Endocrine, Gi, Misc Pharm

Front 1

Serotonin synthetic pathway

Back 1

Tryptophan -> 5-hydroxytryptophan -> 5-HT -> 5-HIAA

Enzymes:
1st) Tryptophan hydroxylase
2nd) L-aromatic amino decarboxylase
3rd) MAO-A

Front 2

bronchospasm, GI cramping and diarrhea, "odd" flushing of the skin, hypotension and increased urinary excretion of 5-HIAA

Back 2

carcinoid syndrome

Front 3

carcinoid tx

Back 3

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.

Front 4

metoclopramide pharm effects

Back 4

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

Front 5

metoclopramide med use

Back 5

4. Used to treat esophageal reflux (GERD) and empty the stomach prior to emergency surgery, etc.

Front 6

odansetron

Back 6

antiemetic drug which blocks 5-HT3 receptors in CTZ and at vagal afferent fibers

Front 7

cisapride

Back 7

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

Front 8

sumatriptan

Back 8

agonist at 5-HT1B and 5-HT1D receptors to inhibit the release of inflammatory peptides, used to treat migraine headache and cluster headache

Front 9

buspirone

Back 9

a partial agonist at 5-HT1A receptors; opens K+ channels to hyperpolarize neurons; used to tx anxiety, slow onset of action, no drug dependence

Front 10

histamine H1-receptors

Back 10

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

Front 11

histamine H2-receptors

Back 11

dilates arterioles
increases gastric H+ secretion

Front 12

cromolyn sodium

Back 12

inhibits mast cell degranulation by preventing inc in intracellular Ca++

Front 13

olopatidine

Back 13

inhibits mast cell degranulation and blocks histamine H1-receptors, used
to tx conjunctivitis assn with seasonal allergy

Front 14

Sedating antihistamines

Back 14

diphenhydramine, meclizine

Front 15

Non-sedating antihistamines

Back 15

terfenadine, fexofenadine, clemastine

Front 16

Prophylaxis of motion sickness (need to block central muscarinic ACh receptors)

Back 16

dimenhydrinate, meclizine and scopolamine

Front 17

DOC for Tx of Meniere’s disease

Back 17

meclizine

Front 18

H2-receptor blockers

Back 18

cimetidine, famotidine, ranitidine – blocks gastric acid secretion,
also blocks allergic responses in the skin

Front 19

A patient exposed to poison oak is given (2 drugs):

Back 19

both diphenhydramine (H1-blocker) and cimetidine (H2-blocker) to prevent itching and pain

Front 20

A patient w GERD is being treated with cimetidine requires allergen testing by a dermatologist.

Back 20

Must d/c cimetidine to ensure accuracy of skin tests. Tx GERD w omeprazole during allergy testing.

Front 21

Patient has insomnia from depression; tx with a TCA but patient still has insomnia

Back 21

Give an antihistamine (e.g., diphenhydramine) to induce sleep, and patient gets urinary retention from combined atropine-like effect of the drug combination

Front 22

ipecac induces vomiting by

Back 22

an action at the CTZ and by an irritant action in the stomach which is not blocked by antihistamines

Front 23

What drug induces emesis by stimulating D2-receptors in the CTZ?

Back 23

apomorphine

Front 24

lactulose (synthetic disaccharide)

Back 24

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.

Front 25

A patient with S/S (confusion/coma) of hepatic portal encephalopathy needs tx

Back 25

lactulose which acidifies the bowel to trap ammonia as ammonium ion; ammonium lost in feces; plasma [ammonia] falls; coma and confusion disappear

Front 26

docusate sodium

Back 26

a stool softener = an anionic surfactant: detergent action allows water to enter feces; softens the stool wo increasing its bulk

Front 27

Diarrhea

Back 27

tx w loperamide or diphenoxylate which stimulate mu opiate receptors

Front 28

Ulcers

Back 28

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)

Front 29

Ulcers with H. pylori

Back 29

triple AB tx = clarithromycin, amoxacillin, omeprazole

Front 30

Which antiulcer drug does not alter stomach pH?

