Pharm vs function 1 Word Scramble

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Question	Answer
What are the actions of parathyroid hormone?	Increases Ca reabs and decrs phosphate reabc in kidney. Incrs Ca abs in intestine. Promotes bone resorption at high doses, bone formation at low dose.
What stimulates release of parathyroid hormone?	Inversely related to serum Ca2+ levels (ie, more PTH released when Ca is low). High phosphate levels also stimulate PTH release
What are the classical actions of Vitamin D?	increases abs of Ca2+ and phos. in intestine. Kidney: incrs. abs of Ca and Phos, and shifts D metabolism toward Secalciferol (24,25). Bone: promotes turnover. Thy/PThy: Decrs PTH activity, decrs calcitonin.
What are the non-classical actions of Vitamin D?	blocks proliferation and increases differentiation in skin, breast tissue. Increases transcription of its own rec. Decreases PTH recs.
What form of Vitamin D is particularly helpful in patients with decr'd kidney fxn?	Dihydrotachysterol (DHT). D3 analog w/flipped ring. Doesn't have to be 1-alpha-OH'd in kidney
Which organs are involved in the manufacture of active Vitamin D (1,25)?	Skin takes 5-dehydrocholesterol-->D3. Liver takes D3-->25OH-D3. Kidney takes 25-OH-D3 to (1,25)OH2-D3. (Intestine makes the 7-dehydrocholesterol from cholesterol.)
How do bisphosphonates work?	Mainly affect osteoclasts. They aAlter the bone mineral surface, inhibit osteoclast recruitment, inhibit osteoclast activity, and shorten osteoclast lifespan.
Name several uses of Vitamin D.	Deficiency (esp. common in northern climes), nutritional issue, metabolic rickets, hypoPTH, pseudohypoPTH, senile osteoporosis, CKD, psoriasis (calcipotriene).
Name 2 IV drugs that can treat hypercalcemia of malignancy.	Mithramycin and gallium nitrate
Where is calcitonin made?	C cells of thyroid
What is the first treatment step in senile osteoporosis?	D2 or D3, Ca supplements, weight-bearing exercise
What are some treatment options for high-turnover osteoporosis (is, post-menopause)?	HRT, raloxifene, bisphosphonates, calcitonin, intermittent teriparatide, Ca2+ supplements
What are some dietary sources of Vitamin A?	egg yolks, milk, liver, fat
In what family are retinoic acid receptors grouped?	sex hormone, glucocorticoid, thyroid, and vitamin D recs
What are the symptoms of vitamin A deficiency?	night blindness, diarrhea, reproductive anomalies, blocked spermatogenesis, slowed growth, fewer RBCs and blood volume, effects on taste/smell/hearing
What are the symptoms of vitamin A excess?	dry, red itching skin with peeling, hepatomegaly, cirrhosis, splenomegaly, hypertrophy of fat-storing cells, congenital abnlities. Can lead to oral leukoplakia and SCC
How is retinoic acid related to leukemia?	acute promyelocytic leukemia (APL) d/t the RAR-alpha gene transloc'd to the PML gene (17:15). Fusion prod. represses gene transcription & diff. of promyelocytes but reproduction continues unabated. Can txt w/high-dose all-trans retinoic acid (ATRA)
How do the topical retinoids trentinoin and adapalene differ?	trentinoin--activates all 3 RARs, adapalene activates RAR-beta selectively to decr SEs
How is growth hormone release controlled?	hypothalamic hormones--somatostatin as a major negative regulator of GH, GHRH stimulates GH release
What are the final hormones in the growth hormone cascade?	GH--stimulates IGF-1 and opposes insulin. IGF-1 promotes growth and differentiation of tissues. IGF-2 has insulin-like activity and is less dep. on GH for release.
How is prolactin release controlled?	Dopamine inhibits release from anterior pituitary (major regulator).
What types of vasopressin receptors are there and what are their actions?	V1a--vasoconstriction. V1b--pituitary, activation stimulates ACTH. V2--in renal DT &CCT to increase aquaporins and concentrate urine. V2 also increase procoag-factors VIII &vWF
What drugs mimic the action of oxytocin and contract the uterus?	prostaglandins (dinoprostone, carbaprost) and ergot alkaloids via alpha-1 activity (ergonovine)
What is the drug of choice in hyperprolactinemia?	bromocriptine--DA agonist
What are the drug options in acromegaly?	octreotide (1st choice--somatostatin analog), pegvisomant (2nd choice--GH rec blocker but might not decrease size of GH-adenoma), bromocriptine has moderate inhibition of GH release
How can you administer FSH and LH to treat infertility?	In women--give hMG or urofollitropin (FSH analogs) to stimulate follicles, then hCG (LH analog) to induce ovulation. In men--give hCG to promote testosterone production, then hMG to stimulate spermatogenesis
Why does clomiphene, an estrogen receptor blocker, treat female infertility?	limits estrogen's feedback on the pituitary to increase LH and FSH release
Why can't estrogen be used alone in HRT or contraception? When might it be okay?	estrogen-->unopposed proliferation of uterine lining, can increase uterine cancer risk. Must use a progestin to keep lining thin. Might be okay to use estrogen alone for HRT if a woman no longer has a uterus.
