52 - Cellular Adaptations (Myocardial Hypertrophy, Valve Defects)

Question 1

Hypertrophy

Answer 1

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

Question 2

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

Answer 2

Permanent cells

Question 3

Hyperplasia

Answer 3

Increase in cell number Occurs in labile cells

Question 4

Example of physiological hyperplasia

Answer 4

Proliferative and secretory endometrium

Question 5

Example of pathological hyperplasia

Answer 5

Parathyroid hyperplasia.

Question 6

*Appearance of parathyroid hyperplasia

Answer 6

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

Question 7

Example of pathological mixed hypertrophy and hyperplasia

Answer 7

Grave’s disease (antibody mimics thyroid stimulating hormone)

Question 8

*Appearance of thyroid in Grave’s disease

Answer 8

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

Question 9

Where does metaplasia often occur?

Answer 9

Junctions between different epithelial cell types.

Question 10

Common stimulus for metaplasia

Answer 10

Altered environment

Question 11

Metaplasia

Answer 11

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

Question 12

Example of physiological metaplasia

Answer 12

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

Question 13

Example of pathological metaplasia

Answer 13

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

Question 14

What triggers metaplasia in Barrett oesophagus?

Answer 14

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

Question 15

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

Answer 15

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

Question 16

When is atrophy irreversible?

Answer 16

When accompanied by cell death or fibrosis

Question 17

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

Answer 17

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

Question 18

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

Answer 18

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

Question 19

Patterns of myocardial hypertrophy

Answer 19

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

Question 20

Normal left ventricle thickness

Answer 20

Under 15mm

Question 21

Normal RV thickness

Answer 21

Under 5mm

Question 22

Normal male and female heart weights

Answer 22

Women over 400g Men over 500g

Question 23

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

Answer 23

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

Question 24

Genetic cause of myocardial hypertrophy

Answer 24

Hypertrophic obstructive cardiomyopathy (HOCM)

Question 25

Nutmeg liver

Answer 25

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

Question 26

Ways to classify valve diseases 1) 2) 3)

Answer 26

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

Question 27

Congenital cause of aortic stenosis

Answer 27

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

Question 28

Example of a mitral valve problem

Answer 28

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

Question 29

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

Answer 29

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

Question 30

Rheumatic heart disease

Answer 30

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

Question 31

Infective endocarditis

Answer 31

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

Question 32

How does infective endocarditis present?

Answer 32

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

Question 33

How can a bacteraemia leading to infective endocarditis come about?

Answer 33

From dental work, invasive surgery, IV drug use

Question 34

Name for cardiac failure arising from hypertension

Answer 34

Hypertensive heart disease

Question 35

Ramipril

Answer 35

ACE inhibitor