Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/43

Click to flip

43 Cards in this Set

  • Front
  • Back
Inherent problems with the the cardiac muscle generally called?

Usual etiology

What do they all have in common?
Cardiomyopathy (CM)

Etiology often unknown

HEART FAILURE is something all etiologies of CM have in common
4 types of CM
1) Dilated

2) Hypertrophic

3) Restrictive

4) Arrhythmogenic
Dilated CM characteristic feature?

Main Hemodynamic Abnormality

Potential Scenerio?
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
Histological presentation of Dilated CM?
Myocyte Hypertrophy interspersed w/ myocyte Degeneration
Causes of Dilated CM (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!
Young, athletic athlete sudden collapses and dies, think?

Main Hemodynamic Abnormality?

Main Etiology
Hypertrophic CM

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

Familial (almost always; 1/500 carrier gene)
Key Pathological presentation of Hypertrophic CM?
Asymmetric defect of Septum -2-2.5x thicker than other ventricular walls

Can block outflow tract (aorta) & pull anterior mitral leaflet (Mitral regurgitation!!)
CM causing a rigid myocardium?

Main Hemodynamic Abnormality?

Sign?
Restrictive CM

Diastolic Dysfunction (^ Diastolic pressure, v Ventricular filling)

**Right Heart Failure - JVD, hepatomegaly, ascities, peri edema
Main causes of Restrictive CM?
1) Genetic - HEMOCHROMATOSIS & glycogen storage diseases (POMPE'S)

2) AMYLOIDOSIS (amyloidosis sarcoidosis)
Restrictive CM (RCM) presents very similarly to Constrictive CM (CCM)..how do you differentiate?
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**
CM that INVOLVES THE RV and Adipose/fibroadipose replaces the ventricular myocardium?

Predominance in?
Arrhythmogenic MC

Cause/etiology unclear

Strong MALE,YOUNG ADULTS predominance
4 Diseases of the Pericardium
1)Acute Pericarditis

2)Pericadial Effusion

3)Cardiac Tamponade

4)Constrictive Pericarditis
2 Main etiologies of Acute Pericarditis
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
Clinical presentation of Acute Pericarditis (6)
*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
Causes of Pericardial Effusion?
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)
Up to how much pericardial fluid is normal?
50 mL
Clinical Features of Large Pericardial Effusion (3)
1)Soft heart sounds
2)Reduce intensity of friction rub
3)Dullness over posterior lung(Ewart's sign)
Caridiac Tamponade causes
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
Clinical features of Cardiac Tamponade? (4)
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
What is Kussmaul's sign

Sign of?
Take in breath and actually causes INCREASED JVD w/ inspiration

Constrictive Pericarditis
Pattern of Right atrial (jugular venous) pressure w/ Tamponade & Constrictive pericarditis?
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
General composition of Lipoprotein?
Protein and phospholipid on surface and help solubulize the triglyceride and cholesterol ester which is in the core of the molecule
Function of the proteins (4)
1)Solublize lipids

2)Serve as binding ligands

3) Activate or inhibit enzymes

4) Involved in lipid transfer
4 Classes of lipoproteins?
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
T/F Small, denser LDL particles appear to bind more effectively to the LDL receptor?
T
Which lipoproteins are syn by LIVER for energy providing purposes?

" syn by Intestinal enterocytes " ?
VLDL

CM
byproduct of VLDL and is the main Atherogenic lipoprotein
LDL

Diabetes and obesity are ass w/ ^ production of VLDL & LDL
T/F As you eat cholesterol converted to LDL, therefore LDL concerntration ^
F

The cholesterol you eat v the syn and expression of the LDL receptor on the surface of the liver cell
Severe hypertriglyceridemia may manifest as ?
Eruptive xanthoma (Gross Shit!) - clusters of TG surrounded by macrophages
Increased TG CONTENT in a NORMAL amount of VLDL

Ass with use of?

*Variability in lipid panel phenotype amongst family?
Familial Hypertriglyceridemia

Oral estrogen replacement therapy

*NO* (key difference!)
In Familial combined Hyperlipidemia is there variability in lipid panel phenotype amongst family?
*YES* (key difference!)

Very athrogneic abnormality
Fxn of HDL (2)
"good cholesterol"

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

2) Also ANTI-INFLAMMATORY
Most important risk factor for CHD?

2ary risk factors?
LDL cholesterol

-low HDL, HTN, smoking, age, family history
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
T
T/F Familial Hypercholesterolemia is a polygenic dz?
T

ass w/ Tendon xanthoma (thickening of Achilles or patellar tendons)
In US, optimal level of total cholesterol is ___ or less with LDL cholesterol ___ or less
total: <200

LDL: <130 (the lower the better/safer)
Statins work by?

Niacin " ?
Statin: Inhibiting Chol syn & ^ LDL-Rc

Niacin: v VLDL
Earliest manifestations of atherosclerosis is what?
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
Earliest leasion of atherosclerosis

next steps? (4)
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
Don't develop angina until the lesion occludes the lumen by how much?
75% (lots of people can have coronary atherosclerosis and be completely asymptomatic)
T/F Most patients who hav edied of MI have had non-occlusive artery disease?

Mech of death?
T

When the plaque ruptures, the CLOT that formed suddenly on TOP suddenly (acutely) occludes the artery -> DEATH
Plaques that get big enough by themselves to occlude artery never present with devastaing, acute types of ischemia because ?
The induce COLLATERALIZATION (gradual occlusion mech)
Good risk marker for Occlusive artery disease?
C-REACTIVE PROTEIN b/c it is a potential player causing the inflammation of the plaque