Hypertension Flashcards
Define hypertension
elevated BPP measured on 3 separate occasions
hypertension classification
normal less than 130 and less than 85 prehypertension 130-139, 85-89 140 above hypertension 90 above
causes of primary hypertension
Family history – Genetic or shared environmental influences
Fetal factors – Low birth weight
Obesity
Environmental factors:
Alcohol
Sodium intake
Poor diet – Generally leads to obesity or increased salt intake
causes of secondary hypertension
Renal Diseases - > 80% Diabetic nephropathy Chronic GN Polycystic disease Chronic tubulointerstitial nephritis Renovascular disease, including renal artery stenosis Endocrine: Phaeochromocytoma – catecholamine secreting tumour Cushing’s syndrome Thyroid disease Conn’s syndrome Acromegaly – Growth hormone excess Vascular: Aortic coarctation
11 beta hydroxysteroid (found in liquor ice)= increased cortisol- increased sodium reabsorption
medications that cause secondary hypertension
estrogen, herbal, NSAIDS, steroids, sympathomimetics
clozapine, TCA ,carbamazepine
blood vessel complications of uncontrolled hypertension
Vascular smooth muscle hypertrophy
Small vessel leak (resulting in proteinuria and retinopathy in kidneys & eyes, respectively)
Atherosclerosis (peripheral artery occlusive disease)
cardiac complications of uncontrolled hypertension
Atrial enlargement
Left ventricular hypertrophy
other complications of uncontrolled hypertension
retinopathy grade 1-4 renal Macroscopic: Atrophic kidneys with scarring Microscopic: Focal sclerosis on glomeruli Changes in large and small arteries (atheroma, elastic re-duplication)
brain Arterioles Sclerosis & aneurysm formation Basal ganglia Small infarcts & hemorrhages Dementia Likely due to small vessel complications
loop diuretics mechanism of action
inhibit Na/K+/ 2CL- symporter and prevent their reabsorption decreasing fluid retention
short lived duration
used in hypertension if there is renal impairment
used in oedema
adverse effects of loop diuretics
hyponatremia hypokalemia- increased risk of V-Tach gout metabolic: dyslipidemia, metabolic alkalosis hearing impairment
Thiazides mech of action
block NaCl co-transporter in the distal convoluted tubule
prevent reabsorption of sodium increasing its excretion
adverse effects of thiazides
hypokalemia
hyponatremia
gout
metabolic changes; lipid and glucose tolerance
erectile dysfunction(reduced flow to penile structures and reduction in zinc which is needed for formation of sex hormones)
Mineralocorticoid antagonist diuretics
inhibit aldosterone receptor action on the ENAC in the distal tubule
ENAC usually reabsorbs Na and exchanges with k+
so if there is inhibition there is K+ sparing
adverse effects of Mineralocorticoid antagonist diuretics
hyperkalemia
erectile dysfunction
high estrogenic leading to gynecomastia
name the 2 types of calcium channel blockers
dihydropyridine- antihypertensive
non-dihydropyridine- anti-arrhythmic properties
mechanism of action of calcium channel blockers
block voltage gated calcium channels (l type)
do not use verapamil with beta blockers
examples of calcium channel blockers
Very- verapamil
nice - nifedipine
drugs- diltiazem
side effects of calcium channel blockers
low BP bradycardia headache AV block constipation, nausea peripheral oedema
adverse effects of ccb
tachy
ankle edema
headache
flushing
contraindications of CCB
tachyarrhythmias
heart failure
AV block( cant use non dihydropyridine)
what are the top 3 drug choices for hypertension
ACE inhibitors
thiazides
CCB
risks of BP control
Hypotension Acute kidney injury Syncope Electrolyte abnormalities (Falls not significantly increased)
benefits of BP control
Decreased rate of CV events: Myocardial infarction Acute coronary syndrome Stroke Acute decompensated heart failure CV death Decreased orthostatic hypotension
cardio selective vs non cardio selective beta blockers
cardio-selective act on B1 (atenolol)
non selective act on b1 and 2 (carvedilol, propanolol, labetalol)
carvedilol has alpha blocking properties
