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MedEd > Renal > Flashcards

Renal Flashcards

1
Q

What is renal function?

A

How much blood flow goes through the glomerulus = Glomerular filtration rate. Should be >90ml/mom

Endogenous marker is blood urea and serum creatinine (this is dependent on age/sex/weight/muscle mass).

Can give EDTA to clinically assess

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2
Q

What conditions raises blood urea levels?

A

GI bleeds, hepatic function and nutrition states

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3
Q

What is normal urea:creatinine ratio?

A

40:1 to 100:1

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4
Q

What does metformin predispose for in poor kidney function patients?

A

lactic Acidosis

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5
Q

Features of AKI?

A

Fluid -> oliguria, volume overload
Electrolyte - > hyperkalae,ia
Acid-base -> metabolic acidosis

Measured by urea or creatinine

Potentially reversible

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6
Q

CKD features?

A

Impaired renal function for >3 months.

Abnormal structure/function or GFR <60ml/min for >3months
+/- evidence of idney damage

usuualy progressive and irreversible

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7
Q

Symptoms of AKI?

A

Underlying cause
Oliguria/anuria

N+V
SOB
Dehydration
Confusion (encephalopathy from uraemia)

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8
Q

Signs of AKI?

A

HTN, distended bladder, dehydration (postural hypotension)

Fluid overload e.g. HF, cirrhosis, nephrotic syndrome) = raised JVP, pulmonary and peripheral oedema

Pallor, rash and bruising from vascular disease

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9
Q

How to classify AKI?

A

Stage 1: 1.4x rise in Creatinine to baseline of urine <0.5ml/kg/hr for >6hours

Stage 2: 2x Cr rise r urine output the same for >12hours

Stage 3: 3x Cr rise of <0.3ml/kg/hour for >24hrs or anuria>12hours

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10
Q

RFs for AKI?

A

Hypovolaemia

CKD, diabetes, HF, renal transplant, ?75YO, contrast administration

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11
Q

Pre-renal causes of AKI?

A

40-70% AKI= reduced urine output and raised urea:creatinine ratio

Hypovolaemia: either renal loss from diruetic overuse or extrarenal loss e.g. V+D, burns, sweating and blood loss

Systemic vasodilation e.g. Sepsis and neurogenic shock

Decreased CO e.g. MI or HF

Intrarenal vasoconstriction

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12
Q

Renal AKI causes?

A

Tubular = acute tubular necrosis

Glomerular = glomerulonephritis

Interstitial = iterstitial nephritis

Vascular = vessel obstruction e.g. thrombosis, vasculitis and haemolytic microangiopathy

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13
Q

What can cause acute tubular necrosis?

A

Paracetamol, NSAIDs, ACEi, contrast and myoglobinuria in rhabdomyolysis

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14
Q

What causes intrarenal vasoconstriction in pre-renal AKI?

A

Renal artery stenosis, fibromuscular dysplasia, cardiorenal syndrome, hepatorenal syndrome,

NSAIDS, ACEi and ARB

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15
Q

How to manage pre-renal AKI?

A

NEWS and identify causitive problem e.g. hypovolaemia and monitor fluid balance, K+, lactate and daily creatinine

Bolus and maintenance fluid

Stop nephrotoxic meds and change medications that are renal excreted
e.g. metformin and LMWH
Avoid contrast

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16
Q

What drugs can commonly cause AKI?

A

Abx such as aminoglycosides e.g. gentamicin and amikacin

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17
Q

What causes Acute Tubular Necrosis (ATN)?

A

> 50% of renal causes of AKI

Renal tubular epithelial cell injury due to ischaemia from shock/sepsis or nephrotoxic agents

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18
Q

What Exogenous substances causes ATN?

A

NSIADS, aminoglycosiides, amphotericin B, contrast media, calcineurin inhibitors, cisplatin

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19
Q

What endogenous substances cause ATN?

A

Myoglobiunuria (rhabdomyolysis), haemoglobinuria, crystals (uric acid) e.g. gout, and myeloma (IgG light chains)

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20
Q

Features of ATN?

A

Urine = muddy brown granular casts, myoglobiunuria and haemoglobiunrura

Features of raised AKI: e.g. urea, creatinine, potassium and metabolic acidosis
Urea:creatinine ratio <40:1

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21
Q

Indicators of rhabdomyolysis?

A

Raised CK, hypocalcaemia and elevated phosphate

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22
Q

Hyperkalaemia management?

A

Escalate + ABCDE
Continuous cardiac monitoring + IV acess and redo bloods
Review drugs e.g. stop neprotoxic
10ml 10% calcium gluconate IV over 10 mins
100ml 20% dextrose with 8U insulin over 15mins
Nebulised salbutamol 5-10mg
Sodium bicarbonate to correct acidosis

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23
Q

ECG changes in hyperkalaemia?

A

Tall tented T wave, small absent p wave, broad QRS, increased PR interval, sine wave, bradycardia

24
Q

What is glomerulonephritis and what can it causes?

A

Inflammation of the glomeruli and nephrons.

Can cause increase in BP to malignant HTN
Urine dipstick can show blood and protein
Decreased renal function due to loss of filtering capacity

25
Q

Features of nephrotic syndrome?

A

Proteinuria?3.5mg/24hours
Hypoalbunaemia <25g/L
oedema
Hyperlidaemia +-hypercoagulative state

26
Q

features of nephritic syndrome?

A

Hypertension
haematuria + red cell casts
Oedema
Oliguria and progressive renal impairment

27
Q

Primary Causes of nephrotic syndromer?

