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Internal Med - Jesse > GI > Flashcards

GI Flashcards

0
Q

abdominal pain + hyperkalemia is seen in __________

A

bowel infarction (represents tissue necrosis).

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1
Q

Abdominal pain + anion gap acidosis DDx (3)

A

bowel infarction, DKA, or severe pancreatitis.

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2
Q

Murphy’s sign - whatever is it, what does it indicate?

A

pain on palpation of right upper quadrant with inspiration; is associated with cholecystitis.

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3
Q

Sonography findings of cholecystitis (3)

A

Gallbladder wall thickening
Sonographic Murphy’s sign (tenderness with pressure applied by probe over gallbladder)
Pericholecystic fluid

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4
Q

Abdominal pain can be caused by: (5)

A

obstruction, perforation, ischemia, infection, or metabolic disturbances.

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5
Q

Abdominal pain referred from the hollow viscera travels via the __________ nerves; the type of pain is ______________.

A

splanchnic (sympathetic); dull, vague, and poorly localized

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6
Q

Diseases involving the parietal peritoneum produce _________ pain.

A

sharp, stabbing, well-localized

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7
Q

DKA can produce ______ (4)

A

abdominal pain, vomiting, ketonuria, and an anion gap acidosis

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8
Q

DDx diffuse or periumbilical abdominal pain (6)

A 
Abdominal aortic aneurysm (AAA)
Ischemic bowel
Bowel obstruction, especially small bowel
Pancreatitis
Gastroenteritis
Metabolic disturbances (see other card)
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9
Q

DDx RUQ pain (4)

A

Cholecystitis
Biliary colic
Hepatitis
Pyelonephritis

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10
Q

DDx RLQ pain (4)

A

Appendicitis
Nephrolithiasis
Crohn disease of terminal ileum
Gynecologic (ovarian torsion, ectopic preg)

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11
Q

DDx LUQ pain (2)

A

Splenic rupture

Pyelonephritis

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12
Q

DDx LLQ pain (4)

A

Diverticulitis
Nephrolithiasis
Inflammatory bowel disease
Gynecologic (ovarian torsion, ectopic preg)

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13
Q

Metabolic disturbances assoc with abdominal pain (5)

A 
Acute intermittent porphyria
Diabetic ketoacidosis (DKA)
Familial Mediterranean fever
Narcotic withdrawal
Lead toxicity
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14
Q

Conditions with severe pain but relatively normal abdominal examinations (pain out of proportion to findings) are: (3)

A

ischemic bowel, pancreatitis, and acute intermittent porphyria.

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15
Q

Abdominal pain physical exam: look for / do: (9)

A

Fever, jaundice, evidence of vascular disease, presence of bowel sounds, rebound tenderness, point tenderness, palpable masses, rectal exam (&occult blood), pelvic exam

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16
Q

4 mechanisms of diarrhea

A

Increased secretion of electrolytes and water
Increased osmotic load
Inflammation leading to exudation of protein and fluid
Altered intestinal motility

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17
Q

Increased secretion diarrhea DDx (5)

A

WATERY STOOL
Enterotoxin producing bacteria (e.g., ADP-ribosylating toxin like cholera toxin, guanylate cyclase activators like E. coli heat stable toxin)
Noninvasive microbial gastroenteritis (e.g., viral gastroenteritis, Giardia)
Carcinoid syndrome
Vasoactive intestinal peptide-secreting tumor (VIPoma)
Villous adenoma

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18
Q

Increased osmotic load diarrhea DDx (7)

A

BULKY, GREASY STOOL
Sorbitol ingestion (sugar-free candy diarrhea)
Bile salt malabsorption
Pancreatic insufficiency (due to lipid malabsorption)
Lactase deficiency (lactose intolerance)
Other malabsorption syndromes (e.g., celiac disease/gluten intolerance)
Postantrectomy rapid gastric emptying (dumping syndrome)
Magnesium-containing laxatives

