Brainscape's Knowledge GenomeTM

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


See full index

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.

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

Epidemiology of lupus?

A

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

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

SLE etiology

A

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

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

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

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

Most common symptom involvement in SLE

A

Constitutional
Joints
Skin

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

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

Constitutional symptoms involvement in SLE

A

▪ Fatigue
▪ Fever
▪ Weight loss

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

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

Less common symptom involvement in SLE

A

Hematological
Musculoskeletal
Serositis
Kidneys
Heart
Lungs
Vascular
Neurological

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

Diagnosis of SLE criteria

A

Consider if constitutional symptoms and > 2 organ manifestations

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

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

Antigen-specific ANAs:

A

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

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

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

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

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

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

Epidemiology of RA

A

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Articular symptoms in RA

A

Polyarthralgia
Morning stiffness
Joint deformity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Extraarticular symptoms in RA

A

Same as SLE + Rheumatoid nodules in skin and lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

General treatment approach in RA

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Acute disease flare in RA treatment

A

GC: Lowest dose <3 months, long term only if no respons to DMARD
NSAIDS: relief pain but does not help in progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Long term RA treatment

A

ALL patients get monotherapy by DMARD
Interfere with RA inflammation and can lead to remission
Reduce morbidity by 30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

DMARD

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Biological treatment in RA

A

▪ TNF-α inhibitors: e.g., adalimumab, infliximab, etanercept
▪ Others: rituximab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Treatment target strategi in RA

A

▪ 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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Diagnostic tools in RA

A

CLINICAL!!
LAbs
Imaging (X-ray)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Criteria of diagnosis in RA (when to consider)

A

Patients with arthralgia, joint stiffness, and synovitis lasting ≥ 6w

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Spesific parameters in lab to diagnose RA

A

▪ Anticitrullinated peptide antibodies (ACPA) (90%)
▪ Rheumatoid factor (RF): IgM autoantibodies against the Fc region of IgG
▪ Serological studies may be negative (seronegative RA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

X-ray findings in RA

A

▪ Early: soft tissue swelling, osteopenia
▪ Late: joint space narrowing, marginal erosions of cartilage and bone, osteopenia, subchondral cysts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Define Seronegative spondylarthritis

A

Include several chronic inflammatory arthritic diseases that affect the vertebral column.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Types of seronegative spondylarthritis

A

▪ Ankylosing spondylitis (most common)
▪ Reactive arthritis
▪ Psoriatic arthritis
▪ Spondyloarthritis associated with inflammatory bowel disease (IBD)
▪ Undifferentiated spondyloarthropathy
▪ Peripheral spondyloarthritis
▪ Juvenile spondyloarthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Diagnosis of Spondylarthritis?

A

▪ Negative for rheumatoid factor
▪ Genetic association with HLA-B27

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Epidemiology of spondylarthritis

A

▪ Generally more commonly affect men
▪ Age of onset: typically between 20–40 years of age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Symptoms of spondylarthritis

A

▪ 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
Q

Define gout

A

Gout is an inflammatory crystal arthropathy caused by the precipitation and deposition of uric acid crystals in synovial fluid and tissues

40
Q

Etiology of gout

A

Primary hyperuricemia
Secondary hyperuricemia

41
Q

Secondary hyperuricemia

A

Decreased uric acid excretion: most common cause
Increased uric acid production

42
Q

what is uric acid

A

An end-product of purine metabolism that is excreted by the kidneys
Has somewhat poor water solubility

43
Q

What trigger urate crystals to form

A

↑ Uric acid (due to insufficient excretion/increased production of purines)
▪ Acidosis
▪ Low temperature (cool peripheral joints)

44
Q

States of increased uric acid production

A

High cell turnover:
▪ Tumor lysis syndrome
▪ Hemolytic anemia
▪ Psoriasis
▪ Myeloproliferative neoplasms
▪ Chemotherapy, radiation

45
Q

states causing decreased uric acid secretion

A

o Medications (pyrazinamide, aspirin, loop diuretics, thiazides, niacin)
o Chronic renal insufficiency
o Ketoacidosis (starvation, diabetes mellitus) and lactic acidosis

46
Q

Symptomes of Gout

A

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
Q

Diagnosis of gout

A
  1. Assess the clinical probability of acute gout.
  2. If relatively low: Arthrocentesis with synovial fluid analysis
  3. If relatively high: Diagnostic tests are not routinely required.
48
Q

treatment of gout

A

▪ Nonpharmacological measures: Rest and ice the joint.
▪ Pharmacotherapy: Initiate within 24 hours of onset.
o First-line agents: GC, NSAIDs, or colchicine

49
Q

when do we give GC + Colchicine in gout?

A

Indicated for attacks involving ≥ 4 joints, > 1 large joint, or severe pain

50
Q

Two large classifications of small artery vasculitis

A

ANCA associated
Non ANCA associated

51
Q

What is small vessle vasculitis

A

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
Q

Granulomatosis with polyangiitis

A

→ 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
Q

Eosinophilic granulomatosis with polyangiitis

A

→ Severe allergic asthma, sinusitis
→ Skin manifestations (e.g., tender nodules)
→ Peripheral neuropathy
→ Gastrointestinal, cardiac, and/or renal involvement

54
Q

Microscopic polyangiitis

A

→ Pauci-immune glomerulonephritis
→ Hypertension
→ Palpable purpura
→ Like granulomatosis with polyangiitis but spares the nasopharynx

55
Q

IgA vasculitis

A

→ 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
Q

Cryoglobulinemic vasculitis

A

→ Fatigue
→ Arthralgia
→ Palpable purpura
→ Glomerulonephritis
→ Most cases are 2nd to cryoglobulinemia due to HCV

57
Q

Large Vessels vasculitis

A

Giant cell vasculitis
Takayasu Vasculitis

58
Q

Giant cell vasculitis clinical

A

→ 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
Q

Giant cell vasculitis diagnosis

A

→ ↑ ESR (≥ 50 mm/hour), ↑ CRP
→ Negative autoantibody studies
→ Temporal artery biopsy (gold standard): granulomatous inflammation

60
Q

Giant cell vasculitis management

A

→ High-dose glucocorticoids to prevent
permanent vision loss

61
Q

Takayasu Vasculitis clinical

A

→ 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
Q

Takayasu Vasculitis diagnosis

A

→ ↑ 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
Q

Takayasu Vasculitis management

A

→ Glucocorticoids
→ PLUS a glucocorticoid-sparing agent
(methotrexate, azathioprine, infliximab)

64
Q

Medium Vessel vasculitis

A

Kawasaki disease
Polyarteritis nodosa

65
Q

Kawasaki clinical

A

→ Most often occurs in children < 5 years
→ “CRASH (Conjunctivitis, Rash, Adenopathy, Strawberry
tongue, Hand-foot changes) and BURN (≥ 5d fever)

66
Q

Kawasaki diagnosis

A

→ ↑ ESR, ↑ CRP, thrombocytosis
→ Echocardiography: coronary artery aneurysms
Criteria: 5d fever + 4 other symptoms

67
Q

Kawasaki management

A

→ High-dose aspirin PLUS IVIG

68
Q

Define Polyarthritis nodosa

A

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
Q

Etiology of polyarthritis nodosa

A

Mostly idiopathic
Hepatitis B
Hepatitis C
HIV
CMV

70
Q

Organ involvement in polyarthritis nodosa

A

▪ 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
Q

Diagnosis of polyarthritis nodosa

A

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
Q

Treatment og polyarthritis nodosa

A

Severe: IV methylprednisolone + cyclophosphamide
Mild: High dose oral prednisone + methotrexate

73
Q

Define Sjogrens syndrome

A

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
Q

Sjogrens diagnosis

A

Consider Sjogren syndrome in patients with features of sicca syndrome without a known cause.
Positive anti-Ro/SSA or anti-La/SSB autoantibodies

75
Q

Gene as with sjogrens

A

HLA-DR52

76
Q

Clinical symptoms

A

Xerostoma
Xeropthalmia
Xerosis (skin)
Vaginal dryness
Nasal dryness
Pharyngeal/laryngeal dryness

77
Q

Systemic Sjogren involvment?

A

▪ 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
Q

treatment of sjogrens

A

Frequent water intake
Caries prophylaxis - frequent dental visits
Artificial salvia
Oral muscarinic agonists (PILOCARPINE)
Eyedrops
NSAIDS
Low dose GC if needed in systemic

79
Q

HS reaction in allergy?

A

Type I

80
Q

Stages of an allergic reaction?

A

Sensitization
Subsequent effective stage

81
Q

Immediate vs late allergic response?

A

Immediate: mast cell degranulation
Late: Chemokine + other mediators cause inflammation

82
Q

Allergy types?

A

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
Q

Allergy testing

A

Skin prick test or skin scratch test
Direct IgE allergen essay
Total serum IgE levels

84
Q

Desensitization in allergy

A

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
Q

Define Anaphylaxis

A

Bronchospasms (wheezing)
Laryngeal edema (dyspnea)
Hypotension (circulatory collapse)

86
Q

Managment of anaphylaxis

A
  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
Q

Define Systemic

A

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
Q

3 main points of scleroderma pathology

A

▪ Autoimmunologic component
▪ Inflammatory synthesis of extracellular matrix: fibrosis
▪ Noninflammatory vasculopathy

89
Q

Limited SSc

A

Neck, face + distal limbs
sparing the trunk
PAH (may occur)
GI involvement (bloating and constipation)
Slow onset years after Reynaud phenomenon

90
Q

Diffuse SSc

A

Trunk, face and limbs
Scleroderma renal crisis may occur
Cardiac disease
ILD
Same time as Reynaud

91
Q

CREST syndrom

A

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
Q

Diagnosis of SSc

A

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
Q

SSc specific markers on lab tests

A

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)

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