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Foundations of Pharmacy Care > Exam I: GI, Antihyperlipidemic and Diuretic drugs > Flashcards

Exam I: GI, Antihyperlipidemic and Diuretic drugs Flashcards

1
Q

Acid secretion in the stomach is stimulated by?

A
  1. Histamine (H2 receptors)
  2. Ach (M3 receptors)
  3. Gastrin (promotes histamine secretion by ECL cells)
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2
Q

If PPIs permanently turn of proton pumps, how is acid produced when PPIs are stopped?

A

New proton pumps must be synthesized

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3
Q

Histamine. Receptor? Synthesis? Antagonists?

A

Receptor - Binds to H2 receptors on parietal cells

Synthesis - Made by Enterochromaffin-like (ECL) cells

Antagonists - Similar structure to histamine reversible competitive inhibitors on H2 receptors

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4
Q

Acetylcholine. Receptor? When is it released?

A

Receptor - Muscarinic III receptors on parietal cells

Released when food is smelled during hunger prior to eating - vagus (vagal) nerve stimulation

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5
Q

Gastrin. Promotes the release of?

A

Promotes histamine secretion by ECL cells - indirect stimulation of acid production

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6
Q

How is gastric acid (HCL) secreted?

A

Secreted by parietal cells in the stomach via the proton pump (H+/K+ ATPase)

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7
Q

Prostaglandin (PGE2). Function in the stomach?

A
  1. Inhibit acid production
  2. Cytoprotective - stimulates epithelial cell to secrete mucous barrier around stomach
  3. Stimulate epithelial cells to release bicarbonate (neutralize acid)
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8
Q

Five causes of Peptic Ulcer Disease (PUD).

A
  1. H. pylori - gram negative bacteria that colonizes beneath mucosal barrier
  2. Chronic NSAID use
  3. Other drugs (ie. Bisphosphonates, corticosteroids, clopidogrel, warfarin)
  4. Hypersecretion of gastric acid like in Zollinger-Ellison syndrome - benign pancreatic tumor that secretes gastrin
  5. Stress ulcers (ie. no PO for ICU patients, disruption in mucous and bicarbonate secretion)
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9
Q

How exactly does H. pylori cause ulcers?

A

Produces an enzyme called urease (converts urea to ammonia which increases pH)

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10
Q

Describe two cytoprotective drugs.

A
  1. Sucralfate - Coat the stomach and ulcer (if present), prevents acid from coming in contact
  2. Misoprostol - synthetic PGE1, acts like prostaglandins (inhibit acid production, stimulate mucous and bicarbonate secretion)
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11
Q

Name two methods to eradicate H. pylori (HPI).

A

Clarithromycin Triple

Bismuth Quadruple

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12
Q

Clarithromycin Triple regimen. Drug names, strengths, duration and directions.

A

14 day regimen

  1. Clarithromycin 500mg po BID
  2. Amoxicillin 1 gram po BID
  3. PPI po QD taken 30 min before breakfast
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13
Q

Bismuth Quadruple. Drug names, strengths, duration and directions.

A

10-14 day regimen

  1. Bismuth subsalicylate 2 tabs po QID
  2. Metronidazole 250 mg po QID
  3. Amoxicillin 500 mg po QID
  4. PPI po QD taken 30 min before breakfast
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14
Q

M of a for H2RAs?

A

Secondary inhibition of vagal (Ach) and gastrin-stimulated acid secretion

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15
Q

When is acid secretion most effectively inhibited by H2RAs?

A

Basal and nocturnal - at bedtime

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16
Q

Treatment durations for H2RA management of PUD for duodenal ulcers (DU) vs gastric ulcers (GU).

A

DU - 6-8 weeks

GU - Full 8 weeks

Add 2-4 weeks to regimen for elderly patients or smokers, ulcers take longer to heal in these patients

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17
Q

Put ranitidine, cimetidine, nizatidine and famotidine in order from longest to shortest duration

A

1 and 2. Famotidine and Nizatidine - 10 hours

  1. Ranitidine - 6-10 hours
  2. Cimetidine - 6 hours
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18
Q

Famotidine comes in 20 mg and 40 mg. There are some patients that take 20 mg po QD.

