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Med Year 3 > Glomerulonephritis and PCKD > Flashcards

Glomerulonephritis and PCKD Flashcards

1
Q

what is interstitial nephritis

A

inflammation of space between cells and tubules = interstitium

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2
Q

what is glomerularsclerosis

A

pathological process of scarring of tissue in glomerulus, caused by GN or obstructive uropathy

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3
Q

what is IgA nephropathy

A

bergers disease = most common cause of glomerulonephritis

  • peak age: 20
    IgA deposits in mesangium
    overalps with HSP
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4
Q

how does IgA nephropathy present and how is it managed?

A

classically: macroscopic haematuria in young people following an UPPER RESP TRACT INFECTION

manage with monitoring 6-12 months, ACE-I if hypertensive

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5
Q

what is nephrotic syndrome?

A

when basement membrane in glomerulus becomes highly permeable to protein so leaks into urine

damaged podocytes, so loss of albumin (main protein that keeps blood in blood vessels)

low albumin = increased lipids by liver

loss of anti-thrombin 3= hypercoaguable

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6
Q

what is the classic triad of nephrotic syndrome?

A

low serum albumin
high urine protein +3 on dipstick
oedema

= also may have hypercholesterolaemia

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7
Q

what causes nephrotic syndrome?

A

minimal change disease in children

in adults: focal segmental glomerularsclerosis (presents in young adults, due to idiopathic reasons, HIV, renal path, heroin etc)

secondary causes: HSP, diabetes, infection

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8
Q

how do you manage nephrotic syndrome?

A 
high dose steroids for 4 weeks 
low salt diet
diuretics 
fluid restriction: 1-1.5L
albumin infusions
antibiotic prophylaxis 
anti-coag?
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9
Q

what is nephritic syndrome?

A

inflammation of kidney = group of symtpoms

 antibody meets antigen to form immune complex
 this complex will lodge itself in capillary and cause an IR against capillary and antigens
 WCC are recruited (hence on FBC, high WCC)
 Areas become inflamed, and breakdown
 Allows RBC and WBC to pour through the opening
• Hence protein gets through as well

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10
Q

what are the features of nephritic syndrome?

A

peripheral oedema
proteinuria
serum albumin <25

oliguria
high BP
granular casts

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11
Q

what would you see on a urine dip for nephritic?

A

proteins, bloods, WC

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12
Q

what are the causes of nephritic syndrome?

A

minimal change disease
focal segmental

primary: IgA, post-strep GN, GPS

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13
Q

main difference between nephritic and nephrotic?

A

only protein in urine = nephrotic

protein, sediments and extra cells = nephritic

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14
Q

what is glomerulonephritis, and what are some examples?

A

conditions that cause inflammation of or around glomerulus and nephron

o	Minimal change disease
o	Focal segmental glomerulosclerosis
o	Membranous glomerulonephritis
o	IgA nephropathy (AKA mesangioproliferative glomerulonephritis or Berger’s disease)
o	Post streptococcal glomerulonephritis (AKA diffuse proliferative glomerulonephritis)
o	Mesangiocapillary glomerulonephritis
o	Rapidly progressive glomerulonephritis
o	Goodpasture Syndrome
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15
Q

what is the pathophysiology of GN

A

immunoglobulin and complement activation within glomeruli

antigens may be trapped and deposited

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16
Q

what is membranous GN

A

most common type
- ages 20 and 60
IgG deposits in basement membrane
idiopathic

secondary to malignancy, NSAIDs, rheumatic disorders

management: ACE-I, immunosuppression if svere (ccs and cyclophosphamide)

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17
Q

what is the prognosis of membranous GN

A

o 1/3 recover spontaneously, 1/3 remain proteinuric, 1/3 develop ESRF

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18
Q

what is membranoproliferative GN

A

= same as membranous but deposits also in mesangium

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19
Q

what is post-strep GN?

A 
patients <30 years 
presents as:
- 1-3 weeks after a strep infection
-develops as acute nephritic syndrome 
- malaise, haematuria, proteinuria, hypertension, oliguria

caused by: immune complex depositition in glomeurli

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20
Q

what causes post-strep GN and what are the investigations?

A

immune complex deposition in glomeruli

- low C3 on bloods, renal biopsy, starry sky appearance

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21
Q

what is GPS?

A

small cell vasculitis

  • anti-GBM antibodies attack glomerulus and pulmonary basement membrane

= GN and pulmonary haemorrhage

  • more common in men, age 20 and 60
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22
Q

what are the tests and management for GPS

A

linear IgG deposits and CO transfer factor is raised

management: plasma exchange, steroids, cyclophosphamide

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23
Q

what differential could you give for GPS

A

wegeners (ANCA vasculitis may present with wheeze and sinus)

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24
Q

what is rapidly progressive GN

A

very acute illness w sick patients

secondary to GPS often
nephritic syndrome features

treated with BP control and steroids

25
Q

what is vasculitis

A

inflammation of the blood vessles, diff sizes

26
Q

what type of vasculitis affects small vessels?

A

Henoch=schonlein purpura
Eosinophilic granulomaosis with polyangiitis (churg-strauss syndrome)
Microscopic polyangiitis = main feature is renal failure
Granulomatosis with polyangiitis (wegener’s granulomatosis)

27
Q

what type of vasculitis affects medium sized vessels?

A

Polyarteritis nodosa
Churg-strauss syndrome
Kawasaki disease

28
Q

what type of vasculitis affects large vessels?

A

GCA and takayasu’s arteritis

29
Q

what is the main complication of GCA?

A

blindness

30
Q

what are some generic presentations of vasculitis?

A 
purpura, joint and muscle pain
peripheral neuropathy
renal impairment 
anterior uveitis and scleritis
GI disturbance and bleeding
hypertension
31
Q

what are the systemic manifestations of vasculitis

A

fever, fatigue, WL, anaemia

32
Q

how do you test for vasculitis?

A

CRP and ESR raised

ANCA blood test

33
Q

what is HSP?

A

IgA vasculitis = affects children
presents as rash on legs and bum

inflammation bc of IgA deposits on BV of affected organs

often triggered by URTI

most common in children under age of 10

rash due to leaking from small BV

34
Q

what are the features of HSP and how do you treat it?

A

purpura, joint pain, abdo pain, renal involvement

= analgesia and hydration

35
Q

explain the ANCA system

A

Antineutrophil cytoplasmic antibodies (ANCA) are a group of autoantibodies produced when a person’s immune system mistakenly targets and attacks its own neutrophil proteins. Two of the most commonly targeted proteins are myeloperoxidase (MPO) and proteinase 3 (PR3)

36
Q

what are p-anca and c-anca?

A

p-ANCA: also called anti-MPO antibodies –> microscopic polyangiitis and churg-strauss syndrome
typical pattern of peri-nuclear staining, specific for myeloperoxidase enzyme

c-ANCA also called anti-PR3 antibodies –>

wegener’s granulomatosis
diffuse cytoplasmic staining

both enzymes are stored in neutrophil granules

37
Q

what is churg strauss syndrome?

A

small and medium vasculitis

lung and skin problems

presents with severe asthma in late teens

eleveated eosinophils on FBC

38
Q

what is granulomatosis with polyangitis?

A

wegeners

CLASSIC SIGN: saddle shaped nose

small vessel

affects resp and kidneys (epistaxis, crusty secretions), cough, wheeze, haemoptysis with consolidation on CXR

leads to rapidly progressing GN

39
Q

what is the pathogenesis of ANCA vasculitis

A

expression of auto-antigeon on surface due to cytokines

binding = activation of neutrophils

cytotoxic injury to vessel wall

apoptosis and necrosis of neutrophils and endothelial cells

40
Q

how do you diagnose ANCA vasculitis?

A

history and examination, ANCA blood test, kidney biopsies, CXR, CO transfer factor differentiates between pulm oedema and presence of blood in alveoli

41
Q

how do you manage ANC vasculitis?

A

Induction of remission: cyclophosphamide and steroids

Maintenance of remission: azathioprine & CCS

42
Q

what is polyarteritis nodosa?

A

Medium vessel

Most associated with hep B = clear cause or hep C and HIV
Affects skin, GI tract, kidneys and heart
Renal impairment, strokes and myocardial infarction

Usually ANCA negative

43
Q

how does PAN present and how is it treated?

A

Presentation: GI bleed, bowel infarction, HTN, renal artery aneurysms
Livedo reticularis = mottled, purplish, lace like rash Diagnosis: angiogram
Treatment: if hep B neg, give CCS and cyclophosphamide
If hep b positive: antiviral and CCS

44
Q

what is kawasaki disease?

A

Medium vessel vasculitis

Common in oriental world

• Young children <5 years
Clinical features:
-Persistent high fever >5 days
-Erythematous and desquamation of palms and soles
-Strawberry tongue (red tongue with prominent papillae)

45
Q

how do you treat kawasaki disease and what is the key complication?

A

Treatment: symptomatic but IV immunoglobulins are used for severe form

Key complication = coronary artery aneurysm

46
Q

what is takayasu’s arteritis?

A

large vessel

aorta, pulmonary arteries

can swell and form aneurysms or can become narrow and blocked

= AKA pulseless disease

47
Q

how does takayasus present and how is it treated?

A

fever, malaise, muscle aches, claudication or syncope

CT, MRI angio or doppler of US carotids

treatment: steroids

48
Q

what is polycystic kidney disease

A

genetic condition where kidneys develop multiple fluid filled cysts

two types are autosomal dominant and autosomal recessive

49
Q

how does ADPKD present?

A

= chromosome 16 or 4

  • extra renal: cerebral aneurysms, cysts on liver, spleen, pancreas etc
  • issues with cardiac valve and colonic diverticula
50
Q

what is the USS diagnostic criteria for ADPKD?

A

Two cysts, unilateral or bilateral, if aged <30 years
2 cycts in BOTH kidneys if 30-59
4 cysts in both kidneys if aged >60 years
- Also, use CT scans to diagnose

51
Q

what are complications of ADPKD?

A 
Chronic loin pain 
Hypertension
Cardiovascular disease
Gross haematuria if cyst ruptures 
Renal stones (common in patients with PKD)
ESRD at age 50
52
Q

what is ARPKD?

A

gene on chromosome 6
rarer and more severe

presents in childhood/infancy

= presents in pregnancy with oligohydraminos as fetus doesn’t produce enough urine

53
Q

how else does ARPKD present?

A
  • may require dialysis in first few years of life

dysmorphia = ears are low set, flat nasal bridge

ESRD before adulthood

54
Q

what does a renal biopsy show for ARPKD?

A

multiple cylindrical lesions at RA to cortical surface

55
Q

how do you manage polycystic kidney disease?

A

tolvaptan = vasopressin receptor antagonist

slows the development of cysts and progression of RF if CKD stage 2 or 3

  • nephrectomy if poor prognosis otherwise
    supportive: anti-hypertensivem analgesia, AB, drainage of INFECTED cysts
56
Q

what is von hippel lindau disease?

A

autosomal dominant condiiton on chromosome 3 (encodes TSG protein)

presents in 20s or 30s with malignancies in retina, CNS, kidneys

renal manifestations: cortical renal cysts, renal cell carcinoma

treatable by surgical intervention

screening in genotype confirmed patients is annual USS and CT every 3 years (for fam members CT too)

57
Q

what are simple cysts

A

non genetic cause of cystic disease

more common with age
Unilocular and located in the cortex
Kidneys do not get enlarged by these cysts
Over the age of 30
Unlikely that on its own this will cause haematuria or pain

58
Q

what is acquired renal cystic disease?

A

Patients who have had a long duration of dialysis can develop acquired renal cysts

Tend to have shrunken kidneys and a negative family history of cystic diseases

Med Year 3 (25 decks)

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