01a: HTN Flashcards by Nuna H

Normal BP according to JNC 7 classification

Systole: under 120
Diastole: under 80

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Pre-hypertension BP according to JNC 7 classification

S: 120-139
D: 80-89

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Hypertension stage I BP according to JNC 7 classification

S: 140-159
D: 90-99

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Hypertension stage II BP according to JNC 7 classification

S: over 160
D: over 100

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List the antihypertensive drug classes

Diuretics
Sympatholytics (affect adrenergic function)
Vasodilators
RAAS affecting agents

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(Thiazide/loop) diuretics are used for HTN. Give the name of the prototype. What’s the mechanism?

Both but mainly thiazide (loop diuretics rarely used);

Hydrochlorothiazide

Enhance Na, K, H2O excretion by preventing reuptake of Na in kidney

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Lisinopril is in (X) class of drugs, used to treat (Y).

X = ACE inhibitor

Y = HTN

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Losartan is in (X) class of drugs, used to treat (Y).

X = ARB (Angiotensin Receptor Blockers)

Y = HTN

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Ca channel blockers are used as anti-HTN agents for their (X) effect.

X = vasodilator

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First-line treatment for uncomplicated HTN.

Thiazide diuretics (hydrocholorothiazide)

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(X) class of drugs is used to treat HTN. It’s very powerful, especially for removal of edema (ex: pulmonary).

X = loop diuretics

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Initial versus chronic use of diuretics will lower BP by which mechanisms?

Initial: lower CO and plasma volume

Chronic: vasodilation (by decreasing Na/Ca exchange and thus lowering intercellular Ca levels)

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T/F: diuretics will allow reduction in RAAS activity.

False - stimulates it due to low volume/Na

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(X) is beta-blocker used to treat HTN. Which receptor(s) does it target?

X = metroprolol

Beta-1 (cardiac, renal)

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What are the mechanisms by which beta-blocker, (X), reduces BP?

X = metroprolol

Cardiac: decrease HR, contractility, CO

Renal: decreases RAAS (thus, decrease TPR/afterload)

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CNS alpha-2 (agonists/antagonists) are used to treat HTN.

Agonists (but not first-line and can be troublesome in elderly patients)

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Alpha-1 (agonists/antagonists) used as anti-HTN therapy. What’s the prototype?

Alpha-1 antagonists;

Prazosin

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T/F: Prazosin is one of the first-line anti-HTN agents.

False, not first-line

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Adverse effect of Prazosin as HTN treatment is (X). Thus, should be avoided in (Y) patients.

X = tachycardia
Y = CHF

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Ca channel blockers can be non-selective or selective for:

Arterial smooth muscle (Vaso-selective) or cardiac tissue (cardio-selective)

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List the Ca channel blockers used to treat HTN. Which ones are selective?

Diltiazem
Nifedipine (Vaso-selective)
Verapamil (cardio-selective)

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Ca channel blockers are preventing Ca (entry/exit) (into/from) (X) cells.

Entry into;

Vascular smooth muscle (Nifidipine) or cardiac myocytes (verapamil)

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First recommended treatment option for HTN is (X). If the BP goal of (Y) is not achieved, what is the next step?

X = lifestyle modification
Y = under 140/90 (unless diabetic or CKD: under 130/80)

Consider initial drug choices

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HTN: Threshold to start pharmacological therapy in patients age 60 and above.

SBP over 150
Or
DBP over 90

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HTN: Threshold to start pharmacological therapy in patients under 60.

SBP over 140 or | DBP over 90

HTN: Threshold to start pharmacological therapy in patients with DM or CKD.

SBP over 140 or | DBP over 90

Patient with BP of 130/95 falls into which category of HTN?

Hypertension stage I (since diastolic BP over 90)

T/F: Systolic (not diastolic) BP more often predicts CV complications.

True

BP is the product of (X) and (Y).

``` X = CO Y = TPR ```

CO is the product of (X) and (Y).

``` X = HR Y = SV ```

T/F: No matter how high the CO or TPR, renal excretion has the capacity to completely return BP to normal.

True - by reducing intravascular volume

T/F: Implantation of a kidney from a normotensive person into a hypertensive one typically improves the BP.

True

Signals from baroreceptors in carotid sinus are transmitted via:

CN IX (Glossopharyngeal)

Signals from baroreceptors in aortic arch are transmitted via:

CN X (Vagus)

Baroreceptors send signals to (X), which raises/lowers (Y) to raise/lower BP.

``` X = solitary tract (medulla) Y = TPR and CO (via HR and contractility) ```

T/F: Rate of HTN among identical twins is nearly the same as that among dizygotic twins.

False - concordance much higher among identical twins (genetic component)

Research shows that Type (I/II) diabetes is RF for HTN via which mechanism?

II; high insulin levels; Increases sympathetic activation or increases TPR via vascular smooth muscle hypertrophy

T/F: Secondary HTN is often curable.

True - most causes known

Causes of secondary HTN:

Acronym: CCCRAP 1. CKD 2. Coarction (narrowing) of aorta 3. Cushing's 4. Renovascular (stenosis) 5. (primary) Aldosteronism 6. Pheochromocytoma

T/F: Secondary HTN has more of a genetic component than Essential HTN.

False - vice versa

Angiotensin II increases BP by which mechanisms?

1. Vasoconstriction | 2. Release of Aldosterone (which causes Na and H2O retention)

Which labs/physical exam findings would make you think HTN in patient is due to renovascular etiology?

1. Abdominal bruit (40-60%) | 2. Unexplained hypokalemia

T/F: Both hypo- and hyper-thyroidism presents with HTN.

True (1/4 of hypothyroid pts and 1/3 of hyperthyroid pts)

Which anti-HTN drug class indicated for patients with CKD?

1. ACE inhibitors | 2. (ARBs) Angiotensin II Receptor blockers

Which anti-HTN drug class indicated for patients with diabetes?

1. ACE inhibitors 2. ARBs (Angiotensin II Receptor blockers) 3. CCBs (Ca Channel Blockers)

Which anti-HTN drug class indicated for patients post-MI?

1. Beta-blockers!!! 2. ACE inhibitors 3. ARBs (Angiotensin II Receptor blockers) 4. Aldosterone Antagonists

Which anti-HTN drug class indicated for patients with CHF?

1. Diuretics 2. Beta-blockers 3. ACE inhibitors 4. ARBs (Angiotensin II Receptor blockers) 5. Aldosterone Antagonists

(X) class of anit-HTN drugs cause an (increase/decrease) in Bradykinin via which mechanism?

X = ACE Inhibitors (Lisinopril) Increase; Inhibit ACE, which promotes degradation of Bradykinin (a vasodilator)

T/F: In HTN patients, ACE inhibitors lower blood pressure with little change in CO or heart rate.

True

How do ACE Inhibitors alter GFR?

They don't - dilation of both afferent and efferent arterioles

Angiotensinogen produced by (X) and acted on by (Y) to form (Z).

``` X = liver Y = renin (from JGA) Z = Angiotensin I ```

Renin secreted by (X) cells in response to:

X = juxtaglomerular 1. Adrenergic (beta-1) stim 2. Low intra-renal blood perfusion 3. Low Na/Cl to macula densa

List the rapid pressor responses of AII.

1. Direct vasoconstriction 2. Enhance peripheral noradrenergic (NE) transmission 3. Increase sympathetic discharge from CNS 4. Increase catecholamine release from adrenal medulla

Release of Aldosterone from (X) is considered (rapid/slow) pressor response of AII.

X = adrenal cortex; | Slow

T/F: Altered renal hemodynamics via AII are considered slow pressor responses.

True

In addition to the rapid and slow pressor responses, which category of effects is brought on by AII?

Cardiac/vascular remodeling (ex: LV hypertrophy)

Lisinopril, a(n) (X) drug, is eliminated via which route?

X = ACE inhibitor Kidney (essentially all ACE Inhibitors are)

Most common adverse effect of Lisinopril, mediated by (X). Which other adverse effect is also mediated by (X)?

Cough (5-20%); X = Bradykinin Angioedema

Lisinopril is contraindicated for:

1. PREGNANCY 2. Intolerance (ex: angioedema) 3. Bilateral renal a stenosis 4. Renal insufficiency (creatinine over 3 mg/dL) 6. Hyperkalemia or hypotension

Local AII synthesis can be dependent of (X), thus allowing (X)-escape via the action of (Y) enzyme.

``` X = ACE Y = Chymase ```

Losartan is 10,000x more specific for (X) receptor than (Y).

``` X = AT1 Y = AT2 ``` (Angiotensin receptors)

T/F: ARBs permit activation of AT2 receptors.

True (AT2 receptors cause vasodilation/antiproliferative action)

T/F: Both ACE and ARB should be avoided in pregnancy.

True - fetal abnormalities

The major determinant of a drug's reduction in CV risk is the amount of (X) it causes.

X = BP reduction

T/F: ACE-I increase renal blood flow.

True - via vasodilation of the afferent and efferent arterioles (but don't increase GFR)

Patients with diabetic kidney disease, with or without | hypertension, should be treated with an (X) anti-HT drugs.

X = ACE-I or ARB

Aliskiren is the only (X) drug approved for clinical use. What's its mechanism?

X = Direct Renin inhibitor (DRI) Inhibits Angiotensinogen conversion to AI (by renin)

Aliskiren has (low/high) bioavailability but (low/high) affinity/potency.

Low; high

T/F: Dual ACEi/ARB therapy both reduces albuminuria and increases CV benefit more than either agent alone.

False - only reduced albuminuria, but additional CV/renal benefits not seen in combo therapy

T/F: Aliskiren used as add-on, not for monotherapy.

True