PharmacoDynamics



Therapeutics II

Exam #1

(Endocrine Pathology, DM, Thyroid, RA, Gout)

4-3-2008 |Yayyy!! Its note-card season again (

,mtyyh | |

|Endocrine Pathology: |Into the Bloodstream |

| |Nuclear (go into the cell’s nucleus) |

|Endocrine means that a hormone is secreted _____. |Anterior & Posterior Lobe |

|Hormones act at a ____ level to affect gene expression. |Anterior Lobe |

|The pituitary gland is made up of what 2 parts? |Posterior Lobe |

|Which lobe gets VENOUS blood supply? |B/c venous supply has significantly lower pressure (compared to arterial). This |

|Which lobe gets ARTERIAL blood supply? |relatively low blood pressure supplying the anterior lobe makes that lobe vulnerable |

|Why do we care about the blood supply to the different lobes of the pituitary gland? |to ischemic injury (if BP drops a lot, the anterior lobe will receive much less |

|*KNOW* |blood, thus less oxygen, thus ischemic injury) |

|What does anterior lobe of the pituitary secrete? |GH (growth hormone), Prolactin, FSH (follicle stimulating hormone), LH (luteinizing |

|Posterior Lobe? |hormone), ACTH, TSH (thyroid stimulating hormone), MSH (melanocyte stimulating |

|T or F? ALL pituitary hormones act as negative feedback regulators @ the pituitary. |hormone) |

| |Vasopressin (ADH) & Oxytocin |

| |True! Each hormone negatively feedsback to the pituitary to stop its own release. |

|Hyperpituitarism: |Excess production of anterior pituitary hormones caused by a Functional Adenoma. |

| |True! (but can secrete more than 1 hormone type) |

|Define. *KNOW* |Growth Hormone |

|T or F? Adenomas are often one cell type secreting 1 hormone excessively. |Kinda true…they can cause gigantism OR Acromegaly. |

|Adenomas known as “Somatotroph Cell” Adenomas hyper-secrete which hormone? |Age & status of epiphyses (open or closed) |

|T or F? Somatotroph Adenomas cause gigantism. |Olga’s were closed. Can tell because only develops gigantism if epiphyses open during|

|What determines if the somatotroph adenoma causes gigantism or acromegaly? *KNOW* |adenoma (like Egor did). *KNOW* |

|Egor has gigantism from a somatotroph adenoma. Olga has acromegaly from the same |Open Epiphyses = Gigantism |

|thing. Who’s epiphyses were CLOSED @ the time when the adenoma developed? How do you |Closed Epiphyses = Acromegaly |

|know? | |

|Briefly describe Gigantism |Develops in children (open epiphyses) who suffer from somatotroph adenoma. Increased |

|Briefly describe Acromegaly |body size w/ disproportionately long arms & legs. |

|T or F? Somatotroph Adenoma is the most common form of hyperfunctioning adenoma. |Develops in adults (closed epiphyses). Growth in soft tissues, skin, viscera & bone |

|Clinical manifestations of Prolactinomas: (4) |enlargement in face, hands, feet, & jaw. |

|T or F? These clinical manifestations are more easily noticed by women who passed |False! Prolactinomas are most common. |

|menopause. |~Amenorrhea ~Galactorrhea (milk leaking) ~Loss of libido ~Infertility |

| |False!! Pre-menopausal women are more likely to notice things like amenorrhea, |

| |infertility, etc… |

|Hypopituitarism: |~Non-secretory pituitary adenomas ~Ischemic necrosis of |

| |pituitary ~Ablation of pituitary by surgery or |

|Name the 3 causes of a hypofunctional pituitary: |radiation |

|T or F? Signs & symptoms of ischemic necrosis of the pituitary develop only after |True! |

|75% of it has been destroyed. |Postpartum necrosis of anterior pituitary. Occurs b/c pituitary enlarges during |

|Define Sheehan’s syndrome: *KNOW* |pregnancy, but blood supply remains the same. This causes the already vulnerable |

| |venous blood supply to the anterior lobe to become too low, resulting in necrosis. |

|Thyroid Gland: |Colloid |

| |The storage form of thyroid hormones (T4 & T3) |

|The thyroid gland is composed of follicles that contain ____. *KNOW* |T4 |

|What is Colloid? *KNOW* |~Normal maturation ~Normal Brain |

|Which is the “main thyroid hormone”? |development *KNOW* ~Normal growth |

|What are the 3 major functions of the thyroid hormones? |A hypermetabolic state caused by high circulating levels of free T3&T4. |

|Define Thyrotoxicosis: |Hyper-functioning thyroid gland (Hyperthyroidism) *can be other causes as well. |

|Thyrotoxicosis is usually caused by what? |Something which stimulates release of T3/T4. (example: iodine) |

|Define Goitrogen: |Acute rise in catecholamines (more common in Grave’s disease) |

|Define Thyroid Storm: | |

|How is Grave’s disease unique from hyperthyroidism? *KNOW* |Grave’s disease is an AUTO-IMMUNE DISORDER characterized by antibodies which |

|Describe the following antibodies which appear in Grave’s Disease |stimulate the TSH receptor, resulting in excess release of T3/T4. |

|TSI |Grave’s disease antibodies: |

|TGI |= Thyroid Stimulating Immunoglobin (binds TSH receptor, activates cAMP pathway cause |

|TBII |increased release of T3/T4) |

|T or F? Clinical features are the same for hyperthyroidism and Grave’s Disease. |=Thyroid Growth stimulating Immunoglobin (proliferation of thyroid follicular |

|Jane has been experiencing heat intolerance, excessive sweating, tremor, tachycardia,|epithelium) |

|& has lid lag. You suspect Hyperthyroidism. T or F? When you run labs, you expect to |= Thyroid Binding Inhibitor Immunoglobin |

|see elevated levels of TSH, T3, & T4. |3.) True! (so cannot tell them apart based solely on s/sx) |

| |4.) FALSE!! Her TSH would NOT be elevated if she has |

| |hyperthyroidism. (the T3 & T4 should be high) |

| |*this is b/c the high T3/T4 will negatively feedback |

| |on the pituitary, preventing TSH release. |

|Describe Cretinism: *KNOW* |Refers to hypothyroidism developing in infancy or early childhood. (when T3/T4 and/or|

|Describe Myxedema: |Iodine are deficient) |

|If someone has primary hyPOthyroidism, we’d expect their TSH levels to be ____. |Refers to hypothyroidism developing in older children or adults. |

|*KNOW* |High (b/c there is no T3/T4 inhibiting its release from the pituitary) |

|If someone has hyperthyroidism, we’d expect their TSH levels to be ____. *KNOW* |Low (b/c there is excess T3/T4 inhibiting TSH release from the pituitary) |

|What are Orphan Annie Nuclei? |Invaginations of cytoplasm often seen in thyroid tumors (non-functional tumors) |

|Adrenal Cortex: |Steroid Hormones (Glucocorticoids, Mineralcorticoids, & Androgens) |

| |~Maintains blood glucose ~Stimulates lipolysis |

|The adrenal cortex synthesizes and secretes ____. |~↓ skeletal muscle glucose absorption ~↓ skeletal muscle |

|Describe the actions of Cortisol (5) *KNOW* |protein synthesis ~↑ skeletal muscle release of amino |

|How is Cushing Syndrome difference from Cushing Disease? *KNOW* |acids |

|Describe some clinical features of hypercortisolism:` |“Syndrome” = any condition that produces elevation in glucocorticoid levels |

| |(hypercortisolism). “Disease” = Pituitary|

| |disease associated w/ hypersecretion of ACTH, also causing hypercortisolism. |

| |(probably from small ACTH-producing adenoma). |

| |HTN, weight gain, truncal obesity, “moon face”, buffalo hump, ↓ muscle mass, |

| |hyperglycemia, etc… |

|Endocrine Pancreas: |Islet of langerhans (composed of Beta cells, Alpha cells, & Delta cells) |

