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142 Cards in this Set

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  • Back
Serotonin synthetic pathway
Tryptophan -> 5-hydroxytryptophan -> 5-HT -> 5-HIAA

1st) Tryptophan hydroxylase
2nd) L-aromatic amino decarboxylase
3rd) MAO-A
bronchospasm, GI cramping and diarrhea, "odd" flushing of the skin, hypotension and increased urinary excretion of 5-HIAA
carcinoid syndrome
carcinoid tx
tx w cyproheptadine (blocks 5-HT1 and 5-HT2 receptors) or the somatostatin analog octreotide which inhibits the release of 5-HT from the tumor.
metoclopramide pharm effects
1. Blocks D2-receptors in CTZ – prevents nausea, also causes S/E’s = EPS, hyperprolactinemia
2. Blocks 5-HT3 receptors in CTZ and at vagal afferents – prevents nausea/emesis
3. Stimulates 5-HT4 receptors on prejunctional cholinergic neurons to amplify the release of ACh, ACh stimulates muscarinic receptors in the GI tract
metoclopramide med use
4. Used to treat esophageal reflux (GERD) and empty the stomach prior to emergency surgery, etc.
antiemetic drug which blocks 5-HT3 receptors in CTZ and at vagal afferent fibers
agonist at 5-HT4 receptors on prejunctional cholinergic neurons - amplifies the release of ACh to increase tone in the LES, used to treat GERD and empty the stomach prior to emergency surgery
agonist at 5-HT1B and 5-HT1D receptors to inhibit the release of inflammatory peptides, used to treat migraine headache and cluster headache
a partial agonist at 5-HT1A receptors; opens K+ channels to hyperpolarize neurons; used to tx anxiety, slow onset of action, no drug dependence
histamine H1-receptors
stimulates afferent pain receptors – pain/itch
contracts bronchial smoth muscle – asthma
contract GI smooth muscle – diarrhea
contracts vascular endothelial cells to increase capillary permeability
dilate arterioles
histamine H2-receptors
dilates arterioles
increases gastric H+ secretion
cromolyn sodium
inhibits mast cell degranulation by preventing inc in intracellular Ca++
inhibits mast cell degranulation and blocks histamine H1-receptors, used
to tx conjunctivitis assn with seasonal allergy
Sedating antihistamines
diphenhydramine, meclizine
Non-sedating antihistamines
terfenadine, fexofenadine, clemastine
Prophylaxis of motion sickness (need to block central muscarinic ACh receptors)
dimenhydrinate, meclizine and scopolamine
DOC for Tx of Meniere’s disease
H2-receptor blockers
cimetidine, famotidine, ranitidine – blocks gastric acid secretion,
also blocks allergic responses in the skin
A patient exposed to poison oak is given (2 drugs):
both diphenhydramine (H1-blocker) and cimetidine (H2-blocker) to prevent itching and pain
A patient w GERD is being treated with cimetidine requires allergen testing by a dermatologist.
Must d/c cimetidine to ensure accuracy of skin tests. Tx GERD w omeprazole during allergy testing.
Patient has insomnia from depression; tx with a TCA but patient still has insomnia
Give an antihistamine (e.g., diphenhydramine) to induce sleep, and patient gets urinary retention from combined atropine-like effect of the drug combination
ipecac induces vomiting by
an action at the CTZ and by an irritant action in the stomach which is not blocked by antihistamines
What drug induces emesis by stimulating D2-receptors in the CTZ?
lactulose (synthetic disaccharide)
slow-acting laxative which is converted to small organic acids in the bowel; these acids exert an osmotic effect to slowly draw water into the feces.
A patient with S/S (confusion/coma) of hepatic portal encephalopathy needs tx
lactulose which acidifies the bowel to trap ammonia as ammonium ion; ammonium lost in feces; plasma [ammonia] falls; coma and confusion disappear
docusate sodium
a stool softener = an anionic surfactant: detergent action allows water to enter feces; softens the stool wo increasing its bulk
tx w loperamide or diphenoxylate which stimulate mu opiate receptors
tx w H2-receptor blockers (cimetidine), antacids, (Al and/or Mg hydroxides), PGE-receptor agonists (misoprostol), proton pump inhibitors (omeprazole) or sucralfate (mixture of AlOH and sucrose whichs forms a viscous gel at acidic pH; gel coats ulcerated tissue)
Ulcers with H. pylori
triple AB tx = clarithromycin, amoxacillin, omeprazole
Which antiulcer drug does not alter stomach pH?
Patient on propranolol takes cimetidine for heartburn and develops severe bradycardia. Why?
Bx cimetidine inhibits CYP450 and thus blocks the metabolism of propranolol
Al OH in GI
Mg OH in GI
Pat being tx w doxycycline; which drug contraindicated?
Al/Mg antacids
Patient needs emergency surgery; need to empty stomach/prevent reflux. Drug = ?
metoclopramide = prokinetic in stomach and bowel and tightens the LES
Cancer chemo patient has n/v and noctural acid reflux Tx w = ?
Patient has post-operative paralytic ileus Tx w = ?
metoclopramide, bethanechol, cisapride
Patient treated with drug for Crohn’s disease or ulcerative colitis develops hepatic damage or bone marrow depression. Drug = ?
sulfasalazine; patient is a slow acetylator.
Sulfasalazine consists of sulfapyridine conjugated to 5-aminosalicyclic acid. Bacterial E's in the large bowel hydrolyze sulfasalazine to free sulfapyridine and free 5-aminosalicyclic acid. The 5-aminosalicyclic acid is an NSAID, and the sulafapyridine, which is metabolized by acetylation,
suppresses the bone marrow.
s/s of laxative abuse w castor oil or bisacodyl =
constipation, hypokalemia, muscle weakness, abnormal architecture inner GI wall
Aspirin effect on platelets
irreversibly inhibiting the COX-1 in platelets via acetylation to prevent the synthesis of thromboxane A2 (TXA2)
Aspirin OD s/s
- n/v, tinnitus
- respiratory alkalosis
– aspirin uncouples oxidative phosphorylation in skeletal muscle
- increases pCO2 -> increases respiration
- metabolic acidosis -> as CO2 production increases, a metabolic acidosis develops
- children skip the alkalosis step and go directly to acidosis w low blood pH and low bicarbonate
Aspirin OD tx
make urine alkaline (acetazolamide or NaHCO3) to enhance the renal clearance of salicylate and infuse bicarbonate to correct acidosis
an inhibitor of PDEase in platelets which potentiates the antiplatelet effect of aspirin and prostacyclin (PGI2)
half-life of aspirin as only 1 h, why does it inhibit platelet inhibition for a longer period?
Aspirin irreversibly acetylates active site of COX-1 in platelets
How does aspirin prevent platelet aggregation when it is not taken in doses large enough to maintain a steady-state plasma concentration?
Aspirin irreversibly acetylates active site of COX-1 in platelets
patient has intermittent episodes of hemiplegia which resolve spontaneously; would like to treat with aspirin, but patient has aspirin “hypersensitivity”; Tx w?
What is the causative compound in aspirin hypersensitivity?
DOC for menstrual cramps
Baby has patent ductus arteriosus
close with indomethacin
Want to keep ductus open prior to surgery: what drug will do this ?
alprostadil = PGE1 analog dilates the ductus arteriosus
pat tx with NSAID develops GI ulceration
what is the MOA?
inhibition of gastric PG synthesis
A patient with nasal polyps who has wheezing with aspirin needs a antipyretic drug
DOC = acetaminophen
Acetaminophen is antipyretic but not
Drug OD; initially blood chemistries normal, but 36 h later see increase in AST and ALT.
what is the drug?
acetaminophen; treat with n-acetylcysteine to replenish glutathione
Adverse effects of NSAID’s
gastric ulceration – results from decreased PG synthesis in stomach; prevent or tx with misoprostol (methyl-PGE1)

interstitial nephritis – hematuria, proteinuria, flank pain

decreased RBF and GFR causing oliguria
Patient on NSAID for tendonitis for 2 weeks develops fever and hematuria: diagnosis?
acute interstitial nephritis
histologic photo of kidney tissue with lots of lymphocytes: diagnosis?
