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Year 2 EMS > MoD lectures 1-7 > Flashcards

MoD lectures 1-7 Flashcards

1
Q

Define hyperplasia

A

increase in cell number

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2
Q

Define hypertrophy

A

cell size increase

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3
Q

Define atrophy

A

cells decrease in size and number

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4
Q

Define metaplasia

A

Cells change their morphology

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5
Q

Define hypoxia

A

not enough oxygen, often caused by ischaemia

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6
Q

Define anoxia

A

no oxygen

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7
Q

What is ischaemia?

A

lack of blood flow

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8
Q

What can cell injury be due to? (5)

A
  • insufficient oxygen availability
  • physical trauma
  • chemical agents
  • infectious organisms
  • exposure to radiation
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9
Q

What is the difference between exo-toxins and endo-toxins?

A

bacteria can produce toxins which are secreted by the cells, these are exo-toxins. The endo-toxins are toxins that are present inside the bacterial cell and is released when the cell disintegrates

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10
Q

What tissues have a high sensitivity to free radicals?

A

Bone marrow as it is high proliferating.

The uterus and pancreas have a low turnover so are not as sensitive

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11
Q

What does damage to the mitochondria cause?

A

oxidative phosphorylation is damaged so there is less ATP causing:

  • the sodium pump is reduced causing an influx of calcium, water and sodium into the cell and increase efflux of potassium –> osmotic gain of water, and acute cellular swelling
  • anaerobic glycolysis increases to generate ATP from glycogen, this lowers the pH due to the increased lactic acid
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12
Q

What is lethal cell death?

A

when cells are unable to achieve a new steady state following environmental insults
due to irrreversible breakdown of energy-dependent interactions between DNA, MEMBRANES AND ENZYMES

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13
Q

How does free radial toxicity damage cells?

A

some escape from the electron transport chain and damage important cellular processes or characteristics e.g. cell membrane. They can react with molecules to produce more free radicals

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14
Q

Which enzymes work together to diffuse oxygen based free radicals?

A

superoxide dismutase and catalse

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15
Q

How does an increase in calcium cause membrane defects?

A

it activates a number of enzymes: ATPases (causes atp depeletion), phospholipases (causes membrane damage), proteases (breakdown membrane and cytoskeletal problems) and endonucleases (DNA fragmentation)

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16
Q

What is necrosis?

A

cell death as a result of lethal cell injury

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17
Q

Is necrosis or apoptosis a passive process?

A

necrosis

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18
Q

How does necrosis incite an inflammatory reaction?

A

when the cells die they release small effector molecules that cause an inflammatory response

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19
Q

What are the 4 types of necrosis and what tissues do they affect?

A

Coagulative: most sorts of solid tissue except brain

caseous: tuberculosis (tissues loses all structure and looks like cottage cheese)
colliquative: brain
fat: the fat become necrotic when it is traumatized, free chain fatty acids are released when the fat breaks down which chelates calcium

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20
Q

What replaces the necrosis tissue in the brain?

A

due to the lack of collagen in the brain it liquidifies and causes a cyst

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21
Q

What necrosis is a sub-group of coagulative?

A

gangrene: there are two types wet and dry

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22
Q

What is apoptosis?

A

programmed cell death, if there is DNA/protein damage the body will stimulate apoptosis

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23
Q

How does chemo/radioherapy work?

A

agents stimulate apoptosis through DNA

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24
Q

How do tumours affect apoptosis?

A

they knock off p53 which allows the cells to recognise it has damage (also affcets bl-2)

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25
Q

What is a neutrophil polymorph?

A

neutophils that have lobed nuclei and granualar cytoplasm and function as phagocytes

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26
Q

What is an inflammatory exudate?

A

a fluid that filters from the circulatory system into lesions or areas of inflammation

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27
Q

What are inflammatory mediators?

A

molecules that are released by immune cells during times when harmful agents invade our body

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28
Q

What is endothelium?

A

the tissue which forms a single layer of cells lining various organs and cavities of our body, it is formed from embryonic mesoderm

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29
Q

What is resolution?

A

The arrest of an inflammatory process without suppuration: the absorption or breaking down and removal of the products of infloammation

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30
Q

What is fibrosis?

A

the thickening and scarring of connective tissue, usually as a result of injury

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31
Q

What is suppuration?

A

the formation or discharge of pus

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32
Q

What is an abcess?

A

a swollen area within body tissue, containing pus

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33
Q

What is pyogenic?

A

pus producing

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34
Q

What are the 4 cardinal features of inflammation?

A

heat (calor), redness (rubor), pain (dolor), swelling (tumor)

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35
Q

Name 4 types of inflammation?

A

serous: outpouring of serous fluid
fibrinous: formation of fibrin
prulent: formation of pus
psuedomembranosus:

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36
Q

What is the vascular reaction to acute inflammation?

A

dilatation

initially the flow increases then decreases due to increased permeability

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37
Q

What mediates the increased permeability in the vascular reaction?

A

histamine, bradykinin, NO, leukotriene B4 and complement components

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38
Q

How does the exudative reaction defeat the initial cause of inflammation?

A

the exudate is constantly turning over so it tends to diltue the noxius agents and it transports clumps of them to lymph nodes, it also increases the supply of oxygen and nutrients

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39
Q

Why does the endothelium become protein rich?

A

it become leaky so immunoglobins and fibrinogen leak out

40
Q

What ways can you quantitate how severe the process of acute inflammation is?

A

measuring pyrexia and acute phase reaction proteins

41
Q

What acute phase reaction proteins are usually measured?

A

C-reactive protein (produced in the liver), ESR (erythrocyte sedimentation rate) and plasma viscosity

42
Q

How do neutrophils phagocytose bacteria?

A

Oxygen dependent myeloperioxidase and oxygen independent (lysozyme, lactoferrin cationic proteins) mechanisms

43
Q

What do pattern recognition recepetors do?

A

recognize foreign cells, just recognises a pthogen, it can’t distinguish a type from another

44
Q

What are cytokines?

A

chemical messengers that the cells of the immune system use to tell each other what they should be doing, allows for communication

45
Q

Name 5 pattern recognition receptors

A 
toll-like receptors (TLR)
NOD-like receptors (ɴʟʀ) 
rigl-like receptos (ʀʟʀ)
C-type lectins (Clr)
scavenger receptors
46
Q

Which receptor recognises
a) ʟps
B) Flagellin

A

a) toll-like receptor 4

b) Tlr5

47
Q

how does complement interact with the pathogenʔ

A
  • it induces the inflammatory response
  • binding of the anitbody with the complement at the surface of the pathogen that produces very effective immune response (same mechanism that hypersensitivity reactions can occur)
48
Q

Which cytokines makes you feel unwell and is the first to be producedʔ

A

ɪʟ1- it incxreases coagulation, inflammation, acute phase proetins and fever

49
Q

What cells are the Prr onʔ

A

plasma

50
Q

What are the primary and secondary lymphoid organsʔ

A

primaryː bone marrow and thymus (lymphocyte development and selection.
secondaryː spleen, lymph nodes, mucosal surfaces (where the immune response takes place)

51
Q

how are B and T cells receptors codedʔ

A

they are coded by genes that are fragmented that can be combined to produce specificity

52
Q 
What human leucocyte antigens does MʜC class 1 molecules displayʔ
And to what kind of T cellsʔ
A

ʜʟa-a
ʜʟa-b
ʜʟa-C
cytotoxic T cells

53
Q 
What human leucocyte antigens does MʜC class 2 molecules displayʔ
And to what kind of T cellsʔ
A

ʜʟa-dp
ʜʟa-dq
ʜʟa-dʀ
helper T cells

54
Q

What is immunosuppressionʔ

A

a natural or artificial process which turns off the immune system, partially or fully, accidentally or on purpose

55
Q

What is immunodeficiencyʔ

A

the lack of an efficient immune system- susceptibility to infection

56
Q

if you have a lack of or damage to neutrophils or macrophages, what infections are you more susceptible toʔ

A

staphylococcus aureus, salmonella, aspergillus

ones that are killed off using macrophages etc/.

