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GI II: Test 1 > Buzzin > Flashcards

Buzzin Flashcards

1
Q

colonizing oral cavity?

A
  1. strep mutans
  2. prevotella intermedia, porphyromonas gingivalis
    late: actinomycetem comitans
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2
Q

PAS stain

A

pseudohyphae, oral candidiasis

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3
Q

Tzanck smear, multinucleated cells

A

HSV

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4
Q

lesion in mouth thats bleeding

A

pyogenic granuloma

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5
Q

what is white and won’t scrape off?

A

hairy leukoplakia - see hyperparakeratosis w/ balloon cells - think EBV

Luekoplakia = premalignant lesion

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6
Q

Tobacco SCC?

A

p53 and NOTCH

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7
Q

pink squamous cells and mucin making cells neoplasia in mouth?

A

mucoepidermoid carcinoma

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8
Q

perineural invasion in mouth?

A

adenoid cystic carcinoma

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9
Q

polyhydramnios

A

think atresia

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10
Q

double bubble sign?

A

duodenal atresia - 30% have trisomy 21

also think annular pancreas

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11
Q

air in stomach on CXR?

A

think fistula

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12
Q

weak posterior/lateral aspect of diaphragm?

A

diaphragmatic hernia

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13
Q

high AFT levels in amniotic fluid

A

think omphalocele (OLDMA) or gastroschisis (YMA)

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14
Q

defect in anterior abdominal wall?

A

gastroschisis

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15
Q

why meckels?

A

failed involuation of vitelline duct

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16
Q

appendicitis you think….

A

maybe meckels in young kids!

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17
Q

projectile non bilious vomiting

A

pyloric stenosis

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18
Q

hirschsprung disease

A

megacolon! - see bilious vomiting

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19
Q

acquired megacolon?

A

chagas disease

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20
Q

pyrosis

A

heartburn

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21
Q

odynophagia

A

pain w/ swallowing

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22
Q

achalasia

A

increased tone of LES

secondarily due to chagas disease: trypanasoma cruzi

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23
Q

hiatal hernias

A

sliding = upper part of stomach –> diaphragm

rolling: upper fundus slids up esophagus

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24
Q

zenker diverticulum

A

pouches of esophagus due to increased pressure

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25
Q

mallory-wess laceration

A

retching/violent vomiting = lengwise tears

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26
Q

boerhaave syndrome

A

perforation of esophagus due to increased pressure

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27
Q

barrets

A

metaplasia (replacement): squamous cell to intestinal glandular mucosa w/ goblet cells

ADCA risk - length is most imp. risk factor >3cm

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28
Q

+mucicarcmine staine

A

ADCA

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29
Q

middle third of esophagus

A

SCC

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30
Q

mets of cancer in upper third esophagus?

A

cervical LNs

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31
Q

cancer in middle esophagus spread?

A

SCC - mediastinal, paratracheal,, tracheobronchial nodes

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32
Q

cancer in lower third esophagus?

A

think ADCA - spread gastric/celiac nodes

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33
Q

curling stress ulcer?

A

burns/trauma - proximal D

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34
Q

Cushing stress ulcer?

A

intracranial disease - see gastric, duodenal, esophageal ulcers

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35
Q

where’s h. pylori?

A

antrum / duodenum

spiral shaped, curved bacilli

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36
Q

chronic inflamm. of fundus?

A

AI diseae

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37
Q

chronic inflamm. or whole stomach?

A

drugs/alcohol

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38
Q

antral gastritis w/ high acid production, no hypergastrinemia

A

H pylori

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39
Q

+ ammonia in breath

A

due to urease in H. pylori infection

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40
Q

cancer assoc. w/ h pylori?

A

ADCA, MALT lymphoma

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41
Q

body/fundus gastritis w/ hypergastrinemia?

A

AI gastritis

AutoAbs to parietal cells and IF - loss of parietal cells

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42
Q

achlorhydria

A

defective gastric acid secretion

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43
Q

oxyntic

A

acid producing mucosa - parietal cells

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44
Q

air under diaphragm in CXR?

A

think PU that punctured through stomach

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45
Q

hematochezia

A

bright red blood in stools

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46
Q

EGD

A

upper GI endoscopy

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47
Q

hypertrophic gastropathies?

A

metetrier disease: xs secretion of TGF alpha: body/fundus ; w/l diarrhea, Peripheral edema

ZE syndrome : gastrin secreting tumor - see chronic diarrhea , multiple peptic ulcers

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48
Q

epithelial dysplasia in gastric tumor?

A

benign gastric adenoma/ a type of polyp

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49
Q

virchows node/ sister mary joseph node, axillary/irish node?

A

think gastric adenocarcinoma

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50
Q

two types of gastric adenomas?

A
  1. Intestinal type (non signet ring) - usual type
    - assoc. w/ H. pylori
    APC/WNT pathway
    - occur in gastric antrum/pulorus
    - form bulky ulcerative tumors
  2. Diffuse-type (signet ring)
    - not assoc. w/ h. pylori
    germline loss of fn. in E-cadherin (CDH1 gene)
    - infiltrate diffusely in wall of stomach
    - linitis plastica
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51
Q

MALToma

A

marginal zone B cell lymphoma - H. pylori related
arise in site of previous inflammation
CD19/20 +

see lyymphoepithelial lesions

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52
Q

GIST

A

mesenchymal gastro-intestinal stromal tumor

arise from interstitial cells of cajal

C-KIT/CD117 or PDGFRA mutations

see spindle cell features

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53
Q

C-KIT/CD117 +

A

mesenchymal GIST

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54
Q

direct vs. indirect hernia?

A 
direct = occur medial to epigastric 
indirect = lateral to epigastric
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55
Q

target sign on US

A

think intussuscpetion

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56
Q

red currant jelly stool

A

intussusception

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57
Q

coffee bean sign?

A

volvulus

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58
Q

primary vascular related GI bleeding?

A

Ischemic bowel disease, mural infarction, angiodysplasia, hemorrhoids

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59
Q

cocaine + abdominal pain/bloody diarrhea?

A

ischemic bowel disease

also think CMV and E. coli

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60
Q

watershed zones?

A

ischemic bowel disease - think splenic flexure, sigmoid colon, rectum

** most often colon!!!

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61
Q

dysentary

A

painful bloody diarrhea

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62
Q

secretory diarrhea

A

persist during fasting - think infectious; viral or enterotoxin

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63
Q

osmotic diarrhea

A

hypertonic fluid - abates w/ fasting - think lactase defic.

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64
Q

exudative diarrhea

A

due to mucosal damage –> purulent bloody stoools that persist w/ fasting - think bacterial or IBD

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65
Q

malabsorptive diarrhea

A

abates w/ fasting : see improper absorption –> bulky stools w/ xs fat

ex. celiac, giardia, CF, chronic pancreatitis

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66
Q

genetics of celiac?

A

HLA-DQ2/DQ8

diffuse/severe blunting of villi in D/J
malabsorption

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67
Q

dermatitis herpetiformis

A

subepidermal blistering of skin seen in 10% of celiac pts.

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68
Q

IgA anti-transglutaminase Ab

A

seen in Celiacs

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69
Q

MTP gene

A

mutated in abetalipoproteinemia:

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70
Q

oil red-o stain

A

abetalipoproteinemia:

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71
Q

acanthocytic red cells/ burr cells

A

abetalipoproteinemia:

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72
Q

guillan barre syndrome

A

campylobacter enterocoloitis

most common bacterial pathogen in developed countries and travelers diarrhea

see watery/blood diarrhea

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73
Q

bloody diarrhea, fever, ab. pain

A

shigellosis

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74
Q

rose spots

A

maculopapular rash on chest and abdomen - typhoid fever - salmonella typhi

may mimic appendicitis

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75
Q

ETEC

A

watery/secretory noninflamm. diarrhea

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76
Q

EHEC

A

O157:H7 –> HUS + bloody diarrhea

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77
Q

EIEC

A

dysentery

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78
Q

EAEC

A

nonbloody diarrhea, prolonged in AIDS

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79
Q

tropheryma whipplei

A

Whipple disease - se w/l, diarrhea/steatorrhea, and polyarthritis

see dense accum. of foamy macrophages in SI lamina propria –> accumulate in nodes and joints

** only one affecting lymphatic transport

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80
Q

which kills many children every year?

