Cardio 1/23/07

Front 1

T/F Hypertension is more predominant in poor countries?

Back 1

F

Front 2

The 2 most common risk factors for HTN?

Back 2

Age & Gender

-both non-modifiable

Front 3

Severe HTN is defined as?

Back 3

systolic > 190

Front 4

T/F Women are affected by HTN more than men?

Back 4

T

Front 5

For every ____ mmHG increase in systolic BP, you double your risk of dying from a stroke

What about diastolic BP?

Back 5

Sys - 20 mmHg increase

Dys - 10 mmHg increase

Front 6

For every 20/10 mmHg increase in BP you __ your risk of dying from a heart attack

Back 6

double

Front 7

What is the trend of BP with aging?

Back 7

Both sys and diastolic BP increase until 60

From there...sys ^ until 80 & dias comes back down

Front 8

Effects of ^ sym tone (5)?

Back 8

1) ^ BP (via vasoconstiction, ^ insulin resistance, favoing dylipidemia, vascular trophic effect)

2) Hyperinsulinemia

3) Elevated Heart Rate

4) Vasoconstiction

5) ^ Thrombosis (^ BP = prothrombotic)

Front 9

Effects of AT1 pathway (5)?

Back 9

1) Vasoconstiction
2)^ Aldosterone
3)^ Catacholamins
4)Hypertrophy/proliferation of target organs
5)^ BP w/ - feedback on RENIN)

Front 10

If AT1 pathway blocked what happens?

Back 10

Take AT2 pathway

1)Vasodilation
2)Inhibiting cell growth/division
3)Promoting cellular differentiation
4)Inhibits injury response
5)Promotes apoptosis
6)Lowers BP - lose - feeback on RENIN

Front 11

ACE acts as a kininase by doing?

Elaborate..

Back 11

Bradykinin degeneration

Therefore ACE Inhibitors inhibit bradykinin degeneration -> ^ Bradykinin -> stimulates B2 receptors on endothelial cells with realease NO -> Vasodilation & growth inhibition

IMPORTANT POINT: ACE inhibitors are a two-pronged attack b/c you 1) inhibit Ang II and stimulate NO at the same time

Front 12

Two problems with bradykinin build-up?

Back 12

1) Cough - common

2) Angioedema - rare but can kill you

Front 13

Alternative to ACE?

Back 13

Chymase

..but isnt present in a lot of animal models

Front 14

Short-term effects of Ang II?

Long-term

Back 14

short-term: Hemodynamic - ^ BP

long-term: Stuctural - end organ damage (ie kidney failure, heart failure, stroke, etc)

Front 15

^ chance of having a heart attack w/ high or low renin?

Back 15

high

Front 16

Normal Endothelium does what to maintian vascular tone?

Back 16

synthesiszes a lot of NO - an anti-growht factor

so if you strippped off teh endothelium, the underlying muscle would tend to proliferate and grow (vasoconstric w/ platelets and leukocyte sticking)

Front 17

Ang II stimulation of enzyme NADPH oxidase facilitates what?

Ultimate effect?

Back 17

formation of SUPEROXIDE anions
(can be inhibited by AT1 receptor blockers)


the oxidizing lipids (ie superoxide & co) get into the athrerosclerotic plaques (also promoted by Ang II at AT1 receptor activition) -> cytokines (IL-6) that alter vascular matrix composition -> STROKE(coronary plaque instability)

Front 18

How does Ang II also play a role in progression of atherosclerosis?

Back 18

superoxides (from Ang II stimulation of NADPH oxidase) also NEUTRALIZES NO and creates PEROXYNITRITES (a powerful oxidant) -> oxidizes LDL (making more atherogenic) -> LOX-1 receptor activation (also by Ang II) uptakes oxidized LDL causing more endothelial injury

ANG II WORKS IN CONCERT WITH ELEVATED LDL CHOLESTEROL LEVELS IN PROMOTING ATHEROSCLEROSIS

Front 19

Aldosterone produced where?

Effect?

Back 19

Adrenal glomerulosa

promotes Na resorption and K excretion

Front 20

T/F Aldosterone receptors are found all over the body, not just the kidney?

Back 20

T

Front 21

High BP damages the heart in what 2 wyas?

Back 21

1)Atherosclerosis

2)Physical forces

Front 22

Angiotensinogen from?

Back 22

liver

Front 23

Renin from?

Back 23

kidney

Front 24

ACE from?

Back 24

lung

Front 25

2 Goals of anti-HTN therapy?

Back 25

1) control BP
2) ultimate goal is to protect the target organs by preventing stroke, heat attack, kidney dz, and cv events

Front 26

What is it called when there is aso much swelling that the optic disk is obscured?

