Cv: 15. Leech : Things To Know

Front 1

what is the most common form of childhood heart disease? (general)

****

Back 1

shunt

remember- shunts are more common left to right

Hint 1

left to right shunt: right sided heart overload with secondary pulmonary hypertension and right ventricle hypertorphy
cyanosis later in the presentation (whereas in a right to left shunt, cyanosis is immediate)

Front 2

what is the most common congenital defect seen in adults?

Back 2

Atrial Septal Defect

Front 3

what is the most common form of congenital defect seen in kids?

Back 3

Ventricular septal defect

Hint 3

that is the most common CONGENITAL defect, but the most common CAUSE of childhood heart disease is SHUNT

Front 4

what happens in Transposition of Great Arteries?

Back 4

aorta from right ventricle; pulmonary artery from left

Hint 4

fetal development occus as a result of mixing venous and systemic blood through the ductus arteriosus (connetion between pulmonary artery and aortic arch) and the foramen ovale (RA and LA); postnatal life depents on continued patency of the ductus as well as a VSD, ASD or patent foramen ovale

Front 5

The aorta arises from the right ventricle and the pulmonic trunk from the left ventricle. A VSD, or ASD with PSA, is needed for extrauterine survival. There is right-to-left shunting.

this describes?

Back 5

Transposition of Great Vessels

Front 6

Commonest cyanotic heart disease…from birth

Back 6

tetralogy of fallot

remember this has to be a right to left shunt... and just for shits...

VSD, Pulmonary Stenosis, RVH, and Overriding aorta

Front 7

what is the most likely cause of congenital heart disease?

Back 7

UNKNOWN!

90% have unknown etiology

mix of genetic and environment

Front 8

are many congenital heart defects a result of enviornment?

Back 8

not really

< 1% of congenital defects are environmental - - best known is maternal rubella in 1st trimester  patent ductus arteriosis, pulmonic & aortic stenosis, tetralogy of Fallot & others

Front 9

are many congenital heart defects a result of genetics?

Back 9

5% associated with multisystem syndromes 2° to chromosomal abnormalities - - trisomy 21 (Down Syndrome) 13, 15,18, & Turner (45X)

Front 10

when does Degenerative Calcific Aortic Valve Stenosis occur (age group)

Back 10

70-80

Hint 10

majority in 70s and 80s
few are secondary congenital bicuspid valves and develop disease in 50s and 60s

Front 11

80 year old patient presents with angina, syncope, and CHF... what does she likely have?

Back 11

Degenerative Calcific Aortic Valve Stenosis

Front 12

a patient with Degenerative Calcific Aortic Valve Stenosis has LVH secondary to pressure overload... what caused this?

Back 12

thickening and immobility of aortic valve cusps with narrowing of the orifice

Front 13

where do subendothelial rigid calcific masses occur in Degenerative Calcific Aortic Valve Stenosis?

Back 13

in the sinuses of Valsalva

Front 14

a patient has regurgitation and arrhytymias secondary to impinging on conduction pathways... what is this likely do to?

Back 14

Mitral Annular Calcification

Front 15

does Mitral Annular Calcification
provide a focus for infective endocarditis?

Back 15

NO!

Hint 15

Mitral Annular Calcification is degenerative, nonimflammatory, calcific deposits within the mitral annulus; you pretty much just get the stenosis, it does not provide a good site for bacteria

Front 16

with Mitral Annular Calcification
you obviously get calcific deposits on the annulus, but is this an inflammatory disease?

Back 16

no

Front 17

what is the pathogenesis of infective endocarditis?

Back 17

blood-borne bacteria 2° to infection elsewhere in the body; IV drug abuse; dental or surgical procedures; micro-injuries to gut, urinary tract, oropharynx or skin

Front 18

what are 2 major risk factors for infective endocarditis?

Back 18

congenital heart anomalies

mitral valve prolapse

Hint 18

infective endocarditis is a blood bourne bacteria secondary to infection

Front 19

with endocarditis, what will you likely see?

Back 19

Direct injury to valves or myocardium & aorta

Front 20

how do you get an embolism with infective endocarditis?

Back 20

Irregular reddish tan vegetations overlie valve cusps that are being destroyed. Portions of the vegetation can break off and become septic emboli.

Front 21

what type of patients will you see non bacterial thrombotic endocarditis?

Back 21

: cancer patients (particularly visceral adeno) prolonged debilitating illness (renal failure, chronic sepsis) thought to be 2° DIC or other hypercoagulable condition; may embolize to brain, heart, or elsewhere

Front 22

do you have valve damage in non bacterial thrombotic endocarditis? what about in bacterial?

Back 22

non bacterial thrombotic endocarditis: no

bacterial: yes

Front 23

is high serum HDL a risk cholesterol risk factor?

Back 23

NO, that is a good thing!

if you have LOW HDL that is a risk factor...

or high LDL

Front 24

 age
Family history
Cigarette smoking
Hypertension
Marked obesity
Sedentary lifestyle

these are all what?

Back 24

risk factors for cholesterol

Front 25

11) Understand the current hypothesis for atherosclerosis

Back 25

The response to injury hypothesis

chronic endothelial injury

accumulation of lipoproteins (LDL mainly)

oxidation of lipoproteins

adhesion of monocytes & other leukocytes

release of platelet factors → migration of smooth muscle cell into intima

proliferation of SMC’s

↑ accumulation of lipids

Front 26

12) Know lab tests for acute myocardial infarct…the GOLD STANDARD

Back 26

increase in serum troponin

Hint 26

may also see an increase in serum creatine kinase MB

Front 27

what are the 3 types of Angina?

Back 27

stable, Prinzmetal, unstable

Hint 27

stable- caused by atherosclerosis, so upon exertion there is an increase in oxygen demand but no increase in supply because the arteries can't dilate
prinzmetal- vasospasm causing a decrease in coronary blood flow
unstable- plaque disruption with mural thrombosis

Front 28

describe stable angina

Back 28

chest pain due to >75% stenosis of major coronary artery

Front 29

describe Prinzmetal angina

Back 29

vasospasm causes problem

happens at rest

Front 30

describe unstable angina

Back 30

plaque disruption with mural thromboses

Hint 30

remember, there are three kinds of angina pectoris:
stable- more than 75% stenoses in major coronary arteries
prinzmetal- vasospasm
unstable- plaque disruption

Front 31

what are the two types of MI? describe

Back 31

transumural: full thickness of ventricular wall

subendocardial: limited to inner 1/3 to 1/2 of ventricular wall, usually in area of diminished perfusion

Front 32

this MI is limited to the inner 1/3 to 1/2 of the ventricular wall - - - usually in an area normally of diminished perfusion

Back 32

subendocardial

Front 33

this MI is full thickness of the ventricular wall, usually 2° to severe coronary atherosclerosis with plaque disruption & superimposed occlusive thrombosis

Back 33

Transmural

Front 34

what normally causes transmural MI

Back 34

90% are 2° to coronary atherosclerosis with one or more stenosing & subsequently disrupted plaques.

Hint 34

those plaquest occur most often in the circumflex arteries adn the right coronary

Front 35

in transmural MI what chamber of the heart is most commonly affected

Back 35

LV

Front 36

what causes subendocardial MI?

Back 36

Diffuse coronary atherosclerosis and global border line perfusion made transiently critical by increase demand, vasospasm or hypotension but without thrombosis

result of locally decreased blood supply, possibly from a narrowing of the coronary arteries

Hint 36

remember,

transmural caused by a disrupted plaque and stenosed coronary arteries

subendocardial caused by coronary atherosclerosis with or without thrombus

Front 37

please describe the gross changes of MI for the following time frames:

6-12 hrs
18-24 hrs
1st week
7-10 days
6 weeks

**TEST

Back 37

6-12: see nothing

18-24: pale to cyanotic

1st week: yellow and soft tissue

7-10 days:rim of hyperemic granulation tissue

6 weeks: white fibrous scar is well established

Front 38

how long does it take to see a white fibrous scar post MI?

Back 38

6 weeks

Front 39

when do you see a yellow tan and soft area post MI (time)

Back 39

1 week after MI

Front 40

6-12 hours post MI what would you see as far as gross change in the heart grossly?

Back 40

listen to mugatu...nothing!!!!

Front 41

1 hr post MI what micro changes would you see?

Back 41

nothing really

Front 42

12-72 hours post MI what micro changes will you see?

Back 42

neutrophilic infiltration into the necrotic tissue -->myocyte coagulative necrosis; dead myocytes become hypereosinophilic with loss of nuclei

Front 43

3-7 days post MI what micro changes will you see?

Back 43

dead myocytes begin to disintegrate and are resorbed by macrophages

Front 44

7-10 days post MI what micro changes will you see?

Back 44

granulation tissue progressively replaces necrotic tissue -->dense fibrous scar