Brainscape's Knowledge GenomeTM

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


See full index

Year 3 OSCE > Case 23- Glomerulonephritis > Flashcards

Case 23- Glomerulonephritis Flashcards

1
Q

Normal urine output

A

<0.5ml/kg/hour

NB- less than this for 6-12 hours is an AKI

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

NSAIDS and ACE-I

A

Can both cause an AKI
ACE-I dilate the efferent arterioles
NSAIDS block prostaglandins causing construction of the afferent arteriole

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

Complications of an AKI

A

Fluid overload
Metabolic acidosis
Hyponatraemia
Hyperkalaemia
Hyperuraemia
Hypocalcaemia
Hyperphosphataemia

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

Nephrotic syndrome

A

Podocyte damage- protein leaking out

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

Features of nephrotic syndrome

A

Proteinuria- urine is frothy
Oedema- starts as periorbital and then develops into pitting
Hypoalbuminaemia
Hyperlipidaemia- hypoalbuminaemia causes liver to increase protein production to compensate and this causes lipid production to increase
Hypercoaguable state due to urinary loss of antithrombin 3
Increased risk of infection- immunoglobulin loss

HHH PIO- hypercoaguable, hypoalbuminaemia, hyperlipidaemia, proteinuria, infection, oedema

NB- can rarely get protein casts also, and reduced T4

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

Causes of nephrotic syndrome

A

Minimal change disease
FSG
Membranous nephropathy
Membranoprolifertiave glomerulonephritis
Secondary causes- SLE, Hep B, Hep C, HIV, DM (nephropathy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Management of nephrotic syndrome

A

Input from renal team
Low sodium and low protein diet
Fluid restriction- 1-1.5L/ hour
Loop diuretic
ACE/ ARB to reduce proteinuria (controversial as ACE can damage the kidney)
VTE prophylaxis
Statins for hypercholesterolaemia
Renal biopsy

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

Nephritic syndrome

A

Inflammation causes breakdown that allows RBC/ WCC/ protein to leak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Features of nephritic syndrome

A

Haematuria- intermittent gross haematuria (cola coloured urine)
Hypertension- low EGFR causes fluid retention
Oliguria- low EGFR
Uraemia- anorexia, n and v, pruritis, pericarditis, CNS abnormalities (confusion)
RBC casts- acanthocytes (dystrophic RBC)
Sterile puris
Mild proteinuria
Mild to moderate oedema

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

Causes of nephritic syndrome

A

IgA nephropathy
Post strep glomerulonephritis
GOODPASTURES (GBM)
Membranoprolifertiave glomerulonephritis (also nephrotic)
HSP- henloch-schenlein purpura

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

Management of nephritic syndrome

A

Input from renal team
Low sodium diet and water restriction
ACE ARB for proteinuria/ HTN
May need immunosuppressive theory (depends on cause)
If severe may need RRT

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

Glomerulonephritis

A

Renal disease characterised by inflammation and damage of the glomeruli- allows protein and or blood to leak into the urine. Immune response causes glomerular injury

May present with;
Isolated haematuria and or proteinuria
Nephrotic syndrome
Nephritic syndrome
AKI
CKD

Non proliferative causes- nephrotic syndrome
Proliferative causes- nephritic syndrome

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

Non proliferative glomerulonephritis

A

Lack of proliferation of cells in the glomeruli

Typically causes nephrotic syndrome

Minimal change glomerulonephritis
Focal segmental glomerulosclerosis
Membranous glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Proliferative glomerulonephritis

A

Increased cells in the glomerulus

Usually presents with nephritic syndrome. Dangerous- can progress to ESRD over weeks to years

IgA nephropathy
Post infectious glomerulonephritis
Membranous glomerulonephritis- BOTH
Rapidly progressive glomerulonephritis
GOODPASTURES
Vasculitic disorders eg. Wegeners granulomatosis/ microscopic polyangitis

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

Minimal change glomerulonephritis

A

Presents as nephrotic syndrome
Often children affected
Supportive care and steroids (cyclophosphamide if non-responsive to steroids)

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

Focal segmental glomerulosclerosis (FSGS)

