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3B General Care > Nephrology > Flashcards

Nephrology Flashcards

1
Q

focal

A

some but not all glomeruli contain the lesion

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2
Q

diffuse (global)

A

most glomeruli contain the lesion

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3
Q

Segmental

A

only a part of the glomerulus contain the lesion (often focal as well)

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4
Q

proliferative

A

an increase in cell numbers due to hyperplasia of one or more of the resident glomerular cells with or without inflammation

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5
Q

membrane alterations

A

capillary wall thickening due to deposition of immune deposits or alterations in the basement membrane

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6
Q

Nephrotic syndrome

What is is?

A

Increased filtration of macromolecule across the glomerular capillary wall
- due to structural and functional abnormalities of glomerular podocytes

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7
Q

Clinical features of nephrotic syndrome

A
  1. Hypoalbuminaemia - as a result of heavy proteinuria & increased renal catabolism of filtered protein
  2. Oedema - due to sodium retention & increased capilliary permeability
  3. Hypercholesterolaemia & hypertriglyceridae,oa - increased synthesis and impaired catabolism
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8
Q

Aetiology

Membranous nephrotic syndrome

A
  • idiopathic
  • drugs (gold, penicillamine, NSAIDs)
  • autoimmune ( SLE, thyroiditis)
  • Neoplasia
  • Infections

–> IgG deposition & complement C3 in the outer glomerular basement membrane

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9
Q

Clinical features of nephrotic syndrome

A

Oedema of the ankles, genitals and abdominal wall

Periorbital oedema and arm oedema may also be features of severe disease

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10
Q

Differential diagnosis for nephrotic syndrome

A
  • Congestive cardiac failure (would also be raised JVP)

- cirrhosis (would also be signs of liver failure)

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11
Q

Management of nephrotic syndrome

A

General oedema- salt restriction, diuretics & amiloride
Proteinuria - ACE-i/ ARB, normal diet
Specific treatment: (of underlying disease), cyclophosphamide, chlorambucil with prednisolone, rituximab in resistant disease

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12
Q

Complications of nephrotic syndrome

A

Venous thrombosis (loss of clotting factors in urine)
Sepsis (loss og Ig in urine increases susceptibility to infection)
AKI (result of progression of underlying renal disease, consequence of hypovolaemia or renal vein thrombosis)

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13
Q

Acute glomerulonephritis

A

caused by an immune response triggered by an infection or other disease
typically post strep (group A, beta-haemolytic strep)
Bacterial antigen becomes trapped in the glomerulus leading to acute diffuse proliferative glomerulonephritis

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14
Q

Acute glomerulonephritis

clinical features

A
  • haematuria
  • proteinuria
  • hypertension and oedema (periorbital, leg or sacral) caused by salt and water retention
  • oliguria
  • uraemia
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15
Q

Management of post strep glomerulonephritis

A

supportive

  • HTN –> salt restriction and loop diuretics & vasodilators
  • Fluid balance & daily weights
  • Fluid restriction if evidence of fluid overload
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16
Q

Rapidly progressing glomerulonephritis

A
  • anti-glomerular basement disease (with lung involvement = Goodpasture’s syndrome)
  • anti-neutrophilic cytoplasmic antibody (ANCA) vasculitis
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17
Q

Pathogenesis of UTI

A

sexual intercourse
urethral catheterisation
cystitis encouraged by urinary obstruction/ stasis, previous damage to bladder epithelium, bladder stones, poor bladder emptying

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18
Q

Clinical features of lower UTI

A 
micturition, 
dysuria, 
suprapubic pain and tenderness, 
Haematuria 
Smelly urine
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19
Q

Clinical features of acute pyelonephritis

A

Loin pain & tenderness
Nausea & Vomiting
Fever

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20
Q

Acute pyelonephritis

A

neutrophil infiltration of the renal parenchyma

small cortical abscesses & streaks of pus in renal medulla

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21
Q

reflux nephropathy

A

childhood UTIs + vesicoureteric reflux –> progressive renal scarring –> hypertension + CKD

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22
Q

Recurrent UTI

A

same or different organism more than 2 weeks after stopping abx = reinfection
Relapse = recurrence of bacteriuria with the same organism within 7 days

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23
Q

TB of the urinary tract

A

symptoms of UTI

sterile pyuria

Culture of mycobacteria from early morning urine sample

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24
Q

Tubulointerstitial nephritis

A

primary injury to renal tubules and interstitium –> decreased renal function

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25
Q

Acute tubulointerstitial nephritis

causes

A

most due to allergic drug reaction (penicillins/ NSAIDs)

Infection less common

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26
Q

Presentation of acute tubulointerstitial nephritis

A 
fever
eosinophila
eosinophiluria
normal/ mildly raised proteinuria 
AKI
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27
Q

Management of acute tubulointerstitial nephritis

A

withdrawal of causative drug

High dose prednisolone

28
Q

Chronic tubulointerstitial nephritis

causes

A

prolonged consumption of large amounts of analgesia (NSAIDs), DM & toxina

29
Q

Presentation of Chronic tubulointerstitial nephritis

A

polyuria
proteinuria
uraemia

(polyuria & nocturia are the result of tubular damage –> inability to properly concentrate urine)

30
Q

Bilateral renal disease

Renal hypertension

A

hypertension complicates bilateral renal disease

(glomerulonephritis, reflux nephopahty or analgesic nephropathy)

  • Activation of renin-angiotensin-aldosterone system
  • Retention of salt and water

–> increase in blood volume and therefore blood pressure

31
Q

Renovascular disease

A

narrowing of renal arteries

  • usually due to atheroma, but may also be due to fibromuscular hyperplasia
  • renal perfusion pressure is reduced
  • renal ischaemia –> reduced pressure in afferent glomerular arterioles
32
Q

Nephrocalinosis

A

diffuse renal parenchymal calcification
painless
hypertension and renal impairment commonly occur

33
Q

Nephrocalcinosis

causes

A

Medullary - hypercalcinaemia, renal tubular acidosis, primary hyperoxaluria, medullary sponge kidney, TB

Cortical - renal cortical necrosis

34
Q

Renal failure

A

failure of renal excretory function
result of reduction in GFR
Accompanied to a variable extent by failure of EP production, Vit D hydroxylation, regulation of acid-base balance & BP control

35
Q

Define AKI

A

abrupt, sustained rise in serum urea & creatinine due to a rapid decline in GFR
- loss of normal water and solute homeostasis

36
Q

Pre-Renal causes of AKI

A

impaired perfusion of the kidneys

  • hypovolaemia
  • hypotension
  • impaired cardiac pump efficiency
  • vascular disease
    ACE-i & NSAIDs impair renal autoregulation so increase tendency to develop pre-renal uraemia
37
Q

Management of pre-renal AKI

A
  • prompt fluid replacement
38
Q

Post- renal AKI

A

both urinary outflow tracts blocked

relieved if obstruction is removed

39
Q

Renal AKI

A

commonly due to acute tubular necrosis –> renal ischaemia or direct renal toxins

Other cuases include diseases that affect the interstitium- drug hypersensistivity infections, renal vasulature and acute glomerulonephritis)

40
Q

Causes of acute tubular necrosis

A

Haemorrhage, burns, D&V, acute pancreatitis, diuretics, MI, congestive cardiac failure, endotoxic shock, snake bite, myoglobinaemia, haemoglobulinaemia, hepatorenal syndrome, radiological contrast, pre-eclapsia

41
Q

Clinical features of AKI

A
  • change in urine output

- biochemical abnormalities - hyperkalaemia, metabolic acidosis, hyponatraemia, hypocalcaemia& hyperphosphataemia

42
Q

Symptoms of AKI

A

weakness
fatigue
anorexia
Nausea & vomiting
confusion, seziures & coma
Pruritus & bruising (impaired platelet function)
Breathlessness from fluid overload & anaemia

43
Q

Management of AKI

A

prevention & fluid expansion

44
Q

Chronic Kidney disease

A

longstanding & progressive impairment of renal function
- persistent (>3/12) evidence of kidney damage ± impaired eGFR

  • fibrosis of remaining tubules, glomeruli & small blood vessels –> renal scarring & loss of renal function
45
Q

Causes of CKD

A

DM, HTN, atherosclerotic renal vascular disease

schistosomiasis (middle east)

46
Q

Clinical features of CKD

A

Anaemia (increased blood loss, reduced EPO production, shortened RBC survival)
Bone disease (renal phosphate retention, impaired production of Vit D 3)
Neurological - polyneuropathy- peripheral paraethesiae & weakness, postural hypotension, disrupted GI motility
CVD- htn, dyslipidaemia & vascular calcification

47
Q

Goals of CKD management

A
  • treat cause e.g. vasculitis, improve DM control
  • slow deterioration of renal function
  • Reduce CV risk
  • treat complications
  • dose adjustment for reno-toxic drugs
48
Q

Renoprotection in CKD

A

BP <120/80

  • ACE-i
  • ARB
  • Diuretics
  • CCB
49
Q

Reducing CV risk in CKD

A
  • optimal control of BP & reduce proteinuria
  • statins to lower cholesterol
  • cessation of smoking
  • optimise diabetic control
  • normal protein diet
50
Q

Correction of CKD complications

Hyperkalaemia

A

restriction of dietary potassium

stop potassium retentive drugs

51
Q

Correction of CKD complications

calcium & phosphate

A

reduce dietary phosphate restriction
oral phosphate binding agents (calcium carbonate)
synthetic Vit D

52
Q

Correction of CKD complications

Anaemia

A

Can supplement with recombinant EPO

53
Q

Correction of CKD complications

Acidosis

A

oral sodium bicarbonate

54
Q

Correction of CKD complications

infection

A

increased risk of infection

vaccination - flu & pneumococcal

55
Q

Complications of dialysis

A

CVD - atheroma
Sepsis (peritonitis from staph aureus/ indwelling access devices)
Amyloidoisis

56
Q

Autosomal- dominant
Poly cystic kidney disease

(ADPKD)

A

cysts increase in size with age –> renal enlargement, progressive destruction of normal kidney tissue, gradual loss of renal function

PKD1 gene mutation, chromosome 16

57
Q

Clinical features of ADPKD

A
  • acute loin pain from cyst haemorrhage/ infection/ UTI
  • abdominal discomfort from renal enlargement
  • hypertension
  • progressive renal impairment (end-stage renal failure in 50% pts by 50-60)
  • liver cyst (pancreas, spleen & ovary as well)
  • subarachnoid haemorrhage
  • mitral valve prolapse
58
Q

Diagnosis of ADPKD

A

Large irregular kidneys, HTN & hepatomegaly

- definitive diagnosis on USS

59
Q

Management of ADPKD

A

contro BP
monitor disease progressuion (seruum creatinine)
renal replacement

60
Q

Medullary sponge kidney

A

uncommon condition

characterised by dilatation of collecting ducts in the papillae with cystic changes

61
Q

Renal Cell Carcinoma

Demographics

A

most common renal tumour in adults
present around 55 with men: women 2:1
arise from proximal tubular epithelium

62
Q

Clinical features of renal cell carcinoma

A 
Haematuria
loin pain 
mass in the flank
malaise, weight loss, fever
left sided scrotal varicoceles if obstruction of gonadal vein
63
Q

RCC mets

A

25% at presentation

  • bone
  • liver
  • lung
64
Q

Management of localised RCC

A

radical nephrectomy

- partial if bilateral disease/ poor contralateral disease

65
Q

Management of locally advanced/ metastatic RCC

A

interleukin 2 and interferon –> remission in 20% of cases

targeted immunotherapy

3B General Care (8 decks)

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