Final Flashcards
What are the thyroid agents used to treat hypothyroidism
Levothyroxine (T4), liothyronine (T3), liotrix (4:1 ratio of T4:T3), thyroid desiccated
What are the anti thyroid agents used to treat hyperthyroidism
Radioactive iodine sodium, methimazole, potassium iodide, propylthiouracil
What is organic inaction
Iodine iodinated tyrosine residues within thyroglobulin molecule to make MIT and DIT
What is the oral bioavailability of T4 vs T3
T4: 80% - half life 7 days
T3: 95% - half life 1 day
What agents inhibit conversion of T4 to T3
Radiocontrast agents: iopanoic acid and ipodate
Amiodarone, beta blockers, corticosteroids
*used for thyroid storm
What drugs decrease T4 absorption
Antacids, ferrous sulfate, cholestyramine, colstipol, ciproloxacin, PPIs, coffee
What increases the metabolism of T3 and T4
CYPinducers: rifampin, rifabutin, phenobarbital, carbamezepine, phenytoin, imatinib, PPIs
What are the features of levothyroxine
Long half life, easy to measure serum level
Why is T3 not used for hypothyroid treatment
Short half life
What are thioamides
Methimazole and PTU
What are the contraindications to PTU and methimazole
Pregnancy; but if used, PTU is choice for first trimester and methimazole in 2nd and 3rd
What is the MOA of PTU and methimazole
Inhibits thyroidal peroxidase catalyze reactions and blocks iodide organification and coupling of MIT and DIT to form T3 and T4; PTU blocks peripheral conversion of T4 to T3
What are the adverse effects of PTU and methimazole
Macupapular pruritic rash, lupus like reaction, hepatitis (more common with PTU), cholestatic jaundice (more with methimazole), *agranulocytosis - reverse with CSF
What are the anion inhibitors used for hyperthyroidism
Perchlorate, pertechnetate, and thiocyanate
*block thyroid gland ups take of iodide by inhibition transport mechanism; can be overcome with large doses of iodides
What is the MOA of iodides used for hyperthyroidism
Inhibit organification and hormone release; used for thyroid storm, preoperative reduction of hyperplastic thyroid, and block thyroid uptake in emergency exposure to radioactive iodine; adverse rxn: acneiform rash, swollen salivary gland, mucinous membrane ulceration, conjunctivitis, metallic taste *avoid during pregnancy
What is the most common beta blocker used to treat hyperthyroid symptoms.
Propranolol
Is methimazole or PTU preferred overall as a treatment for hyperthyroidism
Methimazole
Who is radioactive iodine treatment the treatment of choice for hyperthyroidism
Patients over 21
What is the protocol for treatment of thyroid storm
Beta blockers, potassium iodide to prevent release of thyroid hormones from gland, PTU or methimazole, IV hydrocortisone to protect against shock and block conversion of T4 to 3, if above inadequate, plasmapharesis of dialysis
What is mecasermin
IGF-1 agonist
What is pegvisomant
GH antagonist
What are the FSH analogs
Follitropin alpha and beta, urofollitropin
What is the LH analog
Lutropin alpha
What are the gonadotropin releasing hormone antagonists
Ganirelix, cetrorelix, degarelix, abarelix
What is bromocriptine used for
Parkinson’s, acromegaly, infertility, and galactorrhea
What is cabergoline
Dopamine receptor agonist; use to treat prolactin excess
What are the vasopressin receptor antagonists
Conivaptan and tolvaptan
What hormones use Gs receptors
LH, FSH, TSH, glucagon, PTH, PTHrP, ACTH, GHRH, CRH
What hormones use Gi pathways
Somatostatin
What hormones use a Gq pathway
TRH GnRH
What hormones use a cytokine receptor linked kinase pathway
GH and prolactin (JAK, tyrosine kinases)
What is somatropin
Recombinant human form of GH; CYP450 inducer
What are the effects of GH vs IGF-1 on blood glucose
GH increases it (hyperisulinemia) and IGF-1 will decrease it
What are the adverse effects of GH supplementation
Intracranial HTN, otitis media in patients with Turner syndrome, hypothyroidism, pancreatitis, gynecomastia in kids; in adults: peripheral edema, arthralgia and carpal tunnel; contraindicated in malignancy
How is mecasermin administered
Subcutaneous; adverse effect: hypoglycemia
What are the features of ocreotide
Somatostatin analog; subcutaneous
What is lanreotide used to treat
Acromegaly
What are the adverse affects of the somatostatin analogs
Gallstone, sinus bradycardia, vitamin B2 deficiency
What is urofollitropoin
Purified human FSH extracted from urine of postmenopausal women
What are the uses of urofollitropin and follitropin alpha/beta
Ovulation induction, spermatogenesis induction (urofollitropin),
What is lutropin alpha used for
Only in combo with follitropin alpha for stimulation of follicular development in infertile women with LH deficiency
What is choriogonadotropin alpha used for
Induce ovulation and pregnancy in anovulatory infertile females (pre treated with follicle stimulating hormones), treatment of hypogonadotropic hypogonadism, spermatogenesis inductions
How are all gonadotropin preparations administered
Subcutaneous or IM injection
What are the adverse effects of gonadotropin preparations
Ovarian hyperstimulation syndrome (enlargement, ascites, hydrothorax), multiple pregnancies which increases risk for gestational diabetes, preterm labor and preeclampsia
What does continuous administration of leuporlide produce
During first 7-10 days: agonist
After 7-10 days: antagonist *used more for suppression than agonist
When is leuprolide used for stimulation vs suppression of gonadotropin production
- stimulation: infertility, LH responsiveness
- suppression: ovarian hyperstimulation, endometriosis, uterine leiomyomata, prostate cancer, central precocious puberty
What are the adverse effects of leuprolide
Hot flashes, sweats, HA, depression, diminished libido, vaginal dryness, breast atrophy, decreased bone density
What are GnRH antagonists used for
Abarelix and degarelix are used to treat Advanced prostate cancer; ganirelix and cetrorelix used for ovarian hyperstimulation
How is bromocriptine or cabergoline administere
Oral or vaginal suppository; cabergoline has longer half life
Can dopamine agonists bee used to suppress postpartum lactation
No b/c increases incidence of stroke or coronary thrombosis
What is oxytocin administered for
IV: initiation of labor
IM: control of postpartum bleeding
What is the difference between desmopressin and vasopressin
Desmopressin has minimal V1 activity
How are vasopressin and desmopressin administered
Vaso: IV or IM
Desmo: IV, SQ, intranasally, or PO; longer half life
Besides DI, what else is desmopressin used to treat
Coagulopathy in hemophilia A and von willebrand dz
What is the MOA of conivaptan and tolvaptan
Tolvaptan antagonizes V2; conivaptan antagonizes V1 and V2
How does nuclear binding o f thyroid hormone initiation gene transcription
Dissociates NCoR/SMRT and HDAC and recruits co-activators and HATS
What are the features of propranolol
Non selective beta blocker; also inhibits conversion of T4 to T3
When is methimazole given
Before thyroid surgery; inhibits thyroperoxidase
When is potassium iodide used
To treat hyperthyroidism and prepare thyroid gland for removal - blocks iodine uptake; also used to treat deficiency, protects thyroid from radiation exposure, doesn’t affect heart
What are the indications for use of PTU
Graves, toxic multinodular goiter if intolerant of methimazole or suregery isn’t good option, in prep for thyroidectomy, used in radioactive iodine therapy intolerant of methimazole
Does PTU interfere with thyroid hormones given orally or by injection
No
Who is radioactive iodine therapy or thyroid cancer contraindicated in
Pregnant wom
What is the MOA of perchlorate
Competitive inhibitor of iodide uptake; blocks sodium iodide symporter, controls amiodarone induced thyroid dysfunction*
How does methimazole decrease the serum concentration of T3
Prevents addition of iodine to tyrosine residues
What are the rapid acting insulin’s
Aspart, lispro, glulisine
What are the short acting insulin’s
Regular insulin
What is the intermediate acting insulin
NPH (neutral protamine hagerdorn)
What are the long acting insulin’s
Detemir, glargine
What is the amylin analog
Pramlintide
What are the GLP-1 agonists
Exenatide and lliraglutide
What are the dipeptidyl-peptidase 4 (DPP-4) inhibitors
Sitagliptin, linagliptin, saxagliptin, alogliptin
What are the potassium ATP channel blocker drugs used for diabetes
Sulfonylureas and meglitinides
What are the 2 generations of sulfonylureas
First gen: chlorpropamide, tolbutamide, tolazamide
Second gen: glipizide, glyburide, glimepiride
What are the meglitinides
Nateglinide, repaglinide
What drug falls in the biguanide category
Metformin
What are the thiazolidinediones
Pioglitazone and rosiglitazone
What are the SGLT2 inhibitors
Canagliflozin, dapagliflozin, empagliflozin
What are the inhibitors of alpha-glycosidases
Acarbose and miglitol
What classes of drugs fall under the insulin secretagogues category
Sulfonylureas, meglitinides, GLP-1 agonist, DPP-4 antagonist
What is the clincial use of rapid acting insulin’s
Postprandial hyperglycemia (take before meal as SQ)
What is the clinical use of short acting insulin
Basal insulin maintenance, overnight coverage, postprandial (if inject 45 min before meal), IV in urgent situations
What are the clinical use of intermediate acting insulin
Basal insulin maintenance overnight coverage, use is declining
What are the features of detemir and glargine (long acting)
Detemir: Lys 29 in B chain is a lipid and rapidly absorbed but bound to albumin
Glargine: AA sub in A and B chains enhance crystal stability, change pKa of insulin - soluble at low pH (4) but precipitates at 7; peakless
Clinical use: basal mainteance (1-2 SQ injections daily)
Besides diabetes what is insulin used as a treatment for
Hyperkalemia (in combo with glucose and furosemide)
What are the adverse effects of insulin
Hypoglycemia, lipodistrophy (hypertrophy of SQ fat at injection site, prevent by changing injection site or IM injections), resistance, hypersensitivity, hypokalemia
What are some causes of hypoglycemia while on insulin
Missing a meal, exercise, overdose
How do you treat insulin induced hypoglycemia
Glucose, diazoxide (KATP opener), glucagon
What is the MOA of amylin
Inhibits glucagon secretion, enhances insulin sensitivity, decreases gastric emptying(slows rate of glucose absorption), causes satiety
What is the onset of amylin analog (pramlintide)
Rapid; peaks in 20 min, last 3 hrs, used for T1DM, T2DM who take mealtime insulin, inject SQ before meals in adjunct to insulin
What are the adverse effects of amylin
Hypoglycemia (reduce insulin dose), drug interactions with anticholingergics (enhances their effects)
What regulates insulin secretion
- GPCR Gs ligand: beta2 agonists and GLP-1 agonists
- GPCR Gi ligands: somatostatin and alpha 2 agonists - decrease secretion
What are the features of GLP-1
Synthesized by L cells;; promotes beta cell proliferation, insulin gene expression, glucose dependent insulin secretion; inhibits glucagon secretion, cause satiety and inhibits gastric emptying; *very short half life so not used as a drug
Does exenatide or liraglutide have a longer half life
Liraglutide
When is GLP-1 receptor agonist treatment indicated
T2DM patients who are not controlled by metormin/sulfonylureas/thiazolidinediones; *adminitered parenterally
What are the adverse effects of GLP-1 agonists
Lower risk of hypoglycemia (stimulates insulin release only during hyperglycemia), linked to cases of acute pancreatitis and pancreatic cancer
What is DPP-4
Serine protease
What are the clinical uses of DPP-4 inhibitors
Adjunct therapy to diet and exercise in patients with T2DM, used as monotherapy and in combo with metforin/sulfonylureas and TZDs; taken orally
What are the adverse effects of DPP-4 inhibitors
Upper respiratory tract infections, acute pancreatitis, hypoglycemia if combined with other secretagogues)
What channel do sulfonylurea drugs block
SUR receptor on Kir6. Inwardly rectifying potassium channels
What are the adverse effects of sulfonylureas
Hypoglycemia, weight gain, secondary failure, hypersensitivity - cross reaction with other sulfamides - sulfonamide abx, carbonic anhydrase inhibitors, diuretics
What drug interactions do sulfonylureas have
- enhance hypoglycemia effect:: displace binding with albumin - sulfonamides, clofibrate, salicylates; enhancing effect on KATP: ethanol; inhibiting CYP enzymes: azole antifungal, gemfibrozil, cimetidine
- decreases glucose lowering effect:: inhibiting insulin secretion: Beta blockers, CCBs; KATP channel: diazoxide, inducing CYP: phenytoin, griseofulvin, rifampin
What is the clinical use of meglitinides
Control of postprandial hyperglycemia in patients with T2DM, taken orally, can be alone or in combo
What is the MOA of metformin
Activation of AMP-dependent protein kinase which decreases GNG in the liver, increases glucose uptake, glycogen formation, and FA oxidation, lowers glucose levels, increases insulin activity; inhibitors mitochondrial OxPhos
What is the first line treatment for T2DM
Metformin; does not cause hypoglycemia or weight gain, taken orally, decreases risk of macro and microvascular complications
What are the pharmacokinetics of metformin
Not bound to plasma proteins, not metabolized, excreted unchanged in kidneys
What are the adverse effects of metformin
Decreased absorption of B12, lactic acidosis (esp under conditions of hypoxia, renal and hepatic insufficiency ), contraindiated in CHF, COPD, renal failure, chronic alcoholism and cirrhosis