A

Nephrotic syndrome and CKD
Causes- idiopathic, renal pathology eg. IgA, HIV, heroin, Alport, sickle cell

Biopsy- sclerosis and hyalinosis, effacement of foot processes

Salt restriction and diuretics
Statins
Transplant required (High recurrence rate in renal transplant);

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

Membranous glomerulonephritis

A

Nephrotic syndrome
Slowly progressive
30-50 years commonly affected
Idiopathic but can be associated with Hep B/ malaria/ SLE/ malignancy/ drugs eg. NSAID

Histology;
-basement membrane thickening
-subepithelial spikes on silver stain
-PLA2

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

IgA nephropathy

A

Most common type in adults
Also called BERGERS disease
Presents as nephritic syndrome- macroscopic haematuria
Often appears 24-48 hours after an URTI
Can be benign or lead to ESRD

Renal biopsy
Immunochemistry +ve for IgA deposits in the matrix and glomerular mesangial proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Post infectious/ Post streptocccal glomerulonephritis

A

Nephritic syndrome
Can occur after any infection (but tends to be strep pyogenes)
Typically presents 2 weeks after the URTI (not like 2 days- IgA nephropathy), or 3-6 weeks after a skin infection

Bloods- low complement (C3), raised ASO
Biopsy- subepithelial humps, starry sky (granular) appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Membranoprolifertiave glomerulonephritis

A

Nephrotic syndrome
IgG and complement deposits on the basement membrane
Majority idiopathic
Can be secondary to malignancy rheumatoid disorders (SLE) and drugs (NSAIDS)
Renal biopsy- tram track appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Rapidly progressive glomerulonephritis

A

Also known as crescenteric glomerulonephritis
Poor prognosis

Any type of GN can progress to this, but some may only ever present as this
Typically after GOODPASTURES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

GOODPASTURES syndrome (Anti GBM Disease)

A

Anti GBM antibodies- attack the glomeruli and the alveoli
Present with renal failure (nephritic syndrome) and haemoptysis
Can have rapid progression to ESRD

Anti GBM antibodies and IgG deposited in the basement membrane of the glomerulus
Raised transfer factor due to pulmonary haemorrhage

IV steroids
Plasmapheresis
Can’t reverse kidney damage caused

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Wegeners granulomatosis

A

Affects lungs, kidneys and other organs
Caused by cANCA (test for this)

IV steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Microscopic polyangitis

A

Renal- glomerulonephritis
Systemic- Fever, lethargy, myalgia, weight loss, rash (palpable purpura)
Resp- cough, dyspnoea, haemoptysis
Mononeuritis multiplex

PANCA (test for this)

Steroids
Plasmapheresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

General investigations for glomerulonephritis

A

Urine dipstick and microscopy (MSU)- hameaturia, proteinuria, dysmoephic RBC, leukocytes, RBC casts
24 hour urinary collection, urinary ACR
UE (renal failure or normal), LFT (deranged if related to hepatitis), FBC (anaemia), lipid profile (hypercholesterolaemia)
Specialist- RENAL BIOPSY (required to elucidate cause in nephrotic/nephritic syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

General management of GN

A

Treat underlying cause
Restrict dietary salt and water
Immunosuppression (steroids)
Blood pressure control (ACE or ARB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Sx of ADPKD

A

Chronic renal failure, abdominal and flank pain (cyst rupture, UTI, stone), recurrent UTI, renal stones, palpable kidneys, extra renal manifestations;

Cerebral aneurysms
Hepatic (most common), splenic, pancreatic, prostatic cysts
Cardiac valve disease (MR)
Colonic diverticulum
Aortic root dilation
LVH
Arterial HTN (morning headaches)

NB- but, cerebral events are more liekly to occur than liver ones ie. SAH more common than l;iver failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Investigations for ADPKD

A

Urine dipstick
Bloods- FBC UE fasting lipid profile (raised)
Renal USS (scan of choice), MRI scan head (aneurysm), abdomen and pelvis (other cysts)
Genetic testing- chromosomal involvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Management of ADPKD

