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Year 5 😊✌🏼 > Path: Histopath > Flashcards

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
Q

In what pattern are immune deposits seen in membranous glomerular disease?

A

immune complex deposits along entire GBM

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26
Q

Prognosis if membranous glomerular disease

A

40% ESRF after 2-20 years

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27
Q

Management of membranous glomerular disease

A

ACEi or ARB to control BP

steroids (often poor response)

other immunosuppressants e.g. cyclophosphamide in severe disease

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28
Q

Causes of membranous glomerular disease

A

Primary: anti-phospholipase A2 antibodies (present in `75%)

Secondary: SLE, infection(HBV, HCV, malaria, syphilis), drugs (NSAIDs, penicillamine, gold), malignancy (lung, prostate)

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29
Q

Differentials for asymptomatic haematuria

A

thin basement membrane disease (benign familial haematuria)

IgA nephropathy (Berger’s disease)

Alport Syndrome (would be seen in children?)

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30
Q

Differentials for asymptomatic haematuria

A

thin basement membrane disease (benign familial haematuria)

IgA nephropathy (Berger’s disease)

Alport Syndrome (would be seen in children?)

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31
Q

How can you differentiate thin basement membrane disease and IgA nephropathy?

A

difficult!!!

IgA: more likely to cause frank haematuria; more common in asian population; more likely to cause changes in renal function (raised Cr)

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32
Q

what anitbody is seen in myasthenia gravis?

A

Anti-ACh-receptor antibody

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33
Q

What antibodies are seen in pernicious anaemia?

A

anti-parietal cell antibodies (90%)
anti-IF antibodies (intrinsic factor) - (50%)

34
Q

antibodies in limited cutaneous scleroderma?

A

anti-centromere

35
Q

Histological findings in nephrotic syndrome secondary to diabetes mellitus

A

diffuse glomerular basement membrane thickening

mesangial matrix nodules (aka Kimmelstiel Wilson nodules)

36
Q

When do you see Kimmelstiel Wilson nodules

A

diabetic kidney disease

-> pathognomonic

37
Q

Ddx in diffuse glomerular basement membrane thickening and nephrotic syndrome

A

membranous glomerular disease
diabetic kidney disease

in DM KD you also see: kimmelstiel Wilson nodules (mesangial matrix nodules, hyaline deposits)

38
Q

What are Kimmelstiel-Wilson nodules?

A

seen in Diabetic nephropathy on microscopy of renal tissue

mesangial thickening due to nodular, hyaline deposits within the glomerulus.

39
Q

how does diabetic nephropathy first present ?

A

microalbuminuria

40
Q

demographic for diabetic nephropathy

A

classically found in asians

41
Q

Histology of nephrotic syndrome caused by amyloidosis

A

apple green birefringence with Congo-red stain

42
Q

AA vs AL amyloidosis

A

AA: acute phase protein - associated with chronic inflammation e.g. RA, chronic infections (TB)

AL: light chains - most commonly due to multiple myeloma

43
Q

What is the most common presentation of amyloidosis?

A

nephrotic syndrome

(=secondary cause of NS due to amyloid deposits)

44
Q

What is amyloidosis?

A

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
Q

Features of amyloidosis

A

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
Q

Histopath in amyloidosis

A

apple green birefringence with Congo red stain under polarised light

remember: Amy ate a green apple with her Congo red hair

47
Q

What is ATN?

A

damage to tubular epithelial cells

48
Q

What is the commonest intrinsic/renal cause of AKI?

A

ATN

49
Q

Commonest causes of CKD in the UK

A
  1. Diabetes (20%)
  • glomerulonephritis (15%)
  • HTN and vascular disease (15%)
  • reflux nephropathy (chronic pyelonephritis) (10%)
  • Polycystic kidney disease (9%)
50
Q

What part of the nephron is affected in ATN?

A

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
Q

What are the causes of ATN?

A

ishaemia

toxins

52
Q

Pathophysiology of ATN

A

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
Q

Which nephrotoxins can cause ATN?

A

NSAIDs
aminoglycosides
cisplatin
radiographic contrast agents
myoglobin (secondary to rhabdomyolysis)
haemoglobinuria
amphotericin

lead
ethylene glycol

54
Q

Blood findings in ATN?

A

azotemia
hyperkalemia
metabolic acidosis

55
Q

urine sodium in ATN?

A

high

> 40 mmol/L

56
Q

urine osmolality in ATN

A

<350 mOsm/kg

57
Q

What is the most common type of amyloidosis?

A

primary (AL) amyloidosis

58
Q

What are the different types of amyloidosis?

A
  • primary (AL)
  • secondary (AA)
  • haemodialysis associated (Abeta2M)
  • familial amyloidosis
59
Q

What organs can be affected by amyloidosis most commonly and what is the result?

A
  • 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
Q

How do you manage amyloidosis?

A

chemotherapy with melphalan and corticosteroids

also depends on the type and is managed by specialists

61
Q

What is the pathological hallmark of sarcoidosis?

A

granulomas (non-caseating)

62
Q

How can sarcoidosis affect the heart?

A

It can affect the…
- epicardium -> pericarditis
- myocardium -> heart failure
- endocardium -> valvular lesions

can cause dysrhythmias, conduction defects

63
Q

What is the underlying pathology in amyloidosis?

A

it is a multisystem disorder caused by extracellular aggregation and deposition of amyloid in various organs.

these are misfolded proteins.

64
Q

name 2 types of amyloid proteins seen in amyloidosis

A

beta pleated sheet structure
resistant to enzyme degradation

65
Q

What is amyloid?

A

insoluble protein/protein fragments

66
Q

localised vs systemic amyloidosis

A

localised affects a single organ

67
Q

What is the commonest form of amyloidosis?

A

light chain (AL) amyloidosis

68
Q

What is deposited in AL amyloidosis?

A

Ig light chains

most associated with MM, but some may not have MM

69
Q

What are bence jones proteins and when are they seen>

A

seen in MM / AL amyloidosis / Waldenstroem’s macroglobulinaemia

monoclonal Ig light chain found in the urine

70
Q

What causes AA amyloidosis?

A

buildup of serum amuloid A (acute phase protein)

-> therefore this form of amyloidosis is seen in chronic infections/inflammation

71
Q

What diseases is AA amyloidosis associated with/

A

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
Q

Pathophysiology of haemodialysis associated amyloidosis

A

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
Q

Familial amyloidosis

A

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
Q

how do you diagnose amyloidosis?

A

tissue biopsy -> congo red stain under polarised light should show apple green birefringence.

75
Q

Management of FMF

A

colchicine (inhibits granulocyte function; prevents acute episodes and progression to AA amyloidosis)

76
Q

What vessles are in the portal triad?

A

hepatic portal vein
hepatic artery
bile duct

77
Q

Which liver enzyme may be raised post MI?

A

aspartate aminotransferase (AST)

78
Q

Name of criteria for dx of infective endocarditis

A

modified Duke criteria

79
Q

Troisier sign

A

palpable LN in the L supraclavicular fossa

80
Q

palpable LN in the L supraclavicular fossa - name of this sign

A

Troisier

Year 5 😊✌🏼 (53 decks)

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