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RCS > L23- CVS Pathology IV > Flashcards

L23- CVS Pathology IV Flashcards

1
Q

define systemic hypertensive heart disease and briefly explain pathogenesis

A

-LV hypertrophy, no evidence of other causes besides HTN

Sustained pressure overload –> GFs + local mechanical effects –> upregulate actin / myosin expression => hypertrophy

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2
Q

HTN LV hypertrophy is considered (concentric/eccentric) and the heart will weigh (2). In long-standing cases (3) is often observed. On histology, myocytes will appear (4).

A

1- concentric
2- 400-600g
3- RV hypertrophy and dilatation
4- enlarged with large hyperchromatic, rectangular, ‘box-car’ shaped nuclei

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3
Q

describe the clinical features (and progression) of systemic hypertensive heart disease

A

Early- asymptomatic

  • ->
  • angina
  • signs/sxs of LHF
  • ->
  • CVA, renal failure (via HTN)
  • SCD (sudden cardiac death)
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4
Q

Pulmonary hypertensive heart disease, aka (1), is defined as (2). Note- (3), (4) are excluded from (2).

A

1- cor pulmonale
2- R sided cardiac chamber disease secondary to pulmonary parenchymal or vascular disease
3- pulmonary HTN due to LHF
4- pulmonary HTN due to congenital heart disease

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5
Q

describe the appearance of acute cor pulmonale

A

(pulmonary hypertensive heart disease)
-Pulmonary Embolism => sudden inc of burden on RV / R heart
=> RV dilatation (no hypertrophy)

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6
Q

The most common cause of chronic cor pulmonale is (1), but other causes include (2). The R heart will have the following changes: (3).

A

(pulmonary hypertensive heart disease)
1- COPD
2- idiopathic, pulmonary fibrosis, cystic fibrosis, marked obesity
3- RV hypertrophy, RA hypertrophy and dilatation

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7
Q

(1) is the generalized inflammation of myocardium where (2) is the primary cause to its development and myocardial (3). It is associated with (4) of the myocardium.

A

1- myocarditis
2- inflammatory process
3- myocardial injury
4- necrosis / degeneration of myocytes

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8
Q

The most common cause of myocarditis is (1), specifically (2) in most cases. Pathogenesis involves the following three steps, (3).

A

1- viral
2- coxsackie A/B, enteroviruses
3- direct viral cytotoxicity –> cell-mediated immune rxns against infected myocytes –> CKs released aggrevate myocardial dysfunction

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9
Q

describe the gross and histological appearance of viral myocarditis

A

Gross:

  • dilated, flabby heart (or normal)
  • cut surface that has patchy pallor and mottling
  • possible mural thrombi

Histo:

  • interstitial inflammation, mainly lymphocytes, few plasma cells
  • focal necrosis of myocytes – adjacent to inflammatory cells
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10
Q

describe clinical presentation of myocarditis and the investigation used in diagnosis

A
  • Varies: asymptomatic – sudden acute HF / arrhythmias
  • Nonspecific (mostly): flu-like sxs, fatigue, dyspnea, palpitations, chest pain, fever (may mimic acute MI sxs)

Investigations: PCR for viral nucleic acids, serological studies

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11
Q

list the complications of myocarditis

A
  • acute HF
  • dilated cardiopathy –> chronic HF (viral type)
  • arrhythmias: ventricular is most dangerous, leading to possible SCD
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12
Q

describe the outcomes of myocarditis

A
  • mostly a self limiting disease (spontaneous resolution)
  • if Pt survives acute phase –> inflammation resolves –> healing with total resolution or progressive fibrosis

(majority recover completely)

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13
Q

list the 3 parasites (and theie associated disease) that cause myocarditis

A
  • trichinella spiralis; trichinosis: infects muscle
  • trypanosoma cruzi; Chaga’s disease
  • toxoplasmosis, toxoplasma gondii
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14
Q

Parasitic Myocarditis, indicate the microorganism:

(1) is most common cause
(2) common in immunocompromised
(3) related to cats
(4) endemic in South America

(5) parasitization of scattered myofibers by it with accompanied mixed inflammatory infiltrate
(6) shows eosinophilic predominance on histology

A

Trichella Spiralis (trichinosis): 1, 6

Trypanosoma Cruzi (Chaga’s disease): 4, 5

Toxoplasmosis (toxoplasma gondii): 2, 3

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15
Q

(bacterial/fungal/parasitic/fungal) myocarditis is occurs in immuno-compromised individuals, where it is characterized by the presence of (2) in the myocardium

A

1- fungal (Candida spp.)

2- mixed inflammatory infiltrate: neutrophils, lymphocytes, plasma cells

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16
Q

list the 2 types on noninfectious myocarditis

A
  • immunologically medicated

- giant cell myocarditis

17
Q

Immunological medicated (noninfectious) is related to (1) diseases and (2) drugs. It is described as (3) in nature and severity and the inflammatory response is composed of (4).

A

1- SLE, polymyositis
2- (drug hypersensitivies) methyldopa, sulfonamides
3- mild, self-limiting (resolves spontaneously)
4- lymphocytes, macrophages, high in eosinophils

18
Q

Giant cell myocarditis has a (1) cause and can be associated with (2) diseases. It is dangerous in (3) people as (4) can cause death. Its histological appearance is described as (5).

A 
1- idiopathic (maybe immune origin)
2- SLE, thyrotoxicosis
3- 20-40s people
4- CHF, arrhythmias
5- granulomatous inflammation: giant cells, lymphocytes, eosinophils plasma cells + focal extensive necrosis
19
Q

define Cardiomyopathy and list the three main categories

A

-primary myocardial disease excluding ischemia, HTN, valvular lesions, congenital anomalies, inflammatory disorders as causes

1) dilated CM (includes arrhythmogenic RV CM)
2) hypertrophic CM
3) restrictive CM

20
Q

The most common type of CM is (1), aka (2). It is characterized by progressive cardiac (dilatation/hypertrophy), (concentric/eccentric) hypertrophy, and (diastolic/systolic) dysfunction. It will eventually lead to (6).

A 
1- DCM (dilated)
2- congestive CM
3- dilatation
4- eccentric hypertrophy
5- systolic, contractile dysfunction
6- progressive HF
21
Q

list the common caused of DCM (hint- 8)

A

1) idiopathic (most cases)
2) genetic mutations
3) EtOH: direct cytotoxicity
4) Viral Myocarditis (coxackie B virus)
5) Nutritional disturbances: thiamine/vitB1 deficiency, chronic anemia
6) chemotherapy: doxorubicin
7) pregnancy associated / peripartum DCM
8) stress provoked

22
Q

describe the genetic causes of DCM

A

(25-35% of cases)
Most common: AD mutations affecting cytoskeleton

Less common: X-linked mutations to dystrophin

Uncommon: mutations of mitochondrial proteins in oxidative phosphorylation

23
Q

Peripartum CM (DCM) occurs during (1) and is associated with (2). (3)% of cases will recover spontaneously.

A

1- late gestation to few weeks after delivery
2- volume overload, HTN, nutritional disturbances
3- 50%

24
Q

DCM will be exhibited in (1) heart chambers. In total the heart will appear (2) with (3) sized walls. There will (4) dysfunction, which can lead to (5), which can lead to (6).

A 
1- all four chambers
2- enlarged, flabby, heavy (2-3x)
3- normal, thin, or thick walls
4- contractile dysfunction
5- mural thrombosis
6- embolization
25
Q

DCM Histology:

(1) myocyte appearance
(2) interstitial appearance

(3) is also possibly seen due to (4) dysfunction leading to (5)

A

1- hypertrophied, enlarged nuclei // some thin and stretched out and irregular
2- fibrosis, mainly in endocardium

3- necrosis (myocytes)
4- contractile dysfunction
5- poor perfusion / ischemia

26
Q

DCM:

  • mostly affects (1) individuals
  • fundamental defect is (2)
  • EF of (3)
  • progresses to (4)
  • Tx: (5)
A 
1- 20-50 age group
2- contractile dysfunction
3- <25% (50-65% is normal)
4- CHF
5- cardiac transplantation
27
Q

ARVC, aka (1), is a (2) type disorder in nature / cause. It is characterized by (3) due to (4). (3) can lead to the following progression: (5).

It is associated with a (6) defect and (7) disease.

A

1- arrhythmogenic right ventricular cardiomyopathy
2- AD inherited
3- thin RV
4- myocyte replacement by fatty infiltration
5- RHF, arrhythmia –> SCD
6- desmosomal adhesion protein
7- Naxos Syndrome

28
Q

HCM is characterized by (1- describe effect) and (2), and in 30% of cases (3). HCM will present with (4).

A

1- myocardial hypertrophy –> small LV chamber
2- abnormal diastolic filling
3- intermittent LV outflow obstruction (ant. leaflet of MV)
4- exertional dyspnea or SCD in young adults

29
Q

HCM is inherited in a (1) fashion and is the result of a (2) mutation in one of the following protein: (3). (2) will result in a (gain/loss) of function leading to (5) progression.

A

1- AD
2- point mutation
3- [sarcomeric protein] β-myosin heavy chain (most common), myosin binding protein C, cardiac troponin T
4- gain of function
5- myocyte hypercontractility –> inc energy use –> intense compensatory hypertrophy (myofiber disarray) + fibroblast proliferation

30
Q

HCM will have a (1) appearance on the walls and a (2) appearance of the cavity. (3) is the hallmark feature and (4) is another possible critical feature.

A

1- thick, massive hypertrophy w/o dilatation
2- banana-like configuration (longitudinal section)
3- Asymmetric Septal hypertrophy (most prominent in subaortic region)
4- endocardial plaque/sclerosis in L outflow tract

31
Q

HCM histology:

(1) myocyte appearance
(2) myocyte organization
(3) interstitial appearance

A

1- hypertrophy, diameter >40µm (15µm is normal)
2- myofiber disarray: haphazard arrangement of hypertrophied, abnormally branching myocytes
3- fibrosis

32
Q

list the clinical features and symptoms of HCM and include its treatment

A
  • exertional dypnea
  • angina / MI
  • harsh ejection systolic murmur
  • SCD via arrhythmia
  • CHF

Tx:

i) therapy to relax ventricles
ii) partial septal muscle excision (reduce outflow obstruction)

33
Q

(1) is the least common type of CM. It is characterized by (2) leading to (3) progression and (diastolic/systolic) dysfunction.

A

1- Restrictive CM (RCM)
2- stiff walls
3- loss of ventricular compliance –> impaired ventricular filling during diastole
4- diastolic dysfunction OR systolic if systole is not forceful

34
Q

list the common causes of RCM

A
  • endomyocardial fibrosis (most common)
  • Loffler’s syndrome
  • radiation fibrosis
  • amyloidosis
  • hemochromatosis
  • metastatic tumors
35
Q

list the clinical features and complications due to RCM

**indicate Dx requirement

A

Sxs: exertional dyspnea, fatigue, chest pain

Complications: arrhythmias, CHF

Dx: endomyocardial biopsy

36
Q

RCM Morphology:

(1) ventricle appearance
(2) cavity appearance
(3) myocardium appearance
(4) atrium appearance
(5) interstitial appearance

A 
1- normal or slightly enlarged
2- not dilated
3- firm
4- both atria dilated
5- patchy variable fibrosis
37
Q

EMF is a (1) type of CM commonly found in (2) age group and (3) regions. It is characterized by (4) leading to (5) in the affected chambers.

A 
(endomyocardial fibrosis)
1- restrictive CM
2- children, young adults
3- Africa, tropics
4- dense fibrosis of endocardium and subendocardium (from apex to AV valves)
5- reduced volume and compliance
38
Q

Loefflers Endomyocarditis is a (1) type of CM characterized by (2). It is caused by abundance of (3) in the periphery releasing (4) to damage (5).

A 
1- restrictive CM
2- endocardial fibrosis, with large mural thrombi
3- eosinophils + abnormal degranulation
4- MBP (major basic protein)
5- endocardium --> necrosis, fibrosis

RCS (29 decks)

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