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Pharm 2 > HTN > Flashcards

HTN Flashcards

1
Q

JNC 8 guidelines

A
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2
Q

AHA/ACC

A
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3
Q

When do we treat HTN?

A
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4
Q

Do differences exist among different populations for the tx of blood pressure?

A

HTN pathophys: low renin htn, high/medium htn
Plasma renin activity used to predict bp response to antihypertensive agents
AA: have higher salt sensitivity and MARKEDLY LOWER PLASMA RENIN LEVELS= DECREASED RAAS =use CA CHANNEL BLOCKER AND DIURETICS
South Asians: higher central obesity and insulin resistance-> htn driven by higher sympathetic activity
Caucasian: respond better to BB- ACE or ARBs

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5
Q

Age and HTN tx

A

Younger pts (under 50)= better with ACE, ARB, or BB
Older (over 60)= Diuretic or CCB

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6
Q

Factors that lead to BP elevations

A

Please Think About Common Sources When Practicing

Primary HTN
Technique- bp cuff, back supported
Anxiety
Compliance
Secondary HTN
Withdraw
Pain

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7
Q

Common therapies for htn

A

*1ST LINE. ACE, ARB, THIAZIDES, CCB
*ALTERNATIVE: ALDOSTERONE ANTAGONISTS, bb, alpha blocker

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8
Q

1st line htn jnc 8 guidelines

A

ACE and ARB DONT MIX BC HYPERKALEMIA

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9
Q

Targets for reducing bp

A
  1. BP=CO* TPR-> reduce CO or TPR
  2. decrease bp by reducing HR
  3. decrease bp by reducing SV
  4. decrease bp by reducing PR
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10
Q

Antihtn drug classes

A

A- ACE- pril- inhibit ACE= decrease SVR, SV
A- ARBS- sartan- block angiotensin 2 receptors= SVR, SV
A-Alpha blockers-osin- Doxazosin- block alpha receptors- SVR
B- Beta blocker- lol- Block beta receptors- HR, SV
C- CCB- dipine- block Ca channels- SVR
D- Diuretics- ide- SV

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11
Q

What can I expect from BP meds?

A
  1. Monotherapy @ mean doses= SBP reductions btwn 10-15 mm hg
  2. DBP w/ monotherapy= 5-10 mm hg
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12
Q

Agents that block the production of action of Angiotensin 2

A
  1. ACE
  2. ARBS
  3. Renin Inhibitors
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13
Q

Why do we use ACE inhibitors in htn?

A
  1. increase Vasodilation
  2. most useful when renin is Elevated or when Diuretics/CCB renders bp renin dependent
  3. INDIRECTLY DECREASES ALDOSTERONE SECRETION- higher volume, higher SV
  4. reduce risk of stroke
  5. Slow progression of diabetic nephropathy
    VD OF AFFERENT VESSELS OF KIDNEY= DECREASE DIABETIC NEPHROPATHY
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14
Q

When do we use ACE inhibitors?

A

PPPHHD
Pediatric HTN- doc w/ HTN
Post MI-1st line for all pts to reduce mortality- EVEN IF AA
Proteinuria- 1st line all pts- EVEN IF AA
Hypertension- 1st choice for non AA pts, and YOUNG PTS
Heart failure- 1st line for all pts with reduced Ejection fracture to reduce mortality
Diabetes Mellitus- 1st line for all pts

90% bp effect @ 20 mg lisinopril (dont go up-> add med)

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15
Q

ACE inhibitors- Renal disorders

A
  1. Renally protective= decrease proteinuria, stabilize kidney fxn, decrease pressure in afferent and efferent arterioles thru dilation (improve intraglomerular cap pressure)
  2. Good for HTN pts with renal disease-> Diabetic nephropathy and CKD
  3. Caution with AA pts
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16
Q

ACE inhibitors- Heart disease

A

Prevents LV remodeling after MI and in HF- 1st drug used in pts with LVDysfunction= Reduce preload/afterload/ slows progression of HF

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17
Q

ACE inhibitors- Adverse Effects

A

HACH
COUGH- SECONDARY TO INCREASED BRADYKININ LEVELS
ANGIOEDEMA- SECONDARY TO BRADYKININ
CONTRAINDICATED: PREGO AND BILAT RENAL ARTERY STENOSIS
HYPOTENSION- DIZZINESS
Hyperkalemia
Transient increases in Serum Creatinine at initial therapy-> DC if INCREASE OVER 30% IN 1ST 2 MONTHS OR IF HYPERKALEMIA DEVELOPS ANYTIME-> will decrease GFR and increase Creatinine bc decrease volume

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18
Q

ACE drug interactions

A

PLAN B
Potassium-sparing diuretics/potassium supplements- higher risk of HYPERKALEMIA
Bactrim-> increased HYPERKALEMIA
NSAID-> antagonism
Lithium levels increase
Additive effects with other hypertensives
MONITOR CREATININE AND SERUM POTASSIUM

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19
Q

Angiotensin Receptor Blockers ARBS -sartans

A

Use 1st instead of ACE
MOA: block binding of Angiotensin 2 to AT1 receptor
Target: Renin-angiotensin-aldosterone system (RAAS)
USED FOR DIABETIC NEPHROPATHY and CANT TOLERATE COUGH OF ACE
for AA due to angioedema w/ ACE (lower risk of bradykinin issues)
*Telmisartan (Micardis)- 24 hr half life so less peaks adn troughs
*Olmesartan (Benicar)- 12 hr half life

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20
Q

ARB adverse effects

A

PAL- Potentiate, antagonize, Lithium
No bradykinin effects
Hypotension- monitor
Hyperkalemia
insomnia, cramps, rare rhabdomyolysis
Antagonize NSAIDS-> potentiate CCB, digoxin, lidocaine, lithium levels increased
Monitor Cr/K- initial start increase- slight risk of angioedema

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21
Q

Diuretics

A

Thiazides
loop
Potassium sparring

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22
Q

Thiazides - Water pills

A

thiazides, loop diuretics, potassium sparing diuretics, carbonic anhydrase inhibitors, osmotic diuretics, Antidiuretic hormone antagonists
- increases Urine Volume by acting on diff parts of nephron
- natriuretic causes increase in renal sodium excretion
-lower bp by increasing secretion of sodium and decrease BV

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23
Q

Clinical uses of diuretics

A

Edematous states- loops work
-hf
-kidney disease and renal failure
-hepatic cirrhosis
-idiopathic edema

Non-edematous states- thiazides work
-htn
-nephrolithiasis
-hypercalcemia
-renal and cardiac protection

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24
Q

Common diuretics used in HTN

A
  1. Thiazides
  2. Loop diuretics
  3. Potassium sparing diuretics, including mineralocorticoid receptor antagonist
    CKD ALWAYS NEED DIURETICS, some people hide fluid well
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25
Q

Thiazides and Thiazide like

A

hydrochlorothiazide (HCTZ)(dont use) and chlorthalidone (thalitone)(24h half life and better bp control)
Indications: HTN, peripheral edema, HF
-Mainstay of htn tx -> most widely used diuretic
-1st line: ALL RACES, AA TOO
-Sulfonamide derivative-> caution w/ sulfa allergy
-diminish the use of NSAID bc inhibit prostaglandins which decrease renal bf
-Diuresis immediately but effect bp may take 1-2 months
- give in AM

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26
Q

Thiazides MOA

A

MOA: early part of Distal Convoluted Tubule (DCT)-> inhibit NACL- channel (cotransporter)
- reduce PVR by reducing BV-> reduce CO
-BV returns to normal in few months but antihypertensive effects continue

What happens in the distal convoluted tubule? 5-10% of NACl- reab via the cotransporter-> impermeable to water so filtrate becomes more diluted

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27
Q

Which thiazide should you use?

A

1. Chlothalidone
-half life 40 hr due to slow absorption rate
-preferred bc of longer half life and improve bp control over entire day
2. Hydrochlorothiazide HCTZ- 6-15 hr half life

current tx guidelines do not recommend one thiazide over another

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28
Q

Thiazide Side effects

A

-*Hypokalemia
-Hyponatremia
-Hypomagnesemia
-Hyperuricemia- higher dose diur assoc w/ gout
-Hyperglycemia- unknown- pt specific
- may increase total serum cholesterol and LDLs
Allergic rxn- being sulfonamides

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29
Q

What should you do if the pt develops hypokalemia while taking a thiazide diuretic?

A

-start Potassium Chloride supplement
-change to Dual therapy med-> add ACE or ARB, Triamterene/hydrochlorothiazide (Maxzide)
-stop thiazide and change to a Potassium Sparing Diuretic- can be on multiple diuretics

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30
Q

Thiazide drug interactions

A
  1. Additive/synergistic effects-hypovolemia, electrolyte abnormalities
  2. NSAIDS- decrease diuretic efficacy
  3. Digoxin- see arrhythmias if hypokalemic
  4. Dofetilide (special class 3 antiarrhythmic)- Contraindicated due to life threatening arrhythmias
  5. Li- increased levels with long term use
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31
Q

Loop Diuretics OVERVIEW

A

Furosemide (Lasix), Torsemide (Demadex) (better bioavail, greater potency), Bumetanide (Bumex)(better bioavail, greater potency)
MOA: inhibit NA/K/2Cl transporter int he thick ascending loop of Henle’s loop
Effect: increase Sodium in filtrate -> more water in filtrate-> and Potassium-> decreases water reabsorption
- hepatic metabolism/renal elimination
-pts bcome REFRACTORY TO RX- sometimes add thiazide
-highly PROTEIN BOUND
-GREATEST DIURETIC EFFECTS bc 25% of sodium gets reabsorbed in ascending loop
-ABILITY TO CAUSE DIURESIS IN PT W/ RENAL IMPAIRMENT
-DOSING IS DEPENDENT UPON RESPONSE THRESHOLD- PT SPECIFIC

32
Q

Loop Diuretic Side Effects

A

Diuresis related issues
-Hypokalemia, Hypomagnesemia, Hyperuricema = Electrolytes
-Hypotension
-Hyperglycemia
OTOTOXICITY-> reversible- pts in renal failure/impairment
hypersens rxn bc sulfonamides

33
Q

Potassium Sparing Diuretics overview

A

Mineralcorticoid receptor antag= Spironolactone (Aldactone)
Na+ ion channel inhibitors (ENaC channels)= Amiloride (Midamor)
MOA: antagonists of the effects of Aldosterone in collecting tubules via 2 paths
1. Direct antagonism of mineralcorticoid receptors-> prevent exchange of sodium for potassium- spironolactone
2. Inhibit sodium entrance via ion epithelial sodium channels (ENaC) in luminal mem- Amiloride

GOOD FOR RESISTANT HTN- 3 MEDS AND 1 IS A DIURETIC

34
Q

Why are we targeting aldosterone?

A

-Increases resorption of sodium
-Increases Resorption of water
-Increases renal excretion of potassium
-Causes myocardial and vascular fibrosis

35
Q

Potassium- sparing diuretic indications

A
  • Weak diuretic/antihypertensives when Monotherapy
    For pts with significant edema where two diuretics are needed for htn
    1.Triamterene- Triamteren/hctz (Maxzide)
    2. Amiloride- Amiloride/HCTZ (Moduretic)
    MINERAL CORT ANTAG- USED OFTEN IN RESISTANT HTN AND HF= EFFECTIVE WHEN ASSOC W/ EDEMA FROM HYPERALDOSTERONISM (tumor on adrenal glands, bilateral renal hyperplasia

spironolactone- diuretic for hepatic cirrhosis w/ascites, breast growth in male to female transgender transition, acne (androgen effects), PCOS

36
Q

Potassium sparing diuretic - Adverse Effects

A

-*Hyperkalemia- specifically with Amiloride= caution with DM and Renal disease-> monitor pts on ACE inhibitors/ARB, Bactrim
-Blue urine= Triamterene
-GYNECOMASTIA- Spironolactone

37
Q

Carbonic Anhydrase inhibitors overview

A

one of 1st diuretics
inhibits carbonic anhydrase-> increase amount of sodium remaining in lumen of PCT->decrease reabsorption of Bicarbonate->increases Secretion

Shortcomings: diuretic effect decreases significantly with use over days bc Na reabsorption back into plasma-> reduced bicarb enhances NaCl reabsorption by remainder of nephron

38
Q

Carbonic Anhydrase Inhibitor MOA

A

MOA: diuretic by reducing reabsorption of bicarb in the pct (retained in lumen)->bicarb uses sodium hydrogen exchanger so significant reduction in Na+->Na reabsorbed in distal parts where its exchanged for potassium-> late reabsorption leads to increased potassium secretion- HYPOKALEMIA-> loss of bicarb thru urine= developing METABOLIC ACIDOSIS

39
Q

Urine Acidification and Carbonic Anhydrase

A
  1. In the PCT: H+ combines w/ HCO3- to form carbonic acid (H2CO3)
  2. CAH converts H2CO3 into Water and CO2. CO2 freely diffuses back into the cell.
  3. In the renal tubular cell: CAH converts the CO2 and cytoplasmic H2O into H2CO3. H2CO3 readily dissociates into H+ and HCO3-.
  4. HCO3- transported through cell’s basolateral membrane into the bloodstream

Decrease Bicarb in blood = Acidic-> no H+ exchange for Na-> pee it out tho= Metabolic acidosis-> breathe out CO2 = use for altitude sickness

Blood pH maintained= 7.4 altering urine pH=-> recycle bicarb= stops swing of pH

40
Q

Carbonic Anhydrase uses

A

*Altitude sickness
*Glaucoma
*Idiopathic intracranial htn - pseudotumor cerebri

41
Q

Carbonic Anhydrase inhibitors- Glaucoma tx

A

Dorzolamide opthalmic 2% susp TID
*Acetazolamide- oral tab
MOA: block carbonic anhydrase in the ciliary body of the eye which secretes bicarb-> blocks water flow into eye stopping aqueous humor production-> reduces intraocular pressure by 26%-> TX is Lifelong

42
Q

Carbonic Anhydrase inhibitor- Altitude sickness tx

A

*Acetazolamide - oral- 24hours prior to ascent
USED FOR TX AND PREVENTION OF ALTITUDE SICKNESS
prevents minor and major SE: pulmonary and cerebral edema, dizziness, weakness, n/v
- makes all soda taste flat
IS A SULFA DRUG= USE WITH SALICYLATES CAN CAUSE METABOLIC ACIDOSIS

43
Q

Carbonic anhydrase inhibitors SE

A

*Hypokalemia and makes carbonated beverages taste flat
-type 2 renal tubular acidosis, metabolic acidosis

44
Q

Osmotic Diuretics MOA

A

MOA: increase in urine flow by pulling fluid-> elevates glomerular filtrate osmolarity-> interferes directly with osmosis

45
Q

Antidiuretic Hormone Antagonists

A

Conivaptan (V1a and V2), Tolvaptan (V2) —– Nephrology prescribe
Indications: Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) and HF
MOA: inhibits effects of antidiuretic hormone in collecting tubule

3 vasopressin receptors: V1a, V1b, and V2= V1 is vasculature and CNS, **V2 receptors in Kidney

46
Q

antidiuretic Hormone Antagonists (ADH) - explanation

A

LAST DITCH EFFORT
ADH secretion-> stim by HYPONATREMIA
-adh stops diuresis naturally bc causes significant water retention

SIADH shows elevated levels where dangerous levels of Hyponatremia due to plasma dilution:
-small cell lung cancer-> secretes adh
-2ndary cause of HTN
-Amiodarone

ADH antagonists:
-stop the affects of ADH-> used for HYPONATREMIA

47
Q

Where Meds work in the nephron?

