changes Flashcards

(42 cards)

1
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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2
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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3
Q

Hypertrophy

A

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

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4
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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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

Causes of hyperplasia

A

viral incuduced - 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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10
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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11
Q

Hyperplasia

A

inc in no. of cells resulting in inc size

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12
Q

Mechanisms of atrophy

A

inc catabolism
inc ubiquitin proteosome pathway
inc lysosomal degredation

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13
Q

Physiological hyperplasia

A

lactating breast

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14
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)

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15
Q

Dysplasia

A

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

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16
Q

Pathological hyperplasia

A

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

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17
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

18
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

19
Q

Metaplasia

A

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

20
Q

Anaplasia

A

complete loss of morphological differentiation

21
Q

Alcoholism sublethal changes in the liver (5)

A
fatty change                
alcoholic hyaline              
megamitochondria                  
mitochondrial crystals                
proliferation of endoplasmic reticulum
22
Q

Neoplasia

A

autonomous new growth

23
Q

Pompe

A

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

24
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

25
Benign neoplasia
fibroids
26
Malignant neoplasia
carcinoma
27
Cellular accumulations (5)
lipids (fats and cholesterol) Proteins Hyalin change glycogen pigments
28
Lipofuscin
insolulbe brownish yellow intracellular pigment that accumulates with age complexes of lipid and protein derived from peroxidation of polyunsaturated lipids of subcellular membranes
29
Hyaline in liver
intermediate filaments
30
Mineral and Pigment deposition
hemosiderin
31
Hemosiderosis vs hemochromatosis
no scarring vs scarring
32
Hyaline change
since hyalin is just telling you its pink it can be many substances - mallory's hyaline, hyaline membrane disease
33
hemosiderin in lungs
heart failure
34
Lipofuscin is seen in
long lived cells like cardiac myocytes and neurons
35
Dystrophic Calcification
deposition of Ca in tissues in sites of chronic cell death and inflammation
36
Fewer doubling times of fibroblasts suggests
more clotting, seen in older people or in diseases like werner's
37
Metastatic calcification
percipitation of Ca due to metabolic problem
38
Calories and aging
more calories means more accumulation of unwanted substances so fater aging
39
Mallory Hyaline
in liver due to ethanol
40
hyaline in lung
fibrin
41
Aging
rate at which you age could be a disease -- werner's
42
Enzyme that works against aging
telomerase