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Cardiology > Dx and Tx HTN > Flashcards

Dx and Tx HTN Flashcards

1
Q

What is essential/primary and secondary HTN?

A
  • Primary: chronic elevation in blood pressure without evidence of other disease
  • Secondary: elevation in blood pressure from other disorder.
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2
Q

When do you start thinking about secondary causes of HTN?

A
  • when you cannot get their BP under control alone with medications, if there is a sudden onset or if they start developing sx, if its episodic. Previously well controlled HTN develops sudden increase in BP.
    ex: pheochromocytoma, renal artery stenosis, cushings, kidney failure, sleep apnea, birth control, NSAIDS.
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3
Q

What are some environmental factors that play a role in essential htn? Non-environmental factors?

A
  • obesity
  • alcohol consumption
  • sedentary lifestyle
  • salt intake
Non-environmental: 
-FHX 
-Age
-Gender (generally greater than 65 but becoming more common in children and teenagers) 
-Race (blacks) 
-
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4
Q

Sx of Essential HTN

A

asymptomatic, HA, end organ damage in long term undiagnosed or untreated htn.

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5
Q

Risk factors for HTN

A
  • DM: hyperinsulinemia
  • excess ETOH
  • Cigarettes and Coffee
  • low birth
  • stress, anxiety, depression
  • Oral Contraceptives (estrogen and progesterone)
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6
Q

Complications of HTN

A

END ORGAN DAMAGE
-TIA, stroke, vascular dimentia
-Heart failure, LVH
-Angina, MI
-PVD
-Diabetic Retinopathy (cotton wool spots, neuovascularization, flame hemmorhages, av nicking, silver wiring)
-Renal impairment, proteinuria
(microalbuminemia)

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7
Q

what is isolated systolic htn?

A
  • elevated systolic pressure when the diastolic is normal. May pose significant danger for heart events and stroke.
  • *this increases pulse pressure**
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8
Q

What is pulse pressure? What are some effects of high pulse pressure?

A
  • the difference between systolic and diastolic BP.

- High pulse pressure produces greater stretch of the arteries causing damage to the elastic elements of the vessel

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9
Q

What are the two main types of Secondary HTN?

A
  • Renovascular HTN
  • -renal artery stenosis
  • -fibromuscular dysplasia
  • Adrenal causes of HTN
  • -hyperaldosteronism
  • -pheochromocytoma
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10
Q

What % of all cases of HTN are primary? secondary?

A

95% primary HTN

5% secondary HTN

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11
Q

What medications may cause HTN?

A
  • oral contraceptives
  • corticosteroids
  • NSAIDS
  • OTC cold remedies containing ephedrine or sympathomimetics
  • Caffeine
  • EPO
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12
Q

What is the most common cause of 2ndry HTN? Explain why.

A

-Renal artery stenosis; narrowing of renal artery, kidney senses low O2 when the renal artery is blocked. Renin is then sent from the JG cells out to the blood stream into the lungs where Angiotensin I is converted to AngiotensinII via ACE. AngioII tells the adrenals to release aldosterone, arterioles to constrict, pituitary to release ADH/vassopressin, and renal tubules to absorb Na, Cl and excrete K. Aldosterone retains sodium and therefore water. Volume is increased…..increased BP.

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13
Q

are ACE inhibitors protective or harmful to the kidneys? how?

A

harmful! they will kill the kidneys if you let them!

-AngioII causes vasoconstriction of the efferent glomerular arterioles, which increases perfusion pressure and GFR.WIth stenosed renal arteries afferent flow cannot be increased and efferent arteriole constriction is crucial for maintaining some degree of filtration. ACE inhibitors prevent conversion of Angio 1 to Angio II and therefore remove the kidneys only remaining regulatory mechanism as well as cutting the perfusion pressure and eliminating what little renal function remains.

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14
Q

What are the two processes of Renovascular hypertension?

A
  • Atherosclerotic renal artery disease; common in older men, often bilateral proximal aspect of renal artery.
  • Fibromuscular dysplasia: fibrosis and aneurysm formation in the middle and distal renal arteries, common in young women.
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15
Q

What are some clinical clues of renovascular htn?

A
  • sudden onset w/o FHX
  • drug resistant HTN
  • abdominal bruit
  • renal insufficiency
  • worsening renal function after ACE inhib.
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16
Q

Renovascular HTN

  • diagnostiics
  • tx
A

Dx: renal functions: BUN, creatinine

  • plasma renin levels
  • angiography** definitive

Tx: -balloon angioplasty, surgery with stent

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17
Q

Primary Hyperaldosteronism

  • types
  • what is this?
A
  • unilateral adrenal adenoma (most common in women)
  • bilateral adrenal hyperplasia (most common in men)

What is this?

  • increased aldosterone, stimulates excessive renal Na+ retention with resultant volume expansion and htn.
  • increased intravascular volume augments renal perfusion, thereby renin secretion is suppressed.
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18
Q

Primary Hyperaldosteronism

  • diagnostics
  • tx
A

Diagnostics:

  • serum renin level (low)
  • urine aldosterone levels
  • increased serum aldosterone level that does not suppress after saline-induced volume expansion
  • CT to differentiate between adrenal adenomas and hyperplasia, make sure its at the level of the kidney and not in the pituitary.

Tx:

  • adrenal tumors are resected
  • adrenal hyperplasia: Spironolactone (diuretic, K+ sparing)
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19
Q

Pheochromocytoma

  • signs and sx
  • dx
  • tx
A

Signs and Sx:
-HA, sweating, palpitations, tachycardia, n/v, cyclic HTN

dx: 24hr urine catecholamine and metanephrines (biproduct of catecholamine)

tx:
- Surgical resection: alpha and beta blockage and volume expansion before surgery.

-chronic therapy with phenoxybenzamine (alpha adrenergic blocker)

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20
Q

Aortic Coarctation

  • what is this?
  • what is paradoxical about this?
A

-what: narrowing of the aorta, just distal of the left subclavian artery. congenital defect that obstructs aortic outflow leading to elevated pressures proximal to the coarctation.

  • distal pressures are not reduced as would be expected, reduced systemic blood flow and in particular reduced renal blood flow leads to an increase in the release of renin and the activation of the RAAS.
  • expect aortic coarctation if diff pressures in arms vs legs, right arm vs left arm on a child!!!
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21
Q

How does aortic coarctation effect the barroreceptors?

A

-baroreceptor reflex is blunted due to structural changes in the walls of the vessels, over time they become desensitized to chronic elevation in pressure and become “reset” to the higher pressure.

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22
Q

HTN medication of choice for black Americans?

A
  • calcium channel blockers

* *ARBS AND ACEI are CI!!!!!

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23
Q

JNC VIII adult blood pressure classification

A

Normal: less than 120mmhg systolic, less than 80mmhg diastolic

prehypertension: less than 120mmhg systolic, 80-89mmhg diastolic

HTN 1: 140-159mmhg systolic, 90-99mmhg diastolic

HTN 2: greater than or equal to 160mmgh systolic, greater than or equal to 100mmhg diastolic

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24
Q

Sx of Hypertensive end organ damage

A
  • CHF
  • CVD
  • cerebral vascular disease
  • uremia
  • microalbuminemia
  • aortic dissection
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25
Q

Evaluation of pt with HTN

A

-BP in both arms and compared with pressure in legs
-funduscopic exam: retinal changes, AV nicking, copper wire, retinal hemorrhages and exudates
-heart exam: S4 and S4
-vascular exam: carotid bruits, PVD, abdominal bruits
-neuro exam for evidence of prior strokes
LABS:
-CMP; renal function, glucose, and electrolytes
-fasting lipids
-UA (microalbuminemia)
-CBC (hemochromotosis=iron over load, anemia)
-EKG
-Echo

26
Q

Goal of HTN Tx

A

-reduce risk factors and prevent end organ damage!!!!!

27
Q

beginnig at 115/75mmhg, CVD risk doubls for each increment of _______.

A

20/10mmhg

28
Q

When do you begin treating HTN?

A
  • a patient shouldnt be labeled as having HTN unless the BP is persistently elevated after three to six visits over a several month period.
  • medications should begin if systolic pressure is persistently greater than 140/90 despite attempted nonpharmacologic therapy.
29
Q

primary htn are generally treated with drugs that aim to…
1.
2.
3.

Patients with 2ndry htn are best tread by…..

A
  1. reduce blood volume
  2. reduce systemic vascular resistance
  3. reduce cardiac output by depressing heart rate and stroke volume.

-2ndry are best treated by controlling or removing the underlying disease or pathology

30
Q

Generally speaking, what are the major classes of antihypertensives?

A
  • diuretics
  • beta blockers
  • ACE inhibitors
  • ARBS
  • Ca2+ channel blockers
  • alpha blockers
  • alpha agonists
  • vasodilators
  • direct renin inhibitors
31
Q

Diuretics:

  • MOA
  • most common adverse effect
  • drug names
A

moa: causes diuresis which reduces plasma and stroke volume leading to a decrease in CO and blood pressure
- most common adverse effect is hypokalemia
- drugs: thiazides (HCTZ), loop diuretics(lasix), K+ sparing (Spirinalactone)

32
Q

Thiazides:

  • drug name
  • MOA
  • SE
  • CI
A

Hydrochlorothiazide
-MOA: inhibits NaCl reabsorption in the DISTAL CONVOLUTED TUBULE of nephron.

SE:

  • may cause hypokalemia, but rarely does K+ need to be administered with this drug.
  • may precipitate hyponatremia.

CI:
-sulfa allergy

33
Q 
Loop Diuretic 
-MOA
-SE
-when do you use? 
-drug names
-
A

moa: slectively inhibits NaCl reabsorption in the thick ascending limb of the loop of henle.

SE: stronger incidence of hypokalemia, oral K+ is usually supplemented

Use this: reserved for pts with chronic renal insufficiency/stage 3/4 heart failure to get rid of volume.

Drug Names:

  • Furosemide (lasix)
  • Torsemide (Demedex)
  • Bumetanide (Bumex)
  • Metolazone (Zaroxolyn)
  • go up in power as you move down the list.
34
Q

K+ sparing diuretics

  • MOA
  • drug names
A

moa: antagonize the effects of aldosterone at the LATE DISTAL AND COLLECTING TUBULE.

Drugs:

  • Aldactone (Spironolactone)*
  • Midamor (Amiloride)
  • Dyrenium (Triamterene)
35
Q

which diuretic is used initially?

A

-thiazide type diuretics

36
Q

Beta Blockers

  • MOA
  • where are these receptors located?
  • beta selectivity drug examples
A

MOA: negative inotropic and chronotropic effects, reduces CO

  • receptors: Beta 2 in lungs, liver, pancreas, arteriole smooth muscle, Beta 1 in the lungs and JG cells of the kidney
  • Beta 1 selective: Metoprolol (lopressor, Toprol), Atenolol (Tenormin), Bisoprolol (Zebeta), Acebutolol(sectrol)
  • Non-selective: Propranolol(Inderal), Sotalol(Betapace), TImolol(Blocadren)
37
Q

can beta blockers be combined with diuretics?

A

yes, :) simple as that.

38
Q

Adverse effects of Beta blockers

A
  • bradycardia
  • heart failure
  • Bronchospasm (careful using in asthma or COPD, use Beta 1 selective blockers)
  • Effects on CNS:
  • -impotence
  • -depression
  • -sedation
  • -fatigue
  • -reduced ability to exercise
  • -cold extremities
39
Q

Example Beta and alpha 1 blockers

A

Carvedilol(Coreg) and Labetolol(Trandate)

*good for CHF when you already have a weakened left ventricle. Shown to decrease ventricular scarring and decrease O2 consumption, must start low and slow otherwise their ventricle may give out.

40
Q

Adverse Effects of Beta Blockers

A
  • mask hypoglycemia
  • mask shock
  • lowers HDL
  • hypotension
  • NSAIDS can blunt beta blocker effects
  • epinephrine causes sever HTN in presence of beta blockade.
  • Calcium channel blockers, conduction effects on the heart are additive with beta blockers.
41
Q

ACE Inhibitors
-MOA
-

A

moa; block the conversion of angiotensin 1 to angiotensin II, leading to artery and vein dilatation reducing arterial pressure, preload, and afterload. Promotes renal excretion of Na and H2O by blocking the effects of angiotensin in the kidney and stimulation of aldosterone.
-block the degredation of bradykinin and stimualte the synthesis of other vasodilating substances (causes cough)*

42
Q

What are the ACEI drugs?

A

Captopril (Capoten) Lisinopril(Zestril), Enalapril (Vasotec), Benazpril (Lotensin), Ramipril (Altace), Quinapril (Accupril)

43
Q

ACEI are first line drug of choice to treat HTN in pts with what conditions?

A
  • DM
  • CHF
  • Chronic kidney failure
  • MI
44
Q

Adverse Effects of ACEI

-CI

A
  • cough*
  • acute renal failure** DO NOT USE WITH BILATERAL RENAL ARTERY STENOSIS**
  • angioedema
  • hypotension
  • rash
  • changes in taste
  • hyperkalemia *(dont give with K+ sparing drugs)

-CI in pregnancy

45
Q

Angiotensin II Receptor Blockers (arbs)

  • moa
  • CI
  • examples
A

moa: bind to angiotensin II receptors and block their action.

  • CI in pregnancy!!!
  • -should not be used with bilateral renal artery stenosis!!!!

examples: “sartans”
- Irbesartan (avapro)
- Candesartan (Atacand)
- Losartan (cozaar)
- valsartan(Diovan)
- olmesartan Medoxomil (Benicar)

46
Q

Calcium Channel blockers:

  • MOA
  • effects
A

moa: dilate peripheral arterioles by blocking the influx of calcium into arterial smooth muscles, resulting in muscle relaxation and vasodilation.
effects: reduces PVR and arterial pressure, decrease myocardial contractile force and O2 requirements

47
Q

Which HTN medication is the best single agent for lowering pressures?

A

CALCIUM CHANNEL BLOCKERSSSS

48
Q

What are the Calcium channel blocker classes and the medications in each?

A
  1. Dihydropyridines:
    - vascular selective
    - -amlodipine(Norvasc)
    - -Felopidine (Plendil)
    - -Nicardipine (Cardene)
    - -Nifedipine (Procardia)
    - -Isradipine (Dynacirc)
  2. ) Non-dihydropyridines
    - verapamil(calan, isoptin)
    - Diltiazem(Cardizem)
49
Q

Which class of drugs in CI in CHF?

A

CALCIUM CHANNEL BLOCKERS!!!!…except Norvasc.

50
Q

Adverse Effects of dihydropyridines, non-dihydropyridines

A

dihydro:
- reflex tachycardia
- flushing
- HA
- excessive hypotension
- edema

non-dihydro:

  • constipation
  • excessive bradycardia
  • impaired electrical conduction (AV block)
  • depressed contractility
51
Q

Alpha-1 Blockers

  • MOA
  • when to take
  • medications
A

MOA: block alpha receptors in small arterioles and venules, reduce arterial pressure by dilation, deacreasing PVR

-take at bedtime d/t orthostatic hypotension

Meds:

  • Prazosin (Minipress)
  • Terazosin (hyrin)
  • doxazosin (Cardura)
52
Q

alpha 2 receptor agonists

  • where are these receptors?
  • MOA
  • SE
  • Medications
A

-receptors located in the brain

MOA:
-decrease sympathetic outflow from the vasomotor center=decreased vasoconstriction

  • SE:
  • sedation, dry mouth, depression

meds:
Clonidine(catapres)
Methyldopa(aldomet)*** safe in pregnancy

53
Q

Vasodilators:

  • MOA
  • use
  • medications
A

moa: smooth muscle relaxation by increasing cGMP.
- use: use in emergency when you need to drop someones pressure fairly rapidly.

  • meds::
  • Hydralazine- tachycardia w/ palpitations and hypotension often, may cause lupus-like syndrome!
  • Minoxidil: severe sodium and water retention, may cause hirsutism.
  • Reserpine: depletes NE from nerve endings deceasing PVR and BP, may cause depression d/t loss of serotonin. Oo
54
Q

Hypertensive Crisis:

-urgent vs emergent

A

urgent: no apparent end organ damage
emergent: end organ damage apparent or suspected

55
Q

Hypertensive crisis could be d/t rebound from what drug?

A

clonadine, think gma at the nursing home

56
Q

Hypertensive urgency tx, emergencies tx

A
  • Captorpril
  • Amlodipine
  • Clonidine

Emergency:

  • Nitroprusside: Cyanide toxicity
  • Nitroglycerin
  • -may use Fenoldopan, labetalol, or hydralazine as alternatives.
57
Q

Which two HTN meds do you not want to use together right away because of their additive efffects? Which classes make good combos?

A

Calcium channel blockers and Beta blockers

Combos:

  • beta blocker and diuretic
  • ARB and diuretic
  • ACEI and diuretic
  • CCB and ACEI
  • ACEI and beta blocker
58
Q

What is the DOC for HTN dx during pregnancy?

If HTN diagnosed before pregnancy, which medications are CI during pregnancy?

A

-methyldopa

HTN before: ACEI and ARBS CI, Beta blockers, dont use in early pregnancy.

59
Q

patient whos initial bp is greater than 160/100, initial therapy should be with 2 agents, true or false.

A

True.,

60
Q

Thiazides often potentiate the MOA of ACEs and ARBS, true or false.

A

True.

Cardiology (12 decks)

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