| |Beta cells |

|____ comprise the endocrine portion of the pancreas. |Alpha cells |

|_____ secrete insulin |Delta cells |

|_____ secrete glucagon | |

|_____ secrete Somatostatin | |

|Diabetes: Type 1 vs. Type 2 |Type 2 |

| |Type 1 |

|Which type of DM is being described? *KNOW* |Type 1 |

|Adults |Type 1 |

|Children |Type 1 |

|Anti-islet anti-bodies present |Type 2 |

|Low blood insulin |Type 1 |

|Autoimmune-Immumopathic mechanisms causing beta cell destruction |Type 1 & 2 |

|Insulin resistance |Type 2 |

|Caused by environmental insult and/or genetics |Type 1 |

|Give Insulin |Type 2 |

|Give oral therapy | |

|Insulinitis is seen (inflamed islets) | |

|Caused by Peripheral insulin resistance and/or derangement in beta cell secretion of | |

|insulin. | |

|Describe “derangement of beta cell secretion of insulin”. |The normal pulsatile, oscillating pattern of insulin secretion is lost & rapid first |

|Describe “Beta cell exhaustion”. |phase of insulin secretion triggered by glucose is weakened. |

|Describe “Insulin resistance by peripheral tissues”. |Chronic hyperglycemia causes the beta cells to tire out, resulting in even less |

|List 2 substances which INCREASE insulin sensitivity. *KNOW* |insulin secretion. |

|Why do diabetics have poor wound healing? *KNOW* |The post-receptor signaling by insulin is impaired (so tissues no longer respond to |

|HbA1C levels are helpful for what? |insulin) |

| |Adiponectin & Leptin (tell you when you’re “full”) |

| |Due to Nonenzymatic glycosylation. (the hyperglycemia inhibits collagen deposition @ |

| |injury site) |

| |Monitoring therapy efficacy (it can display glucose levels over past 2-3 months) |

|Endocrine Pathology SUMMARY: *KNOW* |Somatotroph adenoma (↑GH) in child/young adult whose epiphyses are not yet closed. |

|Gigantism results from what specifically? |Sheehan’s syndrome |

|I am postpartum necrosis of anterior pituitary. |Endocrine |

|Hormones secreted into the bloodstream that act @ the nuclear level are called ____. |Functional Adenomas |

|Excessive production of anterior pituitary hormones is most often caused by _____. |Colloid |

|I am the storage form of thyroid hormones. |Prolactinomas (hyperprolactemia) |

|I am the most common hyper-functioning pituitary adenoma. |Cortisol |

|I am secreted by the Adrenal Cortex & help the body maintain its blood glucose. |Hyper-functioning Pituitary (hypersecretion of one hormone, rarely more) |

|Secretory pituitary tumors result in _____. |Hypo-functioning Pituitary ( general hyposecretion) |

|Non-secretory tumors of pituitary result in ____. | |

|Endocrine Pathology SUMMARY cont… |Cushing Syndrome |

|Any disorder causing ↑ glucocorticoid levels. |Thyrotoxicosis |

|Hypermetabolic state caused by high circulating levels of free T3&T4 is known as |HypERthyroidism (b/c the high T3/T4 prevent the release of TSH from the pituitary via|

|_______. |negative feedback) |

|Low TSH levels signify ______. |HyPOthryoidism (b/c there is less T3/T4 circulating which means less negative |

|High TSH levels signify _____. |feedback on the pituitary) |

|A disorder of Hypersecretion of ACTH from the pituitary. |Cushing Disease |

|I am produced in adipose tissue and am able to tell your fat ass when to stop eating |Leptin & Adiponectin |

|(you’re “full”). |Type 1 (usually kids) |

|Diabetes caused by autoimmune/immunopathic mechanisms. |Type 2 (usually adults) |

|Diabetes caused by obesity, insulin resistance, and/or deranged insulin secretion. | |

| | |

|Diabetes Mellitus (DM): |“storage hormone” – b/c it stores glucose as fat |

| |Types of DM: |

|Insulin is known as a “____ hormone”. Why? |Juvenile onset resulting from lack of insulin secretion by beta cells (can be from |

|Describe the following: |cell injury, viruses, genetics, or auto-immune) |

|a.) Type 1 DM |Adult onset due to insulin resistance or deranged insulin secretion by beta-cells. |

|b.) Type 2 DM |DM developed during a pregnancy. |

|c.) Gestational Diabetes |↑ risk for developing diabetes |

|d.) Pre-diabetes |~Impaired glucose tolerance (IGT) = when 2 hour postprandial glucose is 140-199 |

|3.) Pre-diabetes is characterized by what 2 things? |mg/dL. ~Impaired Fasting Glucose (IFG) = fasting|

| |glucose between 100-125 mg/dL (remember: DM is fasting glucose >126 mg/dL) |

|What are some signs & symptoms of DM? (6) |~Classic (3 P’s) – Polyuria, polydipsia, polyphagia ~Blurred vision (DM is leading |

|How can DM be diagnosed? *KNOW* |cause of blindness) ~Dry, itchy skin |

| |~Slow wound healing ~Weight loss |

| |~Fatigue |

| |>Random plasma glucose > 200 mg/dL plus s/sx. OR |

| |>Fasting plasma glucose >126 mg/dL OR |

| |>2-hour postprandial glucose >200 mg/dL during oral glucose test |

| |*Above should be confirmed on 2nd occasion. |

|ADA Goals *Gotta KNOW* |70 – 130 mg/dL |

| |< 180 mg/dL |

|Preprandial plasma glucose goal? |< 7% |

|Postprandial plasma glucose? |< 130/80 |

|HbA1C (glycosylated hemoglobin)? |40 ; Females >50 |

|LDL |1.4 (females) OR contrast dye procedure planned OR Abnormal renal|

| |frunction (shock, acute MI, septicemia) |

|* Meglitinides: |~Non-sulfonylurea secretagogue ~Stimulates insulin release |

| |from B-cells in glucose dependent manner. (basically, same as sulfonylurea) |

|MOA? |>Repaglinide (Prandin) >Nateglinide |

|Name them: |(Starlix) |

|T or F? Only used as monotherapy to avoid duplication of therapies. |FALSE! It can be used as monotherapy, BUT may also be combined w/ other therapies. |

|What may be Meglitinides combined with? |Anything BUT sulfonylureas (Do NOT use w/ sulfonylureas b/c have same MOA) |

|What MUST we remember to tell pts if they are taking Repaglinide (Prandin) or |If you skip a meal, skip your dose (ONLY taken WITH MEALS!!!) (“No Meal, No Meg”) |

|Nateglinide (Starlix)? |Those w/ erratic eating habits |

|Meglitinides are a good choice for which pts? | |

|Alpha-glucosidase Inhibitors: |Inhibits hydrolysis of complex carbs into simple sugars (causes delayed glucose |

| |absorption & ↓ postprandial glucose concentrations) |

|MOA? |~Acarbose (Precose) ~Miglitol (Glyset) |

|Name them: |Those w/ lots of contraindication against some of the better options (its got limited|

|Best in what pts? |efficacy & poor tolerability, so kinda 2nd or 3rd line) |

|What must we remember to tell pts when taking Acarbose or Miglitol? |If become Hypoglycemic, CANNOT just eat a snack!! Must take pure glucose tabs or |

| |milk!!! (Why? b/c med prevents breakdown of the snack into the needed glucose – snack|

| |won’t work!) |

|Thiazolidinediones (TZD’s): |Increase insulin sensitivity (bind to nuclear receptors that regulate |

| |insulin-responsive genes). This helps ↓ hepatic glucose production & ↑ glucose uptake|

|MOA? |into Skeletal muscle. |

|Name them: |~Pioglitazone (Actos) ~Rosiglitazone |

|T or F? Dependent on the presence of insulin to work. |(Avandia) |

|T or F? TZD’s begin to lower blood sugar in about 1-2 days. |True! |

|T or F? First line monotherapy for Type 2 DM. |FALSE! They take 6-8 weeks for full effect!! (Why? b/c they work by altering genes & |

|T or F? When dosing a TZD, start w/ 4mg QD then adjust the dose as necessary every 2|this always takes time) |

|weeks. |False!! It can be used as monotherapy, but is considered 2nd or 3rd line. |

