2. Cellular Injury and Adaption Flashcards Preview

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Flashcards in 2. Cellular Injury and Adaption Deck (48):
1

What is the most common cause of injury at the cellular level?

Hypoxia.

2

What is hypoxia?

It is the lack of oxygen that leads to the inability of the cell to synthesize suficient ATP by aerobic oxidation.

3

What is the most common cause of hypoxia?

Ischemia.

4

What is isquemia?

It is the loss of blood supply due to decreased arterial flow or decrease venous outflow.

5

What is the most common mode of inheritance reguarding genetic defects involving enzymes ?

Recessive manner.

6

What is the most common mode of inheritance reguarding genetic defects involving structural proteins?

Dominant manner.

7

What does Vitamin A deficiency lead to?

Night blindness, squamous metaplasia, immune deficiency.

8

What does Vitamin C deficiency lead to?

Scurvy.

9

What does Vitamin D deficiency lead to?

Rickets and osteomalacia.

10

What does Vitamin K deficiency lead to?

Bleeding Diathesis.

11

What does Vitamin B12 deficiency lead to?

Megaloblastic anemia, neuropathy, and spinal cord degeneration.

12

What does Folate deficiency lead to?

Megaloblastic anemia and neural tube defect.

13

What does Niacin deficiency lead to?

Pellagra (diarrhea, dermatitis, and dementia). [N-word:3D's]

14

What are the four protective factors against free radicals?

Antioxidants, Superoxide dismutase, glutathione peroxidase, catalase.

15

What does release of cytochrome C inside the mitochondria do?

Trigger fo apoptosis.

16

What is pyknosis?

Degeneration and condensation of nuclear chromatin

17

What is karyorrhexis?

Nuclear fragmentation.

18

What is Karyolysis?

Dissolution of the nucleus.

19

What clinical marker is released during biliary tract obstruction?

Alkaline phosphatase.

20

What clinical marker is released during hepatitis?

Transaminases.

21

What clinical marker is released during pancreatitis?

Amylase and lipase.

22

What clinical marker is released during myocardial injury?

Creatine phosphokinase-MB isozyme (CPKMB, lactate dehydrogensase [LDH], Troponin).

23

In what type of cellular injury do we observe massive influx of calcium?

Irrevesible cell injury.

24

What is the most common form of necrosis?

Coagulative necrosis.

25

What is coagulative necrosis?

Denaturing and coagulation of proteins within the cytoplasm, micro: loss of nucleus but preservation of cellular shape. Common in most organs including the heart, liver, and kidney.

26

What is liquefactive necrosis?

Cellular destruction by hydrolytic enzymes, due to autolysis and heterolysis. Occurs in absecesses, brain infarcts and pancreatic necrosis.

27

What is caseous necrosis?

Combination of coagulatoin and liquefaction necrosis, gross: soft, friable, and cottage-cheese like. Characteristic of tuberculosis.

28

What is fat necrosis?

Caused by the action of lipase on fatty tissue. It has a chalky white apperance.

29

What is fibrinoid necrosis?

Necrotic tissue that histologically resembles fibrin. Micro: has an eosinophilic (pink) homogenous apperance.

30

What is gangrenous necrosis?

It is a gross term used to describe dead tissue. Common sites are lower limbs, gallbladder, GI tract, and testes.

31

What is Dry gangrene?

Microscopic pattern is coagulative necrosis.

32

What is Wet gangrene?

Microscopic pattern is liquefactive necrosis.

33

What is apoptosis and what is special about it?

It is programmed cell death; there is a lack of an inflammatory response.

34

What gene inhibits apoptosis?

It is the bcl-2; it prevents release of cytochrome c from mitochondria and binds pro-apoptotic protease activating factor (Apaf-1).

35

What gene stimulates apoptosis?

It is p-53; it is elevated by DNA injury and arrests the cell cycle. If DnA repair is impossible, p53 stimulate apoptosis.

36

How is apoptosis executed?

Mediated by a cascade of caspases; they digest nuclear and cytoskeletal proteins and activate endonucleases.

37

What are Councilman bodies?

It is an eosinophilic globule often surrounded by normal parenchyma found in the liver of individuals suffering from viral hepatitis, yellow fever, or other viral syndrome. It represents a hepatocyte that is undergoing apoptosis.

38

What is atrophy?

It is the decrease in cell size and funtional ability. Micro: small shrunken cells with lipofuscin granules. EM: decreased intracellular components, and autophagosomes.

39

What is hypertrophy?

An increase in cell size and functional ability due to increased synthesis of intracellular components.

40

What is hyperplasia?

An increase in the number cells in a tissue or organ.

41

What is metaplasia?

A reversible change of one cell type to another, usually in response to irritation.

42

What is dysplasia?

An abnormal proliferation of cells that is characterized by changes in cell size, shape, and loss of cellular organization; it is not cancer but may progress to cancer (preneoplastic lesion) like cervial dysplasia.

43

What is a Russell body?

It is a intracytoplasmic accumulation of immunoglobulins in plasma cells.

44

What is Lipofuscin?

It is an endogenous pigment of wear and tear pigment that is perinuclear yellow-brown pigement. It is an indigestible material within lysosomes, common in the liver and heart.

45

What is hyaline change?

A nonspecific term used to describe any intracellular or extracellular alteration that has a pink homogenous appearance on H and E stains.

46

What is dystrophic calcification?

Precipitation of calcium phosphate in dying or necrotic tissues.

47

What is a Psammoma body?

There are laminated calcifications that occur in meningiomas and papillary carcinomas of the thyroid and ovary.

48

What is metastatic calcification?

Precipitation of calcium phosphate in normal tissue due to hypercalcemia (supersaturated solution).