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STEP1 > Gastropatho > Flashcards

Gastropatho Flashcards

1
Q

where are bile salts reabsorbed

A

terminal ileum

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2
Q

Heterotrophic salivary gland trapped in lymph node is

A

Warthin tumor

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3
Q

What is the mneumonic for warthin tumor

A

Warriors in germany love smoking

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4
Q

what is the most common salvary gland tumor

A

pleomorphic adenoma

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5
Q

2 main problems in achalasia

A

1) disordered esophageal motility

2) inability to relax LES ( loss of post ganglionic inhibitory neurons that contain NO and VIP)

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6
Q

what do we see on endoscopy in eosinophilic esophagitis

A

esophageal rings and linear furrows.

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7
Q

boerhave which part of the esophagus

A

distal esophageal rupture

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8
Q

difference between hematamesis of esophageal varices and mallory weis

A

wehde painful wehde painless

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9
Q

sclerodermal esopheag motillity due to what

A

smooth muscle atrophy –> dec LES pressure and dysmotility

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10
Q

what are drugs that cause pill esophagitis

A

bisphosphonates - tetracyclines - potassium chloride - NSAIDS and iron

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11
Q

plummer vinson has increased risk of

A

esopheal squamous cell carcinoma

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12
Q

Obesity can lead to ? cancer ? why?

A

adneocarcinoma due to increase in abdominal pressure that can lead to hiatel hernia –> gerd –> cancer ( adenocarcinoma )

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13
Q

achalasia can lead to what cancer

smoking to what

A

both can lead to squamous and adeno

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14
Q

squamous epithelium? adde mnl esophageous

A

upper 2/3 from esophageous

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15
Q

most common cause of squamous cell carcinoma is

A

alcohol

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16
Q

adult onset GERD . keep in mind

A

asthma

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17
Q

DM and GERD how does it present

A

ma bekun 3ndon heartburn w hal osas krml asln ma be7eso . bas they present as nocturnl cough and hoarsness

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18
Q

GERD histology

A

basal zone hyperplasia

elongation of lamina propria with scattered eosinphils and neutrophils

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19
Q

corpus of stomach is the

A

body

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20
Q

parietal cells location

A

body and fundus

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21
Q

Vit B12 def in a setting of autoimmune disease suggests

A

pernicous anemia

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22
Q

difference between ulcer and erosion

A

erosion : loss of epithelial layer ( can extend to muscularis mucusa y3ni b3dna bil mucusa )
ulcer : extends kela loss of mucusal layer - submucusa

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23
Q

chronic gastritis leads ato atrophy of parietal cells and ?

A

intestinal G cells metaplasia ( increase risk of gastric cancers ) and maltoma

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24
Q

H pylori affect what part of stomach

Autoimmune affect what part

A

H pylori: antrum and duedeum

Autoimmune : fundus / body

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25
Q

hypersensitivity of autoimmune gastritis

A

type 4 hypersensitivity ( CD4 +)

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26
Q

menetrier disease cause - can lead to - histology

A

hypoalbuminenia
gastric adenocarcinoma
hyperplasia not inflammation

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27
Q

type A blood increase risk of what cancer

A

Gastric intestinal

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28
Q

intestinal gastric cancer is more common where in stomach

A

lesser curvature

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29
Q

chronic gastritis increase risk of what >

A

intestinal gastric cancer

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30
Q

Gross image of gastric cancer diffuse

A

stomach wall grossly thickened ( llinitis plastica)

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31
Q

duedenal ulcer hypertrophy of what glands

A

brunner ( found in duedenum

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32
Q

Keef el H pylori bt2ze?

A

1) depletion of somatostain producing cells

release cytotoxins that inhibit proudction of bicarb –> ulcer

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33
Q

celiac disease what hypersenistivity?

A

type 4

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34
Q

dermatitis herpitififomis what layer

A

dermis papilla

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35
Q

celiac what layer

A

lamina propria

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36
Q

celiac increase risk of what cancer . if we control celiac, doe sthe risk decrease?

A

t cell lymphoma - no

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37
Q

Celiac disease HLA

A

HLAQ2 HLAQ8

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38
Q

lactose intolerance : stool ph keef ? why ?

A

decreased due to the colonic bacteria fermenting lactorse and changing it to short fatty acid like acetate w hek –> decrease pH of stool

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39
Q

pancreatic insuffieciency fat voluble be2el and what vit

A

VIT b12 ( unknown mechanism leh)

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40
Q

pancreatic insuffiecncy fe

A

dec in duedenal pH and fecal elastase

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41
Q

fecal elastase is a

A

noninvasive stool marker of pancreatic exocrine function

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42
Q

tropical sprue versus celiac sprue location

A

both deu je bas tropical kamem ileum

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43
Q

tropical sprue assocuated with what anemia

A

megaloblastic anemia ( folate andV12)

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44
Q

treatment of whipple

A

ceftriaxone

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45
Q

perianal disease asssociated with

A

crohn ( sah spares rectum bas ma khas el anus)

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46
Q

bile acid absorbed in

A

terminal ileum

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47
Q

TG absorbed in

A

jejunem

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48
Q

PAS

A

Carb in tissue

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49
Q

theory of tropical sprue

A

infection –> inflammation –> bacterial overgrowth

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50
Q

diverticulum lacks what layer

A

Muscularis layer

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51
Q

mnuemonic for zenker

A

Elderly MIKE

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52
Q

zenker cause

A

cricopharngeal problem inn motility –> increase pressure –> pouch muscle weaknes in psterior hypopharynx

53
Q

omphalomesentric cyst

A

cystic dilation of vitelline duct

54
Q

most common congenital anomaly of GI tract is

A

Meckel

55
Q

hirshprung cause

A

FAILURE of neural crest cell migration that occurs very early and happens caudally

56
Q

cause of intessuption in adults

A

tumor

57
Q

cause of intessuption in chidlren

A

rota virus

adenovirus –> peyer patches hypertrophy –> lead point( lymphooid hyperplasia_

58
Q

thumbprint sign due to mucusal edema seen in

A

colonic ischemia

59
Q

premature formula + postal vein gas

A

necrotizing enterocolitis

60
Q

well demarcated necrotic zones seen in

A

adhesion

61
Q

hirshprung associated with mutation in what?

A

RET

62
Q

which cancer more aggresisve the colitis associated or sporadic

A

colitis because mutifocal and flat earl p53 and late APC . 3ks lsporadic ( early APC and later p53)

63
Q

overexpression of COX 2 has been linked to ?

A

colorectal cancer .

64
Q

example of a mismatch repair gene

A

MLH1

65
Q

histology of cirrhosis

A

diffuse bridging fibrosis ( via stellate cells) and regenerative nodules

66
Q

cirrhosis lead to an increase in estrogen that leads to?

A

1) gynecomastia
2) spider angiomata
3) palmar erythema

67
Q

bil cirrhosis, sho by3mlo el stellate cells

A

they transform into myofibroblasts secrete TGF beta –> deposit type I collagen ( lie beneath the endothelial cells)

68
Q

what are the functional liver markers

A

albuminin- bilirubin - PT - platlets

69
Q

for Spontaneous bacterial peritonitis give C

A

cefotaxime

70
Q

AST is located where in the cell? and this explain why it is more affected by what pathology?

A

AST think inside so mitochondria and since alcohol is a mitochondrial liver toxin then it will be affected in alcoholic liver disease

71
Q

AST> ALT in NASH suggests

A

progression to fibrosis

72
Q

where do we see malory bodies

A

alcoholic hepatitis

73
Q

what are mallory bodies?

A

intracytoplasmic eosinophilic inclusions of damaged keratin filaments

74
Q

fibrosis and regenerative nmodule sthink

A

Alcoholic cirrhosis

75
Q

NASH long term can lead to

A

cirhosis and HCC

76
Q

swollen and necrotic hpatocytes with neurtophilic infiltration

A

alcoholic hepatitis

77
Q

which tumor secreats EPO

A

kidney - liver

78
Q

increase AFP

A

liver cancer, liver diseases

79
Q

aflatoxin from aspergillus induce what mutation

A

p53

80
Q

angiosarcoma

A

malignant associated with arsenic- vinyl chloride

81
Q

UCB or CB water soluble and can be filtered by kdiney out

A

CB loosly bound to albumin

82
Q

dubin johnson due to defect in what

A

MRP2 ( defective canalicular secretion)

83
Q

granulomatous destruction of bile ducts seen in

A

PBC

84
Q

what ethinicty is relayed to gall stone disease

A

Native american

85
Q

brown pigment stones are related to

A

infections ( mnruh 3nd mr.brown besir 3na infection)

86
Q

TPN and alcoholic cirrhois sassociated with what type of stones

A

pigment stones

87
Q

causes of acalculous cholecystitis :

A

gallbladder stasis- hypoperfusion(ischemia) - infection(CMV)

88
Q

failure to visualize gallbladder on HIDA suggest

A

obstruction

89
Q

calcified gallbladder is

A

porcelain

90
Q

ascending cholangitis

raynolds?

A 
jaundice
fever 
RUQ
reynolds:
altered mental status 
shock
91
Q

why does TPN lead to gallstones

A

because no nutrients reach the gut so no secretin-CCK - bile secretion–> cholesterol builds up

92
Q

what stones does crohn lead to ?

A

chol: no absoption of bile acids in terminal ileum .

andpigment since no absoption of Vit B12 –> hemolysis –> pigment stones

93
Q

leh akcoholic cirhosis lead to gallstones

A

liver cannotmake bile acid anymore

94
Q

where do we see suprammamary / impacted teeth

A

gardner syndorme

95
Q

what charactraistic of poly most relate with risk of malignanyc

A

size

96
Q

Villous adenoma release

A

mucus . so secreatry diarrhea

97
Q

which part of the colon is always involved in lynch

A

proximal colon

98
Q

right side tumors more associated with what mutations

left side tumors?

A

right side = microsatellite instability

left side = APC ( which is chromosomal instability pathway )

99
Q

what do we see on barium enema in colon cancer

A

apple core lesions

100
Q

loss of APC bil sura el kalemet ele tahet

A

decrease in intercellular adheson

increase in proliferation

101
Q

CRC with microsatellite instabikity pathway betun what poly

A

serrated

102
Q

APC on what chromosome

A

5

103
Q

in wilson , the mutation is in which gene

A

ATP7B

104
Q

wilson can present with what renal disease

A

Fancomi

105
Q

el deposits in wilson disease besiro bi aya membrane of eye

A

descemet

106
Q

wilson which chromosome/

A

chromosome 13

107
Q

ATP7B gene in wilsone responsible for

A

1) excreates Cu in bile

2) inserts cuppor in ceruloplasmin and release it to blood

108
Q

hallmark of Wilson

A

decrease cerulosplasmin in serum .

109
Q

what exam do we use to detect wilson kleyser fisher

A

slit lamp exam

110
Q

treatment of wilson

A

penicillamase
trientine
oral zinc

111
Q

hemochromastosis on ch . associated with which HLA , C282Y > H63D

A

6

HLA A3

112
Q

wilson increase risk of

A

hcc

113
Q

HISTOLOGY OF hemochromatosis is

A

micro nodular cirrhoisis

114
Q

hemochromatosis can lead to shi khaso bil gonads and shi joints

A 
hypogonadosim 
arthropathy ( callcium pyrophosphate deposition)
115
Q

labs in hemochromo . iron - ferritin - TIBC - saturation

A

high high low high .

116
Q

transfeerin saturation is

A

iron / TIBC

117
Q

treatment if hemochromo

A

chelation with deferasirox , rebeated phlebotomy , deferoxamine , defirprone

118
Q

with primary sclerosing cholangitis , fe increased risk of of 2 cancers

A

cholangiocarcinoma and gallbladder cancer

119
Q

granuloma in bile ducts

A

primary biliary cholangitis

120
Q

2 things increase risk of cholangiocarcinoma

A 
primary sclerosing cholangitis 
clonorchis sinesis( chinese liver fluke)
121
Q

primary biliary cholangitis looks on pathology like

A

graft versus host disease

122
Q

what drugs can increase risk of pancreattis

A 
sulfa drugs 
NRTI 
protease inhibitors 
GLP1 
6 MERCAPTO
123
Q

mneumonic of pancreatitis

A

I GET SMASHED

124
Q

3 complications of chronic pancreatitis

A

pancreatic insuff manifesting as steatorhea , fat soluble vit def , and diabetes - pseudocyst - splenic vein thrombosis

125
Q

gastric veins in fundus think

A

splenic vein thrombosis

126
Q

pancreatitis and child think

first cause pancreatitis and adults think

A

CF

Alcohol

127
Q

pancreatitic adenocarcvinoma when it presents, it presents as

A

abdominal pain radiating to the back

128
Q

courvoiser sign

A

obstructive jaundice with palpable non tender gallbladdder

129
Q

amylase and lipase in chronic pancreatitis can be

A

normal le2ano asln batal fe enzymes

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