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ESA 2 - RJS > MoD > Flashcards

MoD Flashcards

1
Q

What are the eight causes of cell injury?

A 
Hypoxia
Toxins
Heat
Cold
Trauma
Radiation
Micro-organisms
Immune reactions
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2
Q

What is hypoxia?

A

Oxygen deprivation causing atrophy (wasting), cell injury or cell death

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3
Q

What is ischaemia?

A

Loss of blood supply due to decreased arterial supply or decreased venous drainage

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4
Q

What occurs in cell injury that causes depletion of mitochondrial nucleotides and ATP?

A
  1. Decreased oxygen = decreased ATP production in mitochondria
  2. Loss of activity of Na/K pump = increase in intracellular Na = increased H2O
  3. Ca enters cell
  4. Increase in anaerobic respiration = increase in lactic acid = decrease pH = effects enzymes = chromatin clumping
  5. Ribosomes detach from ER = disruption of protein synthesis
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5
Q

What are free radicals and what are the main three?

A

Molecules with a single unpaired electron

OH’, O2-, H2O2

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6
Q

What negative effects do free radicals elicit?

A

Attack lipids in membranes = lipid peroxidation

Damage proteins and nucleic acids = mutagenic

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7
Q

What positive effects do free radicals elicit?

A

Produced by leukocytes for killing bacteria

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8
Q

What are the four defence mechanisms against free radicals?

A
  1. Superoxide dismutase (SOD enzyme) = O2- to H2O2
  2. Catalases and peroxidases = H2O2 to O2 + H2O
  3. Savenger radicals = Vitamin A, C, E & glutathione
  4. Storage proteins sequester transition metals (e.g. Fe and Cu) as they catalyse formation of free radicals
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9
Q

What is the function of heat shock proteins?

A

Ensure correct refolding of proteins that have undergone denaturing due to cell injury

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10
Q

Define oncosis

A

Changes that occur in injured cells prior to death

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11
Q

Define necrosis

A

Morphologic changes that follow cell death, largely due to progressive degradative action of enzymes on cell

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12
Q

Define apoptosis

A

Cell death induced by regulated intracellular programme - cells activate enzymes that degrade cells’ own nuclear DNA and proteins

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13
Q

What are the cellular events seen in necrosis?

A

Cell unable to maintain membrane integrity, contents leak out.
Often causes inflammation
Lysosomal enzymes are released
Dystrophic calcification occurs

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14
Q

How is necrotic tissue removed?

A

Enzymatic degradation & phagocytosis by white cells

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15
Q

What are the two types of necrosis?

A

Coagulative & Liquifactive

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16
Q

What is coagulative necrosis?

A

Protein denaturing which then cause clumping and solidity of dead cells

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17
Q

What is coagulative necrosis most common in?

A

Ischaemia

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18
Q

What is seen under the microscope in coagulative necrosis?

A

Ghost outline of cells as cellular architecture is preserved

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19
Q

What is liquifactive necrosis?

A

Release of active enzymes which generate a viscous mass via enzymatic degradation

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20
Q

When is liquifactive necrosis most common?

A

Associated with massive neutrophil infiltration

Also seen in the brain as it is a fragile tissue with minimal support from robust collagenous matrix

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21
Q

What are the other two, less common, types of necrosis?

A

Caseous necrosis

Fat necrosis

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22
Q

What is caseous necrosis and when does it occur?

A

Cheese-like appearance - amorphous debris

Highly associated with TB

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23
Q

What is fat necrosis and when does it occur?

A

Destruction of adipose tissue

Typically seen with acute pancreatitis (inflammation causes release of lipases)

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24
Q

What can also occur with fat necrosis?

A

Release of free fatty acids that can react with Ca can causes chalky deposits

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25
Q

What is gangrene?

A

Term used to describe necrosis visible to the naked eye

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26
Q

What are the two types of gangrene and what causes them?

A

Dry gangrene - coagulative necrosis - ischaemic limbs

Wet gangrene - liquifactive necrosis - infection

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27
Q

What is an infarction and what are the two types?

A

Refers to the cause of necrosis

Red or white infarct

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28
Q

What are the most common causes of an infarct?

A

Thrombosis/embolism, external compression of vessel, twisting of vessel

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29
Q

What occurs in a white infarct and where do they occur?

A

Coagulative necrosis
Occurs in solid organs with good stromal support, after end artery - limits amount of haemorrhage that can occur
Heart, spleen, kidneys

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30
Q

What occurs in a red infarct?

A

Extensive haemorrhage into dead tissue

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31
Q

What are the five instances that red infarcts occur?

A
  1. Organs with dual blood supply - e.g. lungs
  2. Where capillary beds of 2 separate arterial supplies merge - e.g. intestines
  3. Loose tissue - poor stromal support for capillaries
  4. Previous congestion - e.g. congestive cardiac failure
  5. Raised venous pressure
32
Q

What are the cellular events associated with apoptosis?

A

Nuclear chromatin condensation and fragmentation.
Cytoplasmic budding and phagocytosis of apoptotic bodies
No leakage of cell contents therefore no inflammation

33
Q

What are the macroscopic structural changes of necrosis?

A

Firm or soft

Pale or heamorrhagic

34
Q

What are the microscopic structural changes of necrosis?

A

Pykinosis (Condensation of chromatin)
Karyorrhexis (Destructive fragmentation of nucleus)
Karyolysis (Complete dissolution of chromatin by endonucleases)
Leading to disappearing of nucleus
Glassy, homogenous cells left

35
Q

What are the electron microscopic changes of necrosis?

A

Discontinuities in plasma and organelle membranes
Dilation of mitochondria and large amorphous densities
Membrane blebs

36
Q

What are the mircoscopic changes seen in apoptosis?

A 
Single cells or small clusters
Intensely eosinophilic (lots of chemical mediators)
Dense nuclear fragments
Cell shrinkage
Chromatin condensation
Nuclear fragmentations
Phagocytosis by macrophages
37
Q

What are the electron microscopic changes seen in apoptosis?

A

Cytoplasmic blebs

Fragmentation into membane-bound apoptotic bodies

38
Q

What occurs in cell injury caused by alterations in calcium homeostasis?

A

Raised intracellular calcium due to influx across plasma membrane and release from mitochondria and endoplasmic reticulum
Causes enzyme activation which produces cell injury

39
Q

What are the six main causes of acute inflammation?

A 
Foreign bodies
Immune reactions
Infections & microbial toxins
Tissue necrosis
Trauma
Physical and chemical agents
40
Q

What is the biological purpose of acute inflammation?

A

Response of living tissue to injury, initiated to limit the tissue damage

41
Q

What are the clinical features of acute inflammation?

A 
Rubor - redness
Tumour - swelling
Color - heat
Dolor - pain
Loss of function
42
Q

What are the changes in tissues that occur

A

Vascular phase - vasodilation, increased permeability, vascular stasis
Cellular phase - infiltration of inflammatory cells (fibrin, neutrophils)

43
Q

What occurs in vasodilation in acute inflammation and what are the chemical mediators?

A

Initial vasoconstriction followed by vasodilation to increase blood flow for protein delivery and hydrostatic pressure
Mediated by histamine, prostagladins

44
Q

What occurs in increased permeability of blood vessels

A

Vasodilation causes gaps in membrane therefore escape of protein-rich fluid (exudate)
Mediated by histamine, leukotrienes

45
Q

What are the two types of oedema?

A

Transudate - Low protein content (due to hydrostatic pressure imbalance only)
Exudate - High protein content (types that occurs inflammation)

46
Q

What occurs during neutrophil margination and migration?

A

Neutrophils to line up at the edge of blood vessels (endothelium) = margination
Neutrophils then roll along endothelium, sticking to it intermittently = rolling
Stick more avidly = adhersion
Emigration of neutrophils through blood vessel wall = migration (chemotaxis)
Mediated by C5a and leukotriene B4

47
Q

What type of neutrophils are seen in acute inflammation?

A

Polymorphonuclear leucocytes

48
Q

What do neutrophils do in acute inflammation?

A

Phagocytosis

Release toxic metabolites and enzymes damaging host tissue

49
Q

What chemical mediators cause neutrophil chemotaxis?

A

C5a, LTB4, bacterial peptides

50
Q

What chemical mediators enhance phagocytosis?

A

Opsonins - C3b

51
Q

What are the hallmarks of acute inflammation?

A

Exudate of fluid

Infiltrate of inflammatory cells

52
Q

How does exudation of fluid combat injury?

A

Delivers plasma proteins to area of injury
Dilutes toxins
Increases lymphatic drainage

53
Q

How does pain and loss of function combat injury?

A

Enforces rests, reduces chance of further trauma

54
Q

What are the local complications of acute inflammation?

A

Swelling - blocking of tubes
Exudate - compression
Loss of fluid - burns
Pain and loss of function

55
Q

What are the systemic complications of acute inflammation?

