Week 5 Exam: NR565 / NR 565 (Latest 2026 / 2027) Advanced Pharmacology Fundamentals | Questions & Answers | 100% Correct | Grade A - Chamberlain

Week 5 Exam: NR565 / NR 565 (Latest 2026 / 2027) Advanced Pharmacology Fundamentals | Questions & Answers | 100% Correct | Grade A - Chamberlain Question: How are ACE inhibitors beneficial in treating nephropathy r/t T1DM? Answer They decrease glomerular filtration pressure by decreasing levels of angiotensin II, which lowers BP. Decreased glomerular filtration pressures slows development Question: What are key considerations when initiating ACEIs in DM for diabetic nephropathy? Answer They are not protective against early kidney disease and cannot be used as primary prevention. ACEIs are CI in pregnancy SEs: hyperkalemia, cough, angioedema, renal failure, hypotension Question: What are examples of DDP-4 inhibitor drugs for DM? Answer "Gliptins": sitagliptin (Januvia) saxagliptin (Onglyza) linagliptin (Tradjenta) alogliptin (Nesina) Question: What are the AEs of DDP-4 inhibitors? Answer URIs, HA, sinusitis (most common) pancreatitis - severe abd pain w/ or w/o vomiting hypersensitivity - anaphylaxis, angioedema, SJS Question: What is the MOA of DDP-4 inhibitors? Answer inhibits the enzyme dipeptidyl peptidase-4 which l/t prolonged activity of incretin hormones to enhance their actions incretin hormones help increase insulin release in response to meals and decrease hepatic glucose production without directly releasing insulin Question: What are examples of glucagon-like peptide-1 receptor agonists (GLP-1 RAs)? Answer exenatide (Byetta & Bydureon) liraglutide (Victoza) dulaglutide (Trulicity) semaglutide (Ozempic & Rybelsus) tirzepatide (Mounjaro) Question: What is the MOA of GLP-1 RAs? Answer incretin mimetic that activate GLP-1 receptors like endogenous incretin hormones l/t slowed gastric emptying and insulin release, inhibition of postprandial glucagon release, and suppression of appetite improves glucose control and can induce weight loss Question: What are AEs r/t GLP-1 RAs? Answer GI issues - nausea, vomiting, diarrhea hypoglycemia - esp. when combined with/ sulfonylureas pancreatitis - severe abd pain w/ or w/o vomiting renal impairment - may require hemodialysis or transplant injection site reaction & pruritis - more common w/ Bydureon development of antibodies hypersensitivity - anaphylaxis & angioedema Question: What is the benefit of prescribing Bydureon over Byetta? Answer greater effect on fasting BG as opposed to postprandial BG better tolerated in terms of N/V Question: How can patients decrease N/V when taking Byetta? Answer take at a specific time relative to meals to decrease GI upset - before meals can help reduce nausea stay well hydrated eat smaller, more frequent meals that are low in fat and fiber - easier to digest Question: Why do GLP-1 RAs cause nausea? Answer 1. slowed gastric emptying can l/t feelings of fullness, nausea, & sometimes vomiting 2. increased feeling of satiety, especially initiating med and when increasing dose 3. hormonal effects on the gut can affect digestion & motility l/t symptoms like diarrhea or constipation Question: How would you approach a patient starting on exenatide w/ a hx of pancreatitis? Answer Risk for pancreatitis when using GLP-1 RAs, w/ severe cases manifesting as pancreatic necrosis, pancreatic hemorrhage, and even death If s/s r/t pancreatitis develop (severe abd pain w/ or w/o vomiting), stop immediately & notify provider If pancreatitis confirmed, do not resume If patient has hx or pancreatitis, consider other options Question: What are glycemic control targets? Answer HgbA1c 7.0% (or 8.0% w/ Hx of microvascular/macrovascular complications, older age, etc.) Question: What are examples of sulfonylureas? Answer glyburide (DiaBeta) glipizide glimepiride Question: What is the MOA of sulfonylureas? Answer stimulate insulin release by pancreatic islet cells & may increase target cell sensitivity to insulin w/ prolonged use Question: What are the potential SEs & risks associated with/ sulfonylurea therapy? Answer hypoglycemia - can l/t severe hypoglycemia if coupled w/ other antiDM drugs and/or if BG is already low CV toxicity (1st generation sulfonylureas) Question: How can the risk of hypoglycemia be minimized in patients on sulfonylurea therapy? Answer Patient education s/s of hypoglycemia like sweating, shaking, confusion, and dizziness & how to respond to low BG promptly Regularly monitor BG Start with low dose & adjust based on needs - can prevent excessive insulin release & ¯ risk of hypoglycemia Take w/ meals to stabilize BG levels Consume a balanced diet that includes carbs to help prevent hypoglycemia Avoid alcohol - increased risk of hypoglycemia when combined w/ sulfonylureas Be aware of interactions with drugs that can risk of hypoglycemia - ex: beta blockers mask hypoglycemia symptoms Switch therapy regimen to DDP-4 or GLP-1RAs if patient experiences frequent hypoglycemia episodes Monitor renal function because sulfonylureas are excreted by kidneys & renal impairment can l/t accumulation & subsequent hypoglycemia Question: When considering prescribing a sulfonylurea, how would you decide between a first- or second generation agent for your patient? 2nd generation drugs: Answer - more potent & can achieve desired BG-lowering effects @ lower doses, which decreases risk for SEs like hypoglycemia - shorter duration of action which can help manage BG w/o causing significant hypoglycemia - preferred sulfonylureas in older adults or those w/ renal impairments (at higher risk for hypoglycemia) - better safety profile and less likely to cause adverse CV effects 1st generation drugs: - more cost effective - longer duration of action - increased risk of SEs like hypoglycemia & CV toxicity (concern in hx CVD) Question: Can sulfonylureas be prescribed in pregnancy? Answer No - there is an increased risk for fetal hypoglycemia & animal studies have demonstrated fetal abnormalities How would you explain to a patient w/ T1DM why sulfonylureas are not part of their treatment regimen? Answer sulfonylureas don't work when basal insulin is not present How should DM management work/ sulfonylureas be approached in patients w/ significant renal or hepatic impairment? Sulfonylureas are metabolized by the liver and excreted by the kidneys - impairment increases risk for accumulation l/t hypoglycemia - Liver impairment slows metabolism of the drug - Kidney disease slows excretion of the drug Manage by considering a different drug, decrease dosage, and/or regularly monitoring BG What is the MOA of metformin? inhibits glucose production in the liver decreases glucose absorption in the GI tract l/t less postprandial BG spikes sensitizes insulin receptors in target to issues (fat & muscle cells) l/t increased ability to take in glucose in the presence of insulin What are SEs r/t metformin? GI disturbances - nausea, diarrhea, decreased appetite (lessens over time) altered nutrient absorption - B12 & folic acid metabolic acidosis - increased risk w/ renal impairment If a pregnant woman with type 2 diabetes inquiries about the safety of continuing metformin, how would you discuss the potential benefits and risks with her? Glycemic control in mother, BG & Apgar scores are the same as they are with insulin administration Folic acid deficiency & neural tube defects are not a major concern What are the advantages & disadvantages of using meglitinides for DM management? Same MOA as sulfonylureas - stimulate pancreatic insulin release Shorter acting than sulfonylureas Those who don't respond to sulfonylureas won't respond to meglitinides Beneficial over sulfonylureas for postprandial BG spikes because they can be taken w/ each meal What are the contraindications and potential adverse effects of pioglitazone therapy? AEs: - HF s/t fluid retention (exacerbated w/ combo use of insulin) - Ovulation l/t unintended pregnancy - risk bladder cancer - risk fractures (women) CIs: active bladder cancer or Hx bladder cancer, HF How would you approach the use of thiazolidinediones in a patient with type 2 diabetes and a history of mild heart failure? decrease dosage or D/C use Avoid concurrent use w/ insulin as fluid retention can be exacerbated Report dyspnea, edema, fatigue, & rapid weight gain What is the MOA of TZDs? activate peroxisome proliferator-activated receptor gamma (PPAR gamma) in the cell nucleus, which activates insulin-responsive genes regulating carbohydrate & lipid metabolism increased cellular insulin sensitivity, especially in skeletal muscle & adipose tissue since it enhances responses to insulin, insulin must be present for drug to work What are examples of sodium-glucose cotransporter-2 (SGLT-2) inhibitors? canagliflozin (Invokana) dapagliflozin (Farxiga) empagliflozin (Jardiance) What is the MOA of SGLT-2 inhibitors? block reabsorption of glucose in the kidneys l/t urinary excretion of glucose What are the potential benefits and risks of SGLT-2 inhibitor therapy? benefits: glycemic control, weight loss d/t caloric loss risks: female genital fungal infx & UTIs, increased urination, postural hypotension & dizziness (esp. w/ diuretics) What are the potential consequences of delayed treatment for congenital hypothyroidism? Mental disability will be permanent, but physical effects will reverse How would you explain to parents the importance of early thyroid hormone replacement therapy for their newborn diagnosed with hypothyroidism? Hormone replacement initiated w/in a few days of birth won't result in physical & mental developmental issues Treatment is continued for 3 years, then stopped for 4 wks to assess if deficiency is transient or permanent (TSH= permanent deficiency) How would you identify and manage a patient presenting with symptoms of thyrotoxic crisis in an emergency setting? Manifestations: tachycardia, angina, tremor, nervousness, insomnia, hyperthermia, heat intolerance, sweating Management: IV levothyroxine, beta blockers for symptoms like palpitations/tachycardia How would you counsel a patient on the correct way to take levothyroxine to ensure its efficacy? Take on an empty stomach 30-60 minutes before a meal - best when taken in the morning Space medications that decrease absorption by 4 hours to ensure proper absorption How can the GI SEs of metformin be managed or mitigated? Start the initial dose low & gradually increase it to let the body adjust to the medication and ¯ GI disturbances. Take the medication with food - helps minimize nausea & other GI upset by ¯ the concentration of the drug in the stomach Use an ER version instead of IR - may be better tolerated Stay hydrated If a patient is on both calcium supplements and levothyroxine, how would you instruct them to take these medications to prevent interaction? Take levothyroxine on empty stomach and then take calcium supplement at least 4 hours after taking levothyroxine How would you educate a patient on the importance of taking repaglinide with meals and strategies to ensure adherence? Taking repaglinide with meals ¯ risk for hypoglycemia and should not be taken 30 minutes before meals How would you discuss the risks of pioglitazone with a diabetic patient who has a history of heart failure, and what alternatives might you consider? Pioglitazone (a TZD) can cause or worsen HF s/t fluid retention, especially when coupled with insulin. Monitor for s/s of new or worsening HF like swelling, SOB, and weight gain. Should not be used in Hx HF. Other drugs to consider include: - SGLT-2 inhibitors ("gliflozins") - DPP-4 inhibitors ("gliptins") - GLP-1 RAs Metformin How can overdosage of levothyroxine be prevented and managed? Start dosage low and titrate slowly Take as directed & monitor TSH levels regularly - q6-8 wks until target range is reached and then less frequently Report s/s of overdose like tachycardia, heat intolerance, anxiety, palpitations, etc. How would you address concerns about atrial fibrillation in an older patient who is worried about their levothyroxine dosage? If dosage is too high, it can l/t sx of hyperthyroidism including tachycardia and potentially a. fib Careful monitoring & appropriate dosing are crucial to preventing this How would you explain to a patient the need for dosage adjustment if their TSH levels remain elevated after starting levothyroxine? Dosage would need to be until desired range is reached. If TSH is still elevated, it indicates that TH levels are still too low, and the body is continuing to signal for more hormone production How would you explain to a patient how methimazole works? MOA: inhibits enzyme thyroid peroxidase (crucial for synthesis of T3 & T4), which ¯production of these hormones & lowers their levels in the body - Can take 3-12 wks to see changes in TH & feel full benefits What are the AEs of methimazole? AEs: - Skin rashes - usually mild - Nausea - Agranulocytosis - WBC count decreases significantly & increased risk for infx - Hypothyroidism - if dose too high What is the treatment for hyperthyroidism in pregnancy? propylthiouracil (PTU) in the 1st trimester & methimazole in 2nd and 3rd trimesters If a pregnant patient is diagnosed with hyperthyroidism, how would you discuss the use of PTU over methimazole? PTU is safer in 1st trimester of pregnancy because it poorly crosses the placenta. Methimazole has a higher risk for congenital malformations when used in the 1st trimester Considered a safe option in the 2nd and 3rd trimesters Signs and symptoms of hypothyroidism and hyperthyroidism Hypothyroidism: Thick, coarse, dry Hyporeflexia, "hung up" patella reflex Slow thought process, Weight gain (5 10 lbs./2.25-4.5 kg) Constipation, Menorrhagia, Cold intolerance: Cold all the time Hyperthyroidism (aka graves disease): Smooth, silky Hyperreflexia, Mind racing, Weight loss (10 lbs./4.5 kg) Diarrhea, loose, frequent stools, Oligomenorrhea, Heat intolerance: Hot all the time pg. 418-419 What adjunctive therapy is good