Week 4 GI Part 2 Flashcards
(100 cards)
1
Q
What is hepatitis C?
A
An infection of the liver caused by the hepatitis C virus (HCV)
HCV is an RNA virus and a member of the genus Hepacivirus and the family Flaviviridae.
2
Q
How is hepatitis C transmitted?
A
Through infectious blood or body fluids, during childbirth, IV drug use, or sexual intercourse
Humans are the only reservoir for the virus.
3
Q
What types of hepatitis can hepatitis C cause?
A
Both acute and chronic hepatitis
Chronic hepatitis can lead to liver cirrhosis and hepatocellular carcinoma (HCC).
4
Q
What is the incubation period for hepatitis C?
A
2 weeks to 6 months (median: 8 weeks)
5
Q
What is the most common reason for liver transplantation?
A
Hepatitis C infection
6
Q
What is the global prevalence of chronic hepatitis C?
A
About 70 million people
7
Q
What percentage of individuals infected with HCV know their diagnosis?
A
About 20%
8
Q
Which regions have the highest prevalence of hepatitis C?
A
- Eastern Mediterranean
- South East Asia
- Western Pacific
- Sub-Saharan Africa
9
Q
What are the modes of transmission for hepatitis C?
A
- Parenteral
- Sexual
- Perinatal
- Tattooing, sharing razors, and reusing acupuncture needles
10
Q
What is the role of glycoproteins E1 and E2 in hepatitis C?
A
They mediate the attachment of the virus to the host cell
11
Q
What is the percentage of individuals who develop chronic HCV infection?
A
60% to 85%
12
Q
What are common symptoms of acute hepatitis C infection?
A
- Icterus and jaundice
- Fatigue
- Arthralgias
- Myalgias
- Abdominal pain
- Fever
- Nausea, vomiting, diarrhea
13
Q
What is the initial test for diagnosing hepatitis C?
A
HCV antibodies
14
Q
What indicates active infection in hepatitis C diagnosis?
A
Positive HCV RNA test
15
Q
What are the treatment goals for hepatitis C?
A
- Eradication of HCV
- Prevention of progression to cirrhosis, HCC, and decompensated liver disease
16
Q
What are direct-acting antiviral agents (DAAs) used for?
A
To treat hepatitis C infection
17
Q
What are the main classes of laxatives?
A
- Bulk-forming
- Stimulant
- Osmotic
- Emollient
18
Q
What are the general indications for using laxatives?
A
- Constipation
- Bowel regimen for patients on opioid therapy
- Bowel preparation before colon procedures
19
Q
What is a common side effect of all laxatives?
A
Bloating
20
Q
What is the mechanism of action of bulk-forming laxatives?
A
Absorbs water to form a bulky gel, promoting peristalsis
21
Q
What are examples of bulk-forming laxatives?
A
- Psyllium husk
- Methylcellulose
- Polycarbophil
- Wheat dextrin
22
Q
What are stimulant laxatives used for?
A
To stimulate colonic contractions
23
Q
What are examples of stimulant laxatives?
A
- Senna
- Bisacodyl
- Castor oil
24
Q
What is a contraindication for bulk-forming laxatives?
A
Fecal impaction
25
What is a potential adverse effect of stimulant laxatives?
Abdominal cramps
26
Fill in the blank: Hepatitis C virus is a ______ virus.
RNA
27
True or False: There is currently a vaccine available for hepatitis C.
False
28
What are the adverse effects of stimulant laxatives?
• Abdominal cramps
• Diarrhea
• Intestinal obstruction
• Anaphylaxis (associated with psyllium in susceptible individuals)
## Footnote
Adverse effects tend to be minimal with these agents.
29
Name three agents classified as stimulant laxatives.
• Senna
• Bisacodyl
• Castor oil
## Footnote
These agents stimulate colonic contractions.
30
What is the mechanism of action for stimulant laxatives?
• Myenteric plexus stimulation through direct action on the intestinal mucosa or nerve plexus → colonic contractions
• Alter water and electrolyte secretion in the intestinal mucosa.
31
What is the onset of action for oral administration of stimulant laxatives?
6–12 hours (up to 24 hours with senna)
## Footnote
Approximately 1 hour for rectal administration.
32
What is melanosis coli?
Brown or black discoloration of colonic mucosa on colonoscopy due to pigmented macrophage deposition in lamina propria.
33
What are the indications for osmotic laxatives?
• Constipation
• Preparation for colonoscopy
• Hepatic encephalopathy (specifically for lactulose).
34
What are common agents classified as osmotic laxatives?
• Magnesium citrate
• Magnesium sulfate
• Polyethylene glycol
• Sorbitol
• Lactulose.
35
What is the mechanism of action for osmotic laxatives?
Osmotically active substances draw water into the GI lumen → soft stools.
36
List some adverse effects of osmotic laxatives.
• Bloating
• Flatulence
• Diarrhea
• Nausea
• Dehydration
• Hypermagnesemia (in patients with renal impairment who take magnesium-containing laxatives).
37
What is the main agent used as an emollient laxative?
Docusate (Colace).
38
What is the mechanism of action for emollient laxatives?
• Surfactant: ↓ surface tension along oil–water interface of stool
• Incorporates water and fat in stool → soft stool.
39
What are the contraindications for emollient laxatives?
• GI obstruction
• Concomitant mineral oil use.
40
What are the adverse effects of emollient laxatives?
• Diarrhea
• Abdominal cramps
• Throat irritation
• Dehydration.
41
What virus causes hepatitis E?
Hepatitis E virus (HEV).
42
What is the transmission route for hepatitis E?
Fecal–oral route.
43
Which populations are most affected by hepatitis E?
• East and South Asia
• Resource-poor areas with frequent water contamination
• Areas with unsafe drinking water supplies.
44
What is the mortality rate for pregnant patients with hepatitis E?
20%.
45
What are the clinical symptoms of hepatitis E during the icteric phase?
• Jaundice
• Dark urine
• Grayish stools
• Itching.
46
What serologic test indicates a current or recent infection of hepatitis E?
Anti-HEV IgM antibodies.
47
What is the incubation period for hepatitis E?
2–6 weeks.
48
What are the main preventive measures against hepatitis E?
• Chlorine treatment of water and sewage
• Regular handwashing
• Avoidance of possibly contaminated food, such as uncooked shellfish.
49
What is the primary reservoir for hepatitis E virus?
Animals (zoonotic virus).
50
What is the classification of hepatitis E virus?
RNA virus: genus Hepevirus.
51
True or False: Hepatitis E can cause chronic infection.
True, but chronic cases are very rare and typically occur in immunosuppressed patients.
52
What is alcoholic fatty liver disease?
A condition that ranges from fatty liver (hepatic steatosis) to nonalcoholic steatohepatitis, leading to liver injury, fibrosis, cirrhosis, and potentially primary liver cancer.
## Footnote
Management includes lifestyle modifications such as diet and exercise.
53
What are antispasmodics?
A group of medications used to reduce excessive GI smooth muscle contractility and spasm.
## Footnote
They are helpful in abdominal pain due to conditions like irritable bowel syndrome, although efficacy is controversial.
54
How are antispasmodics classified?
They are classified into:
* Anticholinergics
* Direct smooth muscle relaxants
55
Name three anticholinergic medications.
* Dicyclomine
* Hyoscyamine
* Atropine
56
What is the mechanism of action of anticholinergics?
They block acetylcholine’s action at muscarinic receptors in the enteric nervous system and on smooth muscle cells, resulting in decreased smooth muscle contractions and motility.
57
List common adverse effects of anticholinergics.
* Constipation
* Urinary retention
* Blurred vision
* Xerostomia
* Dizziness
* Nausea
* Drowsiness
* Tachycardia
58
What are contraindications for anticholinergics?
* Hypersensitivity
* GI obstruction
* Severe ulcerative colitis
* Glaucoma
* Myasthenia gravis
* Breastfeeding
59
What is the mechanism of action for direct smooth muscle relaxants?
They act directly on intestinal smooth muscle cells, causing relaxation and decreased motility.
60
Name two direct smooth muscle relaxants.
* Mebeverine
* Peppermint oil
61
What is the primary route of transmission for hepatitis A?
Fecal-oral transmission is the most common route.
62
What are the typical symptoms of hepatitis A?
* Nausea
* Anorexia
* Abdominal pain
* Fever
* Jaundice
63
What is the incubation period for hepatitis A?
2–6 weeks before symptoms appear.