A

Fever - endogenous pyrogens produced, increase prostaglandins
Leukocytosis - increased release from bone marrow
Acute phase response - decreased appetite, raised pulse rate, altered sleep patterns, changes in plasma concentrations of CRP, alpha-1-antitrypsin, fibrinogen
Septic shock

56
Q

What are the sequelae of acute inflammation?

A

Complete resolution (changes gradually reverse) - if collagen framework still intact
Chronic inflammation and fibrous repair, tissue regeneration - if collagen framework not intact
Continued acute inflammation with chronic inflammation - abscess (acute around the edge, chronic in the middle)
Death

57
Q

Give clinical examples of acute inflammation

A

Lobar pneumonia

Acute appendicitis

58
Q

Give one inherited disorder of acute inflammatory process

A

Alpha-1-antitrypsin deficiency
Autosomal recessive disorder - low levels of alpha-1-antitrypsin therefore decreased trypsin breakdown. Trypsin catalyses conversion of proelastase to elastase which breaks down elastin, destorying alveolar walls.

59
Q

How does aspirin modify acute inflammation?

A

Inhibits cyclooxygenase and blocks prostaglandin synthesis resulting in decreased fever, pain and vasodilatation

60
Q

What is chronic inflammation?

A

Chronic response to injury with associated fibrosis

61
Q

How does chronic inflammation arise?

A
  1. Take over from acute inflammation
  2. Arise de novo (no preceeding acute inflammation)
  3. Develop alongside acute inflammation
62
Q

What are the microscopic appearances of chronic inflammation?

A

Macrophages - phagocytosis, presentation of antigen to immune system, synthesis of cytokines and complement
Lymphocytes - B lymphocytes produce antibodies, T lymphocytes produce cytotoxic functions
Plasma cells - differentiated antibody-producing B lymphcytes
Eosinophils - allergic reactions
Fibroblasts/myofibroblasts - recruited by macrophages
Giant cells - multinucleate cells made by fusion of macrophages, frustrated phagocytosis

63
Q

What are the different types of giant cells recognised?

A

Langhans - TB
Touton - Fat necrosis
Foreign body type

64
Q

What are the effects of chronic inflammation?

A

Fibrosis e.g. chronic cholecystitis
Impaired function of tissue e.g. Inflammatory bowel disease
Atrophy e.g. gastric mucosa
Stimulation of immune response e.g. rheumatoid arthritis

65
Q

What is granulomatous inflammation?

A

Chronic inflammation with granulomas (collection of immune cells, macrophages = epithelioid histiocytes)

66
Q

When do granulomas arise?

A

Persistent low-grade antigenic stimulation

Hypersensitivity

67
Q

What are the main causes of granulomatous inflammation?

A

Mildly irritant ‘foreign’ material
Infections - Mycobacterium (TB), leprosy
Unknown causes - sarcoidosis

68
Q

What is regeneration?

A

Replacement of dead or damaged cells by functional, differentiated cells

69
Q

What is the difference, in terms of regeneration of labile, stable and permanent cells?

A

Labile - rapid proliferation (epithelial, heamatopoietic)
Stable (resting state) - speed of regeneration variable (hepatocytes, osteoblasts, fibroblasts)
Permanent (Unable to divide) - neurones, cardiac myocytes

70
Q

What is fibrous repair?

A

Replacement of functional tissue by scar tissue

71
Q

What are the key components of fibrous repair?

A
  1. Cell migration
  2. Blood vessels
  3. Extracellular matrix production and remodelling
72
Q

What are the cell types involved in fibrous repair?

A

Inflammatory cells - phagocytosis (neutorphils, macrophages), chemical mediators (lymphocytes, macrophages)
Endothelial cells - angiogenesis
Fibroblasts/myofibroblasts - extracellular matrix proteins, wound contraction

73
Q

What are the defects of collagen synthesis?

A

Vitamin C deficiency (Scurvy) - inadequate hydroxylation of alpha chains leading to defective helix formation
Ehler-Danlos syndrome - Defective conversion of procollagen to tropocollagen
Osteogenesis imperfecta - mutation in collagen gene

74
Q

What is chronic granulomatous disease?

A

Deficiency of NADPH oxidase therefore unable to produce reactive oxygen species and cannot degrade pathogens engulfed. Causes formation of granulomas (frustrated macrophages forming giant cells)

75
Q

What is angiooedema?

A

Mutation causing deficiency of C1-inhibitor protein
Leads to abnormal activation of complement system by unopposed activation of contact pathway resulting in large amounts of bradykinin causing vasodilation and increase permeability

ESA 2 - RJS (6 decks)

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