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SBL Exam 2 > CT Disorders (McGowan) > Flashcards

CT Disorders (McGowan) Flashcards

1
Q

This test is for autoimmune disease, but is NOT specific. Further testing needs to be done to get a more specific diagnosis. Performed by indirect immunofluorescence, and a titer of < 1:40 is normal/negative (higher the ratio, then it is positive or clinically significant).

A

(+) ANA (anti-nuclear Ab)

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2
Q

Do autoimmune diseases occur mostly in males or females?

A

Females

***Overall! There are individual diseases that appear more in males than females.

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3
Q

Minority populations are more at risk and have increased severity of _________ diseases. Much is unknown as to why.

A

Rheumatologic

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4
Q

What are the major diffuse CT diseases (aka collagen vascular disorders) discussed?

A 
SLE
Scleroderma (aka Systemic Sclerosis) 
Sjogren Syndrome
Dermatomyositis (DM)
Polymyositis (PM) 
Inclusion Body Myositis (IBM) 
RA (***discussed in a later block!)
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5
Q

This disease is multi system, and is classified as an inflammatory autoimmune disorder. It has auto-Abs to nuclear Ags, with immune complexes making it a type III hypersensitivity.

A

Systemic Lupus Erythematosus (SLE)

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6
Q

SLE can have spontaneous remissions and relapses, and its severity varies. Occurs more in females and AA/Hispanics. What are genetic/environmental factors associated with it?

A

Sex hormones/X-linked?
UV light
Viruses (EBV)

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7
Q

What is the main cardiopulmonary feature that SLE patients can have?

A

Pericarditis

***Constant “crushing” sharp chest pain that is worse with cough or deep inspiration. Worse when supine. Diffuse ST elevation on ECG.

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8
Q

Why are SLE patients also at increased risk of myocardial infarction?

A

Due to accelerated atherosclerosis

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9
Q

This is the term for the “butterfly” rash that presents as an erythematous eruption over cheeks and nasal bridge in SLE patients. It spares the nasolabial folds.

A

Malar Rash

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10
Q

When ordering labs (CBC, ESR, ANA, etc.) what are the Ab tests we should use to specify for SLE?

A

(+) anti-ds DNA – means Abs to dsDNA
(+) Sm (Smith) – means Abs to Smith

***Remember, there is (+) ANA but this just means there’s an autoimmune issue. NOT specific!

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11
Q

In SLE, if there are (+) anti-ds DNA Abs, then what does that mean for disease activity?

A

This correlates with disease activity (means the disease is still active at this time).

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12
Q

In SLE, if there are (+) Sm Abs, then what does that mean for disease activity?

A

This does NOT correlate with disease activity (means disease is not currently active).

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13
Q

In SLE, complement activation promotes inflammation. So if there is decreased ______ or ______ that means there is increased consumption of it. Suggests disease activity, and it will return to normal levels when in remission.

A

C3

C4

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14
Q

This is a non-infectious type of endocarditis that can present in SLE.

A

Libman-Sacks Endocarditis

  • **The others are infectious and include:
    • Rheumatic Heart Disease
    • Infectious Endocarditis
    • Non-Bacterial Thrombotic Endocarditis
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15
Q

What are the main treatments used for SLE?

A

– Avoid sun exposure, wear sunscreen

– NSAIDs

– Glucocorticoids (topical or systemic - also called “corticosteroids”)

– Hydroxychloroquine

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16
Q

Briefly explain what happens in the early years after diagnosis of SLE.

A

– Infections occur, especially with opportunistic organisms.

– Active SLE, chiefly due to kidney or CNS disease.

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17
Q

Briefly explain what happens in the later years of SLE.

A

– Accelerated atherosclerosis (linked to chronic inflammation, becomes major cause of death due to myocardial infarction) 5x higher incidence of MI in pts with SLE than general population!

– Thromboembolic events become increasingly frequent causes of mortality

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18
Q

What are ways to manage/prevent SLE?

A

– Minimize other conventional risk factors for atherosclerosis (ie, HTN, obesity, etc.)

– Avoid smoking

– Influenza vaccination every year

– Pneumococcal vaccination every 5 years

– Preventive cancer screening (due to increased risk of malignancy in SLE pts)

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19
Q

What corticosteroid use (in SLE) what needs to be monitored?

A

– Monitor for avascular necrosis of bone (most commonly hips and knees)

– Long term use, need to monitor for osteoporosis

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20
Q

This disease can occur as a primary disease in patients without SLE, or it can occur as a secondary disease in 1/3 of SLE patients.

A

Anti-Phospholipid Antibody Syndrome (APS)

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21
Q

Describe Type One Ab of APS.

A

Causes a biologic false-positive test for syphilis. Need to use non-treponemal tests (RPR and VRDL).

***If testing for syphilis on patient with APS, better to use Treponemal Ab test!

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22
Q

Describe Type Two Ab of APS.

A

Lupus anticoagulant – this is a misnomer because there is actually an increased risk factor for venous and arterial thrombosis and miscarriage.

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23
Q

Describe Type Three Ab of APS.

A

Anti-cardiolipin Abs are present, which are directed at a serum cofactor Beta-2GPI.

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24
Q

How often should Abs be measured for APS?

A

Abs should be measured on two occasions 12 weeks apart.

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25
Q

What is treatment for APS?

A

Anticoagulation – continued indefinitely

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26
Q

What is a characteristic of SLE/APS Retinopathy?

A

Cotton Wool Spots

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27
Q

Lupus-Like Syndrome/Drug-Induced Lupus promotes the _________ of DNA. There is also no _______ or _______ symptoms like in SLE.

A

Demethylation
Renal
Neurologic

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28
Q

Lupus-Like Syndrome/Drug-Induced Lupus will have a (+) ANA and a…

A

(+) Anti-histone Abs

***Occurs in 95%

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29
Q

What are some associated medications that can cause Drug-Induced Lupus?

A
    • Hydralazine
    • Isoniazid (INH)
    • Minocycline
    • TNF Inhibitors
    • Quinidine
    • Chlorpromazine
    • Methyldopa
    • Procainamide
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30
Q

What type of drug can cause flare-ups in SLE (but do not cause Drug-Induced Lupus)?

A

Sulfa Antibiotics

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31
Q

Neonatal Lupus affects children born of mothers with what Abs?

A

Anti-Ro (SSA)

OR

Anti-La (SSB)

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32
Q

Transient symptoms of Neonatal Lupus include rashes, thrombocytopenia, hemolytic anemia, and arthritis. The main symptom that is the most worrisome is…

A

Permanent complete heart block (occurs to infant)

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33
Q

This is a variant of cutaneous lupus, and can occur independently or manifest from SLE. Most commonly occurs on the head.

A

Discoid Lupus Erythematosus (DLE)

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34
Q

DLE is characterized by well-defined inflammatory ________ that evolve into atrophic, disfiguring scars. There is usually concern over the appearance of skin lesions and patients desire treatment.

A

Plaques

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35
Q

What is the treatment for DLE?

A

Photoprotection and topical anti-inflammatory agents or systemic antimalarial drugs.

***Early treatment of DLE is essential to minimize scarring!

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36
Q

This disease occurs most often in 30-60 yo females. It is progressive and has a hallmark of thickening and hardening of the skin. There is also microangiopathy and fibrosis of the skin and visceral organs.

A

Scleroderma (SSc)

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37
Q

In Scleroderma, there is also an obliteration of what? This causes the dry itchy skin.

A

Obliteration of eccrine sweat and sebaceous glands

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38
Q

What are the 3 subtypes of Scleroderma?

A

Localized
Limited (CREST)
Diffuse

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39
Q

Scleroderma is multisystem, the main one being the skin. _______ _______ _______ is seen in virtually all patients (usually the first symptom in Caucasian patients), and there are changes in skin pigmentation (usually first symptom in African Americans).

A

Secondary Raynaud Phenomenon

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40
Q

This type of Scleroderma has the following characteristics:

– Occurs in children

– Discreet areas of discolored skin induration

– NO Raynaud’s

– NOT systemic

A

Localized

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41
Q

Localized Scleroderma is histologically indistinguishable from other forms. Patches are called ________, and coalesced patches are generalized ________.

A

Morphea

Morphea

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42
Q

This type of Scleroderma involves the fingers, toes, face/neck, and distal extremities. Raynaud’s can be one of the first symptoms, and it presents with CREST syndrome.

A

Limited Scleroderma (lcSSc)

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43
Q

This is a major symptom of Limited Scleroderma (systemic) that presents as shortness of breath.

A

Pulmonary HTN

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44
Q

Limited Scleroderma has an indolent course (delayed onset and slow progression) and vascular manifestations are more pronounced. Renal crisis is (COMMON/UNCOMMON).

A

Uncommon

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45
Q

Limited Scleroderma involves CREST syndrome, which is what?

A

C = Cutaneous calcinosis

R = Raynaud’s phenomenon (spasm of blood vessels in response to cold or stress)

E = Esophageal dysfunction (acid reflux, GERD)

S = Sclerodactyly (thickening and tightening of skin on fingers and hands)

T = Telangiectasias (dilation of capillaries causing red marks on surface of skin)

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46
Q

In Diffuse Scleroderma (Diffuse Cutaneous Systemic Sclerosis) there are phases, which are…

A

Inflammatory edematous phase –> Fibrotic phase

Skin induration, hyper/hypo-pigmentation –> loss of body hair and impaired sweating

Fibrotic joints –> stiffness

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47
Q

Diffuse Scleroderma can present with fatigue, stiffness, malaise, arthralgia, weakness, carpal tunnel, and Raynaud (later than in Limited Scleroderma). There is also internal organ involvement, such as _______ ______ and _______ _______ _______.

A

Renal Crisis
***May see hemolytic anemia on labs during renal crisis!

Interstitial Lung Disease

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48
Q

These are the primary causes of morbidity and mortality in Limited and Diffuse Systemic Sclerosis.

A
    • Interstitial lung disease (***Diffuse)
    • Pulmonary A. HTN (***Limited)

***2 others are = Aspiration Pneumonia and Increased incidence of bronchoalveolar carcinoma. Remember top 2 for sure!

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49
Q

What does interstitial lung disease present with and how is it diagnosed (in diffuse scleroderma)?

A

Presents = Chronic dry cough, dyspnea, fine “velcro” crackles (rales)

Diagnosis = Pulmonary function test (PFT) and Lung CT

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50
Q

How can we diagnose PAH in limited scleroderma?

A

2D ECG or Right heart catheterization (gold standard to show elevated pulm artery pressure)

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51
Q

Renal crisis is uncommon but life-threatening. It is more common in Diffuse SSc and is considered a medical emergency. It is characterized by the abrupt onset of…

A
    • Malignant HTN
    • Hemolytic anemia
    • Progressive renal insufficiency
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52
Q

High doses of what medication can induce a renal crisis?

A

Glucocorticoids

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53
Q

A major symptom of GI issues associated with SSc is Barrett Esophagus, which can cause increased risk of…

A

Esophageal Adenocarcinoma

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54
Q

This is the main MSK symptom associated with SSc.

A

Carpal tunnel syndrome

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55
Q

What can happen to the thyroid in SSc?

A

Hypothyroid from thyroid fibrosis

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56
Q

For a diagnostic workup in SSc, we want to pay particular attention to the blood pressure. Why is this?

A

It is a heralding feature of renal disease!

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57
Q

What would the serology look like for Diffuse SSc?

A

(+) ANA
(+) Anti-Scl 70 — also called Anti-(DNA) topoisomerase I
(+) Anti-RNA polymerase III

***Know ALL these names!

58
Q

What would the serology look like for Limited SSc?

A

(+) ANA

(+) Anti-centromere

59
Q

What is the treatment/management for SSc?

A

No therapy to date significantly alters the disease course! Just manage individual organ system involvement.

60
Q

Sjogren Syndrome usually occurs in females in the mid-50s that are postmenopausal. They present with Sicca symptoms, which are…

A 
Dry eyes
Dry mouth (xerostomia) 
Vaginal dryness 
Trachea-bronchial dryness 
Parotid or other major salivary gland enlargement
61
Q

Another major characteristic of Sjogren Syndrome is ________ _______, which is due to inadequate tear production and often feels as if a foreign body is in the eye. A Check Schirmer test can be used to measure the quantity of tears being secreted.

A

Keratoconjunctivitis Sicca

62
Q

Sjogren Syndrome has a strong association with what type of cancer?

A

B-cell Non-Hodgkin Lymphoma (MALT Lymphoma)

63
Q

What are the main characteristics of the serology workup you want to look at for diagnosing Sjogren Syndrome?

A

(+) ANA

Polyclonal Hypergammaglobulinemia

(+) Anti SSA/Ro – presence may lead to newborn complete heart block

(+) Anti SSB/La – never present without Ro

***Remember, Ro and La can also be seen in lupus so you need the WHOLE picture in order to make a diagnosis!

64
Q

This is essential for diagnosis in Sjogren Syndrome. It reveals characteristic lymphoid foci in accessory salivary glands.

A

Lip Biopsy

65
Q

For treatment/management of Sjogren Syndrome, it’s important to have regular follow-ups with…

A

Dentist and Ophthalmologist

66
Q

What drugs are important to avoid for Sjogren Syndrome and why?

A

Avoid atropinic drugs and decongestants, because these will further dry out the patient!

67
Q

For inflammatory myopathies, they most often occur in females more than males, and African Americans more than Caucasians. Myalgias and weakness will present in the…

A

Symmetrical (bilateral) proximal muscles

***Difficulty rising from a chair or bathtub or climbing stairs

68
Q

What muscle enzymes are elevated with inflammatory myopathies?

A 
Creatinine Kinase (CK) 
Aldolase

***EXCEPT – CK is only mildly elevated or normal in IBM!

69
Q

This inflammatory myopathy occurs in two age groups, 7-15 yo and 30-60 yo. It causes weakness without sensory symptoms. Proximal muscles affected first, followed by distal muscles late in the disease course.

A

Dermatomyositis (DM)

70
Q

What are the characteristic skin lesions of DM?

A

– Gottron’s patches/papules (raised violaceous lesions overlying the dorsal of DIP, PIP, and MCP joints)

– Heliotrope rash (periorbital edema, purplish suffusion over eyelids)

– Periungual erythema

– V-neck erythema (Poikiloderma: “Shawl Sign” – erythema over neck/shoulders, upper chest, and back)

71
Q

DM can cause an increased risk of what?

A

Occult malignancy

***As soon as DM is diagnosed, start looking for this! Pretty much any type of cancer can occur. Do age appropriate cancer screenings.

72
Q

What is the main serology component to help diagnose DM?

A

Anti Jo-1

73
Q

This type of inflammatory myopathy occurs in people 30-50+ yo. It is a subacute condition (over weeks to months) and causes proximal muscle weakness. There are NO skin changes, and NO association to occult malignancy.

A

Polymyositis (PM)

74
Q

On a biopsy for PM, there will be ________ ________ with invasion of non-necrotic muscle fibers without features suggestive of another diagnosis (like IBM or muscular dystrophy).

A

Endomysial Inflammation

75
Q

What labs will be elevated in DM?

A

CK

Aldolase

76
Q

What labs will be elevated in PM?

A

Only CK

77
Q

What is the main serology component to help diagnose PM?

A

Anti Jo-1

78
Q

What is the main treatment for DM/PM?

A

Glucocorticoids

79
Q

This type of inflammatory myopathy occurs more often in MALES >40-50 yo. Also occurs more in caucasians than African Americans. Presents with weakness in finger flexion or quadriceps weakness.

A

Inclusion Body Myositis (IBM)

80
Q

In a biopsy to diagnose for IBM, you would see endomysial inflammation, _______ _______, and invasion of non-necrotic muscle fibers.

A

Rimmed Vacuoles

81
Q

What labs will be elevated in IBM?

A

CK will have MILD elevation or be NORMAL

82
Q

What is the main serology component of IBM?

A

Anti-cN1A Auto-Abs

83
Q

What is the main treatment for IBM?

A

It is refractory to treatment (Glucocorticoids are NOT helpful). So treatment is just supportive.

84
Q

What are the systemic vasculitides affecting small vessels?

A

IgAV – aka Henoch-Schonlein Purpura (HSP)
Anti-GMB (Goodpasture Syndrome)
Granulomatosis with Polyangiitis (GPA)

85
Q

What are the systemic vasculitides affecting variable vessel sizes?

A

Eosinophilic Granulomatosis with Polyangiitis (EGPA)

Behcet Syndrome

86
Q

What are the systemic vasculitides affecting medium vessels?

A 
Thromboangiitis Obliterans (Buerger Disease) 
Polyarteritis Nodosa (PN) 
Kawasaki Disease (KD)
87
Q

What are the systemic vasculitides affecting large vessels?

A 
Takayasu Arteritis (TA) 
Giant Cell Arteritis (GCA or Temporal Arteritis)
88
Q

IgA Vasculitis (IgAV) aka Henoch-Schonlein Purpura (HSP) is immune-mediated and occurs in small vessels. It can occur in any age but is more common in kids. What is the tetrad involved with this disease?

A
    • Palpable purpura (NO thrombocytopenia)
    • Arthritis/arthralgia
    • Abdominal pain
    • Renal Disease (glomerulonephritis)
89
Q

When performing a biopsy to diagnose IgAV, what would be seen?

A

IgA deposits

90
Q

What is the treatment for IgAV?

A

Supportive and glucocorticoids

91
Q

Anti-Glomerular Basement Membrane (GBM) aka Goodpasture Syndrome affects small vessels, mainly _________ and ________ capillaries.

A

Glomerular

Pulmonary

92
Q

In GBM, what can be a cause of death if it’s not treated?

A

Pulmonary hemorrhage (due to the affect on the pulmonary capillaries)

93
Q

What would present in a renal biopsy to diagnose GBM?

A

Deposition of anti-basement membrane autoantibodies

94
Q

What is the treatment for GBM?

A

Plasmapheresis (removes Abs)
Glucocorticoids
Cyclophosphamide (dialysis sometimes)

95
Q

Granulomatosis with Polyangiitis (GPA) aka Wegener’s Granulomatosis affects small vessels, most often in males over 40 yo. The major hallmarks of this include…

A
    • Granulomatous inflammation
    • Renal involvement (segmental glomerulonephritis)
    • Respiratory involvement (upper and lower)
96
Q

What is usually affected in the respiratory tract in GPA?

A

90% Nasal involvement! – Saddle nose, crusting, bleeding, obstruction

***Looks like you got HARDCORE punched in the face

97
Q

What would be seen on biopsy to diagnose GPA?

A

Vessel changes with granulomas

98
Q

What is the main serology component of GPA?

A

(+) ANCA

99
Q

What is the treatment for GPA?

A
    • No smoking
    • Cyclophosphamide
    • High dose glucocorticoids
    • Rituximab
    • Methotrexate (if renal function is normal)
100
Q

Eosinophilic Granulomatosis with Polyangiitis (EGPA) aka Churg-Strauss Syndrome affects small and medium vessels. It can damage the ________ ________ and other organs.

A

Respiratory Tract

***This disease is very similar to GPA!

101
Q

What is the main hallmarks of EGPA?

A

Asthma + Eosinophilia –> Vasculitis with granulomas

102
Q

There are 3 phases involved in EGPA, what are they and what occurs in each phase?