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19
Q

Inflammation-mediated diarrhea DDx (5)

A

BLOODY STOOL, with or without leukocytes
Ulcerative colitis
Crohn disease
Radiation-induced enteritis
Invasive microbial gastroenteritis (e.g., Shigella, Entamoeba)
Cytotoxic bacterial infection (e.g., Clostridium difficile, enterohemorrhagic E. coli infection)

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20
Q

Altered intestinal motility diarrhea DDx (3)

A

Thyrotoxicosis
Irritable bowel syndrome (IBS)
Neurologic disease (e.g., diabetes-associated enteropathy)

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21
Q

Triggers for a stool exam in diarrhea (8)

A 
High fever
Evidence of dehydration
Systemic toxicity
Bloody stool
Immunocompromise
Overseas or outdoor (e.g., hiking) travel
Male homosexuality
Recent antibiotic use

NOTE: The presence of blood and/or leukocytes in the stool suggests an invasive microbial (e.g., Shigella, Campylobacter, or Entamoeba) rather than a viral or toxin-mediated cause.

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22
Q

Chronic diarrhea: how to distinguish between osmotic and secretory (2 ways)

A

1 Osmotic diarrhea (which is generally caused by some sort of malabsorption syndrome) improves with fasting, whereas secretory diarrhea persists during fasting.
2 calculate the stool osmotic gap using the following formula:
Osmotic Gap = Osmolality - 2(Stool Na + Stool K)
Stool osmolality is usually estimated using the measured plasma osmolality. An osmotic gap >50 mOsm per kg H2O suggests an osmotic diarrhea.

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23
Q

Definition of diarrhea

A

increase in the volume of stool. (often accompanied by increased stool fluid content and frequency.)

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24
Q

Main causes of dyspepsia (3)

A

Peptic ulcer disease (PUD), gastroesophageal reflux disease (GERD), and gastritis

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25
Q

Ulcerative colitis often presents with bloody diarrhea and abdominal pain +/- tenesmus. Crohn’s presents with similar symptoms except:

A

pain may be more cramplike, with accompanying fever and weight loss.

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26
Q

Patients with IBS may have many similar symptoms to UC/Crohn’s including abdominal pain, bloating, and diarrhea; 3 ways to tell IBS apart:

A

Symptoms have often been prolonged.
There is an absence of bleeding and weight loss.
Bowel movements often relieve symptoms in IBS.

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27
Q

IBD Sx (7) and Chrohn’s specific Sx (3)

A

IBD: Vital sign abnormalities (tachycardia, orthostatic hypotension, fever).
Abdominal tenderness
Pyoderma gangrenosum (ulcerating lesion usually on trunk)
Erythema nodosum (violaceous subcutaneous nodules usually on lower legs)
Uveitis
Arthritis
Other extraintestinal inflammatory conditions

Crohn’s specifically: fullness or palpable masses (adherent loops of bowel).
Rectal fistulas (perirectal abscess).
Aphthous ulcers of the oral cavity

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28
Q

Lower GI bleeding DDx (5)

A 
IBD
diverticulosis
colon cancer or polyps
arteriovenous malformations
hemorrhoids
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29
Q

Hepatobiliary diseases associated with IBD (5)

A 
Sclerosing cholangitis (mostly ulcerative colitis)
Cholelithiasis (mostly Crohn's disease)
Fatty liver
Autoimmune hepatitis
Cholangiocarcinoma

(Increased alkaline phosphatase level may represent underlying liver disease, which occurs at a higher frequency in patients with IBD.)

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30
Q

Colonoscopy findings in UC & Crohn’s

A

Skip lesions and cobblestone mucosa in Crohn’s disease;

Continuous involvement and pseudopolyps in ulcerative colitis.

