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Pathology > Apoptosis/Necrosis > Flashcards

Apoptosis/Necrosis Flashcards

1
Q

A diagnosis based on case history, c/s, physical exam

A

Clinical diagnosis

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2
Q

List of diseases that could account for clinical findings/lesions

A

Differentials

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3
Q

Diagnosis based on changes in biochemistry, hematology, cytology

A

Clinical pathological

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4
Q

Diagnosis based on clonclusive evidence that confirms cause of disease. What may it require?

A

Eitiologic May require ancillary testing

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5
Q

Diagnosis based on predominant lesion or lesion pattern

A

Morphologic diagnosis

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6
Q

Diagnosis based on conclusive evidence from clinical data and observed lesions

A

Definitive

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7
Q

Causes of cell membrane injury

A

1) Transmembrane proteins (hijacked by microbes to enter cell)
2) Oxidative stress from free radicals
3) Loss of phospholipids through decreased synthesis/increased degradation
4) Cytoskeletal abnormalities

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8
Q

Consequences of cell membrane injury

A

1) Loss of Na pump –> cell swelling
2) Increased permeability –> Ca includx - Mitochondrial damage - Apoptosis
3) Injury to RER and ribosome dissociation —> inhibited protein synthesis

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9
Q

Oxidative damage is caused by (3)

A

1) Superoxide anion
2) Hydrogen peroxide
3) Hydroxyl radical

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10
Q

Endogenous source of oxidative damage

A

1) Enzymatic reactions: lipoxygenase, prostaglandin synthetase, lipid peroxidation…etc
2) Transition metal cations (Cu, Fe)
3) Inflammation and tissue injury –> increased free radical production

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11
Q

Exogenous sources of oxidative damage

A

Chemicals

Drugs

Toxins

Radiation

Tissue trauma

Aging

Stress

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12
Q

Antioxidant defense mechanisms (5)

A

1) Superoxide dismutase (SOD)–> catalyzes superoxide anion to hydrogen and oxygen
2) Catalase: catalyzes hydrogen peroxide to water and oxygen
3) Glutathione perioxidase (catalyzes llipid hydroperoxidases to water and oxygen)
4) Vitamin E: neutralizes effects of free radicals
5) Selenium: co-factor of glutathione peroxidase

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13
Q

What is White Muscle Disease caused by

A

Deficiency of Vit E and Selenium Muscle is oxidized, turns necrotic

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14
Q

Implications of oxidative stress on health

A

1) Inflammatory conditions result in chronic oxidative stress causing ORGAN FAILURE and ACCELERATED AGING
2) Chronic oxidative stress can also cause CARCINOGENESIS and NEOPLASTIC DISEASE

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15
Q

Causes of damage to mitochondria (2)

A

1) Oxidative stres
2) Calcium influx

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16
Q

Consequences of damage to mitochondria (2)

A

1) Reduced ATP production
2) Leakage of proapoptopic proteins Cell death/apoptosis

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17
Q

Causes of damage to nucleus

A

1) Oxidative stress: damages nuclear envelope DNA damage:
2) Reactive O2 species, reactive carbonyl species, lipid peroxidation products, alkylating agents, hydrolysis
3) Chemicals, drugs, radiation
4) Random mutations
5) DNA repair malfunction

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18
Q

Cells most susceptible to hypoxia

A

Neurons

Hepatocytes

Cardiac myocytes

Renal tubules

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19
Q

Pathogenesis of hypoxia

A

Lack of oxygen —> reduced ATP —> loss of Na/K pump function—> influx of ions (Na, Ca) and water –> cell swelling

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20
Q

What is first step of reversible cell injury

A

Hydropic degeneration

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21
Q

Types of cell injury

A

Reversible

Irreversible

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22
Q

Gross features of cell swelling

A

Organ enlargement, pallor

Increased fluid in tissues (noticeable during cutting)

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23
Q

Histological features of cell swelling

A

1) Cell enlargement
2) Cytoplasmic vacuolation
3) Cell membrane blebbing

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24
Q

What is ballooning degeneration? What is it associated with?

