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MRCS part B- JMB > Critical Care > Flashcards

Critical Care Flashcards

1
Q

A good anaesthesia?

A

Insensitive to pain
Reversible loc
Muscle relaxation

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2
Q

Types of anaesthetics

A

Amides- lidocaine

Esters- cocaine

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3
Q

Moa of anaesthetics?

A

Reversible inhibition of sodium channels (which are proteins therefore increased protein affinity leads to increased efficacy)
Prevent action potentials

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4
Q

Why does lidocaine not work in bacterial environment

A

Exists as an ionised base- In acidic environment cannot penetrate cell membrane

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5
Q

Lidocaine/bupivicaine/prilocaine dose

A

3 (7 with epi) max 200(500)
2 (3) max 150(150)
6

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6
Q

Indication and complications of spinal anaesthesia?

A 
Surgery below the umbilicus T10
Hypotension-splanchnic pooling
Damage during insertion
Dislodgement/infection via catheter
Haematoma post removal- cord compression
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7
Q

Definition of burns

A

Tri zone injury
Central area of coagulative necrosis
Surrounded by static area of inflam and ischaemia
Surrounded by hyperaemia

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8
Q

How to calculate survival of burns patients

A

Bull chart guides survival
TBSA + age > 100 = >20% mortality

Lund and bower chart for tbsa

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9
Q

Why place a pulmonary artery catheter?

A

Ra pressure assumed to be equivocal to la pressure- no valves
Can calculate temp, o2 sats, ef, co, pressures

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10
Q

Aetiology of brain injury

A

1- at time of injury

2- hypoxia, hypotension, RICP, hypercarbia

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11
Q

Cerebral perfusion pressure equation

A

MAP- ICP

MAP= diastolic + 1/3sbp

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12
Q

What controls cerebral vasodilation

A

Co2 levels

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13
Q

Why dilated pupils in head injury

A 
Cniii palsy
Runs through tentorium cerebellum
Swelling leads to compression of this
Loss of parasympathetic 
Symph from t1
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14
Q

Indications for parenteral nutrition

Complications?

A

Compromised gi tract
Hyper catabolic state

Does not maintain bowel mucosa
Monitoring required
Tpn jaundice- tpn is hepatotoxic?
Line sepsis

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15
Q

Different types of dialysis?

A

Haemodialysis- uses a ppm where small molecules removed by DIFFUSION- cheaper and simpler
Haemofiltration- continuous convection of molecules across membrane
Peritoneal dialysis

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16
Q

Functions of kidneys?

A 
Homeostasis- Electrolyte balance, Acid base balance, Fluid balance
Plasma filtration
Metabolise drugs 
Excrete waste
Hormones- epo, renin, calcitrol(Vit d)
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17
Q

Types and indications for ventilation

A

Bipap- type 2 resp failure
Cpap- splints airways open and overcomes compliance- type 1 resp failure, cardiogenic and non cardiogenic pulmonary oedema

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18
Q

Reasons for itu admission?

A

Pathology reasons
Monitoring/expertise reason
High risk procedure
Preoptimisation

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19
Q

Definition of brain stem death?

A

Patient comatose
Coma cause known
Irreversible damage
Reversible causes excluded

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20
Q

Brain stem death assessment?

A

Cnii light reflex
Cniii & vi occulovestibular reflex (turning head and eyes follow)
Can v & vii corneal
Cnviii oculocephalic reflex (water in ear)
Cn ix x gag reflex
Motor response to pain
Ventilatatory response following apnoea testing

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21
Q

Scoring system for pancreatitis?

A

Glasgow score/Apache/Ransom

Glasgow score: PANCREAS
PaO2 <8
Age>55
Neutrophils>15
Ca <2.0
Renal- Urea >16
Enzymes LDH >600/AST >200
Albumin <32
Sugar >10
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22
Q

Reasons for hyperglycaemia and hypocalcaemia in Acute pancreatitis?

A

Hyperglycaemia- destruction of Beta cells
Hypocalcaemia- fat saponification, exocrine enzymes release due to pancreas destruction, leads to breakdown of fat to free fatty acids which chelate calcium

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23
Q

What are the pancreatic exocrine enzymes?

A

Trypsin, amylase and lipase

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24
Q

What is the pH equations?

A

Henderson-Hasslebach equation
pH= power of hydrogen

=pKa (acide dissociation constant) + log (base concentration)/acid concentration

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25
Q

What is the chloride shift principle?

A

In peripheral capillaries, CO2 is taken into cells via Cl- transporter and converted into HCO3- by carbonic anhydrase
Then excreted again for Cl-
Contributes to buffering process

?Affects Hb affinity for O2

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26
Q

What is a buffer system?

