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Path: Histopath Flashcards

1
Q

Triad in nephrotic syndrome

A

oedema
proteinuria (>3g/24h)
hypoalbuminaemia (<30g/L)

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2
Q

What are features seen in nephrotic syndrome aside from the triad?

A

hyperlipidaemia
thrombotic disease

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3
Q

buzzwords for nephrotic syndrome in SBAs

A

swelling (classically periorbital in children)

frothy urine (occurs due to proteinuria)

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4
Q

Primary causes of nephrotic syndrome

A

Minimal change disease
membranous glomerular disease
focal segmental glomerulosclerosis

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5
Q

secondary causes of nephrotic syndrome

A

Diabetes mellitus
Amyloidosis
SLE

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6
Q

Diagnosis of nephrotic syndrome

A

urine dip (proteinuria; no haematuria)
urine PCR (>300 mg/mmol)
serum albumin - low
total cholesterol - high
immunoglobulins - low
renal biopsy - diagnostic investigation of choice in adults (avoided in children)

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7
Q

What is minimal change disease?

A

a cause of nephrotic syndrome
most common cause of nephrotic syndrome in children

no changes are seen on light microscopy; on electron microscopy loss of podocyte foot processes is seen.

responds well to steroids

no immune deposits

associated with eczema and asthma

recent allergic reaction is a possible trigger

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8
Q

How is minimal change disease managed?

A

1st line: steroids (90% respond)

2nd line: cyclosporine (calcineurin inhibitor)

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9
Q

epidemiology of minimal change disease

A

children (75%)

second peak in elderly

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10
Q

histological changes in minimal change disease

A

no changes on light microscopy
loss of podocyte foot processes on EM

no immune complex deposition (immunofluorescence)

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11
Q

Prognosis of minimal change disease

A

good prognosis
5% ESRF

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12
Q

triggers for minimal change disease

A

Often idiopathic

Secondary causes (rare)
- Immune stimulus (e.g., infection, immunization, allergic reaction)
- Tumors (e.g., Hodgkin lymphoma)
- Certain drugs (e.g., NSAIDs)

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13
Q

In what demographic is FSGS most common?

A

most common in afro-caribbean/afro-american/hispanic

Common in adults (30%)

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14
Q

What can be seen on histology in FSGS?

A

LM:
- focal and segmental glomerular consolidation and scarring
- hyalinosis (hyaline deposits)

EM:
- loss of podocyte foot processes

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15
Q

FSGS

A

focal segmental glomerulosclerosis

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16
Q

What part of the nephron can be affected by disease processes?

A
  1. glomeruli
  2. tubules & interstitium
  3. blood vessels
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17
Q

response rate to steroids in FSGS?

A

50%

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18
Q

prognosis of FSGS

A

50% have ESRF in 10 years

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19
Q

Management of FSGS

A
  1. steroids
  2. plus immunosuppressants if needed (e.g. calcineurin inhibitors second line - cyclosporine, tacrolimus)

ACEi or ARB to control BP

-> ESRF if left untreated

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20
Q

Causes of FSGS

A

mostly primary idiopathic

can be secondary to:
- obesity
- HIV
- drugs (lithium, heroin)
- lymphoma

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21
Q

Do you see immune deposits in FSGS?

A

no

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22
Q

What cause of primary nephrotic syndrome has immune deposits?

A

membranous glomerular disease

-> immune complex deposits along entire GBM

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23
Q

membranous glomerular disease - does it respond to steroids?

A

poor response

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24
Q

What histological findings are seen in membranous glomerular disease?

A

LM: diffuse glomerular BM thickening

EM: loss of podocyte foot processes; sub epithelial deposits = ‘spikey’

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25
In what pattern are immune deposits seen in membranous glomerular disease?
immune complex deposits along entire GBM
26
Prognosis if membranous glomerular disease
40% ESRF after 2-20 years
27
Management of membranous glomerular disease
ACEi or ARB to control BP steroids (often poor response) other immunosuppressants e.g. cyclophosphamide in severe disease
28
Causes of membranous glomerular disease
Primary: anti-phospholipase A2 antibodies (present in `75%) Secondary: SLE, infection(HBV, HCV, malaria, syphilis), drugs (NSAIDs, penicillamine, gold), malignancy (lung, prostate)
29
Differentials for asymptomatic haematuria
thin basement membrane disease (benign familial haematuria) IgA nephropathy (Berger's disease) Alport Syndrome (would be seen in children?)
30
Differentials for asymptomatic haematuria
thin basement membrane disease (benign familial haematuria) IgA nephropathy (Berger's disease) Alport Syndrome (would be seen in children?)
31
How can you differentiate thin basement membrane disease and IgA nephropathy?
difficult!!! IgA: more likely to cause frank haematuria; more common in asian population; more likely to cause changes in renal function (raised Cr)
32
what anitbody is seen in myasthenia gravis?
Anti-ACh-receptor antibody
33
What antibodies are seen in pernicious anaemia?
anti-parietal cell antibodies (90%) anti-IF antibodies (intrinsic factor) - (50%)
34
antibodies in limited cutaneous scleroderma?
anti-centromere
35
Histological findings in nephrotic syndrome secondary to diabetes mellitus
diffuse glomerular basement membrane thickening mesangial matrix nodules (aka Kimmelstiel Wilson nodules)
36
When do you see Kimmelstiel Wilson nodules
diabetic kidney disease -> pathognomonic
37
Ddx in diffuse glomerular basement membrane thickening and nephrotic syndrome
membranous glomerular disease diabetic kidney disease in DM KD you also see: kimmelstiel Wilson nodules (mesangial matrix nodules, hyaline deposits)
38
What are Kimmelstiel-Wilson nodules?
seen in Diabetic nephropathy on microscopy of renal tissue mesangial thickening due to nodular, hyaline deposits within the glomerulus.
39
how does diabetic nephropathy first present ?
microalbuminuria
40
demographic for diabetic nephropathy
classically found in asians
41
Histology of nephrotic syndrome caused by amyloidosis
apple green birefringence with Congo-red stain
42
AA vs AL amyloidosis
AA: acute phase protein - associated with chronic inflammation e.g. RA, chronic infections (TB) AL: light chains - most commonly due to multiple myeloma
43
What is the most common presentation of amyloidosis?
nephrotic syndrome (=secondary cause of NS due to amyloid deposits)
44
What is amyloidosis?
a multisystem d/o caused by deposition of misfiled amyloid proteins as amyloid fibrils in tissues this disrupts the normal function of these tissues
45
Features of amyloidosis
Caused by amyloid deposits in different parts of the body Kidneys: nephrotic syndrome Heart: restrictive cardiomyopathy, conduction defects, heart failure, cardiomegaly Liver/spleen: hepato/splenomegaly Macroglossia in 10% neuropathies incl. carpal tunnel syndrome
46
Histopath in amyloidosis
apple green birefringence with Congo red stain under polarised light remember: Amy ate a green apple with her Congo red hair
47
What is ATN?
damage to tubular epithelial cells
48
What is the commonest intrinsic/renal cause of AKI?
ATN
49
Commonest causes of CKD in the UK
1. Diabetes (20%) - glomerulonephritis (15%) - HTN and vascular disease (15%) - reflux nephropathy (chronic pyelonephritis) (10%) - Polycystic kidney disease (9%)
50
What part of the nephron is affected in ATN?
tubules icshemic: The straight segment of the proximal tubule and the straight segment of the distal tubule (i.e., the thick ascending limb) are particularly susceptible to ischemic damage toxic: The convoluted segment of the proximal tubule is particularly susceptible to damage from toxins.
51
What are the causes of ATN?
ishaemia toxins
52
Pathophysiology of ATN