Back 26

Papilledema

Front 27

As people with HTN live longer, there is a greater chance of dying with what form of cardiac failure?

Back 27

diastolic dysfunction b/c heart fails to dilate adequately as opposed to not being able to contract enough (from hypertrophy perhaps?, never specifically explained in script)

-there's well preserved LV function (not the dilated form of cardiac failure that were familiar with)

Front 28

If you can lower BP by 10/5 mmHg you can prevent each one of these by how much?

1)stroke
2)MIs
3)Heart failure

Back 28

1)Stroke by 35-45%

2)MI's by 25%

3)Heart failure by 50%

Front 29

with CV damage that starts out with high BP (HTN), DM, and maybe insulin resistance, the root physiologic cause of subsequent CV events is?

Back 29

Endothelial dysfunction - vascular disease

Front 30

Normal BP?

Back 30

120/80 or less

Front 31

pre-HTN BP?

Back 31

sys: 120-139 & dias: 80-89

-candidate for lifestyle modification or drug treatment if cormorbid conditions exist (ie DM, heart failure)

Front 32

Stage 1 HTN BP?

Stage 2?

Back 32

sys: 140-159 & dias: 90-99

sys: >160 & dias: >100

-two stages b/c pop data says that BP increase of 20/10 2x risk of dying from heart attack or stroke

Front 33

5 Keys to office BP measurement?

Back 33

1)5 minutes rest in CHAIR (not exam table) with feet on floor

2)Arm @ heart level

3)Appropriate-sized cuff

4)Take it TWICE with at least TWO MINUTES b/w readings

5)Communicate BP # to patients

Front 34

What are you called if your BP doesnt v at night? meaning?

Back 34

"non-dipper"

-you are at an increased risk even if daytime BP is not that high

-usually BP v 10-20% at nights

-cutoff upper limit at night: 120/75; day: 135/85 for 24-hr monitoring or self-measurement

Front 35

During a urinalysis, what is a clue to HTN damage?

Back 35

Microalbuminuria - index of how extensive the damage is, can be followed with treatment (esp w/ DM)

Front 36

As we age, creatnine levels?

Back 36

decrease b/c v in muscle mass (esp women)

Front 37

People w/ kidney disease often ___ aldosterone secretion and may have a low serum ___

Back 37

increase aldosterone; low serum potassium

Front 38

Chronic kidney dz defined as?

Back 38

GFR < 60 ml/min

Front 39

CV dz risk factors

Back 39

Smoking
BMI > 30
Physical inactivity
Lipid abnormalities (dyslipidemia)
DM
Microalbuminria or GRF < 60
Age
Family History

Front 40

Target heart damage by HTN (3)?

Back 40

1)LV hypertrophy
2)Angina prior to MI
3)heart failure

Front 41

2 very common indentifiable causes of HTN?

Back 41

Sleep apnea

Occult Hyperaldosteronism

Chronic kidney dz is becoming more common b/c population is getting older

Front 42

In order to diagnose obstructive sleep apnea you must?

Treatment?

Back 42

Give a sleep study - cant just go by history

1)Weight loss

2) Continuous positive airway pressure

3)sympathetic-driven form of HTN, but Beta Blockers dont work well so use Minerlaocorticoid receptor blockers (spironolactone)

Front 43

3 signs of renal parenchymal dz (chronic kidney dz ass with agin/ and long standing HTN)?

Back 43

1) periorbital/pedal edema

2) ^ creatinine

3) ^ proteinuria & hematuria

Front 44

If HTN onset before 30 or after age 55 think?

another clues?

Back 44

Renal vascular Dz (or any secondary cause of HTN)

-another clue would by if you give ACEI or ARB and the renal function gets worse!

-abdominal bruit

-diffuse vascular dz

-unilateral small kidney, with renin from diseased kidney

Front 45

if someone comes in on 3 or more drungs with uncontrolled BP, no matter what the potassium is, they are considered to have?

Back 45

Aldo excess (possibly primary aldosteronism) causing Resistant HTN (harder to treat - usually must remove gland)

Front 46

Chromaffin cell tumors of neuroectodermal orgin are called?

Signs?

Back 46

Pheochromocytomas

-Anxiety (^ HR, paroxysms, sweating, HA, weight loss, etc)

-Orthostatic hypotension

-Cafe aulait spots or neurofibromas

-An undetected pheochromoytoma can cause a HTN crisis in surgery

Front 47

Most classic anti-HTN medication is? Mech?

Back 47

Thiazide diuretics

-inhibition of the Na/Cl pump in the DCT

-very cheap

-Getting BP down in the importnat thing, not how (ie what drugs you use) you go about doing it?

Front 48

Tonic renin syn and release is stimulated by? Drug for?

