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Drugs- Basic High Yield Stuff for Boards > GI > Flashcards

GI Flashcards

1
Q

Which has a higher drug bioavailability: by mouth or by rectum?
Why?

A

rectum> mouth
Veins of distal rectum drain into pelvic veins and not the portal system so meds reach systemic circulation w/o first pass metabolism.

Meds by mouth–>absorbed in intestines which drain into portal system

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2
Q

Drugs causing Focal to Massive Hepatic Necrosis(4)

A

“liver HAVAc”

  1. Halothane
  2. Amanita phalloides (death cap)
  3. Valproic Acid
  4. Acetaminophen
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3
Q

Zone of the liver most susceptible to INJESTED toxins and viral hepatitis?
Function of this zone?

A
  • Zone 1 (periportal)

- Oxygen-intensive metabolism

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4
Q

Zone of the liver most susceptible to Yellow Fever?

A

Zone II (intermediate)

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5
Q

Which zone of the liver is responsible for cytochrome 450 metabolism?

A

Zone III

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6
Q

Zone of the liver most susceptible to Ischemia/low O2?

A

Zone III

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7
Q

Zone of the liver most susceptible to METABOLIC by products?
Name 2 examples of common drugs.

A

Zone III

Alcohol–>Acetaldehyde
Acetaminophen –>NAPQ1

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8
Q

Antidote to Acetaminophen Toxicity?

A

N-acetylcystein (replenishes glutathione)

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9
Q

Octreotide:
MOA
Uses(4)
Adverse

A

Somatostatin analog (in brain inhibits GH release from ant. pituitary)

  1. Acromegaly
  2. Carcinoid syndrome
  3. Variceal bleeding (esp. esophageal)
  4. VIPoma, gastrinoma, glucaconoma

Adverse: Gallstones and GI upset

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10
Q 
Somatostatin: 
Cell source
Actions(4)
Increased somatostatin release by?
Decrease somatostatin release by?
A

Dcells (pancreatic islets, GI mucosa)

Inhibits secretion of various hormones-“encourages SOMATO-STAsis

  1. decrease Gastric Acid/Pepsinogen secretion
  2. decrease pancreatic and Sm.Intestine fluid secretions
  3. decrease gallbladder contractions
  4. decrease insulin and glucagon release

Increase: by Acid (like FAs and AAs)
Decrease by Vagal stimulation

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11
Q

Compare Oral glucose load to IV glucose

A

Oral glucose load leads to increased insulin compared to IV equivalent due to GIP secretion

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12
Q 
GIP:
What does GIP stand for? (2)
Cell Source
Exocrine Actions
Endocrine Actions
Regulation(3)
A
  1. Glucose-dependent Insulinotropic Peptide
  2. Gastric inhibitory peptide

Kcells (duodenum, jejunum)

Exocrine: decrease Gastric H+ secretion
Endocrine: increase insulin release

increase GIP release via increased FA, AA, oral glucose

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13
Q

Which Abx stimulates the Motilin-R?

A

Erythromycin

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14
Q

Macrolides: Azithromycin, clarithromycin, erythromycin
MOA
MOResistance
Clinical Use (4)

A
  • Inhib 23S (part of 50S) which blocks translockation (‘macroSLIDES’)
  • Methylation of 23S
  1. Atypical pneumonia: Mycoplasma, Chlamydia, Legionella
  2. STIs: Chlamydia
  3. Gram + Cocci: Strep infections in pt allergic to penicillin
  4. B. pertussis
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15
Q

Macrolides: Azithromycin, clarithromycin, erythromycin

Adverse (5)

A

“MACRO’

  1. Motility Issues (GI)
  2. Arrhythmia (prolonged QT)
  3. Cholestatic hepatitis
  4. Rash
  5. eOsinophilia

Clarithromycin/Erythromycin: inhibit P450–>increase serum concentrations of Theophylline and Oral anticoagulants

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16
Q

How does Atropine affect the stomach?

What does Atropine NOT affect?

