Atrophy - semmelweis.hu

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Transcript of Atrophy - semmelweis.hu

Atrophy

Dr. Attila Zalatnai

Normal tissue

Abnormal noxas

degeneration adaptation

hyperplasia

hypertrophy

hyperplasia + hypertrophy

necrosis

death

superinfection

tissue loss

mutilation

resorption

cavitation

fistule

pseudocyst

Reparation

fibrosis

scarring

calcification

ossification

metaplasia

inflamm. atrophy

pseudometaplasia

pseudo-hypertrophy

regeneration

dysplasia

malignant transformation

((

Atrophy

Decrease of the size of organs, accompanied by decreased function

Physiologic atrophy = involution (thymus, breast, ovaries)

Local: Generalized:

- slow narrowing of arteries - senile atrophy

- loss of trophic effects - decreased food supply

- inactivity (muscles, bones) (inanition, malabsorption,

- loss of hormonal effects (adrenal) esophageal tumors)

side effects of steroids! - generalized atherosclerosis

- compression atrophy - tumorous cachexia

- irradiation - hypophysis-insufficiency

--vitamin B12 deficiency (tongue) - anorexia nervosa

- prolonged chronic inflammation (gastritis)

- degenerative processes (brain)

Conditions following atrophy

- function loss

- regeneration: after cessation of the cause

- pseudometaplasia (due to compression; e.g. flattening of columnar epithelium)

- space replace (fat, liquor)

- pseudohypertrophy: overproliferation of other tissues

- compensatory hypertrophy: (paired organs)

(loss of both the organic and inorganic material)

Diffuse Local

Primary Secondary (immobilisation)

- senile - glycocorticoids

- postmenopausal - hypogonadism

- malabsorption

- chr. alkoholism

Normal

CompressionNORMAL

POROTIC

Osteoporosis

Pathological fracture

Hydrocephalus, hydronephrosis

Cushing-syndrome

N

Celiac disease

(gluten-sensitive enteropathy)

genetic disposition + gluten exposition

starch + gluten

wheat

villi

Lieberkühn-

crypts

4

1

NORMAL

CELIAC DISEASE

Celiac disease

Celiac disease

MALABSORPTION

Alzheimer’s disease

- Most common cause of senile dementia

- Slowly progressive accumulation of a toxic, abnormal peptide

(A, -amyloid)

- Interference with neurotransmission

- Neuronal destruction