How are estrogen and testosterone made?	cholesterol--> intermediates--> testosterone by P450 enzymes. Then testosterone--> DHT by 5alpha reductase or testosterone--> estrogen by aromatase.
What are some androgen receptor antagonists and what are they used for?	flutamide (for prostate CA or BPH), cyproterone acetate (for early puberty, acne, severe hirsutism--investigational in the US)
How is androgen synthesis inhibited?	P450 blockers--including ketoconazole (antifungal), spironolactone (diuretic)
What drugs are used to oppose thyroid hyperactivity in Graves' Disease? Which is the DOC in pregnancy and breast-feeding?	Thyroid peroxidase enzyme enzyme inhibitors: propylthiouracil (DOC in preg), methimazole, carbimazole (not available in US)
What are the various forms of iodine used in thyroid disorders?	123-I used for Dx, 131-I used to destroy overactive thyroid tissue, Lugol's solution of nonradioactive I helps harden thyroid before surgery
How is FSH secretion regulated?	major regulator: Inhibin, made in ovarian granulosa cells and testicular Sertoli cells, selectively suppresses FSH synthesis. Minor roles: activins stimulate FSH, follistatin inhibits FSH (poss. by binding activin)
What are some ways insulin may be modfied to make it dissolve more slowly?	addition of a protamine (NPH), precipitate it with Zn2+ (lentes), add extra Arginines (Glargine)
How do sulfonylureas work?	Hypoglycemic--promote insulin release. Bind to the SUR1 subunit of the inward-rectifying ATP-sensitive K+ channel to cause partial depol.--> activates voltage-sensitive Ca2+ channels--> exocytosis of insulin granules
What is the difference between 1st and 2nd-gen sulfonylureas?	1st gen-bind by ionic interactions and might be displaced by other drugs. 2nd-gen--nonionic interactions, effective at 10 to 100X lower concs than 1st-gen
How do meglitinides work?	Hypoglycemic--inhibit conductance of the same inward-rectifying K+ channel as sulfonylureas but at a different subunit. End result is the same--promotes release of insulin
How does GLP-1 work?	GLP-1=incretin, enhances glucose-dep. insulin secretion from beta cells. Also lowers serum glucagon during hyperglycemia, slows gastric emptying to slow glucose rise in serum and to decrease food intake. (Exenatide)
What is DPP-IV?	Main enzyme that metabolizes incretins (GLP-1, GIP). More circulating incretins--> more insulin secretion--> lower glucagon levels. (Sitagliptin)
How does metformin work?	Antihyperglycemic. Decreases glucose output from liver, inhibits gut abs. of glucose, increases GLUT4s in muscle an fat to promote glucose uptake
How do thiazolidinediones work?	Antihyperglycemics. Increase insulin action on lipid and protein metabolism. Also activate PPAR-gamma--> increases mRNA for enzymes and proteins involved in insulin sensitivity. (-glitazone suffix)
How are alpha-glucosidase inhibitors helpful in diabetes?	Antihyperglycemic. Inhibit enzymes that take complex carbs to monosaccharides--> slower rise in serum glucose after meals. (acarbose, miglitol)
What is amylin?	Neuroendocrine hormone made in beta cells of pancreas. Amylin homolog is pramlintide; decr's rate of gastric emptying, prevents post-meal rise in glucagon, and promotes satiety. Useful in T1DM for better control, T2DM for better control with other drugs
What happens when muscarinic receptors are activated?	M recs activated by ACh. M2--K+ channels, mainly in heart, slows HR. M3--GPCRs that increase cytosolic Ca2+; contracts smooth muscle, promotes secretion form glands, and constricts pupil.
What happens when Nm receptors are activated?	Somatic nervous system--NMJ-->muscle movement. Activated by ACh.
What happens when Nn receptors are activated?	PNS--ganglions. Nn are Na+ channels, activation furthers signaling to M recs
Where are alpha-1 recs found, and what occurs with their activation?	Found in blood vessels (constriction), smooth muscle in bladder neck and uterus(contraction), glands (secretion).
Where are alpha-2 recs found, and what occurs with their activation?	presynaptic adrenergic receptors (inhibit NE release), CNS. GI--relaxation, inhibition of secretion; Vessels--reduce vasoconstriction outflow; Beta cells--inhibit insulin secretion
Where are beta-1 recs found, and what occurs with their activation?	Mainly found in heart (increase rate, force, conduction, ventricular excitability). Also in kidney JGA (promote renin secretion)
Where are beta-2 recs found, and what occurs with their activation?	Blood vessels (dilate), smooth muscle (relax), metabolism (promotes), bronchi (dilate)
What happens when beta1 & 2 recs are activated? What drug does this?	beta-1: greater force and rate--> higher SBP. beta-2: vasodilation in periphery--> much lower DBP. Sum: Increased cardiac output, wider pulse pressure. Drug is isoproterenol (also epinephrine--alpha effects too)
Name 2 beta-1 agonists and their uses & effects.	Dopamine and dobutamine. Increase heart contractility, promote renal vasodilation. Helps with CO in CHF, preserves kidney function in shock.
Name 3 drugs used in pheochromocytoma.	alpha blockers--phenoxybenzamine (OR & outpt)and phentolamine (OR only). beta blockers (like propranolol). Combined to protect vasculature from the effects of catecholamines in a pheo.
Name drugs to use and drugs to avoid in glaucoma.	alpha agonists and beta blockers both decrease aqueous humor. Muscarinic agonists and AChE inhibitors increase outflow of humor past the trabecular mesh. Avoid atropine in narrow angle glaucoma--mydriasis can close trabecular mesh.
What are the major actions of PGI2? How is it made?	Opposes TXA2 in vessels, relaxes bronchial sm.m., vasodilates, cytoprotective in gastric mucosa, renal vasodilator. Made in COX pathway, prostacyclin synthase.
What are the major actions of PGE? How is it made?	Promotes uterine contraction, maintains PDA, renal vasodilator, cytoprotective in gastric mucosa. Made in COX pathway, interchanges with PGF2alpha.
What are the major uses of PGE1, PGE2, and PGF2-alpha analogs?	PGE1: Alprostadil and Caverject--ED; Misoprostol--gastric protection w/NSAID, w/ mifepristone (anti-progestin). PGE2--Dinoprostone for cervical ripening. PGF2alpha--carboprost--contracts the uterus to control postpartum bleeding
What are the actions of TXA2? How is it made?	Stimulates platelet aggregation (opposed by PGI2), vasoconstricts. COX pathway, also need thromboxane synthase
Where are COX enzymes found?	COX1--almost everywhere. COX2--mainly in inflammatory cells (esp. activated macrophages); assoc'd w/ colon polyps' progression to cancer.
What is PAF? How is it made?	Platelet aggregation factor--promotes agg, vasodilation, increases vascular permeability, WBC chemotaxis, bronchospasm, and gastric ulcers. Made from membrane phospholipids, free radicals, and PLA2.
What do leukotrienes do? How are they made?	LTC4, LTD4--promote bronchoconstrictors, mucosal edema. (Esp. LTC4). Made in LOX pathway; takes AA-->5HPETE. 12HPETE, another product, is assoc'd w/atherosclerosis, angiotensin-med'd aldosterone synthesis, and inhibition of beta cell release of insulin
What are the major actions of NSAIDs?	Inhibit COX (both or just COX-2) for antipyretic (inhibit PGEs in hypothalamus), analgesic (inhibit nociceptor-sensitizing PGE2 and PGI2), and antiinflammatory (reduce vasodilation in acute phase) actions
Which NSAID inhibits COX and LOX? What is the effect of this?	Ketoprofen. No known benefit to inhibiting LOX as well. If taken w/probenecid--longer duration of action
What is the only COX-2 selective inhibitor left on the market?	Celecoxib
What is the only NSAID marketed as a single enantiomer?	Naproxen
Which NSAID irreversibly inhibits COX?	Aspirin--leads to a persistent decrease in platelet fxn; this is used therapeutically to prevent clots
Which NSAID has a superlong halflife (over 2 days)?	Piroxicam
What are the major differences between 1st, 2nd, and 3rd-gen antihistamines?	1st cross the blood brain barrier whereas 2nd and 3rd don't. 1st generation drugs are likely to produce sedation, nervousness, etc. (CNS histaminergic neurons promoke wakefulness). All are reversible inhibitors of H1 recs
How does colchicine work?	binds to tubulin and inhibits polymerization--paralyzes granulocytes so they can's get into joint space and deposit urate crystals in gout.
