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STEP 1 > 07a: GI > Flashcards

07a: GI Flashcards

1
Q

Between (X) weeks of embryological development, you would expect the physiologic midgut to be herniated outside the abdominal cavity.

A

X = 6-10

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2
Q

Ventral wall defects: failure of rostral fold closure during development

A

Sternal defects (ectopia cordis)

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3
Q

Ventral wall defects: failure of lateral fold closure during development

A
  1. Omphalocele

2. Gastroschisis

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4
Q

Ventral wall defects: failure of caudal fold closure during development

A

Bladder exstrophy

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5
Q

Abdominal protrusion in newborn that’s covered by skin

A

Umbilical hernia (incomplete closure of umbilical ring)

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6
Q

Neonate with abdominal distension and bilious vomiting likely has obstruction before/after which part of GI tract?

A

Small bowel, after second part of duodenum

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7
Q

Duodenal atresia is due to an issue with (X) process. Jejunal/ileal atresia is due to an issue with (Y) process.

A 
X = recanalization 
Y = blood supply (ischemic necrosis and segmental resorption due to disruption of mesenteric vessels)
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8
Q

Neonate presenting with non-bilious projectile vomiting and olive-shaped mass in epigastric region

A

Hypertrophic pyloric stenosis

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9
Q

Hypertrophic pyloric stenosis is associated with (X) exposure.

A

X = macrolide

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10
Q

Which acid/base disturbance is seen in Hypertrophic pyloric stenosis?

A

Metabolic alkalosis (hypokalemic, hypochloremic) due to vomiting acid and volume contraction

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11
Q

Annular pancreas refers to which anomaly?

A

Ventral bud abnormally encircles and compresses/narrows 2nd part of duodenum

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12
Q

Pancreas divisum refers to which anomaly?

A

Failure of ventral and dorsal buds to fuse (common, mostly asymptomatic; may cause pancreatitis)

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13
Q

(X) part of GI tract receives foregut blood supply but actually arose from (Y).

A 
X = spleen
Y = mesoderm (stomach mesentery)
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14
Q

Which part(s) of small/large bowel are retroperitoneal

A
  1. Duodenum (parts 2-4)

2. Ascending and descending colon

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15
Q

(Liver/gallbladder/pancreas/spleen) is/are retroperitoneal

A

Pancreas (except tail)

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16
Q

Portal triad is contained in (X) ligament. Umbilical vein remnant, aka (Y), is contained in (Z) ligament.

A 
X = hepatoduodenal (bile duct, proper hepatic a, portal v)
Y = Round ligament (ligamentum teres)
Z = Falciform (connects liver to anterior abdominal wall)
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17
Q

Which ligaments are part of the lesser omentum?

A

Gastrohepatic and hepatoduodenal

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18
Q

List the layers of gut wall, from inside to outside, as well as their contents

A

“MSMS”

  1. Mucosa (epithelium, LP, muscularis mucosa)
  2. Submucosa (meiSSner plexus, Secretory glands)
  3. Muscularis externa (Myenteric/auerbach plexus for Motility)
  4. Serosa (if intraperitoneal) or adventitia (retroperitoneal)
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19
Q

Basal electric rhythm (number of waves/min) is highest/most frequent in (stomach/duodenum/ileum)

A

Duodenum (12 waves/min); stomach is 3, ileum is 8-9

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20
Q

Brunner glands in (X) part of GI tract are responsible for secreting:

A

X = duodenum

HCO3

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21
Q

Largest number of goblet cells found in which part of small bowel?

A

Ileum

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22
Q

Intestinal crypts (of Lieberkühn) have (X) cells that secrete TNF as well as:

A

X = Paneth

Defensins, lysozyme

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23
Q

Peyer’s patches would most likely be found where in GI tract?

A

Ileum

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24
Q

Abdominal aorta bifurcates into (X) branches at which level of spine?

A

X = common iliacs

L4 (“biFOURcation)

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25
Q

Which branches come off the abdominal aorta laterally before the celiac trunk?

A

Inferior phrenic (off of which branches the superior suprarenal)

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26
Q

Which branches come off the abdominal aorta laterally between SMA and IMA?

A
  1. Renal (off of which branch inferior suprarenal)

2. Gonadal

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27
Q

SMA syndrome: (X) is compressing (Y).

A 
X = SMA and abdominal aorta
Y = transverse (3rd) part of duodenum
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28
Q

Bilious vomiting in neonate and fibrous bands extending from cecum/right colon to retroperitoneum

A

Midgut malrotation (resulting in cecum placement in RUQ and fibrous bands compressing duodenum)

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29
Q

Derivatives of the ventral pancreatic bud:

A

Uncinate process, inferior part of head, and proximal part of main pancreatic duct

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30
Q

Lymph drainage of rectum

A

Prox to dentate line: inferior mesenteric and internal iliac

Distal to line: superficial inguinal

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31
Q

R and L colic lymph nodes drain:

A

R: upper ascending colon
L: splenic flexure and upper descending colon

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32
Q

Where is the location of the duodenal bulb? Ulcer perforation posteriorly will likely affect which vessel?

A 
From pylorus to neck of gallbladder;
Gastroduodenal a (life-threatening hemorrhage)
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33
Q

Portal-systemic anastamosis involved in esophageal varices

A

Left gastric vein to esophageal vein (a branch of azygos v)

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34
Q

Portal-systemic anastamosis involved in caput medusae

A

Paraumbilical v to small epigastric vv (of anterior abdominal wall)

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35
Q

Portal-systemic anastamosis involved in anorectal varices

A

Superior rectal v to middle/inferior rectal vv

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36
Q

Portal hypertension with esophageal/anorectal varices treated with:

A

Transjugular Intrahepatic Portosystemic Shunt (TIPS) between portal v and hepatic v (bypass liver)

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37
Q

Above pectinate line: list arterial supply and venous drainage

A

Arterial: superior rectal a (off IMA)
Venous: superior rectal v (to IMV to splenic to portal v)

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38
Q

Above pectinate line, (X) cancer. Below, (Y) cancer.

A 
X = adenocarcinoma (endoderm)
Y = squamous cell carcinoma (ectoderm)
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39
Q

Below pectinate line: list arterial supply and venous drainage

A

Arterial: Inferior rectal a (off internal pudendal)
Venous: Inferior rectal v (to internal pudendal to internal iliac, to common iliac, to IVC)

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40
Q

Liver: blood flow (from/toward) central vein and bile flow (from/toward) central vein.

A

Toward (from hepatic a and portal v branches)

From (toward bile ductule)

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41
Q

Liver: Zone (I/II/III) most affected by alcoholic hepatitis and (first/last) zone affected by ischemia.

A

III;

First

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42
Q

Liver: Zone (I/II/III) most affected by yellow fever.

A

II (yeLLow fever)

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43
Q

Liver: Zone (I/II/III) most affected by viral hepatitis.

A

I

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44
Q

Liver: Zone (I/II/III) most susceptible to ingested toxins (ex: cocaine). And Zone (I/II/III) most susceptible to metabolic toxins.

A

I;

III

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45
Q

Liver: Zone (I/II/III) contains CYP450 system

A

III

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46
Q

List the layers of the spermatic cord, from inside to outside, and include the structure that each layer is derived from.

A

“ICE tie”

  1. Internal spermatic fascia (transversalis fascia)
  2. Cremasteric muscle and fascia (internal oblique)
  3. External spermatic fascia (external oblique)
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47
Q

Deep inguinal ring is a physiologic opening in (X). And external inguinal ring is opening in (Y).

A 
X = transversalis fascia
Y = external abdominal oblique aponeurosis
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48
Q

Gastrin secreted by (X) cells in (Y)

A 
X = G
Y = antrum (stomach) and duodenum
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49
Q

H. pylori (directly/indirectly) (increases/decreases) Gastrin production.

A

Indirectly increases (via decreasing D cells/somatostatin levels)

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50
Q

Somatostatin, produced by (X) cells, is (increased/decreased) by vagal stimulation and functions to (increase/decrease):

A

X = D (pancreatic islets, GI mucosa); decreased

Decrease nearly everything:

  1. Gastric acid/pepsinogen secretion
  2. Pancreatic/small intestine secretion (including glucagon and insulin)
  3. Gallbladder contraction
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51
Q

Gallbladder contraction and pancreatic secretion is stimulated by (X) substance, produced in (Y) cells.

A 
X = cholecystokinin (CCK)
Y = I cells (duodenum, jejunum)
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52
Q

Which regulatory substance is primarily responsible for both endocrine and exocrine pancreatic secretions?

A

CCK (bicarb from ductal cells, enzymes from acinar cells);

Secretin also helps with bicarb secretion

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53
Q

T/F: Secretin is released from S cells in presence of high pH.

A

False - low pH (decreases gastric acid secretion)

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54
Q

GIP is released from (X) cells and functions to:

A

X = K cells (duodenum, jejunum)

Increase insulin secretion (endocrine) and decrease gastric acid secretion (exocrine)

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55
Q

Motilin is secreted in (fasting/fed) state and functions to:

A

Fasting (from small intestine)

Produce migrating motor complexes (MMCs)

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56
Q

Intestinal water and electrolyte secretion is increased by vagal stimulation and release of:

A

VIP

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57
Q

VIPoma causes which symptoms?

A

“WDHA syndrome”: Watery Diarrhea, Hypokalemia, Achlorydia

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58
Q

List the 3 main stimulators for gastric acid secretion:

A

“GAHstric acid”

  1. Gastrin
  2. ACh
  3. His
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59
Q

Which phase of acid secretion is triggered just by thought/sight/smell of food?

A

Cephalic (first phase)

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60
Q

List the phases of gastric acid secretion

A
  1. Cephalic
  2. Gastric
  3. Intestinal
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61
Q

Peptide YY is released by (X) portions of GI tract and functions to:

A

X = ileum and colon (during intestinal phase of acid secretion)

Binds receptors on ECL (enterochromaffin-like) cells, blocking gastrin action on the cells for His release

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62
Q

Gastric mucosa: large, oxyntic/pale pink cells in glands on histology are secreting (X)

A

X = gastric acid and intrinsic factor

Parietal cells

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63
Q

Gastric mucosa: small, basophilic cells in glands on histology are secreting (X)

A

X = pepsinogen

Chief cells

64
Q

Crohn’s disease: increase risk of (X) urinary stones via which mechanism?

A

X = oxalate

Decreased bile acid reabsorption (terminal ileum) means decreased fat reabsorption; fat binds to Ca, which then can’t bind oxalate for excretion, so increased oxalate reabsorption

65
Q

Which pancreatic enzymes are secreted in active form?

A

Lipase and amylase

66
Q

Enterocytes absorb which carbohydrates? Via which apical and basal transporters?

A
  1. Glucose (SGLT1; Na dependent)
  2. Galactose (SGLT1; Na dependent)
  3. Fructose (GLUT5; passive transport)

All transported to blood by GLUT2

67
Q

Where are folate and vit B12 primarily absorbed in GI tract?

A

Folate: small bowel (jejunum)
B12: terminal ileum

68
Q

Where is Fe primarily absorbed in GI tract?

A

Duodenum

69
Q

Peyer patches location

A

Lamina propria and submucosa of ileum

70
Q

Rate-limiting step in bile act synthesis carried out by which enzyme?

A

Cholesterol 7a-hydroxylase

71
Q

Bruises turn greenish color due to action of:

A

Heme oxygenase (metabolizes heme into biliverdin)

72
Q

Conjugated bilirubin formed by action of which enzyme?

A

UDP-glucoronosyl-transferase

73
Q

Achalasia is due to:

A

Loss of myenteric (Auerbach) plexus and inhibitory neurons (NO, VIP) in esophagus; absent peristalsis and high LES pressure

74
Q

Achalasia may be secondary to (X) infection.

A

X = Trypanosoma cruzi (Chagas disease)

75
Q

T/F: Achalasia is associated with increased risk esophageal cancer.

A

True - both squamous cell and adenocarcinoma

76
Q

Boerhaave syndrome:

A

TRANSMURAL (unlike Mallory-Weiss syndrome), distal esophageal rupture with pneumomediastinum due to violent retching

77
Q

Which X-ray sign would you most commonly find with Boerhaave syndrome?

A

Pneumomediastinum (stripe of air adjacent to heart/aorta)

78
Q

Esophagitis with white pseudomembrane:

A

Candida infection (immunocompromised pts)

79
Q

Esophagitis with punched-out ulcers:

A

HSV-1 (immunocompromised pts)

80
Q

Esophagitis with linear, shallow ulcers

A

CMV (immunocompromised pts)

81
Q

What are some less common symptoms of GERD?

A

“Silent GERD” can present as chronic (nocturnal) cough, hoarseness

82
Q

Which structural abnormality is a predisposing factor to Mallory-Weiss syndrome?

A

Hiatial hernia

83
Q

Plummer-Vinson syndrome increases risk for which esophageal pathology?

A

Squamous cell carcinoma

84
Q

Pathogenesis/mechanism of esophageal complications in Scleroderma:

A

Esophageal smooth muscle atrophy (fibrous replacement of muscularis) decreases LES pressure and causes dysmotility

85
Q

Pt with history of DM II, obesity, and severe GERD presents with new onset odynophagia. Most likely diagnosis?

A

Ulcer formation (erosive esophagitis)

86
Q

Corkscrew shape of esophagus on barium swallow:

A

Diffuse esophageal spasm (disorganized, non-peristaltic contractions due to impaired inhibitory neurotransmission within myenteric plexus)

87
Q

List some causes of acute gastritis

A

(Usually stress-related mucosal damage)

  1. NSAIDs
  2. Burn (Curling ulcer)
  3. Brain injury (Cushing ulcer)
88
Q

Curling ulcer: mechanism of injury

A

Burns lead to hypovolemia and mucosal ischemia (erosion/ulcer and acute gastritis)

89
Q

Cushing ulcer: mechanism of injury

A

Brain injury leading to high vagal stimulation, high ACh, and high gastric acid production (erosion/ulcer and acute gastritis)

90
Q

Chronic gastritis: mucosal (hypertrophy/atrophy/hyperplasia) and (hyper/hypo)-chlorydia. Two main causes, star the most common.

A

Mucosal atrophy (chronic inflammation); hypochlorydia (and hypergastrinemia, leading to G cell metaplasia)

  1. H. pylori*
  2. Autoimmune
91
Q

T/F: Both ulcer formation and gastric adenocarcinoma are more common in autoimmune/atrophic than H. pylori chronic gastritis.

A

False - ulcers more common with H. pylori; adenocarcinoma more common with autoimmune cause

92
Q

(X) disease: precancerous (hyper/hypo)-plasia of gastric mucosa and stomach rugae that look like brain gyri.

A

X = Ménétrier
Hyperplasia (hypertrophied rugae)
Excess mucus production, parietal cell atrophy

93
Q

(Diffuse/intestinal) gastric cancer associated with H. pylori infection as well as which other risk factors?

A

Intestinal;

Nitrosamines (smoked food), tobacco smoking, achlorhydria, chronic gastritis

94
Q

(Diffuse/intestinal) gastric cancer: leathery, thickened stomach wall. What would you see on histology?

A

Diffuse

Signet ring cells (mucin-filled)

95
Q

You would expect weight loss with (gastric/duodenal) ulcer. Why?

A

Gastric;
pain Greater with meals in Gastric ulcer
pain Decreases with meals in Duodenal ulcer

96
Q

NSAIDs can cause (gastric/duodenal) ulcers. H. pylori can cause (gastric/duodenal) ulcers. ZES can cause (gastric/duodenal) ulcers.

A

Gastric;
Both;
Duodenal

97
Q

T/F: Biopsy should be done on all gastric and duodenal ulcers.

A

False - duodenal ulcers rarely malignant, so no biopsy needed

98
Q

Small intestinal bacterial overgrowth associated with increased serum levels of:

A

Vit K and folate (produced by enteric bacteria)

99
Q

Celiac disease histology:

A
  1. Villous atrophy
  2. Crypt hyperplasia
  3. Intraepithelial lymphocytosis
100
Q

T/F: Celiac disease increases risk of malignancy.

A

True - ex: T cell lymphoma

101
Q

Lactose intolerance: what’s the mechanism of the diarrhea?

A

Osmotic

102
Q

Lactose intolerance can be diagnosed via (X) test. What’s the mechanism behind this?

A

X = hydrogen breath test

Bacterial ferment lactose and produce hydrogen (note: this also acidifies the stool)

103
Q

Ito cells are found in (X) and have which functions?

A

AKA hepatic stellate cells
X = liver (space of Disse)

Normally store vit A (quiescent) and can be activated to produce extracellular matrix (ex: collagen scar tissue leading to cirrhosis)

104
Q

T/F: Alcoholic cirrhosis are deficient in vitamin A.

A

True - Ito cell store of Vit A decreases when they’re activated to produce ECM

105
Q

Schilling test used to assess:

A

Vit B12 deficiency cause

106
Q

Tropical sprue is similar to (X) disease, but responsive to (Y). Which vitamin/mineral deficiencies are seen?

A 
X = celiac sprue
Y = antibiotics (unknown cause)

Vit B12 and folate (megaloblastic anemia)

107
Q

Whipple disease symptoms and histological findings:

A

“PASs the FOAMY WHIPPed cream in the CAN”
PAS positive, foamy macrophages in lamina propria; diarrhea/steatorrhea

  1. Cardiac Sx
  2. Arthralgias
  3. Neuro Sx
108
Q

T/F: D-xylose test normal in pancreatic insufficiency.

A

True - no need for pancreatic enzymes for monosaccharide absorption (test used to distinguish pancreatic insufficiency versus mucosa defect/bacterial overgrowth)

109
Q

“Lead pipe” colon on barium enema:

A

Ulcerative colitis (loss of haustra)

110
Q

“String sign” bowel on barium swallow Xray

A

Crohn’s (bowel wall thickening)

111
Q

Crohn’s disease is (TH1/TH2) mediated and UC is (TH1/TH2) mediated

A

TH1 (non-caseating granulomas; IL2, TNF, IFN-g)

TH2 (IL4-6, IL10)

112
Q

Recurrent UTIs and pneumaturia seen in (Crohn’s/UC).

A

Crohns (enterovesical fistula formation)

113
Q

Mechanism of toxic megacolon is increased (X) causing smooth muscle paralysis

A

X = NO

114
Q

Primary sclerosing cholangitis associated with (Crohn’s/UC)

A

UC

115
Q

NOD2 gene mutation increases susceptibility to (X) disease. What’s the mechanism behind this?

A

X = Crohn’s

Decreased NF-kB activation so decreased cytokine production and innate immunity; this impairs intestinal mucosa immune response, so luminal bac penetrate tissue; exaggerated adaptive immune system response causes chronic inflammation

116
Q

Most likely inciting event in appendicitis in kids

A

Lymphoid hyperplasia (ex: post-viral illness) causing obstruction

117
Q

Diverticulitis symptoms and Rx

A

Similar to appendicitis (fever, leukocytosis, localized abdominal pain), but in LLQ and more common in elderly

Rx: antibiotics

118
Q

Zenker diverticulum: herniation at which location?

A

Killian triangle (inferior pharyngeal constrictor, between thyropharyngeal and cricopharyngeal parts)

119
Q

Characteristics of Meckel diverticulum

A

The rule of TRUE 2’s:

  1. True diverticulum
  2. 2x more likely in males
  3. 2% of population
  4. 2 inches long
  5. 2 feet from ileocecal valve
  6. May have 2 types of epithelia (gastric/pancreatic)
120
Q

Pertechnetate study localizing to RLQ

A

Meckel diverticulum (pertechnetate uptake by ectopic gastric mucosa/parietal cells)

121
Q

Most common Sx in meckel diverticulum

A

Painless GI bleeding

122
Q

Key clinical finding that distinguishes meconium ileus from hirschsprung disease

A

Hirschsprung: empty rectum on digital exam and positive “squirt” sign (explosive expulsion of feces)
MI: Negative squirt sign, rectum not empty

123
Q

T/F: Hirschsprung disease treated by resecting affected segment.

A

True

124
Q

Volvulus in infants/children more common in (X) part of GI tract. In elderly, more common in (Y) part

A 
X = midgut
Y = sigmoid
125
Q

Majority of intussusception causes occur in (X) patient population and may be associated with which causes?

A

X = kids (*Most common cause of GI obstruction in kids 3 months - 6 years old)
Meckel div, recent viral infection (adenovirus) and peyer patch hypertrophy

126
Q

Intussusception commonly occurs at (X) part of GI tract and presents with which Sx?

A

X = ileocecal junction

Intermittent abdominal pain (with pain-free periods) and currant jelly stools

127
Q

60 yo patient with hematochezia and thumbprint sign on abdominal Xray

A

Colonic ischemia (thumbprint sign due to edema/hemorrhage of mucosa)

128
Q

65 yo pt with Hx of CAD, angina, and previous MI presents with post-prandial epigastric pain and weight loss. What diagnosis is near the top of your differential?

A

Chronic mesenteric ischemia

“intestinal angina” due to atherosclerosis of celiac a, SMA, IMA

129
Q

Angiodysplasia:

A

Tortuous dilation fo vessels causing hematochezia (AV malformation)

130
Q

Most common cause of bowel obstruction:

A

Adhesions (fibrous bands of scar after surgery)

131
Q

Thick, dehydrated mass obstructing intestine (esp distal ileum) and preventing stool passage in newborn

A

Meconium ileus (cystic fibrosis)

132
Q

Premature infant develops bilious vomiting and imaging shows portal venous gas. What’s the likely diagnosis and mechanism?

A

Necrotizing enterocolitis

Immature immune system allows bacteria to enter/damage intestinal tissues, leading to necrosis of mucosa and perforation

133
Q

Villous adenoma/polyp can cause which electrolyte abnormalities?

A

Hypokalemia (secrete large V of watery mucus causing secretory diarrhea and hypovolemia)

134
Q

Serrated colonic polyps: (malignant/benign) via (X) pathway with microsatellite (stability/instability) and mutations in (Y).

A

Pre-malignant
X = CpG hypermethylation
Instability
Y = BRAF

135
Q

Adenomatous colonic polyps: (X) pathway with mutations in (Y).

A 
X = chromosomal instability
Y = APC and KRAS
136
Q

T/F: All inherited polyposis syndromes are autosomal dominant

A

True

137
Q

FAP: mutation in (X) on chromosome (Y). Which part of GI tract always involved?

A 
X = APC (tumor suppressor)
Y = 5q

Rectum (thousands of polyps arise after puberty)

138
Q

Patient with FAP has (X)% change of colorectal cancer.

A

X = 100

Hence prophylactic colectomy in these pts

139
Q

What’s Turcot syndrome?

A

A polyposis syndrome; FAP/Lynch plus malignant CNS tumors (medulloblastoma, glioma)

“TURcot = TURban (brain involved)”

140
Q

(X) syndrome: hyperpigmented macules on lips, hands, genitalia along with which other key finding?

A

X = Peutz-Jeghers

Numerous hamartomas (benign polyps) throughout GI tract (increased risk of breast and visceral cancers)

141
Q

T/F: Lynch syndrome involves MSH1/MSH2 gene mutation, numerous colonic polyps, microsatellite instability, and 80% progression to CRC.

A

Mostly true, except NOT a polyposis syndrome so no numerous colonic polyps (hence previous name “HNPCC”)

142
Q

Patient with Lynch syndrome is at risk for which cancers?

A

CRC (80%), endometrial, ovarian, skin

143
Q

List the locations of colon where CRC tends to occur, in order of most to least common.

A
  1. Rectosigmoid
  2. Ascending
  3. Descending
144
Q

Chromosomal instability pathway for CRC: which mutations occur, in order?

A

AK-53

APC gene loss (colon at risk)
KRAS mutation (adenoma)
p53 loss (carcinoma; "the last hit")
145
Q

NSAIDs (increase/decrease) risk for CRC because:

A

Decrease

COX2 over-expression has been linked to CRC

146
Q

Esophageal varices, splenomegaly in 48 yo M with normal liver biopsy. Most likely diagnosis?

A

Portal vein thrombosis

147
Q

T/F: One of first signs of cirrhosis is low albumin levels.

A

False - coagulation disorder (esp low F VII) due to shorter half-life than albumin

148
Q

Patient with history of cirrhosis and ascites presents with fever/chills, abdominal pain, and asterixis. What would be the next step in aiding your diagnosis?

A

Paracentesis of ascitic fluid to check for spontaneous bacterial peritonitis (absolute PMN count over 250 cells/mm3)

149
Q

Patient with Hx of liver disease comes in for routine exam. His AST is higher than his ALT. What are two potential reasons for this?

A
  1. Alcoholic liver disease

2. Non-alcoholic but progression of liver disease to advanced fibrosis/cirrhosis

150
Q

Which primary markers for assessing liver function hold the greatest prognostic significance in cirrhosis patients?

A
  1. Bilirubin
  2. Albumin
  3. PT

Note: AST/ALT measure liver intactness/integrity NOT function

151
Q

Reye syndrome: describe the liver changes/damage and the mechanism by which it occurs.

A 
Fatty liver (microvesicular fatty change)
Aspirin metabolites decrease beta-oxidation (via reversible inhibition of mitochondrial enzymes)
152
Q

28 yo missionary, recently returned from South America, presents with fever, anorexia, nausea, and rash. High AST, ALT (ALT > AST), prolonged PT time. Viral serologies are negative. Likely diagnosis?

A

Drug-induced (halothane anesthetic) liver injury (especially if had surgery abroad)

153
Q

Drug-induced liver injury from halothane: what would you expect to see on autopsy/histology?

A

Liver atrophy on autopsy;
Histo: widespread centrilobular necrosis and inflammation of portal tracts/parenchyma (indistinguishable from viral hepatitis)

154
Q

Drug-induced liver injury from halothane: what’s the mechanism?

A

Immune-mediated (attack hepatocytes)

155
Q

Pyogenic liver abscess that got to liver through hepatic artery: most likely organism?

A

S. aureus (systemic hematogenous route)

STEP 1 (21 decks)

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