Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2 MSK > Connective Tissue Disorders > Flashcards

Connective Tissue Disorders Flashcards

1
Q

Sjogrens

A

Autoimmune condition characterised by lymphocytic infiltrates in exocrine organs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Sjogrens Symptoms

A 
Dry mouth, eyes and vagina.
Poor dental health.
Myalgia and Arthralgia.
Raynauds
Parotid gland swelling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Sjogrens associated conditions

A

Peripheral neuropathy and interstitial lung disease

Increased risk of lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Immunology in Sjogrens

A

Anti Ro and Anti La

Raised IgG and plasma viscosity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Diagnosis of Sjogrens

A

Ocular dryness
+ve anti-Ro and anti-LA antibodies
Lip gland biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What test is used to determine ocular dryness?

A

Schirmers test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Sjogrens treatment

A

Largely symptomatic e.g lubricating eye drops etc

Regular dental care

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

If the patient with Sjogrens has arthralgia what can be used?

A

Hydroxychloroquine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Systemic sclerosis

A

Multisystemic autoimmune disease characterised by vasculopathy autoimmunity + fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Systemic sclerosis

Cutaneous Presentation

A 
Raynauds
Skin becomes thickened and tight leading to Beaking of the nose, Atrophy of the fingertips 
Telangiectasia 
Calcinosis
Sclerodactyly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Systemic sclerosis

GI Presentation

A

Dysphagia, malabsorption, fluctuating diarrhoea/constipation, faecal incontinence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Systemic sclerosis

Pulmonary presentation

A

Pulmonary hypertension

Pulmonary fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Systemic sclerosis

Renal Presentation

A

Accelerated hypertension
Proteinuria
Worsening renal function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How can systemic sclerosis be divided?

A

Limited- Skin involvement in hand feet and face.
- Linked to anti centromere
- Organ involvement is later
Diffuse- skin involvement includes trunk.
- linked to Anti Scl-70 antibody
- early significant organ involvement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Systemic Sclerosis treatment

A

No overall treatment instead tailor to specific systemic involvement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Systemic sclerosis treatment - Raynauds

A

Primary Raynauds - Calcium Channel Blockers
- ARB’s Nitrates
Recurrent Digital Ulcers - PDE- 5 Inhibitor Sildenafil
- Bosentan endothelia receptor agonist.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Systemic Sclerosis treatment - Pulmonary hypertension

A

PDE 5 inhibitor Sildenafil
Bosentan
oOxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Systemic Sclerosis treatment - Pulmonary Fibrosis

A

Mycophenolate Mofetil
Cyclophosphamide ( for aggressive fibrosis)
Rituximab
Nintedanib (anti-fibrotic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Systemic sclerosis renal presentation and treatment

A

Associated with Anti RNA polymerase III antibody
Uncontrolled hypertension and renal failure.
ACE or ARB +/- dialysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Systemic sclerosis

GI treatment

A

PPI for for reflux to prevent GORD

21
Q

How does anti-phospholid syndrome manifest?

A

Recurrent venous or arterial thrombosis and/ or foetal loss.

22
Q

Common cutaneous presentation of anti-phospholipid syndrome?

A

Livedo reticularis

Mottled skin

23
Q

Treatment for anti-phospholipid syndrome

A

For those with episodes of thrombosis- Aspirin

Recurrent pregnancy loss- Low molecular weight heparin

24
Q

If patients with antiphospholipid syndrome have positive antibodies but no history of episode of thrombosis what happens?

A

No anti-coagulation is required simply monitor.

25
Q

In systemic sclerosis what is CREST?

A 
Calcinosis
Raynauds
Eosinophilic dysmotility
Sclerodactyly 
Telangactasia
26
Q

Gout causes

A

Renal under excretion

Excessive purine intake

27
Q

Pathogenesis of gout

A

Deposition of urate crystals within joint.

Uric acid is final step in breakdown of purines.

28
Q

Where is uric acid usually excreted?

A

2/3 excreted via renal system

1/3 excreted via gastrointestinal system

29
Q

What foods are rich in purines?

A

Alcohol, red meat and seafood.

30
Q

What causes the precipitation of crystals out into the joint?

A

Dehydration, trauma, surgery and low temperatures.

31
Q

Which joint is affected first in gout?

A

First metatarsalphalangeal joint. Base of the big toe.

32
Q

How does gout present.

A

Asymmetrical inflamed joints. Movement is painful and doesn’t alleviate symptoms.

33
Q

What can gout mimic?

A

Septic arthritis

34
Q

What is the blood concentration of uric acid required for gout?

A

> 0.42 mol/l

35
Q

How long do symptoms in gout persist?

A

7-10 days usually with no treatment.

36
Q

What is gold standard diagnostic method for gout.

A

Aspirate the joint and observe fluid under cross polarised microscopy.
Also stain with gram culture to exclude septic arthritis.

37
Q

What do urate crystals look like under polarised microscopy?

A

Needle shaped negative birefringence.

38
Q

What are gout tophi?

A

Deposition of uric acid within the soft tissue. Large white painless lumps which can burst through the skin.

39
Q

Acute treatment of gout

A

NSAIDs
Colchicine
Steroids

40
Q

Gout prophylaxis

A

Allopurinol however 2-4 weeks after acute episode.

Bridge 2-4 weeks with NSAIDs

41
Q

Why is there a 2-4 week period after acute when allopurinol can’t be used.

A

As for some reason it triggers a more severe acute attack if used during acute phase.

42
Q

What causes pseudo gout?

A

Calcium pyrophosphate deposits

43
Q

Pathogenesis of pseudo gout?

A

Deposition of calcium within hyaline cartilage.

Deposits break out into synovial cavity.

44
Q

Underlying possible causes of pseudo-gout

A

Hyperparathyroidism
Renal osteodystrophy
Haemochromatosis
Previous cartilage injury

45
Q

Pseudo-gout diagnoses

A

Aspirate and remove fluid and examine under polarised microscopy.

46
Q

What does pseudo gout look like in microscopy?

A

Rhomboid crystals

47
Q

Pseudo-gout treatment

A

Only acute NSAIDs Colchicine

Hydration

48
Q

In gout if people can’t tolerate allopurinol what can be used?

A

Febuxostat

Year 2 MSK (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions