Medicine General 02 Flashcards
Malignant Melanoma Types
- Lentigo maligna melanoma: arises from chronically sun exposed skin
- Superficial spreading MM
- Nodular MM
- Acral-lentiginous MM: arising from palm, soles & nail beds
- Ocular MM
- Mucosal MM
< 30% from pre-existing nevus
ABCDE rule for melanoma evaluation
A - asymmetric
B - borders are irregular
C - color variegation
D - diameter > 6 mm
E - evolution ie changing appearance, growing in size
Black box warning: Tacrolimu,s, Pimecrolimus topical
Can cause T cell lymphoma and should be sparingly used. Risk is more with those with HIV, iatrogenic immunosuppressive Rx, past lymphoma etc.
Inherited platelet function disorders
- Glanzman’s disease (GPIIb/IIIa deficiency)
- Bernard Soulier disease (GP deficiency)
- Chediak Higashi syndrome (abnormal platelet granules)
- Grey platelet syndrome (Alfa granule deficiency)
- Storage pool disease
- Secretion defect
Thrombocytopenia - low production
Myelosuppression:
- viral infections
- drugs, alcohol
- infiltration/failure/fibrosis
ITP, 1/3 rd of cases
B12 or folate deficiency
Inherited disorders
Thrombocytopenia- increased destruction/ consumption
Immune:
- Idiopathic, ITP
- drug induced
- SLE
- HIV related
Non Immune:
- massive transfusion
- Hypersplenism
- DIC, TTP
Koebner phenomenon
Psoriatic changes occurs at the site of skin trauma for example at a simple scratch which turns into a plaque like changes.
Obesity worsened psoriasis and good weight loss improves it.
Inverse psoriasis
Psoriasis changes only at the flexures like axilla, groin or popliteal fossa is termed inverse psoriasis( regular one favors extensor surfaces)
Nail pitting, onycholysis, koebner phenomenon seen in both.
Flare triggers - beta blockers, anti malarials, Statins, Lithium.
Medications which can induce Cutaneous SLE
Subacute Cutaneous Lupus:
Anti Ro/SSA +ve
- Hydrochlorothiazide
- Calcium Channel blockers
- H2 blockers
- proton pump inhibitors
- ACE inhibitors
- TNF inhibitors
- Terbinafine
Myogenic Hyperuricemia
Myogenic hyperuricemia, as a result of the purine nucleotide cycle running when ATP reservoirs in muscle cells are low, is a common pathophysiologic feature of glycogenoses, such as GSD-III, which is a metabolic myopathy impairing the ability of ATP (energy) production for muscle cells. In these metabolic myopathies, myogenic hyperuricemia is exercise-induced; inosine, hypoxanthine and uric acid increase in plasma after exercise and decrease over hours with rest. Excess AMP (adenosine monophosphate) is converted into uric acid.
Porphyria cutanea tarra
Genetic,
Triggers: Estrogens, ALD, Hemochromatosis, Hepatitis C
Lesions -
= on dorsum of hand macular rash, painless on exposure to sunlight
= facial hypertrichosis
= facial hyperpigmentation
Lab test -
Urinary porphyrins
Liver function tests
Hepatitis C serology
Hemochromatosis work up
Treatment: barrier sun protection with clothing and sun screens. Wavelength of triggering light is beyond that absorbed by sunscreens SO THEY MAYNOT HELP.
Pseudo porphyria
Similar lesions on dorsum of hand on sun exposure, specially when taking medications like:
- Tetracycline
- NSAIDs: Naproxen
- Voriconazole
Histopathology of lesions same as porphyria but urinary porphyrins normal