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OSCE Facts / Questions Flashcards

1
Q

Causes of hyperthermia

A

Infections - Sepsis, CNS infection, endocarditis, tropical disease

Environment - heat stroke

Endocrine - Thyroid/Phaeo

CNS - Hypothalamic stroke

Drugs - Serotonin, NMS, e, cocaine, Salicylate, benzo withdrawal

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2
Q

Hyperthermia effects on the CVS

A

Tachy and increased SV, along with vasodilation

Decreases MAP

Fluid compartment shift - dehydration, situation worsens, CVP falls

Worsening tachy, met acidosis —> reduced contractility, SV and MAP

Hypotension and infarct

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3
Q

Features of Serotonin syndrome

A

triad of:

Neuromuscular excitability - clonus, hyper reflex is, rigid

Autonomic dysfunction - hyperthermia, tachy, sweat, flushing

CNS dysfunction - anxiety agitation, confusion coma

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4
Q

Diagnosis of Serotonin syndrome

A

Clinical - features emerge when starting or raising the dose of a serotonergic drug, or second drug added

Also - Hunter criteria

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5
Q

Drugs (and catergories) causing Serotonin syndrome

A

Prevent Re-Uptake - SSRI, SNRIs, MAOI, TCA, tramadol/pet hiding

Stimulate release - Tramadol, MDMA, amphetamine

Other - Lithium, Tryptothan

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6
Q

Treatment of Serotonin Syndrome

A

Stop the drug

Sedation/control agitation

Active Cooling

Control HR/BP

Monitor coag/renal

Antedotes: Cyproheptadine (oral 5HT2a)
Chlorpromazine

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7
Q

cooling methods

A

Passive - Cool the room, take clothes off

Active external - wet towels, ice pack, fan, pads

Active interval - Cool if fluids, Cavity lovage, RRT, CPB, ECMO

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8
Q

Fever, hyperthermia and hyper pyrexia

A

Fever - hypothalamic upreguation of set point - cytokine mediated, responds to NSAIDS

Hyperthermia - failure of temperature regulation, does not respond

Hyperpyrex - >41C

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9
Q

Types of Lactic Acidosis

A

Type A - hypoperfusional

B - normal perfusion

B1 - underlying disease (ketoacidosis, leukaemia, lymphoma)
B2 - Drugs (cyanide, beta-agonists, methanol, ethanol, methanol)
B3 - Inborn errors of metabolism

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10
Q

Causes of a raised CK

A 
Muscular dystrophies
Myosotis, Polymyositis,
MH
Acute MI
Cerebrovascular disease
Neurosurgery

Rhabodomyolysis, hypothyroidism (muscle loss)

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11
Q

Metabolic features of PRIS

A

Bradycardia
RBBB

Met acidosis
Raised lactate
Hepatic and renal failure

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12
Q

Definition of PRIS

A

Acute refractory bradycardia

Plus

Met acidosis (BE >10)
Rhabdo
Hyperlipidaemia
Fatty liver

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13
Q

Mechanism of PRIS

A

Direct mitochondrial resp chain inhibition

Impaired fatty acid metabolism at mitochondria

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14
Q

Risks of PRIS

A

Young (paeds)

Severe critical illness (CNS or Resp origin)

TBI

Excess catecholamines

Excess glucocorticoids

Poor carbohydrate intake

Subliminal mitochondrial disease

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15
Q

Tests for PRIS

A

Consider a serum triglyceride level

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16
Q

Dose range of PRIS

A

4mg/kg/hour

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17
Q

Treat PRIS

A

Stop propofol
Switch to alternative sedation agent

HD/HF with CVS support

Early awareness, monitoring

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18
Q

CSF finding of GBS

A

Raised protein

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19
Q

Differential of weakness

A

Brain stem lesions - Acute disseminated encephalomyelitis

Spinal Cord - transverse myelitis

Polyneuropathy - Infectious - Polio Diptheria, Lyme
Polyneuropathy - Non infection - porphyria

NMJ - Myasthenia, botulism
Muscle - rhabdo, myosotis

Electrolytes - low K, PO3

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20
Q

Ix of GBS

A

CSF - protein
NCS - demyelination from atonal types

MRI brain and spine - cord compression, stem lesions

Anti ganglioside antibodies

Infection - campylobacter, mycoplasma, HIV

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21
Q

When to tube GBS

A

Vital capacity <15ml/Kg

Bulbar weakness, can’t protect airway

Autonomic instability - haemodynamic and cardiac arrhythmia

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22
Q

Drugs to tube GBS

A

Carefully titration induction agent

Vasopressin and atropine (Brady/autonomic

AVOID SUX - hyperkalaemia

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23
Q

Treatment of GBS

A

IvIG
PLex

Equally effective, ivig more expensive but easier

NO ROLE FOR STEROIDS

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24
Q

Other issues for GBS management

A 
Tracheostomy
DVT
Pressure sores
Physio
Pain particularly neuropathic
Psych
VAP bundles
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25
Q

Mortality of GBS

A

5%

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26
Q

Features of poor outcome in GBS

A

Elderly
MV
Poor neurology at start and persisting
Prolonged MV

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27
Q

SCoring system for CAP

A

CURB 65

Confusion (new)
Urea > 7
RR >30
BP <90 sys
Age over 65
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28
Q

CURB score mortality

A 
0 0.7%
1 3.2%
2 13%
3 17%
4 41.5%
5 57%
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29
Q

First line ABx for CAP

A

Penicillin plus macrolide

Ben pen/clindamcin

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30
Q

Ix for CAP in immunocomp

A

Try and get BAL

MC&S
Acid Fast Bacilli (TB)
PCP
Aspergillosis

Galactomannan, beta D glucan (blood), IgG/E assessment

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31
Q

Causes of cavitatinig lung lesions

A

Bacterial pneumonia - Klebsiella and S.aureus
(PVL producing strains of aureus)

TB

Aspiration

Immunodeficiency - HIV - infective: TB, atypical, mycobacterium, aspergillosis
Non infective: NHL, Kaposi’

Non infective - vasculitis, sarcoidosis, rheumatoid, malig, pulmonary infarct

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32
Q

What is PVL

A

Extra cellular cytotoxic made by S.aureus

Leuocidal - lytic pores in the cell membrane

Associated with skin/soft tissue infections but can be pneumonia

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33
Q

Treatment of PVL

A

DoH guidance

Linezolid 600mg 12 hourly
Clindamicin 1.2-1.8g 6 hourly

Consider addition of rifampicin

Consider MRSA cover

Micro involvement

IvIG - toxin continues after bacteria killed

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34
Q

Components of q-sofa score

A

RR > 22
Altered mental state
BP sys < 100

Helps

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35
Q

Define sepsis

A

A life threatening organ dysfunction caused by a dysregulated host response to infection

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36
Q

In the sepsis definitions, how is “organ dysfunction” defined

A

Acute change in total SOFA > 2 points

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37
Q

Define sepsis shock

A

Subset of sepsis

Underlying circulatory, and cellular/metabolic abnormalities are profound enough to cause mortality

Clinically:
Hypotension requiring vasopressors to maintain MAP >65

AND

Lactate > 2mmol/L

DESPITE volume resus

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38
Q

Variables of the SOFA score

A 
Resp : PF ratio
Neuro: GCS
GI: bilirubin
Renal: Creatinine/Urine
Haem: Plts
CVS: MAP or vasopressor use
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39
Q

Definition of VAP

A

Pneumonia occur in patients ventilated for 48 hours / within 48 hours of onset of infection

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40
Q

Diagnosis of VAP

A

Vented 48 hours

Clinical signs, changes in lab tests, CXR

CPIS scoring or HELICS

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41
Q

CPIS elements

A 
Temperature
WCC
CXR changes
PF ratio
Type of secretions
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42
Q

What is a ventilator associated event?

A

Significant event that can be infective or not, leading to a deterioration in oxygenation

20% increase in daily lowest FiO2
Increase in PEEP of at least 3 cm from stable baseline

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43
Q

Organisms for a VAP

A

Less than 48 hours in hospital - similar to CAP
More than 5 days - hospital multi-resistant:
Pseudomonas,
Klebsiella
Enterobacter
Acinetobacter
Haemophilia

Gram positives. - s. aureus, streptococcus

Fungi - rare

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44
Q

Preventative measures of VAP

A

Bundles:

Daily sedation hold
30 degree nursing
Chloe hex mouth care
Suction (sub glottis)
Humidification
Maintain cuff pressure 20-30cmH20

