HYPERTENSION Flashcards
Df of HYPERTENSION , and classification
-Definitions: Hypertension is present in an adult if the BP is greater than or equal to 140/90 mmHg. Before a diagnosis of hypertension is made BP should be checked at least 3 times with some weeks apart. Blood pressure levels can be classified as shown in table
—classification:
1-Optimal : s<120 d<80
2-normal : s<130 d<85
-
3-high normal : s130-139 d85-89
4-grad1: s140-159 d90-99
5-grad2:s160-179 d100-109
6-grad3 : s180and higher d110 and higher
-
Isolated systolic hypertension
Grad1 : s140-149 d<90
Grad2 : s>160 d<90
Explain etiology of hypertension and its types
- we have 2 types :
1- primary ( essential)
2- secondary
—————
1-Primary : In more than 95% of cases, an underlying cause cannot
-Pathogenesis:
It is not clearly understood. Proposed mechanisms
be found. include:
1- Excess renal sodium retention
2- Over activity of the sympathetic nervous system
3-Renin angiotensin excess
4-Hyperinsulinemia as part of metabolic syndrome: hyperinsulinemia , glrr”or. intolerange, reduced levels of HDL cholesterol, hypertriglyceridemia and central obesity (all of which are related to insulin resistance).
5- Alterations in vascular endothelium resulting in reduction of vasodilators or increase in vasoconstrictors
—Factors contributing to the development of Essential Hypertension: - Genetic Factors: hypertension is more common in some families and in some ethnic groups like Africans, Americans
- Environmental factors include obesity, alcohol, lack of exercise and excess salt intake.
II- Secondary hypertension:
In about 57o ofcases an underlying cause can be found:
1- Renal:
i. It accounts for 807o ofthe cases of secondary hypertension.
ii. Parenchymal renal diseases like chronic glomerulonephritis, diabetic nephropathy , adult polycystic disease, chronic tubulointerstitial nephritis and renovascular diseases like renal artery stenosis
2- Endocrinal: Hypo or hyperthyroidism, cushing syndrome, primary aldosteronism, pheochromocytoma,hyperparathyroidism, and acromegaly.
3- Drugs and toxins: glucocorticoids, oral contraceptives, cocaine, cyclosporine, erythropoietin
4- Pregnancy-induced hYPertension
5- Vascular: coarctation of aorta, vasculitis.
Explain Clinical Features, sings
-Clinical Features:
-Symptoms: Usually none, occasionally headache (occipital, blurred vision, dizziness and
epistaxis). Obtain a history of over-the-counter medication use, current and previous unsuccessfu I antihypertensive medication trials.
-A history of cardiovascular risk factors e.g hypercholesterolemia, diabetes mellitus, , tobacco use and family history of premature cardiovascular disease.
—Symptoms specific of secondary hypertension:
- New onset hypertension below age of 30 or above 50 years.
- Weakness, polyuria and muscle cramps caused by hypokalemia in primary hyperaldosteronism.
- Weight gain and emotional lability in Cushing’s syndrome.
- Headaches, palpitations and sweating in pheochromocytoma.
- Systemic vasculitis
—symptoms of complications
In chronic or severe hypertension: symptoms of congestive heart failure, coronary artery disease, cerebrovascular disease and chronic kidney injury (uremia)
—Signs:
1- High blood pressure:
• BP should be measured in the sitting or the supine position with the arm supported after 5 minutes resting.
• Standing BP should be measured in the elderly and those suffering from positional hypotension (diabetics and patients on anti-hypertensive medications) to exclude orthostatic hypotension.
“‘White coat hypertension”: apparent hypertension in the clinic, with a normal BP when recorded by automated devices in the patient’s own home. The risk of cerebrovascular disease in these patients is less than that in patients with sustained hypertension.
