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Pathophysiology II > Connective Tissue Disorders > Flashcards

Connective Tissue Disorders Flashcards

1
Q

What is lupus?

A

An auto-immune disorder with connective tissue disease picture

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2
Q

When is the onset of SLE?

A

20-30 years old, think childbearing age

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3
Q

What population is more likely to have lupus?

A

Females

African Americans

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4
Q

What drugs have been known to induce lupus?

A

Hydralazine
Procainamide
Methyldopa

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5
Q

What is thought to cause SLE?

A

Chronic inflammation multi-system disease characterized by a generation of antinuclear antibody production that either directly damage tissue or form an immune complex which deposits resulting in damage

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6
Q

What test is the most sensitive indicator for SLE?

A

Immunofluorescence test for ANA

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7
Q

What causes the inflammatory response throughout the body?

A

Immune complexes causes inflammation and tissue injury as they are deposited throughout the body

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8
Q

How is diagnosis confirmed that SLE is present?

A

Three out of four typical manifestation: ANA, rash, thrombocytopenia, serositis and nephritis

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9
Q

What confirms diagnosis of SLE according to SLICC classifications criteria?

A

At least four criteria including one clinical and one lab criteria OR biopsy proven lupus nephritis with positive ANA or anti DNA

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10
Q

Why is Lupus an independent risk factor for heart disease?

A

Increased LDL and valvular disease

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11
Q

What is the most common pulmonary manifestation of SLE?

A

Pleuritis

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12
Q

Why do providers face such difficulty when ventilating patients with Lupus?

A

Like ventilating restrictive disease

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13
Q

Why should the provider be concerned if a patient with SLE has had a recent episode of pneumonia?

A

Patients with Lupus do not recover well from pneumonia, if recent illness and elective surgery cancel procedure

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14
Q

What is the most common renal complication from lupus?

A

Glomerulonephritis with proteinuria and casts

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15
Q

How are the joints affected in SLE?

A

Mimic arthritis however non erosive disease process

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16
Q

Why are patients with SLE prone to osteoporosis?

A

Long term steroid use contributes to bone loss

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17
Q

What is the primary treatment for SLE?

A

Steroids are considered the mainstay of treatment

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18
Q

What are other pharmacologic agents used in treatment of SLE?

A

NSAIDS
Anti Malarials
IV Gammaglobulin
Immunosuppressive therapy

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19
Q

What stress does of steroids should be given prior to surgery in patients with SLE?

A

Minor surgery: 1.5-2x steroid dose morning of surgery

Moderate & Moderate surgery: 2x steroid dose morning of surgery

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20
Q

What factors determine anesthetic management in patients with SLE?

A

Drug used in treatment
Degree of organ dysfunction
CNS involvement (seizures/stroke)
Neuropathies

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21
Q

What airway considerations should be taken into account on induction of patients with SLE?

A

Cricoarytenoid arthritis
Mucosal ulceration
RLN palsy

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22
Q

What anesthetic agents should be avoided in patients with SLE?

A

Agents that have an active metabolite (renal or liver impairment)

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23
Q

What is Rheumatoid arthritis?

A

A chronic inflammatory disease characterized by symmetric poly-arthropathy and systemic involvement

24
Q

When is RA typically diagnosed?

A

Peak age of occurrence is 20-50y/o

25
Q

What is believed to cause RA?

A

Antigen or microbe that leads to an immunological response in a genetically predisposed individual

26
Q

Where is the target damage in RA?

A

Synovium

27
Q

What can help a provider differentiate RA from osteoarthritis?

A

Osteoarthritis is usually unilateral compared to symmetric involvement in RA

28
Q

What causes the destruction to the articular cartilage?

A

Progressive proliferative synocitis

29
Q

What are the characteristics of chronic synovitis?

A

Infiltrated by CD4 and t cells
Increased osteoclast activity leading to bone erosion
Pannus formation
Pannus replaced by fibrosis and calcification and permanent ankylosis of joints

30
Q

What portion of axial insolvent is present in RA?

