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Y5 Histopathology > CTD, Vasculitides, Sarcoidosis + Amyloidosis > Flashcards

CTD, Vasculitides, Sarcoidosis + Amyloidosis Flashcards

1
Q

What kind of disorder is SLE (Systemic Lupus Erythematosus)?

A

Systemic Autoimmune Connective Tissue Disease

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2
Q

Which gene is associated with SLE?

A

HLA DR3

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3
Q

What type of hypersensitivity reaction is seen in SLE?

A

Type 3

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4
Q

What is/are the aetiologies of SLE?

A

Probably an unknown environmental trigger on someone with genetic susceptibility (e.g HLA DR3)

Can also be drug-Induced (e.g. Hydralazine)

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5
Q

Which 5 drugs are most commonly associated with inducing SLE?

A

Procainamide, Hydralazine, Phenytoin, Isoniazid, Quinidine

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6
Q

Who stereotypically presents with SLE?

What is the common presenting history?

A

Young AfroC. women

Malaise, anorexia, weight loss, PUO (pyrexia of unknown origin)

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7
Q

Which type of autoantibody is seen in 95% of SLE cases?
What 2 subtypes of this autoantibody are most associated with (non drug induced) SLE?
Which is the most specific for SLE?

A

ANA (Anti-nuclear antibody)
Anti-ds DNA - most specific subtype
Anti-Smith

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8
Q

Which autoantibody subtype is associated with drug induced SLE?

A

Anti-histone

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9
Q

What is an LE cell? Can a histological finding of these be used to diagnose SLE?

A

Neutrophil or macrophage that has phagocytosed the denatured nuclear material of another cell.
No longer used for dx - only in 50=75% of SLE cases, and seen in many other CTDs

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10
Q

Histologically, what is seen on an SLE skin biopsy?

A

Lymphocyte infiltration in upper dermis, vacuolization of the basal layer of epidermis, RBCs extravated into the upper dermis

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11
Q

What would IF staining of a histological section of skin, from an SLE patient, show?

A

IgG antibody deposits in the epidermal basement membrane and within the nuclei of the epidermal cells
Anti ds DNA and Anti histone = homogenous staining pattern
Anti Sm = speckled coarse staining pattern

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12
Q

What are the characteristic lesions seen on the spleen of an SLE patient?

A

Onion skin lesions

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13
Q

What is the most common cardiac presentation of SLE? What would a biopsy of the cardiac tissue show?

A

Libman-Sack non infective endocarditis - vegetation on the valves
Strands of fibrin, neutrophils, lymphs and histiocytes

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14
Q

What are the ACR criteria for defining SLE? How many of the criteria have to be present in order to make a diagnosis of SLE? (NB I think this is only used for dx in clinical trials)

A 
Need 4/11 of ACR criteria (SOAP BRAIN MD): 
Serositis - pleurisy or pericarditis
Oral Ulcers
Arthritis - non errosive
Photosensitivity
Blood disorders (AIHA, ITP, leucopenia)
Renal involvement
ANA +ve
Immune Phenomena (dsDNA, anti-Sm, Antiphopholipid)
Neuro symptoms
Malar rash 
Discoid Rash
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15
Q

If a patient with SLE has a history of recurrent miscarriages and thrombosis, which autoantibody are they likely to have (subtype)?

A

Anti-phospholipid antibody

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16
Q

What neurological symptoms can be seen in SLE?

What renal disorder is most commonly seen?

A

Seizures and Psychosis

Nephrosis (proteinuria, hypoalbuminaemia, oedema) - specifically Membranous Glomerular disease

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17
Q

A patient with SLE has an increased incidence of getting other AI disorders. Which AID is it particularly associated with? What subtypes of ANA are seen in this disease?

A

Sjorgen’s syndrome
Anti-Ro
Anti-La

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18
Q

What are the 2 types of scleroderma?

A 
Limited Sceleroderma (CREST)
Diffuse Sceleroderma
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19
Q

Limited scleroderma used to be called CREST, which is helpfully a mneumonic of the symptoms seen in the disease. What does is stand for?

A

Calcinosis, Raynaud’s, Esophogeal dysmotility, Sclerodactyly, Telengiectasia

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20
Q

What autoantibody is seen in Limited Scleroderma/CREST?

A

Anti-centromere

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21
Q

What are the histological presentations of Limited SclerodermaCREST?

A

Increased collagen in skin anad organs
Onion skin
Intimal thickening of the arterioles

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22
Q

What is Morphea?

A

An area of localised skin fibrosis and excess collagen

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23
Q

What genes are associated with Scleroderma?

