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PHRM 825 > Final Exam > Flashcards

Final Exam Flashcards

1
Q

What types of drugs affect gastric secretion?

A
  1. Antacids (weak base to neutralize excess acid in stomach)
  2. H2 histamine receptor antagonists (stop stomach from producing acid)
  3. Proton pump inhibitors (stop stomach from producing acid)
  4. Protectants (protect esophageal lining)
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2
Q

What types of drugs increase GI motility?

A
  1. Laxatives
  2. Prokinetic drugs
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3
Q

What types of drugs reduce GI motility?

A
  1. Antidiarrheals
  2. Anti-emetics
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4
Q

Describe the events that lead to gastric acid secretion starting with the intake of dietary peptides

A
  1. dietary peptides act on G cells
  2. G cells produce gastrin
  3. Gastrin enters bloodstream
  4. Gastrin acts on ECL cells
  5. ECL cell signaling cascade releases histamine
  6. Histamine binds to H2 receptors on parietal cells
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5
Q

What type of cell produces histamine in the GI tract?

A

ECL (enterochromaffin-like) cells

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6
Q

Which antacids have high neutralizing capacity?

A

NaHCO3
Al(OH)3
Mg(OH)2

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7
Q

Which antacid has moderate neutralizing capacity?

A

CaCO3

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8
Q

What is one adverse effect of CaCO3?

A

milk-alkali syndrome

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8
Q

What is one adverse effect of NaHCO3?

A

systemic alkalosis

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9
Q

What is one adverse effect of Al(OH)3?

A

constipation

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10
Q

What is one adverse effect of Mg(OH)2?

A

diarrhea

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11
Q

Why don’t histamine receptor antagonists cause complete deactivation of parietal cells?

A

Parietal cells are activated through other mechanisms aside from histamine, including CNS activation from acetylcholine and from gastrin

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12
Q

What are the 2nd generation H2 receptor antagonists?

A

Ranitidine (Zantac)
Nizatidine (Axid)
Famotidine (Pepcid)

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13
Q

What are the characteristics of 2nd generation H2 receptors antagonists?

A

-longer half-life (HS vs. BID dosing)
-fewer effects on CYP450 system
-greater potency
-absorbed quickly to reduce parietal cell function

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14
Q

What is the mechanism of action of proton pump inhibitors?

A

They irreversibly bind to the H+/K+ ATPase pump

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15
Q

What is the difference between omeprazole and esomeprazole?

A

Omeprazole: racemic mixture, less potent
Esomeprazole: S-enantiomer, more potent

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16
Q

Proton pump inhibitors are substituted ______________

A

Benzimidazoles

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17
Q

Why do proton pump inhibitors have slow onset?

A

They must be absorbed in the small intestine, circulate, and then be taken up by the parietal cells

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18
Q

What activates the prodrug form of a PPI?

A

The acidic pH in the parietal cell

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19
Q

PPIs have a ______ plasma life but _____ duration action

A

short, long

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20
Q

What are the 5 risk factors for GERD?

A
  1. Obesity
  2. Tobacco smoking
  3. Genetic predisposition
  4. Pregnancy
  5. Delayed gastric emptying
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21
Q

What are the 5 characteristics of GERD pathophysiology?

A
  1. Abnormal esophageal clearance
  2. Lower LES pressure (LES = lower esophageal sphincter)
  3. Decrease in esophageal mucosal resistance
  4. Delayed gastric emptying + increase intra-abdominal pressure
  5. Acid pocket formation
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22
Q

What medications are a direct irritant to esophageal mucosa?

A
  1. aspirin + NSAIDS
  2. Bisphosphonates
  3. Iron
  4. Quinidine
  5. Potassium chloride
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23
Q

What is the mechanism of action of H2RAs?

A

Reversible inhibition of histamine receptors on parietal cells

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24
Q

Name two mucosal protective agents

A

sucralfate (Carafate)
misoprostol (Cytotec)

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25
Q

What is sucralfate’s mechanism of action?

A

aluminum hydroxide complex of sucrose polymerizes to form a kind of gel which creates a protective barrier at ulcer site

acidic pH activates complex

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26
Q

What is misoprostol’s mechanism of action?

A

semi-synthetic prostaglandin derivative that enhances mucus and bicarbonate secretion and reduces acid secretion

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27
Q

Name the four types of laxatives and one example for each

A
  1. Bulk-forming - Psyllium (Metamucil)
  2. Osmotic - PEG 3350 (MiraLax)
  3. Stool softener - Docusate (Colace)
  4. Stimulant - Bisacodyl (Dulcolax)
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28
Q

Name 7 prokinetic drugs (not including opioid-receptor antagonists)

A
  1. Metoclopramide (Reglan)
  2. Prucalopride (Motegrity)
  3. Tegaserod (Zelnorm)
  4. Lubiprostone (Amitiza)
  5. Linaclotide (Linzess)
  6. Plecanatide (Trulance)
  7. Tenapanor (Ibsrela)
29
Q

What is metoclopramide’s mechanism of action?

A

D2 dopamine receptor antagonist in the myenteric plexus which leads to acetylcholine release

(the myenteric plexus is responsible for peristalsis which can be stimulated by ACh)

30
Q

Describe the mechanism of action of prucalopride and tegaserod

A

5HT4 serotonin receptor agonist that activates Gs pathway -> increased cAMP, PKA activation and release of acetylcholine

31
Q

Which prokinetic drugs are chloride channel activators?

A
  1. Lubiprostone (stimulates CIC-2 activator in small intestine)
  2. Linaclotide and Plecanatide (peptide activator of guanylate cyclase C)
32
Q

Which prokinetic drug inhibits the sodium/hydrogen exchanger (NHE3)?

A

Tenapanor

*increased Na+ in the gut leads to increased water in the gut accelerating transit of intestinal contents

33
Q

Which anti-emetics antagonize 5-HT3 receptors?

A

Ondansetron (Zofran)
Granisetron (Kytril)
Dolasetron
Palonosetron

34
Q

Which anti-emetics antagonize NK1 receptors?

A

Aprepitant
Netupitant
Rolapitant

35
Q

Which anti-emetics act as antihistamines and anticholinergics?

A

Dimenhydrinate (Dramamine)
Meclizine (Antivert)
Scopolamine

36
Q

Name four D2 dopamine receptor antagonists that act as antipsychotics and anti-emetics

A
  1. Metoclopramide (Reglan)
  2. Prochlorperazine (Compazine)
  3. Promethazine (Phenergan)
  4. Droperidol (Inapsine)
37
Q

What is the preferred regimen for H. pylori treatment?

A

bismuth salt (subsalicylate, subcitrate)
metronidazole
tetracycline
PPI BID
x10-14 days

38
Q

What does the levofloxacin triple therapy consist of?

A
  1. Levofloxacin daily
  2. Amoxicillin BID
  3. PPI BID
39
Q

What does the rifabutin triple therapy consist of?

A
  1. omeprazole
  2. amoxicillin
  3. rifabutin
    q8h x14 days
40
Q

What is one counseling point for metronidazole?

A

avoid alcohol due to disulfiram-like reaction (nausea and vomiting)

41
Q

What is an adverse effect of penicillins?

A

GI upset, take with food

42
Q

What are three adverse effects of fluoroquinolones?

A

tendon rupture
mental status change
QTc prolongation

43
Q

What is an adverse effect of tetracyclines?

A

photosensitivity

44
Q

What are three adverse effects of macrolides?

A

GI upset
photosensitivity
QTc prolongation

45
Q

What are the two key questions for choosing the H. pylori regimen?

A
  1. Is there a penicillin allergy?
  2. Does the patient have previous macrolide exposure for any reason?
46
Q

What are the options if H. pylori treatment doesn’t work?

A
  1. Switch antibiotics (not used in the first regimen)
  2. Salvage regimens
  3. Extend duration of therapy to 14 days
  4. Penicillin skin test if PCN allergy listed
47
Q

What are the three main causes of peptic ulcer disease?

A
  1. H. pylori
  2. NSAIDS
  3. Stress
48
Q

Which causes of ulcer usually result in a stomach ulcer?

A

NSAIDS, stress

49
Q

Which cause of ulcer usually results in a duodenal ulcer?

A

H. pylori

50
Q

Which cause of ulcer creates the deepest ulcer?

A

NSAIDS

51
Q

In which type of ulcer is pain relieved by food?

A

Duodenal ulcer

52
Q

In which type of ulcer is pain worsened by food?

A

Stomach ulcer

53
Q

Is misoprostol used for treatment or prevention of NSAID-induced PUD?

A

prevention (prophylaxis)

54
Q

Is sucralfate used for treatment or prevention of NSAID-induced PUD?

A

treatment

55
Q

For which type of ulcer are H2RAs used for prevention?

A

duodenal ulcers

56
Q

What 5 processes occur in the body in a well-fed state?

A
  1. insulin release
  2. glycolysis
  3. glycogen synthesis
  4. catabolism of amino acids
  5. fatty acid synthesis
57
Q

What 3 processes occur in the body in an early fasting state?

A
  1. glucagon release
  2. glycogen breakdown
  3. gluconeogenesis (cori and alanine cycle)

(no catabolism of amino acids)

58
Q

What 5 processes occur in the body in a fasting state?

A
  1. Glucagon release
  2. Gluconeogenesis
  3. Lipolysis (adipose tissue)
  4. Fatty acid oxidation
  5. Ketogenesis (liver)
59
Q

Define marasmus

A

Inadequate intake of both protein and energy

60
Q

Define kwashiorkor

A

Inadequate intake of protein with adequate energy intake

61
Q

Define pellagra

A

severe deficiency of niacin (B3)

62
Q

Define beriberi

A

severe deficiency of thiamin (B1)

63
Q

What process is inhibiting by a folic acid (B9) deficiency?

A

DNA synthesis

64
Q

infants have _______ heart rates and respiratory rates, but _______ blood pressure

A

high, low

65
Q

postmenstrual age =

A

gestational age + postnatal age

66
Q

corrected age =

A

postnatal (actual) age - weeks born early

67
Q

oliguria is defined as….

A

< 0.5mL urine/kg/hour

68
Q

anuria is defined as….

A

0 mL urine/kg/hour

69
Q

eGFR (mL/min/1.73m^2) =

A

0.413(height in cm/SCr)

PHRM 825 (2 decks)

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