What is the MOA of thiazolidinediones
Ligands of peroxisome proliferator-activated receptor gamma (PPARy) - nuclear receptor expressed in fat, muscle, liver and endothelium; increases GLUT4 in skeletal muscle and adipocytes, increases IRS1/22 PI3K, decrease PEPCK and NFkB, AP-1
What are the pharmacokinetics of thiazolidinediones
Taken orally once daily; onset is delayed (because depends on gene expression) - full effect 3 months; effects persist for months after discontinuing; metabolized by liver; can administer to patient with renal failure
What are the uses of thiazolidinediones
T2DM; can slay progression from prediabtes to diabetes; no hypoglycemia when used alone
What are the adverse effects of thiazolidinedione
Weight gain (doubled if given with insulin), edema (also doubled if given with insulin) - increases vascular permeability and expression of ENaC which allows incrased sodium and water reabsorption in collecting duct; exacerbation of HF - contraindicated if class III or IV;; increased triglycerides and LDL(rosiglitazone); osteoporosis - suppresses differentiation of MSCs to osteoblasts by inhibiting Runx2
What are the effects of SGLT2 inhibitors
Osmotic diuresis, induced weight loss, reduced BP, reduced plasma levels of uric acid, does not cause hypoglycemia
What are the clincial uses of SGLT2 inhibitors
Orally before 1st meal once a day in conjunction with diet and exercise therapy
What are the adverse effects of SGLT inhibitors
Hypotension, UTI, renal function impairment, hyperkalemia (esp if taking ACEIs, ARBs and K sparing diuretics)
How do alpha glycosidase inhibitors work
Prevent absorption of starch from gut by inhibiting breakdown of disaccharides into absorbable monosaccharides; lowers post prandial hyperglycemia and creates insulin sparing effect
What are the adverse effects of alpha glycosidase inhibitors
Flatulance, malabsorption, diarrhea bloating; decreases absorption of digoxin (acarbose) and propranolol and ranitidine ( miglitol)
How do synthetic steroids travel in the blood vs natural
Synthetic bind weakly to albumin so circulate as free steroids; also have a longer half life
Does prednisone or cortisol have more salt wasting effects
Cortisol
What are glucocorticoids metabolized by
CYP3A4
What does prednisone have to be converted to to have any effect
Prednisolone
What are the potent synthetic glucocorticoids
Prednisone, methylprednisolone, triamcinolone, dexamethasone, bethamethasone
What is needed to convert inert steroids into active steroids
11 beta HSD1 (1 ketoreductase); converts cortisone -> cortisol, 11 dehydrocorticosterone -> corticosterone, prednisone -> prednisolone
What do steroids displace when they bind to their receptor
Hsp90
What are the corticosteroid agonists
- glucocorticoids: prednisone
- mineralocorticoids: fludrocortisone
What are the corticosteroid antagonists
- receptor antagonists: glucocorticoid (mifepristone) and mineralocorticoids (spironolactone)
- synthesis inhibitor: ketoconazole
What are inhibitors of 11 bet HSD2
Glycyrrhizin (licorice) and carbenoxolone (used or esophageal ulcers); increases activity of cortisol receptor - increases salt and water retention and potassium loss
What are the metabolic effects of glucocorticoids
- carb: increase GNG, increase glycogen synthesis, decreased glucose uptake
- lipid: increased lipolysis, lipogenesis, increased fat deposition
- protein: decreased AA uptake, decreased protein synthesis, development of myopathy and m wasting
What are the effects of glucocorticoids on the immune system
Decreased production of prostaglandins and leukotrienes, increased apoptosis of immune cells, decreased production of cytokines, decreased migration of neutrophils and macrophages, decreased expression of cell adhesion molecules
What is used to treat addisons
Glucocorticoids (hydrocortisone) and mineralocorticoids (fludrocortisone); also used to treat congenital adrenal hyperplasia
What are the short acting glucocorticoids (<12 hrs)
Hydrocortisone, cortisone, prednisone, prednisolone, methylprednisolone
What are the intermediate acting corticoidsteroids
Triamcinolone
What are the long acting (>36 hrs) corticosteroids
Betamethasone and dexamethasone
What is prednisolone used to treat
Organ transplant, hematologic cancers, inflammatory conditions; toxicities: adrenal suppression, growth inhibition, muscle wasting, osteoporosis, salt rentation, glucose intolerance, behavior changes
What are the most potent anti inflammatory corticosteroids
Dexamethasone and betamethasone; fluprednisolone is most potent intermediate acting
Which corticosteroids are only oral
Cortisone, prednisone, fluprednisolone, fludrocortisone
What is the most potent mineralocorticoids
Fludrocortisone *also most potent salt retention agent
Which glucocorticoid is the most potent salt retaining agent
Cortisone; fluprednisolone is the least
What corticosteroids are available topically
Hydrocortisone, triamcinolone, beta and dexamethasone
What is important about adrenalcorticoid drug dosing
- use lowest dose for shortest duration; use intermediate or short acting vs long acting
- Reduce systemic distribution: ciclesonide is a prodrug activated by esterases in bronchial epithelium - systemically absorbed
- give single daily doses in AM
- alternate short course pulse therapy
- dose tapering
What patient populations is glucocorticoid administration problematic
Immunocompromised, diabetics, patients with infections, peptic ulcers, HTN, CHF, angina, psychiatric conditions, osteoporosis (post menopausal), children
What are the toxicities assoc with mifepristone
Vaginal bleeding, ab pain, GI upset, HA; antagonist of glucocorticoid and progesterone receptors
What is fludrocortisone
Strong agonist at mineralocorticoid receptors; used to treat addisons; long duration of action
What is spironolactone used to treat
Aldosteronism, hypokalemia from diuretics, post MI; slow onset and offset; toxicities: hyperkalemia, gynecomastia
What are the toxicities of ketaconazole
Hepatic dysfunction; CYP interactions
What are the GnRH agonists
Leuprolide, gonadorelin, goserelin, buserelin, histrelin, nafarelin, triptorelin
Which vasopressin receptor agonist has limited V1 activity
Desmopressin
What signaling pathways does insulin act through
MAPK, PI3K
What’s the difference between leuprolide and ganirelix
Ganirelix immediately reduces gonadotropin secretion - leuprolide does so after about a week
What is leuprolide used to teat
Prostate and breast cancer, endometriosis, uterine fibroids, early puberty
What is ganirelix used to treat
Prevent premature ovulation in those undergoing fertility treatment involving ovarian hyperstimulation - prevents ovulation until triggered by injected HCG
What drugs are used for the induction of labor/control postpartum bleeding
Misoprostol, dinoprostone, carboprost, oxytocin, ergot alkaloids
What drugs are used to delay labor (tocolytics)
Terbutaline, indomethacin, nifedipine, MgSO4, atosiban
What drug is used to maintain a patent ductus arteriosus
Alprostadil
What drug is used to close patent ductus arteriosus
Indomethacin and ibuprofen
What are the anti-HTN used in pregnancy
Alpha-methyldopa, labetalol, hydralazine, sodium nitroprusside
What are the FDA teratogenic risk categories
A: controlled studies fail to demonstrate risk to fetus
B: animal studies have no demonstrated fetal risk, but no control studies in humans
C: studies in animals revealed adverse effects; given only if potential benefit justifies risk to fetus
D:evidence of human fetal risk but benefits might be acceptable
X: contraindicated in pregnancy
Describe amnion prostaglandin production
Synthesized because increase in phospholipase A2 and prostaglandin H synthase; during pregnancy, effects on maternal tissue is limited by inactivating enzyme (PGDH) in the chorion; during labor, PGDH levels decease
What stimulates cortisol production in the fetus
Trophoblasts secrete CRH
What factors cause uterine myocyte relaxation vs contraction
Relaxation: CRH, beta2 agonists, prostaglandin E2
Contraction: oxytocin, thrombin, prostaglandin F2alpha
What happens during cervical ripening
Collagen and glycosaminoglycans are broken down by MMPs
What is misoprostol
Prostaglandin E analog; induces uterine contractions and maintains ductus arteriosus patency; used for termination of pregnancy in combo with mifepristone; off label: cervical ripening, labor induction, incomplete abortion, postpartum hemorrhage; contraindication: previous C section
What are the fetal side effects of misoprostol
Hypoxia due to tachysystole (contractions occurring too rapidly)
What is dinoprostone
Prostaglandin E2 analo; induces uterine contractions and promotes cervical ripening; has a gel form, vaginal (used for cervical ripening at term) and suppositories (terminates pregnancy from 12-10th week); more expensive than misoprostol
What are the side effects of dinoprostone
Fever unresponsive to NSAIDs; hypoxia of fetus
What is carboprost
Prostaglandin Falpha analog; induces uterine contractions - prolong duration of action; used to induce abortion btw 13-20 weeks if failure o another; used or postpartum bleeding; *must be given by IM injection
What are the conraindications of carboprost
Hypersensitivity, acute PID, active cardiac, pulmonary, renal or hepatic dysfunction
What are the maternal adverse effects of carboprost
HTN, pulmonary edema (b/c potent vasoconstrictor), reduces body temp
What are contrainditions to oxytocin
Don’t give if fetus’ lungs are immature or cervix is not ripe; maternal side effects: water intoxication
What are the ergot alkaloids
Ergonovine or ethylergonovine; stimulates adrenergic, dopaminergic and serotonergic receptors; causes prolonged tonic uterine contraction and constricts arterioles and veins; used for postpartum bleeding
How must oxytocin be given
IV
What are the contraindications of ergot alkaloids
HTN, hypersensitivity
What are the adverse effects of ergot alkaloids
St Anthony’s fire: mania, psychosis, vomiting; dr gangrene (fingers, nose, penis, toes)
What is the first choice for limiting post partum bleeding
Oxytocin
What is the management protocol for premature rupture of membranes
- > 34weeks: plan delivery; group B step prophylaxis, single corticosteroid course up to 36 weeks
- 32-34 weeks: group B strep prophylaxis, single corticosteroid course, antimicrobials
- 24-32 weeks: group B strep prophylaxis, single corticosteroid use; no consensus on tocolytics; antimicrobials; magnesium sulfate for neuroprotection
- <24weeks: no group B strep prophylaxis, single corticosteroid course, no consenus on tocolytics
What are the indications for antenatal corticosteroids
Women btw 24 and. 36 weeks with threatened pre term labor, antepartum hemorrhage, preterm rupture of membranes, or conditions requiring C section
What can you give to the mother to cause fetal lung maturation
- betamethasone: 2 doses by IM injection in 24 hr intervals
- dexamethasone: 4 doses by IM injection in 12 hour intervals
- not cortisol b/c placenta metabolizes it to cortisone
What is ritodrine
Beta2 agonist used for tocolysis; maternal effects: severe hallucinations
What is magnesium sulfate used for
Prevent eclamptic seizures; decrease risk for cerebral palsy; used for tocolysis (inhibitors Ach release at uterine NMJ); adverse effects skin flushing, HA, resp depression, in the fetus: m relaxation and CNS depression
What is terbutaline
Beta2 agonist; increases cAMP leading to K+ channel mediated hyperpolarization and dephosphorylation of myosin light chain; contraindications: cardiac arrythmias, poorly controlled thyroid dz or DM; maternal effects: pulm edema, MI, hypotension, SOB, hyperisulinemia, hyperglycemia; fetal side effects: hyperisulinemia, hyperglycemia, neonatal hypoglycemia, hypocalemia, hypotension
What is nifedipine
MOA: blocks calcium influx through voltage gated channels; used as tocolytic; contraindications cardiac dz, maternal hypotension *dont use with magnesium sulfate; no fetal side effects
What is indomethacins use as a tocolytic
Inhibits production of prostaglandin F2alpha; side effects: in fetus: bleeding, necrotizing enterocolitis, decreases in renal function with oligohydramnios, pulm HTN; maternal: gastritis bleeding
What is atosiban
Oxytocin inhibitor; used for tocolysis but not available in US
What are the best choices for delaying labor in the US
Nifedipine or indomethacin
What is alprostadil
PGE1; maintains patent ductus arteriosus; parenteral administration; adverse effects: pyrexia (spike in temp), hypotension, tachycardia, apnea
What are the side effects to given NSAIDS for closure of ductus arteriosus
Oliguria, edema, mild HTN due to decreased kidney function
What are the first and second line drugs for HTN during pregnancy
- first line: used for moderate HTN - oral alpha methyldopa (alpha2 agonist) or oral labetaolol (alpha/beta blocker)
- second line: used for severe HTN - parenteral labetolol, hydralazine (arterial vasodilator) or sodium nitroprusside (arterial and venous vasodilator)
What lab values would you see in someone with 21 beta hydroxylase deficiency
Low sodium, high potassium, low chloride, low bicarbonate, high BUN, high-normal creatinine, low glucose
How do you treat CAH secondary to 21 hydroxylase deficiency
Hydrocortisone, fluids, glucose, get potassium level down
What can addisons occur in conjunction with
As part of poolylandular autoimmune syndrome (type 1 or Type 2 - Schmidt syndrome which is addisons + hypothyroid + T1DM)
- X linked recessive disorder of long chain FA metabolism (adrenoleukodystrophy and adrenomyeloneuropathy) - neuro deterioration which can mimic multiple sclerosis
- infection (TB)
What is familial glucocorticoid deficiency
An inherited adrenal unresponsiveness to ACTH; due to mutation in receptors; isolated cortisol deficiency; increased skin pigmentation; mineralcorticoid always normal; AR
What is triple A (allgrove) syndrome
AR; mutation in AAAS gene that codes for ALADIN; sx: alacrima (no tears), achalasia, adrenal insufficiency, neuro disorder
What are the cholesterol biosynthesis disorders
Smith-lemli-optiz, abetalipoproteinemia
What are the sx of adrenal insufficiency
Fatigue, reduced stamina, weakness, anorexia, weight loss, skin hyperpigmentation, pain, psych sx, HA, salt craving, BP usually low and orthostatic
What lab findings will you see with primary adrenal insufficiency
Moderate neutropenia, low serum Na, high serum K, fasting hypoglycemia, hypercalcemia, low 8am plasma cortisol with increased ACTH, confirmatory test* cosyntropin (synthetic ACTH) stimulation test given IM -> then measure serum cortisol (if doesn’t respond, confirms primary adrenal insufficiency); elevated renin, low serum epi
What confirms the disagnosis of autoimmune Addison dz
Serum abs for 21 hydroxylase
What is required for diagnosis of 21 hydroxylase deficiency
Elevated 17-OH progesterone
How do you treat primary adrenal insufficiency
Glucocorticoid replacement: hydrocortisone, prednisone, prednisolone
Mineralocorticoids: fludrocortisone acetate
What tests can you order to diagnose acute adrenal crisis
ACHT stimulation, cortisol level, blood sugar, serum K or Na, serum pH
What is the treatment for acute adrenal crisis
Hydrocortisone, fluids/glucose, treat hyperkalemia
What is alabaster skin
Decreased skin pigmentation due to secondary adrenal insufficiency
What is McCune-Albright syndrome
Polyostotic fibrous dysplasia, cafe au lait spots, endocrine hyperfunction from multiple organs - can cause ACTH independent cushing
What is the screening test of choice for Cushing
Dexamethasone suppression test; low dose given at night and serum cortisol drawn in morning; if serum cortisol below a certain level, cushing excluded; results used in combo with ACTH drawn before dexamethasone given to determine causes
What is the only time cushing will be suppressed by high doses of dexamethasone
Cushing disease (pituitary adenoma)
What are localizing teaching queens for diagnosis of cushing syndrome
CT of adrenals for ACTH independent Cushing, MRI of pituitary for ACTH dependent, CT of chest and abdomen then PET if nothing found or location off ectopic sources of ACTH
When should you resect adrenal incidentelomas
If >4cm, no hx of malignancy and not obviously a benign lesion, cyst, or hemorrhage
What do ALL patients with an adrenal incidentaloma require
Testing for pheochromocytoma with plasma fractionated free metanephrines
What are the lab findings in primary hyperaldosteronism
Metabolic alkalosis (proton loss = H+ with K+)
What imaging is required in patients with primary hyperaldosteronism
Thin-section CT scan of adrenals to screen for adrenal carcinoma; adrenal v sampling required beforehand
What is the treatment for primary hyperaldosteronism
Removal of adenoma in Conn; if adrenal hyperplasia use spironolactone
What does NE vs epi cause with pheochromocytomas/paragangliomas
NE: HTN, epi: tachyarrhythmias; paragangliomas are more likely to met and secrete NE
What is von hippel lindau dz type 22
AD; 20% develop pheochromocytomas that secrete only NE; hemangiomas of retina, cerebellum brainstem hyperthyroidism, pancreatic cysts, endolymphatic sac tumors, cystadenomas of Adnexa or epididymis, pancreatic neuroendocrine tumors, renal cysts, adenomas, carcinomas
What are the sx of pheochromocytomas
Paroxysmal, increase BP, pounding HA, perspiration, panic, palpitations, pallor after its over
What is the most sensitive test for pheochromocytomas
Fractionated free metaneprhines in plasma; urinary is confirmatory
When should you perform a CT or MRI for a pheochromocytoma
Only if suggestive lab findings
What is the treatment for pheochromocytomas
Resection but patient can develop severe hypotension afterward; abdomen can be seeded during surgery resulting in multifocal recurrent tumors known as pheochromocytomatosis *prior to resection, treat with alpha blockers (phenoxybenzamine), calcium channel blockers (nifedipine), beta blocker ONLY after given alpha blocker
Can histopathology determine if a pheochromocytoma is malignant
No; need lifelong follow up
What is length vs height
Length is supine; height is standing
How do you calculate BMI
Mass in kg/height^ in meters
Mass in lbs x 703/height^2 in inches
For children (2-18) what are the BMI categories
Underweight if <5th percentile for age, normal weight if 5th-85th percentile, overweight if 85-95th percentile, obese if >95th percentile, severe obesity if >120 percent of 95th percentile or BMI>35 (class I) or BMI >140 percent of 95th percentile or BMI >40 (class II)
What is the typical growth for kids
- < 4 years old: >7 cm/year
- 4-6 years old: >6cm/year
- 6 years-puberty: >5 cm/year (2inches)
- peak is 13.5 years in boys and 11.5 years in girls
How do you estimate the adult height of a child
Double the height of child at age of 2
-using mid parental height: for boys - dad’s height + mom’s height + 5/2; for girls - dads height + mom’s height - 5/2; target height is =/- 2 inches of mid parental height
What should you think of if weight falls off first in a child
Nutrition: not enough food, emesis, malabsorption, higher than average caloric requirements
What should you think of if length falls off first in a child
Endocrine: GH deficiency, hypothyroidism, Cushing syndrome
What should you think of if head circumference falls off first
Primary failure of brain to grow or severe craniosynostosis
What is bone age
Provides estimate of child’s skeletal maturation by assessing ossification of epiphyseal centers; helps estimate child’s growth potential; X-ray of let hand and wrist *bone age that is 2 standard deviations below the chronological age is considered delayed
How do you evaluate growth based on age
If less than 36 months, measure length while child is supine; if older than 24 months can use 2-20 yo chart but must be measured standing up (stature)
What is catch up or catch down growth
Occurs in 1st 18 months o life; some kids make up to a 25% downward correction on growth curve - occurs as more table food is introduced; after 24 months of age, usually growth along same curve
What does height below 3% indicate
Can be normal if growth is parallel to curve; abnormal if curve is falling progressively below 3% or if height crosses 2 major percentile lines in a downward direction of 6-12 months
How do you adjust growth curves for premature infants
For first 2 years, plot gestational age rather than chronological
What is the definition of short stature
Height 2 standard deviations below the mean height for age and sex (<3 percentile), height more than 2 standard deviations below the mid-parental height
What are causes of short stature
Familial, constitutional growth delay, idiopathic, hypothyroid, precocious puberty, turner, growth hormone def, Cushing, genetic, nutritional, chronic illness
What do you do for initial work up for concerning short stature
CBC with diff, CMP, thyroid function, IGF and IGFBP-3 levels*, UA and urine pH, ESR, CRP, celiac panel, bone age
What does GH def cause in the neonate vs children
- neonate: midline defects, microphallus, hypoglycemia, GH not relevant for growth during first year of life
- children: decreasing growth velocity, low IGF-1 andIGFBP-3 levels, low GH levels during stimulation using insulin, arginine or clonidine
What findings will you see with Turner syndrome
Short stature, delayed puberty, webbed neck, shield shaped chest, low posterior hairline, *check for karyotype, echo, renal US (horseshoe)
What is the definition of precocious puberty
Before 8 yo in girls, before 9 in boys; full activation of HPG axis
When should you consider precocious puberty as a diagnosis
- in girls: if progressive breast development or crossing major percentile lines upward on the linear growth chart
- in boys: if testicular and penile enlargement, or crossing major percentile lines upward on linear growth chart
What causes premature adrenarche
Increase in DHEA; appearance of pubic hair, axillary hair, odor, mild acne; associated with NORMAL rate of linear growth, no clitoromegaly, penile growth, or testicular enlargement
What is the PE findings of severe hypothyroidism in kids
Increased BMI from growth arrest but increase in weight, delayed relaxation of DTRs
What can case tall stature
- Beckwith-wiedemann syndrome: big head, big when young, normal adult height; overexpresion of IGF-2, do renal US
- GH excess: IGF-1, IGFbp-3
- homocystinuria: error of methionine, similar clinically to marfans
- infant of diabetic mother
- klinefelter: test LH, FSH testosterone
- marfans: diagnosis using Ghent nosology; test: fibrillin-1 gene mutation
What abnormal growth findings suggest a need for referral
- height: growth less than the 3rd percentile or greater than 95th percentile
- growth velocity: decreased or accelerated for age
- genetic potential: projected heigh varies from mid-parental heigh by more than 5 cm
- multiple syndromic or dysmorphic features: abnormal facies, midline defeats, body disproportions
- bone age: advanced or delayed by more than 2 SD
What are some etiologies of DKA
Inadequate insulin, infection (pneumonia, UTI, gastroenenteritis, sepsis), infarction, surgery, drugs (cocaine)
What are the initial sx of DKA
Anorexia, n/v, polyuria, thirst
What are signs of DKA
Kussmaul respiration’s, dry mucous membranes, poor skin turgor, tachycardia, hypotension, fever, ab tenderness
What is the effect of acidosis on potassium
Will shift out of the cells resulting in hyperkalemia
What will the sodium lab value be in someone with DKA
Measured (not corrected) sodium will be low secondary to hyperglycemia; for every 100 mg/dL that glucose is over 100 mg/dL, there will be a 1.6 meq reduction in sodium
What will the potassium lab values be in someone with DKA
Serum may be normal or high but actually have total body deficit*
What other lab values will you see in someone with DKA
Hypertriglyceridemia, hyperlipoproteinemia, hyperamylasemia (salivary; can suggest acute pancreatitis), leukocytosis
What is the rule for fluid replacement in DKA
1-2-3 rule; 2-3 liters NS over 1-3 hrs, then .5 NS at 150 ml/hr, when glucose reaches 250 mg/dL switch to D51/2NS at 100-200 ml/hr
What is the initial insulin administration for DKA
Regular insulin - 10-20 units IV* or IM, then 5-10 units/hr continuous IV, increase if no response in 1-2 hrs
What evaluations would you do for underlying causes of DKA
Culture, EKG, CXR, drug screen, additional hx
What is the initial monitoring you should do for someone in DKA
BSG at least hourly, electrolytes q2-4 hrs +/- ABGs, vital signs q1h, mental status and I/O q1h
When should you consider potassium replacement for DKA
If serum <5.5; when supplementing, keep in mind, renal fxn, baseline EKG, urinary output (measure hourly)
What is the glucose goal when treating DKA
150-250
When should you start intermediate or long acting insulin in someone recovering from DKA
When patient is able to eat (mental status improved, no n/v, no ab pain), anion gap normalized, allow overlap timing of IV w/ SQ insulin (30-60 min)
What factors can precipitate non ketotic hyperosmolar syndrome
Sepsis, MI, glucocorticoids, phenytoin, thiazides, impaired access to water
What are the sx of NKHS
Polyuria, thirst, altered mental state, but NO N/V AB PAIN OR KUSSMAUL
What are the lab results of someone with NKHS
Lactic acidosis with mild anion gap, moderate ketonuria from starvation, corrected serum sodium usually increased
What is the fluid deficit in NKHS
8-10 L (more than DKA)
What are the fluid replacement guidelines for NKHS
2-3 liters NS over first 1-3 hours; then .5 NS over 24-48 hrs, when glucose reaches 250, switch to D51/2NS at 100-200 ml/hrs
What are the insulin administration guidelines for NKHS
Regular insulin 5-10 units IV bonus, 3-7 units continuous infusion, transition when eating as with DKA
What is a HbA1C of 7 indicative of in terms of glucose
140; 6 is 110, 8 is 180
What does diabetic gastropathy lead to
Delayed gastric emptying, insulin-glucose mismatch, hyperglycemia
What is the screening for proteinuria
Spot random urine sample; might need to test for microalbuminuria if <300; use microalbuminuria:Cr ratio
When is a 24 hr urine collection used
To quantify large amounts of protein; used to measure protein and Cr clearance; Need to obtain serum Cr at same time to determine clearance
How can diabetes lead to immune compromise
Glucose >150 interferes with neutrophil function, general debilitation, multiple comorbidities
What is neuropathic Arthropathy
Malformations of the foot caused by diabetes
What is important for diabetic foot care
Daily inspection, dont walk barefoot, moisturize but not between or under toes, prescription shoes, podiatry visits
What monitoring should be done on diabetes patients
- quarterly: Hgb A1C, review self glucose monitoring (SGM) log, foot inspection
- annual: dilated eye exam, urine protein screening, monofilament testing
If calcium and phosphorus move in the same direction, what issue do you have
Vit D
If you have high calcium but low PTH, what is your working diagnosis
