MOD S1&2 Cell Injury Flashcards by Jess Sidney

What is cell injury?

When the cell can no longer adapt to changes in its environment, it begins to show evidence of cell injury.

How well did you know this?

Not at all

Perfectly

How may a cell be injured?

Hypoxia
Toxins
Heat
Cold
Trauma
Radiation
Microorganisms
Immune mechanisms
Dietary deficiency/insufficiency
Genetic abnormalities

How well did you know this?

Not at all

Perfectly

What are heat shock proteins?

Produced in response to cell injury due to heat
They refold denatured proteins correctly
Misfolded proteins are destroyed

How well did you know this?

Not at all

Perfectly

What are the main targets of cell injury?

Cell membranes
Nucleus
Proteins
Mitochondria

How well did you know this?

Not at all

Perfectly

What is ischaemia reperfusion injury?

When blood flow is reinstated to an area of ischaemic tissue, the damage sustained is worse that it would have been without circulation.

How well did you know this?

Not at all

Perfectly

Define ischaemia

The interruption of blood supply

How well did you know this?

Not at all

Perfectly

Name the types of hypoxia

Hypoxaemic
Anaemic
Ischaemic
Histeocytic

How well did you know this?

Not at all

Perfectly

What is hypoxia?

Reduced O2

Often due to ischaemia

How well did you know this?

Not at all

Perfectly

What are some reversible changes to cells caused by hypoxia?

Reduced oxidative phosphorylation
Decreased pH
Na accumulation
Cell swelling
Reduced protein synthesis due to ribosome detachment

How well did you know this?

Not at all

Perfectly

Define oncosis

The spectrum of changes that occur in a injured cell prior to death

How well did you know this?

Not at all

Perfectly

What are irreversible changes to cells brought about by hypoxia?

Accumulation of cytosolic Ca2+

Activation of certain enzymes - these result in cell death

How well did you know this?

Not at all

Perfectly

Do all cells react the same way to ischaemia?

Eg nerve cells would last a few minutes in ischaemic conditions whereas fibroblasts could last for hours

How well did you know this?

Not at all

Perfectly

What reversible structural changes may be seen in an ischaemic cell under an electron microscope?

Swelling
Chromatin clumping
Autophagy
Ribosome dispersal
Blebs

How well did you know this?

Not at all

Perfectly

What are blebs?

Small bumps on the cell membrane where the cytoskeleton has detached

How well did you know this?

Not at all

Perfectly

What irreversible effects may be seen with an electron microscope in an ischaemic cell?

Nuclear changes
Lysosome rupture
Membrane defects
Endoplasmic reticulum rupture

How well did you know this?

Not at all

Perfectly

Define apoptosis

Programmed cell death

How well did you know this?

Not at all

Perfectly

What are the stages of apoptosis?

Initiation
Execution
Degradation/phagocytosis

How well did you know this?

Not at all

Perfectly

What are the two methods of initiation of apoptosis?

Intrinsic (mitochondrial)

Extrinsic

How well did you know this?

Not at all

Perfectly

Name an inhibitor of apoptosis

Bcl-2

How well did you know this?

Not at all

Perfectly

What is necrosis?

The changes which occur after cell death in living tissue

Name a death ligand and a death receptor (involved in extrinsic apoptosis)

Ligand: TRAIL
Receptor: TRAIL-R

What are caspases?

Important effector molecules of apoptosis eg caspase 3

What are the important mediators of apoptosis?

Cytochrome c, APAF, caspase 9

Give some examples of types of necrosis

Coagulative
Liquefactive
Fat
Caseous

Describe coagulative necrosis

More protein denaturation that enzyme release Consistency of tissue remains solid Cell structure is somewhat preserved, leaving a "ghost outline" Tend to be due to infarcts (not in brain)

Describe liquefactive necrosis

More enzyme release than protein denaturation Tissue becomes a viscous mass Tissue is lysed and disappears Tends to be due to infarction (eg in brain) Also seen in massive neutrophil invasions

Describe caseous necrosis

Tissue appears amorphous | Halfway between coagulative and liquefactive

Describe fat necrosis

Occurs in cases of cell death in adipose tissue | The fatty acids released react with calcium to form chalky deposits (calcium soaps)

What is p53?

Very important protein in apoptosis | Mediates apoptosis in response to DNA damage

What is pathological calcification?

Abnormal deposition of calcium salts within tissues

What is gangrene? Give types.

The clinical term for grossly visible necrosis Dry or wet

Name and briefly describe the types of pathological calcification

Dystrophic - occurs in areas of dying tissue. No abnormal serum calcium or calcium metabolism Metastatic - occurs in normal tissues secondary to abnormal calcium metabolism

Define "dry" gangrene and give an example

Grossly visible coagulative necrosis An example is the umbilical cord after birth

Give some examples of types of abnormal cellular accumulations

Normal cell constituents eg lipids, proteins Abnormal substances eg minerals or abnormal metabolic bi-products Pigments eg coal dust, bilirubin, tattoos

Describe "wet" gangrene

Clinical term for grossly visible liquefactive necrosis

What is an infarct? Name the types.

Necrosis due to ischaemia | Red or white infarct

Describe white infarcts and give an example of where one could occur

Caused by the occlusion of an end artery There are no peripheral blood vessels Therefore area is left completely without blood Eg kidney

Describe red infarcts and give an example of where one could occur

Occlusion of blood vessels leads to build up of blood All vessels haemorrhage at once Increased pressure causes decreased blood flow This causes ischaemia and red infarct Eg bowel

What are the main effects of chronic excessive alcohol intake on the liver?

Fatty deposits (steatosis) - reversible, can cause hepatomegaly Hepatitis - usually reversible, jaundice, tenderness and fever Cirrhosis - irreversible hardening and shrinking of liver, sometimes fatal, occurs in 10-15% of alcoholics

What are the main effects of aspirin overdose?

Pulmonary alkalosis Metabolic acidosis (caused by overcompensation to alkalosis) Acute erosive gastritis

Describe hypoxaemic hypoxia and when it could occur

Arterial oxygen content is low eg at high altitudes reduced inspired pO2

Describe anaemic hypoxia and when it could occur

Decreased ability of haemoglobin to carry oxygen eg carbon monoxide poisoning

Describe ischaemic hypoxia and when it could occur

Interruption to blood supply eg blockage of a vessel

Describe histeocytic hypoxia and when it could occur

Inability to utilise oxygen due to disabled oxidative phosphorylation enzymes eg cyanide poisoning

How could ischaemia reperfusion injury be explained?

Oxygen free radical production Neutrophils causing inflammation and tissue injury Activation of the complement pathway

If there was TB in the lung, what is the most common type of necrosis?

Caseous

What could cause liquefactive necrosis?

Infection which draws neutrophils, which secrete proteolytic enzymes

What affects the colour of an infarct?

Colour depends on how much haemorrhaging occurred

Where is fat necrosis most commonly seen?

In pancreatitis when lipases are released