Exam 3 - Content Material

Question 1

What is Lipohypertrophy?

Answer 1

The formation of fatty lumps at or around insulin injection sites. It is caused by repeatedly injecting into the same place and by reusing the same needle.

Question 2

What does the Adrenal medulla secrete?

Answer 2

Secretes catecholamines (epi, NE)

Question 3

What does the adrenal cortex secrete?

Answer 3

Secretes corticosteroids (glucocorticoids & mineralocorticoids)

Question 4

What is the Zona reticularis?

Answer 4

region of the adrenal cortex that produces & secretes androgens, progesterone and the estrogens

Question 5

Glucocorticoid synthesis and secretion is regulated by what kind of feedback mechanism?

Answer 5

Negative feedback

Question 6

What classes of hormones does the adrenal cortex secrete?

Answer 6

1. glucocorticoids
2. mineralocorticoids
3. adrenal androgens.

Question 7

What factors cause the hypothalamus to release CRH?

Answer 7

• —stress
• infection
• pain
• hypoglycemia
• trauma
• hemorrhage & sleep

NOTE THESE ARE ALL STRESS FACTORS

Question 8

What effect does ACTH have on the adrenal cortex?

Answer 8

It causes the adrenal cortex to release glucocorticoids, estrogens, androgens and cortisol

Question 9

What should you consider when administering oral glucocorticoids?

Answer 9

• —Orally glucocorticoids inhibit the release of endogenous glucocorticoid by the adrenals.
• Long term glucocorticoids leads to pituitary inability to manufacture ACTH & thus the adrenals stop synthesizing cortisol & other glucocorticoids. (times time to get regain this function
• Taper dose during withdrawal over 7 days
• —Give additional glucocorticoids during times of stress

Question 10

What are the symptoms of glucocorticoid withdraw?

Answer 10

• Hypotension
• hypoglycemia
• myalgia
• arthralgia
• fatigue

Question 11

What are some examples of glucocorticoid durgs?

Answer 11

• cortisone
• prednisone

Question 12

What are some effects of glucocorticoids in general?

Answer 12

• —Increase the availability of glucose (Cortisol) –> can cause hyperglycemia
• —Protein synthesis is suppressed
• fat deposits are mobilized
• —Most glucocorticoids have little mineralocorticoid activity
  
  • So glucocorticoids do not induce significant Na+ retention & K+ loss

Question 13

What are some adverse reactions with high dose Glucocorticoids?

Answer 13

• Usually seen with high doses
• —Adrenal insufficiency
• Osteoporosis
• Infection
• —Glucose intolerance – can inc plasma glucose levels (hyperglycemia)
• —Myopathy – muscle weakness (arms & legs) → fatigue
• Fluid & electrolyte disturbance → K+ loss
• Growth retardation
• Psychologic disturbances
• Cataracts & glaucoma
• Peptic Ulcer Dz
• Iatrogenic Cushing’s syndrome

Question 14

What are low dose glucocorticoids used for?

Answer 14

• Used to tx adrenocortical insufficiency
• no toxic effects at physiologic doses

Question 15

What are the effects of high dose glucocorticoids?

Answer 15

• Used to tx nonendocrine disorders
• Has high anti-inflammatory and immunosuppressive actions:
  
  • allergic rxns, asthma, inflammation, suppress immune response in organ transplant recipients & cancer

Question 16

—Glucocorticoids increase blood glucose concentrations by what 5 methods?

Answer 16

1. Stimulation of gluconeogenesis & glucose secretion by the liver
2. Increasing the hepatic sensitivity to the gluconeogenic actions of glucagon and catecholamines
3. Decreasing glucose uptake and utilization by peripheral tissue (adipose and muscle)
4. Promotion of glucose storage
5. Increasing proteolysis and decreasing protein synthesis in muscles to support the gluconeogenesis activities

Question 17

What is the main pharmacologic effect of glucocorticoids, and how does it do this?

Answer 17

• Main function
  
  • to suppress immune system and inflammation
• Action:
  
  • —inhibiting chemical mediators such as prostaglandins, histamine , leukotrienes, lymphocytes, phagocytic cells, neutrophils & macrophage

Question 18

What are the differences between —Glucocorticoids & NSAIDs?

