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Heart Flashcards

1
Q

Rheumatic fever

  • Define it
  • When does it occur
  • What are the 2 main problams
A
  • Acute inflammaiton
  • immunologically mediated disease
  • Multisystem disease

Occurs few weeks after Phryngitis caused by Group A beta hemolytic streptococcus

  • The becteria grows on the tonsils and its antigen is released into the circulation -> B cells produce Ab (NO BACTEREMIA!)

2 problemes:

  • Ig cross reacts with the 3 layer of the heart
  • Formation of immune complexes -> Vasculitis, glomerulonephritis.
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2
Q

What are the morphological consequences of the problems mentioned before in the Acute RF?

Heart

A

Heart:

  • Aschoff bodies can be found in any of the 3 layers of the heart -> Pancarditis
    • Endocardium: Verrucae
    • Myocardium: Aschoff bodies
    • Pericardium: fibrinous pericarditis

(Aschoff bodies are granulomatous reactions, consisting of a central zone of degenerating, hypereosinophilic extracellular matrix infiltrated by lymphocytes, plasma cells and Anitshschkow cells (/Gaint cells))

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3
Q

What are the morphological consequences of the problems mentioned before in the Acute RF?

in the other organs

A

Joints:

  • due to immune complexes
  • Migratory polyarthritis (affects large joints)

Skin:

  • Nodules (granulomatous reaction on the skin)
  • Erythema marginatum (related to vascular effection)

CNS:

  • Syndenham chorea (Chorea-ataxic)
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4
Q

What are the morphological consequences of the chroinc RF?

A
  • Scarring of the verruca
    • vitium (stenosis and/or insufficiency)
    • Leaflet thickening - “fish-mouth” / “buttonhole” stenosis
  • Aschoff nodules are replaced by fibrous scar
  • Othe consequences: Mural thrombi (dilation of the left atrium), R ventricular hypertrophy due to lung changes.
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5
Q

Describe the clinical picture of a patient with acute/chronic RF

A

Acute??:

  • the symptoms occur 2-3 weeks after an episode of streptococcal pharyngitis. The predominant clinical manifestations are arthritis (migratory polyarthritis + fever) and carditis (arrhythmias, CHF).

Chronic:

  • vitium with complication such as murmurs, hypertrophy and dilation, CHF, arrhythmias, embolism and an increased risk for infective endocarditis
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6
Q

Describe the diagnosis of RF

A

Serologic evidence of a previous streptococcal infection, in conjunction with Jones criteria.

The rule is that we have to have 2 or more criteria or 1 Jones criteria (major manifestation) + 2 minor manifestation.

  • Major manifestation (Jones criteria):
    1. Carditis
    2. Migratory polyarthritis
    3. Subcutaneous nodules
    4. Erythema marginatum
    5. Syndenham chorea
  • Minor manifestation: fever, arthralgia, elevated acute phase proteins.
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7
Q

What is Non-bacterial thrombotic endocarditis?

A
  • Deposition of fibrin, platelets and other blood components on cardiac valves.
  • Can occur on **normal valve as well.

(no microorganisms)**

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8
Q

Describe the morphology of non-bacterial thrombotic endocarditis

A
  • Sterile, nondestructive, small (1mm).
    • along the lines of closure of the leaflets / cusps.
  • Histological appearance: thrombus without inflammation or valve damage.
  • Can form Lambl excrescences = strands of fibrous tissue.
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9
Q

What is the pathogenesis (causes) of non-bacterial endocarditis

A

Typically hypercoagulable states:

  • sepsis + DIC, hyperestorgenic states, malignancy (mucinous adenocarcinomas with its procoagulant effect) and also related to endocardial trauma.
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10
Q

When will non-bacterial endocarditis become clinically sagnificant?

A
  • by embolization to the brain, heart or other organs
  • can also increase the risk for IE
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11
Q

Describe what is Limban-sacks endocarditis

A

Sterile vegetations (patients with SLE).

immune complex deposition and thus have associated inflammation

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12
Q

Describe the morphology of Limban-sacks endocarditis

A
  • Small, sterile, granular pink.
  • valvulitis fibrinoid necrosis adjacent to the vegetation.
  • deformity can occur.
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13
Q

Describe infective endocarditis

A
  • The patient has bacteremia.
    • invade the valves where it proliferates, makes necrosis, inflammation and precipitation of platelets and inflammatory cells -> called vegetation.

Vegetation = bacteria, necrotic tissue, cell debris, fibrin, inflammatory cells and platelets.

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14
Q

What are the possible causative agents of infective endocarditis?

A

Caused by extracellular bacteria (can also be caused by fungi, rickettsiae and chlamydia)

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15
Q

Based on the microbial virulence and whether an underlying cardiac disease is present, we classify IE into….

A
  • Acute endocarditis:
    • usually suggests a destructive infection.
    • frequently involving a highly virulent organism (mostly s.aureus)
    • attacking a previously normal valve.
    • Highly resistance to therapy
  • Subacute endocarditis:
    • refers to infections by organisms of low virulence (s.viridans)
    • colonizing a previously abnormal heart (especially with deformed valves).
    • Good chance for recovery after an antibiotic therapy.
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16
Q

Describe the morphology of infective endocarditis

A
  • friable, bulky,potentially destructive vegetations are present on the valves.
  • erode the underlying myocardium →ring abscess.
  • emboli (virulent) →abscesses develop at the sites of such infarcts (septic infarcts).

The subacute form is milder.

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17
Q

What are the predesposing factors of IE

A
  1. rheumatic fever: (lesions on the valves)
  2. cardiac malformations
  3. prosthetic valves
  4. catheterization
  5. host factors: neutropenia, immunodeficiency, malignancy, immunosuppression, DM, alcohol, intravenous drug abuse
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18
Q

What are the causative agents and the source of the microorganisms of Infective endocarditis?

A

Causative agents (s.viridans and s.aureus)

  • HACEK
    • Haemophilus, Actinobacillus, Cardiobacterium, Eikenella and Kingella.
      • (All are commensals in the oral cavity)

Source:

  • Dental procedure (as brushing of the teeth or oral surgery)
  • Injection of contaminated material
  • Portal entry (stomach, intestine)
  • Skin lesions
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19
Q

What are the possible complications of IE?

A
  1. embolization of the vegetation with development of abscesses at the site of infarct
  2. perforation of the valve
  3. ring abscess
  4. antigens in the circulation -> formation of immune complexes, with resultant: kidney failure, skin eruption, vasculitis, joints disease
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20
Q

What are the clinical features of IE?

A
  • *Non-specific signs!** Diagnosis is based blood culture.

Subacute: fatigue, weight loss, flulike syndrome, sometime fever

Acute: fever, chills, weakness, lassitude.

Due to complications:

  • Hematuria, albuminuria, renal failure, septicemia, arrhythmia
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21
Q

What is carcinoid heart disease?

  • Morphology
A

Cardiac manifestation of a systemic syndrome that includes flushing, diarrhea, dermatitis and bronchoconstriction and is caused by bioactive compounds released by carcinoid tumors.

Morphology

  • Glistening white intimal plaqulike thickening on the endocardial surface.
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22
Q

What is the pathogenesis of carcinoid heart disease?

A

Related to APUD cancers which produce vasoactive amines:

  • serotonin, kalikrein, bradykinine, histamine, prostaglandins
  • (-> neutralized in the pulmonary vessels by the mono-amino-oxidase system).

When the tumor makes liver metastasis, a huge amount of substances reach the right side of the heart before it reaches the lung. (valvular thickening)

(Can occur on the left side a patent foramen ovale or with pulmonary carcinoids)

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23
Q

What is Myxomatous mitral valve?

A

Valves are “floppy” and prolapse (protrude back into the atrium during systole)

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24
Q

What is the morphology of myxomatous mitral valve?

A

enlarged leaflets (thick and rubbery)

elongated chordae tendinae
(thin and sometimes rupture)

Histologically: thining of the fibrosa layer (accompined by desposition of myxomatous material)

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25
Q

What is the pahtogenesis of myxomatous mitral valve?

A

Primary: unknown (probably a CT defect)

Secondary: changes as a respond to chronic hemodynamic forces.

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26
Q

What are the symptoms of myxomatous mitral valve?

A

Most patients are asymptomatic (discoverd incidentally)

minority of the patients: palpitations, dyspnea, atypical chest pain.

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27
Q

What is calcific valve stenosis?

A

The valvular counterpart of age-related atherosclerosis.

“Wear and tear” → Calcification

Most commonly → aortic valve stenosis

typically occurs at age 70-80 (normal valve)

age 40-50 (congenitally defected bicuspid valve)

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28
Q

What are the effects of aortic valve stenosis?

A

Calcific masses on the outflow side of the cusps which mechanically impede valve opening

Consequence: outflow obstruction

  • Leads to left ventricular pressure overload -> Concentric hyperthrophy.

The cusps become secondarily fibrosed and thickend.

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29
Q

What are the consequences (clinical features) of aortic valve stenosis?

A

hypertrophy → ischemia and angina develops

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30
Q

What are the prostetic heart valves and their disadvantages?

A

Mechanical valve

  1. require chronic anticoagulant -> risk for hemorrhage
  2. can cause RBCs hemolysis due to shear stress
  3. subjected to infection

Bioprosthetic valves

  1. less durable
  2. can fail because of matrix deterioration
  3. can perforate or tear -> valvular insufficiency
  4. can stiffen after implantation. Together with calcification -> stenosis
  5. subjected to infection
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31
Q

What is myocarditis?

A

An inflammatory process in the myocardium that results a myocardial injury

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32
Q

What is the morphology of myocarditis?

A

Microscopically:

  • Interstitial inflammatory infiltrate
  • Focal necrosis of myocytes adjacent to inflammatory cells.
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33
Q

What are the 4 different types of myocarditis?

A

Lymphocytic: most common, if survives the acute -> resolve or heal by fibrosis

Hypersensitivity: interstitial and perivascular infiltrates (lymphocytes, macrophages, eosinophils)

Giant cell: infiltrates composed of giant and plasma cells. focal (or extensive) necrosis

Chagas: infiltrates contains trypansomes + inflammatory cells.

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34
Q

What are the causes of myocarditis?

A
  1. Viral infections: (most common)
    • Coxsackieviruses A and B, cytomegalovirus, HIV.
    • The injury is caused by an immune response.
  2. Nonviral agents:
    • Tryposome cruzi, toxoplasma gondii, trichinosis.
    • Lyme disease by Borrelia Burgdorferi
  3. Noninfectious causes:
    • Systemic diseases of immune origin (SLE), drug hypersensitivity reactions.
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35
Q

What are symptomes of myocarditis?

What myocarditis might progress to?

A

Broad range of clinical spectrum (in between: Fatigue, dyspnea, palpitation)

Might progress to dilated cardiomyopathy

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36
Q

What is cardiomyopathy and the forms of it?

A
  • A group of disease with unknown cardiac failure
  • Attributed to an intrinsic myocardial dysfunction
  • Diagnosed when coronary disease, valvular disease and hypertension can be excluded.

Comes in 2 forms:

  • primary: disease is confined to the heart muscle.
  • secondary: part of a generalized multiorgan disorder.
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37
Q

What are the different forms of cardiomyopathies?

A
  • Dilated CM
  • Arrhytmogenic right ventricular CM
  • Hypertrophic CM
  • Restrictive CM
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38
Q

What can be seen in dilated cardiomyopathy?

A
  • Enlargment of the heart - reaching 800gr
  • Reduced contractility -> EF < 25%
  • Dillation of all chambers
  • Additional signs:
    • mural thrombosis (stasis)
    • mitral insufficiency (dilation)
    • hypertrophied muscles with fibrosis

Myocardium Hypertrophies + dilated

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39
Q

What are the causes for dilated CM?

A
  1. Genetic: 25% of cases, Mutation of the contractile elements (actin, laminin)
  2. Alcohol: acetaldehyde is toxic for the myocardium
  3. Viral: coxsackievirus B
  4. Pregnancy: hypertension, volume overload, immune compromised (recover after delivery)
40
Q

What are the clinical features of dilated CM?

  • Result
  • Main problem
  • Prognosis
  • Treatment
A
  • Slowly progressing CHF (some slip from compensated to non-compensated)
  • Ineffective contraction (reducred EF (<25%))
  • Bad prognosis! 50% die within 2 years
  • Transplantation is needed.
41
Q

Describe arrhytmogenic right ventricular CM

A

The patient has sudden arrhythmia and SCD.

the right ventricle becomes thin due to myocyte replacement by fatty infiltration.

This restricts the contraction of the heart.

Most mutations seems to involve desmosomal junctional proteins.

42
Q

Hypertrophic CM is characterized by…

A

myocardial hypertrophy

abnormal diastolic filling

ventricular outflow obstruction

43
Q

What is the morphology of hypertrophic CM

A
  • Hypertrophy without dilation
  • Asymmetrical septal hypertrophy -> left septal hpertrophy
    • Bnana like configuration of the ventricular cavity

Histologically:

  • myocyte hypertrohy
  • myocyte disarray
  • interstitial fibrosis
44
Q

Hyperthrophic CM pathogenesis

A
  • Point mutation in the gene encoding sarcomeric proteins (β-myosin heavy chain)
  • Hypertrophy is the compensatory mechanism for an inffective contraction.
45
Q

Hyperthrophic CM clinical features

A
  • smaller chambers + impaired diastolic filling -> reduced ejection fraction.
  • Obstruction of the left ventricular outflow by the anterior leaflet of the mitral valve.
  • Increased pulmonary pressure -> dyspnea.
  • signs:
    • murmur
    • ischemia with angina
    • atrial fibrillation
    • mural thrombus formation
    • arrhythmia
46
Q

How are the systole and diastole affected by Restrictive CM

A
  • The wall is stiffer -> impaired ventricular filling during diastole.
  • Systolic function is usually unaffected
47
Q

What is the morphology of restrictive CM

A

Normal sized or slightly enlarged ventricles.

No ventricular dilation.

Firm myocardium.

Biatrial dilation is observed.

Microscopically: interstitial fibrosis

48
Q

What are the other forms of RCM?

A

1. Endomyocardial fibrosis:

  • typically a disease of children and young adults in Africa and other tropical areas which is characterized by dense fibrosis of the ventricular endocardium and subendocardium. This causes restriction

2. Loeffler endomyocarditis:

  • not geographically restricted.
  • Endocardial fibrosis and mural thrombi.
  • There is often an associated peripheral hypereosinophilia -> the eosinophils granules content (MBP) is released which causes:
    • endocardial damage -> necrosis -> fibrosis
49
Q

What are the fatal consequence of hypertension?

A
  1. Heart failure
  2. Cerebral bleeding
  3. Renal failure
50
Q

What are the forms of (Benign?) hypertension?

A

There are several forms of hypertension:

  • Essential hypertension (95% of the cases) - mechanism is unknown.
  • Secondary due to renal, endocrine, cardiovascular of neurologic disorders.
51
Q

What is the most important sign of hypertension?

What is another parameter of hypertension?

A
  • when the diurnal alteration of the blood pressure disappears.
  • systolic higher than 140 mmHg and the diastolic higher than 90 mmHg (sustained).
52
Q

What are the 2 factors that determine the blood pressure?

A
  • peripheral resistance
  • volume of the blood
53
Q

Which organs are central players in blood pressure regulation?

A
  • Kidney (primarily)
  • Adrenals (secondarily)
54
Q

What are the steps of blood regulation by the kidney and adrenals?

Which other organ can influence the BP?

A

(picture below)

B.V. decrease →B.P decreases →Juxtaglomerular cells release renin → angiotensinogen to angiotensin 1 →

ACE converts angiotensin 1 to angiotensin 2 ->

angiotensin 2 has two affects:

  1. vasoconstriction -> increased peripheral resistance -> increased blood pressure
  2. stimulating aldosterone secretion in the adrenals -> increased Na reabsorption -> H2O reabsorption -> increased blood volume -> increased blood pressure
  • The kidney also produces a variety of vasorelaxant or antihypertensive substances (NO, Pg) that counterbalance the vasopressor effect of angiotensin
  • other tissues that influence blood pressure:
    • increased volume -> atria of the heart releases ANP -> inhibition of Na reabsorption and global vasodilation
55
Q

Accelerated or malignant hypertension

  • Incidence
  • Severity
  • Prognosis
A

In about 5% of the cases

severe - diastolic > 120 mmHg . Systolic > 200 mmHg

rapidly rising and leads to death within 1 or 2 years if remain untreated.

56
Q

What can malignant hypertension lead to?

Who may develop malignant hyper tension?

A

Apart from the hypertension:

  • renal failure
  • retinal hemorrhages and exudates, with or without papilloedema.

Hyperplastic arteriolosclerosis is characteristic for it

It may develop in:

  • previously normotensive persons
  • superimposed on preexisting benign hypertension (either essential or secondary).
  • in a young age.
57
Q

What are the underline causes for essential hypertension?

A

Increased B.V. and increased T.P.R

renin-angiotensin-aldosteron axis is defected:

  • Reduced renal Na excretion: Increased Na -> increased volume -> increased cardiac output -> increased blood pressure.
    • It leads to a situation in which a new steady state is set.
  • Increased resistance of the vascular wall (functional vasoconstriction) increased sensitivity to angiotensin.
58
Q

Describe Hyaline arteriolosclerosis

  • To which form of hyper tension is it related to
  • Pathogenesis
A
  • essential hypertension
  • hyaline thickening of the walls of arterioles with narrowing of the lumen
  • same as diabetic angiopathy
  • High blood pressure -> physical stress on the endothelial cells -> cell becomes leaky: leakage of plasma component and ECM production by SMCs -> makes narrowing of the lumen.
    • Kidney: scaring on the surface
59
Q

Describe Hyperplastic arteriolosclerosis

  • To which form of hyper tension is it related to
  • Pathogenesis
A
  • Malignant hypertension
  • the hypertension makes an “onion-skin” proliferation:
    • concentric
    • laminated thickening of the wall of arterioles composed of SMCs -> Leads to luminal narrowing.
60
Q

When is systemic hypertensive heart disease diagnosed?

A
  • Left ventricular hypertrophy (concentric) in the absence of other casual cardiovascular pathology

+

  • History / presence of pahtologic hypertension.
61
Q

What is the morphology of systemic hypertensive heart disease? (macro + micro)

A
  • Concentric hypertrophy
    • Wall exceeds 2cm (norm. 6-10mm)
    • Weight may exceeds 500 gr (norm. ~300gr)
  • Mycroscopic:
    • Myocyte diameter increase
    • nuclear enlargement + hyperchromasia
    • increased interstitial fibrosis
62
Q

How does systemic hypertensive heart disease presented?

A
  • Patients are usually asymptomatic
  • LVH on ECG may be a sign
  • may manifest as: AF and/or CHD
63
Q

What are the direct consequences of hypertension? (4)

A
  1. Development of progressive IHD (potentiating coronary atherosclerosis)
  2. HF
  3. Cerebral bleeding
  4. Renal failure
64
Q

ما هذا

Cor pulmonale?

A

= Right ventricular hypertrophy and dilation

65
Q

How does cor pulmonale develop?

A

Primary disorder of the lung parenchyma or pulmonary vasculature ->

Pulmonary hypertension ->

Cor pulmonale.

66
Q

Depending on the tempo by which the pulmonary hypertension develops, we distinguish ______ which develops due to ________ and _______ which develops due to ______

A

acute cor pulmonale: due to pulmonary embolism with more than 50% obstruction

Chronic cor pulmonale: secondary to prolonged pressure overload caused by emphysema, interstitial pulmonary fibrosis, primary pulmonary hypertension.

67
Q

What is the morphology of cor pulmonale?

A

Acute cor pulmonale:

  • dilation of the right ventricle

Chronic cor pulmonale:

  • right ventricular (and often right atrial) hypertrophy. dilation may develop in the setting of ventricular failure.

*Since chronic cases are due to chronically elevated pulmonary arterial pressure, the pulmonary arteries may contain atheromatous plaques and other lesions.

68
Q

What are the large vessels type of vasculitis ?

A

Giant cell arteritis - old age

Takayasu - early age

69
Q

giant cell arteritis is a large vessel vasculitis charechterised by …

A

​chronic granulomatous reaction → granulomas in lumens of SEGMENTS of arteries in the Head such as temporal ,vertebral , ophthalmic →ischemia

-t-cell mediated response against vessel wall antigen

affects old ages - *take large biopsy*

70
Q

Takayasu large vessel vasculitis is charactarised by…

A

“Pulseless disease”-in asian noodle motherfuckers

  • intimal hyperplasia and thickening of vessel wall
  • collagenous scarring → reduced BP ,weaker pulse in upper extremities

-in early ages unlike giant cell arteritis

71
Q

the medium sized vasculitis include …

A

PAN

KAWASAKI

72
Q

Polyarteritis Nodoa (PAN) is charachterized by …

A

-affects **many vessels EXCEPT THE LUNG

-30%**
of patients hepatitis B as antigen

2 forms
acute - segmental transmural necrotizing inflammation → thrombosis/aneurysm/rupture

chronic - necrotizing inflammation → fibrosis → ischemia

kidney failure
MI
small skin hemorrhages

73
Q

Kawasaki is a medium sized vasculitis characterized by …

A

Acute, febrile, self‐limited disease in infant/children

antibodies against endothelial cells especially → coronary arteries → aneurysm/thrombus/rupture/**AMI

“CRASH”
C**
onjunctivits
Rash
Adenopathy
Strawberry tongue
Hands+feet edema+rash

74
Q

types of small vessels vasculitis include …

A

Microscopic Polyangiitis

wegner granulomatosis

Buerger disease

75
Q

Microscopic Polyangiitis aka “leukocytoclastic vasculitis” is characterized by PMNI infiltration with fragmented nuclei as well as …

A

Hypersensitivity reaction to antibiotics, microorganisms or tumor - affects small vessels.

  • no granulomas , P-ANCA in 70% of cases

90% of patients have :

  • necrotizing glomerulonephritis → hematuria,proteinuria
  • ​ pulmonary capillaries→hemoptysis
76
Q

Wegener granulomatosis is characterized by …

A

C-ANCA

Granulomas and Vasculitis of small vessels in the lungs and upper respiratory tract → hemorrhage and hemoptysis.

Chronic sinusitis

Glomerulonephritis

77
Q

Buerger disease is characterized by …

A

develops before age 35.

Strongly associated with smoking tobacco which is toxic to endothel

small microabscesses in vessel wall may result in gangrene of the extremities.

Raynaud phenomenon

78
Q

infectious vasculitis is usually caused by bacteria and fungi , particulary … which can cause…

A

Aspergillus

can cause mycotic aneurysm→thrombosis→infarct

79
Q

Isolated pericardial disease is uncommon. thats meaning …

A

pericardial diseases are almost always associated with disease in other parts of the heart

80
Q

pericarditis can be caused by …

A

primary pericarditis → viral infection

secondary pericarditis →

  • after AMI
  • Uremia
  • ​SLE , RF
  • Surgery
81
Q

what are the fates of pericarditis ?

A

immediate hemodynamic sequences

resolve

progress to chronic fibrotic process

82
Q

morphology of pericarditis comes in 2 forms

A

Acute pericarditis

  • Virus/Uremia →“Bread-Butter” fibrinous exudate
  • ​Bacteria → fibrino-purulent exudate
  • ​Malignancy → Bloody effusion

Chronic pericarditis

delicate adhesions →fibrotic scars →contrictive pericarditis

83
Q

normally , serous fluid in the pericardial sac measures for about 30-50 ml. pericardial effusions exceeding these volumes occur in the following forms …

A

Serous → CHF, hypoalbuminemia

Seroanguinous (serous+blood) → ruptured MI , Trauma , aortic dissection , malignancy

Chylous → lymphatic obstruction

84
Q

a patient previously diagnosed with pericarditis is complaining about atypical chest and dyspnea. his blood pressure was measured and was found to be low. atempts to stabilize his blood pressure with medications failed. this patient may have developed…

A

cardiac tamponade due to fluid accumulation

85
Q

aneurysm is a …

A

abnormal dilation of blood vessel

86
Q

aneurysm are classified as …

A

true aneurysm →involves all 3 layers

false/pseudo aneurysm →breach in vascular wall→hematoma

87
Q

aneurysm can come in two shapes , namely

A

saccular / fusiform

88
Q

name 3 types of aneurysms

A

1) Abdominal Aortic Aneurysm -“AAA”
2) Syphilitic aneurysm
3) Berry aneurysm

89
Q

what are the causes of AAA and where does it usually arise ?

A

Atherosclerosis →compress→necrosis→dilation

Genetic polymorphism in →MMP/ MMPi / inflammatory infiltration

arises between renal arteries above iliac bifurcation

90
Q

what are the 2 types of AAA and my be the consequences of such aneurysms ?

A

Mycotic →bacteria infects atherosclerotic lesions

inflammatory → periaortic fibrosis + inf.inf.

consequences :

thrombosis → ischemia
rupture
embolism
compression on ureter

91
Q

syphilitic aneurysms are caused by which type of spirochaete bacterium?

A

Treponema pallidum →syphillis STD

disease affects vasa vasorum → ischemia of aortic root media→ scaring →dilation

valvular insufficiency → L.V.H

92
Q

Berry aneurysms are most commonly found in the …and are due to …

A

branching points of arteries in circle of willis

develops due to

congenital malformation + hypertension

if ruptures →intracranial pressure increases

treatment clip it ! or insert spiral metal inside it !

93
Q

aortic dissection is a …

A

intimal tear allows blood to flow to space between intima and media so they separate.

94
Q

what are the causes of aortic dissection ?

A

1) hypertension →old ages
2) atherosclerosis
3) C.T. disorders →young ages → Marfan syndrome

95
Q

how are aortic dissections classified ? what are the consequences of such dissections ?

A

A
Type 1/2 → proximal in ascending aorta

  • type 1 - extensive, ascending +descending
  • ​type 2 - focal, in ascending

B

  • type 3 → distal, in descending aorta

consequences :

1) narrow orifices of blood vessels
2) rupture and bleeding inside body cavities →cardiac tamponade

3) sometimes new channels are formed allowing
* *re-entry** of blood to lumen of aorta →chronic dissection

Y Pathology! (20 decks)

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