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MBBS VI - SpC - Medicine > Rheumatology - COMBINED > Flashcards

Rheumatology - COMBINED Flashcards

1
Q

What are the RF for osteoporosis?

A
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2
Q

What is the classification for causes of osteoporosis?

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3
Q

What are the types of bone and there gross structure?

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4
Q

What is the hormonal regulation of osteoclastogenesis from osteoblasts and stromal cells?

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5
Q

What are the history taking and PE for osteoporosis?

A

FRAX (fracture risk assessment tool):
Medical history: history of fall, fracture
Drug history: glucocorticoid/thyroxine/cyclosporine/tacrolimus/anti-convulsants
Family history: family history of osteoporosis
Social history: smoking, alcoholism, physical inactivity, malnutrition

PE: height and weight measurement (vertebral fracture: kyphosis, height loss)
Signs of secondary causes of osteoporosis: Cushing syndrome, thyrotoxicosis
Factors influencing propensity to fall: vision/hearing/gait/postural sway/muscle strength

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6
Q

What Ix (biochemical and imaging) for osteoporosis?

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7
Q

What is the medical treatment for osteoporosis?

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8
Q

What is non pharmacological management of osteoporosis?

A
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9
Q

What are the general features of OA?
Classification

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10
Q

What are the RF of OA?

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11
Q

What are the pathological features of OA?

A

Cartilage loss + bone remodelling due to uneven loading

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12
Q

What are the SS of OA?

A
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13
Q

What are the hand joints and knees affected in OA?

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14
Q

How is the hip and spine affected in OA?

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15
Q

What is the ddx for OA?

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16
Q

What PE done for OA?

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17
Q

What Ix done for suspected OA?

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18
Q

What is the medical treatment of OA?

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19
Q

What is surgical treatment for OA?

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20
Q

What is the complication of OA?

A

OA with calcium pyrophosphate deposition (CPPD)
 General features
* May be present in as many as 30 – 60% of unselected OA patients
* OA with CPPD is not any more rapidly progressive than OA alone but some may develop
rapidly progressive destructive arthropathy
* Presence of CPPD may modify OA symptoms especially with longer early morning
stiffness and more signs of synovitis

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21
Q

What are the general features of RA?

A

 Inflammatory + Symmetrical + Polyarthritis
* Destruction of joints due to erosion of bone and cartilage
* Stretching of tendons and ligaments
 Progresses from periphery to more proximal joints and results in locomotor disability
 Joint distribution
* Affects hands (PIP/ MCP/ IP of thumbs), wrists, feet (MTP) in the early stages
* Involve other synovial joints including shoulder, elbow, knees and ankles

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22
Q

What is the pathogenesis of RA?

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23
Q

What are the SS of RA?

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24
Q

What are the specific joints involvement in hand RA?

A
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25
Q

How are the wrist, elbow, shoulder
Lower extremities: feet, knees
Cervical spine
Others involved in RA

A
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26
Q

What are the systemic and non articular manifestation of RA?

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27
Q

What is the ddx for RA?

A
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28
Q

How to clinically assess RA?

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29
Q

What is the diagnostic criteria for RA?

A

Three ‘A’s and two ‘6’s
1. Arthritis
2. Antibodies (anti-CCP, RF)
3. Acute phase reactants (ESR, CRP)

  1. 6 weeks duation
    <6 weeks duration: 0
    >6 weeks duration: 1
  2. > 6/10 points = Definite RA
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30
Q

What are the Ix done for RA?

A
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31
Q

What is the medical treatment for RA?

A

Mnemonic: ELISA Please Give Her Methotrexate

E-Etanercept
L-Leflunomide
I-Infliximib
S-Sulfasalazine
A-Anakinra

P-Penicillamine
G-Glucocorticoid + Gold salts
H-Hydroxychloroquine
M-Methotrexate

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32
Q

What is the prognostic factors for RA?

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33
Q

What is the disease activity assessment of RA?

A
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34
Q

What is the response criteria for RA?

A
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35
Q

You are examining a pair of hands. Examination reveals there is ulnar deviation, swan neck deformity, Z- shaped thumb, wasting of hand muscles, rheumatoid nodule. The patient appears to be unable to unbutton clothes.

What is the most likely diagnosis?
What are your differential diagnosis?
What important clinical manifestation helps to make the above differential diagnosis less likely?

A

Most likely dx is Rheumatoid arthritis

ddx
 Polyarticular gouty arthritis and elbow gout tophi ± Bursitis
 Nodular osteoarthritis
 Psoriatic arthritis
 Jaccoud’s arthritis of SLE

More likely RA reasons
 Presence of ulnar deviation, Z-thumb and swan neck deformities makes gout arthritis less likely
 Absence of MCP and wrist involvement makes nodular osteoarthritis less like
 Absence of associated skin psoriatic lesions and presence of subcutaneous nodules makes
psoriatic arthritis less likely
 Presence of rheumatoid nodules makes Jaccoud’s arthritis of SLE less likely

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36
Q

What are the complications of long-standing rheumatoid arthritis?

A
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37
Q

Descirbe the types of drugs used to treat RA and their complications?

A
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38
Q

What are the RF for septic arthritis?
Which joint affected most?

A

Knee affected most

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39
Q

What are pathogens causing septic arthritis?

A
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40
Q

What is the mechanism of infection in septic arthritis?
What is the pathogenesis?

A
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41
Q

What are the SS of septic arthritis
What is the ddx?

A
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42
Q

What are the Ix for septic arthritis?

A
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43
Q

What is medical and surgical management for septic arthritis?

A
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44
Q

What are the general features of gout
What is the 3 classical stages?

A
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45
Q

What are the RF for gout?

A
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46
Q

What are the causes of hyperuricemia?

A
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47
Q

What are the precipitating factors for acute gout attack?

A
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48
Q

What is the pathophysiology of gout?

A
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49
Q

What is the clinical manifestation of gout according to stage?

A
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50
Q

What is the ddx of gout?

A
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51
Q

What is the biochem Ix for gout?

A
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52
Q

What are the radiological Ix for gout?

A
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53
Q

What is the acute management of gout?

A
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54
Q

What is the chronic management of gout?

A
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55
Q

What are the complications of gout?

A
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56
Q

What are the general features of ankylosing spondylitis (part of 1/4 seronegative spondyloarthritis)?

A
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57
Q

What are the musculoskeletal manifestation of ankylosing spondylitis?

A
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58
Q

What are the extra-articular manifestations of ankylosing spondylitis?

A

Mnemonic for ankylosing spondylitis

The six “A”s of Ank spond:
Atlanto-axial subluxation
Anterior uveitis
Apical fibrosis
Aortic regurgitation
Amyloidosis (renal)
Achilles involvement (enthesitis)

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59
Q

What is the diagnostic criteria for ankylosing spondylitis?

A
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60
Q

What is the history taking for ankylosing spondylitis?

A
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61
Q

What is the PE done for ankylosing spondylitis?

A
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62
Q

What are the biochemical Ix done for ankylosing spondylitis?

A
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63
Q

What radiological Ix done for ankylosing spondylitis?

A
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64
Q

What is the management of ankylosing spondylitis?

A
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65
Q

What are the 2 important types of back pain in the clinical practice and what are the major differences between them?

A
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66
Q

What are the important extra-articular features to look for in assessing a patient with inflammatory back pain?

A

 Evidence of skin psoriasis
* Located in scalp, behind ears, peri-umbilical, natal cleft, extensor aspects of elbows,
knees and trunk
 Reiter’s syndrome
* Presents with urethritis and painless urethral discharge
 Eye involvement
* Conjunctivitis and iritis
* Common to all forms of seronegative spondylitis
 CVS derangement
* Aortic regurgitation

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67
Q

What genetic marker may be helpful for investigating a patient with back pain?

A
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68
Q

What is the general features of psoriatic arthritis?

A
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69
Q

What is the ddx of psoriatic arthritis?

A
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70
Q

What is the musculoskeletal manifestation of psoriatic arthritis?

A
71
Q

What is the extraarticular manifestation of psoriatic arthritis?

A
72
Q

What is the diagnostic criteria for psoriatic arthritis?

A
73
Q

What are the biochemical tests for psoriatic arthritis?

A
74
Q

What is history taking and PE for psoriatic arthritis?

A
75
Q

What imaging done for psoriatic arthritis and results?

A
76
Q

What is the medical treatment for psoriatic arthritis?

A
77
Q

What are the general features of reactive arthritis?

A
78
Q

What is the micbio of reactive arthritis?

A
79
Q

What is the preceding infections in reactive arthritis

A
80
Q

What is the musculoskeletal manifestation in reactive arthritis?
What is the extraarticular manifestation in reactive arthritiss?

A
81
Q

What is the ddx of reactive arthritis?

A
82
Q

What is the biochemical tests and imaging done for reactive arthritis?

A
83
Q

What is the treatment of reactive arthritis
disease course

A
84
Q

What is the pathogenesis of SLE?

A
85
Q

What is the precipitating factors for relapse of SLE?

A

 Drug non-compliance (most common)
 Infection
 Stress
* Physical stress including surgery
* Psychological stress
 Pregnancy
 Drug-induced
 UV light exposure

86
Q

What is the ddx for SLE?

A

Less common (3):
* Mixed connective tissue disease: overlapping features of SLE, systemic sclerosis and polymyositis (one disease that is mixed). Expresses anti-U1 ribonucleic protein (Anti-U1 RNP)
* Overlap syndrome: distinct entity where patient is diagnosed to have 2 well defined rheumatological syndorme most commonly SLE and RA
* Undifferentiated connective tissue disease (UCTD): interim label and the actual disease should be defined when patient develop more specific clinical manifestation on follow up.

87
Q

What is the cutaneous involvement in SLE?

A
88
Q

What is the resp, cardi and vascular system involvement in SLE?

A
89
Q

What is the GI, UG, MSS and CNS system involvement in SLE?

A
90
Q

What is the haematological, ophtahlmological involvements and constitutional symptoms in SLE?

A
91
Q

What is the diagnostic criteria for SLE?
Clinical criterion?

A

SLICC diagnostic criteria
4 out of 17 criteria including at least 1 clinical criterion and 1 immunological criterion (OR)
Biopsy proven lupus nephritis with +ve ANA or anti dsDNA

Serositis
Oral ulcer
Arthritis
Photosensitivity

Blood (all bloods are low)
Renal protein loss
ANA
Immunologic (DS-DNA)
Neurologic (psych, seizure)

Malar rash
Discoid rash

92
Q

What is the diagnostic criteria for SLE?
Immunological criterion?

A
93
Q

What are the basic blood tests done for SLE?

A
94
Q

What are the specific blood tests for SLE?

A

Direct antiglobulin test (Coombs test): detect antibodies on the RBC –> use of anti human IgG (AHG reagent) and anticomplement antibodies if patients RBC is coated by Ig
Indications: transfusion reaction, hemolytic disease of the newborn, autoimmune hemolysis, drug induced hamolysis. Positive DAT result: suggests presence of immune mediated haemolytic process

Anti-Histone (drug-induced SLE) = hi STONED on drugs

95
Q

What are the absolute contraindications and relative contraindications for renal biopsy in SLE?
What prebiopsy evaluation done
What compliciations?

A
96
Q

What is the classification of lupus nephritis from renal biopsy and the treatment based on class?

A

I - No: Normal kidney
II - Man: Mesangial GN
III - Faces: Focal proliferative GN
IV - Diffuse: Diffuse proliferative GN
V - Menstrual: Membranous GN
VI - Situation: Sclerosing GN

97
Q

What is the imaging Ix for SLE?

A
98
Q

What are the general measures for SLE management?

A

In about 42% of patients with SLE-related PAH there have been detected antibodies against the endothelin receptor type A [19,31]. Those antibodies promote endothelial dysfunction and inhibit prostacyclin production, one of the main vasodilators, which result in elevated pulmonary artery pressure [19].

99
Q

What is the pregnancy management in SLE?

A
100
Q

What is the medical treatment for SLE?

A
101
Q

What is the prognosis for SLE?

A
102
Q
A

 Acute nephritic syndrome secondary to lupus nephritis

103
Q

In addition to those that had been done already, what are the most relevant investigations, and what are the expected findings?

A
104
Q

What drugs commonly used as specific treatment for lupus nephritis?

A

 Corticosteroids
* At moderate to high dose with gradual tapering
 Cyclophosphamide (Oral/ IV)
* Combined with corticosteroids
* Given for 2 – 6 months
 Azathioprine/ Mycophenolate mofetil
* Maintenance therapy following cyclophosphamide

105
Q

Apart from the lupus nephritis, what associated complications require attention (i.e. monitoring, prevention and treatment)?

A

 Hypertension
 Hyperlipidemia
 Complications of treatment
* Leukopenia
* Infection
* Alopecia (Cyclophosphamide)
* Amenorrhea (Cyclophosphamide)

106
Q

Q1: What are the possible causes of fever in this patient?
Q2: What are the possible causes of this patient’s chest pain?

A

 Relapse of underlying SLE
 Infection due to immunocompromised
* SLE itself is immunocompromising
* Patient is taking corticosteroids and azathioprine

 Serositis (Inflammation of serous tissue: pleura/ pericardium/ peritoneum)
* Manifestation of lupus or secondary to a chest infection
 Pulmonary embolism ± infarction
* Can give rise to pleuritic chest pain
* Complication is rare

107
Q

Q3: What further investigations would you undertake for this patient?
Q4: How should this patient be treated if her problem was secondary to her relapse alone?
Q5: What is the likely cause of this patient’s right hip pain?
Q6: How would you control this patient’s right hip pain?

A

3.
 Delineate underlying infection (Septic workup): CXR, Blood cultures, Sputum and urine smears and culture
 Delineate possible SLE relapse: ANA, anti-dsDNA, serum C3/4, Coomb’s test, Hemolysis screen
 Delineate possible renal involvement during relapse: Urine microscopy, 24-hour urinary protein and creatinine estimation, Renal biopsy

 Increase dosage of immunosuppressant
* Increased steroid dosage
* Azathioprine is substituted by a more potent agent such as cyclophosphamide, cyclosporin A or mycophenolic acid

 Bone necrosis of right femoral head
* Related to chronic steroidal usage
* Active SLE can also cause this condition due to underlying vasculitis

 NSAIDs
 Steroid dosage adjustment
* Dosage should be kept to minimum to prevent necrosis of the other hip
 Physiotherapy
 Referral to orthopedic surgeon
* For consideration of surgery

108
Q

What are the general features/hallmarks of systemic sclerosis/scleroderma?

A
109
Q

What is the classification for systemic sclerosis

A
110
Q

What is the skin and vascular involvement of systemic sclerosis?

A
111
Q

What is the extracutaneous organ involvement of systemic sclerosis?

A
112
Q

What is the diagnostic criteria for systemic sclerosis?

A
113
Q

What are the biochemical tests/antibodies for systemic sclerosis?

A
114
Q

What is the imaging ix for systemic sclerosis?

A
115
Q

What are the principles of treatment for systemic sclerosis?

A
116
Q

What is the medical treatment for systemic sclerosis?

A
117
Q

A patient complains of purplish discoloration of her fingers. On physical examination, there is tight skin, small mouth, sclerodactyly and thickened skin.
Q1: What is the most likely diagnosis?
Q2: What tests will you do to confirm the diagnosis?
Q3: What are the complications?

A

 Systemic sclerosis (Scleroderma)

118
Q

What are the general features of Sjogren syndorme?
What is the classification of Sjogren syndrome?

A
119
Q

What is the pathogenesis and histopathology of Sjogren syndrome?

A
120
Q

What is the clinical manifestation (exocrine gland) of Sjogren syndrome?

A
121
Q

What is the extralglandular clinical manifestation of Sjogren syndorme (i.e. resp, cardi, GI, urogenital, musculoskeletal)?

A
122
Q

What is the extralglandular clinical manifestation of Sjogren syndorme (i.e. derm, neuro, haem)?

A
123
Q

What is the ddx for sjogren syndrome?

A
124
Q

What is the diagnostic criteria for Sjogren syndrome?

A
125
Q

What are the biochemical tests for Sjogren syndorme?

A
126
Q

What are the specific tests for clinical manifestation of Sjogren syndrome?

A
127
Q

What are the imaging ix for sjogren syndrome?

A
128
Q

What is the general and medical treatment for sjogren syndrome?

A
129
Q

What is the complications of sjogren syndrome?

A
130
Q

What are the general features of dermatomyositis and polymyositis?

A
131
Q

What is the muscle manifestation of dermatomyositis and polymyositis (PM)?

A
132
Q

What are the skin manifestations of dermatomyositis and polymyositis?

A
  • Gottrons papule: erythematosus or violaceous rash. Located symmetrically on dorsal surface of MCP, PIP and DIPJ
  • Heliotrope eruption: erythematous to violaceous eruption on upper eyelids –> accompanied with eyelid edema
  • Facial erythema
  • Photodistributed poikoloderma: poikiloderma refers to skin that demonstrates hyperpigmentation and hypopigmentation as well as telangiectasia and epidermal atrophy. Photodistributed sites: upper back (shawl sign), neck and upper chest (V sign)
  • Holster sign: poikiloderma in the lateral aspects of thigh which is a photoprotected site
  • Periungual abnormalities: capillary nail beds may be erythematous and show vascular changes observed in systemic sclerosis and SLE. Abnormal capillary nail bed loops may be evident with alternating areas of dilatation and dropout and periungual erythema
  • Psoriasiform changes in scalp: scalp changes in resembling psoriasis or seborrheic dermatitis
  • Calcionosis cutis: deposition of calcium within the skin
133
Q

What are the associated conditions with dermatomyositis and polymyositis?

A
134
Q

What is the ddx of dermatomyositis and polymyositis?

A
135
Q

What is the diagnostic criteria of dermatomyositis and polymyositis?

A
136
Q

What are the basic blood tests for dermatomyositis and polymyositis?

A
137
Q

What autoantibodies tested for in dermatomyositis and polymyositis?

A
138
Q

What are more invasive ix for dermatomyositis and polymyosiits?

A
139
Q

What non basic Ix done for dermatomyositis and polymyositis?

A
140
Q

What is the medical treatment for dermatomyositis and polymyositis?

A
  • Glucocorticoids: imrpoves strength and preserves muscle function
    High dose steroid or pulse steroid as initial function. High dose steroid = PO prednisolone 1mg/kg/day (max = 80mg/day). Pulse steroid = IV methylprednisolone 1g/day for 3 days. Steroid sparing agents should be initially together with glucocorticoid treatment to reduce cumulative dose of steroid and diminish steroid induced morbidity.
  • Azathioprine: antimetablite (purine antagonist): inhibits adenine and guanine ribonucleatide production and hence decreases intracellular purine synthesis. Incorporates into replicating DNA as false nucleotides to stop replication. AE: myelosuppression/hepatotoxicity/pancreatitis
  • Methotrexate: antimetabolite –> irreversibly binds and inhibits dihydrofolate reductase (DHFR), inhibits formation of reduced folates and thymidylate synthetase resulting in reduced purine and thymidylic acid synthesis. AE: pulmonary toxicity, hepatototixicty, nephrotoxicity, myelosuppression
  • Hydroxychloroquine: effective in 75% of patients in controlling skin diseae but without any benefit to muscle disease. AE: GI disturbance most common (nausea/vomiting), hyperpigmentation, myopathy and neuropathy, retinopathy (bulls eye maculopathy)
  • IVIG: reasonable 2nd line agent for patients with refractory disease. Indicated in selected patients with severe life threatening weakness or patients with severe dyspahgia at risk for aspiration. AE: headache, thromboembolism, anaphylaxis in patients with IgA deficiency, transfusion related acute lung injury, transfusion volume overload (TACO)
141
Q

What are the complications of dermatomyosis?

