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General practice > Renal - Glomerulonephritis > Flashcards

Renal - Glomerulonephritis Flashcards

1
Q

Features of nephritic syndrome

A

Haematuria means blood in the urine. This can be microscopic (not visible) or macroscopic (visible).
Oliguria means there is a significantly reduced urine output.
Proteinuria is protein in the urine. In nephritic syndrome, there is less than 3g / 24 hours. Any more and it starts being classified as nephrotic syndrome.
Fluid retention

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2
Q

Criteria for nephrotic syndrome diagnosis

A

Peripheral oedema
Proteinuria more than 3g / 24 hours
Serum albumin less than 25g / L
Hypercholesterolaemia

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3
Q

What does glomerulonephritis refer to

A

Glomerulonephritis is an umbrella term applied to conditions that cause inflammation of or around the glomerulus and nephron

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4
Q

What is interstitial nephritis

A

Interstitial nephritis is a term to describe a situation where there is inflammation of the space between cells and tubules (the interstitium) within the kidney

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5
Q

What is glomerulosclerosis

A

Glomerulosclerosis is a term to describe the pathological process of scarring of the tissue in the glomerulus. It is not a diagnosis in itself and is more a term used to describe the damage and scarring done by other diagnoses

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6
Q

What can cause glomerulosclerosis

A

Glomerulosclerosis can be caused by any type of glomerulonephritis or obstructive uropathy (blockage of urine outflow), and by a specific disease called focal segmental glomerulosclerosis.

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7
Q

What are most types of glomerulonephritis treated with

A

Immunosuppression (e.g. steroids)
Blood pressure control by blocking the renin-angiotensin system (i.e. ACE inhibitors or angiotensin-II receptor blockers)

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8
Q

Most common cause of nephrotic syndrome in children

A

Minimal change disease

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9
Q

Most common cause of nephrotic syndrome in adults

A

Focal segmental glomerulosclerosis

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10
Q

Aetiology of minimal change disease

A

Majority are idiopathic
drugs: NSAIDs, rifampicin
Hodgkin’s lymphoma, thymoma
infectious mononucleosis

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11
Q

Features of minimal change disease

A

nephrotic syndrome
normotension - hypertension is rare
highly selective proteinuria
only intermediate-sized proteins such as albumin and transferrin leak through the glomerulus

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12
Q

What might a renal biopsy show in minimal change disease

A

normal glomeruli on light microscopy

electron microscopy shows fusion of podocytes and effacement of foot processes

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13
Q

Mx of minimal change disease

A

majority of cases (80%) are steroid-responsive

cyclophosphamide is the next step for steroid-resistant cases

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14
Q

What is focal segmental glomerulosclerosis(FSGS)

A

Focal segmental glomerulosclerosis (FSGS) is a cause of nephrotic syndrome and chronic kidney disease. It generally presents in young adults.

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15
Q

Causes of FSGS

A 
idiopathic
secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy
HIV
heroin
Alport's syndrome
sickle-cell
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16
Q

In which patients is FSGS likely to recur

A

Patients with renal transplants

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17
Q

What might a renal biopsy show in FSGS

A

focal and segmental sclerosis and hyalinosis on light microscopy
effacement of foot processes on electron microscopy

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18
Q

Mx of FSGS

A

steroids +/- immunosuppressants

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19
Q

What does nephrotic syndrome predispose patients to

A

Nephrotic syndrome predisposes patients to thrombosis, hypertension and high cholesterol.

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20
Q

Most common cause of primary glomerulonephritis

A

IgA nephropathy(Berger’s disease)

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21
Q

How does IgA nephropathy classically present

A

It classically presents as macroscopic haematuria in young people following an upper respiratory tract infection.

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22
Q

Conditions associated with IgA nephropathy

A

alcoholic cirrhosis
coeliac disease/dermatitis herpetiformis
Henoch-Schonlein purpura

23
Q

Histology in IgA nephropathy

A

Mesangial hypercellularity

Positive immunofluorescence for IgA and C3

24
Q

IgA nephropathy presentation

A

young male, recurrent episodes of macroscopic haematuria
typically associated with a recent respiratory tract infection(1-2 days after URTI)
nephrotic range proteinuria is rare
renal failure is unusual and seen in a minority of patients

25
Q

Differentiation of IgA nephropathy and post-strep glomerulonephritis

A

post-streptococcal glomerulonephritis is associated with low complement levels

main symptom in post-streptococcal glomerulonephritis is proteinuria (although haematuria can occur)

there is typically an interval between URTI and the onset of renal problems in post-streptococcal glomerulonephritis(Posy-strep glomerulonephritis develops 1-2 weeks after URTI)

26
Q

Mx of IgA nephropathy if isolated hematuria with no/minimal proteinuria

A

no treatment needed, other than follow-up to check renal function

27
Q

Mx of IgA nephropathy if persistent proteinuria, a normal or only slightly reduced GFR

A

initial treatment is with ACE inhibitors
if there is active disease (e.g. falling GFR) or failure to respond to ACE inhibitors
immunosuppression with corticosteroids

28
Q

What is the most common type of glomerulonephritis overall

A

Membranous glomerulonephritis

29
Q

How does membranous glomerulonephritis usually present

A

Nephrotic syndrome or proteinuria

30
Q

What might a renal biopsy demonstrate in membranous glomerulonephritis

A

electron microscopy: the basement membrane is thickened with subepithelial electron dense deposits. This creates a ‘spike and dome’ appearance

31
Q

Causes of membranous glomerulonephritis

A

diopathic: due to anti-phospholipase A2 antibodies
infections: hepatitis B, malaria, syphilis
malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
drugs: gold, penicillamine, NSAIDs
autoimmune diseases: systemic lupus, thyroiditis, rheumatoid

32
Q

Mx of membranous glomerulonephritis

A

all patients should receive an ACE inhibitor or an angiotensin II receptor blocker (ARB)

A combination of corticosteroid + another agent such as cyclophosphamide is often used

33
Q

What is post strep glomerulonephritis

A

Post-streptococcal glomerulonephritis typically occurs 7-14 days following a group A beta-haemolytic Streptococcus infection (usually Streptococcus pyogenes).

It is caused by immune complex (IgG, IgM and C3) deposition in the glomeruli. Young children are most commonly affected.

34
Q

Features of post strep glomerulonephritis

A 
headache
malaise
visible haematuria
proteinuria
this may result in oedema
hypertension
oliguria
35
Q

Renal biopsy features of post strep glomerulonephritis

A

endothelial proliferation with neutrophils

electron microscopy: subepithelial ‘humps’ caused by lumpy immune complex deposits
immunofluorescence: granular or ‘starry sky’ appearance

36
Q

What is Anti-GBM/goodpasture’s syndrome

A

Is a rare type of small-vessel vasculitis associated with both pulmonary haemorrhage and rapidly progressive glomerulonephritis. It is caused by anti-glomerular basement membrane (anti-GBM) antibodies against type IV collagen.

37
Q

Features of Anti-GBM disease

A

pulmonary haemorrhage
rapidly progressive glomerulonephritis
this typically results in a rapid onset acute kidney injury
nephritis → proteinuria + haematuria

38
Q

IX for Anti-GBM disease

A

renal biopsy: linear IgG deposits along the basement membrane
raised transfer factor secondary to pulmonary haemorrhages

39
Q

Mx of Anti-GBM disease

A

plasma exchange (plasmapheresis)
steroids
cyclophosphamide

40
Q

Factors that increase likelihood of anti-gbm disease

A 
smoking
lower respiratory tract infection
pulmonary oedema
inhalation of hydrocarbons
young males
41
Q

What does rapidly progressive glomerulonephritis refer to

A

Rapidly progressive glomerulonephritis is a term used to describe a rapid loss of renal function associated with the formation of epithelial crescents in the majority of glomeruli.

42
Q

Causes of rapidly progressive glomerulonephritis

A

Goodpasture’s syndrome
Wegener’s granulomatosis
others: SLE, microscopic polyarteritis

43
Q

Features of rapidly progressive glomerulonephritis

A

nephritic syndrome: haematuria with red cell casts, proteinuria, hypertension, oliguria
features specific to underlying cause (e.g. haemoptysis with Goodpasture’s, vasculitic rash or sinusitis with Wegener’s)

44
Q

Gene associated with Anti-GBM disease

A

HLA DR2

45
Q

What is granulomatosis with polyangiitis (Wegener’s granulomatosis)

A

It is an autoimmune condition associated with a necrotizing granulomatous vasculitis, affecting both the upper and lower respiratory tract as well as the kidneys.

46
Q

Features of wegener’s granulomatosis

A

upper respiratory tract: epistaxis, sinusitis, nasal crusting
lower respiratory tract: dyspnoea, haemoptysis
rapidly progressive glomerulonephritis (‘pauci-immune’, 80% of patients)
saddle-shape nose deformity
also: vasculitic rash, eye involvement (e.g. proptosis), cranial nerve lesions

47
Q

Wegener’s granulomatosis vs Churg-Strauss syndrome

A

Wegener’s granulomatosis - Renal failure, epistaxis/haemoptysis, cANCA

Churg-Strauss syndrome - Asthma, pANCA, eosinophilia

48
Q

IX for wegner’s disease

A

cANCA positive in > 90%, pANCA positive in 25%
chest x-ray: wide variety of presentations, including cavitating lesions
renal biopsy: epithelial crescents in Bowman’s capsule

49
Q

Causes of transient or spurious non-visible haematuria

A

urinary tract infection
menstruation
vigorous exercise (this normally settles after around 3 days)
sexual intercourse

50
Q

Causes of persistent non-visible haematuria

A 
cancer (bladder, renal, prostate)
stones
benign prostatic hyperplasia
prostatitis
urethritis e.g. Chlamydia
renal causes: IgA nephropathy, thin basement membrane disease
51
Q

Spurious causes of haematuria where blood is not present on dipstick

A

foods: beetroot, rhubarb
drugs: rifampicin, doxorubicin

52
Q

When should urgent referral be made for haematuria

A

Aged >= 45 years AND:
unexplained visible haematuria without urinary tract infection, or
visible haematuria that persists or recurs after successful treatment of urinary tract infection

Aged >= 60 years AND have unexplained nonvisible haematuria and either dysuria or a raised white cell count on a blood test

53
Q

What might bloods show in post strep glomerulonephritis

A

bloods:
low C3
raised ASO titre

General practice (26 decks)

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