Interstitial nephritis caused by aspirin or another NSAID
Patient with CHF takes ibuprofen; effect on kidney = ?
Constriction of afferent arteriole lowers RBF and GFR to cause salt\water retention; no PG's to partially inhibit the effects of ADH in the collecting duct = water retention.
Patient tx with NSAID for arthritis exhibits dec [Hb] and Hct and has occult blood in his stool. Which drug could be addded to tx to reverse this pathology?
for gout,
binds to tubulin to block the formation of microtubules and thus inhibit phagocytosis of urate crystals by WBC’s; used to tx the pain of acute attacks
for gout,
inhibits xanthine oxidase to block the synthesis of uric acid from purines
Patient with a renal transplant is taking the immunosuppressant drug azathioprine. Patient develops gout. Which gout drug is contraindicated?
allopurinol bx azathioprine is converted to the cytotoxic agent 6-mercaptopurine (6-MP) which kills antigen presenting cells and T- and B-lymphocytes, and 6-MP is inactivated (metabolized) by xanthine oxidase.
Patient with lymphoma tx with chemo. Which drug will prevent dec in renal function?
allopurinol. Chemo kills lymphoma cells which release nucleic acids which are converted to urate; excessive urate in urine crystalizes to occlude the collecting ducts, pelvis and ureters; rapid, progressive renal dysfunction develops; allopurinol prevents the formation of urate
Probenecid and large doses of aspirin enhance the renal clearance of urate: urate stones may form, so keep the urine alkaline with
sodium citrate
Which drug is not uricosuric?
allopurinol and colchicine
DOC for severe hyperuricemia
Patient with gout treated w probenecid gets remineralization of bone. Why?
increased urinary excretion of urate
patient takiing a small daily dose of aspirin may develop gout whereas a large daily dose of aspirin is used to treat gout. Why the discrepancy?
Small doses of aspirin enhance urate reabsorption in the renal tubule whereas large doses of aspirin are uricosuric
Patient being tx for gouty arthritic develops leukopenia. Which drug ?
Pg woman develops hyperthyroidism. How to treat?
What are the usual causes of hyperprolactinemia and their treatment?
blockade of D2-dopamine receptors and increased TRH in hypothyroidism cause hyperprolactinemia.

in hypothyroidism, tx w thyroxine to suppress plasma [prolactin]
patient w recurrent v. tach/v. fib. develops hyper- or hypothyroidism while taking amiodarone. Why?
Amiodarone is 37% iodide by weight. This iodide can either prevent the conversion of T4 to T3 (hypothyroidism), or it can serve as a substrate for the synthesis of T3 by thyroid peroxidase
Central DI
tx with desmopressin (long t1/2 bx it is resistant to degradation by peptidases; very selective for renal V2-receptors)
Nephrogenic DI
tx w HCTZ; if that doesn’t work, try indomethacin
Li+-induced DI
tx w amiloride (prevents entry of Li+ into principal cells of LDT/CD) or HCTZ
Treat SIADH w
demeclocycline- inhibits action of ADH in LDT/CD
Patient treated with propranolol; which drug will still bronchodilate?
theophylline or aminophylline act via intracellular inhibition of PDEase
Asthmatic patient treated with theophylline develops a sinus infection which requires
tx w an AB; Which AB would require adjustment of the daily dose of theophylline?
Erythromycin because it inhibits CYP450 which is the enzyme that metabolizes theophylline
asthmatic patient taking theophylline develops seizures after taking an OTC drug for heartburn. drug = ?
cimetidine which blocks the CYP450 which metabolizes theophylline
Which drug causes the greatest increase in FEV1 with the smallest increase in HR?
patient w exercise-induced asthma uses cromolyn prophylactically. MOA ?
cromolyn prevents Ca++ influx into mast cells when IgE bridges form = no mast cell degranulation
Glucocorticoids pharm effects
1. Inhibit the production of Il-1 and IL-6 by macrophages and monocytes
2. Inhibit antibody synthesis by B-cells
3. Prevent the functions of cytotoxic T-cells
4. NO bone marrow depression
Which drug suppresses cellular immunity, blocks the synthesis of PG’s and LT’s and increases neutrophil count in blood?
A glucocorticoid

NB: Glucocortiocoids decrease the number of B & T lymphocytes, monocytes, eosinophils and basophils by stimulating their movement from the blood into lymphoid tissue. However, glucocorticoids acutely increase the release of neutrophils from bone marrow and prevent their migration out of the blood into tissues
Cyclosporine MOA
inhibits calcineurin to prevent the production of IL-2 by helper T-cells
Mycophenolate MOA
inhibits inosine monophosphate dehydrogenase which prevents the synthesis of purines in T & B lymphocytes. Unlike other cells from the bone marrow,
T & B lymphocytes lack the enzyme HGPRTase for purine synthesis
Cytotoxic immunosuppressant Azathioprine
converted to 6-mercaptopurine (purine analog = antimetabolite) which interferes with the nucleic acid synthesis that is needed for proliferation of B- and T-cells
Cytotoxic immunosuppressant Cyclophosphamide
alkylates DNA; S/E = hemorrhagic cystitis
Patient with vitamin D toxicity exhibits:
hypercalcemia with hypercalcinuria; hyperphosphatemia; anorexia, nausea, weight loss, weakness; dehydration develops because hypercalcemia impairs the renal concentrating ability of the kidney
Tx of vitamin D toxicity:
aggressive hydration w isotonic saline, furosemide to enhance urinary Ca++ excretion and plicamycin (mithramycin) = a cytotoxic antibiotic drug that inhibits bone resorption
Patient w renal failure has low plasma Ca++ Tx w ?
tx with 1,25 diOH-Vit D
Patient w Paget’s disease (a localized bone dx w uncontrolled osteoclastic bone resorption and secondary in the formation of poorly organized bone) exhibits hearing loss,
bone pain, bone deformity, increased serum alkaline phosphatase, increased urinary hydroxyproline, high output HF and immobilization hypercalcemia. TX w ?
Tx w calcitonin to decrease bone pain, bone deformity, hearing loss and hypercalcemia. Calcitonin will decrease serum Ca++ and PO4- by inhibition of osteoclastic bone resorption and decreasing the reabsorption of Ca++ and PO4- by the kidney.
Alendronate and etidronate
bisphosphonates inhibit the resorption of bone by inhibiting the ability of osteoclasts to dissolve hydroxyapatite crystals. Bisphosphonates increase bone mass and decrease fractures. Used to prevent glucocorticoid-induced osteoporosis and used with calcitonin to treat Paget’s dx; used an alternative to HRT to prevent post-menopausal bone loss
A post-menopausal woman requires tx to maintain bone mass, but cannot take estrogen bx her mother and sister had breast cancer. Tx w ?
alendronate or etidronate
A patient tx with steroids develops hypocalcemia. Why?
Steroids antagonize the effects of vitamin D on the GI absorption of Ca++ ; less Ca++ absorption -> inc [PTH] -> inc bone resorption -> inc renal excretion of Ca++ -> hypocalcemia and osteoporosis
hypochromic, microcytic anemia
Fe-deficiency anemia, only RBCs affected
Fe-deficiency anemia caused by
increased Fe requirment, decreased GI absorption of Fe or blood loss
S/S of Fe-deficiency anemia
pallor, fatigue, feel light-headed; pica = craving for clay, laundry starch, ice
Labs in Fe-deficiency anemia
decreased serum [ferritin] and increased total iron binding capacity (TIBC)
Tx of Fe-deficiency anemia
with ferrous iron; vitamin C enhances the GI absorption of ferrous iron
normochromic, macrocytic (megaloblastic) anemia caused by
deficiency of folate (lack of dietary intake) or vitamin B12 (no GI absorption)
S/S of folate def
diarrhea, anorexia, sore tongue, irritability, forgertfulness
S/S of vitamin B12 def
same as for folate plus a neurological syndrome = paresthesias of distal extremities, sensory disturbances which may progress to spastic ataxia; caused by demyelination of nerves fibers in the dorsolateral spinal column; vitamin B12 is necessary for the conversion of methylmalonyl CoA to succinyl CoA which is needed for the synthesis of myelin; no vitamin B12 = demyelination

methylmalonic acid in the urine
Tx vitamin B12 deficiency with
i.m. injection of cyanocobalamin or hydroxycobalamin; this tx must be continued for life.
A patient with normochromic, macrocytic anemia has distal paresthesias. The patient is treated with p.o. folate and the anemia disppears, but the neurological S/S worsens. What happened?
Folate will correct the megaloblastic anemia, but the neurological syndrome results from B12 deficiency because B12 is needed for the synthesis of myelin.
A patient being treated with phenytoin, isoniazid, pyrimethamine, trimethoprim or methotrexate develops normochromic, macrocytic anemia. Why?
Phenytoin and isoniazid
interfere with the GI absorption of folate. Pyrimethamine, trimethoprim and methotrexate
inhibit DHF reductase.
A patient on hemodialysis develops normochromic, macrocytic anemia. Why and what to do about it?
Hemodialysis removes plasma folate. Patients on hemodialysis must be treated with erythropoetin (EPO), folate and ferrous iron.
A patients with a Hct. 24 is started on hemodialysis. After tx with EPO, folate and ferrous iron, the patient develops HT. Why?
As the Hct is increased by increased production of RBC's, the viscosity of blood rises. According to Poiseuille's law, resistance is directly
related to viscosity. The increase in Hct increases the resistance to flow, so BP increases.
Which drug could be used for "blood doping" (i.e., increased Hct) in competitive cycling?
EPO, epoetin alfa, darbepoetin
from the cortisol pathway
from the testosterone pathway.
Glucocorticoid S/E
glaucoma, osteoporosis, GI ulcers (from decreased gastric PG synthesis), psychosis
Patient with malar (buterfly) rash, arthritis, polyserositis: urine shows proteinuria and microscopic hematuria Dx = ?
Tx = ?
SLE, Tx w prednisone or any other –sone or –lone drug
Which synthetic glucocorticoid is used to differentiate bilateral adrenal hyperplasia from adrenal carcinoma?
dexamethasone because it will depress serum cortisol by 50% in adrenal hyperplasia caused by a pituitary adenoma (Cushing’s dx) but have no effect on serum cortisol in adrenal carcinoma.
Which drug will increase the urinary excretion of 17-ketosteroids (testosterone) in a patient with bilateral adrenal hyperplasia (i.e., Cushing’s dx) wo affecting urinary 17-OH-steroids (cortisol) in a patient with adrenal carcinoma?
Metyrapone blocks the CYP45011 that converts 11-deoxycortisol ( a 17-OH-steroid) to cortisol so there is no cortisol to feedback inhibit the pituitary. ACTH rises and stimulates adrenal steroid synthesis causing even more 11-deoxycortisol to be produced. This generalized increase in adrenal steroid synthesis also increases the synthesis of testosterone which is metabolized to 17-ketosteroids, so the urinary excretion of 17-ketosteroids also increases. In a patient with adrenal carcinoma, cortisol produced by the tumor suppresses ACTH release so the normal adrneal cortex atrophies and thus cannot respond to the increase in ACTH secretion caused by metyrapone
Which drug will suppress plasma cortisol in a patient with normal pituitary/adrenal function?
