Hypertension and AntiHypertensives Flashcards
Normal BP
<120mmHg/<80mmHg
Prehypertension
120-129/<80
stage 1 HTN
130-139/80-89
Stage 2 HTN
> 140/>90
White Coat Hypertension
Normal BP other than doctor’s office, Diagnosis is ambulatory BP, 24hr observation
Primary HTN Pathophysiology
Most common- Essential HTN, 95%
Hypersensitive SNS HTN
Increased SNS activity = Norepi on SM= Vasoconstriction= Inc. TPR= Inc. BP
SNS action on Kidneys HTN (Hyperactive RAA AXIS)
JGA= epi= Renin= AT1=AT2= Vasoconstriction (inc ADH and Aldosetrone)= TPR = high BP
SNS action on HEart
SA node= ic. HR= inc. BP
Ventricular Myocardium= inc. contractility= inc. CO and Inc BP
ELderly and Af-Am
Low renin HTN
DEcrease the excretion of Na+ = More Na in blood= Water moves towards Na= inc. BV= Inc. BP= inhibits RAAS= low Renin= Low AT2= and no effect.
Na Retention
Vasoconstriction= TPR inc = Inc BP
Risk Factors for primary HTN
Diabetes, Obesity, Obst. Sleep Apnea, neurosis, FH, Vitamins, Genetic, Ethnicity
Age range of primary HTN
(25-55)
Secondary HTN
5% (uncommon) younger ind. (<25)
Kidneys (parenchyma) in HTN
damage to the parenchyma of kidney= inc. Na, Water, and inc. BP
Glomerulonephritis
Diabetic nephropathy (most common)
Polycystic Kid. Disease
Kidney (blood vessels)
Stenosis of Renal artery (no ACEinhib) Atherosclerosis Wegner's Granulomatosis Polyarteritis Nedosa Vasculitis Fibro-muscular dysplasia (20-30 year old females)
Endocrine cause of HTN
Conn’s Disease (ZG)= Hyperaldosteronism= inc Na and h2o= inc. BV= Inc BP
Cushing’s (ZF)= inc Cortisol= Inc Nor/epi= Vasoconstriction= inc BP
Pheochromocytoma= Large Epi and NorEpi= inc. Contractility, inc SV, Inc RAAS= Inc.BP
Also, look for Electrolyte imbalances, BUN, creatinine, Low GFR
Thyroid HTN
Hyperthyroidism= inc. Nor/epi rec. sensititivity= Inc. Hr= Inc BP
Hypothyroidism cause= low T3 and T4= acts on kidneys= inc. Na retention= inc BV= Inc.BP
T3 and T4 inc. Diastolic BP
hyperparathyroidism= high levels of PTH= inc. Ca conc= osteoclast activty, SM cells= Vasoconstriction= BP
Turner’s Syndrome
Coarctation of aorta= constriction of a part of arota= inc. pressure
high ICP
Cushing’s Triad- Hypertension, Bradycardia and Slow respiration
Pregnancy HTN
2nd Trimester (>20 wks)= High BP risks= Pre-eclampsia- HTN and proteinuria 24 hr protein test, Protein/creatinine ratio
can lead to eclampsia- HTN, Proteinuria, Seizures (bad)
treat with Magnesium sulphate
drugs
Oral contraceptives- E2 inc= inc. Angiotensinogen= Inc.BP
Sympathomimetics- Aderall; Ritalin, cocaine
SSRI excess- serotonin syndrome too much antidepressants= SSRI, SNRI, St.John’s Wort
MAO inhib
Tyramine (cheese), Selegiline (treat resistant depression)= hypertensive crisis
HYPERTENSIVE CRISIS
Retinopathy (flame haemorrages) LVH Arrythmia A. Dissection Abdominal aor. Aneyrysm Atherosclerosis
. TREATMENT STRATEGIES BP goal
> 130/>80
THiazide, ACE inhib, ARB or Ca blocker
General nonelderly
Non Black :Thiazide. ACE Inhibitor, ARB, CCB
Black: thiazide diuretic or CCB
Elderly >65 yean old
Use clinical judgment on blood pressure goal and
drug choice if serious comorbidities
Diabetes
ACE inhib and ARB
CKD without proteinuria (140/90) and with proteinuria= (130/80)
ACE inhib or ARB
Stable ischemic HD
B blockers, ACE in, ARB and CCB
Diabetic HTN
Diuretics, ACe inhib, ARb and CCB
Recurrent stroke
Diuretcs, ACE inhib and ARB
HEART FAILURE
Diuretics, b blocker, ACe inhib, ARB and Aldosterone antagosist
Prev. MI
b blockers, ACE inhib, Ald. inhib
CCD
Ace inhib and ARBs
Thiazide diuretics
Hydrochlorothiazide, Chlorthalidone
Thiazide diuretics MOA
Lower Na and water retention, Dec.\BV, CO, TPR= Dec. BP
Therapeutic use
Thiazides are useful in combination therapy with a variety of
other antihypertensive agents, including p-blockers, ACE inhibitors,
ARBs, and potassium-sparing diuretics. With the exception of metolazone
TD are not effective in patients
low GFR, use Loop diuretics instead
Side effects of TD
hypokalemia, hyperuricemia,
and, to a lesser extent, hyperglycemia in some patients
Loop diuretics
furosemide, torsemide, bumetanide, and ethacrynic acid
LD, MOA
blocking sodium and
chloride reabsorption in the kidneys, even in patients with poor renal
function or those who have not responded to thiazide diuretics. Loop
diuretics cause decreased renal vascular resistance and increased
renal blood flow
Difference in MOa of TD and LD
Thiazides, they can cause hypokalemia. However,
unlike thiazides, loop diuretics increase the calcium content of urine,
whereas thiazide diuretics decrease it. These agents are rarely used
alone to treat hypertension, but they are commonly used to manage
symptoms of heart failure and edema
Potassium-sparing diuretics
Amiloride, Triamterene ( inhibitors of epithelial sodium transport at the late distal and collecting
ducts)
spironolactone and eplerenone
aldosterone receptor antagonists