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SOE Flashcards

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1
Q

Risk factors AAA?

A

Male, >65, smoking, HTN, MI/stroke, genetic-marfans etc

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2
Q

Atypical symptoms of AAA?

A

back pain (renal colic like), mimicking sciatica, chronic severe back pain (contained), transient LL paralysis

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3
Q

What is a aorto-enteral fistula associated with?

A

a previous graft that has eroded into the GI tract

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4
Q

How prognosticte AAA?

A

APACHE and POSSUM not up to much. Use Hardman index or Glasgow Aneurysm score

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5
Q

Complications following emergency AAA?

A 
Early/late, graft and non-graft related.
Early graft- distal embolism, AKI, leak
Late graft- infection, aorto-enteral fistula, pseudoan
Early non-graft- MI, ARDS, ileus etc
Late non-graft- SBO, incisional hernia
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6
Q

What is the most important factor in predicting outcome post AAA repair?

A

Age followed by shock at presentation and AKI

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7
Q

When is AAA electively repaired?

A

Male >5.5, Female >5cm or >1cm/year

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8
Q

What are the indications for spinal drain insertion post AAA?

A

If complex case and concern or to rescue delayed paraplegia

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9
Q

Where are lumbar drains inserted?

A

Into sub-arach space

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10
Q

Absolute and relative contra-indications for lumbar drain insertion

A

Absolute- pt receving anticoags, bleeding

Rel- non-comm hydroceph, large SOL or infection

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11
Q

Normal IAP?

A

5-7mmHg

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12
Q

Grades of abdominal HTN?

A

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

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13
Q

Define abdominal compartment syndrome

A

IAP>20 with or without APP<60 with new organ dysfn or failure

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14
Q

Risk factors for getting abdominal HTN?

A

Reduced wall compliance -trauma, burn, prone
Inc abdo contents- Intra or extra mural
Capillary leak
Other- Mech vent, high PEEP, inc head of bed, shock

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15
Q

How can measure abdo pressure?

A

Needle though abdo wall (direct)

Or indirect- bladder ut also stomach, colon, uterus

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16
Q

Effect of high abdo pressure on other organ systems?

A

Resp-basal atelectasis- VQ mismatch
CV- reduced venous return, inc afterload
Neuro- says inc ICP but not sure if I believe it
Renal- direct compression, up-reg RAAS
GI/hepatic- hypoperfusion, biliary stasis

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17
Q

Indications for open abdomen?

A

Severe necrosing pancreatitis
Abdo sepsis
Damage control post trauma
Emergent vascular surgery

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18
Q

The complication of open abdomen>

A 
Nursing- skin, pain
Fluid loss
Malnutrition
Infection
Adhesions
Ileus
Longer term hernias
High risk of enterocutaneous fistula
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19
Q

What temporary closure devices for abdomen?

A

Bogota bag- 3L plastic bag fixed to gascia or skin
Negative pressure therapies
Sythetic mesh
Velcro-type sheath Whittmann patch

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20
Q

What is the Bamford classification?

A

TACS/PACS, LACS and POCS s

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21
Q

When does the National Institute of Neurology and Stroke (NINS) say thrombolysis is contra-indicated?

A 
prev ICH
BP >185 or DBP>110
Trauma/stroke in last 3/12
Coagulopathy- plt <100, PT >15 on anticoags
Major surgery within 14/7
GI haem within 21/7
Severe hyper or hypogly
Seizures at onset or SOL
Isolated mild deficits or recent MI
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22
Q

What studies have looked at decompressive craniectomy for malig MCA?

A

DESTINY, DECIMAL and HAMLET <60 and DESTINYII >60

Sig reduction in mortality but nearly all had significant impairment. And over 60 is not recommended.

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23
Q

When should decompressive craniectomy be considered?

A

If <60, MCA infarct, NIHSS >15, CT evidence of infarct of at least 50% MCA territory.

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24
Q

Therapeutic hypothermia in ischaemic stroke?

A

No benefit- hyperthermia should be avoided. Most recent trial EuroHYP-1

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25
Interventional radiology in ischaemic stroke- what can be done and timings?
Clot retrieval can be considered up to 8 hours post in some situations but rare. More common is those with carotid or MCA clots not responding to thrombolysis
26
When does focal cerebral ischaemia result in coma?
Brainstem affecting the reticular activating system Malig MCA with oedema and herniation Cerebral venous thrombosis- raised ICP, cerebral oedmea and seizure
27
Mechanism of contrast induced AKI?
Direct reactive O2 species Imbalance of constriction and dilatation Contrast induced diuresis and increased viscocity of urine
28
Risk factors for getting contrast induced AKI?
Age >75, CKD eGFR<60, nephrotoxic drugs, IV contrast (as opposed to PO)
29
Define KDIGO stages
1- 1.5-2x creat or >26.5micromol/l or <0.5ml/kg urine for 6-12hrs 2. 2-3x < 0.5ml/kg/hr for more than 12 hrs 3- >354micromol/l or >3x creat or on RRT, <0.3 ml urine for 24hrs or anuria for 12 hrs
30
Potential protection from contrast induced AKI?
Fluid NAC- though may reduce creatinine release rather than helping kidney Bicarb- renal alkalinisation
31
What are the diagnostic criteria for contrast induced AKI?
Cr rise >44 or 25% from baseline within 48hrs
32
How manage a patient with AKI?
``` STOP Sepsis and hypoperfusion Toxins Obstruction Primary renal No evidence converting oliguria to polyuria using diuretics helps AKI ```
33
Types of RRT?
CVVHF, CVVHD, CVVHDF, CUF (slow cont ultra-filtration) and SLEDD (sustained low-efficiency daily dialysis)
34
Which trials have looked at dose of effluent in RRT?
RENAL 2009- 25 vs 35ml/kg no benefit | IVOIRE no benefit 70 vs 25
35
Disequilibrium syndrome- what is it and how avoid?
Cerebral oedema from urea shifts. Therefore aim reduce urea by 30% r less in first 24hrs
36
Commonest cause of ALF in developing world vs UK?
HAV, HBV and HEV in developing world. Paracetamol iin UK
37
Causes of ALF?
``` Infective- Hepatitis, CMV, EBV Drugs- paracetamol, AEDs, St John's wort, chemo, recreational drugs Toxins- amatoxin Malignancy Vascular- Budd-Chiari (HVein), ischaemia Preg- HELLP Metabolic- Wilsons Autoimmune ```
38
Kings criteria for paracetamol ALF?
``` pH<7.3 or all three of PT>100s Cr >300 G3 or 4 encephalitis ```
39
King's criteria for non-paracetamol ALF?
``` PT>100s or any three of 1. Age <11, >40 2. Non A, Non B heptatis or idiosynchcratic 3. Jaundice to enceph >7/7 4. PT>50 5. TB >300 ```
40
What is the system for grading encephalitis?
West-Haven criteria
41
What are the mechanisms for renal failure in ALF?
ATN most commonly due to hypo-perfusion or nephrotoxins GN in HBV or HCV is possible Intra-abdo HTN due to ascites HRS
42
What is the management of ALF with regards to other organ systems?
Resp- G3/4 enceph usually need intubation. Low PEEP CV- Use vasopressors and get euvolaemia Neuro- neuro-protective measures CPP 60-80 but controversial as is hypothermia etc Renal- RRT early to avoid overload and acidosis Coag- DIC common
43
Paracetamol mechanism of ALF?
NAPQI is hepatotoxic. Paracetamol is metabolised largely by glucoronidation and sulphation but a very small amount is by CYP450 which is de-toxified by glutathoine. If the glucoronidation and sulphation is saturated more goes down the CYP system overwhelming the glutathione.
44
What are the risk factors for developing paractamol toxicity?
Cytochrome induction- chronic EtOH, inducing drugs | Glutathione depletion- malnutrition or alcohol
45
What is ARDS?
acute, diffuse inflammatory lung injury leading to increased pulmonary vascular permeability, increased lung weight and loss of aerated lung tissue with hypoxaemia and bilateral radiographic opacities associated with increased venous admixture, increased dead space and decreased lung complaince
46
Pulmonary causes of ARDS
Pneumonia, contusion, aspiration, inhalational injury, vasculitis, drowning