A

Prodromal Phase = Allergic disease (asthma/allergic rhinitis) – occurs months-years

Eosinophilia-Tissue Infiltration Phase = High eosinophils in circulating blood. Tissue infiltration in lung/GI/other tissues (extravascular)

Vasculitis Phase = Systemic necrotizing heart/lungs/nerves/skin and palpable purpura

103
Q

If you were to collect a CBC in a patient with EGPA, what would you see that stood out?

A

High eosinophil count

104
Q

What is the main serology component of EGPA? Why is it not very helpful?

A

(+) ANCA – only occurs in <50% patients and could be other disease that also test positive for this (ie, GPA)

105
Q

If a lung biopsy was performed to diagnose EGPA, what would be seen?

A
    • Granulomas and vascular changes

- - Eosinophils in tissue

106
Q

What is the treatment for EGPA?

A
    • No smoking

- - Glucocorticoids

107
Q

Behcet Syndrome involves variable vessel sizes. It occurs worldwide, but is most common in Turkey, Asia, and Middle East. There is multisystem involvement. What can occur in large, small, or venous vessels?

A

Large Vessels = Aneurysms

Venous Involvement = DVT

Small Vessels = Triad: 1) Recurrent mouth ulcers, 2) Genital ulcers, 3) Eye inflammation (uveitis)

108
Q

Another characteristic of Behcet Syndrome is ________, which can form pustules at sites of sterile needle pricks.

A

Pathergy

109
Q

What is the main serology component to diagnose Behcet Syndrome?

A

HLA-B51

***Otherwise, diagnosis is only via thorough history and physical exam!

110
Q

What is the treatment for Behcet Syndrome?

A

Low dose glucocorticoids

111
Q

Thromboangiitis Obliterans (aka Buerger Disease) affects medium vessels and is a segmental disease. It occurs in young males under 35 you and is ONLY in __________.

A

Smokers

112
Q

Thromboangiitis Obliterans moves from distal vessel to proximal. There is thrombosis that leads to loss of digits on hands and feet. Internal organ disease is rare. In diagnosis, the angiography has what appearance?

A

“Corkscrew” appearance

113
Q

What is the treatment for Thromboangiitis Obliterans?

A

STOP SMOKING

***Glucocorticoids and anticoagulation don’t work! `

114
Q

Polyarteritis Nodosa affects medium vessels and is segmental. It occurs more often in males and is associated with what virus?

A

HBV (Hepatitis B Virus)

115
Q

Polyarteritis Nodosa will present with skin conditions like livedo reticular, subcutaneous nodules, ulcers, and digital gangrene. 80% of patients will also have _________ ________ which can cause ________ ________.

A

Vasculitis neuropathy

Foot drop

116
Q

In Polyarteritis Nodosa, a renal symptom can be ________ ________. Also, the _______ are spared in this disease!

A

Renin-mediated HTN

Lungs

117
Q

Polyarteritis Nodosa can be diagnosed by biopsy or angiogram. What would be seen in each of these?

A

Biopsy = Infiltration and destruction of blood vessels by inflammatory cells –> Fibrinoid necrosis, NO granulomas

Angiogram = Micro-aneurysm

118
Q

What would be present in the serology for Polyarteritis Nodosa?

A

Check HBsAg, HBsAb, and HBeAg –> for Hepatitis B

119
Q

What is the treatment for Polyarteritis Nodosa?

A

Glucocorticoids

120
Q

Kawasaki Disease (aka Mucocutaneous LN Syndrome) affects medium vessels and is an acute febrile illness. It most often occurs in males under 5 yo of Asian ancestry (highest incidence in Japan). Patient usually presents with…

A
    • Fever
    • Lymphadenopathy
    • Rash
    • “Strawberry tongue”
121
Q

What can cause morbidity in Kawasaki Disease, even years later?

A

Coronary involvement – can cause aneurysm or MI

122
Q

What is the treatment for Kawasaki Disease?

A
    • IVIG within 10 days of symptoms

- - High dose ASA (yes, aspirin in peds pt)

123
Q

Takayasu Arteritis is an uncommon disease affecting large vessels (aorta and branches). Occurs most often in females under 40 yo. It has a chronic relapsing and remitting course. Angiography shows…

A

Long smooth tapered stenosis

124
Q

Takayasu Arteritis is called the _______ _______ because it obliterates UE peripheral pulses. Collateral damage can be limb loss from ischemia (but this is rare).

A

“Pulseless Disease”

125
Q

What happens to the kidneys and eyes in Takayasu Arteritis?

A

Kidneys = Renal A. Stenosis –> leads to HTN

Eyes = HTN from the kidneys can lead to retinopathy that shows copper wiring infarctions

126
Q

What are the aortic complications of Takayasu Arteritis?

A

Dilations
Regurgitation
Aneurysm
Rupture

127
Q

What can be seen on histology for Takayasu Arteritis?

A

Granuloma with some giant cells

128
Q

What is the treatment for Takayasu Arteritis?

A

Glucocorticoids

129
Q

Giant Cell Arteritis (GCA) aka Temporal Arteritis (TA) and _________ _________ often co-exist with each other. They affect females more than males in ages >40-50 yo. Also more frequent in caucasians than African Americans.

A

Polymyalgia Rheumatica (PMR)

130
Q

GCA and PMR will show a normal WBC count, but they have elevated…

A

ESR and CRP

***Erythrocyte Sedimentation Rate (ESR) and C-reactive Protein (CRP)

131
Q

Giant Cell Arteritis (GCA) aka Temporal Arteritis, affects large vessels including…

A 
Cerebral Arteries (temporal, facial, ophthalmic) 
Aortic Arch
132
Q

GCA occurs in females more than males that are >50 yo. Northern European ancestry is more frequent. The main clinical history/symptoms are…

A
    • Headache
    • Jaw claudication (pain and fatigue in jaw with chewing)
    • Association with PMR
    • Visual abnormalities (amaurosis fugax or diplopia)

***Described as “shades coming down” for visual issues.

133
Q

What is the gold standard for diagnosing GCA?

A

Temporal artery biopsy – will show segmental granulomatous vasculitis with multinucleated giant cells

134
Q

What treatment is used for GCA and why is it vital to start even before biopsy?

A

Glucocorticoids – vital to start before biopsy because it will cause a dramatic improvement. If there is no treatment or if it’s started too late the patient can become blind!

135
Q

Polymyalgia Rheumatica (PMR) is associated with GCA and presents as stiffness, soreness, and muscle pain. Usually proximal (shoulders, neck, and pelvic girdles) and severe. Can last morning or the whole day. Feelings (subjective) of weakness are a result of ________, there is no true (objective) weakness.

A

Pain

***Trouble combing hair, putting on a coat, etc.

136
Q

What is the treatment for PMR?

A

Glucocorticoids

137
Q

(PRIMARY/SECONDARY) Raynaud is benign and symmetric. It is an exaggerated physiologic response to cold or emotion. Occurs most often in females ages 15-30.

A

Primary

138
Q

Secondary Raynaud occurs secondary to something. Occurs in CTD, hematologic and endocrine conditions, use of beta blockers or cancer drugs cisplatin and bleomycin. Typically in people >30 yo and is unilateral. This type is more severe, it can be due to _________.

A

Ischemia

139
Q

To diagnose Raynaud, a nailfold capillaroscopy is done. What are the results in primary and secondary?

A

Primary = Normal

Secondary = Distorted with widened and irregular loops, dilated lumen and areas of vascular “dropout”

140
Q

Raynaud is often called the “Red, White, and Blue Syndrome”. Why is this?

A

Pallor (White) –> Vasoconstriction

Cyanosis (Blue) –> Ischemia

Erythema (Red) –> Reperfusion

SBL Exam 2 (7 decks)

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