S.p. Exam #1 - Heart

Front 1

Steatosis

Back 1

- In cellular pathology, steatosis (also called fatty change, fatty degeneration or adipose degeneration) is the process describing the abnormal retention of lipids within a cell.
- It reflects an impairment of the normal processes of synthesis and elimination of triglyceride fat. - Excess lipid accumulates in vesicles that displace the cytoplasm.

Front 2

necessary components to pump the heart

Back 2

- Blood vessels (arteries and veins)
- Muscle (myocardium)
- Cardiac valves
- Conduction system

Front 3

blood flow of the heart

Back 3

- De-oxygenated blood flows from the superior and inferior vena cavae into the right atrium
- Through the tricuspid valve into the right ventricle
- Through the pulmonic valve into the pulmonary arteries and lungs (exchange of gases)
- Through the pulmonary veins – returning oxygenated blood into the left atrium
- Through the mitral valve into the left ventricle
- Out through the aortic valve into aorta to be distributed to the body

Front 4

Why is the left ventricle thicker than the right ventricle?

Back 4

Form follows function. Why?

- RV pumps blood to the lungs. LV pumps blood to the entire body.

- LV AND THE AORTA ARE THICK WALLED.

Front 5

components of the heart's conduction system

Back 5

- SA node (pacemaker), junction of the right atrial appendage and the superior vena cava
- AV node, at the right atrium along the atrial septum
- Bundle of His and the right and left bundle branches

Front 6

The conductor of the rate and rhythm is the _____

Back 6

SA node (pace maker)

Front 7

Systole

Back 7

contraction (the ventricular muscle contracts during systole)

Front 8

Diastole

Back 8

(the ventricular muscle relaxes during diastole)

Front 9

pericardium

Back 9

Parietal pericardium
- Fibrous tissue (collagen)

Pericardial sac
- Potential space
- Fluid
- completely surrounds the heart and is composed of fibrous connective tissue and acts as a protective membrane

Visceral pericardium – Lines the epicardium
- Single layer of mesothelium

Front 10

Why do you need elastic tissue in the pericardial sac?

Back 10

Because it acts as a pump, that has to be able to expand and contact protects the heart, and holds it in place within the thorax

Front 11

Hemopericardium

Back 11

blood in the pericardial sac – is a pathologic state – abnormal - (MI with myocardial rupture)

- If you look at this in a radiograph you see a huge heart and makes you think is cardiomegaly , but is really blood covering the heart.
- you also see hemopericardium if you have a rupture of the ascending part of the aorta , or rupture of the coronary artery and all the blood escapes into the pericardial sac.

Front 12

Pericarditis

Back 12

an inflammation of the pericardial sac
It can be a uremic pericaritis due to kidney failure , or an infectious pericarditis

Front 13

Chronic epicarditis

Back 13

- Adipose tissue normally covers the epicardial surface of the heart
- the epicardial surface of the heart is no longer smooth
- There Is a purulent exudate, and fibrinous adhesion- this tells you this is pathologic
- most common causes of chronic epicarditis – infectious(bacterial), chemical (uremia) or tumor metastasis (rare)

Front 14

Myocardium

Back 14

- made up of specialized striated muscle fibers
- They are specialized bc they branch, (unlike smooth muscle)
- Cardiac muscle branches bc the myofibrils have to stretch all the way around the heart

- striated muscle (myofibrils) make up most of the volume because they are large fibers
- myocardium also have endothelial cells (within)- they invest all of the valves , papillary muscles, atrial chambers, ventricular chambers

Front 15

5 components of myocytes

Back 15

5 components of myocytes

Sarcolemma (cell membrane)
conduction
- Sarcoplasmic reticulum

Reservoir for electrolytes
- Sarcomere

Contractile elements (actin, myosin)
- Regulatory proteins (Troponin, tropomyosin)

Mitochondria
- Aerobic metabolism

Nucleus
- Single, spindle shaped

Front 16

Sarcolemma

Back 16

5 components of myocytes

Sarcolemma (cell membrane)
conduction
- Sarcoplasmic reticulum

Reservoir for electrolytes
- Sarcomere

Contractile elements (actin, myosin)
- Regulatory proteins (Troponin, tropomyosin)

Mitochondria
- Aerobic metabolism

Nucleus
- Single, spindle shaped

Front 17

sarcoplasmic reticulum

Back 17

5 components of myocytes

Sarcolemma (cell membrane)
conduction
- Sarcoplasmic reticulum

Reservoir for electrolytes
- Sarcomere

Contractile elements (actin, myosin)
- Regulatory proteins (Troponin, tropomyosin)

Mitochondria
- Aerobic metabolism

Nucleus
- Single, spindle shaped

Front 18

sarcomere

Back 18

5 components of myocytes

Sarcolemma (cell membrane)
conduction
- Sarcoplasmic reticulum

Reservoir for electrolytes
- Sarcomere

Contractile elements (actin, myosin)
- Regulatory proteins (Troponin, tropomyosin)

Mitochondria
- Aerobic metabolism

Nucleus
- Single, spindle shaped

Front 19

mitochondria

Back 19

5 components of myocytes

Sarcolemma (cell membrane)
conduction
- Sarcoplasmic reticulum

Reservoir for electrolytes
- Sarcomere

Contractile elements (actin, myosin)
- Regulatory proteins (Troponin, tropomyosin)

Mitochondria
- Aerobic metabolism

Nucleus
- Single, spindle shaped

Front 20

nucleus of myocyte

Back 20

5 components of myocytes

Sarcolemma (cell membrane)
conduction
- Sarcoplasmic reticulum

Reservoir for electrolytes
- Sarcomere

Contractile elements (actin, myosin)
- Regulatory proteins (Troponin, tropomyosin)

Mitochondria
- Aerobic metabolism

Nucleus
- Single, spindle shaped

Front 21

average size of left ventricle

Back 21

Left ventricle – 1.3 to 1.5 cm
Right ventricle – 0.3 to 0.5 cm

*the left ventricle has to be thicker than the right ventricle bc you have to pump the blood up through the aorta.
So there are higher pressures on the left side of the heart

Front 22

average size of right ventricle

Back 22

Left ventricle – 1.3 to 1.5 cm
Right ventricle – 0.3 to 0.5 cm

*the left ventricle has to be thicker than the right ventricle bc you have to pump the blood up through the aorta.
So there are higher pressures on the left side of the heart

Front 23

Cardiomegaly

Back 23

Cardiomegaly (enlarged heart):
- Hypertrophy – same number of cells, just larger
- Dilation – enlarged chamber size
--> In response, will release Atrial Natriuretic Peptide

Front 24

endocardium

Back 24

- Innermost lining of heart chambers, valves, chordae tendineae, papillary muscles and trabeculae carneae
- Endothelium
- Connective tissue
- Smooth muscle
Termination of conduction system

Front 25

Endothelial lining of the endocardium

Back 25

a single layer of squamous epithelium , Fibrous connective tissue, is were you have small capillaries and BV
Capillaries and BV’s protect the innermost myocardium, and supply blood and nutrients

Endocardial layer is critically important

Front 26

Atrio-Ventricular valves

Back 26

- Tricuspid and mitral
- Leaflets, chordae tendinae, papillary muscles, myocardium

Front 27

Semilunar valves

Back 27

- Pulmonic and Aortic
- Cusps

Front 28

coronary arteries

Back 28

- 2 to 4 mm in diameter
- Supply nutrients to the heart
- Arise from the ascending portion of the aorta
--> Sinus of Valsalva
- Course along the epicardial surface and send branches to nearly every myocyte
- Flow during diastole
- Collaterals

Front 29

What happens when the atherosclorotic plaque become very big and cover the coronary ostia?

Back 29

prevents blood flow into the coronary arteries and that leads to myocardial infarcts

Front 30

different coronary arteries

Back 30

Left Main (left anterior descending and left circumflex):

Left Anterior Descending:
- Diagonals
- Supplies the apex, anterior LV wall, anterior 2/3 septum

Left Circumflex:
- Obtuse marginals
- Lateral Left Ventricle

Right Coronary Artery:
- Right Ventricle, posterior 2/3 of septum (post descending) and posterior basal Left Ventricle

Front 31

left main coronary artery branches into....

Back 31

Left Main (left anterior descending and left circumflex):

Left Anterior Descending:
- Diagonals
- Supplies the apex, anterior LV wall, anterior 2/3 septum

Left Circumflex:
- Obtuse marginals
- Lateral Left Ventricle

Right Coronary Artery:
- Right Ventricle, posterior 2/3 of septum (post descending) and posterior basal Left Ventricle

Front 32

LAD supplies...

Back 32

Left Main (left anterior descending and left circumflex):

Left Anterior Descending:
- Diagonals
- Supplies the apex, anterior LV wall, anterior 2/3 septum

Left Circumflex:
- Obtuse marginals
- Lateral Left Ventricle

Right Coronary Artery:
- Right Ventricle, posterior 2/3 of septum (post descending) and posterior basal Left Ventricle

Front 33

Right Coronary Artery supplies...

Back 33

Left Main (left anterior descending and left circumflex):

Left Anterior Descending:
- Diagonals
- Supplies the apex, anterior LV wall, anterior 2/3 septum

Left Circumflex:
- Obtuse marginals
- Lateral Left Ventricle

Right Coronary Artery:
- Right Ventricle, posterior 2/3 of septum (post descending) and posterior basal Left Ventricle

Front 34

left circumflex artery supplies....

Back 34

Left Main (left anterior descending and left circumflex):

Left Anterior Descending:
- Diagonals
- Supplies the apex, anterior LV wall, anterior 2/3 septum

Left Circumflex:
- Obtuse marginals
- Lateral Left Ventricle

Right Coronary Artery:
- Right Ventricle, posterior 2/3 of septum (post descending) and posterior basal Left Ventricle

Front 35

bloodflow of the lungs

Back 35

Deoxygenated blood from right side of heart (return from body) flows to lungs where exchange of CO2 for O2 occurs.

Oxygenated blood then leaves via pulmonary veins to the left side of the heart to be sent to the body.

Front 36

in the lungs... gaseous exchange occurs within

Back 36

alveolar septae

--> Alveolar septa- are very thin wall capillaries that allow for exchange of gas O2 and CO2

Front 37

Alveolar septa

Back 37

are very thin wall capillaries that allow for exchange of gas O2 and CO2

Gaseous exchange occurs within the alveolar septae

Front 38

normal aging of the heart chambers

Back 38

Chambers:
- Increased left atrial cavity size, Decreased left ventricular cavity size, Sigmoid-shaped ventricular septum

Valves:
- Aortic valve calcific deposits, Mitral valve annular calcific deposits, Fibrous thickening of leaflets, Buckling of mitral leaflets toward the left atrium, Lambl excrescences

Front 39

normal aging of the heart valves

Back 39

Chambers:
- Increased left atrial cavity size, Decreased left ventricular cavity size, Sigmoid-shaped ventricular septum

Valves:
- Aortic valve calcific deposits, Mitral valve annular calcific deposits, Fibrous thickening of leaflets, Buckling of mitral leaflets toward the left atrium, Lambl excrescences

Front 40

normal aging of the epicardial coronary arteries

Back 40

Epicardial Coronary Arteries
- Tortuosity, Increased cross-sectional luminal area, Calcific deposits, Atherosclerotic plaque

Myocardium:
- Increased mass, Increased subepicardial fat, Brown atrophy, Lipofuscin deposition, Basophilic degeneration, Amyloid deposits

Front 41

normal aging of the myocardium of the heart

Back 41

Epicardial Coronary Arteries
- Tortuosity, Increased cross-sectional luminal area, Calcific deposits, Atherosclerotic plaque

Myocardium:
- Increased mass, Increased subepicardial fat, Brown atrophy, Lipofuscin deposition, Basophilic degeneration, Amyloid deposits

Front 42

normal aging of the aorta

Back 42

Aorta:
- Dilated ascending aorta with rightward shift (due to a loss of elastic fibers and atheroscleorotic plaque )
- Elongated (tortuous) thoracic aorta
- Sinotubular junction calcific deposits
- Elastic fragmentation and collagen accumulation
- Atherosclerotic plaque

Front 43

Dilated ascending aorta

Back 43

due to a loss of elastic fibers and atheroscleorotic plaque

Front 44

cause of heart failure

Back 44

Systolic
- 65%
- Poor pump

Diastolic
- 35%
- Poor filling

Front 45

majority of heart failure is (systolic / diastolic)

Back 45

Systolic
- 65%
- Poor pump

Diastolic
- 35%
- Poor filling

Front 46

systolic heart failure

Back 46

Compensatory mechanisms:
- Increased end diastolic filling pressure
- Increased end diastolic volume
- Neurohumoral

Frank Starling Law
- Increased volume leads to increased cardiac output
- Greater overlap of sarcomere filaments thus increased force

- Eventually, the length of the sarcomere length will become too long and the actin-myosin bridges will not overlap
- The higher end pressure will cause backup of blood into the pulmonary circulation

Front 47

Neurohumoral Response to Heart Failure

Back 47

Front 48

left vs. right-sided heart failure

Back 48

Left sided:
- More common
- Systemic disease
- Respiratory difficulties

Right sided:
- Less common
- Secondary to left sided failure, pulmonary disease

Front 49

which is more common... L or R sided heart failure?

Back 49

Left sided:
- More common
- Systemic disease
- Respiratory difficulties

Right sided:
- Less common
- Secondary to left sided failure, pulmonary disease

Front 50

etiology of heart failure

Back 50

- Hypertension
- Atherosclerosis / Myocardial infarct(s)
- Valvular disease
- Inflammatory disease
- Tumors

Front 51

on a dead body... if you see a blue green bruise.. what does that signify?

Back 51

tells you something is dead under the skin

Front 52

if you see pitting edema during an autopsy...

Back 52

Pitting edema tells us there was a heart problem

Front 53

Most common cause of mitral valve stenosis is _____

Back 53

rheumatic heart disease

--> causes sclerosis , and narrowing of your mitral valves --- fish mouth appearance
- so the blood is having a hard time getting through that mitral valve- mitral valve is no longer pliable

Front 54

Left atrial fibrosis

Back 54

Left atrial fibrosis c/w regurgitation

Left atrial fibrosis with regurgitation (backflow of blood)- through a stenotic mitral valve from rheumatic heart disease
You may hear a heart murmur (turbulent flow) due to the flow through the stenotic valve
Tx for this will be valve replacement

Front 55

What happens when you have endocarditis affecting the chordae tendinae, and you have ruptured of one of those cherdae tendinae ?

Back 55

Then you have an incompetent valve that wont open or close properly , having regurgitant flow

Front 56

Damage of the AV valves can lead to...

Back 56

Stenosis
Regurgitation
Mixture of both

Front 57

stenosis

Back 57

- Does not open fully
- Impedes forward flow
- Blood and pressure back up

Can be either:
- Acquired aortic and mitral (2/3 of all valvular disease)
- Primary chronic cuspal abnormalities

Front 58

regurgitation

Back 58

- Does not close completely
- Backflow of blood

Can be from:
Dilation of ventricle (affecting papillary muscle)
Dilation of aorta or pulmonary artery (affecting commisures)
Damage to cusps or supporting structures (chordae tendinae)

Front 59

most common valve diseases

Back 59

Aortic stenosis: calcification of anatomically normal and congenitally bicuspid aortic valves

Aortic insufficiency: dilation of the ascending aorta, related to hypertension and aging.

