Panniculitis Flashcards

1
Q

What is the most common panniculitis?

A

Erythema nodosum

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2
Q

What is the most common group of people with of erythema nodosum?

A

Women in the 2nd and 4th decades

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3
Q

What is the pathogenesis of erythema nodosum?

A

Th1 cytokine hypersensitivity reaction to various antigens

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4
Q

Most common etiology of erythema nodosum?

A
  1. Idiopathic
  2. Streptococcal infection (#1 identifiable cause), other infxn (Yersinia, Salmonella, Campylobacter), viral URI’s coccidioidomycosis
  3. Drugs: Estrogens/OCPs, sulfonamides, NSAIDs
  4. Inflammatory conditions: Sarcoidosis and IBD (Crohn’s> UC)
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5
Q

What drugs are associated with erythema nodosum?

A

Estrogens/OCPs, sulfonamides, NSAIDs

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6
Q

What is Lofgren’s syndrome?

A

Sarcoidosis w/ EN, hilar lymphadenopathy, fever, polyarthritis, and uveitis a/w good progress

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7
Q

What is the clinical presentation of erythema nodosum?

A

Acute, tender subcutaneous nodules on pretibial areas (most commonly) bilaterally with overlying erythema to bruises-like patches

Develop over 1-2 weeks, then resolve spontaneously

New lesions can pop up over 1-2 months

Can be a/w fever, arthralgias, malaise (may precede cutaneous findings)

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8
Q

What are the chronic types of erythema nodosum?

A

Subacute nodular migratory panniculitis/erythema nodosum migrans

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9
Q

Characteristics of chronic erythema nodosum?

A

Women usually, unilateral, migrating centrifugally expanding nodules (less ender than acute version)

  • Usually idiopathic, but may be a/w streptococcus infxn
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10
Q

What is the treatment for chronic erythema nodosum?

A

Saturated solution of potassium iodide

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11
Q

What is the histology of erythema nodosum?

A

Septal panniculitis w/ thickening/fibrosis of septae

  • neutrophils seen particularly in early lesions
  • Miescher’s migrogranulomas: small histiocyte aggregates surrounding a central stellate cleft located in the subcutaneous fat septa
  • +/- thrombophlebitis (more common in EN-like lesions seen Behcet’s disease
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12
Q

What is the treatment for erythema nodosum?

A

Lesions tend to resolve w/o scarring in a few days to weeks.

  • Treating underlying medical issue if identified can be helpful
  • Other tx: NSAIDs, elevation, SSKI, colchicine (especially if Behcet’s associated), systemic immunosuppressants
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13
Q

What does erythema nodosum suggest regarding infection with coccidioidomycosis and sarcoidosis?

A

Improved prognosis

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14
Q

What is the pathogenesis of alpha1-antitrypsin deficiency panniculitis?

A

Alpha1-antitrypsin (made in the liver, serine protease inhibitor) is low –> dysregulation of immune system w/ increase in neutrophils –> release of proteolytic enzymes –> fat necrosis

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15
Q

What are the different alleles seen in alpha1-antitrypsin deficiency and what are their significance?

A

M= medium (normal quantities of enzyme)

S = slow (moderately decreased quantities of enzyme)

Z = very slow (severely decreased quantities of enzyme)

So people w/ one copy of Z or S have mild/moderate dz; most severe form is seen with homozygous Z alleles

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16
Q

Clinical features of anti1 antitrypsin deficiency panniculitis?

A

Large erythematous to purpuric, tender nodules or plaques appear especially on lower trunk and proximal extremities(flanks, buttocks, and thighs) Oily discharge can be seen

  • As opposed to EN heals w/ scarring and subcutaneous atrophy
  • preceding trauma in 1/3
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17
Q

Systemic associations of anti1 antitrypsin deficiency panniculitis?

A

A/w chronic liver dz (cirrhosis) , emphysema, pancreatitis, membranoproliferative glomerulonephritis c-ANCA vasculitis, and angioedema

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18
Q

What is the histology of anti1 antitrypsin deficiency panniculitis?

A

Early: neutrophilic panniculitis followed by rapid necrosis and destruction of fat (liquefactive necrosis of fat w/ foamy macrophages and cystic spaces)

Chronic inflammation and hemorrhage may be present at the periphery of involved areas

19
Q

What is the treatment of anti1 antitrypsin deficiency panniculitis?

A

Alpha1-antitrypsin replacement leads to rapid improvement, can also use doxy, colchicine, cyclophosphamide, dapsone, decreased alcohol consumption, plasma exchange, and liver transplant

20
Q

What is the distinction between erythema induratum vs nodular vasculitis?

A

Classically the erythema induratum of Bezin referred to cases associated with TB and then the nodular vasculitis were those caused from other causes/idiopathic

21
Q

What test should be performed on the tissue collected for erythema induratum in regards to TB?

A

PCR should be performed

22
Q

What type of reaction is erythema induratum/nodular vasculitis?

A

Type IV hypersensitivity

23
Q

Clinical features of erythema induratum/nodular vasculitis?

A

Tender, recurrent, red-purple nodules and plaques on calves most commonly

  • may ulcerate and scar
24
Q

What is the histology of erythema induratum/nodular vasculitis?

A

Lobular and septal panniculitis w/ neutrophils, lymphocytes, macrophages, giant cells + (this mix of cells is classic), mixed vessel vasculitis [connective tissue and septa]

  • Main difference between this and PAN is that PAN doesn’t affect the fat lobules themselves
25
Q

What is the histologic difference between PAN and erythema induratum/nodular vasculitis?

A

Main difference between this and PAN is that PAN doesn’t affect the fat lobules themselves

26
Q

What is the treatment of erythema induratum/nodular vasculitis?

A

Treat TB if present, otherwise care needed is supportive + various systemic tx like CS, NSAIDs, TCN, or SSKI

27
Q

What is the pathogenesis of pancreatic panniculitis?

A

A/w pancreatic disorders (pancreatitis/carcinoma, and pseudocysts)

  • Occurs due to hydrolysis of fat by lipase, amylase, and trypsin (increased serum levels of any (or all) of these three enzymes and detectable
28
Q

Clinical features of pancreatic panniculitis?

A

Subcutaneous nodules of legs (most common sites )

  • May occur prior to known pancreatic issues
  • May have systemic symptoms
29
Q

What is Schmid’s triad?

A

Nodular lesions + polyarthritis + eosinophilia in the setting of pancreatic panniculitis –> a/w poor prognosis

30
Q

What is the histology of pancreatic panniculitis?

A

Mixed panniculitis w/ “ghost cells” (anucleate necrotis adipocytes) formation and fat necrosis w/ saponification by calcium salts –> basophilic color of damaged fat lobules

31
Q

Treatment for pancreatic panniculitis?

A

Treat the underlying pancreatic disorder

32
Q

What is the pathogenesis of lipodermatosclerosis?

A

Due to a combination of venous insufficiency and fibrinolytic abnormalities –> increased capillary permeability –> fibrin cuffs form around vessels –> decreased O2 exchange/tissue anoxia –> cystic fat necrosis with or without dermal stasis changes

33
Q

What are the clinical features of lipodermatosclerosis?

A

Acute = rubor, dolor, and color, can look like b/l cellulitis

Chronic= well-defined induration, hyperpigmentation “inverted wine bottle look from sclerosis)

  • Medial lower leg, superior to malleolus is the most commonplace
34
Q

What is the histopathology for lipodermatosclerosis?

A

Septal thickening, fibrosis, cystic fat necrosis / surrounding lipophages, mild non-specific inflammation, lipomembranous change, and you can see stasis changes (angioplasia, inflammation, and fibrosis)

35
Q

What is the treatment for lipodermatosclerosis?

A
  • Leg compression and elevation
  • Systemic options: danazol, oxandrolone, and pentoxifylline
36
Q

What are the panniculitis due to external factors?

A

Cold panniculitis or physical trauma/foreign material

37
Q

What is the clinical presentation of cold panniculitis?

A

acute, firm, painful, cool (in temperature), erythematous plaques/nodules that develop 1-3 days post-cold exposure; most commonly affects areas of prominent fat distribution (central cheek, thighs, and back)

38
Q

What is popsicle panniculitis?

A

Seen in infants on the cheeks mostly (dude to higher saturated to unsaturated fatty acid ratio in that area)

39
Q

What is equestrian panniculitis?

A

Young women equaestions on the thighs form cold exposure

40
Q

What are some risk factors for cold panniculitis in neonates?

A

Head or whole-body hypothermia for hypoxic-ischemic encephalopathy and use of ice therapy for supraventricular tachycardia

41
Q

What is the histology of cold panniculitis?

A

Lobular panniculitis + typical pernio changes (superficial and deep perivascular and peri-eccrine lymphohistiocytic infiltrate w/ papillary dermal edema)

42
Q

What is the prognosis of cold panniculitis?

A

Resolves over several weeks; lipoatrophy may develop in affected areas

43
Q

What is sclerosing lipogranuloma?

A

Male genitalia (penis) due to injection of oil-based materials for augmentation

44
Q

What is the histology of physical trauama/foreign material?

A

Vacuolated spaces, foreign material (Swiss cheese look in sclerosing lipogranuloma) and evidence of needle stick