A

Minimal changes disease
Membranous nephropathy
Focal segmental glomerulosclerosis

28
Q

Secondary causes of nephrotic syndrome?

A

DM - glomerulosclerosis
SLE
Amyloid

29
Q

Primary causes of nephritic syndrome?

A 
Membranoprolifertive (MPGN)
Raid progressive (RPGN) with types:
1=Anti-GBM (goodpastures)
2=Immune complex deposition
3= pauci immune

Thin BM disease
Alports syndrome

30
Q

Secondary causes of nephritic syndrome?

A 
Post-streptococcal
IgA nephropathy (bergers)
HSP
Small vessel vasculitiis
SLE
Anti-GBM disease

Cryoglobineamia (IgM secondary to MM, CLL and waldenstroms)

31
Q

What is minimal change disease?

A

Affects youn population with normal biopsy ecept electron = podocyte effacement

Associated with Hodgkins lymphoma
Steroid responsive

32
Q

Features of membranouse nephropathy

?

A

100% nephrotic
Granular IC depositon with spike and dome pattern on microscopy

Primary= autoimmune (ab for PLA2R)

Secondary = Malignancy, drugs and infection e.g. HEPB/C and SLE

33
Q

What drugs can cause secondary membranous nephropathy

?

A

Gold, penicillamine and captopril

34
Q

What is FSGS?

A

Nephrotic
Focal scarring with IgM deposition

In Afro-caribbeans
Heroin, HIV and HIV-associated hephropathy

Bisphosphonate use e.g. Pamidronate

35
Q

Differences in diabetic and amyloid nephropathy?

A

Nephrotic
Congo red staining = aple green birefringence for amyloid

Diabetic = Nodular glomerulosclerosis and Kimmelstiel-Wilson nodules

36
Q

What us MPGN?

A

nephrotic + nephritic

Immune complex associated with deposition causing mixed nephritic

Type 1 = Hep C>B
Type 2 = C3 nephritic factor (low C3)

Presents tram tacking appearence and mesangial proliferation on microscopy

37
Q

What is IgA nephropathy?

A

Days after URTI causes deposition of complexes and episodic macroscopic haematuria

Nephritic syndrome

38
Q

What is Henoch Schonlein Purpura?

A

Nephritic

variant of IgA nephropathy
Systemic vasculitis and depostion = purpuric rahs and arthralgia

39
Q

What is post-strep GN?

A

1-2 weeks after throat or skin infection causes IgA depostion and high ASOT with Low C3
‘smoky urine’

40
Q

What are the Rapidly progressive GN?

A

Nephritic syndromes

Anti-GBM goodpastures
Immune complex deposition
Pauci immune

41
Q

GFeatures of Anti-GBM type 1 RPGN?

A

Haematuria, haemopysis, proteinuria young M>F

Auto-abs to Type 4 collahen so linear stain

42
Q

Features of Type 2 immune complex mediated RPGN?

A

Any immune complex deposition = granular pattern

SLE< IgA nephrotpathy and HSP

43
Q

Features of Pauci-immune Type 3 RPGN?

A

Negtaive stain and ANCA associated

cANCA = ENT+lungs+kidneys = granulomatous polyangiitis

pANCA=asthma+eosinophilia+mononeuritis multiplex and purpura = eosinophilic granulomatosis with polyangiitis [purpura = microscopic polyangiitis]

44
Q

What drugs cause glomerular damage?

A

Rifampicine, dapsone, penicillins, isonazid

45
Q

What drugs cause post-renal tubular blockage?

A

Aciclovir and sulphonamides

46
Q

What drugs cause acute interstitial nephritis?

A

Penicillins, anti-Tb therapy, sulphadiazine and cephalosporins

47
Q

Symptoms of CKD?

A

Often asymptomatic.

Severe = anorexia, N+V, fatigue, pruritis, peripheral oedema, msucle cramps, pulmonary oedema, sexual dysfunction

48
Q

Signs of CKD?

A

Underlying disease e.g. SLE

Skin pigmentation and excoriations from uraemia, pallor, HTN, peripheral oedem,a peripheral vascular disease and renal bone disease

49
Q

Consequences of CKD?

A

Progressive failure of homeostatic = acidosis and hyperkalaemia

Progressive hormonal failure = anaemia and renal bone disease e.g. osteomalacia

CVD = vascular calcification, uraemic cardiomyopathy

Uraemia, encephalopathy and death

50
Q

CKD Ix?

A

bedside: BP, dipstick urine, fundoscopy, ECG for cardiac changes

Bloods: bicarb for metabolic acidosis, U&Es, Hb for renal normocytic anaemia, PTHCa/phosphate studies
BM and HbA1c

Imaging: USS and CXR, biopsy if no diagnosis

51
Q

CKD management?

A

1) limit progression
2) symptom control
3) Prep for renal replacement therapy

52
Q

How to limit CKD progression?

A

BP target so lifestyle and drugs
Tight sugar control
decreased CVS risk
Diet to reduces phosphate and salts

53
Q

How to symptom control for CKD?

A

Human EPO or iron for anaemia
Sodium bicarb for acidosis
Loop diuretics and fluid restriction for oedema
HTN treatment
Phosphate binders for hyperphosphataemai e.g. sevelamer
HypoCaHyperPth e.g. cholecaliferol, alfa, cincacimet

54
Q

How to renal replacement therapy for CKD?

A

Haemodialysis, peritoneal dialysis and renal transplant

55
Q

Indications for urgent haemodialysis?

A 
AEIOU
Refractory Acidosis
Refractory hyperkalaemia (electrolytes)
Drug OD (ingestion)
Refractory pulmonary oedema
Uraemia with complications

MedEd (32 decks)

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