1.4 Adapatation to Injury and stress Flashcards

1
Q

Hypertrophy

A

increase in size of cells leading to an increase in size of tissue

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2
Q

Physiological hypertorphy

A

Uterus during pregnancy–>SM cells get largers (but note these cells can also divide)
Skeletal muscle–>by over working

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3
Q

Pathological hypertrophy

A

heart because of hypertension–>short term this is good to pump against a pressure gradient but in the long term that’s a problem

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4
Q

Causes of hypertrophy (3)

A

Mechanical stimulus - cardiac and skeletal muscle hypertrophy

Growth factor stimulation - endocrine stimulation at puberty - not a good example

increased functional demad - unilateral nephrectormy –>take out one, other one grows–glomeruli get huge

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5
Q

In Myocardial hypertrophy the size

A

increases

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6
Q

What happens to ANF in myocardial hypertrophy

A

it is normally not expressed but gets expressed to decrease cell volume, lowering load and lowering pressure

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7
Q

Proteins expressed in Myocardial hypertrophy (6)

A

c-fos, jun, EGRF, fetal contractile proteins (beta myosin-more energy efficient but dec atpase activity), growth factors (TGF -beta, IGF -1)

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8
Q

What is the end result of myocardial hypertrophy

A

degeneration

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9
Q

The hearts of well trained athletes have vs myocardial hypertrophy

A

good ability to dialate and increase stroke volume vs only an increase in heart rate

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10
Q

Hyperplasia

A

inc in no. of cells resulting in inc size

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11
Q

Physiological hyperplasia

A

lactating breast

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12
Q

Pathological hyperplasia

A

overstimulation by hormones e.g. enlargement of the prostate; inc risk of cancer

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13
Q

Causes of hyperplasia

A

viral induced - warts

growth factor stimulation - endocrine or stress- induced

ex.
- endometrial proliferation with each menstral cycle
- callus formation
- erythroid hyperplasia under chronic hypoxic conditions

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14
Q

Atrophy

A

decrease in size and often fn of cells, generally associated with a decrease in size and or fn of a tissue or organ

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15
Q

Causes of Atrophy (7)

A

Disues atrophy of muscle - voluntary or denervation-induced
dec blood supply
inadequate nutrition
loss of endocrine stimulation
loss of growth factors
aging
pressure

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16
Q

Mechanisms of atrophy

A

inc catabolism
inc ubiquiting proteosome pathway
inc lysosomal degredation

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17
Q

Metaplasia

A

replacement of one differentiated cell type by another with change in stem cell differentiation

18
Q

causes of metaplasia

A

chronic irritation - squamous metaplasia in respiratory tract in response to tobacco smoke

chronic gerd - distal esophagus change in response to gastric acid (barrot’s esophagus)

19
Q

Dysplasia

A

abnormal or disorderly growth recognized by a change in size shape and or organization of cells within a tissue

20
Q

Anaplasia

A

complete loss of morphological differentiation

21
Q

Neoplasia

A

autonomous new growth

22
Q

Benign neoplasia

A

fibroids

23
Q

Malignant neoplasia

A

carcinoma

24
Q

Cellular accumulations (5)

A

lipids (fats and cholesterol) Proteins Hyalin change glycogen pigments

25
Q

Alcoholism sublethal changes in the liver (5)

A
fatty change                
alcoholic hyaline               
megamitochondria                  
mitochondrial crystals                
proliferation of endoplasmic reticulum
26
Q

Hyaline in liver

A

intermediate filaments

27
Q

Pompe

A

glycogen accumulates in the body, specifically in the heart and child dies by age of 2 from heart failure

28
Q

Protein accumulation

A

proteinuria and resoption in proximal tubules excess secretory protein: russell bodies in plasma cells

defects in folding and transport: alpha1 antitrysin deficiency, cystic fibrosis, familial hypercholesterolemia

protein damage

29
Q

Mineral and Pigment deposition

A

hemosiderin

30
Q

Hemosiderosis vs hemochromatosis

A

no scarring vs scarring

31
Q

hemosiderin in lungs

A

heart failure

32
Q

Lipofuscin

A

insolulbe brownish yellow intracellular pigment that accumulates with age

complexes of lipid and protein derived from peroxidation of polyunsaturated lipids of subcellular membranes

33
Q

Lipofuscin is seen in

A

long lived cells like cardiac myocytes and neurons

34
Q

Dystrophic Calcification

A

deposition of Ca in tissues in sites of chronic cell death and inflammation

35
Q

Metastatic calcification

A

percipitation of Ca due to metabolic problem

36
Q

Hyaline change

A

since hyalin is just telling you its pink it can be many substances - mallory’s hyaline, hyaline membrane disease

37
Q

Mallory Hyaline

A

in liver due to ethanol

38
Q

hyaline in lung

A

fibrin

39
Q

Aging

A

rate at which you age could be a disease – werner’s

40
Q

Fewer doubling times of fibroblasts suggests

A

more clotting, seen in older people or in diseases like werner’s

41
Q

Enzyme that works against aging

A

telomerase

42
Q

Calories and aging

A

more calories means more accumulation of unwanted substances so fater aging