Peri-op pharmacology Flashcards

1
Q

What level ASA status are most patients at?

A

1/2/3

  • 1 - A normal healthy patient
  • 2 - Patient with mild systemic disease
  • 3 - Patient with severe systemic disease
  • 4 - Severe systemic disease, constant threat to life
  • 5 - Moribund patient, not expected to survive over 24 hours with/without surgery
  • 6 - Declared brain dead, organ retrieval
  • add “E” in emergency(except 6)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What drug is the only one that is white?

A

propofol

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

What happens in order to pre-optimise a patient for surgery?

A
admit to a specialised unit (HDU/POSU)
Invasive BP monitoring
Urinary catheter
Central venous access
Ionitropic support
Cardiac output monitoring
Maximise O2 delivery peri-op to supra-normal levels
Surgery school for 'less fit' patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 3 things done pre-operatively?

A

Oxygen, fluids, drugs

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

What drugs are given pre-operatively?

A

Antacids, antiemetics, analgesia, sedatives

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What drugs are important to OMIT pre-surgery?

A

Ace-inhibitors (-prils) 24-72 hrs
Angiotensin receptor antagonists (-sartans) 24-72 hrs
Anti-TNF drugs (2 weeks)
Platlet inhibitors - aspirin, clopidogrel, prasugrel (7-10 days)
DOACS dabiggatran (4days, possible reversal with praxbind)
Rivaroxiban, apixiban, edixoban (3days)
NSAIDS (bar paracoxib which can be given IV)

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

What NSAID can be given IV peri-operatively

A

parecoxib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do NSAIDs work

A

COX-2 inhibitor -> reduce production of prostaglandins, prostacyclin and thromboxanes by inhibiting formation of these from arachidonic acid.

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

What do prostaglandins do?

A

Inflammatory response, temperature regulation, renal blood flow, gastric protection

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

What does prostacyclin do?

A

Vasodilator, inhibits platelet aggregation, prevents coagulation in normal blood vessels

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

What do thromboxanes do?

A

vasoconstriction, causes platelet aggregation, released at site of injury

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

What are the gastric adverse effects of NSAIDS and theory behind this?

A
  • ↓ mucosal protection
  • ↑ gastric acid secretion
  • May lead to peptic ulceration

Prophylaxis with omeprazole/misoprostol

Action
• High index suspicion
• NSAIDs should NOT be given to patients with a history of GI ulceration or bleeding

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

What synthetic prostaglandin prevents GI toxicity of NSAIDS

A

misoprostol

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

What is the difference between COX 1 and COX 2

A

1= constitutive form, present in tissues, inhibition leads to GI side effects

2= inducible form, present at sites of inflammation, inhibition responsible for anti-inflammatory action on NSAIDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What COX-2 inhibitor is commonly used peri-operatively?

A

parecoxib (dynastat 40mg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the coagulation SE of NSAIDS and theory behind this?

A
  • reduced production of thromboxane
  • NSAIDs increase bleeding time
  • displace warfarin increasing the effect

Action: do NOT use if risk of intra-operative bleeding

17
Q

What are the respiratory SE of NSAIDS and theory behind this?

A
  • can precipitate acute asthma
  • associated with chronic rhinitis and nasal polyps

Action: do NOT use in aspirin-sensitive asthma, and use w/ caution in other asthmatics

18
Q

What are the renal SE of NSAIDS and theory behind this?

A
  • normal renal blood flow = little prostaglandin release. Prostaglandin’s release when renal blood flow is low. causes compensatory vasodilation
  • NSAIDs cause renal failure if given during blood loss or hypotension, precipitate fluid retention, lead to hyperkalaemia
19
Q

How do NSAIDs lead to hyperkalaemia?

A

renal blood flow reduced - vasoconstrictors are released (noradrenalin, angiotensin) -> prostaglandins are released (compensatory vasodilatation) ->precipitate fluid retention (exacerbate heart failure)
NSAIDs indirectly supress renin and aldosterone secretion -> hyperkalaemia

20
Q

When must you avoid giving NSAIDs

A
renal impairment
hyperkalaemia
hypovolaemmia
circulatory failure
sever liver dysfunction
pre-eclampsia/eclampsia
21
Q

When should you use NSAIDs cautiously?

A

> 65yrs
diabetes
arteriopathy
cardiac/hepatobiliary/ major vascular surgery

22
Q

What things are given intraoperatively?

A
Oxygen
fluids
blood/blood products
antibiotics
anaesthesia
analgesia
muscle relaxation
23
Q

What drug puts people to sleep ?

A

IV Propofol

24
Q

How is the patient kept asleep?

A

Inhalated desflurane

25
Q

Advantage and Disadvantage of desflurane ?

A

Ad = rapid recovery, particularly in obese pt; reduces cognitive dysfunction post-op

Disad= big globe warming potential

26
Q

What drug can be used to support a pt’s circulation

A

ketamine - used if pt is hypotensive (as propofol reduces BP further) - but more of a continuum the level to use

27
Q

What site to anaesthetic agents work at

A

type A GABA receptors - binding opens transmembrane channel and enhances chloride activity

AND ascending reticular activating system - reduces cerebral cortical activity

28
Q

What is used for muscle relaxation? depolarising and non-depolarising

A

Depolarising: suxamethonium

non-depolarising: atracurium and rocuronium

29
Q

Use and action of suxamethonium

A

Muscle fasciculate and the remain paralysed for 3 minutes to get in airway then it is broken down by acetyl-cholinesterase in the neuromuscular junction

30
Q

What is a rapid-sequence induction and when does it happen?

A

Presumed full stomach case. (And pregnancy)
Pre-oxygenate pt for 5 minutes, de-nitrogenate, sleep dose of propofol. Given 1mg/kg of suxamethonium, paralysed. O2 off. laryngoscope in, endotracheal tube, blow cuff up and lungs are isolated from gastric content -> can’t aspirate.
Not done in elective surgery as pt is starved.

31
Q

How does atracurium and rocuronium work?

A

competetive block - builds up in 3-4mins, paralysed for 20mins. can reflux and aspirate - hence only used in elective when starved

32
Q

What drug can reverse neuromuscular block due to rocuronium

A

Suggammadex
- rescue reversal dose of 16mg/kg. Time to reversal 1.5mins.
Expensive so limited to emergency situations
- encapsulates steroid portion of amino steroid relaxant within hydrophobic interior

33
Q

What things are given post-operatively?

A
analgesia
fluids
blood products
inotropes/vasopressors
anti-emetics
anti-coaguants
antibiotics
oxygen
34
Q

What is a regional block

A

TAP (transverse abdominis plane)

35
Q

What are the advantages and complications with an epidural

A

Ad: avoids respiratory complications associated w/ pain and large amounts of systemic opioids, continuous infusion, patient-controlled form

Complications: hypotension, itching, epidural haematoma