|Adverse Effects? *KNOW* |False!! Must wait longer than 2 weeks before adjusting dose. Takes 6-8 weeks for full|

| |effect. |

| |~Hepatic problems? (monitor LFT’s) ~Fluid retention/edema |

| |(avoid if pt has CHF!!) |

|Dipeptidyl peptidase-4 (DPP-4) inhibitors: |Inhibit DDP-4 enzyme (this enzyme normally breaks down Incretins like GLP-1) ( |

| |results in prolonged action of incretins & ↑ insulin synthesis & release from |

|MOA? |B-cells, ↓ glucagon release, ↓ hepatic glucose production. |

|Name them: |Sitagliptin (Januvia) |

|Dosage adjustments are needed for ____. |Poor renal function |

|T or F? They can be used as monotherapy OR in combination w/ sulfonylureas or |False!! Although they can be used as monotherapy (that part’s true), they have not |

|insulin. |been studied in combo w/ sulfonylurea or insulin. CAN BE COMBINED W/ Metformin or a |

| |TZD. |

|You be the Physician!: |Diane has Diabetes ; Wanda has IFG |

| |Lifestyle modification, weight loss, ↑ activity |

|Diane Soon and Wanda Liv both visited your office today. Here are their labs: |Metformin (ALWAYS 1st LINE!!) *KNOW* along w/ lifestyle modifications, etc… |

|Fastine glucose Diane = 153 ; Wanda = 125 Diagnose each. |Quit! You are obviously a shitty physician!! Try pharmacy school maybe! ( jk, lol |

|What do you suggest for Wanda Liv? |Add Insulin OR Sulfonylurea OR TZD (will depend on the individual pt) *making sure |

|Unfortunately for Diane, she has now been diagnosed w/ Diabetes, what will you |she has no contraindications for whichever u choose. |

|prescribe? |~Metformin = poor renal function (Cr >1.4) ~Insulin = I dunno, are there |

|After 1 year, Diane Soon returns & her diabetes is uncontrolled on the Metformin. |any? ~Sulfonylurea = weight gain (obese?) |

|What do you do? |~TZD’s = CHF, Poor liver function |

|What are the contraindications you would have to consider? | |

|**DIABETES or NOT Game** *KNOW WELL* |Yes, they have DM |

|Can the following diagnose DM or not? |Nope |

|Fasting glucose of 157 mg/dL. |Depends – if they have signs & symptoms consitent w/ DM, then YES. If not, then no. |

|2-hour postprandial glucose of 189 mg/dL. |Nope (maybe they just ate a high sugar meal) |

|Random plasma glucose of 212 mg/dL |Yes |

|Random plasma glucose of 250 mg/dL but no s/sx. |Nope |

|Fasting glucose of 126 mg/dL. |Yes |

|2-hour post-prandial glucose 143 mg/dL. |Nope (but they have pre-diabetes, IFG) |

|2-hour post-prandial glucose of 210 mg/dL |Yes |

|Fasting glucose of 108 mg/dL. | |

|Random plasma glucose of 201 mg/dL with complaints of polyuria and polyphagia. | |

|Diabetes Mellitus SUMMARY *KNOW* |Insulins: |

|What kind of insulin am I? |Long-acting |

|glargine |Long-acting |

|detemir |Rapid-acting |

|lispro |Short-acting |

|regular |Rapid-acting |

|glulisine |Intermediate |

|NPH |Rapid-acting |

|aspart |2.) Detemir (Levemir) & Glargine (Lantus) |

|I CANNOT be mixed w/ any other insulin. |3.) 50 units daily (0.5units x 100kg = 50 units) |

|Jenny weighs 100kg and needs to start insulin therapy. What should her initial daily |4.) 25 – 50 mg/dL |

|dose be? |5.) 70 – 130 mg/dL |

|Every unit of insulin can ↓ glucose by ____. |6.) < 180 mg/dL |

|ADA Goal for preprandial glucose = ____? |7.) < 7% |

|ADA Goal for postprandial glucose = ____? | |

|ADA Goal for HbA1c = ____? | |

|DM Drugs SUMMARY: *KNOW* |Metformin |

|Avoid me if pt has Cr >1.5 (male), >1.4 (female) |Byetta (Exanatide), Sulfonylureas, Meglinitides |

|I stimulate insulin release by B-cells of pancrease. |TZD’s |

|If pt has CHF, do NOT give them me. |Meglitinides |

|If you skip a meal, skip taking me. |Alpha-glucosidase inhibitors (Precose, Glyset) |

|If pt taking me, must tell them that a snack will not help hypoglycemia, they require|Byetta |

|glucose tabs/milk. |Alpha-glucosidase inhibitors (Precose, Glyset) |

|I can ONLY be used for Type II diabetes. |Byetta & PO Drugs |

|I inhibit the hydrolysis of complex carbs into simple sugars |Smylin (pramlintide) |

|I might cause/exacerbate pancreatitis. | |

|I am a synthetic amylin analog. | |

|DM Drugs SUMMARRY Cont… |Metformin (if pt has poor renal function) |

| |Sulfonylureas & Meglinitides |

|I can cause Lactic Acidosis |Alpha-glucosidase inhibitors (Precose, Glyset) |

|We share the same MOA’s. (Don’t use us together! Duplication!!) |Symlin (pramlintide) |

|I cause delayed glucose absorption and thus ↓ postprandial glucose concentrations. |Byetta (Exenatide) |

|When adding me, ALWAYS ↓ the pts insulin dose by 50% to avoid hypoglycemia. |Metformin |

|I am an incretin mimetic. |Metformin, TZD’s |

|I can be used to prevent DM in high risk pts. | |

|I ↑ insulin sensitivity. | |

|Complications of DM: |~Diabetic Ketoacidosis ~Hyperglycemic |

| |hyperosmoler state (HHNS) ~Hypoglycemia |

|Name the 3 main ACUTE complications of DM: |< 60 mg/dL *KNOW* |

|Hypoglycemia is defined as blood glucose < ___. |Shaking, sweating, dizziness, anxiety, tachycardia, hunger, h/a, weakness, impaired |

|What are some signs & symptoms of hypoglycemia? |vision, irritability. |

|Who wins the argument? A diabetic pt comes to the pharmacy with signs of |Intern Elyse! (2 is not enough to work! Must take 4-5 tabs) |

|hypoglycemia. She asks 2 interns what to do. Intern Soomi says take 2 glucose tablets| |

|now. Intern Elyse says take 5 glucose tablets now. Who’s right? |Last emailed here!! |

|Late Metabolic Complications: |Nerve damage caused by prolonged hyperglycemia. 2 types described next. |

| |“Typical diabetic neuropathy”, characterized by paresthesias &/or pain in |

|What is Diabetic Neuropathy? |extremities. Usually begins in feet and progresses upwards (feet ( up legs ( arms) |

|Describe Peripheral Neuropathy: |Changes in function of organs. |

|Describe Autonomic Neuropathy: |~Diabetic gastroparesis (n/v, rapid satiety) ~Diabetic diarrhea (lots of |

|List some specific manifestations of Autonomic Neuropathy: (6) |watery diarrhea) ~Neurogenic Bladder (loss of urinary continence) |

| |~Impotence ~Orthostasis |

| |~Hypoglycemic unawareness (no tachycardia, etc…) |

|Describe Diabetic Retinopathy: |Leading cause of new blindness. Involves retinal changes (microaneurysms, ↑ |

|What is the most fatal complication from long-term DM? *KNOW* |permeability, occlusion, proliferation of new blood vessels). 2 types ( |

|Describe Diabetic Nephropathy: |Non-proliferative vs. Proliferative |

|What is the early manifestation of Diabetic Nephropathy that must be treated? *KNOW* |Diabetic Nephropathy (20-40% of pts) - ↑ morbidity & mortality ( |

|How should microalbuminuria be treated? *KNOW* |Characterized by proteinuria, ↓GFR, ↑ arterial BP. |

|T or F? If a diabetic pt has EITHER HTN or Microalbuminuria, they should be given an|Microalbuminuria (30 – 299 mg/24hr) |

|ACEI or ARB. |With ACEIs OR ARBs AND restrict protein intake to < 0.8gm/kg/day |

|Aspirin therapy should be added to which pts? Y? |True!!! *KNOW* |

| |Type 1 & Type 2 Diabetics that are: -( > age 40 OR |

| |( Family Hx of CVD OR ( HTN OR ( Smoker OR ( Dyslipidemia OR ( Albuminuria |

| |b/c daily aspirin (75-162mg) will ↓ risk for MI & stroke |

|Patient Education |~Diet |

| |~Exercise & wt. management ~Hypo/Hyperglycemia action|

|What non-pharmacologic things must we always discuss w/ diabetic pts? (8) |plan (what to do if pt feels either) |

|T or F? A 10-20lb weight loss can lessen insulin resistance. |~Home Blood Glucose Monitoring ~Complications of DM |

|T or F? For Type 2 diabetics exercise may ↑ chance for hypoglycemia. |~Foot Care (muy importante!!) ~Eye Care |

|T or F? If going to exercise a certain part of the body (ex: abs) you should inject |~Dental care |

|insulin directly into that muscle. |True!! ( |

| |False!! For Type 1 diabetics, it may ↑ risk for hypoglycemia. |

| |False!!! Do NOT inject insulin directly into a muscle that is going to be exercised |

| |(weakens it) |

|DKA & HHNS: |Diabetic Ketoacidosis |

| |Hyperosmolar Hyperglycemic Nonketotic State |

|What is DKA? |Prolonged hyperglycemia |

|What is HHNS? |True |

|Both are caused by what? |Lethargy, weakness, dehydration (losing water), GI symptoms, mental status changes |

|T or F? Ketone bodies are weak acids. |Hyperpnea & Fruity odor on breath (acetone breath) |

|Clinical manifestations of each include: |Infections, Illness, ↓ insulin, d/c of insulin, emotional stress, New onset type 1 |

|What are 2 manifestations specific to DKA? |DM, psychological problems/eating disorders. |

|What can predispose a diabetic pt to DKA or HHNS? | |

|DKA vs. HHNS: Which is being described? |HHNS |

| |DKA (symptoms usually noticeable, so glucose doesn’t get as high as HHNS) |

|Usually >60y/o |DKA |

|Plasma glucose Inhibit sperm enzymes needed for |

|Which progestins are the WORST for causing androgenic side effects? *KNOW* |fertilization >Inhibit implantation by altering FSH/LH peaks >Inhibit |

|Which progestin has the LEAST chance for causing androgenic side effects? *KNOW* |ovulation |

|T or F? All progestins have the ability to cause androgenic side effects. |Levonorgestrel > Norgestrel & Desogestrel |

| |Norgestimate ( |

| |True!! |

|Adverse Effects: |~Breast neoplasia (change color) ~Breast tenderness |

| |~Fluid retention ~Thromboembolism |

|List the estrogens adverse effects: (5 main ones she mentioned) |~Cardiovascular accident ~others: cervical |

|List the progestins &/or estrogens adverse effects: |erosion, cyclic wt. gain, hepatocellular adenomas/cancer, HTN, leukorrhea, nausea, |

| |telangectasia, chloasma |

| |Acne/oil skin, ↑ appetite, breast tenderness, depression, fatigue, lethargy, h/a, |

| |hirsutism, HTN, ↑LDL, ↓HDL, ↓ libido, pruritus, wt. gain. |

|What does “ACHES” describe? |The early warning signs of OC’s (early warning signs of rare, but very dangerous |

|What does it stand for? *KNOW* |adverse effects) |

| |A = Abdominal pain (gall bladder disease, hepatic adenoma, pancreatitis) |

| |C = Chest pain/SOB (pulmonary embolus, MI) H = h/a severe! (stroke, HTN, |

| |migraine) E = Eye problems (stroke, HTN, vascular problem) S = |

| |Severe leg pain (DVT) |

| | |

| |*must counsel pts to be aware that these are signs of serious adverse effects & must |

| |call physician if they appear. |

|Contraindications to COC’s (combo oral contraceptives): |~Cerebrovascular accident (stroke, MI, etc…) ~Known impaired liver|

| |function/liver tumor ~CA of breast/estrogen-dependent |

|List ABSOLUTE CI’s to COC’s: (7) *KNOW* |neoplasm (known or suspected) |

|T or F? If someone has an absolute CI against COC’s, the pt. & physician must weigh |~Over 35 & currently heavy smoker (>15cigs/day) ~Pregnancy (ya think?) |

|the risks vs. the benefits to decide if COC is right for them. (I thought COC was |~Thromboemolic disorder (or history of) |

|right for everyone!?! Lol ( get it?) |~Undiagnosed, abnormal vaginal bleeding |

|List the RELATIVE CI’s to COC’s: (5) |False!! Do NOT use COC’s if the patient has an absolute CI against them!!! Use |

|T or F? If pt has relative CI against COC’s, the pt & physician must weigh risks vs. |minipill or other form of OC instead. |

|benefit to decide if a COC is right for them. |~Active gallbladder disease |

| |~Major surgery req. immobilization (b/c of DVT risk) ~Under 35 & |

| |currently heavy smoker (many MD’s avoid COC’s whenever the pt smokes…) |

| |~Severe h/a |

| |~Uncontrolled HTN |

| |True! look @ each individuals’ risks, wishes, etc… |

|Non-contraceptive Benefits of OC’s: |~PID (pelvic inflammatory disease) ~Ovarian cancer |

| |~Endometrial cancer |

|List some diseases that OC can prevent: (9) |~Ovarian cysts ~Ectopic |

|What other benefits do they have? |pregnancy ~Fibrocystic breast |

| |disease ~PMS (that’s a disease!? So |

| |I can call in sick for it!! () ~Toxic |

| |shock syndrome ~Anemia |

| |Fewer cramps, less flow for fewer days, more predictable menses, elimination of |

| |mittelschmerz (pain during ovulation) |

|What drugs can interact w/ OC’s? |~Antibiotics (inhibit gut bacteria req’d for estrogen recycling) ~Anticoagulants |

|Pts should always use an additional method of contraception during _____. |~Anticonvulsants ~Enzyme |

|T or F? If a pt misses 2 or more pills, they must contact their physician. *KNOW* |inducers |

| |~Pioglitazone, Rosiglitazone (this might be on exam cuz relates to DM! Probly not |

| |though () ~St. John’s Wart |

| |Prom! He he, lol ( During their first pack of birth control. |

| |False!! You must call physician if miss 3 or more. (If miss 1: take ASAP or take 2 |

| |the next day. (If miss 2: take 2 pills for next 2 days |

|Choosing an COC: |< 35ug |

| |Progestational, estrogenic, & androgenic side effects |

|Best to use a COC w/ ____ug ethinyl estradiol. |True! |

|Must always consider what? |The give hormones (30mcgEE, 0.15mgLNG) over 84 days, then 7 days placebo (Seasonale) |

|T or F? Most COC’s are triphasic and most closely mimic a women’s natural cycle. |or 7 days 10mcgEE (Seasonique). Both = menses every 3 months instead of every month. |

|What are “extended cycle” COC’s? |(you get your period once every season) |

|What are “continous cycle” COC’s? |Active pills (20mcgEE, 90mcgLNG) for 365 days. No placebo. No period. |

|Name them: (1) |Lybrel |

|Which OC’s, when taken continuously, can b used as continuous cycle contraception? |Monophasic OC’s |

|(You skip the placebo pills and take the active ones year round) | |

|Name the transdermal system of contraception. |Ortho-evra |

|Does it contain estrogen, progestin or both? |Both |

|How is this patch used? |Apply WEEKLY x 3 weeks. Can be applied to butt, abs, |

|The patch is not as effective if the woman is ____. |arm or torso Week 4 is patch free = menses |

| |Obese |

|T or F? NuvaRing is a vaginal ring contraceptive containing only progesterone. |False!! It contains both estrogen & progestins. |

|How should NuvaRing be used? |Insert on or before Day 5 of menses Keep in place |

|What is the only oral contraceptive option which is progesterone only? |for 3 weeks Week 4 is ring-free|

