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GI DRx > 04a: Pharmacology > Flashcards

04a: Pharmacology Flashcards

1
Q

“-tidine” drugs

A

H2 R blockers

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2
Q

“-prazole” drugs

A

PPIs

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3
Q

List the 3 major substances that stimulate H secretion from parietal cells.

A
  1. Histamine (paracrine) from ECL cells
  2. Gastrin (endocrine) from G cells
  3. ACh (neural) from enteric nerves
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4
Q

T/F: Both PPIs and H2 antagonists are taken in the morning, before breakfast, for max effect.

A

False - H2 antagonists taken once daily at bedtime (inhibit nocturnal acid secretion)

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5
Q

(PPIs/H2 antagonists) are administered as prodrug with enteric coating for absorption/release in (X).

A

PPIs;

X = duodenum

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6
Q

T/F: PPIs have slow onset and long duration of action.

A

True

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7
Q

T/F: PPIs have long elimination half-life.

A

False

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8
Q

T/F: Both PPIs and H2 antagonists used in ZES.

A

False - PPIs

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9
Q

(Ranitidine/Odansetron/Omeprazole) dose should be adjusted for low CYP2C19 metabolizers.

A

Omeprazole

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10
Q

Patient with chronic pain and on chronic NSAIDs presents with GI toxicity. What are Rx options?

A
  1. Switch to COX-2 selective inhibitor
  2. Add PPI to drug regimen
  3. Add prostaglandin analogue (misoprostol) to drug regimen
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11
Q

List risk of long-term PPI use.

A
  1. C. diff diarrhea

2. Hip fracture (esp post-menopausal F smokers)

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12
Q

Prototypic antacids include which salts?

A

Mg(OH)2 and Al(OH)3

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13
Q

Side effects of antacids:

A
  1. Constipation (Al) or diarrhea (Mg)
  2. Systemic alkalosis
  3. Excess cation absorption (Na, Ca)
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14
Q

The emetic center, located in (X), receives inputs from:

A

X = medulla

  1. Area postrema
  2. Tractus solitarius
  3. Cerebellum
  4. Higher centers
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15
Q

Blood-borne cytotoxic drugs and gut bacteria can both cause emesis via (X) pathway to the emetic center.

A

X = small intestine to vagal/sympathetic efferents to area postrema OR solitary tract

Note: blood-borne emetics can also affect area postrema directly

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16
Q

Which four main receptors have been targeted for (activation/inhibition) by anti-emetics?

A

Inhibition (antagonists to:)

D2, M, 5HT3, H1

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17
Q

Odensetron is what kind of drug?

A

Anti-emetic; 5-HT3 (serotonin) R antagonist

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18
Q

T/F: Glucocorticoids can be used as anti-emetic agents.

A

True

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19
Q

Cannabinoid-R (agonists/antagonists) and Substance P (agoinsts/antagonists) can be used as anti-emetic agents.

A

Agonists; antagonists

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20
Q

T/F: Studies have shown that anti-emetics are equally as effective in mono and combo therapies.

A

False - more effective in combo

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21
Q

List some therapeutic uses for laxatives and cathartics.

A
  1. Counteract opioid constipation
  2. Management of chronic constipation in elderly
  3. Prior to colonoscopy
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22
Q

Methylcellulose is a(n) (X) agent that has which MOA?

A

X = bulk-forming laxative

High content of indigestibles (cellulose or its derivatives) soften the stool by increasing the fecal water content and stimulate peristaltic activity

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23
Q

List examples of osmotic cathartics.

A
  1. Mg and phosphate salts

2. Polyethylene glycol

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24
Q

Docusate is example of which drug?

A

“Stool softeners”, aka emollient laxatives

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25
Q

Bisacodyl is example of which drug?

A

Stimulant cathartic

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26
Q

Patient planning to undergo colonoscopy for screening purposes is given (Methylcellulose/Docusate/Polyethylene glycol/Bisacodyl), which has a (slow/fast) onset of action.

A

Polyethylene glycol (osmotic cathartic)

Fast (few hours)

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27
Q

T/F: Naltrexone is effective against opioid-induced constipation.

A

True - but not used for this purpose due to its inhibition of opioid CNS effects as well

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28
Q

(X) drug is used to counteract opioid-induced constipation due to its (tertiary/quaternary) ammonium and selectivity to the periphery.

A

X = methylnaltrexone

Quaternary (limited access into CNS)

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29
Q

T/F: Opioid agonists are used as OTC anti-diarrheal drugs.

A

True (but those with limited CNS distribution)

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30
Q

Loperamide, aka (X), is what type of drug?

A

X = imodium

Anti-diarrhetic (opioid agonist)

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31
Q

Patient with diarrhea should not be given opioids for Rx if he/she presents with:

A

bloody diarrhea (opioids ay prolong infections with invasive bacteria like shigella)

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32
Q

What are the general drug class options for diarrhea in IBD?

A
  1. 5-ASA (5-aminosalicylates)
  2. Corticosteroids
  3. Anti-metabolites (azathioprine)
  4. Biologics
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33
Q

Mesalamine is in (X) class of drugs, used to treat (diarrhea/constipation) caused by (Y).

A

X = 5-ASA
Diarrhea
Y = IBD

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34
Q

List two TNF-alpha (agonsts/antagonists) used to treat diarrhea in IBD.

A

Antagonists;

  1. Infliximab (mouse/human IgG1)
  2. Adalimumab (fully humanized IgG1)
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35
Q

(X) is an Integrin alpha-4 (agonist/antagonist) used to treat (constipation/diarrhea) caused by (Y).

A

X = Vedolizumab
Antagonist
Diarrhea;
Y = IBD (moderate/severe Crohn’s/UC that’s unresponsive to other Rx)

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36
Q

Vedolizumab MOA:

A

Blocks lymphocyte interaction with adhesion molecules (MAdCAM-1) on vascular endothelium in inflamed regions of intestine

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37
Q

Patient with IBD and on (X) drug is at risk of (Y)-virus associated progressive multifocal leukoencephalopathy (PML).

A 
X = Vedolizumab
Y = JC
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38
Q

Intestinal ischemia can be the result of (arterial/venous) obstruction, such as:

A

Either

Embolus (arterial), thrombus (arterial or venous)

39
Q

Aside of obstruction, intestinal ischemia can be the result of:

A

Decreased blood flow

40
Q

List the mechanisms of intrinsic blood flow regulation to the intestines.

A
  1. Sympathetic fibers (splanchnic nerves)

2. NE (artery/arteriole constriction)

41
Q

Digitalis glycosides have which effect on intestinal blood flow?

A

Vasoconstrictive (decrease flow)

42
Q

Following several hours of intestinal ischemia, (X) causes (vasodilation/vasoconstriction) and (increase/decrease) in collateral blood flow.

A

X = hypoxemia
Vasoconstriction
Decrease

43
Q

T/F: Hypoxemia-induced vasoconstriction of splanchnic circulation can be reversed once ischemia has been corrected.

A

False - if vasoconstriction is sustained for a long enough period of time, it will persist despite return of blood flow to the area

44
Q

Intestinal ischemia: cell death occurs in lumen (first/last) and spreads to which layers?

A

First;

Spreads outward from lumen until there is total transmural necrosis

45
Q

List the three categories of intestinal ischemia. How often is each the cause of ischemia?

A
  1. Colonic ischemia (60%)
  2. Acute mesenteric ischemia (30%)
  3. Chronic mesenteric ischemia (5%)
46
Q

You would have high suspicion of AMI in patient that presents with which clinical findings?

A
  1. SUDDEN onset abdominal pain (may be post-prandial)

2. Pain out of proportion to the exam (can’t palpate abdomen due to intense pain)

47
Q

List the top four most common etiologies of AMI.

A
  1. SMA Embolus (50%)
  2. NOMI (Non-occlusive; 25%)
  3. SMA Thrombosis (10%)
  4. Mesenteric venous thrombosis (10%)
48
Q

AMI: Emboli that have passed into (X) artery are no longer (minor/major), but (minor/major) emboli.

A

X = ileocolic
Major
Minor

49
Q

T/F: About 1/5 of patients presenting with AMI will have peripheral emboli.

50
Q

(X) cause of AMI is similar to ACS (Acute coronary syndrome) in that the (embolus/thrombus) forms atop a(n) (Y).

A

X = SMA thrombosis
Thrombus
Y = plaque

51
Q

Patient with hx of stroke and peripheral vascular disease is at risk for which AMI etiology?

A

SMA thrombosis

52
Q

Patient with CHF (HFrEF) presents with sudden confusion and abdominal distension; you worry the cause is AMI. Which etiology may be likely in this patient? Explain.

A

NOMI (non-occlusive);

Poor CO and hypoperfusion causes ischemia and persistent/irreversible vasoconstriction

53
Q

The “string of sausages” sign on SMA angiogram is classic finding in which disease?

54
Q

(X) cause of AMI is seen in younger patients with (Y) deficiencies.

A

X = mesenteric venous thrombosis
Hypercoaguable states
Y = Protein C/S, antithrombin III

55
Q

(X) cause of AMI is commonly superimposed on chronic mesenteric ischemia, so up to half of these patients will report a history of which symptom?

A

X = SMA thrombosis

Post-prandial intestinal angina (weeks/months preceding acute event)

56
Q

AMI: upon admission, about (X)% of patients have a

(leukopenia/leukocytosis) and about (Y)% have which acid/base disorder?

A 
X = 75 
Leukocytosis (above 15,000 cell/mm3)
Y = 50
Metabolic acidosis (GAP)
57
Q

Which X-ray findings are consistent with AMI?

A

Thumb-printing (suggesting submucosal hemorrhage and edema)

58
Q

Gold standard for diagnosis of AMI

59
Q

How might (X) imaging modality be a therapeutic, as well as diagnostic, option for AMI?

A

X = angiogram

Intra-arterial agents (ex: paparavine - a vasodilator)

60
Q

Initial treatment of AMI.

A
  1. Treat underlying cause (CHF, arrhythmia, blood V)

2. Broad-spectrum antibiotics

61
Q

T/F: AMI with infarct has mortality rate as high as 90%.

