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Year 2 > Case 1 > Flashcards

Case 1 Flashcards

1
Q

Mast cells release..

A

Histamine

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2
Q

Factors responsible for angiogenesis:

A

VEGF
FGF-2
PDGF

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3
Q

First stage of wound healing

A

Inflammation

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4
Q

Role of macrophages in wound healing

A 
Removal of tissue debris
Angiogenesis
Antimicrobial
Chemotaxis
Proliferation of fibroblasts and keratinocytes 
Deposition and remodelling of ECM
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5
Q

During wound healing, neutrophils are replaced with macrophages after…

A

48-96hrs

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6
Q

First intention wound healing

A

Small scab consisting of: fibrin clot, neutrophils, and macrophages

Growth factor secreted which brings edges of wound together.

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7
Q

Sutures for first intention wound are removed after…

A

1 week

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8
Q

Second intention wound healing

A

Large scab consisting of: fibrin clot, neutrophils and macrophages.

More granulation tissue formed.

Wound edges brought together by contraction of myofibrils.

Increased risk of infection - requires regular cleaning.

Broader scar formed.

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9
Q

PGE2 and Pain

A

Sensitises A-delta and C nociceptive neurones to serotonin, substance P and Bradykinin
Stimulates chemotaxis.

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10
Q

How do pyrogens cause an increase in body temperature?

A

Cause hypothalamic PGHS2 to generate PGE2

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11
Q

MOA of Ibuprofen

A

Competitive reversible inhibition of COX1 domain of PGHS-1 and PGHS-2

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12
Q

MOA of aspirin

A

Acetylation of COX domain of PGHS. Causes irreversible inhibition.

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13
Q

Pathophysiological effects of PGHS-1

A

Chronic pain

Hypertension

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14
Q

Pathophysiological effects of PGHS-2

A

Inflammation

Chronic pain

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15
Q

Why does ibuprofen (and other NSAIDs) cause gastric ulceration?

A

Inhibition of COX domain of PGHS. Inhibits synthesis of prostaglandins which normally inhibit gastric secretion and protect the mucosa.

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16
Q

Primary Haemostasis

A

Exposed collagen causes activation of integrin receptors. Platelet aggregation to each other and the damaged vessel wall via integrins.
This requires Von Willibrand Factor.
Formation of a platelet plug which stops blood flow from minor wounds and provides a surface for strengthening reactions to occur on.

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17
Q

Extrinsic Pathway of Secondary Haemostasis

A

Tissue damage activates tissue factor III
TF III forms an active complex with VII (VIIa:III) - Ca2+ dependent
VIIa:III activates TF X (Xa)

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18
Q

Intrinsic pathway of Secondary Haemostasis

A

Damage to a vessel causes activation of TF XII (XIIa) - requires HMW-K and kallikrein.
XIIa converts prekallikrein to kallikrein (stimulating more XII activation)
XIIa also activates XI (XIa)
XIa activates IX (IXa)
IXa activates X (Xa)

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19
Q

Final Common pathway in Secondary Haemostasis

A

TF X was activated in extrinsic and intrinsic pathways.
Xa converts Prothombin to thrombin (requires Ca2+, Va and platelet surface)
Thrombin activates TF V and VIII (stimulating more thrombin production)
Thrombin converts fibrinogen to fibrin and activates XIII.
XIIIa stabilises fibrin resulting in clot formation

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20
Q

Haemophilia A

A

TF VIII deficiency

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21
Q

Haemophilia B

A

TF IX deficiency

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22
Q

Haemophilia C

A

TF XI deficiency

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23
Q

Von Willibrand’s Disease

A

I - little vWF
II - poor functioning vWF
III - no vWF

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24
Q

Thrombocytopathia

A

Reduction in platelets

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25
Q

Why does vitamin K deficiency affect the clotting cascade?

A

It is a component of thrombin

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26
Q

Why does vitamin C deficiency affect clotting?

A

Involved in collagen synthesis. Results in weakened blood vessel walls.

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27
Q

Classical Pathway of Complement system

A

Binding of IgM and IgG secreted by B-lymphocytes to the surface of an invading organism.
Resulting in activation of C3 convertase
C3 converted to C3a and C3b

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28
Q

Alternative Pathway of Complement System

A

Spontaneous formation of C3a and C3b

Accelerated at the surfaces of invading organisms.

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29
Q

Lectin Pathway of Complement System

A 
Mannose-binding lectin binds to mannose on bacterial cell walls. 
Activates MASP-1 and MASP-2 (proteases)
Cleavage of C2 and C4 
Generates C4b2a (C3 convertase)
C3 converted to C3a and C3b
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30
Q

Actions C3b

A

Stimulates phagocytes via opsonisation

Cell lysis

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31
Q

Shared action of C5a and C5b

A

Formation of membrane attack complex to cause cell lysis

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32
Q

Shared action of C3a and C5a

A

Proinflammatory

Induce release of inflammatory mediators from mast cells (Mast cell degranulation)

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33
Q

Spinothalamic tract crosses over in…

A

The medulla

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34
Q

How do neutrophils enter site of injury?

A

Histamine and interleukins released from mast cells due to C3a and C5a.
Histamine and interleukins cause cell adhesion molecules (selectins) to move to the apical surface.
Neutrophils adhere to capillary wall via selectins.
Margination - Neutrophils migrate to site of infection/injury between capillary endothelial cells.

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35
Q

Inflammation stage of wound healing:

A

Increased neutrophils at site.
TNF-alpha causes cell proliferation and differentiation and pyrogen stimulation.
Resulting in increased heat/fever.

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36
Q

Second stage of Wound Healing

A

Proliferation

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37
Q

Proliferation stage of wound healing

A

Increased macrophages at site of injury

VEGF causes angiogenesis

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38
Q

Third stage of wound healing

A

Remodelling

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39
Q

Remodelling stage of wound healing

A

Increased fibroblasts and endothelial cells at site of injury.
Increased IL10 causing B cell growth and inhibition of cytokine synthesis by T cells

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40
Q

IgA

A

Found during lactation in milk.

Monomer in blood, dimer when secreted.

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41
Q

IgD

A

Expressed when B cells leave primary lymphoid tissue and migrate to secondary.

42
Q

IgE

A

Facilitates inflammatory response. Combats worm infections.

43
Q

IgG

A

Most abundant antibody in plasma.

Ready made for foetus, able to cross placenta.

44
Q

IgM

A

First antibody produced during development and primary immune response.
Secreted by mature B cells.
Pentamer, joined by disulphide bonds.

45
Q

Langerhans Cells

A

Dendritic cells in skin

46
Q

T helper cells recognise…

A

MHC II

47
Q

Coreceptor for T helper cells

A

CD4

48
Q

MHC II are expressed by

A

Antigen Presenting Cells (APCs)

49
Q

MHC I are expressed by

A

All nucleated cells

50
Q

Cytotoxic T lymphocytes recognise

A

MHC I

51
Q

Coreceptor for cytotoxic T lymphocytes

A

CD8

52
Q

When a T helper cell binds to MHC II…

A

T helper cell becomes activated, proliferates into a clone and released activated cytokines.
Enables invaded cell to kill microbe.

53
Q

When a cytotoxic T lymphocyte binds to MHC I…

A

CTL stimulates apoptosis of target cell
OR
Release of perforins, granulysin and granzymes, forming pores in target cell walls - cell lysis.

54
Q

Effects of TNF

A

Activation of leukocytes resulting in production of cytokines.
Proliferation of fibroblasts causing collagen synthesis.
Procoagulation
Systemic effects - fever. leukocytosis, low appetite, increased sleep

55
Q

Why are tendons over the surface of bones flat?

A

Prevents sublaxation (falling off)

56
Q

Why is it significant that tendons contain fibroblasts?

A

It means that they are not a passive tissue - they can respond to mechanical loading.
Fibroblasts produce extracellular matrix and increase collagen when necessary.

57
Q

What type of epithelium is the epidermis?

A

Keratinised, stratified squamous

58
Q

Layers of epidermis (4)

A 
Innermost to outermost:
Stratum basale 
Stratum spinosum 
Stratum granulosum 
(Stratum lucidum - thick skin only)
Stratum corneum
59
Q

Stratum Basale

A

Innermost layer of epidermis.

Proliferate and move gradually up to the top where they are shed.

60
Q

Stratum spinosum

A

Prickle cell layer of epidermis.

Cells anchored together by desmosomes, when cells shrink, desmosomes remain intact - therefore, cells appear prickly.

61
Q

Stratum granulosum

A

Granule cell layer of epidermis.
Nearer the outer surface of the skin - cells starting to lose their nuclei and organelles.
Cells contain a lipid rich secretion acting as a water sealant.

62
Q

Stratum lucidum

A

Layer of epidermis found only in thick skin.
Between corneum and granulosum.
Thin and transparent.

63
Q

Stratum Corneum

A

Outermost layer of epidermis. Filled with dead cells called squames. Packed with keratin.
Many layers of cells (10-20)

64
Q

Dermal Papillae

A

Assists with adhesion between dermal and epidermal layers.

Has a large surface area to allow it to nourish the avascular epidermis.

65
Q

Contents of Dermis

A

Nerves (thermoregulation and sensation)
Blood supply (thermoregulation)
Collagen, elastin and fibroblasts (protect)
Sweat glands (thermoregulation)
Macrophages (protection)
Adipocytes (thermoregulation and protection)

66
Q

Contents of superficial Dermis layer of skin:

A

Loose connective tissue,
Many capillaries,
Meissner’s Corpuscles - senstitive to touch and temperature

67
Q

Contents of deep dermis layer of skin:

A 
Irregular connective tissue containing collagen and elastin (strength and extensibility)
Fibroblasts
Macrophages 
Adipocytes 
Sweat glands
68
Q

How is the hypodermis layer of the skin adapted to its function?

A

Contains adipose tissue - for vitamin D and triglyceride synthesis.
Sweat glands - regulation of temperature

69
Q

Thermoregulation via the skin.

A

Sweat glands

Superficial cutaneous plexus (reduced blood supply when cold)

70
Q

How are tendons adapted to their function?

A

Make muscle contraction more economical - prevent fatigue
Enable muscle belly to be distant from site of action - reduced bulk.
Can pass through narrow spaces e.g. cubital fossa

71
Q

Weakest part of a tendon

A

Myotendinous junction

Surface is invaginated to increase surface area and maximise strength.

72
Q

Strongest type of cartilage

A

Fibrocartilage - alternating layers of hyaline cartilage matrix and thick layers of dense collagen fibres.

73
Q

Function of ligaments:

A

Limit allowable movements and prohibit unwanted movements.
Proprioception - contain mechanoreceptors
Hold tendons in place i.e. retinaculae in fingers, wrist and ankles

74
Q

Function of bone

A

Protection and support
Assists movement
Mineral homeostasis - stores calcium and phosphorus
Blood cell production - takes place in bone marrow

75
Q

A delta nociceptive

A

High threshold mechanical receptor - respond to intense mechanical stimulus.

Thinly myelinated.

Responsible for first, sharp, well-localised pain

76
Q

C nociceptive fibres

A

Respond to intense mechanical stimulation, temperatures >42C and irritant chemicals.

Unmyelinated axon

Responsible for slow, later-onset, poorly localised pain.

77
Q

How does substance P result in perception of moderate to severe pain?

A

Accumulates in dorsal horn

78
Q

Role of substance P and CGRP release in pain response

A

Substance P: mast cells release histamine = vasodilation, 5-HT release activates nociceptors

CGRP also causes vasodilation

79
Q

Hyperalgesia

A

Histamine, prostaglandins and bradykinin increase sensitivity of nociceptive sensory endings.

