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Pathophysiology - Intro > Autoimmunity > Flashcards

Autoimmunity Flashcards

1
Q

What is the lack of response to the body’s own cells known as?

A

tolerance

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2
Q

What is autoimmunity?

A

when a body develops autoantibodies as a reaction to its own tissues or self-antigens

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3
Q

What do almost all patients with autoimmunity have present in their serum?

A

autoantibodies

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4
Q

What does lupus affect?

A

skin, heart, brain, blood, kidney, lungs and joints

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5
Q

Lupus stats (americans w/ it, worldwide pop, priamry gender, diagnosis age)

A

1.5 Americans
5 million worldwide
90% r women
diagnosed between 15 to 44

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6
Q

What are the 4 types of lupus

A

systemic, cutaneous, neonatal, and drug induced

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7
Q

What is the primary form of lupus + what percent of poel have it?

A

systemic lupus, 70%

aka systemic lupus erythematosus (SLE)

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8
Q

About ____ of SLE patients develop severe disease of the heart, lungs, kidneys, or brain.

A

half

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9
Q

What are the common signs and symptoms of SLE

A

fatigue
arthritis
butterfly rash on cheeks and nose
fever
photosensitivity
secondary Raynaud’s pehnomenon
mouth or nose ulcers
inflammation of the skin, joints, nervous system, kidneys, lungs, and other organs
malaise
wt. loss
discoids skin lesion
polyarthritis without deformity
seizures or psychosis
chronic pleuritis or pericarditis

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10
Q

What is cutaneous (aka discoid) lupus + what % of cases

A

affects only the skin

accounts for 10% of all cases

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11
Q

most common rash caused by cutaneous lupus?

A

red, scaly, raised but NOT itchy

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12
Q

Why is cutaneous lupus known as a discoid rash?

A

bc the rashes r usualy circular

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13
Q

Where else does discoid rashes appear?

A

face, neck, scalp, nose, mouth and vagina

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14
Q

Approximately __% of patients with cutaneous lupus will
develop SLE.

A

10

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15
Q

How many drugs can lead to Drug-induced lupus erythematosus (DILE) + what %

A

70+ drugs and 10% of all lupus cases

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16
Q

Difference between SLE and DILE?

A

DILE rarely affects organs

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17
Q

What are some of the medications known to cause DILE?

A

hydralazine (used to treat high blood pressure)
procainamide
quinidine (used to treat irregular
heart rhythm)

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18
Q

What is the risk of developing DILE on most drugs?

A

less than 1%

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19
Q

What is neonatal lupus?

A

the autoantibodies of the mother affects the fetus/ newborn’s skin, heart and blood

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20
Q

What is the ethiology of lupus?

A

it’s unknown but genetic + envrionmental factors have an impact

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21
Q

Environmental factors of lupus?

A

infections
sulfa antibiotics and penicillin
ultraviolet light
stress
certain drugs
hormones

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22
Q

__% of lupus patients have a parent or a sibling with lupus

A

20

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23
Q

__% of children develop
lupus if their mother has lupus.

A

5

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24
Q

For women when do the signs and symptoms of lupus worsen?

A

before menstrual cycle and during pregnancy so estrogen may have an impact in women

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25
Q

What should lupus patients do?

A

limit exposure to sunlight
never use tobacco
prevent fatigue and stress
eat a healthy diet
exercise
take care of fevers over 100°F promptly

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26
Q

How to diagnos lupus?

A

no single test to confirm so blood test, biopsy, urinalysis, autoantibody testing and measurement of general level of inflammation

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27
Q

Medication to control lupus:

A

NSAIDs
corticosteroids
antimalarial medications
immunosuppressive drugs
monoclonal antibodies

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28
Q

between ___ and ___ % of lupus patients
die prematurely as a result of complications

A

10 and 15

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29
Q

What scleroderma?

A

chronic, progressive autoimmune disease of the connective tissue in with sclerosis of skin, scarring of certain internal organs occurs
- classified as either diffuse or limited, depending on extent and location of skin involvement

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30
Q

What is the word scleroderma dervied from?