damage to tubular cells → necrotic proximal tubular cells (casts) fall into the tubular lumen → debris obstructs tubules → reduced flow and increased haemodynamic pressure in nephron → reduced pressure gradient across BM → decreased GFR and acute renal failure tubular glomerular feedback reduces the BS to kidneys further.
53
Which nephrotoxins can cause ATN?
NSAIDs aminoglycosides cisplatin radiographic contrast agents myoglobin (secondary to rhabdomyolysis) haemoglobinuria amphotericin lead ethylene glycol
54
Blood findings in ATN?
azotemia hyperkalemia metabolic acidosis
55
urine sodium in ATN?
high >40 mmol/L
56
urine osmolality in ATN
<350 mOsm/kg
57
What is the most common type of amyloidosis?
primary (AL) amyloidosis
58
What are the different types of amyloidosis?
- primary (AL) - secondary (AA) - haemodialysis associated (Abeta2M) - familial amyloidosis
59
What organs can be affected by amyloidosis most commonly and what is the result?
- Kidneys (nephrotic syndrome is the commonest presentation) - heart (restrictive cardiomyopathy, conductive defects, heart failure, cardiomegaly) - liver/spleen (hepato/splenomegaly) - tongue (macroglossia in 10%) - neuropathies (incl. carpal tunnel syndrome) -> remember 5 Kidneys are most commonly affected (nephrotic syndrome), amyloidosis is a restrictive (CM) disease, due to the plaques it is hard to conduct and the heart fails and becomes big, the car goes through tunnels and people with amyloidosis have to talk about it a lot so they get a big tongue.
60
How do you manage amyloidosis?
chemotherapy with melphalan and corticosteroids also depends on the type and is managed by specialists
61
What is the pathological hallmark of sarcoidosis?
granulomas (non-caseating)
62
How can sarcoidosis affect the heart?
It can affect the... - epicardium -> pericarditis - myocardium -> heart failure - endocardium -> valvular lesions can cause dysrhythmias, conduction defects
63
What is the underlying pathology in amyloidosis?
it is a multisystem disorder caused by extracellular aggregation and deposition of amyloid in various organs. these are misfolded proteins.
64
name 2 types of amyloid proteins seen in amyloidosis
beta pleated sheet structure resistant to enzyme degradation
65
What is amyloid?
insoluble protein/protein fragments
66
localised vs systemic amyloidosis
localised affects a single organ
67
What is the commonest form of amyloidosis?
light chain (AL) amyloidosis
68
What is deposited in AL amyloidosis?
Ig light chains most associated with MM, but some may not have MM
69
What are bence jones proteins and when are they seen>
seen in MM / AL amyloidosis / Waldenstroem's macroglobulinaemia monoclonal Ig light chain found in the urine
70
What causes AA amyloidosis?
buildup of serum amuloid A (acute phase protein) -> therefore this form of amyloidosis is seen in chronic infections/inflammation
71
What diseases is AA amyloidosis associated with/
AA - secondary Amyloidosis associated with chronic inflammation/infection and deposit of A-SAA (acute phase serum amyloid A) AID - RA, ankylosing spondylitis, IBD infections - TB, osteomyelitis, IVDU (skin infections) Non-immune - renal cell carcinoma, Hodgkin's
72
Pathophysiology of haemodialysis associated amyloidosis
in haemodialysis you get accumulation of beta 2 microglobulin (becuase it cannot cross the dialysis membrane) usually occurs in someone with longstanding CRF, esp if on peritoneal dialysis associated with articular depositions and carpal tunnel syndrome
73
Familial amyloidosis
ATTR mutated transthyretin deposition (it is a protein made in the liver) in the MedEd guide they mention something about AR (FMF) being the commonest one.
74
how do you diagnose amyloidosis?
tissue biopsy -> congo red stain under polarised light should show apple green birefringence.
75
Management of FMF
colchicine (inhibits granulocyte function; prevents acute episodes and progression to AA amyloidosis)
76
What vessles are in the portal triad?
hepatic portal vein hepatic artery bile duct
77
Which liver enzyme may be raised post MI?
aspartate aminotransferase (AST)
78
Name of criteria for dx of infective endocarditis
modified Duke criteria
79
Troisier sign
palpable LN in the L supraclavicular fossa
80
palpable LN in the L supraclavicular fossa - name of this sign
Troisier

Year 5 😊✌🏼 (53 decks)

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