Ambulatory BP over 24 hours is helpful in patients with labile BP, symptomatic hypotension and those with “white coat hypertension”
2- Signs of secondary hypertension:
Radio-femoral delay (coarctation of the aorta)
Enlarged kidneys (polycystic kidney disease)
Abdominal bruits (renal artery stenosis)
Moon face and trunkal obesity (cushing syndrome)
3- Signs of other cardiovascular risk factors:
- Abdominal obesity (metabolic syndrome)
Tendon xanthomas (hyperlipidemia)
4- Signs of end organ damage and complications:
- Retinopathy:
Stage I arteriolar narrowing
Stage II arteriolar irregularity
Stage III hemorrhages and exudates
Stage IV papilledema associated with severe life threatening disease
(Malignant hypertension)
Cardiac: Left ventricular enlargement or failure.
Peripheral vascular disease: weak or absent peripheral pulsations,
Carotid vascular disease (carotid bruit).
CNS: Cerebrovascular disease (stroke).
Explain the diagnosis methods
–Investigations
-All hypertensives:
1.Urine: for blood, protein and glucose
2.Blood urea and serum creatinine. If elevated, more specific renal
investigations are as creatinine clearance
3.Electrolytes (hypokalemia may occur in primary hyperaldosteronism or more commonly due to diuretic therapy)
4.Blood glucose, lipid profile (total and high density lipoprotein cholesterol).
5. ECG: Left ventricular hypertrophy (LVH) & coronary artery disease (cAD).
-In selected cases:
Imaging:
1.Chest x ray: (cardiomegaly,heartfailure, coarctation).
2.Ambulatory BP monitoring: (borderline or white coat hypertension).
3.Echocardiography: left ventricular hypertrophy (LVH).
4.Abdominal ultrasound (possible renal disease).
5.Renal angiography, MR & CT angiography, renal arterial duplex (renal arlery stenosis)
-Laboratory:
1.urinary catecholaminese.g free metanephrins (pheochromocytoma).
2.Urinary cortisol and Dexamethasone suppression test (Cushing’s syndrome).
3.Plasma renin and aldosterone (primary aldosteronism).
4.Sensitive thyroid-stimulating hormone level.
explain the complications of targeted organs
1-Blood vessels:
1.1 Wide spread atheroma formation leading to coronary and or cerebrovascular disease, particularly if other risk factors (e.g. smoking, dyslipidemia, diabetes)
are present.
2-Central nervous system:
2.1 Stroke (due to hemorrhage or thrombosis and transient ischemic attacks
(TIAs) are more common in hypertensive patients
2.2 Subarachnoidhemorrhage
2.3 Hypertensive encephalopathy: a condition of high blood pressure and neurologic symptoms, usually reversible if hypertension is controlled. Symptoms include disturbances of speech and vision, disorientation, fits and loss of consciousness. Papilledema is common.
3-Retina:
3.1 Changes are associated with hypertension include retinal ischemia or infarction and also central retinal vein thrombosis.
4-Heart:
4.1 Higher incidence of coronary artery disease
4.2 Left ventricular hypertrophy (forcible apex and 54, ECG and
echocardiographic evidence)
4.3 Left ventricular failure in severe hypertension even in the absence of coronary artery disease.
5-Kidneys:
5.1 Long standing hypertension may lead to proteinuria and renal failure due to damage of renal vasculature.
explain the Treatment in chronic hypertension
— Studies have demonstrated clear benefits of treatment of hypertension even grade 1. Treatment goal <140 190 for most patients.
–Treatment of hypertension includes:
1- A-Non-pharmacologic therapy (Life sfyle interventions):
- Smoking cessation: smoking accounts for 30%o of all cardiovascular deaths. It decreases the risk to never smoked at2 years.
- Weight reduction: BMI should be < 25Kgn,ln,2
- Diet: low salt :< 6gm/d, adequate potassium: increase fruit and vegetable
consumption, adequate calcium, low saturated fat diet.
- Exercise: moderate exercise 30-40 minutes most days of the week is
beneficial in lowering BP in hypertensive patients.
- Limited alcohol consumption
2- B-Pharmacologic therapy (antihypertensive medications):
Aim: to reduce the risk of complications.
—–Classes of drugs:
l- Angiotensin converting enzyme inhibitors (ACE inhibitors):
e.g. captopril (50-150 mg daily in divided doses, enalapril or lisinopril (10-20
mg daily ), ramipril (2.5-10 mg daily ).
Mechanism:
- They block the conversion of angiotensin I to angiotensin II, which is a potent vasoconstrictor.
- They block the degradation of bradykinin, a potent vasodilator.
—-Indications:
- Patients with diabetes, heart failure, proteinuria and renal
insufficiency. ACE inhibitors reduce proteinuria and delay progression of diabetic
nephropathy beyond that explained by control of hypertension.
—-Side effects:
- Profound hypotension following the first dose particularly in sodium depleted patients or on large doses of diuretics,
- ACEI may induce cough, angioedema.
- Deterioration of renal functions in those with severe bilateral
renovascular disease (as angiotensin II plays a major role in
maintaining renal perfusion. Patients taking them should be monitored (creatinine and K levels) when therapy is first given.
—————————
2- Angiotensin receptor blockers (ARBs):
e.g. losartan (50-100 mg daily), valsartan ( 80-160 mg daily ) and candesartan ( 16 mg daily) .
——Mechanism:
- Selective block of the receptors of angiotensin II.
——Indications:
- Hypertensives who can not tolerate ACEI because of persistant cough.
Similar to ACEIs may preserve renal function and can reduce proteinuria. ARBs do not cause cough as they have no effects on bradykinin. Angioneurotic edema and renal dysfunction are less encountered.
———————
3-Calcium channel blockers:
e.g. felodipine (5-20 mg daily) , amlodipine (5-10 mg daily), and nifedipine
(10-20 mg three times daily ) .
——–Mechanism:
- Arteriolar dilatation, some also reduce the force of cardiac contraction.
——-Indicotions:
- Concomitant ischemic heart disease.
- Second choice after ACEI or ARBs for patients with proteinuria.
——-Side effects:
- Ankle edema, headache, flushing, palpitation and sweating.
- These are seen particularly with the short acting preparations.
side effects can be lessened by co-administration of a beta-blocker.
————————
4- Thiazide diuretics:
Dose: 12.5 -25 mgdaily as hydrochlorothiazide
Duration: up to 24 hrs.
—side effects: Metabolic effects (such as hyperglycemia, hyperuricemia or hypokalemia) which tend to occur with higher doses of dietetic.
Loop diuretics such as frusemide 40 mgld do have a hypotensive effect but are not routinely used in the treatment of essential hypertension. Potassium sparing diuretics are not effective except spironolactone in the treatment of hypertension and hypokalemia associated with primary hyperaldosteronism.
—————————
5- Alpha adrenergic blockers:
e.g. prazosin ( short acting ) , doxazocin ( 1-4 mg daily ).
——–Mechanism:
- Block the post synaptic al-receptors with resulting vasodilatation.
——Side effectsz
- Postural hypotension with the earlier short acting preparations.
Good choice for benign prostatic hypertrophy.
—————————-
6-Beta blockers:
e.g. atenolol, bisoprolol, metoprolol (selective B blocker) and propranolol
(non selective).
—-Indications.’ It is of choice in younger patients < 55 y and not black.
——Mechanism: attenuate the effects of the sympathetic nervous and reninangiotensin systems.
They decrease cardiovascular mortality. They should be used post myocardial infarction. They are especially useful in patients with both hypertension and angina.
——Side effects: bradycardia, bronchospasm, cold extremities, fatigue, bad dreams and hallucinations. They should be avoided in diabetic patients who require insulin and those with asthma,heart block or depression.
—————
7-Combined alpha and beta adrenergic blockers: e.g.: labetalol (dose :200- 240 mg daily ) , carvedilol (6.25-50 mg daily ).
—————–
8-Centrally acting antihypertensives:
* Methyl dopa: used in pregnancy.
- Acts on central cr2 receptors usually without slowing of the heart.
- It has potentially serious hepatic and blood side effects.
——————–
9-Direct vasodilators: e.g. minoxodil (up to 50 mg daily), hydralazine (up to
100 mg daily).
—–Indications:
- Reserved to patients resistant to other forms of treatment.
—–Side effectsz
- Hydralazine may cause SLE like syndrome, It can be associated with tachycardia and fluid retention.
- Minoxidil can cause severe oedema. excessive hair srowth and coarse facial features.
If these agents are used, it is usually in combination with a beta-blocker
EXPLAIN TREATMENT IN Hvpertensive emergencv
