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Intensive Care Medicine > MCQ > Flashcards

MCQ Flashcards

1
Q

What systolic target in trauma? What’s the exception?

A

80-90mmHg, in TBI have to balance needs

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2
Q

What did the PROPPR trial show?

A

pragmatic randomised optimal platelet and plasma ratios trial
showed a sig decrease in exsanguination for 1:1:1 vs 1:1:2 FFP:plt:RBC
BUT no mortality benefit at 1 and 3 days
Sig underpowered

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3
Q

In trauma when should cryo be used?

A

When fibrinogen <1.5-2g/dl

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4
Q

In trauma, if pelvic bleeding what would make surgical packing more appropriate than IR?

A

FAST positive

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5
Q

How does audio-guided USS work when putting in lines?

A

It does not make image just a doppler sound

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6
Q

What are the two complications more likely in landmark vs uss technique for line insertion?

A

PTX and arterial puncture

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7
Q

What are the commonest causes and absolute % for end-stage renal failure in UK?

A 
DM (20-40%)
HTN (5-25%)
Glomerular inc IgA neph (10-20%)
Idiopathic (5-20%)
Intersitial disease (5-15%)
Rare- Renal art stenosis, Polycystic kidneys, vaculitis combined represent <5%
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8
Q

What’s the definition of CKD?

A

A disruption of renal function or structure for >3months

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9
Q

What % of patients with CKD end up with end-stage CKD?

A

1%

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10
Q

What, in addition to eGFR, is a marker of prognosis in CKD? What are the cut offs?

A

Albuminuria

A1 <30, A2 30-300, A3 >300

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11
Q

What efficiency do HME filters work?

A

70%

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12
Q

Wha efficiency of humidification are cold and warm water baths in the circuit?

A

30% and 90%

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13
Q

What efficiency do ultrasonic nebulizers have in terms of generating circuit humidity?

A

100%

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14
Q

Why are ultrasonic humidifiers not commonly used in circuit humidification?

A

Can be too efficient and deposit water droplets into the alveoli, for that reason we use it for meds instead

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15
Q

What is gas in small bowel and rectum only suggestive of?

A

Large bowel obstruction

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16
Q

Gas and fluid levels in small bowel means what?

A

Can be normal or suggest ileus but not necessarily an obstruction

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17
Q

Can Thiopentone cause bronchospasm?

A

Yes and laryngospasm

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18
Q

Which muscle relaxant has the least histamine release associated with it?

A

Vecuronium

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19
Q

At what level does the coeliac trunk arise?

A

T12

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20
Q

What are the first branches of the coeliac trunk?

A

L gastric, common hepatic and splenic art

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21
Q

What does the coeliac trunk supply?

A

Greater curvature of stomach, liver, gallbladder, spleen, pancreas

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22
Q

Where does the portal vein collateralise with the systemic venous network?

A

Oesophgeal, rectal, paraumbilica and a few small connections with colic and retroperitoneal veins

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23
Q

How does the IMA drain?

A

In health via the superior rectal, sigmoidal and L colic veins into the inferior mesenteric vein which then joins the splenic vein

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24
Q

What is first line treatment for Aspergillosis?

A

Voriconazole. Posaconazole is a resue therapy

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25
Q

What is the classic CT sign of Aspergillus infection?

A

The Halo sign which is a nodule surrounded by ground glass

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26
Q

What are the classes of anti-fungals?

A 
Cell membrane
Triazoles- Fluconazole, Voriconazole etc
Imidazoles- Ketoconazole
Polyenes- Amphoterecin (liposomal preparations fewer side effects and have surpassed deoxycholate preparations)
Allylamines- Terbinafine

Cell wall
Echinocandins- Caspo, Andiulafungin

Intracellular
Griseofulvin, Flucytosine

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27
Q

What are the site of action of antifungals?

A

Cell membrane (azoles), Cell wall (fungins), Intracelluar (Griseofulvin, Flucytosine)

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28
Q

If Voriconazole is contraindicated in Aspergilosis what is the next treatment choice?

A

Amphorecin B

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29
Q

What is the treatment of cryoptococcus meningitis?

A

2/52 Amphoterecin and Flucytosine followed by 8/52 fluconazole

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30
Q

Causes of pre-hepatic jaundice?

A

Haemolysis, haematoma absorption
Crigler-Najjar syndrome
Gilberts syndrome
Jaundice of newborn

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31
Q

Cause of hepatic jaundice

A

Cirrhosis, steatohepatitis, genetic-haemochromatosis, alpha 1, Wilsons,
From mets, autoimmune hepatitis, PBC, infection HAV HBV etc, liver abscess, heart failure and backpressure, toxins, HELLP

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32
Q

Drugs that cause hepato-toxicity

A

Hepatocellular- amidoarone, HAART, halothane, NSAIDs, PPI, rifamipicin, SSRI, paracetamol, TPN
Mixed- phenytoin, enalapril, amitriptyline
Cholestasis- steroids, TCA, erythromycin

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33
Q

What equation is used to calculate cardiac output from transpulmonay indicator dilution?

A

Stewart-Hamilton

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34
Q

How does oesophageal doppler measure cardiac output?

A

Measures descending aorta flow velocity and uses either measured or normogram data of aortic diameter to estimate volume. The proportion of cardiac output going to descending aorta is a large source of error

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35
Q

What is Fick’s principle?

A

blood to an organ can be calculated by dividing the amount of a substance taken up by the organ per unit time (A:V concentration difference).

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36
Q

Give a practical example of Fick’s principle in calculating cardiac output

A

The O2 update from lungs divided by the difference between mixed venous and arterial O2

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37
Q

What is the indirect Fick method

A

Uses CO2 instead of O2. The difference between arterial and venous CO2

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38
Q

What is the Penaz technique for cardiac output estimation>

A

A cuff with LED is put on finger. The cuff goes up and down to keep the light going through the finger and hitting the photosensor constant. The pressure changes correspond to the pressure waveform of arterial pulsation. From there through multiple assumptions CO can be calculated

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39
Q

What is first line treatments for non-high risk PE?

A

LMWH or Fondaparinux

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40
Q

When are LMWH and Fondaparinux not first line for non-high risk PE? What is the treatment?

A

If (ESC)creatinine clearance <30->UFH

(NICE) eGFR<30 then use UFH or dose adjusted LMWH with Xa levels

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41
Q

When can Rivaroxiban be used in PE?

A

Can be used as initial treatment in those with non-high risk PE by both NICE and ESC guidelines

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42
Q

What are symptoms of total Ant circulation stroke? What is the definition of partial Ant circ stroke?

A

Unilateral weakness +/- sensory defecit
Homonymous hemianopia
Higher cerebral dysfn (dysphasia, visuospatial disorder)
PACS is 2 of 3 of above

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43
Q

What are the signs of posterior circulation stroke POCS?

A

LOC, isolated homonymous hemianopia, cerebellar symptoms, brainstem signs

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44
Q

What are the cerebellar signs?

A

Ataxia, dysphagia, dysphonia, nystagmus

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45
Q

Lacuna infarcts (LACS) present how?

A

A subcortica stroke due to small vessel disease- unilateral weakness, pure sensory stroke or ataxic hemiparesis

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46
Q

How does malignant MCA infarct present and progress?

A

severe hemiparetic stroke with oedema within 24-48 hours causing raised ICP

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47
Q

How does carotid artery dissection usually present

A

Young people after trauma, headache and neck pain, Horner’s syndrome and CN palsies

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48
Q

What are the groups of pulmonary hypertension set out by Dana Point classification in 2008

A

6 groups
Group 1- PAH- idiopathic, congenital or disease related
1’- secondary pulm venous hypertension (occlusive disease)
2- secondary L heart failure
3- secondary chronic hypoxia or chronic lung disease
4- secondary chronic thromboemobolic disease
5- unknown or secondary multiple mechanisms (haem, vasculitic, metabolic)

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49
Q

What did the TRICC study look at and find?

A

‘Transfusion req in CC’ tested transfusion trigger 70 (aim 70-90) vs 100g/dl (aim 100-120) with non-sig trend to reduced 30day mort in restrictive arm. Those <55 and with APACHEII <20 were statistically sig reductions subgroups.
And increase in MI and pulm oedema in liberal arm

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50
Q

What is the evidence for keeping Hb>100 in ACS?

A

one pilot study (carson, brooks et al 2013 Am heart J)

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51
Q

What did the TRISS study find?

A

70 vs 90g/dl trigger for transfusion in septic shock. Found same as TRICC there was no difference in 90day mortality

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52
Q

In traumatic bleeding how do you decide if you use O neg or wait for cross match?

A

If having transient response to fluid await crossmatch if no response switch to o-neg

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53
Q

How is hyperK and hyperPO4 caused in tumour lysis?

A

Cell lysis

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54
Q

How does HypoCa occur in tumour lysis?

A

Binds with free PO4 and deposits calcium phosphate in tissues

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55
Q

Why do you get hyperuricaemia in tumour lysis?

A

Cell breakdown releases nucleic acids which convert into uric acid

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56
Q

How does renal failure occur in tumour lysis syndrome?

A

Multifactorial but ppt of uric acid and CaPO4 in renal tubules are major contributors

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57
Q

How prevent tumour lysis?

A

Fluid and hopefully pre-treat with rasburicase/allopurinol

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58
Q

How treat established tumour lysis?

A

Correct hyperK and consider phosphate binders for PO4. RRT if needed by standard defn, Ca corrected cautiously as can worsen renal failure through CaPO4 deposition

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59
Q

Defn mild c.diff infection and treatment

A

No WBC, <3 stool/day-> PO metronidazole 10-14/7

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60
Q

Defn moderate c.diff and treatment

A

WBC 10-15 and 3-5 stool/day

Metronidazole 10-14/7

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61
Q

Dfn severe c.diff and treatments

A

WBC>15, AKI (50% up from baseline), T >38.5, severe colitis
PO vanc 125mg QDS 10-14/7 if low risk
Fidaxomicin if frail or receiving abx otherwise

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62
Q

Defn and treatment for life-threat c diff

A

shock, partial/complete ileus, toxic megacolon, CT evidence of severe disease
PO vanc 500mg QDS 10-14/7 and IV metronidazole TDS

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63
Q

What are inclusion criteria for ECMO?

A

Murray score >/=3, >/=2.5 and deteriorating quickly, uncomp resp acidosis pH<7.2 or bronchopleural fistula

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64
Q

Exclusion criteria for ECMO?

A

High vent support >7/7 inc PIP >30 FiO2>0.8
Sig co-morbidity
Contra-indication to anticoag

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65
Q

How do you calcualte the Murray score?

A

The score for each of the below components divided by the number of components
Score 0-4 for:
CXR quadrants involved (0=0, 4=4)
Compliance (Vt/Pplat-PEEP) (0=>80, 60-79, 40-59, 20-39,4=<20)
PEEP- 5=0, 6-8, 9-11, 12-14, 4->14)
PF ratio- >40=0, 30-40, 23.3-30, 13.3-23.3, < 13.2=4

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66
Q

What are predictors of difficult to BVM?

A 
M- mask seal-beard etc
O- obesity/obstruction
A- age>55
N -No teeth
S- sleep apnoea/stiff lungs
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67
Q

How many attempts at intubation should be tried before proceding to LMA in RSI?

A

3

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68
Q

What are subtypes of COPD and how do they manifest?

A

Chronic bronchitis and empysematous change. The former are at risk of CO2 retension, pulm HTN and sleep apnoea.
THe latter have high work of breathing and hyperinflation

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69
Q

Berlin criteria for ARDS?

A

Within a week of known trigger or start of resp symptoms
Bilateral infiltrates in 2 or more quadrants
Not fully explained by another cause

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70
Q

Definition of mild, mod and severe ARDS?

A

PEEP 5 or more
Mild- PF 200-300 (26.7-40kPa)
Mod- 100-200 (13.4-26.6)
Severe <100 (<13.3)

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71
Q

Causes of ARDS

A

Direct (inside lung) and indirect (outside lung)

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72
Q

What cells produce stomach acid?

A

Parietal cells make HCl

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73
Q

What do Chief cells produce in stomach?

A

Pepsinogen which is activated to pepsin a proteolytic by acid conditions

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74
Q

What hormones promote acid environment in stomach>

A

gastrin, histamine and parasymp system

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75
Q

What hormonoes inibit acid production in stomach?

A

Somatostatin, PGE2, PPI/H2 blocker, anti-muscurinics

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76
Q

How does pyloric stenosis result in hypoK?

A

As the body wants H+ it exchanges K+ for H+ in distal tubule

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77
Q

What is in hospital mort for first SBP and 1 year mort?

A

1st presentation 20%, 1 year mort 30-90% depending on where on the journey the patient is. SBP should be a trigger for liver transplant consideration

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78
Q

What bacteria cause SBP?

A

E.coli (40%)
also klebsiella
Less likely G+ve cocci like strep and enterococcus

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79
Q

Definition of cardiogenic shock

A

inadequate tissue perfusion secondary cardiac dysfn

BP<90mmHg, pulm oedema, signs imparied perfusion

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80
Q

Haemodynamic definition of cardiogenic shock

A

CI<2.2l/min/m2, wedge pressure >18mmHg

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81
Q

What drug is a good choice in shock secondary AMI?

A

Levosimendan (inc availablity of intracelluar Ca) is an inotrope that doesn’t increase myocardial O2 demand but in practice NA and Dobutamine are commonly use.

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82
Q

What did IABP-SHOCK-II trial show?

A

no improvement in 12 month mort with use of IABP in patients undergoing early re-vascularisation so IABP not used

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83
Q

Signs of life threatening asthma?

A

reduced resp effort, silent chest, arrhythmia, reduced GCS, hypoxia, normal PaCO2, hypotension, PEF<33%

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84
Q

Signs of severe asthma?

A

PEF 33-50%, HR >110, RR >25, unable to speak in sentences

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85
Q

What is the RR reduction of failure and of complications in USS CVC insertion vs landmark?

A

Failure 86% reduction with 41% reduction in first pass success (IJV)
Complications 57% reduction (90% reduction in subclavian complications!)

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86
Q

Descending from diaphragm what are the main arterial outlets from aorta in abdomen?

A 
Phrenic artery
Coeliac trunk
Supra-renal art
SMA and renal arteries
Gonadal
IMA
Iliacs
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87
Q

What are the branches of the coeliac trunk

A

on L splenic art and coming off at about 1o’clock the L gastric artery
on R common hepatic which gives off gastroduodenal (greater curve and joins splenic) and right gastric which joins the L gastric and supplies the lesser curve. R common hepatic then becomes the hepatic proper

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88
Q

What study demonstrated non-inferiority of Rivaroxiban and Warfarin/LMWH

A

EINSTEIN-PE

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89
Q

What score is used to assess risk of bleeding from anticoagulation as OP? What are it’s constituents?