A

 MOST common fatal complications
* Aspiration pneumonia due to dysphagia
* Interstitial lung disease (ILD)
* Myocarditis
o Leads to conduction abnormalities and fatal arrhythmia

142
Q

What are the general features of vasculitis?
What is the general classification based on size of vessel affected?

A
143
Q

What are the types of large vessel vasculitis?

A

Takayasu Arteritis
- Transmural fibrous thickening of aortic branches
- Japanese women <40 y/o
- ‘Pulseless disease’ (subclavian artery disease = decreased or uneven blood supply to upper limbs)
- Uneven BP in upper extremities + Parasthesia
- Elevated ESR

Samurai getting their arm cut off = transmural fibrous thickening

Giant Cell (Temporal) Arteritis:
- Intimal thickening & fragmentation of lamina
- Increased ESR
- Jaw claudication & temporal headaches
- Polymyalgia Rheumatica
- Visual Problems (ophthalmic artery)

Give high dose corticosteroids BEFORE BIOPSY (prevent blindness)

Give Corticosteroids Ammediately
Gas Claudication Always

144
Q

What are the types of medium vessel vasculitis?

A

Polyaarteritis Nodosa
- Transmural Arteritis w/ fibrinoid necrosis
- Renal, coronary, mesenteric

‘String of Pearls’ appearance on Biopsy
- Fibroid => Necrosis => Fibroid => Necrosis

  • +ve HBsAg

PlaN-B: Give pearls

Kawasaki Disease
- Necrotising vasculitis involving coronary arteries
- Can cause MI in children = give IV immunoglobulin + aspirin (which may cause Reye’s syndrome)
- AdenOpathy
- Oropharyngeal signs
- Desquamation

The cow (Kaw) that Moo’d!

145
Q

What are the types of small vessel vasculitis?

A

HSP:
- AKA IgA vasculitis
+ Haematuria
+ Palpable purpura
+ Arthralgia
+ GI pain, + IgA deposition, follow recents URI (B19 & GaS)
HSP = has stomach pain

Cryoglobulinemic Vasculitis:
- AKA, HepC vasculitis
+ Haematuria
+ Palpable purpura
+ Arthralgia
no GI pain, + HepC & Cryoglobulin deposition, treat underlying HepC
CGV = C gets Viral

Churg-Strauss Syndrome
- AKA Eosinophilic Granulomatosis with Polyangiitis
- Necrotising, eosinophilic, granulomatous infiltration
- p-ANCA
- Asthma/Allergic rhinitis
- Polyps
- Antibodies
- Peripheral neuropathy
(PAPAP)

Wegner Granulomatosis
- AKA Granulomatosis with polyangiitis
- c-ANCA (draw C which overlaps NP, lung, kidney)
- We-C-Ner = nasopharynx, lungs, kidneys

Microscopic polyangiitis
- p-ANCA
- lungs & kidneys (NO nasopharynx)
- Draw P over body, P crosses lungs and kidneys)

146
Q

What are the types of variable vessel vasculitis?

A
147
Q

What are the types of single vessel vasculitis?

A
148
Q

What are the types vasculitis associated with systemic disease?

A
149
Q

What are the types vasculitis associated with probable etiology?

A
150
Q

What are the distinguishing characteristics of vasculitis subtypes?

A
151
Q

What are the general features of eosinophilic granulomatosis with polyangiitis (EGPA) and the comparison of ANCA associated small vesel vasculitis?

A

Churg-Strauss Syndrome
- AKA Eosinophilic Granulomatosis with Polyangiitis
- Necrotising, eosinophilic, granulomatous infiltration
- p-ANCA
- Asthma/Allergic rhinitis
- Polyps
- Antibodies
- Peripheral neuropathy
(PAPAP)

Wegner Granulomatosis
- AKA Granulomatosis with polyangiitis
- c-ANCA (draw C which overlaps NP, lung, kidney)
- We-C-Ner = nasopharynx, lungs, kidneys

Microscopic polyangiitis
- p-ANCA
- lungs & kidneys (NO nasopharynx)
- Draw P over body, P crosses lungs and kidneys)

152
Q

What are the SS of EGPA (eosinophilic granulomatosis with polyangiitis)?

A

Churg-Strauss Syndrome
- AKA Eosinophilic Granulomatosis with Polyangiitis
- Necrotising, eosinophilic, granulomatous infiltration
- p-ANCA
- Asthma/Allergic rhinitis
- Polyps
- Antibodies
- Peripheral neuropathy
(PAPAP)

153
Q

What is the Ix to make dx of EGPA (eosinophilic ganuloatmosis with polyangiitis)?
What is the treatment?

A
154
Q

What are the general features of granulomatosis with polyangiitis (GPA) (Wegeners granulomatosis) and comparison of ANCA associated small vessel vasculitis?

A

Wegner Granulomatosis
- AKA Granulomatosis with polyangiitis
- c-ANCA (draw C which overlaps NP, lung, kidney)
- We-C-Ner = nasopharynx, lungs, kidneys

155
Q

What is the SS of granulomatosis with polyangiitis (GPA) (Wegeners granulomatosis)?

A
156
Q

What is the Ix (basic and imaging) for granulomatosis with polyangiitis (GPA) (Wegeners granulomatosis)?

A
157
Q

What is the treatment principle for granulomatosis with polyangiitis (GPA) (Wegeners granulomatosis)?

A
158
Q

What are the general features of microscopic polyangiitis (MPA)?
Comparison of ANCA associated small vessel vasculitis

A

Microscopic polyangiitis
- p-ANCA
- lungs & kidneys (NO nasopharynx)
- Draw P over body, P crosses lungs and kidneys)

159
Q

What are the SS of microscopic polyangiitis and the Ix done to make dx?

A
160
Q

What is the treatment principle of microscopic polyangiitis?

A
161
Q

What is the general features of amyloidosis?

A

 Deposition of misfolded and insoluble fibrous proteins in normal organs and tissues
* Extracellular tissue deposition of fibrils composed of subunits of a variety of proteins many of which circulate as plasma constituents
 Type of precursor protein, tissue distribution and the amount of amyloid deposition largely determine the clinical manifestation

162
Q

What is the classification of amyloidosis?

A
163
Q

What are the SS of amyloidosis?

A
164
Q

What are the essential Ix to make a dx of amyloidosis?

A
165
Q

What is the treatment of amyloidosis depending on type?

A
166
Q

What is cryoglobulinemia?

A

Cryoglobulinemic Vasculitis:
- AKA, HepC vasculitis
+ Haematuria
+ Palpable purpura
+ Arthralgia
no GI pain, + HepC & Cryoglobulin deposition, treat underlying HepC
CGV = C gets Viral

167
Q

What is cryoglobulinemia syndrome
Essential mixed cryoglobulinemia?

A

 Cryoglobulinemic syndrome
* Form of immune-complex mediated systemic vasculitis involving small and medium- sized arteries and veins
 Essential mixed cryoglobulinemia
* Traditional term for idiopathic (primary) vasculitis caused by circulating CGs that contains both a polyclonal IgG and an IgM with rheumatoid factor (RF) activity which are called mixed CGs

168
Q

What is the Brouet classification for cryoglobulinemia?

A
169
Q

What are the causes of crygoglobulinemia?

A
170
Q

What is the pathogenesis of cryoglobulinemia?

A
171
Q

What are the SS of type 1 cryoglobulinemia?

A
172
Q

What are the SS of type 2 and type 3 (mixed) cryoglobulinemia?

A
173
Q

What are the Ix done for cryoglobulinemia?

A
174
Q

What is the treatment principle of cryoglobulinemia?

A

MBBS VI - SpC - Medicine (80 decks)

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