|T or F? The minipill contains more progestins than the COC’s b/c it lacks the |= menses |

|estrogen component. |Mini-pill |

|The mini-pill is a good choice for patients w/ what? (5) *KNOW* |False!! It actually contains LESS progestins than COC’s (that’s why its called |

|The mini-pill sounds great! Why doesn’t everybody use it? |“mini”) |

| |~History of CVA (stroke, MI, etc…) |

| |~DVT |

| |~Uncontrolled HTN |

| |~Pts who are breastfeeding |

| |~Smokers > 35 y/o |

| |B/c has some major drawbacks… (less |

| |effective, ↑ irregular menses, amennorhea (can be +/-), complicated |

| |instructions/STRICT compliance req’d ( |

|Long-term progestins (the shot), is desirable for which pts? (Depo-provera) |~CI’s to estrogen ~Compliance|

|What are the major risks associated w/ long-term progestins? (4) |issues w/ other methods ~Contraception desired for at least 1 |

|What is Implanon? |year ~Want to breast feed ~Amenorrhea is desired |

|How long does it last? |Breast cancer, ↓ bone density, DELAYED FERTILITY (up to 10 months after!!), weight |

|Who are some good candidates for Implanon? |gain |

|Who cannot use Implanon? |Subdermal etonorgestrel – subdermal implant |

| |3 years! |

| |~Long-term contraception desired ~Desire for prompt |

| |return of fertility upon d/c ~CI’s to estrogen |

| |~Compliance issues w/ other methods |

| |~Joel ( ~Hx of thromboembolic disorders ~Undiagnosed abnormal vaginal bleeding |

| |~Liver disease ~Breast CA ~Pregnant |

|How can a woman use her own body temperature to determine when she’s ovulating? |Body temp ↑ just AFTER ovulation (so ↑ temp = safe sex) |

|Name 2 IUD’s: |HIGH FAILURE RATE!! |

|Why are they not really used that much? |Paraguard (copper IUD) & Mirena (LNG IUD) |

|IUD’s are best for which pts? |b/c can cause scarring, INFERTILITY, ↑ risk for ectopic pregnancy, ↑ risk for PID, |

|Juno just came into your pharmacy asking about Plan B. What do you tell or ask her? |bleeding. |

|She says yes and shows you her license. You verify she is 19 y/o. How should she take|Those who already have children (not teens!) |

|it? |Ask if she is 18 with a proper ID? |

|Juno should only seek emergency contraception if it’s within ____ of unprotected sex.|1 pill now, the 2nd pill 12 hours later. (ex: 1 at 4pm, 1 at 4am – but who is gonna |

| |set an alarm to take a pill in the middle of the night?!?! Pick good times) |

| |72 hours!! |

|Contraception SUMMARY: *KNOW* |LH surge (during ovulatory phase) |

|I stimulate maturation of dominant follicle. |FSH surge (during follicular phase) |

|I stimulate development of follicles. |Menses (this is the end of the luteal/secretory, start of follicular) |

|When hormones drop _____ occurs. |Estrogen |

|Component of OC’s that inhibit ovum implantation |Progestins |

|Component of OC’s that thicken cervical mucus. |Norgestimate |

|I’m the progestin w/ least chance of androgenic side effects. |Levonorgestrel (Norgestrel & Desogestrel are pretty bad also) |

|I am the progestin with the worst androgenic s.e’s |Estrogens |

|I am the component of OC’s which is associated w/ cardiovascular accident. (b/c I ↑ |Abdominal pain, Chest pain/SOB, H/a, Eye problems, Severe leg pain. |

|clotting factors) |Liver (liver impairment/cancer = absolute CI!) |

|“ACHES” stands for what? |Rosiglitazone (Avandia) & Pioglitazone (Actos) |

|Jane wants OC. Do we care about her kidney or liver function? | |

|I am a DM medication which interacts w/ OC’s. | |

|Hyperthyroidism: |activated sympathetic nervous system |

| |Rapid release of TH’s (thyroid hormones) S/Sx = Temp >103, tachycardia, |

|Hyperthyroidism mimics the actions of ____. |tachypnea, delirium, n/v/d. *Can be FATAL!* |

|What is Thyroid Storm? S/Sx? |B-blockers, SSKI, PTU, Steroids |

|How can it be treated? |Grave’s Disease (formation of thyroid receptor antibodies that MIMIC TSH) |

|____ accounts for 85% of all hyperthyroidism cases. |Toxic Nodular Goiter (enlarged thyroid gland due to multiple nodules that |

|What is Plummer’s Disease? |over-secrete T3) – another cause of hyperthyroidism |

|What is a “Hot nodule”? |Toxic adenoma (solitary functioning nodule that secretes T3) – another cause of |

| |hyperthyroidism |

|Signs & symptoms of hyperthyroidism? |Wt loss, ↑ appetite, fatigue, nervousness, tachycardia, palpitations/chest pain, |

|How often should a pt be monitored? |irregular heart beats, SOB/dyspnea, heat intolerance, tremor, pedal edema, light/no |

|France (thin woman) comes in complaining of heat intolerance, heart seems to be |menses, mental disturbances, insomnia, changes in vision, exopthalmos, diarrhea, |

|racing & can’t sleep. When you run her labs, you expect to see what? (b/c she also |warm, smooth velvety skin, hair loss. |

|has exopthalmos & you suspect she has hyperthyroidism) |Monthly – until symptoms disappear & TSH normalizes. |

| |q6-12 months – once pt is stable |

| |↓TSH, ↑TT4, ↑FTI, ↑RAIU (radioactive iodine uptake) |

|Treatment: Thionamides |~Methimazole (QD dosing) |

| |~Propylthiouracil (PTU) (TID-QID dosing) |

|Name them: (2) *KNOW* |inhibits iodide oxidation & coupling |

|What is their MOA? |Skin rash, h/a, drowsiness, loss of taste, vertigo, arthralgia, myalgia |

|ADR’s of Methimazole & PTU? |Neutropenia, thrombocytopenia, hepatitis |

|Severe ADR’s include what? (3) |PTU (“Pregnancy Thyroid Use” () |

|Which is safe to use in pregnancy? | |

|Treatment: Iodides (anion inhibitors) |~Acutely blocks thyroid hormone release ~Over time, inhibits |

| |conversion of iodide ( iodine ~↓ size of thyroid gland |

|MOA? |False!! Don’t do enough to be used alone!! |

|T or F? Can be used as monotherapy. |↓ size of thyroid prior to surgery |

|What is the main use of iodides? |Relieve symptoms w/in 2-7 days. Attain quick euthyroid state. |

|What is an advantage of the iodides? |False!!! That would ruin your RAI test!!!! Use it AFTER (3-7 days after). |

|T or F? Iodides can be given before RAI (radioactive iodine) therapy to prevent | |

|release of thyroid hormones. | |

|Treatment: Adjunctive Therapy |B-blockers ~Iodides (after RAI|

| |given) ~Thionamides (given to elderly or cardiac disease|

|What else can be used? |pts prior to RAI) |

|What is the agent of choice for thyroid ablation? (for pts w/ Grave’s or have |~Corticosteroids |

|single/multi-nodular goiters) *KNOW* |Radioactive Iodine Therapy (RAI, I131) |

|T or F? Can also be used in pregnancy. |FALSE!! Absolute CI |

|RAI therapy causes what? |Euthyroid or Hypothyroid state (b/c destroys thyroid cells) |

|T or F? Effects are seen immediately b/c the thyroid gland is shut down. | |

|T or F? Most pts undergoing RAI therapy require thyroid replacement drugs for the |False! Takes 3-6 months |

|rest of their life. |True!! b/c most develop HyPOthyroidism after the treatment. |

|What are the 2 main symptoms of hyperthyroidism in pregnancy? |~Failure to gain wt despite good appetite ~Tachycardia |

|T or F? Some drugs can induce thyroid diseases (hypo/hyperthyroidism). |True!! |

|Which drugs? |~Amiodarone (structurally related to thyroid hormone, contains iodine) ( can cause |

|Which drugs interact w/ hormones/treatments? |hypo OR hyper |

| |~Lithium (inhibits thyroid hormone release by blocking iodine transport) ( can cause |

| |hypo |

| |Coumadin ( when hyper = ↑ metabolism of clotting factors. |

| |when hypo = ↓ met of clotting factors. |

| |Cholestyramine, Sucralfate, Aluminum |

| |hydroxide & Antacids ( ↓ absorption of thyroid hormone |

| |Estrogen ( ↑TBG levels = less free hormone |

|Thyroid Function Tests: *KNOW* |0.8-1.5 ng/dL |

| |0.25 – 6.7 mcU/mL |

|What is the normal range for FreeT4? *KNOW* |Low! (should know this by now!!) ( |

|What is the normal range for TSH? *KNOW* |Low! (duh!) |

|In Hyperthyroidism, we expect the TSH levels to be ____. | |

|In Hypothyroidism, we expect the Free T4 levels to be _____. |*understand how to easily diagnose a pt based on |

| |lab data + s/sx. |

|Hypothyroidism: |6-7 days |

| |2 days |

|T4 has a half-life of ____. *KNOW* |T4 (T4 is the hormone that reflects functional state of most pts w/ thyroid disease.)|

|T3 has a half-life of ____. |False!! Just the opposite - ↑ oxygen consumption & basal metabolic rate |

|Which is the “main” hormone? |FALSE!! TSH can be low if pt has “CENTRAL hypothyroidism” (meaning the problem is in |

|T or F? Thyroid hormones ↓ oxygen consumption by most tissues and ↓ basal metabolic |the pituitary, not the thyroid gland itself) (BUT usually low TSH signals |

|rate. |HypERthyroidism – be careful when diagnosing w/ TSH values!!!) |

|T or F? TSH levels will never be low if a patient has hypOthyroidism. | |

|Which antibodies, when positive, can confirm the presence of Grave’s Disease? *KNOW* |TRAb (thyroid receptor IgG antibody) |

|Which antibodies, when present in larger than normal amounts, suggest Hashimoto’s |~ATgA – antibodies to thyroglobulin (when >8%) ~TPO – thyroperoxidase antibodies |

|disease? |(when >100) *note: TPO >100 “strongly suggests” hashimoto’s |

|Radioactive Iodine uptake should normally range between _____. |5-15% ------> 10-35% |

|What is Hashimoto’s Disease? |(5 hr) (24 hr) |

|S/Sx of Hashimoto’s Disease? *KNOW* |Form/cause of HypOthyroidism characterized by: (+) ATgA & TPO >100. |

| |>Goiter (due to antibody infiltration) >Throat |

| |fullness/tightness >Trouble swallowing foods |

| |or liquids >Periorbital edema |

| |>Others: intolerance to cold, fatigue, etc… |

|What are some general s/sx of Hypothyroidism? |Fatigue, lethargy, wt. gain, ↓ appetite, cold intolerance, constipation, menstrual |

|Primary Hypothyroidism is diagnosed by what lab values? *KNOW* |irregularities, bradycardia, slowed reflexes/speech, muscle aches/stiffness, (+/-) |

|Central Hypothyroidism (or pituitary insufficiency) is diagnosed by what labs? *KNOW*|goiter, memory/mental impairment, depression, coarseness or loss of hair, puffy |

| |face/eyelids, hoarseness, brittle nails, dry/thin/cool skin, non-pitting edema. (many|

| |are the opposite of the hyperthyroidism s/sx) |

| |↑ TSH levels, ↓FT4 levels, ↓RAIU |

| |↓ TSH levels, ↓FT4 levels. ↓RAIU |

|Treatment: |Synthetic T4 [Levothyroxine (Synthroid or Unithroid)] |

| |7 days |

|What is the DOC for treating hypothyroidism? *KNOW* |B/c T3 has lots more side effects (and T4 gets metabolized into T3 anyways) |

|Half-life of Levothyroxine? *KNOW* |1.6 – 1.7 mcg/kg/day *use IBW!! |

|Why do we use synthetic T4 & not T3 if T3 is more potent? |25 mcg/day |

|Initial dose of levothyroxine if pt generally healthy? *KNOW* |50-75 mcg/day |

|Initial dose if elderly or with CVD? *KNOW* |0.5 – 2 mcU/mL |

|Initial dose if pediatric or > 45 but no CVD? | |

|What is our TSH goal when treating? *KNOW* | |

|Name the T4 & T3 combo products: |~Armour thyroid (freeze-dried porcine/bovine gland) ~Liotrix (Thyrolar) – fixed |

|Name the T3 only preparation: |ratio mimics glandular content, but expensive & still has T3 adverse effects. |

|What is the half-life of Liothyronine (Cytomel)? |Liothyronine (Cytomel) |

|Liothyronine (Cytomel) is used mainly for what? |1.5 days |

| |Myxedema coma (hypothyroidism-induced coma) |

|Patient Counseling: |~Takes about 2-3 weeks for symptoms to resolve ~Full effect of med in 6-8 weeks.|

| |~Know the name, dose & color of your med ~Take on an EMPTY |

|We must always tell pts what when receiving new hypothyroidism treatment? (thyroid |stomach ~Treatment will be lifelong |

|hormone replacement) *KNOW* |~Avoid taking antacids, iron tablets or high fiber meal with tablets |

| |~Know the s/sx of hyperthyroidism to tell if they are taking too much thyroid |

| |hormones. |

|Hyper/Hypothyroidism SUMMARY: *KNOW* |PTU (Propylthiouracil - a thionamide) |

|I can safely be used in pregnancy. |Iodides |

|I can be given AFTER (3-7 days) RAI is given. |Thionimides |

|I am given to elderly/cardiac disease pts BEFORE & AFTER (4 days prior & 4 days |RAI therapy |

|after) RAI is given. |0.8 – 1.5 |

|I am the agent of choice for thyroid ablation. |0.25 – 4.5 |

|FT4 normally should range: |Primary Hypothyroidism |

|TSH normally should range: |Hyperthyroidism (but could have Central Hypo) |

|Kalei’s TSH level is 10.5. She probably has ____. |Hyperthyroidism (IF his FT4 had been low, he would be diagnosed w/ Central |

|Jake’s TSH level is 0.09. He probably has ____. |Hypothyroidism) |

|Tom’s TSH level is 0.23 & his FT4 is 12.5. He has ____. |Mild hypothyroidism (TSH is ↑, but T4 okay) |

|Jan’s TSH level is 8 & her FT4 is 1.0. She has ___. |TRAb |

|I am the antibody that can definitively diagnose Grave’s Dis. |ATgA >8% & TPO >100 |

|I am the antibody’s which suggest Hashimoto’s. |Levothyroxine (synthetic T4) |

|I am the treatment of choice for hypothyroidism. | |

|Levothyroxine Dosing Review: Tell what the initial dosage range is for each of the |1.6 – 1.7 mcg/kg/day (need her weight) |

|following pts… |25 mcg/day (b/c elderly) |

| |50-75 mcg/day (b/c they are young) |

|Norma Lay-Dee is a healthy 29 y/o. |25 mcg/day (b/c has CVD) |

|Elda Lee is 71 y/o. She has no other disease states. |50 – 75 mcg/day (b/c > 45 y/o) |

|Jit Baybee is only 9 y/o. |25 mcg/day (b/c elderly & CVD) |

|Art is 51 & has CVD. |1.6 – 1.7 mcg/kg/day (not elderly & ED doesn’t matter) |

|Al Mostold is 49 y/o & has not other disease states. |1.6 – 1.7 mcg/kg/day (b/c not >45) |

|Notta Youngin is 89 y/o & has CVD. |50 – 75 mcg/kg/day (b/c he is > 45) |

|Plainol Guy is 43 y/o and has erectile dysfunction. | |

|Reg U. Lergirl is 45 y/o and has no CVD. | |

|Reg’s older brother is 46 y/o. Has no CVD either. | |

|Rheumatoid Arthritis: |Synovium |

| |Body views synovium as foreign (“non-self”) and initiates immune attack against it |