A

rotovirus - causes severe wtery diarrhea

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81
Q

AIDS/diarrhea

A

thik cryptosporidium spp.

also MAI - can detect w/ acid fast stain

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82
Q

amebiasis

A

dysentery and liver abscess - caued by entamoeba histolytica seen in india, mexico, colombia –> go to liver, brain and lungs

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83
Q

giardia

A

deacreased expression of brush border enzymes –> steatorrhea

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84
Q

pANCA

A

some UC

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85
Q

ASCA

A

some CD

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86
Q

starts on cessation of smoking

A

UC

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87
Q

UC

A

colon and rectum –> retrograde, no skips
mucosa/submucosa - superficial broad based ulcers
can cause megacolon and pseudopolyps
NO granulomas/strictures
bloody mucoid diarrhea
risk of ADCA

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88
Q

CD

A 
regional enteritis
unaffected, skip areas
transmural 
linear mucosal ulcers - deep ulcers
granulomas!!! 
fissureing/fistula
creeping fat
relatively mild diarrhea, ab. pain, RLQ (ileocecal)
*** erythema nodosum
ADCA 
fat + vit malabsorption
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89
Q

sessile

A

flat

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90
Q

pedunculated

A

polyps w/ stalk

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91
Q

hyperplastic polyps

A

sessile - no malignant potential - most common

92
Q

inflammatory polyps

A

seen in chronic IBD - see rectal bleeding ad mucus discharge - not malignant

93
Q

hamartomatous polyps

A

pedunculated - think PJ syndrome of juvenile polyposis

94
Q

mutated STK11

A

Peutz-Jeghers syndrome -
see hamartomatous polyps, mucocutaneous hyperpigmentation
increased risk of cancer

95
Q

SMAD4, BMPR1a mutations

A

think juvenil polyposis
age <5
see hamartomatous polyps - congenital malformations - digital clubbing - cancer by age 50

96
Q

adenomas

A

neoplastic polyps that are not yet malignant - size >4cm has increased malignancy

97
Q

APC gene mutation

A

Familial adenomatous polyposis - see numerous adenomas >100 to make ddx

colon cancer by age 30 if not treated

autosomal dominant

98
Q

MLH1, MSH2 , microsatellite instability due to repair gene defect

A

think hereditary non-polyposis colorectal cancer HNPCC

see sessile serrated adenomas

autosomal dominant

right sided ADcarcinoma - mucinous subtypes + endometrial cancer

99
Q

mucinous ADCA

A

predominantly on right side - has to do with DNA mismatch repair genes or hypermethlaition: MSH2, MLH1, BRAF — think HNPCC or sporadic colon cancer

100
Q

left sided ADCA?

A

think typical tubular/villous ADCA with APC/WNT pathway defect

change in bowel habits, rectal bleding, melena, LLQ pain : presents w/ obstruction and is caught more quickly

101
Q

right sided ADCA?

A

presents w/ fatigue, w/l, anemia : they don’t often present w/ obstruction

mucinous ADCA

due to MSH2, MLH1, BRAF mutations and DNA mismatch repair problems

102
Q

where does colon ADCA met to?

A

regional LNs, lungs, bones, liver *** most common

103
Q

well differentiated neuroendocrine tumor?

A

carcinoid tumor ** midgut most aggressive

carcinoid syndrome = serotonin release - episodic skin flushing, diarrhea, bramping, asthma

104
Q

zones of rectum?

A

upper zone = columnar epi. (see ADCAs)

middle zone = transitional zone = cloacogenic carcinoma (behaves like SCC but doesn’t make keratin)

lower zone = squamous epi. - see condyloma papilliform - HPV 16/18, mutated E6/E7

105
Q

anal fistulas assoc. w/?

A

CD

106
Q

lymph drainage above dentate line?

A

perirectal and paravertral nodes

107
Q

lymph drainage below dentate line?

A

superficial inguinal /femoral nodes

108
Q

toxin of H. pylori?

A

Vacuolating cytotoxin (VacA) causes cell
injury characterized by vacuolization. Another H. pylori gene from a pathogenicity island encodes cytotoxin-associated
antigen (CagA) and is present in many patients with chronic gastritis and peptic ulcers and increases their risk for gastric
cancer.

109
Q

leather bottle stomach

A

diffuse gastric ADCA - signet rings are seen

110
Q

cobblestone appearance of gastric mucosa

A

leather bottle stomach - diffuse gastric ADCA - signet rings are seen

111
Q

Sclerosing cholangitis associated w/ what?

A

UC sometimes CD

112
Q

Diarrhea with mucus and blood in the stools

A

Shigella dysenteriae and Entamoeba histolytica.

with E. histolytica can see liver abscess

113
Q

ompeprazole + Upper GI endoscopy reveals 3 circumscribed, round, smooth lesions in
the gastric body from 1 to 2 cm in diameter. Biopsies are taken and microscopically show the lesions to consist of irregular
glands that are cystically dilated and lined by flattened parietal and chief cells. No inflammation, H. pylori, metaplasia, or
dysplasia is present.