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31
Q

Complications of Crohn’s disease (3)

A

bowel obstruction, abscesses, and fistulas

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32
Q

Complications of ulcerative colitis (2)

A

toxic megacolon and colon carcinoma

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33
Q

chronic hepatitis is defined as hepatitis that persists for _______

A

6 months

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34
Q

Chronic gastritis is characterized by mononuclear cell infiltrates and lack of mucosal erosions. Chronic infection with H. pylori is associated with at least three types of chronic gastritis:

A

Chronic active gastritis, atrophic gastritis, and so-called type B gastritis.

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35
Q

_______ gastritis is believed to be a precursor to some gastric cancers.

A

Atrophic

36
Q

Acute gastritis can occurs in the setting of a serious systemic illness, such as trauma, burns, sepsis, liver and renal failure, and shock, but is more commonly due to _______

A

direct mucosal injury due to agents such as nonsteroidal anti-inflammatory drugs (NSAIDs), ethanol, steroids (high doses), and strong alkali and acid agents.

37
Q

What amount of gastric acid is required (excess/normal/reduced) to produce duodenal ulcers and gastric ulcers?

A

In duodenal ulcers, excess gastric acid is necessary for ulcer formation (hence the dictum, “no acid, no ulcer”). In contrast, patients with gastric ulcers tend to have normal or even reduced gastric acid secretion.

(H. pylori infection appears to be associated with >90% of duodenal ulcers and 70% to 80% of gastric ulcers.) (PUD usually manifests a chronic epigastric pain.)

38
Q

Epigastric pain DDx (6)

A 
Peptic ulcer disease (gastric, duodenal)
Gastritis (acute, chronic)
GERD
Pancreatitis
Myocardial ischemia
Cholecystitis
39
Q

Traditional pharmacologic treatment is designed to inhibit or neutralize gastric acid or protect the mucosa. The major classes of drugs used are: (4)

A

H2-receptor antagonists (cimetidine, ranitidine, famotidine, nizatidine)—limit both basal and stimulated acid secretion
Antacids (aluminum hydroxide, magnesium hydroxide, calcium carbonate, and others)—neutralize gastric acid and provide relatively prompt relief of symptoms
Proton pump inhibitors (lansoprazole, omeprazole)—most potent antisecretory agents, which limit the terminal step in acid secretion
Sucralfate—mucosal protectant without significant antacid effect

40
Q

Gastritis is _________ mucosal inflammation, as opposed to the ________ damage seen in ulcer disease. (Superficial/deep)

A

Superficial; Deep

41
Q

Tx of peptic ulcers?

A

Treatment of underlying H. pylori infection & antacid therapy with or without mucosal protective agents.

42
Q

Hemochromatosis - which organs fail

A
  • autosomal recessive
  • liver, heart, and gonadal failure.
  • Pancreatic failure, leading to glucose intolerance, combined with increased skin pigmentation (“bronze diabetes.”)
  • Secondary hemochromatosis may occur in patients who are transfusion dependent
43
Q

Wilson disease - organs affected

A
  • autosomal recessive
  • increased accumulation of copper in the liver and brain.
  • may present with fulminant or chronic hepatitis, cirrhosis, psychiatric involvement, or neurologic disease (tremor, rigidity).
44
Q

α1-Antitrypsin deficiency - organs affected (typical presentation)

A
  • autosomal recessive

- early emphysema and asymptomatic cirrhosis.

45
Q

Hepatic encephalopathy characteristics (3)

A 
confusion, personality changes, and asterixis; may progress to obtundation and coma. 
Unknown etiology (increased ammonia?)
46
Q

Cirrhosis complications (4)

A

ascites, portal hypertension, jaundice, and encephalopathy.

47
Q

Cirrhosis findings on phys exam (7 categories)

A

1 liver is enlarged, normal or small; firm.
2 ascites (bulging Flanks, shifting dullness)
3 Portal hypertension –> splenomegaly, internal hemorrhoids, and caput medusae
4 Men: gynecomastia, testicular atrophy.
5 Skin: jaundice and spider telangiectases.
6 hand: Clubbing, Palmar erythema, Dupuytren’s contracture (permanent flexion of the third or fourth metacarpal phalangeal joint)
7 asterixis (hepatic encephalopathy)

48
Q

Ascites DDx (6)

A 
Cirrhosis
Abdominal malignancy (pancreatic, ovarian)
Nephrotic syndrome
Cardiac failure
Peritoneal tuberculosis
Peritoneal mesothelioma
49
Q

Lab findings in cirrhosis (4)

A

Hyponatremia - increased ADH secretion (effective renal blood flow is reduced)
Decreased BUN level - malnutrition and decreased protein production
Decreased albumin level
Increased bilirubin level (mostly direct)

50
Q

Cirrhosis hematological abnormalities (3)

A
  • Increased PT
  • Macrocytic anemia (mean cell volume >100) because of increased RBC membrane in liver disease - may also be caused by concomitant alcohol use or folate deficiency
  • Thrombocytopenia secondary to splenomegaly and decreased production of thrombopoietin
51
Q

serum ascites-albumin gradient - diseases assoc with > and < 1.1 mg/dL (4 and 5, respectively)

A

Less than 1.1: malignancy, TB, pancreatitis, nephrotic

More than 1.1: cirrhosis (portal hyperT), hepatic mets, Budd-Chiari, cardiac disease, myxedema

52
Q

Tx of ascites

A

Sodium restriction (<2 g NaCl per day).
Diuretic therapy: Potassium-sparing diuretics are the drugs of choice. Many patients also require furosemide.
Large-volume paracentesis: Removal of 6 to 8 L of peritoneal fluid (effective, prompt)
Peritoneovenous (LeVeen) shunt: connects the peritoneum to the vena cava.

53
Q

________ is the most important predisposing risk factor for hepatocellular cancer (HCC).

_______ may be elevated in HCC, but its use as a screening test is limited because of its relatively low sensitivity and specificity.

A

Cirrhosis; α-Fetoprotein

54
Q

In the patient with new-onset hepatic encephalopathy, an underlying precipitant should be suspected, including ________ (4)

A

infection, GI bleeding, hypokalemia, and drugs

55
Q

_____ is associated with inflammatory bowel disease (especially ulcerative colitis) in up to 90% of cases.

A

PSC (primary sclerosing cholangitis)

56
Q

Primary biliary cirrhosis (PBC) affects predominantly ________, whereas primary sclerosing cholangitis (PSC) affects mostly ________.

A

PBC = middle-aged women; PSC = men

57
Q

Symptoms of cholestatic liver disease (5)

A 
Pruritus
Fatigue
Steatorrhea
Jaundice
Malabsorption of fat-soluble vitamins (A, D, E, K) may also lead to symptoms
58
Q

Classic triad of pancreatic carcinoma

A

jaundice, weight loss, and back or abdominal pain.

59
Q

Signs of ascending cholangitis (4)

A

Fever and chills
Right upper quadrant pain
Jaundice
Nausea and vomiting

(Ascending cholangitis due to extra hepatic bile duct obstruction)

60
Q

Viral hepatitis type that most commonly becomes chronic

A

Hep C

61
Q

Causes of hepatitis (7 categories)

A

Hepatitis viruses
Other viral infections (cytomegalovirus, herpes simplex virus, Coxsackie viruses, hepatitis G virus, transfusion-transmitted virus (TTV)
Drugs (acute and chronic): Oxyphenisatin (a laxative, no longer used in the US), Acetaminophen, Halothane, Isoniazid, Methyldopa, Azole antifungals
Alcohol
Acute anoxic liver injury
Autoimmune chronic active hepatitis (ACAH)
Hereditary disorders: Wilson disease, hemochromatosis, and α1-antitrypsin deficiency

62
Q

HepA to E are all ssRNA except one - which one and what is it?

A

Hep B, dsDNA

63
Q

AST and ALT findings in acute viral hepatitis and alcoholic hepatitis (2)

A

1 Acute viral hepatitis causes a greater absolute AST and ALT elevation than alcoholic hepatitis.
2 In alcoholic hepatitis, the serum AST is usually elevated out of proportion to the ALT, leading to an AST-to-ALT ratio greater than 2.

