Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

79 Cards in this Set

  • Front
  • Back
what cells do FSH, and LH, respectively, stimulate in the testis?
FSH --> sertoli cells; LH --> leydig cells
what cells release testosterone in the testes?
leydig cells
what genetic element initiates sexual differentiation in males?
TDF on Y chromosome
what if there is no TDF?
baby will be female (have ovaries)
in early fetal development, what is necessary for internal male genitalia to form, and where does it come from?
mullerian inhibiting hormone - comes from sertoli cells
what if there is no mullerian inhibiting hormone?
female internal genitalia
what is necessary for external male genitalia?
what is necessary for external female genitalia?
lack of testosterone
what needs to happen for there to be DHT?
conversion of testosterone to DHT by 5-alpha-reductase
where is type 1, and type 2 5-alpha-reductase found?
type 1 - liver and skin; type 2 - urogenital tract and liver
what can deficiencies of type 2 5-alpha-reductase result in?
ambiguous gender idnetification at birth, usually female
what can be done about this?
dramatic reversal at puberty, as testosterone is converted by type 1 5-alpha-reductase, resulting in male gender assignment
hyperplasia/carcinoma of the prostate is treated by inhibiting what androgen(s)?
acne is treated by inhibiting what androgen(s)?
male pattern baldness is treated by inhibiting what androgen(s)?
precocious puberty in boys is treated by inhibiting what androgen(s)?
sex drive in sex offenders is treated by inhibiting what androgen(s)?
what is the Kd for the androgen receptor with DHT compared to T?
DHT 1000> T
what feature of AR gene increases sensitivity to androgens?
lesser amount of glutamine repeats (12-32 normal - if over 40, spinal/bulbar muscular atrophy)
what are the indications for giving testosterone (2) and how is it given?
given as skin cream for: 1) congenital or acquired hypogonadalism in men; 2) breast carcinoma in posmenopausal women
what drug must we know that is used for prostate cancer, precocious puberty, uterine leiomyoma, and endometriosis?
what type of drug is it, and what is its MOA?
GnRH agonist - continued exposure disrupts pulsatility of gonadotrophs, inhibiting FSH and LH secretion
what are its adverse effects (4)?
1) short term rise in serum testosterone; 2) decreased libido; 3) negative effects on mood; 4) osteoporosis
what is a non-FDA approved use for ketoconazole?
prostate cancer
what are its adverse effects (4)?
1) short term rise in serum testosterone; 2) decreased libido; 3) negative effects on mood; 4) osteoporosis - same as leuprolide
what drug is used for metastatic prostate cancer and BPH, and what type of drug is it?
flutamide - nonsteroidal anti-androgen - directly blocks androgen receptor
what are its adverse effects (4)?
1) short term rise in serum testosterone; 2) decreased libido; 3) negative effects on mood; 4) osteoporosis - same as leuprolide
what is flutamide most effective in combination with?
what drug is used for prostate cancer, BPH, and alopecia, and what is its class/MOA?
finasteride - 4-aza analog of T that acts as competitive, specific inhibitor of type II 5-alpha-reductase
what does finasteride block, and not block?
blocks actions of DHT but not T in prostate, seminal vesicles, hair follicles, epididymis
what are the adverse effects of finasteride like?
generally better tolerated than flutamide
what is a non-FDA approved use of testosterone?
to improve libido in both women and men
what decreases local pH in gouty attacks, and what leads to that?
increased lactate production, from inflammatory response
what exacerbates inflammatory response?
increased synovial phagocytosis of crystallized uric acid
why is there more crystallized uric acid?
drop in local pH (all of these create a vicious cycle)
what are treatment goals of gout (3)?
1) relieving gouty attacks; 2) preventing recurring gouty episodes; 3) preventing urate lythiasis
what drug is a diagnostic indicator of gout, and what type of drug is it?
colchicine - a plant alkaloid - diagnostic because it is only effective against gout - dramatically relieves pain and inflammation of gouty arthritis in 12-24 hours
what is the MOA of colchicine?
inhibits tubulin polymerization, leading to inhibition of leukocyte and phagocyte migration and phagocytosis of crystals in joints
why are NSAIDS often used?
decreased side effects
what is colchicine indicated for?
prophylaxis of recurrent episodes of gouty arthritis
what are adverse effects of colchicine?
diarrhea, N/V, abdominal pain, hair loss, bone marrow suppression, peripheral neuritis, myopathy
what is the normal dosing of colchicine for an acute attack, and what should be avoided?
