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Pete FFICM SOE/OSCE > Gen - Causes, Lists And Definitions 1-11 > Flashcards

Gen - Causes, Lists And Definitions 1-11 Flashcards

1
Q

Outcome scores for AAA

A

Hardman index

Glasgow Aneuyrsm Score. (Score of 84 - 65% pred mortality)

Hardman (1 point each, >2 = 80% mortality)

Age>76
Cr>190
Hb<90
Ischaemic ECG
LOC in Hospital.
Glasgow
Age - year in points
Shock 17
Myocardial disease 7
Cerebr0vascular 10
Renal disease 14
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2
Q

Complications of a AAA repair

A 
Graft Early - 
Massive Transfusion
Distal embolus
Branch involvement - pancreatitis, AKI
ENDOLEAK

Graft Late - Infection, occlusion, Aorto-enteric fistula, pseudoaneury…

Non graft early - MI, renal failure, paraplegia, HAP/VAP/ARDS, transfusion issues, ARDS, ACS, ileus

Non graft late - slow resp wean
Small bowel obstruction
DVT/PE
Hernia

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3
Q

When to electively operate AAA

A

Male >5.5cm
Fem >5cm
Growth >1cm/year

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4
Q

Abdominal pressures

A

Normal 5-7

1 - 12-15
2 - 16-20
3 21-25
4 25+

ACS - >20 with new organ dysfunction (+/- APP<60)

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5
Q

Risk factors for Ab Compartment

A

Diminished Wall Compliance —- tight closure, burns, obese

Increased abdo content - Intra and extra lum

Capillary leak - sepsis, pancreatitis, acidosis, fluid +++

Other - MV, PEEP>10, Shock, increased head of bed

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6
Q

Issues with an open abdomen

A

Nursing - skin, turning, positioning, pain

Fluid loss - ?fluid balance

Malnutrion - loss of protein/nitrogen

Infection

Ileus

Risk of entero-Cutan fistula

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7
Q

When to CT a stroke

A

Thrombolysis or anti coag decisions
Known anti-coag use

Bleeding tendency
GCS <13
Fluctuating or progressive symptoms

Papilloedema, stiff neck, fever

Head at onset

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8
Q

Oxford (bamford class of stroke)

A

TACS - MCA
PACS MCA/ACA
LACS - deep penetrating artery with subcortical
POCS Brainsetm cerebellum

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9
Q

Define Contrast Induced AKI

A

Development of AKI within 48 hours of contrast load

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10
Q

Mechanisms of contrast AKI

A

Reactive Oxygen Species are nephrotoxic

Imbalance vasoconstriction vs dilation

Increased O2 consumption

Contrast diuretics

Increased urine viscosity

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11
Q

KDIGO stages

A

1 - 1.5 to 2x increase in baseline (or 26umol) OR <0.5ml/kg 6-12hrs

2 2-3. OR 0.5ml/kg >12 hours

3 - 3x (or 354 umol) OR <0.3 for 24 or anuria for 12

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12
Q

Indications for RRT

A

Metabolic acidaemia

Hyperkalaemia

Symptomatic uraemia

Fluid overload

Overdose

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13
Q

Types and principles of RRT

A

CVVHF - CONVECTION - bulk flow down hydrostatic gradient

CVVHD - DIFFUSION - countercurrent of blood and diasylate

SCUF

CVVHDF

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14
Q

Things to prescribe on RRY

A

Intermittent or continuous

HF or HD (diffusion better for small solutes)

Dose - how much filtrate produced (25-35ml/kg/hour)

Fluid - pre or post dilution

Fluid balance target

Anticoagualtion

Flow rates

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15
Q

Anti coag methods in RRT

A

None - no bleed short filter life

UFH - Titratable, monitored, reversible. RISK OF HIT

LMWH - no titration. No reversal

Prostacyclin - Less bleeding, short filter, HYPOTENSION

Citrate - Good regional, stays in circuit.

BUT, hypocalcaemia, large sodium load. CI in liver disease. Citrate acid.

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16
Q

Define Acute Liver Failure and its classification

A

Rare life threatening illness usually with liver disease already, with acute deterioration in synthetic function

Presents as jaundice, enceph, coaguloapthy

Hyper acute < 1 week
Acute 1- 4
Sub acute 4-24 weeks

Duration from jaundice to enceph

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17
Q

Causes of ALF

A

Infection - Hep, HSV, CMV, VQV EBV
Drugs - PARACETAMOL, phenytoin, tb - isnoiazid, chemo, amphet.

Toxins - mushrooms

Malignancy

Vascular - budd chiara (vein thrombosis), ischaemia

Pregnancy, HELLP. Acute fatty liver

Wilsons

Autoimmune

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18
Q

King criteria - paracetamol

A

pH< 7.3

OR

All of

PT>100s
Cr>100
Grade 3/4 enceph

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19
Q

Kings - non para

A

PT>100

OR

3 of

Age <11 >40

Non hep a/b

Not hyper acute

PT>50s
Bilirubin >300

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20
Q

Encephalopathy grading

A

West Haven

1 lack of awards, euphoria/anxiert

2 - lethargy, apathy

3 - Somnelence, semi stupour

4 - coma

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21
Q

ARDS definitions - proper

A

Acute and diffuse

Inflammatory lung injury

Causing increased lung vascular permeability

Increased lung weight

Loss or aerated tissue with

Hypoxaemia, bilateral radio graphic opacities, increased venous admin

Increased dead space and decreased compliance

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22
Q

ARDS berlin

A

Within 1 week of acute resp insult

Bilateral opacities that are NOT effusions, collapse or nodules

Resp failure NOT explained by LVF/overload (echo)

Ventilated with PEEP>5

PF<300

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23
Q

Causes of ARDS

A

Pulmonary or Non Pulmonary
:
Pulmonary:

Pneumonia
Contusion
Aspiration pneumonitis
Burns
Vasculititis
Drowning

Extra-pulmonary

Sepsis, 
Burns
Trauma
TRALI
Pancreatitis
Bypass (pump lung)
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24
Q

Pathophysiology of ARDS

A

Exudate, Proliferative, Fibrotic

Exudative - Leakage of fluid in alveoli, microtrombus

Proliferative - type II pneumocytes form, fibrin deposition, exudate&raquo_space; scar

Fibrotic - fibrosis

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25
Q

Vent strageties for ARDS

A

Low Tv 5-7ml/kg IBW
Accept a higher resp rate

Aim Sats 88-95 to reduced FiO2

PEEP>5

Pplat<30

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26
Q

Improving vent in ARDS

A

Vent strategies

NMBDs

Recruitment

Prone

HFOF

ECMO

Inhaled NO

Steroids

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27
Q

Murray score

A

PF ratio
PEEP
Compliaance
CXR quadrants

0-4, average score used..
>3 refer

28
Q

Contra indications to ECMO

A

Irreversible organ damage/MOF

Advanced malignancy

Chronic severe pulm hypertension

29
Q

Indications VA ECMO

A 
Cardiogenic shock - myocarditis, arrhythmia, PE, anaphylaxis
Wean from bypass
Heart transplant
Chronic cardiopmyopathy - bridge to VAD
ECLS
30
Q

Indication VV ECMO

A

Potentialy reversible acute failure

ARDS with bacterial / viral pneumonia

Lung transplant - bridge / graft failure

Pulmonary haemorrage/haemoptysis

Status asthmaticus

31
Q

relative CI to ECMO

A 
Age>75
Polytrauma, multiple bleeds
CPR.60 minutes
MOF
CNS injury
32
Q

VA CIs

A

Severe aortic regurgitation

Aortic dissection

33
Q

VV CI

A

Unsupportable cardiac failure
Pulm Hypertension
Cardiac arrest

34
Q

Complications of ECMO

A

Cannulation - Pneumothorax, vascular injury, infection, emboli, bleed

Anticoag - haemorrhage

EAquipment - pump failure, oxygenation failure

35
Q

Causes of adrenal insufficiency

A

Primary - Addisons (adrenal is destroyed)

Secondary - Insufficient production of ACTH (rare)

Tertiary/relative - Suprresion of HPA axis due to steroids

36
Q

Causes of primary adrenal insufficiency

A

Autoimmune (common)

Infection - TB, fungal, HIV (CMV)

Cancer - mets

Drugs - etomidate, ketoconazole

Other - critical illness insufficiency
Amyloid

37
Q

Causes of secondary adrenal insufficiency

A

Dystruction of pituitary

Sheehans
Malignancy
Bleed

38
Q

Causes of tertiary adrenal

A

Relative

Suppression of exogenous corticosteroids

39
Q

Definition of Addisons

A

Autoimmune disease of cortex, reduced or absent cortisol

Cortisol deficiency = rise in ACTH

MSH rises - pigmentation

ACTH and MSH come from pre-opiomeanoncortin

40
Q

Diagnosing adrenal insuffiency

A

Cortisol and ACTH (primary C low, A high)

Sec/ter : both low

Synacthen test:

Adrenal antibodies

41
Q

When might you use steroids in crit care

A

Treatment of disease - COPD, asthma, adrenal crisis

Organ donor - methy pred

PCP in HIV

Airway oedema

Anaphylaxis

Myxoedemia coma

S.pneumonia bacterial meningitis]

Sepsis

42
Q

Pathology of amniotic fluid embolus

A

Initially thought emboli..tissue in the circulation.

Now - two phase immune response to tissue ANTIGENS

1 - RIGHT heart failure.

Vasoactive substances produced. Pulmonary vasospasm.
Hypotension, hypoxia. 30 minutes

2 - Right recovers, LV fails. Pulmonary oedema
Increased cap. Permeability, DIC, uterine Antony, MOH.

43
Q

Triad of AFE

A

Hypoxia

Cardiovascular collapse

Coagulopathy

44
Q

Define AFE

A

Rare catastrophic emergency presenting as sudden maternal collapse associated with shock, hypoxia and coagulapathy.

Happens with amniotic fluid/cells enter maternal circ

45
Q

Risk factors for AFE

A 
Advanced maternal ages
Polyhydromanios
Induction of labour
Placenta Pravin/abruptions
Multip
Uterine rupture
IUD
Trauma
46
Q

Differential of AFE

A

Obs and non obs

Obs - Placental abruption,
Eclampsia
Uterine rupture
PPH

Non obs - Anaphyalxis, total spinal, sepsis PE

47
Q

Define anaphylaxis

A

A severe life threatening generalised systemic hypersentivity reaction divided in allergic and non-allergic

Allergic: Immune mediated - IgE

Histamine, cytokines, prostaglandins - vasodilation, hypotension, tachy

Non-AllergicL. Mast cell and basophils degranulation with no immune trigger

48
Q

Classify hypersensitivity

A

I - Immune - IgE - Asthma, anaphylaxis

II - antibody mediated IgG/M. Goodpastures

III - Immune complex mediated - IgG and complement. Lupus nephritis, RA

IV - Delayed - T cells, macrophages. Contact dermatitis, coeliac. Transplant reject

V - Idiopathic

49
Q

Drugs causing anaphylaxis

A

NMBD - roc, sux, atra

ABx - penicillins

Thio

Latex

Gelatine/starches

Chlorhex

Iodine contrast

50
Q

Drugs for anaphylaxis

A

IM adrenaline - 1ml of 1:1000
iv 50-100mcg iv of 1:10000

Saline 500 to 1litres

Chlorphenarmine - 10mg

Hydrocortisone - 200mg

51
Q

When to take bloods in anaphylaxis

A

At the time

1-2 hours later

24 hours

52
Q

Tests for anaphylaxis

A

RAST - radioallergosorbant - antigen specific IgE

ImmunoCAP

Skin prick testin

53
Q

Types antibiotics and examples

A

Bacteriostatic and bacteriocidal.

Cidal - causes cell death, hosts undamaged

Penicillins
Carbapenems
Aminoglyc
Rifampicin 
Quinolone

Static - limit growth while immune system removes

Macrolides
Tetracyclines
Sulphonamide
Trimeth

54
Q

Mechanisms of antibiotic activity

A

Inhibit cell wall synthesis

Inhibit DNA synthesis/function

Inhibit Tetrahydrate folate synthesis

Inhibit protein

55
Q

Abx that inhibit cell wall synth

A

Penicillins

Cephalosporins

Glyco - vanc/teic

Polymixin E - Colistin

56
Q

Abx that inhibit DNA

A

Metronidazole. Complexes DNA and strands break

Rifampicin Inhibit DNA dep. RNA polymerase

Quinolone - Cipro - inhibits DNA Tyra sent

57
Q

Abx that inhibit THF

A

Trimethoprim

Co-trimoxazole

Dapsone

Inhibit conversion of Di to trihydrofolate

58
Q

What is septrin

A

Co-trimoxazole

Sulfamethoxazole and trimethoprim.

Sulfa affect different step of folate metabolism

PCP, maltophilia

59
Q

ABx that inhibit protein

A

Tetracycline

Gentamicin
Amikacin (aminoglycs)

Chloramphenicol

Macorlide - eryth/claritth (attached to ribosomal subunits)

Clindamyin. - anti exotoxins

Linezolid

60
Q

Gram positive cocci

A

Staph
Strep - b haem - GAS - pyogenes. GBS -
Y-haem enterococcus

A haem - st.pneumonia/viridian

61
Q

Gram neg cocci

A

Neisseria

Moraxella

62
Q

Gram positive bacilli

A

Actinomycetes
Bacillus
Diptheria
Listeria

63
Q

Mechanism of Abx resistant

A

Intrinsic - there’s no target, no transport mechanism, membrane is impermeable

Acquired - Drug inactivation - beta lactamases
Reduced permeability
Reflux of drugs - gram neg pump them back out, pseudomonas pumps pencilling

                   Altered molecule target/creation of new path
                    E.g MRSA makes a penicillin binding protein
                     VRE - new cell wall substrate
64
Q

How do bacteria acquire these changes

A

Sporadic mutation

OR

Horizontal gene transfer
TRANSformation - Free DNA from listed bacteria
TRANSduction - Bacteriophages (virus transfer DNA from one bac to other)
TRANSposition - Transporons move between plasmids
Conjugation - Plasmids - require contact between two bacteria

65
Q

SSD regime

A

Topical paste
Tobramycin
Polymixin E
Amphotericin B

Gastro cover

Enteral vancomycin (MRSA cover)

Systemic cefotaxime.

66
Q

What is C.diff

A

Gram positive bacillus
Anaerobic
Spore forming

Produces two toxins
A - entero - causes fluid sequestration

B - cyto - detected in the CDT test

Tx - metro/vancomycin

Pete FFICM SOE/OSCE (199 decks)

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