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
How does ROS induce Cell Injury
Lipid Peroxidation Protein Fragmentation Single Strand Breaks in DNA
26
Initation of Lipid Peroxidation
LH+X -> L.+XH
27
Propagation of Lipid Peroxidation
L.+O2->LOO. | LOO.+LH->L.+LOOH
28
termination of Lipid PEroxidtion
L.+L.-> non-radical product
29
what does ROS do to DNA
Single-stranded breaks | greater than 30 different base modifications in both purines and pyrimidnes - thymidine and guanine being major sites
30
what controls ROS
ENzymes Antioxidants Serum Proteins
31
what ENzymes control ROS
Catalase, SOD, and Glutahione peroxidase
32
What Antioxidants control ROS
Vitamins E, A, and C, glutathione, cysteine
33
what do Serum proteins do to control ROS
Reduce/bind iron (transferrin, ferritin) and copper (Ceruloplasmin) needed to catalyze the formation of ROS
34
ROS effect on aging
Loss of antioxidants leads to ROS being more detrimental
35
what does an increase in cytoplasmic ionic ca do
ATPase: decreases ATP Phospholipase: decrease Phospholipids Protease: Protein Disruption Endonuclease: DNA damge
36
normal cyoplasmic Ca
.1 micromolar
37
Normal Extracellular Ca
1.3 millimolar
38
what may also cause cell membrane injury
``` Complement - C5-C9 MAC Cytotoxic T and NK cells - perforin Virus Bacterial Endotoxins and Exotoxins Drugs ```
39
what happens first Biochem alterationsor morphologic changes
Biochemical alterations occur 1st
40
what determines the degree of cell injury
Physiologic state of the cell Intensity of insult Duration of insult number of exposures to insult
41
results of cell injury
Reversed Cell adaptation cell death
42
what causes cell adpatation
lots of small exposures
43
how may a cell adapt
Changes in size number functional modification Intracellular accumulations
44
sefverity of that which causes Reversiible cell injury
Acute process
45
description of reversible cell injuy
Cell injury of short duration and low intensity
46
Causes of Reversible cell injury
Ischemia Exposure to toxin Infectious aagents Thermal injury
47
what does plasma membrane injury lead to
Increased intracellular Na | isosomotic gain in water and cell swelling
48
when does Cell death occur
when an insult overcomes compensation mechanisms
49
what is the signature biochemical event that equates with cell death
It does not exist
50
order of death and injury over time
Cell death Ultrastructural changes Light microscopic changes GRoss morpholoic changes
51
what happens to cell proteins after death
Released
52
what are the morphologic types of necrosis
Coagulative Liquefactive Caseous Enzymatic (fat)
53
what determines necrosis type
Patterns of enzymatic degradation of cells and extracellular matrix the type of necrotic debris bacterial products when present
54
characteristsics in coagulative necrosis
Cell outline Pink cytoplasm Anucleated cells
55
liquefactive necrosis
Turns tissue into liquid
56
caseous necrosis
Gains cheese like appearance as a soft white protein masss