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CVD > 01a: HTN > Flashcards

01a: HTN Flashcards

1
Q

Normal BP according to JNC 7 classification

A

Systole: under 120
Diastole: under 80

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2
Q

Pre-hypertension BP according to JNC 7 classification

A

S: 120-139
D: 80-89

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3
Q

Hypertension stage I BP according to JNC 7 classification

A

S: 140-159
D: 90-99

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4
Q

Hypertension stage II BP according to JNC 7 classification

A

S: over 160
D: over 100

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5
Q

List the antihypertensive drug classes

A
  1. Diuretics
  2. Sympatholytics (affect adrenergic function)
  3. Vasodilators
  4. RAAS affecting agents
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6
Q

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

A

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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7
Q

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

A

X = ACE inhibitor

Y = HTN

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8
Q

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

A

X = ARB (Angiotensin Receptor Blockers)

Y = HTN

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9
Q

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

A

X = vasodilator

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10
Q

First-line treatment for uncomplicated HTN.

A

Thiazide diuretics (hydrocholorothiazide)

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11
Q

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

A

X = loop diuretics

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12
Q

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

A

Initial: lower CO and plasma volume

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

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13
Q

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

A

False - stimulates it due to low volume/Na

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14
Q

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

A

X = metroprolol

Beta-1 (cardiac, renal)

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15
Q

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

A

X = metroprolol

Cardiac: decrease HR, contractility, CO

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

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16
Q

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

A

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

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17
Q

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

A

Alpha-1 antagonists;

Prazosin

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18
Q

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

A

False, not first-line

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19
Q

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

A 
X = tachycardia
Y = CHF
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20
Q

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

A

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

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21
Q

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

A
  1. Diltiazem
  2. Nifedipine (Vaso-selective)
  3. Verapamil (cardio-selective)
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22
Q

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

A

Entry into;

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

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23
Q

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

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

Consider initial drug choices

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24
Q

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

A

SBP over 150
Or
DBP over 90

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25
Q

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

A

SBP over 140 or

DBP over 90

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26
Q

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

A

SBP over 140 or

DBP over 90

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27
Q

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

A

Hypertension stage I (since diastolic BP over 90)

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28
Q

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

A

True

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29
Q

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

A 
X = CO
Y = TPR
30
Q

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

A 
X = HR
Y = SV
31
Q

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

A

True - by reducing intravascular volume

32
Q

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

A

True

33
Q

Signals from baroreceptors in carotid sinus are transmitted via:

A

CN IX (Glossopharyngeal)

34
Q

Signals from baroreceptors in aortic arch are transmitted via:

A

CN X (Vagus)

35
Q

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

A 
X = solitary tract (medulla)
Y = TPR and CO (via HR and contractility)
36
Q

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

A

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

37
Q

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

A

II; high insulin levels;

Increases sympathetic activation or increases TPR via vascular smooth muscle hypertrophy

38
Q

T/F: Secondary HTN is often curable.

A

True - most causes known

39
Q

Causes of secondary HTN:

A

Acronym: CCCRAP

  1. CKD
  2. Coarction (narrowing) of aorta
  3. Cushing’s
  4. Renovascular (stenosis)
  5. (primary) Aldosteronism
  6. Pheochromocytoma
40
Q

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

A

False - vice versa

41
Q

Angiotensin II increases BP by which mechanisms?

A
  1. Vasoconstriction

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

42
Q

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

A
  1. Abdominal bruit (40-60%)

2. Unexplained hypokalemia

43
Q

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

A

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

44
Q

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

A
  1. ACE inhibitors

2. (ARBs) Angiotensin II Receptor blockers

45
Q

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

A
  1. ACE inhibitors
  2. ARBs (Angiotensin II Receptor blockers)
  3. CCBs (Ca Channel Blockers)
46
Q

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

A
  1. Beta-blockers!!!
  2. ACE inhibitors
  3. ARBs (Angiotensin II Receptor blockers)
  4. Aldosterone Antagonists
47
Q

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

A
  1. Diuretics
  2. Beta-blockers
  3. ACE inhibitors
  4. ARBs (Angiotensin II Receptor blockers)
  5. Aldosterone Antagonists
48
Q

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

A

X = ACE Inhibitors (Lisinopril)
Increase;

Inhibit ACE, which promotes degradation of Bradykinin (a vasodilator)

49
Q

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

A

True

50
Q

How do ACE Inhibitors alter GFR?

A

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

51
Q

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

A 
X = liver
Y = renin (from JGA)
Z = Angiotensin I
52
Q

Renin secreted by (X) cells in response to:

A

X = juxtaglomerular

  1. Adrenergic (beta-1) stim
  2. Low intra-renal blood perfusion
  3. Low Na/Cl to macula densa
53
Q

List the rapid pressor responses of AII.

A
  1. Direct vasoconstriction
  2. Enhance peripheral noradrenergic (NE) transmission
  3. Increase sympathetic discharge from CNS
  4. Increase catecholamine release from adrenal medulla
54
Q

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

A

X = adrenal cortex;

Slow

55
Q

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

A

True

56
Q

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

A

Cardiac/vascular remodeling (ex: LV hypertrophy)

57
Q

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

A

X = ACE inhibitor

Kidney (essentially all ACE Inhibitors are)

58
Q

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

A

Cough (5-20%);
X = Bradykinin

Angioedema

59
Q

Lisinopril is contraindicated for:

A
  1. PREGNANCY
  2. Intolerance (ex: angioedema)
  3. Bilateral renal a stenosis
  4. Renal insufficiency (creatinine over 3 mg/dL)
  5. Hyperkalemia or hypotension
60
Q

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

A 
X = ACE
Y = Chymase
61
Q

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

A 
X = AT1
Y = AT2

(Angiotensin receptors)

62
Q

T/F: ARBs permit activation of AT2 receptors.

A

True (AT2 receptors cause vasodilation/antiproliferative action)

63
Q

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

A

True - fetal abnormalities

64
Q

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

A

X = BP reduction

65
Q

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

A

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

66
Q

Patients with diabetic kidney disease, with or without

hypertension, should be treated with an (X) anti-HT drugs.

A

X = ACE-I or ARB

67
Q

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

A

X = Direct Renin inhibitor (DRI)

Inhibits Angiotensinogen conversion to AI (by renin)

68
Q

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

A

Low; high

69
Q

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

A

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

70
Q

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

A

True

CVD (8 decks)

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