A
48
Q

Vasodilators

A

Relax smooth of arterioles-> decreased sys vascular resistance

some relax veins as well - nitroprusside and nitrates

49
Q

Calcium Channel blockers overall

A

Indications: Antianginal effects, antiarrhythmic effects, antihypertensive effects
1. Dihydropyridines (Arteries/arterial)
-Amlodipine (angina, HTN)
-Nifedipine (angina, htn, raynaud, prego)
2. Non-Dihydropyridines (Rate & rhythm)
-Verapamil (angina, htn, ARRYTHMIAS)
-Diltiazem

50
Q

Calcium channel blocker classes

A
  1. dihydropyridines
    - POTENT vasodilators
    -preferred for HTN
  2. non dihydropyridines
    - LESS VD EFFECT
    -Greater inotropic effects-> NOT FOR HF
51
Q

How calcium blockers tx htn, angina, and arrhythmia

A
52
Q

CCB SE/ Toxicity

A

Verapamil and Diltiazem:
-Brady
-AV block
-HF worsen and cause

TOXICITIES-> may require D/C therapy
-PERIPHERAL EDEMA, headache, dizziness-> secondary to DIHYDROPYRIDINES (amlodipine) diuretics wont tx

53
Q

CCB vs CCB with RAS

A

CCB= VD arteries, veins remain VC-> capillary overload forces fluid into surrounding tissue
CCB w/ ACE= RAS inhibitor dilates Arteries and Veins-> reduces CCB induced peripheral edema

54
Q

CCB additional info

A
  • ALL are effective for HTN
  • Doses for angina are similar to HTN doses
    -Best to work in combos
    -best for low renin state

Used in other conditions:
-Migraine prophyl= Verapamil
-Preterm labor inhibition- nifedipine

55
Q

Other Vasodilators

A
  1. Hydralazine- Severe HTN and HF
    -SE: HA, NAUSEA, ANOREXIA, PALPITATIONS, FLUSHING
    -pts with IHD-> reflex tachycardia and symp stim can provoke angina
    -highdoses= Lupus like syndrome (arthralgia, myalgia, skin, rashes, fever)-> MONITOR ANA/CBC
  2. Minoxidil
    -TX resistant HTN
    -SE: hypertrichosis- Wolf man syndrome
  3. Nitroprusside
    -HTN emergencies, severe heart failure
    SE: cyanide toxicity and methemoglobinemia
56
Q

Sympathoplegic (Sympatholytic) agents- alter the sympathetic nervous system function

A

Catecholamines-> Adrenoceptors-> alpha, beta, dopamine
A1: VC
A2: decrease symp
B1: BP
B2: VD

57
Q

Sympathoplegic agents: Peripheral alpha (A1) blockers

A

Doxazosin (Cardura), PRAZOSIN (MINIPRESS), Terazosin (Hytrin)
Indications:
-HTN- combo with first-line agents
-BPH- Tamsulosin Alpha1a target
Nightmares in PTSD (Prazosin off label use)

MOA: Selectively blocks Alpha1 adrenoceptors= blockade leads to relaxation of vascular sm-> VD and Decreased BP (receptors are in sm and heart)

SE:
-FIRST DOSE PHENOMENON: orthostatic hypotension, dizziness, palpitations, especially on 1st dose (give at bedtime)
-HA, NERVOUSNESS, NASAL CONGESTION

NOT FIRST LINE ANTI HYPERTENSIVES

58
Q

Centrally acting alpha 2 agonist agents

A

Clonidine (Catapres TTS) or Methyldopa (Aldomet)
Indications: alt med for htn in non prego adults, htn in PREGO, prego induced hypertension
MOA: Stim alpha 2 in the brain-> decreased symp outflow and increased vagal tone (block norepi)
Benefits: decreased HR< CO, PVR, Renin
AE: CNS DEPRESSION, SLEEP DISTURBANCE, NIGHTMARES
Sodium and water retention
Anticholinergic effects: sedation, dry mouth, constipation
Drug interactions: CNS depressants, Antihypertension= BETA Blockers= compounding

DO NOT STOP ABRUPT-> REBOUND HTN AND TACHY (compensatory norepinephrine release after D/C-> ALWAYS TAPER

Other uses: ANXIETY, ADHD, withdrawl from alcohol and narcotics

59
Q

Beta Blockers -lol= not 1st line unless HF post MI

A

(Preferred for htn) Cardioselective: Atenolol, metoprolol tartrate
mixed alpha and beta: Labetalol= 1st line prego

60
Q

Vasodilating Beta Blockers

A

Carvedilol & Labetalol= also block alpha 1 receptors-> blunting VC effects of norepinephrine
Nebivolol= antagonist on cardiac beta 1 receptors-> increase NO availability
Diabetes: Nebivolol and Carvedilol best choices of beta blocker to add in diabetics

