Cardio 2/2/07

Front 1

Inherent problems with the the cardiac muscle generally called?

Usual etiology

What do they all have in common?

Back 1

Cardiomyopathy (CM)

Etiology often unknown

HEART FAILURE is something all etiologies of CM have in common

Front 2

4 types of CM

Back 2

1) Dilated

2) Hypertrophic

3) Restrictive

4) Arrhythmogenic

Front 3

Dilated CM characteristic feature?

Main Hemodynamic Abnormality

Potential Scenerio?

Back 3

Dilation of ALL FOUR chambers

Systolic dysfxn

Peripartum CM - during 3rd trimester or immediate post-delivery period, if woman survives and becomes pregnant again, almost always fatal

Front 4

Histological presentation of Dilated CM?

Back 4

Myocyte Hypertrophy interspersed w/ myocyte Degeneration

Front 5

Causes of Dilated CM (5)

Back 5

1)Familial (genetic)

2)ALCOHOLIC

3)Acute Viral - Coxsackie & Echo (ENTEROVIRUSES)

4)Chagas - T Cruzi (S American parasite)

5)Peripartum

-note that some are potentially reversible

-also you're going to have REGURGE (b/c of chamber dilation) so expect embolisms!

Front 6

Young, athletic athlete sudden collapses and dies, think?

Main Hemodynamic Abnormality?

Main Etiology

Back 6

Hypertrophic CM

Diastolid Dysfxn (LV contraction vigorus (LV hypertrophy) but relaxation impaired)

Familial (almost always; 1/500 carrier gene)

Front 7

Key Pathological presentation of Hypertrophic CM?

Back 7

Asymmetric defect of Septum -2-2.5x thicker than other ventricular walls

Can block outflow tract (aorta) & pull anterior mitral leaflet (Mitral regurgitation!!)

Front 8

CM causing a rigid myocardium?

Main Hemodynamic Abnormality?

Sign?

Back 8

Restrictive CM

Diastolic Dysfunction (^ Diastolic pressure, v Ventricular filling)

**Right Heart Failure - JVD, hepatomegaly, ascities, peri edema

Front 9

Main causes of Restrictive CM?

Back 9

1) Genetic - HEMOCHROMATOSIS & glycogen storage diseases (POMPE'S)

2) AMYLOIDOSIS (amyloidosis sarcoidosis)

Front 10

Restrictive CM (RCM) presents very similarly to Constrictive CM (CCM)..how do you differentiate?

Back 10

RCM has normal sys fxn (dias disfxn) while CCM has sys dysfxn

**CLINICALLY - CCM responds to vasodilators while there is NO GOOD TXMT for RCM**

Front 11

CM that INVOLVES THE RV and Adipose/fibroadipose replaces the ventricular myocardium?

Predominance in?

Back 11

Arrhythmogenic MC

Cause/etiology unclear

Strong MALE,YOUNG ADULTS predominance

Front 12

4 Diseases of the Pericardium

Back 12

1)Acute Pericarditis

2)Pericadial Effusion

3)Cardiac Tamponade

4)Constrictive Pericarditis

Front 13

2 Main etiologies of Acute Pericarditis

Back 13

1)INFECTIOUS: most commonly VIRAL (used to be TB; can also be bacterial; as can Toxo (watch out for kitty litter))

2)NONINFECTIOUS:
a)post-MI
b)uremic pericardidtis
c)malignant involvment (from lymphomas; radiation)
d)Connective Tissue Dz - LUPUS
e)Drug-induced

Front 14

Clinical presentation of Acute Pericarditis (6)

Back 14

*1)DIFFUSE ST elevation (all except aVR & V1)

*2)PR segment DEPRESSION

3)POSITIONAL Chest Pain

4)Fever

5)Dyspnea

6)Friction rub

also have abnormal ECG

Front 15

Causes of Pericardial Effusion?

Back 15

Anything that ^

1)Capillary permeability (ie Hypothyroidism)

2)Capillary Pressure (ie CHF)

3)Oncotic pressure (ie Cirrhosis & Nephrotic syn)

4)Obstruction of lymph flow

5)Maligancy (BLOODY)

Front 16

Up to how much pericardial fluid is normal?

Back 16

50 mL

Front 17

Clinical Features of Large Pericardial Effusion (3)

Back 17

1)Soft heart sounds
2)Reduce intensity of friction rub
3)Dullness over posterior lung(Ewart's sign)

Front 18

Caridiac Tamponade causes

Back 18

MCC NEOPLASTIC, postviral & uremic

Any etiology of acture pericarditis can progress to cardiac tamponade

Also Acute Hemorrhage from chst trauma, rupture of LV following MI or dissecting aortic aneurysm

Front 19

Clinical features of Cardiac Tamponade? (4)

Back 19

1) Hypotension w/ PULSUS PARADOXUS (take in breath & pulse becomes weaker; measured by inspiratory reduction in systolic pressure >10 mmHg)

2) Jugular venous Distention

3) Quiet precordium on palpation

4) Sinus tachycardia

Front 20

What is Kussmaul's sign

Sign of?

Back 20

Take in breath and actually causes INCREASED JVD w/ inspiration

Constrictive Pericarditis

Front 21

Pattern of Right atrial (jugular venous) pressure w/ Tamponade & Constrictive pericarditis?

Back 21

1)Tamponade = y descent bluncted (impaired ventricular filling from ^ pericardial pressure)

2)Constrictive pericarditis = y descent appears accentuated from higher than normal right atrial pressure - not blunted because the EARLIEST phase of diastolic filling not impaired

Front 22

General composition of Lipoprotein?

Back 22

Protein and phospholipid on surface and help solubulize the triglyceride and cholesterol ester which is in the core of the molecule

Front 23

Function of the proteins (4)

Back 23

1)Solublize lipids

2)Serve as binding ligands

3) Activate or inhibit enzymes

4) Involved in lipid transfer

Front 24

4 Classes of lipoproteins?

Back 24

1)Chylomicrons (CM) - largest; 93% tryglyceride; responsible fo rtransferring dietary fat to peripheral tissue (energy); would basically only raise TG levels

2)VLDL - little less TG and more chol than CM (would rise both TG (more) & Chol (less) levels

3)LDL - mostly Chol w/ little TG

4)HDL - smallest; less Chol than LDL & tries to take Chol back to liver for excretion from the body

Front 25

T/F Small, denser LDL particles appear to bind more effectively to the LDL receptor?

Back 25

T

Front 26

Which lipoproteins are syn by LIVER for energy providing purposes?

" syn by Intestinal enterocytes " ?

Back 26

VLDL

CM

Front 27

byproduct of VLDL and is the main Atherogenic lipoprotein

Back 27

LDL

Diabetes and obesity are ass w/ ^ production of VLDL & LDL

Front 28

T/F As you eat cholesterol converted to LDL, therefore LDL concerntration ^

Back 28

F

The cholesterol you eat v the syn and expression of the LDL receptor on the surface of the liver cell

Front 29

Severe hypertriglyceridemia may manifest as ?

Back 29

Eruptive xanthoma (Gross Shit!) - clusters of TG surrounded by macrophages

Front 30

Increased TG CONTENT in a NORMAL amount of VLDL

Ass with use of?

*Variability in lipid panel phenotype amongst family?

Back 30

Familial Hypertriglyceridemia

Oral estrogen replacement therapy

*NO* (key difference!)

Front 31

In Familial combined Hyperlipidemia is there variability in lipid panel phenotype amongst family?

Back 31

*YES* (key difference!)

Very athrogneic abnormality

Front 32

Fxn of HDL (2)

Back 32

"good cholesterol"

1) Takes the cholesterol from the peripheral tissue back to the liver for excretion from the body

2) Also ANTI-INFLAMMATORY

Front 33

Most important risk factor for CHD?

2ary risk factors?

Back 33

LDL cholesterol

-low HDL, HTN, smoking, age, family history

Front 34

T/F if you have diabetes, you have the same risk of having a CV event as someone hwo has CHD but does not have diabetes

Back 34

T

Front 35

T/F Familial Hypercholesterolemia is a polygenic dz?

Back 35

T

ass w/ Tendon xanthoma (thickening of Achilles or patellar tendons)

Front 36

In US, optimal level of total cholesterol is ___ or less with LDL cholesterol ___ or less

Back 36

total: <200

LDL: <130 (the lower the better/safer)

Front 37

Statins work by?

Niacin " ?

Back 37

Statin: Inhibiting Chol syn & ^ LDL-Rc

Niacin: v VLDL

Front 38

Earliest manifestations of atherosclerosis is what?

Back 38

Endothelial dysfunction (imparied responsiveness to NO and vasodilation)

Atherosclerosis is a "childhood disease" (begins early)

Ass with abnomalities of the INTIMA which allow inflammatory cells to adhere and get into vessel wall

Front 39

Earliest leasion of atherosclerosis

next steps? (4)

Back 39

1) Lipoproteins (modified LDL)begin to enter the vessel wall accompanied by inflammatory cells

2) Released cytokines/chemoattractants from above convert recruited blood monocytes -> macrophage formation

3) Scavenger receptors on Macrophages make MACROPHAGE FOAM CELLS that in turn make proteolytic enzymes (metalloproteinases) that weaken vessel's intima

4)Intimal infiltration of the plaque area with smooth muscle cells from Media

5) Fatty streak formation

Front 40

Don't develop angina until the lesion occludes the lumen by how much?

Back 40

75% (lots of people can have coronary atherosclerosis and be completely asymptomatic)

Front 41

T/F Most patients who hav edied of MI have had non-occlusive artery disease?

Mech of death?

Back 41

T

When the plaque ruptures, the CLOT that formed suddenly on TOP suddenly (acutely) occludes the artery -> DEATH

Front 42

Plaques that get big enough by themselves to occlude artery never present with devastaing, acute types of ischemia because ?

Back 42

The induce COLLATERALIZATION (gradual occlusion mech)

Front 43

Good risk marker for Occlusive artery disease?

Back 43

C-REACTIVE PROTEIN b/c it is a potential player causing the inflammation of the plaque