) Flashcards
Acute mastitis vs periduxtal mastitis
Acute- bacterial (S.aureus) infection from breast feeding; erythematous breast with purulent nipple discharge
Periductal- inflammation of the aubareolar duct due to cigarettes. Leads to columnar becoming squamous due to vitamin a deficiency and the duct gets blocked with keratin causing inflammation. Heals with fibrosis so myofibroblast pulls nipple inwards to ducts
Mammary duct extasía
Inflammation of the subsreolar duxts leads to dilation of the ducts causing inflammatory debris to create a mass and debris leaks out of breast as green brown nipple discharge; plasma cells
Fat necrosis
- presentation
Mass because of inflammatory and giant cells or as calcifications because fat binds calcium
Fibrocystic change
- pathophysiology
- subtypes
- complication
Development of fibrosis and cysts (dilation of lobules and ducts) in premenopausal women due to estrogen
- lumpy breast
Subtypes - fibrosis cysts apocrine metaplasia - no increase risk of invasive cancer
Ducts hyperplasia (>2 layers of cells in the duct and sclerosing adenosis (calcification and fibrosis - increased risk
Atypical hyperplasia - increased atypical cells in lobular or duct/ greatness increased risk of invasive carcinoma
Intraductal papilloma vs papillary carcinoma
Papillary duct growth into large duct
- intraductal- premenopausal; finger like projection is lined by luminal and myoepitheal : blood nipple discharge
- papillary carcinoma- post meno ; finger like projection is lined by luminal only
Fibroadenoma vs phyllodes tumor
Most common benign breasts mass is Fibroadenoma.
- tumor of fibrous tissue and glands in premenopausal ; responds heavily to estrogen so shrinks during menopause ; no increase risk of cancer
Phyllodes- fibroadenoma like tumor with overgrowth of fibrous tissue in postmenopausal ; May be malignant
Ducts carcinoma in situ (+subset)vs lobular carcinoma in situ
Dcis- malig proliferation of cells in ducts which doesn’t cross the basement membrane; present as calcification (no mass usually
- since there’s calcification need to biopsy calcification to distinguish between benign shit like fibrocystic sclerosing adenosis and fat necrosis
- subset is PAGET
Lobular carcinoma in situ - malignant proliferation of cells in lobular ; found incidentally bc no calcifications or mass primoduxed; cells lack ecadherin; treatment- TAMOXIFEN
Invasive Ducati carcinoma (+subtypes) vs invasive lobular
Ductal - most common invasive forms duct like structures ; presents as a mass
- tubular , mucinous , medullary (seen in brca; malignant cells with inflammation cells such as lymphocytes and plasma), inflammatory - grows in dermal lymphatics (so swelling)and presents like a mastitis that doesn’t resolve with antibiotics and
Lobular - lack ecadherin so can’t form duxts ; grows in single file
Male breast cancer
- location
- most common subtype
- possible symptoms
- risk factors
Subseeolar so can produce milk
Males only have ducts and no lobulares therefore more commonly would have invasive distal carcinoma
RF: Klein filter and BRCA2
Acne management
Comedones (whit and black heads ) topical retiñoids
Pustules - benzoyl peroxide
Clindamycin/ doxy/erythomycin antibiotics
Last resort -isoretinoin
Lichen planus association with what GI condition
Chronic hep c infection.
Pemphigus vulagaris vs pemphigoid
Vulgaris- IgG against desmoglein in desmorones; positive Nikolsky; blistering of skin and oral mucosa; iF - fish net
Pemphigoid - IgG against hemidesmisomes - negative nikolsky; blistering of skin only ; IF: liner
Erythema multiforme
- subtypes
- pathophysiology
- causes
Subtypes : SJs and TEN
- SJS (EM with oral mucosa and lip involvement plus fever)
- TEN : severe form of SJs with sloughing of skin at epidermal dermal junction due to adverse drug reaction
Hypersensitivity rxn associated with HSV, mycoplasma infection , AI diseases, malignancy and penicillin and sulfonamide ——-targetoid rash (with white center due to necrosis ) and bullae
Basal cell carcinoma vs squamous
- location; causes, appearance
BCC- top lip , UVB sun exposure , ulcerated ulcer with surrounding telangiectasia
SCC- lower lip; UVB sun exposure , but also immunosuppressive therapy, arsenic , chronic inflammation from burns or draining sinus tract
- dysplasia : actinic keratosis
- subtype : keratoacanthoma——occurs suddenly and resolves spontaneously
Vitiligo vs albinism
V- autoimmune destruction of melanocytes
A - enzyme deficieny (tyrosinase) so can’t make melanin; increased risk of SCC especially and other skin cancers
Freckles pathophysiology
Increases melanosomes( melanocytes are not increased
Pituitary adenoma
-presentation
Functional or non functional
- non functional creates a mass effect therefore headache, bitemporal hemianopsia , hypopituitarism because pituitary gland is compressed
- function
——most common in prolactinoma (prl inhibits Gnrh therefore amenorrhea and low libido
—gag adenoma ——adults have growth of visceral organs such as the heart, diabetes because GH prevents glucose from going into the Cells
MCCOD of acromegaly
Cardiac failure
Causes of hypopituitiarism
Craniopharyngioma, pituitary adenoma compression the pituitary gland, empty sella turcica, apoplexy, sheehan (no lh therefore no axillary or pubic hair, no lactation)
Causes of SIADH
CNS or pulmonary or cyclophosphamide
Presentation of hyperthryroidism
Increase BMR
increase sympathetic via beta1
Hypocholesterolemia
Hyperglycemia
Oligomenorrhea bone resorption
Graves vs hashimotos (HLA, complication )
- pathophysiology
Autoantibody stimulating TSH receptors (type 2 )
Hash - autoantibodies (anti thyroglobulin and antimicrosomal) produced by T cells attack the thyroid gland therefore initially present as hyperthyroidism bc thyroid hormones are release then hypo
—- HLA dr5
——- complication : marginal B cell lymphoma
De quervain thyroiditis ve Reidel fibrosing thyroiditis (associated conditions)
d - presents as hyperthyroidism after a viral infection; tender thyroid
Reidel - presents as hypothyroidism; inflammation leading to fibrosis; nontender
- associated igg4 conditions (pancreas, air gallbladder problem , retropharyngeal fibrosis, bilateral hydronephrosis
- similar to anaplastif but is benign since the fibrosis can invade nearby structures such as airway
Papillary adenocarcinoma
RF
Method of spread
Unique feature
Most common
Spreads via cervical lymph nodes
Psamommas
RF: ionizing radiation due to acne
Follicular carcinoma
- mode of invasion
- how to diagnose
Hematogenous
Fine needle aspiration is not useful bc the capsule will possible look similar to a follicular adenoma was in benign so need to take out the capsule/follicle
Primary hyperparathyroidism
- causes
- labs
- complications
Cause :one gland parathyroid adenoma, Parathyroid hyperplasia or cancer
-labs: increase pth, increase ca , low p043-, high urinary camp, high alkaline phosphatase
- nephrolithiasis (calcium pxalate, neuropsych, cyst and fibrosis in bone because of bone resorption, acute pancreatitis due to the hyper calcium , peptic ulcer disease, nephrocalcibosis
Hypoparathyroidism vs pseudo
Pseudo - mutant Gs protein theeefoew resistant to the PTH. Low ca but high PTH; short with shortened 4/5 fingers
Hypo- causes - damage to parathyroids, surgery , digeorge
T1DM
- pathophysiology
- HLA
Autoantibodies damages the pancreas (type 4
- HLA DR3 and 4
MCCOD IN DIABETICS
Cardiovascular disease
Somatostatinomas
-presentation
Aomatostaun inhibits acid protection therefore achlorydia, inhibits gallbladder contraction therefore gallstones , and affects bile therefore malabsorption/ steatorrhea
Cushing
- pathophysiology
- presentation
Most common cause is exogenous steroids (leads to bilateral adrenal atrophy), adrenal adenoma or adrenal hyperplasia or adrenal cancer leads to atrophy of normal gland and atrophy of gland that’s mass producing then cortisol, acth secreting pituitary adenoma( bilateral adrenal huperplasia and responds to high dose dexa) , acth secreting small lung (bilateral adrenal huperplasia and but doesn’t responds to high dose dexa
- cortisol causes hypertension bc stimulates alpha 1 , affects collagen hence striae, osteoporosis, immune suppression , breaks down muscles to get amino acids for glucose production hence muscle weakness
Conn syndrome
- presentation
Primary - adrenal ádrenoma most likely , or adrenal hyperplasia or cancer—- low renin
Secondary - fibromuscular dysplasia or atherosclerois so high renin
CAH
21- increased. Sex steroids , salt wasting bc no aldosterone and hypotension bc low cortisol; girls virilization and births and precocious puberty for males
17 deficiency required to make sex and cortisol therefore no salt wasting
11 deficiency - still have some minor mineral corticoid action but no cortisol
Adrenal insufficiency
- causes
- symptoms
Acute - n. Meningitis lead to DIC which causes hemorrhagic necrosis of bilateral adrenal glands
Chronic -Tb, autoimmune, metastatic cancer especially from lungs
Hyperpigmentation due to increased acth, low bp, low na , high K
Possible Location of pheochronocytoma
Bladder wall therefore hypertensive when urinating
Achrondoplasia
- pathophysiology
Activating FGFR3 therefore inhibits cartilage growth in endochrondal bone (bones not in head or chest
Osteopetrosis
- pathophysiology
- complications
- treatment
Impaired carbonic anhydrase therefore can’t create H+ required for bone resorption or removal of calcium from bone, this leads to malfunctioning osteoclasts and only the osteoblast work therefore lay down thick but weak bones
- compilation thick bone can infiltrate the bone marrow therefore pancytopenia, compress cranial nerves leading to vision and hearing impairment, compress for foramen magnum (hydrocephalus)
Renal tubular acidosis - Can’t reasorb hco3 therefore metabolic acidosis
Treatment : bone marrow transplant (get monocytes to make good osteoclast)
Osteomalacia (
- associated pediatric manifestation
- pathophysiology
- labs
- complications
-Rickets (<1yo)
- vitamin d deficiency so the osteoid that the osteoblasts create can’t be mineralized
- labs - think vitamin d deficiency the low calcium and phosphate, increased pth increased alk phos since osteoblasts increased
- complications (adult- vertebrae and hip fractures) (child- frontal bossing leg bowing , rachitic rosary , pigeon chest possible bc of osteoid deposition
Osteoporosis
- pathophysiology
- affected areas
- labs
- treatment
Decreased bone mass
Fractures of hip , vertebrae and radius
Normal labs
Tx: exercise,vitamin d, calcium
Bisphosphonates (osteoclasts eats it and are apoptosed
No steroids because will worsen it
Paget
- pathophysiology
- presentation
- labs
- complications
Osteoclast go haywire and eventually the osteoblast starts to put down bone . Osteoclasts die but osteoblast still working creating thick easily fractured
bone
Thick bone affects cranial nerves (hearing and vision impairment , craneofacial bones lion facies , thicken skull especially
Labs- only increased ALK PHOS
complication: high out heart failure and osteosarcoma
Lambert vs MG (interesting unknown things
MG- affects mostly eyes (diplopia and ptosis ; associated with thymoma or thymus hyperplasia so once they’re removed mg resolves
Lambert - proximal muscle weakness, no eye involvement ; acetycholinesterase inhibitors don’t work because the issue is prior the ACH receptor ; treatment removed the cancer causing the paraneoplastix syndrome