A
  • Atropine blocks Vagal stimulation of parietal cells (Ach binding M3)
  • Vagal stimulation of G-cells is not affected by atropine b/c the are stimulated by GRP (not Ach)
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17
Q

D-xylose absorption test:
Use
Mechanism

A
  • distinguishes malabsorption from mucosal damage vs. other causes of malabsorption.
  • D-xylose doesn’t require pancreatic enzyme processing for absorption
  • With pancreatic insuff. : D-xylose would still appear in the blood
  • With GI mucosal damage: No D-xylose would appear in the blood
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18
Q 
Chagas Disease:
infectious agent
GI effect (2)
Radiographic appearance
treatment (2)
A

T. cruzi

  • megacolon, megaesophagus
  • “birdbeak”

Treatment: 1. NifurtiMOX 2. Benznidazole
“MOXie people T.ake CRUZes to South America”

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19
Q

Compare treatment of Celiac sprue vs. Tropical sprue

A

Celiac sprue: gluten free diet

Tropical sprue: Antibiotics

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20
Q

Treatment of Crohn’s disease (5)

A
  1. Corticosteroids
  2. azathioprine
  3. Abx (ciprofoxacin, metranidazole)
  4. Infliximab
  5. Adalimumab
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21
Q

Treatement of Ulcerative Colitis (4)

A
  1. 5-aminosalicylic preparation (like melamine)
  2. 6-mercaptopurine
  3. infliximab
  4. colectomy
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22
Q

Schistosoma:
Transmission
Treatment

A

transmitted by snails and penetrate human skin to form granulomas

tx: Praziquantel

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23
Q 
Reye syndrome:
Definition
Clinical symptoms
Cause
Mechanism
A

Fatal childhood hepatic encephalopathy (rare)

  1. Mitochondrial abnormalities
  2. Fatty liver (microvesicular fatty change)
  3. hypoglycemia
  4. vomitting
  5. Hepatomegaly
  6. coma
  • viral infection (esp VZV & influenzaB) treated with aspirin
  • aspirin decreases B-oxidation by reversible inhib of mitochondrial enzymes
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24
Q

Only childhood illness where it is acceptable to use Aspirin?
Symptoms (6)

A

Kawasaki disease (asian children desquamating)

  1. Adenopathy (cervical)
  2. Strawberry tongue (oral mucositis
  3. Hand-foot changes (edema, erythema)
  4. Fever
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25
Q

Treatment of Hepatic encephalopathy(2)

Why?

A
  1. lactulose (increase NH4+ generation)

2. Rifaximin or Neomycin (decrease NH4+ producing gut bacteria)

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26
Q

treatment of physiological neonatal jaundice

A

-phototherapy (non-UV) which isomerizes unconjugated bilirubin to water-soluble form

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27
Q

treatment of Crigler-Najjar Syndrome, type 1 (2)

A
  1. plasmapheresis

2. phototherapy

28
Q

Treatment of Wilson disease (hepatolenticular degeneration)

(3)

A

chelation w/

  1. penicillamine
  2. trientine
  3. oral zinc
29
Q

Treatment of hemochromatosis (1, 3)

A
  1. repeated phlebotomy

chelation w/

  1. deferasirox
  2. deferoxamine
  3. oral deferiprone
30
Q

GI drug reaction:

Acute cholestatic hepatitis, jaundice

A

Erythromycin

31
Q

GI drug reaction:

Diarrhea(5)

A

“Might Excite Colon On Accident”

  1. Metformin
  2. Erythromycin
  3. Colchicine
  4. Orlistat
  5. Acarbose
32
Q

GI drug reaction:

Focal to massive hepatic necrosis (4)

A

“liver HAVAc”

  1. Halothane
  2. Amanita phalloides (death cap mushrooms)
  3. Valproic acid
  4. Acetaminophen
33
Q

GI drug reaction:

Hepatitis(5)

A
  1. Rifampin
  2. Isoniazid
  3. Pyrazinamide
  4. Statins
  5. fibrates
34
Q

GI drug reaction:

Pancreatitis (6)

A

“Drugs Causing A Violent Abdominal Distress”

  1. Didanosine
  2. Corticosteroids
  3. Alcohol
  4. Valproic Acid
  5. Azathioprine
  6. Diuretics (furosemide, HCTZ)
35
Q 
GI drug reaction: 
Pseudomembranous Colitis(3)
A
  1. Clindamycin
  2. Ampicillin
  3. Cephalosporins
  • antibiotics predispose to superinfection by resistant C.diff
36
Q

H2 blockers:

Name (4)

A 
"Take H2 blockers before you '-dine'"
"think TABLE FOR 2 to remember H2"
1. Cimetidine
2. ranitidine
3. famotidine
4. nazatidine
37
Q

H2 blockers:
MOA
Clinical use (3)

A

Reversible H2-R block–> decrease H+ secretion by parietal cells

  1. peptic ulcers
  2. gastritis
  3. mild esophageal reflux
38
Q 
H2 blockers:
Adverse
1. Cimetidine (4)
2. cimetidine and ranitidine (1)
3. others
A

Cimetidine:

  1. potent P450 inhib (D-D)
  2. Antiandrogenic (prolactin release, gynecomastia, impotence, decreased libido)
  3. CNS effects (Confusion/Dizzy/HA)
  4. crosses placenta

Both Cimetidine and Ranitidine:
1. decrease renal excretion of creatinine

All other H2 blockers are relatively free of these effects

39
Q

Proton Pump inhibitors:

Name (5)

A
  • prozole
    1. Omeprazole
    2. lansoprazole
    3. esmeprazole
    4. pantoprazole
    5. dexlansoprazole
40
Q

Proton Pump inhibitors:
MOA
Clinical Uses (4)
Adverse (3)

A
  • Irreversible inhib H/K+ ATPase of parietal cells
    1. Peptic Ulcers 2. gastritis
    3. GERD 4. Zollinger-ellison syndrome
  1. increase risk of C.diff
  2. Pneumonia
  3. decrease Mg+2 (w/ long term use)–>osteoporosis
41
Q

Triple therapy for H. pylori ulcers

A
  1. PPi
  2. Clarithromycin
  3. Amoxicillin/Metronidazole
42
Q

Antacid Use D-D explanation

A

Affects absorption, bioavailability, or urinary excretion of other drugs by

  1. altering gastric pH
  2. altering urinary pH
  3. delaying gastric emptying
43
Q

All Antacids can cause what adverse side effect

A

hypokalemia

44
Q

Antacids:

Name 3

A
  1. Aluminum hypoxide
  2. Calcium carbonate
  3. Magnesium hydroxide
45
Q

Aluminum Hydroxide:

Adverse(6)

A
  1. Constipation (“AluMINIMUM feces)
  2. hypophosphatemia
  3. prox. muscle weakness
  4. osteodystrophy
  5. seizures
46
Q

Calcium Carbonate:

Adverse (3)

A
  1. Hypercalcemia (milk-alkali syndrome)
  2. Rebound acid increase
  3. Chelate and decrease effectiveness of other drugs (tetracyclines)
47
Q

Magnesium Hydroxide:

Adverse(5)

A
  1. Diarrhea
  2. Hyporeflexia
  3. Hypotension
  4. cardiac arrest

“Mg+2= Must Go 2 the bathroom”

48
Q

Which antacid causes constipation?
Diarrhea?
chelation interactions?
hypokalemia?

