Brainscape's Knowledge GenomeTM

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


See full index

HUMAN HEALTH AND DISEASE > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What is the aetiopathogenesis of rheumatoid arthritis?

A

Unknown but it is recognised that it probably results from a combination of genetic and environmental factors leading to breakdown of immune tolerance.

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

What are the other autoimmune diseases as well as RA associated with in terms of aetiopathogenesis?

A

Associated with MHC:
* Rheumatoid Arthritis (RA): HLA-DR4 (more frequent in smokers)
* Systemic Lupus Erythematosus (SLE): HLA-DR3, complement components
* Progressive systemic sclerosis (PSS): HLA-DR3

  • Immunological associations: serology often positive for a variety of autoantibodies
  • Histology shows evidence of immune involvement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the auto-antibodies present in RA?

A

-RF (rheumatoid factor) present in RA, but non-specific

-95% specific to RA is the anti-CCP (anti-citrullinated protein antibodies)

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

What are auto-antibodies?

A

Antibodies produced by the immune system that mistakenly target and attack the body’s own tissues.

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

What are the auto-antibodies present in systemic lupus erythematosus (SLE)?

A

ANA (antinuclear antibodies), specifically dsDNA antibodies

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

What is the auto-antibody present in progressive systemic sclerosis (PSS)?

A

Scl 70

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

What are the auto-antibodies present in Sjogren’s syndrome?

A

ENA (extractable nuclear antigen) antibodies (Ro, La) as well as RF.

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

What are rheumatoid factors?

A

Auto-antibodies which target and attack IgG antibodies or IgM produced by the body itself.

This leads to inflammation, joint damage etc.

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

How prevalent is RA?

A

1% of population is affected with a female predisposition in the ratio F:M being 2.5:1.

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

What is RA?

A

-Symmetrical polyarthritis which often starts in hands and wrists.

-It’s a systemic disease which may have extra-articular movement.

-This means RA doesn’t only affect joints but also other organs and systems in the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the symptoms and signs of RA?

A

Symptoms:
-Pain
-Swelling
-Morning stiffness
-Malaise (fatigued)
-Non-articular symptoms

Signs:
-Swelling
-Warmth
-Tenderness
-Limited movement
-Deformity

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

What can advanced RA look like?

A

-Bountonniere deformity of thumb (z-shaped)

-Ulnar deviation of metacarpophalangeal joints

-Swan neck deformity of fingers

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

What does the anatomy of a RA joint look like compared to a healthy joint?

A

In the RA joint:

1.The synovial membrane is thickened

2.There’s an overgrowth of the synovia sites (pannus)

3.Marked influx of inflammatory cells; each of those producing cytokines which stimulates inflammation

4.Osteoclasts get activated to eat away at the bone

5.Cartilage overlying the bone is getting damaged and removed

6.Swelling of the overlying soft tissues is caused; there’s damage to the ligaments and structures supporting the joints

7.The joint itself also gets damaged

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

What does the pannus look like histologically?

A

slide 20

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

What are some of the complications of RA?

A

-rheumatoid nodules
-Tendon rupture
-Normochromic, normocytic anaemia
-Nerve entrapment e.g. median nerve
-Vasculitis - a group of conditions that cause inflammation of the blood vessels.
-Atlanto-axial subluxation
-Eye complications

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

How are patients with RA treated?

A

Analgesia (e.g. NSAIDs reduce pain and swelling)

DMARDs especially methotrexate, hydroxychloroquine for mild to moderate

TNFa blockade e.g. Infliximab, Etanercept

Anti-B cell monoclonal ab e.g. rituximab

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

What is the relevance of RA to dentistry?

A

Hand deformity - oral hygiene, blister packs

Carpal tunnel syndrome

Atlanto-axial subluxation during GA

TMJ dysfunction

Sjogren’s syndrome

Anaemia

Complications of systemic treatment

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

What is Sjogren’s syndrome?

A

An autoimmune disease which can cause oral and ocular dryness.

It can either be a primary disease (dry eyes, mouth, vagina, etc.) or it can be secondary to other autoimmune diseases (e.g. RA, PSS, SLE)

19
Q

What is the incidence of Sjogren’s syndrome and who is most likely to get it?

A

It’s quite rare but it’s much more common in females (F>M 9:1) with 2 peaks of onset: mid 30s and then postmenopausal 45-60 due to reduction is oestrogen

20
Q

What are the symptoms of Sjogren’s syndrome?

A

-Sicca symptoms (95%): dryness of mouth, eyes, skin, vagina

-Excessive fatigue (75%)

-Arthralgia - pain in joints without joint inflammation.

-Myalgia - muscle pain/aching

-Dental caries

-Loss of teeth

-Candida

-Swollen salivary glands and Lacrimal glands

21
Q

If you have Sjogren’s syndrome, what is there also an increased risk of?

A

Lymphoma/maltoma

Have to look out for B cell lymphoma, mucosal associated lymphoid tissue

22
Q

What investigations are required in order to diagnose Sjogren’s syndrome?

A
  1. Measure salivary flow, whether it’s stimulated or unstimulated:

-For stimulated parotid flow, normal is >0.4ml/min
-For unstimulated whole salivary flow, normal is >0.2ml/min

  1. Schirmer test
  2. Do bloods: FBC, inflammatory markers, auto-antibodies Ro and La, others as indicated
  3. Ultrasound (has largely replaced sialography & scintigraphy)
  4. Labial gland biopsy
23
Q

What is the relevance of Sjogren’s syndrome to dentistry?

A

-Xerostomia: Dental caries, Loss of teeth, Candida

-Salivary gland enlargement

-Complications of systemic treatment

24
Q

What are the variants of lupus erythematosus?

A
  1. Discoid lupus (DLE)– scarring skin lesions/oral (affects either just skin or just mouth)
  2. Subacute cutaneous (SCLE)- rash, systemic disease (predominantly affects skin but has some features of systemic disease)
  3. SLE (predominantly systemic but might include skin rash/oral lesion)
  4. Anti-phospholipid syndrome (sticky blood, prone to clots)
  5. Drug-induced lupus
25
Q

What is the aetiology of SLE?

A

SLE is a multi-system disease

Pathology- widespread vasculitis (immune system mistakenly attacks blood vessels) of capillaries, arterioles and venules

Aetiology- genetic, complement deficiency

Triggers- UV light, infection, or even drugs

26
Q

What investigations would we undertake in diagnosing lupus?

A

In the bloods, you’re looking for raised ESR, ANA, positive RF etc.

27
Q

What are cerebral micro-infarcts?

A

Blood vessels in the brain affected.

White spots in the brain present

28
Q

What is lupus nephritis?

A

Connective tissue disorder resulting from an abnormal immune system

29
Q

how does lupus nephritis manifest as?

A

Foamy urine = increased protein in urine

Brownish urine due to blood present

Elevated creatine in the blood

High bp

odema of feet, lower legs and eyelids.

5% of patients with SLE will develop some degree of renal involvement

30
Q

What can anti-phospholipid syndrome lead to?

A

Increased tendency to clotting

Venous thrombosis

Arterial thrombosis

Recurrent foetal loss

Thrombocytopenia - low platelet count

Livedo Reticularis - net-like pattern on skin due to change in blood flow affected small blood vessels in the skin.

31
Q

What is the relevance of lupus erythematosus to dentistry?

A

Oral ulceration

Complications of systemic treatment

Candida

+/-Dry mouth (xerostomia)

Main differential is lichen planus (you might think the patient has lichen planus, but it’s actually an oral manifestation of their lupus)

32
Q

What are the subtypes of scleroderma?

A
  • Systemic fibrosis
  • Limited systemic / CREST syndrome
  • Localised to skin - morphoea
33
Q

What can patients with diffuse systemic sclerosis have?

A

Scleroderma - thickening of skin

Skin induration - hardening/thickening of skin

Flexion Fingers: start to bend in and become claw-like and this starts distally & gradually works its way proximally

Digital gangrene may occur

Skin may look shiny

In terms of facial changes, the patient could develop microstomia and struggle to open their mouth wide

Can also have pulmonary fibrosis, diverticula (malabsorption), intimal arterial proliferation (kidney)

34
Q

What is the relevance of scleroderma to dentistry?

A

Microstomia - abnormally Small mouth

Widened periodontal membrane

Severe sclerodactyly- difficulty with oral hygiene

Immunosuppression

35
Q

What is affected in the more limited systemic disease variations of lupus?

A

CREST:

Calcinosis - calcium deposit in fingertips/soft tissues

Raynaud’s phenomenon - episodes of reduced blood flow to fingers and toes = turn white or blue

Esophagus (oesophagus) - difficulty swallowing

Sclerodactyly - thickening and tightening of the skin on the fingers and hands.

Telangiectasia - dilated blood vessels that appear as red spots on skin, particularly on face and hands

36
Q

What treatments are there for these patients with lupus, systemic sclerosis, etc.?

A

Analgesics

Glucocorticoids

Immunosuppressive: cyclophosphamide, azathioprine, mycophenolate mofetil

Biologics

37
Q

How is Raynaud’s treated?

A

Physical: gloves (heated)

Nifedipine: Ca channel antagonist

Losartan: angiotensin II antagonist

38
Q

Who is most commonly affected by Osteoarthritis?

A

The general population >60yrs old
There is a 10% genetic predisposition though

39
Q

What is osteoarthritis (OA)?

A

Non-autoimmune degenerative joint disease

40
Q

What is the pathogenesis of OA?

A

Degenerative disease of cartilage

(may be genetic or mechanical insults, or biochemical abnormalities of cartilage)

41
Q

What do Heberden’s nodes look like?

A

Heberden’s node on the distal interphalangeal joint is a characteristic joint to be affected in OA so it wouldn’t be seen in RA- key differentiating factor

Distal interphalangeal joint is the last joint (closest to nails) in the fingers

42
Q

Compare and contrast primary OA with secondary OA.

A

Primary OA:

-Majority of cases
-Strong family history
-Onset around 50

Secondary OA:

-Congenital abnormality of joints
-Structural disorders in children which can lead to trauma causing OA

43
Q

What are the clinical features of OA?

A

Symptoms:
-Pain– worse with use
-Morning stiffness <30 mins
-Disability

Signs:
-Swelling– hard and bony
-Crepitus - popping, clicking or crackling sound in a joint
-Muscle wasting
-Limited movement
-Joint deformity
-Monoarticular occasionally
-Bilat and symmetrical e.g. knees, hands, hips

44
Q

What is the relevance of OA to dentistry?

A

-Reduced mobility
-Reduced manual dexterity
-TMJ dysfunction

HUMAN HEALTH AND DISEASE (58 decks)

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