|____ normally keeps our cartilage & bones nourished. |(WBC activation) |

|In RA, what is occurring, generally? |~Formation of rheumatoid factors ~TNF-a |

|WBC activation results in what? |production ~synovial thickening |

|What role does TNF-a play in RA? |(Pannus formation) ~local microvasculitis |

|What role do B-cells play in RA? |Stimulates production of T-lymphocytes (which release pro-inflammatory cytokines), ↑ |

|Lots going on in RA. Summarize what’s happening. *KNOW* |cell infiltration, other “bad” stuff |

| |~Present antigens (trigger immune response by stim. T-cells) |

| |~Produce antibodies (auto-antibodies in RA) ~Produce cytokines (promote |

| |inflammation) |

| |Body thinks synovium foreign ( pro-inflammatory mediators/cytokines released (via |

| |TNF-a, T-cells, B-cells) ( synovium enlarges & you loose cartilage & bone |

|Evaluation of RA patients: Criteria |~AM stiffness lasting > 1hr before improvement ~Involves > 3 joints |

| |~Arthritis of the hand or wrist joints ~Bilateral |

|When gathering pt history, we must get the ACR Criteria for Classification of RA. |involvement of joint areas (ex: both wrists) **above 4 criterias must have been |

|What are these specific classifications? (7) *KNOW* |present for > 6wks** |

|A pt must have at least ____ of those 7 complaints in order to be diagnosed w/ RA. |~Rheumatoid Nodules ~(+) serum |

|*KNOW* |rheumatoid factor (IgM) ~Radiographic evidence of RA |

| |**last 3 do NOT require presence for > 6 wks** |

| | |

| |4 (so pt must have at least 4 of the above to diagnose RA based on ACR criteria!!) |

|Evaluation of RA patients: Labs |< 20 – 30 mm/h |

| |Elevated (>30 mm/h) *but NOT specific for RA, it can be elevated in many |

|Which lab test can definitively diagnose RA? |inflammatory diseases. |

|What is the anti-CCP value if pt has RA? |Anti-CCP (cyclic citrullinated antibodies) |

|T or F? Anti-CCP is the first lab value we request when diagnosing RA. |It is present in most pts w/ RA or in healthy people who will eventually develop RA. |

|T or F? Presence of RF can definitely diagnose RA. |IF DETECTED = RA *KNOW* |

|When would we test for anti-CCP? |False!!! Get the RF (rheumatoid factor) first |

|What other labs are sometimes used? |False!! Its presence alone cannot (5% of healthy people have it), but if its presence|

| |along w/ joint inflammation = RA. |

| |If RF test comes back negative, but pt has unexplained joint inflammation. |

| |CBC, Renal/Heptaic function tests, Synovial fluid analysis, Stool guaiac (NSAID use) |

|Treatment Guideline: |Document baseline disease damage/activity (s/sx, labs, imaging, etc…) |

| |Initiate therapy (pt. education, begin DMARDs w/in 3 months of diagnosis, and |

|When treating a pt, what is Step 1? |consider NSAIDs, low-dose steroids, or local injection & physical therapy) |

|What is Step 2? |Periodically assess disease activity (s/sx, labs, x-rays, etc…) |

|What is Step 3? |3 months!! *KNOW* |

|If inadequate response after ____ time of MAXIMAL therapy, you should add or change |Depends on pt – which have they tried?, What effects have they had? Combo therapy? |

|DMARD. |Note: common for single therapy to fail. |

|How do you know what to change or add? |Surgery!!! (last resort after max combo’s fail) |

|What if combo DMARD therapy fails (meaning they still have symptoms &/or structural | |

|joint damage) what do you do? *KNOW* | |

|How do NSAIDs help RA? |↓ joint pain, ↓ joint swelling, ↑ joint function. |

|T or F? They are a great OTC choice b/c they prevent the joint destruction |FALSE!! NSAIDs do NOT alter course of the disease or prevent joint destruction. |

|associated w/ RA. |Relieve symptoms w/in days & may slow rate of joint damage ( |

|How do Glucocorticoids (steroids) help RA? |False!! Even though they sound great, they are ONLY FOR SHORT TERM USE due to their |

|T or F? Steroids are the DOC for RA. |bad side effects. |

|What are some ADRs of glucocorticoids? |Osteoporosis, wt gain/HTN/edema, hyperglycemia, cataracts. |

|What is the main use for glucocorticoids in RA therapy? *KNOW* |Used for 2 weeks for flare-up OR as “bridge therapy” (while waiting for MTX effects) |

| |*SHORT TERM ONLY* |

|ALL RA pts are candidates for ____. |DMARD’s (disease modifying anti-rheumatic drugs) |

|Why are the DMARDs used in every pt w/ RA (unless strictly contraindicated, which is |b/c they are the bomb!! ~↓ or prevent |

|rare) |joint damage ~Preserve joint integrity |

| |& function ~↓ total healthcare costs |

| |~maintain economic productivity of RA pts (allows RA pts to go to work, live daily |

| |lives) |

|DMARD’s: |Methotrexate (MTX) |

| |Retards progression of radiologic erosions (, cheap, can be given w/ other DMARDs. |

|What is the DMARD of choice? *KNOW* |~Given WEEKLY!! ~Give FA supplement |

|Why is MTX so great? |>Signs of infection (b/c suppresses immune system) >CBC |

|What 2 things MUST we always remember about the administration of MTX? *KNOW* |>LFT |

|What should be monitored when pt taking MTX? |*monitor monthly x 1st 6 mnths, then q1-2 mnths. |

|What is the DMARD used if the disease is mild and in early stages? *KNOW* |Hydroxychloroquine (HCQ) – why? b/c it has the least toxic SE’s, but does NOT slow |

|Note: “mild” = < 3 joints affected & no bone erosion. |radiologic damage (therefore, MTX/combo better for more serious, progressed RA) |

|What is the one thing we hafta worry about if pt taking HCQ? |Eyes, if > 60 y/o (eye exam q6 months if so) |

|DMARD’s cont… |Sulfasalazine & Minocycline *note: caution if pt |

| |has sulfa/salicylate allergy!! |

|Name the 2 other main DMARD’s. |True!! |

|T or F? Both slow radiographic progression of RA just like MTX. |False!! Sulfasalazine is a great option (especially when combined w/ MTX), it’s the |

|T or F? Minocycline is considered an very good RA treatment option, but |Minocycline that needs more info… |

|sulfasalazine requires more info/data before we can decide its benefits. |Leflunomide (Arava) |

|Which DMARD is considered 2nd/3rd line due to numerous ADRs & 12 fatal cases of liver|True!! (BUT, it can be combined w/ MTX – even though similar MOA’s) |

|damage? |MTX + SS + HCQ *KNOW* (that triple combo is more |

|T or F? Leflunomide (Arava) should really only be used if pt cannot tolerate MTX. |effective than MTX alone or MTX + HCQ) |

|Which can be safely used in pregnancy? | |

|___ + ____ + ____ = the most effective DMARD combo. | |

|Biologic Agents: |TNF-a inhibitors |

| |True!!! (even though they are usually/almost always used only after MTX fails/gets |

|Which is considered the biological agent of choice (it’s used if MTX fails or cannot |inadequate response as replacement of or combo with MTX) |

|be used). |~Humira (“HUMans ENjoy being alone”) |

|T or F? TNF-inhibitors are new to the RA treatments and can actually be used as a |~Enbrel |

|first drug of choice, in MTX-naïve pts. |Remicade |

|Name the TNF-inhibitors which can be used alone OR in combo. *KNOW* |12 weeks |

|Name the TNF-inhibitors which MUST be combined w/ MTX. *KNOW* |~CHF (caution if class I or II, AVOID if class III or IV) ~Hypersensitivity |

|We can expect to see improvement within ____ time of starting TNF-inhibitor therapy. |~Active infections or live vaccinations |

|Contraindications to TNF-inhibitor therapy? | |

|Which biological RA treatement option is considered to have “modest benefits”? |Kineret (Anakinra) (“KINda works…”) – modest benefits and lots of ADR’s ( |

|T or F? It is most often combined w/ MTX or TNF-inhibitors b/c the combo better than|Kinda true, but…FALSE!! The MTX part is true (Kineret is often combined w/ MTX b/c |