A

Manage complications- ace, ABX for infections, dilaysis in ESRD, cysts drainage, avoid NSAID
Tolvaptan (vasopressin receptor antagonist)- slows progression of the cysts
Other steps- genetic counselling, avoid contact sports, avoid NSAIDS and anticoagulants, regular BP and ultrasounds and UE
Genetic testing for immediate family members
Renal transplant- only curative option

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Henoch schoenlein purpura

A

IgA vasculitis (NOT AN IGA NEPHROPATHY- bergers disease, no rash in latter as it affects kidneys, not all the blood vessels) commonly presenting with a purpuric rash affecting the lower limbs or buttocks in children

Often triggered by an URTI (tonsillitis) or a gastroenteritis

Purpura, joint pain, abdominal pain, renal involvement (affects kidneys 50% of the time- IgA nephropathy)

No thrombocytopenia

NB- exclude other pathology and assess for organ damage;
-FBC, UE, albumin (nephrotic), CRP, ESR
-Blood cultures (rash), urine dipstick, urinary albumin:creatinine, BP etc.

31
Q

Glomerulonephritis

A

Conditions that cause inflammation of or around the glomerulus. A cause of intrinsic AKI

32
Q

Small vessel vasculitides

A

HSP
Eosinophilic granulomatosis with polyangitis (CS)
Microscopic polyangitis
Granulomatosis with polyangitis (wegeners)

33
Q

Medium vessel vasculitides

A

Poly arteritis nodosa
Eosinophilic granulomatosis with polyangitis (CS)
Kawasaki

34
Q

Large vessel vasculitides

A

GCA
Takayasu

35
Q

Non specific features of vasculitides

A

Fatigue
Fever
Weight loss
Anorexia
Anaemia
Arthralgia

36
Q

Vasculitides investigations

A

MSU dipstick and microscopy and analysis, OBS (BP in each arm), BM
Bloods- FBC UE LFT TFT CRP ESR blood viscosity (inflammation) ANA ANCA HBA1c glucose
Imaging- CT angiography, biopsy of affected vessel, CXR (lung manifestations) and XRay of affected joints

37
Q

Other potential features of vasculitides

A

Purpura
Joint and muscle pain
Peripheral neuropathy
Renal impairment
GI disturbance
Anterior uveitis and scleritis
HTN

38
Q

pANCA

A

Microscopic polyangitis
CS (eosinophilic granulomatosis with polyangitis)

39
Q

cANCA

A

Wegners (granulomatosis with polyangitis)

40
Q

Eosinophilic granulomatosis with polyangitis (CS)

A

Paranasal sinusitis
Mononeuritis multiplex ;wrist drop, foot drop etc.)
Presents with severe asthma
Elevated Eosinophils
Joint pain

NB- LTRA may precipitate the disease

41
Q

Microscopic polyangitis

A

Renal failure
Also affects lungs- SOB and haemopytiss

42
Q

Granulomatosis with polyangitis (Wegner)

A

URT- Nosebleeds, crusty secretions, hearing loss, sinusitis, saddle shaped septum
LRT- Cough wheeze and haemoptysis with consolidation on CXR
Renal- Rapidly progressing glomerulonephritis (pauci immune)
Other- Proptosis, cranial nerve lesions etc.

43
Q

Poly arteritis nodosa

A

Associated with Hep B C and HIV
Renal impairment, stroke, MI, skin etc.
libido reticularis

44
Q

Takayasu

A

Aorta and it’s branches (and pulmonary arteries)
Aneurysms and pulselessness
Arm claudication or syncope

45
Q

Kawasaki

A

Young children under 5

46
Q

Renal failure and haemoptysis

A

GOODPASTURES syndrome (anti-GBM disease)
Granulomatosis with polyangitis (Wegner)
(Microscopic polyangitis)- less so.