Answer 18

Glucocorticoids:

• —Bind to DNA and does RNA coding for protein synthesis
• have much greater anti-inflammatory actions

NSAIDs:

• ↓ COX enzymes → ↓ production of prostaglandins (chem. that promote inflammation, pain, and fever) → ulcers in the stomach and intestines, and ↑ risk of bleeding.

Question 19

What are some short acting Glucocorticoids?

Answer 19

• Cortisone
• Hydrocortisone

8-12 min half life

Question 20

What are some intermediate acting Glucocorticoids?

Answer 20

• Prednisone
• Prednisolone
• Methylprednisolone
• Triamcinoclone

18-36min half life

Question 21

What are some long acting Glucocorticoids?

Answer 21

• Bethmethasone
• Deamethasone

36-54min half life

Question 22

What are some uses for Glucocorticoids?

Answer 22

• Rheumatoid Arthritis (reduce inflammation & pain but does not alter dz)
  
  • ​Local injections are effective and less toxic than systemic tx
• Systemic Lupus Erythematosus
• —Inflammatory disorders (inflammatory bowel disease, Ulcerative Colitis & Crohn’s dz)
• Allergic reactions (—bee stings, drug rxn’s, poison ivy etc…)
• —Asthma (PO & inhalation) reserved if β2 agonist not working
• —Dermatologic disorders
• —Neoplasms
• Suppression of allograft rejection to prevent organ transplant rejections (person is on this for life)
• —Prevention of respiratory distress syndrome in preterm infants

Question 23

How do high dose glucocorticoids cause Osteoporosis?

Answer 23

• By inhibiting Ca++ absorption
• Dec bone formation of osteoblast & accelerate the bone resorption of osteoclasts.

Question 24

How do you prevent osteoporosis when giving high dose glucocorticoids?

Answer 24

• Check bone mineral density with long term tx b/4 tx starts
• Give Ca++ with vit D.
• ↓ Na+ intake & give thiazide diuretic with bisphosphonates or calcitonin (↑ bone density)

Question 25

What is lactic acidosis and it is seen most commonly with what?

Answer 25

* Accumulation of lactic acid in blood, resulting in a lower pH in muscle & serum. * Occurs most commonly in tissue hypoxia, liver impairment, resp. failure, burn trauma, neoplasms & CV disease

Question 26

What is ketoacidosis?

Answer 26

—acidosis is accompanied by an accumulation of ketones in the body, resulting from extensive breakdown of fats because of faulty carbohydrate metabolism.

Question 27

What are the symptoms of Ketoacidosis?

Answer 27

Fruity odor of acetone, confusion, dyspnea, N/V, dehydration, wt. loss and, if untreated, coma

Question 28

What is —Cushing syndrome?

Answer 28

—adrenal hormone excess

Question 29

What is addison's disease?

Answer 29

Adrenal hormone deficiency

Question 30

How would high doses of Glucocorticoids cause peptic ulcers?

Answer 30

—glucocort inhibit prostaglandins, inhibit mucus & dec blood flow (watch for black tarry stools)

Question 31

What are the effects of Glucocorticoids on pregnant women?

Answer 31

* —Crosses placenta (cleft palate, spontaneous abortion & low birth weight) * —Lactation – enter breast milk (doses \> 5 mg/day prednisone) cause growth retardation

Question 32

What are some drug interactions with Gluccocorticoids?

Answer 32

* —Digoxin, thiazide & loop diuretics— * NSAID’s * —Insulin & oral hypoglycemics (may need insulin & hypoglycemic agents.— * Vaccines

Question 33

Why would you want to monitor a patient who is taking glucocortiticoids and Digoxin, thiazide & or loop diuretics?

Answer 33

* You would want to monitor a patent taking both of thse medications because they both cause K+ loss. (Glucocorticoids cause retention of Na and H2O and excretion of K+ and so do diuretics). * The loss of potassium can result cardiotoxicity.

Question 34

Why would giving a vaccine to a patient who is taking glucocorticoids be contraindicated?

Answer 34

* Because glucocorticoids supress the immune system this leads to a decreased antibody reaction to antigens. * This can lead to a live otherwise harmless vaccine causing a viral infection * DON'T GIVE THEM BOTH AT THE SAME TIME

Question 35

Why wouldn't you want to give a patient with a systemic fungal infection glucocorticoids?

