Basic concept behind auscultatory method
-Turbulent flow between systolic and diastolic pressures is audible. -Laminar flow returns at diastolic pressure.
#1 COD in the US
Prevalence of hypertension in males vs females and general prevalence at ages 75 and up:
-male greater than female until menopause (55-65) and then reverses -60-75% of those above age 75
-Risk factors for atherosclerosis/ HTN (6)
-smoking -sedentary lifestyle -DM -dyslipidemia (^^ LDL/ HDL ratio) -sex hormones -renal failure *Note, HTN is also a risk factor for atherosclerosis and vice versa
Hypertension predisposes patients to what four conditions?
-Coronary Artery Disease (CAD) -CHF -MI -Stroke/ CVA
Definition of HTN
Blood pressure at which the benefits of therapy outweigh the risk
Most beneficial effect/ strongest correlation to HTN treatment? One other?
#1: reduces risk of stroke by 35% quickly! -also reduces CHF/MI rates
Define Pre-HTN, HTN1, and HTN2 (and what are the very basic treatment reccomendation guidelines for each?)
Pre-HTN: 120-139/ 80-89; no drugs HTN1: 140-159/90-99; mono therapy HTN2: 160/100+; combo therapy *Always recommend lifestyle changes
5 Compelling Indications to treat HTN:
-CHF -CAD -Hx of CVA -DM esp w/ proteinuria -Renal Insufficiency
MAP- CVP is equal to?
BP= CO x TPR ... so increasing BP must increase either CO, TPR, or both
Guyton's major discovery?
BP is proportionate to Na excretion levels; to maintain hypertension, altered renal setpoint is required
Without an altered renal setpoint, what would happen in the presence of HTN?
increased BP = pressure diuresis = urine excretion = decreased BV and therefore BP
Important (but uncommon) causes of secondary hypertension? (5)
-hyperaldosteronism -pheo -renovascular/ chronic renal failure -hypothyroid -aortic coarctation
Basis of hyperaldosteronism/ how it causes HTN (2) Describe the electrolyte changes the condition induces:
-non-supressible aldo (^^^ aldo even in presence of high blood volume) -non-stimulatable renin (low renin even in presence of diuretic/ low blood volume) **Leads to ^ Na/ ECF and BP **DECREASE K+, as aldo induces K+excretion
How does a pheo cause HTN? Where is it located?
Pheochromocytoma= adrenal medulla tumor Produces NE/Epi, leading to vasoconstriction and ^^TPR
Three ways in which chronic kidney failure produces hypertensive state:
-increased renin --> ^ blood volume -inhibited Na pumps --> ^^ serum Na levels -sympathetic activation = vasoconstriction
Of the secondary causes of hypertension, which is most common?
chronic renal failure
Essential hypertension is responsible for what percentage of cases?
When is an evaluation for secondary HTN warranted? (3)
-early hypertension -hypertension with no family history -very severe or refractory hypertension
Causes of "essential" hypertension? (6)
-Genetics -Diet: Na intake, maybe K+/ Ca? -stress -sedentary lifestyle -ETOH -smoking
What is malignant hypertension and how is it detected?
-Blood pressure level at which there is evidence for acute vascular injury. -Most easily detected on retinal fundoscopic exam -BP level may not be what is expected (may be higher or lower than expected HTN state)
Possible causes of hyperaldosteronism: (3)
-Conn's/ adrenal tumor -adrenal hyperplasia (may be glucocorticoid sensitive or insensitive) -pseudohypoaldosteronism
What exactly is pseudohyperaldosteronism? What are two causes?
-Liddle's disease: Na channel mutation; causes excessive reabsorption of Na by kidney (^ blood volume) -Black licorice + Tobacco: enable activation of Aldo receptors by glucocorticoids (more common than Liddle's) *There was something about inactivation of glucocorticoids after liddles written here, but I really think it is a Na channel mutation--Shapiro may have said that, but the review books contradict him*
What is a very good indicator that a patient should be evaluated for hyperaldosteronism? How is it diagnosed?
-hypokalemia esp in the presence of ACEi drugs -diagnosed mainly by supression/ stimluation tests -cannot supress aldo with volume increase -cannot stimulate renin with diuretic/ volume decrease
What are two causes of renovascular HTN? In what population would you expect to see these? Which responds well to correction?
-fibromuscular dysplasia- young, white, female w/ fhx -atheromatous- older person w/ peripheral vascular disease **Fibromuscular dysplasia responds very well to correction
What is the gold standard for diagnosis of renovascular HTN?
How is a pheochromocytoma appropiately diagnosed (2 steps)?
-1st: screen urine and blood If extremely high catechols/ metabolites are found... -2nd: get CT of adrenals
Describe the fundoscopic changes seen in hypertension (grades 1-4)
stage 1: low AV ratio (normal is 2:3), arterioles are narrow stage 2: AV nicking stage 3: hemorrhages and exudates stage 4: papilledema *May be worth taking a peek at the corresponding pictures before exam, Ill try to remember to add them to our path slides.**
Medication class most commonly prescribed for uncomplicated hypertension (w/o compelling indications)
Drugs used to treat HTN in combination with systolic heart failure or DM?
ACEi/ARB *ARB= angiotensin receptor blocker (ie losartan)
Drugs used to treat HTN in patient with a history of MI?