Day 3 Htn

Front 1

class I
classification of recommendation

Back 1

strong recommendation with evidence and/or general agreement that there is a benefit

Front 2

class IIa
classification of recommendation

Back 2

weight of evidence in favor of procedure/treatment

Front 3

class IIb
classification of recommendations

Back 3

usefulness/efficacy less well established by evidence

Front 4

class III
classification of recommendations

Back 4

evidence and/or agreement that a procedure/treatment is not effective, may be harmful

Front 5

level A
level of evidence

Back 5

data derived from multiple randomized clinical trials

Front 6

level B
level of evidence

Back 6

data derived from a single randomized trial

Front 7

level C
level of evidence

Back 7

only consensus opinion of experts or case studies

Front 8

define essential HTN

Back 8

having HTN of an unknown origen
more than 90% of individuals diagnosed with HTN have this version

Front 9

define secondary HTN

Back 9

hypertension related to concurrent medical conditions or is endogenously (has an internal cause/origen)

less than 10% of individuals have this version

Front 10

name the medications that can cause secondary HTN

Back 10

adrenal steroids (prednisone, fludrocortisones)

amphetamines/anorexiants(drug that suppresses the appetite)

a2 agonists (clonidine) when abruptly stopped

calcineurin inhibitors (cyclosporine, tacrolimus)

cocaine/cocaine withdrawel

cox2 inhibitors/NSAIDs

decongestants (phenylpropanolamine)

ephedra alkaloids

venlafaxine

Front 11

name the disease that can cause secondary HTN?

Back 11

chronic kidney disease

Cushing's syndrome (body making excessive cortisol which is a vasoconstrictor)

coarctation of the aorta (obstruction in the aorta)

obstructive sleep apnea (excessive snoring, cause a hypoxic state this can increase sympathetic response so respiratory rate decrease so does oxygen saturation, a and Beta stimulation can worsen blood pressure)

parathyroid disease (increase levels of Ca leads to vasoconstriction of the arteries)

pheochromocytoma (a vascular tumor of the adrenal gland; hypersecretion of epinephrine results in intermittent or sustained hypertension)

primary aldosteronism

renovascular disease

thyroid disease

Front 12

define arterial blood pressure?

Back 12

pressure in the arterial wall of the coronary arteries, measured in mm Hg

Front 13

define: systolic blood pressure (SBP)

Back 13

the peak pressure in the arteries occurring at the end of the cardiac cycle when the ventricles are contracting

Front 14

what two things determine systolic blood pressure?

Back 14

strove volume (the volume of blood pumped out of the left ventricle)

and

aortic compliance (or stretch of the aorta)

aortic compliance (

Front 15

define diastolic blood pressure

Back 15

The arterial BP that occurs after cardiac contraction when the cardiac chambers are filling.

Front 16

what determines diastolic blood pressure?

Back 16

total peripheral resistance(TPR)/systemic vascular resistance (SVR) (The resistance to blood flow that is primarily determined by the vascular tone of the arteriolar blood vessels. )

and diastolic time interval

Front 17

define mean arterial pressure?

Back 17

the average pressure throughout the cardiac cycle

during a cardiac cycle 2/3 of the time is spent in diastole and 1/3 is spent in systole

Front 18

how can you calculate pulse pressure?

Back 18

SBP - DBP

Front 19

how do you calculate blood pressure?

Back 19

BP=CO(SV x HR) x TPR

Front 20

what are the four possible mechanisms of HTN?

Back 20

inravascular volume

autonomic nervous system

atherosclerotic mechanisms

the RAAS system (renin-angiotensin-aldosterone-system)

Front 21

stimulating a1 receptors via norepinephrine in the smooth muscles causes?

Back 21

vasoconstriction so HTN

Front 22

if NE stimulate a2 what hapens?

Back 22

decreases NE outflow will cause vasodilation

Front 23

if EPI stimulates B1 receptors in the heart & kidney what happens?

Back 23

in the heart will increase the heart rate and contractility(inotropy)

in the kidney will stimulate the release of renin to start RAAS

both f these will cause HTN

Front 24

if EI stimulates B2 receptors in the vascular smooth muscle what happens?

Back 24

vasodilation

Front 25

angiotensin II effects AT1 and AT2 what are these effects?

Back 25

AT1 located in the brain, kidney, myocardium, peripheral vasculature, and adrenal glands