47
Non-pulmonary cause of ARDS
Sepsis, burns, trauma, TRALI, pancreatitis, bypass
48
What is the pathophysiology of ARDS?
Triphasic- 1. Exudative- days 2-40 inflammation and leak with microthrombus causing VQ mismatch and reduced complaince 2. Proliferative- days 4-7 proliferation of type II pneumocytes and fibroblasts with fibrin deposition, scar formation 3. days 7-14 fibrotic stage
49
What trials looking at NMBAs in ARDS?
ACURASYS severe ARDS with cisatra or placebo showed a 90day mort benefit in patients with PF<120 and inc ventilator free days with no inc in ICU weakness
50
What studies have looked at prone ventilation in ARDS?
PROSEVA showed 50% reduction in mortality with NNT 6.
51
What trials have shaped the use of HFOV?
OSCAR- no benefit | OSCILLATE- harm NNH 9
52
Steroids in ARDS?
Conflicting evidnce. Thought that low dose long course later in disease process may be of help. in 2006 Steinberg gave methylpred and showed reduced ventilator days but no mort benefit and increase in myopathy and neuropathy. In 2007 Meduri gave steroids early which showed a great improvement but with septic shock as a complication. Underpowered.
53
Components of Murray score?
PF ratio, PEEP, Compliance, CXR findings
54
Types and causes of adrenal insufficiency?
``` 1, 2 and 3ary. Primary is Addison's of which 70-90% autoimmune. Others inclue TB infection, HIV and CMV, mets, drugs (etomidate) and others including waterhouse-Friderichsen syndrome Also 2ary (pituatary) and tertiary (hypothalamus) from seroids down regulation, infarction (Sheehan's) and malig ```
55
Type of shock in Addison's or similar?
High CO distributive
56
Triad of amniotic fluid embolism?
CV collapse, coagulopathy and hypoxia
57
Phases of amniotic fluid embolus
phase 1 RV failure and anaphylaxis type picture followed by LV failure and DIC with sepsis type leaky capillaries
58
Risk factors for amniotic fluid embolism?
No RF but association like mechanical delivery, older mum, placetnal pathology, multiparity, trauma
59
Types of hypersensitivity reactions? What type is anaphylaxis?
Types 1-4 | Type 1 is anaphylaxis IgE mediated
60
What are types 2,3 and 4 hypersensitivity reactions and give examples
2- IgG or M mediated ab-mediated . Eg, autoimmune haemolytic anaemia, Goodpasture's 3- Immune complex mediated- IgG or complement- Lupus, RA 4- Delayed,T-cells- contact derm, chronic rejection
61
How is tryptase taken in anaphylaxis?
ASAP and 1-2hrs post then 24hrs
62
When test for cause if anaphylaxis?
Send all to clinic in 4-6/52 to allow mast cells to make histamine again
63
What other tests apart from prick tests in allergy?
RAST- measures IgE ab in serum | ImmunoCAP- enzyme assay more sensitive than RAST but both of these have a low sensitivity.
64
Examples of bacteriostatic and cidal abx?
bateriacidal- Pens, cephs, aminoglyc, glycopep, quinonlones, nitroimidazole, Rifiampicin, Nitro Static- Macrolides, tetracyclines, Trimethoprim, Clindamycin
65
Mechanism of action of abx?
Inhibit cell wall Inhibit DNA snthesis of fn Inhibit tetrahydrofolate Inhibit protein synthesis
66
What is time dep and conc dep killing of bacteria?
Time dep is time above MIC | Conc dep- killing correlates with peak conc such as aminoglyc
67
Which abx inhibit cell wall?
Penicillin, cephalosporins and glycopeptides (Vanc)
68
What abx inhibit DNA synthesis/fn
Metronidazole Cipro, Rifampicin
69
Which abx inhibit protein synthesis?
Erythro etc, clinda, linezolid, Gent
70
Give G-cocci
Neisseria and Moraxella
71
G+ve rods?
ABCDL | Actinomyces, Bacillus, clostridia, Diptheria and listeria
72
Mechanism of abx resistance?
Intrinsic-lack of target, lack of transport mechanism, impermeable membrane Acquired- Drug inactivation (b-lactamases), efflux of drug (pseudomonas), alternative pathyway or altered molecular target
73
How is resistance to abx acquired?
Mutation or horizontal gene transfer eg free DNA, bacteriophages, plasmid conjugation

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