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Pathology A > Cellular injury and adaption > Flashcards

Cellular injury and adaption Flashcards

1
Q

main ways cells can be injured

A 
genetic derangements
oxygen deprivation 
immunological responses 
nutritional imbalances
infectious agents 
chemical agents and drugs 
physical agents
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2
Q

example of genetic derangement

A

sickle cell anaemia

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3
Q

example of oxygen deprivation

A

brain infarct

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4
Q

eg of immunological reactions

A

rash from poison ivy

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5
Q

eg of nnutritional imbalance

A

anorexia nervosa

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6
Q

eg of infectious agents

A

parasitics infection: leishmaniasis

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7
Q

eg o chemical agents/drugs

A

cough syrup

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8
Q

eg of physical agents

A

burns or shark bite

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9
Q

describe the morpholpgical alterations in cell injury

A 
plasma membrane can bleb
mitochondria can swell
ER and swell and detach from 
ribosomes
nucleus can clump
all are reversible
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10
Q

what are some biochemical mechanisms of cell injury

A

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

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11
Q

what can ROS cause

A

oxidative stress and cell injury

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11
Q

what can ROS cause

A

oxidative stress and cell injury

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12
Q

what are the responses to cellular injury

A

reocery, death, adaptation

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13
Q

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

A

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

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14
Q

what is coagulative necrosis associated with

A

ischaemia (except brain)

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15
Q

what does caogulative necrosis look like macroscopically and microscopically

A 
macro = firm tissue, arhitecture maintined for days after death (looks white)
micro= preserved cell outlines, cells become eosinophilic, loss of nuclei, infiltration by leukocytes
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16
Q

what is liquefactive necrosis associated with

A

infections

ischaemic injury to brain

17
Q

what does liquefactive necrosis look like macroscopically and microscopically

A 
micro = tissue architecture lost -> liquid through enzymatic digestion. cream yellow pus 
microscopically = leukocytes, neutrophils, dead cells and debris
18
Q

what is caseous necrosis associated with

A

TB

19
Q

describe caseous necrosis macro and micro

A 
macro = white, soft, cheesy, encllosed by distinct border
micro= eosinophilic centre, collar of lymphocytes and activated macs => granuloma
20
Q

what is fat necrosis associated with

A

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

21
Q

describe fat necrosis macro + micro

A 
macro = chalky, whitish deposit as a result of Ca soaps 
micro = anucleated adipocytes with Ca deposits
22
Q

what is fibrinoid necrosis associated with

A

vascular damage

23
Q

describe fibrinoid necrosis macro + micro

A

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

24
Q

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

A

used in clinical practise to describe condition

dry is coagulative and wet is liquefactive

25
Q

describe gangrenous necrosis macro and micro

A 
macro = black skin + putrefaction 
micro = coagulative/liquefactive
26
Q

what are some physiological classifications of apoptosis

A

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

27
Q

what are the pathological classifications of apoptosis

A

DNA damage, misfolded proteins, infection, atrophy

28
Q

what are the features of apoptosis

A

single cells, no inflammation, active process

29
Q

what are adaptations

A

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

30
Q

what is chronic adaptation

A

due to persistent, sublethal injury

= changes in cell size/growth + differentiation

31
Q

describe hypertrophy

A

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

32
Q

describe hyperplasia

A

inc in number, reversible, hormonal/inc functional demand

33
Q

describe atrophy

A

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

34
Q

describe metaplasia

A

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

35
Q

describe smokers lung

A

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

36
Q

describe barret’s oesophagus

A

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

37
Q

describe dysplasia

A

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

38
Q

describe dysplastic epithelium of uterine cervix

A

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

39
Q

what is intracellular accumulation

A

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

Pathology A (26 decks)

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