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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
what is necrosis
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
what is apoptosis
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
coagulative necrosis
protein dentauration- they coagulate when they denature - ischaemia of solid organs - ghost outline - features of cell death
28
liquefactive necrosis
neutrophils secrete proteases that breakdown the cells enzyme degradation is substantially greater than denaturation
29
caseous necrosis
contains amorphous debris | particularly associated with infections especially tb
30
what is pathological apoptosis
cytotoxic T cell killing of virus-infected or neoplastic cells -when cells are damaged, particularly with damaged DNA
31
what are the stages of apoptosis
initiation execution degradation & phagocytosis
32
what is the intrinsic pathway of apoptosis
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
extrinsic pathway of apoptosis
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
degradation and phagocytosis
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
what is the difference between apoptosis and necrosis
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
what is gangrene
necrosis visible to the naked eye | -an appearance of necrosis
37
what is infarction
necrosis caused by a reduction of arterial blood flow - a cause of necrosis - can result in gangrene
38
what is an infarct
an area of necrotic tissue which is the result of loss of arterial blood supply -an area ischaemic necrosis
39
what does coagulative necrosis lead to
dry gangrene - necrosis - gangrene
40
what does liquefactive necrosis lead to
wet gangrene - necrosis - infection
41
what causes infarction
atherosclerosis occlusion by thrombus or thromboembolism twisting compression
42
white infarct
'solid organs' occlusion of an end artery often wedge-shaped microscopically you see coagulative necrosis
43
red infarct
haemorrhagic infarct - loose tissue - dual blood supply - numerous anastomoses - prior congestion - raised venous pressure - re-perfusion
44
what is ischaemic-reperfusion injury
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
what causes ischaemic-reperfusion injury
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
what abnormal cellular accumulations occur after cell injury
normal cell components build up abnormal components build up pigment
47
mechanisms of intracellular accumulations
abnormal metabolism- fat alterations in protein folding and transport deficiency of critical enzymes inability to degrade phagocytosed particles
48
what is steatosis
accumulation of triglycerides | commonly seen in liver
49
what causes steatosis
chronic alcohol misuse obesity diabetes mellitus
50
what complications can steatosis lead to
liver and metabolic dysfunction liver function liver cirrhosis sudden death
51
atherosclerosis
cholesterol builds up in smooth muscle cells and macrophages/ histocytes (foam cells) = atherosclerotic plaque
52
xanthoma
cholesterol in macrophages within skin/ tendons, associated with hereditary hyperlipidaemias
53
diseases associated with accumulation of proteins
alcoholic liver disease- mallroys hyaline | alpha1 antitrypsin deficiency
54
pathological accumulation of calcium
localised in dying tissues- dystrophic most common generalised (metastatic) deposition in otherwise normal tissue due to hypercalcaemia due to dysfunction in calcium disturbance
55
what is metastatic calcification
hypercalcaemia secondary to disturbances in calcium metabolism hydroxypatite crystals are deposited in normal tissues throughout the body usually asymptomatic but can be lethal
56
what causes metastatic calcification
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
effects of hypercalcaemia
``` bone disease renal stones confusion, drowsiness, coma, psychosis thirst and polyuria anorexia, nausea, vomiting and abdominal pain ```
58
what is present in the blood after a myocardial infarction and why
* 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
name two other conditions in which fatty liver is commonly seen
``` excessive alcohol intake Diabetes mellitus Obesity Drugs (including alcohol), Carbon tetrachloride toxicity Toxins and infections. ```
60
In addition to fat, what else can accumulate within hepatocytes in patients who drink alcohol to excess?
mallorys hyaline
61
How does | cirrhosis appear histologically?
Bands of fibrosis surrounding nodules of regenerating | hepatocytes

Pathological Processes (10 decks)

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