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Pharm2 > Exam1 > Flashcards

Exam1 Flashcards

1
Q

what is a diuretic

A

drugs that make you pee

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2
Q

diuretics to know (4)

A
  • furosemide
  • hydrochlorothiazide
  • spironolactone
  • mannitol
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3
Q

common uses of diuretics

A
  • edema (peripheral and pulmonary)
  • hypertension (to decrease blood pressure)
  • heart failure
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4
Q

how do diuretics work? (mechanism of action)

A
  • diuretics cause kidneys to excrete more sodium than they normally would.
  • since water likes sodium, this causes an increase in urine volume
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5
Q

nephron anatomy and when the diuretics work

A
  1. proximal convoluted tubule (mannitol)- STRONGEST
  2. loop of henle (furosemide)
  3. early distal convoluted tubule (HCTZ)
  4. late distal convoluted tubule (spironolactone)
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6
Q

what’s the problem with diuretics?

A
  • dehydration
  • hypotension (orthostatic)
  • electrolyte imbalances
  • nocturia (take before 1400)
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7
Q

Furosemide

A

(diuretic med)
-only for edema or heart failure (NOT for hypertension)
-ototoxicity (tinnitus)–> reversible with ethacrynic acid
-***HYPOKALEMIA is a major issue
other issues:
-dehydration
-hyponatremia, hypocloremia
-hypotension
-hyperglycemia, increase LDL, decrease HDL

teach clients:

  • signs of hypokalemia (muscle weakness; tired, cramps)
  • nausea and vomiting
  • eat foods rich in potassium
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8
Q

Hydrochlorothiazide (HCTZ)

A

(diuretic med)–> early distal convoluted tubule

  • often initial drug of choice for hypertension
  • often used with other hypertensive drugs
  • NOT ototoxic
  • promote reabsorption of calcium and reduce risk of postmenopausal osteoporosis
  • can reduce urine production to those with diabetes insipidus

complications:
- hypokalemia, hypochloremia, hyponatremia
- dehydration
- hyperglycemia

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9
Q

Spironolactone

A

(diuretic med)

  • potassium-sparing diuretic (increase K+ level)
  • avoid potassium-rich foods and salt substitutes
  • combined with other diuretics (loop and HCTZ) for hypertension and edema
  • for heart failure

complications

  • hyperkalemia
  • endocrine effects
  • drowsiness, metabolic acidosis

DO NOT COMBINE WITH ACE INHIBITORS AND ARBs because those increases potassium levels

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10
Q

Mannitol

A

(diuretic med)
-reduces intracranial pressure (cerebral edema) by drawing fluid back into the vascular and extravascular space
-can only be administered via IV
-watch out for crystallization/precipitation:
(keep warm or use filters)

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11
Q

what foods are rich in potassium?

A
  • spinach
  • baked potatoes
  • sweet potatoes
  • orange
  • raisins
  • cantaloupe
  • bananas
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12
Q

RAAS meds

A

ACE inhibitors

  • captopril
  • enalapril
  • lisinopril

ARBs:
-losartan

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13
Q

how do ACE inhibitors work? (RAAS meds)

A

ACE inhibitors 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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14
Q

how do ARBs work? (RAAS meds)

A

ARBs 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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15
Q

common uses of RAAS meds:

A
  • hypertension
  • heart failure
  • cardioprotection (primarily ACE inhibitors)
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16
Q

notable problems with RAAS meds:

A
  • first-dose orthostatic hypotension
  • hyperkalemia
  • persistent cough (ACE inhibitors only)
  • angioedema (swelling of face) = medical emergency
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17
Q

calcium channel blocker (CCBs) meds to know:

A
  • nifedipine
  • amlodipine
  • verapamil
  • diltiazem
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18
Q

common uses or calcium channel blockers:

A
  • hypertension
  • angina pectoris
  • cardiac dysrhythmias
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19
Q

mechanism of action of CCBs

A
  • CCBs 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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20
Q

which of the 4 CCBs decrease HR?

A

verapamil

diltiazem

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21
Q

whats the problem with CCBs?

A 
CCBS!
C- canckles (peripheral edema)
C- constipation
B- bradycardia (verapamil and diltiazem)
S- syncope (dizziness; fainting)
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22
Q

which of the CCBs meds can cause constipation?`

A

verapamil

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23
Q

high yield concepts with CCBs

A
  • always check HR and BP before administering
  • verapamil and diltiazem slow HR
  • verapamil causes constipation
  • know nonpharmacologic measures for constipation (fluid, fiber, walking)
  • avoid grapefruit juice with CCBs
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24
Q

what food must you avoid with CCBs

A

grapefruit juice

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25
Q

cardioselective beta blockers (B1 only)

A
  • metoprolol

- atenolol

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26
Q

non selective beta blockers (B1 and B2)

A
  • propranolol
  • carvedilol
  • labetalol
27
Q

adrenergic receptors (beta 1) pertaining to beta blockers

A

heart

  • increases heart rate
  • increases contractile force

beta blockers: will slow heart rate

28
Q

adrenergic receptors (beta 2) pertaining to beta blockers

A

lungs
-causes bronchodilation

beta blockers: will cause bronchoconstriction

29
Q

adrenergic receptors (alpha1) pertaining to beta blockers

A

arteries

-causes vasoconstriction

30
Q

common uses of beta blockers

A
  • hypertension
  • angina pectoris
  • atrial fibrillation
  • cardioprotection (post MI)
31
Q

what’s the problem with beta blockers?

A
  • bradycardia and hypotension
  • can mask hypoglycemia
  • broncoconstriction (nonselectives)
  • fatigue and/or depression
32
Q

clients with respiratory disease (asthma and COPD) should avoid which kind of beta blockers?

A

nonselective:

  • propranolol
  • carvedilol
  • labetalol
33
Q

what does digoxin do? (2)

A
  1. digoxin stimulates the vagus nerve to release MORE acetylcholine, causing the heart to beat SLOWER.
    - great for atrial fibrillation (overly active atria)
  2. digoxin also blocks something called the sodium potassium ATPase pump in the heart. this causes the heart to squeeze HARDER, which is great for client with heart failure (fluid overload)
34
Q

digoxin has a very narrow therapeutic index. what is the levels of digoxin?

A

0.5-2

35
Q

drug interactions with digoxin:

A

-diuretics
-ACE inhibitors and ARBs
-antacids (tums)
and many more

36
Q

early digoxin toxicity

A
  • anorexia
  • nausea
  • vomiting
37
Q

late digoxin toxicity

A
  • bradydysrythmias
  • altered mental status
  • syncope
  • visual changes
  • death
38
Q

digoxin toxicity and potassium correlation

A

think “K”
increase potassium, decreases digoxin levels
decrease potassium, increases digoxin levels

39
Q

check ________ for 60 seconds before giving digoxin; hold if HR is less than 60

A

apical pulse

40
Q

antiangina medications to know

A
  • nitroglycerin

- isosorbide mononitrate

41
Q

stable angina

A
  • doesnt hurt when at rest
  • hurts when exercising or moving around
  • blood still can get through even when theres a plaque
42
Q

unstable angina

A
  • pain can occur at any time
  • clot/platelet formation due to plaque rupture
  • much harder for blood to get by
43
Q

Prinzmetal angina

A
  • coronary artery vasospasm (pushes in and out)
  • blood has trouble going through
  • can happen anytime
44
Q

how do antiangina meds work? (mechanism of action)

A
  • nitroglycerin and isosorbide mononitrate causes the body to produce more cyclic GMP
  • cyclic GMP causes widespread vasodilation
  • this helps client with angina because it decreases preload (less blood gets back to the heart= less work for the heart) and helps open the coronary arteries
45
Q

common problems with antiangina meds

A
  • headache (50% of people)
  • orthostatic hypotension
  • reflex tachycardia (can also increase O2 demand)
  • tolerance
  • tachyphylaxis (a drug losing part or its entire efficacy over time as the body becomes tolerant)
46
Q

nitroglycerin teaching

A
  • sit or lie down
  • place tablet under tongue
  • wait five minutes
  • if pain persists, call 911 and take another
  • wait five minutes
  • if pain persists, take one last tablet

MAX= 3 tabs

47
Q

isosorbide mononitrate teaching:

A
  • DON’T CRUSH
  • only lasts 12hrs
  • must have “nitrate-free interval”
  • improves exercise tolerance
  • take BEFORE chest pain
48
Q

what if the patient actually have a myocardial infarction?

A

give them MONA

M- morphine (helps with chest pain)
O- oxygen
N- nitroglycerine
A- aspirin–> for platelet plug formation; must be chewable for faster absorption

49
Q

dyslipidemia meds to know

A
  • statins
  • cholesterol absorption inhibitors
  • bile-acid sequestrants
  • nicotinic-acid, niacin
  • fibrates
50
Q

mechanism of action of STATINS

A
  • statins 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
51
Q

statins to know

A

(ending in -vastatin)

  • atorvastatin
  • lovastatin (must take with food)
  • rosuvastatin
  • simvastatin
52
Q

best time to give patients statins?

A

nighttime, because we make most cholesterol at night

53
Q

whats the problem with statins?

A
  • hepatotoxicity (0.5-2% of clients)

- myopathy (5-10 of clients); muscle problems

54
Q

rhabdomyolysis (pertaining to statins)

A
  • when muscles are destroyed, they release myoglobin
  • myoglobin can clog up kidneys and lead to kidney failure
  • urine turns into “cola brown” color
  • must check CK levels
55
Q

high yield concepts pertaining to statins

A
  • clients should report muscle pain/weakness
  • watch for hepatotoxicity
  • take statins in the evening
  • statins do not replace diet and exercise
  • avoid grapefruit
56
Q

antidysrhythmic meds

A

Class 1: Na+ channel blockers
Class 2: beta blockers
Class 3: K+ channel blockers (AMIODARONE)
Class 4: Ca2+ channel blockers

57
Q

antidysrhythmic med that is FDA approved for life threatening ventricular dysrhythmias

A

amiodarone

58
Q

what’s the problem with amiodarone (antidysrhythmic med)

A
  • dysrhythmias
  • liver toxicity
  • photosensitivity
  • pulmonary toxicity
  • thyroid dysfunction
  • visual disturbances
59
Q

can amiodarone treat atrial fibrillation?

A

yes, it’s just not FDA approved

60
Q

why is baseline testing need to be performed when client is taking amiodarone?

A

it can cause heart, liver, skin, pulmonary, thyroid, and vision problems

61
Q

adrenergic agonists to know:

A
  • epinephrine
  • norepinephrine
  • dopamine
  • dobutamine
62
Q

how to rapidly increase BP?

A
  • fluid bolus (normal saline, lactated ringer’s)
  • volume expander (hypertonic–> expands vascular space; increases water; increases BP) (ex; hetastarch, albumin)
  • vasopressor
63
Q

problems with adrenergic agonists?

A
  • too much vasoconstriction (necrosis)
  • tachycardia (decreased stroke volume)
  • increase workload on the heart
64
Q

high yield concepts pertaining to adrenergic agonists:

A
  • very powerful and dangerous (for shock)
  • you have to give them centrally (central line; subclavian vein)
  • doses are titrated
  • monitor urine output and perfusion to extremeties

Pharm2 (7 decks)

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