A

Swelling that occurs in EPIDERMIS Cytoplasm becomes clear.

Peripheral nuclei Inclusion bodies (viral)

Usually associated with viral infection

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25
Q

What is cytotoxic edema? Why is this area so susceptible

A

Swelling that occurs in CNS Susceptible to hypoxic injury due to lack of anerobic glycolysis

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26
Q

What are three types of irreverisible cell damage

A

Necrosis

Apoptosis

Post-mortem autolysis

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27
Q

Nuclear condensation, nucleus appears shrunken and dark

A

Pyknosis

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28
Q

Nuclear destruction

A

Karyolysis

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29
Q

Nuclear fragmentation

A

Karyorexis

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30
Q

Nuclear and cytoplasmic changes of necrosis

A

Pyknosis Karyorrhexis Kryolysis Cytoplasmic:

1) Eosinophilia (proteins)
2) Loss of boundaries, cell rupture
3) Loss of cell adhesions, individualization

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31
Q

Which type of necrosis occurs with sudden loss of blood - resulting in severe acute hypoxic injury

A

Coagulation necrosis

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32
Q

Is coagulation necrosis acute or chronic

A

Acute

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33
Q

Which type of necrosis has retention of cell outlines

A

Coagulation

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34
Q

Which type of necrosis has cytoplasmic hypereosinophilia and pyknotic or absent nuclei

A

Coagulation

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35
Q

Which type of necrosis occurs with bacterial infections

A

Caseation necrosis

36
Q

Which type of necrosis manifests in granulomatous nodules?

A

Caseation necrosis

37
Q

Appearance of caseation necrosis

A

Cottage cheese!

38
Q

Which type of necrosis has an inflammatory zone

A

Caseation necrosis

39
Q

What is histological appearance of caseation necrosis

A

Loss of tissue architecture

Granulomatous/pyogranulomatous inflammation and cellular debris

40
Q

Where do you find liquefactive necrosis

A

CNS, abscesses

41
Q

Is caseation necrosis acute or chronic

A

Chronic

42
Q

What is the chronic type of liquefactive necrosis

A

In CNS

43
Q

Where does acute liquefactive necrosis occur

A

Abscess

44
Q

What is malacia

A

Cavities filled with liquid

Common in liquefactive necrosis in brain and spinal cord

45
Q

Is malacia in CNS acute or chronic

A

ACUTE - severe cases result in death

Mild cases will heal with glial scaring (chronic lesions)

46
Q

Viscous, opaque, white/yellow/green fluid is known as what

A

Supparative inflammation

47
Q

Is supparative necrosis associated with inflammation

A

Yes! Hyperemic ring

48
Q

You see histologically an inflammed tissue with lots of degenerative neutrophils and bacteria. What type of necrosis?

A

Supparative (liquefactive)

49
Q

Can supparative necrosis become chronic

A

Yes, if body walls it off

50
Q

What is a combo of coagulative and liquefactive necrosis

A

Moist gangrene

51
Q

Which type of necrosis is associated with bacteira

A

Moist and gas

52
Q

What type of necrosis is coagulation and mummifcation

A

Dry necrosis

53
Q

Which type of gangrene is acute? Which is chronic

A

Acute: dry

Chronic: moist

54
Q

What is a huge risk of moist gangrene

A

Fatal septicemia after tissue sloughing

55
Q

You have a patient with black, shriveled tissue. What is this?

A

Dry gangrene

56
Q

Your patient has malodorous, brown tissue that is soft. What is this

A

Moist gangrene

57
Q

Your patient has black tissue with a hemorrahagic exudate that contains bubbles. What is this?

A

Gas gangrene

58
Q

What type of bacteria are associated with gas gangrene

A

Anerobes such as Clostridium

59
Q

Sequelae of necrosis

A

1) Inflammation - Neutrophils digest and liquify - Macrophages phagocytose
2) Healing/replacement - Regeneration - Fibrosis
3) Seuqestration - Occurs when necrotic tissue doesnt heal and is removed from body via degradation and phagocytosis (bones)

60
Q

T/F cells undergo apoptosis first swell

A

False, they shrink

61
Q

T/F inflammation is an important step in apoptosis

A

False! No inflammation in apoptosis, only in necrosis

62
Q

Morphology of apoptosis (4)

A

1) Chromatin condensed
2) Cytoplasm condensed
3) Apoptotic bodies: fragmentation of cell in small membrane bound segments
4) Continue maintenace of cell membranes, to prevent inflammation

63
Q

Physiological causes of apoptosis (2)

A

Fetal development

Leukocyte apoptosis

64
Q

Causes of pathologic apoptosis

A

1) Hypoxia
2) Withdrawal of growth factors
3) Cell mediated immune responses

65
Q

Intrinsic pathway of apoptosis

A

Regulated by mitochondria

1) Initiated by withdrawal of growth factors/hormones or DNA damage
2) Release of pro-apoptotic factors from mitochondria. Caspase activation —> apoptosis

66
Q

Extrinsic pathway of apoptosis

A

Initated by death receptors/ cytotoxic T-cells

Fas/FADD signalling followed by caspase activation and apoptosis

67
Q

Whats the name of the enzyme cascade in apoptosis

A

Capase enzyme cascade

68
Q

What is autophagocytosis

A

Cellular house-keeping Removes and recycles damaged organelles and protein

69
Q

Two types of pathological calcifications

A

Dystrophic - at site of injury and necrosis

Metastatic - secondary to hypercalcemia

70
Q

Examples of dystrophic calcificaiton (4)

A

1) Necrotic myocardium/skeletal muscle (white muscle disease)
2) Granulomas
3) Calcinosis cutis (collagen degeneration and calcification) due to hydroadrenocorticism )
4) Calicnosis circumscripta : repetitive injury followed by calcification

71
Q

6 causes of hypercalcemia in vet med **

A

1) Renal failure
2) Primary hyperparathyrodism (rare)
3) Paraneoplastic (lymphoma and anal sac adenocarcinoma produced PTH-related protein)
4) Vit D toxicosis
5) Destructive bone tumor
6) Severe granulmatous disease

72
Q

What causes irreversible cell damage

A

Oncotic necrosis

73
Q

Calcinosis cutis is an example of what

A

Dystrophic calcification

74
Q
A
75
Q

What type of necrosis involved anerobic bacteria

A

Gas gangrene

76
Q

What type of necrosis involved intracellular bacteria

A

Caseation necrosis

77
Q

What type of necrosis involves extracellular bacteria

A

Suppurative inflammatory necrosis

78
Q

Whats this

A

Liquefactive necrosis (clear spaces with eosiniphilic precipitate)

79
Q

Whats this

A

Apoptotic bodies

80
Q

Whats this

A

Ballooning degeneration

(Clear cytoplasm; peripheral nuclear; vira inclusion bodies)

81
Q

Whats this

A

Caseation necrosis

(inflammatory zone, granulomatous to pyogranulomatous inflammation, intracellular bacteria)

82
Q

Whats this

A

Coagulation necrosis

(distinct line of necrotic tissue; loss of nuclei; loss of (individual cell) boundaries; hypereosinophilia)

83
Q

Whats this

A
84
Q

Whats this

A

Supparative necrosis

(degenerative neutrophils; bacteria)

85
Q

Which is necrosis and which is apoptosis

A

Left - necrosis (loss of definition, hypereosinophilic)

Right - apoptosis (nuclear condensation)

86
Q

Which nuclear changes are occuring

A
  1. Pyknosis
  2. Karyolysis
  3. Karyohexis

Pathology (8 decks)

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