Pathology - Cell Injury, Cell Death And Adaptations

Front 1

Hyperplasia - types

Back 1

Hormonal hyperplasia --> breast
Compensatory hyperplasia --> liver resection
Pathological hyperplasia --> wound healling

Front 2

Causes of atrophy

Back 2

Decreased workload
Loss of innervation
Diminished blood supply
Inadequate nutrition
Loss of endocrine stimulation
Aging

Front 3

Cachexia

Back 3

Wasting syndrome - loss of body mass that can not be reversed nutritionally

Front 4

Autophagy

Back 4

Starved cell eats its own components

Front 5

Metaplasia definition + cause

Back 5

Reversible change - adult cell type is replaced with another
Genetic ´reprogramming´ of stem cells--> epithelial metaplasia
- response to chronic inflammation

Front 6

Ischemia of myocardial cells

Back 6

1 - 2 min - noncontractile
20-30 min - cell death

Front 7

Reversible injury

Back 7

Cellular swelling
Fatty change

Front 8

Morphology of necrosis

Back 8

Swelling of ER
Lysosome rupture
Nuclear condensation
Swelling of mitochondria
Fragmentation of cell membrane and nucleus
High eosinophilia, pink-due to decreased cytoplasmic RNA
Myelin figures--> large phospholipid masses from damaged membrane
Pyknosis--> nuclear shrinkage
Karyorrhexis--> pyknotic nucleus undergo fragmentation

Front 9

Coagulative necrosis

Back 9

High protein tissues, parenchymatous organ, firm structure.
- heart, liver, spleen, lung
Red--> yellow colour
*old myocardial infarction is therefore coloured yellow.

Front 10

Liquefactive necrosis

Back 10

Digestion of cells due to bacterial or fungal infection.
-brain, fat tissue

Front 11

Coagulative necrosis
- Gangrenous necrosis

Back 11

Involves multiple tissue layers, complicated by bacterial infection--> attreact leukocytes-> ´wet gangrene´

Front 12

Caseous necrosis

Back 12

Tuberculous infection
- center of granulomas.
´cheese-like´
Surrounded by ring of macrophages and giant cells(Langhans cells)

Front 13

Fat necrosis

Back 13

Release of active pancreatic lipase into peritoneal cavity and pancreas--> acute pancreatits
- pancreatic enz. and lipases split TGesters, release FA. FA combine with Ca2+ -->saponification

Front 14

Fibrinoid necrosis

Back 14

Arterial wall and CT are infiltrated by immune complexes, show characteristic of fibrin.

Front 15

Can atrophy be induced?

Back 15

Injection of thyroxinen will decrease the need of thyroid gland. It will shrink.

Front 16

Free radical cell injury

Back 16

Lipid peroxidation of membranes
Cross-linking of proteins
DNA fragmentation

Front 17

Removal of free radicals

Back 17

-Superoxide dismutase
-GSH peroxidase - ratio GSH vs GSSG reflects cells ability to oxidize free radicals
-Catalase in peroxisomes
-Vit A, E, C and beta-carotene

Front 18

Mercury chloride poisoning - mechanisms

Back 18

Binds to sulfhydryl groups of cell membrane proteins --> inhibits ATP-dependent transport

Front 19

Carbon tetrachloride poisoning

Back 19

CCl4-->CCl3 (in liver) by CYP450
Cause phospholipid peroxidation - breakdown of ER
-low hepatic protein synthesis
-swelling of ER
-low lipid export--> fatty liver
End resulat can be Ca2+ influx and cell death.

Front 20

Normal(non-pathological) Apoptosis
-causes

Back 20

Embryogenesis
Implantation
Involution of hormone dependent tissue
Maintain constant nr. of cells
Self reactive lymphocyte elimination
Cell death induced by Tcyt-cells

Front 21

Pathologic Apoptosis
-causes

Back 21

DNA-damage
Accumulation of misfolded proteins
Viral infections
Atrophy in parenchymal cells

Front 22

Two pathways of apoptosis

Back 22

Intrinsic-mitochondrial--> cytochrome C
Extrinsic-death receptor-->Fas-TNF-receptor

Front 23

Atherosclerosis

Back 23

Smooth muscle cells and macrophages are filled with lipid vacuoles --> plaques

Front 24

Xanthomas

Back 24

Accumulation of intracellular cholesterol in hereditary and aquired hyperlipidemic syndromes.
-subepithelial CT of skin or tendons
- arranged in clusters, foamlike

Front 25

"Alcoholoc hyaline"

Back 25

Seen in alcoholic liver disease, accumulation of intracellular cytoskeletal proteins becasue of cell injury - ´Mallorys bodies´ or ´Mallorys hyaline´

Front 26

Russell bodies

Back 26

Accumulation of Immunoglobulins
-seen in nasal polyp slide

Front 27

Glycogen accumulation
- cause

Back 27

Glucose mtb abnormality
-Diabetes Mellitus- accumulation of glycogen in renal tubular cells, cardiomyocytes, beta-cells in islets of Langerhan.

Front 28

Pigments
-exogenous

Back 28

Exogenous: Carbon--> anthracosis, blacken lymph nodes and pulmonary parenchyma

Front 29

Pigments
-endogenous

Back 29

Lipofuscin- marker of past free radical injury(heart, liver, brain)
Melanin
Hemosiderin- stain Prussian blue, (bone marrow, spleen, liver)
Bruise formation
Hemosiderosis-->systemic overload of iron. First liver, bone marrow, spleen, lymph node->->progressive overload of whole body.

Front 30

Hemosiderosis
-cause

Back 30

High absorption of iron
-impaired utilisation
-hemolytic anemias
-transfusions
*hereditary hemochromatosis

Front 31

Dystrophic calcification

Back 31

*atheromas->advanced atherosclerosis
-formation of crystalline phoshate
-dying cells has no Ca2+ regulation+phosphate=insoluble precipitate.

Front 32

Metastatic calcification
- Hypercalcemia, causes

Back 32

1. increased PTH secretion due to tumour.
2. destruction of bone -
Paget´s disease
immobilization
multiple myeloma
leukemia
skeletal metastases
3. Vit. D disorders-->intoxication-sarcoidosis(activated vit.D precipitate)
4. Renal failure ->phosphate retention->secondary hyperparathyroidism

Front 33

Russell bodies

Back 33

Accumulation of Immunoglobulins
-seen in nasal polyp slide

Front 34

Glycogen accumulation
- cause

Back 34

Glucose mtb abnormality
-Diabetes Mellitus- accumulation of glycogen in renal tubular cells, cardiomyocytes, beta-cells in islets of Langerhan.

Front 35

Pigments
-exogenous

Back 35

Exogenous: Carbon--> anthracosis, blacken lymph nodes and pulmonary parenchyma

Front 36

Pigments
-endogenous

Back 36

Lipofuscin- marker of past free radical injury(heart, liver, brain)
Melanin
Hemosiderin- stain Prussian blue, (bone marrow, spleen, liver)
Bruise formation
Hemosiderosis-->systemic overload of iron. First liver, bone marrow, spleen, lymph node->->progressive overload of whole body.

Front 37

Hemosiderosis
-cause

Back 37

High absorption of iron
-impaired utilisation
-hemolytic anemias
-transfusions
*hereditary hemochromatosis

Front 38

Dystrophic calcification

Back 38

1.Necrotic tissue
2.Tissues undergoing slow regeneration
*atheromas->advanced atherosclerosis
-formation of crystalline phoshate
-dying cells has no Ca2+ regulation+phosphate=insoluble precipitate.
*heart valves - stenosis

Front 39

Metastatic calcification
- Hypercalcemia, causes

Back 39

1. increased PTH secretion due to tumour.
2. destruction of bone -
Paget´s disease
immobilization
multiple myeloma
leukemia
skeletal metastases
3. Vit. D disorders-->intoxication-sarcoidosis(activated vit.D precipitate)
4. Renal failure ->phosphate retention->secondary hyperparathyroidism

Front 40

Hemochromatosis

Back 40

Inherited defect on chromosome 6 resulting in uncontrolled absortion of iron. Systems becomes overloaded with iron.
1. pancreas - fibrosis
2. liver - cirrhosis
3. skin - around sweat glands
4. heart muscle
5. mesenteric lymph nodes