to prescribe to control symptoms of hyperthyroidism other than thyroid specific medications? Know drug classes and examples of those drug classes. β-Blockers and nonradioactive iodine may be used as adjunctive therapy. β-Blockers suppress tachycardia by blocking β-receptors on the heart. Nonradioactive iodine inhibits synthesis and release of thyroid hormones. pg. 419 Monitoring needs and intervals for thyroid medications. levothyroxine-Monitoring: Check TSH 6-8 weeks after initiating therapy and after any dosage change. Check TSH at least once a year after serum TSH is stabilized. Methimazole-Monitoring: Check CBC with differential if signs or symptoms of infection. Check LFTs if signs or symptoms of liver dysfunction. Propylthiouracil (PTU)- Treatment continues for 1-2 years PTU has caused rare cases of liver injury. Onset is sudden and progression is rapid. - Propylthiouracil (PTU) carries a risk for liver toxicity. Although rare, the FDA recommends against using PTU as a first-line treatment due to potential for hepatic toxicity. Treatment continues for 1-2 years PTU has caused rare cases of liver injury. Onset is sudden and progression is rapid. pg 421 - Effects of maternal hypothyroidism on offspring and appropriate patient teaching related to need for treatment. Maternal hypothyroidism can result in permanent neuropsychological deficits in the child. can decrease IQ and other aspects of neuropsychological function in the child. teaching: to help ensure healthy fetal development, maternal hypothyroidism must be diagnosed and treated very early. some authorities currently recommend routine screening for hypothyroidism as soon as pregnancy is confirmed. If hypothyroidism is diagnosed, replacement therapy should begin immediately. the signs and symptoms of pregnancy mimics those of hypothyroidism When women taking thyroid supplements become pregnant, dosage requirements usually increase—often by as much as 50%. The need for increased dosage begins between weeks 4 and 8 of gestation, levels off at approximately week 16, and then remains steady until parturition. pg. 418 - Patient teaching for thyroid medications. :levothyroxine: should be taken on an empty stomach in the morning, at least 30 to 60 minutes before breakfast. Inform patients about the symptoms of thyrotoxicosis and instruct them to notify the prescriber if these develop (Sweating, irritability, weight loss, tachycardia)Instruct patients to separate administration of levothyroxine and these drugs by 4 hours Overdose may cause thyrotoxicosis. Symptoms include tachycardia, angina, tremor, nervousness, insomnia, sweating, and heat intolerance. methamizole: Agranulocytosis: Inform patients about early signs of agranulocytosis, including fever or sore throat. If follow-up blood tests reveal leukopenia, methimazole should be stopped. Hypothyroidism: Methimazole may cause excessive reductions in thyroid hormone synthesis. If signs of hypothyroidism develop or if plasma levels of T3 and T4 become subnormal, dosage should be reduced. Radioactive Iodine: Inform patients about symptoms of iodism, including brassy taste, burning sensations in the mouth, and soreness of gums and teeth. Iodine can also cause corrosive injury to the GI tract. Instruct patients to notify the prescriber if severe abdominal distress develops. PTU: can cause rare cases of liver injury What drug class can interfere with the assessment and monitoring of diabetes and why? o You will need connect pathophysiology information of medications and diabetes together. Think about alpha and beta cells. Hypoglycemic agents. Drugs that lower blood glucose levels can intensify hypoglycemia induced by insulin. Among these drugs are sulfonylureas, glinides, and alcohol (used acutely or long term in excessive doses). When these drugs are combined with insulin, special care must be taken to ensure as best as possible that blood glucose does not fall too low. Hyperglycemic agents. Drugs that raise blood glucose (e.g., thiazide diuretics, glucocorticoids, sympathomimetics) can counteract the desired effects of insulin. When these agents are combined with insulin, insulin dosage may need to be increased. β-Adrenergic blocking agents. β-Blockers can delay awareness of and response to hypoglycemia by masking signs that are associated with stimulation of the sympathetic nervous system (e.g., tachycardia, palpitations) that hypoglycemia normally causes. Furthermore, because β-blockade impairs glycogenolysis and because glycogenolysis is one means by which the body can respond to and counteract a fall in blood glucose, β-blockers can make insulin-induced hypoglycemia even worse by preventing the body's natural counterregulatory response. Coadministration of canagliflozin with Uridine 5'-diphospho-glucuronosyltransferase inducers— such as rifampin, phenytoin, or phenobarbital—can decrease canagliflozin efficacy. Accordingly, if used with such an agent, the 300-mg canagliflozin dose should be considered. Because canagliflozin causes a diuretic effect, the risk for dehydration and hypotension may be increased when used in combination with thiazide and loop diuretics. pg. 406 - HgbA1C goals- what are they generally? Review goal guidelines for different age groups within the ADA DM Guidelines linked in the Endocrine Case Studies and on your Student Lesson Plan. Neonatal Diabetes Diabetes diagnosed in the first 6 months of life has been shown not to be typical autoimmune type 1 diabetes. This so-called neonatal diabetes can either be transient or permanent. The most common genetic defect causing transient disease is a defect on ZAC/HYAMI imprinting, whereas permanent neonatal diabetes is most commonly a defect in the gene encoding the Kir6.2 subunit of the β-cell KATP channel. Diagnosing the latter has implications, since such children can be well managed with sulfonylureas. Maturity-Onset Diabetes of the Young MODY is characterized by impaired insulin secretion with minimal or no defects in insulin action. It is inherited in an autosomal dominant pattern. Abnormalities at six genetic loci on different chromosomes have been identified to date. The most common form is associated with mutations on chromosome 12 in a hepatic transcription factor referred to as hepatocyte nuclear factor (HNF)-1α. A second form is associated with mutations in the glucokinase gene on chromosome 7p and results in a defective glucokinase molecule. Glucokinase converts glucose to glucose-6-phosphate, the metabolism of which, in turn, stimulates insulin secretion by the β cell. The less common forms of MODY result from mutations in other transcription factors, including HNF-4α, HNF-1β, insulin promoter factor (IPF)-1, and NeuroD1. Diagnosis Readily available commercial genetic testing now enables a true genetic diagnosis. It is important to correctly diagnose one of the monogenic forms of diabetes because these children may be incorrectly diagnosed with type 1 or type 2 diabetes, leading to