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5th year blocks > Internal medicine - Infecto and rheuma > Flashcards

Internal medicine - Infecto and rheuma Flashcards

1
Q

Define SLE

A

Multisystem AI disease predominantly affects women of childbearing age and is the most common form of lupus.

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2
Q

Epidemiology of lupus?

A

Age of onset in women is 15-44 and
Sex; 10:1 female: male

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3
Q

SLE etiology

A

The exact etiology is unknown, but several predisposing factors have been identified.

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4
Q

Predisposing factors for SLE

A

Genetic predisposition
→ HLA-DR2/HLA-DR3 are commonly present in individuals with SLE.
→ Genetic deficiency of classical pathway (C1q, C2, C4) in10% of

Hormonal factors:
→ Hyperestrogenic states (due to oral contraceptive use, postmenopausal hormonal therapy, endometriosis)

Environmental factors
→ Cigarette smoking and silica exposure increase the risk
→ UV light and EBV infection may trigger disease flares

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5
Q

Mechanism behind SLE

A
  1. Deficiency of classical complement proteins (C1q, C4, C2)
  2. Failure of macrophages to phagocytose immune complexes and apoptotic cell material (plasma and nuclear antigens)
  3. Dysregulated, intolerant lymphocytes targeting normally hidden intracellular antigens → autoantibody production (ANA, anti-dsDNA)
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6
Q

Autoimmune reactions in SLE

A

Type III hypersensitivity (most common in SLE) → antibody-antigen complex formation in microvasculature → complement activation and inflammation → damage to skin, kidneys, joints, small vessels

Type II hypersensitivity → IgG and IgM antibodies directed against antigens on cells (e.g., red blood cells) → cytopenia

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7
Q

Most common symptom involvement in SLE

A

Constitutional
Joints
Skin

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8
Q

Skin symptoms involvement in SLE

A

▪ 85% of cases
▪ Malar rash (butterfly rash)
▪ Raynaud phenomenon
▪ Photosensitivity → maculopapular rash
▪ Discoid rash
▪ Oral ulcers (usually painless)
▪ Nonscarring alopecia (except with discoid rashes)

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9
Q

Constitutional symptoms involvement in SLE

A

▪ Fatigue
▪ Fever
▪ Weight loss

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10
Q

Joint symptoms involvement in SLE

A

▪ 90% of cases
▪ Arthritis and arthralgia
▪ Distal symmetrical polyarthritis
▪ No deformity in MCI PIP like in RA

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11
Q

Less common symptom involvement in SLE

A

Hematological
Musculoskeletal
Serositis
Kidneys
Heart
Lungs
Vascular
Neurological

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12
Q

Diagnosis of SLE criteria

A

Consider if constitutional symptoms and > 2 organ manifestations

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13
Q

MINIMUM diagnostic criteria for SLE

A

Antinuclear antibodies (ANAs)
Antigen-specific ANAs: Request only if ANAs are positive.
Screen all for antiphospholipid syndrome
Laboratory markers of disease activity and/or organ damage

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14
Q

Antigen-specific ANAs:

A

Anti-dsDNA antibodies
Anti-Sm antibodies: Smith antigens (nonhistone nuclear proteins)

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15
Q

General principle of SLE treatment

A

Usually require life-long immunosuppressants.
Management is guided by disease severity and organs affected
Should be frequently monitored: medication-induced adverse effects.
NSAIDS can provide symptomatic relief
Lifestyle change: moking, exercise
Avoid UV light

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16
Q

Pharmacotherapy in SLE

A

All patient use Hydroxychloroquine regardless of activity
Mild to moderate: add oral GC +/- immunosupressants
Severe: Induction and maintenance therapy

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17
Q

Severe SLE: Induction and maintenance therapy

A

Induction therapy
o High-dose IV glucocorticoids (methylprednisolone)
o Immunosuppressive agents (cyclophosphamide)

Maintenance of remission
o Hydroxychloroquine with or without lower dose GC
o AND/OR immunosuppressants
o OR biological agents (rituximab)

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18
Q

Define RA

A

Rheumatoid arthritis (RA) is a chronic, systemic, inflammatory autoimmune disorder that primarily affects the joints.
Causes pain, swelling, synovial destruction, deformities

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19
Q

Epidemiology of RA

A

Affects women (3:1)
Peak incidence: > 65 years.

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20
Q

Risk factors for RA

A

→ Genetic disposition: associated with HLA-DR4 and HLA-DR1
→ Environmental factors (e.g., smoking)
→ Hormonal factors (premenopausal women are at the highest risk)
→ Infection
→ Obesity
→ Family history of RA

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21
Q

Mechanism of RA

A
  1. Conversion of arginin to citrulline (citrullination)
  2. Active CD4+ T- cells gets activated by this
  3. IL secretion and B-cell activation - Anticitrullinated Ab
  4. Type II and III HS reaction
  5. CD4+ cells go to joints causing 3 things
  6. Inflammation, Angiogenesis, Proliferation
  7. Ab against IgG called Rheumatoid factor is made to remove the Ag and immune complexes
  8. RF triggers formation of new complexes and HS III reactions
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22
Q

Articular symptoms in RA

A

Polyarthralgia
Morning stiffness
Joint deformity

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23
Q

Extraarticular symptoms in RA

A

Same as SLE + Rheumatoid nodules in skin and lungs

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24
Q

General treatment approach in RA

A

Acute disease flares: GC and NSAIDS
Long term treatment: Monotherapy with DMARD OR Biological

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25
Acute disease flare in RA treatment
GC: Lowest dose <3 months, long term only if no respons to DMARD NSAIDS: relief pain but does not help in progression
26
Long term RA treatment
ALL patients get monotherapy by DMARD Interfere with RA inflammation and can lead to remission Reduce morbidity by 30%
27
DMARD
1. Methotrexate (MTX): First line in moderate to high disease activity 2. Hydroxychloroquine: If low activity disease 3. Sulfasalazine: If MTX is contraindicated (pregnancy) 4. Leflunomide: if all other DMARD are CI
28
Biological treatment in RA
▪ TNF-α inhibitors: e.g., adalimumab, infliximab, etanercept ▪ Others: rituximab
29
Treatment target strategi in RA
▪ Target at 3 months: ≥ 50% improvement in the disease activity index ▪ Target at 6 months: low disease activity (or remission) ▪ Targets not reached: Consult rheumatology to adjust treatment.
30
Diagnostic tools in RA
CLINICAL!! LAbs Imaging (X-ray)
31
Criteria of diagnosis in RA (when to consider)
Patients with arthralgia, joint stiffness, and synovitis lasting ≥ 6w
32
Spesific parameters in lab to diagnose RA
▪ Anticitrullinated peptide antibodies (ACPA) (90%) ▪ Rheumatoid factor (RF): IgM autoantibodies against the Fc region of IgG ▪ Serological studies may be negative (seronegative RA)
33
X-ray findings in RA
▪ Early: soft tissue swelling, osteopenia ▪ Late: joint space narrowing, marginal erosions of cartilage and bone, osteopenia, subchondral cysts
34
Define Seronegative spondylarthritis
Include several chronic inflammatory arthritic diseases that affect the vertebral column.
35
Types of seronegative spondylarthritis
▪ Ankylosing spondylitis (most common) ▪ Reactive arthritis ▪ Psoriatic arthritis ▪ Spondyloarthritis associated with inflammatory bowel disease (IBD) ▪ Undifferentiated spondyloarthropathy ▪ Peripheral spondyloarthritis ▪ Juvenile spondyloarthritis
36
Diagnosis of Spondylarthritis?
▪ Negative for rheumatoid factor ▪ Genetic association with HLA-B27
37
Epidemiology of spondylarthritis
▪ Generally more commonly affect men ▪ Age of onset: typically between 20–40 years of age
38
Symptoms of spondylarthritis
▪ Non-specific symptoms (fever, fatigue, weight loss) ▪ Arthritis o Insidious, often unilateral onset o Particularly of the sacroiliac joints o Asymmetrical peripheral oligoarthritis o Stiffness and pain is worse in the morning (typically > 30 minutes) o Usually responds well to NSAID therapy ▪ Insertional tendinopathy (e.g., achillodynia) ▪ Dactylitis: fingers have a sausage-like appearance
39
Define gout
Gout is an inflammatory crystal arthropathy caused by the precipitation and deposition of uric acid crystals in synovial fluid and tissues
40
Etiology of gout
Primary hyperuricemia Secondary hyperuricemia
41
Secondary hyperuricemia
Decreased uric acid excretion: most common cause Increased uric acid production
42
what is uric acid
An end-product of purine metabolism that is excreted by the kidneys Has somewhat poor water solubility
43
What trigger urate crystals to form
↑ Uric acid (due to insufficient excretion/increased production of purines) ▪ Acidosis ▪ Low temperature (cool peripheral joints)
44
States of increased uric acid production
High cell turnover: ▪ Tumor lysis syndrome ▪ Hemolytic anemia ▪ Psoriasis ▪ Myeloproliferative neoplasms ▪ Chemotherapy, radiation
45
states causing decreased uric acid secretion
o Medications (pyrazinamide, aspirin, loop diuretics, thiazides, niacin) o Chronic renal insufficiency o Ketoacidosis (starvation, diabetes mellitus) and lactic acidosis
46
Symptomes of Gout
o Acute pain, erythema, decreased motion, swelling, warmth o Possibly fever o Symptoms are likely to occur at night, waking the patient. o Symptoms peak 12–24 hours and regress over days/weeks. o Desquamation of the skin overlying the joint seen during recovery
47
Diagnosis of gout
1. Assess the clinical probability of acute gout. 2. If relatively low: Arthrocentesis with synovial fluid analysis 4. If relatively high: Diagnostic tests are not routinely required.
48
treatment of gout
▪ Nonpharmacological measures: Rest and ice the joint. ▪ Pharmacotherapy: Initiate within 24 hours of onset. o First-line agents: GC, NSAIDs, or colchicine
49
when do we give GC + Colchicine in gout?
Indicated for attacks involving ≥ 4 joints, > 1 large joint, or severe pain
50
Two large classifications of small artery vasculitis
ANCA associated Non ANCA associated
51
What is small vessle vasculitis
Heterogeneous group of rare AI diseases characterized by blood vessel inflammation (vasculitis). Inflammation can lead to ischemia, necrosis, and/or hemorrhage, with subsequent end organ damage.
52
Granulomatosis with polyangiitis
→ Most often in adults 40–60 years of age; ♂ > ♀ → Chronic sinusitis/rhinitis, saddle nose deformity → Chronic otitis media and mastoiditis → Treatment-resistant pneumonia-like symptoms → Rapidly progressive glomerulonephritis
53
Eosinophilic granulomatosis with polyangiitis
→ Severe allergic asthma, sinusitis → Skin manifestations (e.g., tender nodules) → Peripheral neuropathy → Gastrointestinal, cardiac, and/or renal involvement
54
Microscopic polyangiitis
→ Pauci-immune glomerulonephritis → Hypertension → Palpable purpura → Like granulomatosis with polyangiitis but spares the nasopharynx
55
IgA vasculitis
→ Mostly affects children (90% of patients are < 10) → Palpable purpura on lower limbs → Arthritis and/or arthralgia → Abdominal pain → Hematuria if IgA nephropathy is present → Often secondary to URTIs
56
Cryoglobulinemic vasculitis
→ Fatigue → Arthralgia → Palpable purpura → Glomerulonephritis → Most cases are 2nd to cryoglobulinemia due to HCV
57
Large Vessels vasculitis
Giant cell vasculitis Takayasu Vasculitis
58
Giant cell vasculitis clinical
→ Most commonly affects women > 50 years → Visual impairment: may result in blindness → New-onset headache → Tender temporal artery → Jaw claudication → Associated with polymyalgia rheumatica
59
Giant cell vasculitis diagnosis
→ ↑ ESR (≥ 50 mm/hour), ↑ CRP → Negative autoantibody studies → Temporal artery biopsy (gold standard): granulomatous inflammation
60
Giant cell vasculitis management
→ High-dose glucocorticoids to prevent permanent vision loss
61
Takayasu Vasculitis clinical
→ Most commonly affects Asian women < 40 years → Disparity in blood pressure between arms (Takayasu is also known as pulseless disease) → Bruit over subclavian artery or abdominal aorta → Syncope and angina pectoris
62
Takayasu Vasculitis diagnosis
→ ↑ ESR, ↑ CRP → MR angiography: vascular wall thickening with luminal stenosis or occlusion of the aorta and major branches → Angiography: stenosis of aortic arch/great vessels → Biopsy: granulomatous inflammation of the aorta
63
Takayasu Vasculitis management
→ Glucocorticoids → PLUS a glucocorticoid-sparing agent (methotrexate, azathioprine, infliximab)
64
Medium Vessel vasculitis
Kawasaki disease Polyarteritis nodosa
65
Kawasaki clinical
→ Most often occurs in children < 5 years → "CRASH (Conjunctivitis, Rash, Adenopathy, Strawberry tongue, Hand-foot changes) and BURN (≥ 5d fever)
66
Kawasaki diagnosis
→ ↑ ESR, ↑ CRP, thrombocytosis → Echocardiography: coronary artery aneurysms Criteria: 5d fever + 4 other symptoms
67
Kawasaki management
→ High-dose aspirin PLUS IVIG
68
Define Polyarthritis nodosa
A systemic vasculitis of medium-sized vessels that most commonly affects the skin, peripheral nerves, muscles, joints, gastrointestinal tract, and kidneys, but usually spares the lungs.
69
Etiology of polyarthritis nodosa
Mostly idiopathic Hepatitis B Hepatitis C HIV CMV
70
Organ involvement in polyarthritis nodosa
▪ Renal involvement (∼ 60%): hypertension, renal impairment ▪ Coronary artery involvement (∼ 35%); ↑ risk of MI ▪ Skin involvement (∼ 40%): rash, ulcerations, nodules ▪ Neurological involvement: polyneuropathy, stroke ▪ GI involvement: abdominal pain, melena, nausea, vomiting
71
Diagnosis of polyarthritis nodosa
Visceral angiography of affected organ ▪ Findings: mostly in renal, mesenteric, and hepatic arteries ▪ Numerous microaneurysms (1–5 mm in diameter) ▪ Stenosis of small muscular arteries and medium-sized vessels
72
Treatment og polyarthritis nodosa
Severe: IV methylprednisolone + cyclophosphamide Mild: High dose oral prednisone + methotrexate
73
Define Sjogrens syndrome
Chronic inflammatory autoimmune disease that most commonly occurs in middle-aged women. Primary Sjogren syndrome is idiopathic Sjogren syndrome that occurs concomitantly with another autoimmune disease classified as secondary Sjogren syndrome. Sjogren syndrome most commonly manifests with sicca syndrome but can also manifest with systemic symptoms
74
Sjogrens diagnosis
Consider Sjogren syndrome in patients with features of sicca syndrome without a known cause. Positive anti-Ro/SSA or anti-La/SSB autoantibodies
75
Gene as with sjogrens
HLA-DR52
76
Clinical symptoms
Xerostoma Xeropthalmia Xerosis (skin) Vaginal dryness Nasal dryness Pharyngeal/laryngeal dryness
77
Systemic Sjogren involvment?
▪ Arthralgias and/or arthritis (most common systemic symptom) ▪ Raynaud phenomenon ▪ Constitutional symptoms: fever, weight loss, fatigue ▪ GI involvement: dysphagia, dyspepsia, reflux esophagitis ▪ Pulmonary involvement: interstitial lung disease ▪ Vasculitis ▪ Autoimmune thyroiditis ▪ Neurological involvement, e.g., peripheral neuropathy, myelitis
78
treatment of sjogrens
Frequent water intake Caries prophylaxis - frequent dental visits Artificial salvia Oral muscarinic agonists (PILOCARPINE) Eyedrops NSAIDS Low dose GC if needed in systemic
79
HS reaction in allergy?
Type I
80
Stages of an allergic reaction?
Sensitization Subsequent effective stage
81
Immediate vs late allergic response?
Immediate: mast cell degranulation Late: Chemokine + other mediators cause inflammation
82
Allergy types?
Food (nuts, egg, soy, milk, shellfish) Animal source (bee, wasp, cats, insects, rats) Enviromental (dust, mites, latex, pollen, mold) Atopic disease (Allergic asthma, rhinitis, conjunctivitis, dermatitis) Transfusion reaction Drug induced (penicillin, Sulfa-drugs, allopurinol, SNAIDS)
83
Allergy testing
Skin prick test or skin scratch test Direct IgE allergen essay Total serum IgE levels
84
Desensitization in allergy
No relief from treatment or from avoiding allergen Do allergen immunotherapy Introduce allergen in small doses slowly increasing goal is tu make mast cells produce IgG not IgE Called isotype switching and lasts for 3 years
85
Define Anaphylaxis
Bronchospasms (wheezing) Laryngeal edema (dyspnea) Hypotension (circulatory collapse)
86
Managment of anaphylaxis
1. Epi penn with 0.3mg adrenalin 2. In hospital administration og 0-5-1g adrenaline 3. High flow O2 4. IV crystalloids 5. Antihistamins 6. Corticosteroids (IV hydrocortisone or inhaled salbutamol)
87
Define Systemic
Systemic sclerosis (SSc) is a systemic autoimmune disease characterized by vasculopathy and fibrosis of the skin and other organs. Based on the extent of cutaneous involvement, SSc is categorized as limited or diffuse
88
3 main points of scleroderma pathology
▪ Autoimmunologic component ▪ Inflammatory synthesis of extracellular matrix: fibrosis ▪ Noninflammatory vasculopathy
89
Limited SSc
Neck, face + distal limbs sparing the trunk PAH (may occur) GI involvement (bloating and constipation) Slow onset years after Reynaud phenomenon
90
Diffuse SSc
Trunk, face and limbs Scleroderma renal crisis may occur Cardiac disease ILD Same time as Reynaud
91
CREST syndrom
CREST syndrome refers to symptoms associated with limited SSc C: Calcinosis cutis: small white calcium deposits: elbows, knees, fingertips R: Raynaud phenomenon E: Esophageal hypomotility (systemic sclerosis): smooth muscle atrophy and fibrosis → dysphagia, gastroesophageal reflux, heartburn → aspiration, Barrett esophagus S: Sclerodactyly T: Telangiectasia
92
Diagnosis of SSc
CLINICAL! ▪ Skin thickening on hands extends proximal to the MCP joints ▪ Multiple organ system involvement is a hallmark. ▪ Determine disease severity. ▪ Obtain routine laboratory studies: SSc-specific evaluations. ▪ Assess for cardiopulmonary complications (even if asymptomatic).
93
SSc specific markers on lab tests
o Anticentromere antibodies: associated with limited SSc o Anti-Scl-70 (anti-topoisomerase I antibody) associated with severe and rapidly progressive diffuse SSc and limites SSc o Anti-RNA polymerase III: associated with diffuse SSc

5th year blocks (14 decks)

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