Hypertension Flashcards
Complications of HTN
- END ORGAN DISEASE
- Premature cardiovascular disease
- CHF, LVH, ventricular arrhythmia (PMI may be displaced laterally; you WILL see this on EKG), MI
- CVA, intracranial HTN
- Especially with significant fluxuations in BP
- Headache, blurred vision, slurred speech
- Retinopathy - they need to be seen by an ophthalmologist yearly
- Chronic renal insufficiency, ESRD - decreased urine output - Check serum Cr for elevations
- Peripheral vascular disease - claudication (pain or cramping with walking or exercise)
- Also think about ED
- Also look for skin breakdown (painful and dry, over bony areas)
- Extremities will be colder
- Hypertensive emergencies
- With pts with high BP, you want to make sure that they aren’t at cardiovascular risk
- These pts usually feel completely fine because there are no noticeable symptoms
- Screening for BP
- USPSTF recommends BP screening adults starting at age 18 years
- Every year for patients >40 years
- Every year for high risk patients
- Every 3-5 years for normotensive, average risk patients
- Recommends obtaining BP readings outside clinical setting for diagnostic confirmation, treatment
How to treat Stage II HTN
(>140/>90) = lifestyle modification, CV risk reduction, begin 1 medication
leading COD in women
CAD and CVA over all other causes combined
Essential (primary) HTN
- pathogenesis is poorly understood but a variety of factors are implicated:
- Increased sympathetic neural activity, with enhanced beta-adrenergic responsiveness.
- Increased angio II activity and mineralocorticoid excess.
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Genetic: twice as common in subjects who have one or two hypertensive parents
- genetic factors account for ~ 30% of incidence
- Reduced adult nephron mass may predispose to hypertension
- Perinatal factors:
- intrauterine: hypoxia, drugs, nutritional deficiency
- post-natal environment: malnutrition, infections
- The syndrome of apparent mineralocorticoid excess (AME), a genetic disorder, and chronic ingestion of licorice or licorice-like compounds (such as carbenoxolone) can result in findings similar to those in primary aldosteronism: hypertension, hypokalemia, metabolic alkalosis, and low plasma renin activity
- 90-95% of patients have essential hypertension
Secondary HTN
- Renovascular disease
- Renal artery stenosis à MOST COMMON CAUSE OF SECONDARY HTN
- Obstructive Sleep Apnea - STOP BANG
- Primary renal HTN
- Coarctation of the Aorta
- Pheophromocytoma - Catecholamine-secreting tumors from chromaffin cells of adrenal medulla and sympathetic ganglia
- Primary hyperaldosteronism - elevation in blood pressure is dependent upon the mild volume expansion that occurs
- Cushing’s syndrome - moderate diastolic hypertension d/t Increased peripheral vascular sensitivity to adrenergic agonists, increased production of angiotensinogen
- Other endocrine
- Hyper/Hypothyroidism - changes in hypothyroidism include decrease in contractility, reduction in HR, and increase in peripheral vascular resistance
- Hyperparathyroidism
- You start thinking of secondary HTN if you put them on medication and BP is not coming down with medications
Ace Inhibitors
- Highly effective, well tolerated, most patients develop a dry cough
- Block the formation of angiotensin II, decreasing the amount of angiotensin available to both AT1 and AT2 receptors
- Arterial dilation, decreasing resistance to blood flow and consequently decreasing blood pressure
- First-line therapy for heart failure or asymptomatic LV dysfunction, MI, anterior infarct, diabetes, systolic dysfunction, proteinuric chronic kidney disease
- Side effects:
- Approximately 10% of patients develop a chronic nonproductive cough
- Angioedema: Rarely, ACE inhibitors produce a sudden swelling of the lips, face, and cheek areas in an allergic reaction that can occur at any time during therapy
- May affect renal function and raise the potassium level
USPSTF 2015 guidelines for treatment
- For nonblack patients, initial treatment consists of a thiazide diuretic, calcium-channel blocker, angiotensin-converting enzyme inhibitor, or angiotensin-receptor blocker.
- For black patients, initial treatment is thiazide or a calcium-channel blocker.
- Initial or add-on treatment for patients with chronic kidney disease consists of either an angiotensin-converting enzyme inhibitor or an angiotensin-receptor blocker (not both).
- Comparison of Guidelines
- JNC 7 (2003)
- Defined HTN, pre-HTN
- Recommended goal BP <140/90 or <130/80 for DM, CKD
- Recommended treatment goals and medication class based on risk categories, “compelling indications”
- Very specific algorithm and recommendations to follow
- JNC 8 (2014)
- Recommends goal BP <140/90 for everyone <60 yrs, <150/90 for >60 yrs
- Recommends treatment goals, medication class based on pt characteristics (race) or CKD
- Hedges recommendations – “use clinical judgment”
- In persons older than 50 years, SBP > 140 mmHg is a much more important CVD risk factor than DBP.
- The risk of CVD beginning at 115/75 mmHg doubles with each increment of 20/10 mmHg
- Individuals who are normotensive at age 55 have a 90% lifetime risk for developing hypertension.
leading causes of renal failure
DM and HTN
Ambulatory blood pressure monitoring devices
-small, portable machines that record blood pressure at regular intervals over 12-24 hrs while patients go about their normal activities and are sleeping
hypertensive urgency
BP >180/>120 in asymptomatic patient, start on 2 medications
most common reason for medical office visits and use of prescription drugs in the United States
HTN
How to treat BP >160/100
begin 2 medications, ideally a combo pill to improve compliance
Acute Hypertensive emergency (malignant HTN)
- Marked hypertension with retinal hemorrhages, exudates, or papilledema
- May be associated with hypertensive encephalopathy
- Seizure
- Altered mental status
- Headache with visual changes
- Decreased urinary output with rapid increase in renal failure
- Eclampsia in pregnancy/postpartum
Evaluation of HTN pt
- Hx: FH, CVD risk factors, PMH (ever had problems with kidney, any prenatal or postnatal issues), ROS for end organ damage/complications
- PE: VS (RR, BMI), Eyes (look at fundus), Brain, Neck, Heart, Lungs (listening for crackles for evidence of heart failure), Abdomen (listening for bruits), PV (look at feet looking for ulcers, pulses, hair distribution)
- Labs
- CBC, BMP, UA
- CBC - wont really tell you much
- BMP - looking at kidneys, glucose
- UA - specific gravity, glucose
- Fasting (9 to 12 hours) lipid profile
- Electrocardiogram
- Urine microalbuminuria for patients with diabetes to screen for early nephropathy
- CBC, BMP, UA
- Consider TSH, toxicology screen, other labs as dictated by H&P