A

Gre words sklera for hard and derma for skin

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31
Q

When was the word scleroderma first used?

A

In 1836 Giovambattista Fantonetti described a patient who has dark leathery skin that results in loss of joint movement range

32
Q

Stas of scleroderma (ppl in us, worldwide, gender, dagnosis age)

A

300,000 in us
2.5 mill worldwide
women are 4x more likely to get it compared to men
diagnosis age is in 40s

33
Q

2 types of scleroderma + what is more common

A

localized scleroderma (LSc) which only affects the skin

Systemic scleoriss scleroderma (SSc) which affects skin + internal organs

34
Q

How does LSc appear?

A

looks like waxy patches of skin (morphea) or strakes on the skin (linear sclerosis)

stop progresses or regresses w/o treatment

35
Q

What are the 2 types of SSc?

A

limited cutaneous SSC (lcSSc) and diffuse cutaneous SSc (dcSSc)

36
Q

What is lcSSc?

A

has skin tightening on fingers, hands, arms below elbows, feet and les below knees

37
Q

What parts of the body does dcSSC affect?

A

fingers, hands, and arms below the elbows, skin on the feet legs below the knees, skin on the trunk, above the
elbows, and on the knees

38
Q

Do pt with lcSSc or dcSSc have a greater risk for significant organ dysfunction?

A

dcSSc

39
Q

The 10-year survival rate for lcSSc is __%

A

71

40
Q

The 10-year survival rate for dcSSc is __%.

A

21

41
Q

What are the 1st signs and symptoms of scleroderman?

A

seconadray Raynaud’s phenomenon
tightening of the skin of the fingers
pain in 2 or more joints, heartburn
diffulcuty swallowing
SOB

42
Q

Impact of immune system on scleroderma?

A

could stimulate fibroblasts to produce too much collagej = stiffening

43
Q

What are some other factors to scleroderma?

A

exposure to viral infection and certain chemicals can = scleroderma in ppl genetically predisposed to it

may be linked to estrogen

44
Q

How to diagnose scleroderma?

A

no single test - autoantibodies and biopsy
- complete history and physical exam
- lab testing including Scl-70 and centromere antibodies can be supportive of diagnosis
- skin biopsy is only rarely necessary
- blood tests and urinalysis r performed to rule complications or accompanying conditions
- lung function testing and echocardiography

45
Q

What should scleroderma pt do to manage the disease?

A

small frequent meals, no smoking, healthy diet, exercise, avoid exposure to cold, moisturize, protect skin

46
Q

treatments to manage scleroderma

A

anti-inflammatory drugs, immunosuppressive drugs, and vasodilators, corticosteroids
- treatment is directed to area of the body affected
- rheaumatology referral is recommended
- physical therapy helps pt maintain muscle strength but doesnt chagne course of joint disease

47
Q

What is Sjögren’s syndrome?

A

autoimmune disease that causes inflmmation of the exocrine (moisture producing) glands in the body resulting in dryness in affected areas
- cause is unknown but genetic factors seem to play a role in predisposing a person to Sjorgren syndrome

48
Q

stats of Sjögren’s syndrome (ppl in us = gender)

A

4 mill in us
90% r women

49
Q

About ____ of the cases are called primary
Sjögren’s syndrome.

A

half

50
Q

What is secondary Sjögren’s syndrome?

A

Sjögren’s syndrome that occurs with another disease

51
Q

symptoms of Sjögren’s syndrome

A

dry eyes and mouth (xerostomia)
- keratoconjunctivitis sicca
- difficulty talking, chewing and swallowing from dryness of nasal, oral and laryngeal pharynx
- sores in or on mouth and nose
- dental decay may occur
- can cause complications in lungs, heart, GI tract, bv, liver, pancrease and CNS

52
Q

When does Sjögren’s syndrome often affect women?

A

during childbearing years (shows possible link to estrogen)

53
Q

how to diagnose Sjögren’s syndrome?

