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Icm > Renal > Flashcards

Renal Flashcards

1
Q

How do you classify aki

A

Stage 1 : 1.5- 1.9 x baseline
Less < 0.5 ml/kg hour for 6-12 hour

Stage 2: 2-2.9 baseline
<0.5 ml/kg over 12 hr

Stage 3: > 3 baseline
<0.3 mls/kg over 24hrs

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2
Q

What is the classification system for CKD

A

G1-5 based on gfr

A1-3 based on acr

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3
Q

What is the definition of contrast induced nephropathy

A

Development of Aki within 48 hours of a contrast load

Creat > 44 or 25% rise

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4
Q

Mechanism of contrast induced nephropathy

A

Nephrotoxicity from reactive oxygen species
Contrast induced diuresis
Highly viscous urine

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5
Q

Risk factors contrast induced nephropathy

A

> 75
Renal impairment
Nephrotoxic drugs
IV rather oral contrast

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6
Q

How can you prevent contrast induced nephropathy

A 
Avoid contrast
Use low osmolality or non ionic 
Stop nephrotoxics 
Pre hydration saline 1ml/kg 
Mac 600mg bd for 2/7 
IV na bicarbonate
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7
Q

Mechanism of action of cvvhf

A

Convection

Movement of solute and water down hydrostatic pressure gradient

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8
Q

Mechanism of action of cvvhd

A

Diffusion

Countercurrent flow of blood and diasylate with diffusion of solutes down a concentration gradient

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9
Q

How do you prescribe rrt

A 
Dose of effluent ; 25-35mls/kg
Pre post replacement : 30:70
Fluid balance target 
Anticoagulant 
Flow rate - Trieste up to 250mls/ hr
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10
Q

How big is myoglobin

A

16,000 da

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11
Q

Pathophysiology of cerebral salt wasting

A

Tropically occurs following SAH and characterised by renal loss of sodium due to increased ANP and BNP causing increased renal perfusion pressure

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12
Q

Criteria for cerebral salt wasting diagnosis (blood and urine)

A

Hyponatraemia
High urine and serum osmolality
Urinary sodium >40
Hypovolaemia

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13
Q

Criteria for diagnosis of siadh on blood and urine

A 
Hyponatraemia 
Low serum osmolality 
High urine osmolality 
High urinary sodium 
Euvolaemic or hyper
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14
Q

Causes of nephrogenic Diabetes insipidus

A 
Lithium 
Amphotericin B
Demeclocycline 
Amyloid
Pkd 
Sickle cell
Bartter syndrome 
Inherited
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15
Q

Cause of cranial diabetes insipidus

A 
TBI
Brain tumour
Phenytoin ethanol 
Idiopathic 
tB encephalitis
Sarcoidosis
Leukaemia 
Thyroidits 
Genetic
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16
Q

Pathophysiology cranial DI

A

Lack of ADh or vasopressin
Secreted in the post pituitary under hormonal control from hypothalamus

Vasopressin increases water permeability in the dct leading to water reabsorption and salt exertion via aquporins, urea removal in collectin duct snd increase na absorption in loop henle

Peripheral vasoconstriction

17
Q

Diagnosis of cranial di on fluid deprevation test

A

No water for up to 18hours

Urine osmolality < 300

Then give desmopressin

> 800 (50% increase)

18
Q

Diagnosis of nephrogenic di on water deprivation test

A

No water for up to 18hours

Urine osmolality < 300

Then give desmopressin

< 500 (<50% increase)

19
Q

Pathophysiology of nephrogenic di

A

Improper response of the kidney transplant to adh

  • damage to loop henle or collecting ducts
20
Q

Treatment of nephrogenic di

A

Consume enough fluid to equal the amount produced
Treat any reversible causes
Amiloride/ hydrochorothiazide

21
Q

Pathophysiology of DKA

A

Absolute or relative insulin deficiency which when combined with high glucagon, cortisol and catecholamines stimulates lipolysis abs ketogenesis leading to a metabolic acidosis

Hyperglycaemia results from increase hepatic gluconeogenesis and glycolysis

22
Q

Characteristic changes in dka

A

Osmotic diuresis due to hyperglycaemia
Vomiting
Reduced oral intake

23
Q

Causes dka

A

Surgery
Infection
Mi
Non compliance

24
Q

Diagnostic criteria dka

A

Glucose > 11
Ketonuria > 3 or 2+
Bicarbonate <15 or ph <7.3

25
Q

Fluid replacement in dka

A 
Treat hypotension with 500mls of 0.9% 
Then 1l over 1 hr
1l over 2hr
1l over 4hrs 
If k <5.5 supplement
26
Q

Insulin therapy in dka and targets

A

Fixed rate insulin at 0.1 u/ kg /hr
Continue long acting

Ketone 0.5 /hr
Bic 3 / hr
Glucose 3/ hr

27
Q

Define HHS

A 
Hyperglycaemia > 30
Fluid depletion
No or mild ketosis <3 
Without acidosis or low bicarbonate 
Serum hyperosmolality > 320
28
Q

Goals of management of HHS

A

Normalise osmolality
Give 0.9% saline unless osmolality not declining and give 0.45 %

Na <10 in 24hours
Glucose < 5 per hour

Low dose insulin infusion 0.05 u/kg/hr once glucose not falling

29
Q

What is rifle criteria

A

Risk : increase creat 1.5 or uo <0.5ml/kg/hr over 6 hours

Injury : increase creat x 2 or uo <0.5 mls/ kg over 12 hours

Failure increase creat x3 or uo 0.3mls/kg over 12hours

Loss ; persistent - complete loss of function > 4 weeks

Eskd: > 3 months

30
Q

What are the kdigo guidelines

A

1 : 1.5-2 creatinine 0.5/6h

2: 2-3 creatinine 0.5/12hr
3: >3 creatinine 0.3/ 24 hr

31
Q

Pathophysiology compartment syndrome

A

Tissue pressure exceeds perfusion pressure

As pressure increases veins compress, increase hydrostatic pressure forces fluid out and further increases pressure

Stimulates nocireceptors -> pain

Ischaemia

32
Q

Pathophysiology rhabdomyalsis

A

Excessive muscle breakdown (trauma or non traumatic)

Sodium and calcium influx damage pumps
Water drawn into myocyte
K+ leaves cell

Sustained contraction due to calcium
ATP depletion
Further calcium influx-> free radicles + memebrane damage

Potassium phosphate urate myoglobin CK release

33
Q

Electrolytes changes in rhabdo

A

Low ca and sodium

High CK urate phosphate potassium myoglobin

34
Q

How does rhabdo cause Aki

A

Myoglobin forms insoluble casts
-> obstruction

Increased uric acid worsens obstruction

Direct Haem toxicity

Vasoconstriction

35
Q

Risk factors for citrate toxicity

A 
Liver failure
Low cardiac output 
Low calcium
Low albumin
Cold
36
Q

Define ckd

A

Abnormalities of kindbey structure and function for over 3months

37
Q

How does myoglobin cause rhabdo

A

Inhibits exogenous nitric oxide causing vasoconstriction

Icm (16 decks)

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