactant
proteins SP-A, -B, -C, -D)
cholesterol
Produce by type II alveolar
cells
http://www.netterimages.com/images/vpv/000/000/010/10291-
At end-expiration, the volume

of the thorax and lungs tends to
approach residual volume,
produces atelectasis
This results in perfused, but not
ventilated alveolicauses
hypoxia
Hypercapnia:
Decreased lung compliance
small tidal volumes
increased physilogic dead
space
increased work of breathing
insufficient alveolar
ventilation eventually result
in
Pulmonary arterial
vasoconstriction
increased right-to-left
shunting through the foramen
ovale and ductus arteriosus and
within the lung itself
Hyaline Membrane Disease (Respiratory Distress

Syndrome). Nelson Textbook of Pediatrics
http://ocw.tufts.edu/data/51/673802/674886_xlarg
e.jpg
http://trialx.com/curebyte/2011/07/12/clinicaltrials-and-related-photos-for-newborn-respiratory-
UAC: Umbilical artery

Catheter
NG: Nasogastric tube
http://www.uen.org/utahlink/tours/loadimg.cgi?p=/tour/15478/15478bronchog
rams.jpg
Risk factors associated with transient tachypnea of

newborn.
Incomplete
resorption of fluid
from the lungs of
the newborn
This is a diagnosis
of exclusion when
no other cause is
found for the
infant's tachypnea
Guglani L et al. Pediatrics in Review 2008;29:e59-e65
http://pedsinreview.aappublications.org/content/29/11/e59.full
2008 by American Academy of Pediatrics
Mechanism of fetal and neonatal lung fluid transport.

ENaC: type II cell
apical epithelial
sodium channels
K+=potassium,
NKCC=sodium,
potassium, 2 chloride
cotransporter
active secretion of chloride ions

from alveolar cells into the alveolar
space. Sodium (Na+) and water
accompany chloride (Cl-).
(ENaC) activated by adrenergic stimulation.

Na+/K+ ATPase move sodium into the
interstitium, brings chloride and water
passively
2008 by American Academy of Pediatrics
Radiographs of Babies who have transient tachypnea of

the newborn of differing severity
Note the streaky lung opacities and fluid in the minor

fissure on the right side.
http://roentgenrayreader.blogspot.com/2010/11/transient-tachypnea-of2008 by American Academy of Pediatrics

newborn.html
MECONIUM
ASPIRATION
SYNDROME
http://img.medscape.com/pi/emed/ckb/clinical_procedures/7
Frontal chest shows large, ropey and strand-like densities

http://www.learningradiology.com/caseofweek/caseoftheweekpix/cow89.
jpg
Organisms gain entry

to the respiratory
tract by inhalation of
droplets and invade
the mucosa.
Epithelial destruction
redness, edema,
hemorrhage and
sometimes an
exudate.
http://emedicine.medscape.com/article/302460
http://www.ncbi.nlm.nih.gov/books/NBK8142/bin/ch93f1
.jpg
http://www.ncbi.nlm.nih.gov/books/NBK8142/bin/ch93
Abnormal, high-pitched sound produced by

turbulent airflow through a partially obstructed
airway at the level of the supraglottis, glottis,
subglottis, and/or trachea.
It can be:
Inspiratory stridorextrathoracic obstruction
Supraglottic area
Nasopharynx, epiglottis, larynx, aryepiglottic folds, false vocal
cords
Glottic and subglottic area
Vocal cords to the extrathoracic segment of the trachea
Expiratory stridor (wheezing) intrathoracic obstruction

bronchial obstruction
Biphasic stridortracheal (subglottic or glottic anomaly)

critical and fixed airwary obstruction at any level
http://medschool.lsuhsc.edu
EXTRATHORACIC
Ppl : Pleural pressure

Patm: Atmospheric
pressure
Ptr: Intratracheal pressure
INTRATHORACIC
Forced expiration
Forced expiration
(Ptr) exceeds (Patm)lessening the
(Ptr) is less than (Ppl)worsening
obstruction
the obstruction
Forced inspiration
Forced inspiration
(Ptr) falls below (Patm) the
(Ptr) exceeds (Ppl) lessening the
obstruction worsens resulting in
degree of obstruction
flow limitation
neonate
Laryngomalacia
Vocal cord dysfunction
Congenital tumours
Choanal atresia
Laryngeal webs
1st
2nd
Chronic
Chronic
Chronic
Chronic
Chronic
Chilld
Infection -epiglottitis -Laryngitis
Croup : 1-2 days duration less severe
FB
Laryngeal dyskinesia
acute
Acute
Acute
chronic
adult
Infection -epiglottitis -Laryngitis
Trauma acquired stenosis
CA Larynx or Trachea or main bronchus
Acute
Acute
chronic
http://dnbhelp.files.wordpress.com/2011/10/stridor.jpg?w=6
45
Acute inflammatory
injury of the
bronchioles, usually
caused by a viral
infection
Bronchioles
Respiratory Syncytial
Virus (RSV)90%
small airways, less than

2 mm in diameter, and
lack cartilage and
submucosal glands.
Spread
Direct contact with nasal

secretions
airborne droplets
fomites
http://i47.tinypic.com/xc9nxg.p
http://www.scielo.br/img/revistas/rhc/v58n1/15504
f1.gif
The effects of bronchiolar

injury include the following:
Increased mucus secretion
Bronchial obstruction and
constriction
Alveolar cell death, mucus
debris, viral invasion
Air trapping
Atelectasis
Reduced ventilation that
leads to
ventilation/perfusion
mismatch
Labored breathing
Type 1 allergic reactions
mediated by
immunoglobulin E may
account for some clinically
significant bronchiolitis
http://www.urgentcarecmetesting.com/SamplePresentation/Rose%20-
42. PATHOGENESIS
OF ASTHMA
Definition
o Chronic
inflammatory
condition of the
airwayshyperreactiv
ity
o Episodic airflow
obstruction
Main processes
o Inflammatory reaction
o Remodeling
http://www.clivir.com/pictures/asthma/asthma_sympto
ms.jpg
Andrew H. Liu, Joseph D. Spahn, Donald Y. M. Leung.

Childhood Asthma. Nelson Textbook of Pediatrics
Involved:
Dendritic cells and macrophages
present antigens to T-helper cells induce the switching of B
lymphocytes to produce IgE
T-helper lymphocytes
Mast cells
Eosinophils
Leads to
episodes of wheezing
Coughing
tightness in the chest
Breathlessness
shortage of breath specially at night and in the morning

Inflammation causes obstruction of airways

by:
Acute bronchoconstriction
Swelling of bronchial wall
Chronic production of mucous
Remodeling of airways walls
The inflammatory reaction goes on for a long

period
Changes
Epithelial cells
damaged and the cilia are lostsusceptible for infection

goblet cells increasedincrease in the secretions
function of the muco-ciliary escalator lostsecretions
accumulate in the lungs
The basement membrane