True/False

A

False

Doses always add up to the treatment dose for H2RAs (in this case 40 mg)

20 mg po/IV BID

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19
Q

Which H2RA causes the most side effects? What are the most common side effects? (4)

A

Cimetidine

  1. CNS - headache, dizziness, confusion etc
  2. GI (most common) - diarrhea, constipation, nausea
  3. Nosocomial pneumonia
  4. 2.3 times greater risk of community-acquired pneumonia
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20
Q

DDIs for cimetidine specifically. (4)

A
  1. inhibits hepatic CYP enzymes - increased plasma concentration for warfarin, alprazolam, etc.
  2. Decreased hepatic blood flow - increased bioavailability of drugs with a high hepatic extraction ratio
  3. Additive myelosuppression (alkylating agents, antimetabolites, radiation therapy)
  4. Decreased bioavailability when taken with Al/Mg antacids (Mylanta, Maalox)
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21
Q

Famotidine and nizatidine do not inhibit CYP enzymes.

True/False

A

True

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22
Q

DDI for all H2RAs

A

Decreased bioavailability of ketoconazole because it needs acid to dissolve

Salicylates—decreased renal tubular secretion (competitive inhibition by all H2RAs)

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23
Q

PPIs onset of action? How long does acid secretion take to return after discontinued?

A

Onset of action - 1 hour

Full acid secretion returns after 4-7 days from the time a PPI is discontinued

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24
Q

Most common side effects of PPIs. (6)

A
  1. GI (most common) - abd pain, nausea
  2. CNS - headache
  3. 2.5 times higher risk of community-acquired pneumonia
  4. Osteoporosis and increased risk of fracture
  5. Hypermagnesemia
  6. Dose-dependent decrease in vitamin B12
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25
Q

Name the PPIs approved to treat PUD. (3, one is a combo)

A
  1. Omeprazole alone or with NaHCO3
  2. Lansoprazole
  3. Rabeprazole
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26
Q

DDIs of omeprazole specifically.

A
  1. Inhibition of CYP enzymes
    - increased levels of warfarin, phenytoin etc.
    - Decreased levels of omeprazole when taken with Rifampin or St. John’s wort (supplement)
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27
Q

DDIs for all PUD PPIs.

A
  1. Decreased bioavailability of ketoconazole, ampicillin, iron salts, digoxin, atazanavir.
  2. May increase risk of digoxin-associated cardiotoxicity secondary to hypomagnesemia
  3. Sucralfate - binds to GI drugs and delays absorption and decreases oral bioavailability of PPI
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28
Q

What is GERD?

A

Transient relaxation of the esophageal sphincter

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29
Q

What can trigger GERD symptoms? (4)

A

Obesity

Alcohol or tobacco use

Fatty, spicy foods

Some medications/drugs

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30
Q

What are some alarm symptoms of GERD? Why are the alarming?

A

Symptoms: Dysphagia, chronic sore throat, bleeding or anemia, unexplained weight loss

Alarming because the symptoms may be due to Barrett’s esophagus syndrome which increases risk of cancer

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31
Q

Name the PPIs approved to manage GERD. (6)

A
  1. Omeprazole
  2. Esomeprazole
  3. Lansoprazole
  4. Rabeprazole
  5. Pantoprazole
  6. Dexlansoprazole (Dexilant)
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32
Q

What is NERD? More likely to respond to PPIs?

A

Non-erosive reflux disease (NERD) is a type of gastroesophageal reflux disease (GERD) in which the esophagus is unharmed by stomach acid

Less likely to respond to PPIs compared to patients with Erosive Esophagitis (EE)

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33
Q

Use of OTC PPIs for acid reflux should not exceed what time period. Why?

A

No longer than 14 days every 4 months without doctor supervision.

Can mask a serious illness like esophageal cancer

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34
Q

Concerns about long term use of PPIs

A
  1. Osteoporosis and bone fracture (decreased calcium absorption)
  2. Community-acquired pneumonia
  3. C. difficile colitis
  4. Ischemic heart disease and acute MI (PPIs may decrease nitric oxide synthesis)
  5. Dementia (in mice PPIs increase amyloid-beta proteins in brain)
  6. Chronic renal failure (mechanism unclear)
  7. Gastric carcinoid tumors in mice
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35
Q

What is the most effective antagonists for nausea and vomiting?

A

Serotonin (5HT3) receptor antagonists

ie. Ondansetron

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36
Q

Name 4 antiemtics for cytotoxic drug-induced emesis.

A

Ondansetron** (most common antiemetic)

Metoclopramide

Promethazine

Dronabinol nabilone

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37
Q

Name the Neurokinin receptor antagonists used to delay vomiting following cytotoxic drug-induced emesis

A

Aprepitant** (most common antiemetic)

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38
Q

Can dolasetron mesylate be administered IV for CINV? Why or why not?

A

No

Due to the risk of dose-dependent QT interval prolongation

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39
Q

Which Serotonin (5HT3) receptor antagonists are not indicated for RINV?

A

Dolasetron

Palonosetron

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40
Q

Statins derive their name from?

A

Molds or fungi

41
Q

“STATIN” pharmacological class. M of a?

A

HMG CoA Reductase Inhibitors

HMG CoA reductase is the rate limiting enzyme in cholesterol synthesis

By inhibiting this enzyme it leads to a compensatory increase in the expression of LDL receptors which stimulates LDL catabolism

42
Q

“STATIN” drugs have a pleiotropic effect. What does this mean? What are the pleiotropic effects?

A

Pleiotropic effect –> multiple effects with one dose

Decreases inflammation at site of coronary plaque, inhibits platelet aggregation, and anticoagulant effects

43
Q

How do “STATIN” drugs affect HDL, LDL and triglyceride levels?

A

Lowers: LDL (“Bad cholesterol”), Triglycerides

Raises: HDL (“Good cholesterol”)

44
Q

Patients with Atherosclerotic Cardiovascular Disease risk factors do not need to take a “STATIN” if cholesterol levels are normal.

True/False

A

False

If a patient is at risk for ASCVD from a co morbid condition then they need to be on a “STATIN” drug

45
Q

“STATIN” drugs can be used for primary and secondary prevention. What is the difference?

A

Primary prevention – Medication is given for a patient that has never had the targeted disease

Ex. Patient at risk for a heart attack but never experienced

Secondary prevention – Aims to reduce the impact of a disease that has already occurred and prevent it in the future

Ex. Patient has had a heart attack in the past. Medication is used to prevent a future heart attack.

46
Q

Adverse drug reactions to “STATIN” drugs. (5)

A

Diarrhea

Arthralgia (joint pain)

Nasopharyngitis (swelling of nasal passages in the back of the throat)

Insomnia

Malaise (feeling tired, ill or uncomfortable)
Increased hepatic function tests

47
Q

When are “STATIN” drugs most effective? Why? Name the exceptions to this.

A

Most statins should be administered before bedtime because cholesterol is synthesized when dietary intake is at its lowest.

Exceptions - Atorvastatin and Rosuvastatin - can be taken at any time

48
Q

Why can Atorvastatin and Rosuvastatin be taken at anytime in the day as opposed to other “STATIN” drugs?

A

They have a longer half life than other statins

49
Q

Can “STATIN” drugs be given to pregnant patients?

A

No

Category X

50
Q

What to do if a patient complains of myalgia (muscle pain)?

A

Try a different statin

Remember –> the more lipophilic the statin the greater chance of muscle pain

51
Q

What fruit do statins interact with?

A

Grapefruit

52
Q

At certain doses, Simvastatin must be taken concurrently with what other type of drug?

A

Calcium channel blockers (CCBs)

53
Q

High intensity statin therapy. On average how much is LDL lowered with a daily dose? Name the two drugs and dose ranges.