How does allopurinol work?	inhibits xanthine oxidase--the enzyme that converts hypoxanthine to xanthine and xanthine to uric acid in purine degradation. Used in chronic gout
Name 2 uricosuric drugs.	Probenecid, sulfinpyrazone (a metabolite of phenylbutazone--NSAID)
Name several classes of drugs used to treat asthma.	Bronchial dilation: Selective beta-2 agonists, muscarinic antagonists, methylxanthines. Treatment of inflammation: glucocorticoids, LOX path modulators. Prevention of mast cell degranulation: chromolyn sodium, human IgG Ab to IgE
Describe the calcineurin pathway and name 2 modulators.	T cell cascade: TyrK activ--> cleave PIP2--> IP3--> Ca2+ release --> calcineurin--> NFAT active--> transcription of IL-2 & cytokines. Cyclosporine complexes with cyclophilin, tacrolimus complexes with FKBP--either combo inhibits calcineurin activity
How do cytotoxic drugs work?	Inhibit purine synthesis (mycophenolate mofetil), alkylate DNA (cyclophosphamide), inhibit DHF and puring/thymidylate/ methionine synthesis (methotrexate)
What are the effects of activation of different 5HT recs?	5HT1A--anxiolysis in CNS. 5HT1B/D--sensory nerve endings, activation decreases inflammation (triptans). 5HT2A--hallucinogenic. 5HT3 stimulates nausea. (ondansetron, alosetron are blockers). 5HT4 is prokinetic (metoclopramide, domperidone, tegaserod).
What are some ways to inhibit gastric acid? Which is most effective?	H2 blockers--prevent stimulation of H2 recs on parietal cells. PPIs--inhibit H+/K+ ATPase on parietal cells. PPIs are more effective overall; H2 blockers mainly minimize basal acid secretion, as at night.
What are the major side effects of Al and Mg-containing antacids?	Al--delays gastric emptying, leading to constipation. Mg--stimulates CCK and motor function leading to laxation.
How do side effects differ among the 1st-gen antipsychotics?	Lower-potency drugs have more anti-alpha1 and anti-ACh effects but less EPS. Opposite is true for higher potency. DA usu inhibits ACh; DA blockade--> excess ACh firing--> EPS. SO DA block PLUS anti-ACh=less EPS.
How do side effects differ among the 2nd-gen antipsychotics?	2nd gen have some Anti-ACh effects but not the seating anti-alpha1 effects. Clozapine has lots of anti-ACh effects so very little EPS. Olanzapine and Risperdone have some anti-ACh effects and some EPS, but less than most 1st-gen drugs.
Name 2 drug classes used in Alzheimer's Disease.	AChE inhibitors (compensate for early loss of ACh neurons), NMDA rec antagonists (blocks excitotoxicity)
Name several different ways to oppose emesis.	5HT3 antag. (ondansetron, alosetron, high dose metoclopramide); muscarinic antag. (scopolamine), mixed H1/M antag. (dimenhydrinate, promethazine), DA antag. (low dose chlorpromazine, prochlorperazine); misc--dexamethasone, lorazepam, dronabinol, arepipant
Name the NTs affected by these classes of antidepressants: TCAs, SSRIs, MAOIs	TCAs--inhibit NE and 5HT reuptake. SSRIs--mainly 5HT reuptake (a bit of NE). MAOIs--preferential increase in 5HT, some NE and DA
Name benzodiazepines used for insomnia.	Flurazepam (long halflife but fast redistr.); temazepam, triazolam, zolpidem (techn. not a benzo)
How do benzodiazepines work?	Bind to a site on GABA-operated Cl- channels--> enhance Cl- conductance when GABA is bound to its own sites--> more inhibitory postsynaptic potentials
Which benzos are used for EtOH withdrawal?	Chlordiazepoxide (Librium) and Oxazepam
Which benzos are used for status epilepticus?	1o-lorazepam (Ativan); 2o-diazepam (Valium),
What drug can be used in suspected benzo overdose?	flumazenil--benzo rec antagonist
Name 3 drugs used to treat alcohol addiction.	Disulfiram (Antabuse), acamprosate (attenuate craving), naltrexone (attenuates reward effects at opioid recs)
Name various uses of opioids	antitussive, analgesic, slow transit of GI tract (antidiarrheal)
Naloxone vs naltrexone--what's what?	Naloxone--antagonizes effects of injected opiate in overdose. Naltrexone--attenuates rewarding effects of opioid receptor activation.
Name drugs used to prevent migraine and treat acute attacks.	Prevention--beta blockers (1o), TCAs (2o), valproate. Abortives--Triptans (1o), ergot alkaloids, NSAIDs (more mild). Misc--metoclopramide (N/V)
Give 3 halogenated ester anesthetics and discuss their differences.	Isoflurane (most soluble), sevoflurane (middle solubility), desflurane (least soluble). Less soluble=faster acting (less needed to distribute thoroughly) and vice versa.
List the drugs used in a combined-anesthetic general anesthesia strategy.	Benzo pre-op for anxiolysis; fentanyl for pain; induction drug (thipental, propofol, or etomidate); paralytic (NMJ blocker or succinylcholine--NMJ ag/depol blocker); halogenated ester to maintain anesthesia. Antiemetic & analgesic at end of procedure.

Created by: emoboe