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
Q

Describe the timescale of a wound healing

A
  1. Haemostasis. 2. Inflammatory phase. 3. Proliferation and migration. 4. Maturation
26
Q

Describe proliferation and migration

A

Granulation (in granulation tissue fibroblasts produce collagen and ECM, neutrophils and capillaries needed for angiogenesis). Contraction- wound can feel itchy (myofibroblasts) and epithelialisation

27
Q

Why will the timescale on healing be shorter due to having stitches

A

1st intention rather than 2nd intention

28
Q

Describe maturation

A

When the collagen is remodelled from type 3 to type 1, and small blood vessels decrease

29
Q

Describe serous exudate

A

Exudate during inflammatory wound healing stages (excessive is a sign of high bioburden)

30
Q

Describe sanguinous exudate

A

Fresh blood- indicator wound bed has undergone trauma such as dressing change, small amount is usual during inflammation

31
Q

Describe purulent discharge

A

Milky/ green/ yellow colour and thick, indication of infection

32
Q

What does discharge aid

A

Cells t migrate into the affected area e.g. WBCs

33
Q

Describe a fibroclot

A

A scab which contains neutrophils and macrophages which secrete growth factor

34
Q

What are neutrophils replaced by in the wound

A

After 48-96 hours neutrophils are replaced by macrophages as the predominant cells in the wound

35
Q

What type of cut requires a suture

A

Secondary intention, wound 6.5mm deep or 20mm long