Cellular injury and adaption

Question 1

main ways cells can be injured

Answer 1

genetic derangements
oxygen deprivation 
immunological responses 
nutritional imbalances
infectious agents 
chemical agents and drugs 
physical agents

Question 2

example of genetic derangement

Answer 2

sickle cell anaemia

Question 3

example of oxygen deprivation

Answer 3

brain infarct

Question 4

eg of immunological reactions

Answer 4

rash from poison ivy

Question 5

eg of nnutritional imbalance

Answer 5

anorexia nervosa

Question 6

eg of infectious agents

Answer 6

parasitics infection: leishmaniasis

Question 7

eg o chemical agents/drugs

Answer 7

cough syrup

Question 8

eg of physical agents

Answer 8

burns or shark bite

Question 9

describe the morpholpgical alterations in cell injury

Answer 9

plasma membrane can bleb
mitochondria can swell
ER and swell and detach from 
ribosomes
nucleus can clump
all are reversible

Question 10

what are some biochemical mechanisms of cell injury

Answer 10

hyooxia, toxins and ROS
can be seen in depletion of ATP, mitochondrial damage, loss of Ca homeostasis, accumulation ROS, defects in membrane permeability, DNA and protein damage
reversibility is dependent on level of damage

Question 11

what can ROS cause

Answer 11

oxidative stress and cell injury

Question 11

what can ROS cause

Answer 11

oxidative stress and cell injury

Question 12

what are the responses to cellular injury

Answer 12

reocery, death, adaptation

Question 13

what is necrosis, why does it occur, and what happens

Answer 13

death of body tissue
not enough blood flowing to tissue/injury/radiation/chemicals
enxymatic digestions, loss cell membrane integrity, release of products into IC space, inflammatory responses

Question 14

what is coagulative necrosis associated with

Answer 14

ischaemia (except brain)

Question 15

what does caogulative necrosis look like macroscopically and microscopically

Answer 15

macro = firm tissue, arhitecture maintined for days after death (looks white)
micro= preserved cell outlines, cells become eosinophilic, loss of nuclei, infiltration by leukocytes

Question 16

what is liquefactive necrosis associated with

Answer 16

infections

ischaemic injury to brain

Question 17

what does liquefactive necrosis look like macroscopically and microscopically

Answer 17

micro = tissue architecture lost -> liquid through enzymatic digestion. cream yellow pus 
microscopically = leukocytes, neutrophils, dead cells and debris

Question 18

what is caseous necrosis associated with

Answer 18

TB

Question 19

describe caseous necrosis macro and micro

Answer 19

macro = white, soft, cheesy, encllosed by distinct border
micro= eosinophilic centre, collar of lymphocytes and activated macs => granuloma

Question 20

what is fat necrosis associated with

Answer 20

not specific pattern of cell death, but describes destruction of fat due to pancreatic lipases

Question 21

describe fat necrosis macro + micro

Answer 21

macro = chalky, whitish deposit as a result of Ca soaps 
micro = anucleated adipocytes with Ca deposits

Question 22

what is fibrinoid necrosis associated with

Answer 22

vascular damage

Question 23

describe fibrinoid necrosis macro + micro

Answer 23

macro = not grossly discernable
micro = accumulation of fibrin (pink for protein) around BV
inflammation

Question 24

what is gangrenous necrosis associated with and what is dry and wet

Answer 24

used in clinical practise to describe condition | dry is coagulative and wet is liquefactive

Question 25

describe gangrenous necrosis macro and micro

Answer 25

``` macro = black skin + putrefaction micro = coagulative/liquefactive ```

Question 26

what are some physiological classifications of apoptosis

Answer 26

embryogenesis, endometrial breakdown, cell loss in proliferating populations, eliminate potential harmful cells and host cells

Question 27

what are the pathological classifications of apoptosis

Answer 27

DNA damage, misfolded proteins, infection, atrophy

Question 28

what are the features of apoptosis

Answer 28

single cells, no inflammation, active process

Question 29

what are adaptations

Answer 29

reversible changes to number, size, metabolic activity, function, phenotype of cells

Question 30

what is chronic adaptation

Answer 30

due to persistent, sublethal injury | = changes in cell size/growth + differentiation

Question 31

describe hypertrophy

Answer 31

increase in size of cells, inc synthesis of structural components, reversible, hormonal or increased functional demand

Question 32

describe hyperplasia

Answer 32

inc in number, reversible, hormonal/inc functional demand

Question 33

describe atrophy

Answer 33

decrease in cell size/number/activity can progress to irreversible due to reduced demand/dec O2, insufficient nutrients, persistent injury, endocrine insufficiency

Question 34

describe metaplasia

Answer 34

cell replaced by another differentiated cell type (eg common columnar->squamous) replaces stressed cells with better equipped cells reversible stem cells are reprogrammed

Question 35

describe smokers lung

Answer 35

metaplasia normal ciliated columnar epithelium in trache + bronchi replaced by rugged squamous epithelium bc columnar cells are 1 cell thick lose mucus and cilia

Question 36

describe barret's oesophagus

Answer 36

metaplasia normal strat squam replaced with columnar + goblet cells in response to acid reflux columnar cells = more resistant to HCl + pepsin bc mucus

Question 37

describe dysplasia

Answer 37

disordered growth + maturation epithelia sequential mutations reversible or can lead to neoplasia

Question 38

describe dysplastic epithelium of uterine cervix

Answer 38

squamous epi gets infected (HPV) abnormal proliferation -> mutations -> loss growth control disordered maturation from basal to top layer extending full thickness = carcinoma in situ

Question 39

what is intracellular accumulation

Answer 39

build up of substances within cell nomral body substances endogenous = von gierkes disease (glycogen) exogenous = tattoos