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Y3 Medicine > Renal > Flashcards

Renal Flashcards

1
Q

Give 3 common causes of CKD

A
  • renovascular disease
  • hypertension
  • diabetes
  • glomerular nephritis (nephrotic and nephritic syndromes)
  • Hereditary diseases like APCKD
    less common causes in autoimmune disease (SLE), myeloma etc
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2
Q

What are the 3 classic findings in nephrotic syndrome?

A
  • high cholesterol
  • gross protein urea (causes frothy urine)
  • Low serum albumin
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3
Q

How does nephrotic syndrome usually present?

A
  • pitting odema in legs
  • odema in face worse in morning
  • any age
  • predisposing factor eg diabetes, fhx
  • frothy urine
  • incidental finding of gross protein urea
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4
Q

Give 3 secondary causes of nephrotic syndrome?

A
  • diabetes
  • lupus nephritis
  • myeloma
  • amyloid
  • pre- eclampsia
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5
Q

give 3 primary causes of nephrotic syndrome

A
  • FSGS
  • minimal change
  • membranous nephropathy
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6
Q

What are the classical findings of nephritic syndrome?

A
  • blood and small amounts of protein in urine
  • no swelling
  • vague symptoms
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7
Q

How may CKD present?

A
  • vague symptoms like fatigue, malaise, anorexia, weakness
  • swelling of face and legs
  • breathlessness due to pulmonary odema
  • pruritis, lethargy, cramps and headaches due to raised urea
  • insomnia
  • polyurea
  • sexual dysfunction
  • predisposing factors often present
  • usually picked up incidentally by urine dips
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8
Q

How is CKD investigated?

A
  • urine dip
  • 24 hr urine collection/ spot urine collection to look at ACR
  • bloods: u&e, alk phos, parathyroid hormone, plasma glucose and HbA1c, serum ablumin, lipid screen (usually high), FBC (normocytic anaemia), anti nuclear antibodies, serum free light chains, c ANCA and p ANCA, anti GMB if no clear cause
  • ECG and echo as heart failure is often a differential and LVH often occurs due to fluid overload
  • Renal USS if suspect APCKD, obsutruction, haematuria, low GFR
  • renal biopsy when indicated
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9
Q

When should a renal biopsy be done in someone with CKD

A

Progressive disease, nephrotic syndrome, systemic disease, AKI without recovery, unknown cause

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10
Q

When should the GP refer someone with CKD to a nephrologist?

A
  • When reach stage 4
  • ACR>70 mg/mmol unless due to DM
  • ACR >30 with haematuria
  • eGFR decrease by 15% in 12 months or >25% total
  • high BP poorly controlled despite >4 antihypertensives at theraputic dose
  • known or suspected rare or genetic cause of CKD
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11
Q

Describe stage 1-5 CKD

A 
1= eGFR> 90
2= 60-89
3= 30-59
4= 15-29 
5= <15
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12
Q

List 5 complications of CKD

A
  • hypertension
  • odema
  • hyperkalaemia
  • uremia
  • coagulopathies
  • acidosis
  • anaemia of chronic disease
  • hypocalcamia with hyperparathyroidism
  • rugger jersey spine/mineral bone disease (related to above)
  • CVD due to high BP, vascular stiffness, inflammation, oxidative stress, abnormal endothelial function
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13
Q

What treatment is given in CKD to slow disease progression

A
  • ACEi or ARB (not both) and check K+ before and 2 weeks after starting treatment
  • Good glyaemic control
  • lifestyle advice
  • Avoid NSAIDS, nephrotoxic drugs and K+ sparing diuretics (amiloride and spironolactone)
  • Adjust doses of renal metabolised/ excreted drugs
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14
Q

What treatments are given for CKD complications?

A
  • odema: furosemide/ bumetanide, restrict sodium and fluid intake
  • Anaemia: ferrous sulphate or IV iron then EPO if not work
  • Acidosis: sodium bicarb supplements
  • high phosphate and K+: reduce in diet (refer to dietician), calcium acetate works as phosphate binder
  • hyperparathyoidism/ hypocalcaemia: give adcal D3/ alphacalciferol
  • CVD: anti platelets (aspirin) and statin
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15
Q

Describe the management of hyperkalaemia? inc doses

A
  • Do ECG and VBG to confirm
  • If K+> 6.5 or ECG changes, give IV calcium gluconate 10mg 10% over 10 mins and actrapid 10 units and 50mls 50% dextrose immediately
  • Also give calcium resonium (15-45mg) to bind the Ca2+
  • Give 5-10mg salbutamol neb if K+ not coming down
  • sodium bicarb and call renal reg if still refractory
  • Final option is dialysis
  • If k+ 6-6.5 or no ECG changes, give calcium gluconate usually, stop K+ sparing diuretics, give fluids/ hydrate, think about loop diuretics if refractory
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16
Q

Give 2 pre renal, 2 renal and 2 post renal causes of AKI

A

Pre: hypovolaemia, sepsis, cardiac failure, renal artery occlusion, renal vein thrombosis
Renal: small vessel vasculitis, glomerular disease (anti GBM, lupus), ATN (ischaemia, nephrotoxins, rhabdomylosis) acute interstitial nephritis (drugs, infection)
Post: calculi, retroperitoneal fibrosis, bladder outlet obstuction (tumour)

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17
Q

What are the 3 criteria for AKI?

A
  • Rise in serum creatinine of > 26 umol/L over 48hrs
  • 50% or greater increase in creatinine within 7 days
  • fall in urine output to less than 0.5 ml/kg/hr for more than 6 hrs
18
Q

What investigations would you do for suspected AKI?

A

Urinalysis: dipstick for blood, nitrates, leukocytes, glucose, osmolality
Bloods: FBC, Blood film, U&Es, coag studies (DIC), CK, myoglobinurea (?rhabdomyalysis), autoantibody screen virology
USS when ?obstruction
CXR- pulmonary odema, AXR- renal calculi
Doppler USS to look for stenosis or renal arteries and veins

19
Q

How is AKI managed?

A
  • monitor fluid and electrolyte balance closely
  • treat cause
  • pre renal aki: fluid replacment
  • withdraw nephrotoxic drugs
  • identify and treat complications (hyperalaemia, acidosis, pulmonary odema, bleeding)
  • restrict oral K+ and monitor carefully
20
Q

When should renal replacement therapy be used in AKI? (6)

A
  • Hyperkalaemia (>6.5) refractory to medical management
  • pulmonary odema/ fluid overload refractory to medical management
  • metabolic acidosis refractory to medical therapy
  • uraemia complications (pericarditis or uraemic encephalopathy)
  • CKD stage 4/5
  • dialysable nephrotoxin
  • intrinsic renal disease (vasculitis, GN, SLE) suspected
21
Q

When does a pt with CKD need specialist renal care? (7)

A
  • GFR < 30 with or without diabetes (stage 4)
  • ACR 70 or more unless diabetes
  • ACR 30 or less with haematuria
  • sustained decrease in GFR or 25% or more
  • Hypertension which remains poorly controlled despite 4 drugs at theraputic doses
  • known or suspected rare or genetic causes of CKD
  • Suspected renal artery stenosis
  • outflow obstruction should go to urology
22
Q

Describe how youd undertake a fluid assessment?

A

look at tongue, JVP, skin turgor, HR,RR BP, cap refill, pulmonary odema, peripheral odema

23
Q

Give adv and dis avd of haemodialysis

A

Disadv: need to go in hospital 4x 3 hrs a week, need access with central line or fistula, diet restrictions
Adv: can sometimes be done at home, other hrs of week they can do as please, can remove fluid at same time,

24
Q

What are the two types of peritoneal dialysis

A

APD: nightime bags
CAPD: continuous bags
The more concentrated the bags the more fluid is removed

25
Q

What are contraindications of peritoneal dialysis

A

IBD, adhesions due to previous abdo surgery, massive central obesity or very little abdofat

26
Q

What 3 drugs does everyone go on after renal transplant

A

Tacrolimus, azathioprine and cyclosporin
Most also go on mycophenolate and prednisolone. Also need contraception for 1st year and need to monitor U&E, dipstick, PTH, lipids, glucose and screen for malignancies.

27
Q

What are the advantages of renal transplant

A

no diet restriction, normal life afterwards

28
Q

What are the complications of haemo and peritoneal dialysis?

A

peritoneal: peritonitis, thickening of peritoneum leading to small bowel obstruction (encapsulating peritoneal sclerosis) or access failure
Haemo: fistula clotting, SVC obstuction, endocarditis, line sepsis, access failure, shock

29
Q

Give 3 complications of renal transplants

A

infections, rejection, obstuction, thrombosis, delayed graft function, donor derived infections , graft vs host disease, new onset diabetes after transplant, malignancies, damage during operatiion

30
Q

What may cause nephritic syndrome (7)? Give a couple of secondary features associated with each

A
  • ANCA/ small vessel vasculitis (churgg strauss, wengers- rashes, asthma, joint pain)
  • IgA nephropathy (gross haematuria, after infections or strenuous exersize)
  • Anti GBM (pulmonary haemorrhage)
  • Think basement membrane disease (hereditary)
  • Alport (hearing and eye problems)
  • Post Step GN (1-2 weeks after impetigo/ tonsilitis)
  • Lupus
31
Q

How is IgA nephropathy diagnosed and managed?

A
  • increased serum IgA, intermittent visible/ microscopic haematuria and mesangeal immune complex deposition in glomeruli on biopsy
  • treatment is with immmunosurpression, give an ACEi for HTN
32
Q

How is ANCA vasculitis diagnosed and managed?

A
  • +ve c ANCA (GPA) or p ANCA (churgg strauss, MPA)

- immunosurpression

33
Q

How is ANTI GBM diagnosed and managed?

A
  • +ve anti GBM autoantibodies + biopsy and pulmonary infiltrates on CXR
  • manage with immunosurpression and plasma exchange
34
Q

How is alport syndrome diagnosed and managed?

A

alternative thickening and thinning of GBM and sensorineural hearing loss
management is supportive

35
Q

What is the normal anion gap and what is the equation?

A

(Na + K) - (cl + HCO3)

Normal gap is 8-12

36
Q

What is the anion gap useful for?

A

Determining cause of metabolic acidosis - increased acid or decreased alkali?

37
Q

What does a high anion gap suggest?

A

Increase in organic acids- as it means unmeasured ions make up a greater proportion of the anions in the serum.
Organic acids inc lactic acid, ketoacids, methanol or ethanol poisioning, can be due to renal failure also

38
Q

What does metabolic acidosis with a normal anion gap suggest?

A

acidosis is due to decrease in alkali

  • renal loss of bicarb (RTA, addisons)
  • diarrhoea (loss of Cl-)
39
Q

How much K+ does a patient need per day and what’s the fastest you can give it?

A

1mmol/kg/day (for maintanance- increased if vomiting or high output stoma)
Dont give faster than 10mmol/hr, if faster than 20mmol/hr need cardiac monitoring.
If in AKI, they need more fluid and less K+.
(if K+ consistently low, check Mg)

40
Q

Why shouldnt you give too much saline?

A

lots of Na and CL!! can get hyperchloarmic acidosis which will lead to reduced eGFR

41
Q

how should nephortic syndrome be managed

A
  • fluid restriction, furosemide +/- thiazide to reduce odema- monitor body weight
  • treat cause (usually steroids)
  • ACEi/ ARB reduces proteinuria
  • identify/ prevent/ manage complications (VTE, infection, hyperkalaemia, hyper lipidaemia)

Y3 Medicine (9 decks)

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