Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Year 2 > Case 1 > Flashcards

Case 1 Flashcards

(102 cards)

Start Studying
1
Q

Mast cells release..

A

Histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Factors responsible for angiogenesis:

A

VEGF
FGF-2
PDGF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

First stage of wound healing

A

Inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

During wound healing, neutrophils are replaced with macrophages after…

A

48-96hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Sutures for first intention wound are removed after…

A

1 week

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

PGE2 and Pain

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do pyrogens cause an increase in body temperature?

A

Cause hypothalamic PGHS2 to generate PGE2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

MOA of Ibuprofen

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

MOA of aspirin

A

Acetylation of COX domain of PGHS. Causes irreversible inhibition.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pathophysiological effects of PGHS-1

A

Chronic pain

Hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Pathophysiological effects of PGHS-2

A

Inflammation

Chronic pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Haemophilia A

A

TF VIII deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Haemophilia B

A

TF IX deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Haemophilia C

A

TF XI deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Von Willibrand’s Disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Thrombocytopathia

A

Reduction in platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Why does vitamin K deficiency affect the clotting cascade?
It is a component of thrombin
26
Why does vitamin C deficiency affect clotting?
Involved in collagen synthesis. Results in weakened blood vessel walls.
27
Classical Pathway of Complement system
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
28
Alternative Pathway of Complement System
Spontaneous formation of C3a and C3b | Accelerated at the surfaces of invading organisms.
29
Lectin Pathway of Complement System
``` 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 ```
30
Actions C3b
Stimulates phagocytes via opsonisation | Cell lysis
31
Shared action of C5a and C5b
Formation of membrane attack complex to cause cell lysis
32
Shared action of C3a and C5a
Proinflammatory | Induce release of inflammatory mediators from mast cells (Mast cell degranulation)
33
Spinothalamic tract crosses over in...
The medulla
34
How do neutrophils enter site of injury?
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.
35
Inflammation stage of wound healing:
Increased neutrophils at site. TNF-alpha causes cell proliferation and differentiation and pyrogen stimulation. Resulting in increased heat/fever.
36
Second stage of Wound Healing
Proliferation
37
Proliferation stage of wound healing
Increased macrophages at site of injury | VEGF causes angiogenesis
38
Third stage of wound healing
Remodelling
39
Remodelling stage of wound healing
Increased fibroblasts and endothelial cells at site of injury. Increased IL10 causing B cell growth and inhibition of cytokine synthesis by T cells
40
IgA
Found during lactation in milk. | Monomer in blood, dimer when secreted.
41
IgD
Expressed when B cells leave primary lymphoid tissue and migrate to secondary.
42
IgE
Facilitates inflammatory response. Combats worm infections.
43
IgG
Most abundant antibody in plasma. | Ready made for foetus, able to cross placenta.
44
IgM
First antibody produced during development and primary immune response. Secreted by mature B cells. Pentamer, joined by disulphide bonds.
45
Langerhans Cells
Dendritic cells in skin
46
T helper cells recognise...
MHC II
47
Coreceptor for T helper cells
CD4
48
MHC II are expressed by
Antigen Presenting Cells (APCs)
49
MHC I are expressed by
All nucleated cells
50
Cytotoxic T lymphocytes recognise
MHC I
51
Coreceptor for cytotoxic T lymphocytes
CD8
52
When a T helper cell binds to MHC II...
T helper cell becomes activated, proliferates into a clone and released activated cytokines. Enables invaded cell to kill microbe.
53
When a cytotoxic T lymphocyte binds to MHC I...
CTL stimulates apoptosis of target cell OR Release of perforins, granulysin and granzymes, forming pores in target cell walls - cell lysis.
54
Effects of TNF
Activation of leukocytes resulting in production of cytokines. Proliferation of fibroblasts causing collagen synthesis. Procoagulation Systemic effects - fever. leukocytosis, low appetite, increased sleep
55
Why are tendons over the surface of bones flat?
Prevents sublaxation (falling off)
56
Why is it significant that tendons contain fibroblasts?
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
What type of epithelium is the epidermis?
Keratinised, stratified squamous
58
Layers of epidermis (4)
``` Innermost to outermost: Stratum basale Stratum spinosum Stratum granulosum (Stratum lucidum - thick skin only) Stratum corneum ```
59
Stratum Basale
Innermost layer of epidermis. | Proliferate and move gradually up to the top where they are shed.
60
Stratum spinosum
Prickle cell layer of epidermis. | Cells anchored together by desmosomes, when cells shrink, desmosomes remain intact - therefore, cells appear prickly.
61
Stratum granulosum
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
Stratum lucidum
Layer of epidermis found only in thick skin. Between corneum and granulosum. Thin and transparent.
63
Stratum Corneum
Outermost layer of epidermis. Filled with dead cells called squames. Packed with keratin. Many layers of cells (10-20)
64
Dermal Papillae
Assists with adhesion between dermal and epidermal layers. | Has a large surface area to allow it to nourish the avascular epidermis.
65
Contents of Dermis
Nerves (thermoregulation and sensation) Blood supply (thermoregulation) Collagen, elastin and fibroblasts (protect) Sweat glands (thermoregulation) Macrophages (protection) Adipocytes (thermoregulation and protection)
66
Contents of superficial Dermis layer of skin:
Loose connective tissue, Many capillaries, Meissner's Corpuscles - senstitive to touch and temperature
67
Contents of deep dermis layer of skin:
``` Irregular connective tissue containing collagen and elastin (strength and extensibility) Fibroblasts Macrophages Adipocytes Sweat glands ```
68
How is the hypodermis layer of the skin adapted to its function?
Contains adipose tissue - for vitamin D and triglyceride synthesis. Sweat glands - regulation of temperature
69
Thermoregulation via the skin.
Sweat glands | Superficial cutaneous plexus (reduced blood supply when cold)
70
How are tendons adapted to their function?
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
Weakest part of a tendon
Myotendinous junction Surface is invaginated to increase surface area and maximise strength.
72
Strongest type of cartilage
Fibrocartilage - alternating layers of hyaline cartilage matrix and thick layers of dense collagen fibres.
73
Function of ligaments:
Limit allowable movements and prohibit unwanted movements. Proprioception - contain mechanoreceptors Hold tendons in place i.e. retinaculae in fingers, wrist and ankles
74
Function of bone
Protection and support Assists movement Mineral homeostasis - stores calcium and phosphorus Blood cell production - takes place in bone marrow
75
A delta nociceptive
High threshold mechanical receptor - respond to intense mechanical stimulus. Thinly myelinated. Responsible for first, sharp, well-localised pain
76
C nociceptive fibres
Respond to intense mechanical stimulation, temperatures >42C and irritant chemicals. Unmyelinated axon Responsible for slow, later-onset, poorly localised pain.
77
How does substance P result in perception of moderate to severe pain?
Accumulates in dorsal horn
78
Role of substance P and CGRP release in pain response
Substance P: mast cells release histamine = vasodilation, 5-HT release activates nociceptors CGRP also causes vasodilation
79
Hyperalgesia
Histamine, prostaglandins and bradykinin increase sensitivity of nociceptive sensory endings.
80
Mechanism for allodynia (pain response to non painful stimuli)
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
Gate theory of pain
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
How do endorphins and encephalins control pain?
Inhibit substance P release | Suppress activity in spinothalamic neurons
83
How does emotional state affect pain perception?
Serotonin containing neurons in brainstem descend down into dorsal horn. Act on GABAergic neurons to block pain pathways.
84
Pathway responsible for visceral pain
Spinoreticular (to reticular formation in the brainstem)
85
Somatisation
Pain as a result of stress
86
Where do nociceptive inputs enter the spinal cord?
Substantia gelatinosa
87
Periaqueductal gray
Functions in pain modulation. Contains enkephalin producing cells.
88
Apoptosis
Programmed cell death. Involved shrinking of cells which then split up into droplets. Has a 'starry sky' appearance.
89
Necrosis
Degradation and loss of cell membranes. | Contents of cells accumulates and cells die.
90
Chemotaxis
Recruitment and activation of inflammatory cells
91
Inflammatory cells involved in acute inflammation
Neutrophils Platelets Mast cells
92
Inflammatory cells involved in chronic inflammation
Macrophages Lymphocytes Plasma cells
93
Why does scarring not occur in foetuses?
Skin is rich in metalloproteinases. | Skin will re-epithelialise rapidly.
94
Phospholipase A2
Cleaves fatty acids from cell membrane phospholipids. Generates arachidonic acid.
95
MOA of NSAIDs
Reversible nhibition COX domain of PGHS-1 and PGHS-2
96
MOA of paracetamol
Unknown. May affect peroxidase domain activity of PGHS-1 or 3 in CNS. Or its metabolites may have some effects in CNS.
97
Why do NSAIDs cause compromised renal function?
Inhibit synthesis of PGI2, PGE2 and prostacyclins which are involved in maintaining renal blood flow.
98
Reye's Syndrome
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
Initial stage of bruising (contusion/ecchymosis)
Damaged capillary leaks into soft tissue beneath skin. | Accumulation of RED blood beneath skin.
100
Stages of bruising
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
Cells responsible for colour changes in contusions/bruising.
Macrophages - phagocytosis of RBC debris
102
Signs of thrombocytopenia
Platelet deficiency Petechiae - spontaneous tiny haemorrhages in the skin and mucous membranes. Severe bruising

Year 2 (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions