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Medicine block > Renal medicine block > Flashcards

Renal medicine block Flashcards

1
Q

What is AKI staging based on?

A

Serum creatinine which is increased in AKI and urine output which is decreased in AKI

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2
Q

What are the RF of AKI?

A
  • Diabetes
  • CKD
  • HF/CVD
  • Comorbidities
  • > 75
  • Sepsis
  • ACEi/ARBS/NSAIDs/Abx
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3
Q

What are the pre renal causes of AKI?

A
  • Hypovolaemia
  • Liver failure and HF (reduced effective circ vol)
  • Reduced cardiac output
  • NSAIDs, ACEi, ARBs, ciclosporin
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4
Q

What are the intrinsic causes of AKI?

A
  • Ischaemia
  • Glomerulonephritis
  • Vasculitis
  • Malignant HTN
  • Sepsis
  • Nephrotoxins eg. rhabdomyolysis, contrast
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5
Q

What are the post renal causes of AKI?

A
  • Bladder outflow obstruction

- Blockage of ureters

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6
Q

What are the Ix into AKI?

A
  • Dip = haematuria and proteinuria
  • USS KUB, urine MC&S
  • Haemolysis screen if suspect DIC/HUS/TTP
  • Bloods - FBC, U&E, CRP, LFT, CK
  • Cryoglobulins, immunoglobulins and ANA for a cause
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7
Q

What is involved in the haemolysis screen?

A
  • Blood film - reticulocytes
  • LDH
  • Bilirubin
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8
Q

What is the management of AKI?

A
  • Stop nephrotoxic agents
  • Ensure fluid status ok = IV fluid if dehydrated or diuretics if overloaded
  • Careful of third space losses
  • Treat the underlying cause and adjust drug doses for renal func
  • May need RRT and ICU referral
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9
Q

What are the indications for renal replacement therapy?

A
  • Hyperkalaemia, overload and met acidosis resistant to meds

- Uraemic pericarditis and uraemic encephalopathy

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10
Q

What are the clinical features of nephrotic syndrome?

A
  • Proteinuria, urine PCR >300
  • Oedema
  • Albumin <30
  • Hypercholesterolaemia
  • Can have normal kidney function
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11
Q

What are the causes and complications of nephrotic syndrome?

A

Causes - minimal change disease, focal segmental glomerulosclerosis, membrane nephropathy, amyloid
Complications - progression to CKD, VTE (hypercoag state), increased risk infection, HTN, hyperlipidaemia -> CAD

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12
Q

What are the autoimmune causes of nephritic syndrome?

A

Treated with immunosuppression.

  1. Goodpasture’s syndrome - Ab to collagen = GN and haemoptysis due to lung problems
  2. Vasculitis, ANCA associated, only one that can cause AKI, treat w plasma exchange then ciclosporin + tacrolimus
  3. Lupus nephritis - SLE and ANA
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13
Q

What is post infective GN? How is it treated?

A

Usually a few weeks post strep infection eg. tonsiitis. 3-12 = peak incidence.
Treat supportively = ACEi/ARBs as usually self limiting

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14
Q

What is the presentation of nephritic syndrome?

A
  • Haematuria, sometimes vissible
  • +/- oedema and proteinuria
  • AKI
  • HTN
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15
Q

What is IgA nephropathy?

A

Idiopathic cause of nephritic syndrome, gross haematuria, treat supportively.

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16
Q

What is the medical management of GN?

A
  • Supportive treatment - ACEi/ARBs for protein and HTN, statins for hypercholesterolaemia, fluid overload = water and salt restriction and diuretics, if risk VTE = therapeutic LMWH
  • Immunosuppression
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17
Q

What is the invasive treatment of GN?

A
  • Renal replacement therapy/haemodialysis if ESRF or severe AKI
  • Plasma exchange
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18
Q

What are the stages of CKD?

A 
Stage 1 - >90 ml/min
Stage 2 - 55-89 ml/min
Stage 3a - 45-54 ml/min
Stage 3b - 30-44 ml/min
Stage 4 - 15-29 ml/min
Stage 5 - <15 ml/min
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19
Q

What are the causes of CKD?

A
  • DM
  • HTN
  • GN
  • Chronic/recurrent polynephritis
  • Polycystic kidney disease
  • Obstructive nephopathy
  • Reno vasc disese
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20
Q

What are the complications of CKD?

A
  • CVD = highest causes mortality
  • ACD
  • Malnutrition/sarcopenia/dyslipidaemia
  • Bone disease
  • Electrolyte disturb, fluid overload, met acidosis, uraemic pericarditis and encephalopathy
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21
Q

What are the parts of management of CKD?

A
  • Treat underlying disease
  • Reduce risks and complications
  • Prevent progression
  • Discuss for the future
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22
Q

How do you treat underlying disease in CKD?

A
  • DM and HTN control
  • Promptly treat infection
  • Immunosuppressants
  • Tolvaptan for polycystic kidney disease
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23
Q

How do you reduce the risks and complications associated w CKD?

A
  • Reduce CVS risks
  • Supplement - Vit D, folate, B12, Fe
  • Low phosphate/K+ diet
  • EPO
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24
Q

How do you prevent progression of CKD?

A
  • ACEi/ARB for proteinuria and BP

- Monitor bloods

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25
Q

What do you need to discuss for the future in CKD?

A
  • Transplant

- Renal replacement therapy and haemodialysis

26
Q

Diabetic nephropathy:

  • Diagnosis
  • Treatment
A

Dx - increased albumin and PCR, evidence of poorly controlled DM, other microvascular disease.
Treat - ACEi/ARBs, anti HTN, reduce CVS RF, cont screening for other microvascular complications

27
Q

HTN nephropathy:

  • What is it?
  • Ix
  • Treatment
A

Chronic increased BP that causes nephrosclerosis of the kidney, can be causing renal impairment or caused by renal impairment.
Ix - urine metanephrines, cortisol, aldosterone:renin ratio, TSH, MRA (renal artery stenosis)
Treat - anti HTN

28
Q

Polycystic kidney disease:

  • Sx
  • Ix
  • Treatment
A

Sx - asymptomatic, due to size of kidney, infected cysts - fever, haematuria, flank pain
Ix - FH and USS
Treatment - control BP, tolvaptan to slow progression to CKD, genetic testing

29
Q

What causes ACD in CKD?

A
  • Reduced EPO production from kidney
  • Poor absorption and malnutrition = Fe def
  • Inflam and infection = Fe def
  • Blood loss
  • Uraemic suppression of BM
  • Med induced
  • B12 and folate def
30
Q

What is the management of ACD in CKD?

A

First measure levels of B12, folate, ferritin, Fe, trasnferrin and if def replace these IV. Then give EPO. Aim for Hb to be 100-120.
Careful w EPO as increases BP = increase risk VTE.

31
Q

How is mineral bone disease caused in CKD?

A

Don’t make Vit d as it isn’t hydroxylated in the kidney - no Ca absorbed in the gut = reduced serum Ca.
Increased PTH = Ca from bone to normalise serum Ca = reduced bone density and increased likelihood of fracture. Also known as tertiary hyperparathyroidism (persists even when initial cause has been corrected.

32
Q

How does peritoneal dialysis work?

A

Fluid drained into peritoneal cavity through PD tube, solutes move from blood across peritoneal mem down conc grad into dialysate fluid. Conc grad made from high conc glucose.

33
Q

What are the adv and disadv of PD?

A

Adv - QOL and more individualised

Disadv - infection, have to manage technically, unsuitable if had surgery or stoma

34
Q

What are the types of PD?

A
  • Automated PD = overnight
  • Continuous ambulatory PD = 4-5 times a day w overnight indwelling
  • Assisted automated PD = HCA helps
35
Q

How does haemodialysis work?

A

Blood from pt to dialyser and back to pt. Waste solute, salt and excess fluid move across a semi permeable membrane and are removed by the dialyser.

36
Q

What are the adv and disadv of HD?

A

Adv - efficient and lots of support staff

Disadv - infection, reactions, haemodynamic instability, risk of bleed, cramps, anaemia, mortality rates are very high

37
Q

What are the types of HD?

A
  • Home HD
  • Nocturnal HD
  • Cont RRT, used in ICU and HDU
38
Q

What is involved in conservative management as an alt to RRT?

A

In people >80 or w a WHO performance status of 3+ there is no survival benefit w RRT. Instead:

  • Sx control
  • Advanced care plan in preferred place
  • Support pt and fam
39
Q

What are the contraindications of renal transplant?

A
  • Active infection or malignancy
  • Non compliance to treatment
  • Severe heart or lung disease
  • Reversible renal disease
  • Uncontrolled substance abuse or psychiatric illness
  • Short life expectancy
40
Q

What are the different types of donors and outcomes?

A
  • Living related and living non related have comparable outcomes, related is best
  • Deceased non related - little prep time, years long waiting lists, reduced survival vs living donors
41
Q

What is induction treatment in renal transplant?

A

Potent immunosuppression to prevent hyper acute rejection= methyprednisolone + basilixamab and thymoglobulin.

42
Q

What is maintenance treatment in renal transplant?

A

Immediate immunosuppression to prevent acute or chronic rejection:

  1. Anti proliferative agent - mycophenolate (suppresses all immune cells), azathioprine
  2. Calcineurin inhib eg. ciclosporin, tacrolimus - T cell inhibition
  3. Corticosteroid eg. prednisolone
43
Q

What is involved in the long term care of a renal transplant pt?

A
  • Vaccines and infection screen
  • Malignancy screen
  • Follow up - GFR, CNI levels, proteinuria, Ca, phosphate, PTH, lipids, glucose
  • Contraception obligatory in first year
44
Q

What are the main causes of mortality from transplants?

A
  • Malignancy
  • Infection
  • CVD
45
Q

What are the complications of renal transplant?

A
  • Malignancy - skin, cervix, breast, prostate, liver, renal, colorectal, post transplant lymphoproliferative disorder (PTLD)
  • Infection - CMV, EBV, Hep B, pneumocitis jirovecii, TB
  • New onset diabetes after transplant NODAT
  • Rejection
46
Q

What are the simultaneous transplants?

A
  • Liver and kidney if cirrhosis and ESRF

- Pancreas and kidney in some T1DM

47
Q

Give some differentials for oedema/swelling

A
  • Heart failure
  • Liver failure
  • Kidney failure and nephrotic syndrome
  • Anaphylaxis if mins
  • DVT - swelling leg
  • Hypothyroidism
  • Hypoalbuminaemia from malabsorption
48
Q

What is the immediate management of a pt w nephrotic syndrome?

A
  • Diuresis - furosemide
  • ACEi/ARB = reduces pressure in kidney by reducing blood flow = less protein forced into urine
  • LMWH - prevent VTE
  • Statin
49
Q

What are the indications for renal biopsy and what are the risks?

A
  • Significant proteinuria no obvs cause
  • AKI no obvs cause
  • CKD no obvs cause
  • Renal transplant dysfunction
    Risk - bleeding, can be really severe and have interventional radiology backup
50
Q

What are the complications of HD?

A
  • Medical problems - pneumonia, MI, GI bleed, stroke, electrolyte abnormalities, fracture
  • Problems w access eg. line sepsis, thrombosis in fistula
  • Fluid overload
  • Steal syndrome
  • Arrhythmias
51
Q

What is steal syndrome? IN EXAM

A

In HD pt can have a fistula = artery and vein joined together and vein is arterialised so bigger flow of blood, takes 6 weeks to mature. In steal syndrome there is increased blood up the arm through the arterialised vein than goes to the hand so there is cold hand, ischaemia, can get death of digit tissue.
Presentation - numb and cold hand, pain when on HD

52
Q

Thrombosis of fistula

A

Often at an area where the vein is narrowed and stenosed - stasis of blood and thrombosis. Pt will have noticed missing thrill.
Treatment is to remove the clot and open the stenosis as much as possible but recurrence is likely.

53
Q

What is the access used in HD?

A
  • Fistula, normally brachiocephalic

- Perma cath = a central line that passes down IJV and sits in the RA (risk endocarditis and line sepsis)

54
Q

What are the atypical infections a pt can get after a transplant?

A
  • CMV - multisystem disease eg. marrow suppression, ocular, GI = diarrhoea, 1-6 months
  • EBV - related to PTLD, fever, pharyngitis, cervical lymphadenopathy, hepatosplenomegaly
  • Pneumocystis - yeast like fungus, SOB and normal CXR< desaturation of O2 sats when get up and walk about
  • BK nephropathy - haematuria and rising creatinine, causes graft dysfunction and can often trigger rejection
55
Q

How do you treat the atypical infections pt can get after transplant? Q IN EXAM

A

EBV, CMV, BK nephropathy - decrease immunosuppressants, +/- antivirals.
Pneumocystis - co-trimoxazole.

56
Q

What are the complications of PD? Q IN EXAM

A
  • Peritonitis - either infection of tunneled line or through the inside of the tube
  • Leaking
  • Drainage problems
  • Hernia
  • Dialysis failure eg. encapsulating sclerosing peritonitis
57
Q

Peritonitis from PD Q IN EXAM

  • Presentation
  • Ix
  • Treatment
  • Bacterial causes
A

Presentation - cloudy bag and severe abdo pain, guarding, lack of bowel sounds, tense
Ix - all of fluid from bag for gram stain
Treat - don’t wait for results of gram stain, intraperitoneal abx eg. vancomycin + oral abx
Cause - Staph epidermidis most common but also S.aureus, pseudomonas

58
Q

What is ADPKD?

A

Adult polycystic kidney disease - multiple cysts bilaterally in both kidneys. They increase in size and eventually fail. Strong FH component, autosomal dominant. Diagnose on USS.

59
Q

How is ADPKD treated?

A
  • Control HTN to prevent ESRD

- Tolvaptan, may control rate of cyst growth

60
Q

What are the complications of ADPKD?

A
  • Pain and discomfort - from size of kidney
  • Bleed and haematuria - cyst can pop
  • Cysts can become infected
  • Berry aneurysms, screen for them if FH
61
Q

What is the most likely cause of bilaterally enlarged kidneys with CKD?

A

Diabetic nephropathy

62
Q

What is found on bloods in acute interstitial nephritis?

A

Raised eosinophils and AKIy

Usually after an URTI

Medicine block (8 decks)

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