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FFICM > Definitions, Tables, Facts - Renal And Endo > Flashcards

Definitions, Tables, Facts - Renal And Endo Flashcards

1
Q

KDIGO stage 1

A

Increase in creatnine by 26.5mmol/L
Or 1.5x baseline in 7 days

AND

U/O <0.5ml/kg/hr for 6 hours

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2
Q

KDIGO 2

A

Creatinine 2-2.9x baseline

U/O 0.5ml/kg/hr 12 hours

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3
Q

KDIGO 3

A 
Creatinine 3x baseline
OR
Rise by 353.6 umol/litre
OR 
Needing RRT

Urine output 0.3mls/kg/hr for 24 hours
OR
12 hours of anuria

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4
Q

Complications of AKI

A

Metabolic - acidosis, hyperkalaemia, electrtolytes, uraemic enceph

Fluid - tissue overload, resp failure, postive balance

Long term - progress to CKD, need for long term RRT

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5
Q

Risk factors for AKI

A 
Known CKD
CCF, DM, Liver disease
Previous AKI
Any impairment limiting access to fluids (neuro, cognitive)
Age 65
Sepsis and hypovolaemia

NEPHROTOXIC DRUGS - ACEi, ARBS, Gent, diuretics, NSAIDs
Obstructions

Other causes - ?contrast
Rhabdo, HUS, TLS, GN, nephritis

Surgery - 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/1.73m2BSA
2  60-89
3  30- 59 (A 45-59, B 30-44)
4  15-29
5 <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 CVD

Haem
Anaemia
Uraemic plt dysfunction

Impaired immuno

Neuro- polyneuropathy

May 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 membrane

Blood pumps

Pressure sensors and air detectors/traps

Vascular access device

Anit-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 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, bleeding
Absolute urea above 36??

Hyperkalaemia
Met acidosis
Oligo-anuria
Fluid overload

Extra:
Volume removal, prevent overlaoad
?sepsis
Drugs in overdose

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13
Q

Types of RRT

A

Continuous or intermittant (usually IHD), or peritoneal

Continuous - 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 
None
Systemic —> UFH, LMWH
UFH - can monitor and reverse
           Risk of HIT
LMWH - Xa monitoring, but partially reversed only

CItrate - chelates calcium pre filter, therefore hypocalcaemia
Prostaglandins - 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 waves
Broad QRS
PR prolonged
Bundle branch, fasciculuar

Leads to vent arrhythmnia, sine wave, arrest

21
Q

Causes of hyperkalaemia

A

AKI/CKD
Iatrogenic - potasssium supplement,
Nutritional - bananas

Cell lysis - TLS, rhabdo, haemolytic, blood transfusion
Addisons - hypo adrenal

Drugs - sprio, sux, b-blockers, ACEi

22
Q

Treatment of hyperkalemia

A

Treat and remove cause
12 lead ECG
Monitored bed

If ECG changes or K>6
10mls 10% calcium gluconate 2 minutes
+/- nebs salbutatmol
10 units of actrapid in 50mls of 50% dex over 20 minutes

Calcium resonium

RRT

23
Q

Causes of hypophosphataemia

A

Severe critical illness - sepsis, polytrauama, malabsorption, alkalosis, hyporthermia.
Refeeding
RRT
Drugs - diuretics, aluminium salts

24
Q

Causes of hyperphosphatemia

A

Iatrongenic
Vit D toxicity
Acute - AKI, TLS, met acidosis, Rhabdo
Hypoparathyroid

25
Q

Causes of hypercalcaemia

A 
Malignancy
Hyperparathyroidism
CKD
Immobility
Pagets
Granulamotous disease - Sarcoid, TB
Immobility
26
Q

Features of hypercalacemia

A

Lethargy, fatigue, abdo pain, constipation, pacnreatitis

> 3.5 coma, brady

27
Q

Management of hypercalcaemia

A

Treat cause
Vit D and PTH levels
Remove precipitants

Fluid status - fluid resus
Pamidroniate
Furosemide if fkluid repletes
Steroids - sarcoid or Vitamin D

28
Q

Anion Gap eqn

Normal 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

Diarrhoea
Ileostomy
RTA
Parenteral nutirtion
Dilutional
Colonic 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 acid

Acetone

3-beta hydroxy butyrate

34
Q

Precipitants of DKA

A

New undiagnosed DM
Poor treatment compliance
Out of date insulin
Lipohypertrophy of injection sites

Infection, gastroenterisits
Myocardial infaction
Surgery
Trauama

35
Q

Goals of treatment in DKA

A

Glucose fall by 3mmol/l/hr

Ketones fall by 0.5mmol/L/hr

Bicarbonate rises by 3mmol/L/hr

36
Q

Treatment principles

A 
Fluid
Bolus 500mls if hypotensive
1l NaCL over 1 hour
Then 1NaCl with potassium over 2, 2, 4, 4 and 6 hours
Add dextrose once BM <14

Insulin at FRII of 0.1units/Kg/hr

Maintain long acting insulin at night

37
Q

Why admit DKA to crit care

A 
Ketones >6
Bicarb <5
Ph<7.0
K <3.5
GCS <12
SaO2 <92% on air
HR up or down
Anion gap >16
38
Q

When to restart sc insulin after DKA

A

Pt able to take diet and fluids
Ketones <0.6
pH >7.3

Stop insuline infusion 60 minues after first sc dose

39
Q

Diagnostic criteria for DKA

A

Glucose > 11 (or known DM)

K - ketones >3

A - acid, pH <7.3 OR HCO < 15

40
Q

Characteristics of HHS

A

Older patients
Type II DM

Marked hypovolaemia
BM>30 WITHOUT HYPERKETONAEMIA
PH>7.3M BICARB >15

Serum Osm>320 mosmol/kg

There is some insulin deficiency, but still some left to avoid lipolysis

Fluid defecit 100-220ml/kg fluid def

41
Q

Treatment options of HHS

A

Fluid
1 litre over 1 hours
Aim 2-3 litres positive by 6 hours
6 litres postive by 12 hours

Aim 50% of fluid deficit in the first 12 hours

Allow BM to fall by 5mmol an hour

Insulin 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 oedema
VTE
Feet 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

BUT

Inappropriately 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 
Infection
MI, CVA, PE
Peri-op, thyroid surgery
Burns, trauma
Pregnancy

Contrast, amiodarone, excess T4
DKA
Thyroiditis

FFICM (59 decks)

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