|either agent alone. |its more effective than MTX alone) BUT Kineret CANNOT be combined w/ |

|T or F? MTX + TNF-inhibitors is a common therapy choice (when combo is desired) and |TNF-inhibitors!!! |

|seems to work fairly well. |True! (It’s a good mix of DMARD + biological) |

|20-30% pts do not respond to MTX + TNF-inhibitors. What biological options do we have|Rituximab (Rituxan) – inhibits B-cells |

|for those pts? |Abatacept (Orencia) – inhibits T-cells |

|T or F? These drugs (Rituximab & Abatacept) should only be used in pts who have not |True!! |

|responded to MTX + TNF-inhibitors. |True!! (another reason why we try MTX + max TNF-inhibitors first) |

|T or F? Rituximab & Abatacept are IV only. | |

|List the Contraindications to MTX, Leflunomide (Arava), & Anakinra (Kinret) *KNOW* |~Alcoholic or Chronic liver disease ~Active infections |

|Why do we care about these contraindications? |~Blood dyscrasias ~Live |

|What do we give if pt has moderate-severe RA, but has a CI against MTX? |vaccinations ~Pregnant or lactating |

| |~Hypersensitivity |

| |B/c on the exam, there is probly gonna be a RA case where a patient has a CI against |

| |the use of MTX. Therefore, we will have to be able to recognize that this pt cannot |

| |just get the RA DOC. |

| |Good question!! I think it will depend on the pt… (Sulfasalazine is okay option (if |

| |no allergy or obstructions) (Leflunomide is okay option (if wanna die of liver |

| |damage – jk, lol. If their liver is currently ok & no signs of infection) |

| |(TNF-inh. best option (if no III /IV CHF or active infections) |

|RA SUMMARRY: *KNOW WELL* |3 |

| |MTX, Sulfasalazine, Minocycline (& maybe glucocorticoids) |

|Start DMARDs within ____ months of diagnosis |MTX (but takes 2-3 weeks for benefits) |

|I slow radiographic progression of RA. |TNF-inhibitors (but can be used as first line) |

|I am the DOC for treating RA |HCQ (but takes 1-6 months for benefit) |

|I am a “new” DOC (usually used after MTX fails) |RF (rheumatoid factor) |

|I am the DOC for early, mild RA. |Anti-CCP (if present = RA) |

|I am the main lab value used for diagnosis of RA |Kineret (Anakinra) |

|I can definitively diagnose RA if RF negative |3 months!! |

|I CANNOT be combined w/ TNF-inhibitors. |NSAIDs, |

|If inadequate response to MAXIMAL therapy, add/change it after ___ | |

|I am good for symptomatic relief, but I do NOT prevent progression of RA. | |

|RA SUMMARY cont… *KNOW* |Remicade |

| |MTX (give FA!) |

|TNF-inhibitor that MUST be combined w/ MTX. |Humira OR Enbrel (TNF-inhibitors) |

|Which RA treatment requires a folate supplement be given during therapy? |B/c it cannot be used w/o MTX! |

|Jane has moderate RA but cannot take MTX (has chronic liver disease). What do you |~TNF-inhibitors (maybe?, Cat B), ~Hydroxychloroquine (maybe?, also Cat B) |

|suggest? |I dunno! If anyone knows please email me. Its in the objectives that we hafta know |

|Why not Remicade (TNF-inhibitor)? |which are safe during pregnancy?!?! |

|I can be used safely in pregnancy. |MTX |

|I am always given WEEKLY. |Glucocorticoids |

|I am only for SHORT TERM use, maybe to help during a flare-up or as “bridge therapy”.| |

|Last emailed herrrrrreeeeeeeee!!! | |

| | |

| | |

|Gout: |~Hyperuricemia, Recurrent acute attacks, formation of trophy (uric acid crystals that|

| |attach to bone), & nephrolithiasis/renal disease. |

|Describe GOUT: |2 – 7 mg/dL |

|Normal range for uric acid? *KNOW* |> 7 – 7.5 mg/dL |

|Uric acid levels of ____ = GOUT. *KNOW* |~↑ uric acid (↑ protein intake, ↓ elimination, etc…) ~Being Male |

|Risk factors? (7) |~Age (men >30, women > 55) ~↑ |

|T or F? Most cases of GOUT are caused by underexcretion of uric acid. |SCr/BUN ~HTN|

|Define Underexcretion. *KNOW* |~↑ wt |

|How could we tell if pt was overproducing uric acid, causing their GOUT? *KNOW* |~↑ alcohol intake (beer, not wine) |

| |True! |

| |< 300 mg/24hrs |

| |If urate excretion > 1000 mg/24hrs |

|What is an Acute Gouty Attack? |Rapid onset of pain, swelling, and inflammation |

|What drugs can induce an attack? |~Losartan |

|What is “peudogout”? |~Phenofibrate |

| |~Amlodipine *they ↓ uric acid levels quickly, which may INDUCE an attack ( |

| |Gout-like presentation, but w/o elevated uric acid levels. The symptoms are from |

| |accumulation of calcium pyrophosphatate dihyrate or calcium Hydroxyapatite crystals. |

|Treatment: |NSAIDS (any NSAID is fine) |

| |Steroids |

|1st line DOC? |Colchicine |

|2nd line, if the NSAIDs are contraindicated? |Max Dose! (continue for 24hr after resolution of attack) |

|3rd line. If NSAIDs & Steroids are contraindicated? |If NSAID is contraindicated OR if NSAIDs fail |

|What dose of NSAID is appropriate for management of acute gouty attack? |Triamcinolone (intra-articular injection) & Prednisone |

|When would you use Corticosteroids to treat an acute attack? |# of joints affected ( one = triamcinolone (once) |

|Name the available corticosteroids for treatment of acute gout attacks: (2) |Multiple joints = prednisone (over 2 wks) |

|So you are gonna use a corticosteroid, but can’t decide which one. What will help you|8.) < 6 mg/dL |

|make the decision? | |

|What is the GOAL uric acid level? *KNOW* | |

|Prophylaxis: |Colchicine |

| |DON’T Prophylax if 1st attack: ~mild, |

|Which drug is the best option for prophylaxis? |responded to tx ~Sr urate mildly|

|How can you decide if a pt requires prophylaxis? |elevated ~urinary excretion < 1000 |

| |mg/24hrs DO Prophylax if 1st attack: |

| |(Severe (Complicated|

| |course of uric acid lithiasis (Sr urate >10 |

| |(Urinary urate excretion > 1000 mg/24hrs (Frequent attacks (>2/year) |

|Prophylaxis cont… |True!! (maintenance dose = 0.6 – 1.2 mg BID) |

| |CrCl < 50 mL/min *KNOW* |

|T or F? Colchicine is the DOC for prophylaxis of gouty attacks. |False!! It can be d/c’d if Sr urate is normal & pt is symptom free for 1 year ( |

|CANNOT prophylax w/ colchicine if ____. |Uricosurics ( Probenecid & Sulfinpyrazone (note: the |

|T or F? Once we decide to prophylax with colchicine, a pt will take it the rest of |uricosurics only help if problem if underexcretion) Xanthine Oxidase Inhibitor|

|their lives. |( Allopurinol |

|List the UALA’s: (3) |If pt is 7 – 7.5 |

|Uric acid levels which signal GOUT. |> 1000 |

|I excrete ___mg/24hrs of urate, so I must have overproduction problem. |< 300 |

|I excrete ___mg/24hrs of urate, so I must have an underexcretion problem. |Only 1 joint affected ; more than 1 joint affected |

|If giving steroids, give triamcinolone intra-articularly once if ____. Give |> 10 |

|prednisone over 2 weeks. if ____. |Allopurinol |

|Always prophylax if 1st attack had uric acid levels of ____ |Colchicine OR Uricosurics (Sulfinpyrazone or Probenacid). |

|Use ___ as prophylaxis if pt has hx of kidney stones. |Allopurinol |

|Use ____ as prophylaxis if renal function normal. | |

|Use ____ as prophylaxis if CrCl < 50 mL/min | |

| | |

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