MoD

Question 1

What is infarction?

Answer 1

Tissue death caused by obstruction of the blood supply

Question 2

What are some common causes of cell damage?

Answer 2

Hypoxia, immune mechanisms, toxins, trauma, radiation

Question 3

What are the types of hypoxia?

Answer 3

Hypoxic - low O2 content of blood
Anaemic - decreased ability of Hb to carry O2
Ischaemic - Interruption to blood supply
Histiocytic - Inability of the cell to use O2

Question 4

How do free radicals cause cellular damage?

Answer 4

Oxidise lipids of cel membrane and can cause DNA mutation

Question 5

What is the function of heat shock proteins?

Answer 5

Refold damaged proteins

Question 6

What are some reversible cell changes?

Answer 6

Reduced staining due to increased water content
Clumping of chromatin
Blebs
Accumulation of fat/keratin

Question 7

What are some irreversible cell changes?

Answer 7

Nuclear changes
Damage to membranes
Lysosome rupture
Lysis of ER

Question 8

What are the three types of irreversible cell changes?

Answer 8

Pyknosis, karyolysis, karyohexis

Question 9

What is pyknosis?

Answer 9

Shrinking of nucleus

Question 10

What is karyolysis?

Answer 10

Dissolution of nucleus

Question 11

What is karyohexis?

Answer 11

Fragmentation of nucleus

Question 12

What are the types of necrosis?

Answer 12

Coagulative, liquefactive, caseous and fat

Question 13

What is coagulative necrosis - where does this commonly occur?

Answer 13

Necrosis whereby dead tissue has a solid consistency with a ghost outline. Occurs when protein denaturation is the dominant process, in cases of ischaemia. Commonly occurs in the kidney or heart

Question 14

What is liquefactive necrosis?

Answer 14

Necrosis whereby tissues are digested leading to digestion of tissues. Occurs when the dominant process is release of enzymes. Seen in the brain and the lungs

Question 15

What is the cause of caseous necrosis?

Answer 15

Infections such as TB

Question 16

What is the cause of fat necrosis?

Answer 16

Pancreatitis and trauma

Question 17

What is gangrene?

Answer 17

Necrosis that is visible to the naked eye

Question 18

What is a white infarct?

Answer 18

An infarct that occurs after the occlusion of an end artery - so the tissue has no blood supply

Question 19

What is a red infarct

Answer 19

An infarct that occurs in a tissue with a dual blood supply - some blood is present but not enough to sustain the tissue

Question 20

How is apoptosis initiated?

Answer 20

Internal pathway - internal changes such as DNA damage

External pathway - external changes - receptor mediated

Question 21

How is apoptosis executed?

Answer 21

Intrinsic - increased membrane permeability results in release of cytochrome C which interacts with APAF1 gene and caspase 9 protein to form an apoptosome. The apoptosome activates a series of enzymes

Extrinsic - A death ligand such as TRAIL binds to a death receptor resulting in caspase activation

Question 22

Apoptosis - degradation

Answer 22

Caspase breaks down the cell into membrane bound fragments which can be broken down by phagocytes or taken up by neighbouring cells

Question 23

What is p53?

Answer 23

A protein which mediates apoptosis in response to DNA damage, suppressing tumours. It is described as the guardian of the cell

Question 24

What are some key differences between apoptosis and necrosis?

Answer 24

Apoptosis affects single cells, shrinkage occurs, the plasma membrane remains intact, no adjacent inflammation

Question 25

What are some consequences of chronic alcohol intake?

Answer 25

``` Raised AST/ALT levels Alcoholic hepatitis - elevated serum bilirubin and jaundice cirrhosis cardiomyopathy gastritis/pancreatitis growth/mental retardation of children Birth defects ```

Question 26

What is the treatment for a paracetemol overdose

Answer 26

Measure serum paracetemol levels to decide whether to administer n-acetylcysteine

Question 27

What occurs in an aspirin overdose?

Answer 27

Respiratory alkolosis followed by respiratory acidosis GI bleed and gastritis petechaie - red spots caused by haemorrhage

Question 28

What are the common symptoms of acute inflammation?

Answer 28

``` Calor - heat Dolor - pain Rubor - redness tumour - swelling loss of function ```

Question 29

What are some common causes of acute inflammation?

Answer 29

Infection, chemicals, tissue necrosis, hypersensitivity reactions, trauma

Question 30

What is the general progression of acute inflammation?

Answer 30

Changes in blood flow > exudation of fluid > infiltration of inflammatory cells

Question 31

How do changes in blood flow in acute inflammation occur?

Answer 31

Vasodilation - controlled by histamine. Increases vascular permeability

Question 32

What occurs during exudation of fluid in acute inflammation?

Answer 32

Exudation of protein rich fluid into tissues Blood flow slows (stasis) leading to tumour Fluid in tissues causes oedema

Question 33

What is the difference between exudate and transudate

Answer 33

Exudate - protein rich fluid lost during inflammation | Transudate - protein poor fluid lost as a result of hydrostatic pressure

Question 34

What are the chemical mediators for vascular leakage in acute inflammation?

Answer 34

Histamine, IL-1, TNF

Question 35

How do neutrophils enter the tissues in acute inflammation?

Answer 35

margination - stasis causes neutrophils to line up at edge of vessels Rolling - neutrophils roll along endothelium, adhering intermittently Adhesion - stick more avidly Emigration - neutrophils move through gaps between endothelial cells

Question 36

What is chemotaxis?

Answer 36

The movement of a substance towards a high concentration of a chemoattractant

Question 37

What are the chemoattractants for neutrophils in acute inflammation?

Answer 37

C5a, LTb4 or bacterial peptides

Question 38

What are the 'killing mechanisms' of neutrophils in acute inflammation?

Answer 38

O2 dependent - superoxide/h2o2 | O2 independent - hydrolase enzymes/bacteridal permeability increase protein

Question 39

What is shock?

Answer 39

A clinical symptom of circulatory failure - low BP leading to poor cardiac output and therefore tachycardia

Question 40

How is acute inflammation resolved?

Answer 40

Vascular changes stop Exudate drains into lymphatics Neutrophils are phagocytosed by macrophages Mediators have short half lives, and therefore break down Dilution of mediators by exudate treatment: incision and drainage

Question 41

How can chronic inflammation arise?

Answer 41

take over from acute inflammation arise de novo develop alongside acute inflammation in persistent irritation

Question 42

How are macrophages stimulated to enter tissues?

Answer 42

Gamma interferon from T/NK cells

Question 43

What signalling molecules do macrophages release?

Answer 43

IL-8 - chemoattractant for neutrophils NO - vasodilation TNF/IL-1 - fever

Question 44

What are the functions of lymphocytes in chronic inflammation?

Answer 44

B lymphocytes > plasma cells > immunoglobulins | T lymphocytes - release mediators

Question 45

What are giant cells? Include types

Answer 45

multinucleate cells made by fusion of many macrophages Langhans - horseshoe nuclei, TB Foreign body - less organised Touton - fat necrosis

Question 46

What is granulamatus infection?

Answer 46

Infection with presence of granuloma - an aggregation of epitheloid macrophages surrounded by lymphocytes. Functions to wall off substances which are harmful but cannot be removed Giant cells may be present - but not always!

Question 47

What is ulceration?

Answer 47

Necrosis through mucosa - commonly found in the stomach linked to helicobacter pylori