HTN- Leah (6) * Flashcards
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
CVD
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?
90-95%
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?
arteriogram
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)
diuretics
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?
B-blockers
