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pharm 2nd half
Stack #185895
| Question | Answer |
|---|---|
| Sucralfate. What is it? | Sucralfate is a super awesome mucus plug for ulcers. |
| How do stimulant laxitives work? | Stimulant laxatives irritate the intestinal lining |
| Name a stimulant laxative | Ducosate Sodium |
| Which nervous system do stim laxatives affect? | PNS |
| Who shouldn't use stim laxatives? | I dont know. |
| Anticholinergic drugs: MOA? How do you use them in ulcers? | They block ACH receptors. Parietal cells and the stomach smooth muscle itself have ACH receptors. If you block parietal ACH you decrease acid production. If you block Muscarinic recptrs (they're on smooth/cardiac muscle) you block movement of stomach. |
| Fleet enema. Drug class? | Osmotic laxative. Ions in the drug cause water to move into stools. |
| Fibercon. Drug class? | Bulk laxative. Bigger is better. |
| Neocultol. Drug class? | Emollient. Lubricates your poooooooooooo. |
| Docusate sodium. Drug class? | Stimulant laxative. |
| Contrast pituitary gland with hypothalamus. | Hypothalamus is the master of the pituitary. The pituitary is a two-part gland that makes (anterior only) and releases hormones. |
| What hormones are produced/ stored in anterior pit? | FLAT PeG |
| What hormones are made by hypothal and released into posterior pituitary for storage and release? | Oxytocin and ADH |
| Which corticosteroids are produced by adrenal cortex? What do they do? | Adrenal cortex (the outer part) produces two types of corticosteroids: glucocorticoids and mineralocorticoids. Glucocorticoids affect metabolism. Mineralocorticoids affect fluid balance (think aldosterone is a mineralocorticoid.) |
| Why should food be taken with steroids? | Steroids irritate GI. |
| Side effects of steroids? | SE/AE steroids: Changes in wt gain, electrolyte imbalance, cardiac function, mood, sleep patterns, psychotic episodes. Large doses cause GI upset. Causes blood sugar to rise. Watch Diabetics closely! |
| What is methylpenisolone? | Glucocorticoid. |
| What is hydrocortisone, cortisone? | Glucocorticoids |
| What is fludrocortisone? | Mineralocorticoid. Addisions disease. |
| Contraindications of steroids? | Systemic fungal infections, local viral infections, no live virus vaccinations. |
| How do antihyperglycemics work? | Oral drugs. They decrease glucose abdorption and synthesis. |
| Symptoms of DB? | 3 Ps: polyuria, polydypsia, polyphagia. |
| What is insulin? | Hormone that lowers blood glucose levels. |
| What is glucagon? | Hormone that raises blood glucose levels. |
| Where is insulin/glucagon produced? | Both are pancreatic hormones. Insulin is made in beta cells. Glucagon is made in alpha cells. |
| Define ketoacidosis. | Ketoacidosis is a seriuos condition in Type 1 diabetics. (Type 2 generally dont get it.)Inability to access glucose (ie not enough insulin around) causes body to burn fat for fuel. This releases acidic ketone bodies. Result: possible coma. |
| Compare Regular Insulin/ Humulin U/ Humulin N including route of admin and duration of action. | Route of admin is SC. Duration for regular insulin is 6-8, humulin N is 18-24, humulin is >36 |
| Metformin. What is it? | Metformin is an antihyperglycemic. These drugs keep glucose levels from rising too fast after meals but do not lower glucose. MOA decrease liver glucose production and intestinal glucose absorption. |
| Ascarbose. What is it? | Ascarbose: in small intestine inhibits glycoside hydrolase and reversibly ties up alpha amylase causing a delay in blood glucose absorption. More sugar is left in stools. This leads to AE/SE of flatulence, diarrhea, abdominal pain. |
| Oral hypoglycemics. What are they? | Oral hypoglycemics: sulfonylurea compounds useful in Type II DB. Enter Beta cells and cause insulin release. These drugs have no insulin properties so no value in Type 1 DB. |
| What are complications of Diabetes? | Retinopathy, neuropathy, skin infections, atherosclerosis, blindness, retinal hemorrhages. |
| Define bactericidal/bacteristatic. | bactericidal kills bacteria by inhibiting some integral life process like cell wall maintenance or ability to make proteins. Bacteriastatic inhibits viral reproduction. |
| Gram neg vs gram positive. The colors. | Neg is pink/reddish. Pos is dark purple. |
| Beta lactamase. what is it? | Enzyme that some nasty bacteria make. The enzyme destroys beta lactam antibiotics like penicillins and cephalosporins. |
| One drug for each gen of penicillin. | Gen 1: Methicillin Gen 2: Amoxicillin Gen 3: Ticarcillin Gen 4: Piperacillin |
| Which gen of penicillin is broadest spectrum? Which is most narrow? | Broadest spectrum is Piperacillin (Generation 4) Most narrow spectrum is Generation 1. |
| Which gen has resistance to Beta lactamase enzymes? | First generation. Methicillin |
| What do you know about Ampicillin/Sulbactam? Whats the brand name? | Ampicillin is second gen. Sulbactam is really cool. It inhibits enzymes that can destroy penicillin. Use them together and you have a really potent drug called Unasyn. |
| Explain the general qualities of Cephalosporins? | Cephalosporins are used in people allergic to penicillins but there's a 30 percent crossover risk, so you only try them on people with mild allergies to penicillin. 4 generations. Use when bacteria are peniclln-resistant. |
| When do you use aminoglycosides? Are they for gram pos or neg? Whats the MOA? | Antibiotics. Bactericidal. Not absorbed by Gi so use before intestinal surgery or for tough UTIs. usually reserved for serious gram neg bacilli nosocomial infections. Gram neg. Attach to ribosomes. |
| What should your patient avoid when taking amino glycosides? | Pregnancy. May cause fetal harm and deafness. Category D. possess peripheral NeuroMusc activity. careful. increased ototoxic effect with diuretics. Can be nephrotoxic. Careful with other nephrotox drugs like cephalosporins. |
| What is tobramycin? | aminoglycoside. powerful against serious gram neg infections. (nosocomial)DONT CONFUSE TOBY WITH THE MACROLIDES DESPITE SAME ENDING. |
| What is neomycin? | topical aminoglycoside. use for skin and ocular infections. |
| Side effects of aminoglycosides. | NVD. Nephrotoxicity! Ototoxicity presents as tinnitus. |
| Tetracyclines. When are they indicated? Gram pos or gram neg? What is the spectrum? | Use in Gram pos and neg. Cholera. Rocky mountain spotted fever. Lyme. They are occasional alternatives to Penicilins for gram neg infections. Broad spectrum. |
| What should you tell patient about diet with tetracyclines? | No calcium rich food. No milk/ antiacids. Take One hour before or several hours after meals. |
| Are tetracyclines bacteristatic/cidal? How do they work? | Static. They interfere with protein synthesis. |
| What is ceftriaxone | third gen cephalosporin |
| What is ticarcillin | Third gen penicillin. |
| What is Ciprofloxacin | Fluroquinolone |
| What is Azithromycin | Macrolide |
| Antigungals. What are the drug types? | Amphotercin B and Azoles including difluconazole, myconazole, afluconazole, ketoconazole |
| When to use amphotercin B. | OJ. for invasive fungal infections (aspergillis, candidiasis, Cryptococcus, histoplasmosis, blastomycosis) |
| Side effects of fungal drugs | Hard on liver and kidneys. thrombophlebitis. ataxia. |
| Contrast Herpes simplex I, II, Herpes Zoster. | I-fever blisters, mouth sores II-genital Zoster-Chicken pox, shingles. |
| Nystatin class | antifungal-candidiasis. pretty safe drug. |
| HIV stages | acute illness followed by clinical latency. Finally patients develop opportunistic infections. These Clinical symtoms (including tumors)indicate progression to AIDS. |
| How many cases of AIDS a year? | 4.3 million new cases. |
| How do antiviral drugs work? | Block viral DNA before or after viral DNA enters cell. |
| What characterizes AIDS? | Fast replication of virus. Asymptomatic. Immune sys deteriorates especially CD4s |
Created by:
manka