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Pathological Processes > Cell Injury or Death > Flashcards

Cell Injury or Death Flashcards

1
Q

what is hypoxia

A

oxygen depravation

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2
Q

what are some environmental causes of cell injury

A

direct trauma
extremes of temperature
changes in pressure
electric currents

radiation

microorganisms

immune mechanisms

nutritional

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3
Q

what is hypoxaemic hypoxia

A

arterial content of oxygen is low

  • reduced inspired p02 at altitude
  • reduced absorption secondary to lung disease, pneumonia
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4
Q

anaemic hypoxia

A

decreased ability of haemoglobin to carry oxygen

  • anaemia
  • carbon monoxide poisoning
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5
Q

ischaemic hypoxia

A

interruption to blood supply

  • blockage of vessel
  • heart failure
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6
Q

histiotoxic hypoxia

A

inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes
-cyanide poisoning

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7
Q

how does the immune system damage the body’s cells?

A

hypersensitivity reactions- host tissue is injured secondary to an overly vigorous immune reaction - hives

autoimmune reactions- immune system fails to distinguish self from non self

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8
Q

what cell components are the most susceptible to injury

A

cell membranes
nucleus- DNA
proteins
mitochondria

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9
Q

what are the reversible consequences of reduced intracellular ATP during cell injury

A

there is no oxygen so thers no oxidative phosphorylation in the mitochondria so no ATP is being produced.

Na pump cant work as it is ATP dependant, so there is an influx of Ca, water and Na to the cell which causes swelling, loss of microvilli and blebs, ER swelling

decrease in glycolysis which leads to a drop in pH and in glycogen which causes chromatin tO clump

decrease in protein synthesis as ribosomes detach

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10
Q

what are the irreversible consequences to an influx of calcium

A

calcium moves in to mitochondria and ER and water follows so it bursts

increased cytosolic calcium concentration affects the action of important enzymes in the cell

  • ATPase
  • Phospholipase C
  • Protease
  • Endonuclease
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11
Q

what are free radicals

A

single unpaired electron in an outer orbit- an unstable configuration hence react with other molecules often producing further free radicals

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12
Q

what are the biologically significant free radicals and which is the most dangerous?

A
  • OH DOT - hydroxyl- the most dangerous
  • O2 - superoxide
  • H2O2 Hydrogen peroxide
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13
Q

what causes the formation of free radicals

A 
oxidative phosphorylation
radiation
transition metals
drugs and chemicals 
normal part of inflammatory response
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14
Q

how do free radicals affect lipids

A

cell and organelle membranes damaged
lipid peroxidation
extensive damage

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15
Q

how do free radicals affect proteins

A

oxidation of amino acid side chains
protein-protein cross linkages
results in protein fragmentation

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16
Q

how do free radicals affect nucleic acids

A

reaction with thymine
single strand breaks in DNA
mutagenic and therefore carcinogenic

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17
Q

what causes oxidative stress

A

an imbalance between free radical generation and radical scavenging systems

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18
Q

how does the body control free radicals

A

decay spontaneosly

free radical scavengers- anti-oxidants

enzymes that neutralise free radicals

  • superoxide dismutase- 02 minus converted into hydrogen peroxide
  • catalase- hydrogen peroxide into oxygen and water
  • glutathione peroxidase
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19
Q

how does the body control free radical damage IN PROTEINS

A

heat shock proteins that mend mis-folded proteins and maintain cell viability
-protein chaparones and ubiquitin

free radicals cause proteins to cross link and fragment

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20
Q

what is pyknosis

A

shrinkage of chromatin

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21
Q

what is karyorrhexis

A

fragmentation of nucleus

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22
Q

karyolysis

A

dissolution of nucleus

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23
Q

what do you see under an electron microscope when cells are injured or dying

A 
reversible 
blebs
swelling
clumping of chromatin
ER swelling
mitochondrial swelling 
irreversible
rupture of lysosomes and autolysis 
pyknosis 
karyolysis
karyorrhexis
lysis of ER
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24
Q

what is oncosis

A

cell death with swelling, the spectrum of changes that occur in injured cells prior to death

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25
Q

what is necrosis

A

in a living organism the morphological changes that occur after a cell has been dead some time seen after 12-24 Hours

  • coagulative
  • liquefactive (colliquitive)
  • caseous
  • fat necrosis
  • fibrinoid necoris
26
Q

what is apoptosis

A

programmed cell death

  • cell death and shrinkage
  • regulated intracellular program where a cell activated enzymes that degrade its own nuclear DNA and proteins
  • characteristic DNA breakdown

condensation of chromatin, fragmentation and apoptic bodies

27
Q

coagulative necrosis

A

protein dentauration- they coagulate when they denature

  • ischaemia of solid organs
  • ghost outline
  • features of cell death
28
Q

liquefactive necrosis

A

neutrophils secrete proteases that breakdown the cells

enzyme degradation is substantially greater than denaturation

29
Q

caseous necrosis

A

contains amorphous debris

particularly associated with infections especially tb

30
Q

what is pathological apoptosis

A

cytotoxic T cell killing of virus-infected or neoplastic cells
-when cells are damaged, particularly with damaged DNA

31
Q

what are the stages of apoptosis

A

initiation
execution
degradation & phagocytosis

32
Q

what is the intrinsic pathway of apoptosis

A

initiating signal comes from within the cell

Triggers:

  • most commonly irreparable DNA
  • Withdrawal of growth factors or hormones

p53 protein is activated and this results in outer mitochondrial membrane becoming leaky
cytochrome C is released from the mitochondria and this causes activation of caspases

33
Q

extrinsic pathway of apoptosis

A

initiated by extracellular signals

Triggers
-cells that are a danger- tumour cells

signals - TNF-alpha

  • secreted by T killer cells
  • binds to cell membrane receptor (death receptor)
  • results in activation of caspases
34
Q

degradation and phagocytosis

A

both intrinsic and extrinsic pathways cause the cells to shrink and break into apoptotic bodies

the apoptotic bodies express proteins on their surface

they can now be recognised by phagocytes or neighbouring cells

finally degradation takes place within the phagocyte/ neighbour

35
Q

what is the difference between apoptosis and necrosis

A

apoptosis leads to shrinkage and chromatin condensation, budding and apoptotic bodies phagocytosed with no inflammation in single cells. Fragmentation into nucleosome size fragments ; form clumps beneath nuclear membrane, intact plasma membrane

necrosis occurs in contiguous groups of cells and has swelling, blebbing with disruption of cell membrane and the release of proteolytic enzymes with important inflammatory reaction as well as adjacent inflammation
pyknosis, karryorrhexis, karyolysis, disrupted plasma membrane, degradation of cellular contents

36
Q

what is gangrene

A

necrosis visible to the naked eye

-an appearance of necrosis

37
Q

what is infarction

A

necrosis caused by a reduction of arterial blood flow

  • a cause of necrosis
  • can result in gangrene
38
Q

what is an infarct

A

an area of necrotic tissue which is the result of loss of arterial blood supply
-an area ischaemic necrosis

39
Q

what does coagulative necrosis lead to

A

dry gangrene

  • necrosis
  • gangrene
40
Q

what does liquefactive necrosis lead to

A

wet gangrene

  • necrosis
  • infection
41
Q

what causes infarction

A

atherosclerosis
occlusion by thrombus or thromboembolism
twisting
compression

42
Q

white infarct

A

‘solid organs’
occlusion of an end artery
often wedge-shaped
microscopically you see coagulative necrosis

43
Q

red infarct

A

haemorrhagic infarct

  • loose tissue
  • dual blood supply
  • numerous anastomoses
  • prior congestion
  • raised venous pressure
  • re-perfusion
44
Q

what is ischaemic-reperfusion injury

A

paradoxically, if blood flow is returned to a damaged but not yet necrotic tissue, damage sustained can be worse than if blood flow hadn’t been returned

45
Q

what causes ischaemic-reperfusion injury

A

increased production of oxygen free radicals with reoxygenation
increased number of neutrophils resulting in more inflammation and increased tissue injury
delivery of complement proteins and activation of the complement pathway

46
Q

what abnormal cellular accumulations occur after cell injury

A

normal cell components build up

abnormal components build up

pigment

47
Q

mechanisms of intracellular accumulations

A

abnormal metabolism- fat
alterations in protein folding and transport
deficiency of critical enzymes
inability to degrade phagocytosed particles

48
Q

what is steatosis

A

accumulation of triglycerides

commonly seen in liver

49
Q

what causes steatosis

A

chronic alcohol misuse
obesity
diabetes mellitus

50
Q

what complications can steatosis lead to

A

liver and metabolic dysfunction
liver function
liver cirrhosis
sudden death

51
Q

atherosclerosis

A

cholesterol builds up in smooth muscle cells and macrophages/ histocytes (foam cells) = atherosclerotic plaque

52
Q

xanthoma

A

cholesterol in macrophages within skin/ tendons, associated with hereditary hyperlipidaemias

53
Q

diseases associated with accumulation of proteins

A

alcoholic liver disease- mallroys hyaline

alpha1 antitrypsin deficiency

54
Q

pathological accumulation of calcium

A

localised in dying tissues- dystrophic
most common

generalised (metastatic)
deposition in otherwise normal tissue
due to hypercalcaemia due to dysfunction in calcium disturbance

55
Q

what is metastatic calcification

A

hypercalcaemia secondary to disturbances in calcium metabolism
hydroxypatite crystals are deposited in normal tissues throughout the body
usually asymptomatic but can be lethal

56
Q

what causes metastatic calcification

A

increased secretion of PTH resulting in bone resorption- primary hyperparathyroidism, secondary and teritary hyperthyroidism

destruction of bone tissue

  • primary tumours of bone marrow
  • diffuse skeletal metastases
  • Paget’s disease of bone- when accelerated bone turnover occurs
  • immobilism
57
Q

effects of hypercalcaemia

A 
bone disease 
renal stones
confusion, drowsiness, coma, psychosis 
thirst and polyuria 
anorexia, nausea, vomiting and abdominal pain
58
Q

what is present in the blood after a myocardial infarction and why

A
  • Troponin T
  • Troponin I

An area of cardiac muscle has undergone oncosis/necrosis due to lack
of blood supply/infarction (1 mark). In oncosis/necrosis cell
membranes become leaky and intracellular proteins leak out of the
cells and can be measured in the blood

59
Q

name two other conditions in which fatty liver is commonly seen

A 
excessive alcohol intake 
Diabetes mellitus
Obesity
Drugs (including alcohol), Carbon tetrachloride toxicity
Toxins and infections.
60
Q

In addition to fat, what else can accumulate within hepatocytes in
patients who drink alcohol to excess?

A

mallorys hyaline

61
Q

How does

cirrhosis appear histologically?

A

Bands of fibrosis surrounding nodules of regenerating

hepatocytes

Pathological Processes (10 decks)

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