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LAST TEST EVA > Vasculitis > Flashcards

Vasculitis Flashcards

0
Q

Medium vessels

A

Immune complexes : polyartheritis nodusa

Anti endothial cell antibody : Kawasaki

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1
Q

Large vessel vasculitis

A

Granulomatous disease : giant cell , takayasu

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2
Q

Small vessel

A

Microscopic polyangitis
Wegners granulomotosis
Chrug Strauss

Sle, IgA henoch schonlein, cryoglobulin, good pastures

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3
Q

Pr3 - anca

A

C-anca

Wegners, microscopic poly, pan, Chrug, good pastures

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4
Q

MPO- anca

A

P-anca

Primary vasculitis, microscopic polyangitis , Chrug, pan

Felty, sle, sjorgen, uc, crohns, primary sclerosing cholangitis

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5
Q

Microscopic polyarteritis

A

Necrotising vasculitis affecting arteries, capillaries, venules

Glomerulonephritis and pulmonary capillaritis common ( not in PAN)

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6
Q

Presents as palpable purpura

A

Microscopic polyarteritis

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7
Q

Skin biopsy : lesions are all the same stage

Segmental fibrinoid necrosis of media

A

Microscopic polyarteritis

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8
Q

Have fragmented pmns - leucocytoclasia

A

Microscopic polyarteritis

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9
Q

Cause of microscopic polyarteritis

A

Reaction to antigens once antigen is removed it goes away

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10
Q

Triad :acute necrotizing Granulomatous inflammation of medium to small vessels in upper and lower respiratory tract

Affects other body sites- eye and skin

Focal necrotizing glomerulonephritis

A

Wegners granuolmatosis

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11
Q

Age of onset and test for Wegners

A

5th decade m>f and c-anca detectable in 95%

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12
Q

Begins as severe type of asthma

Sinusitis ~>asthma ~> organ involvement

A

Churg Strauss

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13
Q

Diagnostic markers for churg Strauss

A

Blood eosinophilia, eosinophils and granulomas in affected tissue and p- anca . Mainly affects lungs

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14
Q

Segmental transmutation necrotizing vasculitis in medium and small arteries . Doesn’t affect arterioles, capillaries, venules

Aneruysms and thrombosis common

A

Polyarteritis nodosa

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15
Q

Spares the lungs and if a disease of young adults ….m>f

A

PAN

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16
Q

Clinical signs of PAN

A

Ischemia and infarction often episodic. And general symptoms of malaise, fever weightless, etc

30% have HBsAg in serum
Both c-ANCA and p-ANCA but p is more common

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17
Q

Treatment pan

A

Untreated - fatal unless cutaneous

Corticosteroid and cyclophosphamide

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18
Q

Vasculitis of children and infants parents as acute fever rash,viral erythema, red lips and strawberry tongue

A

Kawasaki

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19
Q

Kawasaki diseases symptoms and problems

A

Asymptomatic to mi coronary artery aneurysms with rupture and death

Leading cause of acquired heart disease in the us and japan. Similar lesions as pan .

Cause is thought to be viral induced in genetically susceptible patients

Tx with anti- pyretics and IVIG

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20
Q

Affects medium to to small vessels - mainly radial and tibial arteries ususally young male and women smokers

A

Buergers disease

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21
Q

Buergers disease age and hla type

A

Before the age of 35
Hla -a9 and b5

Common in Japan, Israel, India

Hypersensitive to injected tobacco extract

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22
Q

Inflammation of. Large medium and small arteries.

Usually affects head arteries ( temporal, ophthalmic, vertebral) or aorta

A

Giant cell (temporal) arteritis

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23
Q

Most common vasculitis in adults. You see segmental modular thickenings, lumen is reduced.

A

Giant cell arteritis

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24
Q

Giant cell arteritis clinical symptoms

A 
Usually elderly 70-80 
- half pts have visual symptoms 
- vague constitutional symptoms( fever, fatigue, weightloss, HA) 
Facial pain over the temporal artery
May cause thoracic aortic aneurysm
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25
Q

What do you see on biopsy giant cell

A

Fragmentation of internal elastic membrane

Granulomatous inflammation of emerita near the internal elastic membrane

Multinucleated giant cells

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26
Q

Granulomatous inflammation of large to medium sized arteries. Fibrous thickening of aortic arch and it’s branches and in half of cases the pulmonary arteries are affected

A

Takayasu arteritis

27
Q

Takayasu clincial symptoms and biopsy results

A

Females > 40
Wake pulses and low BP in upper extremities.
Ocular probs , neuro deficits, pulm HTN, HTN, claudication.

Narrowing and obliteration of lumens On angiogram

Biopsy: intimate thickening, mononuclear inflammation, giant cells, lumens occluded by partially organized thrombus

28
Q

Vasculitis that look like micros poco polyarteritis and pan

A

RA, sle , henoch- schonlein purpura , mixed cryoglobulinemia, malignancy

29
Q

Henoch- schonlein purpura

A

Generalized vasculitis of small vessels of the skin (purpura), GI tract,
joints (arthritis), kidneys (rarely - lungs & CNS)

Most common vasculitis in children.
75% of cases occur in children 2-11 years old.
Rare in adults.

IgA antibody– antigen complexes ĺ deposit locally - throughout bodyand activate pathways leading to necrotizing vasculitis.

Bacterial, viral, vaccine, drug, idiopathic causes. No single etiology has been clearly identified.

30
Q

Why is it important to differentiate sle from what

A

APLA syndrome because treatment is different steroids vs anti coagulation

31
Q

Anti phospholipid antibody (APLA) Hughes syndrome

A

3 different antibodies cause both arterial & venous thrombosis (blood clots).

  1. anticardiolipin antibodies
  2. antibodies directed against specific molecules (e.g. beta-2-glycoprotein 1).
  3. lupus anticoagulant (LA)

> 50% patients have primary APLAS. Prevalence in general population ~2-4%. Any age (esp. females with SLE)

Secondary APLAS - ~ 30% of patients with SLE develop.
Anticardiolipin antibodies are more common than lupus anticoagulant (~ 5X)

In patients with 1º APLAS, ~ 10% will eventually be diagnosed with an autoimmune disorder
(e.g. SLE or a mixed connective tissue disorder).
Antibodies induce a thrombophilic state. Exact mechanism is unknown.

APLA react will endothelial cell membrane phospholipids ĺ cell damage ĺ thrombosis
APLAS is associated with miscarriages, preterm labor, preeclampsia, and eclampsia.
Thrombocytopenia (low platelets) observed in 20-40% of patients.
Stroke, MI, kidney damage, PE If multiple clots – catastrophic APS (CAPS)

32
Q

Red papule forms a vesicle
in the center.
Dries, forms a black scab.
No scarring.

Papule is usually on   
face, trunk, extremities.
Palms, soles, and oral 
mucosa may be 
involved.

Papule precedes fever.Serology.

A

Rickettsialpox - R. akari

33
Q

Papule becomes a vesicle
on an erythematous base.
Resembles a “dew drop”
on a rose petal.

Papule begins on head
ĺ progresses to trunk,
arms, then legs.

Vesicles present in all
stages.

Common in children.
Positive Tzanck test or DFA.

A

Chicken pox (VZV)

34
Q 
Red macule or papule with 
central vesiculation
surrounded by a red areola. 
Papule crusts in a few days.
No scarring.

Palmar surfaces and
sides of fingers, hands,
and plantar toe skin.

After fever, in 1-2 days
oral ulcers on the hard palate, tongue, buccal mucosa.
Cell culture & PCR.
RX: symptomatic relief

A

Hand-foot-and-mouth Disease
(enteroviruses, e.g.
coxsackievirus A16)

35
Q 
At tick bite site, an ulcer with 
a red halo forms.
Later becomes generalized 
maculopapular rash.
Rash is generalized, 
involves palms and 
soles, and is rarely 
hemorrhagic.

Fever, headache, and
generalized lymphadenopathy

Symptoms similar to a milder
form of RMSF.
Serology – R. conorii Ab

A

Boutonneuse fever

36
Q

At mite bite site, vesicle or
black scab appears on an
erythematous base.

Vesicles are usually on
trunk or extremities.

Rash fades within a few days.Pneumonitis is frequent.
Serology.

A

Scrub typhus - o. Tsutsugamishi

37
Q

Louse-borne typhus

epidemic

A

R. prowazekii

Human body louse (Pediculus humanus)

38
Q

Murine typus

A

R. typhi
Rat flea
(also endemic CA, HI, TX)

39
Q

African tick bite fever

A

R. africae

Buffalo ticks - usually live on cattle

40
Q

Scrub typhus

A

O. tsutsugamushi

Chigger mite

41
Q

Hands and feet then to trunk

A

Rmsf

42
Q

Extremities to trunk

A

Small pox and kawasakis

43
Q

Lower extremities

A

N. Meningitidis

44
Q

Hair line and downward

A

Measles

45
Q

Head to trunk to extremities

A

Varicella

46
Q

Neck to trunk

A

Scarlet fever group a strep s. Pyogenes

47
Q

Localized or generalized skin desquamation

A

Staph aureus, scalded skin syndrome. Exfoliatins toxin

48
Q

Scarlatina like rash that desquamates

A

Staph aureus TSS . Toxic shock toxin (tsst 1 )

49
Q

Cowdry type a inclusions

A

Intranuclear - VZV - herpes zoster

50
Q

Molluscum contagiosum

A

Benign papular eruption of multiple umbilical end cutaneous lesions

51
Q

H and e stain of Molluscum contagiosum

A

Epidermal acanthosis (hyperplasia) - MC grows into dermis to form multiple lobules.

Eosinophilic intra-cytoplasmic inclusion bodies - at the lobule base,
more basophilic at superficial layer.

Central crater - into which the inclusion bodies discharge their contents.

52
Q

Intracellular growth

A

Rickettsia (RMSF, typhus), VZV, HSV, MCV, rubella

53
Q

Endotoxin

A

Neisseria meningitidis

LPS causes vasculitis & DIC

54
Q

Exotoxin

A

Streptococcus pyogenes (Group A Strep.)Pyrogenic (erythrogenic) toxins A-C

55
Q

Bacteria in vessel wall

A

Treponema pallidum
endothelial proliferation
lymphoplasmocytic vasculitis
endarteritis obliterans (fibrosis/healing)

56
Q

Immune Attack

of infected cells

A

Measles (Rubeola)
T cells attack viral antigen in infected
endothelium of small vessels ĺ Koplick Spots:(oral lesions on mucous membrane enanthem)

57
Q

Complement Activation

[Immune / Autoimmune]

A

Cutaneous Necrotizing Vasculitis:
Microscopic polyarteritis (small vessels)
Giant Cell Arteritis (large temporal art. & aorta)
Polyarteritis Nodosa (PAN) (medium & small)
91

58
Q

Petechia rash

Fulminant disease is Waterhouse friderichsen syndrome what is that

A

N. Meningitidis

non-palpable purpura
ecchymosis
shock
DIC
adrenal gland destruction
Grey/black necrosis with DIC.
59
Q

Septic arthritis ĺ most common initial manifestation (migratory polyarthralgia).

Rash ĺ occurs below the neck (spares scalp, face, mouth).

Small papules or petechiae located on trunk or extremities, palms and soles.- turn into pustules on broad erythematous bases and necrotic centers.
9

A

Neisseria Gonorrhoeae

60
Q

Impetigo

A

Vesicles that crusts

Strep pyogenes, staph aureus

61
Q

Erysipelas

A

Superficial cellulitis variant

Margin sharply demarcated, painful

Step. Pyogenes ans staph aureus

Spreads via lymphatics

62
Q

Gumma

A

Syphilis

63
Q

1° Tiny red papule on legs and other exposed areas,
becomes an elevated erythematous plaque.
Satellite papules form after few months; may fuse together.
No ulceration (unlike syphilis).

2° 5 -12 months after 1° stage, erythematous circular patcheson extremities and face; may go unnoticed.

3° Lesions with blue pigmentation on face, head, neck.
Replaced by depigmented spots resembling vitiligo.

A

T. Careteum -‘blue stain disease

64
Q

1°Skin papules develop on extremities ~ 1 month after infection, Enlarge to form papillomatous “frambesiform” nodules.
Usually children are affected.

2 Yellow crusted granulomatous nodules appear on extremities
and face and usually heal; may reoccur.

3 Long chronic course of remissions and relapses.
Systemic symptoms ~>fever, malaise, LN
May have skin destruction ~>large ulcerated nodules
Disfiguration esp. around nose ~>gangosa
Painful open sores on feet soles~> crab yaws
Later, bone destruction ~>tibias

A

Tp subsp. Pertenue

65
Q

When does the rash appear with measles

A

4th febrile day . Hair line to toes in 2-3 days . Maculopapular

LAST TEST EVA (7 decks)

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