PHARMACOLOGY I – BLOCK 4:
- Anti-Thyroid Drugs
- Adrenal Steroids
- Female Gonadal Hormone Drugs
- Androgen Drugs
- Bone Drugs
- Anti-Thrombotic Drugs
- Hyperlipoproteinemia Drugs
- Antimicrobials – General Principles
- Antimicrobials – Cell Wall Inhibitors
- Antimicrobials – Ribosomally-Active Antibiotics
- Antimicrobials – Sulfonamides and Quinolones
- Antimicrobials – Anti-Mycobacterial Drugs
- Antimicrobials – Anti-Viral Drugs
- Antimicrobials – Anti-HIV Drugs
- Antimicrobials – Anti-Fungal Drugs
- Antimicrobials – Anti-Malarial Drugs
- Antimicrobials – Anti-Parasitic Drugs
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Q: What happens to the TSH level in hypothyroidism?
A: It increases. You don’t have much T3/T4, and so you can’t negatively feedback on the TRH and TSH release. You therefore make more TSH.
Q: What condition increases adrenergic receptor synthesis?
Q: What condition decreases deep tendon reflex?
A: Hypothyroidism. This is Pathognomonic!!
Q: What are the BBB of Thyroid Hormones?
A: Brain, Basal Metabolic Rate, Beta Receptor Synthesis
Q: 5′ monodeiodinase converts Thyroxine to what?
A: 3,5,3′ Triiodothyronine (removes Iodide at outer ring) ACTIVE T3.
5-monodeiodinase converts it to 3,3′,5′ Triiodothyronine (rT3) (removes inner ring) INACTIVE rT3.
Q: What four classes of drugs can treat hyperthyroidism?
A: Thioamides, Potassium Iodide, Radioactive Iodide, Anion Inhibitors
Q: What class of drugs inhibit peroxidase?
Q: What Thioamide inhibit both peroxidase and prevent peripheral conversion of T4 to T3?
A: Propylthiouracil (PTU)
Q: What enzyme does organification of Iodine?
Q: What Thioamide just inhibits peroxidase, and nothing else?
Q: What’s the best drug to treat hyperthyroid patients who are pregnant or breastfeeding?
A: Propylthiouracil (PTU)
Q: Which thioamide is long-acting?
Q: How long does it take for thioamides to be effective?
A: 4 weeks, because you gotta wait for the T4/T3 to deplete
Q: What are the adverse effects of thioamides?
A: AGRANULOCYTOSIS (leading to infections). Also allergic reactions — hepatitis, maculopapular rash, arthralgia, vasculitis.
Q: What is the pros and cons of thioamides?
A: Pros — doesn’t destroy gland (vs. radioactive iodide). Bad — only works for 2-3 yrs.
Q: What hyperthyroid drug takes only 2-5 days to work?
A: Potassium Iodide (Lugol’s Solution)
Q: What drug inhibits proteolysis (release of T3/T4 from thyroglobulin) via Wolff Chaikoff Effect?
A: Potassium Iodide. When you intake a lot of Iodide, you get negative feedback and inhibit T3/T4 release.
Q: What drug can you use to decrease the size and vascularity of the thyroid gland in preparation of surgery?
A: Thioamies, Potassium Iodide.
Q: What drug do you use to prevent thyroid from absorbing radioactive iodide, like from radioactive poisoning?
A: Potassium Iodide, because it saturates the thyroid so other types of iodide can’t get in.
Q: What drug can cause fetal goiter when used during pregnancy?
A: Potassium Iodide.
Q: What drug can cause salivary inflammation?
A: Potassium Iodide.
Q: What drug can cause thyrotoxicosis due to Jod Basedow Effect?
A: Potassium Iodide, Anion Inhibitors (Perchlorate, Pertechnetate, Thiocyanate).
Q: What drug do you take as an alternative to surgery for Thyroid cancer?
A: Radioactive Iodide 131. You also take it to get rid of any microscopic traces of the cancer after surgery.
Q: What drug can destroy the fetus thyroid if you take it during pregnancy?
A: Radioactive Iodide 131, because it can cross the placenta because it is lipid soluble. So you can take it per os as well.
Q: What happens after you take Radioactive Iodide 131?
A: You become permanently hypothyroid, since you don’t have a thyroid anymore. You need to take Hormone Replacement Therapy for the rest of your life, which is easier to deal with than hyperthyroidism.
Q: How long does it take Radioactive Iodide 131 to destroy the thyroid?
A: 1-3 months
Q: What class of drugs competitively block iodine uptake into follicular cells in thyroid glands?
A: Anion Inhibitors (the anion is the iodide)
Q: What are the anion inhibitors?
A: Perchlorate (ClO4-), Pertechnetate, Thiocyanate (SCN-)
Q: What class of anti-thyroid drugs give you aplastic anemia?
A: Anion Inhibitors
Q: What is the drug of choice for Myxedema Coma?
A: Levothyroxine (T4) – because it converts to the active T3 when needed. It’s cheap,stable (since it’s inactive), and has a loooong halflife (vs. active T3).
Q: What Myxedema Coma drug can give you cardiotoxicity like MI, Arrhythmia, and Angina and therefore contraindicated in cardiac patients?
A: Liothyronine (T3)
Q: When would you use T3?
A: Only during EMERGENCIES, in extreme cases of myxedema coma when you need to replenish T3 quickly. T4 you have to wait for it to convert to T3.
Q: What’s the mortality rate for Myxedema Coma?
A: 50%. It’s not really a coma, but you can get unconscious. It is basically extreme hypothyroidism.
Q: What combination of drugs do you use to treat Thyroid Storm?
A: High-Dose Propylthiouracil (which remember inhibits peroxidase and inhibits peripheral T4 to T3 conversion), Propranolol (to prevent MI), and Potassium Iodide.
Q: What type of steroid increases glucose in blood (by increasing gluconeogenesis and decrease glucose uptake in muscle and fat), increase glycogen storage in liver, decrease immunity and inflammation, decrease calcium absorption in GI, and increase gastric acid/pepsin?
Q: What adrenal steroid can give you myopathy?
A: Glucocorticoids, because it catabolizes muscle protein.
Q: What adrenal steroid increase surfactant in fetal lungs (and therefore matures it)?
Q: How do you prevent adrenal crisis (severe adrenal insufficiency due to the decrease in the number of adrenal steroid receptors you have)?
A: By tapering off the dosage of the drug, instead of suddenly withdrawing it.
Q: What does POMC break down into?
A: ACTH, gamma-MSH, and beta-Lipotropin.
Q: What does ACTH breakdown into?
A: CLIP and alpha-MSH (main MSH for skin pigmentation)
Q: What are the layers of the Adrenal cortex and what do they produce?
A: ATII, K+ stimulate Zona Glomerulosa to produce Aldosterone (Mineralocorticoids) – because only zona glomerulosa have 18-hydroxylase
ACTH stimulate Zona Fasciculata to produce Cortisol (Glucocorticoids)
ACTH stimulate Zona Reticularis to produce Androgens
Q: What steroid increase lipocortin, which inhibits phospholipase A2, which decreases Prostaglandin, and therefore decrease inflammation?
Q: What ACTH analogue is used to diagnose CAH and Adrenal Insufficiency (Addison’s)?
A: Cosyntropin. It stimulates Cholesterol Desmolase (Cytochrome P450 SCC), increasing 17-OH-Progesterone if you have CAH.
Q: What time of day is Cortisol the highest?
A: In the morning. Lowest at night when sleeping, just like the Sympathetic Nervous System. So you give doses in the mornings to simulate natural schedule.
Q: If you have increased CRH, increased ACTH, and increased Cortisol, you know the tumor is where?
A: Hypothalamus –> secrete too much CRH.
Q: If you have decreased CRH, increased ACTH, and increased Cortisol, you know the tumor is where?
A: Pituitary –> secrete too much ACTH.
Q: If you have decreased CRH, decreased ACTH, and increased Cortisol, you know the tumor is where?
A: Adrenal Gland –> secrete too much Cortisol.
Q: If you have increased CRH, increased ACTH, and decreased Cortisol, where is the impairment?
A: Adrenal Gland –> can’t secrete Cortisol — Addison Disease, CAH –> more ACTH made to “compensate” for the decreased Cortisol –> ACTH breaks down to alpha-MSA –> increased skin pigmentation.
Q: If you have decreased CRH, decreased ACTH, and decreased Cortisol, where is the impairment?
A: Hypothalamus or Pituitary — Sheehan Syndrome (Hypopituitary during pregnancy)
Q: Which mineralocorticoid is short-acting?
Q: Which mineralocorticoid is long-acting and therefore better for treating Addison’s Disease?
Q: Which glucocorticoid is short-acting and weak?
A: Cortisol (natural) or Hydrocortisone (synthetic cortisol)
Q: Which glucocorticoid has equal mineralocorticoid and glucocorticoid activity?
A: Cortisol — so does both salt retention and increase metabolism/decrease immunity/decrease inflammation/increase gastric acid/decrease calcium absorption
Q: Which glucocorticoids are intermediate-acting?
A: Prednisone (or prednisolone) and Triamcinolone
Q: Which glucocorticoid has some mineralocorticoid activity and therefore may cause some edema?
Q: Which glucocorticoids are long-acting and most active?
A: Betamethasone and Dexamethasone.
Q: Which glucocorticoids are used to mature fetal lungs?
A: Betamethasone and Dexamethasone, because they can penetrate the fetus.
Q: What does a Low-Dose Dexamethasone Suppression Test test for?
A: Tests for Cushing’s Disease, Adrenal Tumor, Ectopic Secretions. If you give Dexamethasone (a long-acting glucocorticoid), and there is no negative feedback, then you know something in your body is secreting all that extra cortisol.
Q: Once you establish you got either Cushing’s Disease, Adrenal Tumor, or Ectopic Secretion, what does doing a High-Dose Dexamethasone Suppression Test test for?
A: If giving a high dose Dexamethasone suppresses your cortisol levels to normal levels, then you most likely have Cushing’s Disease. If there is no suppression, then measure the basal ACTH. If ACTH level stays the same, then you got ectopic ACTH Tumor. If you have decreased ACTH then you most likely have an adrenal tumor (because of negative feedback).
Q: What inhaled Glucocorticoids are used to treat Asthma because it is restricted to the bronchioles (since it is inhaled)?
A: Beclomethasone, Budesonide, Flunisolide, Fluticasone.
Q: What are the adverse effects of Glucocorticoid drugs if you use over 2 weeks?
A: Adrenal Suppression. You can also get Cushingoid Syndrome and Osteoporosis.
Q: What drug should you NOT use if you have Hypertension, Peptic Ulcer, Infections, and Diabetes?
A: Glucocorticoids. Because remember, Glucocorticoids increase gastric acid, decrease immunity, and DECREASE SENSITIVITY TO INSULIN (and increases glucose in blood).
Q: What drugs do you use to treat Cushing Syndrome (before the main treatment of surgery, of course)?
A: Adrenal Steroid Synthesis Inhibitors — Aminoglutethimide, Ketoconazole, Metyrapone, and Mitotane.