47
Q

Difference between GOODPASTURES and Wegners

A

Saddle shaped nose, pANCA, no anti GBM

48
Q

Interstitial nephritis

A

Inflammation of the space in the kidneys between the cells and the tubules (the interstitium)

NB- glomerulonephritis is where there is inflammation around the glomerulus

2 types- AIN & chronic tubulointerstitial nephritis

49
Q

Acute interstitial nephritis

A

Presents with AKI, HTN, and generalised hypersensitivity reaction eg. Rash, fever, eosinophilia

Caused by a hypersensitivity reaction to drugs (NSAID, antibiotics) or an infection

50
Q

Chronic tubulointerstitial nephritis

A

Chronic inflammation of the interstitium- presents with CKD

Underlying cause- autoimmune, infectious, iatrogenic, granulomatous disease

51
Q

ATN

A

Most common cause of AKI
Reversible in early stages

52
Q

Cause of ATN

A

Ischaemia- shock, sepsis

Nephrotoxins- aminoglycosides (streptomycin, gentamicin), myoglobin (secondary to rhabdomyolysis), lead, contrast dye

53
Q

Features of ATN

A

AKI features- raised urea, creatinine, potassium

NB- muddy brown casts in the urine

54
Q

Phases of ATN

A

Oliguric
Polyuric
Recovery

55
Q

Histology features

A

Loss of nuclei and detachment of tubular cells from the basement membrane
Dilated tubules
Necrotic cells obstruct the tubule lumen

56
Q

Causes of AIN

A

Drugs eg. Penicillin, rifampicin, NSAID, allopurinol, furosemide
Systemic disease eg. SLE, sarcoidosis, Sjogrens
Infection

57
Q

AIN investigations

A

Sterile pyuria
White cell casts

58
Q

Drugs that can worsen renal function in AKI and must be stopped

A

NSAID
Aminoglycosides (gentamicin, streptomycin)
ACE and ARB
Diuretics

(DAMN- diuretic, ACE-I/ARB, aMinoglycoside, NSAID (except 75mg aspirin))

59
Q

Drugs that may have to be stopped in AKI as increased risk of toxicity (but doesn’t usually worsen AKI itself)

A

Metformin
Lithium
Digoxin

60
Q

ADPKD Aneurysm screening

A

Offered to people with ADPKD and a family history of brain ameurysm

If no or only small aneurysms are found, you’ll be offered further scans at intervals of 1 to 5 years to check for new haemorrhages or an increase in the size of an existing one.

61
Q

Management of HSP

A

Analgesia
Supportive management for nephropathy

No indication for steroids or immunosuppressants

62
Q

Management of IgA nephropathy

A

Minimal proteinuria- no treatment
Elevated proteinuria and slightly reduced eGFR- ACE-I
Active disease (falling eGFR/ no response to ACE)- immunosuppression with steroids

63
Q

Management of membranous glomerulonephritis

A

ACE or ARB
Immunosuppression if not responding eg. Corticosteroid with cyclophosphamide

64
Q

Minimal change disease

A

Nephrotic syndrome
Idiopathic (small amount of cases- NSAID, malignancy, infectious mononucleosis)
Management- steroids (cyclophosphamide if steroids don’t work)

Biopsy- fusion of podocytes and effacement of foot processes

65
Q

Nephrotic syndrome and thyroid function

A

Low total but not free thyroxine levels

66
Q

Complications of nephrotic syndrome

A

VTE
Hyperlipidaemia
CKD
Infection risk
Hypocalcaemia

67
Q

Nephrotoxicity and contrast media

A

Rise of creatinine 25% 3 days post procedure
Use saline 12 hours pre and post procedure to avoid in high risk patients (or sodium bicarbonate)
If high risk and on metformin, withhold for 48 hours until renal function is normal

68
Q

Complications of peritoneal dialysis

A

Peritonitis (S. epidermidis, then S. aureus)- Vancomycin & ceftazidime (or gentamicin)
Peritoneal sclerosis

69
Q

Causes of renal papillary necrosis

A

Pyelonephritis
Diabetic nephropathy
Obstructive nephropathy
Analgesic nephropathy (NSAID)
Sickle cell anaemia

70
Q

Management of vasculitis

A

Refer to rheumatologist
Steroids eg, oral Prednisolone and immunosuppression (cyclophosphamide) to stop flare up
Continued immunosuppression eg methotrexate

71
Q

LTRA (monteleukast) and EGPA

A

Worsen asthma symptoms in EGPA

72
Q

What to do after an abnormal ACR reading

A

Repeat with a first pass morning urine specimen

73
Q

What is the most important infection to monitor for following solid organ transplant?

A

CMV- treat with Ganciclovir

Year 3 OSCE (61 decks)

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