A

HLA DR5

Drw8

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24
Q

Which subtype of scleroderma is associated with pulmonary fibrosis? and which with pulmonary hypertension?

A 
Diffuse = fibrosis 
Limited = hypertension
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25
Q

Where are the skin changes in limited scleroderma?

A

Face and distal to elbow and knees

If there are trunkal skin presentations, it has to be diffuse scleroderma!

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26
Q

Where do the skin changes in diffuse scleroderma present? Where else can it present?

A

Skin changes can occur anywhere

Will also involve one or more internal organs, commonly the kidneys, oesophagus, lungs and heart

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27
Q

Which autoantibody is most commonly seen in Diffuse scleroderma?
What staining pattern, seen under IF, is associated with this autoantibody?

A

Anti Scl-70 (Anti Topoisomerase-1)

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28
Q

What is the gold standard test for diagnosing scleroderma?

A

There isn’t one! It is predominantly a diagnosis of exclusion, but is defined as:
Symmetrical skin thickening with Raynauds phenomenon (70% of cases), nail fold capillary dilatation and ANAs (mainly Anti Scl-70 and Anti-centromere)

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29
Q

What is Polymyositis? and Dermatomyositis?

A

Polymyositis in an AI inflammatory disorder of muscle
DM is an AI inflammatory disorder of the muscle and skin

Both are commonly associated with underlying malignancy (if >50 years old at presentation)

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30
Q

Which Autoantibody (subtype) is seen in:

a) Polymyositis
b) Dermatomyositis?

What type of autoantibodies are these?

A

a) Anti Jo-1 (Anti-tRNA synthetase)
b) Anti Mi-2 (Anti Jo-1 is also seen in DM but not as common)

ANA

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31
Q

What are the main 2 cutaneous features of Dermatomyositis?

What is a nail sign often seen in DM?

A

Heliotrope (‘lilac’) rash - violacious eruption on upper eyelids
Gottron papules - discrete rythematous papules on MCc and IP joint
Nail sign: Periungal telengiectasia

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32
Q

What is the main overlapping symptom seen in Polymyositis and Dermatomyositis?

A

Symmetrical proximal muscle weakness (pain may or may not be present, but in Juvenile DM it is normally very painful)

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33
Q

What investigations are used to diagnose Dermatomyositis?

Which of these investigations is truly diagnostic?

A

Muscle biopsy, skin biopsy, EMG, bloods

Muscle biopsy is truly diagnostic

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34
Q

On the muscle biopsy, what are the 2 classical histological findings of DM?

A
  1. A mixed B- and T-cell perivascular inflammatory infiltrate
  2. Perifascicular muscle fiber atrophy

‘Drop out’ of capillaries and myofibre damage?

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35
Q

What are the histological signs of DM on the skin biopsy?

A

Perivascular inflammation, hyperkeratosis in the stratum corneum, epidermal atrophy, follicular plugging, and interface dermatitis

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36
Q

How is Polymyositis diagnosed?

A

4 fold: History and physical examination, elevated CK, abnormal EMG, positive muscle biopsy

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37
Q

What are the hallmark clinical features of Polymyositis?

A

Main presentation is Proximal muscle weakness. Dysphagia and muscle pain also common.
25% of patients will also experience cardiac and pulmonary symptoms.

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38
Q

What does sclerosis mean?

A

Hardening of a body tissue

Scleroderma therefore literally means hard skin

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39
Q

What is the most common systemic manifestation of DM and PM?

A

Interstitial lung disease (pulmonary fibrosis) and Cardiac disease (HF, conduction abnormalities)

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40
Q

What are the 3 ways used to classify Vasculitides?

A

Clinical Setting
Histopathological pattern
Vessel size (what we use from now on)

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41
Q

Name 2 large vessel vasculitides?

A

Takayasu’s Arteritis

Temporal Arteritis

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42
Q

What is Takayasu’s arteritis often called, due to its clinical presentation?
What 2 other vascular symptoms are often seen?

A

Pulseless disease

Vascular symptoms: absent pulse + bruits, claudication

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43
Q

Who stereotypically presents with Takayasu’s arteritis?

A

Japanese women

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44
Q

What are the main symptoms of Temporal Arteritis?
With this clinical presentation, what sign (seen on blood test) would further solidify your diagnosis of TA?
What would you do next?

A

Symptoms: Scalp tenderness, temporal headache, pain on chewing/talking (jaw claudication), blurred vision
Sign: high ESR
Mgmt: Urgent biopsy!

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45
Q

What Ix is needed to give a definitive diagnosis of Temporal Arteritis (Gold Standard)?
What would a positive result show?

A

Temporal artery biopsy

Granulomatous transmural inflammation, giant cells and skip lesions

46
Q

What is another name for Temporal arteritis?

A

Giant Cell Arteritis
TA and GCA are now used interchangeably, though technically Temporal arteritis is GCA of the temporal artery (this is also called Horton’s disease)

47
Q

Who stereotypically presents with TA?

Half of all cases of Temporal arteritis coexist with what other disease?

A

Elderly (>55yo), more often women

Polymyalgia Rheumatica

48
Q

What is the treatment for Temporal Arteritis?

A

High dose steroids

49
Q

Name 3 medium vessel vasculitides?

A

Polyarteritis nodosa (PAN)
Kawasaki’s Disease
Buerger’s Disease (Thrombangitis obliterans)

50
Q

Which 3 organs are most commonly affected in Polyarteritis Nodosa? How do each of these present?
Which organ is spared?

A

80% renal - haematuria , HTN
70% cardiac - HF, MI, pericarditis
50% GI (mesenteric arteries) - abdo pain

Lungs are spared

51
Q

In Polyarteritis Nodosa, what characteristic sign is seen on angiography?

A

‘Rosary’ sign - Microaneurysms give a nodular appearnace, like beads on a rosary

52
Q

Common symptoms of Polyarteritis Nodosa?

A

PUO, weight loss, neuropathy, haematuria, HTN, abdo pain, rash, livedo reticularis

53
Q

Which disease is commonly associated with Polyarteritis Nodosa?

A

Hepatitis B (30%)

54
Q

Where is the most common place to take a tissue biopsy in the diagnosis of Polyarteritis Nodosa?
What would a positive biopsy show?

A

Sural nerve
Necrotizing arteritis, focal and sharply demarcated, with areas of fibrosis (from healing). Infiltrates of polymorphs, lymphocytes, and eosinophils.

55
Q

What is another name for Kawasaki’s disease?

Who is most commonly affected?

A

Microscopic Polyangitis

Children (

56
Q

Criteria for diagnosis of Kawasaki’s Disease

A

Fever > 5 days associated with at least 4/5 of:

i) Bilateral non supportive conjunctivitis
ii) 1 + changes to URTI mucosal membrane (strawberry tongue, red lips)
iii) 1 + changed to arms and legs (swelling, redness, skin peeling around nails - desquamation)
iv) Polymorphous rash (normally truncal)
v) Cervical LNs

57
Q

What is a potentially lethal complication of Kawasaki’s disease?

A

MI - coronary artery involvement can lead to aneurysm formation and MI

58
Q

Who commonly gets Buerger’s disease?

A

Heavy smokers, usually men under 35

59
Q

What is the common presentation of Buergers disease?

A

pain; ulceration of toes, feet, fingers

60
Q

In Buerger’s disease, what can be seen on an angiogram?

A

Corkscrew appearance from segmental occlusive lesions

61
Q

Name 4 small vessel vasculitides?

A

Wegeners Granulomatosis
Churg Strauss Syndrome
Microscopic polyangitis
Henoch Schonlein Purpura

62
Q

Which small vessel vasculitide(s) is/are associated with pANCA?
Which particular antibody is involved?

A

Churg Strauss Syndrome
Microscopic polyangitis

Anti-MPO (myeloperoxidase)

63
Q

Which small vessel vasculitide(s) is/are associated with cANCA?
Which particular antibody is involved?

A

Wegener’s Granulomatosis

Anti-PR3 (proteinase)

64
Q

What are triad of symptoms seen in Wegener’s granulomatosis?

A

1) Upper Resp Tract: sinusitis, epitaxis, saddle nose
2) Lower Resp tract: cavitation, pulmonary haemorrhage
3) Kidneys: crescentic glomerulonephritis (see renal histo)

65
Q

What is another name for Wegener’s Granulomatosis?

A

Granulomatosis with polyangitis

66
Q

What is another name for Churg Strauss Syndrome?

A

Eosinophilic Granulomatosis with polyangitis

or Allergic Granulomatosis

67
Q

What are the 3 stages seen in the manifestation of Churg Strauss?
Is there any systemic involvement?

A

1 - Airway inflammation: asthma and allergic rhinitis
2 - Hypereosinophilia: tissue damage (mainly lungs and GI)
3 - Vasculitis: can lead to severe complications

Yes, happens later due to the last 2 stages

68
Q

Who gets Churg Strauss?

A

People with a history of airway allergic hypersensitivity (atopy)

69
Q

What are the diagnostic markers of CSS?

A

Eosinophil granulocytes and granulomas in affected tissue

pANCA (anti-MPO) +ve

70
Q

What does pANCA and cANCA stand for? What is the other form of ANCA?
What are they?/What is their function?

A

Perinuclear Anti-neutrophil cytoplasmic antibody
Cytoplasmic Anti-neutrophil cytoplasmic antibody
aANCA = atypical ANCA

Autoantibodies, mainly IgG, work against antigens in the cytoplasm of neutrophil granulocytes and monocytes.

71
Q

What is the most serious complication of CSS? (accounts for 50% of deaths in CSS patients)

A

Heart disease: normally due to inflammation of the heart muscle (hypereosinophilia), sometimes due to inflammation of the arteries supplying the heart

72
Q

What is microscopic polyangitis?

A

Ill-defined AID, characterized by a systemic, pauci-immune, necrotizing, small vessel vasculitis without clinical or pathological evidence of necrotizing granulomatous inflammation.

73
Q

What does pauci-immune mean?

Which small vessel vasculitides are considered to be Pauci-Immune?

A

Negative Immuno Flourescence: Form of vasculitis associated with minimal evidence of hypersensitivity upon IF (won’t see anything on IF)
Wegener’s, CSS, Microscopic Polyangitis are all Pauci-Immune

After a -ve IF result, an ANCA test should always be done to look for these vasculitides (especially in the presentation of Glomerulonephritis)

74
Q

Who typically presents with Henoch Schonlein Purpura?

A

Children under 10, with a hx of URTI in the past few days

75
Q

How does HSP commonly present?

A

Classic Triad:

  1. Palpable purpuric rash (lower limb extensors and buttocks)
  2. Colicky abdo pain
  3. Arthritis (mainly ankles, knees, elbows)

Can also see: Glomerulonephritis (Type 2 RP Crescentric GN - see renal histo), Orchitis

76
Q

How does Microscopic Polyangitis commonly present?

A

Pulmonary renal syndrome:

a) Pulmonary haemorrhage
b) Glomerulonephritis (RP Crescentric)

Can also get constitutional symptoms: fatigue, weight loss, anorexia, fever etc.

77
Q

Immunostaining of a glomerular biopsy, from a patient with HS Nephritis, will show what characteristic feature?

A

IgA deposition

78
Q

Typical signs on blood test for HSP?

A

High creatinine and urea (kidney involvement)
High IgA, CRP, ESR
May be high platelet count (useful in distinguishing from ITP and TTP)

79
Q

How is HSP diagnosed?

A

Normally diagnosed on clinical presentation (quite specific combination of symptoms).
Blood tests and biopsy of skin lesions can also help aid diagnosis

80
Q

What is the treatment and prognosis of HSP?

A 
Symptom control (analgesia) is normally the only necessary treatment, as HSP should self resolve within several weeks. 
Can relapse in 1/3 of cases and lead to severe kidney damage - treated with IV steroids
81
Q

Fill in the gaps! (Esme is getting lazy…)

Amyloidosis is a multisystem disorder caused by ? that are deposited as ? in ?, disrupting their normal function.

A

Amyloidosis is a multisystem disorder caused by ABNORMAL FOLDING OF PROTIENS that are deposited as FIBRILS in TISSUES, disrupting their normal function.

82
Q

What protein (folding) structure is most commonly seen in Amyloidosis?

A

Beta-pleated sheets

83
Q

Amyloidosis can be Primary or Secondary. What are the other names for these 2 forms of amyloidosis? (Full name, not just initials!)

A 
Primary = AL Amyloidosis = Amyloid Light Chain  
Secondary = AA Amyloidosis = (Serum) Amyloid A Amyloidosis
84
Q

Which form of Amyloidosis is the most common?

A

AL Amyloidosis

85
Q

For both AL and AA Amyloidosis: what is the amyloid derived from? (it’s in the name!)

A

Primary: amyloid is derived from light chains (component of antibodies)
Secondary = amyloid derived from Serum Amyloid A (Acute phase protein)

86
Q

Which form of Amyloid has ‘Bence Jones protein’ in their urine? What is Bence Jones Protein?

A

Primary

Bence Jones protein is a term used to describe abnormal LIGHT CHAINS in the blood and urine.

87
Q

What is Primary/AL Amyloidosis associated with?

A

Plasma Cell Dyscrasias and Paraproteins e.g Multiple Myeloma
N.B most people with Amyloid do not have MM!

