Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

need to knows > Gastroenterology (F.A.) > Flashcards

Gastroenterology (F.A.) Flashcards

1
Q

Gastrin

A

where: G cells in antrum of stomach
action: increase H+ secretion by parietal cell, increase stomach mucus lining, increase stomach motility
regulation (+): food (stomach distension, alklanization, AA/peptides,), vagal stim via GRP,
regulation (-): low pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how does chronic PPI and chronic atrophic gastrtitis (H Pylori) affect Gastrin levels

A

increased gastrin levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Somatostatin

A

where: D cells of Islet of Langerhans (Pancreas)
action: decrease all secretions: gastrin, pancreatic (glucagon, insulin, enzymes), lowers gallbladder motility
regulation (+): low pH
regulation (-): vagal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Cholecystokinin

A

where: I cells of duodenum
action: help pancreatic/biliary secretions enter duodenum (increase gall bladder motility, increase pancreatic secretion via neural muscarinic pathway, soften sphincter of Odi) and decrease gastric emptying
regulation(+): presence of FA/AA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Secretin

A

where: S of the duodenum
action: neutralize acid by secreting HCO3-., decrease gastric acid secretion, increase bile secretion
regulation (+): high acidity, presence of FA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Glucose dependent Insulinotropic peptide

A

where: K cells of duodenum
action: increase insulin release, decrease gastric acid secretion
regulation (+): FA, AA, oral glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Motilin

A

where: small intestines
action: increase migrating motor complexes
regulation (+): FASTING STATES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Vasoactive Intestinal Peptide

A

where: parasympathetic ganglia of sphincters, gallbladder, SI
action: increases H20/electrolyte secretion, relaxes sphincters and smooth muslces
regulation (+) : distension and vagal
regulation (-): sympathetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Ghrelin

A

where: stomach
action: increase appetite
regulation(+) in fasting state
regulation (-) : food

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

when is Ghrelin increased pathologically

A

Prader-Willi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Intrinsic Factor

A

where: parietal cells of stomach
action: bind B12 for absorption in terminal ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Gastric Acid

A

where: parietal cells of stomach
action: release H+ into lumen
regulation (+): gastrin , AcH, histamine
regulation (-): SST, Secretin, GIP, prostoglandin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pepsin

A

where: chief cells of stomach
action: protein breakdown
regulation (+): needs H+ to activate from pepsinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Bicarbonate

A

where: mucosa and Brunner’s glands (SI)
action: neutralize acid
regulation: secretin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the pancreatic secretions?

A

alpha amylase, trypsinogen, lipase, proteases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

explain the role of trypsinogen

A

trypsinogen gets activated by enterokinase/enteropeptidase (brush border enzymes on duodenum/jejunum) and becomes trypsin which can then activate the other zymogens (pro-peptidases) released by pancreas, and further activate itself by cleaving trypsinogen more.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

explain the process of carbohydrate absorption at SI

A

-monosacch only
- glucose and galactose through SGLT1
-fructose through GLUT 5
then everything enters blood via GLUT 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

SI injury leads to deficient absorption of what (3) vitamins/minerals

A

Fe
Folate
B12
“Iron Fist Bro”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Peyer;s Patches role?

A

unencapsulated lymphoid aggregates in Ileum
Uses M cells to sample environment and be APC
causes Bcell to become plasma cells that produce IgA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

whats in bile, anyways?

A

bile salts: bile acid (made by 7 alpha hydroxylase) conjugated to taurine or glycine to be water soluble
bilirubin(broken down heme), phosopholipids, cholesterol, water, ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what does bile do, anywho?

A
  • cholesterol excretion
  • digestion of lipids, and absorption of fat soluble vitamins
  • antimicrobial
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

heme—–> biliverdin

which enzyme???

A

heme oxygenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

direct vs indirect bilirubin

A

direct: soluble, conjugated w/ glucoronic acid (at liver)
indirect: INsoluble, UNconjugated,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what enzyme conjugates bilirubin?

A

UDP glucoronysyl transferase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

fate of conjugated bilirubin?

A

becomes urobilinogen. 80% of which becomes stercobilinogen and is pooed out
20% of urobilogen is reabsorbed and most of this is recycled by liver, and a very small amount is peed out via kidney (urobilin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

naaaame the salivary gland tumor:

  • most common
  • benign
  • mixed : chondromyxoid stroma and epithelium
  • recurs if partially removed
A

pleomorphic adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

naaaame the salivary gland tumor:

  • most common malignant
  • has mucinous and squamous components
A

mucoepidermoid carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

naaaame the salivary gland tumor:
benign cystic w/ germinal centers
smokers
10% bilatera, 10% malignant

A

Warthrin tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Achalasia

A

“bird’s beak”
very HIGH LES resting pressure, because of loss of Auerbach’s plexus (PSNS) so decreased VIP and NO released, uncoordinated/absent peristalsis
progressive dysphagia of solids AND liquids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

achalasia poses an increased risk of what?

A

esophageal ca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Boerhaave Syndrome?

A

transmural tear in esophagus due to retching

  • pneumomediastinum
  • subcutaneous emphysema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

“esophageal rings”
“linear furrows”
unresponsive to GERD

A

eosinophilic esophagitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

caustic ingestions and GERD causes what esophageal problem

A

strictures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Esophageal varices

A

dilated lower 1/3 veins, hematemesis

seen in portal htt, cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Esophagitis in immunocompromised. Name the cause?

  1. white plaque
  2. linear tears
  3. punched out lesions
A
  1. candida
  2. CMV
  3. HSV1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

GERD symptoms? whats going on with LES?

A
  • heart burn, regurg, dysphagia, hoarse, cough

- transient decreases in LES pressures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What syndome is caused by a mucosal tear in esophagus due to severe vomitting (alcholics, bulemics)

A

Mallory Weiss Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Plummer Vinson Syndrome

A

iron deficiency anemia
esophageal webs
dysphagia
(glossitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Plummer Vinson Syndrome causes risk of?

A

esophageal SCC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

esophageal smooth muscle atrophy and fibrous replacement with low resting LES pressures

A

CREST syndrome (sclerodermal esophageal dysmolitity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Barrett’s Esophagus has increased risk of?

A

esophageal adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Barret’e Esophagus path?

A

stratified squamous epithelium (normal in esophagus) has metaplasia with nonciliated goblet cells (of intestines)
due to chronic GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

squamous cell carcinoma of esophagus vs adenocarcinoma

location
risk
prevelance

A

SCC: upper 1/3
A: lower 1/3

SCC:smoking, alcohol, hot tea, betel nuts
A: GERD/Barrett, obesity, smoking

SCC: world
A: USA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Acute Gastritis (3 causes)– think erosions!

A
  1. NSAIDs - b/c they decrease PGE protection
  2. Curling’s Ulcers- result of burns– hypovol– ischemia
  3. Cushing’s Ulcers- result of CNS damage– increased vagal output– increased acidity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Chronic Gastritis (2) causes— think inflammation

A

(1) H Pylori – antrum of stomach, PUD and MALT lymphoma

(2) autoimmine– body/fundus of stomach–parietal cells of stomach attacked

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Menetrier’s Disease

A

excess mucosal hyperplasia causing hypertrophic rugae. Damages parietal cells, decreases acid production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is “intestinal” gastric cancer associated with

A

H Pylori, smoked foods, smoking, chronic gastritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what is “diffuse” gastric cancer associated with

A

NOT H pylori
it looks like the signet ring
leather bottle stomach, linitis plastica

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Virchow Node

A

sign of gastric cancer

L supraclavicular node involvement by mets from stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Krukenberg Tumor

A

bilat mets to ovaries from gastric cancer

mucin secreting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Sister Mary Joseph nodule

A

sign of gastric cancer met to the subcut periumbilical area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Gastric Ulcer vs Duodenal Ulcer
food?
HPylori relation?
other causes apart from HPylori

A

food makes gastric ulcer Greater
food makes duodenal ulcer Decrease

gastric ulcer is 70% relation to HPylori
duodenal ulcer is 90% relation to HPylori

gastric ucler can be caused by NSAID
duodenal ulcer can be caused by ZES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

which type of ulcer is generally benign?

