git Flashcards

1
Q

what are the causes of toxic megacolon

A

pseudomembranous clotiis and ulcerative colitis
Nonsevere: leukocytosis < 15,000/mm3 and serum creatinine < 1.5 of baseline
Severe: leukocytosis ≥ 15,000/mm3 OR serum creatinine ≥ 1.5 of baseline
Fulminant: decreased blood pressure, shock, ileus or toxic megacolon

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2
Q

when do we place a tips

A

we place a tis if the patient has reccurent variceal hemorrhage it impairs ammonia clearnece

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3
Q

how does zollinger ellison syndrom e present

A

ulcers in the gastrium and dudodenum plus inactivation pf pancreatic enzyme = decreased absorption of fats

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4
Q

how does drug induced esophagitis look like

A

The characteristic finding on upper endoscopy is a punched-out ulcer with normal surrounding mucosa, often located at a site of anatomic narrowing

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5
Q

explain pathogensis of hepaticellular accumulation of lipids in obesity

A

In obese individuals, adipokines released from fat depots decrease the insulin sensitivity of peripheral tissue. Increased peripheral insulin resistance causes post-prandial hyperglycemia, which, in turn, increases insulin secretion. This hyperinsulinemia triggers lipid uptake as well as lipogenesis within hepatocytes (non-alcoholic steatosis). The precursors of triglycerides (e.g., fatty acids, glycerols) and the byproducts of lipid metabolism can cause hepatocellular damage (non-alcoholic steatohepatitis, NASH) by inducing oxidative stress

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6
Q

what causes sma syndrome

A
Rapid weight loss, severe burns or other
inducers of catabolism, prolonged bed rest
• Also caused by pronounced lordosis or
after surgical correction of scoliosis
• SMA gets trapped between transverse
portion (3) of duodenum and aorta
• Postpranidal pain, especially in LUQ
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7
Q

retroperitoneal hematoma

A
Retroperitoneal hematoma is a
common complication of abdo
and pelvic trauma. The pancreas
is a retroperitoneal organ, and
pancreatic injury is freq a source
of retroperitoneal bleeding.
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8
Q

pathopys of portal hypertension

A
Vasoactive agents cause venous
dilation of the splanchnic arterial
vasculature further intrahepatic
vasoconstriction > increased portal vein
hydrostatic pressure leading to ascites
• Kidney sense decreased perfusion and
activate RAAS
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9
Q

where is IMV located

A

IMV does not course with IMA
• IMV drains to splenic veins to portal
vein

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10
Q

what supplies the ant iliac crest

A

Deep circumflex iliac art: from external

iliac > supplies ant iliac crest

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11
Q

how does splenic laceration present with

A

Rigid abdomen and left shoulder pain

Kehr sign

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12
Q

what causes phrenc neerve irritation

A

(ruptured spleen,

peritonitis, hemoperitoneum, diaphragm

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13
Q

myocardial contusion

A

Mid anterior chest wall pain
• SOB
• Persistent tachycardia
• New ECG findings

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14
Q

drainage of hemarrhoids

A
hemorrhoids results from abn
distension of a portion of the anal
AV plexus. The vascular
components of internal
hemorrhoids drain into the sup.
rectal vein, which subseq drains
into the IMV. Band ligation of
hemorrhoids cuts off their blood
supply, causing them to degen
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15
Q

what is dynergic defecation

A
Dyssynergic defecation occurs
when the puborectalis muscle or
the int.or ext. anal sphincter fails
to relax during defecation,
leading to chronic constipation.
Dyssynergic defecation is usually
considered a fxnal disorder and
occurs more commonly in the
elderly but may also occur w/
certain neuro disorders (e.g. PD,
MS) or trauma.
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16
Q

why we have constipation in cauda equina

A
The pelvic splanchnic nerves (S2-
S4) provide parasympathetic
innervation to the bowel and
bladder, and their impairment in
CES can cause constipation and
difficulty urinating. Other SSx of
CES incl radicular LBP and leg
weakness (sciatic nerve) as well
as saddle anaesthesia (pudendal,
ilioinguinal nerves).
Gastrointestinal &amp; Nutrition
(GI)
Anatomy (Anat) 3
1525
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17
Q

where does the visceral fibres for appendicitis enter

A

afferent pain fibres entering at the

T10 lvl in the spinal cord.

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18
Q

how to identify appendiz

A
The teniae coli are 3 separate
smooth muscle ribbons that travel
longitudinally on the outside of
the colon and converge at the root
of the vermiform appendix
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19
Q

what are the two anatsomoses present in the intestine

A
the marginal artery
of Drummond, which is the
principal anastomosis, and the
inconsistently present arc of
Riolan (mesenteric meandering
artery).
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20
Q

manifestations of chronic gerd

A

impaired peristalsis, inflammation,

stricture or malignancy

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21
Q

portovaval anastomoses

A

L gastric vein > esophageal vein
• Sup rectal vein > mid and inf rectal vein
• Paraumbilical vein > sup and inf
epigastric vein

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22
Q

explain development of brown pigment stones

A
Brown pigment gallstones are
composed of Ca salts of
unconjugated bilirubin and arise
2° to bacterial or helminthic
infection of the biliary tract. β-
glucuronidase released by injured
hepatocytes and bacteria
hydrolyzes bilirubin glucuronides
to unconjugated bilirubin. The
liver fluke Clonorchis sinensis
has a high prevalence in East
Asian countries and is a common
cause of pigment stones.
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23
Q

explain mechanism of RAS

A

Ras GTP activated MAPK

> enters nucleus and influe

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24
Q

explain lactase deficiency how it works

A

Damaged cells and sloughed off and
replaced with immature cells with low
lactase concentration

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25
Q

what enzyme deficeintin homocystinuria

A

cystathionine synthase

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26
Q

base excision repair chemicals

A

Cytosine deamination to uracil
Excessive nitrite consumption promotes
cytosine to uracil, adenine to hypoxanthine,
and guanine to xanthine

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27
Q

explain the vitelline duct abnormalities

A

Persistent vitelline duct: meconium from
umbilicus
• Meckel: partial closure (patent portion
attached to ileum) > fibrous band may
connect to umbilicus
• Vitelline sinus: partial closure (patent
portion attached to umbilicus)
• Vitelline duct cyst (enterocyst): central
portion remains patent

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28
Q

umbilical hernia

A

Failure of umbilical ring to close

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29
Q

umbilical hernia

A
Failure of umbilical ring to close
defect in the linea alba and Px as
protrusions at the umbilicus that
are soft, reducible, and benign.
Associated with Downs, hypothyroid,
Beckwith Wiedemann
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30
Q

hirschprung disease

A
Make auerbach and meissner plexus
• Move from cranial to caudal
• Proximal colon by week 8
• Rectum by week 12
• Failure to migrate = Hirschsprung
(rectum and anus always involved, sigmoid
involved 75% of the time)
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31
Q

function of b cells in peyer patches

A

B cells migate to lamina propria in

Peyer’s patches > synthesize IgA dimers

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32
Q

Hepatic abscess

A
S. aureus can cause hepatic
abscesses via heme seeding of the
liver. Enteric bacteria (e.g. E.
coli, Klebsiella, and enterococci)
can cause hepatic abscesses by
asc the biliary tract (i.e. asc
cholangitis), portal vein pyemia,
or direct invasion from an
adjacent area
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33
Q

what causes cholangitis

A

E coli or Klebsiella

or enterococci

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34
Q

Isospora belli

A

diarrhea in hiv

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35
Q

hep c genome variation

A

Hypervariable genome coding for 2

envelope glycoprotein

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36
Q

which is the only polymerase with 5-3 activity

explain the hiv env protein

A
DNA Poly 1
• Only poly to have 5' >3' exonuclease
activity
s env GP seqs also contain
an HVR prone to freq genetic
mut.
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37
Q

MOA of shigella toxin

A

Inhibits protein synthesis by removing

adenine of 60S > preventing tRNA binding

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38
Q

salmoella action

A

Penetrates GI tract > travels to mesenteric
lymph nodes > picked up by macrophages
and survives

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39
Q

why ecoli EHEC

A

Do not ferment sorbitol (does not

produce glucuronidase)

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40
Q

MOA of yerseina entroclitica

A

Enterotoxin: increases cGMP causing

diarrhea

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41
Q

clostridium difficile MOA

A

Both inactive Rho regulatory proteins
involved with actin cytoskeletal structure
maintenance

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42
Q

camp jeujeni moa presentation

A

dogs). MFx usually
include fever, cramping
abdominal pain, and watery
diarrhea that may be bloody.

