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IHP 1001 > Ch.1 Cell injury, death, adaptation > Flashcards

Ch.1 Cell injury, death, adaptation Flashcards

1
Q

origin of a disease, including the underlying causes and modifying factors.

A

Etiology

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2
Q

Development of the disease. The HOW

A

Pathogenesis

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3
Q

Steady state

A

Homeostasis

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4
Q

Well cells indergo injurious stimulus so they ___ and achieve new steady state & preserve viability & fx.

A

Adapt

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5
Q

If injury is ___ homeostasis is restored

A

Reversible

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6
Q

If stress is persistent or severe this results in ____ injury

A

Irreversible

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7
Q

Oxgen deficiency

A

Hypoxia

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8
Q

Ischemia

A

Reduced blood supply

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9
Q

Most common cause of hypoxia and ischemia is

A

Blockage of an artery or inadequate oxygenation of blood.

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10
Q

Toxic agents in daily environment

A

Toxins

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11
Q

Infectious pathogens; viruses, bacteria, fungi, parasites that injure cells by diverse mechanisms.

A

Infectious Agents

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12
Q

Rxns that can result in cell injury and tissue injury;
ex. autoimmune rxns, excessive or common immune response to microbe

A

Immunologic reactions

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13
Q

Chromosomal abnormalities or mutations
Ex. Sickle cell anemia
Or even mutations that can result in decrease or increase in protein function.

A

Genetic Abnormalities

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14
Q

Protein-calorie insufficiency remains a major cause of cell injury, and specific vitamin deficiencies

A

Nutritional imbalances

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15
Q

Derangement of function and morphology that cells can recover from if the damaging stimulus is removed

A

Reversible Cell Injury

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16
Q

___ cell injury result in cell and organelle swelling which is main sign.

A

Reversible

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17
Q

____ ____ is another sign of reversible cell injury. Appearance of lipid vacuoles in cytoplasm. mostly occurs in organs that are involved in lipid metabolism ex. Liver

A

Fatty change

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18
Q

A cell becomes ____, turning redder due to injury. Becomes intensely basic.

A

Eosinophilic

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19
Q

4 signs of cell injury

A

-Blebbing (due to loss of surface microvilli)
-appearance of phospholipid rich densities
-dilation of ER-> detachment of ribosomes.
-Nuclear alteration. Myelin figures.

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20
Q

collections of phospholipids resembling myelin sheaths that are derived from damaged cellular membranes.

A

Myelin figures

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21
Q

When the cell passes the point of no return, excessive injury

A

Irreversible injury

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22
Q

1st Phenomena of irreversible injury

A

> inability to restore mitochondrial function= No Ox. Phosphorylation= NO ATP

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23
Q

2nd Phenomena of irreversible injury

A

Alt. structure & loss of function of the plasma membrane & intracellular membranes

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24
Q

3rd Phenomena of irreversible injury

A

Loss if structural integrity of DNA & chromatin

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25
Q

Inevitable end result of severe damage that is beyond salvage and is not thought to be regulated by specific signals or biochemical mechanisms

pathologic

A

Necrosis

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26
Q

pathway of cell death in which cells activate enzymes that degrade the cells’ own nuclear DNA and nuclear and cytoplasmic proteins. Req. ATP

physiologic

A

Apoptosis

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27
Q

Sign of Necrosis or apoptosis?

Swelling & adjacent  inflammation

A

Necrosis

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28
Q

Sign of Necrosis or apoptosis?

Shrinking

A

Apoptosis

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29
Q

Sign of Necrosis or apoptosis?

Pyknosis → karyorrhexis → karyolysis

A

Necrosis

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30
Q

Sign of Necrosis or apoptosis?

Fragmentation into nucleosome-sized fragments

A

Apoptosis

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31
Q

Sign of Necrosis or apoptosis?

Disrupted plasma membrane

A

Necrosis

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32
Q

Sign of Necrosis or apoptosis?

Intact plasma membrane, but orientation of lipids in altered

A

Apoptosis

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33
Q

Sign of Necrosis or apoptosis?

Enzymatic digestion, may leak out of cell

A

Necrosis

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34
Q

cellular function may be lost long before _________ occurs and that the morphologic changes of cell injury (or death) lag behind loss of function and viability

A

cell death

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35
Q

Myocardia cells become non-contractible after 1-2min of ischemia but don’t die until 20-30 min after ischemia has elapsed.

this Is an example that ____ ≠ ____

A

Loss of function ≠ non-viable

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36
Q

increased binding of eosin to denatured cytoplasmic proteins and in part to loss of basophilic ribonucleic acid (RNA) in the cytoplasm

A

Eosinophilia, sign of necrosis in cytoplasm.

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37
Q

____ is Characterized by nuclear shrinkage and increased basophilia; the DNA condenses into a dark, shrunken mass.

A

Pyknosis

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38
Q

Fragmentation of a pyknotic nucleus (shrunken)

A

karyorrhexis

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39
Q

basophilia fades due to digestion of deoxyribonucleic acid (DNA) by DNase.

A

Karyolysis

40
Q

basophilia fades due to digestion of deoxyribonucleic acid (DNA) by DNase.

A

Karyolysis

41
Q

No ATP results in loss of function of the Na+/K+ pump leaving more sodium in the cell resulting in

A

Cell swelling

42
Q

Mitochondrial membrane damage allows ___ to Leak into the cytoplasm, this activates _____

A

Cytochrome C, apoptosis.

43
Q

Lysosome membrane damage= hydrolytic enzymes leak into cytoplasm, becoming activated by _____

A

High intracellular calcium

44
Q

Necrotic tissue retains its gross structure, cell shape, and organ structure. BUT nuclear structures are lost.

A

Coagulative Necrosis

45
Q

Areas of necrosis caused by ischemia (no blood), leaving area pale.

A

Infarcts

46
Q

When blood re-enters the loosely organized tissues.
Blood build up.

Seen in testicular, pulmonary.

A

Red infarction

47
Q

Necrotic tissue liquified due to enzymatic lysis of cells and protein content.

ex. in accesses, proteolytic enzymes from neutrophil ___ tissue

A

Liquefactive Necrosis; liquify

48
Q

Macrophage in CNS

A

Microglial Cell

49
Q

Hallmark of ____ infarction are when proteolytic enzymes from microglial ells liquify the ___

A

Brain

50
Q

Proteolytic enzymes from pancreas liquify surrounding parenchyma.

A

Pancreatitis

51
Q

Liquefaction produces yellow substance

A

Pus

52
Q

Localized collection of pus

A

abscess

53
Q

When limb looses blood supply, has undergone coagulative necrosis of multiple. tissue layers. Mummified tissues. Limbs.

A

Gangrenous Necrosis

54
Q

“cottage cheese like” due to presence of both coagulative & liquefactive necrosis. Tissue architecture destroyed.

A

Caseous Necrosis

55
Q

_____ this disease causes caseous necrosis ion the lungs

A

Tuberculosis

56
Q

Nodular inflammatory lesion

A

Granuloma

57
Q

Necrosis of adipose tissues that results in chalky white appearance due to the build up of calcium in dead adipose tissue.

A

Fat Necrosis

58
Q

When fatty acids or lipases attach to calcium.

A

Saponification

59
Q

Enzymes leak out of damage pancreatic acing cells, digesting peritoneal fat cells + their content.

Released fatty acid + calcium = chalky lesions.

A

Acute Pancreatitis

60
Q

When calcium deposits on necrotic tissues which acts as a collection point.

Normal serum calcium

A

Dystrophic calcification

61
Q

When high serum calcium or phosphate levels lead to calcium deposition on normal tissues;
ex. Hyper-para-thyroidism

A

Metastatic Calcification

62
Q

Necrotic damage to blood vessel wall, leaking of protein (fibrin) into blood vessel walls.

*youll see a ring of fibrin circumferential bright pink area of fibrin**

A

Fibrinoid Necrosis

63
Q

2 causes of damage to blood vessels walls resulting in fibrinoid necrosis

A
  • Malignant hypertension
  • Vessel inflammation (vasculitis)
64
Q

Leaking of what protein in cardiac muscle results in the detection of tissue specific necrosis unison blood or serum samples?

A

Troponin

65
Q

Fragments of the plasma membrane that are altered, and recognized & phagocytose by macrophages. no inflammation

A

Apoptotic Bodiues

66
Q

> Ex. Menstrual cycle -> (cells that have increased in # in preparation fertilization , not used, endometrial shedding.

> Ex. Resorption of cells and cellular cycle

> Ex. Bone remodeling in the mouth, bone cells flagged for being removed.

A

Physiologic Apoptosis

67
Q

Exposure to radiation and cytotoxic drugs results in ____ apoptosis

A

Pathologic

68
Q

Mitochondrial membrane becomes permeable due to Bcl2 is turned off , allowing Cytochrome C to leak into cytoplasm, triggers cause reaction by the cell itself.

A

mitochondrial (intrinsic) pathway

69
Q

Explain the Bcl2 inactivation process in the intrinsic apoptosis.

A

BH3 -only proteins sense lack of survival signals or DNA/protien damage.
They activate effector molecules BAX, BAK which then demonetize to form a membrane channel. + a decrease in BCL-2 & BCL-X = cytochrome c leaks out.

70
Q

> affected cell refuses to undergo apoptosis.
T cels recognize FAS(CD95) death receptor of affected cell
T-cells have the Fas ligand (FasL)
They go to the cell and cross link FasL with the FAS receptor. Binding adaptor proteins as well.
Recruit and activate Caspase-8.