Malignancy, granulomatous dz, drugs, mets, MM, lymphoma, vit D intoxication
What sx would you expect with acute vs chronic hypercalcmia
Acute: polyuria, dehydration, renal impairment
Chronic: stones, bone weakness, psychiatric issues
How do you treat chronic hypercalcemia
Loop diuretics
What are the risks of treating hypercalcemia with loop diuretics
Stones; fluid shifting and volume depletion
What is the corrected calcium equation
Measured Ca + .08(4-serum albumin)
How do you treat hypocalcemia
Calcium and vitamin D; how much depends on how low Ca and sx; mild hypo: 8-8.4, moderate 7.5-8, severe <7.5
What is the effect of immobilization on calcium levels
Increased osteoclasts activity which leads to bone resorption and PTH suppression b/c of high calcium; leads to calciuria
What DEXA is used for screening vs diagnosis
Screening: peripheral
Diagnosis: central - lower spine and hip
What are the classifications for DEXA scan
Normal T score >-1
Osteopenia -1 - -2.5
Osteoporosis: <2.5
What should you give to replace calcium in someone with osteoporosis
1000-3000 mg/day (calcium carbonate - but can get constipated so don’t talk regularly); calcium citrate if low acid in stomach (H2 blockers, PPI, gastric)
What sexual sx can hyperthyroidism have
Oligomenorrhea, loss of libido, gynecomastia
What is needed to diagnose Graves’ disease
ONLY clinical history and physical exam; other tests will confirm but that’s all you need to diagnose
What scan is used to visualize graves
Radioactive iodine;; can use technetium but only iodine determines if uptake is increased
What do you give to someone with hyperthyroidism who has asthma and cannot tolerate beta blockers
Calcium channel blockers
How long to methimazole and PTU take to start working
2-8 weeks *do not use methimazole during pregnancy
If you find a thyroid nodule what tests would you do next if the TSH was low vs normal
If low, do a thyroid scan
If normal, do FNA
What characteristic makes a benign thyroid nodule a more likely diagnosis
Tenderness, family hx of benign nodules, hashimotos, mobile nodule, concomitant diagnosis of hyper or hypothyroidism
What characteristics are more likely to predict a malignant thyroid nodule
Very young, very old, men, history of neck irradiation, firm, fixed nodes, LAD
Most thyroid nodules are _____
Cold
What is the approach to patient with a thyroid nodule
- low TSH -> thyroid scan -> if hot, ablate, resent or rx medically; if cold -> FNA
- if normal TSH -> FNA -> cytopathology -> if benign, monitor by US; if suspicious or malignant, surgery
What is Queen Anne sign
Loss of lateral aspect of eyebrows - seen in hypothyroidism
What are some things you should keep in mind when starting thyroid replacement
Start low recheck very 6-12 weeks, dissipated thyroid or T3 not easy to control and better to avoid, T4 prep provides steady levels of T3 and 4
What is method failure rate vs typical failure rate of contraception
Method: inherent rate if method is used correctly
Typical: rate when method is actually used by patient
What is the most effective reversible contraception
Hormonal contraceptive
What are the different types of hormonal contraceptives
OCP
Injectable: depomedroxyprogesterone acetate
Implantable: etonogestrel rod
IUD: levonorgestrel (Mirena, skyla, liletta, Kyleena)
Patches: orthoevra
Rings: nuva ring
What do combination estrogen and progesterone pills do
Suppression of hypothalamic gonadotropin releasing factors; progesterone suppresses LH (prevents ovulation and thickens mucus); estrogen stabilizes endometrium and allows less breakthrough bleeding (improves cycle control)
What is the progestin only OCP
Mini pill; makes cervical mucus think; ovulation still occurs in 40% of users; used mainly in breastfeeding women and women who have contraindication to estrogen; must be taken at same time everyday starting on first day of menses (if >3 hrs late, use back up for 48 hrs)
What are the benefits of OCPs
Menstrual regularity, improves dysmenorrhea, decrease risk of iron deficiency anemia, lower incidence of endometrial and ovarian cancers, benign breast and ovarian dz (cyst)
What are the side effects of OCP
Breakthrough bleeding, amenorrhea, bloating, weight gain, breast tenderness, nausea, fatigue, HA
SERIOUS Side effects: DVT, PE, cholestasis and GB dz, stroke and MI, hepatic tumors
What is the transdermal patch
Estrogen and progesterone; apply one patch weekly for 3 weeks to buttocks, outer arm or lower ab; caution with use in women > 198 lbs; same side effects as OCP BUT greater risk of thrombosis
What is the vaginal ring
Estrogen and progesterone; assoc with greater compliance bc once a month use - insert into vagina for 3 weeks; can be removed up to 3 hrs without affecting efficacy; better tolerated bc does not get metabolized by liver (less breakthrough bleeding)
Who cannot use combination contraceptives
Women over 35 who smoke, personal hx of thrombosis (patients with family hx need to be tested for thrombophilia), hx of coronary a dz, cerebral vascular dz, CHF, migraine with aura, uncontrolled HTN, sever liver dz; diabeetes chronic HTN, and SLE - individualized prescriptions
What is depo
IM injection every 11-13 weeks; maintains contraceptive level of progestin from 14 weeks; give within first 5 days of menses and if not use back up method for 2 weeks; MOA: thickening of mucus, decidualization of endometrium, blocks LH surge and ovulation; efficacy equal to sterilization and is not altered by weight
What are the side effects of depo
- Alterations of bone metabolism assoc with decreased estrogen; reversible after discontinuation; *over 2 years should consider alternative
- irregular bleeding (can improve with estrogen add back but wait till after second dose)
- weight gain
- exacerbation of depression
What are the indications for use of depo
Desire fo contraception, better compliance, breastfeeding, when estrogen is contraindicated, women with seizure disorders, sickle cell anemia (decreased # of crisis), anemia secondary to menorrhagia, endometriosis, decrease risk of endometrial hyperplasia
What are the contraindictions to depo
Known or suspected pregnancy, unevaluated vaginal bleeding, known or suspected malignancy of the breast, active thrombophlebitis or current/past hx of thromboembolic events or cerebral vascular disease
What are LARCS
Long acting reversible contraceptives
How long does nexplanon last
3 years; insert first 5 days of menses (if not, use back up for 7 days); MOA: thickens cervical mucus and inhibits ovulation
What are the side effects of nexplanon
Irregularly irregular vaginal bleeding, HA, vaginitis, weight increase, acne, breast pain
What are the indications for nexplanon
Convenient effective method of contraception, may be used in breastfeeding patients
What are the contraindications of the nexplanon
Known or suspected pregnancy, current or past hx of thrombosis, liver tumors or active liver dz (poorly metabolized), undiagnosed abnormal uterine bleeding, known or suspected breast cancer (*only absolute contraindication)
What are the complications of insertion of nexplanon
Infection, bruising, deep insertion, migration, persistant pain or paresthesias at insertion site
What are the available IUDs
Copper T (paragard) Levonorgestrel releasing (mirena, liletta, skyla, kyleena)
What are the risks with IUDs
Increased risk of infection w/in first 20 days post insertion, increased risk of ectopic pregnancy, if becomes pregnant, offer removal if strings are visible (decreases risk of spontaneous abortion), uterine perforation at time of insertion (requires laparoscopy for removal), risk of malposition necessitating hysteroscopy for removal
What are the contraindications to IUDs
Breast cancer (only the levonorgestrel containing ones), recent puerperal sepsis, recent septic abortion, active cervical infection, Wilson’s dz (only copper one) uterine malformations (uterine septums, fibroids, significantly enlarged)
How long are each of the levonorgsterel IUDs good for
Mirena/kylena: 5 years
Liletta:3 year’s
Skyla: 3 years; used originally for nulliparous women b/c smaller
What are the benefits of the hormonal IUDs
Decrease in menstral blood loss, less dysmenorrhea, protection of endometrial lining from unopposed estrogen, convenient and long term
How long does copper T IUD work
10 years; MOA: copper interferes with sperm transport or fertilization and prevention of implantation
What must you do with a vaginal condom after intercourse
Leave it in there for 6-8 hrs
What must you use in addition to a diaphragm
Spermicide; may be inserted up to 6 hrs before intercourse and left in for 6-8 hrs after (no more than 24 hrs); must be fitted by doctor (fit may change after birth, weight change or surgery); *more likely to get UTIs (puts pressure on urethra and causes urinary stasis and altered vaginal flora from spermicide)
What is the Caya
A one size fits all diaphragm
What is the cervical cap
Smaller version of diaphragm applied to cervix itself; high risk of displacement and TSS; left in place for 6 hrs after (no more than 48)
What is the sponge
Sponge containing spermicide with dimple that fits over cervix; only one size; more effective in nulliparous women; left in place for 6 hrs (no more than 30 hrs)
What is the basal body temp method
Take temp and when notice temp diff avoid sex for 3 days
What is the cervical mucus method
Assess cervical mucus and note changes around ovulation (spinnbarketi) and avoid sex for 4 days
What is the symptothermal method
Combines cervical mucus and basal body temp; awareness of other signs of ovulation (breast tenderness, cramping)
Is there any contraindication to emergency contraception
No
What is plan B
Progestin only (levonorgesterel); 2 pills taken 12 hrs apart; OTC for women >17; must be used within 120 hrs; failure rate worsens after 72 hrs
What is Ella
Ulipristal acetate; indicted for up to 5 days after unprotected intercourse; postpones follicular rupture/inhibit or delay ovulation
How should you counsel patients seeking permanent sterilization
Address all other options (LARCS), reasons for choosing sterilization, discuss risk/benefits, screen for indicator of regret, possibility of failure and increase risk of ectopic, need to use condoms to prevent against STIs
What are the complications of vasectomy
Bleeding, hematomas, acute/chronic pain, local skin infections
Are vasectomies immediately effective
No; complete azoospermia within 10 weeks
How is female sterilization done laparoscopically
Occlude Fallopian tubes by
- electrocautery: fast, increase risk of thermal injury to surrounding tissue, poor reversibility, greater risk of ectopic
- clips: hulka is most reversible but greatest failure rate, filshie has lower failure rate
- bands: falope rings - intermediate reversibility and failure rate, higher incidence of post op pain, increased risk of bleeding
- salpingectomy
What is the most common approach for female sterilization
Mini laparotomy; infra umbilical incision in postpartum period or suprapubic incision as interval
What makes up the pelvic diaphragm l
Levator ani and coccygeus
What is an anterior vaginal prolapse
Cystocele
What is a lower posterior vaginal prolapse
Rectocele
What is a vaginal vault prolapse
When uterovagial canal sags (usually b.c uterus was removed)
What is the treatment for a cystocele
Do nothing, pelvic floor PT, Pessary, surgical correction (anterior colporrhaphy - pubocervical fascia is sutured in the midline and laterally to the Arcus tendinous fascia)
What are the treatments for uterine prolapse
Pessary, hysterectomy, colpocleisis
What is the diff btw Pessary used for cystocele vs uterine prolapse
Cystocele: support - ring or gehrung
Uterine prolapse: gelhorn, donut, cube
What is the Q tip test
Insert a Q tip into urethra and have them valsalva: if moves >30 degrees, stress urinary incontinence
What are the treatments for urethrocele
Topical estrogen, pelvic floor PT, Pessary, surgery (suburethral sling - transvaginal or transobturator tape for vaginal approach; ab approach with Marshall-marchetti-krantz or Burch procedure)
What is the best treatment option for rectocele
Surgery
How do you treat urge incontinence/overactive bladder
- behavior modification: decrease caffeine, limit fluids after 7 pm, bladder training
- antispasmodic: oxybutynin, tolterodine
What hormonal changes occur to the breast
- estrogen: growth of adipose tissue and lactiferous ducts
- progesterone: lobular growth and alveolar budding
What are the risk factors for breast cancer
Hx of atypical hyperplasia, high breast tissue density, first degree relative with breast or ovarian cancer, early menarche <12, late menopause >55, no term pregnancies, never breastfed, recent and Long term use of OCP, postmenopausal obesity, personal hx of endometrial or ovarian cancer, alcohol consumption, height (tall), high SES, ashkenazi Jewish
When will you always bx in the breast
If palpable mass
Who gets a mammogram
> 40 years
When is MRI used for breast imaging
Adjunct to diagnostic mammography, post cancer diagnosis for evaluation and staging, used with implants, women at higher risk for breast cancer (BRCA)
What do you do if bloody fluid shows up on FNA
Send to cytology and need mammogram or US
What happens if a cyst reappears or does not resolve with FNA
Need mammogram/US and bx
When does cyclic breast pain occur
Starts at luteal phase and ends after onset of menses
What meds can cause breast pain
Anti-HTN, anti-depressants
