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Pharmacology #3 Carrington College -Dr.Dave

Terms in this set (263)

GnRH
stimulates pituitary production of LH and FSH. Pulsatile release at different frequencies selects the gonadotroph transcripted.
LH
primarily responsible for regulation of gonadal steroid production. In the ovary, acts with FSH to stimulate follicular development
hCG
produced by the placenta, structurally very similar to LH, causes increased production of progestins by the ovaries. It is used to treat LH deficiency. It has become a popular agent for weight loss. White somewhat effective, the weight re-gain is almost universal. Bottom line; it does not really solve the problem of obesity
Oxytocin
posterior pituitary, stimulates milk ejection in lactating women, increases and maintains urine concentrations
Vasopressin aka ADH
Stimulates renal vascular vasoconstriction (V2) to restrict diuresis and causes general vascular vasoconstriction via V1 receptors.
Bromocriptine
PO; as a dopamine agonist, it is used to inhibit PRL release. Aggressive.
Desmopressin
IV, Nasal; a vasopressin synthetic analogue, has greater AGH properties vs. vasoconstriction properties. Drug of choice for diabetes insipidus In high doses it is used to treat Von Willebrand disease and enhance factor VII.
Octreotide
synthetic analogue of somatostatin. Used to treat hypersecretory diarrhea, enteric fistulas. Inhibits release of hormones. reduces digestion in the liver
Types of Adrenal Steriods
Glucocorticoids - release stimulated by ACTH
Mineralcorticoids - release stimulated by angiotensin and ACTH
Adrenal Androgenoids - principally DHEA
Glucocorticoids
stress hormones. Effects are body wide. Profound effects on carbs, protein, and fat metabolism. Anti-inflammatory and immunosuppresive properties are principal reasons for their therapeutic use. They also provide feed-back regulation by suppressing ACTH secretion.
Limitations: Chronic exogenous administration or cushing's leads to a whole hose of undesirable effects:rounded face, weight game, protein loss, skin thinning.
Corticosteriod Medications
Hydrocortisone (Sulucortef)
Prednisone (Deltasone)
Cortisone (Cortone)
Prednisolone (Orapred)
Methylpredinsolone (SoluMedrol)
Triamcinolon (Kenalog)
Betamethasone (Celestone)
Fludrocortisone (Florinef)
Mineralcorticoids
salt management
effects: promote reabsorption of Na from the renal filtrate, increasing fluid retention. Excess aldosterone secretion leads to hypernatremia, hypokalemia, metabolic alkalosis, increased plasma volume and HTN.
uses: adrenal insufficiency
meds: Aldosterone -endogenous prototype & Fludrocortisone (Florinef)
Adrenocortical Insufficiency
Chronic (Addison's disease) : hyper pigmentation, weakness, fatigue, weight loss, hypotension, and inability to maintain fasting serum glucose. Relatively minor stress can precipitate acute insufficiency with shock and death. Both glucocorticoid and mineral corticoid activity is needed. Baseline dosing with hydrocortisone and fludrocortisone is necessary.
Hyperglucocorticoid activity
Cushing's syndrome, congenital
Hypermineralocorticoid activity
Spironolactone
Estrogen
Endogenous: Estradiol, Estriol, Estrone
Effects: trasmembrane transport to nucleus, site of estrogen receptor
Female maturation: secondary sexual characteristics
Endometrium: development
Metabolic effects: decrease bone resorption, maintenance of skin, vascular structure and changes in the liver.
Blood: enhances coagulation, lowers LDLs and raises HDLs
* it has feedback effects on the hypothalamus resulting in decreased secretion of LH and FSH*
Progesterones
Endogenous: Progesterone is a chemical precursor to all other gonadal hormones. It has feedback effects on the hypothalamus resulting in decreased secretion of LH and FSH.
Effects: little effect on lipid metabolism. factors fat deposition. it increases basal insulin levels.
Endometrium: stops further development but maintains it.
Hormonal Contraception
Types: combination of estrogen and progesterone in mono, bi and triphasic versions; PO protestants only
Mechanism: selective pituitary inhibition, resulting in inhibition of ovulation.
Efficacy: 0.5 to 1 per 100 years.
S/E: (mild) N/V, breakthrough, bleeding, edema, HA, breast changes. (moderate) weight gain, increased skin pigmentation, acne, and hirustism. (severe) vascular disorders: CVA, MI, cancer, jaundice
Cautions: age, cardiovascular risk, smoking.
Post Menopausal Hormonal Therapy
Symptoms: more than just hot flashes.. osteoporosis, changes in lipid metabolism, vaginal atrophy etc.
Estrogen & Progesterone
Post Menopausal Hormone therapy; reduces the risk of endometrial hyperplasia (cancer?) vs. estrogen alone.
Androgens & Anabolic Steroids
Androgenic (male sexual characteristics)
Anabolic (muscle mass, increase bone density) - controlled substance schedule II, modified testosterone, as the dose goes up the selectivity goes down.
Spermidcidals
usually used in combo w/ barrier methods
Barrier Methods
Condon, diaphragm, sponge. Rates of efficacy are dependent on technique. "safe sex"
Sterilization
must be considered permanent when making the decision even though it can sometimes be reversed.
Iodine
an essential nutrient for the production of the principle thyroid hormone
T3
triidothyronine, more potent, smaller fraction, metabolized peripherally from T4
T4
levothyroxine, less potent, majority of circulating hormone
Hypothyroidism
lack of thyroid circulating hormone
Hashimoto's thyroiditis
autoimmune destruction of gland
Drug induced hypothyroidism
several drugs can inhibit hormone formation
Dyshormonogenisis
due to enzyme defieciency
Treatment for Hypothyroidism
Mild myexedema- oral replacement
Severe myexedema - IV replacement
Hypothyroid medications
Levothyroxine (Synthroid)
Liothyronine (Cytomel, Triostat)
Liotrix (Euthroid, Thyrolar)
Thyroid desiccated [U.S.P] (Armour Thyroid)
Graves
hyperthyroidism; autoimmune disorder where the body produces an antibody that mimics the effects of TSH which binds to the TSH receptor even more tightly than TSH, causing and increased release of thyroid hormone.
Toxic Goiter
can present with normal T4 but elevated T3
Subacute Thyroiditis
secondary to viral infection. it appears to resolve on its own.
Hyperthyroidism medications
Propythiouuracil (PTU)
Methimazole (Tapazole)
Potassium iodine solution (SSKI)
Alternative therapy to hyperthyroidism
Radiation I131, surgical: risk of damage to parathyroid glands. Radiation & surgery require exogenous replacement of thyroid hormone after therapy.
Intestine
Parathyroid hormone: Increased Ca & PO4 absorption by increased amounts of active vitamin D.
Vitamin D: Increased Ca & PO4 absorption
Kidney
Parathyroid hormone: Decreased Ca excretion, increased PO4 excretion.
Vitamin D: Ca & PO4 decreased
Bone
Parathyroid hormone: Ca & PO4 reabsorption increased in high doses, decreased by low doses.
Vitamin D: Increased Ca & PO4 resorption(1,25) decreased (24,25) vitamin D
Serum Levels
Parathyroid hormone: Ca increased & PO4 decreased
Vitamin D: Both Ca & PO4 increased
Secondary Hormones to Bone Homeostasis
Calcitonin
Glucocorticoids
Estrogens
GERD Causes/ risk factors
causes: lower esophageal sphincter tone: negative pressure chest vs. positive pressure abdomen
Risk factors: hiatus hernia, atony
GERD - Reduce LES tone
types of foods - fat , chocolate
smoking, ethanol
other drugs: morphine, meperidine, calcium blockers, theophylline
Estrogen, progesterone
Gastric acidification
GERD therapeutic approaches Phase I
Phase I : Elevate HOB 6-8" w/ blocks
dietary modifications
decrease or stop smoking
decrease alcohol consumption
avoid complication medications
take antacids - therapeutic amounts : schedule 1 & 3 hrs pc & hs for healing
GERD therapeutic approaches Phase IIa
H2 antagonists - at standard doses
Cimetidine 300mg AC & HS, Rantidine 150mg BID etc.
Prokinetic agents - increase gastric emptying rate
Metoclopromide (Reglan)
Bethanecol
Sucralfate - as slurry
GERD therapeutic approaches Phase IIb
H2 antagonist - at high doses
PPIs: Omeprazole, Lansoprazle, Pantoprazole
GERD therapeutic approaches Phase III
surgery
Peptic Ulcer Disease (PUD)
Acid Secretion
Parietal cell - gastric proton pump
Histamine = increases cAMP
Acetylcholine, gastrin = increases intracellular calcium
Basal = 15%
Cephalic = 30%, the sight and smell of food
Gastric = 50%, the direct stimulation of food
Intestinal = 5%, stimulation & inhibition components
Pepsin - activated at low pH
Peptic Ulcer Disease (PUD)
Mucosal protective mechanisms
Mucus secretion
Bicarbonate secretion
Mucosal blood flow
Rapid cellular repair
Prostaglandins - stimulate mucus & bicarbonate secretion and increase intestinal blood flow.
Peptic Ulcer Disease (PUD) Etiology & Pathogenesis
Imbalance between destructive and protective mechanisms
Some cause overproduction of acid - Zollinger Ellison Syndrome (ZES)
Some increase acid and decrease protection - smoking, stress, genetics
Some decrease protection - NSAIDs, H pylori
Gastric Ulcer (GU) - often normal acid secretion. Duodenal, pancreatic reflux a factor. H pylori are significant contributors, especially in recurrence.
Duodenal Ulcer (DU) - can have normal or elevated acid secretion (ZES). Most commonly located in the duodenal bulb
Treatment of PUD
Non-Pharmacologic
Non-pharmacologic:
Reduce or stop smoking, alcohol consumption
Avoid foods that aggravate symptoms
Stress management
Treatment of PUD
Pharmacologic
Pharmacologic: Stop offending drug use: NSAIDs, steroids, where possible
Antacids: therapeutic doses - 30ml 1 & 3 hours pc & hs and/or
H2 blockers: normal doses or Proton pump inhibitors
Protectives:

