NAPLEX Complete Study Outline A Topic-Wise Approach DIABETES (2019)
- North American Pharmacist Licensure Examination
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Copyright Johanna Kristin Ellerup, PharmD Contributing Editor: Olga Kalugina, PharmD 2019 Johanna Kristin Ellerup PharmD All rights reserved. No part of this book may be reproduced, or stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, nor in any language without the express written permission of the author. Printed in the United States of America
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Table of Contents Diabetes Epidemiology and Generalized Informa on: Recommenda ons Pa ent Counseling points: Cover terms Clinical Pearls & Notes: Signs and symptoms of associated disease states: Pathophysiology: Treatment op ons: Lifestyle Interven ons – DPP-4 GLP-1 Alpha-Glucosidase Megli nides Sulfonylureas First Genera on Second Generation Sodium Glucose Transporter Protein2 – Inhibitors Thiazolidinediones Biguanides Amylin Analog Insulin An -Hypoglycemic Agent/Glycogenoly c Clinical Guidelines: References:
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Diabetes Epidemiology and Generalized Information: Prevalence 1.25 million Americans. Incidence is 40,000 new diagnoses each year. 2013 – 33-49% of patients not meeting general targets for glucose 33-49% of patients not meeting general targets for glucose, BP or cholesterol & only 14% met goal while not smoking. 2012-17 – cost of diabetes (w/adjustments for inflation) increased 26% Social determinants of health are economics, environment, political & social conditions in which people live. 14% of Americans suffer from food insecurity & increased risk of T2DM, suboptimal glycemic control, psychosocial conditions and low treatment adherence 79. Recommendations A—Clear evidence from well-conducted, generalizable randomized controlled trials that are adequately powered B—Supportive evidence from well-conducted cohort studies C—Supportive evidence from poorly controlled or uncontrolled studies E—Expert consensus or clinical experience - BMI - >=25Kg/m2 or >=23 Kg/m2 in Asian Americans. Consider testing [Level B recommendation] - Everyone gets tested at 45 years of age [B] - Repeat testing, if normal and conditions listed, roughly every 3 years [C] - In patients w/pre-diabetes & T2DM – test & if needed treat for cardiovascular issues [B] - Pre-diabetes risk screening in children or adolescents who are overweight (BMI >=85%) [B]
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- Patient centered, open-ended positive response, collaborative health care team approach. [B] - Multidisciplinary team with interactive communication [E] 79 Patient Counseling points: 1) Do not double doses. If close to the time of the next, subsequent dose, skip the dose you missed and continue regimen. Consider making a note (i.e., in diabetes diary) of missed dose to reconcile any blood glucose fluctuations. 2) Swallow tablets/capsules whole. Do not crush or chew. 3) Store all injectables out of direct sunlight. Refrigerate, do not freeze, prior to use and maintain within acceptable room temperature once vial is punctured or pen is utilized. 4) Do not shake injectables; instead hold between both palms and gently swirl. 5) Use alcohol swabs to clean vials and skin prior to puncturing and rotate injection sites to reduce injection site reactions and lipodystrophy. 6) Report any unusual or elevated reactions or side effects to your doctor immediately. If in doubt, call 911. 7) Carry identification somewhere on your person at all times indicating that you are diabetic for emergency purposes. 8) Keep portable candies and long acting carbohydrates/protein on hand and utilize mobile apps for guidance. 9) Contact your provider during illness as physiologic needs may change. 10) Notify all providers of medical history, including history of gallstones, ethanol, smoking, pancreatitis, hepatic/renal disease, cholesterol level and current medications including Over-the-Counter items, herbals and supplements. 11) Check all vials and pens (where possible) for cloudiness, changes in color or particulate matter. Dispose of safely in sharps containers. 12) Unless otherwise stated in the package insert, cloudy insulins (glargine, isophane, etc.) should not be given intravenously. 13) Vials follow ISMP (Institute for Safe Manufacturing Practices), US Pharmacopeia standards of 28 days stability
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after puncturing a multi-dose vial unless otherwise stated in the package insert. 14) Those with diabetes should check their feet routinely and protect from cuts, corns, blisters and injuries that may compromise skin integrity. Diabetic patients are more prone to fungal and bacterial infections of the extremities, especially if they suffer from diabetic neuropathy which can decrease awareness. Suggest they make a habit of doing a quick, yet thorough, inspection while changing their socks, shoes. IF the patient notices any changes to their feet or calves, advise them to notify their primary care physician, podiatrist and/or dermatologist immediately.