suboptimal treatment regimens and delays in diagnosing other family members (49). The diagnosis of monogenic diabetes should be considered in children with the following findings: ○ Diabetes diagnosed within the first 6 months of life ○ Strong family history of diabetes but without typical features of type 2 diabetes (nonobese, low-risk ethnic group) ○ Mild fasting hyperglycemia (100-150 mg/dL [5.5-8.5 mmol/L]), especially if young and nonobese ○ Diabetes with negative autoantibodies and without signs of obesity or insulin resistance - Review diagnostic criteria and process for DM Fasting plasma glucose ≥126 mg/dLaOrRandom plasma glucose ≥ 200 mg/dL plus symptoms of diabetesbOrOral glucose tolerance test (OGTT): 2-h plasma glucose ≥200 mg/dLcorHemoglobin A1c 6.5% or higher pg398 - Know mechanism of action and contraindications for DM drug classes. Mechanism of action. Metformin lowers blood glucose and improves glucose tolerance in three ways. First, it inhibits glucose production in the liver. Second, it reduces (slightly) glucose absorption in the gut. And third, it sensitizes insulin receptors in target tissues (fat and skeletal muscle) and thereby increases glucose uptake in response to whatever insulin may be available. In contrast to the sulfonylureas (see later), metformin does not stimulate insulin release from the pancreas. As a result, metformin does not actively drive blood glucose levels down and hence poses little if any added risk for hypoglycemia when used alone. metformin is contraindicated for people with failing hearts. Mechanism of action. Sulfonylureas act primarily by stimulating the release of insulin from pancreatic islets. If the pancreas is incapable of insulin synthesis, sulfonylureas will be ineffective—which is why they do not work in patients with type 1 diabetes. With prolonged use, sulfonylureas may increase target cell sensitivity to insulin. Sulfonylureas promote insulin release by binding with and thereby blocking adenosine triphosphate (ATP)-sensitive potassium channels in the cell membrane. As a result, the membrane depolarizes, thereby permitting influx of calcium, which in turn causes insulin release. The extent of release is glucose dependent and diminishes when plasma glucose declines. Sulfonylureas are contraindicated during pregnancy and breast-feeding. Use these drugs with caution in patients with renal or hepatic dysfunction. Metlitinides (Glinides) Facilitates calcium influx in pancreatic β cells, which leads to increased insulin release α-Glucosidase Inhibitors Delays absorption of dietary carbohydrates Mechanism of action. Acarbose (Precose, Glucobay ) delays absorption of dietary carbohydrates and thereby reduces the rise in blood glucose after a meal. To be absorbed, oligosaccharides and complex carbohydrates must be broken down to monosaccharides by α-glucosidase, an enzyme located on the brush border of cells that line the intestine. Acarbose inhibits this enzyme and thereby slows digestion of carbohydrates, which reduces the postprandial rise in blood glucose. Dipeptidyl Peptidase-4 Inhibitors Enhances actions of incretin hormones to stimulate glucose dependent insulin and suppresses glucagon release Sodium-Glucose Cotransporter 2 Inhibitors Reduces the reabsorption of glucose, increasing urinary excretion of glucose Glucagon-like Peptide-1 Receptor Agonists Activates receptors for GLP-1- slowing gastric emptying, inhibits glucagon, suppresses appetite, and stimulates glucose-dependent release of insulin Thiazolidinediones Thiazolidinediones are contraindicated in patients with severe heart failure and should be used with caution in patients with mild heart failure or symptoms of heart failure. These drugs are also contraindicated in patients with bladder cancer or history of bladder cancer. - Know examples of DM drug classes. Alpha-glucosidase inhibitors Biguanides Bile Acid Sequestrants Dopamine-2 Agonists DPP-4 inhibitors Meglitinides SGLT2 Inhibitors Sulfonylureas TZDs Oral combination therapy - Be able to calculate the total daily dose of insulin based on weight. Calculate with the lowest possible dose unless otherwise specified. For example, the total daily dose (TDD) of insulin can be calculated by taking the total weight of the patient's weight in kilograms (kg), which is 80 kg (184 pounds) multiplied by 0.6 units equals 48 units. This means 24 units of the TDD is the basal insulin dose of glargine (Lantus) (50%) and the other 24 units of rapid-acting bolus/mealtime insulin (50%). 80x0.6= 48 (tdd) - Be familiar with treatment algorithm for DM and when to increase or decrease insulin. Slide 1: The first-line treatment for all patients with diabetes is Metformin and lifestyle changes. Comprehensive lifestyle management is key to improving health. Slide 2: Next, it is important to consider specific comorbidities, especially those that are related to the heart and kidneys. The presence of or high risk for atherosclerotic cardiovascular disease, chronic kidney disease, or heart failure will impact the selection of agents used. Slide 3: It is also important to consider patient A1C goals, which are individually considered. For example, patients who experience severe hypoglycemia or have a limited life expectancy may have an A1C goal of 8 rather than the typical goal of 7. The blue box on the left and subsequent boxes in that chart lane refer to patients with heart and renal influences. The right lane refers to patients who are meeting their A1C goals; for these patients maintain the current treatment of metformin and lifestyle changes. Slide 4: The guidelines inform the treatment of diabetic patients with or at risk for atherosclerotic cardiovascular disease. Specific drug classes are listed; insulin is not included for those individuals who are meeting their A1C goal. However, if the patient is above their A1C goal, insulin is a treatment option. In practice, you may see providers managing diabetic patients differently. Remember, clinical practice guidelines are guidelines and not absolute actions that must be followed. The patient's unique needs must take priority. Also, more than one guideline exists. However, the ADA guidelines are referenced on board exams and are the preferred guideline in the course and program. Slide 5: The right side of the algorithm also guides the treatment of individuals who do not have heart or renal concerns. These considerations represent rationale drug selection. Notice three goals are emphasized: minimize weight gain, promote weight loss, or reduce costs. Cost may be a concern; looking up drug costs on GoodRX and discussing costs with patients is essential before making a shared decision on a treatment plan. Slide 6: The ADA also provides guidance on when and how to start insulin as well as how to manage titration. Additionally, you'll notice in this algorithm there is also information available on selecting the best insulin for your patient. Notice, it is recommended that a