Answer 35

* Because glucocorticoids supress the immune system this leads to a decreased antibody reaction to antigens from the fungal infection. * Giving a patient with a systemic fungal infection glucocorticoids would supress the immune system that is needed to fight off the fungal infection. * Giving a patient glucocorticoids with a systemic fungal infection **IS CONTRAINDICATED**

Question 36

You should take precaution giving glucocorticoids to what kind of patients?

Answer 36

* —Pediatric patients * pregnant women * breast feeding women * With HTN & heart failure * With renal impairment * With esophagitis, gastritis, or PUD, * With myasthenia gravis * With diabetes * With osteoporosis * Taking diuretics, digoxin, insulin, hypoglycemics & or NSAIDs * —**If have high mineralocorticoids DO NOT administer systemically for long periods of time**

Question 37

How are Glucocorticoids administered?

Answer 37

* —PO, IV, IM, SQ, topically, local injection or inhalation * Usually given in morning before 9:00am * Doses are usually tapered if taking for long perioids of time * Prolonged treatment with high doses usually only given if there are life threatening circumstances

Question 38

What are tye metabolic effects of the glucocorticoids?

Answer 38

1) A mobilization of fatty acids, converting cell metabolism from using glucose for energy to using fatty acids for energy 2) Antagonistic effect on antidiuretic hormones to maintain water balance 3) Reduction in the amount of new bone synthesis 4) Allows the body to deal with stress by allowing epi and glucagon to activate gluconeogenesis and glycogenolysis

Question 39

How are aldosterone levels controled?

Answer 39

1. Extracellular Na+ & K+ levels – when serum Na+ levels are low or K+ levels are high, aldosterone levels rise 2. Renal renin release – a reduction in renal blood flow inc aldosterone levels by the renin-angiotensin-aldosterone system (RAS) 3. Pituitary ACTH – the glucocorticoid hormones produced in the adrenal cortex have mineralocorticoid effects

Question 40

What does aldosterone do?

Answer 40

* Regulates K+, Na+ & H2O balance—In the distal renal tubules * aldosterone promotes the reabsorption of Na+ into the blood in exchange for K+ secreted into the renal tubules for excretion

Question 41

Where are Mineralocorticoids produced?

Answer 41

in the outer layer of the adrenal cortex (zona glomerulosa)

Question 42

What type of drug is Fludrocortisone and what is it used for?

Answer 42

* Mineral corticosteroid * Has both high minealocorticoid and glucocotricoid activity * —Used for adrenocortical insufficiency (Addison dz)—and for tx of salt-losing adrenogenital syndrome

Question 43

What are the pharmacokinetics of Fludrocortisone?

Question 44

What is the MOA of fludrocortidone?

Answer 44

* —Acts on the distal renal tubule to enhance the reabsorption of Na+ and to inc the urinary excretion of both K+ & H+ ions— * Low doses – mineralocorticoid effect K+ excretion and Na+ retention which inc blood pressure— * High dose – glucocorticoid activity

Question 45

What are some contraindications for mineralcorticoids?

Answer 45

* —Systemic fungal infection— * Conditions not requiring mineralocorticoid activity

Question 46

What are some adverse effects of Mineralcorticoids?

Answer 46

* Small dose – Na+ retention, K+ excretion causing inc blood pressure * Large dose - * ​Inhibits endogenous adrenal cortical secretion & pituitary corticotropin excretion— * promotes the deposition of liver glycogen

Question 47

What are some complications of Diabetes?

Answer 47

* —HTN, * heart disease, * renal failure, * blindness, * neuropathy, * amputations, * impotence * stroke

Question 48

When does Type I diabetes usually develop?

Answer 48

* —Accounts for 5 to10% of all cases (approx. 1.2 to 2.4 million) * —Most develop during childhood, usually abruptly from destruction of pancreatic beta cells (autoimmune disorder)

Question 49

When does Type II diabetes usually develop?

Answer 49

* —Begins at middle age & progresses gradually— * Usually obese with low risk of ketoacidosis, but can be normal weight—Has same long-term risk of complications as type 1 diabetes— * Sx’s are from insulin resistance & decreased insulin secretion * —Capable of insulin synthesis

Question 50

What are some characteristics of type I diabetes?

Answer 50

* due to destruction of pancreatic beta cells (r/t autoimmune process-development of antibodies against the patient’s own beta cells) which are responsible for insulin synthesis and release into the bloodstream. * Genetics plays a role, but the trigger for the autoimmune process has not yet been uncovered

Question 51

What are some characteristics of type II diabetes?

Answer 51

They have normal or slightly high insulin levels (hyperinsulinemia).

Question 52

What are some complications of Diabetes?

Answer 52

* —Macrovascular damage – heart dz, HTN & stroke usually due to artherosclerosis (hyperglycemia & lipid metabolism) * —Microvascular damage – damage to small blood vessels & capillaries * —Retinopathy (blindness)— * Nephropathy— * Sensory & motor neuropathy (tingling in finger, toes)— * AutonomicNeuropathy (Gastroparesis)— * Amputations r/t infections— * Erectile dysfunction

Question 53

People with diabetes should be expected to be on what kind of medications?

Answer 53

* ACEIs * ARBs * CCBs * low-dose diuretics * Insulin

Question 54

What are two types of complications that can occur with Diabetes? (duration)

Answer 54

* —Long term problems usually occur because of dec blood flow * Short term complications w type 1 DM: hypoglycemia & hyperglycemia & ketoacidosis (potentially fatal). * Ketoacidosis occurs w/ prolonged, severe hypoglycemia. It is relatively common in type 1 but rare in type 2 DM

Question 55

How is diabetes diagnosed?

Answer 55

* **—Fasting plasma glucose** – at least 8 hours after last meal. Normal is \< 100 mg/dl diabetes if \> 126 mg/dl * **—Casual plasma glucose** – test at any time \> 200 mg/dl but must also display signs & sx (polyuria, polydypsia, ketonuria & rapid wt. loss * —**Oral glucose tolerance test** – used when first 2 test not definitive. Give glucose load of 75 g of glucose & measure plasma level 2 h later. Normal is \< 140 mg/dl diabetes if \> 200 mg/dl * **—Hemoglobin A1c** – at or higher than 6.5%

Question 56

For what type of patients would you use Self-monitor blood glucose?

Answer 56

* Type I and Type II Diabtetes patients * This should be done before meals & hs.

Question 57

What is the target blood pressure for a patient with diabetes?

Answer 57

* systolic \< 140 mm Hg * diastolic \< 90 mm Hg

Question 58

How would you prevent complications with type I diabetes?

Answer 58

* —Diet – caloric intake should be spread throughout the day— * Exercise – inc response to insulin & inc glucose tolerance— * Insulin replacement – Since pancreas is basically not working, it produces no insulin, so daily doses of insulin are imperative to have glycemic control.— * ACE inh or ARB – helps prevent diabetic nephropathy & diabetic HTN (goal 130/80 mm/Hg) * —“Statins” – reduce high levels of LDL (prevents CV events) & should be given to all diabetic pts.

Question 59

How would you prevent complications with type II diabetes?

Answer 59

* —Glycemic control (diet & exercise) – In type 2 most pts are obese and diet & exercise can normalize insulin release & dec insulin resistance— * Glycemic control with drug tx – PO, insulin & injectable— * Initiate diet, exercise (TLC) & one drug therapy (metformin HCl)— * TLC & Add second drug (metformin plus sulfonylurea or basal insulin)— * TLC & metformin & switch from sulfonylurea or basal insulin to intensive insulin therapy

Question 60

What is the 1st line drug of choice for the treatment of type II Diabetes?

Answer 60

Metformin **in particular for overweight & obese people and those with normal kidney function.**

Question 61

What is Hemoglobin A1c?

Answer 61

A measure of the total hemoglobin over 3 months; this value reflects the average glucose level over those 3 months.

Question 62

What is the ideal level that Hemoglobin A1c should be kept at with patients with diabetes?

Answer 62

HbA1c \< 7%

Question 63

Where is insulin synthesized and how is it secreted?

Answer 63

* **Synthesized:** Insulin synthesized in the pancreas by beta cells within the islets of Langerhans * **Secreted: **—secreted by **_sympathetic activation_** of beta receptors in the pancreas. * —**_Main stimulus**_ for insulin release _**is glucose_** but amino acids, fatty acids & ketone bodies can also stimulate release * —Activation of alpha cells in the pancreas **_inhibit_** release of insulin

Question 64

What does insulin do?