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Cover terms Fasting Blood Glucose (FPG) – Macrovascular disease – Metformin, Insulin. Fasting – greater than 6 hours between meals – 70-100 (up to 130) Post-Prandial Glucose (PPG) and A1C – Microvascular disease – GLP-1, DPP4, Insulin & SGTP. Peak postprandial – (peak – 1-2 Hrs after initiation of meal) = <=180mg/dl. Preprandial – Similar to trough – just prior to eating 70-130 HbA 1 C – Normal non-diabetic patients 4-6%. Very strict control is <7. Some patients may require <8 to prevent hypoglycemia. Primary failure – Inability to achieve disease remission/optimal effect with evidence based drug treatment and doses. Secondary effect – After initial success, the agent loses effectiveness which may be neutralization by pathogen enzyme secretion, alternate pathway or irreversible over-saturation of receptors (down regulation). 75g oral glucose tolerance test (OGGT) – With either fasting plasma glucose (FPG) or 2HR plasma glucose. The 2Hr plasma glucose diagnoses, overall, more patients than either the FPG or A 1 C. Diagnosis requires, at least, two elevated and separate test results (even A1c) unless there’s obvious signs of hyperglycemia – 3P’s – polyuria (urine), polyphagia (eating) & polydypsia (drinking), etc. Repeat testing in 3-6 months.8 This distinguishes transient hyperglycemia (temporary alteration in diet, infection, drug treatment, etc.) from diabetes. Pre-diabetes – Not a clinical diagnosis, but rather a warning to increase monitoring and non-pharmacologic pathways. 8 Pediatric and geriatric patients display altered pharmacokinetic/dynamics and therefore require different treatment, dosing or increased monitoring. Start low and go VERY slow. For example, pediatrics have different Vd and an immature GI tract/hormone secretions, so that a drug may have greatly reduced serum levels or have a higher level excreted unchanged. Geriatrics
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may have greatly reduced renal or hepatic function not fully evident on labs, so that the duration of action of a 6 hour tablet that undergoes second pass effect may be increased to 24 plus hours in this patient population. The ‘Incretin Effect’ is defined as the insulin response difference in oral versus IV dosing of glucose. A possible explanation for this increased effect, in some cases a three-fold increase, is the digestive enzyme secretion in saliva. By the time food has entered the stomach via the lower esophageal sphincter, the pancreas has been actively stimulated in preparation whereas an IV injection bypasses this mechanism. Under normal conditions, glucagon is secreted by the alpha cells of the Isle of Langerhans, which also secretes beta and delta cells, of the pancreas in response to fasting conditions and maintains glucose concentration within the plasma. Insulin is secreted by the beta cells of the Pancreas, in response to meals and stimulates the uptake of glucose to peripheral tissue and out of the plasma circulation thereby reducing solutes in plasma.31 Clinical Pearls & Notes: Categories of diabetes: Think - 3P’s – Poly-urea (urinating/micturating), Poly-dypsia (drinking), Poly-phagia (eating). Think – increased osmolarity (dissolved particles in solute) of blood for pathogenesis of primary and secondary disease. All agents that induce the secretion of insulin can lead to pancreatitis. Genetic missense variants: Known pathogenicity in the GCK (highly overrepresented in DM) , HNF1A , HNF4A , ABCC8 , and INS genes.11 DNA amino acids: G (guanine), T (thymine), C (cytosine), A (arginine). SNP – Single Nucleotide Polymorphisms – change to one specific nucleotide in an open-reading frame that may alter the translation/transcription of that sequence. T1DM = Immune mediated or idiopathic – AKA Juvenile Diabetes.8 T2DM = Insulin resistance peripherally w/relative insulin deficiency or more commonly effect on insulin secretion with insulin resistance. AKA adult diabetes. In this class, hyperglycemia may follow metabolic
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syndromes = obesity, HTN, hyperlipidemia and impaired fibrinolysis. (AHFS,3211) HbA 1 C – “…nonexzymatic glycosylation of other proteins throughout the body as a result of recent (eg. previous 6-8 weeks) hyperglycemia.” (AHFS, 3212) Microvascular complications include blindness, retinopathy, and nephropathy, co-morbid with dyslipidemia, blood pressure and vascular thrombosis. Most associated with PPG. AHFS Agents that have CYP 450, OAT/OCT, PgP interactions, etc – even when ‘not clinically significant’ may play an important role to individual patients displaying unexpected sides or reactions. Don’t dismiss them. Agents that are excreted in bile and/or unabsorbed from the GI tract is eliminated in feces. Consider this if agent affects GI transit time or binds to the GI tract excessively. In general, the insulin or sulfonylurea dose is reduced preferentially over DPP-4, GLP-1 or SGTP. Beta blockers, hypothyroid agents, anxiolytics, catecholamines agonists/antagonists may mask hypoglycemic signs and alter glucose metabolism. Insulin is preferred in pregnancy and pediatrics due to increased Vd, decreased muscle and altered adipose tissue. In general, oral agents are reserved for 18+. Geriatric patients (70+) have reduced renal, hepatic and cardiac function and therefore, in general, may use lower dosages or increased intervals with all agents to reduce hypoglycemia which can lead to falls, dizziness, altered mental status, etc. Insulin is needed in ketonuria and glucosuria. Hypoglycemia treatment protocol – IV D50W 50mL Bolus with D10W titrated to glucose >100mg/dl. Glucocorticosteroids, such as dexamethasone, may be added.
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Signs and symptoms of associated disease states: Hepatic Failure: ALT/AST >120 (3 times upper limit of normal [ULN]); elevated Alk Phos (indicative of liver, bone disease), yellowing of sclera, skin (jaundice), abdominal pain, nausea, vomiting, fatigue, anorexia, dark urine, ascites. Pancreatitis: Serum & urine amylases increased, amylase/CrCl ratio, electrolyte imbalance, sCa 2+ , glucose and lipase. Thyroid Tumors: Malignant or benign, lump on base of neck that (key characteristic) bobs up and down with swallow mechanism (follows thyroid), hoarseness, dysphagia, dyspnea). Prevalence ~ 6% female, 1-2% male. Up to 95% are benign, but must be evaluated. Consist of cysts, goiter (commonly in hypothyroid), adenomas and nodules. 57 Lactic Acidosis: Fatigue, headache, mental instability, increased lactase dehydrogenase and liver function tests (LFT’s). Metabolic Acidosis: Tachypnea, anorexia, nausea, vomiting, lethargy, mental status changes and abdominal pain. Diabetic ketoacidosis: Blood glucose levels needn’t be >200, but an increased anion gap, elevated blood and/or urine ketones, mental status changes may be present. Potential factors include hypovolemia, acute renal failure, hypoxemia, reduced oral intake, ethanol ingestion, acute illness (infection) and reduced insulin dosage. Renal labs: Hgb/Hct, electrolytes, BUN/sCr, CBC. Signs: Increased water retention (edema), HTN/hypotension, unconcentrated urine, skin turgor, appetite changes, digestion alterations, addition of NSAIDs, ACEI, diuretics, digoxin, etc. Fournier Gangrene : Necrotizing fasciitis, tenderness, swelling, redness of genitals, back to the rectum, 100.4+ fever, malaise, increased LDL-c hypoglycemia. Alcohol consumption in Diabetes – Alcohol displays varying effects depending on fed/fasting state of patient and whether acute or chronic ingestion. It can increase blood glucose in the fed state, due to a reduced
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inhibition (I.e., person may consume more carbohydrates calories), the sugar content of the drink itself, an alteration in fat metabolism, and an increase in peripheral insulin resistance. Whereas in chronic or starvation states the depletion of glycogen and alcohol preventing hepatic gluconeogenesis can cause blood glucose levels to plummet to dangerously low levels. This is compounded by the fact that hypoglycemia awareness is blunted during alcohol consumption and, due to the above listed events, there is an attenuated response to correction of hypoglycemia.80
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Pathophysiology: 1) Type 1 Diabetes – Polygenic form. Attributed to several genes, including HLA-DQA1, HLA-DQB1, and HLA-DRB1 genes contribute 5% toT1DM population. HLA is human leukocyte (white blood cell) antigen (a pathogenic cell). Considered auto- immune – where immune cells are attacking Isle of Langerhans- Pancreatic Beta Cells that secretes insulin. Pancreatic alpha-cells secrete glucagon.16 Signs – 3P’s, unexplained weight loss, excessive fatigue. Signs of DKA – “Sweet fruity breath” – Hallmark feature, dry or flushed skin (also thyroid or CHF), stomach pain (variety, including liver, bowel obstruction, etc), disoriented, SOB. Number 1 treatment is insulin replacement. Several agents- DPP4, GLP-1, Sulfonylureas, Meglitinides- are not compatible with T1DM because they stimulate the secretion of insulin from the pancreas which is the key feature separating Type 1 from Type 2. Hence, the side effect of pancreatitis for these agents.13 2) Type 2 Diabetes – Polygenic form. Think – overuse/over- stimulation disease. IGF2BP2 -SNP rs4402960 (Insulin-like growth factor 2 mRNA-binding protein 2; single Nucleotide Polymorphism) G/T, TERT rs2735940 T/C, TERT rs2736098 G/A.15 T2DM is also associated with Metabolic Syndrome (hypercholesterolemia, hyperglycemia, hypothyroidism, hypertension), which doesn’t rule out an inflammatory disorder. Evidence shows that the DASH and Mediterranean diets may have positive outcomes. - This is the only type of diabetes that is amenable to diet and exercise alone. Signs – 3P’s, increased fungal infections, sores that don’t heal (may also indicate cancer, psoriasis, etc). 