52 - Cellular Adaptations (Myocardial Hypertrophy, Valve Defects) Flashcards

1
Q

Hypertrophy

A

Increase in size of cells without increasing cell number Increased production of intracellular structures with an increase in nucleus size and shape

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2
Q

Which cells take the hypertrophy pathway in response to mechanical stress, growth factors, etc?

A

Permanent cells

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3
Q

Hyperplasia

A

Increase in cell number Occurs in labile cells

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4
Q

Example of physiological hyperplasia

A

Proliferative and secretory endometrium

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5
Q

Example of pathological hyperplasia

A

Parathyroid hyperplasia.

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6
Q

*Appearance of parathyroid hyperplasia

A

Normal parathyroid is speckled with white, which is fat, In hyperplasia, fat is lost.

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7
Q

Example of pathological mixed hypertrophy and hyperplasia

A

Grave’s disease (antibody mimics thyroid stimulating hormone)

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8
Q

*Appearance of thyroid in Grave’s disease

A

Normal thyroid has cuboidal epithelial-bound follicles filled with acellular colloid. This is lost in Grave’s disease. Cuboidal epithelium becomes columnar.

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9
Q

Where does metaplasia often occur?

A

Junctions between different epithelial cell types.

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10
Q

Common stimulus for metaplasia

A

Altered environment

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11
Q

Metaplasia

A

A reversible change in which one adult cell type is replaced with another

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12
Q

Example of physiological metaplasia

A

Pre-menarche epithelium is mucosal (simple columnar). At onset of menarche, tissues swell and expose mucosa to acidic vaginal environment. Becomes stratified non-keratinising stratified squamous epithelium

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13
Q

Example of pathological metaplasia

A

Barrett oesophagus. Acid reflux from stomach causes non-keratinising stratified epithelium to become intestinal columnar epithelium with goblet cells.

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14
Q

What triggers metaplasia in Barrett oesophagus?

A

Bile acid stimulates NF-kB in epithelial cells, causing them to differentiate to intestinal columnar epithelial

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15
Q

Hyperplasia and metaplasia vs neoplasia 1) 2) 3) 4)

A

1) Hyper/meta are controlled division in response to a stimulus. Neoplasia is uncontrolled that can occur without stimulus. 2) Gene expression in hyper/meta is unchanged. Neo is result of genetic change. 3) Hyper/meta are benign, but can predispose to neo. Neo can be benign or malignant. 4) Hyper and meta can be reversible

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16
Q

When is atrophy irreversible?

A

When accompanied by cell death or fibrosis

17
Q

Characteristics of physiological myocardial hypertrophy 1) 2) 3) 4)

A

1) Growth of ventricle wall in proportion to chamber 2) Increased capillary density 3) No loss of systolic or diastolic function 4) Reversible

18
Q

Characteristics of pathological myocardial hypertrophy 1) 2) 3) 4)

A

1) Growth of ventricle wall with reduced or enlarged cavity 2) Reduced function, progression to heart failure 3) Deposition of matrix 4) Does not regress

19
Q

Patterns of myocardial hypertrophy

A

1) Concentric - from excessive pressure 2) Eccentric - from excessive volume

20
Q

Normal left ventricle thickness

A

Under 15mm

21
Q

Normal RV thickness

A

Under 5mm

22
Q

Normal male and female heart weights

A

Women over 400g Men over 500g

23
Q

Microscopic appearance of hypertrophied cardiac muscle 1) 2) 3)

A

1) Enlarged, rectangular (box-shaped) nuclei 2) Bi-nucleated myocytes 2) Increased connective tissue

24
Q

Genetic cause of myocardial hypertrophy

A

Hypertrophic obstructive cardiomyopathy (HOCM)

25
Q

Nutmeg liver

A

From high right heart pressure. Blood is pushed back into hepatic veins, which haemorrhage.

26
Q

Ways to classify valve diseases 1) 2) 3)

A

1) By pathological process (EG: degenerative, infectious) 2) By result (EG: stenosis, regurgitation) 3) By valve affected (EG: mitral, aortic)

27
Q

Congenital cause of aortic stenosis

A

Congenital bicuspid aortic valve. Valve wears out, becomes calcified over time

28
Q

Example of a mitral valve problem

A

Myxomatous mitral valve, aka sloppy valve. Causes mitral valve prolapse. Can be related to connective tissue disease

29
Q

What is acute rheumatic fever? 1) 2) 3)

A

1) Streptococcus pyogenes infection, typically in children 2) Infection of throat. 3) ~3% develop carditis and arthritis

30
Q

Rheumatic heart disease

A

1) Aberrant immune response to strep infection because of molecular mimicry (of cardiac myosin) 2) Causes fibrosis of any valve, multiple valves at once 3) Most common global cause of mitral valve stenosis

31
Q

Infective endocarditis

A

When there is a dysfunctional valve and bacteraemia, there is a change of a thrombus forming on valve with bacteria in it - a vegetation.

32
Q

How does infective endocarditis present?

A

1) Fever 2) Worsening of, new onset of murmur 3) Symptoms of embolism

33
Q

How can a bacteraemia leading to infective endocarditis come about?

A

From dental work, invasive surgery, IV drug use

34
Q

Name for cardiac failure arising from hypertension

A

Hypertensive heart disease

35
Q

Ramipril

A

ACE inhibitor