Back 30

sucralfate

Front 31

Patient on propranolol takes cimetidine for heartburn and develops severe bradycardia. Why?

Back 31

Bx cimetidine inhibits CYP450 and thus blocks the metabolism of propranolol

Front 32

Al OH in GI

Back 32

constipation

Front 33

Mg OH in GI

Back 33

diarrhea

Front 34

Pat being tx w doxycycline; which drug contraindicated?

Back 34

Al/Mg antacids

Front 35

Patient needs emergency surgery; need to empty stomach/prevent reflux. Drug = ?

Back 35

metoclopramide = prokinetic in stomach and bowel and tightens the LES

Front 36

Cancer chemo patient has n/v and noctural acid reflux Tx w = ?

Back 36

metoclopramide

Front 37

Patient has post-operative paralytic ileus Tx w = ?

Back 37

metoclopramide, bethanechol, cisapride

Front 38

Patient treated with drug for Crohn’s disease or ulcerative colitis develops hepatic damage or bone marrow depression. Drug = ?

Back 38

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.

Front 39

s/s of laxative abuse w castor oil or bisacodyl =

Back 39

constipation, hypokalemia, muscle weakness, abnormal architecture inner GI wall

Front 40

Aspirin effect on platelets

Back 40

irreversibly inhibiting the COX-1 in platelets via acetylation to prevent the synthesis of thromboxane A2 (TXA2)

Front 41

Aspirin OD s/s

Back 41

- 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

Front 42

Aspirin OD tx

Back 42

make urine alkaline (acetazolamide or NaHCO3) to enhance the renal clearance of salicylate and infuse bicarbonate to correct acidosis

Front 43

dipyridamole

Back 43

an inhibitor of PDEase in platelets which potentiates the antiplatelet effect of aspirin and prostacyclin (PGI2)

Front 44

half-life of aspirin as only 1 h, why does it inhibit platelet inhibition for a longer period?

Back 44

Aspirin irreversibly acetylates active site of COX-1 in platelets

Front 45

How does aspirin prevent platelet aggregation when it is not taken in doses large enough to maintain a steady-state plasma concentration?

Back 45

Aspirin irreversibly acetylates active site of COX-1 in platelets

Front 46

patient has intermittent episodes of hemiplegia which resolve spontaneously; would like to treat with aspirin, but patient has aspirin “hypersensitivity”; Tx w?

Back 46

ticlopidine

Front 47

What is the causative compound in aspirin hypersensitivity?

Back 47

leukotrienes

Front 48

DOC for menstrual cramps

Back 48

ibuprofen

Front 49

Baby has patent ductus arteriosus

Back 49

close with indomethacin

Front 50

Want to keep ductus open prior to surgery: what drug will do this ?

Back 50

alprostadil = PGE1 analog dilates the ductus arteriosus

Front 51

pat tx with NSAID develops GI ulceration
what is the MOA?

Back 51

inhibition of gastric PG synthesis

Front 52

A patient with nasal polyps who has wheezing with aspirin needs a antipyretic drug

Back 52

DOC = acetaminophen

Front 53

Acetaminophen is antipyretic but not

Back 53

antiinflammatory

Front 54

Drug OD; initially blood chemistries normal, but 36 h later see increase in AST and ALT.
what is the drug?

Back 54

acetaminophen; treat with n-acetylcysteine to replenish glutathione

Front 55

Adverse effects of NSAID’s

Back 55

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

Front 56

Patient on NSAID for tendonitis for 2 weeks develops fever and hematuria: diagnosis?

Back 56

acute interstitial nephritis

Front 57

histologic photo of kidney tissue with lots of lymphocytes: diagnosis?

Back 57

Interstitial nephritis caused by aspirin or another NSAID

Front 58

Patient with CHF takes ibuprofen; effect on kidney = ?

Back 58

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.

Front 59

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?

Back 59

misoprotol

Front 60

Colchicine

Back 60

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

Front 61

Allopurinol

Back 61

for gout,
inhibits xanthine oxidase to block the synthesis of uric acid from purines

Front 62

Patient with a renal transplant is taking the immunosuppressant drug azathioprine. Patient develops gout. Which gout drug is contraindicated?

Back 62

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.

Front 63

Patient with lymphoma tx with chemo. Which drug will prevent dec in renal function?

Back 63

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

Front 64

Probenecid and large doses of aspirin enhance the renal clearance of urate: urate stones may form, so keep the urine alkaline with

Back 64

sodium citrate

Front 65

Which drug is not uricosuric?

Back 65

allopurinol and colchicine

Front 66

DOC for severe hyperuricemia

Back 66

allopurinol

Front 67

Patient with gout treated w probenecid gets remineralization of bone. Why?

Back 67

increased urinary excretion of urate

Front 68

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?

Back 68

Small doses of aspirin enhance urate reabsorption in the renal tubule whereas large doses of aspirin are uricosuric

Front 69

Patient being tx for gouty arthritic develops leukopenia. Which drug ?

Back 69

colchicine

Front 70

Pg woman develops hyperthyroidism. How to treat?

Back 70

PTU

Front 71

What are the usual causes of hyperprolactinemia and their treatment?

Back 71

blockade of D2-dopamine receptors and increased TRH in hypothyroidism cause hyperprolactinemia.

in hypothyroidism, tx w thyroxine to suppress plasma [prolactin]

Front 72

patient w recurrent v. tach/v. fib. develops hyper- or hypothyroidism while taking amiodarone. Why?

Back 72

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

Front 73

Central DI

Back 73

tx with desmopressin (long t1/2 bx it is resistant to degradation by peptidases; very selective for renal V2-receptors)

Front 74

Nephrogenic DI

Back 74

tx w HCTZ; if that doesn’t work, try indomethacin

Front 75

Li+-induced DI

Back 75

tx w amiloride (prevents entry of Li+ into principal cells of LDT/CD) or HCTZ

Front 76

Treat SIADH w

Back 76

demeclocycline- inhibits action of ADH in LDT/CD

Front 77

Patient treated with propranolol; which drug will still bronchodilate?

Back 77

theophylline or aminophylline act via intracellular inhibition of PDEase

Front 78

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?

Back 78

Erythromycin because it inhibits CYP450 which is the enzyme that metabolizes theophylline

Front 79

asthmatic patient taking theophylline develops seizures after taking an OTC drug for heartburn. drug = ?

Back 79

cimetidine which blocks the CYP450 which metabolizes theophylline

Front 80

Which drug causes the greatest increase in FEV1 with the smallest increase in HR?

Back 80

albuterol

Front 81

patient w exercise-induced asthma uses cromolyn prophylactically. MOA ?

Back 81

cromolyn prevents Ca++ influx into mast cells when IgE bridges form = no mast cell degranulation

Front 82

Glucocorticoids pharm effects

Back 82

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

Front 83

Which drug suppresses cellular immunity, blocks the synthesis of PG’s and LT’s and increases neutrophil count in blood?

Back 83

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

Front 84

Cyclosporine MOA

Back 84

inhibits calcineurin to prevent the production of IL-2 by helper T-cells

Front 85

Mycophenolate MOA

Back 85

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

Front 86

Cytotoxic immunosuppressant Azathioprine

Back 86

converted to 6-mercaptopurine (purine analog = antimetabolite) which interferes with the nucleic acid synthesis that is needed for proliferation of B- and T-cells

Front 87

Cytotoxic immunosuppressant Cyclophosphamide

Back 87

alkylates DNA; S/E = hemorrhagic cystitis

Front 88

Patient with vitamin D toxicity exhibits:

Back 88

hypercalcemia with hypercalcinuria; hyperphosphatemia; anorexia, nausea, weight loss, weakness; dehydration develops because hypercalcemia impairs the renal concentrating ability of the kidney

Front 89

Tx of vitamin D toxicity:

Back 89

aggressive hydration w isotonic saline, furosemide to enhance urinary Ca++ excretion and plicamycin (mithramycin) = a cytotoxic antibiotic drug that inhibits bone resorption

Front 90

Patient w renal failure has low plasma Ca++ Tx w ?

Back 90

tx with 1,25 diOH-Vit D

Front 91

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 ?

Back 91

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.

Front 92

Alendronate and etidronate

Back 92

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

Front 93

A post-menopausal woman requires tx to maintain bone mass, but cannot take estrogen bx her mother and sister had breast cancer. Tx w ?

Back 93

alendronate or etidronate

Front 94

A patient tx with steroids develops hypocalcemia. Why?

Back 94

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

Front 95

hypochromic, microcytic anemia

Back 95

Fe-deficiency anemia, only RBCs affected

Front 96

Fe-deficiency anemia caused by

Back 96

increased Fe requirment, decreased GI absorption of Fe or blood loss

Front 97

S/S of Fe-deficiency anemia

Back 97

pallor, fatigue, feel light-headed; pica = craving for clay, laundry starch, ice

Front 98

Labs in Fe-deficiency anemia

Back 98

decreased serum [ferritin] and increased total iron binding capacity (TIBC)

Front 99

Tx of Fe-deficiency anemia

Back 99

with ferrous iron; vitamin C enhances the GI absorption of ferrous iron

Front 100

normochromic, macrocytic (megaloblastic) anemia caused by

Back 100

deficiency of folate (lack of dietary intake) or vitamin B12 (no GI absorption)

Front 101

S/S of folate def

Back 101

diarrhea, anorexia, sore tongue, irritability, forgertfulness

Front 102

S/S of vitamin B12 def

Back 102

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

Front 103

Tx vitamin B12 deficiency with

Back 103

i.m. injection of cyanocobalamin or hydroxycobalamin; this tx must be continued for life.

Front 104

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?

Back 104

Folate will correct the megaloblastic anemia, but the neurological syndrome results from B12 deficiency because B12 is needed for the synthesis of myelin.

Front 105

A patient being treated with phenytoin, isoniazid, pyrimethamine, trimethoprim or methotrexate develops normochromic, macrocytic anemia. Why?

Back 105

Phenytoin and isoniazid
interfere with the GI absorption of folate. Pyrimethamine, trimethoprim and methotrexate
inhibit DHF reductase.

Front 106

A patient on hemodialysis develops normochromic, macrocytic anemia. Why and what to do about it?

Back 106

Hemodialysis removes plasma folate. Patients on hemodialysis must be treated with erythropoetin (EPO), folate and ferrous iron.

Front 107

A patients with a Hct. 24 is started on hemodialysis. After tx with EPO, folate and ferrous iron, the patient develops HT. Why?

Back 107

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.

Front 108

Which drug could be used for "blood doping" (i.e., increased Hct) in competitive cycling?

Back 108

EPO, epoetin alfa, darbepoetin

Front 109

17-OH-steroids

Back 109

from the cortisol pathway

Front 110

17-ketosteroids

Back 110

from the testosterone pathway.

Front 111

Glucocorticoid S/E

Back 111

glaucoma, osteoporosis, GI ulcers (from decreased gastric PG synthesis), psychosis

Front 112

Patient with malar (buterfly) rash, arthritis, polyserositis: urine shows proteinuria and microscopic hematuria Dx = ?
Tx = ?

Back 112

SLE, Tx w prednisone or any other –sone or –lone drug

Front 113

Which synthetic glucocorticoid is used to differentiate bilateral adrenal hyperplasia from adrenal carcinoma?