GLP-1 be considered before starting insulin. Slide 7: The information in this box is important to know and remember. To start insulin, patients should be started on 10 IU a day OR 0.1-0.2 IU/kg a day and then titrated up from there based on fasting glucose results. And, of course, there's another algorithm to decide what process to use for titration. The algorithm for insulin therapy continues but this is the last box of information you need to be familiar with at this point. - Be familiar with frequency of Hgb A1C monitoring timeline. Perform the A1C test at least two times a year in patients who are meeting treatment goals (and who have stable glycemic control). E Perform the A1C test quarterly in patients whose therapy has changed or who are not meeting glycemic goals. E Point-of-care testing for A1C provides the opportunity for more timely treatment changes. E pg. 398 - Know when to start insulin. (LAG) Short Duration: Rapid Acting insulin: lispro (SubQ inj: within 15 min before or just after meals) SubQ inf: continuous, with bolus just before meals), aspart (SubQ inj: 5-10 min before meals SubQ inf: continuous, with bolus 5-10 min before meals), glulisine (SubQ inj: within 15 min before meals or within 20 min after. SubQ inf: continuous, with bolus 15-20 min before meals) Short Duration: Short Acting insulin: regular (if sub q inj. 30 minutes before meals or 20 minutes after) (if sub q. inf 15 to 20 minutes before meals) Intermediate Duration: Neutral protamine Hagedorn insulin (twice daily at same time each day) Long Duration Insulin: glargine (U-100), detemir (once or twice daily take at same time each day) Ultralong Duration Insulin: glargine (U-300), degludec (once daily take at same time everyday) - Know how insulin is mixed (combination and amount) when Total Daily Dose is calculated (TDD). Mixing Insulins Mixing should be done only with insulins of proven compatibility. Of the three longer-acting insulins in current use, only NPH insulin is appropriate for mixing with short-acting insulins (i.e., regular, lispro, aspart, and glulisine insulins). When a mixture is prepared, the short-acting insulin should be drawn into the syringe first to avoid contaminating the stock vial of the short acting insulin with NPH insulin. For example, the total daily dose (TDD) of insulin can be calculated by taking the total weight of the patient's weight in kilograms (kg), which is 80 kg (184 pounds) multiplied by 0.6 units equals 48 units. This means 24 units of the TDD is the basal insulin dose of glargine (Lantus) (50%) and the other 24 units of rapid-acting bolus/mealtime insulin (50%). Know what type of insulin and how much is needed according to carbohydrate intake. The mealtime carbohydrate-to-insulin dose is calculated using the 450 rule for regular insulin and the 500 rule for rapid-acting insulin; thus 500 is divided by the TDD insulin, 48 equals 10.4 (this is rounded down to 10). The carbohydrate-to-insulin ratio is 1:10. If the meal is 60 grams of carbohydrates, 60 is divided by 10, which equals 6 units of rapid-acting insulin for carbohydrate coverage. - Know insulin types with examples. Short Duration: Rapid Acting insulin: lispro, aspart, glulisine (LAG) Short Duration: Short Acting insulin: regular Intermediate Duration: Neutral protamine Hagedorn insulin Long Duration Insulin: glargine (U-100), detemir Ultralong Duration Insulin: glargine (U-300), degludec pg. 402 Be familiar with step therapy and asthma treatment so you know when which medication would be appropriate for which type of asthma. -Know the description of each type or degree of asthma look at flash cards Be familiar with examples of drug classes Antiinflammatory Drugs: Glucocorticoids Beclomethasone (inhaled) Prednisone (oral) Antiinflammatory Drugs: Others Cromolyn (mast cell stabilizer, inhaled) Zafirlukast (leukotriene modifier, oral) Antiinflammatory Drugs: Monoclonal Antibodies Omalizumab (anti-IgE antibody) Antiinflammatory Drugs: Phosphodiesterase-4 Inhibitors Roflumilast (oral) Bronchodilators: Anticholinergic Drugs Ipratropium (inhaled, short acting) Tiotropium (inhaled, long acting) Bronchodilators: β2-Adrenergic Agonists Albuterol (inhaled, short acting) Salmeterol (inhaled, long acting) Bronchodilators: Methylxanthine Theophylline (oral) - Know Lifespan considerations for methylxanthines Methylxanthines are approved for children of all ages, including neonates. It is important to consider variable drug clearance across age ranges when dosing. pregnant women Methylxanthines have been associated with adverse effects in some animal reproduction studies. breastfeeding Labeling for methylxanthines warns against breastfeeding only if the mother may have toxic levels. older adults Older patients are at much higher risk for toxicity when taking methylxanthines. - Know risk factors for fatal asthma attacks - Be familiar with benefits of various nicotine replacement options Nicotine Chewing Gum (Nicotine Polacrilex): Nonprescription; user controls dose Nicotine Lozenges (Nicotine Polacrilex): Nonprescription; user controls dose; easier to use than nicotine gum Nicotine Transdermal Systems (Patches): Nonprescription; provides a steady level of nicotine; easy to use; unobtrusive Nicotine inhaler: User controls dose; mimics hand-to-mouth motion of smoking Nicotine nasal spray: User controls dose; fastest nicotine delivery and highest nicotine levels of all nicotine-based products - Know contraindications and length of treatment of smoking cessation medications Nicotine patch: Nicotine gum: Use beyond 6 months is not recommended Nicotine lozenge: Dosing should decrease over a period of 12 weeks Dosing should stop after 12 weeks Nicotine nasal spray: After 3 months, taper use to complete cessation over additional 2-3 months nicotine inhaler: Decrease use after 4-6 weeks Know patient teaching needed for the various types of nicotine replacement options Nicotine Chewing Gum (Nicotine Polacrilex): Patients should be advised to chew the gum slowly and intermittently for approximately 30 minutes. Rapid chewing can release too much nicotine at one time, resulting in effects similar to those of excessive smoking (e.g., nausea, throat irritation, hiccups). Because foods and beverages can reduce nicotine absorption, patients should not eat or drink while chewing or for 15 minutes before chewing (see Table 34.1). After 3 months without cigarettes, patients should discontinue nicotine use. Withdrawal should be done gradually. Use of nicotine gum beyond 6 months is not recommended. Nicotine Lozenges (Nicotine Polacrilex): The most common adverse effects are mouth irritation, dyspepsia, nausea, and hiccups—all of which can be made worse by taking two lozenges at once or by taking several lozenges in immediate succession. Administration consists of placing the lozenge in the mouth and allowing it to dissolve, which takes 20 to 30 minutes. Users should not eat or drink for 15 minutes before dosing and while