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NURS 2514 > Week 3 - Meds > Flashcards

Week 3 - Meds Flashcards

1
Q

what are the 3 categories of diuretics?

A
  • loop
  • thiazide
  • K+ sparing
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2
Q

what is the prototype of loop diuretic

A

furosemide

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3
Q

what is the MOA of furosemide

A
  • inhibits the reabsorption of sodium & chloride from the ascending loop of henle = prevents reabsorption of water
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4
Q

list some uses of furosemide (4)

A
  • pulmonary edema associated w HF
  • edema
  • hypertension
  • severe renal impairment
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5
Q

why is furosemide especially useful for patients with severe renal impairment?

A
  • it can promote diuresis even when renal blood flow and GFR are low
  • thiazides do not do this
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6
Q

list some adverse effects of furosemide (8)

A
  • hypotension
  • hypovolemia
  • hyponatremia
  • dehydration
  • hypokalemia
  • hypocholemia
  • ototoxicity
  • hyperglycemia
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7
Q

describe assessment for someone taking furosemide (7)

A
  • weight
  • I&O
  • bp
  • improvement of edema
  • urine output
  • electrolytes
  • assess for hearing loss
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8
Q

describe patient education for someone taking furosemide (6)

A
  • need high K+ diet
  • rise slowly from sitting or lying
  • use sunscreen to protect from photosensitivity
  • take earlier in day to avoid nocturia
  • monitor weight
  • BG may be increased for diabetics = may need to increase insulin
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9
Q

what is the prototype of thiazide diuretics

A

hydroclorothiazide

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10
Q

what is the MOA of hydrochlorothiazide

A
  • blocks reabsorption of Na and Cl at the early segment of the distal convoluted tubule
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11
Q

what is a con to hydrochlorothiazide

A
  • only 10% of filtered sodium and chloride is normally absorbed at the site where thiazides act = not as potent as loop diuretics
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12
Q

note: pre much everything for loop & thiazide diuretics are the same so i did not make flashcards on this; one thing to note is thiazides do not cause ototoxicity & are less potent

A

…

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13
Q

what is the MOA of statins

A
  • inhibits HMG-CoA reductase enzyme = decreased cholestrol synthesis
    = lowered LDL, lowered total cholestrol, lower TG, increase HDL
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14
Q

what is the prototype for statins

A
  • lovastatin
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15
Q

list some uses of statins (4)

A
  • hypercholesteremia
  • atherosclerosis
  • prevention of CV events (MI, angina, stroke, etc.)
  • diabetes –> to help reduce mortality by controlling HTN & cholestrol
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16
Q

list some adverse effects of statins (6)

A
  • myopathy
  • rhabdomyolysis
  • hepatotoxicity
  • GI symptoms
  • blurred vision
  • dizziness
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17
Q

describe assessment for someone taking stains (4)

A
  • diet: fat, cholestrol
  • fasting cholestrol, LDL, HDL, triglyceride levels
  • hepatic studies
  • renal function
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18
Q

what are some classes of antihypertensives (4)

A
  • diuretics
  • antiadrenergic drugs/sympatholytics
  • calcium channel blockers
  • drugs that suppress the RAAS
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19
Q

what is the MOA of beta-blockers

A
  • blocks stimulation of beta1 adrenergic receptors
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20
Q

what effects do beta-blockers have (4)

A
  • block cardiac beta1 receptors = decreased HR & contractility
  • suppress reflex tachy
  • block beta1 receptors on juxtaglomerular cells = reduced renin secretion = decreased RAAS effect
  • long term use = reduced peripheral vascular resistance
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21
Q

what is the suffix for beta blockers

A
  • olol
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22
Q

what are some adverse effects of beta blockers (5)

A
  • bradycardia
  • decreased AV conduction
  • reduced contractility
  • blockage of beta2 in lungs = bronchoconstriction
  • hypotension
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23
Q

what is the MOA of alpha 1 blockers

A
  • prevent stimulation of elpha1 receptors on arterioles & veins = prevent sympathetically mediated vasoconstriction = vasodilation = reduced peripheral resistance & venous return to heart
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24
Q

what is the main side effect of alpha1 blockers

A
  • orthostatic hypotension
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25
Q

what is a significant side effect with vasodilators

A
  • reflex tachy
26
Q

what is the MOA of calcium channel blockers

A
  • block calcium channels = dilation of arteries
27
Q

what is the MOA of ACE inhibitors

A
  • lower BP by preventing ACE which is responsible for the conversion of angiotensin 1 to angiotensin 2
    = blocks all the effects of angio 2
28
Q

what effects does angiotensin 2 have (3)

A
  • stimulates the release of aldo (which says to keep Na and H2O
  • increases bp by constricting the efferent arteriole
  • increase pressure in the afferent arteriole (increases systemic BP)
29
Q

what is the suffix for ACE inhibitors

A
  • pril

ex. captopril

30
Q

what are some side effects of ACE inhibitors (5)

A
  • tachycardia
  • hypotension
  • persistent cough , bronchospasm
  • angioedema
  • hyperkalemia
31
Q

what is the MOA of angiotension 2 receptor blockers

A
  • lower bp the same way ACE inhibitors do but it is done by blocking the action of angio 2, not preventing the formation
32
Q

what is the suffix for ARBs

A
  • sartan
33
Q

what is the MOA of direct renin inhibitors

A
  • suppression of the entire RAAS by acting directly on renin, inhibiting the formation of angiotensinogen to angio 1
34
Q

what is the difference in side effects for ACEI vs ARBs`

A
  • arbs do not cause angioedema

- and have lower risk of cough & significant hyperkalemia

35
Q

what is the suffix of direct renin inhibitors

A

-ren

36
Q

what is the MOA of aldo antgaonists

A
  • lower BP by promoting release of Na and water (typically tells us to keep it)
37
Q

what is a significant side effect of aldo antagonists

A
  • promotes renal retention of K+ = risk of hyperkalemia
38
Q

what is the suffix for aldo antagonists

A
  • one

ex. spironolactone, eplerenone

39
Q

what are 2 nursing considerations for ACEI

A
  • have been shown to slow the progression of nephropathy

- GFR must be checks on initiation & with dose increase –> expect ~15% decrease

40
Q

what is kayexelate

A
  • sodium polystyrene sulfonate

- potassium binding agent

41
Q

what is the MOA of kayexelate

A
  • slower method to lower serum potassium

- removes potassium by exchanging sodium for potassium in the body, primarly in the large intestine

42
Q

what is kayexelate used for

A
  • for hyperkalemia
43
Q

what are some adverse effects of kayexelate (3)

A
  • hypokalemia
  • sodium retention = hypernatremia
  • GI effects –> NVD, constipation, anorexia, fecal impaction
44
Q

describe assessment for someone of kayexelate (3)

A
  • monitor electrolytes
  • monitor bowel function
  • monitor I&O, weight
45
Q

describe patient education for someone of kayexelate (2)

A
  • follow low-potassium diet

- avoid laxatives, electrolyte based products, antacids

46
Q

how fast does kayexelate work? how is it administered?

A
  • it is a slower method of lowering serum potassium

- administered oral or rectal route

47
Q

what are 2 types of phosphate binders

A
  • calcium carbonate (ApoCal, Tums)

- sevelamer carbonate (renagel)

48
Q

what is the MOA of sevelamer carbonate

A
  • prevents hyperphosphatemia by binding to dietary phosphate in the gut, preventing its absorption
  • thus, decreases parathyroid hormones
49
Q

list uses of sevelamer

A
  • control of hyperphosphatemia in ESRD patients
50
Q

what are some adverse effects of sevelamer (5)

A
  • infection
  • GI effects (NVD, constipation)
  • obstruction
  • peritonitis
  • perforation
51
Q

describe assessment for someone taking sevelamer

A
  • asses GI status (signs of obstruction, perforation, NVD, bowel function)
  • S&S of infection
  • phosphorus levels
52
Q

describe patient education for sevelamer

A
  • not to chew, cut, or dissolve tabs

- swallow whole w water

53
Q

does sevelamer contain calcium?

A
  • no
54
Q

what is erythropoietin

A
  • a hematopoietic agent given to increase the production of RBCs
55
Q

how is erythropoietin administered? how often for a pt in ESRD

A
  • subcut

- 3 times/week

56
Q

why is insulin/glucose used to treat hyperkalemia? how is it administered

A
  • it is used to rapidly shift K+ into the cell

- administered IV

57
Q

what are 2 types of vit D supplements

A
  1. calcitrol

2. alfacalcidol

58
Q

what is the MOA of calcitrol (3)

A
  • increases intestinal absorption of calcium
  • provides calcium for bones
  • increases renal tubular reabsorption of phosphate
59
Q

what are the uses for calcitrol

A
  • active form of vit D given when phosphate levels are controlled, but calcium remains low
  • hypocalcemia
60
Q

what is replavite

A
  • a vitamin supplment for B, C, and folic acid
61
Q

what is the use for replavite

A
  • used to replace vitamin B & C and folic acid that is lost during dialysis
62
Q

what is alfacalcidol? what does it do

A

type of vitamin D supplement

- helps regulate the amt of calcium and phosphate

NURS 2514 (75 decks)

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