A
  • Aluminum hydroxide
  • Magnesium Hydroxide
  • Calcium Carbonate
  • All antacids cause hypokalemia
49
Q

Bismuth, Sulcralfate:
MOA
Clinical Use(2)

A

“the ‘B’and-aids for the ‘S’tomach”

  • Binds ulcer base–>provide physical protection & allows HCO3- secretion –>reestablish pH gradient in Mucous layer
  1. increase ulcer healing
  2. traveler’s diarrhea
50
Q 
Misoprostol:
MOA
Clinical Use
Adverse (1)
Contra (1)
A
  • PGE1 analog
  • increase production/secretion of gastric mucous (decrease acid)

Use: prevention of NSAID-induced peptic ulcers
Adverse: Diarrhea
Contra: women of childbearing potential

51
Q

Octreotide:
MOA
Clinical Use (4)
Adverse (3)

A
  • Long-acting Somatostatin analog
  • Inhib secretion of various splanchnic vasodilatory hormones
  1. Acromegaly
  2. Carcinoid syndrome
  3. Variceal bleeding (esp. esophageal)
  4. VIPoma, gastrinoma, glucaconoma

Adverse: 1. N/cramp 2. Steatorrhea 3. increase risk of cholelithiasis (CCK inhib)

52
Q

Osmotic Laxatives:

Name (4)

A
  1. Magnesium hydroxide
  2. Magnesium citrate
  3. Polyethylene glycol
  4. Lactulose
53
Q

Osmotic Laxatives:
MOA
Clinical Use
Adverse(2)

A
  • providee osmotic load to draw water into GI lumen
  • Use: constipation
  • Adverse: Diarrhea & dehydration
54
Q

Lactulose:

special use & why

A

Hepatic encephalopathy

- gut flora degrades lactulose into lactic acid/acetic acid–> this promotes NH4+ excretion

55
Q

Who typically abuses osmotic laxatives?

56
Q

Sulfasalazine:
MOA
Clinical Use(2)

A

-combo of Sulfapyridine +5-aminosalicyclic acid–>activated by colonic bacteria
(antibacterial + anti-inflam)

Use: IBD (both Ulcerative Colitis, Crohn’s colitis)

57
Q

Sulfasalazine:

Adverse (4)

A
  1. Malaise
  2. Nausea
  3. Sulfonamide toxicity
  4. Reversible oligospermia
58
Q

Classic vignette of Bulemic on laxative

A
  • Female, overweight (increase eating, no weight gain)
  • decreased energy
  • Met. acidosis
  • Electrolyte abnormalities
59
Q 
Loperamide:
MOA
CNS penetration?
Use (1)
Adverse (2)
A
  • Agonist at u-R –> slows gut motility
  • Poor CNS penetration

Use: Diarrhea
Adverse: Constipation, Nausea

60
Q

Ondansetron:
MOA (2)
Clinical Use(2)
Adverse (3)

A

Powerful central-acting Anti-emetic
- 5-HT3 antagonist & decrease vagal stimulation

  1. post-op vomiting control
  2. chemo pt nausea control

Adverse: HA, constipation, prolonged QT

61
Q

Metaclopramide:
MOA
Effect on colon transport time?
Clinical Use (2)

A

D2-R antagonist

  1. increase resting tone, LES tone
  2. increase contractility, motility
    * Doesn’t alter Colon transport time
  3. Diabetic & postsurgery
  4. anti-emetic
62
Q

Metaclopramide:
Adverse (5)
D-D (2)

A
  1. Parkinsonian effects & Tardive dyskinesia
  2. Restlessness
  3. Drowsy, Fatigue
  4. Depression
  5. Diarrhea

DD: 1. digoxin 2. diabetic agents

63
Q

Metaclopramide:

Contra (2)

A
  1. sm. bowel obstruction

2. Parkinson disease

64
Q

Orlistat:
MOA
Clinical Use (1)
Adverse (2)

A
  • inhib gastric&pancreatic lipase –> decrease breakdown/absorption of dietary Fats

Use: weight loss
Adverse: Steatorrhea, decrease Fatty-Vitamins

65
Q

Ursoliol (ursodeoxycholic acid):
MOA(3)
Clinical use(2)

A
  1. nontoxic bile acid
  2. increase bile secretion
  3. decrease cholesterol secretion and reabsorption

Use:

  1. Primary Biliary cirrhosis (anti-mitochondrial abs)
  2. Gallstone preventionor dissolution

Drugs- Basic High Yield Stuff for Boards (20 decks)

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