01a: HTN Flashcards
Normal BP according to JNC 7 classification
Systole: under 120
Diastole: under 80
Pre-hypertension BP according to JNC 7 classification
S: 120-139
D: 80-89
Hypertension stage I BP according to JNC 7 classification
S: 140-159
D: 90-99
Hypertension stage II BP according to JNC 7 classification
S: over 160
D: over 100
List the antihypertensive drug classes
- Diuretics
- Sympatholytics (affect adrenergic function)
- Vasodilators
- RAAS affecting agents
(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
Lisinopril is in (X) class of drugs, used to treat (Y).
X = ACE inhibitor
Y = HTN
Losartan is in (X) class of drugs, used to treat (Y).
X = ARB (Angiotensin Receptor Blockers)
Y = HTN
Ca channel blockers are used as anti-HTN agents for their (X) effect.
X = vasodilator
First-line treatment for uncomplicated HTN.
Thiazide diuretics (hydrocholorothiazide)
(X) class of drugs is used to treat HTN. It’s very powerful, especially for removal of edema (ex: pulmonary).
X = loop diuretics
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)
T/F: diuretics will allow reduction in RAAS activity.
False - stimulates it due to low volume/Na
(X) is beta-blocker used to treat HTN. Which receptor(s) does it target?
X = metroprolol
Beta-1 (cardiac, renal)
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)
CNS alpha-2 (agonists/antagonists) are used to treat HTN.
Agonists (but not first-line and can be troublesome in elderly patients)
Alpha-1 (agonists/antagonists) used as anti-HTN therapy. What’s the prototype?
Alpha-1 antagonists;
Prazosin
T/F: Prazosin is one of the first-line anti-HTN agents.
False, not first-line
Adverse effect of Prazosin as HTN treatment is (X). Thus, should be avoided in (Y) patients.
X = tachycardia Y = CHF
Ca channel blockers can be non-selective or selective for:
Arterial smooth muscle (Vaso-selective) or cardiac tissue (cardio-selective)
List the Ca channel blockers used to treat HTN. Which ones are selective?
- Diltiazem
- Nifedipine (Vaso-selective)
- Verapamil (cardio-selective)
Ca channel blockers are preventing Ca (entry/exit) (into/from) (X) cells.
Entry into;
Vascular smooth muscle (Nifidipine) or cardiac myocytes (verapamil)
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
HTN: Threshold to start pharmacological therapy in patients age 60 and above.
SBP over 150
Or
DBP over 90
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
- CKD
- Coarction (narrowing) of aorta
- Cushing’s
- Renovascular (stenosis)
- (primary) Aldosteronism
- Pheochromocytoma
T/F: Secondary HTN has more of a genetic component than Essential HTN.
False - vice versa
Angiotensin II increases BP by which mechanisms?
- 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?
- 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?
- ACE inhibitors
2. (ARBs) Angiotensin II Receptor blockers
Which anti-HTN drug class indicated for patients with diabetes?
- ACE inhibitors
- ARBs (Angiotensin II Receptor blockers)
- CCBs (Ca Channel Blockers)
Which anti-HTN drug class indicated for patients post-MI?
- Beta-blockers!!!
- ACE inhibitors
- ARBs (Angiotensin II Receptor blockers)
- Aldosterone Antagonists
Which anti-HTN drug class indicated for patients with CHF?
- Diuretics
- Beta-blockers
- ACE inhibitors
- ARBs (Angiotensin II Receptor blockers)
- 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
- Adrenergic (beta-1) stim
- Low intra-renal blood perfusion
- Low Na/Cl to macula densa
List the rapid pressor responses of AII.
- Direct vasoconstriction
- Enhance peripheral noradrenergic (NE) transmission
- Increase sympathetic discharge from CNS
- 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:
- PREGNANCY
- Intolerance (ex: angioedema)
- Bilateral renal a stenosis
- Renal insufficiency (creatinine over 3 mg/dL)
- 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