Back 48

Sympathetic acivation

Beta blocker - inhibit mainly inotropy (contractility) and chronotropy (rate/timing) by v renin release

Front 49

What anti-HTN drug do you avoid in patients with heart failure?

Back 49

Calcium channel blockers

Front 50

Dont use diuretics as anti-HTN drug for what 2 patients?

Back 50

1) Post MI

2) Renal Dz

Front 51

What anti-HTN drug can you almost always use and is especially good for those with CV conditions

Back 51

ACEI

-ARBs are becoming more popular too

-Post MI BB helpful too!

Front 52

What do you do if initial therapy doesnt work?

Back 52

Optimize doses or ADD extra drugs

DO NOT ENGAGE IN SERIAL MONOTHERAPY

Front 53

What anti-HTN drug is esp good for older women? why?

Back 53

Thiazide diuretics b/c the promote Ca retention

Front 54

What anti-HTN drug is esp good for patients with heart problems (ie tachyarrhythmias, nervousness, hyperthyroidsm etc)?

Back 54

BBs

Front 55

What anti-HTN drug is esp good for benign prostatic hyperplasia?

Back 55

Alpha blockers

Front 56

What anti-HTN drug is esp good for Raynaud's syndrome?

Back 56

Ca Channel Blockers

Front 57

What anti-HTN drug is esp BAD for gout? why?

" Hyponatremia?

Back 57

Thiazide - causes hyperuremia

also thiazide

Front 58

What anti-HTN drug is esp BAD for Reactive ariway dz (ie asthma)

Heart block

Anyone taking Verapamil (a CCB)

Back 58

BB bad for all

Front 59

What anti-HTN drug is esp BAD for young women? why?

History of Angioedema

Back 59

ACEI and ARB - fetal malforamtions

ACEI

Front 60

Normally main mech for ^ CO is? why?

Exceptions (2)?

Back 60

^ HR b/c HR directly proportional to CO

1)Mitral stenosis

2)Severe coronary artery dz - imbalance in supply and demand of O2 to the myocardium -> ^ ischemic tissue (cant contract)

Front 61

Pulsus paradoxus is?

causes (2)?

Back 61

a drop in blood pressure > 10mmHg during inspiration

-usually drops a little on inspiration as blood filling the RV pushes on the IVS and v the LV volume

1)Pericardial effusion (ie cardiac tamponade)

2)v Lung compliance (consisting of..)
-interstitial edema (even asthma)
-severe pulmonary edema
-interstitial fibrosis

Front 62

ejection click?

Back 62

aortic stenosis

-crescendo-decrescendo

Front 63

opening snap?

Back 63

mitral stenosis
-usually CHRONIC rheumatic heart dz

Front 64

midsystolic click?

Back 64

mitral prolapse

Front 65

Austin-Flint murmur

Back 65

Aoric reguritation

-strike the anterior leaflet of the mitral valve, which often results in preclosure of the mitral leaflets

Front 66

Ascites caused by?

Back 66

Pulmonary HTN; R-sided heart faiulure

Front 67

Right ventricle is only visible on what view of the X-ray?

Back 67

Lateral view

-RV is the anterior surface anatomically

Front 68

Enlargement of the LA will cause?

Back 68

referred pain to the ESOPHAGUS

Front 69

Shadow of the heart shouldnt be more than ___ of the thorax (cardiothoracic ratio)

Back 69

50%

Front 70

If vessels are prominent and visible on both sides then they represent arterial flow and indicate?

Back 70

ASD

-L to R shunt; R side of heart can handle 3-4x as much blood as L side

Front 71

Bouncing carotids caused by?

Back 71

Aortic stenosis

-causes enlarged aorta in post-stenotic area due to turbulent flow past the narrowed portionq

Front 72

CHF causes (5)?

Back 72

1) vascular redistribution from bases to apices

2)interstitial and alveolar edema (NO EDEMA IN BRONCHI)

3)Perihilar hazing

4)Peribronchiolar cuffing

5)Pleural effusions

Front 73

Describe the 4 levels of Echocardiogram?

Give you what 2 descriptions

Back 73

Level 1: ventricle and septum, no vlaves

Level 2: level of mitral valve (best to study valves)

Level 3: RV, LV (pre-aorta) outflow tracts & LA (but not mitral valve)

Level 4: Aorta, aortic valve and LA


1) How big the chambers are

2)How well the walls are contracting

Front 74

What does the Doppler show?

Back 74

Blood fluw and turbulence

Front 75

Disappeance of the x wave in the pulmonary-capillary wedge means?

Back 75

Mitral/tricuspid regurge

Front 76

ST depression upon exercise almost guarantees?

other evident showings on test?

Back 76

CAD (coronary ischemia)

Stress test w/ syncope, angina, dyspnea, pulmonay rales, hypotension or v HR