A

HAS-BLED
HTN, renal disease (Cr>200), Liver disease (TB x2 and ALTx3), stroke, major bleeding or concern, labile INR, >65, anti-plt/NSAID, alcohol >8 ‘drinks’/wk

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90
Q

what is NICE guideline for IVC filters?

A

Not recommeneded unless confirmed PE and anticoag is contra-indicated. Should be removed as soon as anti-coag starts

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91
Q

If PE diagnosed, anticoag given and dyspnoea/functional limation persists at 3-6/12 what pathway should be followed?

A

ESC PE guidelines suggest TTE for anyone with symptoms or those at high risk of CTEPH. Probability of pulm HTN is then rated low, medium,high. If intermediate do BNP, CPET and consider if risk for CTEPH high any one requires VQ scan and if defect for pulm HTN specialist work up

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92
Q

What are risk factors for CTEPH

A

T4 replacement, malignancy, prev or recurrent VTE, anti-phos, infected pacemaker, splenectomy, non-O blood groups

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93
Q

Head and neck (usually extra-cranial) dissections account for 20% of all strokes between 20-45. What are the risk factors?

A

Classically think of trauma but also chest infectinos, smoking, HTN, OCP but also Ehler’s-Danlos, high homocysteine levels and alpha 1 def.

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94
Q

How do extra-cranial internal carotid artery dissections present?

A

the commonest type of head/neck dissection 2.5% of all first strokes.
Classic triad:
1. Pain on side of head, face, neck
2. partial Horner’s
3.followed in hours/days later by cerebral/retinal ischaemia (intimal tear causes clot and emobolism)

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95
Q

Why is the vertebral artery most likely to dissect in trauma?

A

Most mobile of arteries and likely to go at C1/2

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96
Q

Whats the evidence for treating carotid/vertebral artery dissection with antiplt/warfarin to prevent embolic events?

A

None, no RCT. A trend toward more events in aspirin only but not significant. Who knows whats best

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97
Q

What are the components of the APACHE II score?

A 
A-Age
B- RR, FiO2
C- HR, MAP
D- GCS
E- Temp
Bloods- WBC pH, Na, K, Cr, AKI (clnical judgement), hct
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98
Q

what are the qSOFA criteria?

A

GCS <15, RR>/=22, SBP <100

2 or more= 10% hosp mort

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99
Q

Definition of sepsis?

A

Life threatening organ dysfunction caused by disregulated host response to infection

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100
Q

How is organ dysfunction defined in sepsis 3 defn?

A

EIther 2 or more points on qSOFA

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101
Q

How is septic shock defined in sepsis 3?

A

pressor to maintain map 65, lactate >2 and not hypovolaemic

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102
Q

What did the ALBIOS study find?

A

ALBIOS comapred albumin 20% and crystalloid with crystalloid alone. No mortality benefit for aiming albumin >30 but was safe.

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103
Q

What subset is ALBIOS knowns for?

A

In a post-hoc subset analysis there was a significant mortality benefit to those with septic shock. That was the same for sepis-2 and sepsis 3 criteria

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104
Q

What did CESAR looks at?

A

Is ECMO safe, efficacious and cost-effective cf standard practice?

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105
Q

Findings and limitations of CESAR?

A

Single centre really, sig cross-over and poor followup data. Only recommendation is Murray>3 or pH<7.2 despite optimum vent (lung protective) should be referred to ECMO centre

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106
Q

According to DAS, how many intubation attempts?

A

3, changing something with each attempt, +1 from a more qualified person

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107
Q

What interventions after Loraz and phenytoin in status epilepticus?

A

Propofol induction
Then Midaz 0.1-0.2mg/kg bolus followed by 0.05-0.5mg/kg/hr
Then Thio

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108
Q

Define status epilepticus and refractory status

A

Status is seizure for over 30min despite mx or multiple seizures within 30min without recovery
REfractory 30-90min

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109
Q

What is the management of status epilepticus in children?

A

Loraz 0.1mg/kg
Phenyoin 20mg.kg over 20min
Can give Praldehyde 0.8mg.kg if required

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110
Q

Why do cirrhotic patients hold onto (or not excrete enough) Na?

A

Splanchnic arterial vasodilatation from portal htn causes a decrease in effective arterial blood volume with activation of the sympathetic system and up-regulation of RAAS.

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111
Q

What does a SAAG >11 g/L mean in terms of ascites?

A

97% accuracy of saying it is due to portal HTN

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112
Q

Why measure total protein in ascitic tap?

A

If <15g/L at high risk of SBP and may benefit from prophylactic abx

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113
Q

With development of ascites there is a 40% 1 year mortality. What are the predictive factors that would mean poor prognosis?

A

HypoNa, low BP, inc Creatinine, low urine Na (note only creatinine in MELD and none in CPugh)

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114
Q

What diuretics for ascites?

A

First presentation Spiro 100->400mg then Furosemide. If recurrent give 100 Sprio, 40 furosemide and increase both stepwise over 7 days

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115
Q

What is the cutoff for positive neutrophil count for SBP?

A

250cells/mm3 though it is more specific at 500

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116
Q

What are the common organisms to cause SBP>

A

Culture +ve in only 40%

E.coli, strep and enterococci most likely

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117
Q

What is bacterascites?

A

When WBC <250 but positive culture. If other signs/symptoms treat otherwise re-sample

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118
Q

What’s first line abx for SBP according to EASL 2010 guideline?

A

cepholasporin- mostly cefotaxime though Taz is what I have seen used

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119
Q

When may albumin be useful in SBP?

A

HRS in 30% with abx only, but reduces to 10% if 1.5g/kg on day 1 and 1g/kg on day 3 if TB at baseline >68 and Cr >88. Not a great study so A2 guideline

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120
Q

Define hepatorenal syndrome

A

occurrence of renal failure in a patient with advanced liver diseas in the abscence of a cause for renal failure

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121
Q

Criteria for HRS diagnosis?

A 
Cirrhosis with ascites
Cr >133
no shock, no hypovolaemia
Albumin 1g/kg/day for 2 days tried
No nephrotxics
NO renal parenchymal disease
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122
Q

What are the four factors that contribute to HRS?

A
  1. Splanchnic arterial dilatation
  2. Sympathetic nervous and RAAS activation causing shift of renal auto-regulation curve and more susceptible to MAP changes
  3. Impaired cardiac fn secondary cirrhotic cardiomyopathy which cannot respond to 1.
  4. increased synthesis of vasoactive substances such as thromboxane A2 and endothelin 1
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123
Q

Definition of neutropenic sepsis?

A

<0.5 neuts and fever >38 or signs/symptoms

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124
Q

Symptoms hyperK

A

> 6.5 muscle weakness, malaise, nausea, parasthesia

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125
Q

What causes the characteristic changes on ECG for HyperK?

A

hyperpolarisation of excitable membranes

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126
Q

What is the earliest and most sensitive change to ECG in hyperK?
What other abnormalities eventually with same?

A

Tented T-waves (T>R)

Eventually wider and flat P and QRS lengthens

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127
Q

When do you see J waves on ECG?

A

hypothermia

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128
Q

What is the Marshall score and what is it used for?

A

Pancreatitis

PF ratio, Cr, BP and pH

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129
Q

What % of pancreatitis is severe and of those what % get ARDS?

A

15-20% develop severe panc

Of those 33% get ARDS and account for 60% of early deaths

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130
Q

What is thought to be the mechanism of ARDS in pancreastitis?

A

SIRS and neutrophilic activation and release of pancreatic protelytic enzymes (elastase) which then damages lung microvasc and cause third space losses in lungs

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131
Q

What is Well’s score for PE?

A

Signs of DVT (3), Alternative diag lesslikely than PE (3), Tachy (1.5),immobile >3days or surgery within 4/52 (1.5), prev VTE (1.5), Haemoptysis (1), Active cancer (1)
Therefore most emphasis on clinical exam and what clincian thinks
Score >4 ->CTPA

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132
Q

Well’s score for DVT?

A

All of equal weight (1) except last one (-2):
Reason for it -Ca, recent immonilisation and surgery within 3/12, had it before
signs of it- localised calf ternderness, swelling of whole leg >3cm, pitting oedema in symptomatic leg, varicose veins,
Dont’ think they have it - an alternative diagnosis is at least as likely
Score >2 for USS within 4 hours

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133
Q

If DVT suspected using Well’s score and USS is negative what are the next steps? If the test is positive what then>

A

DVT -ve on USS but Well’s high then do D-dimer. If positive repeat scan in 1/52

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134
Q

When should local thrombolysis be offered to someone with a ilio-femoral DVT?

A

If they’ve had it for less than 2 weeks and are low risk of bleeding with at leat 1 year of life expectancy.

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135
Q

When would you use heparin in DIC?

A

For thrombotic complications usually chroni

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136
Q

What are the transfusion thresholds in DIC for plt and FFP

A

If bleeding correct plt if <50, if not replace when <20. If overtly bleeding correction with FFP appropriate

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137
Q

What is the triad of DIC?

A

Fibrin deposion, plt aggregation and microvasc occlusion

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138
Q

What bacteria are more likely to cause DIC?

A

G-ve and those that produce endo-toxins

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139
Q

What are non-infective causes of DIC?

A

trauma, burns, long-bone fractures, obstetric complictations (eclampsia, amniotic embolus), malignancy, transplant rejection

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140
Q

What is the mechanism of DIC?

A

Thought to feature one or more pro-coagulant factor such as intra-cellular contents, endoxtoin, tissue factor or lipopolysaccharide

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141
Q

What is the key to treat DIC?

A

Treat the cause

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142
Q

What heparin is used in DIC if microvascular clots predominate?

A

LMWH rather than UFH

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143
Q

What is dose of Thiopentone?

A

1-5mg/kg

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144
Q

Which causes more hypotension Thiopentone or Propofol?

A

Propofol

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145
Q

What are the classes of lactataemia?

A

Type A and B

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146
Q

What is the cause of type A lactataemia?

A

increased production due to lack of O2 for whatever reason (hypoperfusion, severe anaeamia, exercise, CO poisoning)

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147
Q

What are the causes of type B lactataemia? What are the subcategories?

A

Non- hypoperfusion
B1- underlying disease such as phaeo, leukaemia, organ failures, pancreatitis, short bowel
B2- drugs (Beta agonists, arenaline, alcohol, bacterial endotoxins, paracetamol)
B3 - inborn errors of metabolism

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148
Q

Lactate is produced from glycolysis, what can that sometimes cause a lactataemia?

A

Endogeous of exog catecholaemines increase glyolysis, along with sepsis and trauma/burns so more lactate is made

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149
Q

Lactate is also made anaerobically from pyruvate. What states increase pyruvate concentrations therefore pre-disposing to lactate formation?

A

Thiamine deficiency, critical illness, malignancy esp lymphoma and leukaemia

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150
Q

Where is lacate metabolised?

A

Largely 70% liver but also anywhere with mitochondira. Renal is only 5% but can go up when lactaemia is present.

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151
Q

How does phentolamine work?

A

Predom alpha 1 receptors

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152
Q

How does methyldopa exert its cardiovascular effects?

A

Alpha 2 receptors reducing SVR

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153
Q

How does increasing alpha 2 receptor agnoism affect SVR?

A

Reduces NA production

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154
Q

List some Alpha 1 receptor blockers

A

phentolamine, phenoxybenzamine, prazocin

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155
Q

List some alpha 2 blockers

A

methyldopa and clonidine

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156
Q

What drugs work by increasing locally produced nitric oxide?

A

GTN, ISMN causes direct relaxation of smooth muscle tone

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157
Q

How to Beta blockers work?

A

act on G-protein coupled adrenoreceptors which competitively inhibiting cell membrance receptor which in turn reduces cAMP and reduction of intracellular Ca therefore reduces contractility.

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158
Q

What is the acute treatment for thombotic stroke once thrombolysis complete? When should statins be started?

A

Aspirin 300mg for 2/52
No statin in acute phase
(PPI only if previous dyspepsia wiht aspriin)

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159
Q

What is the BODE index and how is each part scored?

A

Used in mortality prediction in COPD
B-BMI <21 (1),
O- obstructive FEV1 >65% (0), 50-64% (1), 36-49% (2), <35% (3)
D- Dyspnoea MMRC dyspnoea scale dysp on walking on flat (1), stops after 100yds/ few min (2), housebound on dressing (3)
E- 6min ET- >350m (0), 250-349 (1), 150-249 (2), < 149 (3)

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160
Q

What is the mortality associated with acute TTP?

A

10% though another card says 50% which seems more plausible

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161
Q

What is the cause of primary TTP?

A

related to enzyme deficiency in breakdown pathway for large von Willibrand factor multimers leading to plt aggregationand microvas coag

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162
Q

Causes of acquired TTP?

A

idiopathic (autoimmune), malig, HIV, preg, drugs (immunosuppressants, antiplt agents)

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163
Q

What are the forms of MAHA?

A

TTP, HUS, DIC, HELLP

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164
Q

Classic presentaion of TTP

A

Fever, neuro symptoms, renal failure (with MAHA and thrombocytopenai)

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165
Q

Treatment of TTP?

A

Plasma exchange but can use steroids, stop when normalised bloods. Plt treatment avoided unless life threatening bleed.

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166
Q

If plasma exchange and steroids are already in use for TTP what else can be added in extremis?

A

Rituximab (steroid sparing and as adjunct)

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167
Q

What does SDD (selective decontamination of the digestive tract) target?

A

15 most common pathogens on ICU:
MSSA, s.pneumonia, H. influenzae, maroxella, e.coli, candida all normal flora. And abdnormal flora Klebsiella, Enterobacter, Citrobacter, Serratia, Proteus, Morganella, Pseudomonas, Acinetobacter, MRSA

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168
Q

What is SDD (selecgive decontam digestive tract)

A

The idea from 80s is to prevent overgrowth of 15 common pathogens and has been shown to reduce infections in ICU (means infections are overgrowth of flora). Cost and resistance means its not really used.

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169
Q

What is the SDD protocol?

A

4/7 PO cefotaxime 100mg/kg/day! And PO tobramycin, amphotericin B, polymyxin and Vancomycin

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170
Q

What are the CSF variables normally?

A

Open pressure <20, clear, glucose 2/3 blood, protein 35mg/dl, WCC 0-3, no cells predominate

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171
Q

What are the CSF variables seen in viral meningitis?

A

Normal/high open pressure, clear, normal glucose, 50-100mg/dl protein, 5-1000 WCC lymphocytes

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172
Q

What are the CSF variables in bacterial meningitis?

A

Opening pressure high, cloudy, low glucose, >100 protein, 100-50K WCC mostly neurophils

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173
Q

What does fungal meningitis look like on CSF?

A

Very high opening pressure, clear or cloudy, low-normal glucose with 20-50 protein, 0-1000 WCC mostly lymphoctes

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174
Q

What does a TB CSF sample come back with from lab?

A

High opening pressure, yellow colour, very low glucose, 100-500 protein and 25-500 WCC mostly lyphocytes

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175
Q

How does TB meningitis usually present?

A

Insidious course over weeks, similar story to acute meningitis, chronic headache, low grade fever

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176
Q

What viruses commonly cause meningitis?

A

enterovirus, HSV, chicken pox, HIV, mumps

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177
Q

What organisms cause meningitis <3months of age?

A

G B strep, E.Coli, Listeria, Neiserria, S. pneumonia, S. aureus

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178
Q

What organisms cause meningitis in children?

A

Neiserria, H. influ, s. pneumonia

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179
Q

What organisms cuase meningitis in adults?

A

S. pneumonia, N meningitidis, s.auraus, Listeria (>65), Klebiella

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180
Q

What organisms more likely to cause meningitis post trauma and in neurosurgical settings?

A

Aerobic G-ve eg E.coli

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181
Q

What is the incidence of N.meningitidis, s.pnuemonia, s.aureus causing meningitis?

A

22% N.men
18% S.pneumoina
10% S. Aureus
5% both E.coli and GBS

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182
Q

What are the complications and the incidence of complications in ECMO?

A

Major bleed 41%, Death 40%, sign infection 30%, circuit clot 19%, lower limb iscahemia 17% oxygenator failure 15%, compartment syndrome 10%, stroke 9%,DVT, 8%, LL amputation 5%, ICH 2%, air embolus 2%, major vessel rupture 2%

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183
Q

When would you do a pleural fluid amylase?

A

Pancreatic or oesophageal pathology

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184
Q

Causes of exudative pleural effusion

A

Malig, pneumina, TB, PE, autoimmune such as RA, asbestosis, pancreatitis

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185
Q

When would you do a pleural fluid pH?

A

If suspect inection/empyema

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186
Q

When is glucose a useful test of pleural fluid?

A

If RA suspected (usually young men early in disease) would be low

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187
Q

When is CT warranted in pleural effusion?

A

CT with pleural enhancement should be done before drainage in all complicated infective and undiagnosed exudative effusions

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188
Q

What are the four main categories of indication for PPM?

A

Brady 2 nodal dysfn
Avoidance or treatment of arrhythmia (overdirve eg)
CV optimisation
Specific conditions like heart transplant

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189
Q

What % population have a PFO?

A

20-30%

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190
Q

What is the sensitivity of TTE and TOE for IE?

A

TTE 50%, TOE 90-100%

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191
Q

Which heart chamber is usually affected first in pericardial effusion?

A

RA filling

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192
Q

What two wavelengths of light are used in pulse oximetry?

A

660 (deoxy) and 940nm (oxy)

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193
Q

What are the findings in TURP syndrome?

A

Hyponatraemia from fluid absorption and glycine toxicity, most people absob 1L during procedure

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194
Q

TURP syndrome is caused by irrigation fluid, why is the fluid so hypotonic?

A

Electrolytes would make it conduct the diathermy current

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195
Q

What is the loading and infusion rate of aminophylline in asthma?

A

5mg/kg over 20min then 0.5mg/kg/hr

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196
Q

What is the frequency of a persistent left SVC?

A

0.5% of population, higher in those with cardiac defects where it can be 1:5

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197
Q

Where do persistent L SVC usually drain?

A

Coronary sinus usually but can go straight into LA

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198
Q

The commonest cause of nec fasciitis? And other causes?

A

Group A strep (60%) (and group B, S. aureus and coliforms such as Klebsiella, Enterobacter and E.coli

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199
Q

Why is Clindamycin included in first line regimen for nec fasc?

A

It has an additional benefit over penetrance that it reduces the production of strep super-antigen

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200
Q

What are the treatment priorities as listed in the guideline for anaphylaxis?

A
  1. Remove trigger
  2. IM adrenalin
  3. High flow O2
  4. IV fluid challenge
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201
Q 
Give afferent and efferent CN for the following reflex
1. pupillary light
2. corneal
3. oculovestibular
4. Gag
5. Cough
6 Motor response to pain
A
  1. II and III
  2. V and VII
  3. VIII, III IV and VI
  4. IX and X
  5. X and X
  6. V abd VII
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202
Q

If only one ear is available for the oculovestibular reflex can the test be conducted?

A

Yes

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203
Q

What is the starting CO2 in an apnoea test for brainstem testing?

A

> 6 or >6.5 if a chronic retainer

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204
Q

What must happen to CO2 and pH in apnoea brainstem death test for it to be failed by a dead patient?

A

pH <7.4 and pCO2 >0.5kPa cf start

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205
Q

What are the points of the Glasgow-Imrie score?

A 
PANCREAS
pO2<7.9
Age>55
Neut>15
Ca <2
Renal Ur >16
Enzyme LDH >600
ALb <32
Sugar >10

PPV 79%
The transition point is between score 3 and 4

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206
Q

What are the types of acute pancreatitis?

A

Necrotising and intersitial oedematous

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207
Q

What is required for diagnosis of pancreatitis?

A

Two of

1. typical history and pain, 2. Amylase at least 3x normal, 3. characteristic findings on CT/MRI

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208
Q

In what situation is the amylase likely to be less than 3x normal in someone who has pancreatitis?

A

If they are are a delayed presentation

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209
Q

What percentage of people with acute pancreatitis have necrotising pancreatitis?

A

5-10%

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210
Q

Is there a link between the extent of pancreatic necrosis and the probability of it becoming infected?

A

No

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211
Q

What gives the most reliably early indicator of mortality in pancreatitis?

A

Persistent organ failures, not the presence of absence of local complications of the pancreatitis itself

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212
Q

What is the modified Marshall score and when is it used?

A

Pancreatitis, can be done daily
PF ratio, renal function and BP off inotropes, score 2 or more means persistent organ failure which confers a mortality risk

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213
Q

Define pancreatic pseudocyst

A

A walled off collection outside the body of the pancreas only can be called such 4 weeks after initial symptoms

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214
Q

What is CARS?

A

Compesnatory anti-inflam response syndrome (can increase risk of infection apparently)

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215
Q

Should pancreatitics be NBM

A

No unless good reason, start feed within 72 hrs, anecdotal to give NJ as better tolerated

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216
Q

What are the three underlying pathological causes of pancreatitis and some examples of each?

A
  1. Ductal dysfunction- GS, malig, post ERCP (alcohol)
  2. Acinar injury - trauma, ischaemia, drugs (alcohol)
  3. Defective intracellular transport- hyperCa, hypertrigs (alcohol)
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217
Q

What is the sequence of events leading to pancreastitis?

A

Acinar cell damage leads to early conversion of trysinogen to trypsin and local digestion

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218
Q

There are three phenotypes of DIC what are they and what is the underlying pathophysiology?

A

You can have high fibrinolysis (bleeding) or high thrombosis (clots). The former usually seen in malignancy particularly haematological and results in bleeding, the latter in sepsis (and results in organ failure due to microvascular thombi). If however you have both you get massive bleeding and a consumptive picture. You can have a little bit of either which is termed pre-DIC

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219
Q

What does Pre-DIC look like and is it worth treating

A

Difficult to identify but it is worth treating

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220
Q

What is the scoring system for DIC and what values are included?

A

ISTH overt-DIC

Plt count, D-dimer, PT and Klauss

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221
Q

When is heparin given in DIC?

A

When microvessel thrombosis dominates, not when someone is bleeding. Small RCT favours LMWH with Xa measurements

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222
Q

What should be done with VTE prophylaxis in DIC?

A

Cont it

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223
Q

GIven DIC is partly microvessel thombi can you give TXA?

A

Yes if the bleeding/major bleeding phenotype

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224
Q

What is the untreated mortality of TTP?

A

90%, even with treatment the mortality is still 50%, half of which in the first 24hrs of presentation

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225
Q

TTP can be congenital and acquired, what does ADAMTS13 do that makes its absence pathognomonic?

A

ADAMTS13 cleaves ultra large vWF, if it’s absent then the ultra large structure causes massive shear forces and major platelet activation and aggregation in all organ systems

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226
Q

What is the pentad of TTP symptoms and signs? What are its short comings?

A

Thrombocytopenia, MAHA, neuro symptoms, renal impairment and fever. 35 % of people don’t have neuro features at presentation and fever and renal impairment are variable.

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227
Q

If you are convinced you have TTP but early need for RRT what may be the alternative diagnosis?

A

Unusual for TTP to need RRT straight away, consider HUS

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228
Q

Whats issue with not being able to use pupillary reflexes in brainstem death testing?

A

Its the only mid-brain nerves we test

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229
Q

Apart from pentad of signs and symptoms of TTP what other issue can the patient have?

A

Abdo pain from mesenteric ischaemia

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230
Q

What is seen on blood film in TTP?

A

Schistocytes

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231
Q

Why test troponin in TTP work up?

A

Sinister sign of coronary occlusion and is a leading cause of early death

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232
Q

What can cause a false positive ADAMTS13 result?

A

Activity usually low <40% but >5% in uraemia, sepsis, post op, pregnancy

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233
Q

What viruses do you look for in TTP workup?

A

Autoimmine screen and also HIV, HAV, HBV and HCV

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234
Q

When is TTP particularly difficult to diagnose?

A

Post-partum, 25% of all TTP is pregnancy related. Seems to be more neuro involvement and less renal cf HUS

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235
Q

Which drugs should be avoided in TTP because they may be the cause or ppt another attack?

A

Quinine and oestrogen containing OCP

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236
Q

Which cell type of malignancy is most associated with TTP

A

adenoca

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237
Q

What is treatment for diarrhoea +ve HUS and diarrhoea -ve

A

D+ve is supportive +/- RRT secondary verotoxin

D-ve is similar to TTP and is treated with PEX and eculizumab

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238
Q

What dose of steroid would you give alongside PEX in TTP?

A

1g Methylpred BD for 3/7 or 1mg/kg/d pred

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239
Q

When is Rituximab considered in TTP?

A

If neuro symptoms on admission

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240
Q

What is the tira of HUS?

A

MAHA, thrombocytopenia and renal failure

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241
Q

Do you need a PPM if you have a sinus pause during sleep test for OSA?

A

No it is usually reversible as long as no symptoms

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242
Q

Which AV blocks require PPM?

A

3rd degree and any second degree with symptoms even if the bradycardia is iatrogenic because of meds needed for something else.
Also any AV block that has a pause >3s even without symptoms or any escape rate <40 even if asymptomatic

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243
Q

If you have 2nd or 3rd degree HB with AF when would you insert PPM?

A

If you have a pause of 5 or more seconds

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244
Q

What about a PPM if AV block only present during exercise?

A

Yes, PPM needed as long as there is no inducible ischaemia

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245
Q

What is pacemaker syndrome?

A

No universal definition but is the loss of improvement in symptoms due to the pacemaker. Used to be single wires cause AV dissassociation and retrograde flow. Now can happen if threshold for capture changes (usually in A lead as we would notice if the V lead stopped doing its thing). This leads to the same thing, AV dissassociation

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246
Q

Is PPM needed in 1st degree HB?

A

Not usually but if PR>0.3s then yes

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247
Q

If you have a bundle branch block is PPM indicated?

A

No unless the bundle branch block is alternating the caveat being that you must also be asymptomatic. If symptoms for any weirdness then PPM should be considered

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248
Q

If you’re post MI and have a transient 3rd or 2nd degree block what should be done?

A

As EP study may be needed + PPM or simply a PPM

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249
Q

Carotid sinus becomes more sensitive with age and may ppt syncope, when would PPM be advised?

A

When pause >3s or sig bradycardia from spont carotid pressure or on tilt table

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250
Q

When would you use overdrive pacing?

A

When someone has SVT or VT that is demonstrably terminated by overdriving after ablation and drugs have failed

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251
Q

When is cardiac resynch therapy indicated?

A

Someone who is NYHA III or IV with LVEF<35% and QRS>0.12s and SR (class I), and AF (class II recommendation). CRT with or without defib is equal though with defib may be better we don’t know. If you’re putting in a PPM for something else and the above applies by NYHA I or II CRT should be considered

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252
Q

When is PPM useful in HOCM?

A

If given with a small AV delay the LVOT gradient is reduced (most useful if grad >30mmHg at rest or>50 on exercise) and even when pacing removed it persisted meaning remodelling may have occurred. That said subsequent RCT showed ++ placebo effect and no objective correlation

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253
Q

What are the class I indications for ICDs

A

Anyone who survives a VF or VT arrest/instability if no completely reversible cause
Structural heart disease if VT even if stable
VT on ESP but unexplained symptoms
LVEF<35% with MI after40 days if NYHA IIor III or <30% and NYHA I
Non ischaemic DCM with EF<35% and NYHA II or III

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254
Q

What are the main differences between child and adult airways?

A

Children- narrowest point immediately below vocal cords and is most open in the neutral rather than head tilt position. Children have larger tongues and nasal passages are smaller

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255
Q

If you are a lone resus responder to an arrested child what should you do? Why is that different to adults?

A

Check for signs of life if safe, then give five rescue breaths and check for life again. If not then do 1min CPR before going to get help.
Adults you should go for help before CPR because you need a defib

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256
Q

What drugs are most likely to cause long QTc?

A

Anti-dysrhythmics class Ia and III are most likely. Sotalol (and quinidine) causes Torsades in 2-4% of patients receiving it. Amiod does prolong QTc but TdP is unlikely

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257
Q

Amiodarone causes long QT as often as Sotalol (2-4%) why do we use Amiodarone and not really Sotalol?

A

Sotalol degenerates into TdP, Amiodarone less so

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258
Q

Give some drugs commonly used in ICU that cause long QTc

A 
TCA and SSR
Cipro, Erythro (etc), metronidazole,co-trimox
Haloperidol
Ondansetron
Dexmetatomidine
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259
Q

What size molecules down haemodialysis filter?

A

Small molecules

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260
Q

What size molecules does haemofiltration filter?

A

Medium and large molecules using convection

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261
Q

What are the characteristics of drugs that are more easily cleared by RRT?

