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MRCS > crit care > Flashcards

crit care Flashcards

1
Q

Causes of obstructive lung disease

A

Asthma
bronchiectasis COPD
bronchiolitis obliterans

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2
Q

Causes of restrictive lung disease

A

pulmonary fibrosis
kyphsclerosis
ARDS
neuromuscular causes

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3
Q

Spirometry findings in obstructive LD:
FEV1
FVC
FEV1/FVC

A

Reduction in FEV1>FVC
hence FEV1:FVC reduced <70%

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4
Q

Spirometry findings in RESTRICTIVE LD:
FEV1
FVC
FEV1/FVC

A

Reduction in FEV1<FVC
hence FEV1:FVC normal/ raised >70%

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5
Q

Anaesthetic agent that has both anaesthetic and analgesic properties but causes dissociative anaesthetic effect (hallucinations/ nightmares)

A

Ketamine

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6
Q

Anaesthetic agent causing the most and least myocardial depression

A

most= sodium thiopentone (squeezy)
least= Etomidate

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7
Q

Anaesthetic agent causing adrenal suppression

A

Etomidate

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8
Q

Anaesthetic agent that has anti-emetic properties

A

Propofol

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9
Q

Anaesthetic agent which is used in RSI

A

Sodium thiopentone (speedy)

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10
Q

Why are sodium thiopentone and etomidate unsuitable for maintaining sedation

A

ST= metabolites build up quickly
E= causes adrenal suppression even with brief use

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11
Q

Side effect of using Etomidate

A

PONV

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12
Q

Causes of neuropathic pain

A

damage to nervous system:

diabetic neuropathy
trigeminal neuralgia
post-herpetic neuralgia
prolapsed IV disc

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13
Q

First and second line mx of neuropathic pain

A

1= amitriptyline/ pregabalin
2= add amitriptyline/ pregabalin
3= refer to pain specialist, neurectomy

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14
Q

Mx of diabetic neuropathy

A

Duloxetine

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15
Q

Mx of trigeminal neuralgia

A

Carbamazepine

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16
Q

How much calories should be given to a non-severely ill patient with BMI<25

A

25-35kcal/kg/day

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17
Q

What is the daily requirement of protein

A

0.8-1.5g/kg/day

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18
Q

How much calories should be given to a severely ill patient

A

50% of 25-35kcal/kg/day in the first 24-48hrs

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19
Q

How many calories should be given to a patient at risk of refeeding syndrome

A

10kcal/kg/day

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20
Q

What other supplements should be given to those at risk of refeeding syndrome

A

Pre-feeding and during feeding:
Thiamine (200-300mg)
Vitamin B complex strong 1tab TDS

Potassium (2-4)
Magnesium (0.2-0.4)
Phosphate (0.3-0.6)

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21
Q

causes of refeeding syndrome

A

reduced intake:
eating disorders
chemo
vomiting
post-op
fasting
prolonged NBM

reduced absorption
chemo
IBD
short bowel syndrome
pancreatitis
cystic fibrosis

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22
Q

describe the pathophysiology of refeeding syndrome

A

prolonged reduced nutrients= reduced levels of body phosphate, K, Mg (serum levels normal)

Start eating= increase in glucose + insulin= rapid shift of phosphate, Mg, K into cells for use= decrease in serum phos, Mg, K levels= seizures, arrthymias

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23
Q

What are the types of muscles relaxants

A

(all end in -ium)

Suxamethonium
Atracurium
Vecuronium
Pancuronium

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24
Q

Which muscle relaxant causes generalised muscle contractions and why

A

Suxamethonium

Because it is a depolarizing Neuromuscular blocker hence prior to paralysis the depolarization of the NM membrane causes muscle fasciculations

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25
Q

How is sux broken down in the body

A

By cholinesterase and acetylcholinesterase

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26
Q

What does sux act on to produce muscle paralysis

A

Acetylcholine receptors at the NM junction

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27
Q

What are the adverse effects of sux

A

-malignant hyperthermia

-increased intraocular pressure

-prolonged paralysis (in those with reduced pseudocholinesterase levels )

