Case 1 Unveil Independent Learning Flashcards

1
Q

What do NSAIDs do

A

Inhibit PGHS-2 dervied prostaglandins (e.g. PGE2) which reduces the extend and duration of local inflammation caused by vasodilation and increased vascular permeability

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2
Q

What two effects do NSAIDs have

A

Analgesic and anti-pyretic

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3
Q

What does analgesic mean

A

Decrease in pain and swelling

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4
Q

What does anti-pyretic mean

A

Decrease in temperature

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5
Q

How do NSAIDs exert their anti-pyretic property

A

NSAIDs inhibit hypothalamic PGHS-2 which normally generates PGE2 in response to circulating pyrogens. So by blocking PGE2 you stop pyrexia

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6
Q

How do NSAIDs decrease pain and swelling

A

Largely due to PGH2. PGH2 supercharged the pain response

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7
Q

What is the full name form aspirin

A

Acetyl salicylic acid

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8
Q

What is the only irreversible inhibitor of PGHS-1 and PGHS-2

A

Aspirin

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9
Q

Describe the mechanism of action of aspirin

A

Acetylation of serine reside in the COX domain active site

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10
Q

What is the origin of aspirin

A

Willow tree bark containing salcin

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11
Q

Describe ibuprofen

A

It is produced as a racemate, the S-enantiomer is the active NSAID

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12
Q

Describe the mechanism of action of ibuprofen

A

It competes with AA for the COX domain site of PGHS-1 and PGHS-2. It is a reversible, competitive inhibitor

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13
Q

Describe the origin of ibuprofen

A

Derived from propanoic acid

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14
Q

Why may paracetamol be chosen over NSAIDs

A

It can have better analgesic and anti-pyretic effects

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15
Q

What is one thing paracetamol doesn’t do that NSAIDs do

A

Little anti-inflammatory activity

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16
Q

What is the mechanism of action of paracetamol

A

May affect peroxidase domain activity in PGHS-2 or PGHS-3 in the CNS or its metabolites may be having affects in the CNS>

17
Q

Describe the WHO pain ladder

A

Mild pain- paracetamol. Moderate pain- paracetamol/ weak opiods (codine). Strong pain- strong opiods (morphine/ heroine)

18
Q

What converts phospholipids to AA

A

Phospholipase A2

19
Q

Describe stage 1 of a bruise

A

Red bruise- fresh blood from capillaries, well oxygenated

20
Q

Describe stage 2 of a bruise

A

Blue bruise (around 24 hours later), oxygen is used up

21
Q

Describe stage 3 of a bruise

A

Purple bruise (2-4 days later) RBCs break down and release Hb

22
Q

Describe stage 4 of a bruise

A

Green bruise (5-7 days later) Hb broken down into verdin

23
Q

Describe stage 5 of a bruise

A

Yellow bruise (1-2 weeks later) verdin is converted to bilirubin

24
Q

Describe stage 6 of a bruise

A

(2-4 weeks later) pale discoloration of bruise

25
Describe the timescale of a wound healing
1. Haemostasis. 2. Inflammatory phase. 3. Proliferation and migration. 4. Maturation
26
Describe proliferation and migration
Granulation (in granulation tissue fibroblasts produce collagen and ECM, neutrophils and capillaries needed for angiogenesis). Contraction- wound can feel itchy (myofibroblasts) and epithelialisation
27
Why will the timescale on healing be shorter due to having stitches
1st intention rather than 2nd intention
28
Describe maturation
When the collagen is remodelled from type 3 to type 1, and small blood vessels decrease
29
Describe serous exudate
Exudate during inflammatory wound healing stages (excessive is a sign of high bioburden)
30
Describe sanguinous exudate
Fresh blood- indicator wound bed has undergone trauma such as dressing change, small amount is usual during inflammation
31
Describe purulent discharge
Milky/ green/ yellow colour and thick, indication of infection
32
What does discharge aid
Cells t migrate into the affected area e.g. WBCs
33
Describe a fibroclot
A scab which contains neutrophils and macrophages which secrete growth factor
34
What are neutrophils replaced by in the wound
After 48-96 hours neutrophils are replaced by macrophages as the predominant cells in the wound
35
What type of cut requires a suture
Secondary intention, wound 6.5mm deep or 20mm long