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Pharm > Pharm 2 exam 1 > Flashcards

Pharm 2 exam 1 Flashcards

1
Q

Furosemide

A

Diuretic

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2
Q

Hydrochlorothiazide (HCTZ)

A

Diuretic

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3
Q

Spironolactone

A

Diuretic

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4
Q

Mannitol

A

Diuretic

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5
Q

Diuretic common uses

A
  • Edema (peripheral (right) &pulmonary (left))
  • Hypertension
  • Heart failure (kidney goes first)
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6
Q

Diuretic mechanism of action

A

Cause the kidney to excrete more sodium than they normally would. Since water likes to follow sodium, this causes an increase in urine volume.

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7
Q

Which part of the kidney does mannitol start working?

A

Proximal convoluted tubule

- Starts the earliest so it is the most powerful

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8
Q

Which part of the kidney does furosemide start working?

A

Ascending limb of loop of Henle

- Starts second earliest so its the second most powerful

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9
Q

Which part of the kidney does Hydrochlorothiazide (HCTZ) start working?

A

Early distal convoluted tubule

- third strongest

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10
Q

Which part of the kidney does spironolactone start working?

A

Late distal convoluted tubule

- least strongest

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11
Q

All Diuretic common themes

A
  • Dehydration
  • Orthostatic hypotenstion
  • Electrolyte imbalances
  • Nocturia (take before 1400)
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12
Q

Furosemide specific common themes and teaching clients

A
  • Only for edema or heart failure
  • Hypokalemia (low potassium) is a major issue
  • Ototoxicity (tinnitus)

Teach clients

  • Signs of hypokalemia (feel weak, tired, cramps, nausea and vomiting)
  • Eat foods rich in potassium
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13
Q

Hydrochlorothiazide (HCTZ) specific common themes

A
  • Often initial drug of choice for hypertension
  • Hypokalemia is a major issue
  • Not ototoxic
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14
Q

Spironolactone specific common themes

A
  • Potassium-sparing diuretic (increases)

- Avoid potassium-rich foods and salt substitutes

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15
Q

Mannitol specific common themes

A
  • Reduces intracranial pressure
  • Watch out for crystallization (precipitation)
    - Keep warm
    - Use filters
  • Use filter needle and patient usually has a foley catheter
  • Makes blood hypertonic (fluid goes into the blood stream)
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16
Q

What types of drugs are Renin-Angiotensin-Aldosterone System (RAAS)?

A
  • ACE inhibitors

- Angiotensin II Receptor Blockers (ARBs)

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17
Q

ACE inhibitors mechanism of action

A

Block the enzyme that converts angiotensin-I to its active form. This causes vasodilation and prevents the release of aldosterone from the adrenal glands, causing excretion of sodium and water.

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18
Q

Angiotensin II Receptor Blockers (ARBs) mechanism of action

A

Block angiotensin-II receptors in the adrenal glands. This causes vasodilation and prevents the release of aldosterone from the adrenal glands, causing excretion of sodium and water

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19
Q

Captopril

A

ACE inhibitor

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20
Q

Enalapril

A

ACE inhibitor

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21
Q

Lisinopril

A

ACE inhibitor

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22
Q

Losartan

A

Angiotensin II Receptor Blocker (ARBs)

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23
Q

RAAS meds common uses

A
  • Hypertension
  • Heart Failure
  • Cardioprotection (following MI) (ACE inhibitors)
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24
Q

Notable Problems with RAAS meds

A
  • First-dose orthostatic hyotension
  • Hyperkalemia
  • Persistent cough (ACE inhibitors only) 10%
  • Angioedema (swelling of the face, lips, tongue) (0.1% in Caucasians and 0.2% in African Americans)
  • Dry, persistent cough (ACE inhibitors)
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25
Q

Calcium Channel Blockers mechanism of action

A

Block calcium channels in arteries/arterioles. This causes them to relax, decreasing blood pressure. Some CCBs also block calcium channels in the heart, causing the heart rate to decrease

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26
Q

Nifedipide

A

Calcium Channel Blockers

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27
Q

Amlodipine

A

Calcium Channel Blockers

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28
Q

Verapamil

A

Calcium Channel Blockers

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29
Q

Dilitiazem

A

Calcium Channel Blockers

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30
Q

Calcium Channel Blockers common uses

A
  • Hypertension
  • Angina pectoris (chest pain)
  • Cardiac dysrhythmias (only verapamil & dilitiazem)
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31
Q

Calcium Channel Blockers notable problems

A
  • C= Cankles (peripheral edema)
  • C= Constipation (verapamil)
  • B= Bradycardia (verapamil & dilitiazem)
  • S= Syncope (dizziness)

Always check HR and BP before administering
Nonpharmacologic measures for constipation (fluid, fiber, walking)
Avoid Grapefruit juice with CCBs

32
Q

Metroprolol

A

Cardioselective (beta 1 only) Beta Blocker

33
Q

Atenolol

A

Cardioselective (beta 1 only) Beta Blocker

34
Q

Propranolol

A

Nonselective (beta 1 and beta 2) Beta Blocker

35
Q

Carvedilol

A

Nonselective (beta 1 and beta 2) Beta Blocker

36
Q

Labetalol

A

Nonselective (beta 1 and beta 2) Beta Blocker

37
Q

Beta blockers common uses

A
  • Hypertension
  • Angina pectoris
  • Atrial fibrillation
  • Cardioprotection (post MI)
38
Q

Beta blockers notable problems

A
  • Bradycardia and hypotension
  • Can mask hypoglycemia (blocks Adrenalin)
  • Bronchoconstriction (nonselectives)
  • Fatigue and/or depression
39
Q

