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FFICM > Causes, Lists And Definitions 1-11 > Flashcards

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
Vent strageties for ARDS
Low Tv 5-7ml/kg IBW Accept a higher resp rate Aim Sats 88-95 to reduced FiO2 PEEP>5 Pplat<30
26
Improving vent in ARDS
Vent strategies NMBDs Recruitment Prone HFOF ECMO Inhaled NO Steroids
27
Murray score
PF ratio PEEP Compliaance CXR quadrants 0-4, average score used.. >3 refer
28
Contra indications to ECMO
Irreversible organ damage/MOF Advanced malignancy Chronic severe pulm hypertension
29
Indications VA ECMO
``` Cardiogenic shock - myocarditis, arrhythmia, PE, anaphylaxis Wean from bypass Heart transplant Chronic cardiopmyopathy - bridge to VAD ECLS ```
30
Indication VV ECMO
Potentialy reversible acute failure ARDS with bacterial / viral pneumonia Lung transplant - bridge / graft failure Pulmonary haemorrage/haemoptysis Status asthmaticus
31
relative CI to ECMO
``` Age>75 Polytrauma, multiple bleeds CPR.60 minutes MOF CNS injury ```
32
VA CIs
Severe aortic regurgitation | Aortic dissection
33
VV CI
Unsupportable cardiac failure Pulm Hypertension Cardiac arrest
34
Complications of ECMO
Cannulation - Pneumothorax, vascular injury, infection, emboli, bleed Anticoag - haemorrhage EAquipment - pump failure, oxygenation failure
35
Causes of adrenal insufficiency
Primary - Addisons (adrenal is destroyed) Secondary - Insufficient production of ACTH (rare) Tertiary/relative - Suprresion of HPA axis due to steroids
36
Causes of primary adrenal insufficiency
Autoimmune (common) Infection - TB, fungal, HIV (CMV) Cancer - mets Drugs - etomidate, ketoconazole Other - critical illness insufficiency Amyloid
37
Causes of secondary adrenal insufficiency
Dystruction of pituitary Sheehans Malignancy Bleed
38
Causes of tertiary adrenal
Relative Suppression of exogenous corticosteroids
39
Definition of Addisons
Autoimmune disease of cortex, reduced or absent cortisol Cortisol deficiency = rise in ACTH MSH rises - pigmentation ACTH and MSH come from pre-opiomeanoncortin
40
Diagnosing adrenal insuffiency
Cortisol and ACTH (primary C low, A high) Sec/ter : both low Synacthen test: Adrenal antibodies
41
When might you use steroids in crit care
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
Pathology of amniotic fluid embolus
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
Triad of AFE
Hypoxia Cardiovascular collapse Coagulopathy
44
Define AFE
Rare catastrophic emergency presenting as sudden maternal collapse associated with shock, hypoxia and coagulapathy. Happens with amniotic fluid/cells enter maternal circ
45
Risk factors for AFE
``` Advanced maternal ages Polyhydromanios Induction of labour Placenta Pravin/abruptions Multip Uterine rupture IUD Trauma ```
46
Differential of AFE
Obs and non obs Obs - Placental abruption, Eclampsia Uterine rupture PPH Non obs - Anaphyalxis, total spinal, sepsis PE
47
Define anaphylaxis
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
Classify hypersensitivity
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
Drugs causing anaphylaxis
NMBD - roc, sux, atra ABx - penicillins Thio Latex Gelatine/starches Chlorhex Iodine contrast
50
Drugs for anaphylaxis
IM adrenaline - 1ml of 1:1000 iv 50-100mcg iv of 1:10000 Saline 500 to 1litres Chlorphenarmine - 10mg Hydrocortisone - 200mg
51
When to take bloods in anaphylaxis
At the time 1-2 hours later 24 hours
52
Tests for anaphylaxis
RAST - radioallergosorbant - antigen specific IgE ImmunoCAP Skin prick testin
53
Types antibiotics and examples
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
Mechanisms of antibiotic activity
Inhibit cell wall synthesis Inhibit DNA synthesis/function Inhibit Tetrahydrate folate synthesis Inhibit protein
55
Abx that inhibit cell wall synth
Penicillins Cephalosporins Glyco - vanc/teic Polymixin E - Colistin
56
Abx that inhibit DNA
Metronidazole. Complexes DNA and strands break Rifampicin Inhibit DNA dep. RNA polymerase Quinolone - Cipro - inhibits DNA Tyra sent
57
Abx that inhibit THF
Trimethoprim Co-trimoxazole Dapsone Inhibit conversion of Di to trihydrofolate
58
What is septrin
Co-trimoxazole Sulfamethoxazole and trimethoprim. Sulfa affect different step of folate metabolism PCP, maltophilia
59
ABx that inhibit protein
Tetracycline Gentamicin Amikacin (aminoglycs) Chloramphenicol Macorlide - eryth/claritth (attached to ribosomal subunits) Clindamyin. - anti exotoxins Linezolid
60
Gram positive cocci
Staph Strep - b haem - GAS - pyogenes. GBS - Y-haem enterococcus A haem - st.pneumonia/viridian
61
Gram neg cocci
Neisseria | Moraxella
62
Gram positive bacilli
Actinomycetes Bacillus Diptheria Listeria
63
Mechanism of Abx resistant
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
How do bacteria acquire these changes
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
SSD regime
Topical paste Tobramycin Polymixin E Amphotericin B Gastro cover Enteral vancomycin (MRSA cover) Systemic cefotaxime.
66
What is C.diff
Gram positive bacillus Anaerobic Spore forming Produces two toxins A - entero - causes fluid sequestration B - cyto - detected in the CDT test Tx - metro/vancomycin

FFICM (57 decks)

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