It it is recurrent, consider treating H pylori
Antacids
Magnesium hydroxide (MOM): also laxative
Aluminum hydroxide (Amphojel): constipates & binds PO4 in diet-(renal)
Aluminum and magnesium hydroxide combinations (Maalox, Mylanta)
Calcium carbonate (Tums, Rolaids) and many more!
H2 blockers
Cimetidine (Tagamet): OTC PO, Rx IV
Famotidine (Pepcid): OTC PO, Rx IV
Ranitidine (Zantac): OTC PO, Rx IV
Nizatidine (Axid): OTC PO
Proton Pump Inhibitors
Omeprazole (Pilosec, generic): 20 - 40 mg daily OTC, PO $
Esomeprazole (Nexium) 20 - 40 mg daily PO and IV $$$$ Lansoprazole (Prevacid) 15 - 30 mg daily OTC, PO $$$
Pantoprazole (Protonix) 40 mg daily PO and IV $$$
Dexilansoprazole (Dexilant) 30 - 60 mg PO $$$
Rabeprazole (Aciphex) 20 mg PO $$$
Protectives
Sucralfate (Carafate): 1g ac & hs (on empty stomach) $
Nausea and Vomiting; Mechanism
chemoreceptor trigger zone (CTZ) coordinating center: dopaminergic and serotoninergic receptors.
Antiemetics
Antihistamines: (H1) good at inhibiting effects of motion sickness. Meclizine (Antivert), Hydroxyzine (Atarax, Vistaril)
**Phenothiazines: block dopamine receptors in the CTZ
Promethazine (Phenergan) [H1 too], Prochlorperazine (Compazine)
**Trimethobenzamide (Tigan): dopamine blocker, not a phenothiazine but...
**Metoclopramide (Reglan): dopamine blocker in addition to gastric emptying.
**Droperidol (Inapsine): dopamine blocker. IM, IV
** ALL dopamine blockers can and will prolong the QT interval, with the potential of serious dysrrhytmias. Black box warning in package inserts.
Dronabinol (Marinol): CII - contains the active ingredient of cannabis. It appears to work in patients that are refractory to conventional therapy.
5-HT3 blockers: have revolutionized chemotherapy n/v control. Also effective for post-op
Ondansetron (Zofran): PO, IV $ (now available generic)
Granisetron (Kytril): PO, IV $$$$
Dolasetron (Anzemet): PO, IV $$$
Laxatives
Irritants or Stimulants
Bisacodyl (Dulcolax): PO, PR
Senna (Senokot): PO
Bulk Laxatives
Bulk laxatives: indigestible sugars - cellulose, hold water by osmosis
Psyllium seed (Metamucil): PO
Lactulose (Cephulac)
Sorbitol
Bran (a.k.a. fiber)
Laxatives - Saline cathartics
dissolved salts in liquid, draw water into lumen
Magnesium citrate (Citroma): PO
Stool Softeners
Stool softeners:
Docusate (Colase, Surfak): "soap"
Mineral Oil
Combination Stool Softeners
Docusate and Senna (Senkot S and Pericolace)
Laxative Abuse
OTC, aging, decreased GI tone. Eating disorders.
Electrolyte disturbances. Chronic bowel irritation. Luminal erosion.
Diarrhea Mechanism
Balance between secretion (small bowel) and reabsorption (colon).

1. A change in the active ion transport: decreased sodium or increased chloride
2. A change in intestinal motility
3. An increase in luminal osmolarity
4. An increase in tissue hydrostatic pressure
Diarrhea Types
1. Secretory - a stimulating substance either increases secretion or decreases absorption of large amounts of electrolytes: excessive dietary fat, stimulatory laxatives, bacterial toxins, excessive bile salts: large stool volumes, with normal ionic contents. Fasting does not change stool volume.
2. Osmotic - poorly absorbed substances retain intestinal fluids: lactose intolerance, malabsorption, osmotic laxatives. Stops with fasting.
3. Exudative - generally associated with inflammatory gut diseases. Mucus, serum protein, and blood are discharged into the gut.
4. Altered Intestinal Motility - hypermotility decreases the contact time for chyme to have electrolytes reabsorbed. Ineffective motility increases contact time and can lead to bacterial overgrowth.
5. Chronic vs. Acute
Diarrhea Therapy
1. Diarrhea, like a cough, can be the body's mechanism to rid itself of harmful substances. The end goal is not necessarily stopping the diarrhea at all costs.
2. Diet: Stop solid foods and avoid dairy products if possible for 24 hours. Advance slowly as tolerated (n/v?). Feeding should continue in children in acute bacterial diarrhea.
3. Search for iatrogenic causes: excessive laxatives in the elderly, antibiotics.
4. Repletion: maintenance of water and electrolyte balance. If n/v are not present then oral route is preferred. WHO-ORS is probably the best. Its use in third world countries has saved millions of lives. Glucose can be absorbed even during diarrhea, drawing electrolytes and water with it.
Diarrhea Drugs
Opiates:
Diphenoxylate/Atropine (Lomotil): PO and controlled substance (V)
Loperamide (Imodium): PO and OTC
Patho of Diabetes Mellitus
Production of insulin: the pancreas produces two opposing products: glucagon and insulin. The alpha islet cells produce glucagon and the beta islet cells produce insulin. Glucagon is catabolic and insulin is anabolic.
Proinsulin
metabolic precursor to insulin
C protein
cleaned off of proinsulin leaving the active hormone insulin
Insulin
a polypeptide hormone with two chains linked together by disulfide bridges between the cysteine amino acids.
Metabolic effects of insulin
: insulin receptors are widely dispersed on cell membranes. They have only been clearly identified in muscle, fat, and liver tissue. They are G protein mediated receptors. Phosphorylation of proteins appears to be the key second messenger mechanism. Insulin is necessary for the transmembrane transport of glucose by many tissues, including the liver in glycogen formation. Insulin is not required by the brain, nerves or kidneys. Several glucose transporters have been identified.
DM I
There are no functioning, secreting beta islet cells. Due to the absence of insulin there is a tendency towards ketoacidosis. Onset of the disease generally occurs in juveniles and young adults but can occur up to 40+ years of age. Rate: 10% of diabetics.

Cause: antibody formation against beta islet cells? It may be triggered by viruses, chemicals or other environmental agents in genetically susceptible individuals. Immunosuppressants have been used experimentally during early onset to inhibit progression of disease. There is familial risk.

Treatment: diet, exercise, INSULIN
DM II (non-obese)
The pancreas can secrete some insulin, but response is delayed and or inadequate. Ketoacidosis is rare due to presence of some insulin. Onset generally occurs over the age of 25 years and comprises 10% of diabetics.

Cause: unknown, but it does run in families.

Treatment: diet, exercise, sulfonylureas and/or insulin if necessary
DM II (obese)
The pancreas can secrete near normal amounts of insulin especially in the early phases of the disease. The effects of the insulin are inadequate. Again, there is little tendency toward ketoacidosis. Type II DM generally occurs in the mature population, comprising 80% of diabetics.

Cause: obesity leading to a decrease in the number of insulin receptors and or a post receptor defect leading to diminished peripheral glucose uptake and post-prandial hyperglycemia. Excess hepatic glucose production occurs because gluconeogenesis is not sufficiently inhibited by the insulin resulting in fasting hyperglycemia.

Glucotoxicity: Chronic hyperglycemia causes a desensitivization or resetting of the glucose "thermostat" upward. A higher percentage of the secreted product is proinsulin.

These over-used beta islet cells "age" faster than in the non-diabetic resulting in a gradual advance of the disease toward a type I like character.

Treatment: diet, exercise, oral hypoglycemic and/or insulin.
Acute complications of DM
Diabetic ketoacidosis (DKA)
Hyperglycemic, hyper osmolar non-ketotic coma (HHNC)
Hypoglycemia
Chronic complications of DM
Nephropathy
Retinopathy
Neuropathy
Peripheral vascular disease
Monitoring of blood glucose
Urine vs. blood monitoring
Value of tight control: glycosylated hemoglobin
Non-Pharmacological Interventions (Diet)
Calories - They need to be restricted in the obese to improve responsiveness. However it is important in young individuals to provide sufficient for normal growth and development.

Content - Fat should comprise 30% of total calories at most. Carbohydrates ideally will run 55-60% and protein 10-20% of total. Soluble fiber slows absorption of the carbohydrates. Alcohol should only be used in moderation with food.
Non-Pharmacological Interventions (Exercise)
improves muscle utilization of glucose and lipids. It is an important adjunct to diet in achieving weight loss and improves cardiovascular function.

Cautions: hypoglycemia, cardiovascular disease
Pharmacological Interventions - Oral Hypoglycemics - First and Second Sulfonylureas
First generation sulfonylureas

Tobutamide (Ornase): PO
Tolazamide (Tolinase): PO
Chlorpropamide (Diabinese): PO

Second generation sulfonylureas
*more potent*
Glyburide (DiaBeta, Micronase): PO
Glipizide (Glucotrol): PO
Glimepiride (Amaryl): PO

Uses: Type II DM, alone or in combination with insulin.
Cautions: The most common problem is hypoglycemia. Once dosed, food must be consumed. There are a number of drug interactions associated with some. Disulfiram reaction can occur with chlorpropamide.
Pharmacological Interventions - Oral Hypoglycemics
Glinides
Repaglinide (Prandin): PO
Nateglinide (Starlix): PO

Glinides: similar in action to sulfonylureas, but not structurally related. Same cautions as sulfonylureas.
Use : Type II DM
Pharmacological Interventions - Oral Hypoglycemics
Biguanide
Metformin (Glucophage): PO

Biguanide: mechanism is not well defined. It may include: direct stimulation of glycolysis in peripheral tissues, reduced hepatic gluconeogenesis, slowed absorption of glucose from the intestinal tract, reduction of glucagon levels and increased insulin binding to receptors. Metformin tends to be more "euglycemic". It does not really lower a normal glucose level.

Uses: Type II DM, gestational diabetes

Cautions: Earlier related compound are associated with lactic acidosis. This side effect caused withdrawal from US market. Metformin was just released. Most frequent problems are nausea, vomiting and diarrhea which can be transient.
Pharmacological Interventions - Oral Hypoglycemics
Alpha-glucosidase inhibitors
Acarbose (Precose): PO
Miglitol (Glyset): PO

Alpha-glucosidase inhibitors: inhibit the intestinal enzyme involved in the breakdown of carbohydrates into simple sugars (single ring) thereby delaying the absorption of the sugars.

Uses: an adjunct to sulfonylureas in type II DM

Cautions: Must be taken with first bite of each meal. Compliance is a pain. Sucrose (like in candy) does not work well to treat acute episodes of hypoglycemia, therefore glucose must be used. Excess luminal sugar can lead to diarrhea.
Pharmacological Interventions - Oral Hypoglycemics
Thiazolidinediones
Rosiglitazone (Avandia): PO (going off market too?)
Pioglitazone (Actos): PO

Thiazolidinediones (glitazones) potentiate the action of insulin to increase glucose uptake and glucose oxidation and reducing hepatic glucose output (gluconeogenisis) and lipid synthesis in muscle and fat cells. Lowers insulin resistance!

Uses: for patients with insulin resistance that are receiving insulin.

Cautions: hepatic disease. They may cause some hepatic toxicity. Troglitazone (Rezulin) withdrawn from market for hepatic toxicity.
Pharmacological Interventions - Oral Hypoglycemics
Incretin mimetics
Sitagliptin (Januvia): PO (DPP-4 inhibitor)
Exenatide (Byetta): Sub Q (GLP-1 analogue)

Incretin mimetics increase the level of incretin hormones, increases insulin secretion and decreases glucagon secretion to reduce gluconeogenesis.
Use: Type II diabetes
Pharmacological Interventions - Oral Hypoglycemics
Amylin mimetic
Pramlintide (Symlin): Sub Q

Amylin mimetic: acts like the endogenous beta-islet cell product: slows gastric empyting, suppresses glucagons secretion and hepatic gluconeogenesis, and increases satiety.
Uses: Type I or II diabetes requiring meal-time injections of insulin without satisfactory response.
Insulin
Human - recombinant DNA technology; least antigenic, standard for new patients.
Extra Rapid Acting Insulin
Insulin lispro (Humalog) onset: 5-15 minutes peak: 30-90minutes Duration: 2-5hours
Insulin aspart (Novolog) onset: 5-15 minutes peak: 1-3hours Duration 3-5 hours
Insulin glulisine (Apidra) onset: 5-15 minutes peak: 30-90min Duration 1-2.5hours
Rapid Acting (Short) Insulin
Insulin regular (Humulin R, Novolin R) onset: 30 minutes peak:2-4 hours Duration 6-8 hours
Intermediate Insulin
NPH (Humulin N, Novolin N) onset: 1-2 hours peak 6-12 hours Duration 18-24 hours
Insulin lente (Humulin L, Novolin L) onset: 1-2 hours peak 8-12 hours Duration 18-24 hours
Long acting Insulin
Insulin ultralente (Humulin U) onset: 5-8 hours peak 14-20 hours Duration 30-36 hours
Insulin glargine (Lantus) onset: 1 hour no peak Duration 24 hours
Insulin detemir (Levemir) onset: 1hour no peak Duration 22-26 hours
Insulin Subcut Admin
Based on S.C. administration. Varies from patient to patient, site to site. Regular is the only form that can be administered I.V.: onset 10-30 minutes, peak 15 - 30 minutes, duration 30 - 60 minutes.
Storage and Handling of Insulin
Long term - refrigerate

Short term - 28 days at room temperature
The vials in active use should be stored at room temperature. The room temperature insulin may cause fewer skin reactions than cold insulin.
Administration of Insulin
IV: only regular! There are specially buffered versions available for low volume continuous infusion pumps. (Humulin BR, Velosulin)

SQ: locations, differences

Extemporaneous mixing:
1. Regular insulin may be mixed with NPH, lente and ultralente.
2. NPH, lente and ultralent can be mixed only with regular insulin.
3. Lentes can be mixed with other ultralente.

4. Never shake the vial, roll between hands. Always draw up regular insulin first. Use within 5 minutes. If it sits for more than a few minutes, the ratio of regular to long acting will change
Premixed Products
NPH/Reg as 70/30 and 50/50.
NPH/Novolog or Humalog as 70/30, 75/25, 50/50
Sliding Scales
based on FSBS or blood glucose
Hypoglycemia
Rapid decline from high levels can give patients hypoglycemic symptoms.
the most life threatening short term:

Mild - Blood glucose <60 mg/dL.

Severe - Blood glucose < 40 mg/dL.
S/S Hypoglycemia
Mild symptoms - Anxiety, shakiness, nausea, increased pulse rate and palpitations: all related to sympathetic stimulation. Other symptoms include difficulty concentrating, confusion, and headache (CNS dysfunction).

Severe symptoms - Disorientation, shallow respirations, inability to respond to stimuli, loss of conscious, and seizures (CNS)

Nocturnal - A.M. headaches, night sweats, restlessness, nightmares
TX of Hypoglycemia
• In conscious patient give sugar cubes, honey, hard candy, etc.

• If swallowing impaired and at home give: glucagon - hormone produced by alpha islet cells of pancreatic. Clinical Uses - Insulin overdosage - Increases blood glucose levels. Family members need to be taught how to administer.

• In acute care setting - IV glucose
Hypoglycemia Info
Occasional mild episodes of hypoglycemia may occur in most every diabetic. Frequent mild or occasional severe reactions are unacceptable, may cause brain damage & require alteration in insulin treatment. Loss of early signs and symptoms may also occur increasing the risk of hypoglycemia.

Golden Rule of Hypoglycemia - Leaving patient untreated is more dangerous than causing a mild hyperglycemia with overtreatment.
Patient Education On Hypoglycemia
Recognize limitations: Focus, Individualize, Review and Practice
Involvement of family members: Diet
Periodic Reassessment: glycosylated hemoglobin

Assess for and enhance therapeutic effects: decreased blood glucose levels to 80-120 mg/dl (fasting), absent ketones in urine, no polyphagis, polydipsia, and polyuria. Normal energy levels. Time both meals & insulin administration strictly. Assess for and minimize adverse effects. Assess for S&S of hypoglycemia at appropriate times for particular insulin. Clarify insulin or oral hypoglycemic agent orders for patients that are NPO for surgery or tests or are vomiting.
Essential Fatty Acids
Linoleic and linolenic acid: 18 carbon fatty acids
Arachidonic acid: a 20 carbon fatty acid that can be made from linoleic acid.
Biogenesis of the Eicosanoids
The first step: Arachidonic acid (a fatty acid) undergoes cyclization by the enzyme type cyclooxygenase (COX). The is a type I and a type II.
Divergent synthesis by various enzymes to respective products: prostaglandins, thromboxanes and leukotrienes.
Cyclooxygenase inhibitors (NSAIDs) and corticosteroids do inhibit synthesis of eicosanoids.
Mechanism of Action: Eicosanoids
All receptors appear to be G protein mediated. Variation in action may have more to do with receptor distribution, quantity and cell types than by mechanism.
Effects: Eicosanoids
depends on which one and where in the body:
PGE2 & PGF2a are potent oxytocics. They may be mediators during dysmenorrhea. PGE2 is used commercially to soften the cervix during labor
Agents: Eicosanoids
Alprostadil (Prostin VR Pediatric): IV- maintain patency of ductus arteriosus
Dinoprostone (Prostin E2): vaginal suppository- effacement of cervix
Misoprotol (Cytotec): PO protection of GI mucosa, vaginal effacement
Latanoprost (Xalatan): ophthalmic, treatment of glaucoma
Bimatoprost (Lumigan, Latisse): ophthalmic, treatment of glaucoma
Travoprost (Travatan): ophthalmic, treatment of glaucoma
Unoprostone (Rescula): ophthalmic, treatment of glaucoma
Asthma Definition
A disease characterized by hyperreactivity of bronchial tissue resulting in a decrease force expiratory rate. Histological changes are marked by:
A. Hypertrophy and hyperplasia of airway smooth muscle.
B. Increased airway wall thickness caused by an exudative inflammatory reaction and edema.
C. Mucous gland hypertrophy and mucus hypersecretion.
D. Epithelial damage, denudation (due to eosinophilia?).
The basic underlying feature to the hyperreactivity is the inflammatory process.
Asthma Triggers: Respiratory Infections
RSV, rhinovirus, influenza, Mycoplasma pneumonia
Mechanism: Inflammation and epithelial damage sensitizing cholinergic irritant receptors: virus-induced relative β blockade possibly contributes
Asthma Triggers: Allergens
airborne pollens, house dust, animal dander, dust
Mechanism:IgE mediated mast cell histamine release.
Asthma Triggers:Enviroment/Occupational
chemicals, dusts, cold air, ozone, sulfur dioxide, nitrogen dioxide
Mechanism:IgE mediated and or epithelial damage with neutrophil infiltration.
Asthma Triggers: Exercise
Mechanism: Hyperventilation with loss of water and cooling of the airways and mast cell histamine release.
Asthma Triggers: Emotions
anxiety, fatigue, stress, laughter
Mechanism: Parasympathetic stimulation; augments pre-existing event, generally not a primary event.
Asthma: Diagnosis
• History - cough, timing, events, description
• Physical assessment -
• Pulmonary Function Test - abnormal, or normal but + for reactivity
• Skin Tests - identifying potential triggers
Pathogenesis : Asthma
• Early asthmatic response (EAR): Prompt onset with spontaneous improvement after about 1 hour. Due to release of pre-formed cellular mediators in mast cells.
• Late asthmatic response (LAR): Second bronchconstrictive event occurring 4 to 12 hours after initial exposure. Duration 2 to 4 hours. LAR is cause by infiltration of inflammatory cells.
• Exercise induced asthma (EIA): Similar to EAR but infrequently associated with LAR.
Non-Pharmacologic Management: Asthma
- Identification and avoidance of triggers: skin tests, careful history
- Vaccination, allergy shots (if applicable)
- Early oxygen therapy to mitigate LAR. Hypoxia increases inflammation.
Pharmacologic Management: Asthma; Mast Cell Stabilizers
Cromolyn (Intal, Gastrocrom): Inh, PO
Nedocromil (Tilade): Inh

Mech: Inhibit the mast cell release of histamine and leukotrienes.

Uses: Prophylaxis; useful in pre-treatment before trigger exposure (i.e.: exercise). They reduces baseline inflammation with chronic treatment, which reduces reactivity.

Limitations: Not effective for bronchoconstrictive phase. They are poorly absorbed orally. Do not appear to stabilize dermal mast cells.
Pharmacologic Management: Asthma; Methyxanthines
Aminophylline: PO, IV
Oxtriphylline (Choledyl): PO
Theophylline (Theo-Dur, Slo-Phyllin, Uniphyl, Theo-24): PO

Mech: Not clearly defined. Elevation of cAMP by inhibition of phosphodiesterase appears to be part of the mechanism. Principal effect is on smooth muscle, resulting in bronchodilation. It does have some effects on striated muscle with strengthening of diaphragmatic contraction. While caffeine is more noted as a CNS stimulant, theophylline will increase alertness. Effects of Methylxanthines can be additive.

Uses: Treatment of moderate to severe acute episodes of bronchoconstriction as well as chronic states.

Limitations: While quite safe, toxicity will frequently include nervousness, tremors, and occasionally seizures, tachycardia, dysrrhythmias. Does increase SVR probably through catecholamine release. Nausea and vomiting can occur.

There are numerous drug interactions:
Inhibit elimination - Cimetidine (-35 to 60%), Erythromycin (-25%), Allopurinol (-20%), BCPs (-10 to 30%), Propranolol (-30%), Quinolones (-25 to 30%)

Increase elimination - Rifampin (+50%), Carbamazepine (+50%), Phenobarbital (+30 to 90%), Phenytoin (+70%), Smoking (+40%)
Pharmacologic Management: Asthma; Beta Agonists
Albuterol (Proventil, Ventolin): PO, Inhaled - β2
Terbutaline (Brethine, Bricanyl, Brethaire): PO, Injectable, Inhaled - β2
Metaproterenol (Alupent, Metaprel): PO, Inhaled - β1 & 2
Isoetharine (Bronchometer, Bronchosol): Inhaled - β1 & 2
Isoproterenol (Isuprel): Inhaled, Injectable - β1 & 2
Epinephrine (Primatene Mist): Inhaled - α and β
Salmeterol (Serevent): Inhaled - β2 - long acting, slower onset? Not for rescue!
Fomoterol (Foradil): Inhaled - β2- long acting, slower onset? Not for rescue!

Mech: As discussed previously, β2 receptors in the lungs trigger bronchodilation. β1 receptors lead to increased heart rate and forcefulness of contraction.

Uses: First line treatment of acute episodes and chronic prophylaxis by reduction of underlying inflammation. Salmeterol is not indicated for acute therapy (rescue).

Limitations: Receptor selectivity is concentration dependent: tachycardia, nervousness, etc. β2 selective agents are generally better tolerated, with less risk of tachyphylaxis. Epinephrine (Primatene Mist) is trouble, especially since it is OTC.
Pharmacologic Management: Asthma; Antimuscarinics
Ipratropium (Atrovent): Inhaled - immediate onset, short acting
Tiotropium (Spiriva): Inhaled - long acting, delayed onset

Mech: Competitive inhibition of vagal muscarinic receptors, decreasing vagal tone of bronchial smooth muscle and decreasing secretions, especially mucus.

Uses: Second line bronchodilator which can be nearly as effective as beta agonists. It is quite useful in patients intolerant of beta stimulation and perhaps more effective in COPD. It can be a second agent to β stimulators due to its different mechanism. Since it is a quaternary compound, there is poor absorption, resulting in little or no systemic effect.

Limitations: Not as useful in acute bronchoconstriction and is limited to the extent of cholinergic tone. Tiotropium should not be considered for rescue.
Pharmacologic Management: Asthma; Corticosteroids
Prednisone (Deltasone): PO
Methylprednisolone (Medrol, SoluMedrol): PO, IV
Beclomethasone (Beclovent, Vanceril): Inhaled
Triamcinolone (Azmacort): Inhaled
Flunisolide (AeroBid): Inhaled

Mech: Modify the inflammatory response possibly by inhibiting eicosanoid production; including prostaglandins, thromboxanes and leukotrienes.

Uses: First line drug in newly diagnosed asthmatics. High oral or intravenous doses followed by tapering doses in moderate to severe episodes. Switch to inhaled agent as tolerated for less systemic effects.

Limitations: Classic Cushingoid symptoms are problems in long term systemic doses: weight gain, fat re-deposition, hyperglycemia, skin thinning, etc. Most desirable to switch to inhaled agent when possible or if oral is necessary, then the smallest effective dose.
Pharmacologic Management: Asthma; Leukotriene Receptor Antagonists
Montelukast (Singulair): PO
Zafirlukast (Accolate): PO
Zileuton (Zyflo): PO

Mech: All block the inflammatory processes associated with asthma by interfering with inflammatory signals mediated by leukotriene D4. Zileuton inhibits 5-lipoxygenase, the enzyme responsible for the synthesis of leukotienes. Montelukast and zafirlukast block the LTD4 receptor.

Uses: These drugs are intended for prophylaxis or as preventative agents, where they reduce the underlying inflammation and hopefully educe the required steroid dose. Improvement in symptoms can take 7 to 10 days and is usually gradual.

Limitations: None are indicated for acute symptoms. All are metabolized through the liver and a number of drug interactions are noted. Montelukast: occasional reports of mild headache, fatigue, dizziness, GI upset, cough and elevation of transaminases (hepatic). Rare reports of severe behavior/mood changes, angioedema and heptatitis were found on post-marketing surveys. Zafirlukast: similar reports but headaches are more common. Zileuton: more reports of CNS pain, chest pain, myalgias and respiratory symptoms but behavior/mood changes are rare.
Release Mechanisms- Histamine - Immunologic: mast cells
granules contain inactive form mixed with heparin, ATP, or other proteins. Release mediated by IgE result in immediate (type I) reactions or release mediated by IgG or IgM activation
Release Mechanisms- Histamine - Neurotransmitter
some tissues, notably the brain have nerve fibers that release histamine as a neurotransmitter. The mechanisms are nearly identical to those of adrenergic fibers
Histamine Receptors
o H1: Predominantly found in vascular endothelial and smooth muscle cells, which causes an increase of intracellular calcium.
o H2: Predominantly in gastric mucosal cells, cardiac muscle, and some immune cells increases intracellular cAMP.
o H3: Presynaptic in the brain and other areas of the CNS and inhibits histamine release.
Histamine Effects
Cardiovascular - decrease in blood pressure, increase in heart rate, edema (vascular endothelial cell leak)
Gastrointestinal - smooth muscle contraction of intestine (H1), parietal cell secretion (H2)
Nerve endings - powerful stimulant of sensory nerve endings and is involved in the pain of stings
H1 Blockers
antihistamines: competitive inhibition of the H1 receptor

Uses: allergic reactions, motion sickness (not related to H1 blockade), sleep aid (not related to H1 blockade), antiparkinsonism effects (not related to H1 blockade). Many have antimuscarinic effects too.

Agents:
Diphenhydramine (Benadryl): PO, IV - sleep, EPSE
Dimenhydrinate (Dramamine): PO, IV - motion sickness
Tripelennamine (PBZ): PO
Cyclizine (Marezine): PO - motion sickness
Meclizine (Antivert, Bonine): PO - motion sickness
Brompheniramine (Dimetane): PO
Chlorpheniramine (Chlor-Trimeton): PO
Promethazine (Phenergan): PO, PR, IV, IM (a phenothiazine) - N/V
Cyproheptadine (Periactin): PO - also serotonin blocker
Loratadine (Claritin): PO - causes little sedation, longer acting
Fexofenadine (Allegra): PO - ditto
H2 blockers - competitive inhibitors
Uses: Suppress acid secretion of the stomach - gastritis, duodenal ulcers, gastric ulcers, stress ulcers, hyper secretory disorders

Cimetidine (Tagamet): PO, IV - drug interactions cytochrome P450, gynecomastia, mental confusion in elderly
Ranitidine (Zantac): PO, IV - few side effects
Famotidine (Pepcid): PO, IV - few side effects
Nizatidine (Axid): PO - few side effects
Decongestants
Think VASOCONSTRICTION
Agents:
Ephedrine (various) po, topical, IV. Not particularly centrally acting. Vasoconstrictor, decongestant, pressor. Controlled substance.
Pseudoephedrine (Sudafed) po. Decongestant. Not particularly centrally acting. Isomer of ephedrine. OTC, but requires signature.
Oxymetazoline (Afrin) topical. Long duration. Tendency to rebound congestion and prolonged use.
Phenylephrine (Neosynephrine, Sudafed PE) PO, topical, iv. Available in various strengths for topical application, even for pediatric use.

Uses: nasal congestion, treating sinus infections, nasal bleeding, eustacian tube congestion
Nasal Glucocorticoids
Reduce chronic inflammation, drainage and fuction. Helps stabilize mast cells, reduce reactivity. Inhibit allergy symptoms by immunosuppression
Agents:
Beclomethasone (Vancenase, Beconase)
Budesonide (Rhinocort)
Dexamethasone (Decadron)
Flunisolide (Nasalide)
Fluticasone (Flonase)
Triamcinolone (Nasacort)
Antitussives
Most commonly available in combinations with other drugs for multiple symptom relief.

Agents:
Codeine (in Robitussin AC)
Hydrocodone (in Hycotuss, Hycodan)
Dextromethorphan (in Robitussin DM)
Benzonatate (Tessalon): Non-opiate!!!!!!!

Expectorant: Only one of significance: Guaifenesin (Robitussin, Mucinex)

Combination products: This is an area of considerable confusion and controversy. OTC commercial products contain often 4, 5 and sometimes 6 different drugs together: analgesics, decongestants, antihistamines, antitussive and expectorant for good measure. Focus on what you are treating. Naming of these products is VERY unhelpful. Repeated brand names are used with variants in additives!
Innate Immune System: Nonspecific Body Defence
First line of defence
Mechanical
Skin/epidemis
Mucus
Inflammation is triggered when mechanical barriers are defeated by non-self items
Biochemical
Complement
Enzymes
Interferons
pH
Free radicals (oxygen source)
Cellular recruitment by cytokines: cellular immunity turned on
Neutrophils
Monocytes
Macrophages
Natural Killer
Dendritic cell
Adaptive Immune System
• Mobilzed by cues from the innate response when innate is incapable of coping
• Antigen presenting cells- phagocytes present to T cells
• T helper cells "instruct" B cells, and others select out self immune
• Memory B cells, memory T cells confer future immunity and reducing time to respond to future exposures
• Bell cell plasma cell produce specific antibody
• Antibody response to antigen optimizes cellular reponse
Vaccines: active immunity
• Trigger immune activation before exposure to a real pathogen
• Types of vaccines:
• Attenuated (live): weakened and unable to produce full disease but can produce subclinical symptoms; generally produce strong immunity (MMR, OPV). Do not use in pregnancy or immunocompromized.
• Inactivated (killed): unable to reproduce or cause disease, made from viral parts and protein, bacterial toxins and recombinant partial organisms and proteins. Boosters are often necessary.
Diphtheria, tetanus, pertussis - child
IM 0.5 mL @ 2 mo, 4 mo, 6 mo, 18 mo
Killed Vaccine
Diphtheria, tetanus, pertussis - adult
IM 0.5 mL adult booster
Killed Vaccine
Haemophilus influenza type B
IM 0.5 mL 2 mo, 4 mo, 6 mo, 15 mo
Killed Vaccine
Hepatitis A- child
IM 0.5 mL 12 mo, booster 6-12 mo later
Killed Vaccine
Hepatitis A- adult
IM 1 mL, booster 6-12 later
Killed Vaccine
Hepatitis B - child
IM 0.25 mL at birth, 0.5 mL at 1-4 mo, 6-18 mo
Hepatitis B - adult
IM 0.5 mL, booster 1 mo, 6 mo
Killed Vaccine
Human papillomavirus - child
IM 0.5 mL at age 11-12 years
Killed Vaccine
Influenza vaccine - child
IM 0.5 mL annual, booster 1 mo
Killed Vaccine
Influenza vaccine - adult
IM 0.5 mL annual, booster?
Killed Vaccine
Influenza vaccine - 5y to adult
Nasal annual
Live Vaccine
Measles, mumps, rebella (MMR)
SQ 0.5 mL @ 15 mo
Live Vaccine
Pneumococcal 7 valent - child
IM 0.5 mL 2 mo, 4 mo, 6 mo, 12-15 mo
Killed Vaccine
Pneumococcal 23 valent - adult
SQ or IM 0.5 mL once, at risk adults
Killed Vaccine
Poliovirus (IPV) - child
SQ 0.5 mL 1-2 mo, 2-4 mo, 6-12 mo
Killed Vaccine
Poliovirus (OPV) - adult
PO 1 dose, once (limited use)
Live Vaccine
Rabies preexposure
IM 0.5 mL days 0, 7, 21 or 28
Live Vaccine
Rabies postexposure
IM 0.5 mL days 0, 3, 7 and 14
Live Vaccine
Rotavirus
PO 3 doses between 14 weeks to 32 weeks
Live Vaccine
Varicella
SQ 0.5 mL, booster 1-2 mo if after 13 y
Live Vaccine
Zoster
SQ 0.5 mL once
Live Vaccine
Passive immunity
• Preformed antibody is donated or transferred
• Maternal to fetus, child
• Immune globulin, general, mixed immunity:
o Used to treat immune deficiencies
o Used to treat auto-immune disorders
• Immune globulin, specific:
o Used to prevent disease
o Used after exposure: antivenin
• Temporary benefit
Immune Modifiers
boost specific functions of the immune system
• Interferons
• Interleukins
• Used to treat numerous disorders: Hepatitis B, C; Kaposi's sarcoma, bladder cancer
Immmunosuppressants
• Used to dampen imune response in transplant rejection
• Control autoimmune disorders
Antibodies; Basiliximab
Mechanism/Use: Inhibits interleukin II/organ rejection
Adverse Reactions:Local reaction to anaphylaxis
Antibodies; Infliximab
Mechanism/Use: TNF blocker/rheumatoid arthritis, Crohn's
Adverse Reactions:Local reaction to anaphylaxis
Antibodies; Antithymocyte globulin
Mechanism/Use: Renal rejection, severe aplastic anemia
Adverse Reactions:Local reaction to anaphylaxis
Cytotoxic; Azathioprine
Mechanism/Use: Inhibit DNA synthesis/renal rejection, rheumatoid arthritis
Adverse Reactions:N/V, thrombocytopenia, anemia, alopecia
Cytotoxic; Cyclophosphamide
Mechanism/Use: Alkylating agent/rheumatic arthritis
Adverse Reactions:N/V, thrombocytopenia, hemorrhagic cystitis
Cytotoxic; Methotrexate
Mechanism/Use: Inhibit DNA synthesis/rheumatic arthritis
Adverse Reactions:N/V, stomatitis, alopecia
Immune modulators; Mycophenolate
Mechanism/Use: Inhibits B T cell proliferation/ renal rejection
Adverse Reactions:N/V, hypertension, edema, hyperglycemia
Immune modulators; Sirolimus
Mechanism/Use: Inhibits cytokine, antibody / organ rejection
Adverse Reactions:Renal failure, CHF, neuropathy
Immune modulators; Temisirolimus
Mechanism/Use: Inhibits cytokine, antibody / organ rejection
Adverse Reactions:Renal failure, CHF, neuropathy
Immune modulators; Tacrolimus
Mechanism/Use: Supress B, T cells/ organ rejection
Adverse Reactions: Hypertension, edema, diabetes
Immune modulators; Cyclosporin
Mechanism/Use:Inhibit inerleukin II / organ rejection
Adverse Reactions:Renal failure, hypertension, endocrine
Etiology of Cancer
• Carcinogens can act as initiators and promoters. They include chemical, physical (radiation) or biological (viral) agents.
• Oncogenes: non-random chromosomal changes in genes that normally are involved in regulation of cellular function, such as tumor suppressor genes.
• Controllable causes: environmental, predisposing disease.
• Uncontrollable causes: familial traits, unidentified causes.
• Tumor development: initiation, promotion, progression, metastasis.
Tumor Burden
the numbers that count
Clinically detectable tumor is about 1 g in mass = 109 cells. That is about 30 doublings from 1 cell. A lethal tumor is about 1 kg in mass = 1012 cells. That is only another 10 doublings. A drug that kills 99.9% of the cells in a tumor leaving only 1 in a 1000 cells alive only reduces the exponent by 3. In the majority of a tumor's life, it is undetectable.

Resistance: primary and acquired. Some tumor types do not respond at all, showing primary resistance. Many tumors are heterogenous. Once mutation begins, the process continues. Cells with resistance mutations are selected and continue to multiply. These tumors respond initially then later fail, showing acquired resistance.
The Cell Cycle
G0 - resting phase of the cell. Most normal cells live the majority of their lives in this phase.

G1 - the cells prepares for DNA synthesis by preparing the enzymes and necessary substrates for DNA synthesis. (40%)*

S - DNA synthesis takes place. (39%)*

G2 - the cells produce RNA, specialized enzymes and the mitotic spindle apparatus. (19%)*

M - the cells splits (mitosis). (2%)*

*portion of the growth phase only (G1- M)

The cell cycle is normally regulated by lymphokines, hormones and growth factors.
The Cell Cycle
Some agents attack the cell during a specific phase of growth. They are known as cell cycle specific (CCS) agents. Others attack without regard to the phase. They are known as cell cycle nonspecific (CCNS). CCS agents tend to be more effective with tumors with a high percentage growth fraction such as hematologic malignancies. CCNS agents are useful in low growth fraction malignancies such as solid tumors. CCS agents include the antimetabolites, the podophyllin alkaloids, the vinca alkaloids and bleomycin. CCNS agents include the alkylating agents, antibiotics, nitrosoureas and cisplatinum and related compounds.
Nucleic Acid Chemistry : DNA
the "zipper", is coded by a precise sequence of nucleotides. Each nucleotide is made up of a sugar (deoxyribose), phosphoric acid and a base. There are four bases in DNA: adenine (A), thymine (T), guanine (G) and cytosine (C). A and G are chemically purines. T and C are pyrimidines. Two strands are held together by chemical bonding between two bases. Only A bonds with T, and only G bonds with C in what is called complementary base pairing. DNA is read or transcripted when an enzyme "unzips" a specific portion of a gene, another enzyme using base pairing, creates an RNA "mirror" image of the DNA. An enzyme then "rezips" the DNA back together.
Nucleic Acid Chemistry : RNA
consists of a sugar (ribose), phosphoric acid and four bases. The four bases are the same except that uracil (U) is substituted for T. There are three known types of RNA: messenger RNA (mRNA), transfer RNA (tRNA) and ribosomal RNA (rRNA). mRNA is the product of DNA transcription, and it is "read" during protein synthesis. tRNA retrieves the appropriate aminoacid for the ribosome during protein synthesis.
Nitrosoureas (alkylators)
Carmustine (BiCNU, Gliadel Wafer) [po] - Irritant, Leukopenia, thrombocytopenia, secondary malignancies
Lomustine (CeeNU) [po only] - Irritant, Leukopenia, thrombocytopenia, secondary malignancies
Alkylating Agents and related compounds
Alkylating agents act by forming chemical bridges between the two sides of the DNA zipper. The zipper becomes stuck. This can occur during any phase of the cell cycle, but cell death occurs when the cell enters or is in one of the growth phases. Active alkylating agents are vesicant. An exception is cyclophosphamide which has to be activated metabolically and is not vesicant. Most are CCNS.
Classic alkylating agents
Mechlorethamine (Mustargen) - Vesicant, Bone marrow depression
Bendamustine (Treanda)- Vesicant, Bone marrow depression
Chlorambucil (Leukeran) [po only]- Vesicant, Bone marrow depression + pulmonary fibrosis
Melphalan (Alkeran) [po] Irritant, Same
Busulfan (Myleran, Busulfex) [po] Irritant, Same + pulmonary fibrosis, skin pigmentation, adrenal insufficiency
Cyclophosphamide (Cytoxan) [po] Irritant, Same + alopecia, hemorrhagic cystitis
Platinum Analogs
Cisplatin (Platinol) - Vesicant, Bone marrow depression + renal & acoustic nerve damage
Carboplatin (Paraplatin)- Irritant, Same but less renal and nerve damage
Oxaliplatin (Eloxatin) - Irritant nearly vesicant, Bone marrow depression + neuropathy
Antimetabolites; Analogue of : Folic Acid
Methotrexate (MTX) [po] -Delayed Toxicity: enteric mucosal ulceration, bone marrow depression
Pemetrexed (Alimta)- Delayed Toxicity: enteric mucosal ulceration, bone marrow depression
Pralatrexate (Folotyn)- Delayed Toxicity: enteric mucosal ulceration, bone marrow depression
Nonclassic Alkulating Agents
Dacarbazine (DTIC) Irritant, Bone marrow depression
Procarbazine (Matulane) [po only] Bone marrow depression + MAOI substrate
Antimetabolites
Antimetabolites are structural analogs (close but no cigar) to many compounds that are important in the synthesis of nucleic acid synthesis. They "mess with" the various enzyme systems involved in the synthesis of nucleic acid and/or provide a false substrate for their synthesis. This results in inhibition of nucleic acid synthesis or a defective product. Most are S phase specific.
Antimetabolites; Analogue of : Pyrimidine
Fluorouracil (5-FU, Adrucil) - Delayed Toxicity: enteric mucosal ulceration, bone marrow depression
Cytarabine (ara-C, Cytosar-U)
Capecitabine (Xeloda) - Delayed Toxicity: N/V, bone marrow depression, alopecia
Cytarabine - Delayed Toxicity: N/V, bone marrow depression, alopecia
Gemcitabine (Gemzar) - Delayed Toxicity: N/V, bone marrow depression, alopecia
Antimetabolites; Analogue of : Purine
Fludarabine (Fludara) - Delayed Toxicity: Myelosuppression, neurotoxicity
Thioguanine (6-TG) [po]- Delayed Toxicity: Bone marrow depression
Mercaptopurine (6-MP) [po] - Delayed Toxicity: Bone marrow depression
Fludarabine (Fludara) - Delayed Toxicity: Bone marrow depression
Cladribine - Delayed Toxicity: Bone marrow depression
Topisomerase I inhibitors: affect the S phase of the cell cycle.
Topotecan ( Hycamtin)- Delayed Toxicity: Irritant, alopecia, nausea and vomiting, peripheral neuropathy, stomatitis
Irinotecan (Camptosar)- Delayed Toxicity: Irritant, same plus diarrhea
Plant Alkaloids
The vinca alkaloids are found in the plant Vinca rosea or the periwinkle. They are M phase specific agents that act on the microtubules which are an important part of the cytoskeleton, especially during mitosis.
Plant Alkaloids; Agents
Vincristine (Vincasar) - Vesicant, mild bone marrow depression, alopecia, neurotoxicity
Vinblastine (Velban)- Vesicant, bone marrow depression, alopecia, loss of reflexes
Vinorelbine (Navelbine)- Vesicant, same
Tyrosine Kinase inhibitors
inhibit the signal transmission between normal and tumor cells inhibiting cellular proliferation and angiogenesis.
Paclitaxel is an alkaloid derived from the Western yew (Taxus brevifolia) and the European yew (Taxus baccata). The original question was: how many forests would be required to produce enough drug? The trees had to be killed (debarked) to extract the drug.
Paclitaxel (Taxol)- Delayed Toxicity: Irritant, near vesicant, bone marrow depression
Docetaxel (Taxotere, Docefrez)- Delayed Toxicity: Irritant, near vesicant, same
Antibiotics
Doxorubicin (Adriamycin)
Doxorubicin liposomal (Doxil, Lipodox)- Vesicant, bone marrow depression, enteromucosal ulceration, cardiotoxicity
Daunorubicin (Cerubidine)
Daunorubicin liposomal (DaunoXome)- Vesicant, same
Idarubicin (Idamycin)- Vesicant, same
Bleomycin (Blenoxane)- Irritant, Pulmonary toxicity, severe allergic reactions, edema of hands, alopecia, enteromucosal ulceration
Dactinomycin (DTIC, Cosmegen)- Vesicant, bond marrow depression, enteromucosal ulceration
Mitomycin (Mutamycin)- Vesicant, same
Tyrosine Kinase inhibitors: Agents
Gefitinib (Iressa): oral only- Hypertension, pruritis, skin erumpsion, asthenia, anorexia, hemoptysis (rare), GI hemorrhage
Imatinib mesylate (Gleevec): oral only- Edema, renal function decreased,
Sorafenib (Nexavar) oral only - Hypertension, rash, hypocalcemia
Sunitinib (Sutent) oral only- Hypertension, rash, hyperglycemia, electrolyte disturbances, diarrhea
Dasatinib (Sprycel) oral only- Edema, rash, diarrhea, thrombocytopenia
Nilotinib (Tasigna) oral only- Edema, hypertension, rash, neutropenia, thrombocytopenia
Hormones and Steroids
Hormones and related compounds have receptors of the membrane of the nucleus. They affect gene expression. In the case of some malignancies such as some prostate and breast cancers, they are promoted by their respective sex hormones. Anti-hormone therapy is a useful adjunct. Glucocorticoids have been found to be useful in hematologic cancers are not listed here.
Hormones and Steroids; Agents
Flutamide (Eulixin)
Abirateron (Zytiga)
Bicalutamide (Casodex)
Enzalutamide (Xtandi)
Tamoxifen (Nolvadex)
Raloxifene (Evista)
Fulvestrant (Faslodex)
Toremifene (Fareston)
Leuprolide (Lupron)
Anastrozole (Arimadex)
Letrozole (Femara)
Megestrol (Megace)
Prostate Cancer
Several types of cells are found in the prostate, but almost all prostate cancers develop from the gland cells (the cells that make the prostate fluid that is added to the semen). The medical term for a cancer that starts in gland cells is adenocarcinoma. Some prostate cancers can grow and spread quickly, but most grow slowly. In fact, autopsy studies show that many older men (and even some younger men) who died of other causes also had prostate cancer that never affected them during their lives. In many cases neither they nor their doctors even knew they had it
Combination Chemotherapy
A. Heterogenous nature
B. The cell cycle
C. Toxicities
D. Resistance
E. Synergy
F. Growth fraction
G. Tumor load
Common Adverse Reactions to Chemotherapy
Most have narrow therapeutic range!
A. Nausea & Vomiting - May cause fluid & electrolyte imbalances. Caused by direct gastric irritation by oral drugs or by stimulation of chemoreceptor trigger zone in CNS: also from psychogenic causes?

B. Toxicity to High Growth Fraction Tissues - "Collateral damage"

• Alopecia - Hair loss may be partial or complete; may affect scalp, eyebrows, eyelashes & body hair.
• GI irritation & ulceration - Occurs throughout GI Tract but particularly in mouth (stomatitis) and esophagus.

Bone marrow depression: the most common and potentially serious adverse reaction.