Q: Which drug blocks desmolase (blocking the conversion of cholesterol –> pregnenolone) and aromatase (blocking androgen –> Estrogen)?
A: Aminoglutethimide… therefore it can be used to treat both Cushing’s Syndrome and Breast Cancer.
Q: Which drug blocks desmolase and 17-20 lyases?
Q: Which drug inhibits adrenal steroid synthesis at low doses but both adrenal and gonadal synthesis at high doses?
Q: Which drug blocks 11-beta hydroxylation, which is the final step in cortisol synthesis?
A: Metyrapone. Because it blocks this enzyme, 11-Deoxycortisol accumulates, which has mineralocorticoid action –> AE: water and sodium retention
Q: What drug destroys the adrenal cortex, and therefore can be used to treat adrenal carcinoma?
A: Mitotane — not used anymore because it can destroy the adrenal cortex, and carcinomas can be surgically removed.
Q: Which drug blocks progesterone receptors and blocks glucocorticoids at high dose and therefore used to treat adrenal carcinoma?
Q: Which drug blocks both aldosterone and androgen?
Q: Which drug treats Primary Hyperaldosteronism (hypersecretion of cortisol from adrenal gland) as well as Hirsutism?
A: Spironolactone — used for both of these because blocks both aldosterone and androgen.
Q: Which drug is an aldosterone antagonist only?
A: Eplerenone — used as adjunct for chronic heart failure.
Q: What are the natural Estrogen drugs?
A: Conjugated Equine Eestrogen
Q: What are the synthetic steroidal estrogens?
A: Ethinyl Estradiol, Mestranol
Q: What are the synthetic non-steroidal estrogens?
A: Diethylstilbestrol (DES), Dienestrol
Q: What estrogen drug gives you vaginal adenocarcinoma in your female offsprings, and therefore taken off the market?
A: Diethylstilbestrol (DES)
Q: What are the five actions of Estrogen?
A: 1. Clotting: increase factors 2,7,9,10, Fibrinogen. decrease antithrombin (AE: Pulmonary Embolism)
2. Hyperplasia of endometrium –> AE: Endometrial/Breast cancer
3. Decrease LDL. Increase HDL
4. Decrease Bone Resorption –> Rx Osteoporosis
5. Sensitizes myometrium to oxytocin before labor
Q: What are the adverse effects of Estrogen?
A: Gall stones, Pulmonary Embolism, and Endometrial/Breast Cancer
Q: What are the three SERMs?
A: Clomiphene, Tamoxifen, Raloxifene
Q: Which SERM inhibits the estrogen receptors in the hypothalamus and pituitary rather than in the gonads and therefore inhibit negative feedback by estrogen on FSH/LH production (increasing FSH/LH), and therefore used to treat Infertility?
Q: Which SERM gives you multiple pregnancies as an adverse effect?
Q: Which SERM is an agonist in bone and lipid, antagonist in breast, and partial agonist in endometrium?
A: Tamoxifen. Because it is a partial agonist in endometrium, it has risk of endometrial cancer.
Q: Which SERM is an agonist in bone and lipid, antagonist in breast AND endometrium, and therefore has no risk of endometrial cancer?
Q: Which drug can you use to treat breast cancer?
A: Tamoxifen and Raloxifene
Q: Which SERM can be used to treat both breast cancer and osteoporosis in post-menopausal women?
Q: Which SERM has AE of blood clot?
Q: Which drugs inhibit aromatase, and therefore can’t convert testosterone to estrogen?
A: Anastrazole, Letrozole, Exemestane
Q: Which drug can you use to treat breast cancer if tamoxifen doesn’t work?
A: aromatase inhibitors — anastrozole, letrozole, exemestane
Q: What type of drug do you use as contraceptives for patients who are at risk of thrombosis (and therefore shouldn’t use estrogen)?
A: Progestins (Progesterone only hormonal contraceptives)
Q: What type of drug proliferates mammary glands and therefore used if you want to keep breastfeeding?
Q: What type of drug decrease endometrial proliferation and therefore used alongside estrogen (which causes endometrial hyperplasia) in contraceptives?
Q: What drug puts a cap on estrogen’s effects, downregulating estrogen receptors and increasing estrogen metabolism, and therefore good in hormone replacement therapy?
Q: Which drug has adverse effects of acne, hirsutism, increased temperature, PMS, increased insulin levels, and increased fat?
A: Progestins (EXCEPT Desogestrel, which has no acne or hirsutism, and therefore preferred)
Q: What drug is a progesterone receptor partial agonist and a glucocorticoid receptor antagonist (at high dose)?
A: Mifepristone — used to terminate pregnancy within 49 days after intercourse, and treats Cushing Syndrome and Adrenal Carcinoma!!
Q: What drug do you take to induce abortion (when egg already implanted) 49 days after intercourse?
A: Mifepristone, which is an anti-progestin drug. Unlike progestin, which is used to prevent pregnancy before implantation of egg, mifepriston is an ANTI-progestin, which would induce menstruation, getting rid of any eggs after they are implanted.
Q: What are the first generation Progestins?
A: Norethindrone, Ethynodiol diacetate
Q: What are the second generation Progestins?
A: Levonorgestrel, Norgestrel
Q: What are the third generation Progestins?
A: Desogestrel, Norgestimate
Q: What is the fourth generation Progestin?
Q: Which progestin has some anti-mineralocorticoid activity, and therefore decreases water retention?
A: Drospirenone, fourth generation progestin.
Q: Which Progestin does not cause hirsutism or acne that is typical of progestins?
Q: Which Progestin-only contraceptive is given orally?
Q: Which Progestin-only contraceptive is given via skin implant and IUD, and therefore lasts for a long time (5 yrs)?
Q: Which Progestin-only contraceptive is given via injection and last for three months?
Q: Which post-coital contraceptive do you use within 12 hrs after sex?
A: Levonorgestrel (which in this case is taken orally rather than via skin graph or intra-uterine device)
Q: What class of drugs can cause cholestatic jaundice?
Q: What are the androgen drugs you give intramuscularly?
A: Testosterone Cypionate, Testosterone Enanthate
Q: What oral androgen drugs give you hepatic toxicity?
Q: Which oral androgen is safe?
A: Testosterone Undecanoate
Q: Which androgen drug have anti-estrogen activity and therefore can be used to treat Endometriosis and Fibrocystic Breast Disease?
Q: Which androgen drug increase C-1 Esterase inhibitor (in complement) and therefore can treat Hereditary Angioedema?
Q: Which anabolic agent has 1:1 androgen-to-anabolic activity?
Q: Which anabolic agent has 1:2 androgen-to-anabolic activity?
Q: Which anabolic agent has 1:3 androgen-to-anabolic activity?
A: Oxymethalone, Nandrolone
Q: Which anabolic agent has 1:7 androgen-to-anabolic activity?
Q: Which anabolic androgen drug doesn’t get converted to estrogen?
Q: Which anatbolic androgen drug can treat hereditary angioedema and anemia?
Q: Which androgen receptor antagonist is non-steroidal and therefore does NOT suppress gonadotropin and therefore can treat prostate cancer without the unwanted side effects of decreased testosterone?
A: Bicalutamide, Flutamide
Q: Which androgen receptor antagonist is steroidal and therefore SUPPRESS gonadotropin/testosterone production, and therefore good to treat Hirsutism?
A: Cyproterone acetate.
Q: What drugs are GnRH agonists used to treat prostate cancer via the negative feedback effect it has on decreasing testosterone levels?
A: Goserelin, Buserelin — initially there is an increase in FSH and LH levels due to the “flare effect” but eventually downregulated.
Q: What enzyme converts Testosterone to DHT, used in external virilization, prostate development, and pubertal maturation?
Q: Which drug inhibits 5-alpha-reductase II and therefore used to treat Benign Prostate Hypertrophy, but gives you the adverse effects of erectile dysfunction and gynecomastia?
Q: What do you get if you are a woman and you have increased LH or insulin, leading to too much androgen, leading to decreased menstruation and ovulation + hirsutism + infertility?
A: Polycystic Ovarian disease
Q: What drugs can you use to treat Polycystic Ovarian Disease by lowering insulin?
A: Pioglitazone, Rosiglitazone (both of which are Thiazolidenediones) as well as Metformin (which is a Biguanide)
Q: What drugs can you use to restore fertility in patients with Polycystic Ovarian Disease?
A: Clomiphene Citrate or FSH
Q: What drugs can you use to treat the Hirsutism and Acne found in Polycystic Ovarian disease?
A: Anti-androgens like spironolactone (which remember is antagonist for androgens as well as aldosterone)
Q: Which drugs can you use to restore menstruation and prevent endometrial hyperplasia in Polycystic Ovarian disease?
A: Oral contraceptives
Q: Normal bone density has a T-score of what?
A: -1 to +1
Q: Osteopenia has a T-score of what?
A: -1 to -2
Q: Osteoporosis has a T-score of what?
A: less than -2.5
Q: What increases Calcium and decreases phosphate in the plasma?
Q: PTH works mainly in what organ and Vitamin D works mainly in what organ?
A: PTH works in kidneys. Vitamin D works in intestines.
Q: What drug is a recombinant PTH and makes use of PTH’s property of increasing bone formation at low intermittent doses?
Q: What increases calcium and phosphate in plasma but doesnt do it by destroying bone?
A: Vitamin D
Q: What decreases PTH secretion, increases immunity, and has anti-cancer properties?
A: Vitamin D.. it’s funny that PTH increases Vitamin D but Vitamin D decreases PTH.
Q: What happens with excessive dose of Vitamin D?
A: you actually get bone resorption.
Q: Which drug can treat Osteoporosis, Osteomalacia (soft bones due to decreased calcium and phosphate), Rickets (which is osteomalacia in kids), and Psoriasis?
A: Vitamin D
Q: What are the three ways to treat Psoriasis?
A: From least to most toxic/effect:
1. Topical (Corticosteroids, Calcipotriol, Anthralin, Coal Tar)
2. Photo (UV A, UV B)
3. Systemic (Biologics, Cyclosporin, Methotrexate, Retinoids) — don’t use because it’s too toxic!!
Q: What class of drugs attach and become part of the bone and can’t be hydrolyzed by osteoclasts because it has Phos-C-Phos rather than the Phos-O-Phos structure of natural bone?
A: Bisphosphonates — Alendronate, Risedronate, Ibandronate, Pamidronate, Zoledronate
Q: What drug decreases bone pain?
Q: What drug blocks FPP Synthase (which converts Mevalonate –> Farnesyl PPi) and so you can’t prenylate membranes or glycosylate proteins and therefore inhibit osteoclast attachment to bone?
Q: What drug is used to treat Osteoporosis, Paget’s Disease of Bone, and Hypercalcemia of Malignancy (which is due to proliferation of osteoclasts)?
A: Bisphosphonates — because it blocks FPP Synthase, which inhibit osteoclast from attaching to bone. So even if you get a proliferation of osteoclasts, they can’t attach to bone.
Q: What drugs can treat Paget’s Disease of Bone?
A: Bisphosphonates and Calcitonin
Q: What class of bone drugs cause Esophagitis and GI Distress, and therefore you tell patient to take lots of water with it and don’t lay down?