A

Upper cervical spine

31
Q

What lab value may indicate RA and why?

A

90% of patients will have circulating autoantibody levels of Rheumatoid Factor (RF)

32
Q

What lab value could also indicate RA but isn’t as sensitive?

A

Anti CCP antibody will be present in 1/3 of patient

33
Q

What structure acts as a pivot point for the rotation of C1??

A

Dens

34
Q

What joint allows flexion-extension, side bending and rotational movements of the head?

A

Zygapophyseal (facet) joints

35
Q

What organ system is affected by RA that isn’t in SLE?

A

Eye, scleritis and corneal ulceration

36
Q

What are the treatment goals for RA?

A

Relieve pain, preserve joint function, prevent deformity and limit systemic complications

37
Q

What class of drugs are the primary treatment for RA?

A

Drugs that alter immune response
Methotrexate
Sulfasalazine
Azathioprine

38
Q

What additional treatments can be used for RA?

A

Drugs that treat pain and inflammation (ASA, NSAIDs)
Surgical treatment
Biological agents (Humira, Embril)

39
Q

What cardiac pathology us most often seen in patients with RA?

A

Dysrhythmias resulting from nodules in the cardiac conduction system
Aortic regurgitation
Pericarditis
CAD

40
Q

What is the most common pulmonary complication from RA?

A

Pleural effusion and restrictive lung disease due to rheumatoid nodules in the lung tissue

41
Q

Why are patients with RA a potential for a difficult airway?

A

Erosion of ligaments by rheumatoid involvement of the bursar around the odontoid process of C2 causes atlanto-axial subluxation

42
Q

What can occur if care is not taken to avoid neck flexion with DVL?

A

May push odontoid into foramen magnum which could potentially reduce vertebral artery blood flow

43
Q

At what level is atlanto-axial stability expected and at what level should FOI be done due to chance of paralysis with flexion?

A

Greater than 3mm suspect subluxation

Instability greater than 5mm requires FOI with inline stabilization or awake

44
Q

When should the provider suspect cricoarytenoid arthritis in patients with RA?

A

If hoarseness, inspiratory stridor, dyspnea or tenderness over the larynx is present

45
Q

How should the provider process if the patient has cricoarythnoid arthritis?

A

Potential difficult airway and use smaller ETT

46
Q

What is Ehler-Danlos syndrome?

A

Inherited connective tissue disorders caused by abnormal production of procollagen and collagen

47
Q

What are the three main manifestations of Ehler Danlos syndrome?

A

Joint hyper mobility and instability
Skin texture anomalies
Vascular and internal organ fragility

48
Q

How many subtype of Ehler Danlos syndrome are there?

A

Six subtypes

49
Q

What are the three most common subtypes of Ehler Danlos syndrome?

A

Classic (V)
Hyper mobility
Vascular (III)

50
Q

How are mature collagen cells formed?

A

Procollagen precursor for hydroxylation and glycosylation to yield mature collagen molecules

51
Q

What are the major required to diagnosis classic Ehler Danlos syndrome?

A
  • Skin hyper extensibility (excessive skin over eye)
  • Widening atrophic scars
  • Joint hyper mobility (muscle hypotonia)
52
Q

What are some of the minor criteria to diagnosis Classic Ehler Danlos syndrome?

A
  • Smooth velvety skin
  • Easy bruising
  • Muscle hypotonia
53
Q

What are the major required to diagnosis vascular Ehler Danlos syndrome?

A
  • Thin translucent skin
  • Arterial, intestinal, uterine rupture
  • Extensive bruising
  • Facial features (prominent eyes, thin nose, small lips)
54
Q

What are some of the minor criteria to diagnosis Vascular Ehler Danlos syndrome?

A
  • Tendon/muscle rupture
  • Early varicose veins
  • Gingival recession
55
Q

Which subtype of Ehler Danlos has the worst prognosis?

A

Vascular due to propensity to rupture arteries

56
Q

Why is pregnancy such a high risk in patients with vascular Ehler Danlos?

A

Risk of uterine rupture

Pathophysiology II (6 decks)

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