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* Year 2 EMS > MOD week 2-4 > Flashcards

MOD week 2-4 Flashcards

1
Q

what is metaplasia?

A

the reversible replacement of one differentiated cell type with another mature differentiated cell type.

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2
Q

why does hypoxia causes cell lysis?

A

sodium-potassium pump stops working (as needs ATP)

–> more sodium diffuses into cell

–> water goes into cell by osmosis

–> cell swells –> lysis

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3
Q

what effect does UV light have on DNA?

A

causes thymine molecules which are next to each other to fuse together –> thymine dimer

normally: exonucleases cleave out thymine dimers and replace with original nucleotides

but if:
- replace with wrong nucleotides
OR
- don’t replace at all

–> when the DNA is replicated, it will be done incorrectly –> mutation –> cancer

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4
Q

what is involution?

A

the shrinkage of an organ in old age or when inactive (e.g. uterus post-menopause)

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5
Q

what effect does lead have in red blood cells?

A

blocks the synthesis of haemoglobin –> anaemia

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6
Q

what does cyanide do in the body?

A

blocks the electron transport chain –> no oxidative phosphorylation can occur and electron back up until no respiration can occur (even anaerobic as all cofactors are reduced) –> death

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7
Q

describe apoptosis

A

‘programmed cell death’ (signals cause death)

no harmful products released (so doesn’t damage adjacent cells)

takes energy

cell shrunken

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8
Q

describe necrosis

A

abnormal, unintended cell death in response to injury

causes release of harmful products (therefore there is damage to surrounding tissue) –> inflammation

does not expend energy

cell swollen

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9
Q

what is a FAS receptor?

A

‘death receptor’

a cell-surface receptor, which, if something binds to it, triggers the cell to go into apoptosis

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10
Q

what are caspases?

A

a group of enzymes which are active in apoptosis

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11
Q

what does the BCL-2 protein do in normal cells? what happens if it is over expressed?

A

a protein which inhibits apoptotic cell death

it is over expressed in follicular lymphoma –> cells accumulate

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12
Q

what are the 4 different types of necrosis?

A

coagulative

caseous

colliguative

gangrene

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13
Q

describe coagulative necrosis

A
  • most common form of necrosis
  • normally caused by hypoxia/ischaemia
  • dead tissue becomes firm + slightly swollen

ischaemia –> reduced ATP –> increased cytosolic Ca2+ and free radical formation –> membrane damage

(nb tissue shows retention of microscopic architecture)

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14
Q

describe colliquative necrosis

A
  • occurs in brain
  • neural tissue has little supporting tissue, thus liquifies upon cell death

“colLIQUative necrosis is LIQUid”

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15
Q

describe caseous necrosis

A
  • dead tissue lacks any structure
  • often seen in granulomatous inflammation (e.g. in TB)

“looks like cheese”

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16
Q

describe gangrene

A

Gangrenous necrosis can be considered a type of coagulative necrosis that resembles mummified tissue. It is characteristic of ischemia of lower limb and the gastrointestinal tracts. If superimposed infection of dead tissues occurs, then liquefactive necrosis ensues (wet gangrene)

(dry = without infection, wet = with infection)

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17
Q

what are the 5 physical characteristics of acute inflammation?

A 
redness (rubor)
heat (calor)
swelling (tumor)
pain (dolor)
loss of function
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18
Q

what is the characteristic cell found in acute inflammation?

A

neutrophil polymorph

stains neutral pink colour with lobed nucleus
(2-5 lobes)

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19
Q

what are the 5 causes of acute inflammation?

A

physical agents (e.g. trauma, frostbite, sunburn etc)

infections

hypersensitivity reactions

chemicals

tissue necrosis (get inflammation around necrosis)

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20
Q

what is exudate?

A

extravascular fluid with high protein concentration, contains cellular debris

implies inflammation

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21
Q

what is the difference between exudate and transudate? 4

A
  1. Exudate is cloudy while transudates are clear.
  2. Exudate is a result of inflammation and injury while transudate is brought about by imbalanced hydrostatic and osmotic pressure (e.g. in heart failure or kwashiorkor)
  3. An exudate has a higher protein content compared to a transudate.
  4. an exudate has higher cell/cell debris content compared to a transudate
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22
Q

what are the 3 major components of acute inflammation?

A
  • changes in vessel calibre
  • increased vascular permeability –> fluid exudate formation
  • cellular exudate formation
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23
Q

what changes in vessel calibre occur in acute inflammation? and what 2 things is this mediated by?

A

local vasodilation (initial transient vasoconstriction)

  • -> increased blood flow
  • -> heat + redness

mediated by histamine and NO on vascular smooth muscle

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24
Q

how is the fluid exudate formed in acute inflammation?

A

increased permeability of microvasculature results in escape of protein-rich fluid into tissue

caused by:

  • chemical mediators (e.g. histamine, NO, leukotriene)
  • direct vascular injury (eg in trauma)
  • endothelial injury - bacteria and toxins
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25
Q

what effects does the presence of fluid exudate have? 6

A

dilution of toxins

increased entry of antibiotics

increased transport of drugs to area

increased fibrin formation (acts as a scaffold for later granulation)

delivery of nutrients and oxygen

stimulation of the immune response

ie FLUID EXUDATE IS USEFUL!!

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26
Q

how does the cellular exudate form?

ie neutrophil emigration and accumulation

A

loss of fluid into tissues and increased calibre of vessels

  • -> slower blood flow + increased viscosity of blood
  • -> stasis

–> neutrophils line up along vascular endothelium, stick to endothelium + migrate through walls into tissues

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27
Q

what is the role of selectins in cellular exudate formation?

A

as the neutrophil rolls along the blood vessel wall, the selectin binds to certain carbohydrate groups presented on proteins on the neutrophil, which slows the cell and allows it to leave the blood vessel and enter the site of infection.

The low-affinity nature of selectins is what allows the characteristic ‘rolling’ action attributed to neutrophils before they exit the blood vessels

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28
Q

what are the 5 cell-derived mediators of acute inflammation?

A

histamine (vasodilator)

prostaglandins (vasodilator)

lysosomal components

leukotrines (produced by leukocytes)

cytokines

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29
Q

what common respiratory condition is associated with inappropriate leukotrines?

A

asthma

leukotrines trigger contractions in the smooth muscles lining the bronchioles; their overproduction is a major cause of inflammation in asthma

Leukotriene antagonists are used to treat asthma by inhibiting the production or activity of leukotrienes.

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30
Q

what are the 4 plasma-derived mediators of acute inflammation?

A

complement system

kinin system

coagulation system

fibrinolytic system

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31
Q

what is a kinin

A

family of polypeptides which induce vasodilation and contraction of smooth muscle

eg bradykinin

32
Q

what are the 4 systemic effects of acute inflammation?

A

pyrexia

lymph node enlargement

nausea, malaise, anorexia

leukocytosis (high white blood cell count)

33
Q

what is a non-specific marker of inflammation picked up in blood tests?

A

c-reactive protein (CRP)

34
Q

What happens is there is excessive exudate formed as a result of acute inflammation?

A

suppuration (aka formation of abscess, due to accumulation of pus) occurs

35
Q

what happens if there is excessive necrosis?

A

repair and organisation –> fibrosis

36
Q

what happens is the causal agent of acute inflammation persists?

A

develops into chronic inflammation –> fibrosis

37
Q

what is chemotaxis?

A

transportation of something (neutrophils, in case of acute inflammation) to correct place due to chemical stimulus

38
Q

what can acute epiglottitis cause?

A

respiratory distress

39
Q

what is diapedisis?

A

endothelial cells contract, so gaps form between them, so neutrophils can pass –> tissue

40
Q

how do you treat an abscess?

A

drain it

can’t use antibiotics as they can’t reach middle of abscess

41
Q

what 3 things does granulation tissue consist of?

A
  • lots of blood vessels
  • fibroblasts
  • white blood cells
42
Q

what are the three things that pus consists of?

A

living + dead neutrophils

bacteria

cell/tissue debris

43
Q

what part of the lung does TB normally occur in?

A

top of the lungs

44
Q

what’s another name for neutrophils?

A

polymorphic neutrocytes

45
Q

what are the 7 causes of cell injury?

A

hypoxia (most common)

physical agents (e.g. trauma)

chemical agents (incl. drugs + poisons)

infections

immune-mediated cell injury

genetic disorders

nutritional imbalances

46
Q

what is an area affected by coagulative necrosis called?

A

infarct

47
Q

what causes pain in acute inflammation? 3

A

release of mediators (e.g. histamine)

tissue damage by neutrophils

physical pressure on nerves from swelling

48
Q

what are the 4 possible outcomes of acute inflammation?

A

resolution

fibrosis

chronic inflammation

suppuration

49
Q

what is margination?

A

accumulation and adhesion of leukocytes to the epithelial cells of blood vessel walls at the site of injury in acute inflammation

50
Q

what are the 3 different types of selections and where do they originate from?

A

E-selectin (from endothelium)

P-selectin (from platelets + endothelium)

L-selectin (from leukocytes)

51
Q

what molecules allow for leukocytes to transmigrate out of blood vessels? (i.e. diapedesis)

A

up regulation of integrins (role is to attach cells to extracellular matrix)

52
Q

what do you call a reduction in the number of blood cells?

A

cytopenia

53
Q

what do you call an abnormal increase in the number of cells?

A

cytosis

54
Q

what do you call inflammation of the rectum?

A

proctitis

55
Q

what is the term used to describe secondary pathological conditions arising from a disease?

A

sequelae

56
Q

what are pattern recognition receptors (PRR)?

what part of the immune system are they a part of?

A

antigen recognition receptors

2 types:

  • cell surface+ intracellular recptors
  • fluid-phase soluble molecules

not specific - just tell immune system that there’s danger in the vicinity (is the fastest response)

innate system

57
Q

what does the PRR TLR4 recognise?

A

lipopolysaccharides

(ie on gram -ve bacteria)

it triggers cell to produce inflammatory cytokines

58
Q

what do the PRRs TLR7 and TLR9 recognise?

A

single-stranded DNA molecules

this indicates presence of virus
(cell produces cytokines in response)

nb TLR7+9 are intracellular

59
Q

name a large ‘family’ of fluid-phase recognition molecules

A

C-type lectin family

(eg collectins, such as mannan(aka mannose)-binding lectin + surfactant protein A + D)

  • they recognise microbial complex carbohydrates
  • then bind to them, via carbohydrate-recognition domains (CRDs)

roles:

  • neutralisation of pathogen
  • recruitment of adaptive response
60
Q

what do plasmacytoid dendritic cells (DCs) produce large amounts of?

what does this do?

A

interferon (IFN-)

antitumour + antiviral properties

61
Q

what do myeloid (aka interstitial) dendritic cells produce large amounts of?

A

interleukin 10 + 12

62
Q

what type of organism do eosinophils act against?

A

eosinophils

63
Q

what is the function of primary lymphoid organs?

what are the 2 found in humans?

A

lymphocyte development and selection

bone marrow (b cells)
thymus (t cells)
64
Q

what is the function of secondary lymphoid organs?

what are the 3 found in humans?

A

to produce an immune response

  • spleen
  • lymph nodes
  • mucosal surfaces
65
Q

what is the name of the process which results in such a great variety in t and b cell receptors being transcribed?

A

V(D)J recombination

66
Q

what is the mechanism of antigen presention on an APC?

A

antigen bind to specific innate (or B) cell receptor on cell membrane (basically an antibody embedded in membrane)

antigen is internalised (so signal is transmitted into cell)

antigen is broken down -> peptides

peptides are bound to newly-synthesised class 2 molecules + bought to cell surface

if peptide is foreign, it is recognised by helper T cells which are then activated

helper T cells produce cytokines needed by B cells, T cells, etc

67
Q

what are major histocompatibility complexes?

what are they also known as?

A

glycoproteins on cell surface membranes of cells

Human Leucocyte Antigens (HLAs)

(unique to each person but vary more the less you are related to a person, eg diff ethnic groups)

  • if endemic disease in an area people become more resistant as their HLAs adapt (via darwinian evolution)

diff HLAs are better at recognisisng diff diseases
- also play a role in certain autoimmune diseases (eg RA)

68
Q

what are the two types of MHC/HLAs?

what’s the difference?

A

class 1

  • found on ALL cells
  • presents peptides to cytotoxic T cells

class 2

  • found only on Antigen Presenting Cells
  • presents peptides to helper T cells
69
Q

what are the 4 ways in which the binding of antibodies to antigens inactivates said antigens?

A

1) neutralisation
2) agglutination of microbes
3) precipitation of dissolved antigens

1, 2 + 3 enhance phagocytosis by macrophages

4) activation of complement system

4 leads to cell lysis

70
Q

what is perforin produced by? and what does it do?

A

cytotoxic T cells

creates cores in infected host cells

The pores formed allow for the passive diffusion of a family of pro-apoptotic proteases, known as the granzymes, into the target cell -> apoptosis

71
Q

what is the difference between a basophil and a mast cell?

A

Mast cells are fixed in the tissues while basophils circulate in the blood

“MASTs are firmly FIXED onto boats”

72
Q

what is the function of mast cells/basophils?

A

regulation of vascular permability

(a protective response to pathogens)

allergic responses

73
Q

what is the definition of a hypersensitivity reaction?

A

undesirable, damaging, discomfort-producing and sometimes fatal reactions produced by the normal immune system (directed against INNOCUOUS ANTIGENS) in a PRE-SENSITISED (immune) host

74
Q

what are the 4 types of hypersensitivity reactions?

A

1 - IgE mediated

2 - cytotoxic

3 - immune complex

4 - cell-mediated

75
Q

describe type 1 hypersensitivity reaction

A

classic anaphylaxis + allergic reactions
(incl hayfever, allergic asthma)
(common antigens incl: pollen, bee venom etc)

  • happens fast (15-30mins)

sudden degranulation of mast cells + basophils
-> release of inflammatory mediators

FINISH TYPE 1!!!!

* Year 2 EMS (7 decks)

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