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Exam 1 > MoD week 1 - cell injury > Flashcards

MoD week 1 - cell injury Flashcards

1
Q

what causes hypoxia?

A

reduced oxygen supply due to ischaemia (lack of blood supply)

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2
Q

what are the 4 types of hypoxia?

A

anaemic hypoxia
hypoxic hypoxia
histiocytic hypoxia
ischaemic hypoxia

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3
Q

what is hypoxaemic hypoxia?

A

low arterial oxygen content

e.g. altitude & lung disease

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4
Q

what is anaemic hypoxia?

A

lack of RBC so reduced O2 carrying capacity

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5
Q

what is ischaemic hypoxia?

A

obstruction / interruption in blood flow (PE, tumour)

lack of blood flow

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6
Q

what is histiocytic hypoxia?

A

poison - no ox/phos

cynaide, disabled ox/phos (from binding to complex 4 - higher affinity than oxygen so e-, H+ and O2 can’t bind)

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7
Q

what are reversible changes in cellular injury?

A

no oxygen, so ox/phos so no ATP production (decrease Na+/K+/ATPase),
no Na+/K+/ATPase leading to cell swelling from Na+ withint cell,
no oxygen leading to increase anaerobic glycolysis (increased production of lactic acid) = pH acidic
ribosomes detach due to lack of ATP (reversible)
chromatin clumping (no ribosomes to produce proteins)
autophagy (protein degradation for survival)

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8
Q

what are irreversible changes in cell injury?

A

oncosis (cell death by swelling) leading to necrosis
membrane disturbance (from swelling) - affects Ca2+ channels (activating), increase [Ca2+] activating ATPase, phospholipases, proteases, endonucleases (DNA)
intracellular substances leak into circulation (detectable)
ER organelles swell causing blebbing (necrosis & oncosis)
nucleus: pyknosis (shrinkage) / karryohexis (fragmentation) / karryolysis (dissolution)
cell death

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9
Q

What is reperfusion?

A

return of blood flow to an ischaemic tissue

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10
Q

What is reactive hyperaemia?

A

during ischaemia, metabolites are released e.g. K+/H+/Pi/ADP etc. to cause vasodilation, but when you reperfuse the tissues, the metabolites will be washed away causing vasoconstriction which increases cell injury

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11
Q

What is ischaemic reperfusion injury?

A

when the metabolites spread around the body cuasing widespread vasodilation and distributive shock
there is also a large production of ROS and neutrophils that the body isn’t ready to defend itself agains, leading to increased inflammation
Ca2+ influx can damage cells

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12
Q

what are some of the body’s protection against antioxidants

A

enzymes: SOD (O2.- –> H2O2) & catalase (H2O2 –> H2O + O2)
vit ACE
glutathione & NADPH

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13
Q

what is oncosis?

A

cell death with swelling, changes that occur prior death

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14
Q

what is necrosis?

A

morphological changes that occur after death

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15
Q

what is apoptosis?

A

energy dependent programmed cell death with shrinkage

physiological: sculpt digits of fingers and toes & uterus contraction
pathological: cell damage in tumours

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16
Q

What are the light microscopic changes of a cell under apoptosis?

A

chromatin condenses, pyknosis, karryhexis, karrylysis

cell appears to be shrunken and intensely eosinophilic (basic stained pink)

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17
Q

what are the electron microscopic changes of a cell under apoptosis?

A

cytoplasmic budding –> fragmentation –> membrane budding (apoptotic bodies) - (contains cytoplasm, organelles & nuclear fragments), removed by macrophage in phagocytosis

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18
Q

what is the extrinsic pathway of apoptosis?

A

external ligands e.g. TRAIL & Fas

binds to ‘death-receptors’ –> caspase activation via cas 8 (independent of mitochondria)

19
Q

what is the intrinsic pathway of apoptosis?

A

triggered by DNA damage / withdrawal of growth factors / hormones
protein p53 is the ‘guardian genome’ activates apoptosis during DNA damage
trigger leads to increased mitochondrial permeability –> release of cytochrome C (from mito)
cytochrome interacts with APAF1 + cas 9 to form apoptosome (which activates a downstream cascade)
all activation happens within mitochondria

20
Q

what is coagulative necrosis?

A 
protein denaturisation & coagulate, solid and white, ghost outline (cell architecture preserved), normally in solid organs e.g. MI, pancreas
mostly ischaemic (lack of blood), incites acute inflammation (phagocytosis)
21
Q

what is liquifactive necrosis?

A

active enzymes released causing autolysis (proteins dissolution by own enzymes)
dead tissues liquefy - large number of neutrophils
rich in proteolytic enzymes e.g. proteases
in organs with no robust collagenous matrix support - becomes a viscous mass
in bacterial infection / ischaemic necrosis of brain
can have pus if acute inflammation arise

22
Q

caseous necrosis

A

amorphous debris, cheesy appearance, no structure

associated with infections e.g. TB and granulomatous inflammation

23
Q

fat necrosis

A

destruction of adipose tissues,
pancreatitis due to lipase release
lipase act on fatty tissue of pancreas for release of fatty acids
fatty A can react with Ca2+ –> calcium soaps (chalky deposits)
e.g. after direct trauma to fatty tissue e.g. breast

24
Q

gangrene

A

visible necrosis

25
Q

dry gangrene

A

exposure to air (dry out) bacteria can’t grow when environment dehydrated so no infection
coagulation
e.g. umbilical
coagulative necrosis is underlying process

26
Q

wet gangrene

A

necrosis modified by infection
overgrown with fungi and bacteria
if get into blood - septicaemia

27
Q

gas gangrene

A

a type of wet gangrene
infected with anaerobic bacteria
produce visible bubbles of gas
e.g. motorbike accident

28
Q

infarction

A

necrosis caused by ischaemia (thrombus, embolism, compression, vovulus)

29
Q

white infarct

A

solid organs / end artery

e.g. heart, spleen, kidney

30
Q

red infarct

A

extensive haemorrhage into dead tissue due to dual blood supply
numerous anastomoses or secondary arterial supply
normally loose tissue with poor stromal support
e.g. lung & brain anastamosis

31
Q

what do molecules released by injured, dying & dead cells cause?

A

molecules leaked out can cause local irritation & inflammation, can be toxic to body but can help aid diagnoses (when appear in blood - give site)

32
Q

what are molecules released by injured, dying & dead cells?

A
  1. K+ e.g. from severe burns / tourniquet shock, can cause MI or massive necrosis if reach heart, tumour lysis syndrome (chemotherapy releases K+)
  2. enzymes: shows organ involved and timing
  3. myoglobin: from dead myocardium & straited muscles
33
Q

what are the main groups of cellular accumulations?

A 
water & electrolytes
lipids
proteins
pigments
cholesterol
34
Q

what do water and electrolytes accumulations cause?

A

oedema (osmotic distrubance)

if in brain, can’t swell as skull, so blood vessels squeezed and blood supply reduced

35
Q

what do lipids accumulation cause?

A

steatosis (fatty change - accumulation of TAGs)
normally in liver (metabolise fat - alcoholic liver disease)
can be reversible within 10 days of alcohol withdrawal, liver becomes golden yellow and not red

36
Q

What does cholesterol accumulation cause?

A 
cholesterol can't be broken down in body, insoluble, eliminated through liver
atherosclerotic plaque (fatty streaks - accumulate in smooth muscle & macrophages - foam cells)
santhoma, xanthelasma, corneal arcus
37
Q

What does accumulation of proteins cause?

A

mallorys hyaline: proteins in hepatocytes damaged due to altered keratin (alcoholic liver)
a1-antitrypsin deficiency: incorrectly folded, therefore not packaged by ER and never secreted by liver, deficiency means proteases acts unchecked and cause emphysema (from breaking down proteins in lungs)

38
Q

what does accumulation of pigments in the cells cause?

A

normal cellular pigments - melanin
endogenous pigments: coal/carbon/soot (when inhaled cause blackened lung tissue, macrophage migrated from lungs to lymph nodes
if high dose becomes fibrotic lung / emphysematous (damaged alveoli)
lipofuscin: age pigment
haemosiderin (from Fe2+ buildup) e.g. haemorrhage into tissue from bruise
bilirubin in jaundice (bile pigment) heme from haemoglobin

39
Q

what is dystrophic calcification?

A

in areas of dying tissue, in atherosclerotic plaques (buildup of fatty deposits)
local changse favour hydroxyapatite crystals
metastatic due to calcium abnormalties e.g. PTHrP, or leukaemia destroying bones

40
Q

metastatic calcification

A

widespread calcium disturbance as opposed to localised

hydroxyapatite crystals

41
Q

alcohol fatty change

A

alcohol causes up regulation of lipogenesis causing steatosis (fatty liver) and hepatomegaly (enlargement from the fats)

42
Q

what is acute alcoholic hepatitis?

A

increased aldehyde causes focal hepatocyte necrosis forming mallory bodies (damage to proteins in hepatocytes)
neutrophil infiltrate
usually reversible
symptoms: fever, tenderness & jaundice (protein haem damaged)

43
Q

what is cirrhosis?

A

results in hard, shrunken liver
histological: micronodules of regenerating hepatocytes surrounded by bands of collagen
irreversible

Exam 1 (39 decks)

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