Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

FFICM > SOE > Flashcards

SOE Flashcards

1
Q

Risk factors AAA?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Atypical symptoms of AAA?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is a aorto-enteral fistula associated with?

A

a previous graft that has eroded into the GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How prognosticte AAA?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

Age followed by shock at presentation and AKI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When is AAA electively repaired?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the indications for spinal drain insertion post AAA?

A

If complex case and concern or to rescue delayed paraplegia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where are lumbar drains inserted?

A

Into sub-arach space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Normal IAP?

A

5-7mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Grades of abdominal HTN?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Define abdominal compartment syndrome

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How can measure abdo pressure?

A

Needle though abdo wall (direct)

Or indirect- bladder ut also stomach, colon, uterus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Indications for open abdomen?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the Bamford classification?

A

TACS/PACS, LACS and POCS s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Therapeutic hypothermia in ischaemic stroke?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Interventional radiology in ischaemic stroke- what can be done and timings?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

When does focal cerebral ischaemia result in coma?

A

Brainstem affecting the reticular activating system
Malig MCA with oedema and herniation
Cerebral venous thrombosis- raised ICP, cerebral oedmea and seizure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Mechanism of contrast induced AKI?

A

Direct reactive O2 species
Imbalance of constriction and dilatation
Contrast induced diuresis and increased viscocity of urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Risk factors for getting contrast induced AKI?

A

Age >75, CKD eGFR<60, nephrotoxic drugs, IV contrast (as opposed to PO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Define KDIGO stages

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Potential protection from contrast induced AKI?

A

Fluid
NAC- though may reduce creatinine release rather than helping kidney
Bicarb- renal alkalinisation

31
Q

What are the diagnostic criteria for contrast induced AKI?

A

Cr rise >44 or 25% from baseline within 48hrs

32
Q

How manage a patient with AKI?

A 
STOP
Sepsis and hypoperfusion
Toxins
Obstruction
Primary renal
No evidence converting oliguria to polyuria using diuretics helps AKI
33
Q

Types of RRT?

A

CVVHF, CVVHD, CVVHDF, CUF (slow cont ultra-filtration) and SLEDD (sustained low-efficiency daily dialysis)

34
Q

Which trials have looked at dose of effluent in RRT?

A

RENAL 2009- 25 vs 35ml/kg no benefit

IVOIRE no benefit 70 vs 25

35
Q

Disequilibrium syndrome- what is it and how avoid?

A

Cerebral oedema from urea shifts. Therefore aim reduce urea by 30% r less in first 24hrs

36
Q

Commonest cause of ALF in developing world vs UK?

A

HAV, HBV and HEV in developing world. Paracetamol iin UK

37
Q

Causes of ALF?

A 
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
Q

Kings criteria for paracetamol ALF?

A 
pH<7.3
or all three of
PT>100s
Cr >300
G3 or 4 encephalitis
39
Q

King’s criteria for non-paracetamol ALF?

A 
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
Q

What is the system for grading encephalitis?

A

West-Haven criteria

41
Q

What are the mechanisms for renal failure in ALF?

A

ATN most commonly due to hypo-perfusion or nephrotoxins
GN in HBV or HCV is possible
Intra-abdo HTN due to ascites
HRS

42
Q

What is the management of ALF with regards to other organ systems?

A

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
Q

Paracetamol mechanism of ALF?

A

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
Q

What are the risk factors for developing paractamol toxicity?

A

Cytochrome induction- chronic EtOH, inducing drugs

Glutathione depletion- malnutrition or alcohol

45
Q

What is ARDS?

A

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
Q

Pulmonary causes of ARDS

A

Pneumonia, contusion, aspiration, inhalational injury, vasculitis, drowning

47
Q

Non-pulmonary cause of ARDS

A

Sepsis, burns, trauma, TRALI, pancreatitis, bypass

48
Q

What is the pathophysiology of ARDS?

A

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
Q

What trials looking at NMBAs in ARDS?

A

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
Q

What studies have looked at prone ventilation in ARDS?

A

PROSEVA showed 50% reduction in mortality with NNT 6.

51
Q

What trials have shaped the use of HFOV?

A

OSCAR- no benefit

OSCILLATE- harm NNH 9

52
Q

Steroids in ARDS?

A

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
Q

Components of Murray score?

A

PF ratio, PEEP, Compliance, CXR findings

54
Q

Types and causes of adrenal insufficiency?

A 
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
Q

Type of shock in Addison’s or similar?

A

High CO distributive

56
Q

Triad of amniotic fluid embolism?

A

CV collapse, coagulopathy and hypoxia

57
Q

Phases of amniotic fluid embolus

A

phase 1 RV failure and anaphylaxis type picture followed by LV failure and DIC with sepsis type leaky capillaries

58
Q

Risk factors for amniotic fluid embolism?

A

No RF but association like mechanical delivery, older mum, placetnal pathology, multiparity, trauma

59
Q

Types of hypersensitivity reactions? What type is anaphylaxis?

A

Types 1-4

Type 1 is anaphylaxis IgE mediated

60
Q

What are types 2,3 and 4 hypersensitivity reactions and give examples

A

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
Q

How is tryptase taken in anaphylaxis?

A

ASAP and 1-2hrs post then 24hrs

62
Q

When test for cause if anaphylaxis?

A

Send all to clinic in 4-6/52 to allow mast cells to make histamine again

63
Q

What other tests apart from prick tests in allergy?

A

RAST- measures IgE ab in serum

ImmunoCAP- enzyme assay more sensitive than RAST but both of these have a low sensitivity.

64
Q

Examples of bacteriostatic and cidal abx?

A

bateriacidal- Pens, cephs, aminoglyc, glycopep, quinonlones, nitroimidazole, Rifiampicin, Nitro
Static- Macrolides, tetracyclines, Trimethoprim, Clindamycin

65
Q

Mechanism of action of abx?

A

Inhibit cell wall
Inhibit DNA snthesis of fn
Inhibit tetrahydrofolate
Inhibit protein synthesis

66
Q

What is time dep and conc dep killing of bacteria?

A

Time dep is time above MIC

Conc dep- killing correlates with peak conc such as aminoglyc

67
Q

Which abx inhibit cell wall?

A

Penicillin, cephalosporins and glycopeptides (Vanc)

68
Q

What abx inhibit DNA synthesis/fn

A

Metronidazole Cipro, Rifampicin

69
Q

Which abx inhibit protein synthesis?

A

Erythro etc, clinda, linezolid, Gent

70
Q

Give G-cocci

A

Neisseria and Moraxella

71
Q

G+ve rods?

A

ABCDL

Actinomyces, Bacillus, clostridia, Diptheria and listeria

72
Q

Mechanism of abx resistance?

A

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
Q

How is resistance to abx acquired?

A

Mutation or horizontal gene transfer eg free DNA, bacteriophages, plasmid conjugation

FFICM (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions