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MEDICINE NEW > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

How to classify causes of chronic polyarthopathies

A

Rheumatoid like:
symmetrical and proximal-stiffness of 30 mins +
Psoriatic
RA

Osteroarthritis (worse at evening)

Spondyloarthropathy: asymmetric oligoarthritis + spine

Gout

Connective tissue- SLE, Sjögrens

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2
Q

Causes of acute polyarthropathies

A

Infective:
Viral- migratory joint arthritis (rheum fever)
Gonococcal

Non-infective:
Reactive + Reiter’s

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3
Q

Acute causes of a monoarthropathy:

A 
Gout
Haemoarthropathy
Osteoarthritis
Septic joint
Trauma
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4
Q

Common sites of psoriasis to check:

A 
Elbows
Hair line/ scalp
Umbilicus
Natal cleft
Genitalia
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5
Q

Cause of monoarthritis:

A 
vITAMin
Infective- septic arthritis
T- haemarthrosis, OA
Autoimmune- early RA
Metabolic- gout/pseudogout
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6
Q

Causes of oligoarthritis (<5 joints)

A

Seronegative arthropathies- psoriatic, reactive, ank spond
OA
Crystal arthropathies

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7
Q

Symmetrical vs Asymmetrical polyarthropathy causes?

A

Symmetrical- vITAmin:
Infection- Hep A, B, C, mumps (athralgia)
Trauma- OA
Autoimmune- RA

Asymmetric-
Seronegative arthropathies

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8
Q

What is Schober’s test?

A

Mark on back at level of posterior iliac spine
Measure 5cm below to 10cm above
Bend forward
Should increase by 5cm

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9
Q

How do neutrophil levels help to determine cause of swollen joint, once aspirated?

A

< 50% osteoarthritis or haemoarthrosis
~ 80% crystal arthropathies
> 90% septic arthritis

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10
Q

Radiological features of RA vs OA vs Gout:

A

OA: LOSS
Loss of joint space, osteophytes, subchondral cysts, subchondral sclerosis

RA: LOSED
Loss of joint space, osteopenia, soft tissue swelling, erosions, deformities

Gout: NOSE
No loss of joint space, soft tissue swelling, erosions

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11
Q

Back pain red flags:

A

Under 20, over 55, acute in the elderly

PC: SOCRATES
S- thoracic
O- pain at night
C- constant
R- bilateral/alternating sciatica
A- fever, night sweats, weight loss, abdo mass, neuro disturbance, sphincter disturbance, leg claudication, morning stiffness
T- progressive
E- worse when supine, exercise-related (spinal stenosis)
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12
Q

3 clinical tests for sacroiliitis:

A
  1. Direct pressure
  2. Lateral compression
  3. Sacroiliac stretch test- hip + knee flexed + adduction = pain
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13
Q

Cauda equina compression signs:

A

Pain: alternating or bilateral leg pain
Sensation: saddle anaesthesia
Power: loss of anal tone on PR
Functional: bladder + bowel incontience

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14
Q

How is cauda equina compression differentiated from acute cord compression?

A

Spinal level in cord compression with UMN and LMN signs

In cauda equina there’s only LMN signs

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15
Q

How does OA differ from RA in symptom presentation?

A

OA:
S- distal hand joints, knees; monoarthritis, oligoarthritis, polyarthritis
O- evening;
E- exercise, stiffness after rest

RA:
S- proximal joints of hands feet; symmetric polyarthitis
O- worse in morning, stiffness >30 mins
A- extra-articular + systemic features

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16
Q

Management of osteoarthritis:

A

Conservative: exercise- aerobics, weight loss, PT, OT, walking aids, heat/cold packs, TENS machines

Medical: PO Paracetamol ± NSAIDs topical
2. Short term NSAIDs (+PPI), codeine, capsaicin, intra-articular steroids

Surgical: joint replacement

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17
Q

Patient has a red hot joint, what risk factors of septic arthritis should be asked about:

A

Over 80
PMH: joint disease-RA, diabetes, CKD, immunosupression
PSH: recent joint surgery, prosthetic joint
SHx: IVDU

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18
Q

Things to tell patients about NSAIDs:

A

Take lowest dose for shortest time, may not need every day
Don’t take additional over the counter NSAIDs

Look out for: malaena (GI bleeding), oliguria (renal impairment)
DHx: Avoid if already taking Aspirin
PMH CI: severe heart failure
SEs: increased risk of MI + stroke

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19
Q

How do the following drugs work?

A. NSAIDs
B. Aspirin
C. Paracetamol

A

A. Cyclooxygenase competitive inhibitor- preventing formation of prostaglandins and thromboxane from arachidonic acid
(COX1 in stomach makes prostaglandins that are protective)
Prevents fever by reduction of PGE2 signalling (acts on CNS)

B. Cyclooxygenase irreversible inhibitor

C. COX2 inhibitor ?Central actions + ?acting on endocannabinoid pathways

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20
Q

Hand signs of RA

A

Hands:
Swollen or red proximal small joints of hand (MCP, PIP, wrist)
Swan necking, Boutoniére’s, Z thumb deformity
Ulnar deviation, dorsal wrist subluxation

Elbow:
Bursitis, rheumatoid nodules

Tenosynovitis

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21
Q

Extra-articular features of RA:

A

Hands- Raynaud’s, carpal tunnel syndrome

Neck- lymphadenopathy

Face- episcleritis, scleritis, scleromalacia (conjuctiva degeneration) or keratoconjunctivitis sicca (dry eye)
Amyloidosis (glossitis)

Chest- bronchiectasis, basal fibrosis, obliterative bronchiolitis
Pleural + pericardial effusion

Abdominal- splenomegaly

Osteoporosis

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22
Q

Tests for rheumatoid arthritis?

A

Bloods: Anticyclic-citrullinated peptide, rheumatoid factor (70%)
Platelets, ESR, CRP

X rays: late disease
MRI or USS: synovitis

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23
Q

What 4 things make up the diagnostic criteria for diagnosing RA?

A

J-ASS score of 6/10 is diagnostic

  1. Joint involvement (swelling or tenderness) max score 5
  2. Acute phase reactants (abnormal CRP or ESR) max score 1
  3. Serology (anti-CCP or RF, high or low titres) max score 3
  4. Symptoms duration (>6 weeks) max score 1
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24
Q

Management of rheumatoid arthritis:

A

Conservative: PT, OT, help to stop smoking (increases symptoms), NSAID analgesia

Medical: Methotrexate + 1 DMARD (sulfasalazine, hydroxychloroquine)
Short term steroids (oral or intra-articular)

Surgical: to prevent pain or deformity, or improve function

After 6 months, DAS28 score >5.1

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25
Q

What is the DAS28 score?

A

An assessment of tenderness and swelling at 28 joints:
MCPs, PIPs, wrists, elbows, shoulders, knees
ESR and patient’s self-reported symptom severity

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26
Q

Main SEs of the rheumatoid arthritis DMARDS
A. Methotrexate
B. Sulfasalazine
C. Hydroxychloroquine

A

A. Pneumonitis, liver cirrhosis, myelosupression
B. S for skin rash, U for ulcers (oral), L for low sperm count
C. Irreversible retinopathy

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27
Q

What are the 4 ways biological agents may act to help treat rheumatoid arthritis?

A
  1. TNFa inhibitors (infliximab, etanercept, adalimumab)
  2. B cell depletion (Rituximab)
  3. IL-1 and IL-6 inhibition (Toclizumab = IL 6)
  4. Disrupted T cell function (Abatacept)
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28
Q

SE of biological agents:

A

Serious infection
TB reactivation and Hep B

Hypersensitivity
Heart failure worsening

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29
Q

Aside from the typical presentation of RA, name 6 other ways it can present:

A
  1. Sudden onset widespread arthritis
  2. Palindromic RA- recurrent arthritis, lasts days to hours, visiting and revisiting different joints (precedes RA, SLA, Whipple’s, Beçet’s)
  3. Persistent mononeuritis- knee, shoulder, hip
  4. Systemic illness with initially few joint problems, fever, fatigue, weight loss, pericarditis
  5. Polymyalgic onset, vague limb girdle aches
  6. Recurrent soft tissue problems- frozen shoulder, carpal tunnel, tenosynovitis
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30
Q

Causes of gout:

A

What goes in: alcohol, purines, diuretics (from blood, enter tubular cell, excreted into tubular lumen in exchange from urate)

What happens inside: leukaemia, cytotoxics- tumour lysis

Hereditary

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31
Q

Rx of acute attack of gout

Include options for renal impairment

A
  1. NSAIDs
  2. Colchicine
  3. Steroids (PO, IM, intraarticular) if AKI/CKD
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32
Q

Long term Rx of gout and it’s indications:

A

Conservative: lose weight
avoid fasts + EtoH + red meats + low dose aspirin

Medical:
allopurinol if 2 attacks in one year, tophi, or urate stones
Start 3 weeks after acute attack, give NSAID cover for 6 months

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33
Q

What are the 3 patterns of calcium pyrophosphate joint disease?

A
  1. Acute calcium pyrophosphate crystal arthritis- large joints often
  2. Chronic calcium pyrophosphate deposition- symmetrical RA like polyarthritis
  3. Osteoarthritis with calcium pyrophosphate deposition- OA with acute pseudogout attacks superimposed
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34
Q

Rx of calcium pyrophosphate deposition in joints?

A

Acute: NSAIDs, intra-articular steroids ± colchicine
Chronic: methotrexate might have a role

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35
Q

7 features of seronegative arthropathies:

A

Who:

  1. Seronegativity (RF -ve)
  2. HLA B27 associated

What joint:

  1. Axial arthritis- spine + sarcoiliitis
  2. Asymmetric large joint oligoarthritis or monoarthritis

What other stuff:

  1. Enthesitis- inflammation of insertion site of tendon/ligament (plantar fasciitis, Achilles tendonitis, costochondritis)
  2. Dactylitis- sausage digit from oedema, tenosynovial + joint inflammation
  3. Extra-articular manifestations: psoriaform rashes, uveitis, oral ulcers, aortic valve incompetence, IBD
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36
Q

How do joint problems present in ankylosing spondylitis?

A

15-30 year old man
Gradual lower back pain
Worse at night, stiff in the morning, better with exercise

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37
Q

Best imaging for ankylosing spondylitis?

A
  1. MRI (most sensitive and better for detecting early disease)
  2. Xray- sacroiliitis with irregularities, erosions, sclerosis
    syndesmophytes (bone forming from enthesitis of ligament)
    bamboo spine- calcification of ligaments

Bloods: FBC, ESR, CRP, HLA-B27 (non-diagnostic)

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38
Q

Management of ankylosing spondylitis:

A

Conservative: Exercise with PT guidance, NSAIDs

Medical: TNFa-blockers, temporary steroids

Surgical: hip replacement if involved

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39
Q

Which conditions affecting the gut are associated with enteric arthropathy (seronegative arthritis)?

A

IBD
GI bypass
Coeliac disease
Whipple’s disease (trophema whippleii)

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40
Q

Nail features of psoriasis?

A

Pitting
Oncholysis (separation from nail bed)
Subungal hyperkeratosis
Thickening

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41
Q

What are the forms of psoriasis?

A
  1. Plaque psoriasis
  2. Small plaque psoriasis (guttate- drop like papules on trunk)
  3. Palmoplantar psoriasis (yellow pustules on a brown base)
  4. Erythrodermic psoriasis (desquamation of 90% of skin)
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42
Q

Management of psoriatic arthritis:

A

NSAIDs
DMARDs: methotrexate, sulphasalazine, ciclosporin
Anti-TNFa biologics

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43
Q

Patient has aysmmetric painful swollen elbow, back and MCP points. What features in the history would suggest a reactive arthritis is the cause?

A

Is it a seronegative arthritis?
Enthesitis- plantar fasciitis, achilles tendonitis, costochondritis
Dactylitis, uveitis, oral ulcers, rashes

Is it secondary to recent:
Urethritis- chlamydia or ureaplasma (may have circinate balanitis = chlamydial painless ulcers)
Dysentery- campylobacter, shigella, salmonella, yersinia

± Keratoderma blenorrhagia (brown raised plaques on soles and palms)

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44
Q

What is the different between diffuse and limited cutaneous systemic sclerosis?

A

Both are due to increased fibroblast activity increasing deposition of connective tissue

Limited cutaneous (CREST)
Slow progression of calcinosis, Raynaud’s, esophageal + gut motility, sclerodactyly, telangiectasia
Anti-centromere (less central organ involvement)

Diffuse cutaneous- organ fibrosis
Rapid progression of lung, cardiac, renal, GI fibrosis
Anti-Scl70 and Anti-RNA polymerase

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45
Q

What is relapsing polychondritis?

A 
Chondritis- inflammation of cartilage
Affects pinna (floppy ears), nasal septum, larynx (stridor) and joints
46
Q

Features of dermatomyositis:

A

Symmetrical proximal muscle weakness- dysphonia, dysphagia, resp weakness

Shawl sign- macular rash over shoulders and back
Helitrope rash ± eyelid oedema
Gottron’s papules- hands, elbows + knees
Nailfold erythema (redness at base of nail)
SC calcifications

Also: fever, arthralgia, Raynaud’s, lung fibrosis, myocarditis

47
Q

Tests for dermatomyositis:

A

Muscle enzymes (ALT, AST, CK, LDH, aldolase)
Electromyography- fibrillation potetnials
Anti-Mi2, Anti-Jo (mijositis? No, myositis)

48
Q

Which autoimmune conditions are often positive for ANA antibodies?

A

(ANA Seager is noisy so SLEep = SHh)
SLE
Srögren’s
Autoimmune hepatitis

49
Q

Which antibodies are associated with SLE?

A

Specific: Anti-dsDNA
Most specific: Anti-Smith

Others: Rheumatoid factor, ANA, Anti-Ro, Anti-La, Anti-RNP
Drug induced: antihistone (better take a good HISTory)

Don’t Stop agent SMITH, R-AN, RoLa-ed and RuNPast

50
Q

Srögren’s is associated with which antibodies:

A

Rheumatoid factor
ANA
Ro
La

(How they’d love to ROw ANA LAke of tears)

51
Q

Liver antibodies to check for?

A

Antimiiiiitochondrial Abs- priiiimary biiiiilary ciiiiirhosis, autoimmune hepatitis

Smoooooth muscle Abs- Autoooooooimmune hepatitis, PBC

52
Q

Antibodies often +ve in diabetes mellitus type 1:

A

Anti-Islet cell Ab

Glutamic acid decarboxylase Ab

53
Q

Antibody associated with thyroid disease?

A

Thyroid peroxidase Ab- Hashimoto’s thyroiditis + Graves

54
Q

What vasculitidies are associated with c-ANCA vs p-ANCA?

A

Most are c-ANCA
imagine a C connecting your node and kidneys (= Wegener’s)

All C have polyangiitis in them-
Granulomatosis Polyangiitis
Microscopic Polyangiitis
Polyangitis nodosum

Main P-ANCA is Churg-Strauss (p for pulmonary as asthma occurs)
Pulmonary-renal aka Goodpasture’s

55
Q

What vasculitidies are C-ANCA +ve?

A

Like a C connecting your nose and kidney (Wegener’s)
All have polyarteriitis in them:

Granulomatous polyarteriitis
Microscopic polyarteriitis
Polyarteritis nodosum

56
Q

What vasculities are P-ANCA positive?

A

P for pulmonary:

Churg Strauss (asthma involvement)
Pulonary-renal vasculitidies (Goodpasture's)
57
Q

What is limbic encephalitis and what antibodies is it associated with?

A

Autoimmune-mediated inflammation of the brain parenchyma

Anti-voltage gated K+ channel Abs

58
Q

10 diagnostic criteria for SLE:

3 skin, 3 blood, 2 surfaces, 3 miscellaneous

A

Skin:
1 malar rash
2 discoid rash
3 photosensitivity

Blood:
1 haem (HAMA, low Plts, 2x low WCC, 2x low lymphocytes)
2 Abs (ds-DNA, Smith, phospholipid)
3 ANA+ve

Surfaces:
1 oral ulcers
2 serositis

Miscellaneous
1 CNS (seizures or psychosis)
2 Bone (proteinuria or cell casts)
3 Non-erosive arthritis x 2 joints
59
Q

What is the pathophysiology of SLE?

A

Polyclonal B cell’s secrete pathological autoantibodies which:

Form immune complexes
Activate complement
Have direct Ab-effects

60
Q

Tests for SLE:

A 
Bloods: 
Coombs +ve haemolytic anaemia
FBC- low WCC,lymphocytes, platelets
ESR, CRP (often normal)
C3, C4 (low)
Antibodies: dsDNA, Smith, RhF, ANA, Ro, La, RNP

BP
Urine microscopy- protein + casts

61
Q

Causes of drug-induced lupus:

A

Drug Induced Problem

Diltiazem (non-hydropyridine for HTN + angina)
Isoniazid (TB)
Phenytoin (epilepsy)

62
Q

Rx of SLE:

A

Acute induction of remission: IV cyclophosphamide + pred
-haemolytic anaemia, severe pericarditis, nephritis
Maintenance: DMARDS- azathioprine, methotrexate, low dose steroids

Skin: topical steroids, sunblock
Kidneys: careful BP control

Biologics- disappointing outcomes so far

63
Q

Features of antiphospholipid syndrome:

A 
CLOTS:
Clots- may cause arterial thrombosis under age 50, or recurrent VTE, or unusual sites (mesenteric, portal vein thrombosis)
Livedo reticularis
Obstetric- 3 miscarriages
Thrombocytopenia
64
Q

What are the different vasculitidies according to vessel size?

A

Large- giant cell arteritis + Takayasu’s arteritis

Median- polyarteritis nodosum + Kawasaki disease

Small- ANCA negative: Henoch Schönlein, ?Goodpasture’s

C ANCA: Granulomatosis polyangiitis (Wegener’s), microscopic polyangiitis

P ANCA: Churg Strauss

65
Q

What are the subtle differences in management if a patient has a large vessel vasculitis vs medium or small vessel?

A

Acute vasculitic attack- everyone gets steroids

Medium or small vessel- add IV cyclophosphamide

66
Q

Symptoms to ask about that suggest giant cell arteritis?

A

Headache
Jaw claudication
Amaurosis fugax
Scalp tenderness

PMR in 50%- bilateral aching, tenderness,morning stiffness

67
Q

In Takayasu’s arteritis, granulomatous inflammation causes which 3 abnormalities in vessels?

A

Stenosis, thrombosis and aneurysms

68
Q

40 year old woman is suspected to have renal artery stenosis, you notice her arm pulses are weak and she has been getting fever, fatigue + feeling dizzy.
What may be the unifying diagnosis + tests to do?

A

Takayasu’s arteritis
HTN from renal artery stenosis + weak pulses

ESR + CRP
MRI or PET

69
Q

Which type of vasculitidies do you get glomerulonephritidies in?

A

ANCA+ve like granulomatous polyangiitis (Wegener’s)

Or Churg Strauss

70
Q

Features of Granulomatosis Polyangiitis (Wegener’s):

A

Eyes- conjunctivitis, scleritis, episcleritis, uveitis
Nose- nasal obstruction, epistaxis, destruction of nasal septum, saddle shaped, sinusitis
Mouth- ulcers
Lungs- cough, haemoptysis, pleuritis
Skin- purpura or nodules

71
Q

Patient age 46 has recently been diagnosed with asthma, recently her creatinine has been increasing and her urine dipstick shows haematuria. What is the diagnosis?

A

Churg Strauss syndrome
Adult onset asthma, eosinophilia and vasculitis
Septic shock picture may occur with glomerulonephritis/renal failure if ANCA +ve

72
Q

65 year old woman comes to her GP surgery with 2 weeks of bilateral aching, tenderness and morning stiffness in shoulders and proximal limb muscles. Feels fatigued, denies weakness or sensation changes.

Differential?

A

Polymyalgia rheumatica (CRP up, CK normal)

Vascular- spinal stenosis
Infection- occult infection
Trauma- osteoarthritis (Cervical spine or shoulder), bilateral impingement
Autoimmune- Recent onset RA, polymyositis
Metabolic- hypothyroidism
Idiopathic- PMR
Neoplasm- occult malignancy

73
Q

How can polymyalgia rheumatica be distinguished from myositis with blood tests?

A

Creatinine Kinase is normal

74
Q

Rx of Polymyalgia Rheumatica?

A

Prednisolone 15mg OD

Consider PPI + bone protection (Vit D/Calcium) as steroids for long ter

If not responding to steroids, revisit diagnosis

75
Q

Diagnostic features of fibromyalgia:

A

Chronic pain >3 months
Widespread- left, right, above and below waist, axial skeleton
Absence of inflammation
11/18 tender points

± morning stiffness, fatigue, poor concentration, low mood, sleep disturbance

76
Q

Where are the 18 ‘tender’ points in fibromyalgia?

A 
On the back: 
2 base of skull
4 base of neck
2 natal cleft
2 posterior to hip trochanter
On the front:
2 base of neck
2 at 2nd rib (midline)
2 lateral elbow in anterior cubital fossa
2 medial knee
77
Q

Management of fibromyalgia:

A

CBT, long term graded exercise programmes
Low dose TCAs + SNRIs which act through noradrenergic system?

Not SSRIs

78
Q

What is chronic fatigue syndrome?

A 
Disabling fatigue >6 months
Affecting physical and mental function
Present 50% of time
And 4 of:
Unrefreshing sleep
Reduced memory

Fatigue after exercise for more than 24 hours
Myalgia
Polyarthralgia

Persistent sore throat
Tender cervical/axillary lymph nodes

79
Q

Difference in diagnostic criteria of fibromyalgia and chronic fatigue?

A

Fibromyalgia >3 months
Chronic fatigue >6 months

Fibromyalgia- physical symptoms for diagnosis: 11/18 tender points
Chronic fatigue- criteria included mental symptoms of reduced memory, unrefreshing sleep, physical criteria include polyarthralgia, myalgia, fatigue

80
Q

Which inflammatory disorders are associated with scleritis and episcleritis?

A

RA
SLE
Vasculitis

81
Q

How are dry eyes tested for?

A

Schirmer filter paper test (<5mm of tear formation in 5 minutes)

= Keratoconjunctivitis sicca

82
Q

Shiny ‘silver wiring’ arteries are seen on fundoscopy of the eye, what is this a sign of?

A

Hardening of the arteries, occurs with atherosclerosis secondary to hypertension.

May also get AV nipping or cotton wool spots if narrowed arteries become blocked

83
Q

Fundoscopy signs of hypertensive retinopathy

A

Think of a hyper tense sheep caught on barbed wire fence, trying to nip it’s way free- might get eaten (flames)

Silver wiring (shiny looking arteries)
AV nipping
Cotton wool spots

Leaks from oedema leave behind hard exudates
Flame haemorrhages = accelerated hypertension

84
Q

What causes amaurosis fugax?

A

Emboli in retinal vasculature causing retinal artery occlusion

Retina may appear pale as reduced blood supply

85
Q

Which rheumatological diseases cause anterior uveitis and which cause scleritis?

A

Anterior uveitis- Ank Spond + Reiter’s (seronegative arthropathies)

Scleritis- RA, SLE, Vasculitis (Wegener’s- GPA)

86
Q

Causes of erythema nodosum?

A

Painful red blue lesions on shins ± arms, thighs

NODOSUM:
No cause- 50%
Drugs- sulphonamides, Dapsone
Oral contraceptives
Strep infections + Sarcoid
UC, Crohns, Beçhet's
Microbiology- viruses, fungi, TB
87
Q

Causes of erythema multiforme?

A

Symmetrical target lesions on palmes, soles, limbs
Forms a spectrum with Stephen-Johnson syndrome (fever + mucosal involvement)

DRUG HIM
Herpes
Idiopathic 50%
Mycoplasma

Drugs- NSAIDs, sulfonamides, allopurinol

88
Q

Which rash is Lyme disease associated with?

A

Erythema marginatum

Small papules at tick site, spreading into erythematous ring with central fading

89
Q

What is the difference between erythema multiforme, migricans and marginatum?

A

Multiforme- occurs on soles, palms and limbs more = DRUG HIM aka drugs (allopurinol, sulphonamides) herpes, idiopathic, mycoplasma

Migrans- centre has a small papule (tick bite site) and centre fades = Lyme

Marginatum- on trunk more, rings come and go = rheum fever associated

90
Q

Pyoderma gangrenosum is associated with:

A

Autoimmune- IBD, Vasculitis (Wegener’s GPA), Autoimmune hepatitis

Neoplastic- myeloma + others

91
Q

Derm manifestations associated with Crohns?

A

Erythema nodosum (the U in NODOSUM is UC, Crohns, Bechet’s)

Pyoderma gangrenosum

92
Q

What is diabetes insipidis?

A

Impaired resorption of water due to lack of ADH (cranial DI) or failure of the kidney to respond to ADH (nephrogenic DI)
ADH is like a bath plug, without it mass amounts of water are lost

Causes hypovolaemic hypernatraemia

93
Q

Causes of cranial diabetes insipidis?

A 
Cranial:
Vascular- Sheehan's syndrome
Infection- meningioencephalitis
Trauma- may be temporary
Autoimmune- autoimmune hypophysitis
Metabolic- iron deposition in pituitary
Idiopathic- 50%
Neoplastic- pituitary tumour, craniopharyngeoma, mets

Congenital- DIDMOAD (diabetes insipidis, diabetes mellitus, optic atrophy, deafness)

94
Q

Causes of nephrogenic diabetes inspidis?

A

No ADH response (no bath plug):

Drugs- lithium
Metabolic- low K+, high Ca+
CKD
Post-obstructive uropathy

95
Q

How is serum osmolality measured?

A

2 x (Na + K) + urea + glucose = 285-295mOsmol/kg

96
Q

Patient is polyuric, dehydrated and polydipsic, their sodium is high. What tests should be done to elucidate endocrinological causes?

A

Glucose- diabetes mellitus
U+E- safety
Ca- a cause of nephrogenic diabetes inspidis
Serum + urine osmolality- osmolality should be 2:1 in urine compared to serum if salt is high, so if urine is more dilute than it should be in light of hypernatraemia suggests diabetes insipidis

97
Q

Test for diagnosing diabetes inspidis?

A

Preliminary: check that daily urine volume >3L (if plasma Na+ plasma osmolality are normal) otherwise not diabetes inspidis

8 hour water deprivation test:

Stage 1- Empty bladder, deprive of fluids for 8 hours
1 hourly weight, ordering serum osmolality if 3% weight loss
2 hourly urine osmolality
4 hourly serum osmolality

If urine is concentrated (>600) not diabetes inspidis

Stage 2- give desmopressin (ADH analogue)
Water can be drunk
See if urine osmolality becomes more concentrated = cranial diabetes inspidis

98
Q

Management of diabetes inspidis, depending on broad type?

A

Cranial DI (on water deprivation test Stage 2, giving desmopressin concentrates urine)

Head MRI
Anterior pituitary function
Rx: Desmopressin

Nephrogenic DI:
Rx: cause
if persistent bendroflumethiazide (inhibits sodium chloride channel)
± NSAIDs (lower urine volume)

99
Q

How is emergency hypernatraemia managed?

A

Lower Na+ very gradually, no more than 12mmol a day to prevent cerebral oedema

0.9% sodium IV to keep up with urine output (where diabetes insipidis is the cause)

100
Q

Complications of acromegaly:

A

Impaired glucose tolerance or insulin resistance (GH phosphorylate insulin R) > DM or ketoacidosis

Hypertension, LVH ± CCF, cardiomyopathy (±arrhythmias)

Colon cancer risk increase

101
Q

Causes of acromegaly:

A 
Pituitary adenoma (5% MEN1)
Ectopic carcinoid tumour
102
Q

Features of acromegaly:

A

Growth of bone- hands, jaw, coarsening face, widened nose
Growth of soft tissue- macroglossia, carpal tunnel, wide spaced teeth, puffy lips/eyelids, snoring

Endo related- low libido, subfertility, goitre, acanthosis nigricans (DM), hypertension

103
Q

Tests for acromegaly:

A

Oral glucose tolerance test: measuring GH levels every 30 minutes during the test

(GH should normally be suppressed by glucose)

104
Q

What causes a false +ve on oral glucose tolerance testing for acromegaly?

A 
Pregnancy
Puberty
Problems with kidneys or liver
Purging- Anorexia nervosa
DM
105
Q

Rx of acromegaly:

A
  1. Transphenoidal surgery
  2. Somatostatin analogues (octreotide) ± radiotherapy
  3. GH antagonist (pegvisomat)
106
Q

Symptoms of hyperprolactinaemia:

A

Women:
Menstrual disturbance- oligomenorrhoea, amenorrhoea
Low libido, dry vagina, infertility (prolactin inhibits GnRH + oestrogen therefore)
Galactorrhea

Men:
Erectile dysfunction (prolactin inhibits GnRH)
Galactorrhea

107
Q

3 causes of hyperprolactinaemia:

A
  1. Excess production by pituitary (levels >5000)
  2. Reduced dopamine inhibition from pituitary stalk, from compression
  3. Use of a dopamine antagonist (antipsychotics)
108
Q

Tests to do in suspected hyperprolactinaemia?

A

Basal prolactin level
Pregnancy test (high normally)
TFTs (hypothyroidism)
U+Es

MRI head if can’t find cause

109
Q

Rx of hyperprolactinaemia?

A
  1. Bromocriptine (DA agonist) to cause inhibition of secretion
  2. Transphenoidal surgery (if Rx resistant)
110
Q

Definition of a macroprolactinoma and how it may be identified from blood tests?

A

Tumour >1mm on MRI
Can cause prolactin levels 10000-100000

Whereas microprolactinomas give levels ~5000

111
Q

Features of Ank Spond

A 
All the A's:
Apical fibrosis
Anterior uveitis
Aortic regurgitation
Achilles tendonitis
AV node block
Amyloidosis
and cauda equina syndrome
peripheral arthritis (25%, more common if female)

MEDICINE NEW (22 decks)

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