the lozenge is in the mouth. In addition, they should not chew or swallow the lozenge Nicotine Transdermal Systems (Patches): Nicotine patches are applied once a day to clean, dry, nonhairy skin of the upper body or upper arm. The site should be changed daily and not reused for at least 1 week. NicoDerm CQ patches are left in place for 24 hours and then immediately replaced with a fresh one. Most patients begin with a large patch and then use progressively smaller patches over several weeks. Starting patch size is typically determined based on the number of cigarettes smoked daily. Certain patients (those with cardiovascular disease, those who weigh less than 100 pounds, and those who smoke less than one-half pack of cigarettes a day) should begin with a smaller patch. Adverse effects are generally mild. Short-lived erythema, itching, and burning occur under the patch in 35% to 50% of users. In 14% to 17% of users, persistent erythema occurs, lasting up to 24 hours after patch removal. Patients who experience severe, persistent local reactions (e.g., severe erythema, itching, edema) should discontinue the patch and contact a medical provider. Nicotine Inhaler: The nicotine inhaler consists of a mouthpiece and a sealed, tubular cartridge. Inside the cartridge is a porous plug containing 10 mg of nicotine. Inserting the cartridge into the mouthpiece breaks the seal. Puffing on the mouthpiece draws air over the plug and thereby draws nicotine vapor into the mouth. Adverse effects are mild. The most frequent are dyspepsia, coughing, throat irritation, oral burning, and rhinitis. The inhaler should not be used by patients with asthma. Because the cartridges contain dangerous amounts of nicotine, they should be kept away from children and pets. Nicotine Nasal Spray: Adverse effects are mild and temporary. At first, most users experience rhinitis, sneezing, coughing, watering eyes, and nasal and throat irritation. Fortunately, these effects abate in a few days. Nicotine nasal spray should be avoided by patients with sinus problems, allergies, or asthma. - Know life span considerations of TB drugs including children, pregnancy, and breastfeeding. children First-line antitubercular drugs with the exception of rifapentine are approved for children; rifapentine is approved for children 12 years of age and older. Ethambutol is usually reserved for children older than 8 years. pregnant women Rifabutin is deemed the safest during pregnancy. The CDC reports that the benefit justifies the risk for isoniazid, rifampin, and pyrazinamide. The CDC does not recommend rifapentine due to insufficient data in pregnant women. Ethambutol has caused teratogenesis in animal studies and there have been reports of eye abnormalities in children; therefore ethambutol should be given only if the benefits are judged to be greater than the risks. breastfeeding According to the CDC, mothers taking isoniazid and rifampin should be encouraged to breastfeed. For other drugs, it is important to weigh the benefits of breastfeeding against any possible risks to the infant. The amounts of drugs excreted in milk are not sufficient for neonatal treatment against TB. older adults No contraindications are identified for older patients. Dosing may need to be adjusted for patients with decreased renal function. - Isoniazid (INH) is a drug that can be used to prevent TB in people that have been exposed. - Know MOA and examples of long acting Beta-2 Receptor Agonist (B2RA) The β2 agonists are sympathomimetic drugs that activate β2-adrenergic receptors. By activating β2 receptors in smooth muscle of the lung, these drugs promote bronchodilation and thus relieve bronchospasm. In addition, β2 agonists have a limited role in suppressing histamine release in the lung and increasing ciliary motility. Arformoterol (Brovana)cFormoterol (Foradil Aerolizer, Perforomist, Oxeze Turbuhaler ) Indacaterol (Arcapta Neohaler, Onbrez Breezhaler ) Olodaterol (Striverdi Respimat) Salmeterol (Serevent Diskus)b - Know patient instructions needed for respiratory drugs Glucocorticoids: If patients are prescribed both a short-acting β2 agonist (SABA) and a glucocorticoid, explain that delivery of glucocorticoids to the airways can be enhanced by inhaling a SABA 5 minutes before inhaling the glucocorticoid. Teach patients with chronic asthma to monitor and record peak expiratory flow (PEF), symptom frequency and symptom intensity, nighttime awakenings, effect on normal activity, and SABA use. Advise patients to rinse their mouth and gargle after dosing to minimize dysphonia and oropharyngeal candidiasis. Cromolyn: For acute prophylaxis, instruct patients to administer cromolyn 15 minutes before exercise and exposure to other precipitating factors (e.g., cold, environmental agents). For long-term use, instruct patients to administer cromolyn on a regular schedule. Be sure to inform them that full therapeutic effects may take several weeks to develop. Teach patients with chronic asthma to monitor and record peak expiratory flow, symptom frequency and symptom intensity, nighttime awakenings, effect on normal activity, and short acting β2 agonist use. β2-Adrenergic Agonists: Advise patients with asthma to assess peak expiratory flow daily and compare with personal best. Counsel patients to keep a record of these assessments along with symptom frequency and symptom intensity, nighttime awakenings, effect on normal activity, and short-acting β2 agonist (SABA) use. Inform patients who are using metered-dose inhalers or dry-powder inhalers that, when two inhalations are needed, an interval of at least 1 minute should elapse between inhalations. Instruct patients to report chest pain associated with changes in heart rate or rhythm. This could indicate cardiac stress secondary to adrenergic effects. Warn patients against exceeding recommended dosages. If worsening symptoms require more frequent use of a SABA, the provider should be notified. Inform patients that inhaled LABAs (formoterol, arformoterol, and salmeterol) should be taken on a fixed schedule—not as needed (PRN)—and always in combination with an inhaled glucocorticoid. Instruct patients to take oral β2 agonists on a fixed schedule—not PRN. Sustained-release preparations should be swallowed intact, without crushing or chewing. Theophylline: Warn patients that, if a dose is missed, the following dose should not be doubled. Instruct patients to swallow enteric-coated and sustained-release formulations intact, without crushing or chewing. Warn patients against consuming caffeine-containing beverages (e.g., coffee, many soft drinks) and other sources of caffeine. Explain that caffeine can intensify adverse effects while decreasing theophylline breakdown. Instruct patients to call the clinic if they start to develop symptoms of nausea, vomiting, abdominal discomfort, diarrhea, insomnia, restlessness, or palpitations, because these may signify theophylline toxicity. Warn patients that smoking tobacco or marijuana can increase theophylline clearance, resulting in ineffective dosing. - Know when it would be appropriate to prescribe an oral corticosteroid in respiratory patients Its use is restricted to patients with either eosinophilic asthma or with dependence on oral glucocorticoids. After resolution of the crisis and hospital discharge, an oral glucocorticoid is taken for 5 to 10 days. Oral glucocorticoids may be required for patients with moderate to severe persistent asthma or for management of acute exacerbations of asthma or COPD. Because of their potential for toxicity, these drugs are prescribed only when symptoms cannot be controlled with safer medications (inhaled glucocorticoids, inhaled β2 agonists). Because the risk for toxicity increases with duration of use, treatment should be as brief as possible. - Be familiar with roflumilast - Know when to use LABA, SABA, Combo drugs in COPD One phosphodiesterase 4 (PDE4) inhibitor, Roflumilast (Daliresp. Daxas) is approved for management of COPD. In patients with severe, chronic COPD with a primary chronic bronchitis component, the risk for exacerbations may be reduced with this drug. Mechanism of action. Roflumilast is a selective inhibitor of PDE, an enzyme that inactivates cyclic adenosine monophosphate (cAMP). By raising levels of cAMP in lung cells, the drug reduces inflammation by suppressing cytokine release and by decreasing pulmonary infiltration by neutrophils and other white blood cells. As a result, cough and excessive mucus production are reduced and mucociliary clearance is improved. Therapeutic use. Romflumilast is approved only for management of COPD. It is not a first-line drug; rather, it is used for exacerbation prophylaxis in patients with severe COPD with a primary chronic bronchitis component and a history of frequent exacerbations. Pharmacokinetics. Romflumilast has a bioavailability approximating 80%. It peaks in approximately 1 hour, although this is delayed if taken with food. It is 99% protein bound with a half-life of 17 hours. Metabolism to its active metabolite is via CYP3A4 and CYP1A2 isoenzymes. Excretions is primarily through urine. Adverse effects. Adverse effects include diarrhea, reduced appetite, weight loss, nausea, headache, back pain, and insomnia. It should be prescribed with caution for patients with depression. Safety in pregnancy has not been established; however, adverse events occurred in animal reproduction studies. Breastfeeding is not recommended when taking this drug. That being said, because COPD is uncommonly among women of child-bearing age, this is not typically a concern. Know which GI drugs interact with CYP450 enzyme system Cimetidine H2 receptor antagonist, Omeprazole PPI, Alosetron (IBS-D) Know which nutritional deficiencies are associated with long term PPI use Long term nutritional def: magnesium, calcium, b12. Can cause renal complications, dementia, and bone fractures. Know risks of short-term PPI use hypocalcemia/hypomagnesemia, community acquired pneumonia, can lead to c-diff, acid rebound, fractures. Know how to treat constipation Infants Docusate, lactulose, and glycerin suppositories have been used to treat constipation safely in infants. Children/adolescentsMilk of magnesia, mineral oil, senna, docusate, and bisacodyl can be used to treat constipation in children and adolescents. Pregnant womenLaxatives should be used cautiously in pregnancy because gastrointestinal stimulation can induce labor. Breastfeeding womenSenna is safe for use during breastfeeding. Data are lacking regarding the use of polyethylene glycol and bisacodyl (Dulcolax); caution is advised. Older adults All laxatives discussed in this chapter can be used in the older-adult population. The older adult should be monitored closely for dehydration. Know which medications are contradicted according to life span considerations. Misoprostol is contraindicated during pregnancy. Because prostaglandins stimulate uterine contractions, the use of misoprostol during pregnancy has caused partial or complete expulsion of the developing fetus. Know how to assess and monitor treatment. We can evaluate ulcer healing by monitoring for relief of pain and by radiologic or endoscopic examination of the ulcer site. Unfortunately, evaluation is seldom straightforward because cessation of pain and disappearance of the ulcer rarely coincide—in most cases, pain subsides before complete healing. However, the converse may also be true—pain may persist even though endoscopic or radiologic examination reveals healing is complete. Eradication of H. pylori can be determined with several methods, including breath tests, serologic tests, stool tests, and microscopic observation of a stained biopsy sample. H2 Receptor Antagonists Monitoring: Consider monitoring of gastric pH (should increase to 5 or above). Monitor for relief of pain. Eradication of H. pylori infection. Proton Pump Inhibitors Follow magnesium levels periodically. Monitor for relief of pain. Eradication of H. pylori infection. - Be familiar with treatment of GERD Famotidine (Pepcid) Cimetidine PPI's Omeprazole Antacids Histamine 2-Receptor Antagonist (H2RA) Cytoprotective Agents - Know examples of the different types of antidiarrheals and how they work opioids By activating opioid receptors in the GI tract, these drugs decrease intestinal motility and thus slow down intestinal transit, which allows more time for absorption of fluid and electrolytes. In addition, activation of opioid receptors decreases secretion of fluid into the small intestine and increases absorption of fluid and salt. Diphenoxylate Loperamide - Be familiar with metoclopramide's use, MOA, side effects, monitoring and patient teaching. Metoclopramide (Reglan) has two beneficial actions: (1) it suppresses emesis (by blocking receptors for dopamine and serotonin in the CTZ), and (2) it increases upper GI motility (by enhancing the actions of acetylcholine). Indications depend on the route (oral or intravenous). Oral metoclopramide has two approved uses: diabetic gastroparesis and suppression of gastroesophageal reflux. Intravenous metoclopramide has four approved uses: suppression of postoperative nausea and vomiting, suppression of CINV, facilitation of small bowel intubation, and facilitation of radiologic examination of the GI tract. Off-label uses include the treatment of hiccups and nausea and vomiting of early pregnancy. Adverse Effects With high-dose therapy, sedation and diarrhea are common. Long-term high-dose therapy can cause irreversible tardive dyskinesia, characterized by repetitive, involuntary movements of the arms, legs, and facial muscles. Older adults are especially vulnerable and can develop involuntary movement disorders after a single dose. To reduce the risk for tardive dyskinesia, treatment should be as brief as possible using the lowest effective dose. Owing to its ability to increase gastric and intestinal motility, metoclopramide is contraindicated in patients with GI obstruction, perforation, or hemorrhage. Of note, exposure to metoclopramide during the first trimester of pregnancy is not associated with an excess risk for congenital malformations. - Know how to prevent ulcers when someone is taking NSAIDs Antisecretory agent that enhances mucosal defenses Prophylaxis. For patients with risk factors for ulcer development (e.g., older than 60 years, history of ulcers, high-dose NSAID therapy), prophylactic therapy is indicated. PPIs (e.g., omeprazole) are preferred. Misoprostol is also effective but can cause diarrhea. Antacids, sucralfate, and H2 receptor blockers are not recommended. Treatment. NSAID-induced ulcers can be treated with any ulcer medication. However, H2 receptor blockers and PPIs are preferred. If possible, the offending NSAID should be discontinued to accelerate healing. If the NSAID cannot be discontinued, a PPI is the best choice to promote healing. - Know when to test for H. Pylori and patient teaching for treatment regimens. when patient is on PPI and H2 Receptor Antagonists consider testing for H.pylori Antibacterial drugs should be given to all patients with gastric or duodenal ulcers and confirmed infection with H. pylori. Antibiotics are not recommended for asymptomatic individuals who test positive for H. pylori. clarithromycin, amoxicillin, bismuth, metronidazole, and tetracycline. None is effective alone. Furthermore, if these drugs are used alone, there is increased risk for developing resistance. - Know treatment options for H. Pylori and lifestyle habits that will impact which therapy is selected. - Know patient teaching information for H2RA, PPIs, antacids, lifestyle management strategies for GERD. - Be familiar with what drugs are used to treat symptoms of IBS. Alosetron (Lotronex) Eluxadoline (Viberzi) Lubiprostone (Amitiza) Linaclotide (Linzess) lifespan tx of GERD and ulcers Infants Both PPIs and H2 receptor antagonists are used safely in infants as young as 1 month to treat GERD and duodenal ulcers. Children/adolescents PPIs and H2 receptor antagonists can be used safely in children, just in smaller doses. Side-effect profiles resemble those of adults. Pregnant women Misoprostol must be avoided at all costs. Some PPIs (esomeprazole) and H2 receptor antagonists (ranitidine) are safe for use in pregnancy. Breastfeeding women Use of drugs such as omeprazole, esomeprazole, and ranitidine is not predicted to cause any adverse effects in breastfed infants.Older adults PPIs are associated with increased risk for fractures from osteoporosis. PPIs can also cause medication interactions and vitamin or mineral deficiencies. There should be a clear indication for prescribing these medications in this older population. Know who can receive live attenuated vaccines and which vaccines are live attenuated. live vaccines: MMR, Varicella, Influenza, Rotavirus Avoid in immunocompromised (HIV, leukemia, lymphoma, malignancy, congenital immunodeficiency, therapy with radiation, cytotoxic cancer drugs, high-dose glucocorticoids) & pregnant women. Anaphylactic reaction, moderate or severe illness with or without fever. - Know contraindications for vaccines MMR - gelatin allergy, neomycin allergy, thrombocytopenia, eggs DTaP - i A shocklike state • Fever (105°F or higher) occurring within 48 hours of vaccination and not attributable to another identifiable cause • Persistent, inconsolable crying lasting 3 or more hours and occurring within 48 hours of vaccination • Seizures (with or without fever) occurring within 3 days of vaccination children with moderate or severe febrile illness, administration should be postponed until the illness has resolved. DTaP is contraindicated if a prior vaccination with DTaP produced (1) an immediate anaphylactic reaction or (2) encephalopathy within 7 days of vaccination. Varicella - pregnant patients, individuals with certain cancers (e.g., leukemia, lymphomas), and individuals with hypersensitivity to neomycin or gelatin, both of which are in the vaccine. In addition, the vaccine should generally be avoided by individuals who are immunocompromised, including those with HIV infection or congenital immunodeficiency and those taking immunosuppressive drugs. Children receiving the vaccine should avoid aspirin and other salicylates for 6 weeks. Hep B - but aspirin should be avoided. The only contraindication to HepB is a prior anaphylactic reaction either to HepB itself or to baker's yeast. Rotarix - contraindicated for infants with SCID. contraindicated for infants with any uncorrected congenital malformation of the gastrointestinal tract that could predispose to intussusception. Both vaccines are contraindicated for children with a history of intussusception. - Know who can safely receive the Hepatitis B vaccine one of the safest vaccines - everyone even immunocompromised should receive - only if had previous anaphylaxis or allergic to baker's yeast - avoid. - Know which vaccines tuberculin purified protein derivative can be given with can be given with live vaccines same day, if not, must wait 1 month after d/t possible interference with reactions. - Be familiar with the rabies vaccination schedule. 4 1-mL doses of HDCV or PCECV IM. First dose ASAP after exposure (day 0), followed by days 3, 7, 14. Along with RIG (rabies immune globulin). If patient immunocompromised, 5 injections on days 0, 3, 7, 14, and 28. Previous vaccine, 2 doses on day 0 and day 3 with no RIG. - Who should receive a Tdap vaccine? one dose after age 11, then every 10 years or each pregnancy between weeks 27-36, or if injury with wound occurs. For clean minor wounds, if 10 years or all other wounds, if more than 5 years since last. - Know expected side effects from vaccines. MMR: anaphylaxis, thrombocytopenia DTaP: acute encephalopathy, convulsions, shock-like state Hep A/B: anaphylaxis Influenza: flu like symptoms Rotavirus: intussusception (rare) Poliovirus PO: paralytic poliomyelitis In general: local reactions, swelling, erythema, fever, diarrhea, vomiting, anorexia, fatigue. - Be familiar with routine recommended vaccination schedules- not catch-up schedules - Know signs and symptoms of: o Measles o Mumps o Rubella o Varicella o Pertussis Measles: rash, high fever (103-105) initial cough, headache, sore throat, conjunctivitis, rash develops 3-5 days after. Mumps: 5-15 years, initial swelling parotid glands, local pain tender. Fever 100- 104. Orchitis in 1/3 males. Rubella: sore throat, mild fever, swelling lymph nodes behind ears and neck. Rash all over. Arthritis. If occurs in pregnancy, severe consequences miscarriage, stillbirth, congenital defects such as cataracts, heart disease, hearing loss, delay. Pertussis: rhinorrhea, mild fever, persistent cough. Intense cough lasting 4-6 weeks. Varicella: "chicken pox" vesicular lesions, fever, malaise, loss of appetite. More severe in adults. Can lead to varicella PNA. Shingles later in life. Blister lesions following a nerve path.