?SSD
Stress ulcer prophylaxis
Silver ETT

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45
Q

Treatment of VAP with MRSA in sputum

A

Glycopeptides - vancomycin

Oxazolidinone - Linezolid

Linez - better lung penetrence but not convincing evidence of superiority

Vanc - renal monitor

46
Q

Treatment of VAP

A

Tazocin
Gentamicin for MDR
Vanc if MRSA
Teic if VRE colonised

47
Q

Factors for consideration for VAP

A

Local policy
Local pathogens
Prevalence of MDR, ESBL, MRSA

Prior therapies, allergy status
Duration of ventilation

Micro results and BALs

48
Q

Methods of working out daily energy requirements

A

Weight based - 25-30kcal/kg/day (IBW)
20-25 in acute illness

Protein - 1.2-1.5G/kg/day

Indirect calorimetry

Eqns - Schofield, Benedict Harris equation based on age, sex, height, weight

49
Q

Energy from protein, carbs and fat

A

Protein 4kcal/g
Carb 4kcal/g
Fat 9 kcal/g

50
Q

What is the RQ, and what is it for carbs, fat and protein

A

Ratio of CO2 produced to Oxygen consumed

Carbs 1
Fat 0.7
Protein 0.8

51
Q

What is refeeding syndrome

A

A collection of features that describe the rapid re-institution of feed in patients who have been starved.

Starvation - carbs metabolism switches to fat and protein breakdown.
Start feed. Insulin surge.

Shift of electrolytes - K, PO3, Mg intra cellular

Also altered sugar homeostasis, thiamine deficiency and salt/water retention

52
Q

Life threatening features of refeeding

A 
muscle weakness
resp failure
Cardiac dysrhythmias
Hypotension
Heart failure
Coma
Death
53
Q

Prevent refeeding

A

Establish who is at risk (NICE guidelines)

Careful re-establish feed at 10kcal/kg/day
Gradually increase

Monitor electrolytes and replace

Multivit replacement, thiamine

Dietician input

54
Q

Risk for refeeding

A

1 of: 2 of:
BMI<16. BMI <18.5
Weight loss >15% in 3-6/12. 10% weight loss
Little/no intake for 10 days. 5 days
Low K/PO3/Mg prior to feed. Hx of alcohol, drugs (insulin, chemo)

55
Q

Differential for low platelets and renal failure +/- neurological changes

A

MAHA - TTP/ HUS
Pre-eclampsia
HELLP
DIC

Autoimmune disease
Vasculitis
Infection - CMV, HSV, HIV, Hep B, sepsis

56
Q

Evidence of haemoloysis

A

Low Hb

Film - schistocyes (fragments)
Spherocytes (rounder smaller)

Reticulocyte count
LDH high
Low Haptoglobins
Raised bilirubin and urobilinogen

57
Q

Test for TTP

A

ADAMTS 13 reduced

Coombs test - negative

58
Q

How does TTP differe from HUS

A

TTP less likely to have renal failure

But more likely to have Neuro abnormalities

59
Q

Pathophys of TTP

A

ADAMTS 13 cleaves vWF

Reduction in ADAMTS means less cleavage

Large vWF factor - platelets aggregation and shearing, haemolysis

Triggers - congenital OR, acquired e.g. haemorrhagic colitis - e.coli, shigella

60
Q

Treatment of TTP in pregnancy

A

Involve haem and obs

Early delivery of foetus (+/- steroids for lung maturation)

FFP infusions as a temporary measure

DO NOT GIVE PLATELETS

Plasma exchange (removes auto-antibodies and replenish enzymes)

IV methyl-pred.

61
Q

Name some indications for plasma exchange

A

GBS
MG
Chronic inflammatory deyelinating poly

Renal: Goodpastures, ANCA vasculitis

62
Q

Process of plasma exchange

A

Blood drawn
Cellular components separated from plasma

Done by centrifuge or filter

Substitute patients plasma with done FFP, or HAS

63
Q

Complications of PLEX

A 
Bleeding
Infection
Allergic reaction
Fluid overload
Hypocalcaemia (infused citrate)
64
Q

Causes of SAH

A

85% aneurysm
10% non-aneurysmal
5% trauma, AV malformation

65
Q

Grading severity of SAH

A

WFNS Score - based on GCS and deficit

Fisher - 4 point radiological scale

Hunt and Hess - 5 point clinical scale

66
Q

WFNS class for SAH

A 
1 - GCS 15, no def
2 - 13-14, no def
3  13-14, def
4- 12-7 +/- def
5 3-6 +/- def
67
Q

Neurological complications of SAH

A

Rebleed - 24 hours - Coil or clip
Risk of intra cerebral haematoma
Hydrocephalus - EVD

DCI due to vasospasm - 5 to 10 days

68
Q

Diagnosis of vasospasm

A

Clinical - Neuro - reduced GCS +/- focal neurology
CVS - Hypertension, brady, arrhythmia

Cerebral angiography - gold standard

CT/MR angio
TCD - Lundegaard Ratio

69
Q

Treatment of vasospasm

A

Nimodipine, both prophylactic and tx
Mg - little evidence

IR - Balloon angio/intra arterial injections

HHH - (though not hypervol) drive the MAP, and haemodilute

70
Q

BP target in initial SAH tx

A

Aim of <180 until coiled/clipped

71
Q

Secondary measures in SAH

A 
Ventilate to normocapnoea
PaO2>10
Normal BM
Treat seizures
Get to Neuro centre
Sit up, loose ties etc
72
Q

Causes of thrombocytopenia

A

Reduced prodcuction
Increased destruction
Increased sequestration

Reduced: 
Bone marrow hypoplasia
Alcoholism
B12 loss
Methotrexate/valproate

Destructions
Immune - ITP/SLE/penicillin
Non - TTP/HUS/DIC
Sepsis/CVVH

Sequestration
Hypersplenism

73
Q

What is heparin

Where is it made

What does it do

A

Naturally occurring glycosaminoglycan

Made by mast cells and basophils from tissues rich in mast cells

Increases antithrobmin 3, in turn inhibit thrombin and Xa

74
Q

Pathophysiology of HIT

A

Type 1 and 2
1 - non immune, 2 immune
1 - more common
1 - 3 days, 2 5-10 days

IgG antibodies form to the heparin/platelet factor 4 complex
Causes platelets activation and thrombosis, subsequent depletion

75
Q

Diagnose HIT

A

4 T’s score (Thrombocytopenia, timing, thrombosis, oTher)

Specific ELISA testing for antibodies

76
Q

Management of HIT

A

STOP HEPARIN
Change to something else - argatroban
Or fondaparinux/danaparoid

Avoid warfarin until platelets recover
DO NOT GIVE PLATELETS
Avoid hep for 100 days

77
Q

4 T’s score

A

0-3 low prob
4-5 intermediate
6-8 high risk

78
Q

Criterial for brain stem death - pre-conditions

A

Cause of coma known (CT)
Irreversible
Deeply unconscious needing mechanical vent
Cardiovascularly stable

79
Q

BSD criteria - exclusions

A

No muscle relaxants or sedatives (may need to do benzo/thio levels)

Normal temp (34C)

Na 115-160
K>2
Mg/PO3>0.5

BM 3-20

80
Q

What should you do if there is benzos/thio on board

A

Observe for 2-3x the half like of the drug
Give antagonists
Plasma analysis (>10ug/L midaz, >5mg/L thio)

81
Q

Who does BSD

A

2 doctors
1 more than 5 years GMC registered
1 consultant

82
Q

Time of death in BSD

A

Completion of first set of test

83
Q

When might you not be able to do tests

A

High cervical cord injury - affects apnoea test

Facial trauma - can’t examine cranial nerves

84
Q

If you can’t do BSD, what other tests are there

A

Consider ancillary tests

Two types - electrical and flow

Electrical - EEG and SSEP

Flow - Cerebral angio (four vessel test)
TCD

PET scan??

85
Q

Describe the apnoea test

A

Increase FiO2 to 1.0

ABG - check PaCO2 and SaO2 similar to monitored value

Change ventilation to get an etCO2> 6.0 and pH < 7.4

Place suction catheter at 5l/m O2 into tube or CPAP

Leave for 5 minutes

Observe

Do another gas

CO2 rise by 0.5

86
Q

ECG features of a TCA overdose

A 
Prolonged QTc
Wide QRS
Arrhythmia
R/S ratio > 0.7 in aVR
Terminal R wave > 3mm in aVR
Right axis deviation
Sinus tachy
87
Q

Why do ECG changes happen in TCA overdose

A

Blocks fast Na channels —> wide QRS

Blocking of K —> long QTc interval

88
Q

Biochemical features of TCA od

A

Metabolic acidosis

89
Q

Features of TCA overdose

A

Neuro and Cardiac

Neuro - Reduced GCS, seizures, coma
CVS - sinus tachy, hypotension, prolonged QRS

Sympathetic - pupillary dilation, dry mouth and skin, retention and agitation

90
Q

Tx of TCA od

A

ABC
Tube if low GCS
Activated charcoal in 1 hour - needs an airway

Sodium bicarbonate

Seizures - benzo’s AVOID Phenytoin

Lipid emulsion

Treat hypotension - fluid/vasopressors (adrenaline over norad)

91
Q

Why does bicarb work on TCA overdose

A

Aim pH 7.5

Alkalinization reduces the affinity for the drug to the sodium channel

92
Q

Drugs to avoid in TCA

A

Anything potentiating a Na block

Phenytoin/flecanide, disopyramide

93
Q

Classify aortic dissections

A

Stanford
A - Ascending aorta +/- arch
B - Descending aorta distal to left subclavian

DeBakey
1 - Starts in ascending and propogates into arch
2 - ascending only
3 - descending only

IIIA - above diaphragm
IIIB - extends below

ESC groupings

94
Q

Why do type A need repairing

A

Typically involve it aortic valve - incompetent
Valve needs repair/reseat
Thoracic aorta is grafted

95
Q

Management features of type B dissections

A

Uncomplicated - BP reduction
Complicated - left thoracotomy
Complex endovascular procedures

96
Q

Convservative tx of a dissection

A

BP control - beta-block (verapamil if CI)
GTN/SNP (reduce BP but reflex tachy alone)

Aim MAP 60-65 (or lowest MAP to maintain perfusion)

If no joy:

Treat pain and anxiety
Consider clonidine
Consider dissection to renal vessels

97
Q

Goal of SSD

A

Prevent or eradicate oro-pharyngeal/gastric carriage of Potentially Pathogenic Microorganisms.

Thought to preserve non-pathological flora, which protect against overgrowth

98
Q

Four components of SSD

A

1 - selective eradication of PPM, use of orobase and NG ABx

2 - Systemic prophylaxis - cefotaxime - prevent resp infections from commensuals

3 - Hygiene and cross-contamination

4 - Regular throat swabs and faeces cultures

99
Q

Benefits of SDD

A

Reduce risk of nocosomial infection

Most ICU infections are opportunistic, aerobic, gram neg, bacilli.

Klebsiella, proteus, pseudomonas, these are present already and proceeded by colonisation

100
Q

Problems with SDD

A

Resistance

Diarrhoea

101
Q

Examples of nocosomial infections

A

UTI
HAP
Line infections/bloodstream
SSI

MRSA/VRE/C.diff

102
Q

What is C.diff

A

Gram pos
Spore forming
Bacteria

Causes illness when competitions bacteria wiped out by Abx
Normal component of gut flora

Causes pseudomembranous colitis —> toxic mega

103
Q

Risk factors for c.diff

A

Use of broad spec ABx
Increasing length of stay in hospital
Use of PPIs
Poor infection control processes

104
Q

Severity of c diff

A

Mild - normal WCC, 3 stools of type 5-7/day

Mod - WCC raised, 3-5 stools/day

Severe - WCC > 15, Temperature 38, Creatinine 50% rise, abdominal/radiology

Life threatening - Hypotension, ileus, megacolon, CT evidence

105
Q

Tx of C diff

A

Mild/mod - 14 days oral metronidazole

Severe - vancomycin oral. Refractory - oral plus iv metronidazole.
Conisder IvIG or rifampicin

Surgical input, bloo lactate, colectomy

106
Q

When to do a colectomy in c diff

A

Caecal dilation 10cm

107
Q

Causes of alveolar infiltration/ground glass

A

Infective - pneumonia, bacterial/viral/fungal

Non-infective 
  Cardiac - pulmonary oedema
   Idiopathic pneumonia syndrome
   Diffuse alveolar haemorrhage
   Bronciolitis obliterans (pulm complication of graft vs host)
108
Q

Investigate patient with alveolar ground glass from stem cell transplant

A 
Culture/infection:
   Blood, sputum, urine, BAL - MC&S
   Throat swabs, viral screen (adeno/rhino, EBV, influenza, RSV, HSV, CMV)
   Atypical
   Aspergillosis: galactomannan/ PCR
   PCP from sputum

Cardiac causes:
12 lead ECG
TTE

HRCT thorax

109
Q

Causes of deranged LFTs in stem cell transplant

A

Sepsis
Drugs - anti virals/anti fungal/abx

Viral - EBV
Fungal

GvHD (hepatitis, dermatitis, enteritis)

Veno-occlusive disease (thrombosis after chemo)

CCF - hepatic engorgement

110
Q

Cause of low platelets in stem cell transplant

A 
Reduced survival:
Sepsis
GvHD
Veno-occlusive
HIT
TTP
Decreased production:
Insufficient transplant
Poor marrow, made worse by drugs
Marrow fibrosis
Persistent/recurrent malignancy
111
Q

Classify haemopoetic stem cell transplants

A

Source of donor - autologous (own), allogenic

Matched or unmatched to HLA (human leukocyte antigens)

Source of cells (peripheral, bone marrow or cord blood)

Intensive of pre-transplant chemo regime:
Myeloblative (total destruction of patients marrow)
Reduced intensity conditioning

112
Q

Poor prognostic features in critical illness of HSCT

A 
MOF
MV
RRT
GvHD
Relapse of malignancy

FFICM (57 decks)

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