Smooth muscle cells
Hyperplasiaability to secrete
contractility increased airway hyper-responsiveness.
The neurons
developed local reflexes

http://www.public.asu.edu/
~shaydel/research_001tb_2.ht
ml
http://ars.els-cdn.com/content/image/1-s2.0-S1369527409001866gr2.jpg
Latent TB
infection (LTBI)
tubercle bacilli are

in the body
inactiveno
disease
the Mantoux
tuberculin skin test
TB disease
immune system
cannot keep the
tubercle bacilli
under control
the bacilli begin to
multiply rapidly
Clinical
manifestation
http://www.eac.int/health/images/tb/ex
posure.jpg
62. PHYSIOLOGY OF THE HORMONE
http://wmaresh.wikispaces.com/file/view/antpostpit.JPG/167267823/antpostp
it.JPG
Growth
Hormone
Physiology of Growth Hormone Secretion. Aysun Bideci, Orhun

amurdan.2008. in http://www.jcrpe.org/sayilar/27/buyuk/29132-1-GH.pdf
Secreted in pulsatile
fashion anterior
pituitary gland
Regulated by:
Growth hormonereleasing hormone

(GHRH)
stimulates both the
synthesis and the

release of GH
Somatostatin
inhibits the release of
GH
IGF
end product of GH
bioeffect
negativefeedback effect
on GH secretion
http://pharmaxchange.info/press/wpcontent/uploads/2011/03/pharm2009.08.fig1_.gi
f
Allen DB. Growth Hormone Treatment. In: Lifshitz, F (eds). Pediatric Endocrinology. 4th edition. New York, NY. Marcel Dekker Inc.
2003;87-111.
http://www.healio.com/~/media/Images/News/Online/Endocrinology/2009/06_June/01/Sperling_fig2_450_288_42087.gif
BIOEFFECTS
http://novocrine.com/images/stories/ho
w-gh-works.jpg
Growth Hormone
Deficiency
Proportional short stature

Below-normal velocity of
growth
Delayed physical
maturation
The child may look
younger than other
children his or her age
Delayed bone age
Increased amount of fat
http://trialx.com/curetalk/wparound the waist
content/blogs.dir/7/files/2011/05/diseases/Growth_
Delayed tooth development Hormone_Deficiency-3.jpg
http://en.wikipedia.org/wiki/Growth_hormone_defic
Delayed onset of puberty iency#Pathophysiology
http://www.emedicinehealth.com/growth_hormone_d
eficiency/page3_em.htm#growth_hormone_deficiency_
symptoms
http://en.wikipedia.org/wiki/Thyroid
Thyroglobulin synthesized in the rough endoplasmic reticulum enter the colloid

in the lumen of the thyroid follicle
Sodium-iodide (Na/I) symporterpumps iodide (I-) actively into the cell enters the
follicular lumen by the pendrin
In the colloid(I-) is oxidized to iodine (I0) by an enzyme called thyroid peroxidase.
Iodine iodinates the thyroglobulin at tyrosyl residues in its protein chain
In conjugation, adjacent tyrosyl residues are paired together
The entire complex re-enters the follicular cell by endocytosis.
Proteolysis by various proteases liberates thyroxine and triiodothyronine molecules,
which enters the blood by largely unknown mechanisms.
http://en.wikipedia.org/wiki/Th
http://www.montp.inserm.fr/u632/images/TRCAR1.gif
Causes:
Deficient production of thyroid

hormone
Disgenesis congenital
Hypothyroidism
Iodine deficiencyendemic
goiter
http://indianclinicalknowledge.com/wpcontent/uploads/2012/07/20120730-092014.jpg
Defect in thyroid hormonal

receptor activity
Enlargement of the thyroid gland

Fuctions:
Normal function of the gland (euthyroidism)
Thyroid deficiency (hypothyroidism)
Overproduction of the hormones (hyperthyroidism)
Cause:
Congenital or acquired
Endemic or sporadic
Increased pituitary secretion of thyrotropic hormone in
response to decreased circulating levels of thyroid
hormones.
Infiltrative processes inflammatory or neoplastic
Thyrotropin receptor-stimulating
antibodiesthyrotoxicosis
Goiter. Nelson Textbook of

Pediatrics
http://findmeacure.com/2008/04/13/growthdisorders/
Disorder
Definition
Primary
amenorrhea
Absence of menstruation in a woman by the age of 16.

Women by the age of 14 who still have not reached
menarche, plus having no sign of secondary sexual
characteristics such as thelarche or pubarche
Secondary
amenorrhea
An established menstruation has ceased for 3 months in

a woman with a history of regular cyclic bleeding, or for
9 months in a woman with a history of irregular periods
Despopoulos A, Silbernagl S. Color atlas of physiology. 5th ed. Thieme;
Amenore bisa terjadi akibat kelainan di otak,

kelenjar hipofisis, kelenjar tiroid, kelenjar adrenal,
ovarium maupun bagian dari sistem reproduksi
lainnya.
Dalam keadaan normal, hipotalamus
mempengaruhi kelenjar hipofisis untuk
melepaskan hormon-hormon yang merangsang
dilepaskannya sel telur oleh ovarium.
Pada penyakit tertentu, pembentukan hormon
hipofisis yang abnormal bisa menyebabkan
terhambatnya pelepasan sel telur dan
terganggunya serangkaian proses hormonal yang
terlibat dalam terjadinya menstruasi.
Penyebab amenore primer:

1. Tertundanya menarke (menstruasi pertama)
2. Kelainan bawaan pada sistem kelamin (misalnya
tidak memiliki rahim atau vagina, adanya sekat pada
vagina, serviks yang sempit, lubang pada selaput yang
menutupi vagina terlalu sempit/himen imperforata)
3. Penurunan berat badan yang drastis (akibat
kemiskinan, diet berlebihan, anoreksia nervosa, bulimia,
dan lain lain)
4. Kelainan bawaan pada sistem kelamin
5. Kelainan kromosom (misalnya sindroma Turner atau
sindroma Swyer) dimana sel hanya mengandung 1
kromosom X)
6. Obesitas yang ekstrim
7. Hipoglikemia
Penyebab amenore sekunder:

1. Kehamilan
2. Kecemasan akan kehamilan
3. Penurunan berat badan yang drastis
4. Olah raga yang berlebihan
5. Lemak tubuh kurang dari 15-17%extreme
6. Mengkonsumsi hormon tambahan
7. Obesitas
8. Stres emosional
Istilah
Definisi
Menorrhagia
Menstruasi yang memanjang (> 7 hari) atau lebih banyak

dari biasanya (>80 mL)
Metrorrhagia
Perdarahan di antara siklus menstruasi
Hypomenorrhea
Menstruasi yang memendek atau lebih sedikit dari

biasanya
Oligomenorrhea
Siklus menstruasi dengan lama siklus >35 hari
Endometrium
Myometrium
Penebalan endometrium
akibat
penambahan/pembesaran
kelenjar endometrium
merupakan prekursor dari
keganasan endometrium
Faktor risiko:
Obesitas overproduksi estrogen endogen pada premenopausal

menyebabkan feedback negatif abnormal oligo/an-ovulasi
endometrium terpapar estrogen menstimulasi the transcription of genes
for cyclin D, protooncogenes, growth factors, dan growth factor receptors
Unopposed estrogen therapy
Faktor menstruasi: usia menarche terlalu awal dan usia menopause terlalu
tua meningkatkan risiko
Lingkungan
Usia tua
Riwayat keluarga
Mutasi BRCA1 atau BRCA2
Tamoxifen (obat kemoterapi) meningkatkan risiko
Penyakit penyerta, eg: DM, HT
Penggunaan pil kontrasepsi oral menurunkan risiko
Perokok memiliki risiko lebih rendah
Klinis
Diagnosis hiperplasia endometrium dapat dicurigai pada:
Wanita pasca menoupose (50-60 thn) dengan perdarahan uterus yang

banyak, lama, dan sering (< 21 hari)
Perdarahan uterus yang tidak teratur pada wanita menopause, atau
menjelang menopause.
Setelah disingkirkan adanya keganasan
Neoplasma jinak otot polos yang berasal dari

myometrium.
Berasal dari satu myosit progenitor
Perdarahan per
vaginam, menorrhagia
Dismenore
Berhubungan dengan
infertilitas
Kemungkinan karena
inflamasi/perubahan
vaskular endometrium
Bila penyebab organik dari perdarahan uteri

tidak dapat ditemukan, disebut DUB
Penyebab:
DUB anovulasi (~90% kasus)
Disfungsi aksis hipothalamus-thalamus-ovarium
anovulasi progesteron tidak dihasilkan
proliferasi endometrium perubahan vaskular
endometrium & penurunan prostaglandin
perdarahan
DUB ovulasi
Akibat dilatasi vaskular endometrium
Kelainan ginekologi jinak di mana terdapat

kelenjar endometrium dan stroma di luar
lokasi normal
Dapat ditemukan di peritonium pelvis,
ovarium, septum rektovaginal, ureter, vesika,
perikardium, dan pleura
Endometriosis di myometrium dinamakan
adenomyosis
Gejala utama: nyeri pada pelvis
Definisi
Terdapatnya Jaringan
endometrium diluar
rahim
Endometriosis di
myometrium
dinamakan
adenomyosis
Symptoms
Pelvic Pain (acute or
chronic)
Dyspareunia (painful
intercourse)
Painful bowel
movements
Premenstrual staining
and abnormal bleeding
Difficult urination
and/or blood present in
the urine
Infertility
Patofisiologi
Genetic, runs in the
family
Retrograde
menstruation
Lymphatic or vascular
spread
Coelomic metaplasia
Problems in the
immune system
Estrogen (natural and
synthetic)
Side Effect on Body

Linked to infertility
Miscarriages
Loss of reproductive
organs (hysterectomy)
Psychologically damaging
Chronic pain
Diagnosis
Most cases diagnosed

because of other
complication(s)
Laparoscopy is best detector
and treatment option
Klasifikasi
Mild- Rare, scattered
lesions, no scarring
Moderate- Minimal
adhesions and
superficial implants
Severe- Reproductive
organs are bound down
by growths, bladder
and/or bowel may also
become affected
Treatment
1. Surgical
2. Non-Surgical
Gonadotropin-releasing hormone agonists,
Danazol, Norethindrone, Gestrinone
All acyclic, some high androgen, others high
progesterone, all low estrogen
Negative side effects such as accelerated bone
loss, weight gain, nausea, breakthrough
bleeding
Pain killers (aspirin, morphine, and codeine)
Rongga panggul dibagi

atas dan bawah oleh
apertura pelvis superior
(pintu atas panggul,
PAP), dibentuk oleh :
promontorium os sacrum
di bagian posterior
linea iliopectinea (linea
terminalis dan pecten
ossis pubis) di bagian
lateral
symphisis os pubis di
bagian anterior
Pintu keluar panggul

disebut apertura pelvis
inferior (pintu bawah
panggul, PBP),
merupakan dua segitiga
yang bersekutu pada
alasnya (pada garis yang
menghubungkan kedua
tuber ischiadica)
Diameter anteroposterior pintu atas panggul (conjugata interna,

conjugata vera) (CV 12 cm)
Jarak antara promontorium os sacrum sampai tepi atas
symphisis os pubis. Tidak dapat diukur secara klinik pada
pemeriksaan fisis. Secara klinik dapat diukur conjugata
diagonalis, jarak antara promontorium os sacrum dengan
tepi bawah symphisis os pubis, melalui pemeriksaan
pelvimetri pervaginam.
Diameter transversa pintu atas panggul ( 13,5 cm)
Diameter terpanjang kiri-kanan dari pintu atas panggul.
Bukan sungguh "diameter" karena tidak melalui titik pusat
pintu atas panggul.
Diameter obliqua pintu atas panggul
Jarak dari sendi sakroiliaka satu sisi sampai tonjolan
pektineal sisi kontralateralnya (oblik/menyilang).
Diameter / distantia interspinarum pada rongga panggul ( 10,5 cm)
Jarak antara kedua ujung spina ischiadica kiri dan kanan.
Diameter anteroposterior pintu bawah panggul ( 7,5 cm)
Jarak antara ujung os coccygis sampai pinggir bawah
symphisis os pubis.
Diameter transversa pintu bawah panggul ( 10,5 cm)
Jarak antara bagian dalam dari kedua tuberositas os ischii.
Diameter sagitalis posterior pintu bawah panggul
Jarak antara bagian tengah diameter transversa sampai ke
ujung os sacrum.
Bidang Hodge I
Bidang Hodge II
Bidang sejajar H-I setinggi tepi

bawah simfisis
Bidang Hodge III
Bidang pintu atas panggul, dengan

batas tepi atas simfisis.
Bidang sejajar H-I setinggi spina

ischiadica
Bidang Hodge IV
Bidang sejajar H-I setinggi ujung

bawah os coccygis
Habitus
Situs
Letak memanjang
Letak melintang
Letak oblik
Presentasi
Fleksi mengikuti jalan lahir
Memanjang: kepala, sungsang

Melintang/oblik: bahu, punggung
Posisi
Hubungan antara bagian tertentu fetus

(ubun-ubun kecil, dagu, mulut, sakrum,
punggung) dengan bagian kiri, kanan,
depan, belakang, atau lintang, terhadap
jalan lahir
Two theories on the onset of human

parturition.
A.
Corticotropin-releasing hormone
prouduced by the placenta is secreted into
the fetal circulation and stimulates
corticotropin secretion from the anterior
pituitary of the fetus. Placental CRH,
through fetal ACTH, stimulates the fetal
adrenal to produce cortisol, which binds to
the placental glucocorticoid receptors to
block the inhibitory effect of progesterone,
further stimulating CRH production in
stimulative fashion.
B.
The fetal hypothalamic-pituitary-adrenal

axis is quiescent during the first half of
gestation because of its suppression by the
maternal influx of cortisol, but during the
second half of gestation, the rise in
estrogen gives rise to the placental enzyme
11b- hydroxysteroid dehydrogenase,
causing cortisol to be converted into its
inactive metabolite, cortisone. The
resulting negative glucocorticoid feedback
on the fetal pituitary gland (less cortisol
passes from mother to fetus) would result
in increased secretions of fetal ACTH,
cortisol and DHEA sulfate, resulting both
in fetal maturation and stimulation of
parturition.
PERSALINAN dipengaruhi
3 FAKTOR P UTAMA
1.
2.
3.
Power
His (kontraksi ritmis otot
polos uterus), kekuatan
mengejan ibu, keadaan
kardiovaskular respirasi
metabolik ibu.
Passage
Keadaan jalan lahir
Passenger
Keadaan janin (letak,
presentasi, ukuran/berat
janin, ada/tidak kelainan
anatomik mayor)
(++ faktor2 P lainnya :
psychology, physician,
position)
PEMBAGIAN FASE /
KALA PERSALINAN
Kala 1
Pematangan dan pembukaan
serviks sampai lengkap (kala
pembukaan)
Kala 2
Pengeluaran bayi (kala
pengeluaran)
Kala 3
Pengeluaran plasenta (kala
uri)
Kala 4
Masa 1 jam setelah partus,
terutama untuk observasi
HIS
Gelombang kontraksi ritmis

otot polos dinding uterus
yang dimulai dari daerah
fundus uteri di mana tuba
falopii memasuki dinding
uterus,
Resultante efek gaya
kontraksi tersebut dalam
keadaan normal mengarah
ke daerah lokus minoris
yaitu daerah kanalis
servikalis (jalan laihir) yang
membuka, untuk
mendorong isi uterus ke
luar.
Terjadinya his, akibat :

1. kerja hormon oksitosin
2. regangan dinding uterus oleh isi
konsepsi
3. rangsangan terhadap pleksus
saraf Frankenhauser yang tertekan
massa konsepsi.
His yang baik dan ideal meliputi :
1. kontraksi simultan simetris di
seluruh uterus
2. kekuatan terbesar (dominasi) di
daerah fundus
3. terdapat periode relaksasi di
antara dua periode kontraksi.
4. terdapat retraksi otot-otot
korpus uteri setiap sesudah his
5. Ostium uteri eksternum dan
internum terbuka
Kala 1
Fase laten :
pembukaan sampai mencapai 3 cm (8 jam).
Fase aktif :
pembukaan dari 3 cm sampai lengkap (+ 10 cm), berlangsung sekitar 6
jam. Fase aktif terbagi atas :
1. fase akselerasi (sekitar 2 jam), pembukaan 3 cm sampai 4 cm.
2. fase dilatasi maksimal (sekitar 2 jam), pembukaan 4 cm sampai 9 cm.
3. fase deselerasi (sekitar 2 jam), pembukaan 9 cm sampai lengkap (+ 10
cm).
Kala 2
Dimulai pada saat pembukaan serviks telah lengkap, berakhir pada saat
bayi telah lahir lengkap.
His menjadi lebih kuat, lebih sering, lebih lama, sangat kuat.
Kala 3
Dimulai pada saat bayi telah lahir lengkap, berakhir dengan lahirnya
plasenta.
Kala 4
Sampai dengan 1 jam postpartum.
Sifat his pada berbagai fase persalinan
Kala 1 awal (fase laten)

Timbul tiap 10 menit dengan amplitudo 40 mmHg, lama 20-30 detik.
Serviks terbuka sampai 3 cm. Frekuensi dan amplitudo terus meningkat.
Kala 1 lanjut (fase aktif) sampai kala 1 akhir
Terjadi peningkatan rasa nyeri, amplitudo makin kuat sampai 60 mmHg,
frekuensi 2-4 kali / 10 menit, lama 60-90 detik. Serviks terbuka sampai
lengkap (+10cm).
Kala 2
Amplitudo 60 mmHg, frekuensi 3-4 kali / 10 menit. Refleks mengejan
terjadi juga akibat stimulasi dari tekanan bagian terbawah janin (pada
persalinan normal yaitu kepala) yang menekan anus dan rektum.
Tambahan tenaga meneran dari ibu, dengan kontraksi otot-otot dinding
abdomen dan diafragma, berusaha untuk mengeluarkan bayi.
Kala 3
Amplitudo 60-80 mmHg, frekuensi kontraksi berkurang, aktifitas uterus
menurun. Plasenta dapat lepas spontan dari aktifitas uterus ini, namun
dapat juga tetap menempel (retensio) dan memerlukan tindakan aktif
(manual aid).
Non farmakologi
Bila kontraksi uterus dan dilatasi serviks
menimbulkan nyeri hebat dapat diberikan
analgesia kuat parenteral
Pudendal block
Spinal (subarachnoid
block)
Epidural block
Induksi persalinan adalah suatu

upaya stimulasi mulainya
proses persalinan (dari tidak
ada tanda-tanda persalinan,
distimulasi menjadi ada)
berbeda dengan akselerasi
persalinan
Indikasi:
Janin: kondisi ekstrauterin

akan lebih baik daripada
intrauterin, atau kondisi
intrauterin lebih tidak baik
atau mungkin membahayakan
Ibu: menghindari / mencegah
/ mengatasi rasa sakit atau
masalah2 lain yang dapat
membahayakan nyawa ibu
Metode:
Surgikal
Melepaskan / memisahkan
selaput kantong ketuban dari

segmen bawah uterus (stripping)
Manual (jari tengah/telunjuk)
Foley cathether
Memecahkan selaput kantong
ketuban (amniotomi)
Obat-obatan
Spartein sulfat, prostaglandin
(misoprostol), oksitosin
Obstetric Ilustrasi
Sixth ed dan
Williams Obstetric
Siklus Hormon
dan Menstruasi
Siklus Menstruasi
Akhir Siklus Mens
(LH <<)
Stimulasi FSH (anterior ptuitari)
FSH (stimulus folikel)
Folikel Hasilkan Estrogen >>
Siklus Endometrium
Awal Endometrium tipis (2mm)

Estrogen (Fase Poliferasi)
Hari 12 ( Ovulasi) tebal 10-12 mm
Feed back (-) FSH << dan LH >>

Folikel Pecah Corpus Luteum
Progesteron (Fase Sekresi)
Corpus luteum Progesteron
Endometrium hipertrofi, sekresi (utk

nidasi)
Progesteron >> Feed back

negatif LH << dan Prolaktin >>
Nidasi gagal, Proges << Mens
Kontrasepsi
1. Kontrasepsi hormonal
A. Kombinasi :
1. Oral
2. Transdermal
patch
3. Intravaginal ring
4. Injectables
B. Progesteron
1. Injectables
2. Susuk KB
(implant)
2. Alat kontrasepsi
dalam rahim
(Akdr = IUD)
a. Mengandung cu
b. Mengandung
levonorgestrel
3. Lain2 : kondom,
diafragma, pantang
berkala dll
Mekanisme
Estrogen
1.
Mencegah ovulasi (menekan
FSH)
2.
Mencegah implantasi (pengaruh
pada endometrium)
Progesteron
1.
Mencegah ovulasi ( menekan
LH)
2.
Mencegah sperma masuk ke
cervix (perubahan lendir cervix)
3.
Mencegah implantasi
(endometrium)
4.
Merangsang Hormon Prolaktin
Kontra indikasi
Thrombophlebitis
Penyakit cerebrovaskuler
atau coronaria
Diabetes dengan
kelainan vaskuler
Hypertensi
Kanker buah dada
Gangguan fungsi hati
Hamil
KOMPLIKASI IUD
Perforasi uterus
Abortus
Kram uterus
Perdarahan
Menorrhagia
Infeksi
KONTRA INDIKASI
IUD
Kehamilan
Infeksi pelvis
Kelainan Bentuk
Uterus
Genital actinomycosis
Cervicitis dan
vaginitis
Cervical dysplasia:
abnormal changes in the cells on the

surface of the cervix that are seen
underneath a microscope
Histology
cervical intraepithelial neoplasia