Mitral stenosis: rheumatic heart disease (99%)

Mitral insufficiency: myxomatous degeneration (mitral valve prolapse)

Front 60

Aortic stenosis

Back 60

calcification of anatomically normal and congenitally bicuspid aortic valves
--> mainly an aging problem

Front 61

Aortic insufficiency

Back 61

dilation of the ascending aorta, related to hypertension and aging

Front 62

Mitral stenosis

Back 62

rheumatic heart disease (99%)

Front 63

Mitral insufficiency

Back 63

myxomatous degeneration (mitral valve prolapse)

--> Myxomatous- softening of the leaflets of mitral valves – is soft bc is a mix of mucous and loose collagenous tissue
This occurs in young females (she mentioned a 30 y/o)

Front 64

what is THE most common valvular disease ?

Back 64

CALCIFIC AORTIC STENOSIS

- Most common valvular disease
- Repetitive mechanical stress
- Calcification of damaged valve from wear and tear
- Dystrophic deposits of calcium phosphate

Front 65

Calcific Aortic Stenosis

Back 65

- Most common valvular disease
- Repetitive mechanical stress
- Calcification of damaged valve from wear and tear
- Dystrophic deposits of calcium phosphate

Front 66

Tx for rheumatic heart disease or aortic stenosis from normal aging is __________

Back 66

valve replacement

Front 67

**bicuspid aortic valve

Back 67

- found in only ~1% of the population
- Instead of having three nice cusps they only have 2
- Eventually the valve will become stenotic and fibrotic bc of the undo stress and increase pressure on the valve
- Predisposed to calcification – any valve that is damaged and under a lot of stress

Front 68

calcific aortic stenosis

Back 68

- Heaped up calcifications
- Within the cusps, free edge usually uninvolved
- Commisures not fused (as opposed to rheumatic disease)
- Protrude into sinuses of Valsalva thus preventing complete opening

Front 69

difference between calcific aortic stenosis & rheumatic disease

Back 69

- in calcific aortic stenosis, Commisures not fused (as opposed to rheumatic disease)

Front 70

aortic regurgitation

Back 70

Intrinsic Valvular Disease
- Postinflammatory scarring (rheumatic heart disease)
- Infective endocarditis

Aortic Disease
- Degenerative and hypertensive aortic dilation
- Syphilitic aortitis
- Ankylosing spondylitis
- Rheumatoid arthritis
- Marfan syndrome

Front 71

aortic regurgitation

Back 71

- Left ventricle hypertrophies and dilates to accommodate the regurgitant volume and provide adequate cardiac output
- Often asymptomatic, and if normal LV function these patients get medical treatment (BP lowering)
- Symptomatic patients require surgery. Pts with subnormal EF and symptoms <1 yr do very well

Front 72

mitral stenosis

Back 72

postinflammatory scarring
--> rheumatic heart disease

Front 73

Clinical symptoms : of mitral stenosis

Back 73

- Dyspnea on exertion: sitting on a chair and they cant breath
- Orthopnea- trouble breathing
- Atrial fibrillation– an irregular heart beat
- Pumonary hypertension- pressure on the right side of the heart are increasing
- Cor pulmonale- heart and lung condition - lungs are being affected that’s why you are having trouble breathing

Front 74

Angina

Back 74

narrowing of the coronary arteries due to the decrease in blood flow through the coronary arteries , causing myocardial ischemia, and infarction

Angina NOT involved with mitral stenosis

Front 75

**rheumatic fever

Back 75

- affects young people (5-15 y/o) with pharyngitis
- Follows β-hemolytic Strep group A pyogenes pharyngitis (2 - 3 weeks)
Anti-streptolysin O antibodies in serum
- Immune mediated (Ab against M protein)
- Fibrinoid necrosis along chorda tendinae and lines of closure of valves
- May lead to chronic rheumatic heart disease

Front 76

major symptoms of rheumatic fever

Back 76

Major:
- Migratory polyarthritis (inflammation of the big joints)
- Pancarditis
--> “Bread and butter” pericarditis -- the exudate of the pericardial surface of the heart
- Subcutaneous nodules
- Eryhtema marginatum
- Syndenham chorea

Minor:
- Fever, elevated ESR or C reactive protein, EKG changes

Front 77

minor symptoms of rheumatic fever

Back 77

Major:
- Migratory polyarthritis (inflammation of the big joints)
- Pancarditis
--> “Bread and butter” pericarditis -- the exudate of the pericardial surface of the heart
- Subcutaneous nodules
- Eryhtema marginatum
- Syndenham chorea

Minor:
- Fever, elevated ESR or C reactive protein, EKG changes

Front 78

Aschoff body

Back 78

During acute RF, focal inflammatory lesions are found in various tissues. Distinctive lesions occur in the heart, called Aschoff bodies, which consist of foci of lymphocytes (primarily T cells), occasional plasma cells, and plump activated macrophages called Anitschkow cells (pathognomonic for RF).

- they can involve the endocardium, myocardium, and paricardium

Front 79

rheumatic mitral stenosis

Back 79

- Chronic stage of RHD
- Thick fibrotic valvular disease with organization (neo-vascularization) of acute inflammation
- Fusion of commisures “Fishmouth”
- Short, thick chorda tendinae
- Affects- Mitral (65 – 70%), Mitral + Aortic (25%)
- Nearly eradicated in industrialized world

Front 80

Mitral annulus

Back 80

The mitral annulus is a ring that is attached to the mitral valve leaflets. Unlike prosthetic valves, it is neither circular nor continuous. The annulus contracts and reduces its surface area during systole to help provide complete closure of the leaflets. Annular dilatation can result in poor leaflet apposition, leading to mitral regurgitation.

Front 81

Mitral Regurgitation

Back 81

Mitral leaflets
- Rheumatic heart disease with retraction
- Mitral valve prolapse

Mitral annulus
- Dilation of annulus because of ventricular enlargement from CHF
- Mitral annulus calcification

Infarct of Papillary muscle

Front 82

mitral valve prolapse

Back 82

- 3% of adults (young women)
- “Floppy valve”
- Mostly incidental finding
- Midsystolic click (most times you dont hear this)
- Echocardiography
- Rubbery, redundant leaflets
- Long, thin chorda tendinae
- Prone to rupture with flail valve
- Dilated annulus
- Myxomatous degeneration (diffuse softening of the leaflets )
- Fibrosa – attenuated
- Spongiosa – thick (myxoid)

Front 83

complications of mitral valve prolapse

Back 83

- Thick leaflets
- Endocardial fibrosis atrium and ventricle
- Atrial surface thrombi
- Calcification
- Infective endocarditis
- Systemic infarcts
- Arrhythmias

Front 84

artificial valve complications

Back 84

- 60% within 10 years
- Thrombo-embolism:
- Mechanical valves
- On anticoagulants (complications themselves)

- Heart valve replacement complication might be that can cause blood clots so pts might be in anticoagulant medications
Can deteriorate overtime – specially seen in cadaver replaced valves

Front 85

common artificial valve complication

Back 85

infective endocarditis
- Most common in first 5 to 6 weeks
- Prosthesis-tissue interface or cusps
- Ring abscess
- Staph epidermidis, Staph aureus, strep, fungi
- Surgery may be needed

Front 86

infective endocarditis

Back 86

- Most common in first 5 to 6 weeks
- Prosthesis-tissue interface or cusps
- Ring abscess
- Staph epidermidis, Staph aureus, strep, fungi
- Surgery may be needed

Front 87

non-bacterial thrombotic endocarditis

Back 87

- Fibrin, platelets and other blood products
- No infectious organisms
- Not invasive or destructive
- Associated with chronic illnesses

Front 88

infective endocarditis

Back 88

Entry of bacteria into bloodstream
-Invasive (dental, surgical) procedures
-Intravenous drug abuse

Colonization of endocardium (valves)

Superimposed on early thrombus (platelets and fibrin)
-Sites of damage to endothelium of endocardium

Front 89

*acute vs. subacute infective endocarditis

Back 89

Acute:
-Fever Normal valves
-Chills Rapid course
-Weakness Highly virulent organisms
Staph aureus, Strep pyogenes

Subacute:
-Fatigue Abnormal valves
-Loss of weight Protracted course
-Flu-like symptoms Low virulence organisms Strep viridans, Staph epiderm

Front 90

*acute infective endocarditis

Back 90

Acute:
-Fever Normal valves
-Chills Rapid course
-Weakness Highly virulent organisms
Staph aureus, Strep pyogenes

Subacute:
-Fatigue Abnormal valves
-Loss of weight Protracted course
-Flu-like symptoms Low virulence organisms Strep viridans, Staph epiderm

Front 91

*subacute infective endocarditis

Back 91

Acute:
-Fever Normal valves
-Chills Rapid course
-Weakness Highly virulent organisms
Staph aureus, Strep pyogenes

Subacute:
-Fatigue Abnormal valves
-Loss of weight Protracted course
-Flu-like symptoms Low virulence organisms Strep viridans, Staph epiderm

Front 92

predisposing factors to infective endocarditis

Back 92

- Rheumatic heart disease
- Mitral Valve Prolapse
- Calcific stenosis
- Congenital heart disease (bicuspid aortic valve)
- Prosthetic valves
- DM, malignancy, IVDA, immunosuppression

Front 93

infective endocarditis

Back 93

Deformed or damaged valves:
--Strep Viridans (Oral bleeding)
Normal or deformed:
--Staph aureus (IVDA)
Prosthetic valves:
--Staph epidermidis
Enterococcus
HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikinella, Kingella)

Front 94

HACEK

Back 94

(Haemophilus, Actinobacillus, Cardiobacterium, Eikinella, Kingella)

Front 95

complications of infective endocarditis

Back 95

Systemic emboli (ischemic lesions)

Glomerulonephritis

Front 96

you would give anti-coagulation therapy to people who:

Back 96

Foreign material:
- coronary artery stents
- valve replacements

Prone to form blood clots:
- Atrial fibrillation/ Left ventricle dysfunction
- Coagulation defects
- Deep vein thrombosis

- Individuals that don’t move a lot, confined to wheel chairs , dehydrated, diabetics, atrial fibrillation, coagulation defects, DVT, obesity are all prone to form blood clots
- Obese people- die because of blood clots in their legs due to bad circulation traveling to the lungs

Front 97

Different Anticoagulant Medications

Back 97

- Different medications effect different parts of the coagulation cascade
- They require different laboratory tests
- They all effect the ability of the body to form blood clots
- They all carry a risk of bleeding especially when the level is high
- Any patient on anticoagulants needs to have proper levels before undergoing a procedure that can cause significant bleeding (dental, surgical, hip replacements etc.)

Front 98

Heparin

Back 98

- Acts by enhancing the activity of antithrombin, a natural anticoagulant made by the body
- Overdose of heparin can be treated with Protamine
- The test for Heparin is the Partial Thromboplastin Time (PTT)
- Therapeutic levels are about 1.5 times the mean of the normal baseline
- Effect is immediate

Front 99

Overdose of heparin can be treated with _____

Back 99

Protamine

Front 100

heparin acts by...

Back 100

Acts by enhancing the activity of antithrombin, a natural anticoagulant made by the body

Front 101

The test for Heparin is the ______

Back 101

Partial Thromboplastin Time (PTT)

Front 102

Warfarin (Coumadin)

Back 102

- Acts by inhibiting Vitamin K
- Overdose of Warfarin can be treated by giving Vitamin K
- The test for Warfarin is the Prothrombin Time (PT)
- More typically Warfarin is monitored by the International Normalized Ratio (INR)
- The usual therapeutic goal is an INR of 2-3 International sensitivity index (ISI)
- It takes about 4-5 days for the anticoagulant affect of Warfarin to take effect
- Warfarin is for long term management

Front 103

warfarin acts by inhibiting

Back 103

vitamin K

Front 104

Overdose of Warfarin can be treated by giving _____

Back 104

Vitamin K

Front 105

which is immedate ad long term use.. warfarin vs heparin

Back 105

Warfarin is for long term management

Effect of heparin is immediate

Front 106

Acts by enhancing the activity of antithrombin, a natural anticoagulant made by the body

Back 106

heparin

Front 107

Overdose of _____ can be treated with Protamine

Back 107

heparin

Front 108

Acts by inhibiting Vitamin K

Back 108

warfarin (coumadin)

Front 109

Overdose of _____can be treated by giving Vitamin K

Back 109

Warfarin

Front 110

Aspirin (salicylate)

Back 110

blocks prostaglandin formation by inhibiting cyclooxygenase (COX)

In clotting, COX activates thromboxane A-2, (prevents platelets from sticking together)

Aspirin is frequently available in combination with other medications such as antacids, pain relievers, and cough and cold medications.

Front 111

** What does aspirin (salicylate) do?

Back 111

blocks prostaglandin formation by inhibiting cyclooxygenase (COX)

In clotting, COX activates thromboxane A-2, (prevents platelets from sticking together)

Front 112

blocks prostaglandin formation by inhibiting cyclooxygenase (COX)

Back 112

Aspirin (salicylate)

Front 113

Heart Murmurs

Back 113

The sound generated by the turbulent flow of blood

Results from one of the following mechanisms:
- Flow across a partial obstruction (aortic valve stenosis)
- Ejection into a dilated chamber (aortic systolic murmur associated with an aortic aneurysm)
- Regurgitant flow across an incompetent valve (mitral valve regurgitation)
- Shunting of blood from a high to low pressure chamber through an abnormal passage (Ventricular Septal Defect)

Front 114

Murmurs are described by their:

Back 114

- Timing (systole, diastole or continuous)
- Intensity (Systolic murmur 1-6/6 and diastolic murmur 1-4/4)
- Location (Point where maximal intensity is heard on the body)
- Shape (Crescendo, decrescendo, diamond shaped or pansystolic)
- Radiation and maneuvers

Front 115

A heart murmur is an indication of:

Back 115

- underlying valvular (mitral or aortic) disease
- congenital heart abnormality

Front 116

Ventricular Assist Devices (VADs)

Back 116

- VADs improve the length and quality of life but at the expense of an increased incidence of inappropriate shocks, strokes, bleeding, and infection/sepsis.
- VADs are for patients who are not candidates for a heart transplant (destination therapy) or to bridge patients until a heart becomes available.
- Even without the unintended consequences, these therapies can extend patients’ lives to the point of developing other diseases, e.g., dementia or cancer.

Front 117

one of the major complications of VAD

Back 117

strokes

Front 118

Ethical Principles

Back 118

- Respect for patient autonomy and informed consent
- If patients lack an understanding of the benefits and burdens of device therapy, they are less capable of making informed decisions.
- Nonmaleficence—One ought not to inflict evil or harm—Some patients may experience decrements in quality of life leaving them worse off than before device implantation
- Distributive justice—fair and equitable distribution of resources—”To each his or her equal share”. Substantial justification is required for more than an equal share.

Front 119

nonmaleficence

Back 119

- Nonmaleficence—One ought not to inflict evil or harm—Some patients may experience decrements in quality of life leaving them worse off than before device implantation

- Distributive justice—fair and equitable distribution of resources—”To each his or her equal share”. Substantial justification is required for more than an equal share.

Front 120

Distributive justice

Back 120

- Nonmaleficence—One ought not to inflict evil or harm—Some patients may experience decrements in quality of life leaving them worse off than before device implantation

- Distributive justice—fair and equitable distribution of resources—”To each his or her equal share”. Substantial justification is required for more than an equal share.

Front 121

Alcoholism also affects the heart muscle how

Back 121

it causes cardiac hypertrophy (hypertensive cardiovascular disease), and cardiac arrhythmias

Front 122

if pts skin is VERY dry in an autopsy... what could it be

Back 122

diabetes? dehydration from hyperglycemia / and or renal failure). Well groomed.

Front 123

Dilated cardiomyopathy

Back 123

a condition in which the heart becomes weakened and enlarged. As a result, the heart cannot pump enough blood to the rest of the body. There are several different types of cardiomyopathy. Dilated cardiomyopathy is the most common form.

Front 124

Most vulnerable part of the myocardium-

Back 124

the inner third of the myocardium (subendocardial region )

In the inner third of the myocardium (subendocardial region) this is were most of the MI’s and ischemia will start

Front 125

Atherosclerosis

Back 125

- ‘hardening of the arteries’
- Accumulation of fat, cholesterol, and other substances build up and damage the vessel
- Calcification and plaque formation
- Over time, plaques block the arteries, may rupture and / or break off

starts from damage to the ENDOTHELIAL lining --> then invades the muscularis

Front 126

- ‘hardening of the arteries’
- Accumulation of fat, cholesterol, and other substances build up and damage the vessel
- Calcification and plaque formation
- Over time, plaques block the arteries, may rupture and / or break off

Back 126

Atherosclerosis

Front 127

where does atherosclerosis start?

Back 127

damage to the ENDOTHELIAL lining --> then invades the muscularis

Front 128

What does atherosclerosis affect?

Back 128

- The large elastic arteries... like the aorta
- medium and large muscular arteries (coronary arteries )
- It is a Disease of the intima (where it starts) – can involve media
- It’s the leading cause of death in developed nations and is becoming the leading cause of death in developING nations as diet changes
- Commonly referred to as ‘ischemic heart disease’ (IHD)- bc it goes from ischemia to infarction

Front 129

What is the leading cause of death in developed nations and is becoming the leading cause of death in developING nations as diet changes

Back 129

atherosclerosis

Front 130

atherosclerosis is a Disease of the ______ (where it starts) – can involve ____

Back 130

intima ... can involve media

Front 131

intima

Back 131

Intima
- Endothelium to internal elastic lamina
Media
- Smooth muscle
- Internal to external elastic lamina
Adventitia
- Collagen, smooth muscle, vessels, nerves

Front 132

media

Back 132

Intima
- Endothelium to internal elastic lamina
Media
- Smooth muscle
- Internal to external elastic lamina
Adventitia
- Collagen, smooth muscle, vessels, nerves

Front 133

adventitia

Back 133

Intima
- Endothelium to internal elastic lamina
Media
- Smooth muscle
- Internal to external elastic lamina
Adventitia
- Collagen, smooth muscle, vessels, nerves

Front 134

What is the purpose of the internal elastic layer of blood vessels?

Back 134

it is so the vessel can constrict and relax

Front 135

Separates blood stream from vessel wall

Back 135

endothelium

Front 136

*** endothelium

Back 136

- Separates blood stream from vessel wall
- Non-thrombogenic

Vasoregulatory factors
- Nitric Oxide (EDRF, vasodilates, prevents aggregation of platelets)
- Endothelin-1 (Vasoconstricts, normal response to injury)
- Prostacyclin (Vasodilates, prevents aggregation of platelets
- Platelet derived growth factor

Front 137

*** vasoregulatory factors of the endothelium

Back 137

- Separates blood stream from vessel wall
- Non-thrombogenic

Vasoregulatory factors
- Nitric Oxide (EDRF, vasodilates, prevents aggregation of platelets)
- Endothelin-1 (Vasoconstricts, normal response to injury)
- Prostacyclin (Vasodilates, prevents aggregation of platelets
- Platelet derived growth factor

Front 138

**an important point about endothelium

Back 138

it is NON-THROMBOGENIC

--> thats why it needs to be damaged in order to form blood clots

Front 139

insults to the endothelium

Back 139

Front 140

the results of anything that will cause insult to the endothelium....

Back 140

- atherosclerosis
- thrombosis
- ischemia
- infarct
- death

Front 141

**risk factors

Back 141

*Cigarette smoking
- Endothelial damage, hypoxia
Hypertension
- Accelerates atherogenesis
Lipoproteins (LDL)
- Cholesterol, hyperlipidemia
*Diabetes Mellitus
Obesity

Front 142

risk factors

Back 142

Family (parent or sibling, cardiac death < 55 year old)
Estrogen via lipoproteins
Age (Men > 45 year old, Women > 55 year old)
Exercise
Lifestyle
Synergism of the above

Front 143

Three stages of atherogenesis:

Back 143

Initiation
Adaptive
Clinical

Front 144

initiation of atherogenesis

Back 144

- Endothelial dysfunction and / or accumulation of smooth muscle cells (predisposition at branching points)
- Disruption of endothelium
- LDL internalized by intimal smooth muscle cells
- Reactive oxygen species
- Further endothelial disruption
- Buildup of macrophages
- Macrophages ingest lipid and become foamy
- Cytokines released
- Macrophage accumulation and smooth muscle proliferation

Front 145

fatty streak

Back 145

- IN the beginning of atherosclerosis
- We start to see Fatty streaks in the aorta (in the large elastic vessels)
- Can start early in age
- Yellow flat intimal lesion
- Lipid laden macrophages
- Few lymphocytes and smooth muscle cells
- Regression or progress to fibrofatty plaque

Front 146

intimal thickening

Back 146

increase in smooth muscle cells and connective tissue

Front 147

FIBROFATTY (ATHEROMATOUS) PLAQUE

Back 147

- Elevated, white/yellow
- Often eccentric
- Eventually fuse
- Neovascularization – new vessels are thin and delicate and may rupture leading to an acute expansion of the plaque

Front 148

cells involved in fibrofatty (atheromatous) plaque

Back 148

- endothelium
- foam cells
- smooth muscle
- macrophages
- lymphocytes
- lipids, lipoproteins
- serum proteins

Front 149

matrixes involved in fibrofatty (atheromatous) plaque

Back 149

- collagen
- proteoglycans
- elastin
- glycoproteins

Front 150

2nd stage of atherogenesis - adaptive

Back 150

- As lumen size decreases, the vessel remodels to try and maintain normal caliber
- Collaterals
- Once the lumen is narrowed to 45% of its original diameter, cannot compensate (there will be no more collateral flow)

Front 151

3rd stage of atherogenesis - clinical (complicated plaque)

Back 151

- Stenosis >75%
- Ulceration, Fissure, Thrombus
- May have intraplaque hemorrhage
- Dystrophic calcification
- Aneurysm
- Rupture (thrombus = acute)
- Lifestyle change and medications may cause regression of plaque

Front 152

syndromes of atherosclerosis

Back 152

- Angina pectoris (chest pain):
---> Stable – Atheroma which limits blood flow, especially under stress
---> Unstable – Thrombus overlying plaque, not fully occlusive
- Myocardial infarct
- Sudden death

Front 153

angina pectoris

Back 153

- chest pain from the heart muscle itself bc of a lack of blood flow (ischemia , infarct )
-usually occurs when Occlusion > 75%
- No death of myocytes
- Ischemia leads to pain:
---> Substernal, down LEFT arm
---> Pressure on chest
---> “Heartburn”

Front 154

ACUTE CORONARY SYNDROMES

Back 154

Front 155

complications of atherosclerosis

Back 155

Occlusion of vessel, thrombus or embolus:
- Myocardial infarct
- Stroke (intracerebral hemorrhage)
Peripheral Vascular Disease (lower extremities)
Aortic Aneurysm

Front 156

acute myocardial infarction

Back 156

- Increased morbidity and mortality
- Same symptoms as angina but more severe and lasting at least 20 minutes
- Sweating, shortness of breath, nausea, radiating pain , Pale
- Diagnosis made by ECG, laboratory tests (troponins, CK)

Front 157

Location of the myocardial infarct will depend upon what

Back 157

the artery that is occluded.

Front 158

What happens if you have a blockage of the left anterior descending coronary artery?

Back 158

Have ischemia and infarct of the anterior wall of LV, and apex

Front 159

*Most vulnerable part of the myocardium?

Back 159

Inner 1/3rd *

Front 160

Zone of perfusion

Back 160

the initial insult of the myocardial wall (inner 1/3rd most vulnerable part of the myocardium)

Front 161

Zone of necrosis

Back 161

when it fans out and my become transmural

Front 162

Cardiac Myocytes

Back 162

Myocytes- the specialized cells of the myocardium
Fibroblast- provide structure and support for the myocytes ( they are like an infrastructure)

- Ischemic changes within seconds
- Buildup of noxious substances (lactate)
- Loss of contractility within 60 seconds
- Still reversible until 30 minutes when myocyte coagulation necrosis
- Classic MI in 2 to 4 hours, irreversible damage
- Necrosis complete within 6 hours (unless collaterals)

Front 163

what happens when you lose myocytes?

Back 163

they will NOT regenerate
--> replaced by fibrous scar tissue

Front 164

CONSEQUENCES OF ISCHEMIA

Back 164

Cardiac arrhythmia

Sudden death due to Ventricular Fibrillation

Front 165

*** Factors affecting the severity and outcome of the myocardial infarction

Back 165

- The location, severity, and rate of development of coronary atherosclerotic obstructions
- The size of the vascular bed perfused by the obstructed vessels
- The duration of the occlusion
- The metabolic/oxygen needs of the myocardium at risk
- The extent of collateral blood vessels
- The presence, site, and severity of coronary arterial spasm
- Other factors, such as alterations in blood pressure, heart rate, and cardiac rhythm

Front 166

when looking at a cross-section of a heart... how can you tell between the anterior and posterior walls?

Back 166

posterior wall is always flat

Front 167

how long is a reversible MI

Back 167

Front 168

MI for 1/2 - 4 hours....

Back 168

Front 169

MI for 4 - 12 hours....

Back 169

Front 170

MI for 12 - 24 hours....

Back 170

Front 171

MI for 1-3 days...

Back 171

Front 172

how long would you have to have a MI infarction before it shows up on gross look... and you can see the beginning of coagulation on light microscope ?

Back 172

4 - 12 hours

Front 173

how long before you would see a dark mottle in the heart.. and under light microscope see pyknosis of the nuclei and myocyte hypereosinophilia & contraction band necrosis?

Back 173

12 - 24 hours

Front 174

how long before you would see a mottle, yelllow-tan infarct on heart and under microscope, see coagulative necrosis, loss of nuclei and striations

Back 174

1-3 days

Front 175

general outline of an evolving MI

Back 175

couple of dats --> increase of neutrophils

couple of weeks --> increase of granulation tissue

couple of months --> scar tissue

Front 176

when is scarring complete in a MI

Back 176

> 2 months

Front 177

when does granulation tissue form during an evolving MI

Back 177

10-14 days

Front 178

when, during an evolving MI, would you see a hyperemic order, yellow-tan soft center.. and under a microscope see beginning of the disentigration of dead myofibers & dying neutrphils

Back 178

Front 179

Coagulative necrosis

Back 179

the myofibrils are breaking apart bc the normal adjacent myocardium is pulling on he fibers and the fibers start to break apart

Front 180

Complications of Myocardial Infarction

Back 180

Contractile dysfunction
- Heart failure, cardiogenic shock
Arrythmias
- Relies on location of infarct
Cardiac rupture
- Free wall, septum and papillary muscle
- 3 to 7 days most often
Pericarditis

Front 181

When are you most vulnerable to rupture the periocardium?

Back 181

3-7 days you are most prone to get cardiac rupture b/c that when you have intense coagulative necrosis , and the fibroblast have still not come in to lay down that fibrous scar tissue

Front 182

therapy for MIs

Back 182

- Thrombolytics:
---Streptokinase, t-PA (tissue type plasminogen activator)
- PTCA (balloon angioplasty)
- CABG (Coronary artery bypass grafts)
- Stents
- Long term anticoagulants!

Front 183

difference between atherosclerosis and hypertension

Back 183

in atherosclerosis... there are SYMPTOMS
- angina pectoris
- impedes perfusion

hypertension
- NO symptoms (no pain)
- pressure IN the vessels
- does NOT impede perfusion

Front 184

what is important about the fact that hypertension is "systemic"

Back 184

HTN is systemic !!

not only affects the smaller vessels of the heart.. but ALSO the brain and the kidneys !!!

the "end" organs

Front 185

myocytes increase in _____ , NOT ______

Back 185

myocytes increase in SIZE, not in NUMBER

Front 186

hypertension (definition)

Back 186

- a chronic condition in which the blood pressure in the arteries is elevated.
- Blood pressure is determined by two measurements - systolic and diastolic - which depend on whether the heart muscle is contracting (systole) or relaxed between beats (diastole).

- HTN / HBP IS HEART DISEASE!!!!!

Front 187

is hypertension / high blood pressure heart disease?

Back 187

YES !!!

- a chronic condition in which the blood pressure in the arteries is elevated.
- Blood pressure is determined by two measurements - systolic and diastolic - which depend on whether the heart muscle is contracting (systole) or relaxed between beats (diastole).

- HTN / HBP IS HEART DISEASE!!!!!

Front 188

blood pressure = ??

Back 188

Blood Pressure = Cardiac Output x Peripheral Vascular Resistance

- Alteration in either CO or PVR can alter BP
- If Cardiac Output is low, need to increase Peripheral Vascular Resistence to maintain blood pressure
- Thus low renal perfusion
- Cycle continues

Front 189

What factors affect cardiac output?

Back 189

Front 190

What are the 3 types of factors that affect peripheral vascular resistance?

Back 190

1) humoral
2) local
3) neural

Front 191

What are the humoral factors that affect peripheral resistance?

Back 191

Front 192

What are the local factors that affect peripheral resistance?

Back 192

Front 193

What are the neural factors that affect peripheral resistance?

Back 193

Front 194

Clinical parameters of High Blood Pressure

Back 194

Systolic pressure >140 mm Hg
Diastolic pressure > 90 mm Hg
Malignant HTN >200 / 120 mm Hg
- Rapid onset
- Complications within 1 to 2 years

- The higher the BP, the greater risk of complications
- Control significantly decreases morbidity and mortality

Front 195

hypertension

Back 195

- “Silent killer”
---> Asymptomatic (UNLIKE atherosclerosis)
---> 25% of population
- Idiopathic (essential) – 95%
- Secondary (tumors, syndromes) – 5%
- Genetic / Familial / Racial Predisposition
- Environmental / Lifestyle (obesity, stress, cocaine)
- Hypertension is a Systemic Illness
---> Causes blood vessel and organ dysfunction and damage

Front 196

What affects cardiac output (autoregulation) ?

Back 196

Front 197

What affects total peripheral resistance?

Back 197

Front 198

What kind of effect do defects in renal sodium hemostasis have on blood pressure?

Back 198

Front 199

What effect does functional vasocstriction have on blood pressure?

Back 199

Front 200

What effects do defects in vascular smooth muscle growth and structure have on hypertension?

Back 200

Front 201

What would increase plasma and ECF volume? And what effect would that have on blood pressure?

Back 201

Front 202

What kind of effect would a decrease in natrieuretic hormone have on blood pressure?

Back 202

Front 203

What kind of effect would increasing vascular reactivity have on blood pressure?

Back 203

Front 204

What kind of effect would increasing the vascular wall thickness have on hypertension?

Back 204

Front 205

Impact of HTN on Blood Vessels

Back 205

Accelerates atherogenesis
Degenerative changes
Arteriosclerosis

Front 206

Systemic Effects of HTN

Back 206

- Myocardial Infarct
- Cardiac Arrhythmias
- Congestive Heart Failure
- Intracerebral Hemorrhage (stroke)
---> Basal Ganglia
---> Pons
- Chronic Renal Failure
---> Dialysis

Front 207

How does HTN affect the heart?

Back 207

- Cardiac hypertrophy
- Concentric left ventricular hypertrophy
---> Leads to stiffness of the wall and poor compliance
- Hypoperfusion to heart itself
- Abnormal function

Front 208

Myocyte hypertrophy

Back 208

the muscle fibers themselves increase in size NOT number = hypertrophy

we know they are cardiac muscle cells bc they are branching and they have a single centrally placed nucleus

Front 209

Prevention of HTN

Back 209

- Regular Blood Pressure Check-Ups
- Diet
- Exercise
- Lifestyle changes (cig’s, ETOH, cocaine)
- Medication (diuretics AKA water pills)

Front 210

Can HTN be successfully treated?

Back 210

YES !! can be successfully treated and prevented !

Front 211

risk factors are (additive / synergistic) ?

Back 211

synergistic
--> by eliminating one, you can significantly uncouple the risk

Front 212

what does "pre-cordial" mean

Back 212

"pre-cordial" means "before the heart" --> in front of the heart

also called sub-sternal

Front 213

EKG shows an infarct.. WHAT is an infarct ?

Back 213

- tissue is DEAD
- will NOT conduct

Front 214

what kind of necrosis is an infarct?

Back 214

coagulative

Front 215

why do people get myocardial infarctions?

Back 215

- NO blood supply
--> b/c of blockage of an artery

Front 216

what is the most common cause of blockage of a coronary artery?

Back 216

a thrombus
(NOT an embolis.. thats rare)

Front 217

what are the 3 coronary arteries?

Back 217

1) LAD coronary artery
---> feeds the apex of the heart (the distal end of the ventricles), the anterior wall of L ventricle, 2/3 of ant. Ventricular septum that separates R & L ventricles
2) Left circumflex artery
---> feeds the post. 1/3 of ventricular septum, and (along with LAD), feeds L ventricular wall
3) Right coronary artery
---> feeds entire R ventricular wall, posterior 1/3 of ventricular septum, postero-basal portion of L ventricle

Front 218

what does the LAD supply blood to?

Back 218

1) LAD coronary artery
---> feeds the apex of the heart (the distal end of the ventricles), the anterior wall of L ventricle, 2/3 of ant. Ventricular septum that separates R & L ventricles
2) Left circumflex artery
---> feeds the post. 1/3 of ventricular septum, and (along with LAD), feeds L ventricular wall
3) Right coronary artery
---> feeds entire R ventricular wall, posterior 1/3 of ventricular septum, postero-basal portion of L ventricle

Front 219

what does the circumflex artery supply blood to?

Back 219

1) LAD coronary artery
---> feeds the apex of the heart (the distal end of the ventricles), the anterior wall of L ventricle, 2/3 of ant. Ventricular septum that separates R & L ventricles
2) Left circumflex artery
---> feeds the post. 1/3 of ventricular septum, and (along with LAD), feeds L ventricular wall
3) Right coronary artery
---> feeds entire R ventricular wall, posterior 1/3 of ventricular septum, postero-basal portion of L ventricle

Front 220

what does the right coronary artery supply blood to ?

Back 220

1) LAD coronary artery
---> feeds the apex of the heart (the distal end of the ventricles), the anterior wall of L ventricle, 2/3 of ant. Ventricular septum that separates R & L ventricles
2) Left circumflex artery
---> feeds the post. 1/3 of ventricular septum, and (along with LAD), feeds L ventricular wall
3) Right coronary artery
---> feeds entire R ventricular wall, posterior 1/3 of ventricular septum, postero-basal portion of L ventricle

Front 221

what is ischemia?

Back 221

LESS bloodflow because of a decrease of the size of the vessel.. perhaps because of atherosclerotic heart

Front 222

can you die from ischemia?

Back 222

YES

Front 223

what is CPK?

Back 223

creatinine phospho-kinase (aka creatine kinase)

found in a # of tissues... including the heart

if your heart dies... myocardial cells die, releasing CPK into the blood
--> when you see elevated CPK levels in serum, must be heart damage

Front 224

what do elevated CPK levels in serum indicate?

Back 224

creatinine phospho-kinase (aka creatine kinase)

found in a # of tissues... including the heart

if your heart dies... myocardial cells die, releasing CPK into the blood
--> when you see elevated CPK levels in serum, must be heart damage

Front 225

what is the principle cell in a thrombus?

Back 225

platelet
--> ONLY stick on abnormal, rough surfaces

Front 226

what is the most common cause of having emboli

Back 226

from thrombi

Front 227

where would emboli from the left ventricle go?

Back 227

- would go down the aorta
- could travel down the abdominal aorta
- could travel far and go to the kidney
- could could up into the ascending aorta into the carotid and give you a stroke

Front 228

what is THE MOST COMMON outcome following an M.I. ?

Back 228

ventricular fibrullation

--> when the tissue dies, it no longer conducts current

Front 229

what kinds of cells are PNMs

Back 229

acute

Front 230

in chronic disease... what cell types are expected

Back 230

monocytes, macrophages & kymphycytes
--> phagocytoze fat --> when they digest lipids, they become more aggressive and start secreting enzymes (i.e. colalgenase, protease --> further destroying arterail wall) and secrete cytokines that will cause the smooth muscle cells from the media to come over

Front 231

foam cells

Back 231

macrophages that digest lipids

--> phagocytoze fat --> when they digest lipids, they become more aggressive and start secreting enzymes (i.e. colalgenase, protease --> further destroying arterail wall) and secrete cytokines that will cause the smooth muscle cells from the media to come over

Front 232

what types of cells primarily make up the media

Back 232

smooth muscle cells

Front 233

vasa vasorum

Back 233

blood vessels that feed other blood vessels

The vasa vasorum are found in large arteries and veins such as the aorta and its branches. These small vessels serve to provide blood supply and nourishment for tunica adventitia and outer parts of tunica media of large vessels

Front 234

diabetes has 2 major outcomes

Back 234

1) damage to the small blood vessels (microvascular disease --> eyes, kidneys & nerves)
- controlled by controlling blood glucose
2) macrovascular disease = medium + large size arteries
- in diabetes, most common COD is myocardial infarction --> coronary artery diseaase
---> control of blood glucose makes NO DIFFERENCE in this

Front 235

why would you refer to a diabetic as "brittle"

Back 235

means they're not stable
--> blood glucose goes up and down

Front 236

what is SGOT

Back 236

Aspartate transaminase AKA serum glutamic oxaloacetic transaminase (SGOT)

a pyridoxal phosphate (PLP)-dependent transaminase enzyme (EC 2.6.1.1). AST catalyzes the reversible transfer of an α-amino group between aspartate and glutamate and, as such, is an important enzyme in amino acid metabolism. AST is found in the liver, heart, skeletal muscle, kidneys, brain, and red blood cells, and it is commonly measured clinically as a marker for liver health.

--> if elevated.. can indicate a problem in one of those organs

Front 237

troponin test

Back 237

The troponin test measures the levels of certain proteins called troponin T and troponin I in the blood. These proteins are released when the heart muscle has been damaged, such as a heart attack. The more damage there is to the heart, the greater the amount of troponin T and I there will be in the blood.

Front 238

what would cause the tissues to separate during a myocardial infarction?

Back 238

- tissue is dead
- there is inflammation --> edema --> fluid buildup

Front 239

most of the time when people get MI...

Back 239

thrombi in coronary arteries

Front 240

3 types of arteriosclerosis

Back 240

1) atherosclerosis
--> aorta, coronary, cerebral
2) medial calcinosis
--> muscular arteries
3) arteriolat sclerosis
--> arterioles

Front 241

medial calcinosis

Back 241

doesnt really do any damage

3 types of arteriosclerosis

1) atherosclerosis
--> aorta, coronary, cerebral
2) medial calcinosis
--> muscular arteries
3) arteriolat sclerosis
--> arterioles

Front 242

arteriolar sclerosis

Back 242

these small arterioles do not have plaques, but does narrow the lumen to them (i.e. kidney)

3 types of arteriosclerosis

1) atherosclerosis
--> aorta, coronary, cerebral
2) medial calcinosis
--> muscular arteries
3) arteriolat sclerosis
--> arterioles

Front 243

most common site for atherosclerosis

Back 243

abdominal aorta

Front 244

what is a stroke

Back 244

atherosclerosis in a cerebral artery --> thrombus forms --> infarct = stroke

this is liquifactive necrosis

Front 245

diplopia

Back 245

"seeing double"

a result of severe ischemia of the cerebral arteries in the brain

Front 246

transient ischemic attacks

Back 246

when cerebral arteries are occluded.. but not fully blocked off (infarct)

can lead to a major stroke in a short amount of time

Front 247

What can cause pericarditis?

Back 247

- viral common

- fibrinous (acute MI, post MI caleld Dresslers, rheumatic fever)

- purulemt or supperative; infections

--> friction rub on phys exam (goes away when pt leans forward)

Front 248

Dressler's Syndrome

Back 248

fibrinous pericarditis days after MI

Front 249

bruit

Back 249

turbulent bloodflow in a large vessel

Front 250

prophylaxis

Back 250

Amoxicillin 500mg caps
Disp: 4 caps
Sig: take 4 caps po 1 hour before dental appt
Refills: 0

**for pen allergy

Clindamycin 150mg caps
Disp: 4 caps
Sig: Take 4 capsules po 1 hour before dental appt
Refills: 0

Front 251

prophylaxis for pt with penicillin allergy

Back 251

Amoxicillin 500mg caps
Disp: 4 caps
Sig: take 4 caps po 1 hour before dental appt
Refills: 0

**for pen allergy

Clindamycin 150mg caps
Disp: 4 caps
Sig: Take 4 capsules po 1 hour before dental appt
Refills: 0

Front 252

Jaw claudication

Back 252

Jaw claudication is pain in the jaw or ear while chewing. This is caused by insufficiency of the arteries supplying the jaw muscles, associated with giant cell arteritis.

--> could be from giant cell arteritis

Front 253

giant cell arteritis

Back 253

- elderly people
- chronic granulamatous inflammation of large to small sized arteries
- NOT continuous... 9areas of disease / norml / disease etc)
-->> so has "skip areas"

***opthalmic arterial involvement can lead to permanent blindness !! medical emergency !!!

usually UNILATERAL

Front 254

amarousis fugax

Back 254

- fleeting darkness
- sudden loss of vision
- partial OR complete
- one OR both eyes
- mild blurring or fogging or complete blackness, and may involve a part of or all of visual field

**NEEDS EMERGENCY EVALUATION !!!

Front 255

- fleeting darkness
- sudden loss of vision
- partial OR complete
- one OR both eyes
- mild blurring or fogging or complete blackness, and may involve a part of or all of visual field

**NEEDS EMERGENCY EVALUATION !!!

Back 255

amarousis fugax

Front 256

mechanism of injury for amarousis fugax

Back 256

granulamatous !!!!!!

Front 257

Takayasu aortitis

Back 257

- younger than 50
- like Giant cell arteritis
- etiology unknown
- large and small vessels
- used to be sseen in Japanese now in other groups worldwide

--> "pulseless disease) .. associated w. women

Front 258

difference between Takayasu aortis and giant cell artiritis

Back 258

GCA --. elderly

Takayasu - younger than age 50

Front 259

what cells are in a granuloma

Back 259

giant cells

macrophages

Front 260

buergers disease

Back 260

- segmental thrombosing
- medium and small arteries
- acute and chronic inflammation + luminal thrombosis
- especially tibial and radical
- can extend into veins and nerves of extremities
- associated with heavy cigarette smokers < 35 y/o males
- tobacco usage essential for initiation and pregression of disease
- reported in cigar smokers marijuana users and smokeless tobacco users

--> ** 2/3 of people with burgers have periodontal disease

Front 261

what is buerges disease strongly linked with

Back 261

- segmental thrombosing
- medium and small arteries
- acute and chronic inflammation + luminal thrombosis
- especially tibial and radical
- can extend into veins and nerves of extremities
- associated with heavy cigarette smokers < 35 y/o males
- tobacco usage essential for initiation and pregression of disease
- reported in cigar smokers marijuana users and smokeless tobacco users

--> ** 2/3 of people with burgers have periodontal disease

Front 262

wegners granulomatosis (w/ poly angiitis)

Back 262

- granulomatous inflammation involving respiratory tract
- necrotizing
- small vessels including kidney
- nasal or oral ulcers
--. painless or painful. >1 month duration
- bloody or purulent nasal discharge
- CXR: nodules, infiltrates or cavities
- urine with hematuria

Front 263

R to L shunt

Back 263

- blood leaves right heart, bypasing lung
- thru shunt
- mixes with deoxygenated blood in R heart & oxygenated blood in L heart

Front 264

cardinal features of Tetrology of Fallot

Back 264

- large VSD
- obstruction of RV outflow tract
- RVH
- aorta overrides VSD

Front 265

what is the most common form of cyanotic congenital heart disease?

Back 265

teratology of fallot

Front 266

transposition of great arteries (TGA)

Back 266

- aorta arises from RV
- not compatible ith life
- ignoring LV
- survive with shunt

Front 267

Total anomalous pulmonary venous circulation (TAPVC)

Back 267

- pulmonary veins may not form
- atresia

Front 268

for congenital defects... which are blue... L to R or R to L ?

Back 268

ONLY R to L

ONLY ones that make you blue require prophylaxis

Front 269

PDA (patent ductus aerteriosis)

Back 269

allows blood to go away from the lungs when they re in utero
-->

Front 270

which congenital heart diseases require prohylaxis?

Back 270

the ones that cause caynoiss !!

aka all the R to L shunt disorders !!!

"take time to prophylax the T's"

Front 271

"take time to prophylax the T's"

Back 271

any congenital heart disorder with a R to L shunt causes cyanonis and needs prohylaxis

Front 272

what is the most common cyanotic CHD?

Back 272

teratolgy of fallot

Front 273

what is the most common CHD?

Back 273

Ventricular Septal Defect (VSD)