88
Q

What can AA Amyloidosis be secondary to?

3 categories; 2 examples for each.

A

The amyloid is formed from an acute phase protein, so, understandably, it is secondary to chronic infections/inflammation:

  1. AID: RA, Ankylosing Spondylitis, IBD
  2. Chronic Infections: TB Osteomyelitis, IVDU
  3. Non-Immune: Renal Cell Carcinoma, Hodgkin’s
89
Q

What is the most common kind of Familial Amyloidosis?

A

Familial Mediterranean Fever (AR)

90
Q

What is seen in Haemodialysis associated Amyloidosis?

A

Deposition of beta2-microglobulin

91
Q

What form of amyloid is deposited in the kidneys in Familial Amyloidosis?

A

AA amyloid

92
Q

What gene is associated with Familial Amyloidosis? What does this gene encode for?

A

TTR - encodes for pyrin

93
Q

What are the clinical features of Amyloidosis? (Caused by amyloid deposits in various organs)

A
  1. Kidney: nephrotic syndrome (most common presentation)
  2. Heart: conduction defects, heart failure (restrictive cardiomyopathy)
  3. Liver/Spleen: hepatosplenomegaly
  4. Tongue: macroglossia (10%)
  5. Neuropathies: incl carpal tunnel syndrome, autonomic neuropathy
94
Q

Alzheimers Addociated Amyloidosis has deposition of which protein?

A

Abeta 2 protein

95
Q

How is Amyloidosis diagnosed?

A

Tissue biopsy: most commonly viewed with Congo Red stain under polarized light - see Apple Green Birefringence

96
Q

What form of Cardiomyopathy is associated with Amyloidosis?

A

RESTRICTIVE Cardiomyopathy

97
Q

What happens (basic pathophysiology) in Familial Mediterranean Fever (form of Familial Amyloidosis)?

A

+++ production of IL-1,, casues attacks of fever and inflammation of serosal surfaces (pleura, peritoneum, synovium)

98
Q

Fill in the Gaps:

Sarcoidosis is a multisystem disease of ? causes, commonly affecting ?, characterized by ? in many ?.

A

Sarcoidosis is a multisystem disease of UNKNOWN causes, commonly affecting YOUNG ADULTS, characterized by NON-CASEATING GRANULOMAS in many TISSUES.

99
Q

What might be seen in the blood results of a patient with Sarcoidosis? How might these blood signs present clinically (symptoms)?

A

High calcium (also Hypercalciuria): renal calculi + nephrocalcinosis
High ESR
High ACE
Low Hb: all signs of anaemia

100
Q

What are the skin manifestations of Sarcoidosis?

A

Skin: erythema nodosum, lupus pernio, skin nodules

101
Q

What are the joint manifestations of Sarcoidosis?

A

Joints: arthritis, bone cysts

102
Q

What are the eye manifestations of Sarcoidosis?

What is Uveoparotid fever?

A

Anterior uveitis - mistin gof vision and painful red eye
Posterior uveitis - progressive visual loss
Keratoconjunctivitis

Uveoparotid fever = bilateral uveitis, parotid enlargement +/- facial nerve palsy

103
Q

What are the Cardiac manifestations of Sarcoidosis?

A

Cardiac: dysrhythmias, cardiomyopathy, conduction defects
CNS: meningitis, cranial nerve lesions

104
Q

What are the CNS manifestations of Sarcoidosis?

A

CNS: meningitis, cranial nerve lesions

105
Q

What might you notice on abdominal examination of a patient with Sarcoidosis

A

Painless, rubbery lymphadenopathy

Hepatosplenomegaly

106
Q

What organ is most commonly involver in Sarcoidosis?

A

Lung

107
Q

What is commonly seen on a CXR of a patient with Sarcoidosis?

A

Bilateral Hilar Lymphadenopathy!!

Fibrosis + fine nodular shadowing in mid zones (due to pulmonary infiltrates)

108
Q

What are the DDx of a CXR with Bilateral Hilar Lymphadenopathy?

A

TB, Lymphoma, Bronchial Ca

109
Q

What 2 groups of people are more at risk of having Sarcoidosis?

A

Female, Afro-Carribbean

110
Q

Histopathology signs of Sarcoidosis?

A

Non-caseating granulomas = histiocytes, multinucleated giant cells of Langhans and lymphocytes
Schaumann bodies
Asteroid Bodies

111
Q

What is the most common presentation of Sarcoidosis?

A

Insidious SOB, dry cough, chest pain, night sweats

Often asymptomatic

Y5 Histopathology (3 decks)

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