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ESA 2 > MoD > Flashcards

MoD Flashcards

1
Q

What is infarction?

A

Tissue death caused by obstruction of the blood supply

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2
Q

What are some common causes of cell damage?

A

Hypoxia, immune mechanisms, toxins, trauma, radiation

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3
Q

What are the types of hypoxia?

A

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

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4
Q

How do free radicals cause cellular damage?

A

Oxidise lipids of cel membrane and can cause DNA mutation

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5
Q

What is the function of heat shock proteins?

A

Refold damaged proteins

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6
Q

What are some reversible cell changes?

A

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

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7
Q

What are some irreversible cell changes?

A

Nuclear changes
Damage to membranes
Lysosome rupture
Lysis of ER

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8
Q

What are the three types of irreversible cell changes?

A

Pyknosis, karyolysis, karyohexis

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9
Q

What is pyknosis?

A

Shrinking of nucleus

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10
Q

What is karyolysis?

A

Dissolution of nucleus

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11
Q

What is karyohexis?

A

Fragmentation of nucleus

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12
Q

What are the types of necrosis?

A

Coagulative, liquefactive, caseous and fat

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13
Q

What is coagulative necrosis - where does this commonly occur?

A

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

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14
Q

What is liquefactive necrosis?

A

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

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15
Q

What is the cause of caseous necrosis?

A

Infections such as TB

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16
Q

What is the cause of fat necrosis?

A

Pancreatitis and trauma

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17
Q

What is gangrene?

A

Necrosis that is visible to the naked eye

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18
Q

What is a white infarct?

A

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

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19
Q

What is a red infarct

A

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

20
Q

How is apoptosis initiated?

A

Internal pathway - internal changes such as DNA damage

External pathway - external changes - receptor mediated

21
Q

How is apoptosis executed?

A

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

22
Q

Apoptosis - degradation

A

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

23
Q

What is p53?

A

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

24
Q

What are some key differences between apoptosis and necrosis?

A

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

25
Q

What are some consequences of chronic alcohol intake?

A 
Raised AST/ALT levels
Alcoholic hepatitis - elevated serum bilirubin and jaundice
cirrhosis
cardiomyopathy
gastritis/pancreatitis
growth/mental retardation of children
Birth defects
26
Q

What is the treatment for a paracetemol overdose

A

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

27
Q

What occurs in an aspirin overdose?

A

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

28
Q

What are the common symptoms of acute inflammation?

A 
Calor - heat
Dolor - pain
Rubor - redness
tumour - swelling
loss of function
29
Q

What are some common causes of acute inflammation?

A

Infection, chemicals, tissue necrosis, hypersensitivity reactions, trauma

30
Q

What is the general progression of acute inflammation?

A

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

31
Q

How do changes in blood flow in acute inflammation occur?

A

Vasodilation - controlled by histamine. Increases vascular permeability

32
Q

What occurs during exudation of fluid in acute inflammation?

A

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

33
Q

What is the difference between exudate and transudate

A

Exudate - protein rich fluid lost during inflammation

Transudate - protein poor fluid lost as a result of hydrostatic pressure

34
Q

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

A

Histamine, IL-1, TNF

35
Q

How do neutrophils enter the tissues in acute inflammation?

A

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

36
Q

What is chemotaxis?

A

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

37
Q

What are the chemoattractants for neutrophils in acute inflammation?

A

C5a, LTb4 or bacterial peptides

38
Q

What are the ‘killing mechanisms’ of neutrophils in acute inflammation?

A

O2 dependent - superoxide/h2o2

O2 independent - hydrolase enzymes/bacteridal permeability increase protein

39
Q

What is shock?

A

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

40
Q

How is acute inflammation resolved?

A

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

41
Q

How can chronic inflammation arise?

A

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

42
Q

How are macrophages stimulated to enter tissues?

A

Gamma interferon from T/NK cells

43
Q

What signalling molecules do macrophages release?

A

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

44
Q

What are the functions of lymphocytes in chronic inflammation?

A

B lymphocytes > plasma cells > immunoglobulins

T lymphocytes - release mediators

45
Q

What are giant cells? Include types

A

multinucleate cells made by fusion of many macrophages

Langhans - horseshoe nuclei, TB
Foreign body - less organised
Touton - fat necrosis

46
Q

What is granulamatus infection?

A

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!

47
Q

What is ulceration?

A

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

ESA 2 (4 decks)

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