A 
Vol dist <1l/kg
Low protein binding
High water solubility
up to 40kDa (only 500Da by dialysis)
low endogenous clearance (<4ml/min/kg)
extraction ratio exceeds endogenous elimination
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262
Q

What common toxins can be cleared by RRT?

A 
Salicylates
Li
Theophy/Aminoph
Alcohols
Ethylene glycol 
Some BB (sotalol, atenolol)
Anticonvulsants (cabemaz, phenytoin, Na val)
Abx- most B lactams, aminoglycosides and metronidazole
metformin
MTX
paraquat and mushroom toxin
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263
Q

What is a common definition of major trauma?

A

ISS>15

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264
Q

What is the estimated blood loss for each class of haemorrhagic shock?

A

Class 1-4

  1. <750ml (<15%)
  2. 750-1500 (15-30%)
  3. 1500-2000 (30-40%)
  4. > 2l (>40%)
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265
Q

How does HR vary in haemorrhagic shock for each class (in general)?

A

Class:

  1. <100bopm
  2. 100-120
  3. 120-140
  4. > 140
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266
Q

What classes of haemorrhagic shock generally have hypotension?

A

Class 3 or 4

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267
Q

What RR would you expect in each class of haemorrhagic shock?

A

Class 1 normal
2 20-30
3 30-40 and class 4 >40

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268
Q

What are the main risk factors for a significant (>2g Hb drop with transfusion requirement) in ICU stress ulcers

A 
48hrs ventilated for resp failure (OR 15.6)
Coagulopathy (OR 4.3)
Other causes are:
head injury
spinal trauma and polytrauma
Major >35% burn
renal/hepatic failure
severe sepsis/shock
Organ transplant
Steroids
Previous ulcer
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269
Q

What are the strong inhibitors of cytochrome p450 with regards to warfarin?

A

Fluconzole

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270
Q

In SAH what BP should you aim for?

A

BP<160

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271
Q

What is the advantage of coiling SAH over clipping?

A

If both technically possible then coiling increases the rate of independent survivors by at least 7 years!

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272
Q

Should TXA be used in SAH if coiling is delayed?

A

Yes but side effects outweigh benefits if started after 48hrs or if cont for more than 72hr

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273
Q

How does Nimodipine reduce neurological deficit in SAH>

A

Vasospasm is no reduced, the effect is through another unknown mechanism

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274
Q

Phenytoin not recommended as prophylaxis in SAH but what duration of non-phenytoin agent is allowed?

A

3-7 days

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275
Q

How do you calculate a child’s weight based on age between ages 1-5(APLS calculation) What weight would you expect for a 4 year old?

A

weight= (2xage)+8

Therefore 16kg

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276
Q

How do you calculate weight when 1-12 months?

and 6-12 years?

A

1-12 months 0.5*age in months +4 kg

6-12 3*age +7

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277
Q

What is the simple weight for age calculation the resus council advocates?

A

(age+4) x2

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278
Q

What defib energy is used in children?

A

4J/kg

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279
Q

how calculate ETT size in children?

And insertion length?

A

age/4 +4

Length (age/2) +12

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280
Q

What bolus of crystaloid is given in trauma and non-trauma in children?

A

trauma 10ml/kg

non-trauma 20ml/kg

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281
Q

What is the dose of adrenalin for children?

A

10microg/kg

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282
Q

What dose of Fentayl used in children

A

1-5microg/kg

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283
Q

Which blood group is considered the universal receipient?

A

AB patients as they have no ABO antibodies

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284
Q

Patients who are Rh + can have Rh -ve blood but who should preferably not?

A

Women of child bearing age

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285
Q

If you are blood group B which blood types can you receive?

A

O and B

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286
Q

What are Duke’s major criteria for IE?

A

Major and minor

Major- positive blood culture typically causing IE (HACEK) from two sources 12 hours apart, positive TTE

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287
Q

What constitutes a positive TTE for IE?

A

Oscillating mass on a valve without an alternative anatomical explanation or abscess seen
New partial dehiscence of prosthetic valve
New regurg

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288
Q

What are the minor Duke’s criteria for IE?

A

Heart condition or IVDU that makes it likely
Fever >38
vasc phenom- Janeway, pulm infarcts/mycotic, splinters
Immunological- GN, Osler’s, Roth spot
micro or TTE not fulfilling major criteria but fit

289
Q

When is proning useful in ARDS?

A

When PF<150

290
Q

How long should someone be proned if it is deemed a useful intervention?

A

16-18hrs

291
Q

Which pathologies are more likely to benefit from prone positioning?

A

Those with dependent consolidation and diffuse alveolar collapse. Fibrotic conditions are less likely to respond

292
Q

What are reported complications of prone positioning?

A

Airway- loss, obstruction
loss of CVC etc
Hypoxia and haemodynamic instablity esp on turning
Facial oedema and pressure injuries/nerve injuries
Retinal/corneal damage

293
Q

According to KDIGO guidelines what are the referral criteria to renal?

A

AKI, GFR<30, ACR>300mg, red cell casts, CKD +HTN on 4 agents, Persistent K+ abnormalities, recurrent nephrolithiasis, hereditary kidney disease, >5 reduction GFR per year

294
Q

Define CKD

A

GFR<60 for >3/12 +/- ACR >30mg/g, histological/structural abnormalities or tubular disorders that cause electrolyte imbalance

295
Q

What affects amount of fluid removed in PD? And the number of larger molecule?

A

Fluid removal depends on electrolytes in PD fluid

The dwell time dicates how many large molecules are removed

296
Q

Complications of PD?

A

Over or under hydration
Raised abdo pressure- hernias,orthopnoea
Also adhesions, sclerosis and peritonitis

297
Q

What is the mortality of peritonitis secondary PD? How is it defined?

A 
Mort 3.5-10%
Two of
signs/symptoms
WBC >100 per ml of effluent with >50% neuts after 2 hour dwell
Positive dwell culture
298
Q

What organisms cause peritonitis in PertonealD?

A

coag neg staph (30%)
gram -ve
S.aureus

299
Q

What are the constituents of post-cardiac- arrest syndrome?

A

Anoxic brain injury- worsened by hypotension, pyrexia, hyperglycaemia
Arrest related myocardial dysfn- all patients regardless of underlying cause
Reperfusion injury/ischaemia- SIRs immune pathways activate and adrenal suppression. Vasoregulation is lost and microcirculation clots. Un-coupling of oxidative phosphorilation

300
Q

Which electrolyte contributes most to resting membrane potential

A

K+
Every cell membrane has a potential of about 70mV
K+ has the greatest intra-cellular concentration and the greatest permeability at rest

301
Q

What is the intra-cellular concentration of Na, K, Mg, Cl, HCO3-

A 
Na 15
K 150
Mg 0.5
Cl 10
HCO 15
302
Q

What are the risk factors for getting contrastinduced AKI?

A

CKD, DM, HTN, heart failure, age, volume deplete, use of nephrotoxics, recent contrast

303
Q

What treatments reduce contrast-induced AKI?

A

IV hydration Na2HCO3 or 0.9% NaCl is most evidence based +/- NAC PO (not IV because of anaphylaxis risk) and use of iso or low osmolar contrast
weak evidence for theophylline but given side effects not recommended in the guideline

304
Q

What is the process of deciding if someone should go to a MTC?

A

If they have any of the pre-hospital trauma triage tool outcomes and the MTC is within 45min

305
Q

What is on the pre-hospital trauma triage tool?

A

Abnormal physiology- low GCS, RR high/low, BP <90
Anatomical- penetrating, chest injury with abnormal physiology, bone(pelvis/ >1 long bone, open skull, crush
Mechanism- fall >6m Ad, >3m Child, car (intrusion, ejection, death of other), vs ped/bike (>20mph, thrown over vehicle), motorbike >20mph, burns.
Those likely to bleed

306
Q

How does the ISS score?? Over which score should mean MTC involvement?

A

1->75

Over 8 should be MTC and major trauma >15, mod 9->15

307
Q

What is the triad of DKA?

A

Ketone >3mmol/l (2+ ketostick)
Gluc >11 or known DM
Bicarb <15 +/- pH <7.3

308
Q

What are the high risk groups in DKA?

A

<25yrs, elderly, preg, heart/renal failure

309
Q

When and at what rate is 10% glucose added in DKA?

A

When gluc <14 start 10% glucose at 125ml/hr

310
Q

What is the dose of the fixed rate insulin used in DKA?

A

0.1units/kg/hr up to 15units

311
Q

What are the recommended correction rates for blood abnormalities in DKA?

A

Ketone dec by 0.5mml/l/hr
Bicarb inc by 3mmol/hr
Glucose dec 3mmol/hr

312
Q

If the recommended correction rates for blood abnormalities in DKA aren’t met what do you do?

A

Increase the fixed rate insuline by 1 unit/hr

313
Q

What factors predict severe disease in DKA?

A 
pH<7.1
HCO3 <5
Ketone >6
K <3.5 on admission
GCS <12
O2 <92%
SBP <90
HR >100, <60
AGap >16
314
Q

Which NMBD is most likely to cause histamine release?

A

Atracurium

315
Q

What happens in CO poisoning?

A

CO with high affinity causes left shift of dissociation curve further impairing O2 offloading. CO also competitively impairs mitochondrial enzymes impairing O2 utilisation

316
Q

What % CO poisonining is symptomatic and likely to cause coma?

A

<10% ok
10-50% headache, visual disturbance etc
>50% coma

317
Q

What is the half life of CO? And if 100% O2 given to patient?

A

6 hours, 90min if 100% O2

318
Q

If child comes in in status already on phenytoin at home and have had lorazepam what is the next drug?

A

Phenobarbitol 20mg/kg (the thio)

319
Q

Why do femoral lines have the highest infection rate?

A

The density of skin flora is highest there. The caveat being that in children there is no greater risk of infection at the femoral site and more recent research has suggested the rates aren’t higher

320
Q

How often should clear and gause type CVC coverings be changed and with what?

A

use chlorhex every 7 (clear) or 2 days gause)

321
Q

What is the minimum frequency for changing caps and administration sets for CVCs?

A

72 hours minimum, any more will cause infection

322
Q

How often should giving sets that contain blood/lipids be changed?

A

Every24 hrs

323
Q

Are sututres advised or not for CVC placement?

A

Teh recommendation from the guidelines is to use a securing device but the risk of CVC falling out should be balanced

324
Q

What conditions have raised Hb transfusion targets and what are the individual targets?

A

Ischaemic stroke (>90), TBI (90), SAH (80-100), ACS (80-90), early stages severe sepsis with evidence of tissue hypoxia (90-100)

325
Q

What are the components of CHA2DS2VASc score? When is anticoagulation advised?

A

CCF, HTN, Age (65 (1)-74 (2)), DM, vasc disease (2 for stroke/TIA/VTE), female
Anticoag advised when one risk factor in addition to gender (>1 men, >2 women)

326
Q

What are the factors in HAS-BLED the

A

HTN (>160), renal dysfn, liver disease, prev stroke, prev or maj bleeding, unstable INR, Age >65, NSAIDs/anti-plt, EtOh/drugs

327
Q

What do the scores for HASBLED mean in terms of bleeding?

A

score 0 is 1% risk over 1 year, score 1 its 3.5%, score 3 6%, score 5 9%

328
Q

Who is at risk of dying from asthma attacks?

A

prev ventilation, recent admission or recurrent admissions, heavy use B2 agonists, emotional/MH/ learning difficulties

329
Q

What is the evidence behind using Mg in acute severe asthma?

A

Reduces intubation rate and improves lung function

330
Q

What are the final line agents in acute severe asthma?

A

Aminophylline, montelukast, abx, heliox, nebulised furosemide- none recommended but have been studied. Case reports of Ketamine, inhaled anaesthetic

331
Q

What are the three most common reaons people with HIV come to ICU?

A

Resp failure (30-40%), sepsis (15-20%), then very low numbers for neuro, cardiac or GI disease

332
Q

What is the leading cause of resp failure in those with immunocompromise secondary HIV

A

PCP but also bacterial pneumonia and COPD are increasingly seen

333
Q

What causes PCP?

A

An atypical fungus, thought to lie dormant in 20% of people

334
Q

What CD4 count is required to see PCP usually?

A

<200

335
Q

What are the typical CXR findings of PCP?

A

Up to 25% are normal but classically bilateral perihilar interstitial infiltrates that becomes more diffuse as the disease progresses

336
Q

What is the first and second line treatement for PCP?

A

Co-trimoxazole +/- steroid (if hypoxic pO2 <9.2 on air) and second line dapsone and others

337
Q

What is the steroid dose for PCP?

A

Pred 40mg BD for 5/7

338
Q

When should HAART be started/restarted in PCP? Why not straight away?

A

Immune reconstitution syndrome could be fatal. Restart after 2/52

339
Q

Can FAST be used to exclude haemorrhage in trauma?

A

No, whilst its PPV is good, its NPV is poor

340
Q

When is a peritonealtap or lavage recommended in trauma (not that you would do it)

A

If there is a negative or equivocal FAST scan as there is a lower false positive for a tap so that would be first

341
Q

What is first line for candidaemia in non-neutropenic patients?

A

Either fluconazole or echinocandin (caspo/Anidula)

342
Q

What is the treatment for a candidaemia in a neutropenic patient?

A

Caspo/Anidulafungin

343
Q

If you get a candidaemia what should be done with indwelling lines?

A

If not neutropenic it is the likely source and should be removed.
If neutropenic could have another source but consideration should be given to its removal

344
Q

What investigatios are required in candidaemia?

A

Echo, Ophtal review (though less important), and USS renal for fungal balls (though would expect +ve urine cultures) which is more often seen in children.

345
Q

Define AKI

A

An abrupt (within 48hrs), reduction in kidney fn with absolute increase in Cr >26.4 micromol/L or >50% increase or <0.5ml/kg/hr for 6 hrs urine output

346
Q

What are the commonest causes of AKI in ICU?

A

Sepsis, major surgery, low CO, hypovolaemia/renal hypoperfusion, medications

347
Q

What are the concentrations of NA, Cl, K Ca, Mg, acetate, bicarb, lactate and glucose in haemodialysis fluid?

A

Na 136-140, Cl 99-110, K 0-4, Ca 2.5, Mg 0.5-1, Acetate 2.5-5, bicarb 27-39, lactate 0, glucose 11

348
Q

What is the cut off for using RRT for toxin removal?

A

If the removal can be increased by 30% or more then it is usually recommended

349
Q

What are the classic toxins that are easily dialysed?

A

Li, Ethylene glycol, salicylate, paracetamol, ethanol, methanol, theophylline, carbamazepine

350
Q

What is metabolised by CYP1A2?

A

Theophylline and Haloperidol

351
Q

What drug inhibits CYP1A2 and may potentiate haloperidol and theophylline?

A

Ciprofloxacin

352
Q

What drugs are metabolised by CYP2C9

A

Warfarin, phenytoin, voriconazole

353
Q

What inhibits CYP2C9 and therefore potentiates warfarin, phenytoin and voriconazole?

A

Metronidazole, amiodarone

354
Q

What does CYP2D6 metabolise?

A

Codeine, tramadol, haloperidol, metoprolol

355
Q

What inhibits CYP2D6 and therefore potentiates codeine, tramadol, haloperidol and metoprolo?

A

Fluoxetine, Amiodarone

356
Q

CYP3A4 is the big one in terms of p450s in ICU, what does it metabolise?

A

Fentanyl, clarith, eryth, warfarin, carbamaz, haloperidol, midaz, amlod, diltiazem, verapamil, statins, hydrocort, methyl pred, anti-retrovirals

357
Q

What drugs inhibit and therefore potentiate drugs metablised by CYP3A4?

A

clari, flucon, amlod, amiodarone

358
Q

What is the big inducer of enzymes p450 and therefore reduce efficacy od drugs?

A

Rifampicin, carbamazepine, phenytoin

359
Q

What did the ISAT trial look at? How many patients and outcome?

A

Coil vs clips in SAH, 1k in each group followup at 2/12 and 12/12
23.7% vs 30.6% dead at one year in favour of coiling

360
Q

What are the causes of intra-renal AKI?

A

Intrinsic renovascular - HTN, small vessel vasculitis, TTP/HUS
Glomerular disease- Goodpastures, post infectious GN etc
Tubulointerstitial- ATN (sepsis, contrast rhabdo, pro-longed pre-renal hypotension) or AIN (drugs)

361
Q

What is the effect of ACEi and ARB on renal glormerualr afferent and efferent?

A

The efferent arteriole is preferentially afeced by these drugs. The inhibition of angiotensin II means the efferent arteriole dilates, this reduces the pressure at the glomerulus meaning GFR is reduced

362
Q

How do NSAIDs affect kideny?

A

Prostoglandins vasodilate the afferent arteriole, NSAID inhibits this effect

363
Q

How do Tacrolimus and cyclosporin affect the kidney

A

They constrict afferent and efferent arteriole through unknown mechanism

364
Q

What drugs causses ATN classically?

A

Aminoglycosides

365
Q

What drugs cause AIN?

A

Beta-lactam, co-trimoxazole, NSAIDs, vancomycin

366
Q

What drugs cause crystallopathies in the kidney?

A

Aciclovir, cipro, MTX

367
Q

Where is Renin secreted?

A

The juxtaglomerular cells in the afferent arteriole

368
Q

How do you differentite between an AKI and ATN?

A

Fractional excretion of Na (excreted/filtered)

369
Q

How does FE Na differentiate between AKI and ATN

A

Low in AKI, high in ATN (<1% pre-renal), >2% ATN not useful if diuretics used but can use FE urea in that situation

370
Q

Where is acid excreted in kidney?

A

Distal tubule largely

371
Q

What viruses are affected by aciclovir?

A

HSV and VZV

372
Q

What disease is Ritonavir used for?

A

HIV

373
Q

Ganciclovir is used in which condition?

A

CMV

374
Q

What are the three drugs that affect influenza?

A

Influenza A, B and C. Flu A is the one that causes the problems
We have Oseltamivir, Zanamivir and amantadine (amantadine not recommended) The other two are equally effective so it comes down to cost

375
Q

What are level 2 (moderatesly strong) recommendation for TBI?

A

Keep BP>90, ICP<20, but CPP>70 is bad, mannitol in emergency but hypertonic may be as effective with fewer side effects. Avoid pCO2 <3.3 prophylactically, barbiturates as last resort, prophylactic AEDs to reduce O2 demand during seizure

376
Q

What is the only level 1 (strongest) recommendation regarding TBI?

A

Avoid steroids as increases mortality

377
Q

What are the level 3 (weakest) recommendations for TBI?

A

SpO2 <90% avoided, CPP<50 is bad, can use hyperventilation to control ICP in first 24 hours

378
Q

What is the evidence for therapeutic hypothermia in TBI>

A

Mixed data for prophylactic use but probably a role in rescue of a high ICP….doesn’t make much sense to me though…

379
Q

What are the two most likely causative organisms in IE?

A

S.Aureus (40%)

Strep 33% (S. Bovis 10%)

380
Q

What are the two main risk factors for developing IE?

A

Cardiac damage- valve replace or rheumatic fever etc and bacteraemia (dentition, IVDU, in-dwelling something, chronic infection)

381
Q

What is first line abx for IE with a native valve?

A

Co-amox and Gent (Vanc Gent and Cipro for pen allergic)

382
Q

What is the first line abx for IE in prosthetic valve?

A

Vanc, Gent, Rifampicin

383
Q

What is the ARDSnet formula for predicted body weight given height?

A

Male - 50 + 0.91(height (cm) -152.4)

Female = 45.5 + 0.91(height-152.4)

384
Q

In a spinal injury what are the pre-requisites for the commencement of weaning?

A

FiO2 <0.4, lung compliance >50ml/cmH2O and VC >150ml, no pain awake and co-operative

385
Q

What would be the biggest factor affecting clearance of a drug that is 98% protein bound and has a high hepatic extraction ratio?

A

Liver blood flow.
If low extraction ratio and high protein binding then clearance is dependent on protein binding
If low extraction and protein binding then hepatic enzyme fn predominates

386
Q

What are the concerns about using bicarb in a met acidosis and when is it appropriate to use it?

A

Worry is that it makes breathing harder due to CO2 produced but also makes intra-cellular acidosis worse. If there acidosis is due to bicarb loss/non-production however then replacement is reasonable.
On balance pH<7.1 would mean bicarb is likely of use

387
Q

What are the causes of a NAGMA?

A

Renal- RTA I, II, IV, carbonic anhydrase inhibitors or aldosterone antagonists
Extra-renal- TPN, Cl rich fluid, GI loss, Ileal conduit

388
Q

How does an ileal conduit cause a metabolic acidosis/

A

Te urea is degraded but bacteria and the resultant NH3 and H+ are absorbed.

389
Q

What does the area under the receiver operator curve of 0.5 mean?

A

Means the test, if positive (or neg in this case) has a 50:50 chance of being a true positive or a false positive

390
Q

Where should an IABP be placed, what % of aortic diameter should it occlude and when does in inflate/deflate?

A

2-3cm distal to L subclav, 80-90% occlude aorta when up.
Inflate either on middle of T wave/dicrotic notch and deflates at start of R wave/ just before pressure comes up for systole

391
Q

How does IABP improve CO?

A

reduced after load with reduced LVEDP and therefore LV wall tension therefore improving CO

392
Q

When have IABPs traditionally been used?

A

In cardiogenic shock post MI

393
Q

What did the IABP-SHOCK II trial study and show?

A

600ptsin cardiogenic shock post MI who were going for early revascularisation. No change in 30 day mortality or 12 month mortality.

394
Q

What is the triad of acute liver failure?

A

Jaundice, coagulopathy and encephalopathy

395
Q

What is the definition of hyperacute, acute and subacute disease in acute liver failure>

A

hyper <7days
acute 1-4 weeks
subacute- 4-12 (some say 6/12)

396
Q

What are the commonest causes of liver failure?

A

70% is paracetamol overdose and presents as hyperacute

397
Q

What are the Kings criteria for liver transplant if from paracetamol OD?

A 
pH<7.3 with adeuqate resus
or lactate >3
or all of:
PT>100s
Cr >300
G3-4 enceph
398
Q

What are the Kings criteria for liver transplant in non-paracetamol OD?

A 
PT>100s or
any three of 
age <10, >40
PT>50
Bili >300
enceph >7 days after jaundice
Unfavourable dises- non-HAV/HBV, DILI
399
Q

What does a FIBTEM look for in ROTEM?

A

Estimates the effect of fibrinogen by activating cytochalasin D which is a platelet inhibitor

400
Q

Whats the difference between TEG and ROTEM?

A

In TEG the cup rotates and the wire is dipped in. As the clot forms the wire moves more and more.
In ROTEM the wire moves and as the clot forms slowly starts to move the cup.

401
Q

What is the clotting time and clotting formation time and alpha angle in TEG/ROTEM?

A

Clotting time is the time it takes for a clot to start to form.
Alpha angle is the rate at which the clot forms and the time it takes for the alpha angle to get to zero (clot formed) is the clot formation time

402
Q

What does a HEPTEM and a FIBTEM measure?

A

HEPTEM- Heparinase

FIBTEM- removes plt fn and only looks at fibrinogen

403
Q

What are the signs of hyperoxia?

A

mild neuro signs, seizure (>2.8atm) but at normal pressures depends on time of exposure. Acute tracheobronchitis is earliest followed by starnal pain, coug and thick secretions, later diffuse alveolar damage

404
Q

What are the potential benefits of hyperoxia in hyperbaric setting (not seen outside of this setting)

A

inc periphe VR, suppression of inflamatory process, anti-microbial effect esp on anerobic organisms, enhanced tissue repair

405
Q

When does alveolar damage start if FiO2>0.5?

A

after about 48hrs

406
Q

Why may surgery precipitate a thyroid storm and how would it manifest?

A

Stress response from infection/trauma causes additional thyroid hormone to be released.
Manifests as pyrexia, tachycardia and HYPOtension. Hypertension is possible but only sometimes. Usually go into AF and get diarrhoea

407
Q

How do you treat a thyroid storm?

A

Correct fluid loss, and glucose
Carbimazole (reduces T3/T4 production), propylthiouracil (reduces converstion of T3/T4 peripherally) and Propranolol for sympathetic effects.
May need active cooling and Dantrolene 1mg/Kg may be useful

408
Q

What other medications should you be careful of in thyroid storm?

A

Mostly protein bound so anything that competes with that eg aspirin will make things worse

409
Q

What dose of propranolol do you give in thyroid storm and repeat every how many min?

A

1-2mg bolus every 10-15min

410
Q

Why use propranolol in preference to other BB in thyroid storm?

A

It also prevents peripheral conversion of T4 to T3

411
Q

What is the evidence for NIV in ECOPD?

A

Halves mortality with NNT 10

412
Q

When should NIV be offered in exac COPD?

A

If after starting standard therapy remain acidotic and pCO2>6 after 1 hr

413
Q

What are the contr-indictions for NIV?

A

Coma or moribund, ++ secretions, vomting, undrained PTX, UGI surgery, facial trauma burns

414
Q

If unsure where the gastric balloon is on a Sengstaken tube what do?

A

50ml air or contrast and XR to see where it is

415
Q

At what OG distance would you expect the GOJ?

A

about 38-40cm

416
Q

What weight should be applied to a Sengstaken tube>

A

either 500 or 1000ml bag

417
Q

How do you inflate the oesophgeal balloon in Sengstaken

A

If present inflate with air until 35-40mmHg reached, this should be deflated every 2few hours to check if bleeding on going. The risk is necrosis

418
Q

What is the Goldman RIsk Index used for?

A

For cardiac complications from non-cardiac surgery

419
Q

Define NYHA classification

A

NYHA 1 -normal
2- mild impairment
3- comfortable only at rest
4- symptoms all time

420
Q

According to surviving sepsis, in septic shock how much fluid should someone get before you admit defeat and start pressors?

A

30ml/kg

421
Q

Who should get an ICP monitor?

A

Those with a chance of survival, GCS<9 and CT proven TBI

422
Q

When shouldan ICP monitor be placed if CT head normal?

A

If two of age>40, BP<90,abdnormal posturing

423
Q

What drugs can cause acute pancreatitis?

A

Na Valproate, metronidazole, steroids, cisplatin, furosemide, azathioprine, NSAID, statins

424
Q

If someone has secondary PTX for >72 hrs where should they be referred?

A

Surgeons for a pleurectomy

425
Q

What is the cutoff for large/ small pneumothorax?

A

> 2cm at level of hilum would be large

426
Q

In PTX the surgical options are a open pleuretomy and a VATS led pleurectomy, what are the recurrence rates for each?

A

1% open, 5% VATS

Medical pleurodesis in those not fit for surgery but inferior to both

427
Q

Why do we use prasugrel and ticagrelor in preference to clopidogrel?

A

More potent and more reliable that clopidogrel

428
Q

When can you not use Ticagrelor?

A

Haem stroke in past, mod hepatic dysfn

429
Q

What is the alveolar gas eqn?

A

P(alveolar)O2=FiO2(P(atm)-P(H2O))-p(blood)CO2/RQ
Where at 37C and normal diet reduces to
PAO2= FiO2(101-6.25)- PaCO2/0.8
=FiO2(94.75)-1.2*PaCO2

430
Q

How is respiratory quotient defined?

A

Vol CO2 released/Vol O2 absorbed during respiration of a particular food

431
Q

What are the two tests for capacity?

A

Test if there is a disturbance of mind/brain and if so does it impair their ability to make the specific decision?

432
Q

When can a lasting power of attorney speak as the patient on medical matters?

A

If the ability to make life-sustaining treatment decisions has been specifically noted within the agreement

433
Q

What are the markers of decompensated liver cirrhosis?

A

ascites, varceal bleeds, encephalopathy, jaundice

434
Q

What is the median survivl for a compensated cirrhotic liver disease patient and one who has decompensated?

A

12 years median if compensated, 2 years if decompensated. 5-7% decompensate per year

435
Q

What is the best score to use in prognosis of hepatic cirrhosis?

A

Child-Pugh

436
Q

What is the AUROC (sensitivity) for APACHE III, IV, ICNARC 2007, SAPSII and MPMIIo?

A 
III- 0.9
IV - 0.88
ICNARC - 0.87
SAPSII- 0.86
MPMIIo- 0.82
437
Q

What is the best measure of deterioration in neuromuscular disease like GBS?

A

Vital capacity

438
Q

What is thought of as a good volume that predicts the need for intubation in GBS or similar with regards FVC?

A

15-20ml/kg or reduction of 30% from baseline

439
Q

Why is vasopressin thought superior to NA in the DBD patient?

A

ICS guidelines state less likely to cause pulmonary HTN and metabolic acidosis.Not sure if I’m sold.

440
Q

What is the usual history of hypercalcaemia?

A

Short history of renal, neuro and abdo symptoms

441
Q

What % patients get delayed ischaemic injury in SAH?

A

60%

442
Q

Vasospasm causes delayed ischaemia in SAH mostly between days 4 and 14. Occurs in 70% but only half have signs (does that mean we undertreat?) How can trans-cranial doppler be used to diagnose?

A

Flow velocity >120cm/s or ratio >3 between MCA and ICA

443
Q

What % of patients get hydrocephalus post SAH?

A

20-30%

444
Q

How do you differentiate between CSW and SIADH?

A

Two ways clinical difference is volume state (Eu/hyper in SAIDH and hypo in CSW) and oliguria in SIADH and polyuria in CSW

445
Q

Once HypoNa corrected how best to differentiate between CSW and SIADH?

A

FE of Urate is the best, if >11% post correction then CSW if returns to normal 4-11% then SIADH

446
Q

Which is best, NG or NJ feeding in pancreatitis?

A

Both equal but obv NG easier to achieve, TPN should be used in those intolerant but is inferior

447
Q

What is a parametric statistical test?

A

That which is applied to a normal distribution (non-parametric being a skewed distribution)

448
Q

What test is used in qualitative data when<10 data points and >10 data points?

A

<10 Fisher’s exact test

>10 Chi squared

449
Q

What stats test in quantitative data when parametric and non-parametric?

A

Parametric (normal dist) Student’s T-test

If non-para- Mann-Whitney U test

450
Q

If you have a parametric and non parametric dataset with quantitative multiple groups which stats test is best?

A

Paramet- ANOVA

Non-para Kruskal-Willis

451
Q

If a paired dataset (same people before and after intervetion) what stats test would you use?

A

Para- paired-t or ANOVA

non-para- Wilcoxon signed rank

452
Q

What electrode is used to detect CO2 in ABG machine?

A

Severinghaus

453
Q

What electrode measures the partial pressure of O2 in a liquid?

A

Clark

454
Q

How is pH measured in ABG machine?

A

silver/silver chloride electrode within a buffer is referenced against a Calomel electrode

455
Q

How does a CO2 electrode work?

A

Its a silver/silver chloride electrode protected by bicarb solution. The CO2 diffuses across much like the BBB and changes the pH of a known solution therefore you know the CO2

456
Q

What does a paramagnetic analyzer measure?

A

Found in ventilators and measures O2

457
Q

In APACHE score what makes up the majority of the score?

A

65.5% is acute physiology, followed by 16.5% chronic health, 5% age, 9.4% admission source, lengthof stay 2.9% and need for IPPV 0.6%

458
Q

Does Mg have a role in phaeochromocytoma?

A

Yes, improves stability

459
Q

What did the MAGPIE study find?

A

Reduced rate of eclampsia with use of Mg in those with severe pre-eclampsia or eclampsia

460
Q

What is the treatment for Eclamptic seizure?

A

4g over 5min Mg follwed by 1g/hr for 24 hrs. If recurrent seizure give 2-4g additional Mg

461
Q

How does magnesium exert its analgesic effect?

A

It is an NMDA antagonist

462
Q

Which NMBDs are metabolised by plasma cholinesterases?

A

Sux and mivacurium (can inc or dec in preg and liver disease)

463
Q

How is atracurium and cis-atra degraded?

A

Hofmann degredation, therefore limited by temp and pH

464
Q

What about a clinical history confers a poor prognosis on OOHCA?

A

Factors that increase time to ROSC and initial non-shockable rhythm

465
Q

What are the neurophysiological investigation outcomes that are poor prognosis in OOHCA?

A

Isoelectric baseline on EEG or burst suppression/refractory status after 72 hrs, absence of SSEP >72 hrs if cooled, >24hrs if not

466
Q

Which biomarker is best (though not good enough to be used in isolation) in OOHCA?

A

Neurone specific enolase

467
Q

What is the most clear cut sitation in OOHCA on day 3 post rewarming and ensuring nothing else could be causing the problem

A

M1-2, no pupil/corneal reflex and bilateral absent SSEPs. If not met then repeat after 24hrs

468
Q

If the criteria of M1-2, no pupil/corneal reflex and no SSEPs not met after 72-96hrs in OOHCA what are the other components of poor prognosis?

A

Two of
myoclonic status <48hrs post ROSC
High NeuroneSpecificEnolase levels 48-72hrs post ROSC
Unreactive malignant EEG
Diffuse anoxic injury on CT <24hrs or on MRI 2-5days

469
Q

If synced DCCV fails in AF with compromise what do you do?

A

Inc from 100 ->150J and if still noting given 300mg Amio and try again after 15min

470
Q

Which recreational drugs can cause serotonin syndrome?

A

Ecstacy, cocaine and LSD

471
Q

What is the major differentiating factor between NMS and serotonin syndrome?

A

Onset- SS usually hours, NMS in days to weeks

472
Q

Which common drugs sshould be avoided when treating serotonin syndome?

A

Tramadol, fentanyl and ondansetron

473
Q

What serotonin antagonist can be used as last ditch attempt in serotonin syndrome?

A

Cyproheptadine (only eneteral preparation available)

474
Q

When should a CT head be done within 1 hour of presentation?

A 
>1 episode of vomiting
GCS<13
GCS <15 2 hours after injury
Likely skull fracture
Seizure
possible base of skull
focal neurology
475
Q

If someone is well after a head injury but takes warfarin how long do you have to do the CT head?

A

8 hours

476
Q

What complication of heparin confers the greatest risk of death?

A

type 2 immune mediated thrombocytopenia (HIT-2)

477
Q

What types of HIT are there?

A

HIT 1 and 2, type 1 is non-immune medated and occurs within a few days and resolves without stopping heparin. Type 2 is immune mediated so takes longer to develop 4-14 days (sooner if previous exposure) and confers the risks known with HIT

478
Q

What is the HIT scoring system?

A

‘4 T’s’
Thrombocytopenia- 0 points <30% reduction, 1pt 30-50%, 2 >50%
Time to thrombocytopenia- 0pts <3days no prev exposure, >4 days but uncertain 1 pt, 5-10days 2pts
Thrombosis?- 0pts none, 1pt, suspected, 2pts definite
Other possibility? 0pts definite 1pts maybe, 2pts none

479
Q

Other treatments for anticoagulatoin if HIT develop are what?

A

Danaparoid (Xa inhib), Fondapariunux. Interestingly, they also cause heparin antibodies but not HITs

480
Q

How do you change the resonant frequency of an arterial BP circuit?

A

Use a shorter or fatter cannula to change the resonant frequency away from 40Hz

481
Q

Define pre-eclampsia

A

HTN after 20/40 gestation resolving within 3/12 of delivery with SBP>140 or DBP>90 on two occasionals >4 hrs apart or >160 or >110 on one reading plus one of
>0.3g/24hr urine protein
AKI
liver disease- epigstric pain, liver tenderness, abnorml LFT
Neuro- seizure, visual disurbance
Haem- haemolysis, low plt, DIC
IUGR

482
Q

When is pre-eclampsia severe?

A

SBP >160, DBP >110

483
Q

Risk factors for pre-eclampsia?

A 
prev pre-ec
older mother and mother<20
multiple preg
high BMI
protein C and S deficiency
Facor V leiden
hyperhomocysteinaemia
484
Q

What to pre-eclamptics die from?

A

ICH and pulmonary oedema (seizure)

485
Q

What is the causative organ of pre-eclampsia?

A

placenta

486
Q

There is an early and late pre-eclamptic phenotype, whilst they are likely to be both present in varying derees within one woman what is the pathophysiology of early pre-eclampsia?

A

Nobody really knows but oxidative stress of the syncytiotrophoblast (cells that are the blood/placenta interface) is one hallmark. If stressed pro-inflammatory cytokines and free foetal DNA is leaked into the maternal bloodstream. This is due to a blood/demand mismatch through defective remodelling of the placental spiral arteries

487
Q

What is the draw back of irradiated RBC?

A

Shorter shelf life and more K+, enough to cause death in massive transfusion

488
Q

What are the hunter seretonin toxicity decision rules?

A
  1. if spont clonus then Seretonin syndrome
    2 else if inducible clonus and agitiation/sweating->SS
  2. Else if occular clonus +agitated/sweat->SS
  3. Else if tremor +hyperreflex->SS
  4. Else if hypertonic+T>38+ occular/inducible clonus->SS
  5. Else not SS
489
Q

What are the crieria for CT within 1 hour at risk of c-spine injury?

A 
GCS<13
Has been intubated
plain XR not good enough
Urgency-prior to surgery
Having other areas scanned
Stable patient but >65, dangerous mechanisms of injury, focal peripheral neurology, parasthesia in UL
490
Q

What counts as a dangerous mechanism of injury with regards C-spine injury?

A

Fall >1m
Fall 5 stairs
Axial load to head (RTA, rollover, ejection, off-road accident)

491
Q

What does CONSORT stand for?

A

consolidation standard of reporting trials

492
Q

What does QUORUM stand for?

A

Quality of reporting of meta-analyses

493
Q

What does MOOSE stand for?

A

meta-analysis of observational studies in epidemiology

494
Q

What does SQUIRE stand for?

A

Standards for quality improvment reporting excellence (of course)

495
Q

What are the top 5 hospital acquired infections?

A 
Resp-23%
UTI- 17%
Surgical site infection 16%
Sepsis 10%
GI 9%
496
Q

When should fixed rate insulin be given in HHS?

A

When glucose is not decreasing with fluid resus and ketones still >1

497
Q

When do you change from 0.9% to 0.45% NaCl in HHS?

A

When blood osmolality stops falling, aim 250-500ml/hr for 12 hours, deficit may be 20L

498
Q

When should HHS be considered for ICU/HDU?

A

Biochem-Os >350, Na>160, pH<7.1, abnormal K, Cr>200

Clinical- GCS<12, O2<92%, BP<90, HR abnormal, Urine <0.5ml/kg/hr, hypoT, macrovascular event (stroke,MI)

499
Q

What variables does the MDRD (modification of diet in renal disease) calculation consider when calculating eGFR?

A

Sex, Cr and ethnicity

500
Q

Define delirium

A

an acute fluctuating disorder of consciousness and cognition which is reversible

501
Q

What are the risk factors for developing delirium in ICU?

A

dementia, alcoholism, HTN and severity of illness at admission

502
Q

What are the parts of a CAM ICU screen?

A

if acute change in last 24 hours
Inattention- Squeeze hand on each A of SAVEAHAART if >2 errors (where squeeze or no squeeze incorrectly is a mistake) then do RASS.
If 0 ask 4 disordered thinking questions

503
Q

What is the mortality associted with fever in neutropenia (without sepsis)

A

15%

504
Q

What is beta-D-Glucan?

A

Its a component of fungal cell wall but is quite non-specific

505
Q

Cause false +ve BDGlucan?

A

surgical gause, GI leak

506
Q

What is Galactomannan

A

Its part of the cell wall of Aspergillus

507
Q

What is the classic aspergilloma CXR appearance?

A

Ball with a crescent of air around it

508
Q

Whats does ADAMSTS13 do?

A

Cleaves ultralarge VWF to normal VWF, if UL VWF is left in the circulation then it causes microthrombi and clot everything off

509
Q

How long do you have to start plasmaexchange if TTP

A

4 hours idealy but up to 8

510
Q

What is Caplacizumab?

A

Used in TTP, stops VWF binding with plt and improves plt count quickly. Now approved by NICE

511
Q

Why does plasma more likely cause TRALI?

A

Anti-leucocyte ab in plasma

512
Q

Why use heparin CVVH in tumour lysis?

A

The hyperPO4 will ppt with Ca and perhaps cause more problems than is solves

513
Q

Causes of isolated raised APTT?

A

Lupus anticoag, factor XII, XI, IX, VIII deficiency, Heparin

514
Q

In massive transfusion when should factor VII be considered?

A

When 10PRBC, 8FFP, 2Plt, 2 Cryo and triangle of bleeding is corrected as much as possible. 10% coronary artery thrombus rate in >65

515
Q

What is FEIBA?

A

Factor eight inhibitor bypassing activity is the original PCC with II, VII, IX and X but only small amounts of activated components apart from VIIa therefore used in haemophiliacs

516
Q

Why is novoseven used in preference to FEIBA in acute setting?

A

Half life of FEIBA shorter so chance of re-bleed higher if you don’t get the dosing exactly right

517
Q

Why do you not add allopurinol to rasburicase?

A

It increases LOS and hospitalisation costs

518
Q

What are the main physiological changes of pregnancy?

A

A- laryngeal oedma
B- splint diaphragm low FRC
C- CO x2 by term, increased circulating volume, aorto-caval compression after 20/40. Placenta 10% of CO
E- pH in stomach lower increasing risk of aspiration, lower oesoph sphincter relaxes

519
Q

What is the best scoring system for predicting maternal outcome if admitted to critical care?

A

CIPHER, though not used much

520
Q

What are the factors that make up the maternal CIPHER mortality prediction calculation?

A

Admission following surgery, external transfer, highest T, highest Cr, highest HR, highest RR, highest WBC if mech vent, lowest Hb, lowest plt

521
Q

How is HELLP defined?

A

Haemolysis- LDH>600, TB >20
Elevated liver enzyme- ALT>70 (AS/GGT>70)
Low plt- <100

522
Q

What are the classes of HELLP?

A

Class I, II and III

523
Q

Which is the most severe form of HELLP? Class I or III?

A

Class I is worst with 40-60% morbidity

524
Q

How is class I, II and III HELLP defined?

A 
Haemolysis is universal- LDH>600
Liver enzymes- >40 in class III, >70 in the other classes
Platelets seem to be more important, 100-150 in III, 50-100 in II and 0-50 in I
525
Q

Are steroids used in HELLP?

A

Used to be but after Cochrane review have fallen away

526
Q

When is eclamptic seizure most likely to present?

A

Post partum (usually within 12 hours of delivery) 44%, 38% antenatal and 18% intrapartum. 20% have no diagnossi

527
Q

How do you treat magnesium toxicity in cardiac arrest? Say someone in obsterics with eclampsia?

A

Stop infusion and give calcium chloride/gluconate

528
Q

What are the two physiological phases of amniotic fluid embolus?

A

First is vasoactive substances causing massive pulm HTN then later it causes LV failure which puts you at risk of pulm oedema
At the same time the circulating vasoactives cause uterine atony and coag factor consumption leading to massive haemorrhage through DIC

529
Q

What % cases of amniotic fluid embolus lead to seizure?

A

10-50%

530
Q

What are the risk factors for amniotic fluid embolus?

A

Older mother, induction of labour, fast labour, operative delivery, abruption, IUfoetal death

531
Q

Whats the triad of symptoms in amniotic fluid embolus?

A

Not useful at all

Hypottension, hypoxia, coagulopathy…good luck spotting coagulaopathy!

532
Q

What are the four Ts of primary (<24hr) and secondary (>24hr) post partum haemorrhage?

A

Tone-atony
Trauma- intruments/delivery itself
Tissue- retained clots/placenta
Thrombin- coagulopathy

533
Q

Whats the defn of major obstetric blood loss?

A

> 1L for RCOG, but other sources suggest 1.5L no real consensus. Point is circulating volume goes up in pregnanc likely for this very reason

534
Q

Can TXA be used in maternal haemorrhage?

A

Yes, WOMAN trial showed decreased mortality give1g if >500ml vaginal or 1L caesarean delivery

535
Q

What is the dose of syntocinon to improve uterine contractility if there’s bleeding?

A

5 units +5 units + infusion

Causes hyptension so inject slowly

536
Q

What frequently accompanies peri partum cardiomyopathy?

A

Most have it before delivery but name persists.

Thromboembolism

537
Q

What is the outcome for women with peri partum cardiomyopathy?

A

Half recover, half are left with a problem. 1.5% need mechanical support and 0.5% get transplant

538
Q

What do pregnant mothers die from?

A

Cardiac disease 2 per100K followed by VTE 1.5/100K, neuro, sepsis, psych, haemorrhage is 0.5 per100K with others between 1.5 and 0.5

539
Q

what is the most common reason for a still pregnant motherto be admitted to ICU?

A

Resp failure- still get CAP, flu, asthma etc

540
Q

What is the most common reason for admitting a post-partum mother?

A

Haemorrhage

541
Q

What do you do if a mother is on a Mg infusion and becomes oliguric?

A

Review the Mg as it may accumulate!

542
Q

What are the risks with a maternal airway?

A

x8 risk of difficulty, increased risk of aspiration

543
Q

What happens with breathing during pregnancy?

A

Increased MV secondary larger Vt, RR stable, reduced FRC of course

544
Q

What are the segments of the RUL?

A

Apical, Ant, post

545
Q

What does the bronchus intermedius divide into?

A

RLL and RML

546
Q

What are the segments of the RML and RLL?

A

RML into two-medial and lateral, RLL into five superior and four basal- ant,post, med, lat)

547
Q

What does the L main bronchus divide into?

A

LUL and LLL

548
Q

What are the segments f the LLL?

A

Superior and 3 or four basal like RLL, ant, post, lat, medial

549
Q

The LUL bronchus gives of LUL proper and lingula, what are the lobes of the lingula?

A

Sup and inf

550
Q

What is the time and BP cut off for thrombolysis in stroke?

A

4.5hrs, BP >185/110 should be treated first (NICE), <180/110 from AHA

551
Q

How long should aspirin be held if thrombolyse for stroke?

A

24 hrs

552
Q

How does clonidine exert its effect?

A

Alpha 2 agonist which acts centrally to reduce exogenous NA

553
Q

What is the maximum number of patients one registrar should be responsible for?

A

8

554
Q

How many patients can a cons ICU be responsible for?

A

8-15

555
Q

When does the ICS recommend you have one supernumerary nurse?

A

For every 10 patients

556
Q

According to GPICS 2 how quickly should a consultant be available?

A

Within 30min

557
Q

What infarct in particular benefits from ACEi?

A

Anterior ? why

558
Q

What aldosterone antagonistsare recommended post STEMI?

A

Eplerenone if HF with EF<40% or DM. Spiro does not feature

559
Q

When can verapamil/diltiazem be used post STEMI?

A

Not initially, useful if BB contraindicated

560
Q

If acute UGIB what drugs do we give?

A

Blood, FFP etc as needed
Terlipressin-evidence for reduced rebleed and mort
Somatostatin (superior to octreotide) has been used but not common place
Abx- reduce rebleed and mort

561
Q

Is intubating a potentially infectious patient in a side room recommended by epic3?

A

Yes but with huge caveat that it should not delay intubation if it is required. That essentially means no, unless they are already in one!

562
Q

Which dugs are associated with pleural effusion?

A

MTX, phenytoin, amiodarone, BB, nitrofurantoin

563
Q

Howwork up a pleural effusion?

A

BTS 2010 suggest if transudate treat cause, if exudate speak to resp and do a tap.

564
Q

What is electrical alternans?

A

The axis of the heart changes wit each beat thought to be due to the heart moving within the pericardial fluid in tamponade

565
Q

What are the four types of exravasation injury?

A

Vasoconstrictor, hyperosmolar (TPN), extreme of pH (amio, phenytoin) and cytotoxic

566
Q

What type of extravasation injury can thiopentone, ketamine and atracurium cause?

A

All very alkaline so causes ischaemia

567
Q

Which extravasations should you not spread and dilute?

A

Cytotoxic agents

568
Q

Over what pH range is feeding allowed in NG tube placement?

A

pH<5.5

569
Q

What can be done to try and get NG aspirate and avoid CXR?

A

Nurse on one side, move NG in or out by 20cm(!) and give mouth care to stimulate secretions

570
Q

When is peripheral cannula ok for someone with TPN?

A

If <14 days and no need for central line otherwise

571
Q

When is a tunnelled line for TPN recommended?

A

After 30 days or expected to need for more than 30 days

572
Q

Which artery supplies the SA and AV node in 60 and 85% of population respectively?

A

RCA

573
Q

How do you size and length an ETT in a paeds pt?

A

Size- (age/4)+4

Length- (age/2)+12

574
Q

What is Parkland’s formula and how is the volume calculated adinistered?

A

Volume=weightx4xsurface area of burn
Half over 8 hours, the rest over 16
Useless in my opinion-need constant review, airway burns need ++ fluid

575
Q

What wavelength is absorbed by CO2?

A

428nm

576
Q

What are the major and minor risk factors for refeeding syndrome?

A

BMI<16 major,<18.5 minor
Weight loss over 3-6/12- 15% maj, 10% min
Day without food- 10maj, 5minor
Other- Low Mg, K, PO4 major, EtOh, diuretics, insulin, cehmo minor

577
Q

How do you start feeding someone at risk of re-feeding?

A

5-10kcal/kg/day slowly increasing to requirement over 7 days

578
Q

What is the evidence for paralysis in ARDS?

A 
Study is if PF<150 to give for 48hrs.
If you get to the point where it may be useful, the initial data is in cis-atracurium strictly speaking though is probably a class effect
579
Q

In a 16year old what is the most likely causative organism in meningitis?

A

Neisseria menand strep pneumonia

580
Q

At what ages is Listeria covered for in meningitis?

A

<3/12 and >50

581
Q

When is dexamethasone given in meningitis? What dose in kids?

A

0.15mg/kg max 10mg QDS given before or alongside the first dose of abx in all those >3/12 with suspected bacterial meningitis
Evidence in s.pneumonia.

582
Q

If a trauma patient has a positive FAST scan and is unstable do you go to CT?

A

Group decision but the recommendation is no, go straight to theatre-not sure how you can make a recommendation on this

583
Q

Above what level do you expect autonomic dysreflexia?

A

Above T6. Worse in higher and complete rather than incomplete transection

584
Q

How does autonomic dysregulation work later on in spinal injury?

A

Sympathetic stimulus from pain/distended bowel/bladder is un-inhibited causing massive HTN below and vasodilatation above with reflex bradycardia

585
Q

What drugs can be used prophylactically in autonomic dysreg?

A

Nifedipine and prazosin have been used

586
Q

How do you treat someone with a hypertensive crisis secondary autonoic dysreg?

A

Sit them up and identify the cause of sympathetic stimulation.
Watch for complications- MI ICH..etc all pressure realted
Used short acting fast onset meds to control if BP>150. Hydralazine, labetalol, nifedipine

587
Q

Why is Foscaranet a second line agent in HSV?

A

Is active aginst but can be toxic

588
Q

What does Ribavirin treat?

A

HCV

589
Q

What are the causes of encephalitis?

A

Can be infective or non-infective. Non-infective is usually autoimmune. Infection likely due to virus but can also be bacteria, fungi or parasite

590
Q

Which HSV causes encephalitis?

A

Usually HSV 1 90% and HSV 2 10%

591
Q

What does daptomycin and Tigecycline largely cover?

A

G+ve

592
Q

What are the ESKAPE bacteria, most likely to be problematic in terms of resistance?

A

Enterobacter, S.aureus, Klebsiella, Acinetobacterm Pseudomonas, Enteroccocus
These also account for more tha 80% of infection in ICU

593
Q

What is the sensitivity of BAL for PJP before and after abx start?

A

90-98% before and 64% if already had abx. With advent of PCR testing BAL is less required and not first line

594
Q

What is the maintenance fluid requirement for children?

A

Holliday Segar formula
4ml/kg/hr for first 10kg
then 2 for the second and 1 thereafter

595
Q

Which has the larger volume of distribution, morphine or fentanyl?

A

Fentanyl 4L/kg but morphine 3.5, Diamorph is 5

596
Q

Define volue of distribution

A

theroretical volume of plasma into which the drug would dissolve in order to give the plasma concentration achieved by administration of a bolus dose

597
Q

Whatis the mortality associated with GI bleed whilst in hospital when admitted with another condition?

A

23%

598
Q

What is attrition bias and how do you avoid it?

A

It is the failure to account for the withdrawals from a research project. To avoid it you do an intention to treat analysis

599
Q

How is performance bias guarded against?

A

If you think you’ve had the drug and know what effect it should have you may do other things make sure it works. Blinding helps

600
Q

What is detection bias and how do you guard against it?

A

If those collecting data know which group is which theymay round up or down as they expect the result to go..blinding

601
Q

If a patient has tachyarrhythmia and fails to respond to three escalating shocks what is the next step?

A

Amio 300 over 10-20min then try again.

602
Q

What are the contrindications to adenosine?

A

Ashma or bronchospasm of any cause, 2nd/3rd egree HB, sick sinus with symptomatic bradys (unless PPM)

603
Q

Which drug antagonises adenosine?

A

Diparydamole

604
Q

By how much should a BB be reduced once eGFR<30?

A

By 50%

605
Q

What does PCC contain?

A

II, VII, IX and X

606
Q

What does activated PCC contain?

A

II, VIIa, IX and X (may be useful in Dabigatran reversal)

607
Q

What colour is sputum in s.pneumonia? H. influenzae?, Klebsiella?

A

S.pneumnia rust colour
H.inf- green
Kleb- red currant jelly

608
Q

How do you get leptospirosis?

A

Contaminated water- pigs, cows, bats etc

609
Q

How does leptospirosis cause problems?

A

You feel ok for 0-3/52 then get spiraemic and feel awful but then the immunogenic phase kicks in and you get a widespread vasculitis and endothelial damage potentially leading to MOF

610
Q

What is a HAP?

A

Infection that develops >2days after admission or on admission if been admitted to care home or similar for >2 days in last 90 days

611
Q

Risk of death x4 if inhalational burn, what are the mechanisms of inhalational injury?

A

direct heat, irritation from inhaled particles, biochemical toxicity

612
Q

Why are burns below the vocal cords unusual?

A

The humidification process in the oropharynx efficiently moves heat to those structures. It’s usually inhaled soot in the airways. Unless steam was about for obvious reason

613
Q

What compound is most likely (80%) to be implicated in death due to fire?

A

CO
Binds Hb
Left shift O2 dissociation curve preventing O2 liberation
Competitive inhibitor of cytochrome oxidase

614
Q

Featrues of severe CO poisoning?

A

Acute neuro symptoms, coma, MI on ECG, significant acidosis, COHb >30%

615
Q

CO is often present when CN is also therefore picking up CN poisioning is difficult. When should it be suspected?

A

Lact >7, Elevated anion gap, reduced AV O2 gradient (high SvO2)

616
Q

How treat CN poisoning? How does it work? Dose?

A

Hydroxycobalamin directly binds HCN to cyanocobalamin which is then renally excreted. Dose 5g over 15min. s/e red gums, urine, can falsely elevate hbCO by 5%

617
Q

How would you treat a post phaeo patient with hypotension?

A

Alpha agonism may be ineffective because phenoxybenzamine will linger. THerefore NA and Phyenl and metaraminol may be ineffective. Could give Vasopressin

618
Q

What apart from hypotension is a post op complication of removing a phaeochromocytoma?

A

hypoglycaemia because eh lack of cortisol reduces the amount of glycogenolysis

619
Q

What is the accepted reference point for BP?

A

The RA

620
Q

What is an ideal BP cuff size?

A

20% larger than the diameter of the arm

621
Q

Which Korotkoff sound is systolic and diastolic?

A

1st systolic

5th- which is loss of 4th sound

622
Q

What are daily nutritional needs (kcal, water, protein)

A

30kcal/kg/d
30ml/kg water/day
1g/kg protein

623
Q

No gold standard definition of VAP but what are the constituents of any system?

A

Clinical
Micro
Radiological

624
Q

What is the VAP care bundle and what does it consist of?

A 
2007 and updated in 2010
Daily sedation hold
Bed head up
ulcer prophylaxis
oral hygiene with antiseptics
Sub glottic aspiration
cuff monitoring
625
Q

How do you correct Na for glucose?

A

Corr[Na]= measured[Na]+2.4*(gluc-5.5)

626
Q

What is a primary spont pneumothorax and a secondary?

A

Primary is anyone F+W<50

Anyone >50 is assmed to have lung disease and is secondary

627
Q

How treat primary spont PTX?

A

Small assymptomatic <2cm can be aspirated or just left

628
Q

How treat a symptomatic spont PTX?

A

drain, seldinger

629
Q

How des furosemide help in HF?

A

Transient but helpful venodilatation and also the diuresis

630
Q

When should dobuatmine be considered?

A

If signs of hypoperfsuion or SBP<85

631
Q

Define heart failure

A

Syndrome of typical symptoms and signs caused by structural or functional cardiac abnormalities resulting in reduced cardaic output and/or elevated intra-cardiac pressures

632
Q

Define HFmrEF (mid-range)

A

Have symptoms +/- signs, LVEF 40-49%, high BNP, LVH of LA enlargement, diastolic dysnfn

633
Q

Define HFrEF (reduced)

A

Symptoms +/- signs with EF<40%

634
Q

Define HFpEF (preserved)

A

Symptoms +/ signs with EF>50%, raised BNP, LVH/LA enlarge and diastolic dysnfn

635
Q

Which causes of HF should prompt genetic counselling?

A

HCM, DCM, arrhythmogenic RV cardiomyop

636
Q

What are the most specific signs of HF?

A

Raised JVP, Hapatojug reflex, S3, lateral displacement of apex

637
Q

What is the NPV of BNP for HF in non-acute and acute settings?
PPV?

A

94-98% NPV
acute PPV 67%
so good rule out test
Not good in renal failure, obese AF and high age

638
Q

In what order do you add drugs for HF?

A

ACEi +BB and if still signs/symptoms HF add spiro/eplerenone

639
Q

In HF when would you add Ivabradine and ARNI?

A

If have ACE, BB and mineralocortocoid anatag and still symptomatic with EF<35%, then swap the ACEi for ARNI and if SR>70 add ivabradine.

640
Q

When is CRT considered in HF?

A

IF ACEi, BB, spiro/eplerenone and HR<70 and considered for ARNI and QRS >130ms resync is considered

641
Q

What does ARNI stand for?

A

Angiotensin receptor neprilysin inhibitor

642
Q

How does an ARNI work?

A

The neprilysin inhibition slows degredation of BNP (and bradykinin) therefore allowing it to exert its diuretic and natriuretic properties for longer. In addition it has myocardial relaxation and anti-remodelling charateristics. The AR bit selectively targets the AT1 receptor and in addn to ARB more generally also reduces myocardial hypertrophy

643
Q

Can ACEi and ARB be used together?

A

Yes but only in HF patients who are on BB and can’t tolerate sprio/eplerenone and then only under strict supervision

644
Q

Who should be considered for CRT?

A

If QRS>130ms and EF<35% and on optimum medical management
If RV paced and deteriorating despite optimum meds
If HFrEF and need pacing for anything else go for CRT

645
Q

How treat exac HFpEF/HFmrEF

A

No real evidence, BB seem to not work for AF i these patients. Give diuretics

646
Q

What is the flow chart for angina treatment?

A

BB first, add Ivabradine or instead of BB if BB not tolerated if HR>70. Add nitrate/amlodipine/ nicorandil. Can attempted revascularisation

647
Q

What angina treatments should not be used together?

A

Nicorandil and nitrate because of lack of additional efficacy

648
Q

What are teh causes of acute HF?

A 
'CHAMP'
Coronary syndrome
HTN emergency
Arrhythmia
Mechanical
PE
649
Q

What did the DOSE study find?

A

furosemide at home dose or 2.5 times the previous oral dose intermittently or cont infusion. Trend toward higher Cr in high dose. No difference in primary end point which was subjective. Secondary end points were stat sig- fluid loss, weight loss, congestion free etc. Therefore higher dose either bolus or cont are recommended. Guidelines suggest home dose and uptitrate

650
Q

What is the complication of IVIG?

A

Sterile meningitis

651
Q

What is given to patients in subsequent pregnancies if they get HELLP or PET?

A

Aspirin 150mg

652
Q

What is the dose range for GTN infusion?

A

0.1-0.8mcg/kg/min

653
Q

Dose range for dobutamine?

A

2-20mcg/kg/min

654
Q

How much Na and gluc in 0.18%NaCl with 4% glucose?

A

Na=31mmol

Gluc- 40g

655
Q

What BIS number do you aim for to ensure anaesthesia?

A

40-60

656
Q

What structures do you pass through to get an LP?

A

Skin, sub cut, supra-spinatusligament, interspinous liganment, ligamentum flavum, extra dural, dura mater, arachnoid mater

657
Q

Where does the line connecting the iliac crests cut the spine?

A

L3/4

658
Q

What is the standard error of the mean?

A

It is the SD/square root of the sample size

659
Q

What contribution do albumin and PO4 have to anion gap?

A

AG= Na+K-HCO3-Cl but also -0.2(alb)+1.5PO4
This means alb contributes 2-8
PO4 contrubutes 0.5-1.5 so low albumin could squeeze you into a falsely low AG

660
Q

Unusual causes of HAGMA?

A

urea acid cycle inherited disorders, salicylates which impair oxidative phosphorylation, glycols, pyroglutamic acid (paracetamol and fluclox), CN, formaldehyde

661
Q

When can pyroglutamic acid cause an acidosis?

A

Glutathione plays important role. When depleted like in malnut, preg, sepsis, paracetamol use levels of pyroglutamic acid rise. Fluclox inhib 5-oxoprolinase to further prevent breakdown.->give NAC and stop ppt drugs

662
Q

What causes right shift of oxygen dissociation curve?

A

high T, low pH, high pCO2

663
Q

Causes of left shift oxy dissociation curve?

A

low T, high pH,

664
Q

What is the p50 for myoglobin?

A

0.4kPa! Myoglobin always get the oxygen

665
Q

What is the context sensitive half life of the following drugs at steady state?
Fentanyl
Thiopentone
Propofol

A

Fent at 12 hours is 300min
Thio is 100min
Prop<50min

666
Q

What are the risks from art line?

A

20% transient occlusion
14% bleeding/haematoma
infection1%

667
Q

According to surviving sepsis, which order should management me instigated in someone who needs everything?

A

1hr bundle -lacate, BCx2 before abx and abx within 1hr, if hypotension give 30ml/kg fluid and cont whilst still fluid responsive and give vasopressors if MAP>65 (pressors in less than 1 hr?)

668
Q

What is in the surviving sepsis 6 hour bundle?

A

It as the followingbut now no longer exists Vasopressors for MAP>65, CVC if lact initially >4 or septic shock and measure CVP and ScvO2 and on going lactate

669
Q

In surviving sepsis guidelines the aims are to achieve normality: MAP 65, CVP 8-12, U/O >0.5ml/kg/hr but what ScvO2 and SvO2 are they aiming for?

A

ScvO2 70% and SvO2 65%- hands up who knows how to reliably control these variables…. now defunct

670
Q

What did the ProCESS and ARISE trial show?

A

Showed that measuring CVP and ScvO2 in sepsis does not confer a survival benefit but it’s still in the guidelines

671
Q

If eclamptic seizure lasts >5min after Mg what do you do?

A

Give loraz as usual but if still refractory think that something else is going on ?ICH
Next would be intubation and propofol or keppra. Avoid phenytoin

672
Q

In SAH where are the aneurysms usually found?

A 
30-35% ACOM
30-35% ICA/PCOM
20% MCA
5% bifurcation of basilar
8% posterior circ
673
Q

What is the difference between HELLP and acute fatty liver of pregnancy?

A

HELLP has LDH rise and AFLP are generally unwell

674
Q

Intrahepatic cholestasis of pregnancy can occur in third trimester with intractable itch and nausea. What danger does it pose to the child?

A

Fetal complications including death but no long term impact on mother

675
Q

How does hypoPO4 present?

A

Refeeding/rhabdo/ haem anaemia usually, global weakness (inc ocular causing diplopia), resp muscle weakness (classically tachypnoea and resp alkalosis), confused,coma

676
Q

What hormone controls phosphate?

A

PTH, if high PO4, PTH high to increase renal losses

677
Q

How does reintroducing carbohydrate to diet after starvation cause hypoPO4?

A

Insulin activtes Na/K ATPase pumps and proteins are again made intracellularly. Both of these proceses shift PO4, K and Mg as co-factors into cells making serum conc fall.

678
Q

Nec fasc can be divided into three types based on the causative organism. What is are they?

A

Type 1- polymicrobial- mixture of G+ve and -ve, aerobic and anaerobic
Type 2- G+ve monobacerial classically strep pyogenese, S. aureus (in particular MRSA)
Type 3- Gas gangrene- Clostridium perfringens

679
Q

Give an example of nec fasc abx treatment

A

Mero, Clindamycin and Vanc/Linez. (Hyper baric O2 and IVIG (neutralise exotoxins) in small number of cases)

680
Q

How is warm ischaemic time defined in organ transplantation>

A

Time that has passed since BP<50 for 2 min until organ is cooled in theatre
SpO2 <70% has been in the guideline previously and can still make up the definition along with other factors

681
Q

What is the allowed warm ischaemic time for liver, pancreas, lungs, kidney?

A

Liver <20min (up to 30min allowed)
Panc 30min
Lung 60min
Kidney 120min

682
Q

What is the investigation of choice in dissection?

A

ECG gated CT, TOE obviously usefl but not as sens/specific as CT

683
Q

When TEVAR placed a concern is the spinal arteries, if a patient develops neuro symptoms how do you treat it?

A

Increase MAP but obviously not tht high given the indication for the procedure. A lumbar drain can improve spinal perfusion pressure

684
Q

What are the two main aortic dissection classification systems?

A

Stanford (Type A and B)

DeBakey (Type I, II, III where II=A III=B and I is everything)

685
Q

What proportion of dissections are type A and B?

A

A=70-80%, B 20-25%

686
Q

What are the three pathophysiological findings in aortic dissection

A

Atherosclerotic ulcer leading to tear
disruption of vasavasorum causing haematoma
de novo tear

687
Q

What is meningococcus? What is pneumococcus?

A

Neisseria meningitidis is meningococcus wheras bacteria like strep pneumoniae is pnuemococcus (90 types of pneumococcus)

688
Q

Are steroids usedul in meningocococcal meningitis?

A

No, N. Meningitidis is not the indication, pneumococcal is.

689
Q

How do steroids help in meningitis in adults?

A

They must be given before the first dose of abx as they work by reducing inflammation to cell lysis that is induced by abx treatment

690
Q

How is steroid treatment for paediatric meningitis different to adults?

A

There is some evidence that H.Influenzae along with pneumococcal meningitis respond favourably to steroid

691
Q

What are the stages of abdominal hypertension?

A

Grade 1 12-15mmHg
2 16-20
3 21-25
4 >25

692
Q

What is the definition of iof abdominal compartment syndrome?

A

abdo htn >20mmHg with organ dysnfn

693
Q

How is abdominal HTN treated?

A

Each factor that plays a role has a primary, secondary and tertiary management plan

694
Q

How is abdominal pressure measured?

A

Catheter in bladder with 25ml saline, supine with no abdo muscle movement zeroed at the mid-axillary line

695
Q

How are intra-luminal contents modified in abdo HTN?

A

Step 1 NG/rectal tube and start pro-kinetics
step 2 reduce feed and give enemas
step 3 colonoscopic decompression and stop feed
4. decompressive lapartotomy

696
Q

In abdo HTNwhat are the steps of removing intra-abdo SoL? (what a term!)

A

Abdo USS to see if there is one
CT to characterise
then drain if possible or surgery if not possible

697
Q

How is abdo wall compliance improved in a step wise appraoch to abdo HTN?

A

step 1 - analgesia and sedation, remove dressings that may be restrictive
2 consider reverse Trendelenbory position, head up 20 degrees
3. Muscle relaxant

698
Q

How is fluid optimised in abdominal HTN?

A
  1. Avoid excess fluid (good one), aim zero balance by D3
  2. Resus with hypertonic fluid, diuretics
  3. CRRT
699
Q

What abdominal perfusion pressure do you aim for in abdominal HTN?

A

APP>60

700
Q

If intra-arterial injection of a medication what are the first steps? What are the next steps possible?

A

Flush with saline to dilute the drug. Thio is the classic one where crystals block small arterioles. Give analgesia to reduce sympathetic response and further vasoconstriction, keep limb warm but elevated. Heparin useful if ischaemia

701
Q

When is a stellate ganglionblock used?

A

I’m sure in other cases but also if pt has intra-art injection of a drug that has caused ischaemia. The block makes limb lose sympathetic innervation dilating the vessels

702
Q

How long should UFH, LMWH, aspirin and clopidogrel be stopped before doing an LP or epidural?

A

UFH 4 hrs
LMWH- 12 hrs for prophylactic, 24 for therap
Clopid/Prsugrel-7 days
Aspirin-no effect

703
Q

What is the mortality beenfit of treating T2RF 2 COPD with NIV?

A

50% reduction in mortality with NNT 10

704
Q

When should NIV be considered in AECOPD?

A

pH <7.35 pCO2 >6 after 1 hr of medical mx

705
Q

How often should a trahe inner tube be changed?

A

Every 8 hours in non-ventilated pts. In ventilated pts the risk of derecruitment etc needs to be weighed

706
Q

What cuff pressure should be aimed for in trache?

A

Check every 8 hours and should be 20-25cmH2O

707
Q

Trauma resus centres on permissive hypotension and low volume blood product resus, when is this not appropriate?

A

If TBI/spinal injury aim MAP 80

If not though can aim SBP 80-90

708
Q

What did CRASH1 show?

A

Steroids are not good for head injuries an should be avoided

709
Q

What did CRASH2 show?

A

TXA reduced death NNT 68, its safe so has been incorporated into practice

710
Q

What did CRASH 3 show?

A

No reduction in death at 28days to those with TBI and getting TXA within 3 hrs but in mild-mod group there was a tiny reduction in mortality…on balance if in that group it causes no harm so give it

711
Q

Beta blocker overdose can be treated with glucagon but what two blockers should you be most worried about?

A

Propranolol causes Na blockade which widens QRS, this an be treated with bicarb
Sotalol causes K efflux blockade which can cause Torsades

712
Q

What abdnormalities would you see in BB overdose?

A

bradycardia and hypotension, AV block
bronchospasm
Hypoglycaemia and hyperK
comas seizures

713
Q

What are the antidotes to BB overdose? How do they work?

A

Glucagon 50mcg/kg up to 10mg then 2-10mg/hr is traditional but is inferior to high dose insulin euglycaemic therapy. Glucagon is a positive inotrope by a non-catecholaime mechanism, it also counters the B3 effects and subsequent hypoglycaemia
Consider intralipid

714
Q

How is high dose insulin euglycaemic therapy given in BB and CCB overdose?

A

Given 50ml 50% glucose with 1unit/Kg insulin short acting initially then titrated to effect

715
Q

What are the admitting criteria for a burns centre? Burns unit? Burns fascility?

A

Centre- BSA>25% + airway burn or >40% if not ( if >25% should be discussed with burns centre)
Unit- Any BSA>10% should be d/w burns unit also if it is non-blanching, circumferential or to face/feet/hand/perineum/gentials
Facilities- More than 2% but <10% discuss if chemical or electrical burn

716
Q

What are the interventions suggested by KDIGO in those ith stage 1 AKI?

A

Avoid nephrotoxics, adequate volume status, maintain perfusion pressure with vasopressors if required, use of functional haemodynamic monitoring should be considered. Normal glucose. Non-invasive work up for the cause

717
Q

What are the recommendations for Stage 2 AKI?

A

All drugs reviewed and adjustments made. RRT/ICU needed?

718
Q

What are the KDIGO stage 3 AKI recommendations?

A

Avoid subclavian lines

Intensive Care Medicine (11 decks)

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