(CIN) I (mild) a benign viral
infection
CIN II (moderate),
CIN III (severe).
Cytology
low-grade SIL (squamous

intraepithelial lesion)low-grade
lesions
high-grade SIL (HSIL) highgrade dysplasia
Sexual activity
Number of sexual partners
Male partners with multiple
sexual partners
Uncircumcised male partner
Early sexual activity
(especially <16 years old)
Sexually transmitted
diseases
Human papillomavirus
Herpes simplex virus
Chlamydia trachomatis
Early age of first pregnancy
Parity
Low socioeconomic class

Cigarette smoking
Human immunodeficiency
virus
Immunosuppression from
any cause
Vitamin deficiencies and
nutritional factors
Interval since last Pap smear
Oral contraceptive use
greater tthan 5 years
Previous history of
squamous intraepithelial
lesion
http://media.jaapa.com/Images/2009/
E6 and E7 :
the oncogenic
proteins
Accuracy of the Papanicolaou Test in Screening for and Follow-up of Cervical Cytologic
Abnormalities: A Systematic Review
Kavita Nanda, MD, MHS; Douglas C. McCrory, MD, MHSc; Evan R. Myers, MD, MPH; Lori A. Bastian,
MD, MPH; Vic Hasselblad, PhD; Jason D. Hickey; and David B. Matchar, MD
http://www.sh.lsuhsc.edu/fammed/Images/PAP-
http://www.stevenchan.us/sites/default/files/goody/cervical-dysplasia-handout-without-notes.png
Hypertensive disorders
due to pregnancy are more
likely to develop in whom:
Are exposed to chorionic villi

for the 1st time.
Are exposed to a
superabundance of chorionic
villi (twins or mole).
Have preexisting vascular
disease.
Are genetically predisposed
to hypertension developing
during pregnancy.
Cunningham FG, et al. Williams obstetrics. 22nd ed.

McGraw-Hill.
Cytokines
(TNF & IL)
ROS & free

radicals
Self-propagating
lipid peroxidase
Production of
foam cells
Atherosis
Activation of
microvascular
coagulation
Trombocytopenia
Increased
capillary
permeability
Edema &
proteinuria
Oxidative stress
Increased interest in the potential benefit of antioxidants to prevent

preeclampsia: vitamin E, vitamin C, & carotene.
Other prevention: Cochrane Collaboration small to moderate benefit of
low-dose aspirin in preventing preeclampsia.
Cunningham FG, et al. Williams obstetrics. 22nd ed. McGraw-Hill.
For statistical purposes, fetal losses are

classified according to gestational age.
A death that occurs prior to 20
weeks' gestation is usually classified
as a spontaneous abortion;
those occurring after 20 weeks
constitute a fetal demise or stillbirth.
Missed abortion
the pregnancy has been retained
following death of the fetus
it is possible that normal
progestogen production by the
placenta continues while estrogen
levels fall, which may reduce
uterine contractility
Cunningham FG, et al. Williams obstetrics. 22nd ed.

McGraw-Hill.
The exposure of
procoagulant tissue extracts
to blood is a major
contributory factor in most
forms of DIC and is of
major pathogenetic
importance in cases
associated with abruptio
placentae & intrauterine
fetal death.
The active component of
such extracts is tissue factor
(thromboplastin); that is,
tissue factor interacts with
factor VIIa to activate the
extrinsic pathway of
coagulation.
Wintrobe Hematology. 12th ed.
Wintrobe Hematology. 12th ed.
Sheehan syndrome, is hypopituitarism, caused by

necrosis due to blood loss and hypovolemic shock
during and after childbirth
Most common initial symptoms of Sheehan's

syndrome are agalactorrhea and/or difficulties with
lactation.
Many women also report amenorrhea or

oligomenorrhea after delivery
Secondly, the anterior pituitary is supplied by a low
pressure portal venous system.
These vulnerabilities, when affected by major
hemorrhage or hypotension during the peripartum
period, can result in ischemia of the affected pituitary
regions leading to necrosis.
The posterior pituitary is usually not affected due to its
direct arterial supply.
Definisi Lama
Definisi Fungsional
Kehilangan darah > 500 mL setelah persalinan

pervaginam
Kehilangan darah > 1000 mL setelah persalinan
sesar (SC)
Setiap kehilangan darah yang memiliki
potensial untuk menyebabkan gangguan
hemodinamik
Insidens
5% dari semua persalinan
4T
Tone
- Atoni uterus
Tissue
- Sisa plasenta/bekuan
Trauma
- laserasi, ruptur,inversio
Thrombin - koagulopati
Gejala dan tanda

yang selalu ada
Gejala dan tanda yang

Kadang-kadang ada
Diagnosis
kemungkinan
Uterus tidak berkontraksi dan lembek

Perdarahan setelah anak lahir
(perdarahan pascapersalinan primer)
Syok
Atonia uteri
Perdarahan segera
Darah segar yang mengalir segera setelah
bayi lahir
Uterus kontraksi baik
Plasenta lengkap
Pucat
Lemah
Menggigil
Robekan jalan
lahir
Plasenta belum lahir setelah 30 menit

Perdarahan segera (P3)
Uterus kontraksi baik
Tali pusat putus akibat traksi

berlebihan
Inversio uteri akibat tarikan
Perdarahan lanjutan
Retensio
plasenta
Plasenta atau sebagian selaput

(mengandung pembuluh darah) tidak
lengkap
Perdarahan segera
Uterus berkontaksi tetapi

tinggi
fundus tidak berkurang
(kontraksi hilang-timbul)
Tertinggalnya
sebagian
plasenta
Gejala dan tanda

yang selalu ada
Uterus tidak teraba
Lumen vagina terisi massa
Tampak tali pusat (jika plasenta belum
lahir)
Perdarahan segera
Nyeri sedikit atau berat
Gejala dan tanda yang

Kadang-kadang ada
Syok neurogenik
Pucat dan limbung
Diagnosis
kemungkinan
Inversio uteri
Sub-involusi uterus
Anemia
Nyeri tekan perut bawah
Demam
Perdarahan > 24 jam setelah persalinan.
Perdarahan sekunder atau P2S. Perdarahan
bervariasi (ringan atau berat, terus menerus
atau tidak teratur) dan berbau (jika disertai
infeksi)
Perdarahan
terlambat
Endometritis
atau sisa
plasenta
(terinfeksi atau
tidak)
Perdarahan segera (Perdarahan

intraabdominal dan / atau pervaginam
Nyeri perut berat atau akut abdomen
Robekan
dinding uterus
(Ruptura uteri
Syok
Nyeri tekan perut
Denyut nadi ibu cepat
Postpartum
Hemorrhage
Management - Bimanual Massage
Replacement of Inverted Uterus
Replacement of Inverted Uterus
Bila
terjadi
perdarahan
terus-menerus,
kemungkinan gangguan koagulopati
Disseminated Intravascular Coagulation (DIC)
adalah suatu keadaan dimana bekuan-bekuan
darah kecil tersebar di seluruh aliran darah,
menyebabkan penyumbatan pada pembuluh
darah kecil dan berkurangnya faktor
pembekuan
yang
diperlukan
untuk
mengendalikan perdarahan
PENYEBAB
Keadaan ini diawali dengan pembekuan darah
yang berlebihan, yang biasanya dirangsang
oleh suatu zat racun di dalam darah.
Karena jumlah faktor pembekuan berkurang,
maka terjadi perdarahan yang berlebihan.
Salah satunya wanita dengan HPP
Tinggi fundus
uteri berdasarkan
usia kehamilan
Bells palsy
merupakan paresis nervus fasialis perifer yang
penyebabnya tidak diketahui (idiopatik) dan bersifat
akut.
Penyebab tersering dari kelemahan wajah unilateral
yang muncul tiba-tiba adalah stroke dan Bells palsy.
Penyebab yang paling umum dari kasus Bells palsy
adalah HSV tipe 1, diduga akibat reaktivasi virus dari
tempat latennya.
Selain itu, yang banyak diperdebatkan adalah iritasi
terus-menerus dalam durasi yang cukup lama
menyebabkan pembengkakan nervus fasialis sehingga
terjepit diduga juga sebagai penyebab Bells palsy.
Sumber: Gilden DH. Bells palsy. N Engl J Med. 2004;351(13):1323-1331.
Ada 4 teori yang dihubungkan dengan etiologi Bells palsy yaitu :

1. Teori Iskemik vaskuler
Nervus fasialis dapat menjadi lumpuh secara tidak langsung karena
gangguan regulasi sirkulasi darah di kanalis fasialis.
2. Teori infeksi virus
Virus yang dianggap paling banyak bertanggungjawab adalah
Herpes Simplex Virus (HSV), yang terjadi karena proses reaktivasi
dari HSV (khususnya tipe 1).
3. Teori herediter
Bells palsy terjadi mungkin karena kanalis fasialis yang sempit pada
keturunan atau keluarga tersebut, sehingga menyebabkan
predisposisi untuk terjadinya paresis fasialis.
4. Teori imunologi
Dikatakan bahwa Bells palsy terjadi akibat reaksi imunologi
terhadap infeksi virus yang timbul sebelumnya atau sebelum
pemberian imunisasi.
PATOFISIOLOGI
Kerusakan pada endotelium dari kapiler menjadi edema dan
permeabilitas kapiler meningkat
kebocoran kapiler edema pada jaringan sekitarnya
Terjadi gangguan aliran darah sehingga terjadi hipoksia dan asidosis
yang mengakibatkan kematian sel.
Kerusakan sel ini mengakibatkan hadirnya enzim proteolitik,
terbentuknya peptida-peptida toksik dan pengaktifan kinin dan
kallikrein sebagai hancurnya nukleus dan lisosom.
Jika dibiarkan dapat terjadi kerusakan jaringan yang permanen.
No. 32
Batang otak terdiri dari

1. Mesencephalon
2. Pons
3. Medulla Oblongata
Bagian otak yang pendek & terkontriksi, yg

menghubungkan pons & cerebellum
Fungsi: jalur penghantar & pusat refleks
Korpora quadrigemina kolikulus superior
(berkaitan dgn refleks visual) & inferior (berkaitan
dengan refleks auditori)
Pedunkulus cerebralis dua berkas serabut silindris yg
terbentuk dari traktus ascenden & descenden yg
membentuk bagian dasar mesencephalon
Mengandung aquaductus Sylvius saluran yg
menghubungkan ventrikel 3 dgn ventrikel 4.
Mengandung nuklei saraf cranial III, IV dan V

(sebagian)
Terdapat substansi Nigra area neuron
berpigmen yg penting dlm fungsi motorik
Terdapat nukleus merah masa neuron merah
muda berbentuk oval berperan dlm tonus otot
& postur
Terdiri dari substansi alba

Menghubungkan medulla dgn berbagai bagian otak melalui
pedunkulus cerebralis
Pusat respiratori, mengatur frekuensi & kedalaman
pernafasan
Terdapat nuklei saraf kranial V, VI, VII & VIII
Panjang sekitar 34 cm
Berawal dari pons foramen magnum
Bagian depan medulla pyramid (tonjolan
substansi putih, yg merupakan lanjutan dari
akson pada pedunkulus cerebri
Bagian belakang sebagian lanjutan traktus
sensorik. Nuklei pusat pemancar informasi
yg dikirim ke pusat otak yg lebih tinggi atau ke
cerebellum
Pusat medulla nuklei yg brperan dlm

pengendalian fungsi spt frekuensi jantung, TD,
pernafasan, batuk, menelan & muntah
Dalam medulla terdapat nuklei N IX, X, XI & XII
Decussatio pyramid di area

superior MS
Pyramida menonjol keluar krn
85% serabut piramida
bersilangan ke sisi lain medulla
spinalis
Traktus
pyramidalis/kortikospinalis
lateral jalur motorik utama
dari cerebrum ke MS
Sisa 15% akson akan memanjang
pada traktus kortikospinalis, dan
bersilangan di MS
Merupakan jaring2 serabut saraf & badan sel yg

tersebar di keseluruhan bagian MO, pons &
mesencephalon
Berfungsi untuk memicu & mempertahankan
kewaspadaan & kesadaran
is a progressive, neurodegenerative
disease that occurs when the
neurons within the brain
responsible for producing the
chemical dopamine become
impaired or dies
Symptoms:
Tremor
Rigidity stiffness and inflexibility
of the limbs, neck and trunk
Akinesia/bradykinesia slow
movement, hypofoni, mask face
Postural instability a tendency to
be unstable when standing upright
excitatory
inhibitory
The increased
inhibition of the
thalamus is central
to PD's effects.
Reduced input to
the motor cortex
leads to rigidity,
bradykinesia, and
the other PD
symptoms.
Guillain-Barre Syndrome (GBS)

Salah satu penyakit demyelinasi saraf. Juga
merupakan salah satu polineuropati, karena
hingga sekarang belum dapat dipastikan
penyebabnya.
Namun karena kebanyakan kasus terjadi
sesudah proses infeksi, diduga GBS terjadi
karena sistem kekebalan tidak berfungsi.
Gejalanya
Kelemahan otot (parese hingga plegia),
biasanya perlahan, mulai dari bawah ke atas.
Jadi gejala awalnya biasanya tidak bisa
berjalan, atau gangguan berjalan.
Sebaliknya penyembuhannya diawali dari
bagian atas tubuh ke bawah, sehingga bila ada
gejala sisa biasanya gangguan berjalan
(Fredericks et all 1996).
Fase progresif.
Umumnya berlangsung 2-3 minggu, sejak
timbulnya gejala awal sampai gejala menetap,
dikenal sebagai titik nadir. Pada fase ini akan
timbul nyeri, kelemahan progresif dan
gangguan sensorik; derajat keparahan gejala
bervariasi tergantung seberapa berat serangan
pada penderita.
Fase plateau.
Fase infeksi akan diikuti oleh fase plateau yang
stabil, dimana tidak didapati baik perburukan
ataupun perbaikan gejala. Serangan telah
berhenti, namun derajat kelemahan tetap ada
sampai dimulai fase penyembuhan.
Fase penyembuhan
Sistem imun berhenti memproduksi antibodi
yang menghancurkan myelin, dan gejala
berangsur-angsur menghilang, penyembuhan
saraf mulai terjadi.
Sebagai akibat dari gangguan motorik dan sistem saraf

otonomik, terjadi gangguan kardiopulmonari.
Berawal dari nafas berat, oleh karena kelemahan otot
pernafasan (baik otot intercostal maupun diafragma),
hingga gangguan ritmik oleh karena gangguan saraf
otonomik.
Akibatnya fungsi paru menjadi terganggu. Paru tidak
bisa mengembang secara maksimal akibatnya
kapasitas vital menurun, dan bisa menimbulkan
atelektasis.
Bila kondisi ini berlanjut, bisa terjadi infeksi paru,
pneumonia, yang akan memperburuk kondisi.
Bila fungsi glotis terganggu, akibat terganggunya
sistem otonomik, penderita mungkin akan tersedak.
Sehingga makanan masuk ke saluran pernafasan, dan
akan menambah infeksi paru.
MG merupakan kelainan transmisi neuromuskuler

dengan karakteristik kelemahan dan fatigue otot
skeletal.
Kelainan yang mendasari MG adalah berkurangnya
jumlah reseptor asetilkolin (AChR) pada membran otot
postsinaptik akibat reaksi autoimun didapat yang
menghasilkan antibodi anti-AChR.
90% pasien MG mengalami manifestasi oftalmik. Ptosis
sendiri merupakan tanda yang prominen dari MG.
Fatigue merupakan karakteristik kelopak mata
myasthenik, dan biasanya disertai variasi diurnal atau
variasi aktivitas, dan bertambah berat setelah menatap
(terutama ke atas) dalam jangka waktu yang lama.
Sumber: Awwad S. Ophthalmic manifestations of Myasthenia Gravis. 2011.
Penyebab ptosis secara patofisiologis antara lain:

Aponeurotic or mechanical ptosis
Floppy eye syndome biasanya disertai keratitis atau
konjungtivitis, sensasi benda asing, injeksi konjungtiva, dan
ada kotoran mata. Biasanya berhubungan dengan OSA
(obstructive sleep apneu).
Neurogenic ptosis (n. III) biasanya disertai defisit neurologis
lainnya
Myopathic ptosis
Disorder of neuromuscular junction myasthenis
gravis. Ptosis merupakan tanda yang prominen
dari myasthenia gravis.
Disorder of the muscle chromic progressive external
ophthalmoplegia, biasanya disertai gerakan ektraokuler yang
lambat dan terbatas, kedua mata biasanya simetris
Traumatic ptosis
Pseudoptosis
Increased of ICP
(mass in one of the hemispher,

the fossa posterior, SAH)
Mechanical distortion of the

lower brainstem
Stimulating mechanically
sensitive region in
paramedian cauda medulla
Triad: hypertension,
bradycardia, & slow, irregular
breathing
When ICP is elevated, there

is a reduction of cerebral
perfusion pressure (CPP) &
ultimately of cerebral blood
flow.
Fluctuation in mean arterial
pressure (MAP) also affect
CPP according to the
formula: MAP-ICP = CPP.
When ICP is elevated, an
increased of MAP may
maintain the CPP.
Ropper AH, Brown RH. Adam & Victors principles of neurology. 8th ed. McGraw0Hill; 2005.
Brust JCM. Current diagnosis & treatment neurology. 1st ed. McGraw-Hill; 2007.
Seizure:
episodes of temporary brain
dysfunction secondary to abnormal
electrical activity.
Epilepsy
two or more unprovoked seizure
(having no identifiable acute,
Inhibitory
proximal cause).
Excitatory
glutaminergic
activity
Population
ofpathologically
excitable neurons
GABA-nergic
projections
Seizure
1. Brust JCM. Current diagnosis & treatment neurology. 1st ed. McGraw-Hill; 2007.
2. Harrisons principles of internal medicine. 18th ed. McGraw-Hill;
3. Silbernagl S, Lang F. Color atlas of pathophysiology. 1st ed. Thieme; 2000.
Rohkamm R. Color atlas of neurology. 1st ed. Thieme: 2004.
Antiepileptic drugs appear to act primarily

by blocking the initiation or spread of
seizures through a variety of mechanisms:
Inhibition of Na+-dependent action
potentials (e.g., phenytoin,
carbamazepine, lamotrigine, topiramate)
inhibition of voltage-gated Ca2+

channels (phenytoin, gabapentin,
pregabalin),
attenuation of glutamate activity

(lamotrigine, topiramate, felbamate),
potentiation of GABA receptor function
(benzodiazepines & barbiturates),
increase in the availability of GABA
(valproic acid, gabapentin, tiagabine),
modulation of release of synaptic vesicles
(levetiracetam),
inhibiting T-type Ca2+ channels in
thalamic neurons (ethosuximide &
valproic acid)
Ropper AH, Brown RH. Adam & Victors principles of neurology. 8th ed. McGraw-Hill; 2005
Acute bacterial meningitis
MENINGITIS
the meninges
ENCEPHALITIS
confined to the
parenchyma
diffuse and/or focal
neuropsychological
dysfunction
acute onset
neutrophilic pleocytosis
Etiology:
Pneumococcal meningitis
Haemophilus influenzae
meningitis
Staphylococcal meningitis
Meningococcal meningitis
Viral meningitis
Etiology:
enterovirus meningitis
herpes simplex virus [HSV]
Chronic meningitis
Etiology:
M. Tb
Fungal
Bacterial entry into the CNS

Elicits the release of many factors
from host cells (macrophages,
microglia, astrocytes, endothelial
cells and infiltrating inflammatory
cells)
Exacerbate host cellular responses
Resulting in neuronal injury
BBB: bloodbrain barrier;

EAA: excitatory amino acids
ICAM: intercellular adhesion molecule
MMP: matrix metalloproteinases
NO: nitric oxide
ROS: reactive oxygen species
TACE: tumour necrosis factor- (TNF)converting enzyme.
http://www.nature.com/nrn/journal/v4/n5/images/nrn1103f5.jpg
http://www.medicinesia.com/wp-content/uploads/2012/01/Fisiologi-Meningitis-Bakteri.jpg
Meningitis
Distinguishing
the benign from
the serious JAAPA.htm
Etiology
Viral
HSV types 1 and 2 (the latter much more common in
neonates than adults)

VZV
EBV
measles virus
mumps virus
rubella virus
Bacterial pathogensMycoplasma species

Toxoplasma gondii
The virus replicates outside the CNS

Gains entry to the CNS
Across the blood-brain barrierenters neural cells
Disruption in cell functioning

perivascular congestion
Hemorrhage
diffuse inflammatory response that disproportionately affects gray matter
over white matter
Regional tropism associated with certain viruses is due to neuron

cell membrane receptors found only in specific portions of the
brain, with more intense focal pathology in these areas
hematogenous spread
travel along neural pathwaysrabies virus, HSV, VZV
HSV predilection for the inferior and medial temporal lobes
Acute disseminated encephalitis and postinfectious

encephalomyelitis (PIE)measles infection,Epstein-Barr virus
(EBV) and CMV infections
immune-mediated processesmultifocal demyelination of perivenous

white matter.
http://emedicine.medscape.com/article/791896-overview#a0104
Jaras
syaraf
Traktus
Cortikospinal
ACA: anterior
Cerebry Artery
PCA: Lobus
Oksipital, serebri
ACA: Lobus Frontalis,

parietal, korpus
kalosum, baal
ganglia anterior,
kapsula interna
http://en.wikipedia.org/wiki/Lateral_medullary_syn
Latin origin: vertere, to spin

the illusion that the environment is spinning
a subtype of dizziness, where there is a feeling
of motion when one is stationery
Classification :
Peripheral
Central
Complex interaction of visual, vestibular

and proprioceptive inputs that the CNS
integrates as motion and spatial orientation
Normally there is balanced input

from both vestibular systems
Vertigo develops from
asymmetrical vestibular activity
Abnormal bilateral vestibular
activation results in truncal ataxia
Peripheral
1.
2.
3.
Physiological (motion sickness)

Benign paroxysmal positional vertigo (BPPV) most
common
Vestibular neuronitis
Labyrinthitis
Menire disease
Perilymph fistula
Central
Brainstem TIA/infarct
Posterior fossa tumors
Multiple sclerosis
Syringobulbia
Arnold - Chiari deformity
Temporal lobe epilepsy
Basilar migraine
Other
Cardiac, GI, psycogen, toxins, medications, anemia,

hypotension
Peripheral vertigo :
caused by problems
within the inner
ear/vestibular system;
also called otologic or
vestibular vertigo.
The most common
cause : BPPV (32%)
Central vertigo : arises from injury to the

balance centers of the CNS; less prominent
movement illusion and nausea.
Has accompanying neurologic deficits (e.g.
slurred speech and double vision), and
pathologic nystagmus (pure vertical/ torsional)
Is it true vertigo?
Autonomic
symptoms?
Pattern of onset and
duration
Auditory
disturbances?
Neurologic
disturbances?
Was there syncope?
Unusual eye
movements?
Any past head or neck
trauma?
Past medical history?
Previous symptoms?
Prescribed and OTC
medications?
Drug and alcohol
intake?
Vital Signs
Orthostatic BP Changes supine
and standing and look for a
change in pulse
Complete HEENT and Neuro
Exam
Otoscopy (Cerumen in EAC;

Tympanosclerosis/perforation;
Otitis Media)
Funduscopic exam.
Nystagmus
Pupillary abnormalities
EOM movements
Cranial Nerves exam.
Internuclear ophthalmoplegia
Auscultate for carotid bruits

Orthostatic vital signs
BP and pulse in both arms
Dix-Hallpike maneuver
Weber-Rinne test
Muscle strength
Gait and Cerebellar function
Rombergs test
Ask patient to stand

with the heels
together, first with the
eyes open, then with
eyes closed.
Note any excessive
postural swaying or
loss of balance
(+) when open or
closed : cerebellar
deficit (cerebellar
ataxia)
(+) only when closed :
propioceptive deficit
(sensory ataxia)
Vertigo associated with a characteristic mixed

torsional and vertical nystagmus provoked Dix
Hallpike test
A latency (1-2 sec) between the completiton of
the test and onset of vertigo and nystagmus
Paroxysmal nature of the provoked vertigo and
nystagmus (an increase and then a decline over
10-20 sec)
Fatigability (a reduction in vertigo and
nystagmus if the test is repeated)
Pain or discomfort between the orbit and

occiput, arising from pain-sensitive structures
Intracranial pain-sensitive structures : venous
sinuses, cortical veins, basal arteries, dura of
matter, middle and posterior fossae
Primary headaches
OR Idiopathic headaches
THE HEADACHE IS
ITSELF THE DISEASE
NO ORGANIC LESION IN
THE BEACKGROUND
TREAT THE HEADACHE!
Secondary headaches
OR Symptomatic headaches
THE HEADACHE IS ON LY
A SYMPTOM OF AN
OTHER UNDERLYING
DISEASE
TREAT THE UNDERLYING
DISEASE!
Tension type of
headache
Migraine
Cluster
headache
Other, rare
types of
primary
headaches
Was felt to be caused by excessive muscle contraction

with constriction of pain-sensitive extracranial
structures
However, no correlation between muscle contraction
and presence of TTHA
Vascular reactivity felt to play a role

However, temporal muscle flow is unaltered compared
to controls
Platelet 5HT is lower in patient with TTHA

some overlap with pathophysiology of migraine

Pembahasan TO1 Reguler PDF

Diunggah oleh

Informasi Dokumen

Judul Asli

Hak Cipta

Format Tersedia

Bagikan dokumen Ini

Bagikan atau Tanam Dokumen

Opsi Berbagi

Apakah menurut Anda dokumen ini bermanfaat?

Apakah konten ini tidak pantas?

Hak Cipta:

Format Tersedia

Pembahasan TO1 Reguler PDF

Diunggah oleh

Hak Cipta:

Format Tersedia

Pasien , 48 tahun

Blood Urea Nitrogen

Urea dihasilkan dari metabolisme

Produk pemecahan keatinin fosfat

Chronic renal failure

Laki-laki dewasa mudah merasa lemas. Sulit

Bilirubin direk = conjugated bilirubin

Excreted from the

Color Atlas of Pathophysiology

Color Atlas of Pathophysiology

Color Atlas of Pathophysiology

Hemostasis (hemo=blood; sta=remain)

Following an injury to blood vessels several

Injured blood vessel

Anemias are defined based on cell size (MCV) and

Anemia of folic acid

Iron deficiency anemia

Anemia (of macrocytic

Folate and vitamin B12

an X-linked recessive hereditary disease

Loud P2 (pulmonic) component

The sounds waves

Symptoms of heart failure

Diastole process by which

Nyeri kepala hilang timbul selama 1 minggu,

Keluhan 1 jam yang lalu nyeri dada seperti

Left coronary artery

Right coronary artery

Right ventricle (RV)

Obstructive lung disease reduced ventilation the ratio of the

Asma sudah 10 tahun

GINA Report 2011

-First third of exhaled gases mix

Two valves added to prevents:

GINA report 2011

Adrenal tuberculosis is a manifestation of

s the clinical condition resulting from chronic exposure

The most common cause: excess ACTH secretion from

Silbernagl S, et al. Color atlas of pathophysiology. Thieme; 2000.

Acute Effect of Diabetes

Silbernagl S, et al. Color atlas of pathophysiology. Thieme; 2000.

Silbernagl S, et al. Color atlas of pathophysiology. Thieme; 2000.

Dengue Infection: Classification

B. Physical exam : head to toe

An incised wound that is clean and sutured closed is

Blood loss (ml)

Blood loss (%)

Occurs when pleural space fills with blood

May put pressure on the heart

Where does the blood come

Lots of blood vessels

ABCs with c-spine

Monitor Cardiac Rhythm

Opening in lung tissue

Air builds in pleural

Each time we inhale,

Each time we inhale,

Accessory Muscle Use

ABCs with c-spine as indicated

Locate 2-3 Intercostal space midclavicular line

Urinary tract stone disease

Results from the absence

approximately 1 per 5000