A
  • lip and salivary gland biopsy, tears and saliva tests, autoantibody testings
  • screen for med side effects, autoimmune thyroid disease, RA, SLE, sarcidosis, scleroderma associated with Sjorgen syndrome
  • schirmer (tests for dry eyes)
  • enlarged salivary glands = lower lip bopsy, which may indicate characteristci infiltration of lyphmocytes
  • blood studies often demonstrate anemia, decreased WBC count and elecated ESR
  • test for Sjogren syndrome antibodies (SSA and SSB antibodies) and high rheumatoid factor titers
54
Q

Drugs for Sjögren’s syndrome

A

treatment is directed toward releiving symptoms esp dryness in oral cavity & eyes
- increasing fluid intake, chewing sugarless gum, using oral sprays to help relieve oral dryness
- artifical tears + wearing sunglasses
- sometimes ophthalmologists block tear ducts w/ silicone or by cautery to maintain adequate eye moisutre
- occasionally prednisone and/or antimalarial med such as hydroxychloroquine r used to lessen immune inflammation

eye drops, NSAID, immunosuppressive drugs and vasodilators

55
Q

etiology of autoimmune disorders?

A

thought to be acquired, not genital, however certain gene markers identify pt at increased risk for many autoimmune disorders

56
Q

What is autoimmune hemolytic anemia?

A
  • autoimmune condition in which RBCs r destroyed by antibodies
57
Q

s/s of autoimmune hemolytic anemia?

A
  • pt experience fatigue, weakness, chills, fever, dyspnea, itching
  • skin is pale and jaundiced and bruises easily (pt may be hypotensive
58
Q

etiology of autoimmune hemolytic anemia?

A
  • b cell-produced antibodies don’t identify RBCs as self, resulting in agglutination of RBCs and an attack on and destruction of the red corpuscles
  • 2 types r warm antibody (agglutinin) anemia and cold antibody anemia (agglutinin)
59
Q

What is warm antibody anemia

A
  • excess of IgG antibodies that react with protein antigens on the RBC surface at body temp (most cases r idiopathic, some may be activated by certain drugs (eg penicillins), autoimmune diseases (eg SLE) or malignancies (esp chronic lymphocytic leukemia)
60
Q

What is cold antibody anemia

A
  • results from fixation of complement proteins on IgM that occurs at colder temp (best around 30F)
  • type is regularly seen in conjunction with infectious mononucleosis or Mycopasma pneumonia
61
Q

How to diagnose autoimmune hemolytic anemia?

A
  • direct Coombs test indicates antibody-coated RBCs that agglutinat when atinglobulin is added to medium
  • some RBCs appear spherical (spherocytes) as visualized under microscope
  • serum bilirubin levels r elevated
  • RBC count, platelet count, hemoglobin concentration, hematocrit usually are all decreased
  • reticulocytet (immature RBC) count is usually elevated
  • examination of peripheral blood smear for agglutination of RBCs and flow cytomentry may be performed
62
Q

How to diagnose autoimmune hemolytic anemia?

A
  • direct Coombs test indicates antibody-coated RBCs that agglutinat when atinglobulin is added to medium
  • some RBCs appear spherical (spherocytes) as visualized under microscope
  • serum bilirubin levels r elevated
  • RBC count, platelet count, hemoglobin concentration, hematocrit usually are all decreased
  • reticulocytet (immature RBC) count is usually elevated
  • examination of peripheral blood smear for agglutination of RBCs and flow cytomentry may be performed
63
Q

how to treat autoimmune hemolytic anemia?

A
  • 1st treat underlying disease or drug use
  • for warm antibody anemia, corticosteroids and cytotoxic drugs r administered to reduce antibody production, splenectomy, IVIG
  • avoidance of cold by dressing warmly, plasmapheresis
64
Q

What is SLE?

A
  • chronic, inflammaotry autoimmune disease characterized by unusual autoantibodes in the blood that targets tissues of the body
65
Q

lab tests for SLE?

A
  • false-positive serologic test result for syphilis
  • DNA or Sm (Smith) antibodies in blood or cardiolipin antibody
  • greater than 0.5 protein in urine in 24 hr periods, cellular casts in urine
    hemolytic anemia, thombocytopenia, persence of abn antibodies in bloodstream, LE cells (WBCs) that r created in lab as part of ttesting, CBC w/ differential leukocyte count, platelet count, erythrocyte sedimentation rate (ER), antinuclear antibody determination, anti-DNA antibody, anti-Sm antibody and anti-chromatin antibody
66
Q

how to treat SLE?

A
  • antiinflammatory drugs: aspririn, NSAIDs, prednisone
  • antimaralarial agents to control skin involvement and arthralgia
  • corticosteroids
  • immunesuppressive meds
67
Q

s/s of scleroderma?

A
  • sclerosis and shrinking of skin and certain internal organs such as GI tract, heart, lungs and kidneys
  • onvolved skin becomes taut, firm, edematous and is firmly attached to subcutaneous tissue
  • skin feels touch and leather, mau itch and pigmented patches
  • raynaud phenomenon is often first s/s, follsoed by swelling, stiffness and pain in joint s
68
Q

What is vasculitis?

A
  • inflammation in walls of blood vessels
  • affected vessel become necrotic when obstructed b y thrombus and an infarct of adjacent tissue results
  • bopsy of involved vessel can demonstrate presence of inflammation in blood vessel
  • classified into 2 main types: small vessel vasculitis and systemic necrotizing vasculitis
69
Q

What is small vessel vasculitis?

A
  • primarily affects capillaries, arterioles and venules
70
Q

s/s of small vessel vasculitis

A
  • petechiae (nonblanching)
  • purpura
  • erythema
  • ulcerations and edema (most often on skin of lower extremities)
  • pain and burning sensation can accompany these lesions
  • ocular lesions
  • genital or oral ulcerations
  • abd pain
  • arthralgia
  • weakness
71
Q

diagnosis and treatment of small vessel vasculitis

A

diagnose - histology and often immunoflouroscence studies of biopsied tissue, presence of Ig and complement in blood vessels, pattern of vascular involvement and the cell types presents can help define subtype of small vessel

treatment - corticosteroid therapy, analgesics and rest

72
Q

What is systemic necrotizing vasculitis + etiology?

A
  • tends to primarily affect medium and large arteries
  • etiology is unknown but autoimmune respones play a role and r mediated by cellular and humoral immunity (illicit drug use, includign cocain and amphetamines, hepatitis B and C r associated w/ development of some forms of systemic vasculitis)
73
Q

s/s of systemic necrotizing vasculitis

A
  • impaired tissue perfusion causes ischemic pain
  • paralysis of an affected nerve can lead to weakness or numbness
  • ulceration of skin
  • headaches
  • fever
  • weakness
  • fatigue
  • malaise
  • anorexia
  • wt loss
  • muscle and joint pain
  • angina
  • dyspnea
  • hypertension
  • visual disturbances
74
Q

diagnose of systemic necrotizing vasculitis

A
  • comprehensive blood studies including CBC, ESR, RA factor determinatioon and serum tests for Ig
  • CBC indicates anemia and usually elevated WBC and platelet counts
  • ESR is elevated durign acute stage
  • CRP test shows an earlier and more intese increasecompareed with ESR
  • chest radiographs show pulmonary infiltrates
  • hematuria and proteinuria
  • aneurrysm and myocardial ischemia
  • biopsy confirms diagnosis by demonstrating invasion of leukocytes in blood bessels
  • angriography
75
Q

treatment of systemic necrotizing vasculitis

A
  • decreasing inflammation of arteries and improving the function of affected organs
  • addresses underlying causative factors and systemic involvement
  • corticosteroids and analgesics
  • immune-suppressing meds such as azathioprine and cyclophsphamide
  • plasmapheresis
  • antihypertensive drugs such as angiotensin-converting enzyme (ACE) inhibitor

Pathophysiology - Intro (15 decks)

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