Q: What type of drug inhibits IL-1 and TNF and therefore decrease osteoclast differentiation and activity, and therefore used to prevent osteoporosis in post-menopausal women?
Q: What SERM is used to prevent osteoporosis in post-menopausal women?
Q: What hormone is released from parafollicular cells in thyroid when plasma calcium increases and decreases BOTH calcium and phosphate levels in the plasma?
A Calcitonin (“tones” down calcium and phosphate in blood)
Q: What type of calcitonin is 100x more potent than regular human calcitonin?
A: Salmon calcitonin (Miacalcin)
Q: What drug treats both Paget’s Disease of Bone, prevents Osteoporosis in post-menopausal women, and hypercalcemia (though not first choice)?
Q: What drug stimulates new bone formation, increase bone crystal size, and used to prevent dental caries?
Q: What drug is a human monoclonal antibody that inhibits RANKL (found on osteoblasts to activate osteoclast maturation), and therefore osteoclasts can’t mature, and therefore used to treat osteoporosis?
Q: What are the first and second line of treatments for osteoporosis?
A: First line — Bisphosphonates, Raloxifene
Second line — Teriperatide, Calcitonin (but only use these if patient can’t use bisphosphonates due to Esophagitis, GI Distress etc.)
Q: What class of antithrombotic drugs work on preventing venous clots (from DVT, Pulmonary Embolism)(red thrombus) from blood stasis, immobilization?
A: Anti-coagulant drugs (the largest group)
Q: What class of antithrombotic drugs dissolve existing clots?
A: Fibrinolytic drugs
Q: What class of antithrombotic drugs work on preventing arterial clots (like from Myocardial Infarction) (white thrombus) from platelet aggregation in vessel injury?
A: Anti-platelet drugs
Q: What type of drug do you give to prevent clotting if patient is immobilized after surgery?
A: Anticoagulant drugs, which work on venous clots (remember blood more immobile here).
Q: What is the strongest organic acid in the body (because it has a sulfate group)?
Q: What drug enhances antithrombin, which binds and inhibits Factors 2 (thrombin), 9, 10, and 11, especially Factor 10?
Q: What is the anticoagulant of choice for pregnancy?
A: Heparin, becuase it is ionized and can’t cross placenta. It can’t be taken orally as well for the same reason.
Q: What drug has risk of thrombocytopenia (along with the usual, like bleeding, osteoporosis)?
A: Heparin — known has HIT — heparin-induced thrombocytopenia
Q: What test do you use to monitor heparin levels so you don’t get Heparin-Induced Thrombocytopenia (HIT)?
A: aPTT (Active Partial Prothrombin Time, which measures efficacy of intrinsic + common pathway).
Q: Why don’t you give anticoagulants intramuscularly?
A: Because your muscles have a lot of vessels and therefore if you puncture through here and prevent clotting, you’ll get a hematoma!!
Q: What do you give to treat Heparin overdose (i.e. person bleeding profusely)?
A: Protamine Sulfate, which is a strong base, so it neutralizes heparin, which is a strong acid.
Q: What type of anticoagulant drugs SELECTIVELY inhibit Factor 10a?
A: Low Molecular Weight Heparins (Enoxaparin, Dalteparin, Tinzaparin)
Q: What type of anticoagulant drug has better bioavailability, longer-lasting, and lower risk of HIT than heparin, and doesn’t require aPTT test to monitor?
A: Low Molecular Weight Heparin.
Q: You give heparin via what and you give LMWH via what?
A: Heparin — give via IV
LMWH — give via Subcu
Q: What drug acts just like LMWH’s, inhibiting 10a, but is a different type of molecular (a synthetic pentasaccharide) and has lower risk of HIT than LMWH?
Q: What drugs inhibit thrombin directly and used when patients can’t use heparin (like if they have HIT or something)?
A: Direct Thrombin Inhibitors — Hirudin, Argatroban, Lepirudin
Q: What anticoagulant drug is derived from leeches?
A: Hirudin — that’s how they suck your blood without clotting!
Q: What drug is similar to LMWH in that it selectively inhibits Factor 10a but is made up of Heparan Sulfate + Dermatan Sulfate + Chondroitin Sulfate (all GAG’s), but it’s not used anymore because it gives you stroke?
Q: What are the three Vitamin K Antagonists?
A: Warfarin, Dicumoral, and Phenindione
Q: What factors need Vitamin K to be synthesized?
A: Factors 2, 7, 9, and 10 AND Protein C (which is actually an anticoagulant)!!!
Q: Why is there an initial transient clotting risk if you use Vitamin K Antagonist?
A: Because Protein C in liver is depleted before the clotting factors. So there’s a short period of time after you take the drugs where you can’t prevent clots and you still have the clotting factors. Therefore you treat concurrently with heparin initially for 3-5 days to prevent these risks.
Q: What drug inhibits Vitamin K Reductase, which normally converts inactive oxidized Vitamin K to active hydroquinone (reduced Vitamin K)?
Q: What adverse effects is caused by the transient initial increase in thrombi in warfarin use?
A: Skin necrosis, purple toe.
Q: What anticoagulant drug is lipid-soluble and therefore you can take orally but because of the same reason it can cross placenta and cause fetal warfarin syndrome?
Q: What values do you test for to monitor bleeding risks (measures extrinsic pathway)?
A: PT (Prothrombin Time) or INR (International Normalized Ratio)
Q: What do you give to treat Warfarin overdoses?
A: Vitamin K (more specifically K1 aka “Phytonadione”). Also give fresh frozen plasma if there is severe hemorrhage)
Q: What class of anti-thrombotic drugs activate plasminogen to become plasmin, which breaks down fibrin (which connect platelets together via GPIIb/IIIa)?
A: Fibrinolytic Drugs — Streptokinase, Anistreplase, Urokinase, Alteplase, Reteplase, Tenecteplase (“USA ART”)
Q: What fibrinolytic drugs are non-selective plasmin activators?
A: Streptokinase, Anistreplase, and Urokinase (“USA”)
Q: What fibrinolytic drugs are selective plasmin activators (recombinant tissue plasmin activators), meaning that they bind specifically to clots and then activate the plasmin?
A: Alteplase, Reteplase, and Tenecteplase (“ART”)
Q: What fibrinolytic drugs are derived from bacteria and therefore antigenic?
A: Streptokinase, Anistreplase
Q: What fibrinolytic drugs are derived from human sources and therefore NOT antigenic and less risk for immune reaction?
Q: What are the two major anti-fibrinolytic drugs, used to prevent activation of plasmin, preventing menstrual and post-delivery bleeding?
A: Aminocaproic Acid, Tranexamic Acid — increases clotting, decreases bleeding.
Q: What class of Anti-platelet drugs block ADP receptors on platelets?
A: Thienopyridines — Ticlopidine, Clopidogrel, and Prasugrel.
Q: What anti-platelet drug causes neutropenia and thrombocytopenia and therefore not used anymore?
Q: What is the best anti-platelet drugs for people who can’t take aspirin (because they have GI bleeding or peptic ulcers)?
Q: What anti-platelet drug blocks COX, and therefore prevents synthesis of TXA2 (thromboxane, which CAUSES clotting) but also PGI2 (prostacyclin, which PREVENTS clotting) at high doses?
A: Aspirin. Give at low doses to spare the PGI2 needed to prevent clotting.
Q: What anti-platelet drugs are PDE Inhibitors, preventing the breakdown of cAMP (which inhibits platelet activation). Your cAMP increases, and so you inhibit platelet aggregation even more.
A: Dipyridamole, Cilastazol
Q: Along with aspirin, what drug is used to prevent thromboembolism in prosthetic hearts?
A: PDE Inhibitors — Dipyridamole, Cilastazol.
Q: What lipoprotein carries triglycerides from GI to tissue (exogenous pathway)?
A: Chylomicrons — therefore has mainly triglycerides
Q: What lipoprotein carries triglycerides from liver to tissue (endogenous pathway)?
A: VLDL — therefore mainly has triglycerides
Q: What lipoprotein carries cholesterol to cells?
A: LDL — therefore mainly has cholesterol.
Q: What lipoprotein does reverse transport of cholesterol to liver?
A: HDL — therefore it reduces cholesterol in blood — lotsa proteins in there.
Q: What are the five main types of hyperlipoproteinemia drugs?
A: Resins, Statins, Fibrates, Nicotinic Acid (niacin, Vit B3), and Ezetimibe. Resins and Ezetimibe are used as adjuncts while the other ones are main drugs.
Q: What two major adverse effects do Statins, Fibrates, and Nicotinic Acid have in common?
A: Hepatotoxicity and Rhabdomyolysis — the lysed muscle tissue can clog up kidney and cause kidney failure. Monitor the hepatotoxicity with liver function tests, and monitor for any increase in CK levels in the blood to detect rhabdomyolysis. If the patient has muscle pains, STOP THE TREATMENT!!
Q: With what class of drugs do you have to watch out for inability to absorb Vitamins A,D,E,K?
A: Resins — because they remove bile salts from your system, which are needed to carry vitamin ADEK into your body.
Q: What hyperlipoproteinemia drugs bind bile salts, and increase their fecal excretion and causes liver to compensate by converting cholesterol to bile and therefore decreasing the overall cholesterol level in your blood?
A: Resins — Cholestyramine and Colestipol
Q: What drug causes an increase in HMG CoA reductase (rate-limiting enzyme in cholesterol synthesis) and therefore increases VLDL and therefore increases triglyceride levels as an adverse effect?
A: Resin (Cholestyramine and Colestipol) — therefore not good as a long-term treatment
Q: What drug decreases cholesterol but increases triglyceride levels?
A: Resins — Cholestyramine, Colestipol
Q: What class of drug do you need to treat with HMG CoA Reductase blockers in order to prevent the adverse effects of increased triglycerides (which is at the expense of decreased cholesterol levels that you want)?
A: Resins — Cholestyramine and Colestipol
Q: What class of hyperlipoproteinemia drugs are contraindicated in patients who have hypertriglyceridemia?
A: Resins — Cholestyramine and Colestipol
Q: What class of hyperlipoproteinemia drug is also used for treating obstructive jaundice because it removes bile salts from your body?
A: Resins — Cholestyramine and Colestipol
Q: What class of drugs inhibit HMG CoA Reductase (rate limiting enzyme in cholesterol synthesis, can’t make mevalonic acid) and also increases LDL receptors in liver, causing decreased cholesterol in the blood?
A: Statins — Lovastatin, Simvastatin, Atorvastatin, Rosuvastatin
Q: What class of hyperlipoproteinemia drug is contraindicated in pregnancy because it prevents the synthesis of cholesterol, and therefore prevents the synthesis of progesterone?
A: Statins — Lovastatin, Simvastatin, Atorvastatin, Rosuvastatin
Q: What class of hyperlipoproteinemia drugs also have cardioprotective properties (increase in NO leading to vasodilation, stabilize plaques, Antioxidant properties by increasing paraoxonase, Anticoagulant properties)?
A: Statins — Lovastatin, Simvastatin, Atorvastatin, Rosuvastatin
Q: What drugs or substances should you NOT use with statins?
A: Don’t use with fibrates or niacin, because they all have the same adverse effects. Also don’t use with substances/drugs that inhibit CYP3A4 (i.e. grapefruit juice), which is needed to metabolize statins.
Q: Which statin drug has a very long half-life and therefore can be used anytime of day and also has antioxidant properties?
Q: Which statin drug is known to be very potent?
Q: Which class of hyperlipoproteinemia drugs are PPAR-alpha agonists (increases glucose/lipid metabolism) and therefore decreases triglyceride levels in your body?
A: Fibrates — Fenofibrate, Gemfibrozil.
Q: Besides the usual hepatotoxicity and rhabdomyolysis, what other adverse effect do fibrates have?
A: Gall stones
Q: What fibrate drug activates lipoprotein lipase, which degrades VLDL (which carries a lot of triglycerides), and therefore decresae triglyceride levels?
Q: What drug is BEST for decreasing triglyceride levels?
Q: What drug is used to treat Type III Hyperlipoproteinemia (aka Dysbetalipoproteinemia, due to ApoE defect causing increased chylomicrons, VLDL, and therefore increased triglycerides)?
Q: Which fibrate drug has less myopathy adverse effects?
Q: What hyperlipoproteinemia drug blocks Adenylyl Cyclase in adipose tissue and therefore decreases free fatty acid production, leading to decreased triglycerides/VLDL and INCREASED HDL?
A: Nicotinic Acid (aka Niacin aka Vitamin B3)
Q: What’s the best treatment to INCREASE HDL?
A: Nicotinic Acid (aka Niacin aka Vitamin B3)!!
Q: What drug has the adverse effect of releasing prostaglandin, causing flushing, itching?
A: Nicotinic Acid.
Q: How do you prevent the itching and flushing adverse effects in nicotinic acid?
A: give aspirin along with the drug. Aspirin blocks COX, so prostaglandin can’t be made.
Q: Which hyperlipoproteinemia drug decreases cholesterol absorption in the GI and increases LDL uptake into the cells, causing an overall lowering of LDL in the plasma?
A: Ezetimibe — use as an adjunct. adverse effect is diarrhea.
Q: What anti-obesity drug inhibits pancreatic lipase (and therefore can give you oily stool as an adverse effect)?
Q: What anti-obesity drug is an SNRI, and therefore can give you MI and stroke, and therefore not used anymore?
Q: What anti-obesity drug decreases your appetite, but can give you depression and suicidal thoughts and therefore not used anymore?
Q: What anti-obesity drug releases norepinephrine only?
Q: What anti-obesity drug releases norepinephrine as well as dopamine?
Q: What is the best way to increase HDL and decrease LDL, more than anything else?
Q: What’s the difference between Prophylactic vs. Empiric vs. Therapeutic Treatment?
A: Prophylaxis = give beforehand to prevent disease. Empiric = give when your patient is at risk of dying and you don’t have time to find out what it is yet. Therapeutic = give when you know what condition the patient has.
Q: Why don’t you typically give bacteriostatic and bacteriocidal drugs together?
A: Because bacteriocidal drugs (like cell-wall inhibitors) require cell division to work. Bacteriostatic drugs stop cell division, making bacteriocidal drugs useless.
Q: What law is it that says drugs need to get to the site of infection?
A: Larry Sutton’s Law: “why do you rob banks?” “because that’s where the money is”
Q: Strep pneumo, H. influenza, Neisseria meningitidis are the top three causes of what?
Q: Strep agalactiae, E. coli, Listeria monocytogenes are the top three causes of what?
A: Neonatal Meningitis
Q: What drug do you give to treat meningitis under 28 days old?
A: Cefotaxime, because has less adverse effects. If over 28 days old, give Ceftriaxone.
Q: How do you calculate therapeutic level?
A: Drug level/MIC (minimal inhibitory concentration)
Q: Why would sub-inhibitory concentration be useful?
A: Because it can enhance host immune defenses, leading to resolution, but only when the host has a strong immunity and not immunocompromised.
Q: What is the name of the effect that states that the more pathogen concentration you have, the more drug concentration you need to resolve?
A: Innoculum Effect
Q: What effect do you see when the drug binds to an organelle or ribosome in the bacteria, leading to continuous killing, even after stopping the dose?
A: Post-Antibiotic Effect — so must give in bolus dosing to give patient the time to recover from the toxicity. i.e. Aminoglycosides
Q: When would you use concentration-dependent drugs?
A: When the drug must enter the organism, like ribosomal drugs. You must give enough so that the drug can enter the cells.
Q: When would you use time-dependent drugs?
A: When the drugs target a certain time period during the cell cycle, like those targeting cell-wall synthesis. You give the drug over a long period of time to ensure that the bacteria will be exposed to the drug at a time when it is dividing.
Q: How do beta-lactam and amikacin work in synergy?
A: Beta-lactams poke holes in the bacterial cell and amikacin enter and bind to the 30s ribosome to do its job.
Q: What two drugs are given together in synergy because they sequentially block the folate pathway?
A: Sulfomethoxazole and Trimethoprim (SMX-TMP or Cotrimoxazole) — SMX blocks dihydropteroate Synthase and TMP blocks dihydrofolate reductase.
Q: What drug is given with penicillin drugs in synergy to block the bacteria’s drug-inactivating enzymes?
A: Clavulanic Acid, Sulbactam, Tazobactam.
Q: In what kind of treatment should you limit to using only a single drug?
A: Prophylaxis, because you want to prevent resistance from forming. On the contrary, yet for the same reason, you would want to give multiple drugs for therapeutic treatment to fully kill the bacteria.
Q: What prophylaxis do you give to prevent rheumatic fever in Group A Strep?
A: Penicillin G
Q: What prophylaxis do you give to prevent Staph aureus or Neisseria meningitidis in patients undergoing CNS shunt surgery?
Q: What prophylaxis do you give to prevent meningococcal meningitis in doctors who may have contact with meningitis patients (like that lady doctor story Dr. Frenkel told in class)?
Q: What prophylaxis do you give to prevent pneumocystis pneumonia (PCP) in HIV patients?
A: TMP-SMX aka “Cotrimoxazole”
Q: Neisseria, Diphtheria, and Group A Strep are the most common causes of what condition?
Q: Staph developed Beta-lactamases, making them resistant to what drug?
Q: Staph mutated penicillin-binding protein (PBP), making them resistant to what drug?
Q: Staph mutated D-ala-D-ala on penicillin-binding protein, making them resistant to what drug?
Q: What kind of bacteria can get beta-lactamase gene via plasmid?
A: gram neg
Q: What kind of beta-lactamases are NOT blocked by clavulanic acid?
A: Extended-Spectrum Beta-Lactamases (ESBLs)
Q: When a bacteria mutates its folic acid pathway, it becomes resistant to what drug?
Q: What drugs is used to block the excretion of penicillin and prolong it’s effects in the body?
Q: What test do you need to do to see if a patient is allergic to penicillin?
A: RAST blood test.
Q: Any drug with sulfa group, like Sulfonamides, penicillin, or cephalosporin could give you what severe allergic reaction in extreme cases?
A: Steven Johnson Syndrome
Q: What is the prophylaxis for rheumatic fever?
A: Penicillin G
Q: What is the drug of choice for treponema pallidum (syphilis)?
Q: What penicillinase-resistant penicillin especially gives you nephrotoxicity and therefore not used anymore?
Q: What penicillin drugs are excreted in bile and therefore useful for treating hepatic abscess and cholangitis?
A: Nafcillin and Ampicillin.
Q: What extended-range penicillins is taken orally only?
A: Amoxicillin. Ampicillin is both parenteral and oral.
Q: What extended-range penicillin is the drug of choice for Listeria (meningitis in neonates)?
Q: What penicillin cannot cross CNS, and therefore cannot be used to treat meningitis?
A: Penicillin G
Q: What extended-range penicillin can be used to treat pseudomonas or mixed intra-abdominal infections but is not the drug of choice?
A: Ticarcillin and Piperacillin.
Q: What cell wall inhibitor drugs can give you disulfiram reaction and bleeding diathesis?
A: Cephalosporins (Cefomandole, Cefoperazone)
Q: What cephalosporins can treat gram positive only and is least permeable to blood brain barrier?
A: First generation cephalosporins — Cefazolin, Cephalexin, Cefadroxil
Q: What cephalosporin drugs are the drug of choice for Gram negative anaerobes (like abdominal infections or obstetrical (PID) where there is no O2?
A: Cefoxitin and Cefotetan — both are second generation cephalosporins
Q: What drugs have no effect on MRSA, Enterococcus, or Listeria?
A: Cephalosporins, Carbapenems (like imipenem, meropenem, ertapenem)
Q: What is the drug of choice for liver abscess and cholecystitis?
A: Cefotaxime (third generation broad spectrum cephalosporin), also used to treat meningitis in neonates under 28 days old.
Q: What is the drug of choice for lyme disease?
A: Ceftriaxone (third generation broad spectrum cephalosporin)
Q: What cephalosporin drug causes biliary obstruction because it is excreted in the biliary tract (and therefore you should infuse over 1-2 hours to prevent cholecystitis)?
Q: What is the drug of choice for pseudomonas?
A: Ceftazidime (“Taz the Tazmanian Devil is a Pseudo-Devil”)
Q: What is the fourth generation cephalosporin?
A: Cefepime, treat Pseudomonas.
Q: What generation of cephalosporins crosses the blood brain barrier, and therefore can penetrate the CNS and treat meningitis?
A: Third generation — Cefotaxime, Ceftriaxone, Ceftazidime, Cefdinir, Cefpodoxime, Cefepime
Q: What bacterial agent would beta-lactamase inhibitors not work against?
A: MRSA, because the method of resistance is due to mutated PBP, not beta-lactamases. It would also not work with any organism with ESBLs, like Gram-neg bacteria with plasmid
Q: What combo drugs are there with clavulanic acid?
A: Clavulanic acid + Amoxicillin (Augmentin). Clavulanic acid + Ticarcillin (Timentin)
Q: What combo drugs are there with Sulbactam?
A: Sulbactam + Ampicillin = Unasyn
Q: What combo drugs are there with Tazobactam?
A: Tazobactam + Piperacillin = Zosyn
Q: What other cell wall inhibitors can you use for empiric therapy for crash patients?
A: Monobactam (Aztreonam) and Carbapenem (Imipenem, Meropenem, Ertapenem).
Q: What is the drug of choice for animal bites?
Q: What drug treats gram-negative aerobes only and is the second drug of choice for pseudomonas?
A: Aztreonam, like aminoglycosides. In contrast, carbapenems are broad spectrum, and good for both gram positive and negative
Q: What drug inhibits the excretion of imipenem, making you require less dose of it, so you can prevent the adverse effects of seizures and renal failure?
Q: What carbapenem can you use to treat UTI, but at the same time can give you renal failure?
Q: What is the BEST carbapenem to use because it goes to the CNS and can use against ESBLs but there is not much supply of it somehow?
Q: What drugs can also be used to fight bacteria with ESBLs like meropenem but doesn’t cross CNS like meropenem?
Q: What cell wall inhibitor is a glucopolypeptide?
Q: What cell wall inhibitor is a lipopeptide?
Q: What cell wall inhibitor irreversibly inhibits synthesis of peptidoglycan (blocks glycation) in cell walls of gram positive organisms?
Q: What drug binds D-ala-D-ala in the PBP of the bacteria, which can be mutated as their mechanism of resistance?
Q: What is the drug of choice for MRSA?
Q: What drug can be used to treat pseudomembranous colitis due to Clostridium dificile (like from Clindamycin use)?
A: You could use vancomycin, BUT metronidazole is used today. We won’t start using vancomycin until the bacteria becomes resistant to metronidazole.
Q: If vancomycin fails to treat VRSA, what’s the next drug you should use?
Q: If Linezolide doesn’t work, what do you use to treat staph aureus?
A: Daptomycin or Tigecycline
Q: What drug can give you renal toxicity because of its renal excretion, Ototoxicity, and Red Man Syndrome?
Q: What is the condition where you get hypertension and facial flushing, after being infused with drug too quickly and too much H2 released?
A: Red Man Syndrome — it is NOT an allergic reaction.
Q: What drug doesn’t actually inhibit the cell wall but the cell membrane of the bacteria, and therefore indirectly inhibit cell wall?
Q: What drug may give you transient muscle weakness or even necrosis, and therefore should be given just 1/day rather than 2/day.
Q: What drugs have disulfiram reaction?
A: Cephalosporins, Metronidazole, and Griseofulvin
Q: What drugs can cause hemolytic anemia in G6PD deficient patients?
A: Sulfonamides, Isoniazid, Primaquine, and Furazolidone
Q: What drugs can cause Kernicterus?
A: Sulfa drugs, Ceftriaxone, Chloramphenicol
Q: What drugs can cause ototoxicity?
A: Aminoglycosides, Vancomycin, Macrolides (but temporary), Loop Diuretics
Q: What drugs can cause Steven Johnson Syndrome?
A: Sulfa drugs, Neviripine, Tipranavir, Fosamprenavir, Darunavir
Q: What drugs can block Neuromuscular Junction?
A: Aminoglycosides, Macrolides, Pyrantel Pamoate.
Q: What drugs can cause nephrotoxicity?
A: Methicillin, Imipenem, Vancomycin, Aminoglycosides, because of renal excretion!
Q: What drugs can cause osteotoxicity?
A: Tetracyclines, Tigecyclines (because it is calcium chelator)
Q: What drugs are bad for your cartilage and therefore can cause Achilles tendon rupture?
A: Quinolones. “Quinolones can break your bones” except it’s really cartilage. It actually helps bones because it treats osteomyelitis.
Q: What drugs go through biliary excretion?
A: Nafcillin, Ampicillin, Ceftriaxone, Cefoperazone, Tigecycline
Q: What does “Buy AT 30, CCELS at 50” stand for?
A: Aminoglycoside and Tetracyclines bind to 30S ribosomal subunit. Chloramphenicol, Clindamycin, Erythromycin (all macrolides really), Linezolide, Synercid work on 50S ribosomal subunit.
Q: Which of the ribosomally active antibiotics are bacteriocidal?
A: Aminoglycosides and Synercid.
Q: What drug binds P site of 30S and inhibits initiation complex formation?
Q: What drug binds 50S and inhibits initiation complex formation?
Q: What drug binds A site of 30S and inhibits amino acid incorporation?
Q: What drug binds 50S and inhibits amino acid incorporation?
Q: What drug binds 50S and inhibits peptide-bond formation?
Q: What drugs bind 50S and inhibits peptide translocation?
A: Macrolides and Clindamycin.
Q: What drug gives you nephrotoxicity (because of renal excretion), ototoxicity (irreversible, dose-related), NMJ block, and is contraindicated in pregnancy?
A: Aminoglycosides — Kanamycin, Neomycin, Streptomycin, Tobramycin, Netilmycin, Amikacin, and Gentamycin.
Q: What drug must be given at 7.4 pH because it doesn’t kill bacteria well in acidic environment?
A: Aminoglycosides — Kanamycin, Neomycin, Streptomycin, Tobramycin, Netilmycin, Amikacin, and Gentamycin.
Q: Which drug does NOT treat anaerobic bacteria because it requires O2-dependent pumps to get into the cells?
Q: What aminoglycoside gives you Type IV hypersensitivity reaction (contact dermatitis)?
Q: What aminoglycoside is the second drug of choice for TB?
Q: What ribosomally-active drug’s absorption is impaired by dairy, antacids, and iron?
Q: Tetracyclines can treat VACUuM THe BedRoom (VACUM TH BR) — what are they?
A: Vibrio cholera, Acne, Chlamydia, Ureaplasma, Mycoplasma, Tularemia, H. Flu, Borrelia, Rickettsia
Q: Which tetracycline drug should you use to treat VACUM TH BR organisms if the patient has renal failure?
A: Doxycycline, because it is excreted in FECES!! (“Doxycycline = Doodoocycline”)
Q: What drug is osteotoxic (becuase is Ca chelator), gives you pseudotumor cerebri (from increased intracranial pressure), and Jarisch-Herxheimer reaction (when bacteria lysed too much and releases endotoxins)?
Q: What drug is similar to tetracyclines and synergistic with Rifampin?
Q: What drug can treat VRE, Acinebacter, and other gram-negative bacteria but NOT pseudomonas?
Q: What drug has very similar mechanisms and adverse effects as tetracyclines, but does not have any known mechanisms of resistances yet?
Q: What drug is so lipid soluble that it needs to go through enterohepatic circulation in order to be conjugated in the liver to albumin by glucuronosyl transferase so it can become more water-soluble and extreted?
A: Chloramphenicol… but this can prevent bilirubin from binding, which goes to brain, and gives you kernicterus and gray baby syndrome.
Q: What drug causes gray baby syndrome?
Q: What ribosomally active antibiotic inhibits Cytochrome P450?
Q: What ribosomally-active drug is used to treat brain abscesses?
A: Chloramphenicol, becuase it has high lipid solubility, going to the brain easier.
Q: What ribosomally-active drug causes irreversible aplastic anemia, gray baby syndrome (cyanosis, green stool, gray skin), and is considered drug of last choice?
Q: What drug class is made of lactone rings + sugar?
Q: What ribosomally active antibiotic class concentrates in the respiratory secretions and therefore can be used to treat upper respiratory tract infection?
Q: What drug class got resisted by bacteria because the bacteria methylated 23S rRNA with the ERM-beta gene?
Q: What drug class can bind motilin, increasing peristalsis and causing abdominal pain and pyloric stenosis?
Q: What Macrolide causes cholestatic hepatitis and there should not be used in pregnancy (which also causes some cholestasis)?
Q: What macrolide is the drug of choice for Mycobacterium avium intracellulare (MAI) in AIDs patients?
Q: What macrolide concentrates in phagocytic cells?
Q: What macrolide is safe in pregnancy because it does not inhibit P450?
Q: What is the drug of choice for Salmonella typhi (Typhoid Fever)?
Q: What macrolide can cause blurry vision and prolonged QT?
Q: What macrolide can potentially unmask Myasthenia gravis and potentially become fatal?
Q: What ribosomally active drug kills bacteroides fragilis (part of your normal flora) and therefore causes an overgrowth of clostridium difficil (which is inherently resistant to this drug) , leading to pseudomembranous colitis (which you treat with metronidazole)?
Q: What class of drug does clindamycin belong to, which destroy normal flora?
Q: What is the only exception where you can use a static and cidal drug together?
A: Penicillin + Clindamycin, treating strep and anaerobes
Q: What drug is a combo of Quinupristin and Dalfopristin, and binds 50S inhibiting amino acid incorporation, and is BACTERIOCIDAL, and used to treat MRSA and VRE?
Q: What drug can treat osteomyelitis due to staph aureus?
Q: What ribosomally active drug is the next treatment for staph if vancomycin doesn’t work?
Q: What ribosomally active drug has good lung penetration and 100% oral bioavailability and thus can be taken with food without any worry?
Q: What two ribosomally-active drugs are bacteriocidal?
A: Aminoglycoside and Synercid
Q: What ribosomally active drug can give you thrombocytopenia and neutropenia but reversible, unlike chloramphenicol?
DRUG OF CHOICES
Q: What is the drug of choice for painful chancroid due to H. ducreyi (vs. painless chancroid due to syphilis)?
A: Erythromycin or Azithromycin (Macrolides)
Q: What is the drug of choice for meningitis?
A: Cefotaxime if under 28 days old. Ceftriaxone if over 28 days old.
Q: What is the drug of choice for anaerobes?
A: Cefotetan and Cefoxitin (“Tin, Tan, Metro and Clinda are Ann’s friends”)
Q: What is the drug of choice for pseudomonas?
A: Ceftazidime (“Taz is the Pseudo-devil”)
Q: What is the drug of choice for syphilis?
A: Penicillin G
Q: What is the drug of choice for UTIs?
A: TMP/Sulfa. 2nd drug of choice is Ciprofloxin
Q: What is the drug of choice for Whooping Cough (Bordetella pertussis)?
A: Macrolides (Erythromycin adn Clarithromycin)
Q: What is the drug of choice for Legionaire’s Disease or Pontiac Fever (both caused by Legionella)?
A: Macrolides (Erythromycin). Quinolones work too.
Q: What is the drug of choice for Salmonella typhi (Typhoid Fever)?
Q: What is the drug of choice for Borrelia burgdoferi (Lyme Disease)?
A: Ceftriaxone for late stage Lyme disease, and Doxycycline for early stage Lyme disease.
Q: What is the drug of choice for Liver Abscess and Cholecystitis?
Q: What is the drug of choice for MRSA?
Q: What is the drugs of choice for Enterococci?
A: Vancomycin, Linezolide, Tigecycline
Q: What is the drug of choice for Listeria?
Q: What is the drug of choice for Rocky Mountain Spotted Fever (Rickettsia)?
A: Doxycycline (“Rocky Mountain boondocks”)
Q: What drugs should you avoid in pregnancy?
A: “SAFE Moms Take Really Good Care”
S – Sulfonamides –> Kernicterus
A – Aminoglycosides –> Ototoxicity
F – Fluoroquinolones –> Cartilage Damage
E – Erythromycin –> Cholestatic Hepatitis in Mom
M – Metronidazole –> Mutagenesis
T – Tetracyclines –> inhibits bone growth (because it’s a Ca Chelator)
R – Ribavirin –> Teratogenic
G – Griseofulvin –> Teratogenic
C – Chloramphenicol –> Gray Baby Syndrome
Q: What are the Atypical bacteria and their treatments?
A: Mycoplasma (walking pneumonia, or rarely meningitis) — Macrolides, Tetracyclines, Quinolones
Chlamydia — Macrolides (in neonates), Tetracyclines (in adults)
Legionella — Macrolides (DOC), Quinolones
Pertussis — Macrolides (Azythromycin)
Borrelia — Ceftriaxone, Tetracycline, Amoxicillin
Rickettsia — Doxycycline
Q: What all can Ceftriaxone treat?
A: Lyme disease, Gonorrhea, Typhoid fever.
Q: What are the STDs and their treatments?
A: Chlamydia — Azythromycin, Doxycycline
Gonorrhea — Ceftriaxone, Azythromycin
Urethritis/Cervicitis — Azythromycin, Doxycycline
Epididymitis — Ceftriaxone, Doxycycline
PID — Cefotetan and Clindamycin (if anaerobe), Doxycycline (if chlamydia)
Trichomonas — Metronidazole, Tinadazole
Syphilis — Penicillin G
Chancroid — Macrolides (Azithromycin, Erythromycin), Ceftriaxone
HSV — Acyclovir
Q:What drugs resemble and compete with PABA (needed for bacteria to synthesize folic acid) and inhibits Dihydropteroate Synthetase (which is only found in bacteria, not humans)?
Q: What is the most frequently used sulfonamide?
A: Sulfamethoxazole. the other two are sulfisoxazole and sulfadiazine.
Q: What drug is excreted by the kidneys but has limited solubility in the urine and therefore can crystallize in the renal tubules?
A: Sulfonamides — so tell patient to drink a lot of water.
Q: What happens when drugs compete with albumin, displacing its conjugation with bilirubin, letting the unconjugated bilirubin go to the brain in the fetus or newborn?
A: Kernicterus.. happens in sulfonamides, Ceftriaxome, Chloramphenicol.
Q: What drug inhibits dihydrofolate reductase (which is found in humans) from combining two dihydrofolate acids together to form tetrahydrofolate in the folate pathway?
A: Trimethoprim (TMP)
Q: What drug is made of sulfa drug + TMP?
A: Cotrimoxazole — it decreases resistance risks, and since it inhibits folate, it has anti-cancer effects.
Q: What drug got resisted when the bacteria increased PABA production, or decreased sensitivity of dihydropteroate synthetase to the drug?
Q: What is the drug of choice for strep pyogenes if the patient has penicillin allergies?
A: TMP, because TMP has no sulfa group.
Q: What drug can treat Nocardia, pneumocystis, toxoplasma, and conjunctivitis due to chlamydia in children, urethritis/cervicitis due to chlamydia in mothers?
Q: What drug do you use to treat uncomplicated UTI, Topical Burn Prophylaxis, and prophylaxis for opportunistic infections in HIV patients (i.e. toxoplasma when CD4<100, PCP when CD4<200)
Q: What drug do you use for Rheumatic Fever prophylaxis in strep pyogenes if the patient is allergic to penicillin?
Q: What drug has anti-cancer effects and can give you pancytopenia?
Q: What drug can increase your transaminase (ALT) levels and give you hepatotoxicity if you have HLA-B 5701 genes?
Q: What drug can cause neonatal hyperbilirubinemia, kernicterus, G6PD Deficiency hemolytic anemia, phototoxicity, and is contraindicated in pregnancy?
Q: What drugs are hindered by antacids?
Q: What is the mechanism of action for quinolones?
A: Inhibits DNA Gyrase, Topoisomerase 2 and 4, and therefore prevents supercoils from forming, killing the bacteria and having post-antibiotic effects.
Q: What drug treats penicillin-resistant strep pneumonia, respiratory infections from atypical agents, and community-acquired pneumonia, and osteomyelitis?
Q: What quinolones can you use for community-acquired pneumonia?
A: Levofloxacin or Moxifloxacin.
Q: What drug causes rupture of achilles tendon (and degenerates cartilage) and therefore contraindicated in kids under 18 and in pregnancy?
Q: What can quinolones do to your heart?
A: Prolong QT
Q: Women taking quinolones have to watch out for what?
A: Candida overgrowth
ANTIMICROBIALS — ANTI-MYCOBACTERIAL DRUGS
Q: What are two unique features of the cell wall of tuberculosis?
A: high-lipid content (and therefore not killed in phagocytes), and acid fast cell wall (resistant to gram staining). “Myco” in latin means “waxy” …. Mycobacterium means “waxy bacteria.”
Q: How long does it take to treat TB and how long does it take before it gains resistance?
A: takes loooong time to treat (i.e. 2 years) but it rapidly gains resistance (can gain as fast as 2 weeks)… so stick with the treatment and be patient!
Q: What are the five drugs used to treat TB?
R — Rifampin
I — Isoniazid (DOC)
P — Pyrazinamide
E — Ethambutol
S — Streptomycin
Q: What is the drug of choice for TB?
Q: What drug inhibits Mycolic Acid Synthesis, and is therefore cidal to mycobacterium?
Q: Isoniazid is similar to what vitamin?
A: Vitamin B6 — Pyridoxime
Q: What gene responsible to the activation of the isoniazid prodrug does the TB delete to become resistant to isoniazid?
A: Kat G Gene
Q: What gene encoding the binding site of isoniazid prodrug does the TB delete to become resistant to isoniazid?
A: INH A Gene
Q: What anti-mycobacterial drugs form anti-nuclear antibodies, especially if you are a slow acylator?
Q: What are the two major age-related adverse effects of isoniazid?
A: Hepatitis, Jaundice
Q: What adverse effects are you preventing by giving Vitamin B6 with Isoniazid?
A: Peripheral and Central Neuropathy. B6 is used in CSF production. Also, obviously, you are preventing vitamin B6 deficiency.
Q: What deficiency are you at risk of getting when you are taking isoniazid to treat TB?
A: Vitamin B6 deficiency
Q: What is the second drug of choice for TB treatment?
Q: Why don’t you use Rifampin when you’re on oral contraceptives
A: Because Rifampin induces CYP450, which metabolizes oral contraceptives.
Q: What is the mechanism of action for rifampin?
A: Inhibits DNA-dependent RNA polymerase in bacteria –> cidal against both intra and extracellular organisms.
Q: Besides treating Mycobacteria, rifampin is good as as prophylaxis against what organisms?
A: Staph, Neisseria meningitidis, H. influenza, Enterobacteriae, and Pseudomonas… therefore good for CNS shunt surgery.
Q: Why don’t you take rifampin with isoniazid?
A: Because they both have the adverse effect of hepatitis, because it is metabolized in the liver.
Q: What drug causes orange urine and tears?
A: Rifampin — orange urine and tears are not harmful.
Q: What anti-TB drug inhibits fatty acid synthesis and therefore inhibits TB from producing its fatty-acid rich cell wall?
Q: What is pyrazinamide (prodrug) activated into?
A: Pyrazinoic acid.
Q: What is the biggest adverse and most unique effect of pyrazinamide besides hepatitis?
A: It causes hyperuricemia and gout
Q: What drug do you give to young women and teenage girls who have rapidly progressing TB?
Q: How does streptomycin interact with other TB drugs?
A: It is synergistic with other TB drugs
Q: What is the biggest adverse effect of streptomycin?
A: ototoxicity and vestibular dysfunction (remember “OtoVAM”)
Q: All anti-TB-drugs are cidal except this one drug… what is it?
Q: What is the mechanism of action of Ethambutol?
A: Inhibits arabinose transferase, increasing the permeability of the TB’s cell wall.
Q: Besides TB what two other mycobacterial organisms do Ethambutol treat?
A: M. avium and M. kanasii.
Q: What is the biggest adverse effect of ethambutol?
A: Retrobulbar neuritis, leading to red/green color-blindness.
Q: What are the two phases of the standard regimen for TB treatment?
A: Initial 2-month phase followed by a 4-month sterilizing phase.
Q: What drugs do you use during the initial 2-month phase if the patient is less symptomatic for TB?
A: INH/RIF/PZA — Isoniazid, Rifampin, Pyrazinamide (“IRP”)
Q: What drugs do you add to the initial 2-month phase if the patient is more symptomatic for TB?
A: INH/RIF/PZA + SM/EMB — Streptomycin and Ethambutol (“IRPSE”)
Q: What drugs do you use during the 4-month sterilizing phase?
A: INH/RIF — Isoniazid and Rifampin (“IR”)… so in total for the whole standard regimen, remember “IRP or IRPSE, then IR”
Q: What drugs do you alternate every 9 months for the Alternative regimen for TB treatment?
A: alternate between INH and RIF — Isoniazid and Rifampin — remember “IRIRIRIRIRIRIRI”
Q: What do you do if a patient tests positive for TB but has no evidence of symptoms, or if the patient has had recent contact with a TB patient?
A: put them on an INH monotherapy for 6-9 months — preventative chemotherapy
Q: What drugs do you use to treat Leprosy (from mycobacteriae leprae)?
A: Dapsone, Rifampin, Clofazime
Q: What anti-leprosy drug is very similar to sulfonamides in that it inhibits Dihydropteroate Synthase of the folic acid pathway?
ANTIMICROBIALS — ANTI-VIRAL DRUGS
Q: What two drugs are neuraminidase inhibitors?
A: Zanamivir and Oseltamivir
Q: What four drugs are viral DNA polymerase inhibitors?
A: Acyclovir, Valacyclovir, Ganciclovir, Foscarnet.
Q: What two drugs are viral RNA polymerase inhibitors?
A: Ribavirin and Foscarnet
Q: What two drugs bind M2 protein, preventing the viruses from uncoating?
A: Rimantadine and Amantadine
Q: What four drugs are used to treat Influenza?
A: ZORA — Zanamivir, Oseltamivir, Rimantadine, Amantadine
Q: Which influenza virus drug is inhaled, and therefore can give you bronchospasm?
Q: Zanamivir is contraindicated in what type of patients?
A: Asthma patients — because it is inhaled
Q: What influenza antiviral drug causes behavioral problems in kids?
A: Oseltamivir, also known as Tamiflu
Q: What influenza viral enzyme cleaves the host sialic acid that the virus binds to in order to release itself from the host cell?
Q: What drugs treats Influenza A only?
A: Rimantadine and Amantadine
Q: Which drugs treat both Influenza A and B, as well as H1N1?
A: Zanamivir and Oseltamivir (neuraminidase inhibitors)
Q: Which strain of Influenza have recently lost sensitivity to neuraminidase inhibitor drugs?
A: Influenza B
Q: What influenza viral protein is an ion channel that brings in H+ to form the acidic environment of endosomes needed for uncoating?
A: M2 Protein
Q: Which flu drug does NOT cross BBB?
Q: Which flu drug crosses BBB?
Q: Which uncoating drug is longer-lasting?
Q: What are the three causes of death due to Hepatitis B Virus?
A: Acute Hepatitis Necrosis, Chronic Hepatic Disease, Hepatocellular Carcinoma
Q: What four drugs treats mainly Hep B virus?
A: Telbivudine, Adefovir, Lamivudine, Entecavir
Q: What drug treats mainly Hep C virus?
Q: What drug mainly treats both Hep B and C?
Q: What three hepatitis drugs are approved in kids?
A: Ribavirin, Interferon, and Lamivudine
Q: What viral hepatitis drug is known as 3TC?
Q: What viral hepatitis drug can also treat Parainfluenza, HIV, RSV, Measles, Lassa, and Hanta virus?
Q: What viral hepatitis drug is teratogenic?
Q: Which viral hepatitis drug is an adenosine analog and therefore inhibits DNA polymerase?
Q: What is the drug of choice for chronic viral hepatitis?
Q: What viral hepatitis drug can give you flu-like symptoms (fever, chill, muscle pain)?
Q: What herpes virus can cause Herpetic Whitlow, Dendritic Lesions in eyes, and Tactile Hyperesthesia due to Encephalitis?
A: Herpes Simplex Virus
Q: What four drugs treat Herpes Simplex Virus?
A: Acyclovir, Valacyclovir, Famciclovir, and Foscarnet
Q: What is the drug of choice for HSV when given IV?
Q: What is the “oral form of acyclovir”?
A: Valacyclovir, which is the L-valyl ester of acyclovir.
Q: Why isn’t acyclovir effective against CMV?
A: because CMV doesn’t have Thymidine Kinase needed to activate the drug. Instead, you would use Ganciclovir.
Q: What do you do if a baby is born to a mother with genital herpes and has or is at risk of neonatal HSV?
A: Give the baby 21 days of high dose acyclovir
Q: What drug is a guanosine analogue that works by inhibiting DNA polymerase?
Q: What drug is used to treat HSV, Varicella, CMV, or EBV if all other drugs do not work?
Q: Which drug is a pyrophosphate analogue (PPi) and works by inhibiting DNA polymerase and HIV reverse transcriptase?
Q: What is the biggest and most unique adverse effect of foscarnet?
A: Hypocalcemia. It also penetrates the blood brain barrier, giving you seizures.
Q: What disease is treated with the same drugs as HSV except with a higher dose?
A: Varicella Zoster
Q: What drug is used to treat post-zoster neuralgia?
Q: What two viral diseases are normally self-limiting and are treated when one is immunocompromised?
A: CMV and EBV
Q: What virus causes micro-ophthalmia, microcephaly, and jaundice when infected congenitally?
Q: What cells are infected in EBV?
A: B cells
Q: What are Downy cells?
A: T cells that engulfed infected B cells in EBV infection.
Q: What is the drug of choice for CMV?
Q: What drug is a deoxyguanosine analogue that initially requires phosphorylation from the virus, but subsequent activation steps by host?
Q: What is the biggest adverse effect of Ganciclovir?
A: Neutropenia. Also thrombocytopenia and aspermatogenesis.
Q: What drug is used as a CMV prophylaxis in renal transplant patients?
A: Valganciclovir, which is the oral prodrug of ganciclovir.
Q: Besides Foscarnet, what other drug can be used for resistant CMV strains?
Q: What is the adverse effect of Cidofovir?
A: Severe renal dysfunction
Q: Does Cidofovir require thymidine kinase to be activated?
A: No, like Ganciclovir, it doesn’t require TK to be activated.
Q: If your patient has pharyngitis with exudates but lab tests come back negative for strep pneumo, what else could it be?
Q: What do you use to treat EBV?
A: Acyclovir, Valacyclovir, Foscarnet
ANTIMICROBIALS — ANTI-HIV DRUGS
Q: How does HIV attach to host cell?
A: gp120 on virus attach to CD4 on T-cell. GP120/CD4 then binds to either CCR5 on macrophage or CXCR4 on T cells. The GP41 on the virus fuses with host T cell.
Q: Why is HIV difficult to treat?
A: Because it mutates really fast. As a retrovirus, it has to constantly convert RNA to DNA then back to RNA, and this is process if imperfect, causing a high chance of mutation.
Q: What three Anti-HIV drugs are contraindicated in pregnancy?
A: Didanosine (DDI), Stavudine (D4T), and Efavirenz (EFV)
Q: What are the two types of HAART treatments?
A: 2 NRTI (ZDV, 3TC) + 1 NNRTI (EFV or ETR)
or 2NRTI (ZDV, 3TC) + 1 PI (LPV) + Ritonavir (needed to decrease the dose needed for PI)
Q: What HAART do you give during pregnancy?
A: ZDV, 3TC + NVP
Q: What is the treatment of choice for preventing verticle transmission of HIV from mother to child?
Q: What is the second and third treatment of choice for preventing verticle transmission of HIV?
A: 2nd DOC = ZDV. 3rd DOC = NVP
Q: How do half of children with HIV die? Explain.
A: autoimmune disease, because HIV hyperstimulates T cells, which release B cell growth factor and B cell transfforming factor. This causes the kid to become hypergammaglobulinemic (increased IgG levels). This IgG is not functional and causes autoimmune antibody disease.
Q: What are the four goals of retroviral treatment?
A: Decrease viral load, decrease opportunistic infections, increase CD4 count, decrease symptoms
Q: What are the four major opportunistic infections in HIV patients?
A: PCP, CMV, MAI, Candida — use prophylaxis!!
Q: What are the six types of HIV drugs?
A: Nucleoside Reverse Transcriptase Inhibitors (NRTI), Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTI), Protease Inhibitors (PI), Fusion Inhibitors, CCR5 Antagonist, and Integrase Inhibitor.
Q: Which HIV drug class works by competing with RNA to bind to the reverse transcriptase, causing chain termination, but does NOT require phosphorylation for its activation?
A: NNRTI (vs. NRTI, which works the same way but is a prodrug that requires phosphorylation by the host,, except Tenofovir)
Q: What drug class inhibits its own metabolism by inhibiting CYP3A4, which also metabolizes it?
A: Protease Inhibitors.
Q: Zidovudine (ZDV) is also known as what?
A: Azidothymidine (AZT)
Q: What drugs are the first-line NRTI for treatment of HIV in pregnancy or pediatrics?
A: Zidovudine, Lamivudine
Q: What NRTI causes lactic acidosis, mitotoxicity, and cardiomyopathy?
Q: What NRTI do you need to test for the HLA-B 5701 gene for hypersensitivity risks (like sulfonamides)?
A: Abacavir (ABC)
Q: What NRTI should you be cautious when usign with abacavir?
A: Lamivudine (because it can cause virologic failure)
Q: Which NRTI should you NOT use with ZDV?
A: Stavudine (D4T). They are antagonists.
Q: What NRTI causes lactic acidosis like Zidovudine but also causes peripheral neuropathy?
A: Stavudine… another reason why you shouldn’t use it with ZDV.
Q: What NRTI gives you pancreatitis, hyperuricemia, and gout?
A: Didanosine (DDI)
Q: What is the best-tolerated NRTI because it has very minor adverse effects (skin discoloration)?
Q: What NRTI is basically a “long-acting 3TC”?
A: Emtricitabine. It has no additive effect when used with 3TC.
Q: What is the only NRTI that doesn’t require activation?
A: Tenofovir (TDF), because it is a nucleotide, not a nucleoside, and so it is already phosphorylated.
Q: What HIV drug class is “unforgiving” because it can develop rapid resistance if used solo or if you miss a dose?
Q: What are the four NNRTIs?
A: “NEED” — Nevirapine, Efavirenz, Etravirine, Delavirdine
Q: What two NNRTI’s can you use together?
A: NONE!!! Don’t use 2 NNRTI’s together!!
Q: Whcih NNRTI can be used to prevent vertical transmission of HIV from mother to child?
A: Nevirapine (NVP)
Q: What NNRTI causes Steven-Johnson Syndrome?
A: Nevirapine (NVP)
Q: What NNRTI is teratogenic and can cause nightmares?
A: Efavirenz (EFV)
Q: What NNRTI is the DOC in HAART?
A: Efavirenz (EFV)
Q: What NNRTI is not commonly used becuase of its short half-life?
A: Delavirdine (DLV)
Q: What NNRTI is teratogenic in animals and therefore be careful when using it?
A: Delavirdine (DLV)
Q: What drug class inhibits the enzyme that cleaves HIV polyproteins into core structural proteins?
A: Protease inhibitors
Q: What is the major adverse effect found in all PIs?
A: delay in carbohydrate/lipid metabolism, leading to hyperglycemia, diabetes, hyperlipidemia.
Q: What PI can especially cause lipodystrophy and central obesity?
A: Saquinavir (SQV)
Q: What PI can boost serum levels of other PIs at low doses because it inhibits P450, which metabolizes the PIs?
A: Ritonavir, and therefore it is given with almost all other PIs (Lopinavir, Fosamprenavir, Darunavir, Atazanavir)
Q: Which PI tastes bad?
Q: Which two PIs has sulfur and therefore causes Steven-Johnson Syndrome?
A: Fosamprenavir and Darunavir (DRV)
Q: What PI gives you nephrolithiasis?
Q: Which anti-HIV drug binds GP41 on the virus, preventing HIV fusion with the host?
A: Enfuvirtide (T20) (Fusion Inhibitor)
Q: What gene does the HIV mutate to make it resistant to enfuvirtide (T20)?
A: env gene, needed to make GP41.
Q: Which anti-HIV drug inhibits CCR5 (on macrophage)?
A: Maraviroc (CCR5 Antagonist)
Q: Which anti-HIV drug blocks HIV DNA integration with the host DNA?
A: Raltegravir (RAL) (Integrase Inhibitor)
ANTIMICROBIALS — ANTI-FUNGAL DRUGS
Q: What are the three big adverse effects of amphotericin B?
A: Flu-like symptoms, Kidney problems, and ERYTHROPOIETIN SUPPRESSION!!
Q: What are the two drugs of choice for Sporothrix?
A: Amphotericin B and Itraconazole (an azole)
Q: How does Amphotericin B work?
A: By binding to ergosterol on the fungal membrane and then creating pores and killing the cell… fungicidal!
Q: Does amphotericin B cross the BBB?
Q: What kind of molecule is amphotericin B?
A: Polyene, which is unsaturated with alternating double and single bonds. Nystatin (for oral thrush in babies) is also a polyene.
Q: Why does 5-flucytosine affect fungi and not humans?
A: Because only fungi can convert 5-flucytosine to 5-FU, which is what will inhibit thymidylate synthase.
Q: What are the adverse effects of 5-Flucytosine?
A: Reversible Neutropenia and Thrombocytopenia.
Q: Amphotericin B can treat a wide spectrum of fungi. But Amphotericin B + 5-Flucytosine is used narrowly to treat what two fungi?
A: Candida and Cryptococcus
Q: If you have cryptococcus or candida with meninigitis and other CNS symptoms, what do you use?
A: Fluconazole (an azole), because it can cross BBB. Amphotericin B cannot.
Q: What class of antifungals inhibit 14-alpha-demethylase, needed for fungi to make ergosterol?
A: Azoles — Itraconazole, Fluconazole, Voriconazole, Posiconazole.
Q: What three organisms do Fluconazole treat best?
A: CCC — candida, cryptococcus, and coccidioides — and since it crosses BBB, it can treat CNS symptoms.
Q: What is the adverse effect of fluconazole?
A: Hepatotoxicity in pregnancy!!! Don’t give to pregnant women! Also Steven Johnson Syndrome.
Q: What is the drug of choice for histoplasma?
Q: What is the adverse effect of itraconazole?
A: negative ionotropic effect in heart.
Q: What is the drug of choice for mucor?
Q: What is the adverse effect of Posiconazole?
A: Hematologic effects (like penia)
Q: What is the adverse effect of voriconazole?
A: CNS effects
Q: What can potassium iodide be used for in terms of antifungal treatments?
A: It can kill sporotrix.
Q: What is the drug of choice for non-CNS candida?
Q: So far, what are the treatments for candida that we have covered?
A: Amphotericin B + 5-Flucytosine (non-CNS), Fluconazole (esp with CNS symptoms), and Caspofungin (non-CNS, DOC)
Q: What drug inhibits fungal cell wall synthesis by inhibiting beta-glycans?
Q: Caspofungin is cidal against what and static against what?
A: Cidal against Candida and Static against Aspergillus
Q: What is the adverse effect of Caspofungin?
A: Bronchospasm (due to histamine release)
Q: What antifungal drugs accumulate in keratin-making cells?
A: Griseofulvin and Terbinafine
Q: What is the mechanism of action of Griseofulvin?
A: Inhibits fungal cell mitosis via microtubule structures.
Q: What does griseofulvin treat?
A: Dermatophytes, which grow in places with keratin — hair, nail, skin.
Q: What is the mechanism of resistance for griseofulvin?
A: decreased uptake of drugs via porins.
Q: What antifungal drug is teratogenic?
Q: What antifungal drug gives you Steven Johnson Syndrome?
Q: What antifungal drug gives you disulfiram reaction?
Q: What antifungal drug interferes with ergosterol synthesis by inhibiting squalene epoxidase, leading to toxic accumulation of squalene in the keratin?
A: Terbinafine (compare this with azoles, which also interferes with ergosterol synthesis but by inhibiting 14-alpha-demethylase)
Q: What treats ring worm (superficial mycosis)?
Q: What are the two interesting adverse effects of terbinafine?
A: Taste disturbance, Steven Johnson Syndrome
Q: What drug like amphotericin B also binds ergosterol, and is also a polyene?
Q: What is Nystatin used for?
A: Swish and Swallow Therapy — oral candida thrush in babies.
Q: What can Gentian Violet treat?
A: Candida… but it makes your skin purple and a lot of folks don’t like that.
ANTIMICROBIALS — ANTI-MALARIAL DRUGS
Q: Which malarias are found in blood only?
A: P. falciparum and P. malariae — therefore you must treat with systemic drug.
Q: Which malarias are found in liver as well as blood?
A: P. vivax and P. ovale (vivax and ovale both have the letter V. Liver has the letter V.) — therefore you must treat with both systemic and a liver drug
Q: What are your systemic malarial drugs?
A: Chloroquine (1st), Quinine (2nd), Tetracycline, Atovaquone, etc.
Q: What are your liver malarial drugs?
Q: What is the malarial prophylaxis drug?
Q: What is prophylaxis against chloroquine-resistant malaria?
Q: A traveler came back to the U.S and developed chills + fever that showed a cyclic pattern of every 72 hrs… what is it?
A: P. malariae!! It is a systemic malaria so you treat it with a systemic drug, like Chloroquine or Quinine
Q: A traveler came back to the U.S and developed chills + fever that showed a cyclic pattern of every 48 hrs… what is it?
A: P. vivax or ovale!! It is a liver malaria so you treat with systemic + liver drugs (primaquine)
Q: Which anti-malarial drug is contraindicated in G6PD deficient patients?
Q: What are the four ways of treating malaria?
A: 1. Impairing parasitic utilization of heme — Artemesinin (which alkylates heme via free radicals), Chloroquine, Mefloquin, Quinine (which prevents detox of heme, killing the plasmodium)
2. Inhibiting electron transport chain — Atovaquone (inhibits cytochrome bc complex, inhibiting pyrimidine synthesis)
3. Inhibiting protein synthesis — Doxycycline, Tetracycline, Clindamycin (which remember are ribosomally active drugs)
4. Impairing synthesis or utilization of folate — Sulfadoxine, Dapsone, Pyrimethamine, Proguanil
Q: What malarial combo treatments are for both adults and kids?
A: Quinine + Tetracycline or Clindamycin (definitely know this one)
Atovaquone + Proguanil (and probably this one too)
Artemether + Lumefantrine
Q: What malarial combo treatments are for adults?
A: Chloroquine + Sulfadoxine
Artesunate + Amodiaquine
Q: Mefloquine, the prophylaxis for chloroquine-resistant malaria, should not be given to who?
A: Mental patients.. because the drug causes neuropsychiatric symptoms… you don’t want to worsen them. Also don’t give to pregnant women during first trimester… can lead to stillbirths.
Q: How did malaria gain resistance to chloroquine?
A: By increasing efflux pump, decreasing the drug’s entrance into the organism.
Q: What antimalarial drugs inhibit synthesis of folate by competing with p-aminobenzoic acid?
A: Sulfadoxine, Dapsone
Q: What antimalarial drugs inhibit dihydrofolate reductase, inhibiting the conversion of dihydrofolate to tetrahydrofolate?
A: Pyrimethamine and Proguanil.
Q: Why is the combo pyrimethamine+sulfodoxine no longer used?
A: Because it causes Steven-Johnson Syndrome and Toxic Epidermal Necrolysis.
Q: What is the drug of choice for Malaria?
Q: What if chloroquine doesn’t work, like in those strains of P. vivax in New Guinea and Indonesia?
A: Treat with Hydroxychloroquine (don’t get confused with mefloquin, which is used for chloroquine-resistant malaria PROPHYLAXIS).
Q: What antimalarial drug works by increasing toxic levels of reactive oxygen species and H2O2 (like nifurtimox in antiparasitic drugs)?
A: Primaquine, which is the malarial liver drug. Because it increases reactive oxygen, it is contraindicated in G6PD deficient patients, who also have an increased reactive oxygen level in their blood system, causing hemolysis.
Q: How did Atovaquone-resistant malaria develop resistance?
A: by mutating the cytochrome b gene.
ANTIMICROBIALS — ANTI-PARASITIC DRUGS
Q: What parasitic drug increases membrane permeability for calcium in the parasite, causing the parasite to contract and become paralyzed?
Q: What does Praziquantel treat?
A: Cestodes (especially Taenia solium aka cysticercosis) and Trematodes
Q: When is Praziquantel contraindicated?
A: When the parasite is in the invasion stage, or when the parasite is in the eye or cerebrum.
Q: What do you give if the parasite is in the eye or is in the tissue invasion stage?
Q: What three parasitic drugs block glucose uptake into the parasite by interferring with microtubular function?
A: Albendazole (eye, tissue invasion treatment), Mebendazole, Thiabendazole
Q: What is the best drug for nematodes?
Q: What is the adverse effect of praziquantel?
Q: What is the adverse effect for mebendazole?
Q: What does a patient have when they took a parasitic treatment and developed pneumonia, fever, and eosinophilia?
A: Loeffler’s Syndrome — shows that the work has already penetrated the blood and has become invasive, and that the drug you gave didn’t work.
Q: What drug interferes with microtubule polymerization and used to treat strongyloides and cutaneous larva migrans (migrating nematodes, cyclostoma)?
A: Thiabendazole (think of “threads” — microtubules, strong thread)
Q: What drug binds metals and therefore good for lead and mercury poisonings?
Q: What is the drug of choice for Loa Loa and Filariasis?
A: Diethylcarbamazine (“DECarb”)
Q: What is the adverse effect of Diethylcarbamazine and Ivermectin?
A: Mazzotti Reaction (from allergic reaction to the parasitic debris). It is a papular skin rash.
Q: What drug intensifies GABA in parasites, leading to its immobilization?
Q: What does Ivermectin treat?
A: Onchocerca (river blindness) (“Iver = River”)
Q: What is the drug of choice for Giardia in adults?
Q: What is the drug of choice for Giardia in children?
Q: What is the drug of choice for Giardia in children with G6PD deficiency?
Q: What drug causes lipid peroxidation, leading to DNA damage?
Q: What two drugs are the drugs of choice for Trichomonas vaginalis?
A: Metronidazole or Tinidazole
Q: What drug gets activated into ferredoxin in the cytosol, disrupting DNA synthesis in the parasite?
A: Metronidazole (“metro ferry”)
Q: Metronidazole is used in both enteric and invasive forms of the parasite. What drug is used for only enteric?
A: Diloxanide (think of it as “diluted metronidazole”)
Q: What is the adverse effect of metronidazole?
A: Disulfiram reaction
Q: What is the drug of choice for Cryptosporidium?
A: Nitazoxanide (like DOC for Giardia in kids with G6PD deficiency)
Q: What drugs do yo use for Cryptosporidium in HIV patients?
A: Paromomycin and Azythromycin
Q: What is the treatment for Toxoplasma?
A: Pyrimethamine + Sulfadiazine (or Spiramycin if you are pregnant)
Q: What is the treatment for PCP?
A: TMP-SMX or Pentamidine Isothionate
Q: What is the adverse effect of TMP-SMX (cotrimoxazole)?
Q: What is the adverse effect of sulfadiazine?
A: Steven Johnson Syndrome (because has sulfur)
Q: What is the mechanism of action for Pentamidine Isothionate?
A: Interferes with RNA, DNA, and protein synthesis.
Q: Trypanosoma causes what two diseases?
A: Chagas Disease (in South America) and African sleeping sickness (in Africa)
Q: What is the treatment of Chagas disease?
Q: What is the treatment of African Sleeping Sickness?
A: T. rhodesiense is melarsoprol, and T. gambiense is Pentamidine and Suramin.
Q: What is the mechanism of action of melarsoprol?
A: It interacts with SH groups of enzymes.
Q: What is the mechanism of action of suramin?
A: inhibits energy metabolism enzymes (glycerol phosphate dehydrogenase)
Q: What do niclosamides treat?
Q: What is the mechanism of action of niclosamides?
A: inhibits parasite mitochondrial phosphorylation
Q: What is the drug of choice for Leishmania?
A: Stibogluconate dosium
Q: What is the mechanism of action for Stibogluconate dosium?
A: It is an antimony analogue that inhibits glycolysis and fatty acid metabolism, starving the parasite.
Q: How does Pyrantel Pamoate work?
A: They depolarize the neuromuscular junction, causint a persistent activation of nicotinic receptors, leading to paralysis of the worm. The pinworms, roundworms, and hookworms detach from your intestinal wall and you poop it out.
Q: What drug causes host cell to produce superoxide and H2O2, leading to peroxidation of the parasite?
Aminoglycosides treats G- aerobes
Clindamycin treats anaerobes and Strep/Staph, but not Enterococcus.
Linezolid treats G+ aerobes
Quinolones treat aerobes
Natural Penicillins (G, V) treat G+ aerobes
Methicillins (Oxicillin, Cloxicillin, Dicloxicillin, and Nafcillin) treat G+
Aztreonam treats G- aerobes
Vancomycin treats G+
Daptomycin treats G+
Metronidazole treats anaerobic bacteria and protozoans.
1st Generation Cephalosporins treat G+
2nd Generation Cephalosporins treat G- (Cefoxitin and Cefotetan also treats anaerobes)
3rd Generation Cephalosporins treat both G+/G-
4th Generation Cephalosporins treats G- (pseudomonas)
Drugs that treat both G+/G- : Extended Spectrum Penicillins, Third Generatioin Cephalosporins, Carbapenems, Tetracyclines, Chloramphenicol, Macrolides, Clindamycin (but mainly anaerobes and staph/strep), Sulfonamide/TMP, Quinolones (rx PCN-resistant strep pneumo, but contraindicated in kids because of it’s cartilage damaging effects).