Brainscape's Knowledge GenomeTM

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


See full index

STEP1 > GASTRO 2: BOARDS AND BEYOND > Flashcards

GASTRO 2: BOARDS AND BEYOND Flashcards

1
Q

What demographic is primarily affected by autoimmune hepatitis (AIH)?

A

Women in their forties and fifties.

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

How is AIH commonly identified?

A

Through incidental findings of elevated aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels on blood work.

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

What are potential complications of AIH?

A

Chronic liver disease and, rarely, cirrhosis.

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

What are the diagnostic criteria for AIH?

A

Presence of antinuclear antibodies (ANA) for sensitivity and anti-smooth muscle antibodies (ASMA) for specificity, especially in type I AIH.

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

What is the management strategy for acute episodes of AIH?

A

Treatment typically involves steroids and immunosuppressants.

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

Are highly specific for systemic lupus erythematosus (SLE) and are believed to be implicated in the pathogenesis of lupus nephritis.

A

Anti-double stranded DNA antibodies

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

Are specific for CREST syndrome, a limited cutaneous form of systemic scleroderma. The five main features (as indicated by the acronym) are calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasias.

A

Anti-centromere antibodies

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

Are associated with drug-induced lupus. Common drugs implicated include procainamide, penicillamine, isoniazid, and methyldopa.

A

Anti-histone antibodies

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

Are found in patients with anti-phospholipid syndrome, a hypercoagulable state that causes thrombosis in arteries and veins. It causes a number of pregnancy-related complications, including miscarriage, stillbirth, preterm delivery, and preeclampsia.

A

Anti-cardiolipin antibodies

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

Are specific for primary biliary cholangitis. Like autoimmune hepatitis, this condition primarily affects middle-aged women. ANA antibodies are also sensitive markers for this disease. Unlike autoimmune hepatitis, patients generally present with signs and symptoms consistent with cholestasis, including itching, fatigue, and jaundice. Primary biliary cholangitis more often progresses to cirrhosis.

A

Anti-mitochondrial antibodies

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

What is a pyogenic liver abscess?

A

A walled-off infection of the liver.

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

What is the most likely cause of a pyogenic liver abscess in a patient with diverticulitis?

A

Seeding of the portal venous system with bacteria from the diverticulitis episode.

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

Which organisms are most commonly responsible for pyogenic liver abscesses?

A

Enteric flora, particularly gram-negative rods like E. coli and Klebsiella pneumoniae.

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

What characterizes acute alcoholic hepatitis?

A

Hepatitis occurring after acute binge drinking in individuals with a history of alcohol-use disorder.

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

What are common symptoms of acute alcoholic hepatitis?

A

Right upper quadrant abdominal pain, fever, and jaundice.

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

What is the main toxic by-product involved in the pathophysiology of acute alcoholic hepatitis?

A

Acetaldehyde, produced during alcohol metabolism.

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

How does acetaldehyde affect hepatocytes?

A

It damages intermediate filaments within the cells.

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

What is a classic histopathological finding in acute alcoholic hepatitis?

A

Mallory bodies, which are cytoplasmic inclusions representing damaged intermediate filaments in hepatocytes.

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

In alcoholic liver disease, nuclei may be pushed aside by fat accumulation with cells, but

A

Nuclear abnormalities are not a classic feature of alcoholic hepatitis.

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

An overabundance of microtubules can be seen in cardiac myocytes in patients with

A

Hypertrophic cardiomyopathy

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

Structural and functional alterations of the Golgi apparatus are seen in several neurodegenerative, diseases including

A

Amyotrophic lateral sclerosis (ALS), Parkinson’s disease, Alzheimer’s dementia, and Huntington’s disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is Budd-Chiari syndrome?

A

Hepatic vein thrombosis leading to abdominal pain, ascites, and hepatomegaly.

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

How is Budd-Chiari syndrome diagnosed?

A

Doppler imaging showing obstruction of the hepatic vein.

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

What conditions are associated with Budd-Chiari syndrome?

A

Hepatocellular carcinoma, polycythemia vera, and hypercoagulable states.

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

What comprises the portal triad?

A

A bile duct, hepatic artery, and portal vein, surrounded by zone I (periportal).

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

Describe the zones of the liver acinus

A

Zone I (periportal), Zone II (midzone), Zone III (centrilobular).

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

What happens in Zone III during hepatic vein thrombosis?

A

Congestion occurs first, leading to potential hepatic necrosis.

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

Why is Zone III particularly susceptible to injury?

A

It is vulnerable to ischemic damage, fatty infiltration, and fibrosis.

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

What are common etiologies of cirrhosis?

A

Alcoholic liver disease, viral hepatitis, autoimmune conditions (e.g., autoimmune hepatitis, primary biliary cholangitis, primary sclerosing cholangitis).

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

How does cirrhosis affect liver function?

A

It impairs synthetic functions like albumin and clotting factor production.

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

What laboratory findings would indicate cirrhosis?

A

Decreased serum albumin and prolonged prothrombin time (PT), partial thromboplastin time (PTT), and INR.

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

How are Factor VIII levels affected in chronic liver disease?

A

Factor VIII levels are usually normal or increased due to synthesis by endothelial cells outside the liver.

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

Where else is von Willebrand factor (VWF) synthesized?

A

By endothelial cells outside the liver, similar to Factor VIII.

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

Evidence of hypervolemia:
- Distended abdomen (ascites)
- Bilateral pitting edema

A

Cirrhosis Overview

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q
  • Vasodilation
  • Low systemic vascular resistance (SVR)
A

Hemodynamic Changes in Cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Low SVR activates:
- Sympathetic nervous system (SNS)
- Renin-angiotensin-aldosterone system (RAAS)
Results in:
- Sodium and water retention
- Hypervolemia

A

Cirrhosis: Activation of Compensatory Systems

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

Low albumin → decreased plasma oncotic pressure
Fluid leakage from capillaries →
Reduces circulating volume
Causes ascites and peripheral edema

Impact on Renal Blood Flow
Low circulating volume → decreased renal blood flow (RBF)
Increased serum antidiuretic hormone (ADH) levels

A

Plasma Oncotic Pressure in Cirrhosis

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

Total body sodium is increased in hypervolemia (e.g., cirrhosis, heart failure)
Serum sodium = sodium in blood
Can be elevated, normal, or low in hypervolemia
Hyponatremia risk:
Due to water retention and dilution of serum sodium

A

Total Body Sodium vs. Serum Sodium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q
  • Activation of SNS and RAAS → sodium and water retention
  • Excess fluid increases total body sodium
  • Retention of water can lead to hyponatremia
A

Summary of Fluid and Sodium Dynamics

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

Internal hemorrhoids are a consequence of congestion of the

A

Superior rectal veins

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

In cirrhosis, venous collaterals form between the left gastric vein and the esophageal veins. Congestion of this vessel leads to

A

Esophageal varices

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

What are Varices?

A
  • Dilated, tortuous veins
  • Hallmark of end-stage liver disease and cirrhosis
    Can rupture, leading to life-threatening hemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Cause of Varices

A
  • Result from portal venous congestion
    Secondary to obstructed blood flow in cirrhotic liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Gastric Varices Explained

A
  • Dilated veins due to congestion in short gastric veins
  • Located along the greater curvature of the stomach
  • Short gastric veins drain into the splenic vein, then the portal vein

Congestion in the splenic vein leads to dilation of short gastric veins
Visible during endoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Risks of Bleeding Varices

A
  • High morbidity and mortality in cirrhosis
  • Screening endoscopy performed to evaluate and treat when bleeding risk is high
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

The superior rectal veins drain into the inferior mesenteric vein, which then drains to the portal vein. Note that the other rectal veins (middle and inferior rectal veins) bypass the portal-venous system. Blood from these veins eventually drains into the inferior vena cava.

A

Dilation of these vessels in portal hypertension does not occur.

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

The umbilical vein is present during fetal development. This structure closes after birth and becomes the

A

Ligamentum teres (also called the round ligament of the liver).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q
  • Drug of choice for managing ascites in cirrhosis after salt and fluid restriction
  • Aldosterone receptor antagonist
A

Spironolactone Overview

49
Q
  • Blocks aldosterone action at the distal tubule
    Results in:
  • Decreased sodium and water retention
  • Increased excretion of salt and water (diuresis)
  • Improvement of ascites
A

Mechanism of Action: Spironolactone

50
Q
  • Spironolactone is a potassium-sparing diuretic
  • Requires monitoring for hyperkalemia
A

Potassium-Sparing Diuretic: Spironolactone

51
Q

Common ECG changes:
- Peaked T waves (classic finding)
Severe hyperkalemia can lead to:
- Broadening of QRS
- Absence of P-waves
- Conversion to sinusoidal wave pattern

A

Hyperkalemia Monitoring: Spironolactone

52
Q

Polyuria and volume loss occurs with

A

Hypercalcemia

53
Q

Tetany occurs in

A

Hypocalcemia

54
Q

Calciphylaxis occurs in

A

Hyperphosphatemia

55
Q

Parathyroid inhibition occurs in ?. Severe hypomagnesemia suppresses parathyroid hormone release, leading to hypocalcemia.

A

Marked hypomagnesemia

56
Q
  • Impairment of neuropsychiatric function due to impaired hepatic function
    Often associated with hyperammonemia
A

Hepatic Encephalopathy Overview

57
Q

Common in many cases of hepatic encephalopathy
Neurologic manifestations include:
- Asterixis
- Confusion
- Coma

A

Role of Hyperammonemia

58
Q

Synthetic disaccharide and osmotic laxative
- Used to lower elevated serum ammonia in hepatic cirrhosis

A

Lactulose as Treatment

59
Q
  • Increases excretion of ammonia via the GI tract
  • Fermented by colonic flora → release of fatty acids
A

Mechanism of Lactulose

60
Q
  • Increases free fatty acid and hydrogen ion concentration in the colon
  • Acidifies colonic environment, converting NH3 to NH4+
  • NH4+ cannot be reabsorbed and is excreted in stool
A

Effects of Lactulose Fermentation

61
Q
  • Ammonium excretion via stool lowers serum NH3 levels
  • Helps improve symptoms of hepatic encephalopathy
A

Impact on Serum NH3 Levels

62
Q

Increase in free fluid in the peritoneal cavity
- Defined as >25 ml of fluid

A

Definition of Ascites

63
Q

Portal hypertension

A

Primary Cause of Ascites in Cirrhosis

64
Q

Blood flows from the portal venous system → liver → hepatic veins → inferior vena cava

A

Normal Blood Flow Pathway

65
Q
  • Normal liver tissue is replaced by fibrous tissue
  • Disrupted blood flow leads to portal hypertension
A

Changes in Cirrhosis

66
Q
  • Increased capillary hydrostatic pressure in the abdomen
  • Fluid shifts from intravascular space to extravascular space
A

Mechanism of Ascites Formation

67
Q

The most common cause of liver malignancy is metastasis. Common primary sites include the pancreas, breast, lung, and colon. Metastasis to the liver is more likely to present as multiple lesions, but a single lesion can also occur. Colonic adenocarcinoma is most likely in this case, given the

A

Coexisting microcytic anemia and heme positive stool.

68
Q

Hepatocellular carcinoma (HCC) is less common than metastasis to the liver. HCC generally presents as a single lesion; however, this patient has no apparent risk factors. Risk factors include infection with ?.

A

hepatitis B, hepatitis C, cirrhosis, alcohol abuse, and exposure to aflatoxins

69
Q

Hepatic adenomas are benign lesions that generally present as solitary nodules in the right lobe of the liver and occur in

A

Younger women on oral contraceptives.

70
Q

Hepatic angiosarcomas are rare, highly malignant lesions whose primary risk factors include exposure to

A

Polyvinyl chloride or arsenic.

71
Q

Rare, highly malignant primary tumor of the liver
- Vascular in nature

A

Hepatic Angiosarcoma Overview

72
Q
  • Atypical endothelial cells
  • Disorganized vascular structures
A

Hepatic Angiosarcoma Histological Features

73
Q

Death often secondary to rupture of liver nodules

A

Hepatic Angiosarcoma Cause of Death

74
Q

Generally poor prognosis
- Less than one year from diagnosis

A

Hepatic Angiosarcoma Prognosis

75
Q

Common metastasis to the lungs and spleen

A

Hepatic Angiosarcoma Metastatic Sites

76
Q

Toxic exposures, notably:
- Polyvinyl chloride
- Arsenic

A

Hepatic Angiosarcoma Primary Risk Factors

77
Q

Most common primary malignancy of the liver

A

Hepatocellular Carcinoma (HCC) Overview

78
Q
  • Alcohol use
  • Cirrhosis
  • Chronic hepatitis B
  • Exposure to aflatoxins (e.g., from contaminated homegrown vegetables)
A

Hepatocellular Carcinoma (HCC) Risk Factors

79
Q
  • Commonly associated with polycythemia
  • Elevated hematocrit due to secretion of erythropoietin (EPO)
A

Hepatocellular Carcinoma (HCC) Lab Abnormalities

80
Q
  • EPO increases bone marrow production of red blood cells
  • Normally secreted by the kidney in response to anemia
A

Erythropoietin (EPO) in HCC

81
Q

Is a tumor marker elevated in pancreatic cancer.

A

Ca 19-9

82
Q

Is a tumor marker that is elevated in multiple malignancies including colonic, gastric, breast, lung, and medullary thyroid cancer.

A

Carcinoembryonic antigen (CEA)

83
Q

This man has cirrhosis with no evidence of portal hypertension, such as ascites. Patients with cirrhosis of any cause are at increased risk for hepatocellular carcinoma (HCC). For this reason, abdominal imaging with

A

Ultrasound, CT scan, or MRI is performed at regular intervals, usually every six months.

84
Q

A contrast agent, is injected into the rectum via enema to visualize the distal colon and rectum by X-ray. This can be useful in disorders of the distal colon, including colon cancer, inflammatory bowel disease, and Hirschsprung’s disease.

A

Barium

85
Q

Occurs in end-stage liver disease when the liver can no longer synthesize sufficient clotting factors.

A

Coagulopathy with elevated prothrombin time

86
Q

Alanine aminotransferase (ALT) is a liver enzyme. Its levels are elevated in many forms of liver disease, and may be low in ? when the liver is replaced by fibrous tissue.

A

Cirrhosis

87
Q

Occurs in end-stage liver disease with liver failure when the liver can no longer perform gluconeogenesis.

A

Hypoglycemia

88
Q
  • Autosomal recessive disorder of copper metabolism
  • Characterized by impaired copper transport and excretion in bile
A

Wilson’s Disease Overview

89
Q
  • Caused by mutation of the ATP7B gene on chromosome 13
  • ATP7B is a copper transport protein
A

Genetic Cause of Wilson’s Disease

90
Q
  • Impaired function of ATP7B leads to copper accumulation in the liver and other organs
  • Results in free radical production and tissue damage
A

Mechanism of Copper Accumulation

91
Q
  • Pathological hallmark of Wilson’s disease
  • Corneal copper deposits along Descemet’s membrane at the limbus (corneoscleral junction)
A

Kayser-Fleischer Ring

92
Q

Copper accumulation in the brain leads to symptoms such as:
- Ataxia (leading to falls)
- Difficulty speaking

A

Neurologic Impairment in Wilson’s Disease

93
Q

Total body copper is increased compared to normal
Copper is trapped in organs (liver, brain, eye, kidneys)