57
Q

if you have damage to or lack of Prr what infections are you more susceptible toʔ

A

pneumococcus or hSV

58
Q

What are you more susceptible to if you have a problem with complementʔ

A

neisseria meningitis

59
Q

What does a lack of B cell make you more susceptible toʔ

A

recurrent pulmonary problems/infections mainly

60
Q

What is hypersensitvityʔ

A

undesirable, damaging, discomfort-producing and sometimes fatal reactions produced by the normal immune system (directed against innocuous antigens) in a pre-sensitized (immune) host
includes allergy and utoimmunity

61
Q

What are the 4 types of hypersensitivity reactionʔ

A

type 1ː ɪgE mediated reaction
ʇype 2ː cytotoxic reaction
type 3ː immune complex reaction
type 4ː cell mediated reaction (DTh)

62
Q

What is the allergic/anapylactic responseʔ

A

igE Ab mediated mast cell and degranulation- release of inflammatory mediators

63
Q

What occurs in an inflammatory responseʔ

A

hypotension, bronchospasm, mucous glands produce alot of secretions, diarrhoea

64
Q

What are the pre-formed mediators that are released during degranulation as part of the intial response after the allergen binds to the mast cell (cell filled with basophil granules)ʔ

A

histamine (stimulation of irratant nerve receptors, smooth muscle contraction and increase in vascular permeability)
kallikrein (activates bradykinin)
tryptase E

65
Q

What are the end products from the late-phase reaction of an allergic responseʔ lipid mediators

A

leukotrienes and prostoglandins

they are arachidionic acid derivatives

66
Q

name 4 examples of an allergic response

A

astham
rhinitis
dermatitis
food allergy

67
Q

What occurs during a type 2 hypersensitivity reactionʔ

A

antibodies produced by the immune response bind to antigens on the patient’s own cell surfaces.
These cells are recognized by macrophages or dendritic cells, which act as antigen-presenting cells. This causes a B cell response, wherein antibodies are produced against the foreign antigen.

68
Q

how is the complement pathway initiated in type 2 hypersensitivity reactionsʔ

A

IgG and IgM antibodies bind to these antigens to form complexes that activate the classical pathway of complement activation to eliminate cells presenting foreign antigens. e.g. if penicillin were to bind to rBC then the rbc would be destroyed

69
Q

What are type 3 hypersensitivity reactionsʔ

A

overproduction of immunoglobulin G (IgG) and IgM to a foreign or self‐antigen can lead to the formation and deposition of excessive amounts of insoluble intermediate‐sized immune complexes, which can be difficult to remove from various tissues by phagocytosis. This in turn may trigger classical complement activation, leading to overproduction of other inflammatory mediators

70
Q

What is the end consequence of type 3 hypersensitivity reactionsʔ

A

tissue damage (vasculitis) due to attempted phagocytosis of complexes causing the release of enzymes and free radicals

71
Q

name a condition that is an example of type 3 hypersensitivity reaction

A

systemic lupus erythematosus

72
Q

What hypersensitivity reaction is T cell mediated and give examples?

A

type 4. Examples: contact dermatitis (nickel, poison ivy), mantoux test, multiple sclerosis

73
Q

What type of hypersensitivity reaction is graves disease and myasthenia gravis a part of?

A

type V (can also be classed as being in type II) Instead of binding to cell surface s, the antibodies recognise and bind to the cell surface receptors, which either prevents the intended ligand binding with the receptor or mimics the effects of the ligand, thus impairing cell signaling.

74
Q

What are granulomas?

A

masses of immune cells that form at sites of infection or inflammation

75
Q

What is CGD?

A

chronic granulomatous disease
This is when phagocytes are unable to kill some types of bacteria and fungi. This disorder leads to long-term (chronic) and repeated (recurrent) infections.
it is sex-linked

76
Q

What is granulation tissue?

A

an important component of healing and compromises of small blood vessel in a connective tissue matric with myofibroblasts

77
Q

What are monocytes?

A

newly formed cells of the mononucelar system

78
Q

What are macrophages?

A

monocytes which have entered tissue (after being in the blood) and then undergo further differentiation in macrophages. Kupffer cells ad histocytes are examples

79
Q

What does caseating mean?

A

necrosis with conversion of damaged tissue into a soft substance

80
Q

What are fibroblasts?

A

type of cell that synthesizes the extracellular matrix and collagen and plays a cricial role in wound healing. They are the most common cells of connective tissue in animals

81
Q

What are the dominant cells in chronic inflammation?

A

lymphocytes (b and t cells), plasma cells and macrophages

82
Q

What can result in primary chronic inflammation (5)?

A
  • some infection - TB, leprosy
  • endogenous tissue
  • exogenous material
  • some autoimmune diseases e.g. rheumatoid arthritis, SLE, pernicious anaemia
  • primary granulomatous diseases e.g. crohn’s, sarcoidosis
83
Q

What is pernicious anaemia?

A

auto-antibodies to intinsic factor and gastric parietal cells leads to no B12 absorption causing anaemia

84
Q

What is sarcoidosis?

A

granulomas collecting in organs, often lungs and lymph nodes, viewed as an immune response to an infection usually

85
Q

What is the most common acute inflammation that can become chronic inflammation?

A

supportive (pus forming)

86
Q

How does acute inflammation become chronic inflammation?

A

If the pus forms as abscess cavity that is deep seated, and drainage is delayed or inadequate, then by the time the drainage occurs the abscess will have developed thick walls composed of granulation and fibrous tissues
The rigid walls of the abscess cavity will therefore fail to come together after drainage, and the stagnating pus within the cavity becomes organised by the ingrowth of granulation tissue, eventually to be replaced by a fibrous scar
Recurrent cycles of acute inflammation and healing can lead to chronic

87
Q

Name an example of acute becoming chronic inflammation

A

cholecystitis (gall bladder inflammation)
This is usually due to gall stones. Multiple episodes of acute inflammation can lead to the replacements of the gall bladder by fibrous tissue and the predominant cell type becomes the lymphocyte rather than the neutrophil polymorph

88
Q

What are 5 macroscopic appearances of chronic inflammation?

A
  1. chronic ulcer
  2. chronic abscess cavity
    3 thickening of the wall of a hollow viscus (singular of viscera- organs in abdo) by fibrous tissue in the presence of a chronic inflammatory cell infiltrate
  3. granulomatous inflammation changes
  4. fibrosis
89
Q

What are microscopic features of chronic inflammation?

A

the cellular infiltrate consists of lymphocytes, plasma cells and macrophages.
Exudation of fluid is not a prominent feature
there may be production of new fibrous tissue rom granulation tissue

90
Q

What does histamine do and where does it come from?

A

increases permeability of blood vessels to white blood cells and proteins. they are from mast cells

91
Q

What are Polymorphonuclear leukocytes?

A

granulocytes.
Types include neutrophils, basophils, eosinophils, mast cells
produced in bone marrow

92
Q

What do macrophages induce and what are they stimulated by?

A

induce: angiogenesis (development of blood vessels in embryo), cells to re-epthelialise the wound and create granulation tissue, angiogenesis factors for bood vessel formation in granulation tissue

93
Q

What do macrophages do if they cannot kill myocabacterium?

A

hold and contain viable organsisms

they are long lived

94
Q

What is granulation tissue?

A

new connective tissue and blood vessels that form on the surface of a wound during healing. consists of connective tissue cells and ingrowing young cells, it ultimately forms cicatrix

95
Q

What is fibrosis?

A

formation of excess fibrousw connective tissue during repair of damaged tissue. it is called fibroma if arises from 1 cell line

96
Q

What is a granuloma?

A

aggregate (nodule) of epithelioid histiocytes (macrophages when they are in cells) and other cells; lymphocytes and histiocytic giant cells

97
Q

Name examples of granulmatous disease arising from these different causes:

a) bacterial
b) parasitic
c) fungal
d) synthetic material
e) unkown

A

a) TB, leprosy
b) schistomiasis
c) cyrtococcal in immunocompromised
d) scilicosis
e) sarcoidosis, Crohn’s

Year 2 EMS (5 decks)

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