64
How is hepatitis A diagnosed?
By detecting anti-HAV IgM antibodies in serum or positive PCR for HAV RNA.
65
What is the management for hepatitis A?
Supportive management as the infection is self-limiting.
66
What vaccination is recommended for hepatitis A?
Routine vaccination for all children > 12 months and individuals at increased risk.
67
What is the structure of the hepatitis A virus?
An icosahedral non-enveloped enterovirus with single-stranded, positive-sense linear RNA.
68
What is a key feature of hepatitis A virus epidemiology?
Incidence is about 1.4 million per year worldwide.
69
True or False: Hepatitis A can lead to chronic liver disease.
False
70
What is the pathophysiology of hepatitis A infection?
Ingestion of contaminated food leads to replication in the liver, resulting in immune-mediated hepatic injury.
71
What are related risks for hepatitis A infection?
* Institutionalization
* International travel
* Age > 50 years
* Underlying liver disease
* Men who have sex with men
72
What is Drug-induced liver injury (DILI)?
Occurs when drugs cause injury to hepatocytes directly or through idiosyncratic reactions
73
What are the potential presentations of DILI?
Acute or chronic, with severe toxicity manifesting as fulminant liver failure
74
What is required for the diagnosis of DILI?
A thorough history and laboratory tests
75
What is the management for DILI?
Early diagnosis, discontinuing the drug, and supportive therapy
76
What is autoimmune hepatitis (AIH)?
Liver inflammation when the immune system attacks its own liver cells
77
How is autoimmune hepatitis diagnosed?
Testing for characteristic autoantibodies and liver biopsy
78
What is the management for autoimmune hepatitis?
Corticosteroids and azathioprine
79
What causes Wilson disease?
Autosomal recessive disorder from a mutation in the ATP7B gene regulating copper transport
80
What are the neuropsychiatric manifestations of Wilson disease?
Help differentiate it from other causes of hepatitis
81
What physical finding is associated with Wilson disease?
Kayser-Fleischer rings
82
What is nonalcoholic fatty liver disease (NAFLD)?
Spectrum of liver pathology due to accumulation of triglycerides in hepatocytes
83
What can nonalcoholic fatty liver disease progress to?
Nonalcoholic steatohepatitis, cirrhosis, and possibly primary liver cancer
84
What is the management approach for NAFLD?
Lifestyle modifications (diet and exercise)
85
What are gastric acid medications?
Proton pump inhibitors (PPIs) and H₂ receptor antagonists
86
What is the mechanism of action of proton pump inhibitors (PPIs)?
Irreversibly inhibit the H+/K+ ATPase pump in gastric parietal cells
87
What are the common indications for PPIs?
Peptic ulcer disease, GERD, and dyspepsia
88
What are the adverse effects of PPIs?
Diarrhea, headache, abdominal pain, malabsorption of vitamin B12, and increased risk of infections
89
What is the primary route of administration for PPIs?
Oral, but can also be given intravenously
90
What are H₂ receptor antagonists?
Competitive inhibitors of H₂ receptors in parietal cells to reduce acid secretion
91
What are common H₂ receptor antagonists?
*Famotidine*
*Cimetidine*
*Nizatidine*
*Ranitidine* (withdrawn from the market in 2020)
92
What is the mechanism of action of H₂ receptor antagonists?
Block histamine from binding to H2 receptors, reducing cAMP and acid secretion
93
What are the indications for H₂ receptor antagonists?
GERD, dyspepsia, PUD, and stress-ulcer prophylaxis
94
What are the adverse effects of H₂ receptor antagonists?
Diarrhea, headache, fatigue, confusion, and gynecomastia
95
What are the pharmacokinetics of H₂ receptor antagonists?
Well absorbed, onset of action 30–60 minutes, renal elimination
96
What drug interactions are associated with PPIs?
Interaction with CYP450 enzymes affecting warfarin, theophylline, and others
97
What is the role of carbonic anhydrase in acid secretion?
Combines water and CO₂ to produce hydrogen ions and bicarbonate
98
What is the function of H+/K+ ATPase in parietal cells?
Transports H+ ions to the lumen of the stomach
99
What is the role of acetylcholine in acid production?
Stimulates acid production via muscarinic receptors
100
What is the primary method of excretion for proton pump inhibitors?
Renal (primary) and feces