ketoconazole blocks the CYP450scc
Which drug can cause a “medical adrenalectomy”?
aminoglutethimide blocks all adrenal and extra-adrenal steroid synthesis bx it prevents the conversion of cholesterol to pregnenolone; it can be used to tx Cushing's syndrome
A patient tx wih steroids develops a GI ulcer. MOA:
inhibition of gastric PG synthesis
S/E’s of estrogens
thromboembolic disease
MOA of RU-486 (mifepristone)
progesterone receptor antagonist
A patient with S/S of hyperestrogenism (breast tenderness) is on a drug to enhance fertility. Drug = ?
clomiphene. Clomiphene blocks CNS estrogen receptors causing increased putsatile release of GnRH which enhances the secretion of FSH – ovulation.
Estradiol contraindicated in a patient w a history of thromboembolic dx (DVT's). Why?
Bx estradiol increases the synthesis of clotting factors
Patient has breast cancer. TX = ?
tamoxifen which blocks estrogen receptors
Why do OCP's which contain an estrogen also contain a progestin?
prevents the endometrial hyperplasia caused by the estrogen
Which compound can be used to maintain bone mass in a postmenopausal woman who has had breast cancer?
raloxifene (a SERM) or alendronate (a bisphosphonate)
tx with an estrogen decreases the risk of
osteoporosis and colorectal cancer
A body builder treats himself w fluoxymesterone (an anabolic steroid). How his
spermatogenesis be affected?
Spermatogenesis is suppressed bx the fluoxymesterone stimulates hypothalamic androgen receptors which inhibit the release of GnRH so no FSH is secreted by the pituitary
A body builder has an enlarged heart and spleen, borderline DM and mild HT, but androgenic steroids are not present in his urine. What drug is he abusing?
growth hormone which increases the production of insulin-like growth factors (IGF's)
Older man has arthralgia, fluid retention and hyperglycemia. What drug has the effect?
growth hormone (GH)
What drug will suppress the secretion of GH hormone in a patient with acromegaly?
bromocriptine or octreotide
Patient with BPH or hair loss. Tx w ?
Finasteride blocks the synthesis of dihydrotestosterone (DHT) by inhibiting 5alpha-reductase
Which drugs is a androgen receptor antagonists?
How to tx a young boy w cryptorchidism?
Leuprolide, goserelin and nafarelin
GnRH analogs
Glucagon (CAMP) pharm effects
metabolic effects = increase in plasma glucose at the expense of liver glycogen stores, increases hepatic CAMP to activate phosphorylase a activity and the enzymes of gluconeogenesis. NO effect on glycogen stores in skeletal muscle.

Cardiac effect = increased dp/dt and HR via increased CAMP
Glucagon (CAMP) med uses
- tx of severe hypoglycemia
- tx of poisoning w beta-blocker; increases dp/dt independent of beta-receptors
- diagnosis of type 1 DM, large doses of glucagon increase insulin and C-peptide release from beta-islet cells: no C-peptide released in type 1 DM
patient with diabetic ketoacidosis, tx w?
lispro or regular insulin i.v., i.v. fluids for rehydration, potassium to prevent hypokalemia as insulin drives glucose into liver, skeletal muscle and fat cells.
tolbutamide, chlorpropamide, glyburide, glipizide; what class?
Sulfonylurea MOA
depolarize beta-islet cells by blocking ATP-sensitive K+ channels: insulin released
Sulfonylurea S/E
metformin and rosiglitazone med use
the glitazones decrease insulin resistance primarily in skeletal muscle and fat cells
used to tx type 2 DM
A patient with type 2 DM develops lactic acidosis while taking a drug. drug = ?
metformin bx metformin increases glucose utilization via anaerobic pathways (glucose -> lactate -> lactate)
Which drug decreases hepatic glucose production in a type 2 diabetic patient without enhancing the pancreatic secretion of insulin?