62
Q

T/F: Diagnosis of both occlusive and non-occlusive AMI can be made with angiography.

63
Q

Patients with CMI (chronic mesenteric ischemia) are typically (obese/cachectic) with PMHx of which diseases?

A

Cachectic (develop sitophobia/fear of eating due to post-prandial pain)

CAD, PVD

64
Q

List some clinical and angiography findings that would support diagnosis of CMI (chronic mesenteric ischemia).

A
  1. Unexplained weight loss, abd pain, food aversion

2. Occlusion of 2+ splanchnic arteries on angiogram

65
Q

CMI (chronic mesenteric ischemia) therapy.

A

Revascularization via:

  1. Surgery
  2. Percutaneous angioplasty/stenting
66
Q

Colonic ischemia: typically (life-threatening/benign) and seen frequently in (younger/older) patients. What are some clinical findings?

A

Benign; older

Pain (LLQ), urge to defacate, some blood in stool

67
Q

If an acute AKI due to mesenteric venous thrombosis (MVT) is suspected, which test should you order right away?

A

CT with contrast (diagnoses 90% of patients with MVT)

68
Q

Patient with AMI due to MVT would be treated with (X) unless showing signs of (Y), in which case immediate surgery required.

A 
X = heparin (potentially after prompt laparotomy/bowel resection) 
Y = infarct
69
Q

Nonocclusive colon ischemia tends to occur in which areas of the colon?

A

Watershed areas, with less collaterals (splenic fixture and rectosigmoidal junction)

70
Q

T/F: Angiogram is gold standard for diagnosis of cholonic ischemia.

A

False - not typically needed; endoscopy (colonoscopy) is diagnostic

71
Q

Which endoscopy/colonoscopy finding is consistent with colonic ischemia?

A

“Single stripe sign” - single linear colonic ulcer

72
Q

Natural history of colonic ischemia:

A

Symptoms subside 24-48h, healing in 2 weeks

more severe damage may take months

73
Q

Nitazoxamide is active against (protozoa/helminths) and has which mechanism of action?

A

Both;

Active metabolite interferes with e-transfer reaction (PFOR), which is essential to anaerobic metabolism

74
Q

Metronidazole-resistant protozoa can be treated with (X). Give example of protozoal species that (X) is used for.

A

X = nitazoxanide

Giardia and Cryptosporidium parvum

75
Q

T/F: Metronidazole has very large Vd.

76
Q

(Metronidazole/paromomycin/nitazoxamide) is poorly absorbed and works in GI lumen.

A

Paromomycin

77
Q

T/F: Nitazoxanide is approved for treatment in adults only.

A

False - kids too (over 1 y.o.)

78
Q

Praziquantel is Rx for (trematodes/nematodes/cestodes).

A

Trematodes (flukes) and cestodes (flatworms/tapeworms)

79
Q

Which GI nematodes can be treated with either albendazole or (X)?

A

X = ivermectin

  1. Ascaris lumbricoides
  2. Strongyloides stercoralis
80
Q

Which tissue nematodes are treated with albendazole?

A
  1. Trichinella spiralis

2. Toxocara canis

81
Q

Which tissue nematodes are treated with diethylcarbamazine?

A
  1. Wuchereria bancrofti

2. Loa loa

82
Q

Which tissue nematodes are treated with ivermectin?

A

Onchocerca volvulus

83
Q

Albendazole is active against helminth (larvae/adults/eggs).

A

Larvae, adults, and some eggs (Ascaris lumbricoides)

84
Q

Albendazole mechanism of action.

A

Inhibits MT polymerization (immobilization and death of parasite)

85
Q

T/F: Albendazole oral absorption is decreased if taken with fatty meals.

A

False - improved

86
Q

T/F: Albendazole is not recommended for pregnancy until after 1st trimester.

A

False - that’s metronidazole; albendazole isn’t recommended in pregnancy at all

87
Q

Ivermectin mechanism of action.

A

Enhances Cl influx through Glu-gated Cl channels, causing hyperpolarization of nerve/muscle cells and paralysis/death of parasite

88
Q

T/F: Ivermectin and diethylcarbamazine are contraindicated in pregnancy.

A

False - only ivermectin is

89
Q

Ivermecting: (oral/IV), (well/poorly)-absorbed, (small/large) Vd, and (does/doesn’t) enter CNS.

A

Oral; well-absorbed and large Vd but doesn’t enter CNS

90
Q

Mazzotti reaction is seen with (X) drug(s) when used against (Y) parasite.

A

X = ivermectin, diethylcarbamazine

Y = onchocerca volvulus

91
Q

What occurs in the Mazzotti reaction?

A

Potentially life-threatening allergic response caused by killing microfilaria

92
Q

Diethylcarbamazine mechanism of action.

A

Immobalizes microfilariae and alters surface structure

93
Q

Praziquantel mechanism of action.

A

Increases permeability of trematode and cestode cell membranes to Ca (paralysis, dislodgement, death)

94
Q

T/F: Praziquantel is contraindicated in pregnancy.

A

False - safe in pregnancy

GI DRx (11 decks)

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