Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Nephrology > Renal manifestations of systemic disease > Flashcards

Renal manifestations of systemic disease Flashcards

Diabetic nephropathy Lupus nephritis Small vessel vasculitis (Wegener's granulomatosis, microscopic polyangiitis, Churg-Strauss syndrome) Myeloma Amyloid Haemolytic uraemic syndrome Thrombotic thrombocytic purpura Atherosclerotic renovascular disease Scleroderma renal crisis Sickle cell nephropathy

1
Q

What is the commonest cause of ESRF

A

Diabetic nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the pathophysiology of diabetic nephropathy

A

hyperglycaemia leads to increase in Bfs -> RAAS activation -> production of glycosylation end products + oxidative stress
There is increased glomerular capillary pressure, podocyte damage and endothelial dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does diabetic nephropathy present?

A

1st - albuminuria

later - scarring (GS), nodule formation + fibrosis w loss of renal function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What accelerates the course of diabetic nephropathy

A

raised BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is a diagnosis of diabetic nephropathy made?

A

microalbuminuria -> A:CR 3-30mg/mmol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the treatment of diabetic nephropathy?

A
  1. INTENSIVE DM CONTROL - prevents microalbuminuria and lowers risk of macroalbuminuria (ACR >30)
  2. BP <130/80 - ACEi/ARBs, no dual therapy
  3. Na+ restriction <5g NaCl <2g Na
  4. Statins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is lupus?

A

Systemic autoimmune disease w abs against nuclear components -> deposition of ab complexes -> inflammation and tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does lupus present?

A 
Rash
Photosensitivity
ulcers 
Arthritis
Serositis
CNS effects
Cytopenias
Renal disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Does lupus present as nephritis or nephrosis?

A

EITHER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hows a diagnosis of lupus made?

A

Clinical
Ab profile - ANA (sensitive not specific)
Anti-dsDNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the treatment of lupus?

A

Depends on histological class
Class I + II
1. ACEi/ARB - renal protection
2. Hydroxychloroquine - for extra renal disease
Class III + IV
Immunosuppression: mycophenolate, glucocorticoids, cyclophosphamide, rituximab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does ANCA stand for?What is it?

A

Anti-Neutrophil Cytoplasmic Antibodies

Serological marker, presence characterises a group of vasculitides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the different types of AAV?

A
  1. Wegeners granulomatosis
  2. Microscopic polyangiitis
  3. Churg-strauss syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does AAV stand for?

A

ANCA associated vasculitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the main types of ANCA?

A
  1. Cytoplasmic - cANCA - Wegeners

2. Perinuclear - pANCA - Churg-Strauss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is a diagnosis of AAV made?

A

Clinical
ANCA
Biopsy
Rapidly progressive GN w/o immune deposits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the treatment of AAVs?

A

High dose glucocorticoids + cyclophosphamide or rituximab

Plasma exchange if presents w RF or pulmonary haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Wegener’s also known as?

A

Granulamatosis w polyangiitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q
  1. What is Wegener’s?

2. what parts of the body does it affect?

A
  1. Autoimmune condition associated w necrotising granulomatous vasculitis
  2. URT + LRT + kidneys
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the clinical features of Wegener’s?

A
  1. URT - epistaxis, sinusitis
  2. LRT - SOB, haemoptysis
  3. Rapidly progressive GN
  4. Saddle shaped nose deformity
  5. Vasculitis and rash, proptosis, CN lesions
21
Q

What are the Ix for Wegener’s?

A

cANCA +ve in 90%, pANCA +ve in >25%
CXR - wide variation including cavitating lesions
Renal biopsy - epithelial crescents

22
Q

What are the features of microscopic polyangiitis?

A

Renal impairment - raised Cr, haematuria and proteinuria
Fever, lethargy, weight loss
Rash: palpable purpura
Cough SOB haemoptysis

23
Q

What is churg-strauss also known as

A

Eosiniphilic granulomatosis w polyangiitis

24
Q

What are the features of churg-strauss

A

asthma
blood eosinophilia
paranasal sinusitis
Mononeuritis multiplex - isolated damage to 2 or more separate nerve areas

25
Q

What are the differences and similarities between wegeners and churg-strauss

A 
W:
- renal failure 
- Epistaxis
- cANCA
CS:
- Asthma
- Eosinophilia
- pANCA
Similarities:
- vasculitis
- sinusitis
- SOB
26
Q

How does myeloma cause renal disease?

A

There is tubular obstruction due to light chain casts

There is deposition of Ig/light chains in glomerulus leading to proteinuria

27
Q

How does myeloma w renal disease present?

A

proteinuria
hypercalcaemia
renal tract infection due to immunosuppression

28
Q

What is the treatment for the renal disease caused by myeloma?

A

adequate hydration
bisphosphonates for hypercalcaemia
anti-myeloma Rx including glucocorticoids

29
Q

How does amyloid cause renal disease?

A

pathological folding of proteins - extracellular accumulation + organ dysfunction including kidney

30
Q

how is amyloid classified?

A

AL amyloid - light chains in myeloma

AA amyloid - serum amyloid A in chronic inflammation

31
Q

How is amyloid diagnosed?

A

Congo red stain gin gon biopsy

SAP scan

32
Q

What are the main features of haemolytic uraemic syndrome (HUS)?

A
  1. AKI
  2. Microangiopathic haemolytic anaemia
  3. Thrombocytopenia
33
Q

How is HUS classified and what are their causeS?

A
  1. Typical HUS (secondary):
    - Shiga toxin producing Escherichia Coli (STEC) 0157:H7
    - Pneumococcal infection
    - HIV
  2. Atypical HUS:
    - Dysregulation/uncontrolled activation of complement
34
Q

Which cause of HUS is mostly seen in children

A

E.Coli shiga toxin producing

35
Q

What is the pathophysiology underlying HUS

A

Glomerular endothelial cells cause damage to rbcs, platelets

As toxins bind to endothelial cells rbc breakdown -> anaemia

36
Q

What are the investigations for HUS?

A 
FBC - anaemia, low platelets
Peripheral blood film - schistocytes 
Stool culture
U+E - AKI
LDH
37
Q

What are the signs and sx of HUS?

A

Bloody diarrhoea
N+V
NO fever
Colitis

38
Q

What is the treatment of HUS?

A

good hydration w IV fluids
Rx renal failure
Atypical - plasma infusion/ exchange, eculizumab

39
Q

How does TTP present?

A
  1. Microangiopathic haemolytic anaemia
  2. Thrombocytopenia
  3. AKI
  4. Neuro sx: headache, palsy, seizure, coma, confusion
  5. Fever
40
Q

What is the pathophysiology behind TTP

A

Congenital deficiency of or acquired abs to ADAMTS13 protease which normally cleaves multimers of vWF
Large vWF multimers lead to platelet aggregation and fibrin deposition in small vessels
Ultimately leads to: MULTI-SYSTEM THROMBOTIC MICROANGIOPATHY

41
Q

What is the treatment of TTP

A

Medical emergency!!
1 plasma infusion/exchange - removes abs/ replaces ADAMTS13
2. CS
3. Rituximab for non-responders or relapse

42
Q

What is atherosclerotic renovascular diseasee?

A

part of systemic atheromatous vascular disease where plaques develop in the main arteries to the kidneys and they can become stenotic

43
Q

How is a diagnosis of atherosclerotic renovascular disease made?

A

> 1.5cm in asymmetry in renal size

CT/MRI angiography

44
Q

How is atherosclerotic renovascular disease treated?

A

control CV risk factors:
ACEi/ARBs
Statins
Aspirin

45
Q

How is scleroderma renal crisis diagnosed

A

accelerated HTN >150/85 plus AKI

Biopsy - shows collapsed glomeruli and onion skin thickening of arterioles

46
Q

What is the treatment of scleroderma renal crises?

A

ACEi/ARBs

IV vasodilators

47
Q

What are the features of sickle cell nephropathy?

A

hyperfiltration (reduced creatinine) and albuminuria

48
Q

What is the treatment of sickle cell nephropathy?

A

ACEi/ARB

transplant

Nephrology (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions