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1
Q

Acute mastitis vs periduxtal mastitis

A

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

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2
Q

Mammary duct extasía

A

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

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3
Q

Fat necrosis
- presentation

A

Mass because of inflammatory and giant cells or as calcifications because fat binds calcium

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4
Q

Fibrocystic change
- pathophysiology
- subtypes
- complication

A

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

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5
Q

Intraductal papilloma vs papillary carcinoma

A

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

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6
Q

Fibroadenoma vs phyllodes tumor

A

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

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7
Q

Ducts carcinoma in situ (+subset)vs lobular carcinoma in situ

A

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

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8
Q

Invasive Ducati carcinoma (+subtypes) vs invasive lobular

A

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

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9
Q

Male breast cancer
- location
- most common subtype
- possible symptoms
- risk factors

A

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

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10
Q

Acne management

A

Comedones (whit and black heads ) topical retiñoids

Pustules - benzoyl peroxide

Clindamycin/ doxy/erythomycin antibiotics

Last resort -isoretinoin

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11
Q

Lichen planus association with what GI condition

A

Chronic hep c infection.

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12
Q

Pemphigus vulagaris vs pemphigoid

A

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

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13
Q

Erythema multiforme
- subtypes
- pathophysiology
- causes

A

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

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14
Q

Basal cell carcinoma vs squamous
- location; causes, appearance

A

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

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15
Q

Vitiligo vs albinism

A

V- autoimmune destruction of melanocytes

A - enzyme deficieny (tyrosinase) so can’t make melanin; increased risk of SCC especially and other skin cancers

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16
Q

Freckles pathophysiology

A

Increases melanosomes( melanocytes are not increased

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17
Q

Pituitary adenoma
-presentation

A

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
18
Q

MCCOD of acromegaly

A

Cardiac failure

19
Q

Causes of hypopituitiarism

A

Craniopharyngioma, pituitary adenoma compression the pituitary gland, empty sella turcica, apoplexy, sheehan (no lh therefore no axillary or pubic hair, no lactation)

20
Q

Causes of SIADH

A

CNS or pulmonary or cyclophosphamide

21
Q

Presentation of hyperthryroidism

A

Increase BMR
increase sympathetic via beta1
Hypocholesterolemia
Hyperglycemia
Oligomenorrhea bone resorption

22
Q

Graves vs hashimotos (HLA, complication )
- pathophysiology

A

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

23
Q

De quervain thyroiditis ve Reidel fibrosing thyroiditis (associated conditions)

A

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

24
Q

Papillary adenocarcinoma
RF
Method of spread
Unique feature

A

Most common
Spreads via cervical lymph nodes
Psamommas
RF: ionizing radiation due to acne

25
Q

Follicular carcinoma
- mode of invasion
- how to diagnose

A

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

26
Q

Primary hyperparathyroidism
- causes
- labs
- complications

A

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
27
Q

Hypoparathyroidism vs pseudo

A

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

28
Q

T1DM
- pathophysiology
- HLA

A

Autoantibodies damages the pancreas (type 4
- HLA DR3 and 4

29
Q

MCCOD IN DIABETICS

A

Cardiovascular disease

30
Q

Somatostatinomas
-presentation

A

Aomatostaun inhibits acid protection therefore achlorydia, inhibits gallbladder contraction therefore gallstones , and affects bile therefore malabsorption/ steatorrhea

31
Q

Cushing
- pathophysiology
- presentation

A

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
32
Q

Conn syndrome
- presentation

A

Primary - adrenal ádrenoma most likely , or adrenal hyperplasia or cancer—- low renin

Secondary - fibromuscular dysplasia or atherosclerois so high renin

33
Q

CAH

A

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

34
Q

Adrenal insufficiency
- causes
- symptoms

A

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

35
Q

Possible Location of pheochronocytoma

A

Bladder wall therefore hypertensive when urinating

36
Q

Achrondoplasia
- pathophysiology

A

Activating FGFR3 therefore inhibits cartilage growth in endochrondal bone (bones not in head or chest

37
Q

Osteopetrosis
- pathophysiology
- complications
- treatment

A

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)

38
Q

Osteomalacia (
- associated pediatric manifestation
- pathophysiology
- labs
- complications

A

-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

39
Q

Osteoporosis
- pathophysiology
- affected areas
- labs
- treatment

A

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

40
Q

Paget
- pathophysiology
- presentation
- labs
- complications

A

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

41
Q

Lambert vs MG (interesting unknown things

A

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

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