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Year 5 😊✌🏼 > Path 6 > Flashcards

Path 6 Flashcards

1
Q

Features of SLE

A

can affect any organ!!

fever, fatigue, weight loss - flare ups

skin - e.g. malar rash
oral ulcers
joints (arthritis)
neurological (e.g. seizures, psychosis)
serositis (e.g. pericarditis, pleuritis; recurrent abdo pain)
renal (glomerulonephritis, protein +)
haematological (pancytopenia)
immunological (autoantibodies)

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2
Q

40yo female with pancytopenia and proteinuria - dx?

A

SLE

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3
Q

Antoantibodies in SLE

A

ANA - used for screening, does not show which antibody specifically is involved

Anti-dsDNA

Anti-Smith (ribonucleoprotiens) - most SPECIFIC (if +ve, v likely to have SLE) but not very sensitive (30% people with SLE have it)

Anti-histone (seen in drug induced lupus e.g. hydrazalazine

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4
Q

What medications can cause drug induced lupus?
Which antibody is positive?

A

hydralazine
procainamide

anti histone antibody

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5
Q

if a number is stated along with ANA, what does it mean?

A

the dilution of the serum at which the test is +ve, e.g. with 1/1000 dilution -> significantly high ANA

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6
Q

What is the underlying skin histology in a malar rash/SLE skin?

A

lymphocytic infiltration of the upper dermis

basal epidermis has undergone vacuolisation

red cells extraposition in the dermis

Immunofluorescence: immune complex deposition at epidermis-dermis junction

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7
Q

SLE skin - where are immune complexes deposited?

How can you see them (method)?

A

epidermis dermis junction

seen with immunofluorescence (Immunoglobulin binding)

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8
Q

What histological changes can you see lupus nephritis?

A
  • thickening of glomerular capillaries (thick wall, wire loop pathology appearance) - due to immune complex deposition in BM
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9
Q

What causes wire loop pathology in lupus nephritis?

A

deposition of immune complexes in the BM leading to thickening of glomerular wall

can be seen on immunofluorescence or electron microscopy

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10
Q

What is Libman sacks?

A

non-infective endocarditis seen in SLE

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11
Q

How does Libman sacks endocarditis present?

A

emboli
stroke
murmurs

the vegetations on the valves are lymphocytes, neutrophils, eosinophils, fibrin strands etc.

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12
Q

What is the problem in Scleroderma?

A

fibrosis and excess collagen in the skin

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13
Q

what is the localised form of scleroderma called?

A

morphoea in the skin (patch of tight skin)

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14
Q

What are the 2 types of systemic sclerosis/scleroderma?

A

diffuse

limited

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15
Q

are scleroderma and systemic sclerosis synonymous?

A

yes

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16
Q

What is the difference between diffuse and limited scleroderma/systemic sclerosis?

A

diffuse - trunk is involved

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17
Q

What is more common, diffuse or limited scleroderma?

A

limited is more common

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18
Q

What autoantibodies are diffuse and limited scleroderma associated with?

A

Diffuse: anti-scl70 (antibodies to DNA topoisomerase)

Limited: anticentromere

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19
Q

What is CREST syndrome?

A

Term no longer used!!

describes limited scelroderma

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20
Q

CREST - what does it stand for?

A

Calcinosis
Raynauds
Oesophageal dysmotility
Sclerodactyly
Telegiectasia

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21
Q

oder of colour change in raynauds?

A

white
blue
crimson

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22
Q

What is sclerodactyly?

A

thinkening of the skin of the fingers+hand causing them to curl inwards causing a claw deformity and limitation in movement

seen in scleroderma

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23
Q

What pattern can be seen on IF in scleroderma?

A

nucleolar pattern

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24
Q

How common is raynauds in the general population (females)?

A

1 in 10

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25
feautures of systemic sclerosis
calcinosis raynauds oesophageal dysmotility sclerodactyly telangiecstasia nail fold capillary dilatation microstomia (difficulty opening small mouth) onion skin - intimal proliferation of arterioles +/- obliteration of the lumen. may have thrombi.
26
What causes skin tightening in scleroderma?
excess collagen deposition in the dermis
27
stomach changes in scleroderma
excess collagen and fibrosis -> causes oesophageal dysmotility
28
What is mixed connective tissue disease?
Patients have features of: SLE scleroderma polymyositis dermatomyositis OVERLAP
29
What enzyme is elevated in poly/dermatomyositis and why?
CK it is leaking out of inflamed muscle
30
What pattern of ANA can you see in mixed connective tissue disease?
speckled pattern
31
ANA - speckled pattern - dx?
mixed connective tissue disease
32
ANA - nucleolar pattern - dx?
scleroderma
33
ANA - entire nucleus stained pattern - dx?
SLE
34
What ANA patterns can you see and what conditions are they suggestive of? What type of test is ANA?
whole nucleus involved - SLE nucleolar pattern - scleroderma speckled pattern - mixed connective tissue disease ANA is a screening test, you would want to do further testing for autoantibodies.
35
What are Gottron's papules and what condition are they a feature of?
erythematous rash over knuckles on dorsal aspect of hands dermatomyositis
36
Dermatomyositis features
Tender, inflamed muscles raised CK Gottron's papules
37
Features of sarcoidosis
Joints (e.g. back pain) skin (nodules, papules, lupus pernio, erythema nodosum) lungs (BHL, fibrosis, cough, lymphocytosis - CD4+ on BAL) lymphadenopathy parotids (bilateral enlargement) heart eyes (uveitis, conjunctivitis) neuro (meningitis, cranial nerve lesions) liver (hepatitis, cirrhosis, cholestatis )
38
What is the pathological hallmark of sarcoidosis?
non-caseating granulomas
39
What conditions give you erythema nodosum?
sarcoidosis IBD Bechets
40
Causes of bilateral parotid enlargement
Infection: mumps Inflammation: sarcoidosis, Sjorgens syndrome alcoholism
41
BHL
bilateral hilar lymphadenopathy
42
histopathological features of sarcoidosis
non-caseating granulomas epithelioid looking cells (with elongated nuclei) Langhans cells (multinucleate giant cells with horse shoe appearance/distribution of nuclei; multiple macrophages fusing)
43
what does non-caseating mean?
there is no necrosis occurring
44
Test findings in sarcoidosis?
- hypergammaglobulinaemia - raised ACE due to abnormalities of capillaries in the lungs where ACE is made - hypercalcaemia (vit D hydroxylation by activated macrophages)
45
What causes hypercalcaemia in sarcoidosis?
increased Vitamin D3 hydroxylation by activated macrophages
46
Types of vasculitis (3)
large vessel medium vessel small vessel
47
types of large vessel vasculitis
Giant cell arteritis takayasus arteritis
48
types of medium vessel arteritis
kawasaki's polyarteritis nodosa
49
types of small vessel vasculitis
Immune Complex SVV - cryoglobulinaemic vasculitis - IgA vasculitis (Henoch Schonlein) - Hypocomplementeric urticarial vasculitis ANCA-associated SVV - microscopic polyangiitis - granulomatosis with polyangiitis (Wegener's) - eosinophilic granulomatosis with polyangitis (Churg-Strauss)
50
What infection is polyarteritis nodosa associated with?
Hep B
51
What vasculitis is Hep B infection associated with?
polyarteritis nodosa (medium vessel vasculitis)
52
What can be seen on angiogram in polyarteritis nodosa?
multiple beads (small aneurysms)
53
What kind of rash is characteristic of vasculitis?
palpable purpuric rash can be seen in any type of vasculitis
54
primary and secondary vasculitis
primary vasculitis (large, medium, small vessel) OR secondary to infective endocarditis, RA, SLE...
55
histology of temporal arteritis
narrowing of lumen granulomas multinucleate giant cell with horseshoe arrangement of nuclei lymphocytic infiltration of tunica media
56
Histopath of polyarteritis nodosa
necrotising arteritis inflammatory cell infiltrates around vessels: polymorphs, lymphocytes and eosinophils seen arteritis is focal and sharply demarcated heals by fibrosis
57
what vessels are most commonly affected by polyarteritis nodosa?
renal and mesenteric arteries
58
3 hallmarks of granulomatosis with polyangitis
ENT Lung kidneys
59
What antibody to test for in ?GPA
C-ANCA (cytoplasmic ANCA) directed against proteinase 3
60
What does C-ANCA bind to?
proteinase 3
61
When is C-ANCA positive?
GPA small vessel ANCA vasculitis ENT, lung and kidney issues (used to be called Wegeners)
62
What is the triad of sx in eosinophilic granulomatosis with polyangitis?
asthma eosinophlia vasculitis
63
What ab is +ve in eosinophilic granulomatosis with polyangitis?
P-ANCA (perinuclear ANCA) directed against myeloperoxidase
64
What is P-ANCA directed against?
myeloperoxidase
65
What ab to test for in ?eosinophilic granulomatosis with polyangitis (Churg Strauss)
P-ANCA
66
How do you manage Church Strauss syndrome?
glucocorticoids PLUS cyclophosphamide Goal is induction of remission
67
What do 1% of children affected by Kawasaki die off? What happens with the rest?
MI 99% have self limiting course
68
onion skin - what is it a histopathological feature of?
onion skin - intimal proliferation of arterioles +/- obliteration of the lumen. may have thrombi. systemic sclerosis
69
What does anisopoikilocytosis mean?
there is a variation size (aniso) and shape (poikilo) of RBCs
70
hypersegmented neutrophil - ddx
B12 deficiency folate deficiency drugs (e.g. methotrexate, 5-FU, hydroxyurea, hydroxycaarbamide)
71
def of hypersegemnted neutrophils
>5 nuclear segments
72
codocytes
target cells central area of increased haemoglobin
73
target cells - ddx
iron deficiency thalassemia hyposplenism liver disease
74
Howell Jolly bodies - what are they and when are they seen?
remnants of nucleus usually removed by spleen -> seen in hyposplenism
75
features of iron deficiency on blood film
microcytosis hypochromia anisopoikilocytosis
76
hyposplenic features on blood film
target cells Howell jolly bodies
77
Causes of iron deficiency
blood loss - major cause other causes: - poor diet - malabsorption - combinations of the above
78
Causes of megaloblastic change
B12 and folate deficiency drugs
79
causes of hyposplenism
absent spleen (therapeutic, trauma) poorly functioning spelen IBD ceoliac disease SLE sickle cell disease
80
Deficiency seen in coeliac
iron b12 folate fat ca
81
deficiency seen in Crohn's disease
b12 bile acids
82
pancreatic disease deficiency
83
xxx deficiency
84
where is tissue traanssglutaminase expressed?
endomysosal layer therefore also called
85
also check IgA levels (some peeople are IgA deficient)
86
also check IgA levels (some peeople are IgA deficient)
87
antibody disappears as people stop eating gluten
88
Why would you perform an endoscopy in ?coeliac disease?
baseline
89
Gold standard for coeliac disease diagnosis
(disstal) duodenal biopsy
90
endoscopy findings in coeliac disease
scalloping of ridges in duodenum (lumps rather than villi)
91
normal villous : crypt ratio
3-5 : 1 villii are the majority of the biopsy
92
normal duodenal vili intro epithelial lymphocyte number
20 intraepithelial lymphocytes / 100 epithelial cells
93
Brunners glands - where are they ?
in the proximal half of the duodenum they may distort villous architecture
94
histopathology in coeliac disease
Villous atrophy - villous height is reduced (atrophy) Crypt hyperplasticity - crypt thickness is increased (hyperplasticity) increased IEL : >25 IEL / 100 epithelial cells these changes disappear if they stop eating gluten
95
Causes of increased IEL
coeliaca infections bacterial overgworh drugs IBD Immune dysregulation
96
most specific test for coeliac disease?
anti-tissue transglutaminase IgA
97
Long term complications of coeliac disease
- malabssorption - osteomalacia - osteoporosis - neurological disease (epilepsy, cerebral calcification) - T-cell lymphoma of the bowel - hyposplenism Important to stick to the diet to prevent these complications
98
genetic components of coeliac diesase
HLA-DQ2 increased risk to family members
99
how often DEXA scan of hip in coeliac disease?
every 3-5 y b/c of the risk of osteomalacia/osteoporosis
100
Lambert-Eaton myasthenic syndrome - what malignancy is it associated with?
Small cell Lung cancer
101
What syndromes is SCLC associated with?
SIADH (15% of patients) Cushing's syndrome (5%) Lambert-Eaton Myasthenic syndrome (3%) acromegaly
102
What infection does the presence of galactomannan in the serum of a septic patient suggest?
Aspergillus
103
Beta-D-Glucan in serum - what does it indicate?
candida aspergillus PCP
104
Glucuronoxylomannan (GXM) in serum - what does it indicate?
cryptococcus

Year 5 😊✌🏼 (53 decks)

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