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Anti- HTN & Chronic HF > Day 1 > Flashcards

Day 1 Flashcards

1
Q

Epidemiology

A

Affects 76.4 million Americans
1 in 3 adults has HTN
Lifetime risk is 90%

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2
Q

Risk Factors for HTN

A 
Cigarette smoking
Obesity (BMI ≥ 30)
Physical inactivity
Dyslipidemia
Diabetes mellitus
Renal dysfunction
Age: men > 55 years, women > 65 years
family history of premature cardiovascular disease (age: men < 55, women < 65)
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3
Q

Etiology for 2 types of HTN

A

Essential Hypertension:
> 90% of cases
Hereditary component

Secondary Hypertension:
< 10% of cases
Common causes: chronic kidney disease, renovascular disease

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4
Q

Total Peripheral Resistance (TPR)

A

Sum of peripheral resistance in peripheral vasculature (represents DBP)

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5
Q

Cardiac Output

A

Amount of blood pumped out by the ventricles (represent the SBP)

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6
Q

Systolic and Diastolic BP

A

Systolic BP (SBP): Number that represents the cardiac contraction

Diastolic BP (DBP): Number that represents nadir (lowest point)…filling of the heart

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7
Q

JNC 8 New BP Goals

A

Patients older than 60 = less than 150/90
Patients younger than 60= less than 140/ 90
Patients with DM and CKD= less than 140/90

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8
Q

Mechanism of Pathogenesis for HTN

A

Increase Peripheral Resistance:
Functional Vascular Constriction/Structural Vascular Hypertrophy:
Over activity of sympathetic nervous system
Genetic components

Increased cardiac output (CO):
Increased Preload: 
Increased fluid volume 
Excess sodium intake
Renal sodium retention

Venous Constriction:
Excess RAAS stimulation
Sympathetic nervous system over activity

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9
Q

Non-Pharmacological Therapy for HTN

A 
Smoking Cessation
Weight loss in overweight and obese
DASH diet
Dietary sodium reduction
Increased physical activity
limit alcohol intake to no more than 1-2 drinks/day
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10
Q

First Line Treatment Approaches for HTN

A

First line options:
Thiazides, CCB’s, ACE-I, ARB’s (all equal in choice)
Note: not the best choice to use ACE-I or ARB’s in a black patient

DM or chronic kidney disease:
ACE-I or ARB’s
JNC 8 states do not use them together

Cardiac history:
Beta-blocker

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11
Q

3 Options for Treating HTN

A

1st option:
Start with 1 drug and max the dose and then add on a 2nd agent if still not at goal, and then add on a 3rd agent once the 2nd drug is maxed out if pt. still not at goal.

2nd option:
Start with 1 drug and if not at goal add a 2nd drug prior to maxing out the dose on the first. Then max the dose on both drugs and if not at goal add a 3rd agent

3rd option:
Start with 2 drugs from the beginning if the SBP >160 and/or the DBP >100. Max out the drug doses and add on a 3rd agent if needed.

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12
Q

Thiazide Diuretics MOA

A

Drugs: Hydrochlorothiazide (HCTZ), chlorthalidone, metolzaone
MOA: Inhibits sodium reabsorption in the distal tubule.

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13
Q

Precautions for Thiazide Diuretics

A

Caution in sulfa allergic patients
Ineffective in patients with severe renal disease
Avoid in patients taking lithium– may increase serum lithium concentrations
Avoid in patients with GOUT

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14
Q

Adverse Effects for Thiazide Diuretics

A

Orthostatic Hypotension
Electrolyte abnormalities: ↓ K, ↓ Na, ↑ Ca, ↑ uric acid, ↑ glucose
Photosensitivity
Increase urination (initially)

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15
Q

Place in Therapy and Dose for Thiazide Diuretics

A

One of the first line drug classes used to treat HTN

Dose: Typically 25mg (can start at 12.5mg)

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16
Q

Loop Diuretics

A

Drugs:
Furosemide (Lasix™)
Bumetanide (Bumex™)
Torsemide (Demadex™)

Mechanism of action:
Inhibits active transport of sodium, chloride and potassium in thick ascending limb of Loop of Henle, causing excretion of these ions
Collecting duct excretes more water in response

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17
Q

Place in Therapy for Loop Diuretics

A

NOT 1st LINE TREATMENT
CHF (preferred diuretic)
Edema (both peripheral and pulmonary)
HTN

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18
Q

Adverse Effects for Loop Diuretics

A

Electrolytes abnormalities: ↓ K, ↓Na, ↓ Ca, ↓ Mg, ↑ uric acid
Dehydration
Ototoxicity
Increase in SCr

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19
Q

Precautions for Loop Diuretics

A

Caution in sulfa allergic patients
Nephrotoxicity
Avoid in patients with GOUT

20
Q

Potassium Sparing Diuretics—Aldosterone Receptor Blockers MOA

A

Aldosterone Receptor Blockers:
Spironolactone (Aldactone™)
Eplerenone (Inspra)

Mechanism of Action: Competes with aldosterone, prevents sodium reabsorption and potassium excretion

21
Q

Potassium Sparing Drugs

A

Triamterene
Amiloride
Mechanism of action: blocks sodium reabsorption and potassium excretion, effect independent of aldosterone

22
Q

Potassium Sparing Diuretics Place in Therapy

A

Hypertension, often in combination with thiazide

Spironolactone – Class IV heart failure

23
Q

Adverse Effect for Potassium Sparing Diuretics

A

General: Hyperkalemia (caution in patients with renal failure)
Spironolactone: Gynecomastia, menstrual irregularities
Eplerenone: More selective thus less side effects

24
Q

10 ACE- Inhibitor Drugs

A 
Benazepril (Lotensin)
Captopril (Capoten)
Enalapril (Vasotec)
Fosinopril (Monopril)
Lisinopril (Zestril, Prinivil)
Moexipril (Univasc)
Perindopril (Aceon)
Quinapril (Accupril)
Ramipril (Altace)
Trandolapril (Mavik)
25
Q

MOA of ACE- Inhibitors

A

Inhibits ACE to block production of AT II
Inhibits breakdown of bradykinin (vasodilator)
Benefit: lowers blood pressure
Disadvantage: inflammatory mediator, probably some common adverse effect of ACE-I
Dilate the efferent arteriole of kidney

26
Q

ACE- Inhibitor Place in Therapy

A

One of the first line drug classes in HTN
First line option for CKD
Used in CHF

27
Q

What is the Dose and what do you have to monitor with ACE inhibitors

A

Dose: Often once a day, sometimes twice daily

Monitor:
Serum K+ & SCr within 4 weeks of initiation or dose increase. You will likely see a benign increase in Scr (<30% from baseline)
Angioedemia

28
Q

Adverse Effects of ACE Inhibitors

A

Cough
Up to 20% of patients
Due to increased bradykinin
Angioedema (rare)
Hyperkalemia: particularly in patients with CKD or DM
Other: Neutropenia, agranulocytosis, proteinuria, glomerulonephritis, acute renal failure

29
Q

Contraindications for ACE inhibitors

A

Pregnancy category C/D- contraindicated
Angioedema with other ACE-inhibitors
Renal artery stenosis (increased risk of renal toxicity)

30
Q

Drug Interactions for ACE inhibitors

A

Potassium supplements
Potassium-sparing diuretics
NSAIDs

31
Q

ACE-I Clinical Differences

A

All can be dosed once daily except captopril
Captopril is dosed twice to three times daily
Most may be dosed more than once a day for efficacy

Enalapril is a prodrug of enalaprilat (only one that is available IV)
Most commonly used ACE-I: lisinopril
Dose is 10-40 mg daily
Captopril absorption decreased by 30-40% when given with food

32
Q

Angiotensin II Receptor Blockers (ARB) 7 Drugs

A 
Candesartan (Atacand)
Eprosartan (Teveten)
Irbesartan (Avapro)
Losartan (Cozaar)
Olmesartan (Benicar)
Telmisartan (Micardis)
Valsartan (Diovan)
33
Q

ARB MOA

A

Inhibits angiotensin II at its receptor sites

Does NOT inhibit the breakdown of bradykinin

34
Q

ARB Place in Therapy

A 
Place in Therapy:  
One of the first line drug classes in HTN
First line option for CKD 
Used in CHF
Dose:  Often once daily
35
Q

Adverse Effects of ARB

A 
Hypotension/orthostatic hypotension
Angioedema
Hyperkalemia
Dizziness
Cough (only case reports)
36
Q

What needs to be monitored with PT taking ARB’s

A

Potassium

Angioedema

37
Q

Contraindications for ARB’s

A

Pregnancy category C/D- should not be used
“Caution” in pts with renal artery stenosis
ARBs CAN be used in patients who have experienced angioedema when taking an ACE inhibitor- but use caution.

38
Q

Drug indications for ARB’s

A

Potassium supplements
Potassium-sparing diuretics
NSAIDs

39
Q

Renin inhibitor- Aliskiren

A

First oral agent that directly inhibits renin
Role in treatment of hypertension is unclear as it is a new agent
Can be used as monotherapy or in combination
ADRs are similar to ACE inhibitors; and similar to ACE inhibitors, this drug should not be used in pregnancy

40
Q

MC Beta Blockers

A 
Most common:
Atenolol: once a day
Metoprolol Succinate:  Once a day
Metoprolol Tartrate:  Twice a day
Sotalol (Betapace)
Class III anti-arrhythmic  agent

Dose: Depends on the beta-blocker

41
Q

Beta Blockers Place in Therapy

A 
Place in Therapy:  Not a first line
Reserved for patients that have significant cardiac history
Heart failure
Post-MI
High coronary artery disease
CKD
42
Q

MOA for Beta Blockers

A

Beta-1 receptors; located in heart and beta-2 receptors are located in the lungs
Beta-blockers block beta-1 receptors thus decreasing the effects of epinephrine, and nor-epinephrine which therefore decrease BP and HR

43
Q

Beta Blocker Differences

A

Cardioselectivity (dose-dependent)
AMEBBA: Atenolol, metoprolol, esmolol, bioprolol, betaxaolol, acebutolol

Mixed α and β blockers
Carvedilol and labetalol

ISA (intrinsic sympathomimetic activity)
CAPP: (Carteolol, acebutolol, penbutolol, and pindolol)

Non-Specific
Nadolol, propranolol, timolol

44
Q

Common Adverse Effects for Beta Blockers

A

Initial: “Beta-blocker blues”: tired, fatigued, depressed, and their chest might feel “different” due to change in heart beat
Other: Sexual dysfunction, rebound HTN if suddenly discontinued

45
Q

Relative Contraindications for Beta Blockers

A

Asthma and COPD (bronchospasm)
Diabetes (masks hypoglycemic response except sweating)
Severe peripheral vascular disease (decreased output can worsen symptoms)
Heart block
Severe acute heart failure
Pregnancy category C

Anti- HTN & Chronic HF (4 decks)

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