3) Diabetes Insipidous – Polygenic form. “Sweet Urine.” Insipidus – (think – insipid) light and odorless. Normally, adults pass approximately 1-2 quarts (1/2 gallon, app 1890ml) of urine daily. DI patients can pass up to 20 quarts (app 5 gallons) of unconcentrated urine, due to an abnormality in renal tubular
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filtering. Important difference - Normal blood glucose levels (normoglycemic). Four major types of DI: a. Centrally mediated – Hypothalamus or pituitary. Vasopressin, a vasoconstricting agent that increases plasma sodium leading to increased water retention and increased blood pressure, does not concentrate the urine. Causes include central trauma, infection, meningeal inflammation, etc. b. Nephrogenic – Adrenally mediated. Vasopressin does not concentrate urine. BUN/sCr can be utilized to discern whether there is pre-renal implications (blockage), lithium and other exogenous xenotropic causes, altered electrolyte status. c. Dipsogenic – Excess fluid intake, especially water. An altered mental or physiologic status that causes more fluid intake than the body can normally process, thereby unfiltered excretion of the excess. Causes include all those previously listed.18 d. Gestational – Transient. May be caused by prostaglandin or oxytocinase/vasopressinase that inactivates vasopressin. Treatment of choice is DDAVP (desmopressin) that mimics the effects of vasopressin without inactivating or attenuating oxytocin (Pitressin – used to reduce pre-term labor).19 4) Gestational Diabetes – Treatment is insulin, as transport of oral agents across the placenta, risk of hypoglycemia and their varied side effects on the developing fetus is controversial at best. Co- morbid diseases include pre-eclampsia (very elevated blood pressure that is dangerous to both the mother and fetus), enlarged baby (possible developmental and/or physiological disorders), 20 At-risk mothers - age >35, previous gestational diabetes or primary family member, previous high birth weight delivery, pre-pregnancy obesity, hormonal disorders (ie., Polycystic Ovarian Syndrome). May be managed with non-pharmacologic factors and insulin. If
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uncontrolled, infants have a higher predisposition of developmental disorders (learning disabilities), heart disease, hyperlipidemia and diabetes later in life. 5) Monogenic Diabetes Syndromes – A form of non-autoimmune, early-onset diabetes that arises from a variant in one gene. It accounts for 1-4% of all DM cases in the US. May or may not be germline or a spontaneous mutation.11 , 12 a. Neonatal – May be transient, occurring only as the neonate begins to mature, or may be lifelong. Occurs in ~1 out of 400,000 US infants. Key determinant is that T1DM is rarely seen before 6 months of age, but NDM exists at birth. May also appear slightly later, ie toddler onward. b. Maturity Onset Diabetes of the Young (MODY) – A monogenetic disease that is heritable. Historically, these patients have chronically elevated blood glucose, but not necessarily peripheral or end-organ disease or overweight. Diagnosed via genetic testing. Medications are not necessarily preferred in this patient class. 6) Secondary Diabetes : Exocrine Pancreas (cystic fibrosis, pancreatitis, etc), Drug/Chemical induced, neonatal diabetes (non- NDM form), etc.
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