A

Base and acid system that resists changes in pH

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27
Q

Aetiology of metabolic acidosis?

A

Gain of H+ ions or loss of bicarb

High anion gap- Methanol, uraemia, DKA, lactic acidosis (Mud Piles)

Normal anion gap- Addisons, Bicarb loss- RTA , Chloride excess , Diarrhoea

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28
Q

Causes of metabolic alkalosis?

A

Gain of bicarb or loss of H+

Vomiting, blood transfusions (citrate),
Diuretics/genetic renal conditions= Barrters

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29
Q

Causes of respiratory alkalosis?

A

Anxiety/Pain
PE
Paracetamol
Asthma

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30
Q

When to use CPAP vs BiPAP?

A

CPAP- recruits collapsed alveoli
Pulmonary oedema/type 1 resp failure

BiPap- type 2 resp failure with acidosis

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31
Q

Categorisation of acute limb ischaemia?

A

Stage I- Not threatened
Stage 2a- salvagble if prompt- decreased CRT, partial sensory loss, inaudible doppler, good power
Stage 2b- slow CRT, partial sensory loss, decreased power, inaudible doppler
Stage 3- Nil CRT, paralysis, parasthetsia, no doppler

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32
Q

What is ARDS?

A

Acute resp failure and non cardiogenic pulmonary oedema
Resulting in hypoxia decreased lung compliance
Diffuse pulmonary infiltrates, normal PAWP, hypoxia

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33
Q

What are the causes and management of ARDS?

A

Lung- infection, aspirate, smoke, drowning
Systemic- DIC, polytrauma, CPB, massive transfusion, acute pancreatitis, sepsis, Fat emobolus

Management- Supportive, PEEP and proning

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34
Q

What is the mortality of ARDS?

A

30-60%

90% if associated with sepsis

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35
Q

Indications for surgical airway?

A

Cant intubate, cant ventilate

Laryngeal trauma/oedema/FB/Upper airway obstruction

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36
Q

Complications of poorly controlled pain?

A 
Sympathetic response- tachycardia and increased metabolic demand
Decreased resp effort
Decreased GI motility- ileus
Decreased mobility
Psychological effects
Chronic Pain
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37
Q

What is the process of pain transmission?

A

Painful/damaging stimuli
Identified by nocioceptors
AP transmitted by A-Delta/C fibres
To spinal cord and up via spinothalamic tract
To thalamus and then to somatosensory cortex

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38
Q

What is the MOA of paracetamol/NSAIDs?

A

Paracetamol- unknown aetiology

NSAIDs- Inhibit COX => decreased prostagladins

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39
Q

Alternatives to medical pain relief?

A 
Hot and cold packs
Rubbing- gated theory of pain
Acupuncture
TENS Machine
Splinting #s
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40
Q

What is the management of new acute AF?

A

Rhythm control if indicated first
Within first 48 hours of presentation
DC cardiovert if haemodynamically unstable/ electively
Chemical cardioversion- flecanide vs amidodarone if not
Or Ablation

Rate control if not for rhythm control

Anticoagulate- CHASDVASC vs HASBLED

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41
Q

What are the complications of a blood transfusion?

A

Immune complications:
Acute haemolytic reaction-ABO incompatibility
Acute febrile reaction- minor histocompatability complex reactions
Anaphylaxsis
TRALI
GvHD

Non-immune
Overload
Hypocalcaemia (citrate)
Hyperkalaemia (broken down cells)
Hypothermia
Infections
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42
Q

How many pints/litres of blood in an average human?

A

4-5 litres

8/9 pints/units

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43
Q

What is a massive transfusion?

A

In 4 hours >/ 50% of circulating volume replaced

In 24 hours >/ 100 % of circulating volume replaced

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44
Q

What can you do for a Jehovah’s witness?

A 
All blood products?
Involve Watchtower representative
Rehydrate- IVT
EPO/Iron tablets
TXA
Good haemostasis intra operatively
Cell saver device
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45
Q

Medical management of IBD?

A

Sulfasalazine
Methotrexate
Azothioprine
Infliximab

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46
Q

Reversible brain stem death differential Dx?

A 
Hypothermia
Hypoglycaemia
Hypothyroidism
Addisons
Toxins
C spine injury
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47
Q

Formulas for calculating burns resuscitation?

A

Parkland’s formular- 4ml x TBSA x weight
Resusication over first 24 hours

Mount Vernon

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48
Q

When to refer to a specialist burns unit?

A

> 5%/>10% TBSA affected in adults/kids
<5yo/NAI/>60yo
Strange burn type- high pressure/electrical/steam/chemical
Hands, face, perineum, flexures, cicrumfrential burns
Inhalation injuries
Immunosuppressed/pregnant

49
Q

Levels of burns?

A

Superfisical epidermal- Sunburn, red, painful, peels, good CRT, no blisters
Superficial dermal- Red, painful, delayed CRT, blistering, moist
Deep dermal- mottled red, sort of painful, non blanching
Full thickness- scortched leathery skin, no pain, no crt

50
Q

What are should you do post CV line insertion?

A

CXR to exclude pneumothorax and check position

US scan to ensure in tip of SVC

51
Q

What muscles lie over subclavian vein on approach to insert line?

A

Pec Major and subclavius

52
Q

How is CO measured?

A

Fick’s principle

HR x SV

SV = afterload = preload

53
Q

Draw a CVP trace?

A

Like JVP wave

54
Q

Definition of compartment syndrome?

A

Elevated interstitial pressure in a closed osteofacial compartment leading to microvascular comprimise

Downward spiral of decreased venous return leading to decreased aorto-venous gradient and therefore decreased perfusion

55
Q

Chance of full function returning when fasciotomies performed for compartment syndrome?

A

<12 hour- 2/3 patient get full function back
>12 hour- only 10%

Sheridan et al.

56
Q

What is rhabdomyolysis?

A

Release of toxic muscle cell components (myoglobin) into systemic circulation

57
Q

Aetiology of Rhabdomyolysis and complications?

A

1o- congential- duchennes
2o- Trauma, burns, hypothermia, ischaemic reperfusion injury, excessive excerise, toxins

Myoglobin release

Complications- AKI =>failure, DIC, Electrolyte abnormalities

58
Q

Commonest level of C spine #?

A

C5

59
Q

What to check for if c spine #?

A

Vertebral artery injury- CTA and MRA needed

60
Q

What is a hangman’s #?

A

Bilateral pars interarticularis # of C2 (Between pedicle and lamina)

61
Q

Difference between spinal shock and neurogenic shock?

A

Spinal shock- 2o to trauma, complete transection of spinal cord
Neurogenic shock- loss of symphathetics => bradycardia and hypotension

62
Q

What is autonomic dysfunction

A

Spinal injury above T6
Leading to symphathetic response below level- peripheral vasoconstriction
And parasymph above lesion- vasodilation and bradycardia

63
Q

Why does biliary pathology lead to prolonged clotting time?

A

As decrease functionality of gall bladder
Therefore decreased biliary production/secretion from GB
Therefore less fat breakdown and vitamin absorption
Vitamin K clotting factors (require Vit K for activation) affected
2,7,9,10

64
Q

Where are ALT/AST produced?

Which is more liver specific?

A

Produced by hepatocytes

ALT more liver specific
AST produced by heart, kidney, liver, brain, intestine, placenta

65
Q

Where are ALP and GGT produced?

A

ALP by bile duct epithelium/bones/placental tissue

GGT by hepatocytes and bile duct epithelium

66
Q

What is the function of bile?

A

Excretory route for lipophilic substances
Emulsifier of fats
Elimination of cholesterol

67
Q

What is the lifecycle of bilirubin?

A

RBCs broken down by spleen to Haem and globin
Haem broken down to Biliverdin
Then to bilirubin and iron
Bilirubin then bound to albumin and brought to liver
Conjugated by enzymes with glucuronic acid in Liver
Thus making it water soluble and allowing it to be excreted in the bile
Bile is then either converted to stercobilinogen and excreted in faeces
Or reabsorbed in distal ileum and converted in urobilinogen and excreted in urine

68
Q

What microorganisms are screen for routinely on a blood transfusion?

A

HIV
Hep B/C
CMV
Syphilisi

69
Q

What is CCK?

A

Produced by duodenum when fat detected

Leads to gall bladder contraction sphincter of oddi relaxation

70
Q

What are the causes of DIC?

A 
Infection
Trauma 
Malignancy
Massive blood transfusion
Placental abruption
71
Q

What are the consequences of hypothermia?

A

Hypoxia- left shifting of Hb-O2 curve
SNS activation- vasodilation and shviering
Enzyme dsyfunction
Coagulopathy

72
Q

How to classify diverticulitis?

A 
Hinchley classification
Stage 0- mild diverticulitis
Stage 1- + pericolic abscess
Stage 2- distal abscess
Stage 3- purulent peritonitis
Stage 4- faeculent peritonitis

Stage 3/4- Operative drainage
Stage 0/1/2- IR

Suitable for Abx if abscess <3cm

73
Q

What are the causes of a fat emoblism?

A 
Trauma/long bone reaming/massive soft tissue injury
Bone marrow transplant
Liposuction
Acute pancreatitis
Intralipid infusion
74
Q

What is the pathophysiology of fat emoblism syndrome?

A

Fat globules gain access via damaged vasculature
Plaltelet bound lipids brokendown leading to free fatty acids in blood
Intravascular coagulation leads to emboli

75
Q

What is the role of MRI in FES

Mortality of FES?

A

Looks for cerebral Oedema- can R/O FES

5-15%

76
Q

What is the definition of a high output stoma and what are the consequences?

A

> 500ml/day

Dehydration, electrolyte imbalance, malnutrition

77
Q

How do you manage a high output fistulas?

A

A2E then MDT

SNAP

Sepsis control
Nutritional support- dieticians
Anatomical assessment- fisutlogram/CT
Adequate IVT/electrolytes
Protect skin
Plan- conservative vs surgical (tract excision)
78
Q

Indications of central line?

A

CVP monitoring/CO monitoring

Interventions- TPN, vasoirritant medication, failed cannulation, haemodialysis

79
Q

How do you manage variceal bleeding?

A 
Endoscopy- band ligation/sclerotherapy
Terlipressin
Balloon tamponade
TIPSS
Surgical shunt
Liver transplant
80
Q

What is the rule of 2/3s with portal htn?

A

2/3 of cirrhotic patients develop portal htn
2/3 of patients with portal htn develop varices
2/3 of patients with varices present with an acute bleed

81
Q

What are the causes of hydrocephalus?

A

Increased production- choroid plexus carcinoma
Decreased circulation- malignancy, infection, haematoma
Decreased reabsorption- thrombosis/haemorrhage

82
Q

What does pulse oximetry detect?

A

Ratio of unsaturated vs saturated haemoglobin

83
Q

What are the side effect of colloids?

A

Anaphylaxsis and affect platelet aggregation

84
Q

What are the pathophysiology of the hypersensitivity reactions?

A

Type 1- IgE => mast cell degranulation leading to heparin, histamin and platelet activating factor release
Leads to profound vasodilation, increased vascular permeability and smooth muscle spasm

Type 2- cell mediated- Ag and ab- acute transfusion reactions

Type 3- immune complex mediated- goodpastures/lupus

Type 4- delayed- contact dermatitis- t cell

Type 5- stimulatory- grave’s, TSH receptor autoAbs

85
Q

What are the causes of hyponatraemia?

A

Hypertonic (hyperglycaemic)
Isotonic (pseudohyponatraemia (myeloma))
Hypotonic

Hypervolaemic- failures
Hypovolaemic- D/V or diuretics/ burns/trauma

Euvolaemic
SIADH
SCLC
Infection
Addisons
Drugs
HypoT
86
Q

When do you gain immunity from tetanus?

A

Tetanus immunisations
After 5 doses

3 given at a couple of months old
1st booster at 5 years old
2nd at 15yo

87
Q

What is an exotoxin/endotoxin?

A

Exotoxin produced by gram +/- bacteria
Immunogenic proteins
With specific effects

Endotoxins
Just produced by gram -ve
Lipopolysacchorides from cell wall leading to general stress response

88
Q

What is the mortality of NEC Fasc?

A

30%

89
Q

What are the different types of adrenergic receptors?

A

alpha 1- vascoconstrioction and increased myocardial contraction duration
beta 1- intropy and chemotropy
beta 2- vasodilation/bronchoconstriciton
Dopamine 1/2- diuresis

90
Q

What is starling’s law?

A

Myocardiac contractility is proportional to myocardial stretch

91
Q

Make up of hartmannas and NaCl?

A

Hartmanns
Na 131, cl 111, bicarc 29, Ca 2, K 5

NaCl
Na 154, Cl 154

92
Q

Where is hartmanns, nacl, dextrose and blood distributed?

A

Blood just intravascularly
NaCl and Hartmanns just ECF
Dextroses everywhere

93
Q

Indications for intubation?

A

Airway- decreased GCS, facial/laryngeal trauma, inhalation injury
Breathing- resp failure, prevention of 2o brain injury

94
Q

How to confirm ETT is in correct position?

A 
Look listen feel
Waveform capnography is gold standard
Face mask misting
Air entry
No stomach rise
CXR
95
Q

How do you calculate ventilation?

A

Tidal volume x RR = 7ml/kg x 12/min

96
Q

Why does tachycardia put one at increased risk of an MI?

A

Coronary artery filling occurs during diastole

Diastole shortens during tachycardia

97
Q

Why RJV preferential site for CVP measurement?

A

No valves between it and RA

Less NV damage risk

98
Q

Causes of normal anion gap metabolic acidosis?

A

Addisons
Bicarb loss- RTA
Chloride excess
Diarrhoea/diuretics

99
Q

RFs for AF?

A 
Age/alcohol
CXS disease
Thyroid status
Valvular disease
DM

Hypovolaemia/hpoxia
Potassium
Acute MI
Sepsis

100
Q

What is the MI re infarction rate when performing surgery?

A

<1 month = 30%

<6 months= 5%

101
Q

What is the MOA of aspirin and clopidogrel?

A

Both prevent platelet aggregation

Clopidogrel via inhibition of ADP receptors

Aspirin via COX antagonism

102
Q

Side effects of NSAIDs?

A 
Heart failure- fluid retention
AKI
Stomach ulcers
Coagulopathy
Decreased inflammation
Bronchospasm
103
Q

Types of Nec Fasc?

A

1- polymicrobial- staph/hi
2- monomicrobial- GAS
3- clostridium
4- fungal

104
Q

What is a pancreatic psuedocyst?

A

fluid filled collection with fibrous capsule

due to leakage of enzyme rich fluids

105
Q

How do you manage a pancreatic pseudocyst?

A

Conservatively
50% resolve
10% infected

Drain- radiologically, endoscopically, open

106
Q

What is a steroid?

A

Organic compounds with characterisitic four rings

Cholesterol/aldosterone/cortisol/testosterone/progesterone/thyroid hormone

107
Q

What affect does aldosterone have?

A

Na/K/ATPase pump activity increase

Increase H20 retention and alkalosis

108
Q

What hormones are produced by the anterior and posterior pituitary?

A 
Anterior:
ACTH
TSH
FSH
LH
GH
Prolactin

Post pituitary:
Oxytocin
ADH

109
Q

What are the effects of gluccocorticoids and how are they controlled?

A

Metabolic- hyperglycaemic effect- inhibit insulin

Non metabolic- Na in/K out- fluid retention
Anti inflam
immunosuppressant
Decrease stress response

CRH produced by hypothalamus leads to ACTH production by ant pituitary leading to cortisol production by cortex

Stimulated by low cortisol levels

110
Q

Complications of gluccocorticoids?

A 
Weight gain
DM
Ulcers
Osteoporosis
Bruising/muscle weakness
Mood changes
Cushing's
Sick day rules!
111
Q

What are the general principles for operating on someone taking glucocortiocoids?

A

Double dose day of surgery
IV hydrocortisone at induction
Alert anaesthetist- pre assessment
Beware of Addison’s

Abdo pain, N/V, shock, hypothermia

112
Q

Criteria for day surgery?

A

Social factors- someone to take them home and keep an eye on them
Medical factors- patient fit
Surgical factors- Op generally doesnt result in serious post op complications
Able to mobilise post op
Good length of op/anaesthetic time

113
Q

What is the ASA criteria?

A 
1- fit and well
2- mild systemic disease
3- severe systemic disease
4- severe systemic disease at constant risk to life
5- moribund
6- Brain dead, organ transplantation
114
Q

When to refer to the coroner?

A

Death <24 hours since admission
Suspicious/accidental/violent death
After op/procedure
Unknown cause of death

115
Q

What to do facing a tracheostomy airway problem?

A 
Help- anaesthetics/senior
A2E
O2 to face and trachy
Trachy box- inner tubes/suctio catheters/scissors & tape
Remove valve/inner tube
Attempt to pass a suction catheter
Deflate cuff if needed
Remove trachy- if in doubt take it out
Ventilate via mouth/nose- cover trachy with gauze
116
Q

What are the types of transplant rejection?

A

Hyperacute- ABO mismatching
Acute- HLA mismatching
Chronic- MHC mismatching?

117
Q

What is in FFP and cryoprecipitate?

A 
FFP= all clotting factors, albumin, fibrinogen, vWF
Cryo= F8, F13, fibrinogen and vWF
118
Q

How does an osmotic diuretic work?

A

Eg. Mannitol

Filtered by the glomerulus but can not be reabsorbed
Leads to increased oslamlality which therefore is balanced out by diuresis

119
Q

Why does Aortic stenosis lead to problems intraoperatively

A

AS leads to hypertrophied ventricle, which is stiff with decreased compliance
Therefore this ventricle has an increased metabolic demand- so is sensitive to changing arterial pressure
And has a lesser ability to respond to a changing afterload

MRCS part B- JMB (10 decks)

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