Ultimate Merge Flashcards
(345 cards)
Conjunctivitis:
Viral vs Bacterial vs Allergic
a) UL vs BL
b) “stuck shut”
c) dcg
d) dcg reappear after wiping
e) other complaints
f) conj. appearance
tx and MoA for each
a) UL->BL vs UL——> vs BILATERAL
b) all
c) serous, thick/purulent, serous
d) no, YES, no
e) burning/gritty vs unremitting dcg vs itchy
f) bumpy vs non-bumpy vs bumpy/chemosis [bumpy=follicular] [edema=chemosis]
Viral: tx compresses +/- anti-hist/decongestant
Bacterial: tx topical abx (erythromycin, polymyxin-TMP, azithromycin); CONTACT lens (FLUOROQUINOLONE drops)
ALLERGIC: tx mast cell stabilizer (olopatadine, azelastine), antihistamine/decongestant drops
What dz’s do you see tau protein in but what types of aggregates?
Alzheimers-NFTs of tau
Pick’s-round aggregates of tau
Common complication in those with treated Hodgkin’s Lymphoma?
secondary malignancy (often in Lung but many others)
PROLACTINOMA (3) popluations and px and detection
Management of Prolactinoma?
1) premenopausal - detected early
- galactorrhea, infertility, oligo/amenorrhea, hot flash, bone loss
2) postmenopausal - detected late
- visual deficits/headache (2/2 mass effect)
3) men - detected late
- vLibido, gynecomastia, impotence, infertility (h/a, visual)
DOPAMINE AGONIST
surgery if refractory
1) dx. benign vs malig? potential? no mass, mass, or other?
a1) intermittent, UL bloody discharge in PREmenopausal woman? hist?
a2) bloody dcg in POSTmenopausal woman? hist?
b) BL cyclical (menstrual) breast pain
c1) painless, firm, mobile lump in young woman
c2) overgrowth of c1 (>5cm) and older pt than c1
d1) asymp/bloody discharge+lump
d2) eczematous changes of the nipple
e) smoker/vitA def. nipple retraction
1)
a1) benign intraductal papilloma; epithelial+MYOepithelial; no mass
a2) malig intraductal papillary carcinoma; ONLY epithelial
b) benign fibrocystic change; lumpiness; NO MALIG POTENTIAL unless sclerosing calc. adenosis (2x), ductal hyperplasia (2x), or atypical hyperplasia (5x) is present
c1) benign fibroadenoma [MC in premenopausal females]; mobile, well-circumscribed mass; NO MALIG POTENTIAL
{um, estrogen sensitive, but is it non-cyclical?}
c2) Cystosarcoma Phyllodes
d1) DCIS
d2) malig Paget’s Dz of Breast (underlying DCIS has spread to nipple)
e) PERIDUCTAL mastitis
Which type of breast cancer does Tamoxifen treat?
What is the most important prognostic factor in breast CA?
LOBULAR carcinoma in situ (which is a RF for invasive lobular carcinoma)
TNM staging (tumor burden)
Explain the benefits;risks of the following SERMs and think through each:a) Tamoxifen b) Raloxifene !
tx?
(2) risk modifications
(3,2) MoA
a)
- tx breast CA
- reduces osteoporosis risk; predisposes endometrial CA-
- estrogen receptor ANTagonist in breast (tx and ppx)
- estrogen receptor AGONIST at osteoclasts; inhibits bone turnover
- estrogen receptor (partial) AGONIST on endometrium
b)
- tx osteoporosis
- reduces breast CA risk; predisposes VTE
- estrogen receptor AGONIST on bone
- estrogen receptor ANTagonist in breast and vagina
nipple discharge* and breast mass in multiparous postmenopausal woman 2 ddx
- BENIGN plasma cell MAMMARY DUCT ECTASIA (*GREEN/BROWN dcg)
- malig Ductal CA in Situ (*bloody dcg)
Fat embolus vs Pulmonary Contusion
FE= AMS+petechiae following a 12-72 hour latency
PC= blunt chest trauma: dyspnea, tachypnea, chest pain, hypoxemia worsened with IVF
Natural infection immunity vs Vaccine immunity?
-- Levels during the following? a) early b) window c) recovery
sAg+anti-c
(elevated both during initial infx and window)
–
Vaccine - anti-S (IgM)
Nat. Imm- anti-S (IgM) + anti-C (IgG!)
a) E, S, anti-C (IgM)
b) anti-C (IgM) only!
c) anti-C (IgG), anti-E, anti-S
[DNA in all 3]
NBS in suspected gout or pseudogout?
What condition do you typically see pseudogout in and why?
What is a weird cause of CPPD/chondrocalcinosis/pseudogout? What else can this cause and is it reversible? What is chondrocalcinosis?
How treat gout? (2)
Arthrocentesis (joint aspirate, fluid analysis)
Hyperthyroidism predisposes pseudogout development.
Hemochromatosis;
lol restrictive cardiomyopathy that’s reversible (vs amyloidosis, sarcoidosis, scleroderma)
Chondrocalcinosis is calcified articular cartilage.
1) ACUTE:
a) NSAID
b) Colchicine
c) Corticosteroids
2) PREVENTION:
a) allopurinol, febuxostat (XOi; decreases uric acid production)
b) Probenecid (inhibits uric acid reabsorption)
c) Rasburicase (metabolizes uric acid) [tx TLS]
Ocular, Vascular, and Cardiac manifestations of opioid use? What are these mediated by?
MiOsis, hypOtension, BRADYcardia
histamine release
Compare/contrast the nodes:
a) Osteoarthritis
b) Gouty Arthritis
c) RA
a) H/B Nodes: bony nodules
b) TOPHI: can ulcerate and drain a chalky material (dist. calcinosis cutis)
c) Flesh-colored, nontender
c) “volcano” with central keratotic plug
d) another name for skin tag
c) keratoacanthoma
d) acrochordon
Initial treatment strats for RA.
What do you give if unresponsive for 6 months?
Classify this category of drugs. What do you need to test for prior to starting?
non-biologic DMARD (methotrexate!) + NSAID/celecoxib/glucocorticoids (relief while awaiting DMARD response)
Add biologic (anti-tnf alpha) or a second non-bio if refractory.
DMARD = non-biologic (methotrexate, hydroxychloroquine, sulfasalazine, leflunomide, azathioprine) + biologic (etanercept, infliximab, adalimumab, toclizumab, rituximab)
[TEST FOR HEP B/C and TB!]
EM vs SJS vs TEN
targetoid s/p HSV infx vs
bullae/desquamation 2/2 “triggers”
v10% = SJS ^30% = TEN
triggers = sulfonamides, carbamazepine, lamotrigine, phenytoin, sulfasalazine, NSAIDs, allopurinol, mycoplasma
What is senile purpura? mech
Suppurative hidradenitis
““acute” SH-looking things
Explain why purulent vesicles can form in allergic contact dermatitis?
BENIGN ecchymoses in elderly patients (nasty hands) due to loss of perivascular CT
Chronic follicular occlusive disease; painful inflammatory nodules and draining sinus tracts. ODORUS (“rotten stretchmarks”)
Intertrigo. More erythematous.
Scratching can lead to 2ndary infxn
Tx frostbite?
Warm water rewarming. Only debride later
What are the two types of scaphoid fractures and how to tx each?
a) NON-displaced (fine radiolucent line or nL xray; v2mm displacement and no angulation) : wrist immobilization for 6-10 wks
b) DISPLACED: open reduction, internal fixation
What is osteonecrosis and what causes almost all of these cases? What are 4 synonyms?
gold standard dx?
Osteochondritis dessicans, aseptic necrosis, avascular necrosis, ischemic necrosis
Corticosteroid, alcohol
also SLE and sickle cell
MRI! (commonly hip. ttp + predinosone/SLE etc. )
What is scleroderma crisis? What does it present with (3)?
What GI issue are scleroderma ppl (as well as DM) at risk for?
Pulmonary manifestation of scleroderma?
Sudden RF (urinalysis can be nL)
MAHA (schistocytes!)
Malig HTN
Sm. Intestinal Bacterial Overgrowth (2/2 lack of proper motility); also angiodysplasia
INTERSTITIAL LUNG DZ! (FIBROSIS)
pulmonary arterial HTN
Burr Cells (echinocytes)
HJ bodies
Spur Cells (acanthocytes)
Target Cells
Spiculated/serrated; Liver dz / ESRD
Basophilic remnants; functional asplenia/splenectomy
Irregular projections; Liver dz
Bull’s eye; hemoglobinopathy (thallasemia); obstructive liver dz
ACLS
How are the (2) different forms of persistent tachyarrythmias treated based on the (2) broad category of symptoms?
What to avoid in WPW?
1) Wide or narrow (qrs) complex
2) STABLE - MEDICINE (amiodarone); UNSTABLE-CARDIOVERT
a) narrow-complex (ex. paroxysmal SVT) tx vagal
b) wide-complex (ex. sust. monomorphic VT) tx (2)
in WPW avoid drugs that increase conduction thru the accessory pthwy (BB, CCB, digoxin, adenosine [av block]); instead tx with procainamide or ibutilide
PALPABLE KIDNEYS, hepatomegaly, nephrotic syndrome, LVH, recurrent pulmonary infection.
tx?
Secondary amyloidosis
tx colchicine