HTN- Leah (6) * Flashcards Preview

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Flashcards in HTN- Leah (6) * Deck (31):
1

Basic concept behind auscultatory method

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

2

#1 COD in the US

CVD

3

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

4

-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

5

Hypertension predisposes patients to what four conditions?

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

6

Definition of HTN

Blood pressure at which the benefits of therapy outweigh the risk

7

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

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

8

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

9

5 Compelling Indications to treat HTN:

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

10

MAP- CVP is equal to?

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

11

Guyton's major discovery?

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

12

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

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

13

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

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

14

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

15

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

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

16

Three ways in which chronic kidney failure produces hypertensive state:

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

17

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

chronic renal failure

18

Essential hypertension is responsible for what percentage of cases?

90-95%

19

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

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

20

Causes of "essential" hypertension? (6)

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

21

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)

22

Possible causes of hyperaldosteronism: (3)

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

23

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*

24

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

25

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

26

What is the gold standard for diagnosis of renovascular HTN?

arteriogram

27

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

28

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.**

29

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

diuretics

30

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

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

31

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

B-blockers