-hyperkalaemia (not good in burns/ necrosis pt= hyperk= cardiac arrest)

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28
Q

Which muscles relaxant is the quickest acting and shortest duration

A

suxamethonium

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29
Q

How quickly do atracurium, vecuronium and pancuronium act

A

atra + vecronium= 30-40mins
pancuronium= 2-3mins

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30
Q

Which muscle relaxant is broken down in the liver/ kidneys

A

pancuronium + vecuronium

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31
Q

How is atracurium broken down

A

by hydrolysis in tissues and causes histamine release

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32
Q

Adverse effects of atracurium

A

Histamine release= flushing, tachycardia, hypotension

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33
Q

Reversal agent for non-depolarizing muscle relaxants

A

non-depolarizing= neostigmine

34
Q

Which muscle relaxant is the only depolarising neuromuscular blocker

A

suxamethonium

35
Q

Sx of malignant hyperthermia

A

hyperpyrexia
muscle rigidity

36
Q

Pathophysiology of malignant hyperthermia

A

genetic defect:

administration of anaesthetic/ anti-psychotic/ anti-emetic= excessive release of Ca from sarcoplasmic reticulum in skeletal muscles= muscle rigidity + pyrexia

37
Q

Mx of malignant hyperthermia

A

Dantrolene-inhibits ca release from sarcoplasmic reticulum

38
Q

Drugs that can cause malignant hyperthermia

A

anaesthetic/ muscle relaxants/ anti-psychotic/ anti-emetic

haloperidol
prochloperazine
metaclopramide
risperidone

39
Q

What is the gene + chromosome involved in malignant hyperthermia

A

Chromosome 19, ryanodine receptor (controls Ca release from SR)

40
Q

How can malignant hyperthermia be diagnosed

A

raised CK

Contracture tests on muscle biopsy exposed to halothane/ caffeine

41
Q

Side effect of neostigmine and how can this SE be countered

A

SE= Bradycardia

Given with atropine

42
Q

WHat is cryoppt made of?

A

Factor 8
Factor 13
vWB factor
fibrinogen

43
Q

Pathophysiological changes seen in ARDS

A

b/l pulmonary infiltrates
(non-cardiogenic)
hypoxaemia (due to reduced diffusion)

44
Q

Causes of ARDS

A

sepsis
pancreatitis
directly injury/ trauma
fat embolism (long bone/ multiple #)
aspiration

45
Q

Features of ARDS

A

hypoxia
tachypnoea
tachycardia

46
Q

Mx of ARDS

A

treat underlying problem:
sepsis= IV ABx

negative fluid balances (diuretics)

recruitment manoeuvres (prone ventilation/ positive and expiratory ventilation)

mechanical ventilation with low tidal volumes (prevent alveolar damage)

47
Q

Why is midazolam preferred as a procedural sedative

A

amnaesia effect

48
Q

What class of drug is flumazenil

A

selective GABA receptor antagonist

49
Q

How is midazolam excreted

A

in the liver (via cytochrome P450 path)

50
Q

What does TPN consist of

A

lipids
glucose
electrolytes

(NO FIBRE)

51
Q

complications of TPN

A

fatty liver + deranged LFT

thrombophlebitis (if admin through small vessels)

sepsis

refeeding syndrome

52
Q

What are the 2 types of neuromuscular blocking drugs and what is their MOA

A

deplorazing and non-depolarizing neuromuscular agents

block Ach from acting on receptor at the NM junction

53
Q

What is the pulmonary artery occlusion pressure

A

Measures the pressure of the LEFT atrium

54
Q

Target values for:
urine output
MAP
CVP

A

URINE O/P: 0.5ml/kg/hr
MAP >65
CVP 8-12

55
Q

What are the different vassopressors available

A

Adrenaline
noradrenaliine
dopamine
dobutamine
metaraminol
milrinone

56
Q

Which vasopressors are alpha agonists

A

noradrenaline, metaraminol

57
Q

Which vasopressors are alpha and beta agonists

A

adrenaline

58
Q

Which vasopressors are beta 1 agonists

A

dopamine

59
Q

Which vasopressors are beta 1 & 2 agonists

A

dobutamine

60
Q

Which vasopressors cause increased SVR

A

adrenaline, noradrenaline

(those that DO NOT act on beta receptors)

61
Q

Which vasopressors cause increased cardiac output

A

all that act on beta receptors

adrenaline
dopamine
dobutamine

62
Q

What effect does dobutamine have on cardiac output and SVR

A

b1 +b2 agonist:

increases cardiac contractility + rate+ BP =increased cardiac output

vasodilation= reduced SVR

63
Q

What is the MOA of Milrinone and what are its effects

A

phosphodiesterease inhibitor =
increased muscle contractility + vasodilator

(same as dobutamine)

64
Q

What are the effects of alpha agonists on the heart and SVR

A

no effect on cardiac output
increase SVR

65
Q

What variables can the swan ganz catheter be used to measure

A

oxygen delivery

pulmoary artery resistance

systemic vascular resistance

stroke volume

66
Q

Where would a swan ganz catheter be sited

A

pulmonary artery

67
Q

Adverse effects of Dextrans for fluid resuscitation

A

Anaphylaxis
Acute renal failure

68
Q

Indication for using an uncuffed ET tube

A

in children
to prevent damage to larynx

69
Q

Which ionotrope can be given through a peripheral vein

A

metaraminol

70
Q

How long does the effect of clopidogrel last

A

120 days

(need to stop 5-7 days pre-op)

71
Q

MOA of clopidogrel

A

anti platelet= acts on ADP to inhibit plt aggregation

72
Q

ECG features of hyperkalaemia

A

Tall T waves
broad QRS
flattened P waves
VF

73
Q

When would you test for brain stem death

A

-Unexplained deep coma
-reversible causes have been excluded
-normal electrolytes
-not under sedation

74
Q

What is involved in testing for brain stem death

A

-fixed pupils, not reactive to light
-no corneal reflex
-no rxn to supra-orbital pressure
-no oculo-vestibular reflex*
-no cough reflex to bronchial stimulation
-no gag reflex to pharyngeal stimulation
-no visible respiratory effort when taken off ventilator for atleast 5min (to allow for adequate arterial partial pressure of CO2 -6-6.5kPa)

*no eye movements to the slow injection of atleast 50ml of ice-cold water into each ear in turn

75
Q

Who can test for brain stem death

A

need 2 doctors to carrying out test on 2 separate occaisions

-Both need to be >5yrs post grad
-1 needs to be a cons
-neither can be part of the transplant team

76
Q

Complications caused by massive transfusion

A

hypothermia (blood stored in the cold)

hypocalcaemia (FFP + plt have citrate antioaoagulant= causes chelation of Ca)

hyperkalaemia (older blood= higher K)

transfusion associated lung injury

coagulopathy (causes dilution and reduced plt, fibrinogen, clotting factors)

77
Q

Describe the pathophysiology of transfusion associated lung injury

A

transfused plasma contains antibodies to leukocytes

leukocytes aggregate and breakdown in the lungs causing damage to alveoli

Inflammatory infiltrates in b/l pleura

78
Q

Which anaesthetic agent is associated with hepatotoxicity

A

halothane

79
Q

Patient presents with an acute dystonic rxn (due to anti-psychotic meds + metoclopramide given), what meds can reverse this

A

procyclidine
benzhexol

80
Q

What are the features seen in an acute dystonic rxn

A

acute torticolis
oculogyric crisis
oromandibular dystonia

81
Q

What is included in the enhanced recovery programmes

A

Admission on the day of surgery

Reduced starvation times (if under GA= carbohydrate loading drink 2 hrs pre-op)
Not for diabetics with complex insulin regimens

Intra-op DO NOT give IV fluids= can cause interstitial oedema and increase complication rates

Post-op:
early ambulation
eat orally within 24hrs
reduced IV fluids= ileus
take out IV/ drains/ catheters
encourage getting dressed and walking around ward

MRCS (21 decks)

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