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Kol- Pharm 323 Spring > Hypertension > Flashcards

Hypertension Flashcards

1
Q

3 mechanisms the body uses to control BP

A
  1. blood volume
  2. Peripheral resistance/diameter of arterioles
  3. Cardiac output
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2
Q

what is the preload?

A

= volume of blood coming back into the ventricles of the heart at the end diastole (diastolic pressure)

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3
Q

what is afterload?

A

peripheral vascular resistance left ventricles must overcome to circulate blood

-how much resistance heart has to pump against to get blood flowing out to the body

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4
Q

5 classes of antihypertensives:

A
  • –Diuretics
    1. Thiazide
    2. Loop
    3. Potassium Sparing
  • –Adrenergic Agents
    1. Alpha Blockers
    2. Beta Blockers
    3. Alpha2 Agonist
    4. Alpha Beta Blockers
  • –Calcium Channel Blockers (CCB)
    1. “dipines”
    2. verapamil & diltiazem
  • –Renin-angiotensin system (RAAS)
    1. ACE inhibitors
    2. Angiotensin II Receptor Blockers (ARBs)
    3. Direct Renin Inhibitors
    4. Aldosterone Inhibitors

—Vasodilators

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5
Q

3 types of classes of diuretics

A
  1. Thiazide
  2. Loop
  3. Potassium Sparing
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6
Q

4 classes of adrenergic agents

A
  1. Alpha 1 Antagonist
  2. Beta Blockers
  3. Alpha2 Agonist
  4. Alpha Beta Blockers
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7
Q

classes of calcium channel blockers

A
  1. “dipines”

2. non-dipines: verapamil & diltiazem

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8
Q

4 classes of RAAS drugs for HTN

A
  1. ACE inhibitors
  2. Angiotensin II Receptor Blockers (ARBs)
  3. Direct Renin Inhibitors
  4. Aldosterone Inhibitors
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9
Q

2 ways diuretics fxn in body to decrease BP

A
  1. Decrease BLOOD VOLUME by urinary excretion of water and electrolytes
    • inhibit absorption of sodium and chloride in kidney –> excrete h2o electrolytes
  2. Decrease arterial resistance due to loss of volume
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10
Q

which drug is our first line therapy for HTN?

A

diuretics!

  • -> most efficacious is loop/furosemide
  • -> most widely used = thiazide/ hydrochlorothiazide
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11
Q

where do loop diuretics work?

A

Inhibits reabsorption of Na & Cl at loop of Henle (early on in tubule)

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12
Q

prototype for loop diuretics?

A

furosemide (Lasix)

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13
Q

which diuretic gives us the most diuresis?

A

furosemide (Lasix) b/c it has more impact on more volume of solute

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14
Q

which diuretic will we use to treat acute pulmonary edema?

A

furosemide (Lasix)

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15
Q

Iv vs PO onset for loop diuretics

A

PO: 1hour
IV: 5 min

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16
Q

Side effects for loop diuretics?

A
  • electrolyte imbalances (Na, Cl, K+) (hypo)
  • hypotension, dehydration, postural hypotension
  • ototoxicity- transient: IV push too quick or very high dose
  • increases risk of digoxin toxicity, lithium toxicity –> lose salt, and body keeps lithium (monitor bipolar meds)
  • increases uric acid (gout) –> if patients already have gout can cause gout attack, usually not a problem for causing new gout
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17
Q

which HTN drugs can cause ototoxicity?

A

furosemide - if given too fast or too high of a dose

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18
Q

Furosemide and hydrochlorothiazide (HCTZ) both have risk for what 2 toxicities?

A

litium and digoxin

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19
Q

where does hydrochlorothiazide (HCTZ) fxn in kidney?

A

-works on the distal tubule.

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20
Q

prototype for Thiazide Diuretics

A

hydrochlorothiazide (HCTZ)

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21
Q

how does hydrochlorothiazide (HCTZ) work? (2)

A

1) reduces BLOOD VOLUME -works on the distal tubule.
- ->Results in excretion of H20, Na, K+
2) Reduces arterial resistance (over time)

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22
Q

onset/peak and duration for hydrochlorothiazide (HCTZ)

A

Onset: 2 hrs., peak 4-6, lasts 12 hours

less sudden onset than loop

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23
Q

side effects of hydrochlorothiazide (HCTZ)

A
  • electrolyte imbalances (K+, Na, Cl) (hypo)
  • dehydration, hypovolemia
  • Hyperglycemia ( w/ DM)
  • increases uric acid (gout)
  • risk for digoxin toxicity and lithium toxicity
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24
Q

which diuretic has risk for hyperglycemia w/ DM?

A

hydrochlorothiazide (HCTZ)

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25
Q

which diuretic will work if GFR is <15-20?

A

loop/furosemide will work

thiazide will not work with severe kidney impairment

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26
Q

thiazide vs fursoemide- whats goin on with K?

A 
thiazide = increase K in diet
furosemide = K supplement
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27
Q

how/were do potassium sparing diuretics fxn?

A

Competes with aldosterone at receptors in the distal tubule (at very end) blocking aldosterone (fluid lost, K remains)
-Aldosterone usually makes body hold onto fluid and loose potassium, if BLOCK aldosterone will lose fluid and keep potassium

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28
Q

what is prototype for potassium sparing diuretic?

A

spironolactone (Aldactone)

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29
Q

how long does spironolactone (Aldactone) take to work?

A

Takes up to 48 hours to work

*do not use with fluid volume overload and struggling to breathe

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30
Q

which diuretic is least efficacious?

A

spironolactone (Aldactone)

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31
Q

side effects of spironolactone (Aldactone)

A
  • Risk for hyperkalemia (high K+) (especially if using a salt substitute which replaces salt with potassium)
  • Endocrine effects: gynecomastia, impotence, hirstruism, deepening of voice
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32
Q

spironolactone (Aldactone) + salt substitute =

A

risk for hyperkalemia

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33
Q

What drugs do we typically not give with Potassium sparing diuretics and why?

A

RAAS b/c of risk of hyperkalemia

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34
Q

who is definitely not taking furosemide?

A

pregz in the eggz

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35
Q

Adrenergic agents- SNS or PNS?

A

SNS - right side of the chart

adrenergic = norepi/epi , betaz n alphaz

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36
Q

how do 1. Alpha1 Adrenergic Antagonists fxn? (2)

A
  • blocks the sympathetic nervous system action on arterioles and veins resulting in vasodilation
  • causes relaxation of smooth muscles in bladder neck and prostatic capsule (BPH)
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37
Q

what is the prototype for Alpha1 Adrenergic Antagonists

A

prazosin (Minipress) “osins”

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38
Q

side effects of prazosin (Minipress)?

A
  • orthostatic hypotension (due to vasodilation)
  • **Ist dose phenomenon (don’t get up for 3 hours) - give at night time
  • reflex tachycardia (due to vasodilation)
  • nasal congestion (due to vasodilation)
  • inhibits ejaculation due to activation of Alpha 1 receptors, reversible
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39
Q

prototype for Alpha2 Adrenergic Agonist

A

clonidine (Catapres)

40
Q

how does clonidine (Catapres) fxn?

A

Alpha2 Adrenergic Agonist

centrally acting on alpha2-adrenergic receptors in the brain

  • reduces sympathetic outflow to heart and blood vessels
  • Results–> vasodilation and decreased cardiac output
41
Q

clonidine (Catapres) routes

A
  • pill-PRN, reduce HTN w/in 30 minutes

- patch changed every 7 days

42
Q

who is taking clonidine (Catapres)

A

Used in severe HTN management (PRN orders) , older patients who struggle with pills

43
Q

side effects of clonidine (Catapres)

A

Alpha2 Adrenergic Agonist

  • dry mouth and sedation (gets better with time- develop tolerance like all CNS drugs)
  • Rebound Hypertension if stop cold turkey
44
Q

Adrenergic Agents: Beta Blockers prototype

A

Metoprolol (Lopressor, Topol XL) - cardioselective

45
Q

how does Metoprolol (Lopressor, Topol XL) fxn?

A

-Decreases HR (NEGATIVE CHRONOTROPE)
-Slows conduction through myocardium (NEGATIVE DROMOTROPE) , slow conduction from SA node to AV node
-Decreases force of contraction (NEGATIVE IONOTROPE)
Other actions: decreases peripheral vascular resistance over time and block beta1 on juxtaglomerular cells that release renin

46
Q

side effects of Metoprolol (Lopressor, Topol XL)

A
  • Bradycardia, AV heart block
  • Decreased cardiac output
  • Watch for S/S of heart failure
  • Rebound cardiac excitation- beta blocker is blocking excitation, stop taking it then sympathetic nervous system comes back with full force –> angina
  • May mask SNS (tremors/jittery) s/s of hypoglycemia in diabetics : prefer to put them on cardioselective
  • Prolongation to sa-av node = prolongation of PR interval
  • Nonselective BetaBlocker (1/2)—can actually cause hypoglycemia b/c glycogen is not getting broken down b/w meals
  • fatigue
  • drowsy
  • dizzy
  • HA
  • sexual dysfunction
  • depression
47
Q

which HTN drug causes -Prolongation to sa-av node = prolongation of PR interval ?

A

Metoprolol (Lopressor, Topol XL)

48
Q

Hold beta blockers is apical pulse is > ________

A

60

49
Q

Can you stop metoprolol suddenly?

A

no, risk of rebound tachy

50
Q

Prototype for alpha/beta blocker

A

carvedilol (Coreg)

51
Q

what receptors is carvedilol (Coreg) blocking

A

A1, B1, B2

52
Q

how does carvedilol (Coreg) fxn?

A
  • Alpha blockade: Dilation of arterioles and veins

- Beta blockade: dec. HR, contractility and conduction

53
Q

side effects of carvedilol (Coreg)

A

bradycardia, AV block, bronchoconstriction (beta 2- don’t use in asthmatics), postural hypotension

54
Q

which patient population should not take carvedilol (Coreg)

A

asthmatic

55
Q

2 Ca channel blockers=

A

Very Nice Drugs

  1. Verapamil
  2. Nifedipine
  3. Diltiazem
56
Q

how does Ca Channel blockers fxn in general?

A

inhibiting the influx of Ca into cells, preventing muscular contraction–> Vasodilation occurs when Ca is blocker and muscle is relaxed

  • -works on peripheral arterioles, arteries, arteries/arterioles of heart –> increases coronary perfusion
  • no effect on veins !!
57
Q

do Ca Channel blockers work on veins?

A

no! only work on peripheral arterioles, arteries, arteries/arterioles of heart

58
Q

NORMAL Ca channels in heart have 3 actions

A
  1. causes positive inotropic effect = stronger contraction
  2. pacemaker activity
  3. AV node excitability regulated by Ca
59
Q

if Give Ca BLOCKADE….

A

= negative inotropic effect in heart - decrease contraction
=negative chronotropic effect = decrease HR
= decrease conduction

60
Q

Ca Channel blockers have same action as what other drug?

A

Beta blockers!

do not give Ca Channel blocker and beta blocker at same time

VND + Metoprolol = sadness

61
Q

Dihydropyridines prototype

A

Nifedipine (Procardia)

(Ca Channel Blocker

62
Q

how does Nifedipine (Procardia) fxn?

A

Ca Channel blocker

- Work primarily on blood vessels: vasodilation of arterioles and arteries , not in heart!

63
Q

if someone gets reflex tachycardia AFTER STOPING a Ca Channel Blocker like Nifedipine (Procardia) we give them

A

beta blocker!

64
Q

Non-Dihydropyridines Verapamil & Diltiazem act on….

A
  1. arterioles
  2. heart:
    - Decrease contractility (neg inotrope )
    - DecreaseHR (neg chronotrope)
    - Decrease conduction through AV node (neg dromotrope)

Plus: Vasodilation
Plus: increases coronary perfusion

65
Q

prototype for Non-Dihydropyridines

A

verapamil (Calan)

66
Q

side effects of verapamil (Calan)

A
  • constipation
  • dizziness
  • facial flushing,
  • edema in ankles/feet,
  • Cardiac: bradycardia, heart block and heart failure
67
Q

Considerations for Ca Chennal blockers

A
  • Check BP and pulse (verapamil & diltiazem)
  • Watch for reflex tachy (nifedipine)
  • IV administration-tachy and hypotension
  • Don’t give with grapefruit juice
68
Q

grapefruit juice does not mix with which class of HTN drugs?

A

Ca Channel Blocker

69
Q

The story of Angie and Al:

A

-ANGIOTENSINOGEN is made by the liver and lives in blood vessels
-When juxtoglomerular cells of kidney sense low BP then release RENIN
-Renin converts Angiotensinogen –> ANGIOTENSIN I
-ACE covers Angiotensin I –> ANGIOTENSIN II
(ACE= Angiotensin Converting Enzyme)
-Angtiotensin II = vasoconstriction + causes Adrenal cortex to release ALDOSTERONE
-Aldosterone causes retaining water/sodium which increases BP

70
Q

Another name for ACE, what else does it work on?

A

Kinase II

works on : bradykinin

71
Q

When we block ACE are we getting rid of all the Angiotensin II?

A

Nope, Angie II is made by other pathways so there is still some hanging around

72
Q

What is wrong with Angie II and Aldosterone?

A

–Increases inflammation in the arteries
Prothrombotic- more likely to clot- MI/stroke
-Increases insulin resistance at the tissues
-Causes cardiac hypertrophy and vascular remodeling by making tissue more fibrotic

73
Q

How do Ace Inhibitors fxn?

A

stop Angie II from being formed

74
Q

times to definitely use an Ace inhibitor

A
  • HTN
  • Post MI
  • HF
  • Diabetes
  • Diabetic Nephropathy prevention
  • Stroke and MI prevention
75
Q

Diabetic Kidneys and Ace inhibitors

A
  • Decrease Angtionensin II with ace inhibitor–> vasodilation of the efferent arteriole –> pressure in glomerulus fall–> slows the progression to chronic kidney disease
  • Some recommend all diabetics to be on an ACE inhibitor even if BP normal to protect the kidney from diabetic nephropathy
76
Q

prototype for ace inhibitor

A

lisinopril (Zestril)

77
Q

fxn of lisinopril

A
  1. Blocks the conversion of angie 1 to angie 2-> vasodilation and decreased fluid volume
  2. Block aldosterone
  3. Increase bradykinin - causes dry cough and angioedema (women and black)
78
Q

side effects of lisinopril

A

side effects of lisinopril Dry cough, angioedema (will go away after 2-3 weeks in most people), 1st dose hypotension, Increased K+

79
Q

who is not taking any RASS drugs?

A

pregz in the eggz

80
Q

angioedema related to lisinopril- what is it? who is getting it? when does it happen?

A
  • Hypersensitivity response Caused by bradykinin
  • May occur at any time during therapy
  • May be life threatening emergency
  • Most common in women, smokers and African-American individuals
81
Q

prototype for Angiotensin II Receptor Blockers

A

valsartan

82
Q

how does valsartan fxn?

A

Angiotensin II Receptor Blockers

– block receptors for AT2 after it is formed

  • Potent vasodilator
  • Prevents bad effects from AT2
  • Blocks aldosterone
  • Not as good as ACE Inhibitor
83
Q

side effects of valsartan?

A
  • Decreased risk of cough compared to lisinopril (not working on Bradykinin)
  • 8% cross-sensitivity with ACE for angioedema
84
Q

direct renin inhibitor prototype

A

aliskiren (Tekturna)

85
Q

how does aliskiren (Tekturna) fxn?

A

Blocks the entire RAAS process by binding with Renin and prevent ATI turning into AT II

86
Q

which HTN must you avoid taking with high fat meal?

A

aliskiren (Tekturna) Direct Renin inhibitors

decrease absorption

87
Q

side effects of Direct Renin inhibitors-aliskiren (Tekturna)

A

angioedema, cough, diarrhea

88
Q

prototype for Aldosterone Receptor Blockers

A

spironolactone (Aldactone)

also our potassium sparing diuretic

89
Q

2 prototypes for direct vasodilators

A

hydralazine (Apresoline)

nitroprusside (Nitropress)

90
Q

how does nitroprusside (Nitropress) differ from hydralazine (Apresoline) in its function?

A

Prototype: hydralazine (Apresoline)
Action: Causes direct relaxation of arteriole smooth muscle

Prototype: nitroprusside (Nitropress)
Action: Causes venous and arteriolar dilation
*Drug of choice for HTN emergency

91
Q

side effects of hydralazine (Apresoline)

A

reflex tachy (give with BB), increased bld. volume (give diuretic), SLE syndrome (lupus syndrome)

-vasodilation throughout system - decrease kidney blood- kidney holds onto fluid - increase blood volume

Serious Adverse effects:

  • Severe hypotension
  • Reflex tachycardia
92
Q

route and indication for hydralazine (Apresoline)

A

Use: Primarily used in emergency situations to quickly decrease BP.
Route: Given IV

93
Q

nitroprusside (Nitropress) route and duration of use

A

Given by IV continuous infusion

  • Effects begin in seconds
  • Not used longer than 72 hours
94
Q

side effect of nitroprusside (Nitropress)

A
  • toxic accumulation of thiocyanate

- If increased blood volume occurs–> manage with furosemide.

95
Q

drug of choice for HTN emergency

A

nitroprusside (Nitropress)

Defined as diastolic greater than 120 mmHg

Kol- Pharm 323 Spring (41 decks)

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