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

GI Flashcards

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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
Treatment of Hepatic encephalopathy(2) | Why?
1. lactulose (increase NH4+ generation) | 2. Rifaximin or Neomycin (decrease NH4+ producing gut bacteria)
26
treatment of physiological neonatal jaundice
-phototherapy (non-UV) which isomerizes unconjugated bilirubin to water-soluble form
27
treatment of Crigler-Najjar Syndrome, type 1 (2)
1. plasmapheresis | 2. phototherapy
28
Treatment of Wilson disease (hepatolenticular degeneration) | (3)
chelation w/ 1. penicillamine 2. trientine 3. oral zinc
29
Treatment of hemochromatosis (1, 3)
1. repeated phlebotomy chelation w/ 1. deferasirox 2. deferoxamine 3. oral deferiprone
30
GI drug reaction: | Acute cholestatic hepatitis, jaundice
Erythromycin
31
GI drug reaction: | Diarrhea(5)
"Might Excite Colon On Accident" 1. Metformin 2. Erythromycin 3. Colchicine 4. Orlistat 5. Acarbose
32
GI drug reaction: | Focal to massive hepatic necrosis (4)
"liver HAVAc" 1. Halothane 2. Amanita phalloides (death cap mushrooms) 3. Valproic acid 4. Acetaminophen
33
GI drug reaction: | Hepatitis(5)
1. Rifampin 2. Isoniazid 3. Pyrazinamide 4. Statins 5. fibrates
34
GI drug reaction: | Pancreatitis (6)
"Drugs Causing A Violent Abdominal Distress" 1. Didanosine 2. Corticosteroids 3. Alcohol 4. Valproic Acid 5. Azathioprine 6. Diuretics (furosemide, HCTZ)
35
``` GI drug reaction: Pseudomembranous Colitis(3) ```
1. Clindamycin 2. Ampicillin 3. Cephalosporins * antibiotics predispose to superinfection by resistant C.diff
36
H2 blockers: | Name (4)
``` "Take H2 blockers before you '-dine'" "think TABLE FOR 2 to remember H2" 1. Cimetidine 2. ranitidine 3. famotidine 4. nazatidine ```
37
H2 blockers: MOA Clinical use (3)
Reversible H2-R block--> decrease H+ secretion by parietal cells 1. peptic ulcers 2. gastritis 3. mild esophageal reflux
38
``` H2 blockers: Adverse 1. Cimetidine (4) 2. cimetidine and ranitidine (1) 3. others ```
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
Proton Pump inhibitors: | Name (5)
- prozole 1. Omeprazole 2. lansoprazole 3. esmeprazole 4. pantoprazole 5. dexlansoprazole
40
Proton Pump inhibitors: MOA Clinical Uses (4) Adverse (3)
- 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
Triple therapy for H. pylori ulcers
1. PPi 2. Clarithromycin 2. Amoxicillin/Metronidazole
42
Antacid Use D-D explanation
Affects absorption, bioavailability, or urinary excretion of other drugs by 1. altering gastric pH 2. altering urinary pH 3. delaying gastric emptying
43
All Antacids can cause what adverse side effect
hypokalemia
44
Antacids: | Name 3
1. Aluminum hypoxide 2. Calcium carbonate 3. Magnesium hydroxide
45
Aluminum Hydroxide: | Adverse(6)
1. Constipation ("AluMINIMUM feces) 2. hypophosphatemia 3. prox. muscle weakness 4. osteodystrophy 5. seizures
46
Calcium Carbonate: | Adverse (3)
1. Hypercalcemia (milk-alkali syndrome) 2. Rebound acid increase 3. Chelate and decrease effectiveness of other drugs (tetracyclines)
47
Magnesium Hydroxide: | Adverse(5)
1. Diarrhea 2. Hyporeflexia 3. Hypotension 4. cardiac arrest "Mg+2= Must Go 2 the bathroom"
48
Which antacid causes constipation? Diarrhea? chelation interactions? hypokalemia?
- Aluminum hydroxide - Magnesium Hydroxide - Calcium Carbonate - All antacids cause hypokalemia
49
Bismuth, Sulcralfate: MOA Clinical Use(2)
"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
``` Misoprostol: MOA Clinical Use Adverse (1) Contra (1) ```
- 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
Octreotide: MOA Clinical Use (4) Adverse (3)
- 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
Osmotic Laxatives: | Name (4)
1. Magnesium hydroxide 2. Magnesium citrate 3. Polyethylene glycol 4. Lactulose
53
Osmotic Laxatives: MOA Clinical Use Adverse(2)
- providee osmotic load to draw water into GI lumen - Use: constipation - Adverse: Diarrhea & dehydration
54
Lactulose: | special use & why
Hepatic encephalopathy | - gut flora degrades lactulose into lactic acid/acetic acid--> this promotes NH4+ excretion
55
Who typically abuses osmotic laxatives?
Bulimics
56
Sulfasalazine: MOA Clinical Use(2)
-combo of Sulfapyridine +5-aminosalicyclic acid-->activated by colonic bacteria (antibacterial + anti-inflam) Use: IBD (both Ulcerative Colitis, Crohn's colitis)
57
Sulfasalazine: | Adverse (4)
1. Malaise 2. Nausea 3. Sulfonamide toxicity 4. Reversible oligospermia
58
Classic vignette of Bulemic on laxative
- Female, overweight (increase eating, no weight gain) - decreased energy - Met. acidosis - Electrolyte abnormalities
59
``` Loperamide: MOA CNS penetration? Use (1) Adverse (2) ```
- Agonist at u-R --> slows gut motility - Poor CNS penetration Use: Diarrhea Adverse: Constipation, Nausea
60
Ondansetron: MOA (2) Clinical Use(2) Adverse (3)
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
Metaclopramide: MOA Effect on colon transport time? Clinical Use (2)
D2-R antagonist 1. increase resting tone, LES tone 2. increase contractility, motility * Doesn't alter Colon transport time 1. Diabetic & postsurgery 2. anti-emetic
62
Metaclopramide: Adverse (5) D-D (2)
1. Parkinsonian effects & Tardive dyskinesia 2. Restlessness 3. Drowsy, Fatigue 4. Depression 5. Diarrhea DD: 1. digoxin 2. diabetic agents
63
Metaclopramide: | Contra (2)
1. sm. bowel obstruction | 2. Parkinson disease
64
Orlistat: MOA Clinical Use (1) Adverse (2)
- inhib gastric&pancreatic lipase --> decrease breakdown/absorption of dietary Fats Use: weight loss Adverse: Steatorrhea, decrease Fatty-Vitamins
65
Ursoliol (ursodeoxycholic acid): MOA(3) Clinical use(2)
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
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