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76 Cards in this Set

  • Front
  • Back
T/F Hypertension is more predominant in poor countries?
The 2 most common risk factors for HTN?
Age & Gender

-both non-modifiable
Severe HTN is defined as?
systolic > 190
T/F Women are affected by HTN more than men?
For every ____ mmHG increase in systolic BP, you double your risk of dying from a stroke

What about diastolic BP?
Sys - 20 mmHg increase

Dys - 10 mmHg increase
For every 20/10 mmHg increase in BP you __ your risk of dying from a heart attack
What is the trend of BP with aging?
Both sys and diastolic BP increase until 60

From there...sys ^ until 80 & dias comes back down
Effects of ^ sym tone (5)?
1) ^ BP (via vasoconstiction, ^ insulin resistance, favoing dylipidemia, vascular trophic effect)

2) Hyperinsulinemia

3) Elevated Heart Rate

4) Vasoconstiction

5) ^ Thrombosis (^ BP = prothrombotic)
Effects of AT1 pathway (5)?
1) Vasoconstiction
2)^ Aldosterone
3)^ Catacholamins
4)Hypertrophy/proliferation of target organs
5)^ BP w/ - feedback on RENIN)
If AT1 pathway blocked what happens?
Take AT2 pathway

2)Inhibiting cell growth/division
3)Promoting cellular differentiation
4)Inhibits injury response
5)Promotes apoptosis
6)Lowers BP - lose - feeback on RENIN
ACE acts as a kininase by doing?

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
Two problems with bradykinin build-up?
1) Cough - common

2) Angioedema - rare but can kill you
Alternative to ACE?

..but isnt present in a lot of animal models
Short-term effects of Ang II?

short-term: Hemodynamic - ^ BP

long-term: Stuctural - end organ damage (ie kidney failure, heart failure, stroke, etc)
^ chance of having a heart attack w/ high or low renin?
Normal Endothelium does what to maintian vascular tone?
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)
Ang II stimulation of enzyme NADPH oxidase facilitates what?

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

Aldosterone produced where?

Adrenal glomerulosa

promotes Na resorption and K excretion
T/F Aldosterone receptors are found all over the body, not just the kidney?
High BP damages the heart in what 2 wyas?

2)Physical forces
Angiotensinogen from?
Renin from?
ACE from?
2 Goals of anti-HTN therapy?
1) control BP
2) ultimate goal is to protect the target organs by preventing stroke, heat attack, kidney dz, and cv events
What is it called when there is aso much swelling that the optic disk is obscured?
As people with HTN live longer, there is a greater chance of dying with what form of cardiac failure?
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)
If you can lower BP by 10/5 mmHg you can prevent each one of these by how much?

3)Heart failure
1)Stroke by 35-45%

2)MI's by 25%

3)Heart failure by 50%
with CV damage that starts out with high BP (HTN), DM, and maybe insulin resistance, the root physiologic cause of subsequent CV events is?
Endothelial dysfunction - vascular disease
Normal BP?
120/80 or less
pre-HTN BP?
sys: 120-139 & dias: 80-89

-candidate for lifestyle modification or drug treatment if cormorbid conditions exist (ie DM, heart failure)
Stage 1 HTN BP?

Stage 2?
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
5 Keys to office BP measurement?
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
What are you called if your BP doesnt v at night? meaning?

-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
During a urinalysis, what is a clue to HTN damage?
Microalbuminuria - index of how extensive the damage is, can be followed with treatment (esp w/ DM)
As we age, creatnine levels?
decrease b/c v in muscle mass (esp women)
People w/ kidney disease often ___ aldosterone secretion and may have a low serum ___
increase aldosterone; low serum potassium
Chronic kidney dz defined as?
GFR < 60 ml/min
CV dz risk factors
BMI > 30
Physical inactivity
Lipid abnormalities (dyslipidemia)
Microalbuminria or GRF < 60
Family History
Target heart damage by HTN (3)?
1)LV hypertrophy
2)Angina prior to MI
3)heart failure
2 very common indentifiable causes of HTN?
Sleep apnea

Occult Hyperaldosteronism

Chronic kidney dz is becoming more common b/c population is getting older
In order to diagnose obstructive sleep apnea you must?

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

2) ^ creatinine

3) ^ proteinuria & hematuria
If HTN onset before 30 or after age 55 think?

another clues?
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
if someone comes in on 3 or more drungs with uncontrolled BP, no matter what the potassium is, they are considered to have?
Aldo excess (possibly primary aldosteronism) causing Resistant HTN (harder to treat - usually must remove gland)
Chromaffin cell tumors of neuroectodermal orgin are called?


-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
Most classic anti-HTN medication is? Mech?
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?
Tonic renin syn and release is stimulated by? Drug for?
Sympathetic acivation

Beta blocker - inhibit mainly inotropy (contractility) and chronotropy (rate/timing) by v renin release
What anti-HTN drug do you avoid in patients with heart failure?
Calcium channel blockers
Dont use diuretics as anti-HTN drug for what 2 patients?
1) Post MI

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

-ARBs are becoming more popular too

-Post MI BB helpful too!
What do you do if initial therapy doesnt work?
Optimize doses or ADD extra drugs

What anti-HTN drug is esp good for older women? why?
Thiazide diuretics b/c the promote Ca retention
What anti-HTN drug is esp good for patients with heart problems (ie tachyarrhythmias, nervousness, hyperthyroidsm etc)?
What anti-HTN drug is esp good for benign prostatic hyperplasia?
Alpha blockers
What anti-HTN drug is esp good for Raynaud's syndrome?
Ca Channel Blockers
What anti-HTN drug is esp BAD for gout? why?

" Hyponatremia?
Thiazide - causes hyperuremia

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

Heart block

Anyone taking Verapamil (a CCB)
BB bad for all
What anti-HTN drug is esp BAD for young women? why?

History of Angioedema
ACEI and ARB - fetal malforamtions

Normally main mech for ^ CO is? why?

Exceptions (2)?
^ 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)
Pulsus paradoxus is?

causes (2)?
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
ejection click?
aortic stenosis

opening snap?
mitral stenosis
-usually CHRONIC rheumatic heart dz
midsystolic click?
mitral prolapse
Austin-Flint murmur
Aoric reguritation

-strike the anterior leaflet of the mitral valve, which often results in preclosure of the mitral leaflets
Ascites caused by?
Pulmonary HTN; R-sided heart faiulure
Right ventricle is only visible on what view of the X-ray?
Lateral view

-RV is the anterior surface anatomically
Enlargement of the LA will cause?
referred pain to the ESOPHAGUS
Shadow of the heart shouldnt be more than ___ of the thorax (cardiothoracic ratio)
If vessels are prominent and visible on both sides then they represent arterial flow and indicate?

-L to R shunt; R side of heart can handle 3-4x as much blood as L side
Bouncing carotids caused by?
Aortic stenosis

-causes enlarged aorta in post-stenotic area due to turbulent flow past the narrowed portionq
CHF causes (5)?
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
Describe the 4 levels of Echocardiogram?

Give you what 2 descriptions
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
What does the Doppler show?
Blood fluw and turbulence
Disappeance of the x wave in the pulmonary-capillary wedge means?
Mitral/tricuspid regurge
ST depression upon exercise almost guarantees?

other evident showings on test?
CAD (coronary ischemia)

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