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ESA 2 > Mechanisms of Disease > Flashcards

Mechanisms of Disease Flashcards

1
Q

Disease

A

A consequence of failed homeostasis with consequent morphological and function disturbances

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2
Q

degree of injury in disease depends on

A

type of injury
severity of injury
type of tissue

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3
Q

continuum of cell change dependant on severity of stimulus

A

homeostasis, cellular adaptation, cellular injury, cell death

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4
Q

hypoxia

A

body or some tissue within the body is deprived of oxygen

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5
Q

causes of hypoxia (4)

A

hypoxaemic hypoxia
anaemic hypoxia
ischaemic hypoxia
histiocytic hypoxia

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6
Q

main consequence of hypoxia

A

decreased aerobic oxidative respiration

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7
Q

ischaemia

A

loss of blood supply

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8
Q

hypersensitivity reaction

A

host tissue is injured secondary to an overly vigorous immune reaction.

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9
Q

autoimmune reaction

A

immune system fails to distinguish self from non self

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10
Q

principal structural targets for cell damage

A

cell membrane- plasma or organellar
nucleus- DNA
proteins- structural (enzymes)
Mitrochondria- oxidative phosphorylation

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11
Q

enzymes activated by ca 2+ influx and effect

A

protein kinase - unnecessary phosphorylation of proteins
phospholipase- causes membrane damage when in exess
proteases- cytoskeleton disassembles
endonucleases- nuclear chromatin damage
ATPase- decreased ATP

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12
Q

ischamia reperfusion injury

A

sudden restoration of blood flow into an area that has previously had insufficient supply causing the production of ROS

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13
Q

when ROS are produced

A

chemical and radiation injury
cellular ageing
ischaemia reperfusion injury
high oxygen concentartion

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14
Q

free radical use

A

used by leukocytes to kill bacteria

cell signalling

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15
Q

3 oxidative species

A

o2-
h2o2
oh.

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16
Q

fentons reaction

A

(Fe2+) + (H2O2) —> (Fe3+) + (OH-) +(.OH)

17
Q

haber weiss reaction

A

(O2-) + (H+) + (H2O2) —> (O2) + (H2O) + (.OH)

18
Q

free radical generation

A

oxidative phosphorylation
cystolic reactions
p450 enzymes
[yields (O2- H2O2)]

Exogenous chemicals can be metabolised to freee radicals

19
Q

lipid peroxidation

A

oxidative degeneration of lipids

leeds to further production of ROS ( autocatylytic chain reaction)

20
Q

ROS interaction with proteins and DNA

A

cause protein fragmentation and cross links

single strand breaks in DNA ( genomic and mitochondrial)

21
Q

ways free radicals can be removed from the body (anti oxidant system)

A

spontaneous decay
enzymes (superoxide dismutase, catalases, peroxidases)
free radical scavengers (Vit E,A,C)
storage protein sequester

22
Q

function of heat shock proteins

A

in cell stress (heat) proteins are denatured (misfolded) heat shock proteins are involved in refolding, if the misfolding is to grear the protein is degraded

23
Q

nuclear changes in cell injury viewed with a light microscope

A

clumped chromatin (reversible)
pyknosis- shrinkage ( irreversible)
karyohexis- fragmentation (irreversible)
karryolysis- dissolution (irreversible)

24
Q

cytoplasmic changes in cell injury viewed with a light microscope

A

reduced pink staining- water accumulation (reversible)

increased pink staining- ddetachment and loss of ribosomes and accumailation of denatured proteins (irreversible)

25
Q

reversible change in cell injury viewed with an electron microscope

A 
swellin
clumped chromatin
autophagy
ribosome dispersion
cytoplasmic blebs
26
Q

irreversible change in cell injurt viewed with an electron microscope

A 
nuclear change (pyknosis, karyolysis, karyohexis)
lysosomal rupture
membrane defects
myelin figures
lysis of ER
27
Q

oncosis

A

spectrum of changes in injured cells to death

28
Q

necrosis

A

morphological changes that follow cell death in living tissu, largely due to progressive degradative action of enzymes on lethally injured cell

29
Q

apoptosis

A

cell death induced by regulated intracellular program- cells activate enzymes that degrade cells own nuclear DNA and proteins

ESA 2 (3 decks)

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