Back 113

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.

Front 114

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?

Back 114

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

Front 115

Which drug will suppress plasma cortisol in a patient with normal pituitary/adrenal function?

Back 115

ketoconazole blocks the CYP450scc

Front 116

Which drug can cause a “medical adrenalectomy”?

Back 116

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

Front 117

A patient tx wih steroids develops a GI ulcer. MOA:

Back 117

inhibition of gastric PG synthesis

Front 118

S/E’s of estrogens

Back 118

thromboembolic disease

Front 119

MOA of RU-486 (mifepristone)

Back 119

progesterone receptor antagonist

Front 120

A patient with S/S of hyperestrogenism (breast tenderness) is on a drug to enhance fertility. Drug = ?

Back 120

clomiphene. Clomiphene blocks CNS estrogen receptors causing increased putsatile release of GnRH which enhances the secretion of FSH – ovulation.

Front 121

Estradiol contraindicated in a patient w a history of thromboembolic dx (DVT's). Why?

Back 121

Bx estradiol increases the synthesis of clotting factors

Front 122

Patient has breast cancer. TX = ?

Back 122

tamoxifen which blocks estrogen receptors

Front 123

Why do OCP's which contain an estrogen also contain a progestin?

Back 123

prevents the endometrial hyperplasia caused by the estrogen

Front 124

Which compound can be used to maintain bone mass in a postmenopausal woman who has had breast cancer?

Back 124

raloxifene (a SERM) or alendronate (a bisphosphonate)

Front 125

tx with an estrogen decreases the risk of

Back 125

osteoporosis and colorectal cancer

Front 126

A body builder treats himself w fluoxymesterone (an anabolic steroid). How his
spermatogenesis be affected?

Back 126

Spermatogenesis is suppressed bx the fluoxymesterone stimulates hypothalamic androgen receptors which inhibit the release of GnRH so no FSH is secreted by the pituitary

Front 127

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?

Back 127

growth hormone which increases the production of insulin-like growth factors (IGF's)

Front 128

Older man has arthralgia, fluid retention and hyperglycemia. What drug has the effect?

Back 128

growth hormone (GH)

Front 129

What drug will suppress the secretion of GH hormone in a patient with acromegaly?

Back 129

bromocriptine or octreotide

Front 130

Patient with BPH or hair loss. Tx w ?

Back 130

Finasteride blocks the synthesis of dihydrotestosterone (DHT) by inhibiting 5alpha-reductase

Front 131

Which drugs is a androgen receptor antagonists?

Back 131

flutamide

Front 132

How to tx a young boy w cryptorchidism?

Back 132

hCG

Front 133

Leuprolide, goserelin and nafarelin

Back 133

GnRH analogs

Front 134

Glucagon (CAMP) pharm effects

Back 134

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

Front 135

Glucagon (CAMP) med uses

Back 135

- 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

Front 136

patient with diabetic ketoacidosis, tx w?

Back 136

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.

Front 137

tolbutamide, chlorpropamide, glyburide, glipizide; what class?

Back 137

Sulfonylureas

Front 138

Sulfonylurea MOA

Back 138

depolarize beta-islet cells by blocking ATP-sensitive K+ channels: insulin released

Front 139

Sulfonylurea S/E

Back 139

hypoglycemia

Front 140

metformin and rosiglitazone med use

Back 140

the glitazones decrease insulin resistance primarily in skeletal muscle and fat cells
used to tx type 2 DM

Front 141

A patient with type 2 DM develops lactic acidosis while taking a drug. drug = ?

Back 141

metformin bx metformin increases glucose utilization via anaerobic pathways (glucose -> lactate -> lactate)

Front 142

Which drug decreases hepatic glucose production in a type 2 diabetic patient without enhancing the pancreatic secretion of insulin?

Back 142

metformin