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Em's ESA 2 > MoD Cell Injury > Flashcards

Flashcards in MoD Cell Injury Deck (28):

What causes cell injury/death?

- hypoxia (common)
- toxins
- physical agents e.g. trauma, temp
- radiation
- MO's
- immune mechanisms
- diet (insufficiency and excess)


What are the causes of hypoxia?

Hypoxaemic hypoxia: arterial O2 is low
Anaemic hypoxia: decreased ability of Hb to carry O2
Ischaemic hypoxia: lack of blood supply
Histiocytic hypoxia: unable to use O2 due to lack of oxidative phosphorylation (cyanide)


What are the targets for cell damage?

Cell membranes, nucleus/DNA, proteins, mitochondria


Describe the mechanisms of both reversible and irreversible hypoxia

Reversible: decreased oxidative phosphorylation leads to less ATP.
1. Less ATP = reduced sodium pump activity causing cell swelling.
2. Less ATP=more glycolysis, decreasing cellular pH.
3. Less ATP=less protein synthesis

Irreversible: the cell membrane becomes more permeable so there is an increase in CA2+.

Increased cytosolic calcium activates destructive enzymes.


What is ischaemia-reperfusion injury?

If blood returns to ischaemic tissue (not yet necrotic), the damage can be worse than if the blood wasn't returned.

Reoxygenation causes increased production of free radicals and increased no. of neutrophils resulting in more inflammation.


List the 3 most important free radicals and the body's defences against them.

hydroxyl radical (most dangerous)
hydrogen peroxide

Body's defence system: Storage proteins, free radical scavengers (Vits ACE), and enzymes


What types of cellular structures are damaged by free radicals?

Main target is lipids in the membranes. This causes lipid peroxidation and production of more free radicals.

They also attack proteins and DNA (can cause malignancy).


What are heat shock proteins and what do they do?

They aim to repair misfolded proteins to protect against cell injury e.g. unfoldases or chaperonins


What is the microscopic appearance of injured cells? (Light and electron)

Light microscopy:
Cells are swollen, shrunken nucleus, clumping of chromatin

Electron microscopy:
All of the above + blebs, defects in membrane, dispersion of ribosomes, organelle swelling


Define oncosis

Cell death with swelling.


Define necrosis and list the types

The morphologic changes that occur in a living organism after a cell has been dead a long time. Often inflammation.



Define apoptosis

Cell death with shrinkage. (membrane integrity preserved unlike oncosis)
Regulated program where the cell activates enzymes that degrade its own DNA and proteins
Can be pathological e.g. if a cell is infected by a virus and needs to be removed


What is the microscopic appearance of coagulative necrosis and when does it occur?

Occurs in the first few days
Involves denaturation of proteins
Appears as a 'ghost outline' of cells
Increased pink staining of cyto


What is the microscopic appearance of liquefactive necrosis and when does it occur?

Mostly enzyme digestion of tissues
Seen in brain
Only parts of cells visible - cellular architecture is not intact


What is the microscopic appearance of caseous necrosis and when does it occur?

Associated with infections, particular tuberculosis
Contains structureless debris
Cheesy appearance


What is the microscopic appearance of fat necrosis and when does it occur?

Destruction of adipose tissue


What are the types of gangrene?

Dry gangrene - exposed to air
Wet gangrene - infection (v serious as it can cause septicaemia)

Gas gangrene (a type of wet gangrene) - bubbles form where the tissue has been colonised by anaerobic bacteria


What are the types of infarction and causes?

Causes - thrombosis and embolism, twisting of an organ which compresses the blood supply

Red - occurs where there is a dual blood supply e.g. brain and lung, there is bleeding into the infarct

White - coagulative necrosis, solid organs with a single blood supply e.g. spleen and kidneys


What molecules are released by injured and dying cells?

Calcium enters damaged membranes causing other molecules to leak out

Potassium e.g. from extensive necrosis from burns. Very toxic on the heart - can cause MI

Enzymes - smallest released first, type depends on the type of damage and the type of tissue

Myoglobin is released from dead striated muscle e.g. myocardium, urine dark


Outline the mechanism of apoptosis

1. Initiation - DNA damage activates p53, or binding of death ligands
2. Execution
3. Degradation and phagocytosis


What are the 5 main groups of abnormal intracellular accumulations?

Water and electrolytes


Give an example of an accumulation of water and electrolytes and why this may occur.

Accumulation of fluid in the brain caused by cell injury. Lack of ATP = accumulation of NA+ = swelling


Give an example of an accumulation of lipids and why this may occur.

Steatosis - accumulation of lipids in the liver caused by alcohol, diabetes, obesity. Liver appears enlarged and yellow.
Cholesterol can accumulate in atherosclerotic plaques and xanthomas.


Give an example of an accumulation of proteins and why this may occur.

Mallory body found in hepatocytes of people suffering from alcoholic liver disease. The bodies are eosinophilic so stain a bright pink colour.


Give an example of an accumulation of pathological pigments and why this may occur.

Accumulation of coal dust in the lungs of a miner
Tattoo pigments carried by macrophages and accumulate in lymph nodes
Lipofuscin is a brown pigment in ageing cells
Heamosiderin is an iron storage molecule found in bruising
Bilirubin accumulation (jaundice) occurs when bile flow is obstructed


What are the two types of pathological calcification and why do they occur? (broad)

Dystrophic: calcification occurring in response to degenerated or necrotic tissue e.g. ageing Whaheart valves, arteries damaged by plaques

Metastatic: calcification occurring in normal tissues due to elevated serum calcium levels, as seen in hyperparathyroidism. Can occur where there is a tumour of bone marrow.


What happens during cellular ageing?

Cells accumulate damage to their DNA and misfolded proteins.
They reach replicative senescence which is where they can no longer divide. (with every replication the telomeres shorten until they reach a critical length where no more replication can occur).
Telomerase is an enzyme which maintains the original length of the telomeres - present in germ cells and many cancer cells.


Describe 3 effects on the liver of chronic excessive alcohol intake.

1. Fatty liver: fat metabolism is disturbed resulting in steatosis and hepatomegaly. Acute, reversible and generally asymptomatic.
2. Acute alcoholic hepatitis: alcohol and metabolites are toxic so a binge can result in acute hepatitis with hepatocyte necrosis and formation of mallory bodies. Usually reversible - tenderness, fever and jaundice.
3. Cirrhosis: hard shrunken liver. Appears as nodules of regenerating hepatocytes surrounded by collagen bands. Irreversible and sometimes fatal.

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