Cardiovascular Drugs Flashcards

1
Q

What % is reabsorbed through the proximal tubule? What ions?

A

65% Na, K, H20 reabsorbed

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2
Q

What is reabsorbed in the descending loop of henle?

A

H20

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3
Q

what % is reabsorbed and what ions in the ascending loop of henle?

A

25% Na, Cl, K

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4
Q

What percent and ions are reabsorbed in the distal convoluted tubule?

A

4-8% Cl, Na

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5
Q

What % and ions are reabsorbed in the cortical collecting duct?

A

2-5% Na, H20

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6
Q

what are edematous states you would use a diuretic for?

A

Heart failure, Hepatic Ascites, nephrotic syndrome, premenstrual edema

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7
Q

what are nonedematous states you would use a diuretic for?

A

hypertension, hypercalcemia, Diabetes insipidus

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8
Q

What are the two main clinical uses for diuretics?

A

Abnormal fluid retention
hypertension

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9
Q

What are the loop diuretic drugs?

A

Furosemide
Torsemide
Bumetanide

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10
Q

Furosemide
Torsemide
Bumetanide

A
  • act on ascending loop of henle
  • ## highest efficacy for removing Na and Cl
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11
Q

When would you use loop diuretics?

A
  • Edema associated with heart failure, hepatic and renal disease.
  • mod to severe hypertension
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12
Q

What channel do loop diuretics block?

A

NKCC2

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13
Q

What are the important actions of loop diuretics?

A

increase urine output
increase prostaglandin synthesis

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14
Q

Adverse effects of loop diuretics?

A

ototoxicity
hyperuricemia
acute hypovolemia
hypokalemia
hypomagnesemia
allergic reactions

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15
Q

What are the thiazide drugs?

A

Hydrochlorothiazide
Chlorthalidone
Metolazone

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16
Q

Hydrochlorothiazide
Chlorthalidone
Metolazone

A

act on the distal tubule
Block NCCT channels
acts similarly to loop diuretics

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17
Q

what are clinical applications for Thiazides?

A

Hypertension
Heart Failure
Hypercalciuria (inhibits Ca excretion)
Diabetes insipidus
Premenstrual edema

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18
Q

Thiazide actions

A

decrease in Ca excretion
decrease in PVR

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19
Q

What is half life of Chlorthalidone

A

40-60 hours

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20
Q

Metalozone

A

most potent
Na excretion in advance of kidney failure

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21
Q

Adverse effects of Thiazides

A

Hypokalemia
hyponatremia
metabolic alkalosis
hyperuricemia
hyperglycemia
hyperlipidemia
hypersensitivity
sexual dysfunction

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22
Q

K-sparing drugs (aldosterone antagonists)

A

Spironolactone and Eplerenone

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23
Q

Spironolactone
Eplerenone

A

used when there is excess aldosterone
monitor potassium, can be fatal
acts in collecting tubule

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24
Q

What are the clinical applications of K-sparing drugs?

A

Heart failure (spironolactone)
Hypertension
Primary Hyperaldosterone
Edema

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25
Q

What is MOA of Ksparing drugs

A

antagonizes aldosterone receptors preventing the nuclear complex , thus decrease in Na reabsorption and decrease in K excretion (two way street)

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26
Q

Adverse effects of Ksparing drugs

A

Peptic ulcers
Endocrine effects
hyperkalemia
Nausea, lethargy, mental confusion

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27
Q

Ksparing (na inhibitors)

A

Amiloride
Triamterene

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28
Q

Amiloride
Triamterene

A

blocks Na transporter
not relient on aldosterone
can prevent K loss associated with thiazides and furosemide

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29
Q

Ksparing (na inhibitor) MOA

A

blocks the ENaC
decrease in Na reabsorption
decrease in K excretion

30
Q

Adverse affects of Ksparing (na inhibitors)

A

Hyperkalemia
Hyponatremia
leg cramps
GI upset
Dizziness, pruritus, headache, minor visual changes

31
Q

What is the Carbonic Anhydrase Inhibitor drug?

A

Acetazolamide

32
Q

Acetazolamide

A

CA inhibitor
acts on epithelial cells in proximal tubule
not as efficacious than other diuretics

33
Q

Clinical applications of CA inhibitor

A

Glaucoma
Epilepsy
Mountain sickness prophylaxis
metabolic alkalosis

34
Q

MOA of CA inhibitor

A

inhibits CA
decreases ability to exchange Na for H
decrease ATPase activity
HC03 retained in lumen increasing pH of urine

35
Q

Adverse effects of CA inhibitors

A

Metabolic Acidosis
hyponatremia
hypokalemia
crystalluria
malaise, fatigue, depression

36
Q

What are the osmotic diuretics?

A

Mannitol

37
Q

Mannitol

A

raises osmotic pressure of plasma, drawing water out of the tissues. Directly increases urine volume.

Given IV

38
Q

Clinical applications of Osmotic Diuretics

A

increase urine flow pts with acute renal failure
reduce intracranial pressure & tx of cerebral edema
excretion of toxic substances

39
Q

Osmotic diuretics contradictions

A

Congestive Heart Failure
Pulmonary Edema

40
Q

Adverse effects of Osmotic Diuretics

A

Extracellular water expansion
tissue dehydration

41
Q

ADH Antagonists

A

Conivaptan

42
Q

Conivaptan

A

ADH controls permeability
Conivaptan is a ADH antagonist, so there will be a decrease in water permeability, making dilute urine
V1 and V2 receptors

43
Q

What are the functions of V1 and V2 receptors?

A

V1 -> increases smooth muscle contraction
V2 -> increases h20 permeability and reabsoprtion via aquaporins

44
Q

Clinical applications of ADH antagonists

A

Euvolemic and hypervolemic hyponatremia
syndrome of inappropriate ADH secretion (SIADH)

45
Q

ADH Adverse affects

A

Infusion site reactions (only given IV)
Thirst
Atrial Fibrillation
GI and Electrolyte disturbance
Nephrogenic Diabetes insipidous

46
Q

ADH contradictions

A

Hypovolemic Hyponatremia
Renal Failure

47
Q

What is hypertension?

A

SBP over 130 sustained
DBP over 80 sustained

48
Q

What are antihypertensives supposed to control?

A

Decrease CO
Decrease PR

49
Q

What are the 4 ways in which an antihypertensive can act?

A

Resistance Arterioles
Capacitance venules
Pump output of heart
Volume of kidneys

50
Q

What are the compensatory mechanisms for decreased blood pressure using drugs?

A

Baroreceptor reflex will engage and increase it again

51
Q

How is stage 1 hypertension patients treated?

A

single drug
lifestyle recommendations

52
Q

How are stage 2 hypertension patients treated?

A

multiple drugs
lifestyle recommendations

53
Q

What are first line treatments for hypertension?

A

Ace inhibitors
ARBs
Calcium channel blockers
Thiazides

54
Q

Second line treatment for HTN?

A

B-blockers
Aldesterone Antagonists

55
Q

Captopril
Enalapril
Lisinopril

A
  • ace inhibitors
  • first line for diabetics or pts with Chronic kidney disease
  • inhibit ACE -> cleaves angiotensin 1 to for angiotensin 2
  • decreases PVR by decreasing sodium retention (aldost.)
  • increase bradykinin
  • NO reflex involved in ACE inhibitors
56
Q

Clinical Applications of ACE inhibitors

A
  • hypertension
  • Preserve renal function in pts with diabetic or non diabetic nephropathy
  • effective in tx of heart failure
  • Standard care for pts with MI
57
Q

ACE and ARBS Preserves renal function how?

A

causing dilation to decrease GFR

58
Q

Adverse effects of Ace Inhibitors

A

Dry hacking cough
hyperkalemia
hypotension
angioedema
Acute renal failure
Rash, fever, alter taste

59
Q

When are Ace inhibitors contradicted?

A

Pregnancy -> 1st bc congenital malformation and 2/3 due to fetal hypotension, anuria, and renal failure

Pts with bilateral renal artery stenosis

Pts with history of angioedema with hx of ACE inhibitors

60
Q

Losartan
Valsartan

A

Angiotensin Receptor blockers
first line agents -> if pt is intolerable to ACEI
Blocks angiotension 2 type 1 recp. -> decrease BP -> blocks Aldosterone release -> decreases Na and H20 retention
decrease diabetic nephropathy
NO INCREASE IN BRADYKININ

61
Q

ARBS adverse side effects

A

NO dry cough
angioedema risk is lower
Losartan reduces uric acid by inhibiting URAT1
similar side effects to ACEI

62
Q

Contradictions for ARB

A

Pregnancy
pts with bilateral renal artery stenosis

63
Q

Aliskiren

A
  • renal inhibitor
  • Not first line
    MOA
  • inhibits enzyme activity of renin, prevents conversion of angiotensinogen to angiotensin 1, resulting in inhibition of angiotensin 2 and aldosterone release
64
Q

Adverse effects of Aliskiren

A

similiar to ACEI
Dry cough no not occur-> due to no increase in bradykinin
Angioedema but low rist

65
Q

Verapamil
Diltiazem
Nifedipine
Amlodipine

A

First line agents for black or elderly people
Two classes:
1) Non- dihydropyridines -> verapamil, Diltiazem
2) Dihydropyridines -> Nifedipine, Amlodipine

66
Q

Verapamil

A

Non-dihydropyridine
works mainly on heart and smooth muscle
tx angina, supraventricular tachyarrhythmias, HTN, migraines, and cerebral vasospasm

67
Q

Diltiazem

A

non-dihydropyridine
for heart and smooth muscle
has better side effect profiles
tx same as Verapamil

68
Q

Amlodipine
nifedipine

A

Dihydropyridines
high affinity for vascular calcium channels vs cardiac
txs HTN ( not great for cardiac arrhythmias)
reduces Ca into smooth muscles to cause vasodilation and lower BP

69
Q

Clinical applications for Ca channel blockers

A

Hypertension for black/ elderly pts

70
Q

what can increase risk of MI when referring to Ca Channel blockers?

A

High doses short acting dihydropyridine can incrase MI
sustained release is preffered

71
Q

Adverse side effects of channel blockers

A

Verapamil -> constipation, gingival hyperplasia, inotropic effects
Diltiazem-> negative inotropic effects
Dihydropyridines -> reflex tachycardia, headache, fatigue hypotension, edema