(A single measurement of aminotransferase level, however, is a poor indicator of the absolute degree of hepatic damage.)

64
Q

Tx for acute viral hepatitis

A

For acute viral hepatitis, there are no well-accepted specific therapies. In many cases, close outpatient follow-up with laboratory monitoring to document resolution of hepatic injury.

65
Q

1 Chronic viral hepatitis Tx

2 chronic hepatitis (infectious and noninfectious) can lead to ______

A

1 chronic HBV and HCV: interferon alpha (bolster immune response)
Chronic HCV: + ribavirin (antiviral)
Chronic HBV: + antiviral agents lamivudine, adefovir dipivoxil, or entecavir.

2 cirrhosis and end-stage liver failure

66
Q

Cirrhosis definition

A
  • irreversible hepatic injury
  • fibrosis that distorts the normal hepatic architecture
  • presence of regenerative nodules.
67
Q

Underlying causes of cirrhosis (7)

A

Alcohol
Chronic hepatitis B or C
Biliary disease (including primary biliary cirrhosis)
Cardiac disease
Autoimmune hepatitis
Inherited diseases (hemochromatosis, Wilson disease, α1-antitrypsin deficiency)
Nonalcoholic fatty liver disease (often in pts with diabetes mellitus or metabolic syndrome).

68
Q

MUDPILERS

A 
Methanol
Uraemia
Diabetic ketoacidosis
Propylene glycol
Isoniazid
Lactic acidosis
Ethylene glycol
Rhabdomyolysis
Salicylates
69
Q

Jaundice DDx

A 
Cholestasis
Hepatocellular injury
Hemolysis
Acute and chronic pancreatitis
Gilbert disease
70
Q

extrahepatic bile duct obstruction/cholestasis DDx (6)

A

Pancreatic carcinoma
Cholangiocarcinoma
Parasitic infections (e.g., Ascaris, liver flukes)
Bile duct strictures
Choledocholithiasis
Primary biliary cirrhosis (but usually causes intrahepatic obstruction)

71
Q

intrahepatic bile duct obstruction/cholestasis DDx (5)

A 
Primary biliary cirrhosis (can also cause extrahepatic obstruction)
Primary sclerosing cholangitis
Drug reactions
Viral hepatitis
Nonalcoholic steatohepatitis
72
Q

Most common and less common causes of pancreatitis

A

Alcohol and gallstones are the underlying etiology in 80% of cases.

Less common causes (10% of cases) include:

  • direct injury (postoperative, traumatic, post-endoscopic retrograde cholangiopancreatography [ERCP])
  • viral infections (mumps, Coxsackie virus, hepatitis, cytomegalovirus)
  • vascular injury (cholesterol embolism, vasculitis)
  • metabolic abnormalities
  • pancreatic cancer
  • pancreas divisum (unclear - under debate)
73
Q

Pancreatitis Sx/findings (6)

A
  • abdominal pain (characteristically epigastric, steady and boring, radiating to the back, and relieved with sitting)
  • Nausea and vomiting are usually present
  • Vital sign abnormalities in unstable pts (hypotension and tachycardia in volume depletion, high temp with infection)

In severe disease:

  • Erythematous skin nodules (because of fat necrosis)
  • Dullness to percussion and decreased breath sounds (indicating pleural effusion, most often on the left)
  • Blue periumbilical discoloration (Cullen sign) and bruising on the abdominal flanks (Grey-Turner sign), both suggesting severe necrotizing disease
74
Q

Pancreatitis DDx

A 
Perforated viscus*
Cholecystitis*
Small bowel obstruction*
Mesenteric ischemia/thrombosis*
Dissecting aneurysm
Renal colic
Diabetic ketoacidosis
Ruptured ectopic pregnancy*

(*also have elevated serum amylase, like pancreatitis)

75
Q

Consequences of pancreatitis (5)

A

1 Death (most often: infection or multiorgan system failure)
2 ARDS (worsening hypoxemia and bilateral pulmonary infiltrates).
3 Pancreatic abscess/infected necrosis (Dx with CT)
4 Pancreatic pseudocyst: Diagnosed by CT. Often resolves on its own within 6 weeks.
5 Chronic pancreatitis: Seen most often as a consequence of alcohol-induced or idiopathic pancreatitis. Symptoms include recurrent pain and malabsorption. Diagnosis confirmed by ERCP, showing beaded dilated pancreatic duct (“chain of lakes”). Treatment is mainly symptomatic, with pancreatic enzyme replacement if needed.

76
Q

Dx of pancreatitis (3)

A
  • typical picture of abdominal pain
  • increased amylase and lipase levels.
  • Imaging studies, such as radiograph and US, may be used to rule out other abdominal pathology.
77
Q

Tx of pancreatitis (general)

A

Treatment is mainly supportive with IV fluids and analgesia.

78
Q

To confirm a hepatic source of elevated alkaline phosphatase due to cholestasis, ______ is measured (confirmed if elevated).

A

5-nucleotidase or gamma glutamyl transpeptidase (GGT).

79
Q

In cholestasis, ________ bilirubin may also be increased and indicates more advanced obstruction. (Direct or indirect)

A

direct (conjugated); hemolysis causes indirect hyperbilirubinemia

80
Q

Serum transaminases (aspartate aminotransferase and alanine aminotransferase) are usually mildly elevated in cholestasis except if cholestasis is due to ___________.

A

acute viral hepatitis

hepatocellular dysfunction alone causes transaminases to be elevated more than alkaline phosphatase.

81
Q

__________ antibody is positive in 95% of patients with PBC and not present in PSC.

60% of PSC cases have positive ____________ antibody.

A

Antimitochondrial antibody (AMA) in PBC

Perinuclear antineutrophil cytoplasmic antibody (P-ANCA) in PSC

82
Q
  • The initial test in evaluating cholestatic liver disease is __________.
  • Tx of cholestatic obstructions?
A

the right upper quadrant ultrasound to determine whether the obstruction is intrahepatic or extrahepatic.

Extrahepatic obstruction will require an intervention to relieve the obstruction, whereas intrahepatic obstructions are treated medically (ursodiol).

83
Q

Primary biliary cirrhosis main characteristics (3)

A

1 occurs mostly in middle-aged women
2 often presents with pruritus or asymptomatic elevations in alkaline phosphatase
3 antimitochondrial antibody is present in most cases.

84
Q

Primary sclerosing cholangitis main characteristics (3)

A

1 usually seen in association with inflammatory bowel disease
2 patients may present with ascending cholangitis (fever, right upper quadrant pain, jaundice).
3 usually (60%) p-ANCA positive

85
Q

Colon cancer Tx

A

Surgery (colectomy).
For more extensive disease (if nodal metastases are present), this is followed by adjuvant chemotherapy (5-FU and levamisole) +/- high-dose pelvic radiation.

86
Q

IBD subtype assoc with higher risk of colorectal ca; screening recommendation in this population?

A

Ulcerative colitis

Colonoscopy after 8 to 10 years of disease, then surveillance colonoscopy every 1 to 2 years

87
Q

Freq of surveillance colonoscopy after removal of colonic adenomatous polyp

A

Surveillance colonoscopy every 3 to 5 years after excision—every 1 to 3 years if multiple, large (>1 cm), villous, malignant (noninvasive)

88
Q

Type A gastritis primarily affects the _______ of the stomach, and is commonly assoc with _______.

Type B gastritis (most common overall) primarily affects the ______ of the stomach, and is more commonly assoc with __________.

A

A: body/fundus; pernicious anemia
B: antrum; H. pylori infection

Internal Med - Jesse (8 decks)

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