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cell injury Necrosis Flashcards

1
Q

what is pathology

A

Study of disease and suffering

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2
Q

What is etiology

A

Origin of disease and its underlying causes and modifiers

Why a disease occurs

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3
Q

what is pathogenesis

A

Development of a disease from molecular/cellular changes to functional and structural abnormalities
How a disease occurs

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4
Q

are cause and effect relationships easy for etiology

A

no

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5
Q

does CEll injury occur in all pathology

A

Yes

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6
Q

when does clinical signs and symptoms of disease occur

A

several steps after the biochemical changes associated with cell injury

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7
Q

Why does Cell injury occur

A

from disruption of 1 or more components that maintain viability

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8
Q

what does cell injury lead to

A

a cascade of effects

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9
Q

what happens to the cell after cell injury

A

May be reversible

may result in cell adpatation or lead to cell death

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10
Q

causes of cell injury for a patient’s view

A 
Hypoxia
Infectious agents
Physical injury
Chemicals/drugs
Immune response
Genetic abnormalities
Nutritional imbalances
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11
Q

what is a hypoxic injury

A

Injury due to lack of oxygen (often due to a lack of blood flow)

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12
Q

do all tissues respond to hypoxic injury the same

A

No, bone needs less oxygen, where-as hearts and brain need more

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13
Q

what, in general, can lead to cell injury

A

Different factors acting at the same cellular site producing injury

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14
Q

what are the usualy cellular targets of injury

A

Cell membranes
Mitochondria
Cell proteins
DNA

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15
Q

what are some of the cell injury mechanisms

A 
ATP Depletion
Generation of Reactive oxygen species
Loss of Ca++ homeostasis
Altered membrane permeability
Mitochondrial damage
DNA and Protein damage
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16
Q

How does Hypoxia-Ischemia affect ATP

A

leads to a decrease in oxidative phosphorylation which ultimately decreases ATP

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17
Q

the decrease in ATP from the Hypoxia-Ischemia leads to

A

Decrease in the activity of Na pump
an increase in anerobic glycolysis
Detachment of ribosomes from the RER

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18
Q

decrease in action of the Na pump from hypoxia-Ischemia

A

Influx of Ca, H2O and Na
Efflux of K
- leads to ER swelling, cellular swelling, loss of microvilla and Blebs

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19
Q

the increase in Anaerobic glycolysis from hypoxia-ISchemia leads to

A

Decrease in glyogen

increase in lactive acid, lowering pH, and clumping of nuclear chromatin

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20
Q

the detachment of ribosomes from hypoxia-ISchemia leads to

A

Decrease in PRotein synth and lipid deposition

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21
Q

what are Reactive OXygen Species

A

Free Radicals

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22
Q

why do REactive Oxygen Species exist

A 
Inflammation
Oxygen toxicity
Chemical/drug - metabolism
Radiation - UV, X-rays
Aging
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23
Q

how is superoxide and hydrogen peroxide produced

A

By auto-oxidation in mitochondria by cytoplasmic oxidases

24
Q

what reaction eventually forms free radical OH

A

the fenton reaction

25
Q

How does ROS induce Cell Injury

A

Lipid Peroxidation
Protein Fragmentation
Single Strand Breaks in DNA

26
Q

Initation of Lipid Peroxidation

A

LH+X -> L.+XH

27
Q

Propagation of Lipid Peroxidation

A

L.+O2->LOO.

LOO.+LH->L.+LOOH

28
Q

termination of Lipid PEroxidtion

A

L.+L.-> non-radical product

29
Q

what does ROS do to DNA

A

Single-stranded breaks

greater than 30 different base modifications in both purines and pyrimidnes - thymidine and guanine being major sites

30
Q

what controls ROS

A

ENzymes
Antioxidants
Serum Proteins

31
Q

what ENzymes control ROS

A

Catalase, SOD, and Glutahione peroxidase

32
Q

What Antioxidants control ROS

A

Vitamins E, A, and C, glutathione, cysteine

33
Q

what do Serum proteins do to control ROS

A

Reduce/bind iron (transferrin, ferritin) and copper (Ceruloplasmin) needed to catalyze the formation of ROS

34
Q

ROS effect on aging

A

Loss of antioxidants leads to ROS being more detrimental

35
Q

what does an increase in cytoplasmic ionic ca do

A

ATPase: decreases ATP
Phospholipase: decrease Phospholipids
Protease: Protein Disruption
Endonuclease: DNA damge

36
Q

normal cyoplasmic Ca

A

.1 micromolar

37
Q

Normal Extracellular Ca

A

1.3 millimolar

38
Q

what may also cause cell membrane injury

A 
Complement - C5-C9 MAC
Cytotoxic T and NK cells - perforin
Virus
Bacterial Endotoxins and Exotoxins
Drugs
39
Q

what happens first Biochem alterationsor morphologic changes

A

Biochemical alterations occur 1st

40
Q

what determines the degree of cell injury

A

Physiologic state of the cell
Intensity of insult
Duration of insult
number of exposures to insult

41
Q

results of cell injury

A

Reversed
Cell adaptation
cell death

42
Q

what causes cell adpatation

A

lots of small exposures

43
Q

how may a cell adapt

A

Changes in size
number
functional modification
Intracellular accumulations

44
Q

sefverity of that which causes Reversiible cell injury

A

Acute process

45
Q

description of reversible cell injuy

A

Cell injury of short duration and low intensity

46
Q

Causes of Reversible cell injury

A

Ischemia
Exposure to toxin
Infectious aagents
Thermal injury

47
Q

what does plasma membrane injury lead to

A

Increased intracellular Na

isosomotic gain in water and cell swelling

48
Q

when does Cell death occur

A

when an insult overcomes compensation mechanisms

49
Q

what is the signature biochemical event that equates with cell death

A

It does not exist

50
Q

order of death and injury over time

A

Cell death
Ultrastructural changes
Light microscopic changes
GRoss morpholoic changes

51
Q

what happens to cell proteins after death

A

Released

52
Q

what are the morphologic types of necrosis

A

Coagulative
Liquefactive
Caseous
Enzymatic (fat)

53
Q

what determines necrosis type

A

Patterns of enzymatic degradation of cells and extracellular matrix
the type of necrotic debris
bacterial products when present

54
Q

characteristsics in coagulative necrosis

A

Cell outline
Pink cytoplasm
Anucleated cells

55
Q

liquefactive necrosis

A

Turns tissue into liquid

56
Q

caseous necrosis

A

Gains cheese like appearance as a soft white protein masss

general path (16 decks)

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