2mg is given as a single dose IV - not to exceed 4 mg, not to be repeated within 7 days
how much is lethal?
8mg/24 hours
what NSAID is used in gout, and how does it help besides being anti-inflammatory?
indomethacin - inhibits urate crystal phagocytosis
what NSAID is better than others at lowering serum uric acid, and what is the problem?
oxaprozin may be better at this, but its use, like other uricosuric agents, is not recommendeed in patients with uric acid stones
what drug is effective for treatment of primary uricemia caused by antineoplastic therapy, and what is its MOA?
allopurinol - competitive inhibitor of xanthine oxidase - inhibits urate synthesis
what is the main use of allopurinol?
effective for treatment of primary hyperuricemia and that secondary to antineoplastic therapy
what are other indications for allopurinol?
reserved for more severe forms of gout - high urinary urate (600-700), gouty nephropathy, recurrent renal sotnes, elevated serum urate
allopurinol is used in situations when what two drugs are contraindiicated?
sulfinpyrazone, probenecid
why is probenecid contraindicated with allopurinol?
allopurinol increases the half life of probenecid, which itself increases clearance of oxypurinol (an active allopurinol metabolite)
what problem may allopurinol induce in the short term, and how?
gouty arthritis - as serum levels of uric acid fall, crystal previously phagocytosed by synovocytes will be released, initiating gouty attack
what may be required during initial treatment?
coadministration of colchicine, sulfinpyrazone, or probenecid
what are other adverse effects of allopurinol (5)?
1) depression of bone marrow; 2) hepatic toxicity; 3) interstitial nephritis; 4) allergic skin reactions; 5) cataracts
what is the name of agents used to increase the rate of uric acid excretion, and what two must we know?
uricosuric agents - used to increase rate of uric acid secretion - 1) probenecid; 2) sulfapyrazone
what treatment course does probenecid have?
should begin with goal of lifelong treatment (like allopurinol)
what is probenecid mainly used for?
to decrease the bodies pool of urate in patients with increasingly frequent gouty attacks
what is probenecid not effective in doing?
relieving acute gouty attack (may exacerbate)
what is the MOA of probenecid and where does it act?
potent inhibitor of uric acid reabsorption at renal tubules
what drugs inhibit the actions of probenecid and sylfinpyrazone?
what happens when probenecid and sulfinpyrazone are used together?
their effects are additive
what AE is associated with probenecid, and who should it not be used in?
uric acid stones - avoid in patients with nephrolithiasis, and with caution in patients with high serum urate levels
what is the primary complication of probenecid?
precipitation of acute gouty attack
what is the toxicity of sulfinpyrazone?
gastric distress/peptic ulcers
what drug interaction was mentioned for sulfinpyrazone?
can increase hepatic toxicity of acetaminophen
what are the primary agents for managing acute gouty attacks?
NSAIDs, colchicine, and other anti-inflammatory agents (allopurinol and uricosuric agents do not alter course, and actually increase gouty attacks)
what drug is used to reduce frequency of gouty attack during early chronic treatment?
what NSAIDS are DOC for acute gouty attacks (2)?
indomethacin, naproxen
how do salicylates affect gout?
they elevate serum urate concentration and antagonize probenecid and sulfinpyrazone
what things minimize intrarenal deposition of uric acid (2), why, and when is this essential?
since pKa is 5.6, and solubility of undissociated form is low, maintaining plasma volume, alkaline urine minimizes its intrarenal deposition - this is important in first few weeks of therapy
what are the adverse effects of allopurinol in the chart (4)?
1) skin rash; 2) N/V; 3) kidney abnormalities; 4) diarrhea
what are the main adverse effects of colchicine (2)?
1) GI distress; 2) bone marrow depression
what are the side effects/toxicity of probenecid?
1) increase risk of stones; 2) may cause attacks during early treatment
what are often the first line drugs in gout, and what are they used in conjunction with?
NSAIDS - used in conjunction with uricosurics