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43
Q

tell histopath of pseudomembranous colitis and most severe complication

A
associated with white, patchy
pseudomembranes on the bowel
mucosa. These pseudomembranes
consist of a neutrophilpredominant
inflammatory
infiltrate, fibrin, bacteria, and
necrotic epithelium. Patients may
develop a nonobstructive colonic
dilation known as toxic
megacolon, which can lead to
colonic perforation.
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44
Q

what bacteria can affect perforation of small bowel

A

candida

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45
Q

which bacteria causes intraabdominal abscess

A
B Fragilis is most common anaerobic
gram neg involved
• Forms abscess (special polysaccharide
forms abscess)
• E coli > enterococci > and strep are also
common
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46
Q

lethal complication of strongyloides stercalis

A

This can result in a
hyperinfec syndrome char by
massive dissem of the organism,
leading to MOD and septic shock

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47
Q

when do you have increased chances of hyperinfection

A

Hyperinfection also with
immunosuppression and HTLv 1 due to
lack of Th2 > no IgE and IgA

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48
Q

hepatic adenoma

A
regresses with ocp
right
lobe
• Associated with contraceptive and
anabolic steroids
• Prone to rupture
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49
Q

what base translocation alphatoxin causes

A

aflatoxin

exposure is a/w a G:C → T:A

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50
Q

explainn metastasis of ct

A

Multiple hypodense masses on CT
• Often outgrow vasculature > central
necrosis

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51
Q

pathogensis of gallbladder obstuction

A
Gallbladder outflow obstruction promotes
hydrolysis of luminal lecithin to
lysolecithin > disrupts mucusa >
epithelium expose to bile salts >
gallbladder hypomotility > increased
pressure > ischemia > bacteria (E coli,
Enterococcus, Klebsiella or Enterobacter
52
Q

weird causes of pleural effusion

A

Pancreatitis, esophageal rupture, chronic

hepatic and renal disease

53
Q

talk abt different ulcer locaion

A

ulcers
located in the oesophagus,
stomach (gastric), and colon

54
Q

where is cea levels increased

A

pancreatic ca,

COPD, cirrhosi

55
Q

diffuse esophegal spasm

A
Impaired inhibitory neurotransmission of
myenteric plexus
• Corkscrew on barium study
• Intermittent dysphagia to solids/liquids,
chest pain, heart burn
56
Q

what does manometry show on sclrdoerma

A
Manometry shows absent perstaltic wave
and low LES tone
incompetence of the LOS due to
atrophy and fibrous replacement
of the oesophageal muscularis.
57
Q

in zollinger ellison syndrome what is the effect of secretin on the gastrin
why do we have diarrhea

A

secretin increeases gastrin reelease

58
Q

pathophys of hpulori

A

Antral dominant gastritis
• Decrease somatostatin and increased
gastrin
• Secretin will decrease gastrin release

59
Q

pathophys of hpulori

A
Antral dominant gastritis
• Decrease somatostatin and increased
gastrin
• Secretin will decrease gastrin release
Diffuse gland atrophy and intestinal
metaplasia
60
Q

explain pathogensis of abetalipotreinmia

A
Accumulation of lipids in GI tract cells
(manifests in 1st year of life)
• Normally lipids are absorbed in
enterocytes and secreted as chylomicrons
(apoB48)
• Microsomal Triglyceride Transfer
Protein (MTP) funcations as chaperone
protein for apoB foliding
• MTP gene mutation > no apoB
• Very low plasma TAG (no VLDL due to
no apoB100)
• High risk of Vit E def > acanthocytes,
retinitis pigmentosa and subacute combine
degeneration
61
Q

what is bronchopulmonary sequesteration

A

Congenital malformation with extra,
nonfunctional lung tissue without
communication to tracheobronchial tree

62
Q

what is dubin johnson/why black liver

A

Conjugated hyperbilirubinemia

• Black liver due to epi metabolites

63
Q

explain cholestasis and its complications

A
Dilated bile canliculi with green brown
plugs and
yellowish green accumulations of pigment in
hepatic parenchyma
Causes
• Intrahepatic
• OCP and erythromycin
• Primary biliary cholangitis
• Pregnancy
• Primary sclerosing cholangitis (also
extra)
• Extrahepatic
• Choledocholithiasis
• Malignancy
Risk of fat soluble vit def
64
Q

Hep A histopath

A

hepatocyte swelling with wispy/clear
cytoplasm), councilman bodies and
mononuclear infiltrates

65
Q

hep b histopath and hep c histopath

A

dull eosinophilic
inclusions that fill the cytoplasm of
hepatocytes

Lymphoid aggregates within the portal
tracts and focal areas of macrovesciular

66
Q

biochemical mechanism of alcohol on liver

A
Decrease in FFA oxidation secondary to
NADH excess made during alcohol
metabolism
• Impaired lipoportein assembly and
secertion
• Increased TAG synthesis, increase
peripheral FA catabolism
• Lipid can be stained with oil red O or
67
Q

Pathogenesis of hemochromatosis

A

HFE mutation cause defecting transferrin
receptor > no hepcidin produced which
normally downregulates ferroportin

68
Q

what does viral hepatitis present with

A

fever,abdominal pain and jaundice

69
Q

acute cholecystitis

A

Fever, long RUQ pain after fatty meal

70
Q

mesentric adenitis

A

Yersinia

• Fever, RLQ pain, N/V

71
Q

complication of ulcerative colitis

A

fulminant colitis, toxic
megacolon, perforation, colon
adenocarcinoma

72
Q

presentation of toxic megacolon

A
typically present w/ abdo
pain/distension, bloody diarrhoea,
fever, and SSx of shock. Plain
abdo XR is the preferred Dx
imaging study. Barium contrast
studies and colonoscopy are c/i
due to the risk of perforation.
73
Q

ulcerivative colitis carcino, vs acs

A
MC malignancy in pt with IBD
(specifically UC) Colitis associated
carcinoma
• Multifocal by nature
• Affect younger pt
• Progress from flat and non polypoid
dysplasia
• Mucinous and have signet ring
• Early p53 mutation, late APC loss
• Distributed within proximal colon
74
Q

complications of mesentric ischemia

A

Complication: acidosis, gangrene,

perforation

75
Q

pathogensis of colonic diverticula

explain 3 different esophegal diverticula

A
sigmoid colon and develop
due to exaggerated contractions
of colonic smooth muscle
segments. This results in ↑
intraluminal pressure, causing
outpouching of the mucosa and
submucosa through the
muscularis (false diverticula).
Individuals (typically age >60)
may be aSSx or have
hematochezia or diverticulitis.
76
Q

classic signs seen in intussception

A
Impaired venous return causing ischemia
and necrosis
• MC at ileocecal junction
• Can be cause by Meckle diverticulum,
lymphoid hyperplasia due to infection,
foreign body, intestinal tumor
• Colicky pain, N/V, bloody "currant jelly"
diarrhea
• Palpable sausage like mass
• Barium enema is diagnostic and could be
therapeuti
77
Q

pathogensis of adenocarcsequence what is function of kras

A

Loss of APC > Upregulation of KRAS

and COX2 > inactivation of DCC and p53

78
Q

classify polpys

A

Hyperplastic: welL differentiate
• Inflammatory: UC and Crohns
• Submucosal: lipoma or lymphoid

79
Q

how does colon cancer present with how does rUC present with

A

constipation /uc Recurrent grossly bloody stool with low
grade fever
Tenesmus (painful straining on defecation
• Rectal adenocarcinoma

80
Q

apart from gallstones how to determine wehther patient has chronic pancreatitis

A
ast:akt +macrocytosis
Alcohol caues high protein
concentrate secertion from pancreas >
plugs up pancreas
• Direct toxic effect on acinar cell
• Will likely see macrocytosis
Can see hypernatremia due to large
third space fluid loss
81
Q

how long it takes to form pancreatic pseudocyst

A

Fibrosis around pseudocyst takes 4• 6
weeks
• MC location: lesser peritoneal sac

82
Q

pathogensis of pancreatitis and mesentric ischemia hitopath

A

Ischemia causes release of trypsin
causing autodigestion > now acute necrotic
pancreatitis

Dusky red and congested, subserosal
echymoses

83
Q

what is hepatocarcinoma present with

A

CD31 which is PECAM1

84
Q

presentation of glucagonoma

A

Necrolytic migratory erythema, DVT,

depression, diabetes

85
Q

cmv infection in git

A
CMV is a common cause of
colitis in pts w/ advanced AIDS.
It is the 2nd most common CMV
reactivation disease in this
population (CMV retinitis is the
most common). Pts w/ CMV
colitis often have abdominal pain,
fever, diarrhea, and weight loss.
Colonoscopy usually shows
erythema, erosions, and
ulcerations; coloni
86
Q

Intergluteal pilonidal disease

A

Skin infection of upper natal cleft or
buttocks
• Draining sinus tracts in the intergluteal
region

87
Q

vit e deficiency

A
Protects against lipid oxidation
• Neurons with long axons are most
susceptible
• Skeletal myopathy, spinocerebellar
ataxia, polyneuropathy, dorsal column
issues
• Hemolytic anemia
88
Q

differentiate between acute and chronic gastritis

A
Acute Helicobacter pylori
infection initially causes
nonatrophic antral gastritis and an
↑ risk for duodenal ulcers.
Chronic infection results in
patchy, multifocal, atrophic
gastritis w/ loss of parietal cells
and G cells in the gastric body;
this is a/w ↓ acid secretion and an
↑ risk of gastric ulcers, GAC, and
MALT lymphoma.
89
Q

what are council man bodies

A

round eosinophilic apoptotic bodies

90
Q

how is the histopathy of acute viral hepatitis

A
Acute viral
hepatitis is marked by panlobular
inflammation and hepatocyte
necrosis and ballooning. Tc cellmediated
signals also cause
hepatocyte apoptosis w/ the
formation of intensely
eosinophilic Councilman bodies.
91
Q

how does cmv colitis present with

A
colitis often have abdominal pain,
fever, diarrhea, and weight loss.
Colonoscopy usually shows
erythema, erosions, and
ulcerations intranucelar basophilic inclusion
92
Q

how do you chataceroize necrotizing entroclitis

A
affecting newborns.
It's characterised by bacterial
invasion and ischemic necrosis of
the bowel wall, and is a/w
prematurity and initiation of
enteral feeding
93
Q

explain pathophys of malrotation/volvulus and ladd bands

A

Lad bands
• Risk of volvulus
the ladl bands is a narrow mesentry that causes duodenal obstruction as well

94
Q

why do pregnant woman develop gerd

A
Pregnant women often develop
GERD due to ↑ lvls of estrogen
and progesterone, which relax the
smooth muscle of the LES. Later
in pregnancy, GERD can also
develop when the gravid uterus
presses on the stomach and leads
to an altered LES angle or ↑
gastric pressure.
95
Q

where do u see hsv esophagitis/esoinophilic esophagitis

A
HSV esophagitis is most common
in those w/ impaired cellmediated
immunity   EOO is a Th2 cell-mediated
disorder leading to eosinophilic
infiltration of the oesophageal
mucosa
96
Q

what is nutmeg liver

A
The centrilobular
necrosis, combo w/ relatively
normal-appearing periportal
regions (zone 1), creates an
overall heterogenous appearance
sometimes referred to as 'nutmeg
liver'.
97
Q

explain focal nodular hyperplasia

A

FNH is a benign liver tumor
marked by a central stellate scar
containing an abnormally large
artery.

98
Q

why prolonged fasting and TPN increases risk of gallstones

what decreases risk of gallstones

Aggregation of gallstones precipated by mucus hypersecretio, calcium, hypomotility

how is cholesterol excreted?excretion of free cholesterol into bile and conversion of cholesterol into bile acids.

A
The absence of normal enteral
stim in pts receiving TPN leads to
↓ CCK release, biliary stasis, and
↑ risk of gallstones. Resection of
the ileum can also ↑ the risk of
gallstones due to disruption of
normal enterohepatic circulation
of the BAs.

high bile salts and high PDC

99
Q

dubin johnson pathophys

A
defective hepatic
excretion of bilirubin
glucuronides across the
canalicular membrane, resulting
in direct hyperbilirubinaemia and
jaundice.
100
Q

how can mastocytosis cause PUD

A
Systemic mastocytosis is
characterised by the abn
proliferation of mast cells and ↑
hist release. Hist causes
hypersecretion of GA by parietal
cells in the stomach as well as a
variety of other SSx (e.g.
hypotension, flushing, pruritus
101
Q

explain biliary atresia

A
Obstruction of extrahepatic bile ducts
• Immune or viral destruction
• Jaundice within firs 2 months
• Dark urine and pale stools
• Hepatomegaly
• Elevated direct bili and GGT
• Intrahepatic bile duct pr
102
Q

exaplan jaundice in bresats milk

A

Breast milk jaundice peaks at 2 weeks
• Beta glucurondiase of milk deconjugates
bilirubin (indirect bilirubinemia

103
Q

how do you screen for fat malabsorption

A
Fats are easiest and first macro to be
effected
• Sudan Black 3 stain for qualitative stool
assay to confirm fat presence in stool
Ultrasound, CT or MRI
104
Q

why woman present with hematochromatosis later what happens if you take vitamin c

A

arthritis)
• Women present significantly later due to
blood loss during menstruation

105
Q

explain how cu is absorpbed

A
60% of Cu absorbed in stomach and
duodenum > binds to albumin and goes to
liver > binds to alpha2• globulin to for
ceruloplasmin
• Unabsorbed Cu is secreted in bile and
stool (main route of elimination)
• 15% of Cu excreted in the urine
106
Q

graft vs host reaction of liver

A

Lymphocytic infiltration and destruction

of the intrahepatic bile ducts of the liver

107
Q

what causes gallbladder hypomotility

A

Spinal cord injury, somatostatinoma, TPN

108
Q

pathophys of pancreatitis why vitmin A causes pancreatic insufficiency

A

Damage to pancreatic acinar cells >
activation a trypsin > activates other
zymogens (Chymotrypsinogen,
prophospholipase A2, proelastase)

109
Q

gastric bypass surgery side effects

A

colicky abdominal
pain, nausea, diarrhea > eat more frequent
smaller meals with low carbs

110
Q

how to differentiate between pancreatic causes of malabsroption vs mucosal

A
mucosal D xyulose not absroped 
pancreatic absorbed 
• Over 90% must be destroyed before
malabsorption
• Proteins, carbs and fats need enzymes
produced by pancreas to be absorbed
• d xylose test will be normal because it
is already a monosaccharide (will be
abnormal in malasorption due to
mucosal issue)
111
Q

new onset of esophagitis wit chronic gerd

A
New-onset odynophagia in the
setting of chronic GORD should
raise suspicion for erosive
oesophagitis w/ oesophageal
ulcers. Dx is made by upper
endoscopy.
112
Q

explain SIBO

A
Gastric bypass Sx can cause
SIBO due to excessive bacterial
proliferation in the blind-ended
gastroduodenal segment. SIBO
results in defic of most vits (B12,
A, D, and E) and Fe, but ↑
production of vitB9 and vitK
113
Q

speak about diabetic gastropariesis

A
Diabetic gastroparesis results
from the destruction of enteric
neurons due to chronic
hyperglycaemia, leading to
impaired relaxation and
disordered and ineffective
peristalsis. This causes delayed
gastric emptying, which presents
as postprandialfullness, regurgof
undigested food, nausea, and
vomiting.
114
Q

explain benefit of fish oil

A

Increase bile acid synthesis, decrease
cholesterol in bile, increased gallbladder
motility

115
Q

which two drugs is associated with blurry vision and dry mouth

A

meclizine, promethazineurinary retention, constipation

116
Q

what sort of diarrhea you have from crohns

A

secretary type because decreased absorption and inflamed mucosa =increased losses

117
Q

where do you see rectal prolapse

A

Protrusion of rectal mucosa through anus
• Pregnancy, constipation, cystic fibrosis
(kids)
• Can be seen in severe diarrhea

118
Q

how to prevent euphoria in morphine ppl

A
motility
• Can cause morphine like euphoria >
given with atropine to prevent abuse
(atropine causes blurred vision, nausea, dry
mouth)
• Adverse: rebound constipation
119
Q

which antibiotic i would use in diabetic gastroparesis

A

erythromycinErythromycin stims upper GI
motility by acting as an ag on
motilin receptors in the
muscularis externa

120
Q

fidoxamicin benefits

A

Used in recurrent C diff infections will

little effect on normal colonic flora

121
Q

how estrogen and progestrone cause stones what is the function of urosedxoycolic acid

A

Ursodeoxycholic acid: reduces biliary
cholesterol and more bile acid > promotes
stone dissolution
• High rate of recurrence
Estrogen: increase cholestrol production
Progesteron: decreases bile acid secretion
• Both cause stone
Phosphate binders: chronic kidney
disease/dialysis Severe weight loss: causes
bile stasis > stone

122
Q

explin intestinal phase of gastric acid production

A

Protein and low pH in duodenum
• Ileum and colon release petide YY
which binds to enterochromaffin like cells
to decrease acid secretion

123
Q

how to treat hepatic encephalopathy why rifaximin not recommended and why kcl is recommented

A

we want to prevent alkalosis so anything that reduces volume or use directic precopating factors

124
Q

why we need to measure bone density in PBC

A

osteoprorisis is adisease that accompanies bone density

125
Q

if an indicidual has a hepatitis c infection can he develop fulminant hepatitis

A

yes if hep A infection occurs