A

Copper Metabolism in Wilson’s Disease

94
Q
  • Total serum copper is paradoxically decreased
  • Ceruloplasmin (copper transport protein) is low due to impaired copper incorporation
A

Wilson’s D: Serum Copper and Ceruloplasmin Levels

95
Q
  • 24-hour urinary copper excretion is increased
  • Increased free copper in serum is filtered at the glomerulus and excreted
A

Urinary Copper Excretion in Wilson’s Disease

96
Q

Increased urinary copper excretion does not reverse total body copper accumulation in tissues

A

Impact of Urinary Excretion on Copper Accumulation

97
Q
  • Ceruloplasmin is the copper transport protein in serum
    Levels are low because copper cannot be incorporated and released from the liver
A

Ceruloplasmin in Wilson’s Disease

98
Q
  • Hepatomegaly
  • Increased serum aminotransferase levels
A

Clinical Features of Wilson’s Disease

99
Q
  • Oral chelation therapy with penicillamine
  • Aids in copper excretion via the kidneys
A

Treatment for Wilson’s Disease

100
Q

Condition characterized by excess total body iron

A

Hemochromatosis Overview

101
Q
  • Can be hereditary due to mutation of the C282Y gene
  • Gene codes for the HFE protein
A

Genetic Cause of Hemochromatosis

102
Q
  • Can develop from excessive blood transfusions
    Associated with disorders like:
  • Sickle cell anemia
  • Beta thalassemia major
  • Myelodysplastic syndromes
A

Acquired Causes of Hemochromatosis

103
Q

Skin: Dark bronze discoloration from iron deposition
Pancreas: May lead to diabetes (“bronze diabetes”)
Heart: Common manifestation is dilated cardiomyopathy

A

Organ Systems Affected by Hemochromatosis

104
Q
  • New complaint of dyspnea on exertion
  • Pitting edema
  • Extra heart sound
A

Symptoms Supporting Dilated Cardiomyopathy

105
Q

Enlarged cardiac silhouette due to increased size of the left ventricle

A

Chest X-ray Findings in Dilated Cardiomyopathy

106
Q

Condition of iron overload with deposition in multiple organs

A

Hemochromatosis Overview

107
Q
  • Elevated serum iron
  • Elevated ferritin
  • Elevated transferrin saturation
  • Transferrin levels may be decreased or normal
A

Iron Studies in Hemochromatosis

108
Q
  • Dilated cardiomyopathy (most common)
  • Rarely, restrictive cardiomyopathy
A

Cardiac Manifestations of Hemochromatosis

109
Q

Skin may turn bronze from iron interaction with melanin

A

Skin Changes in Hemochromatosis

110
Q
  • Iron deposition can lead to diabetes mellitus
  • Often referred to as “bronze diabetes” due to concurrent skin changes
  • Symptoms include polyuria and polydipsia
A

Pancreatic Effects of Hemochromatosis

111
Q

Iron deposition may lead to:
- Hepatomegaly
- Abnormal liver function tests
- Cirrhosis
- Increased risk of hepatocellular carcinoma

A

Liver Complications in Hemochromatosis

112
Q

arthralgias

A

Joint Symptoms in Hemochromatosis

113
Q
  • Erectile dysfunction and small testes indicate testicular atrophy
  • Leads to decreased serum testosterone
A

Endocrine Effects in Hemochromatosis

114
Q
  • Increase in ferritin and hemoglobin A1C
  • Decrease in serum testosterone
A

Expected Laboratory Changes in Hemochromatosis

115
Q

Avoid Alcohol: Protects the liver.
Avoid Vitamin C: Increases iron absorption.

A

Dietary Recommendations for Hemochromatosis

116
Q

Heme Iron: Found in red meat; easily absorbed.
Non-Heme Iron: Absorbed as Fe2+; enhanced by Vitamin C (converts Fe3+ to Fe2+).

A

Iron Absorption Forms

117
Q

Avoid vitamin C to limit dietary iron absorption.

A

Implications for Hemochromatosis Patients

118
Q
A

STEP1 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions