Cardiovascular Tl 1 Pathology Koles/rolitsky Lecture

Front 1

Post capillary venules, vein, or lymphatic?
Exchange fluids with interstitium, site of leukocyte epigration, NO MEDIAL LAYER

Back 1

Post capillary venule

Front 2

Post capillary venules, vein, or lymphatic?
Thin walls, no internal elastic lamina, much less medial thickness compared to arteries of same diameter.

Back 2

Vein (sml, med or large)

Front 3

Post capillary venules, vein, or lymphatic?
Very thin walls, resembling venules, one-way conduits for delivering interstitial fluid into venous blood.

Back 3

Lymphatics

Front 4

Arteriole vs Vein
Which has thicker media

Back 4

ARTERIOLE

Front 5

What kind of capillaries are found in the endothelial layer of the heart, lungs, skin, muscle and CNS?

Back 5

Continuous

Front 6

What kind of capillaries are found in the endocrine glands, renal glomeruli, some digestive tract capillaries?

Back 6

Fenestrated

Front 7

What kind of capillaries are found in the liver, spleen, marrow?

Back 7

sinusoids

Front 8

How many layers of endothelia line the cardiovascular system?

Back 8

One
When they are activated, they round up

Front 9

CD___ also known as PECAM 1 is localized to inter endothelial jxs, and is critical for transmigration in acute inflammation.

Back 9

CD31

Front 10

CD___: expressed on activated high endothelial cells in lymph node for binding naive T-cells

Back 10

CD34

Front 11

The following are ultrastructural features of ____________ cells.
Pinocytotic vesciles near cell membrane, jx complexes w/ neighbors, Weibel-Palade bodies

Back 11

Endothelial

Front 12

Endothelial cells produce what two parts of the extracellular matrix?

Back 12

Proteoglycans and collagen

Front 13

Endothelial cells modulate blood flow by producing vasoconstrictors and vasodilators. List two of each.

Back 13

Constrictors: endothelin, ACE
Dilators: nitric oxide, prostacyclin

Front 14

Endothelin cells produce 4 types of anti thrombotic molecules:

Back 14

Prostacyclin
Thrombomodulin
Plasminogen activator
Heparin- line molecules

Front 15

Endothelin cells produce 3 types of pro thrombotic molecules:

Back 15

vWF
Tissue factor (factor III or thromboplastin), which activates factor 7
Plasminogen activator inhibitor

Front 16

Does TGF beta (made by endothelial cells) stimulate or inhibit growth?
What about heparin?

Back 16

Inhibit, inhibit

Front 17

How are the following involved in inflammation and immunity?
IL 1, IL 6, IL 8

Back 17

Chemotaxis of neutrophils

Front 18

Try to list five adhesion molecules for leukocyte emigration:

Back 18

VCAM 1, ICAM, E-selectin, CD31

Endothelial tissue expresses VCAM 1 so T cells know to bind here.

Front 19

Explain metamorphosis of smooth muscle cells esp, a shift from normal contractile phenotype to a proliferative synthetic phenotype.

Back 19

Migration of SMC from media to intima, loss of capacity to contract, increased mitotic activity, increased synthesis of ecm....(stenosis)

Front 20

What is involved in 1/3 of all US deaths?

Back 20

Atherosclerosis (heart disease and stroke)

Front 21

Monckeberg medical calcific sclerosis is uncommon and clinically insignificant....anyways...2 bullets

Back 21

1. calcium deposits in the media of medium sized muscular arteries in folks over 50
2. Does not cause stenosis alone, but affected arteries may develop atherosclerosis in addition to Monckeberg

Front 22

smooth muscle cells + macrophages + lymphocytes + collage + elastic fibers + proteoglycans + intracellular and extracellular lipid + neovascularization in peripheral plaque ===

Back 22

Atheromatous

Front 23

What are foam cells?

Back 23

Lipid filled macrophages

Front 24

Atherosclerosis Classification
I
II
III
IV
V
VI

Back 24

I: isolated foam cells
II: fatty streak
III: II + sml extracellular lipid pool
IV: atheroma (core of excellular lipid)
V: Fibroatheroma (lipid core and fibrotic layer)
VI: Complicated lesion with surface defect (ulceration) plus hematoma or thrombosis
**Virtually all clinically apparent disease results from V and VI

Front 25

The follow are complication of atherosclerosis AHA type _____
Dystrophic calcification
Rupture or ulceration of intimal surfaces
Hemorrhage into plaque
Thrombosis: the most serious complication

Back 25

Type VI

Front 26

Clinical sequelae of atherosclerosis most often involve ________ arteries.

Back 26

Coronary arteries

And in descending order:
Coronary
Cerebral
Aorta
Lower extremity
Mesenteric

Front 27

What layer of the smaller arteries is affected by atherosclerosis?

Back 27

Mainly the intima

Front 28

What layer of the medium/large arteries is affected by atherosclerosis?

Back 28

variable atrophy of the MEDIA w. loss of elastic fibers and calcification. Medial atrophy may produce sufficient weakness to deform the artery leading to an aneurysm.

Front 29

A fatty streak is composed of lipid-filled macrophages + __ ________ + extracellular lipid

Back 29

T lymphocytes

Front 30

Insudated LDL cholesterol is oxidized in arteries a sites of fatty streaks: it is chemotactic for _____________, ingested by ___________ and cytotoxic to _____________ cells.

Back 30

monocytes
macrophages
endothelial

Front 31

Heterozygous familial hypercholesterolaemia?
Affected Gene:
Chromosome:
Frequency:

Back 31

Affected Gene: LDL receptor
Chromosome: 19
Frequency: 1:500

Front 32

familial defective apoprotein B?
Affected Gene:
Chromosome:
Frequency:

Back 32

Affected Gene: Apo B 100
Chromosome: 2
Frequency: 1:700

Front 33

familial combined hyperlipidemia?
Affected Gene:
Chromosome:
Frequency:

Back 33

Affected Gene: ?
Chromosome: ?
Frequency: 1:200

Front 34

familial hypetriglyceridemia?
Affected Gene:
Chromosome:
Frequency:

Back 34

Affected Gene: ?
Chromosome: ?
Frequency: 1:500

Front 35

Elevated levels of this reflect the chronic inflammatory component of atherosclerosis.

Back 35

C-reactive protein

Front 36

Inborn errors of this can lead to premature atherosclerosis and higher levels are associated with more risk of ischemic heart disease.

Back 36

Homocysteine

Front 37

_________ = apo B100 portion of LDL linked to apo A
Elevated levels correlates with increased risk for atherosclerosis, independent of LDL cholesterol levels, particularly in men.

Back 37

Lipoprotein (LPa)

Front 38

The worst adverse outcomes associated with CRP and LDL cholesterol are:
LDL < __ mg/dl
CRP < __ mg/liter

Back 38

LDL < 70 mg/dl
CRP < 2 mg/liter

Front 39

Berry aneurysms are found in 2% of population upon autopsy. 90% in anterior and middle cerebral arteries near branch points. What three inherited syndromes increase risk of rupture?

Back 39

Marfan
Ehlers Danlos
Neurofibromatosis I

** And smoking & HTN

Front 40

African Americans are __X's more likely to have HTN than Caucasians.

Back 40

2X's

Front 41

In order, what are the 4 most common secondary causes of hypertension.

Back 41

Renal
Cardiovascular
Endocrine
Neurologic

Front 42

What is the most common lesion associated with HTN? Besides in HTN, where else does this occur?

Back 42

Hyaline arteriolosclerosis (Theory: HTN leads to endo damage, which causes leakage of plasma into the media, which stims ecm synthesis by smc.

HTN, Diabetes, and elderly

Front 43

What is the uncommon lesion in HTN, associated with malignant HTN?

Back 43

Hyperplastic arteriolosclerosis

Front 44

What is Hyperplastic arteriolosclerosis?

Back 44

"onion skin" concentric thickening of arteriolar media and intima, causing marked stenosis, may occur in folks w/ BP > 120

Front 45

What are the causes of the following?
True Aneurysms
False Aneurysms

Back 45

True: atherosclerosis, cystic medial degen of aterial wall
False: trauma and surgery

Front 46

What are the most likely locations of athero aortic aneurysms?

Back 46

abdominal aorta below the renal arteries, common illiac, the aortic arch and the descending thoracic aorta.
Rare B4 age 50, if it ruptures it will most likely do so retroperitoneal - ly.
1% risk if 4.0 to 4.9 cm
11% risk if 5.0 to 5.9cm....elective surgery is recommended for this group, but has an operative mortality rate of 3-5%

Front 47

The tertiary stage of what STD can cause obliterative enarteritis of vasa vasorum and ischemic injury of the media to aneuryysm

Back 47

syphilis, in aortic arch and aortic root

Front 48

Aortic Dissection
Before arch
Before and after arch
After arch only

Back 48

Type A/ Type I
Type A/ Type II
Type B/ Type III

Front 49

_ _ _ (______ _______ ___________) of elastic fibers is usually present with aortic dissection, and is always present in Marfan syndrome

Back 49

CMD Cystic medial degereation

HTN is a risk factor
Currently survival is 60-75% for all types but type A has higher mortality than type B

Front 50

Name the following blood vessel type that each of the following are involved with most frequently.
Vasculitis, GC arteritis, Takayasu:
Vessel vasculitis, polyardertitis nodosa, Kawasaki:
Good pasture syndrome:
Wegner granulomatosis, Churg-Strauss syndrome:

Back 50

Vasculitis, GC arteritis, Takayasu: Aorta, arteries

Vessel vasculitis, polyardertitis nodosa, Kawasaki: Arteries, arterioles

Good pasture syndrome: Capillary

Wegner granulomatosis, Churg-Strauss syndrome: Capillaries, venules, veins

Front 51

Vasculogenesis:

Back 51

de novo blood vessel formation

Front 52

Describe Giant cell arteritis (temporal arteritis)

Back 52

Mst common vasculitis in the US
Prediliction for extracranial branches of carotid artery...concern for vision
Focal inflammation of inner media with giant cells, nodular lesions, variable stenosis, nonspecific panarteritis w/o giant cells

Front 53

Takayasu Arteritis (pulseless disease)

Back 53

13-48 left off

Front 54

True systemic vasculitis with Transmural necrotizing inflammation of medium/small arteries in almost any organ except lung.

Back 54

Polyarteritis Nodosa (PAN)

Front 55

Pan like arteritis of medium sized vessels in young children (80% cases under 4 years old) Cardiac sequelae

Back 55

Kawasaki syndrome

Front 56

Pressure-overload hypertrophy or Volume-overload hypertrophy?
Chronic ischemic heart disease, mitral insufficiency
Eccentric hypertrophy
Myocyte width and length increase
Increased muscle mass with cavity volume increase (dilation)
Wall thickness may or may not increase

Back 56

Volume-overload hypertrophy

Front 57

Pressure-overload hypertrophy or Volume-overload hypertrophy?
Hypertension, aortic stenosis
Concentric hypertrophy
Myocyte width increases
Wall thickness increases
Left ventricular cavity volume may decrease

Back 57

Pressure-overload hypertrophy

Front 58

Left ventricular hypertrophy is an independent risk factor for ________ _____.

Back 58

Sudden death.

But exercise hypertrophy is not.

Front 59

Increases or Decreases?
Norepi _________ heart rate, contractility and vascular resistance.

Back 59

Increases

Front 60

What causes right sided heart failure?

Back 60

Caused by left-sided heart failure most often
Caused by chronic pulmonary hypertension (Cor pulmonale)

Front 61

Why is ischemia worse than simple hypoxia?

Back 61

Because in ischemia there is oxygen, nutrient and waste removal insufficiency while in hypoxia it is only lack of oxygen.

Front 62

Describe some of the pathophysiology of Ischemic Heart Disease.

Back 62

Fixed coronary artery lesion
Acute plaque change
Coronary artery thrombosis
Vasoconstriction

Front 63

What are the three most frequent locations for fixed coronary artery lesion plaques?

Back 63

LAD
Left circumflex
RCA

Front 64

Soft Atheroma

Back 64

Vulnerable plaque”
Abundant foam cells and lipids
Thin fibrous cap and little smooth muscle
Inflammatory cell clusters

Front 65

How does adrenergic stimulation affect Acute Plaque Change?

Back 65

It causes HTN and vasospasm, explains why most MI's happen btwn 6am and noon, and why they seem to be stress related.

Front 66

Which has higher mechanical stress, moderate stenosis or severe stenosis?

Back 66

Moderate stenosis
Severe stenosis has low flow and low mechanical stress.

Front 67

85% of occlusive thrombi occur in stenoses <___%

Back 67

<70%

Front 68

Occlusive vs Non-occlusive?thrombus
Unstable angina
Subendocardial infarction
Sudden cardiac death
Distal embolization with microinfarcts

Back 68

Non-occlusive thrombus

Front 69

Occlusive vs Non-occlusive thrombus?
Transmural infarction
Sudden cardiac death

Back 69

Occlusive thrombus

Front 70

Occlusive vs Non-occlusive thrombus?

Mural thrombus

Back 70

Non-occlusive thrombus

Front 71

Often referred to atheromatous plaques, atheroma's are -

Back 71

An accumulation and swelling in artery walls that is made up of cells, or cell debris, that contain lipids, calcium and a variable amount of fibrous connective tissue.

Front 72

There is often vaso____________ stimuli at atheromas such as:
Platelet products (thromboxane)
Circulating adrenergic agonists
Endothelin
Perivascular inflammatory cell mediators

Back 72

Vasoconstriction

Front 73

Endothelial chemokines and adhesion proteins attract T-cells and macrophages
T-cell cytokines stimulate _________ cells and activate macrophages
LDL-cholesterol accumulation

Back 73

endothelial

Front 74

Macrophage metalloproteinases digest _________.

Back 74

collagen

Front 75

__-___________ _________ (____)
Serum acute phase reactant
Independent predictor of coronary heart disease

Back 75

C-reactive protein (CRP)

Front 76

_______ ________ - chest discomfort from transient myocardial ischemia.

Back 76

Angina Pectoris

Front 77

Stable angina - Chronic severe coronary artery stenoses, Relieved by rest or vasodilator.

Prinzmetal variant angina - Coronary artery spasm, Not related to activity, HR, or BP, Relieved by vasodilator

What might you use as a vasodilator?

Back 77

Nitroglycerin

Front 78

Unstable angina - Crescendo angina, Worsening discomfort with (more or less) effort, Plaque rupture with mural thrombus, Possible embolization and vasospasm
Often heralds ___________ __________

Back 78

Less, or even at rest.
Subsequent infarction

Front 79

All of the following are factors that may lead to ________ ________ within minutes.
Acute plaque change
Exposure of thrombogenic basement membrane or plaque contents
Platelet adhesion/aggregation/activation
Vasospasm
Coagulation with thrombosis

Back 79

Myocardial Infarction

Front 80

Discuss the progression in MI complete ischemia:(5)
Reperfusion within 30 minutes can prevent necrosis.

Back 80

Anaerobic glycolysis within seconds
Loss of contractility within one minute
Irreversible cell injury in 20-40 minutes
Microvascular injury in about an hour
Geographic necrosis after 2 hours

Front 81

40-50% of MI's involve the LAD. What parts of the heart will this affect? (3)

Back 81

Anterior left ventricle
Apex
Anterior interventricular septum

Front 82

30-40% of MI's involve the RCA. What parts of the heart will this affect? (2)

Back 82

Inferior/posterior ventricles
Posterior interventricular septum

Front 83

15-20% of MI's involve the Left Circumflex artery. What parts of the heart will this affect? (1)

Back 83

Lateral left ventricle

Front 84

Can an MI continue to cause new problems after the initial infarct?

Back 84

yes,....for example....
Thrombus retrograde propagation
Proximal vasospasm
Impaired myocardial contractility
Platelet-fibrin microthrombi
Arrhythmias

Front 85

Which is more common, a subendocardial or transmural infarction?

Back 85

Transmural

Front 86

Does the following describe a subendocardial or transmural infarction?
Full thickness necrosis
Thrombotic occlusion of single coronary artery after acute plaque change
10% due to Prolonged vasospasm &
Emboli

Back 86

Transmural

Front 87

Does the following describe a subendocardial or transmural infaction?
Infarct of inner 1/3 to 1/2 of ventricular wall
Can cross perfusion territories and be circumferential
Usually from diffuse stenosing atherosclerosis
Therapeutic thrombolysis before transmural necrosis
Shock or severe hypotension can cause circumferential infarct

Back 87

Subendocardial Infarction

Front 88

Describe the apparent gross morphological changes at the site of MI for the following time points.
<12 hrs
12-24 hrs
1-3 days

Back 88

< 12 hours: not grossly recognizable
triphenyltetrazolium chloride after 2-3 hours
Leaked dehydrogenases
12-24 hours: mottling (coagulation necrosis)
1-3 days: mottling with yellow center (inflammation)

Front 89

Discuss the progression of gross morphological changes for the following time points.
3-7 days:
7-10 days:
10-14 days:
2-8 weeks:
> 2 months:

Back 89

3-7 days: soft yellow center with hyperemic border (phagocytosis and granulation tissue)
7-10 days: maximum yellow softening with depressed red margin
10-14 days: red-gray depressed border (collagen deposition)
2-8 weeks: centripetal gray-white scarring
> 2 months: scarring complete

Front 90

Inside out vs outside in

How to infarctions occur?
How to infarctions heal?

Back 90

Infarctions occur from inside-out but heal from outside-in

Exception: infarct extension, Center appears older than periphery

Front 91

Via Electron Micrograph, the earliest indication of infarction (@ 4 hrs) is irreversible ______________ damage.

Back 91

mitochondrial

Front 92

Myocardial Infarction Microscopy

Back 92

< 4 hours: Fiber waviness at border
4-12 hours: Early coagulative necrosis
12-24 hours: Coagulative necrosis with contraction bands and neutrophils
1-3 days: Maximum neutrophils

Front 93

Myocardial Infarction Microscopy

Back 93

3-7 days: early macrophage phagocytosis at border
7-10 days: maximum macrophage phagocytosis and early granulation tissue at border
10-14 days: maximum granulation tissue with blood vessels and collagen
2-8 weeks: Increased collagen and decreased cellularity
> 2 months: Dense collagenous scar

Front 94

List 3 methods for Myocardial reperfusion.

Back 94

Thrombolysis
Percutaneous transluminal coronary angioplasty (PTCA)
Coronary artery bypass grafting (CABG)

Front 95

What are three ways that myocardial reperfusion can cause damage.

Back 95

1. Via the generation of free oxygen radicals from the neutrophils
2. Infarction becomes hemorrhagic due to damaged blood vessles
3. Cells fx poorly for hours-days.

Front 96

75% of folks who have an MI have complications. List 5-10

Back 96

Contractile dysfx
Arrhythmias
Myocardial rupture
Pericarditis
RV infarction
Extension of infarct
Expansion of infarct
Mural thromboembolus
Ventricular aneurysm
Papillary muscle dysfx w/ mitral regurgitation

Front 97

Cardiac Creatine Kinase (CK-MB)
Isoenzyme predominantly in myocytes
Composed of two dimers: M and B
_-_ hours post MI: rises
__ hours post MI: peaks
__ hours post MI: normalizes
Reperfusion accelerates peak

Back 97

Cardiac Creatine Kinase (CK-MB)
Isoenzyme predominantly in myocytes
Composed of two dimers: M and B
2-4 hours post MI: rises
24 hours post MI: peaks
72 hours post MI: normalizes
Reperfusion accelerates peak

Front 98

Troponins (TnI, TnT)
Cytoplasmic proteins regulating calcium-mediated muscle contraction
Not normally detectable in serum
TnI more specific for heart than TnT
_-_ hours post MI: rises
__ hours post MI: peaks
_-__ days post MI: normalizes
Reperfusion accelerates peak

Back 98

Troponins (TnI, TnT)
Cytoplasmic proteins regulating calcium-mediated muscle contraction
Not normally detectable in serum
TnI more specific for heart than TnT
2-4 hours post MI: rises
48 hours post MI: peaks
7-10 days post MI: normalizes
Reperfusion accelerates peak

Front 99

Sudden Cardiac Death is defined as asymptomatic or symptoms for less than 1 hours prior to death, the mechanism is lethal arrhythmia. In 80-90% of cases the cause is severe ____________ _____________.

Back 99

coronary atherosclerosis


others: Coronary artery structural abnormality, aortic stenosis, mitral valve prolapse, cardiomyopathy, myocarditis, pulmonary hypertension, cardiac conduction abnormality

Front 100

Is it possible to get systemic hypertensive heart disease from mild but prolonged hypertension?

Back 100

Yep

Front 101

The following are microscopic signs of ________ __________ _______ _________.
Myocyte hypertrophy
Myocyte irregularity and variability
Increased interstitial fibrosis

Back 101

Systemic Hypertensive Heart Disease

Front 102

This is know as ______ __________.
Pulmonary hypertension with right ventricular hypertrophy (up to 600g) and dilation

Back 102

Cor Pulmonale

Front 103

Chronic cor pulmonale
Parenchymal disease: COPD, interstitial lung disease, pneumoconioses, cystic fibrosis, bronchiectasis
Vascular disease: Recurrent PE, primary pulmonary hypertension, Wegener granulomatosis
Chest movement disorders: kyphoscoliosis, obesity, neuromuscular diseases
Pulmonary artery constriction: acidosis, hypoxemia, altitude sickness, airway obstruction

Back 103

Especially: Parenchymal disease: COPD, interstitial lung disease, pneumoconioses, cystic fibrosis, bronchiectasis

Front 104

Valvular Heart Disease

Which valves are most often affected? What are the causes cases?

Back 104

Aortic and mitral valves most often affected, Rheumatic heart disease is the # 1 cause, followed by MVP, infective endocarditis, and Fen Phen.


Stenosis and/or insufficiency (regurgitation)
Insufficiency is acute or chronic, intrinsic valve cusp disease, damage to supporting structures
Stenosis is usually chronic, Intrinsic valve cusp defect

Front 105

Name the following:
Most common valve abnormality
Age-related dystrophic calcification
>70 year old
Base calcification greater than free cusp edge
No commissure fusion
Concentric left ventricular hypertrophy
Angina and syncope

Back 105

Senile Calcific Aortic Stenosis

Front 106

Name the following:
1.4% of births
Increased risk for infective endocarditis and aortic dissection
Age-related dystrophic calcification
<70 years old
Midline raphe on larger cusp
No commissure fusion

Back 106

Calcified Congenital Bicuspid Aortic Valve

Front 107

Name the following:
Women >60 year old, myxomatous mitral valve, elevated LV pressure
Degenerative calcification of mitral valve ring
Valve function usually normal
Uncommonly causes stenosis, insufficiency, arrythmias
Can thromboembolize
Can predispose to infective endocarditis

Back 107

Mitral Annular Calcification

Front 108

GIve two names for the following:
Usually asymptomatic
Chest pain, dyspnea, fatigue, depression, anxiety, and personality disorders
Rare infective endocarditis, mitral insufficiency, embolic infarcts, or arrhythmia
Rare sudden death

Back 108

Myxomatous Degeneration of Mitral Valve, or Mitral Valve Prolapse (MVP)

Front 109

Give two names for the following:
Thick rubbery valve leaflets ballooning into atrium
Spongiosa myxoid degeneration
Fibrosa thinned
Thin elongated or ruptured chordae
Annular dilation
Secondary atrial and ventricular endocardial thickening
Thrombi on superior valve surfaces
Can involve other valves

Back 109

Myxomatous Degeneration of Mitral Valve, or Mitral Valve Prolapse (MVP)

Front 110

GIve two names for the following:
3% of U.S. adults
Women > Men
20-40 years
Possibly connective tissue disorder
Associated with Marfan syndrome

Back 110

Myxomatous Degeneration of Mitral Valve, or Mitral Valve Prolapse (MVP)

Front 111

What may fowllow a Group A strep phyaryngitis by 10 days to 6 weeks?
What type of disease is it?
Predominant age group?

Back 111

Acute Rheumatic Fever
Acute immune-mediated multisystem disease.
Anti-strep M protein antibodies
Andtibodies cross react w, body glycoproteins.
Most often kids 5-15, increased susceptibility to repeat disease.

Front 112

What are the JONES criteria for Acute Rheumatic Fever?

Back 112

JOINTS: migratory painful polyarthritis
♥: acute pancarditis
NODULES: painless subcutaneous
ERYTHEMA MARGINATUM: truncal rash
SYDENHAM’S CHOREA: abrupt movements

Front 113

What is ♥ Acute Pancarditis?

Back 113

Acute inflammation of the entire heart (the epicardium and the myocardium and the endocardium)

Front 114

What has a "bread and butter" appearance?

Back 114

Fibrinous/Serofibrinous pericarditis

Front 115

What do Anitschkow cells look like?

Back 115

Caterpillars or owls eyes

Front 116

Affects 9-39% of acute valvulitis patients
Organization of acute valvulitis
Leaflet fibrotic thickening
Commissural fusion (“fishmouth”)
Chordae thickening and fusion
Causes stenosis more than insufficiency
Mitral valve alone: 65-70%
Mitral and aortic valves: 25%
Tricuspid valve less common

Back 116

Chronic Rheumatic Heart Disease

Front 117

The following are forms of ___________
Infective
Acute
Subacute
Non-Bacterial Thrombotic
SLE
Carcinoid Heart Disease

Back 117

Endocarditis

Front 118

In infective endocarditis of native valves, 50% of cases are caused by what 'bug''?

Back 118

Strep viridans

Front 119

In infective endocarditis of prosthetic valves, most cases are caused by what 'bug''?

Back 119

Coag neg staphylococci

Front 120

In infective endocarditis are left or right sided valves more often affected?

Back 120

Left

Front 121

_________ __________ non-tender, small erythematous or haemorrhagic macular or nodular lesions on the palms or soles only a few millimeters in diameter that are pathognomonic of infective endocarditis.[1] Pathologically, the lesion is described to be a microabscess of the dermis with marked necrosis and inflammatory infiltrate not involving the epidermis, which is due to the deposition of circulating immune complexes in small blood vessels.

Back 121

Janeway lesions

Janeway: nontender sepic emboli macules on palms and soles
Osler nodes: tender subcutaneous nodules on fingers
Roth spots: oval retinal hemorrhages with pale centers

Front 122

Either pathologic confirmation or clinical criteria (2+0, 1+3 or 0+5 major + minor)
Major: blood cultures, diagnostic echocardiogram, new valvular regurgitation
Minor: predisposing heart lesion/IVDU, fever, vascular lesions (e.g., Janeway lesions), immunologic findings (e.g., Osler nodes, Roth spots), microbiologic evidence with uncharacteristic organism, suggestive echocardiogram

Back 122

Duke Criteria for Infective Endocarditis

Front 123

Acute Infective Endocarditis
Abrupt, rapidly progressive, destructive infection
Spiking fever, chills, petechiae
Highly virulent organisms
S aureus, S pneumoniae, gram – enterics, fungi
Often affects normal valves
Common with IV drug abuse
What is the mortality rate?

Back 123

Mortality is >50% regardless of therapy.

Front 124

Subacute Infective Endocarditis
Insidious, protracted, less-destructive infection
Fever, flulike symptoms
Low virulence organisms
S viridans, S faecalis, S bovis
Involves previously abnormal valves
Myxomatous mitral valve, degenerative calcific valvular stenosis, bicuspid aortic valve, prosthetic valves
History of dental/minor surgical procedure
What is the mortality rate?

Back 124

Most recover with antibiotics

Front 125

Non-bacterial Thrombotic Endocartditis
Associated with debilitated patients with systemic ______________ state. Ex (4)

Back 125

Associated with debilitated patients with systemic hypercoagulable state
Cancer (mucinous adenocarcinoma, APL)
High estrogen states
Burns
Sepsis
Also associated in endocardial trauma.

Front 126

Libman Sacks Disease is another name for:
What do they look like?
Where are they found (valves and location)?
What can they cause?

Back 126

SLE Endocarditis
Small sterile pink vegetations of fibrinous hematoxylin bodies
Can be on underside of mitral or tricuspid valves
Can cause destructive valvular fibrinoid necrosis