• Neutropenia - <1,000 per mm3 = increased risk of infection: calculate an ANC!
• Thrombocytopenia - <50,000 per mm3 = increased risk of bleeding.
• Anemia - decreased oxygen carrying capacity
• Damage to fetus & germinal tissues in ovaries & testes
Monoclonal Antibodies
: manufactured antibody designed to target specific receptors, enzymes or growth factors involved with tumor growth, development or cell type. Types include chimeric, humanized and fully human antibodies. Suffixes in generic name indicate which type: chimeric = "-ximab", humanized = "-zumab", fully human = "-umab".
Monoclonal Antibodies; Agents
Bevacizumab (Avastin): IV; angiogenesis inhibitor: binds to vascular endothelial growth factor. Toxicity: GI perforation, impaired wound healing, pulmonary hemorrhage, thromboembolism, hypertensive crisis
Rituximab (Rituxan): IV; binds to CD20 receptor found on > 90% of B cells. Toxicity: Transfusion reactions, tumorlysis syndrome, mucocutaneous reactions, hypersensitivity, leukopenia, thrombocytopenia, neutropenia
Cetuximab (Erbitux): IV; binds to human epidermal growth factor. Toxicity: Neuropathy, rash, infection
Trastuzumab (Herceptin): IV; binds to human epidermal growth factor receptor 2. Toxicity: Cardiovascular, pain, neuropathy
Ranibizumab (Lucentis): IV; angiogenesis inhibitor, vascular endothelial growth factor inhibitor. Toxicity: Transfusion reactions, embolic events
Asparaginase
used to treat childhood ALL. Derived from Escherichia coli or Erwinia chrysanthemi. An ALL cell cannot synthesize L-asparagine because they lack the enzyme. Asparaginase hydrolyzes L-asparagine in the circulation depriving the tumor cells of this essential nutrient. Most other cells in the body can synthsize L-asparagine from other amino acids.
Immunomodulatory Derivative of Thalidomides (IMiDs):
inhibit angiogenesis, inhibit tumor necrosis factor-alpha (TNF-α), reduce phagocytosis by neutrophils, increases production IL-10, enhances T-cell mediated interactions, and has anti-inflammatory properties. Some of the derivatives are more potent. Thalidomide or derivatives are used in the treatment of multiple myeloma are being studied in a number of other cancers. Needless to say: DO NOT GIVE TO PREGNANT WOMEN!!
Thalidomide
Lenalidomide (Revlimid)
Pomalidomide (Pomalyst)
Acute lymphoblastic leukemia (ALL):
most common form of childhood leukemia. Prognosis is relatively good: over 90% of children enter complete remission. Typical therapy frequently includes vincristine, prednisone, doxorubicin, and aspariginase. Leukemic cells often migrate to sanctuary sites located in the brain and testes. Intrathecal methotrexate is usually included to cover those cells.
Acute myelogenous leukemia (AML):
most common form of adult leukemia. Complete remission rate of 70% is experienced. Typical therapy includes cytarabine and idarubicin and supportive measures such as granulocyte colony-stimulating factor filgrastim. Adults < 55 years can be considered for allogeneic bone marrow transplantation if a suitable HLA-matched donor is available. Cure rates are up to 35-40% in these patients. Patients over age 60 years respond less well to the aggressive chemotherapy and and whole body radiation in transplantation with higher infection rates.
Chronic myelogenous leukemia (CML):
comes from a chromosomally abnormal hematopoietic stem cell. White cell counts > 50,000 are treated with the goal of reducing granulocytes to normal levels and raising hemoglobin concentration levels to normal. Cure is not a goal. Typical first line treatment includes the tyrosine kinase inhibitor imatinib. Other treatment options include interferon-α, busulfan and hydroxyurea.
Chronic lymphocytic leukemia (CLL):
Patients with early-stage CLL have a relatively good prognosis, but therapy does not change the course of the disease. Where there is high-risk disease or the presence of disease-related symptoms, treatment is indicated. Chlorambucil and cyclophosphamide are the two most widely used alkylating agents for this disease. COP and CHOP are also used. In treatment refractory disease, monoclonal antibodies rituximab (CD20) and alemtuzumab (CD52) are used.
Hodgkin's lymphoma
is a B-cell lymphoma with Reed-Sternberg cells that have rearranged VH genes. Up to 80% of tumor specimens have the Eptein-Barr virus genome. Staging drives therapy. Stage I and IIa are usually treated with radiation therapy. Advanced stage III an IV are now treated with ABVD with complete response rates of 80-90% and cure rates of up to 50-60%.
Non-Hodgkin's lymphoma
is a heterogenous lymphoma and the clinical characteristics are related to the cell type (histopathlogic) and the extent of disease involvement. Nodular lymphomas have a better prognosis than diffuse lymphomas: median survival 7 years vs. 1-2 years prior to the advent of rituxan. Standard treatment for diffuse disease is CHOP-R and supportive therapies to improved nadir recovery rates. Some advance stage nodular forms are considered incurable and treatment is palliative. Often watchfull waiting is excercised.
Multiple myeloma
This cancer arises from a single tumor stem cell that produces a marker protein (myeloma immunoglobulin) and primarily involves bone marrow and bone, causing bone pain, lytic lesions, bone fractures, anemia and increased susceptibility to infection. The original combination of melphalan and prednisone (MP) showed a response rate of 40% with a median duration of 2-2.5 years. Lenalidomide plus dexamethasone or bortezomib and melphalan and prednisone have been shown to be more effective. Autologous BMT is a therapy option and if considered, alkylating agents are generally avoided to improve the harvesting of stem cells.
Breast Cancer
Staging is central in the treatment options of breast cancer. Stage I (local, negative lymph nodes) is treated with surgery alone with an 80% cure rate. Stage II (local, positive lymph nodes, the fewer the better!) is often treated with six cycles of CMF, FAC, or FEC and if the cells are positive for the HER-2/neu receptor, adding tratuzumab (Herceptin). Tamoxifen is beneficial in postmenopausal women when used alone after surgery or in combination chemotherapy regimens.

Stage III and IV cancers remain palliative with overall response rates of only 40-50% and a complete response rate of 10-20%. Complete response does not equal a cure!
Gastrointestinal Cancer
cancers that affect the digestive system. This includes cancers of the oesophagus, gallbladder, liver, pancreas, stomach, small intestine, bowel (large intestine or colon and rectum), and anus.
Lung Cancer
Lung cancer is a type of cancer that begins in the lungs. Your lungs are two spongy organs in your chest that take in oxygen when you inhale and release carbon dioxide when you exhale.

Lung cancer is the leading cause of cancer deaths in the United States, among both men and women. Lung cancer claims more lives each year than do colon, prostate, ovarian and breast cancers combined.

People who smoke have the greatest risk of lung cancer.
Ovarian Cancer
Ovarian cancer begins in the ovaries. Ovaries are reproductive glands found only in females (women). The ovaries produce eggs (ova) for reproduction. The eggs travel through the fallopian tubes into the uterus where the fertilized egg implants and develops into a fetus. The ovaries are also the main source of the female hormones estrogen and progesterone. One ovary is on each side of the uterus in the pelvis.
Testicular Cancer
Cancer that starts in the testicles is called testicular cancer. To understand this cancer, it helps to know about the normal structure and function of the testicles.

Testicles (also called the testes; a single testicle is called a testis) are part of the male reproductive system. These 2 organs are each normally a little smaller than a golf ball in adult males and are contained within a sac of skin called the scrotum. The scrotum hangs beneath the base of the penis.
Malignant Melanoma
The most dangerous form of skin cancer, these cancerous growths develop when unrepaired DNA damage to skin cells (most often caused by ultraviolet radiation from sunshine or tanning beds) triggers mutations (genetic defects) that lead the skin cells to multiply rapidly and form malignant tumors. These tumors originate in the pigment-producing melanocytes in the basal layer of the epidermis. Melanomas often resemble moles; some develop from moles. The majority of melanomas are black or brown, but they can also be skin-colored, pink, red, purple, blue or white. Melanoma is caused mainly by intense, occasional UV exposure (frequently leading to sunburn), especially in those who are genetically predisposed to the disease. Melanoma kills an estimated 9,710 people in the US annually.
Brain Cancer
Brain cancer is a disease of the brain in which cancer cells (malignant) arise in the brain tissue. Cancer cells grow to form a mass of cancer tissue (tumor) that interferes with brain functions such as muscle control, sensation, memory, and other normal body functions.
Skin Cancer
Skin cancers include melanoma, basal cell, and squamous cell. Basal and squamous cell are common and treatment is very effective. Malignant melanoma can be difficult to treat. Early diagnosis and treatment can increase the survival rate from melanoma.
While being prepared for a biopsy of a lump in the right breast, the patient asks the nurse what the difference is between a benign tumor and a malignant tumor. The nurse explains that a benign tumor differs from a malignant tumor in that benign tumors
a. do not cause damage to adjacent tissue.
b. do not spread to other tissues and organs.
c. are simply an overgrowth of normal cells.
d. frequently recur in the same site.
B
Rationale: The major difference between benign and malignant tumors is that malignant tumors invade adjacent tissues and spread to distant tissues and benign tumors never metastasize. Both types of tumors may cause damage to adjacent tissues. The cells differ from normal in both benign and malignant tumors. Benign tumors usually do not recur.
A patient who has been told by the health care provider that the cells in a bowel tumor are poorly differentiated asks the nurse what is meant by "poorly differentiated." Which response should the nurse make?
a. "The cells in your tumor do not look very different from normal bowel cells."
b. "The tumor cells have DNA that is different from your normal bowel cells."
c. "Your tumor cells look more like immature fetal cells than normal bowel cells."
d. "The cells in your tumor have mutated from the normal bowel cells."
C
Rationale: An undifferentiated cell has an appearance more like a stem cell or fetal cell and less like the normal cells of the organ or tissue. The DNA in cancer cells is always different from normal cells, whether the cancer cells are well differentiated or not. All tumor cells are mutations form the normal cells of the tissue.
A patient who smokes tells the nurse, "I want to have a yearly chest x-ray so that if I get cancer, it will be detected early." Which response by the nurse is most appropriate?
a. "Chest x-rays do not detect cancer until tumors are already at least a half-inch in size."
b. "Annual x-rays will increase your risk for cancer because of exposure to radiation."
c. "Insurance companies do not authorize yearly x-rays just to detect early lung cancer."
d. "Frequent x-rays damage the lungs and make them more susceptible to cancer."
A
Rationale: A tumor must be at least 1 cm large before it is detectable by an x-ray and may already have metastasized by that time. Radiographs have low doses of radiation, and an annual x-ray alone is not likely to increase lung cancer risk. Insurance companies do not usually authorize x-rays for this purpose, but it would not be appropriate for the nurse to give this as the reason for not doing an x-ray. A yearly x-ray is not a risk factor for lung cancer.
During a routine health examination, a 30-year-old patient tells the nurse about a family history of colon cancer. The nurse will plan to
a. teach the patient about the need for a colonoscopy at age 50.
b. ask the patient to bring in a stool specimen to test for occult blood.
c. schedule a sigmoidoscopy to provide baseline data about the patient.
d. have the patient ask the doctor about specific tests for colon cancer.
D
Rationale: The patient is at increased risk and should talk with the health care provider about needed tests, which will depend on factors such as the exact type of family history and any current symptoms. Colonoscopy at age 50 is used to screen for individuals without symptoms or increased risk, but earlier testing may be needed for this patient because of family history. For fecal occult blood testing, patients use a take-home multiple sample method rather than bring one specimen to the clinic. The health care provider will take multiple factors into consideration before determining whether a sigmoidoscopy is needed at age 30.
Which statement by a patient who is scheduled for a needle biopsy of the prostate indicates that the patient understands the purpose of a biopsy?
a. "The biopsy will tell the doctor whether the cancer has spread to my other organs."
b. "The biopsy will help the doctor decide what treatment to use for my enlarged prostate."
c. "The biopsy will determine how much longer I have to live."
d. "The biopsy will indicate the effect of the cancer on my life."
B
Rationale: A biopsy is used to determine whether the prostate enlargement is benign or malignant and determines the type of treatment that will be needed. Biopsy does not give information about metastasis, life expectancy, or the impact of cancer on the patient's life; the three remaining statements indicate a need for patient teaching.
A patient with a large stomach tumor that is attached to the liver is scheduled to have a debulking procedure. The nurse explains that the expected outcome of this surgery is
a. control of the tumor growth by removal of malignant tissue.
b. promotion of better nutrition by relieving the pressure in the stomach.
c. relief of pain by cutting sensory nerves in the stomach.
d. reduction of the tumor burden to enhance adjuvant therapy.
D
Rationale: A debulking surgery reduces the size of the tumor and makes radiation and chemotherapy more effective. Debulking surgeries do not control tumor growth. The tumor is debulked because it is attached to the liver, a vital organ (not to relieve pressure on the stomach). Debulking does not sever the sensory nerves, although pain may be lessened by the reduction in pressure on the abdominal organs.
Which action by a nursing assistant (NA) caring for a patient with a temporary radioactive cervical implant indicates that the RN should intervene?
a. The NA places the patient's bedding in the laundry container in the hallway.
b. The NA flushes the toilet once after emptying the patient's bedpan.
c. The NA stands by the patient's bed for an hour talking with the patient.
d. The NA gives the patient an alcohol-containing mouthwash for oral care.
C
Rationale: Because patients with temporary implants emit radioactivity while the implants are in place, exposure to the patient is limited. Laundry and urine/feces do not have any radioactivity and do not require special precautions. Cervical radiation will not affect the oral mucosa, and alcohol-based mouthwash is not contraindicated.
A patient who is receiving interleukin-2 (IL-2) therapy (Proleukin) complains to the nurse about all of these symptoms. Which one is most important to report to the health care provider?
a. Generalized aches
b. Dyspnea
c. Decreased appetite
d. Insomnia
B
Rationale: Dyspnea may indicate capillary leak syndrome and pulmonary edema, which requires rapid treatment. The other symptoms are common with IL-2 therapy, and the nurse should teach the patient that these are common adverse effects that will resolve at the end of the therapy.
A 32-year-old male patient is to undergo radiation therapy to the pelvic area for Hodgkin's lymphoma. He expresses concern to the nurse about the effect of chemotherapy on his sexual function. The best response by the nurse to the patient's concerns is
a. "Radiation does not cause the problems with sexual functioning that occur with chemotherapy or surgical procedures used to treat cancer."
b. "It is possible you may have some changes in your sexual function, and you may want to consider pretreatment harvesting of sperm if you want children."
c. "The radiation will make you sterile, but your ability to have sexual intercourse will not be changed by the treatment."
d. "You may have some temporary impotence during the course of the radiation, but normal sexual function will return."
B
Rationale: The impact on sperm count and erectile function depends on the patient's pretreatment status and on the amount of exposure to radiation. The patient should consider sperm donation before radiation. Radiation (like chemotherapy or surgery) may affect both sexual function and fertility either temporarily or permanently.
Interleukin-2 (IL-2) is used as adjuvant therapy for a patient with metastatic renal cell carcinoma. The nurse teaches the patient that the purpose of therapy with this agent is to
a. protect normal kidney cells from the damaging effects of chemotherapy.
b. enhance the patient's immunologic response to tumor cells.
c. stimulate malignant cells in the resting phase to enter mitosis.
d. prevent the bone marrow depression caused by chemotherapy.
B
Rationale: IL-2 enhances the ability of the patient's own immune response to suppress tumor cells. IL-2 does not protect normal cells from damage caused by chemotherapy, stimulate malignant cells to enter mitosis, or prevent bone marrow depression.
The home health nurse is caring for a patient who has been receiving interferon therapy for treatment of cancer. Which statement by the patient may indicate a need for a change in treatment?
a. "I have frequent muscle aches and pains."
b. "I rarely have the energy to get out of bed."
c. "I take acetaminophen (Tylenol) every 4 hours."
d. "I experience chills after I inject the interferon."
B
Rationale: Fatigue can be a dose-limiting toxicity for use of biologic therapies. Flulike symptoms, such as muscle aches and chills, are common side effects with interferon use. Patients are advised to use Tylenol every 4 hours.
The sympathetic system evokes responses characteristic
"fight-or-flight" response: pupils dilate, muscle vasculature dilates, the heart rate increases, and the digestive system is put on hold.
inhibit bladder contraction
secretion of adrenaline and noradrenaline
dilates bronchi
The parasympathetic system has many specific functions
including slowing the heart, constricting the pupils, stimulating the gut and salivary glands, and other responses that are not a priority when being "chased by a tiger".

stimulate peristalsis and secretion
release of bile
contracts bladder
nicotinic receptor
ACh-acetylcholine
adrenergic receptors
norepinephrine
How do you "turn off" the Ach signal?
Acetylcholinesterase
How do you "turn off" norepinephrine?
Re- uptake
Alpha 1 selective receptor Blockers
-zosin
Prazosin
Doxazosin
Terazosin
ACE Inhibitors
-pril
Benazepril
Enalopril
Lisinopril
Angiotensin II blockers
-sartan
Irbesartan
Losartan
Olmesartan
Class Ia : Antiarrhythmics
Quinidine
Procainamide
Disopyramide
Class Ib : Antiarrhythmics
Lidocaine
Tocainide
Class Ic : Antiarrhythmics
Fecainide
Propafenone
Class I : Miscellaneous
Amidodarone
Class II: Antiarrhythmics
Beta Blockers
Class III: Antiarrhythmics
Bretylium
Sotalol
Class IV: Antiarrhythmics
Verapamil
Dilitiazem
What will you give a diabetic with CHF?
ACE Inhibitor
plan b --- ARB
What beta blockers are given for CHF?
Carvedilol
Metoprolol
Nebivilol
Angina Treatment: Nitrates
Nitroglycerine
Isosorbide dinitrate
Isosorbide mononitrate
Angina Treatment: Ca Channel Blockers
Nifedipine
Amlodipine
Nimodipine
Verapamil
Diltiazem
Niacin
Inhibits VLDL secretion, resulting in LDL reduction
Competitive Inhibitors of HMG-CoA Reductase
-statin
Lovastatin
Simvastatin
Pravastatin
Fluvastatin
** used in treating elevated LDL levels
Gram positive cocci
Streptococcus pairs, chains
Staphylococcus clusters
Enterococcus singles, pairs, chains
Gram positive bacilli
Corynebacterium club shaped
Listeria flagellae
Bacillus spores
Lactobacillus
Gram negative cocci
Neisseria
Moraxella
Natural Penicillins
Penicillin G: IV, IM; Penicillin V (Pen VK, Veetids): PO
Amino-penicillins
Ampicillin (Omnipen): PO, IM, IV; Amoxicillin (Trimox, Amoxil): PO
Extended Spectrum Penicillins
Carbenicillin (Geocillin): PO, IV; Ticarcillin (Ticar): IV; Piperacillin (Piperacil): IV $$$$
Beta-lactamase resistant penicillins
Nafcillin (Unipen, Nafcil): PO, IV, Dicloxicillin (Dynapen): PO
Anti-beta-lactamase combinations
Ampicillin/sulbactam (Unasyn): IV;
Ticarcillin/clavulanate (Timentin): IV;
Piperacillin/tazobactam (Zosyn): IV;
Amoxicillin/clavulanate (Augmentin): PO
Cephalosporins
First generation: Cephalexin (Keflex): PO; Cefazolin (Ancef): IV
Second generation: Cefaclor (Ceclor): PO; Cefuroxime (Zinacef): IV (Ceftin): PO; Cefoxitin (Mefoxin): IV; Cefotetan (Cefotan): IV
Third generation: Cefotaxime (Claforan): IV; Ceftriaxone (Rocephin): IV; Ceftazidime (Fortaz): IV; Cefdinir (Omnicef): PO; Cefpodoxime (Vantin): PO
Fourth generation: Cefepime (Maxipime): IV
Flouroquinolones
Levofloxacin (Levaquin): PO, IV; Ciprofloxin (Cipro): PO, IV; Moxifloxacin (Avelox): PO, IV and more
Antifungals
-azole -fungin
Clotrimazole (Lotrimin, Mycelex)
Ketoconazole (Nizoral)
Miconazole (Monistat, Micatin)
Fluconazole (Diflucan)
Voriconazole (Vfend)
Caspofungin (Cancidas)
Micafungin (Mycamine)
Anidulafungin (Eraxis)
Antivirals
-vir
Acyclovir (Zovirax)
Valacyclovir (Valtrex)
Famciclovir (Famvir)
Ganciclovir (Cytovene)
THIS SET IS OFTEN IN FOLDERS WITH...

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