A

Death-receptor (extrinsic) pathway of apoptosis via FAS Ligand

71
Q

2 prototypic death receptors:

A

Type I TNF receptor & Fas (CD95)

72
Q

What is an example of a situation where the FAS ligand pathway is used?

A

Elimination of self-reactive lymphocytes.

73
Q

TNF binds to TNF receptor on target cell, cross linking & activating caspases.

Apoptosis

A

Death-receptor (extrinsic) pathway of apoptosis via TNF

74
Q

Apoptosis pathway that has both intrinsic and extrinsic elements .
>perforins secreted by CD8+ T cells, Create holes in membrane of target cell, insert granzyme, activate capases. Kills viral infected cells.

A

Immune Pathway, cytotoxic T-cell mediated.

75
Q

Activated Caspase-3 will fluoresce what color?

A

Red

76
Q

Cellular damage induced by the accumulation of reactive oxygen species (ROS), a form of free radical.

A

Oxidative Stress

77
Q

4 Effects of mitochondrial dysfunction & damage that lead to failure of oxidative phosphorylation and therefore no ATP.

A
  1. No sodium pumps= cell swelling cause Na+ accumulates inside cell.
  2. Increased aerobic glycolysis= lactic acid buildup= low pH= enzymes loose fxn.
  3. Structural disruption of RER, ribosomes detach= reduced protein synthesis
  4. Damage to mito & lysosomal membrane,
78
Q

chemical species with a single unpaired electron in an outer orbital. Extremely unstable and can react with in & organic compounds. Attacking them!

A

Free Radicals

79
Q

Incomplete reduction of O2 produces what three radical species?

A
  1. Superoxide O2
  2. Hydrogen Peroxide H2O2
  3. Hydroxyl Radicals OH-
80
Q

Enzyme that will get rid of superoxide (O2-) converting it to H2O2

A

Superoxide Dismutase (SODs)

81
Q

Enzyme that converts hydrogen peroxide H2O2 into O2

A

Catalase gluthione peroxidase

82
Q

No enzyme to get rid of OH-, what do you do instead to convert it to H2O? They block formation of free radicals or scavenge them.

A

Endogenous or exogenous antioxidant

83
Q

4 Diff. pathological ways free radicals are generated?

A
  1. Inflammation; NADPH oxidase generates O2- during oxygen dependent killing by neutrophils
    2.Ionizing radiation causes H20 -> OH-
    3.Fenton reaction (metals Fe2+)
  2. Chemical compounds (medicine) broken down in liver P450, generating free radicals.
84
Q

Combine and alter cellular structures by peroxidation of lipids and oxidation of DNA and proteins. (thus, DNA constant damage and repair by these ROS is implicated in aging & neoplasms)

A

Affect of free radical

85
Q

Pt. comes in with infection, what can you tell them to do?

A
  1. take antioxidants (glucothianine, vitamin A,C,E) = reduce damage
  2. Anti- inflammatory = reduce amount to repair (NSAIDS)
    3.Enzymes
  3. Metal carrier proteins.
86
Q

They are aspartate-specific cysteine proteases.
They breakdown cytoskeleton and activate endonucleases

A

Caspases

87
Q

Return of blood (oxygen) to ischemic (oxygen deprived) tissue results in high influx of O2- derived free radicals (backed up breathing/electron transport), produces unstaggered production of ROS which further damages, to already STRESSED or INJURED tissue.

A

Ischemia Reperfusion Injury

88
Q

Ex of Ischemia Reperfusion Injury

A

Continued increase of troponin in heart even after resolving ht blockage and reperfusion of infarcted myocardial tissue.

89
Q

Misfolded protein deposits in extracellular space of tissues, causes tissue damage.

Systemic or localized deposition

A

Amyloid

90
Q

Beta-pleated sheets, Congo red & apple green birefinginence when view microscopically cannot be removed

features of what?

A

an amyloid

91
Q

systemic deposition of AL amyloid, which is derived from immunoglobulin light chain.

As. with plasma cell dyscrasias (e.g., multiple myeloma)

A

Primary Amyloidosis

92
Q

systemic deposition of AA amyloid, which is derived from serum amyloid-associated protein (SAA).

As. w/chronic secretion.

A

Secondary Amyloidosis

93
Q

Chronic inflammation (RF) and Familial Mediterranean Fever (FMF) are associated with

A

Secondly Amyloidosis (AA)

94
Q

Genetic autosomal recessive dysfunction of neutrophils typically in med. region.

Symptoms: episodic fevers, sudden serial inflammation.

A

Familial Mediterranean fever (FMF),

95
Q

4 different most SAA sensitive tissues w/symptoms

A
  1. Kidney/nephrotic syndrome (most common)
  2. Heart res. cardiomyopathy or arrhythmia
  3. Tongue enlargement, malabsorption, heptaosplenomegaly

affected organs must be transplanted, amyloid cannot be removed

IHP 1001 (18 decks)

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