A

Daily dose lowers LDL on average 50% or greater

Atorvastatin 40-80mg
Rosuvastatin 20-40mg

54
Q

Low intensity statin therapy.. On average how much is LDL lowered with a daily dose? Name the four drugs and dose ranges.

A

Daily dose lowers LDL on average less than 30%

Simvastatin 10mg
Pravastatin 10-20 mg
Lovastatin 20 mg
Fluvastatin 20-40 mg

55
Q

Name the combination statin drugs. (3)

A

Advicor® - lovastatin + niacin ER

Simcor® - simvastatin + niacin ER

Vytorin® - simvastatin + ezetimibe

56
Q

Name the three “Choles-“ drugs. Pharmacological class.

A

Bile acid sequestering agent

Cholestyramine

Cholestipol

Cholesevelam

57
Q

Mechanism of action for Choles- drugs.

A

Forms a non-absorbable complex with bile acids and releases chloride ions in the process

Inhibits reuptake of intestinal bile salts and increases fecal loss of LDL-C

58
Q

“Off label” uses of CHOLES drugs

A

Chronic diarrhea due to bile acid malabsorption (most common)

Hyperthyroidism

Pruritus associated with cholestasis

59
Q

Adverse reaction to CHOLES drugs. (6)

A

Abdominal pain

Constipation

Flatulence

Abnormal hepatic function tests

Myalgias

Osteoporosis

60
Q

Interactions and monitoring necessary for patients taking CHOLES drugs. (3)

A

Warfarin – monitor for decreased INR

Statins/fibrates – monitor for increased incidence of myalgias

Amiodarone – may decrease availability/effectiveness of amiodarone

61
Q

Name the three FIBRATE drugs.

A

Gemfibrozil

Fenofibrate

Fenofibric Acid

62
Q

Mechanism of action for FIBRATE drugs

A

Exact mechanism is unknown

In theory, inhibits lipolysis and decreases hepatic fatty reuptake as well as inhibit secretion of VLDL

63
Q

FIBRATE drugs effects on LDL, HDL and triglyceride levels.

A

Very good triglyceride lowering agents

Also decrease LDL and increase HDL

64
Q

FDA approved indications for FIBRATE drugs. (2)

A

Hypertriglyceridemia

Hypercholesterolemia

65
Q

Off-label use of FIBRATE drugs.

A

Primary biliary cholangitis – autoimmune disease of the liver, the bile ducts in your liver are slowly destroyed

66
Q

Adverse reactions to FIBRATE drugs. (4)

A

Increased serum transaminases (can be a signal of liver damage)

Abdominal pain

Abnormal hepatic function tests

Myalgias

67
Q

DDIs for all FIBRATE drugs

A

All can increase incidence of myalgias when combined with statins

68
Q

Gemfibrozil DDIs

A

Contraindications - All statins, ezetimibe, any CYP2C8 substrates (many antiretrovirals)

Also use with caution in patient on warfarin

69
Q

OCUMABS drugs mechanism of action

A

PCSK-9 inhibitors

Human monoclonal antibodies that aid in clearance of LDL

70
Q

Adverse effects of OCUMAB drugs

A

Pain/redness at injection site, flu or flu-like symptoms

71
Q

Name the two OCUMAB drugs available.

A

Alirocumab (Praluent®)

Evolocumab (Repatha®)

72
Q

Niacin (nicotinic acid, Vitamin B3) mechanism of action

A

Not fully understood, potentially related to inhibition of release of free fatty acids from adipose tissue

Increases HDL while lowering LDL and TG

73
Q

Niacin (nicotinic acid, Vitamin B3) adverse reactions. (6)

A

Flushing

Pruritus (itch)

GI distress

Vomiting

Diarrhea

Hepatotoxicity

74
Q

Omega-3 polyunsaturated Fatty acids mechanism of action

A

Reduction in hepatic production of TG-rich very low-density lipoproteins + reduction in hepatic synthesis of TG

Secondary - only used if 1st options fail

75
Q

Omega-3 polyunsaturated Fatty acids adverse reactions

A

Diarrhea, nausea, fishy burps

76
Q

Omega-3 polyunsaturated Fatty acids products available.

A

Lovaza® – high grade fish oil

Vascepa® – Icosapent Ethyl

77
Q

Ezetimibe (Zetia®) mechanism of action

A

Cholesterol absorption inhibitor at the brush border of the small intestine

78
Q

Ezetimibe (Zetia®) adverse reactions (4)

A

Diarrhea

Arthralgia (joint pain)

Fatigue

Increased serum transaminases

79
Q

Clinical pearls for Ezetimibe (Zetia®) (2)

A

Generally used as adjunctive therapy with statins or in addition to dietary changes

Works primarily lowering LDL but also slightly lowers TG and raises HDL

80
Q

PIB drugs are not currently on the market. Name three drugs that haven’t been approved.

A

Torcetrabpib

Anacetrapib

Evacetrapib

81
Q

Mechanism of action for PIB drugs

A

Inhibits cholesterol ester transfer protein resulting in increases in HDL and decreasing LDL

82
Q

Thiazides are 1st line of therapy for what disorder? Which drug is the exception?

A

Hypertension (HTN)

Metolazone is used for CHF patients to assist in fluid management

83
Q

Loop diuretics are first line for what disorder?

A

Fluid management in CHF and other disorders with fluid retention such as cirrhosis

Alternative agent to treat hypertension

84
Q

K-sparing diuretics are primarily indicated in patients with what disorder?

A

Systolic CHF

or resistant hypertension

85
Q

Osmotic diuretics are generally used for what disorder?

A

Intracranial pressure reduction

Not hypertension

86
Q

Off label used for diuretics. (3)

A

Calcium nephrolithiasis

Diabetes Insipidus

Osteoporosis

87
Q

What is Diabetes Insipidus?

A

Condition in which the kidneys are unable to prevent the excretion of water resulting in extremely dilute urine

88
Q

What is Nephrolithiasis?

A

Kidney stone disease

A condition in which individuals form calculi (stones) within the renal pelvis and tubular lumens.

Stones form from crystals that precipitate (separate) out of the urine.

89
Q

Name the 4 THIAZIDE diuretic drugs. (Two don’t end in thiazide)

A

Chlorothiazide

Hydrochlorothiazide

Chlorthalidone

Metolazone

90
Q

Thiazide drugs mechanism of action.

A

Inhibits reabsorption in the distal convoluted tubules causing increased excretion of sodium, potassium and water

Block reabsorption of Na+ and Cl- increasing their excretion

Also decrease Ca2+ excretion

91
Q

FDA approved indications for thiazide drugs. (3)

A

Hypertension (HTN)

Fluid retention in HF – heart failure (mild)

Edema

92
Q

Adverse drug reactions for THIAZIDES (6)

A

Orthostatic hypotension

Dizziness

Photosensitivity

Hyponatremia

Hyperuricemia

Leg cramps

93
Q

When do patients taking THIAZIDE drugs need to be monitored?

A

Monitor patient closely if they are concurrently using dofetilide or lithium

94
Q

Loop diuretics generally end in what suffix? What is the exception?

A

“-semide”

i.e. Furosemide, Torsemide

Exception: Bumetanide

95
Q

Loop diuretics mechanism of action.

A

Inhibits reabsorption of sodium and chloride in the ascending loop of Henle which causes its natriuretic effect (sodium loss)

96
Q

Loop diuretics adverse reactions. (6)

A

Similar to the thiazide diuretics

Orthostatic hypotension

Dizziness

Photosensitivity

Hyponatremia

Hyperuricemia

Leg cramps

97
Q

Name the 5 potassium sparing diuretics.

A

Spironolactone

Triamterene

Eplerenone

Amiloride

98
Q

Potassium sparing diuretic mechanism of action.

A

Competes with aldosterone for receptor sites in the distal renal tubules increasing sodium and chloride excretion while preserving potassium

99
Q

Potassium sparing diuretic adverse reactions.

A

Similar to the thiazide diuretics with the exception of potentially causing gynecomastia

Foundations of Pharmacy Care (12 decks)

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