Mechanisms of Disease

Question 1

Disease

Answer 1

A consequence of failed homeostasis with consequent morphological and function disturbances

Question 2

degree of injury in disease depends on

Answer 2

type of injury
severity of injury
type of tissue

Question 3

continuum of cell change dependant on severity of stimulus

Answer 3

homeostasis, cellular adaptation, cellular injury, cell death

Question 4

hypoxia

Answer 4

body or some tissue within the body is deprived of oxygen

Question 5

causes of hypoxia (4)

Answer 5

hypoxaemic hypoxia
anaemic hypoxia
ischaemic hypoxia
histiocytic hypoxia

Question 6

main consequence of hypoxia

Answer 6

decreased aerobic oxidative respiration

Question 7

ischaemia

Answer 7

loss of blood supply

Question 8

hypersensitivity reaction

Answer 8

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

Question 9

autoimmune reaction

Answer 9

immune system fails to distinguish self from non self

Question 10

principal structural targets for cell damage

Answer 10

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

Question 11

enzymes activated by ca 2+ influx and effect

Answer 11

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

Question 12

ischamia reperfusion injury

Answer 12

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

Question 13

when ROS are produced

Answer 13

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

Question 14

free radical use

Answer 14

used by leukocytes to kill bacteria

cell signalling

Question 15

3 oxidative species

Answer 15

o2-
h2o2
oh.

Question 16

fentons reaction

Answer 16

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

Question 17

haber weiss reaction

Answer 17

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

Question 18

free radical generation

Answer 18

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

Exogenous chemicals can be metabolised to freee radicals

Question 19

lipid peroxidation

Answer 19

oxidative degeneration of lipids

leeds to further production of ROS ( autocatylytic chain reaction)

Question 20

ROS interaction with proteins and DNA

Answer 20

cause protein fragmentation and cross links

single strand breaks in DNA ( genomic and mitochondrial)

Question 21

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

Answer 21

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

Question 22

function of heat shock proteins

Answer 22

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

Question 23

nuclear changes in cell injury viewed with a light microscope

Answer 23

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

Question 24

cytoplasmic changes in cell injury viewed with a light microscope

Answer 24

reduced pink staining- water accumulation (reversible)

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

Question 25

reversible change in cell injury viewed with an electron microscope

Answer 25

``` swellin clumped chromatin autophagy ribosome dispersion cytoplasmic blebs ```

Question 26

irreversible change in cell injurt viewed with an electron microscope

Answer 26

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

Question 27

oncosis

Answer 27

spectrum of changes in injured cells to death

Question 28

necrosis

Answer 28

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

Question 29

apoptosis

Answer 29

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