Renal Pharm Flashcards

1
Q

What are the indications for -afil medications?

A

sildenafil, tadalafil, vardenafil, avanafil = erectile dysfunction

tadalafil can also be used to benign prostatic hyperplasia

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2
Q

What is the MOA and effects of -afil medications?

A

sildenafil, tadalafil, vardenafil, avanafil

MOA - 5PDE inhibitors
- increases cGMP = increased smooth muscle relaxation in reaction of NO activation

Effects:
- pulmonary vasodilation
- penile smooth muscle relaxation
- increased blood flow

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3
Q

What are the AEs and contraindications of -afil medications?

A

silfenafil, tadalafil, vardenafil, avanafil

AEs
- headache, lightheadedness
- exanthema, flushing
- visual changes: photophobia, optic neuropathy
- runny nose, nasal congestion
- RARE: MI, stroke, hearing loss

Contraindications
- NITRATES: hypotension
- alpha blockers
- pregnancy category X

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4
Q

What is the injectable medication for erectile dysfunction? What’s its MOA?

A

alprostadil
injection into the corpus cavernous or into urethra via catheter

MOA: vasodilation via direct effect on vascular + ductus arteriosus

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5
Q

What are the AEs of alprostadil being injected into the penis? What are its contraindiactions?

A

AE
- hypotension/syncope
- penile fibrosis
- priapism/prolonged erection

contraindications:
priapism
anatomic/fibrotic conditions of penis
penile implants
issues with urethra
pregnant partner

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6
Q

What are the drugs that can exacerbate ED?

A

blood pressure medications
antidepressants
opioids
antihistamines
NSAIDs
parkinson’s meds
antiarrhythmics
Histamine H2 receptor antagonists
muscle relaxants
prostate cancer meds
chemotherapy drugs

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7
Q

What are the drugs that can exacerbate BPH/LUTS?

A

opioids
tricyclic antidepressants
antihistamines
decongestants
phenothiazine
alpha-adrenergic receptor agonists
testosterone
anticholinergics

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8
Q

Describe the carbonic anhydrase inhibitors and their MOA. What kind of med is it?

A

acetazolamide - diuretic

MOA: prevents reabsorption of sodium bicarbonate in the PROXIMAL TUBULE

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9
Q

Describe the thiazide medications. What are their MOA and early and late effects?

A

HCTZ, chlorothiazide, chorothiadone, metolazone

MOA: inhibits Na-Cl cotransporter on the DISTAL CONVOLUTED TUBULE
- early: decrease volume via natriuresis
- late: decrease systemic vascular resistance

general:
increases EXCRETION of Na, Cl, K
increases RESORPTION of Ca + decrease excretion of Ca

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10
Q

Describe the thiazide medications. What are their applications and adverse events?

A

HCTZ, chlorothiazide, chorothiadone, metolazone

applications:
HTN
edema secondary to CHF, cirrhosis, CKD
prevention of Ca kidney stones, hypercalciuria
osteoporosis
nephrogenic diabetes insipidus

AE:
hyponatremia
hypokalemia + metabolic acidosis
hyperglycemia
hypomagnesium

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11
Q

Describe the loop diuretics. What is their MOA and effects?

A

furosemide, bumetadine, torsemide, ethycrynic acid

MOA: inhibits Na/K/2Cl symporter on the THICK ASCENDING LOOP OF HENLE

general effects:
loss of Na, Ca, H2O (loops lose Ca)
hypokalemic metabolic acidosis

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12
Q

Describe loop diuretics. What are their applications and AEs?

A

furosemide, bumetadine, torsemide, ethycrynic acid

Applications:
HTN
hypercalcemia management
management of edema with HF, cirrhosis, CKD
ACUTE PULMONARY EDEMA

AEs
hypokalemia, hypo magnesium
cramping
hypotension
OTOTOXIC: hearing decrements - potential permanent hearing damage

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13
Q

Describe the K sparing diuretics. What is their MOA?

A

spironolactone, epleronone, triamterene, amiloride

MOA: blocks aldosterone-mediated Na-K anti porter in the COLLECTING DUCT

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14
Q

Describe alpha blockers. What are their uses and MOA?

A

tamsulosin, doxazosin, terazosin, silodosin, alfuzosin

MOA: alpha blocker
- inhibits a1 receptors in the bladder neck + prosthetic urethra = relaxes smooth muscle
- decreases resistance to urinary flow

first line for small prostate BPH
- immediate effect to help LUTS

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15
Q

Describe alpha blockers. What are there AEs and contraindications?

A

tamsulosin, doxazosin, terazosin, silodosin, alfuzosin

AE
- dizziness, orthostatic HTN, syncope
- fatigue, asthenia
- effects on ejaculatory function
- inoperative floppy iris syndrome: progressive, miosis despite preoperative dilation (tamsulosin)

contraindications - no absolute
- some metabolized by CYP3A4
- alfuzosin/siludosin with meals
- tamsulosin 30 min after meal

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16
Q

Describe the 5-alpha reductase inhibitors. What is their MOA and uses?

A

finasteride, dutasteride

MOA: 5-alpha reductase inhibitor = decreases conversion of T to DHT
- decreased DHT in prostate = decreased growth + increased apoptosis
- reduces prostate volume + decreases risk of acute urinary retention

first line for large prostate BPH
- takes about 6 months for effects to be seen

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17
Q

Describe 5-alpha reductase inhibitors. What are their AEs and contraindications?

A

finasteride, dutasteride

AEs
- nausea, abdominal pain, flatulence
- headache, dizziness
- asthenia, muscle weakness
- decreased libido, ED, gynecomastia
- decreases serum PSA by 50%

contraindications - pregnancy category X

18
Q

Describe the anticholinergic meds. What is their indication of BPH? Describe their MOA

A

tolterodine, darifenacin, oxybutynin, trospium, solifenacin

MOA: inhibits parasympathetic muscarinic receptors on detrusor smooth muscle cells
- decreased muscle tone = symptomatic improvement of overactive bladder

indication: consider in pts with irritable BPH-LUTS in men without an elevated post-void residual

19
Q

Describe the anticholinergic meds. What are their AEs and contraindications?

A

tolterodine, darifenacin, oxybutynin, trospium, solifenacin

AEs
- dry mouth
- constipation
- micturition difficulties
- nasopharyngitis
- dizziness

contraindications
PVR volume > 250 mL: can decreased bladder strength + care urinary retention

20
Q

Describe the beta agonists. What are their indications, MOA, and AEs

A

mirabegron, vibegron

MOA: relaxation of the bladder detrusor muscle + increases bladder capacity

can be user in combination with alpha blockers for BPH

AEs
- increased post-void residual
- HTN

21
Q

Describe the K sparing diuretics. What are their applications and AES?

A

spironolactone, eplerenone, triamterene, amilodride

applications:
spironolactone
- ascites (cirrhosis)
- HFrEF
- Chronic HTN
- hyperaldosteronism

Eplerenone: chronic HTN, post MI with HFrEF

AEs:
- hyperkalemia
- spironolactone: gynecomastia
- triamterene: kidney stones

22
Q

Describe the vasopressin agonist diuretics. What is this MOA, indication, and AEs?

A

tolvaptan, conivaptan

MOA - blocks V2 to promote aquaresis in the COLLECTING DUCT

indication: correction of hyponatremia

AEs: hepatotoxicity, hypernatremia, third

23
Q

Describe the osmotic diuretics. What are their MOA, indication, and AES?

A

mannitol

MOA: non-metabolized sugar increases the osmotic pressure of glomerular filtrate
- inhibits the tubular reabsorption of water and electrolytes
- promotes diuresis

indication:
- elevated intracranial/intraocular pressure
- urogenital irrigation

AE:
- hypotension
- hypovolemia
- can crystalize at room temp
- nephrotoxic

24
Q

Describe the -pril medications. What are their MOAs

A

ACE inhibitors: lisinopril, benazepril, captopril, -pril

MOA: blocks angiotensin converting enzymes
- prevents conversation of angiotensin I to II = decreased vasoconstriction
- decreases afterload + lowers BP

25
What are the -pril medications, their AEs and their contraindications?
ACE inhibitors: lisinopril, -prils AEs: - hypotension/syncope - dizziness - first dose hypotension - hyperkalemia - AKI - cough - angioedema contraindications: BLACK BOX WARNING - pregnancy
26
Describe the -sartan medications. What is their MOA?
ARBs: valsartan, losartan, -sartan MOA: selectively blocks angiotensin II from binding to angiotensin II receptor - decrease angiotensin II mediated vasoconstriction - decreases afterload = lowers BP
27
Describe the -sartan meds. What are their AEs and contraindications?
ARBs: valsarta, losartan, - sartan AEs - first dose hypotension - hyperkalemia - AKI - angioedema contraindications: BLACK BOX WARNING - pregnancy
28
Describe the drug aliskiren. What is its MOA, AEs and contraindications?
MOA: selectively blocks renin from activating RAAS - decrease angiotensin II-mediated vasoconstriction upstream - decreases afterload = lowers BP AEs: - diarrhea - hyperkalemia - hypotension contraindications: Black box warning - pregnancy
29
What are the dihydropyridine calcium channel blockers? Describe their MOA
DHP-CCB: amlodipine (long), nitrendipine (intermediate), nifedipine (short) MOA: binds to + blocks L-type calcium channels in myocardium and vascular smooth muscles - potent vasodilators with minimal myocardial depressant activity - decrease afterload + contractility
30
What are the AEs and contraindications for dihydropyridine calcium channel blockers?
DHP-CCB: amlodipine (long), nitrendipine (intermediate), nifedipine (short) AE - related to hypotension: - headache - peripheral edema (esp amlodipine) - flushing - reflex tachycardia (esp nifedipine) - gingival hyperplasia contraindications: - symptomatic hypertension - acute coronary syndrome - pedal edema - hypertrophic obstructive cardiomyopathy - severe stenotic heart valve defects
31
Describe the nondihydropyridine calcium channel blockers. What are their MOAs?
nondihydropyridine CCB: verapamil, diltiazem MOA: bind + block L-type calcium channels in myocardium + vascular smooth muscle - potent myocardial depressant - decreases afterload + contractility - diltiazem: moderate vasodilatory activity - Class IV anti arrhythmic
32
What are the AEs and contraindications for nondihydropyridine calcium channel blockers?
nondihydropyridine CCB: verapamil, diltiazem AEs: - decreased contractility - bradycardia - AV block - gingival hyperplasia - verapamil: constipation, hyperprolactinemia contraindications: - BETA BLOCKERS: AV block - symptomatic hypertension - acute coronary syndrome - preexisting cardiac conduction disorder: bradycardia, AV blocks
33
Describe the alpha 1 blockers. What are their MOA and their indication?
alpha 1 blockers - doxazosin, prazosin MOA: antagonize alpha 1 receptor on vascular smooth muscle - vasodilator peripheral vascular smooth muscle = decreased afterload adrenergic agent used in hypertension
34
What are the alpha 2 receptor agonists? What are their MOAS?
general MOA: activate the alpha 2 receptors in the presynaptic sympathetic NS - increased presynaptic feedback = decrease NE release - causes centrally-mediated vasodilation selective agents: methyldopa, guanfavine, guanibenz non-selective: clonidine - alpha 2 receptor - imidazoline receptor
35
Compare and contrast the nondihydropyridine and dihydropyridine calcium channel blockers
MOA: block the L-type calcium channels in myocardium and vascular smooth muscle dihydropyridines: amlodipine, nitrendipine, nifedipine - preferentially dilates vascular smooth muscle non-DHP: diltiazem, verapamil - preferentially depresses conducting at the AV/SA node; Class IV antiarrhytmic - this is why they cannot be used with beta blockers: can cause heart block
36
Renin inhibitors and ACEi/ARBs are contraindicated. Why?
can induce hyperkalemia aliskiren + -prils/-sartans
37
List the 5 types of antihypertensives. Give some examples
1. diuretics: thiazides, furosemide, spironolactone 2. RAAS inhibitors: ACEi (-prils), ARBs (-sartans) 3. Calcium channel blockers: - dihydropyridines: amlodipine (-pines) - nondihydropyridines: verapamil, diltiazem 4. adrenergic agents: - alpha 1 blockers: -zosins - alpha 2 agonists - clonidine - beta blockers: -olols 5. direct-acting vasodilators: hydralazine, minoxidil
38
What are the first line recommendations for someone starting anti-HTN therapy?
All ages with/out DM: thiazide, ACEi, ARB, CCB CKD with/out DM: ACEi, ARB Lifestyle recommendations for all
39
What is step 1 of hypertensive therapy and who is it for?
step 1 - mono therapy - elevated BP with high-risk condition - ≥ 75 - 140-159/99 with ASCVD ≥ 10% general: begin and proceed with the same med class until the class if no well tolerated
40
What is step 2 hypertensive therapy and who is it for?
Step 2 - dual therapy - 160/110 dual therapy > high doses of mono therapy - shown to achieve BP target with lower incidence of side effects - DON'T use ACEi/ARB together