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Smmlws > Patho Semi Cardiovascular > Flashcards

Patho Semi Cardiovascular Flashcards

1
Q

Atherosclerosis

A

mural change of elastic and middle sized to large muscular

arteries

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2
Q

Arteriolosclerosis

A

mural change of small muscular arteries and arteioles

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3
Q

Medial sclerosis of Mönckeberg

A

mural change with special characteristics

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4
Q

Degenerative vascular diseases

A

Arteriosclerosis
Vascular changes in diabetes m
Aneurysm
Dissection of vascular layers

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5
Q

Functions of intact endothelium

A

Provision of a non-adherent, non-thrombogenic vascular inner surface
Regulation of:
vascular wall permeability
fibrinolytic and coagulation characteristics of the vascular wall
adhesion of leukocytes and thrombocytes (so-called homing)
lipid oxydation
Production of chemoattractants
Proliferation stimulus for vascular smooth muscle cells
Production of extracellular matrix components
Metabolic activity (e.g. LDL-oxydation)
Maintenance of elasticity (vessel tonus through NO, PGI2, Endothelin, Angiotensin II, TXA 2and structure (e.g. basal membrane) of vessels
Effectuation of inflammatory and immunologic reactions

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6
Q

Functions of monocytes/macrophages

A 
Imp in atherogenesis
Role in lipid metabolism , oxidation and ingestion of extracellular lipid (form foamy cells)
Cytokines and growth factors production
Antigen presentation for t cells
Scavanger function
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7
Q

Functions of smooth muscle cells

Contractile phenotype

A

rich in myofilaments

lipid uptake and excretion in equilibrium: no lipid accumulation, no foamy cells

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8
Q

Functions of smooth muscle cells

Synthetic phenotype

A

rich in rough endoplasmatic reticulum (RER)
on cytokine stimulation (PDGF, bFGF, TGFß) production of extracellular matrix components and expression of LDL- and ‘scavanger’ receptors&raquo_space;
» disbalanced lipid-uptake and -excretion: lipid accumulation and formation of foamy cells
Migration from media layer to intima layer

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9
Q

Theories on atherosclerosis

A

1) The «response to injury» theory
2) The lipid theory
3) The theory of monoclonal growth
4) The thrombogenic theory
5) The infection-inflammation / autoimmnune theory

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10
Q

The «response to injury» theory

A

Atherogenesis is stereotype counter reaction of vascular wall to harmful effect of any kind.
Resulting in vessel wall change to atherosclerotic plaque.

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11
Q

Atherosclerosis is loss of original vascular :

A

Morphologic composition
Elasticity
Patency (altered hemodynamics)

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12
Q

Hemodynamic factors of plaque formation

A

Turbulent flow
Slow passage of blood particles
Lengthened activity time for atherogeneous agents on a given vessel segment

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13
Q

In response injury theory plaque stability is defined as

A

Plaque components
Dimensions of the plaques lipid core
Proteolytic enzyme activity of cellular inflammatory plaque elements
Calcification

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14
Q

According to response injury theory adhesion and intimal gathering of circulating cellular elements

A

Leukocytes
Thrombocytes
Monocytes
T lymphocytes

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15
Q

Main categories of vascular changes

A

Stenosis/occlusion: arteriosclerosis, thrombosis, embolism
Structural weakening:dilation,dissection,rupture
Inflammation

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16
Q

Pathogenesis of atherosclerosis

A 
Endothelial stimulation
Inflammatory response - permeability increase
Lipid accumulation ( oxi ldl and scavenger receptors)
Macrophages turn on to foamy cells
Cytokine and growth factors
Smooth muscle cell migration to intima
Sm muscle cell proliferation
Extra cellular matrix formation
Ecm remodelling 
Calcification
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17
Q

Stages of atherosclerosis

A 
Normal
Fatbubbles, fatty streak
Smooth muscle migrate, ECM remodelling
Atheromatous lipid core and fibrous cap
Complicated vulnerable plaque with calcification
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18
Q

Arteriolosclerosis

A
  • Hyalin arteriolosclerosis homogeneous thickening , increased ecm production of sm muscle cells
  • Hyperplastic arteriolosclerosis, onion skin like thickening, severe hypertension
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19
Q

Forms of ischemic heart disease

A

Angina pectoris
Acute myocardial infarction
Chronic isch heart disease
Sudden cardiac death

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20
Q

Acute myocardial infarction

A

Coagulation necrosis of myocardium

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21
Q

Ami modifiable risk factors

A 
Hyperlipidemia
Hypertension
Diabetes
Smoking (oxidative endothelial damage)
Obesity
Lack of physical activity
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22
Q

Ami novel risk factors

A

elevated serum fibrinogen level
hyperhomocystinaemia
elevated resting heart rate
decreased estrogen levels
oral anticoncipients
psychic stress

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23
Q

Causes of coronary stenosis

A 
Atherosclerosis and complications 90%
Embolism
Coronary spasm (prinzmetal angina)
Inflammations, autoimmune diseases
Iatrogenic, catheters
24
Q

Subendocardial ami

A

Coronary stenosis and increased oxygen demand

Crescendo angina, NSTEMI

25
Q

Transmural Ami

A

Sudden and complete occlusion of a coronary branch
Plaque rupture and thrombosis/embolism/coronary dissection
STEMI

26
Q

Localisation of ami and affected artery branches

A

40-50% left anterior descending (LAD)
-left ventricle anterior wall, frontal 2/3rd of septum, right ventricle area near septum,apex
30-40% right coronary art (RCA)
-right ventricle and posterior interventr. branch
15-20% circumflex artery
-left ventricle, lateral part (and posterior intrv branch )
1-3%isolated right ventricle

27
Q

Proper blood flow in coronaries only happen in this stage (especially left ventricle)

A

End diastole

28
Q

Acute myocardial infarction rare causes

A

Coronary development disorder
Myocardial bridge over a coronary segment
Coronary steal syndrome
Extremely altered hemological parameters (DIC,polycysthaemias,thrombocytosis)

29
Q

0-30min ami

A

Only in electron microscopy
Glycogene depletion
Mitochondrial swelling
Relaxed myofibrillar structure

NOT visible to naked eye nor light microscopy

30
Q

30 min - 4 h ami

A 
Can be seen by light microscopy 
Relaxed muscle strings
Wavy strings in the infarction border
Glycogen depletion and cellular swelling
Pale nuclei (?)
31
Q

Ami irreversible phase

A

4-12h beginning coagulation necrosis, hemorrhage
After 9 hours incipient neutrophil granulocyte infiltration, low cell count visible
12-24h pycnotic cell nuclei, hypereosinophilia, contraction band necrosis

32
Q

Nitro blue tetrazolium cloride reaction

A 
Loss of staining in damaged areas 
Detection of 3-4 hour infarction
Based on intracellular oxidative reactions in living cells
Violet: viable myocardium
Gray:zone of infarction
33
Q

Ami morphology 1-3 days

A 
Progression of coagulation necrosis
Intensive neutrophil gran. Infiltration
Loss of nuclei
Loss of myocyte striations 
Mottling yellow tan infarct center
34
Q

Ami histology

A

Neutrophyl granulocytes infiltrated
Loss of myocyte nuclei
Loss of striation
Homogeneous, hypereosinophilic cytoplasm

35
Q

7-10 days mi

A

Hyperemic border , yellow tan center
Beginning disintegration of dead myofibers with dying neutrophils
Phagocytosis of death cells
Mechanical complications like myocardial rupture occur most commonly within. 3-7 days after infarction

36
Q

Ami early complications

A

Decreased contractility –> left ventricular failure
Arrythmia…bradycardia, conductance disorders,ventricular fibrillation or flutter—sudden cardiac death
Rupture. :
free wall tamponade
ventricular septum shunt
papillary muscle –> acute valvular insufficiency
Mural thrombus
Fibrinous pericarditis

37
Q

Ami expansion affected by

A 
Coronary reserve = resting /max volume
Localisation of coronary lesions
Collaterals
Reperfusion (0-6h): 
    Own fibrinolytic system
    Thrombolysis
    Percutan coronary intervention
    Coronary artery bypass grafting
38
Q

