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Pete FFICM SOE/OSCE > Renal/Endo > Flashcards

Renal/Endo Flashcards

1
Q

KDIGO stage 1

A

Increase in creatnine by 26.5mmol/LOr 1.5x baseline in 7 daysAND U/O <0.5ml/kg/hr for 6 hours

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2
Q

KDIGO 2

A

Creatinine 2-2.9x baselineU/O 0.5ml/kg/hr 12 hours

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3
Q

KDIGO 3

A 
Creatinine 3x baselineORRise by 353.6 umol/litreOR Needing RRT
Urine output 0.3mls/kg/hr for 24 hoursOR12 hours of anuria
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4
Q

Complications of AKI

A

Metabolic - acidosis, hyperkalaemia, electrtolytes, uraemic encephFluid - tissue overload, resp failure, postive balanceLong term - progress to CKD, need for long term RRT

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5
Q

Risk factors for AKI

A 
Known CKDCCF, DM, Liver diseasePrevious AKIAny impairment limiting access to fluids (neuro, cognitive)Age 65Sepsis and hypovolaemia
NEPHROTOXIC DRUGS - ACEi, ARBS, Gent, diuretics, NSAIDsObstructionsOther causes - ?contrastRhabdo, HUS, TLS, GN, nephritisSurgery - emergency, intraperitoneal
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6
Q

Summary of management with AKI

A

Initial resus Assess fluid status Replace with isotonic crystalloids Haemodynamic support

Hx and Exam	D&V - hypovol	Bloody diarrhoea - HUS	No urine - obstruction	Haematuria - GN, stones, Ca	Haemoptyiss - Wegeners, vasculitis	Joint pain/rask - SLE
Ix -	Urinalysis, protein, blood, micropscopy	FBC, U&E, LFT, CRP, CK, Glucose, Ca, PO3, Mg, 	ANtibodies - ANCA, GBM, ANA (SLE)	Renal US
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7
Q

Stages of CKD

A 
1 >90 mls/min/1.73m2BSA2  60-893  30- 59 (A 45-59, B 30-44)4  15-295 <15
Prognositcally worse if proteinuria
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8
Q

Problems with CKD in ITU

A

PK - Altered Vd Decreased clearence Decreased protein binding

Fluid/Electro	Hyperparathyroidism	Hyperphosphate	Acidosis	Hyperkalaemia	Overload
CVS Hyptertension Risk of CVDHaem Anaemia Uraemic plt dysfunctionImpaired immunoNeuro- polyneuropathyMay need dialysis OR conversion from intermittant to continuous
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9
Q

Components of an RRT circuit

A

Extracorporeal circuit including semi permeable membraneBlood pumpsPressure sensors and air detectors/trapsVascular access deviceAnit-coaguation

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10
Q

Basic principles of RRT

A

HF - Convection
HD - Diffusion (solutes down a gradient)
HF - hydrostatic pressure gradient across a semi permeable membrane solvent drag carries low weigh solutes with water —> ultrafiltrate fluid replaces ultrasfiltrate —> determines net fluid
HD - Blood and diasylate fluid run countercurrent to each other seperated by a membrane Solutes diffuse across Fluid removed by increasing pressure

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11
Q

What are filter membranes made of

A

Cellulose or Semi synth
Celluose - low permeability, good for HD
Activate inflammation, less useful in critical illness
Semi-synth - high permeabiliry to water, less inflammation, both HF and HD
Thinner large area membrances —> more diffusion/convection

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12
Q

Indications for RRT

A

Ureamia - enceph, pericarditis, bleedingAbsolute urea above 36??HyperkalaemiaMet acidosisOligo-anuriaFluid overloadExtra: Volume removal, prevent overlaoad ?sepsis Drugs in overdose

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13
Q

Types of RRT

A

Continuous or intermittant (usually IHD), or peritonealContinuous - HF, HD, HDF

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14
Q

Flows needed for CVVHF

A

100-200ml/min

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15
Q

Recommended dose

A

Effluent rate - 20-25mls/kg/hour

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16
Q

Types of anticoag in RRT

A 
NoneSystemic —> UFH, LMWHUFH - can monitor and reverse           Risk of HITLMWH - Xa monitoring, but partially reversed only
CItrate - chelates calcium pre filter, therefore hypocalcaemiaProstaglandins - inhibits platelets —> hypotension
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17
Q

FWD in hypernatraemia

A

= 0.6 x weight x ((current Na/Target Na)-1)

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18
Q

Causes of hypokalaemia

A

Low intake - eating disorders, nutrition, malignancy

Increased loss - GI (D&V), 	Renal loss		Dieuretics, Conn’s, Cushings, liquorice		RTA releated to amphoetricin B		Osmotic diuresis with hyperglycama
Movement into cells	Alkalosis	Sympathetics - salbut			Insulin	Refeeding
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19
Q

ECG hypokalaemia

A

Prolonger PR
Flat T wave
Increased p wave amplitudfe
U waves
Apparent QT prolonged (QU)

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20
Q

ECG in hyperkalaemia

A

Peaked T wavesBroad QRSPR prolongedBundle branch, fasciculuarLeads to vent arrhythmnia, sine wave, arrest

21
Q

Causes of hyperkalaemia

A

AKI/CKDIatrogenic - potasssium supplement, Nutritional - bananasCell lysis - TLS, rhabdo, haemolytic, blood transfusionAddisons - hypo adrenalDrugs - sprio, sux, b-blockers, ACEi

22
Q

Treatment of hyperkalemia

A

Treat and remove cause12 lead ECGMonitored bedIf ECG changes or K>610mls 10% calcium gluconate 2 minutes+/- nebs salbutatmol10 units of actrapid in 50mls of 50% dex over 20 minutesCalcium resoniumRRT

23
Q

Causes of hypophosphataemia

A

Severe critical illness - sepsis, polytrauama, malabsorption, alkalosis, hyporthermia.RefeedingRRTDrugs - diuretics, aluminium salts

24
Q

Causes of hyperphosphatemia

A

IatrongenicVit D toxicityAcute - AKI, TLS, met acidosis, RhabdoHypoparathyroid

25
Q

Causes of hypercalcaemia

A 
MalignancyHyperparathyroidismCKDImmobilityPagetsGranulamotous disease - Sarcoid, TBImmobility
26
Q

Features of hypercalacemia

A

Lethargy, fatigue, abdo pain, constipation, pacnreatitis>3.5 coma, brady

27
Q

Management of hypercalcaemia

A

Treat causeVit D and PTH levelsRemove precipitantsFluid status - fluid resusPamidroniateFurosemide if fkluid repletesSteroids - sarcoid or Vitamin D

28
Q

Anion Gap eqnNormal range

A

(Na+K) - (Cl + HCO3)4-12 (one book says 14-17)

29
Q

What causes raised anion gap met acidosis

A

Strong acid accumulation
Lactic acidosis
Ketoacidosis - DM, starvation, alcohol AKI/CDK Methanol/ethylene glycol Glutathoine deficiency Salicylate Cyanide

30
Q

What causes normal anion gap metabolic acidosis

A

Loss of bicarbonate, loss of renal excretion, ingestion of acids

DiarrhoeaIleostomyRTAParenteral nutirtionDilutionalColonic ureteric implant/diversionb
31
Q

How to correct AG for albumin

A

= measured AG + (0.25 x (40-albumin)Every 1g/L fall in albumin decreases Anion gap by 0.25 mmol

32
Q

Causes of hyperglycaemia in crit care

A

Increased gluconeogenesis
Insulin resistance
Catecholamine administation
Corticosteroid use
Glucose in the drugs

33
Q

In DKA what does the lipolysis lead to

A

Acetoacetic acidAcetone3-beta hydroxy butyrate

34
Q

Precipitants of DKA

A

New undiagnosed DMPoor treatment complianceOut of date insulinLipohypertrophy of injection sitesInfection, gastroenterisitsMyocardial infactionSurgeryTrauama

35
Q

Goals of treatment in DKA

A

Glucose fall by 3mmol/l/hrKetones fall by 0.5mmol/L/hrBicarbonate rises by 3mmol/L/hr

36
Q

Treatment principles in DKA

A 
FluidBolus 500mls if hypotensive1l NaCL over 1 hourThen 1NaCl with potassium over 2, 2, 4, 4 and 6 hoursAdd dextrose once BM <14
Insulin at FRII of 0.1units/Kg/hrMaintain long acting insulin at night
37
Q

Why admit DKA to crit care

A 
Ketones >6Bicarb <5Ph<7.0K <3.5GCS <12SaO2 <92% on airHR up or downAnion gap >16
38
Q

When to restart sc insulin after DKA

A

Pt able to take diet and fluidsKetones <0.6pH >7.3Stop insuline infusion 60 minues after first sc dose

39
Q

Diagnostic criteria for DKA

A

Glucose > 11 (or known DM)K - ketones >3A - acid, pH <7.3 OR HCO < 15

40
Q

Characteristics of HHS

A

Older patientsType II DMMarked hypovolaemiaBM>30 WITHOUT HYPERKETONAEMIAPH>7.3M BICARB >15Serum Osm>320 mosmol/kgThere is some insulin deficiency, but still some left to avoid lipolysisFluid defecit 100-220ml/kg fluid def

41
Q

Treatment options of HHS

A

Fluid1 litre over 1 hoursAim 2-3 litres positive by 6 hours6 litres postive by 12 hours Aim 50% of fluid deficit in the first 12 hoursAllow BM to fall by 5mmol an hourInsulin ONLY if - ketosis in which case treat as DKA OR BM not falling with fluid at FRII 0.05

42
Q

Complications of HHS

A

Cerebral oedemaVTEFeet problems

43
Q

When should HHS go to crit care

A

Osm >350
Na >160
PH <7.1
GCS <12
SpO2 < 92%
U/O less than 0.5mls/kg/hour
Creatinine>200
Hypothermia
Significant co-morbidites

44
Q

What happens to the thyroid in critical illness

A

Total and free T3 falls
Reverse rT3 increases
Transient rise in T4, but may fall
TSH may rise transiently
THEN
Depression of HPT axis, decreased T4
Decreased TBG
These change are the LOW T3 SYNDROME, NONTHYROID ILLNESS or SICK EUTHYROID STATE
TSH falls

45
Q

TFTs in a sick euthyroid

A

Low circuliating T3/4 BUTInappropriately low TSH (even normal is low)Now evidence for supplementation

46
Q

Drugs affecting thyroid

A

Glucocorticoids - TSH suppresion, reduced peripheral conversion
Contrast - inhibit synthesis/secretion
Propanolol - inhibit peripheral conversion
Amiodarone - same
Dopamine - TSH suppresion
Furomide - interferes with binding proteins

47
Q

How is thyroid storm characterised

A

Triad of
Hypermetabolic state
Increased sympathetic activity and excess catecholaminwes
Increased oxygen consumption

48
Q

Causes of a thyroid storm

A 
InfectionMI, CVA, PEPeri-op, thyroid surgeryBurns, traumaPregnancy
Contrast, amiodarone, excess T4DKAThyroiditis

Pete FFICM SOE/OSCE (199 decks)

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