80
Q

Mechanism for allodynia (pain response to non painful stimuli)

A

Chronic/prolonged activation of nociceptors.
Build up of substance P in dorsal horn.
‘Wind up’ - progressive increase in neuronal responsiveness.
Results in low threshold mechanoreceptors generating the sensation of pain.

81
Q

Gate theory of pain

A

Spinothalamic neurons are contacted by nociceptive and touch sensitive fibres.
Activation of low threshold mechanoreceptors (e.g. rubbing area), activates the interneuron which inhibits the pain pathway

82
Q

How do endorphins and encephalins control pain?

A

Inhibit substance P release

Suppress activity in spinothalamic neurons

83
Q

How does emotional state affect pain perception?

A

Serotonin containing neurons in brainstem descend down into dorsal horn.
Act on GABAergic neurons to block pain pathways.

84
Q

Pathway responsible for visceral pain

A

Spinoreticular (to reticular formation in the brainstem)

85
Q

Somatisation

A

Pain as a result of stress

86
Q

Where do nociceptive inputs enter the spinal cord?

A

Substantia gelatinosa

87
Q

Periaqueductal gray

A

Functions in pain modulation. Contains enkephalin producing cells.

88
Q

Apoptosis

A

Programmed cell death.
Involved shrinking of cells which then split up into droplets.
Has a ‘starry sky’ appearance.

89
Q

Necrosis

A

Degradation and loss of cell membranes.

Contents of cells accumulates and cells die.

90
Q

Chemotaxis

A

Recruitment and activation of inflammatory cells

91
Q

Inflammatory cells involved in acute inflammation

A

Neutrophils
Platelets
Mast cells

92
Q

Inflammatory cells involved in chronic inflammation

A

Macrophages
Lymphocytes
Plasma cells

93
Q

Why does scarring not occur in foetuses?

A

Skin is rich in metalloproteinases.

Skin will re-epithelialise rapidly.

94
Q

Phospholipase A2

A

Cleaves fatty acids from cell membrane phospholipids. Generates arachidonic acid.

95
Q

MOA of NSAIDs

A

Reversible nhibition COX domain of PGHS-1 and PGHS-2

96
Q

MOA of paracetamol

A

Unknown.
May affect peroxidase domain activity of PGHS-1 or 3 in CNS.
Or its metabolites may have some effects in CNS.

97
Q

Why do NSAIDs cause compromised renal function?

A

Inhibit synthesis of PGI2, PGE2 and prostacyclins which are involved in maintaining renal blood flow.

98
Q

Reye’s Syndrome

A

Caused by treatment of under 16s with aspirin.
Initial signs: Rash on palms and feet, heavy vomiting, lethargy, confusion, nightmares, pyrexia and headaches.

Can lead to deep comas, seizures, organ failure, flacidity.

99
Q

Initial stage of bruising (contusion/ecchymosis)

A

Damaged capillary leaks into soft tissue beneath skin.

Accumulation of RED blood beneath skin.

100
Q

Stages of bruising

A

Immediately appears RED due to bleeding beneath skin.
Turns BLUE after 24hrs as swelling restricts O2 supply to damaged area.
2-4 days after bruising is PURPLE due to breakdown of RBCs, release of Hb.
5-7 days after, bruising appears GREEN as Hb is broken down into biliverdin.
1-2 weeks after, bruise is YELLOW as biliverdin is converted to bilirubin
2-4 weeks later, pale discolouration of bruise.

101
Q

Cells responsible for colour changes in contusions/bruising.

A

Macrophages - phagocytosis of RBC debris

102
Q

Signs of thrombocytopenia

A

Platelet deficiency

Petechiae - spontaneous tiny haemorrhages in the skin and mucous membranes.
Severe bruising

Year 2 (17 decks)

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