HTN- Leah (6) * Flashcards

1
Q

Basic concept behind auscultatory method

A

-Turbulent flow between systolic and diastolic pressures is audible. -Laminar flow returns at diastolic pressure.

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2
Q

1 COD in the US

A

CVD

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3
Q

Prevalence of hypertension in males vs females and general prevalence at ages 75 and up:

A

-male greater than female until menopause (55-65) and then reverses -60-75% of those above age 75

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4
Q

-Risk factors for atherosclerosis/ HTN (6)

A

-smoking -sedentary lifestyle -DM -dyslipidemia (^^ LDL/ HDL ratio) -sex hormones -renal failure *Note, HTN is also a risk factor for atherosclerosis and vice versa

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5
Q

Hypertension predisposes patients to what four conditions?

A

-Coronary Artery Disease (CAD) -CHF -MI -Stroke/ CVA

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6
Q

Definition of HTN

A

Blood pressure at which the benefits of therapy outweigh the risk

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7
Q

Most beneficial effect/ strongest correlation to HTN treatment? One other?

A

1: reduces risk of stroke by 35% quickly! -also reduces CHF/MI rates

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8
Q

Define Pre-HTN, HTN1, and HTN2 (and what are the very basic treatment reccomendation guidelines for each?)

A

Pre-HTN: 120-139/ 80-89; no drugs HTN1: 140-159/90-99; mono therapy HTN2: 160/100+; combo therapy *Always recommend lifestyle changes

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9
Q

5 Compelling Indications to treat HTN:

A

-CHF -CAD -Hx of CVA -DM esp w/ proteinuria -Renal Insufficiency

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10
Q

MAP- CVP is equal to?

A

BP= CO x TPR … so increasing BP must increase either CO, TPR, or both

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11
Q

Guyton’s major discovery?

A

BP is proportionate to Na excretion levels; to maintain hypertension, altered renal setpoint is required

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12
Q

Without an altered renal setpoint, what would happen in the presence of HTN?

A

increased BP = pressure diuresis = urine excretion = decreased BV and therefore BP

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13
Q

Important (but uncommon) causes of secondary hypertension? (5)

A

-hyperaldosteronism -pheo -renovascular/ chronic renal failure -hypothyroid -aortic coarctation

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14
Q

Basis of hyperaldosteronism/ how it causes HTN (2) Describe the electrolyte changes the condition induces:

A

-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

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15
Q

How does a pheo cause HTN? Where is it located?

A

Pheochromocytoma= adrenal medulla tumor Produces NE/Epi, leading to vasoconstriction and ^^TPR

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16
Q

Three ways in which chronic kidney failure produces hypertensive state:

A

-increased renin –> ^ blood volume -inhibited Na pumps –> ^^ serum Na levels -sympathetic activation = vasoconstriction

17
Q

Of the secondary causes of hypertension, which is most common?

A

chronic renal failure

18
Q

Essential hypertension is responsible for what percentage of cases?

A

90-95%

19
Q

When is an evaluation for secondary HTN warranted? (3)

A

-early hypertension -hypertension with no family history -very severe or refractory hypertension

20
Q

Causes of “essential” hypertension? (6)

A

-Genetics -Diet: Na intake, maybe K+/ Ca? -stress -sedentary lifestyle -ETOH -smoking

21
Q

What is malignant hypertension and how is it detected?

A

-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)

22
Q

Possible causes of hyperaldosteronism: (3)

A

-Conn’s/ adrenal tumor -adrenal hyperplasia (may be glucocorticoid sensitive or insensitive) -pseudohypoaldosteronism

23
Q

What exactly is pseudohyperaldosteronism? What are two causes?

A

-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*

24
Q

What is a very good indicator that a patient should be evaluated for hyperaldosteronism? How is it diagnosed?

A

-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

25
Q

What are two causes of renovascular HTN? In what population would you expect to see these? Which responds well to correction?

A

-fibromuscular dysplasia- young, white, female w/ fhx -atheromatous- older person w/ peripheral vascular disease **Fibromuscular dysplasia responds very well to correction

26
Q

What is the gold standard for diagnosis of renovascular HTN?

A

arteriogram

27
Q

How is a pheochromocytoma appropiately diagnosed (2 steps)?

A

-1st: screen urine and blood If extremely high catechols/ metabolites are found… -2nd: get CT of adrenals

28
Q

Describe the fundoscopic changes seen in hypertension (grades 1-4)

A

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.**

29
Q

Medication class most commonly prescribed for uncomplicated hypertension (w/o compelling indications)

A

diuretics

30
Q

Drugs used to treat HTN in combination with systolic heart failure or DM?

A

ACEi/ARB *ARB= angiotensin receptor blocker (ie losartan)

31
Q

Drugs used to treat HTN in patient with a history of MI?

A

B-blockers