Some HIgh yield concepts for beta blockers

A
  • Always check HR and BP before administering (hold if HR < 50)
  • Clients with diabetes need to check their glucose more frequently
  • Clients with respiratory disease should avoid nonselective beta blockers
  • Do not abruptly stop beta blockers
40
Q

Digoxin mechanism of action

A

Stimulates the vagus nerve to release more acetylcholine (ACh), causing the heart to beat slower. Digoxin also blocks the Na, K- ATPase pump in the heart. This causes the heart to squeeze harder - which is great for client with heart failure

41
Q

Digoxin notable problems

A
  • Short therapeutic window (0,5-2)
  • Many drug interactions
    - Diurectics (Because of potassium level changes)
    - ACE inhibitors and ARBs (because of potassium
    level changes)
    - Antacids
    - Many more…
  • Inverse relationship with potassium
  • Check apical pulse for 60 seconds before giving digoxin: hold if HR less than 60
42
Q

Digoxin toxicity

A

Early toxicity- Anorexia, nausea and vomiting

Late toxicity- Bradydysrythmias, altered mental status, syncpe, visual changes, death

43
Q

Angina pectoris definition

A

Angina is reversible ischemic injury that occurs when the heart’s oxygen demand is greater than the supply

44
Q

Types of Angina

A
  1. Stable angina
  2. Unstable angina
  3. Prinzmetal (variant) angina
45
Q

Stable angina

A

Need more oxygen when exercising and is predictable

46
Q

Unstable angina

A

Plaques ruptures

47
Q

Prinzmetal angina

A

Coronary artery vasospasms

48
Q

Nitroglycerin

A

Antiangina med

49
Q

Isosorbide mononitrate

A

Antiangina med

50
Q

Antiangina medication mechanism of action

A

Cause the body to produce more cyclic GMP. Cyclic GMP causes widespread vasodilation. This helps clients with angina, because it decreases preload and helps open the coronary arteries.

51
Q

Antiangina medication common problems

A
  • Headache (50% of people)
  • Orthostatic hypotension
  • Reflex tachycardia
  • Tolerance
  • Tachyphylaxis
  • Don’t combine with erectile dysfunction drugs
52
Q

Nitroglycerin teaching

A
  1. Sit or lie down
  2. Place tablet under tongue
  3. Wait five minutes
  4. If pain persists, call 911 and take another
  5. Wait five minutes
  6. If pain persists, take one last tablet
  7. 3 is max
  8. Patch is for 10-12 hours
53
Q

Isosorbide Mononitrate teaching

A
  • Don’t crush
  • Only lasts 12 hours
  • Must have “nitrate-free interval”
  • Improves exercise tolerance
54
Q

If they actually have a myocardial infarction (MI) give them what?

A

M- Morphine
O- Oxygen
N- Nitroglycerin
A- Aspirin (chewable)

55
Q

What is dyslipidemia

A

Too much bad lipids in the blood

56
Q

Dyslipidemia meds

A
  • Statins
  • Cholesterol absorption inhibitors
  • Bile-acid sequestrants
  • Nicotinic-acid, niacin
  • Fibrates
57
Q

Statins mechanism of action

A

Block the action of an enzyme called HMG-CoA reductase. This halts a crucial step in the formation of cholesterol, causing a decrease in LDL and VLDL cholesterol

58
Q

Atorvastatin

A

Statin

59
Q

Lovastatin

A

Statin

60
Q

Rosuvastatin

A

Statin

61
Q

Simvastatin

A

Statin

62
Q

Statin notable problems

A
  • Hepatotoxicity (0.5-2% of clients)

- Myopathy (5-10% of clients)- muscle problems

63
Q

What is Rhabdomyolysis

A
  • Clog up kidneys and turn urine cola brown
64
Q

Antidysrhythmic medications 4 classes

A
  • Class 1= Na channel blockers
  • Class 2= Beta blockers
  • Class 3= K channel blockers
  • Class 4= Ca channel blockers
65
Q

Amiodarone

A

Antidysrhythmic (Class 3)

66
Q

Amiodarone toxicity

A
  • Dysrhythmias
  • Liver toxicity
  • Photosensitivity
  • Pulmonary toxicity
  • Thyroid dysfunction
  • Visual disturbances
67
Q

Amiodarone High yield concepts

A
  • Amiodarone can treat atrial fibrillation
  • It can cause heart,liver, skin, pulmonary, thyroid, and vision problems
  • Baseline testing needs to be performed
  • Educate clients on what to report
68
Q

Types of shock

A
  • Hypovolemic (dehydration/bleeding (cullen and turner sign)
  • Cardiogenic (heart weak, no pumping)
  • Distributive (Anaphylactic, Neurogenic, Septic)
  • Obstructive (major arterial obstruction)
69
Q

How to rapidly increase BP

A
  1. Fluid bolus
  2. Volume expander
  3. Vasopressor
70
Q

Epinephrine

A

Adrenergic Agonist (nonselective)

71
Q

Norepinephrine

A

Adrenergic Agonist (more selective, mainly alpha)

72
Q

Dopamine

A

Adrenergic Agonist (causes tachycardia)

73
Q

Dobutamine

A

Adrenergic Agonist (mainly given to make the heart pump harder)

74
Q

Adrenergic Agonist problems

A
  • Too much vasoconstriction (necrosis)
  • Tachycardia (decreased stroke volume)
  • Increased workload on the heart
75
Q

Adrenergic Agonist high yield concepts

A
  • These drugs are powerful (and dangerous)
  • You have to give them centrally
  • The doses are titrated
  • Monitor urine output and perfusion to extremities

Pharm (7 decks)

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