Cardio 1/29/07

Front 1

Leading cause of death in the US?

Back 1

Heart dz

Front 2

Birth weight of heart?

Adult heart weight?

Hypertrophic hearts?

Back 2

birth: 20 grams

adult: 300-350 grams (15x increase)

hypertrophic: 500-700 grams

Front 3

Name the stress increases that deal with hemodynamic burden (3)?

Back 3

1) Frank-Starling mechanism - increasing filling pressures and volumes (acute)

2) increase beta-adrenergic stimulation -> inotropic response (acute)

3)Cardiac hypertrophy (gradual)

Front 4

3 major morphologic changes in cardiac hypertrophy?

Back 4

1) cells get bigger (hyperTROPHY not hyperplasia)

2) increased interstitial fibrosis, most prevalent in pressure overload but can can be seen in volume overload

3) Decreased coronary reserve - ^ O2 demand from hypertrophy so ^ vasculature, however eventually ^ diffusion distance -> relative cardio myocyte hypoxia

Front 5

Difference b/w physiologic and pathologic (pressure overload) hypertrophy?

Back 5

Physiologic - stress and then relaxation (heart has time to recover and "wash out" cytokines and inflammatory mediators

Pathologic - stress on heart ALL THE TIME

Front 6

4 major changes with cardiac hypertension

Back 6

1) morphologic - cellular hypertrophy & fibrosis

2) structural - contracdtile proteins

3) metabolic - fetal isozymes

4) Altered Ca handling

Front 7

Aerobic Exercise produces ___ hypertrophy

Tension exercise (Weights) produces ___ hypertrophy

Pregnancy produces ___ hypertrophy

Back 7

aerobic - eccentric hypertrophy

tension - concentric hypertrophy

pregnancy - concentric hypertrophy

Front 8

Pressure (tension process) overload produces ___ hypertrophy

Volume overload produces ___ hypertrophy

Back 8

^ pressure = concentric

^ volume = eccentric

Front 9

Pathologic hypertrophy metablic effects?

Back 9

Altered glycolysis and glycogen oxidation - more susceptible to ischmic events or cardiac failure

Front 10

LaPlace's Law states that you v wall stress by ?

Back 10

increaseing wall thickness

Front 11

Sarcomere cell pattern in response to pressure overload?

Back 11

^ x-sectional AREA (DIAMETER)

produced in PARALLEL pattern

-to develop more tension

Front 12

Sarcomere cell pattern in response to volume overload

Back 12

individual cells LENGTHEN

produced in SERIES

Front 13

2 results of ^ interstitial fibrosis in concentric hypertrophy?

Back 13

1) makes chamber stiffer (inhibits relaxation)

2) affects diffusion distance

Front 14

3 Functional changes in cardiac hypertrophy

Back 14

1)Ventricular fxn - sys & dias dysfunction, alterations in Ca handling can bare consequences on both

2) Coronary vasculature - increased need for O2 consumption + increaseed diffusion distance = ^ O2 demand with v O2 supply (ANGINA even w/ normal coronary arteries...even worse with artherosclerosis)

3) Electrophysiology - with ^ tissue, there are more electrical abnormalities

Front 15

Final outcome of pathologic hypertrophy?

Back 15

CHF

Front 16

Atheroscclerosis is initiated by ?

Tends to occur?

Back 16

endothelial injury

at points of arterial bifurcation

Front 17

4 major risk factors of atherosclerosis?

Back 17

1) smoking

2) hypertension

3) diabetes

4) male gender

Front 18

3 chronologic steps in the progrssion of atherosclerosis?

Back 18

1) Fatty streak - can be seen in men as young as mid to late teens

2) Fibrofatty (atheromatous) plaque

3) Advanced/vulnerable (comples) Plaque - tends to ulcerate or rupture and progress to thrombosis

...can progress to aneurysm, occlusion by thrombus (mc detected when patient has heart attack, or critical stenosis

Front 19

Eccentric Atherosclerosis plaques composed of?

How do the plaques become more stable? less stable?

Back 19

1) Fibrous Caps

2) Necrotic Center - made of cholesterol, necrotic debris, and macrophages in the center


More stable = ^ thickness of fibrous cap

Less stable = v fibrous caps & more central lipids/necrosis

Front 20

MC structure for aneurysm to occur?

Back 20

Aorta

Front 21

True aneurysm?

False aneurysm?

Back 21

True = expansion of ALL 3 LAYERS of the vessel wall (intima, media & adventitia)

False = contained only by the adventitia

Front 22

False aneurysms are usually caused by

Back 22

hemorrhage

Front 23

Aneurysms of the aorta are predominantly (95-99%) secondary to ?

Other causes?

Back 23

Atheroscleosis

Syphilis, Marfan's, vasculitis and other CT diseases

Front 24

Most common type of aneurysm?

Back 24

Abdominal aneurysm (just inferior to the renal arteries and just superior to the iliac arteries

...followed by descending and ascending thoracic aorta aneurysms

Front 25

Aneurysm with symmetric widening of vessel?

Back 25

Fusiform

Front 26

Aneurysm where one wall is dilated?

Back 26

Saccular

"nutSAC hangs to one side"...yes you like that one ;)

Front 27

Asymptomatic, pulsatile masses felt on abdominal palpitation

Back 27

Clinical presentation for abdomnial aneurysm

Front 28

Aneurysms are a disease of what age range?

Back 28

Elderly, mos people are >60 yrs

Front 29

What size aneurysm is there a major risk factor for rupture?

Back 29

> 6 cm (50% will rupture in 10 yrs)

Front 30

Aortic dissection is?

Back 30

An intiaml tear allowing hemorrhage (through endothelial layer) into the media layer

Front 31

Pathologic process of aortic dissection?

Back 31

Cystic medial necrosis (though no cyst or necrosis...yea, wtf) - fragmentation of the elastic fibers in the wall of the elastic areteries and degeneration of the extracellular matrix

Front 32

Key difference in pain w/ ADis and MI?

Back 32

ADis = pain in BACK
-can also present with aneurysm if dilates posteriorly onto spinal roots

MI = more anterior and ARM

Front 33

MC location for an Adis?

Back 33

Ascending thoracic aorta

...as opposed to aneurysms, which usually occur in the abdominal aorta

Front 34

3 Major complications with Adis?

Back 34

1) lethal hemorrhage into the body cavity

2) Obsturction of major artery branches

3) Expand the aortic valve annulus and cause valvular incompetence (least dangerous)

Front 35

Therapy for Adis?

Back 35

LOWER BP and then surgically close intimal tear & medial dissection

Front 36

Arteriosclerosis obliterans from (2)

Back 36

1) Atherosclerotic plaques directly occuldding arteries

2)Emboli may be genreated from complex plaques

Front 37

Peripheral artery disease (PAD) prevalence MC in?

Back 37

Elderly men UNTIL 75, thereafter men and women have same prevalence

PAD not common in people younger than 60

Front 38

Most common occlusion in PAD?

Back 38

Iliofemoral occlusion - pain in large leg muscle adn buttocks induced by exercise (claudication)

Front 39

Common sites of Claudication for pain in...

1)buttocks, hips & thighs

2)calf & foot

3)thigh & calf

Back 39

1)buttocks, hips & thighs
AORTIC or ILIAC artery

2)calf & foot
POPLIEAL artery

3)thigh & calf
FEMORAL ARTERY

Front 40

Major reason it is difficult to exercise with syndromes of chronic occlusion (PAD)?

Back 40

Not sufficient blood flow with collateral circulation

May be fine at rest but aerobic stress produces ischemic symptoms

Front 41

PAD Physical exam may show (4)?

Back 41

1) v pulses

2) arterial bruit

3) pallor

4) cyanosis

Front 42

Ankle-brachial index used to diagnose what?

Steps?

Back 42

Chronic occlusion (PAD)

1) Take BP at the ankleand the arm

2) Ankle BP should be > or = to that of the arm (gravity)

3) Ankle BP drops below 90% of the brachial artery, then the patient ahs significant arterial disease somewhere b/w ankle and heart

Front 43

Treatment of PAD (3)

Back 43

1)Revascularization by stents

2)Dialating arteries DOESNT work! Must v the VISCOSITY of the blood so that it flows better through arteries

3)Surgery - to bypass area of atherosclerosis

* is dont bypass problem, patients will get ISCHEMIC ULCERATION of the feet -> amputation!

Front 44

Acute arterial obstruction usually caused by?

result?

Back 44

Thrombosis in-situ
...but can ocur from embolization

May result in widespread necrosis b/c there is no time for collaterals to form

Front 45

Acute arterial obstuction treated by (2)?

Back 45

1)Thrombolytic therapy

2)Pulling the clot out directly with catheter

-May result in WIDESPREAD NECROSIS b/c there is no time for collateerals to form

Front 46

*Symptoms of acute arterial obstruction (5)?*

Back 46

1)Pain

2)Pulselessness

3)Palor

4)Paresthesia

5)Paralysis

"5P's"

Front 47

Eggshell calcification in the media of the arterial wall

Back 47

Monckeberg's sclerosis

-arteries become stiff, so patients wont have good vascular reactivity

...Seen in breat biopsies after a mammogram that showed calcification

Front 48

Failure of the venous valves in the legs

Most common in?

Back 48

Varicose veins

Women

Front 49

Predisposing factors for thrombosis (3)?

Back 49

Virchow's triad:

1)stasis

2)hypercoagulability

3)endothelial injury

Front 50

Thrombosis MC in what people(4)?

Back 50

1)Neoplastic diseases

2)Pregnant

3)post-operative

4)immobilized

Front 51

Kidney disease always goes together with?

Back 51

Hypertension

"hyptertensionand kidney disease are like the chicken adn the egg: they always go together"

Front 52

New-onset (acute) glomerulonephritis typically comes with symproms of?

Back 52

Hematuia, pain, sediments

Front 53

Remember: Right outflow occurs when in life?

Back 53

very EARLY (PA stenosis)

Front 54

Hypertension and CHF share what similarities?

Back 54

-pathologic activiation of the alpha-adrenergic nervous system

-pathologic activation of the renin-angiotensin system

-^ synthesis of extracellular matrix that impairs normal fxn

-salutary (favorable) response to ACE inhibitors

Front 55

Most typcial drug that prolongs QT?

Predisposes users to?

Back 55

Quinidine

Torsades de Pointes

Front 56

Does anemia cause cyanosis?

Other causes of cyanosis?

Back 56

No, b/c ALL of RBC (though there are less) are saturated

POLYCYTHEMIA - a person must have approximately 5g of deoxygenated hemoglobin to be cyanotic

Front 57

What do you give to treat meconium babies?

Back 57

NO to facilitate vasodilation

Front 58

The MCC for cyanosis that does not improve with supplemental O2 is?

Back 58

VSD with right to left shunt (ie Tetralogy of Fallot)

Front 59

Olfactory hallucination is a symptom of ?

Back 59

grand-mal seizures

Front 60

The two "shapes" of renal vascular disease?

Back 60

1)20-30 YO often FEMALE pt with problem of SMOOTH MUSCLE OF RENAL ARTERY, called FIBROMUSCULAR DYSPLASIA, manifests with severe hypertension (as high as 220/110)

2)Atherosclerotic plaques within the renal artery often occurring in MEN

Front 61

TIMI measures?

Grades?

Back 61

amount of flow through a vessel (Thrombolysis In Myocardial Infarction)

0 = no flow (bad)
3 = normal (GOOD!)
(1-2 are in between)

Front 62

Lead II, III, AvL & AvF w/ ST segment elevation?

Back 62

Inferior wall MI

Front 63

V1 & V6 ST segment elevation?

Back 63

Anterior/lateral wall MI

Front 64

Retrostenal discomfort during strenuous exercise is most likely?

Back 64

Stable angina