Morphology of mi 10-14 days

A

Red gray infarct
Depressed borders
Granulation tissue well formed

39
Q

Morphology of ami 2-8 weeks

A

Gray white scar
From border toward core
Increased collagen deposition
Decreased cellularity

40
Q

Morphology of mi 2 months +

A

Dense collageneous scar

41
Q

Late complications of mi

A

Ventricular remodelling
Persisting arrythmia
Dressler syndrome (postinfarct. pericarditis)
Ventricular aneurysm
-mural thrombosis—>embolism
-calcification
Chronic heart failure

42
Q

Chronic infarction

A

Collagen formation (replacement fibrosis)
Decreasing cellularity
Hypertrophy of surrounding surviving myocytes on borders

43
Q

Aneurysm of left ventricle

A

Extended akinetic or dyskinetic (paradoxically pulsating) area in the ventricular wall, that decreases ejection fraction.

Localisation : anterior + apical (88%)
Few inferior , rarest is posterior
They do evolve in percutaneous coronary intervention-era , 10%
Aneurysm expansion —>remodelling

44
Q

Endocarditis localisation

A

Parietal or valvular

45
Q

Endocarditis types

A

Infective (acute or subacute)
Non infective
Rheumatic endocarditis
Non bacterial thrombotic : hypercoagulative state and malignant tumors
Libman sacks endocarditis (sterile) (immune complex depositions in systemic lupus erythematosus) (ventricular side of valves)

46
Q

Infective endocarditis determined by

A

Type of virulence of the pathogenic agent
Underlying heart disease
Clinical diagnosis : echocardiography and blood culture tests

47
Q

Infective acute endocarditis symptoms and complications

A

Pathogens high virulence, pyogenic bacteria
Fever
Destruction of valves —acute insufficiency
Spreading
Myocardial abcesses
Intracardial fistula
Pericarditis , pleuritis

48
Q

Sub acute infective endocarditis symptoms

A

Fever („FUO”), exhaustibleness, splenomegaly…
Inflammation in joints
Nail bed (splinter) hemorrhages
Painful fingertip nodules (Osler nodes)
Painless palm or sole erythematous lesions (Janeway lesions)
Retinal hemorrhages (Roth spots)
Mycotic aneurysm (vasa vasorum embolisation)
!Schottmüller triad: cardiac murmur, splenomegaly (septic infarctions), hematuria

49
Q

Schottmuller triad

A

Cardiac murmur, splenomegaly (septic infarctions ), hematuria

50
Q

Infective endocarditis pathogens

A

•Staphylococcus (mostly aureus)
•Streptococci ( alfa hemolysing, oral flora)
•HACEK group (Haemophilus, Actinobacilus, Cardiobacterium, Eikenella, Kingella)
•Gram negative bacteria
•Enterococci (faecalis / faecium
•Rarely: fungi, Rickettsia, Chlamydia
!!!Bartonella, Coxiella, Legionella, Nocardia… (culture negative)

51
Q

Infected valve histology

A

Thickened valve
Fibrinous depositions
In tissue ; neutrophil granul. Cell debris, Clouds of bacteria

(You can see gram positive cocci for ex)

52
Q

Rheumatic fever

A

Can cause valvular , myocardial disease ( pancarditis)

Antibodies directed against group A streptoccoci molecules cross react to host cell antigens (2weeks after infection)

53
Q

Acute rheumatic fever Jones criteria

A 
Carditis 
Migrating polyartiritis
Migrating erythema
Subcutaneous nodules
Chorea
(+nephritis)
54
Q

Rheumatic fever histology acute

A

-Anichkov giant cells
-Aschoff nodules
-Fibrinous exudate in the pericardium
-Myocarditis
-Valves: fibrinoid necrosis and fibrin deposition

55
Q

Rheumatic fever chronic

A

Organisation of acute inflammation and scarring
Most prominant of valves;
-thickening
-leaflet and chordea fusion and shortening
-(mitral valve fish mouth stenosis)
Microscopically, fibrosis and neovascularisation
75% mitral valve and 25% aortic valve
Consequence; stenosis and or insufficiency

Smmlws (4 decks)

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