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Msk > Autoimmune Msk Problems > Flashcards

Autoimmune Msk Problems Flashcards

0
Q

What is the lab work of non-infectious inflammatory myopathies

A

Positive ANA
Anti-Jo-1 AB
Anti-Mi-2 AB’s
Increased creatinine and aldolase

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1
Q

Give two examples of non-infectious inflammatory myopathies. What are they?

A

Don’t matter myositis + polymyositis

Immune-mediated disorders with symmetrical muscle involvement and involvement of other organs

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2
Q

What does muscle biopsy show for polymyositis

A

Necrotic and regenerating muscle with the lymphocytic and macrophage infiltrate

atrophy not prominent

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3
Q

What does muscle biopsies show for dermatomyositis

A

Inflammatory reaction i.e. lymphocytic

Atrophy of muscle fibres = prominent

Capillary damage + muscle – >ischaemia + atrophy

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4
Q

If a patient presents with the matter my situs what else do you need to consider the possibility of?

A

Gastric carcinoma

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5
Q

What is the aetiology of dermatomyositis

A

CD4 cells target capillaries + skeletal muscle

Antibodies + complement damage capillaries

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6
Q

What are the clinical features of the dermato myositis

A

Rash + upper eyelid = purple = heliotrope/raccoons

Malar rash

Red GOTTRON papules + elbows knuckles knees

Hallmark bilateral proximal muscle weakness – Can’t come hair due to weak shoulders

Morning stiffness fatigue + dysphagia @ upper oesophagus

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7
Q

Inside the muscle fascicle where exactly does the information occur in dermatomyositis?

A

Inflammation of the perimysium ->

perifascicular atrophy

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8
Q

In polymyositis is their proximal or distal muscle weakness?
Is the skin involved?
Where is inflammation occurring?
What immune cell is hallmark?

A

Proximal muscle weakness
Skin not involved
Inflammation @endomysium with necrotic muscle fibres
CD8+

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9
Q

What are antibodies directed against in polymyositis?

A

Transfer RNA synthetases

Nuclear + cytoplasmic antigens @ skeletal muscle

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10
Q

What initiates the CD8 positive cells?

A

HIV,

HTLV – 1,

coxsackie B

Alter MHC 1 MHC 2 antigens

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11
Q

Give the two types of X-linked muscular dystrophies

A

Duchenne muscular dystrophy

Becker muscular dystrophy

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12
Q

What is Duchenne muscular dystrophy the characterised by

A

Muscle wasting: skeletal muscle –> adipose tissue

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13
Q

Explain the genetics of Duchenne muscular dystrophy

A

X-linked

Frameshift mutation –Deletion of dystrophin gene – >

cannot anchor muscle fibres in skeletal + cardiac muscle– >

Can’t connect intracellular muscle cytoskeleton (actin)
to
transmembrane proteins alpha + beta dystroglycan. Which are connected to the extracellular matrix

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14
Q

What does the truncated dystrophin protein lead to

A

Inhibited muscle regeneration

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15
Q

Where does the muscle weakness begin from?
@ what age?
where does it progressed to?

A

Proximal muscle weakness @ 1 year old – >progress to distal muscle

E.g. begins in pelvic girdle muscle – >progress superiorly

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16
Q

Explain the Hallmark issue related to the leg in Duchenne muscular dystrophy

A

Pseudohypertrophy of the calf

Learn to walk + Proximal muscle starts to we can – >child puts more force on calf muscle to walk – >hypertrophy

Overtime disease progresses – >
Muscle weakens as disease moves distally and affects calf – >convert calf muscle to fat– > calf looks big but is full of fat

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17
Q

What does the damaged muscle cell release into the Serum?

A

Creatinine kinase + aldolase

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18
Q

Why does the child normally die from Duchenne muscular dystrophy?

A

Cardiac/respiratory (diaphragm) failure

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19
Q

Explain the difference between Becker muscular dystrophy + Duchenne muscular dystrophy

A

In Becker muscular dystrophy disorder is due to non-frameshift insertion in dystrophin Jean i.e.

Protein is partially functional instead of truncated like Duchenne

Onset in Beckers is @adolescence/early adulthood
Onset intuitions is before 5 years old

Beckers is milder

20
Q

Explain the genetics behind myotonic type one muscular dystrophy

A

Autosomal dominant

CTG trinucleotide repeat @DMPK gene ->

Abnormal expression of mytonin protein kinase – >

atrophy type 1 fibres –>

MytoniA + cAtArAct
my tEsticles – Atrophy
My tIcker - arrhythmia
my tOUpee – Frontal balding

21
Q

What is the pathogenesis of SLE

A

Look at pic on 04/03/15

22
Q

What are the genetic and environmental aetiologies?

A

Genetic – (HLA–DR 2+3) & (compliment deficiency)

Environmental

Drugs = isoniazid procainamide hydralazine – >
bind to histones –>histones become immunogenic
->
auto-AB against histones = positive ANA test – > lupus like syndrome -
see all symptoms except CNS + renal involvement

Infections e.g. HIV/CMV/EBV -> polyclonal activation of B lymphocytes – >formation of autoAB against host tissue

Estrogen – > 
DECREASES p(apoptosis of self reactive B cells)

UV light

23
Q

What is epitope spreading

A 
Self reactive lymphocyte – >
react against self-antigen – >
destroyed tissue – >
expose new antigens immune system hasn't seen before – >
produce new self reactive lymphocytes
24
Q

Who does systemically lupus Erythematosus affect?

A

Middle-aged females

Africans + Hispanics

Happens to children and OLD ADULTS

@Kids + older adults: 2 females: 1 male
@Middle aged people: 10 females: 1 male

25
Q

In lupus what does type 3 HSR rxn lead to?

In lupus what does type 2 HSR rxn lead to?

A

Immune complexes = Information @
skin, BM, glomeruli, joints, vessels

Auto antibodies = cytopenias
E.g. anaemia thrombocytopenia leukopenia

26
Q

What are the symptoms of SLE

A

Look at pic on 04/03/15

27
Q

What are the pregnancy related findings in SLE

A

Heart block in the newborn as
IgG anti-Ro/SS-A AB crosses placenta and attacks cardiac conduction system

Antiphospholipid antibody binds to proteins on the trophoblast and causes abortion

28
Q

Explain drug induced lupus in comparison to systemic lupus erythematosus

A 
anti HHHHistone antibodies form
decreased IIIIIncidence of renal + CNS issues
No AAAAB against native DNA
No decreased serum CCCCCompliment
SSSSSSymptoms disappear when drugs stop
29
Q

Treatment for lupus

A

Corticosteroids NSAIDs immunosuppressants hydroxychloroquine

30
Q

What are the common causes of death due to lupus

A

Renal failure

Infection – due to immunosuppressants/auto antibodies against white blood cells

Later on in life = increased p(accelerated coronary atherosclerosis)

31
Q

What is Sjogren’s syndrome

A

Autoimmune destruction of exocrine glands especially lacrimal + salivary glands

mediated by lymphocytes type 4 HSR + fibrosis

32
Q

What does destruction of lacrimal + salivary glands result in?

A

Kerato conjunctivitis sicca / xerophthalmia -
⬇️ tear production – > dry eyes – > corneal damage

Dental Caries

Xerostomia - ⬇️ saliva production - dry mouth

33
Q

Like every other autoimmune disease who is most likely to be affected by Sjogren’s syndrome

A

Older women

34
Q

Sjögren’s can be a primary or a second airy disorder. As a secondary syndrome what can it be associated with?

A

Rheumatoid arthritis

35
Q

What Ab can be present in the blood in sjogrens?

Can this be associated with rheumatoid arthritis

A

Rheumatoid factor

No not necessarily

36
Q

What are the extraglandular manifestations of Sjogren’s syndrome

A

Joint pain CNS/skin issues

37
Q

What are the lab findings and Sjogren’s syndrome

A

Rheumatoid factor

Positive ANA

Anti ribonucleoprotein = anti SSA/SSB
Anti-SSA: crosses placenta – >
attack fetus –> neonatal lupus – >
congenital heart block

38
Q

Is the anti-SSA/SSB enough to make a diagnosis of Sjogren?

What do you need to confirm Sjogrens?

A

Biopsy of minor saliva gland @lip – >

look for lymphocytic SIALADENTIS =
lymphocytes attack minor salivary glands = MALT

39
Q

Explain the relationship between Sjogren’s syndrome and parotid gland

A

Sjogren’s syndrome = inflame parotid gland – >

enlarged parotid gland – >

B cell lymphoma cause unilateral enlargement of parotid gland

40
Q

How do you treat Sjögren’s syndrome

A

Artificial tears

Cyclosporine/pilocarpine eyedrops

Civimeline

41
Q

What does the schimear test and Rose Bengal staying reveal for Sjögren’s

A

Filterpaper placed inside of lower eyelid

Wetting of <10 mm @ 5 minutes = ⬇️ tear problem

Rose Bengal stain shows
FILAMENARY keratitis + PUNCTATE keratitis

42
Q

Explain the pathogenesis of systemic sclerosis scleroderma

A

AI rxn against AG @connective-tissue / endothelial cell – >
endothelial cell dysfunction – >increased expression of Cellular adhesion molecules –>

Th2 enter skin –> the endothelial cell secrete:

PDGF + TGF beta – > activate fibroblast –>
fibrosis around BV –>
organ damage = systemic sclerosis

Endothelin = vasoconstrictor –> ischaemia – >
more fibrosis – >organ damage

43
Q

What are the two forms of systemic sclerosis

A

Limited and diffuse

44
Q

Explain limited systemic sclerosis scleroderma

A

Skin involvement = minimal = distal to knee + elbow
Late visceral involvement

Calcinosis = calcium deposition @ subcutaneous connective-tissue anticentromere Ab

Raynaud phenomenal

Esophageal dysmotility

Sclerodactyly - fibrosis of skin + hands: tight skin – >lose wrinkles – >constrict blood vessels

Telangiectasia– Dilated capillaries

45
Q

Explain the pathogenesis of mixed connective-tissue disease

A

B + T-cell activation – >Ab against U1-ribonucleoprotein

46
Q

What are the lab findings for mixed connective-tissue disease

A

Positive ana

Auntie ribonucleoprotein against you U1-RNP

47
Q

Clinical findings of mixed connective-tissue disease

A 
Hypertension + pleuritis
Arthralgia + arthritis of hands
Raynaud
Pericarditis
Oesophageal dysfunction/dysmotility
Neuralgia Trigeminal
Sclerodactyly
48
Q

Lab findings for systemic sclerosis

A

Positive ana

For diffuse scleroderma –
anti DNA topoisomerase 1 Ab = anti-Scl – 70 Ab

Msk (10 decks)

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