61
Q

Beta blockers in general

A

Common uses: htn, hf, arrhythmias, Post MI, MIGRAINE PROPHYL & tremors (PROPRANOLOL)
AE: hypotension, bradycardia, FATIGUE, SEXUAL DYSFXN, MASKED HYPOGLYCEMIA
Interactions: other cardiac drugs-> hypotension and iatrogenic heart failure

62
Q

Sympathoplegic agents: BB and HTN- not 1st line BP

A

MOA: reduce bp by reducing CO and inhibit renin angiotensin aldosterone system
Indications w/ htn: NEVER 1ST LINE-> only 1st line with Compelling indications= HFrEF or stable ischemic heart disease (chronic stable angina)

AVOID IN PTS OVER 60 YRS OF AGE UNLESS COMORBIDITY-> falls, depression, fatigue
MORE SENS TO SYMP INHIBITION-> ORTHOSTATIC HYPOTENSION, DIZZY-> INCREASED FALLS

63
Q

Specific indications for BB- all highlighted

A

htn: Atenolol and Metoprolol
Cardiac dysrhythmias: Metoprolol
HF: Bisoprolol, Carvedilol, Metoprolol sustained release
Glaucoma: Timolol
MI: Carvedilol, metoprolol (tartrate or succinate), bisoprolol
Pre eclampsia: Labetalol
MIGRAINE PROPHYL, TREMORS, PORTAL HTN, BLEEDING ESOPHAGUS, MARFAN’S, PHEOCHROMOCYTOMA: Propanolol

64
Q

BB relative contraindications

A

active asthma
av block
brady
COPD
Labile diabetes

65
Q

Med combos to avoid if possible

A
  1. no ACE AND ARBS
  2. No direct renin inhibitor should be with ACE or ARB
  3. BB not with CCB
  4. No Alpha blocker and central alpha2 agonists
66
Q

Hypertensive Urgency

A

> 180/120 mm Hg w/ no acute end organ injury
MC is not taking meds
Goals: lower bp <160/100 mm hg -> adjust maintenance therapy, add one, treat compound factors (pain anxiety)

Agents used: any normal long term meds or short acting to lower quickly
-clonidine
-captopril
-nifedipine
-hydralazine

67
Q

Hypertensive Emergency

A

bp > 180/120 mm Hg w/ Organ Damage: encephalopathy, nephropathy, MI, aortic dissection, vision disturbance, HA, dizziness, nausea
#1 CAUSE IF FORGETTING TO TAKE BP MEDS OR UNABLE TO AFFORD MEDS

Goals: tx primary site of end organ damage
SBP < 180/120 in first hour -> <160/110 for the next 24 hours
<100-120 for pts with Aortic Dissection w/in 20 min
Ischemic stroke= not lowered unless >= 185/110 who are candidates for reperfusion therapy

IV agents: hospital specific

68
Q

HTN in pregnancy

A

antihypertension in pregnant w/ chronic htn= bp < 140/90
Maintenance therapy:
Labetalol- beta blocker
Nifedipine- CCB

Acute therapy of severe htn:
-labetalol
-hydralazine

Pre-eclampsia= NO ACEs or ARBs

69
Q

HTN special populations

A
  1. CKD/DM= ACE or ARB
  2. African Americans= diuretics and CCB vs ACE/ARB
  3. No BB for pulmonary issues
  4. 4 meds for Prego= labetalol, methyldopa, hydralazine, nifedipine
  5. NO ACE OR ARB FOR PREGO
  6. No ACE/ARB for bilateral renal artery stenosis
  7. NO ACE AND ARBS TOGETHER
70
Q

Special populations

A
71
Q

meds that benefit lowering B/P and managing secondary condition

A
72
Q

supplements that may show reductions

A

CoQ10
Soluble fiber
Vitamin C
Omega- 3
Magnesium
Garlic cloves

73
Q

Summary ACE and ARBs

A
74
Q

Summary aldost, diuretics

A
75
Q

summary bb and ccb

A
76
Q

summary alpha blockers

A

Pharm 2 (15 decks)

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