A

fundic gland polyps

114
Q

typhoid fever

A

Salmonella typhi

abdominal pain and diarrhea during week 1 of their illness. By week 2, these patients had splenomegaly
and elevations in serum AST and ALT levels. By week 3, they were septic and had leukopenia. At autopsy, the patients
who died were found to have ulceration of Peyer’s patches.

115
Q

centrilobular

A

zone 3 - acetiminophen toxicity

116
Q

periportal

A

zone 1

117
Q

microvesicular steatosis?

A

pregnancy, Reye syndrome, tetracycline/salicylate toxicity, alcohol

118
Q

macrovesicular

A

obesity, diabetes, hep C, EToH

119
Q

skin/body changes of chronic liver failure?

A

jaundice, palmer erythema, spider angiomata, terry nails, finger clubbing, “fector hepatis”” - sweet/musty breath, edema/ascities, hypogonadism/gynecomastia

120
Q

asterixis

A

hepatic enceophalopathy - “flapping” tremor of hands - jerky irregular flexion patterns - due to ammonia accumulation and liver failure

121
Q

macronodular cirrhosis

A

think viral

122
Q

micronodular cirrhosis

A

think ethanol

123
Q

causes of liver cirrhosis?

A

hep C * most common
alcohol * also really common
hep B* sometimes

124
Q

mediators causing myofibroblast transformation?

A

PDGF (migration of stellate cells) and TNF activates stellate cells
TGF beta –> stimulates fibrinogenesis in myofibroblasts

stellate cells secrete VEGF/ANG1 –> vascular remodeling

125
Q

portal HTN?

A

due to liver cirrhosis - b/c of fibrosis and sinusoidal remodeling of myofibroblasts –> intrahepatic vascular reistance

pre-hepatic: portal occlusion
Intra-hepatic: due to liver cirrhosis: alcohol + hep
post hepatic: RSHF, hepatic v. outflow obstruction

see varices, ascites, congestive splenomegaly, heptic encephalopathy

126
Q

high protein ascities?

A

TB, carcinoma = exudate

127
Q

low protein ascites?

A

transudate = albumin loss

128
Q

eruptive xanthomas, pruritis, jaundice

A

think cholestasis - inability to excrete bile - backs up showing jaundice

no bile salts to break down fats –> cholesterol retention and xanthomas

bile salts deposit in skin –> pruritis

129
Q

UDP

A

uridine diphosphatase = conjugates/ makes direct bilirubin

130
Q

choluria

A

dark colored urine - due to bilirubin excretion

131
Q

rotor/DJ syndrome

A

mpaired biliary excretion of bilirubin glucuronides is due to a mutation in the canalicular multidrug resistance protein 2 (MRP2)

see elevated conjugated bili/jaundice w/out AST/ALT elevation

DJ has black liver

132
Q

high unconjugated bili levels?

A

think Gilbert/Crigler Najar - due to UDP problems

133
Q

AST/ALT

A

meausres hepatocyte membrane disruption
ALT found in liver
most common cause of just ALT/AST elevation = NASH

higher AST/ALT ratio is likely ETOH
see very high levels w/ viral infection

134
Q

ALK Phos and GGT

A

induced enzymes - think biliary things

seen w/ cholestasis and EtOH

isolated elevated GGT = EtOH
isolated ALK Phos: must rule out bone and placenta

135
Q

high IgA

A

alcoholic liver disease

136
Q

diffuse hypergammaglobulinemia?

A

cirrhosis, AI hep

137
Q

IgM high

A

primary biliary cirrhosis

138
Q

IgG high

A

AI hep

139
Q

Hep A

A

F-O contamination
1 mos. incubation
third world epidemic - shellfish in US
ACUTE ONLY - does not cause chronic disease

see spike in fecal HAV
see anti-HAV Ab in those having had vacc.
see IgM- anti-HAV after 1 month in those that have been infected

140
Q

Hep B

A

ACUTE and CHRONIC (only minority go to chronic)

  • horizontal transmission: sex most common
  • vertical: seen in Asia!
  • 5% progresses to chronic hepatitis, 1% of total gets cirrhosis, .5% of total gets hepatocellular carcinoma

3 mos incubation

histo: “gorund glass appearance” of HBsAg
portal inflatmmion, apopostis w/ acidophil bodies

141
Q

Dane particles

A

incomplete dsDNA - think HBV

142
Q

indicative of active infection of HBV?

A

HBsAg

143
Q

Acutely infected w/ HBV?

A

see HBsAg, IgG Anti-HBc, IgM Anti-HBc**

144
Q

chronically infected w/ HBV?

A

see HBsAg, IgG Anti-HBc - don’t see Anti-HBc IgM!!!

145
Q

what shows if pt. has ever been infected w/ HBV?

A

IgG Anti-HBc

146
Q

what shows if pt. has only had HBV vaccination and never been infected?

A

IgG Anti-HBs - shows immunity to HBV

147
Q

only thing present during window period indicating acute infection?

A

IgM - anti-HBc

won’t see anything during 3 mos. incubation gap

148
Q

chronicity of Hbv?

A

persistence of HBsAg for more than 6 mos, along with HBeAg and HBV-DNA ::: see it waver

149
Q

what denotes high infectivity of HBV?

A

presence of HBeAg and high levels of HBV DNA

150
Q

what is best indcator of chronicity of HBV?

A

age - younger age at time of infection = larger chance of increased chronicity

151
Q

1 cause of cirrhosis in US?

A

Hep C

152
Q

Hep C

A

ACUTE and CHRONIC!!!! - most
parenteral transmission
2 mos incubation

no vaccine - genome is unstable

see HCV RNA - in case of infection - stays w/ chronicity
see anti-HCV in case of resolution

    • most common cause of Hep C = Stable chronic hepatitis (not cirrhosis)
    • only 15% of total go to cirrhosis

Histo: portal inflammation, bridging fibrosis, lobular inflammation

153
Q

Hep D

A

Acute infection
3 mos incubation
parenteral

Absolutely dependent on HBV infection –> superinfection or co-infection

154
Q

Hep E

A

“hepatitis A of india”
1 mos incubation
F-O route

same serology as hep A:
Fecal HEV seen during infection
Anti-HEV Ab indicates vaccine / clearance
IgM- anti-HEV - indicates infection - DDx

155
Q

clonorchis sinensis

A

think cholangiocarcinomas - these are helminths

156
Q

AMA

A

primary biliary cirrhosis (PBC) (a scarring of liver tissue, confined primarily to the bile duct drainage system of the liver).

157
Q

ASMA

A

think AI hepatitis

histology same as viral hep - see cluster of periportal plasma cells
Female = Type 1
Children = Type 2

sometimes also 80% have associated high titers of various autoantibodies, including (Type 1) ANA, ASMA, but negative for AMA (Type 2) ALKM1, ACL-1*
Increased frequency HLA-B8 or HLA-DRw3
60% have other forms of autoimmune disease

158
Q

vinyl chloride

A

angiosarcoma

159
Q

zone 1 hepatoxocitiy

A

think FE overload, Allyl alcohol

160
Q

Zone 3 hepatoxicity

A

think CCl4 (carbon tetrachloride), acetaminophen, ethanol

aceta: give n-acetyl cystein as antidote - toxicity due to NAPQ1 –> depletion of GSH

161
Q

MTX

A

used to tx. psoriasis/ RA

see periportal fibrosis and cirrhosis

162
Q

Isoniazid

A

anti-TB metabolite –> causes liver damage with increased ALT

163
Q

alcoholic liver disease

A

all changes begin in zone 3 –> portal tracts

  1. Fatty liver: micro/macrovesicular
  2. alcoholic hepatitis: ballooning and mallory bodies - see neutrophils surrounding necrotic hepatocytes
    - see fever, jaundice, RUQ pain, high AST:ALT, high alk phos and GGT
  3. cirrhosis
164
Q

non-alcoholic fatty liver

A

metabolic syndrome; hyperlipidemia with high TG’s, insulin resistance, high BP

see aST cirrhosis (non alcoholic steatohepatitis)

165
Q

C2Y82Y, H63D, TF2R

A

mutations in these genes –> genetic adult hereditary hemochromatosis (autosomal recessive) –> causes gene defect in HFE

hepatocytes unable to recognize iron thus don’t make hepcidin = iron overload! –> ** cirrhosis, bronze skin, ARTHRALGIA

** prussian blue stain **

166
Q

mutations in juvenile hemochromatosis?

A

HAMP, HJV

167
Q

anemia of CD?

A

chronic inflammm – IL6 –> activates production of hepcidin

168
Q

Wilson Disease

A

high copper levels! ATP7B deficiency (controls copper excretion in bile duct)

levels accumulate in liver (cirrhosis/hepatitis), brain (parkinsonian/CNS disorders), eyes (Kayser-Fleischer rings)

on labs see increased urine copper

169
Q

ATP7B deficiency

A

Wilson Disease- high copper levels!

170
Q

ATP7A deficiency

A

Menkes disease = copper deficiency = “kinky hair disease” –> severe neuro disease

171
Q

alpha1AT

A

Autosomal recessive

Pizz gene mutation –> A1AT is a protease normally inhibits neutrophil elastase (this protein is made in liver –> accumulates in liver and causes disease )

seen in neonatal hepatitis and cirrhosis in 40’s assoc. w/ smoking

172
Q

causes of neonatal cholestasis?

A

extrahepatic biliary atresia
idiopathic neonatal hep
A1AT

173
Q

PBC

A

primary biliary cirrhosis = cholestatis liver disease of destruction of small/medium bile ducts in liver

AMA+ : directed against PCD-E2 in herings canal

seen in middle aged women: pruritis and jaundice

** destruction of midde bile ducts –> periportal hepatocellular damage

174
Q

PSC

A

primary sclerosing cholangitis = cholestasis w/ obliterative fibrosis of intra and extrahepatic bile ducts

seen in IBD!!! UC - 90%

male disease - see acute ascending cholangitis

pANCA and ANA elevated!!!

“beading” on ERCP and onion skin fibrosis

175
Q

beading

A

PSC

176
Q

ciliopathies

A

mutation in polycystin Pc1/Pc2 –> bile duct cystic changes/ fibrosis

Von Meyenberg complex and caroli disease (autosomal recessive) think about ADPKD and manifestations in brain and kidneys

177
Q

nutmeg liver

A

acute liver congestion at zone 3

178
Q

budd-chiari syndrome

A

obstruction of more than 2 hepatic vv or IVC

sen in polycythemia or clotting disorders

see RUQ pain, ascites, hepatomegaly

zone 3 congestion

179
Q

HELLPP

A

hemolysis, elevated liver enzymes, low platelets - seen in pregnancy

180
Q

which virus has increased risk during pregnancy?

A

HEV

181
Q

nodular hyperplasia of liver

A

most common benign hepatic mask that isn’t vascular - see central scar of stellate cells

assoc. w/ osler-weber-rendu disease

182
Q

Cavernous hemangioma of liver

A

commonest hepatic tumor/mass

bleed when disrupted and are benign neoplasms

183
Q

Hepatic adenoma

A

rounded smooth borders, no central scar

seen in women on OC’s: prone to rupture

184
Q

hepatocellular carcinoma

A

think HBV, HCV, alcohol

elevated AFP!!!

see liver failure, cachexia, varices, hemorrhage

185
Q

what could get mistaken as focal nodular hyperplasia?

A

fibrolamellar variant of hepatocellular carcinoma - seen in young females and males, not assoc. w/ HBV, HCV, or cirrhosis

see single large mass w/ malignant hepatocyes

186
Q

Klatskin tumor

A

arises from perihilar region of bile duct eptihelium

187
Q

cholelithiasis

A

gallstones

188
Q

5 F’s

A

cholesterol stones - female, fat, flatulent, fertile, forty

189
Q

stone formation?

A
  1. Increased production/saturation → supersaturatiohn
  2. Crystallization (nidus)
  3. Flow (volume, turbulence) – hypomotility leads to sludge
  4. Accretion (matrix/sludge) – sludge gives nidus something to crystalize on → accretion of cholesterol forming stones
190
Q

strawberry gallbladder?

A

Cholesterolosis of the Gallbladder: cholesterol in mucosa
- supersaturated bile and ↑mucosal uptake…can present clinically like acute/chronic cholecystitis
- usually with stones (mechanism unknown if stone absent)
- often called “strawberry gallbladder”
o can cause gallbladder biliary pain
o accumution of cholesterol in mucosa gives it the white/yellow dot background in the pattern of red

191
Q

black pigement stones

A

unconj bilirubin - due to chronic hemolysis, SS, thalassemia , CD

192
Q

brown pigment stones

A

bili + cholelsterol

e. coli infection, liver flukes (C. sinensis )

193
Q

cholelithiasis

A

stones in gallbladder

194
Q

cholecystitis

A

inflamm. of gallbladder

195
Q

choleocholithiasis

A

stones in bile duct

196
Q

acalculous cholecystitis

A

seen in ill - HIV pts - no stones

197
Q

+ revound, murphys sign

A

acute cholecystitis

see necrosis, hemorrhage, inflammation/edema

198
Q

hydrops of gallbladder

A
  • obstruction of cystic duct without inflammation

- results in mucin filled gallbladder

199
Q

HIDA scan

A 
radioactive dye (given IV) is excreted by the liver (GB not seen in acute cholecystitis …even up to 3 hrs…stone blocks duct)
a.	pt injected w/ die into vein – fills gallbladder and later will be seen in small bowel – if there is obstruction then die won’t go into gall bladder and will continue into small bowel ---- + study means there is a stone
200
Q

ECRP

A

used to evaluate the biliary tree

a. tube is inserted down esophagus, into small bowel – at tip of scope there is alight to visualize the ampulla – can pass a needle into the ampulla and send it up into the biliary tree → inject die into biliary tree and examine for causes of obstruction
b. can also go in a grab stones and pull them out of the ampulla of vater
c. can also use ECRP to place a stent

201
Q

acute/ascending cholangitis

A

• Cholangitis = bacterial infection superimposed on an obstruction of the biliary tree most often due to gallstone → ascending cholangitis
- There is secondary bacterial infection…organism is typically from duodenum
- E. coli, Klebsiella, enterobacter ….
• Infection moves up the biliary tree into the liver bile duct system…sometimes resulting in multiple small liver abscesses
• Typically causes: 1)Fever, 2)Jaundice, 3)Abdominal pain (Charcot’s Triad)
- with Hypotension, Mental status changes (Reynold’s Pentad)….increased mortality – watch out!
• Histology: shows inflamm. process due to stone, will see bile ducts are expanded and filled with pus → spills out into liver parenchyma and forms microabscesses and enzymes skyrock → super elevated ALT/AST

202
Q

rokitanski -aschoff sinuses

A

Chronic Cholecystitis:
• >90% associated with gallstones (same epidemiology)
• Pathophysiology: repeated bouts of acute inflammation, chemical or bacterial
• Pathology: stiff, thickened wall with variable inflammation and Rokitanski-Aschoff sinuses
• R-A sinus (seen on right) = areas where gallbladder has constricted and surface mucosa is pulled down into wall
• Clinical: highly variable symptoms of pain and “dyspepsia”
• Pathologic findings and clinical symptoms do not correlate well
• Porcelain gallbladder: chronic cholecystitis with calcified wall, higher risk of adenocarcinoma → mandatory surgery
• see fibrotic thickened gray-white wall due to fibrosis and inflammation with many gallstones present in the lumen
• see calcified wall prominently on the CXR/ CT scan
• Have high risk for developing ADCA, MUST COME OUT!

203
Q

cacinoma of gallbladder

A

• 2 Xs more common in women, peaks in 7th decade
• Native Americans and Hispanics
• Usually assoc. with gallstones
• Rarely diagnosed preop. or when resectable
– no symptoms until advanced disease
– rare ddx in time
• Vast majority are Adenocarcinoma
• Terrible prognosis; <10% 5 year survival!
• ERBB2 (Her-2/neu) overexpressed (2/3)
• can results in direct liver invasion!

204
Q

klatskin tumor

A

cholangiocarcinoma located at jn. or right and left hepatic ducts

205
Q

PRSS1 mutations:

A

code for a variant of trypsin that is resistant to inhibitor deactivation

206
Q

pancreas divisum

A

ducts do not fuse
- - predisposes to chronic pancreatitis
o see that tail and body (dorsal portion) drains through minor sphincter through the “minor duct of santorini”
o Duct of Wirsung does not develop and very little drains out of papilla of vater (when use ERCP and inject into duct of wirsung – see no flux into the pancreas, only up into the biliary tree)

207
Q

annular pancreas

A
    • normal pancreas encircles 2nd part of duodenum
    • presents with obstruction and other developmental defects
  • presents with “double bubble sign” : stomach and proximal duodenum fill w/ air
  • see bilious green tinged vomit – due to bile still entering into the small bowel (obstruction is usually below the ampula)
    o – may or may not be complete obstruction, and less commonly may present later in adulthood
208
Q

defects leading to increased pancreatitis?

A
  • PRSS1: mutated trypsinogen resistant to antitrypsin
  • SPINK1: SPINK 1 protein is a trypsin inhibitor
  • CFRT: some cystic fibrosis variants get pancreatitis
209
Q

two main causes of acute pancreatitis?

A

alcohol: seen in males, 40
biliary stones: seen in women, 70

  • Alcohol → damage of ductule that’s producing HCO3-
  • Drugs → damage of acinus: CCK → zymogens, lipase, amylase
210
Q

elevated serum amylase and lipase***

A

DDx of Acute Pancreatitis: clinical DDX!
- epigastric pain radiating to the back
- fever, nausea, vomiting
- elevated serum amylase and lipase***
Morphology:
- Early stages: see diffuse swelling from edema with redness from vasodilation, but no necrosis
- Mid stages: see areas of hemorrhage and peripancreatic fat along with fat necrosis= “saponification”
- Later stages: see complete fat necrosis = complete saponification

211
Q

most common cause of chronic pancreatitis?

A

alcohol

see excruciating pain, diabetes, ascities, fat malab, pseudocyts formation and duct obstruction

212
Q

TRUE CYST

A
  • Have an epithelial lining.
  • As all epithelia secrete fluid, the cyst will continue to grow in size, and impinge on adjacent anatomical stuctures (a type of neoplasm)
  • Treatment must include excision of epithelium, or they will recur
  • Squamous cysts fill with keratin (because keratin is greasy, they were named as though the contents were fatty (i.e. sebaceous cyst of skin and cholesteatoma are misnomers)
    o epidermal inclusion cyst of skin, keratocyst of jaw, cholesteatoma of external ear canal/mastoid bone
  • Serous cysts secrete a watery clear fluid, mucinous cysts mucin
213
Q

PSEUDOCYST

A
  • Have no epithelial lining Will not grow in size unless connected to a duct
  • Treatment is by drainage
  • examples include pancreatic pseudocyst, adrenal pseudocyst and old abscess
  • represents 75% of all pancreatic cysts – usually occur after a bout of acute pancreatitis
  • histology: there is smooth borders no lining of the epithelium – instead is lined by fibrin and granulation tissue
214
Q

serous cystadenoma

A

cyst mass w/out atypica- seen in elderly females, straw colored serous yellow fluid in it

neg. mucin stain

215
Q

mucinous cystic neoplasms

A

slow growing, painless mass in adult females
makes mucinous fluid
see smooth borders w/ cysts lined by columnar mucinous epithleium

216
Q

Intraductal papillary mucinous neoplasms

A

• Typically arise in the main duct of the head of pancreas of males
• May be benign, borderline or malignant
• presents w/ obstruction, that is not a stone
• histology:
– see papillary neoplasm that distends the pancreatic duct
– neoplasms behave like a stone and continue to grow and expand – must be removed in order to keep them from progressing to chronic pancreatitis
– considered “intraductal neoplasm”

217
Q

pancreatic carcinoma

A

• 4th leading cause of Cancer Death in US
– Median survival 9 months; 5% 5 year survival
– only 20% completely resectable → s shelf: rectal pouch mass – metastasis
• Diagnosis
– Imaging: CT scan commonest, endoscopic US best (can do biopsy at the same time with US)
– Tissue ddx: FNA cytology or needle core biopsy
– Laboratory: CA 19-9 only for monitoring (classically elevated in pancreatic cancer – a marker to follow tx)
• CANCER IS A TISSUE DIAGNOSIS
• Pathology
– Typically metastasize regional lymph nodesà then liverà then lungs
– Direct local invasion (along nerves, duodenum, stomach, colon, vessels)
– Peritoneal spread with ascites
• Staging for possible surgery

218
Q

migratory thrombophelbtisi

A

pancreatic cancer

219
Q

palpable gallbladder

A

think pancreatic cancer

220
Q

STK11 mutation

A

peutz-jeghers syndrome = inherited risk of pancreatic carcinoma

221
Q

common somatic alterations in pancreatic ADCA?

A
  • KRAS – growth factor signal transducer

- p16/CDKNA: (cell cycle regulator: tumor suppressor)

222
Q

Necrosis with portal bridging in liver

A

chronic hepatitis. Mild steatosis is seen in HCV infection. The incidence of
chronic hepatitis is highest with HCV infection.

223
Q

AST

level that is higher than the ALT level

A

characteristic, however, of liver cell injury associated with chronic alcoholism

224
Q

Piecemeal hepatocellular necrosis

A

think HCV

225
Q

ceruloplasmin

A

Ceruloplasmin is an α2-globulin that
carries copper in plasma. Because copper cannot be secreted into plasma, ceruloplasmin levels are low. in Wilson’s disease

226
Q

K-RAS

A

K-RAS mutations are found in more than 90% of pancreatic adenocarcinomas

GI II: Test 1 (6 decks)

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