A

duodenal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

how do you diagnose a gastric ulcer vs a duodenal ulcer

A

gastric: biopsy margins to rule out malignancy!
duodenal: just check for hypertrophy of Brunner’s glands (no biopsy required)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

if ulcer ruptures on lesser curvature of stomach? wheres the bleed?
how about posterior duodenal wall?

A

(1) L gastric A

(2) gastroduodenal A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

celiac’s disease

A

autoimmune against gliadin (most present in duodenum+ jejunum).. IgA anti-tissue transglutaminase
path: crypt hyperplasia and villous atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

HLADQ2 and HLADQ8

A

Celiac’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

dermatitis herpetiform

A

Celiac’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

celiac has increased risk of

A

T cell lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Lactose Intolerance

A

normal villi
decrease stool pH
osmotic diarrhea
breath H test >20 ppm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

pancreatic insufficiency

A

decrease absorption of ADEK and B12

causes: chronic pancreatitis and CF (as well as cancers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Tropical Sprue

A

looks like Celiac’s but responds to antibiotics
megaloblastic anemia assn bc of folate and later B12 def
hint: someone from or visitng the tropics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what causes Whipple Disease

A

cause: TROPHERYMA WHIPPLEI
INTRACELLULAR GRAM + PAS+
foamy macrophages in intestinal lamina propria

64
Q

what are the symptoms of whipple’s disease?

A

Foamy Whipped cream in a “CAN”

  • cardiac
  • arthralgia
  • neurologic

with diarrhea and steatorrhea occurring later in the disease

65
Q

UC vs Crohn’s Disease: where?

A

UC: continuous lesions, always includes rectum: mucosal/submucosal

Crohn’s: skip lesions (seen in terminal ileum often) and SPARES rectum: transmural

66
Q

pathological finds: UC vs Crohn’s

A

UC: bleeding, crypt abcess, no granuloma, TH2, “lead pipe” no haufsta

Crohn’s: granulomatous(noncaseating)TH1, lymphoid aggregates, “creeping fat” “cobblestone mucosa” “string sign” (= a string connecting two parts of GI)

67
Q

complications of UC vs Crohns

A

UC: toxic megacolon, fulminant colitis, perforation

Crohn’s: fistulas, strictures, perianal disease

68
Q

Bloody diarrhea: Crohn’s or UC

A

UC!

69
Q

name the common extra-intestinal manifestations of Crohn’s and UC

A

Pyoderma Gangrenosum
Erythema Nodosum
inflammmation of eye and joints
mouth ulcers

70
Q

+ ASCA (anti-sacchromyces cervisiae ab)

A

Crohn’s

71
Q

what is UC + for? what else is UC associated with

A

p-ANCA +

primary sclerosing cholangitis (90% have UC)

72
Q

Crohn’s management

A

corticosteroids, Azathioprines, antibiotics, infliximab, adalimumab

73
Q

UC management?

A

5 ASA (like mesalamine), 6MP, infliximab, colectomy

74
Q

IBS

A
  • change in form of stool
  • change in frequency of stool
  • abdominal pain
75
Q

Appendicitis

A

caused by obstruction of appendix which leads to basterial invasion and inflammation

76
Q

what two things present like appendicitis?

A

diverticulitis

ectopic pregnancy

77
Q

diverticulum

A

Meckels: true: has all 3 gut layers

most are acquired: false: have only mucosa and submucosa

78
Q

Diverticulosis

A

occurs in elderly, false diverticuli in sigmoid colon, can be due to increased intraluminal pressure, low fiber diet, and weak colonic wall

79
Q

diverticulitis

A

inflammationof diverticuli

LLQ pain

80
Q

Zenker’s diverticulum

A

a false diverticulum due to cricopharyngeal muscles not moving correctly
seen in Killian’s triangle in inferior pharyngeal constricter
seen in old men

81
Q

Meckel’s Diverticulum

A

patency of the vitelline duct prox to the midgut
can be cause of infection due to ectopic tissue (gastric or pancreatic)
true diverticulum
RLQ pain
2x likely in males under 2 yo
diagnosis: pertechnate study

82
Q

pain location of diverticulosis vs Meckels

A

diverticulosis– LLQ

Meckel’s– RLQ

83
Q

Hirschsprung Disease

A

lack of ncc migration causes no autonomic ganglia in lower GI tract
assn w/ RET, increased risk with Down’s
causes congential megacolon

84
Q

presentation of Hirschsprung Disease

A

Bilious Vomit
explosive (squirt sign) feces expulsion
no meconium within 48 hours

85
Q

Malrotation

A

anomaly of midgut rotation during detal devlopment causes wrong positioning of bowel
“Ladd bands” are characteristic, they can lead to volvulus and duodenal obstruction

86
Q

volvulus

A

twisting of bowel around mesentery
midgut volvulus in children
sigmoid volvulus- in elderly
“coffee bean”

87
Q

intussusception

A

lead point causes proximal intestine to fit into distal intestine
common lead points: ilio-cecal junction, Meckel’s, can be associated with virus (like adeno or rota)
“currant jelly stool”

88
Q

“thumb print sign”

A

colonic ischemia

89
Q

h(x) of atherosclerosis+ pain after eating?

A

chronic mesenteric ischemia

90
Q

out of proportion abdominal pain+ currant jelly stool

A

acute mesenteric ischemia

91
Q

tortuous vessel dilation of right sided colon? older patient?

A

angiodysplasia

92
Q

intestinal hypo-motility sans obstruction

A

ileus

93
Q

CF+ constipation in baby

A

meconium ileus

94
Q

premie baby + formula food+ air in abdomen?

A

necrotizing enterocolitis

95
Q

Peutz-Jegher and Juvenile Polyposis causes what kind of polyps in colon?

A

hamartomatous

96
Q

what are the two types of colonic polyps with malignany potential

A

(1) serrated

(2) adenomatous

97
Q

what are the types of adenomatous polyps?

A

(1) villous (worse prognosis)

2) tubular (better prognosis

98
Q

what do serrated colonic polyps look like

A

saw toothed pattern of crypts

99
Q

chromosomal instability leads to what kind of polyp

A

probs w/ APC, KRAS are “chromasomal instability” lead to adenomatous polyps(=neoplastic)

100
Q

what does microsatellite instability lead to in type of polyp?

A

cpg methylation, BRAF mutations= microsatellite instability

cause serrated polyps (pre-malignant)

101
Q

FAP

A

AUTOSOMAL DOM MUT IN APC

multiple colonic polyps after puberty, 100% will become cancer

102
Q

what is Gardner’s syndrome

A

FAP+ bone/soft tissue tumors (+ hypertophy of retinal pigment)

103
Q

extra teeth or impacted teeth a sign of?

A

Gardner’s Syndrome

104
Q

Turcot Syndrome

A

FAP/ Lynch + malignancy CNS tumor

105
Q

peutz jeghers apart from hamartomatous GI polyps has increased risk of what cancers?

A

breast+ GI

106
Q

many hamartomatous polyps before age of 5

A

Juvenile Polyposis syndrome

107
Q

Lynch Syndrome

A

autosomal dominant mutation in mismatch repair genes (MSH1/2) causes microsatellite instability
linked to ovarian, endometrial, skin and colonic cancers

108
Q

most common location of colorectal cancer

A

rectosigmoid> ascending> descending

109
Q

how do ascending CRC and descending CRC present differently?

A

ascending:bloody stool, “exophytic mass”

descending : obstruction “infiltrating mass”

110
Q

whats the marker for CRC

A

CEA

111
Q

“apple core lesion”

A

CRC

112
Q

molecular pathogenesis of CRC?

A

“firing order of events” AK53
APC
KRAS
p53/ DCC

113
Q

why is it thought that NSAIDS can protect against CRC?

A

bc overexpression of COX2 has been seen in CRC

114
Q

what does a cirrhotic liver look like

A

diffuse bridging fibrosis and regenerative nodules distrupting normal liver architecture

115
Q

cirrhosis increases the risk for what?

A

HCC

116
Q

causes of cirrhosis?

A 
(1) alcohol(70%)
nonalc fatty liver disease
chronic viral hepatitis
autoimmune hepatitis 
biliary disease
metabolic diseases
117
Q

causes of portal htt?

A

(1) cirrhosis
vascular obstruction of portal v
Budd Chiari
schistosomiasis

118
Q

what are the neurologic signs of cirrhosis

A

hepatitis encephalopathy

asterixis

119
Q

what do AST and ALT show

A

hepatic injury

alcohol AST»ALT (or progression to advanced cirrhosis)

120
Q

what do ALP and yGT show?

A

biliary injury

note ALP is also increased in bone conditions (but not yGT) yGT is also more closely associated with alcohol use

121
Q

Reye syndrome

A

when you give a kid aspirin it causes irreversible mitochondrial damage( due to decreased B-ox), encephalopathy, and microvesicular fatty change of liver

122
Q

what is the progression of alcoholic liver disease

A

(1) hepatic steatosis : macrovesicular fatty change, reversible with alcohol cessation
(2) alcoholic hepatitis: due to chronic alc use, shows as swollen and necrotic hepatocytes, neutrophilic infiltrate, Mallory bodies
(3) alcoholic cirrhosis: final and irreversible, regen nodules with bands of fibrsosis

123
Q

what is a mallory body?

A

its seen in alcoholic hepatitis (intermediates stage of alcoholic liver disease) and its a intracytoplasmic inclusion of an eosinophilic staining keratin filament

124
Q

NAFLD pathology?

A

cellular ballooning and necrosis
associated with insulin resistance and metabolic syndrome
can cause cirrhosis and CRC

125
Q

hepatic encephalopathy physiology?

A

cirrhosis and shunting of blood away from liver causes decreased metabolism of ammonia. this ammonia can cross BBB
can be exscerbated by increase in ammonia (GI bleed, protein in diet, renal failure)
treatment is: lactulose (increases ammonia to ammonium) and rifaximin (decreases gut NH3 production)

126
Q

HCC marker?

A

AFP

127
Q

HCC caused by?

A

(1) Hep B

2) cirrhosis and its causes: Hep c, hemachromatosis, NAFLD, alcohol, a1antitrypsin, aflatoxin

128
Q

whats the most common benign liver tumor

A

cavernous hemagioma

DONT BIOPSY– it might bleed

129
Q

what liver cancer is related to OCP and steroid use?

A

hepatic adenoma

130
Q

arsenic and vinyl chloride cause

A

angiosarcoma of liver (malignant)

131
Q

if you see multiple liver tumors?

A

METS

132
Q

Budd-Chiari syndrome

A

blockage of hepatic veins.
“nutmeg liver”- centrilobular congestion/necrosis
absent JVD

133
Q

a1antitrypsin deficiency

A 
problem with liver+ lung (dyspnea)
panacinar emphysema (bc of no inhibition on elastase) and misfolded proteins(AAT) aggregating in liver (PAS+)
134
Q

jaundice

A

yellowing of skin or sclera bc of hyperbilirubinemia

135
Q

causes of unconjugated hyperbilirubinemia

A

unconjugated= insoluble = Indirect

  • hemolytic
  • physiologic : baby doesnt have mature UDP glucoronosyl transferase
  • Criggler Najar I- no UDP GT (II is less severe and responds to phenobarbital)
  • Gilbert’s– mildly decreased UDPGT
136
Q

causes of conjugated hyperbilirubinemia

A

conjugated= soluble=direct
bile tract obstruction (PSC, PBC)
excretion defect: Rotor’s and Dubin-Johnson

137
Q

causes of mixed hyperbilirubinemia

A

cirrhosis, hepatitis

138
Q

black liver + conjugated hyperbilirubinemia is?

A

DubinJohnson.
the black pigment is epinephrine
(note this is not seen in Rotor’s)

139
Q

Wilson’s disease?

A

Copper overload due to decreased Cu excretion in bile bc autorecmut in ATP7B.
decreased serum ceruloplasmin
t(x): penacillamine, or trientine, oral zinc

140
Q

wilson’s disease symptoms?

A

Kayser-Fletcher rings, hemolytic anemia, renal problems (Fanconi) liver/neuro/psych involvement

141
Q

What is the cause of Hemochromatosis

A

Autosomal recessive mutation in the HFE gene (transferrin receptor accessory) which causes faulty liver sensing of iron- telling the body iron is low when its not. this leads to increased iron absorption from intestines

142
Q

What are the symptoms of Hemochromatosis

A
  • “bronze diabetes”
    • skin pigmentation
  • -DM
    • arthopathy
    • dilated or restrictive cardiomyopathy
  • -hypogonad
143
Q

Hemochromatosis is a risk factor for what?

A

HCC

144
Q

Primary Sclerosing Cholangitis

who? histology? assn?

A
  • affects middle aged men
  • inflamm and sclerosis (“onion skin thickening”) of biliary tree (“beads of a string”)
  • p-ANCA, Ulcerative Colitis , increased IgM
145
Q

Primary Biliary Cholangitis

who? histology? assn?

A
  • affects middle aged women
  • association to autoimmune conditions (Sjogren, Hashimoto, CREST, RA, Celiac)
  • histology: lymphocytic infiltrate with granulomas of the bile ducts.. its an AUTOIMMUNE rxn!
  • anti-mitochondrial ab +, increased IgM
146
Q

secondary biliary cholangitis

A

due to obstructive lesion (gallstone, biliar strictures, head of pancreas tumor) of the extrahepatic ducts. which causes an increased pressure in the intrahepatic ducts, and leads to innjury, fibrosis, and stasis
(can be complicated by ascending cholangitis infection)

147
Q

black stone=

brown stone =

A

hemolysis

infection

148
Q

choledocolithiasis

A

stone in the CBD, causes increase in ALP, GGT, direct BR, (and or AST and ALT)

149
Q

cholecystitis and its 2 causes

A

inflamm of gall bladder usuallly due to stone in cystic duct

(1) calculus: gallstone in fuct
(2) acalculus: being very sick ex: sepsis, burns CMV causes gallbladder STASIS and hypoperfusion

150
Q

Porcelain Gallbladder

A

blue and brittle gallblader (lights up on CT) due to calcification from chronic cholecystits.
this risk is gallbladder cancer, so get rid of the gallbladder!!!

151
Q

whats the traid, and pentad of ascending cholangitis

A

Charcot triad: jaundice, fever, RUQ pain

Pentad: shock, and altered mental status

152
Q

acute pancreatitis

A

(1) gallstone (2) alcohol (high TGs Mumps, autoimmune, scorpion sting, high calcium, ERCP)
- injury causes activation of trypsinogen which activates all other zymogens while still in pancreas causing autodigestion.

153
Q

what does acute pancreatitis present like

A

acute epigastric pain radiating to back
INCREASED serum amylase and lipase
can be complicated by formation of a psuedocyst: covered in granulation tissue not epithelium. many other complications like hemorrhage, ARDS etc

154
Q

chronic pancreatitis

A

chronic inflamm/atrophy/calcification of pancreas.
cause: alcohol abuse and idiopathic
note that amylase and lipase may not be elevated
pancreatic insuff will cause low ADEK absorption, DM, and steatorrhea
pseudocysts can occur here too

155
Q

Pancreatic Adenocarcinom

A

CA19-9
Trousseau Sign- migrating thrombophlebitis
Courvoisier’s Sign- palpable but not tender gallbladder

if at head of pancreas- can cause CBD obstruction
wt loss w/ abdominal pain radiating to back

need to knows (31 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions