Cell Injury

Question 1

Hypoxaemic hypoxia

Answer 1

Arterial content of oxygen is low

Question 2

Anaemia hypoxia

Answer 2

Decreased ability of haemoglobin to carry oxygen

Question 3

Ischaemic hypoxia

Answer 3

Interruption to blood supply

Question 4

Histiocytic hypoxia

Answer 4

Inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes

Question 5

Enzymes that catalyse free radicals

Answer 5

Superoxide dismutase, catalase, glutathione peroxidase

Question 6

Pyknosis

Answer 6

Irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis

Question 7

Karyorrhexis

Answer 7

Destructive fragmentation of the nucleus of a dying cell whereby its chromatin is distributed irregularly throughout the cytoplasm

Question 8

Karyolysis

Answer 8

Complete dissolution of the chromatin of a dying cell due to the enzymatic degradation by endonucleases

Question 9

Oncosis

Answer 9

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

Question 10

Necrosis

Answer 10

In a living organism the morphologic changes that occur after a cell has been dead some time

Question 11

Coagulative Necrosis

Answer 11

Protein denturation

Question 12

Liquiefactive Necrosis

Answer 12

Enzyme release

Question 13

Gangrene

Answer 13

Necrosis visible to the naked eye

Question 14

Infarction

Answer 14

Necrosis caused by reduction in arterial blood flow

Question 15

Infarct

Answer 15

An area of necrotic tissue which is the result of loss of arterial blood supply

Question 16

Dry gangrene

Answer 16

Necrosis modified by exposure to air (coagulative necrosis)

Question 17

Wet gangrene

Answer 17

Necrosis modified by infection (liquiefactive necrosis)

Question 18

Gas gangrene

Answer 18

Wet gangrene caused by anaerobic bacteria

Question 19

Apoptosis

Answer 19

Cell death with shrinkage, induced by a regulated intracellular program where a cell activates enzymes that degrade it’s own nuclear DNA and proteins

Question 20

Role of p53 protein

Answer 20

Causes outer mitochondrial membrane to become leaky

Question 21

Role of cytochrome c

Answer 21

Causes activation of caspases

Question 22

What is TNFalpha

Answer 22

Secreted by T killer cells, binds to cell membrane receptor, results in activation of caspases

Question 23

Five main groups of intracellular accumulations

Answer 23

Water and electrolytes, lipids, carbohydrates, proteins, ‘pigments’

Question 24

Causes of steatosis

Answer 24

Alcohol, diabetes mellitus, obesity, toxins(carbon tetrachloride)

Question 25

When do lipids accumulate in cells?

Answer 25

Cannot be broken down and is insoluble – Can only be eliminated through the liver – Excess stored in cell in vesicles -Accumulates in smooth muscle cells and macrophages in atherosclerotic plaques = foam cells – Present in macrophages in skin and tendons of people with hereditary hyperlipidaemias =
xanthomas

Question 26

α1-antitrypsin deficiency

Answer 26

Liver produces incorrectly folded α1-antitrypsin protein, cannot be packaged by ER, accumulates within ER and is not secreted, systemic deficiency, proteases in lung act unchecked resulting in emphysema

Question 27

What does haemosiderin store and when is it formed?

Answer 27

Stores iron, formed when there is a local(e.g bruise) or systemic excess of iron

Question 28

What is systemic excess of iron called and in which cases is it seen in?

Answer 28

Haemosiderosis, deposited in many organs. Seen in haemolytic anaemia, blood transfusions and hereditary haemochromatosis

Question 29

Hereditary haemochromacytosis: what is it? Symptoms? Treatment?

Answer 29

Increased intestinal absorption of dietary iron, results in liver(cirrhosis) and pancreas scarring. Symptoms include liver damage, heart dysfunction and multiple endocrine failures, especially of the pancreas. Treatment is repeated bleeding.

Question 30

What is accumulating in jaundice?

Answer 30

Bilirubin, breakdown product of heme, found in all cells. Taken from tissues by albumin to liver, excreted in bile. If bile flow is obstructed or overwhelmed, bilirubin in blood rises and jaundiceresults, deposited in tissues extracellularly or in
macrophages

Question 31

Mechanisms of intracellular accumulations

Answer 31

Abnormal metabolism, alterations in protein folding and transport, deficiency of critical enzymes, inability to degrade phagocytosed molecules

Question 32

Why does dystrophic calcification occur?

Answer 32

No abnormality in calcium metabolism, or serum calcium or phosphate concentrations, local change/disturbance
favours nucleation of hydroxyapatite crystals, can cause organ dysfunction, e.g., atherosclerosis, calcified heart valves

Question 33

Stellate cells and liver cirrhosis

Answer 33

In liver cirrhosis, hepatic stellar cells lose their vitamin A storage capability and differentiate into myofibroblasts, which synthesise and deposit collagen within the perisinusodial space. This collagen surrounds the central vein, constricting it and leading to portal hypertension