Answer 64

* —Stores and builds up energy and is good for cell growth & division by:— * stimulating cellular transport of glucose, AA, nucleotides & K+— * Insulin is converted into glycogen, AA converted into proteins & fatty acids into triglycerides

Question 65

Insulin deficiency promotes hyperglycemia by what 3 ways?

Answer 65

1. —Glycogenolysis (breakdown of glycogen to glucose) 2. —Gluconeogenesis (breakdown of protein & fats to form amino acids & fatty acids). 3. —Reduced glucose utilization (dec cellular uptake of glucose & dec conversion from glucose to glycogen)

Question 66

—Insulin deficiency puts the body in catabolic state (breakdown of complex molecules into simple ones), as a result of this what occurs?

Answer 66

—In absence of insulin glycogen is broken down into glucose (hyperglycemia), proteins into amino aicds (muscle fatigue) & fats into glycerol (glycerin) & free fatty acids (ketoacidosis from the free acid). **THIS IS WHAT CONTRIBUTES TO THE S/SX OF DIABETES**

Question 67

Severe insulin deficiency is manifested by?

Answer 67

* —hyperglycemia * production of ketoacids * hemoconcentration * acidosis & coma

Question 68

How should pre-filled syringes of insulin be stored and how long are they stable?

Answer 68

* Pre-filled syringes store in vertical position in refrigerator. * Stable x1 week-max 2 wks

Question 69

What types of insulin are there, and what is the onset and duration for each?

Answer 69

1. —Rapid acting/Short duration (10-30min / 3-6.5hr) 2. Slower acting/Short duration (30-60min / 6-10hr) regular & (15-30min / 6.5hr) exubera 3. —Intermediate duration (60-120min / 16-24hr) 4. —Long duration (70min / 24 hr)

Question 70

What are some Rapid acting/Short duration insulins?

Answer 70

* —lispro (Humalog) * aspart (NovoLog) * glulisine (Apidra)

Question 71

What are some nursing implications of Rapid acting/Short duration insulins?

Answer 71

* —Give with meals to control postprandial rise in glucose to control glucose between meals & HS * **If no food is given within a short perioid of time pt. will get in a hypoglycemic state.** * All of them are clear solutions— --\> look out for cloudiness * All 3 require prescriptions (Insulin Lispro, Aspart & Glulisine) * **—Do NOT give IV**

Question 72

What are some adverse effects of insulin?

Answer 72

* —Hypoglycemia * edema * weight gain

Question 73

What are some Slower acting/Short duration insulins?

Answer 73

* Humulin R (regular human insulin) * Novolin R * Exubera

Question 74

What are some nursing implications of Slower acting/Short duration insulins?

Answer 74

* Humulin & Novolin R do not need an Rx to get, **except Exubera ** * —SQ inj, SQ infusion, IM inj, oral inhalation & off label IV— * Only insulin given by IV * —Can be inhaled or injected AC to control postprandial hyperglycemia * —Infused SQ to provide basal glycemic control

Question 75

What are some Intermediate duration insulins (NPH insulins)?

Answer 75

* Humulin N * Novolin N

Question 76

What are some nursing implications of Humulin N & Novolin N insulins?

Answer 76

* —Cloudy suspension should be gently shaken b/4 administration— * **Available without prescription—** * The protamine component slows absorption & delays DOA— * Do not administer at mealtime but use bid between meals & at bedtime— * **Is the only long acting insulin that can be mixed with a short acting insulin** * **​—**Draw short acting insulin into syringe first to avoid contamination of NPH vial. * —If have to give a short acting & long acting insulin mix the preparations rather than inject them separately.

Question 77

What are some nursing implications of Insulin Detemir (Levemir)?

Answer 77

* —Clear colorless solution, dosed qd-bid SQ injection. **Do NOT give IV nor mixed with other insulins—** * **Available by prescription only—** * Slow onset & dose dependant DOA. At low doses(0.2 units/kg) persist about 12 h. At higher doses (0.4 units/kg) persist 20-24 h. * —Because of slow onset it is used for basal glycemic control * —It is not given before meals for postprandial hyperglycemia— * Give at same time daily

Question 78

What are some long duration insulins?

Answer 78

—Insulin Glargine (Lantus)

Question 79

What are the nursing implications of —Insulin Glargine (Lantus)?

Answer 79

* —Clear colorless solution, **do NOT mix with other insulins and do NOT give IV**— * **Long DOA 24 h,** qd dosing SQ injection * —Because of long DOA and a stable steady state there is less risk of hypo or hyperglycemia.

Question 80

You should —Discard insulin that has any precipitate except for which type of insulin?

Answer 80

NPH insulins (Humulin N & Novolin N)

Question 81

What are the SQ injection sights for insulin?

Answer 81

* —upper arm, thigh (slowest) & abdomen(fastest)

Question 82

What type(s) of insulin can be given IV and why is it given?

Answer 82

* **—ONLY** Regular insulin can be given IV. * Usually given for ketoacidosis or hyperkalemia * —Insulin is given to ALL pts. that have type I

Question 83

In what situations would you want to supplement additional doses of insulin?

Answer 83

* —During infection * stress obesity * the adolescent growth spurt * pregnancy (after 1st trimester)

Question 84

What drugs lower blood glucose when combined with insulin?

Answer 84

* —sulfonylureas * meglitinides * beta blockers * alcohol

Question 85

What drugs counteract the actions of insulin & produce hyperglycemia?

Answer 85

* thiazide diuretics * glucocorticoids * sympathomimetics

Question 86

What drug(s) can mask the signs and symptoms of hypoglcemia?

Answer 86

* Beta blockers * —(tachycardia, palpitations) & also cause further hypoglycemia by blocking glycogenolysis.

Question 87

What causes hypoglycemia?

Answer 87

* insulin overdose * reduced intake of food * vomiting/diarrhea * excess alcohol * unaccustomed exercise * childbirth

Question 88

Hypoglycemia is defined by what blood glucose level?

Answer 88

\< 50 mg/dl

Question 89

What are the signs and symptoms of a rapidly falling blood glucose levels?

Answer 89

* —activation of the sympathetic nervous system leading to --\> * tachycardia, palpitations, sweating, nervousness

Question 90

What are the signs and symptoms of a slowly falling blood glucose levels?

Answer 90

—HA, confusion, drowsiness & fatigue

Question 91

What can be used to treat falling blood glucose levels (rapid or slow)?

Answer 91

* —Take fast acting sugar * glucose tablets, OJ, sugar cubes, honey, corn syrup, non diet soda * —If pt has severe hypoglycemia IV glucose is preferred

Question 92

What produces glucagon and what are it's effects?

Answer 92

* —Glucagon is produced by alpha cells in the pancreas. * ↑ plasma levels of glucose & relaxes smooth muscle in the GI tract.— * ↑ blood glucose levels following insulin overdose. * It promotes breakdown of glycogen, ↓ glycogen synthesis & stimulates biosynthesis of glucose.

Question 93

How can glucagon be administered?

Answer 93

—IM, SQ & IV

Question 94

What is the MOA for Sulfonylureas?

Answer 94

—Stimulates the release of insulin from pancreas depending on how much glucose there is (insulin sensitivity) --\> can lead to hypoglycemia

Question 95

What are some nursing considerations for sulfonulureas?

Answer 95

* —Only works in type 2 diabetes— * Can be used alone or in combo— * Avoid during pregnancy/nursing mothers

Question 96

What are some side effects of sulfonylureas?

Answer 96

* —Hypoglycemia (fatigue, excessive hunger, profuse sweating, palpitations)— * Weight gain

Question 97

What are the Drug interactions for sulfonylureas?

Answer 97

* —Alcohol (disulfuram rxn)— * Drugs that intensify hypoglycemia: NSAIDS’s, sufonamide antibiotics, ranitidine & cimetidine— * Beta blockers – beta rec promote insulin release & mask S/Sx of hypoglycemia

Question 98

What are some 1st generation Sulfonylureas?

Answer 98

* Tolbut**amide** * Acetohe**amide** * Tolaz**amide** * Chlorop**amide**

Question 99

What are some 2nd generation Sulfonylureas?

Answer 99

Glipizide Glyburide Glime

Question 100

What are some Metglitinides/Short-Acting Secretagogues?

Answer 100

* —Repa**glinide** (Prandin) * nate**glinide** (Starlix)

Question 101

What is the MOA for Metgilitinides/Short-acting Secretagogues

Answer 101

* —Stimulates the release of insulin from pancreas depending on how much glucose there is (insulin sensitivity) --\> can lead to hypoglycemia * It is glucose dependant (if no glucose no insulin is produced) pt **MUST eat no longer than 30 min after drug intake** * **_Works exactly the same as Sulfonylureas_**

Question 102

What are some nursing implications for Metglitinides/Short-Acting Secretagogues?

Answer 102

* —Only approved for type 2 * **—If no response with sulfonylureas there will be no response with metglitinides—** * Approved for monotx or combo with metformin or a glitazone * Use this drug if pt. has allergic reaction to sulfonlureas

Question 103

What are the side effects and drug interactions of Metglitinides/Short-Acting Secretagogues?

Answer 103

* Side effects: * —Hypoglycemia (Less than with sulfonylureas), weight gain * ​​​Drug interactions * ​—Gemfibrizol (causes hypoglycemia)

Question 104

What are the different types of Biguanides?

Answer 104

—Metformin (Glucophage, Fortamet, Glumetza, Riomet)

Question 105

What is the MOA for metformin?

Answer 105

* —Dec glucose production in the liver & enhances glucose uptake & utilization by muscle. * Does NOT promote insulin release * Dec LDL and triglyceride levels.

Question 106

What are the nursing implications for metformin?

Answer 106

* —Because of MOA could possibly use it in pts with type 1 also— * Can be used alone or with sulfonylureas or Exenatide— * Absorbed slowly from small intestine and excreted unchanged in the kidneys (Check renal fxn, creatine cl)

Question 107

What are the contraindications for metformin?

Answer 107

* —Males with creatine clearance \> 1.5— * Females with creatine clearance \> 1.4— * Liver dz, severe infection, alcohol excess or pt. with shock (cause hypoxemia), alcohol use— * Heart Failure

Question 108

What are the side effects of metformin?

Answer 108

* —Weight loss, Dec appetite, nausea, **diarrhea**, dec absorption of vit B12 & folic acid— * can cause lactic acidosis (rare, but mortality rate of 50%) S/Sx are: hyperventilation, myalgia, malaise & unusual somnolence

Question 109

What are some Type 2 Thiazolidinediones (**Glitizones**)?

Answer 109

* —Rosi**glitazone** (Avandia) * Pio**glitazone** (Actos)

Question 110

What is the MOA for Thiazolidinediones (**Glitizones**)?

Answer 110

* —Dec insulin resistance by inc insulin sensitivity of skeletal muscle, liver & adipose tissue (cellular response to insulin inc). * Insulin must be present for drug to work.

Question 111

What are some nursing implications for Thiazolidinediones (**Glitizones**)?

Answer 111

* —Only approved for type 2— DM * Approved for monotx & for combo with metformin, sulfonylurea or insulin (carefully b/c insulin & glitizones cz edema).

Question 112

What are some adverse effects of Thiazolidinediones (**Glitizones**)?

Answer 112

* —Fluid retention (edema & wt gain), inc HDL, LDL and triglycerides * —Contraindicated in Class III or IV heart failure or hepatoxicity

Question 113

What are the drug interactions for Thiazolidinediones (**Glitizones**)?

Answer 113

—Strong CYP2C8 inhibitors (atorvastatin, ketoconazole)& inducers (Rifampin)

Question 114

What are some Alpha-glucosidase inhibitors?

Answer 114

* —Acarbose (Precose) * Miglitol (Glyset)

Question 115

What is the MOA for Alpha-glucosidase inhibitors?

Answer 115

—Dec absorption of carbohydrates, by preventing their breakdown into monosaccharides, in the small intestine. It dec the rise in glucose after a meal.

Question 116

What are the nursing implications for Alpha-glucosidase inhibitors?

Answer 116

—Can be used in monotherapy or with insulin, sulfonylurea or metformin (try to avoid metformin & alpha-gluc together b/c of GI affects)

Question 117

What are the Adverse effects for Alpha-glucosidase inhibitors?

Answer 117

* —Flatulence, cramps, abdominal distention, borborygmus (rumbling bowel sounds) & diarrhea— * Dec absorption of iron (anemia), liver dysfunction

Question 118

What are some Amylin Mimetics drugs?

Answer 118

—Pramlintide (Symlin)

Question 119

What is the MOA for Amylin Mimetics?

Answer 119

—Delays gastric emptying and suppresses glucagon secretion. Also acts to inc sense of satiety, and can thereby lower caloric intake.

Question 120

What are some nursing implications for Amylin Mimetics?

Answer 120

* —Can be used in type 1 or 2— * Used as an adjunct to insulin in type 1 & 2 in pts that have no glucose control even with insulin * —In type 2 in combo with metformin &/or a sulfonlyurea * Peaks in 20 min after SQ injection

Question 121

What are some adverse effects of Amylin Mimetics?

Answer 121

* —Hypoglycemia (esp. when used in combo with insulin & usually develops within 3 h) * Nausea, Injections site rxn’s

Question 122

What are some drung interactions of Amulin Mimetics?

Answer 122

* —PO drugs should be taken 1 h before injecting Pramlintide * drugs that slow motility (anticholinergics) * drugs that slow absorption of nutrients (acarbose, miglitol)

Question 123

What are some Incretin Mimetics/ Glucagon-like Peptide-1 Agonist (GLP-1) durgs?

Answer 123

—Exenatide (Byetta)

Question 124

What is the MOA of Exenatide (Byetta)?

Answer 124

* —Slows gastric emptying * stimulates glucose-dependent release of insulin * inhibits postprandial release of glucagon & suppresses appetite

Question 125

What are some nursing implications for Incretin Mimetics/ Glucagon-like Peptide-1 Agonists (GLP-1)?

Answer 125

* —Give oral drugs at least 1h before Exenatide— * Used to improve glycemic control of type 2 taking metformin or a sulfonylurea— * Suppresses appetites * —Should not be used in pts with end-stage renal dz.

Question 126

What are the adverse effects of Incretin Mimetics/ Glucagon-like Peptide-1 Agonist (GLP-1)?

Answer 126

—Hypoglycemia esp in combo with a sulfonylurea but not w metformin

Question 127

What are the drug interactions with Incretin Mimetics/ Glucagon-like Peptide-1 Agonists (GLP-1)?

Answer 127

—Oral contraceptives & antibiotics

Question 128

Amylin Mimetics and Incretin Mimetics/ Glucagon-like Peptide-1 Agonist (GLP-1) are both what kind of drugs?

Answer 128

Injectables

Question 129

What are the 5 —principle actions of Thyroid hormones?

Answer 129

**—1) stimulation of energy use**, which elevates basal metabolic rate resulting in inc O2 & inc heart rate production. Speeds metabolism of fats, carbs & proteins— **2) stimulation of the heart**, which stimulates both rate & force of contraction resulting in inc cardiac output and an inc in O2 demand.— **3) promotion of growth & development during fetal stages,** maturation of skeletal muscle, reproductive system, development of the brain & CNS. —**4) increases the production & release of other hormones,** estrogen, testosterone, insulin catecholamines (epi, NE) & glucocorticoids (esp. cortisol) **—5) stimulates appetite**

Question 130

What would you want to educate your pt. on when taking medications for hypothyroidism?

Answer 130

* Educate to take only as directed * That replacement therapy is for life * Never discontinue without talking to provider first!

Question 131

What are some characteristics of thyroid hormones?

Answer 131

* **T3** (triiodothyronine) is the **more potent ** * —The amount of T4 released is **GREATER** than T3. Much of the T4 undergoes conversion to T3 which counts for 80% of T3 in plasma * —99.5% of T3 & T4 in plasma is bound to protein. So **only a small amount of thyroid is free** * —All thyroid hormones are protein bound to thyroxin-binding globulin (TBG)— * Half-life 1 day for T3 and 7 days for T4 * —Metabolized in liver & excreted in the urine * **—May produce inhibitory effects if pt. using adrenergic antagonist**

Question 132

When is thyroid hormone usually given?

Answer 132

In the morning

Question 133

A thyroid over dose can cause what manifestations in the pt.?

Answer 133

* —irritability * insomnia * tachycardia * arrhythmias * inc. blood pressure * anxiety * wt. loss ## Footnote **Thyroid hormone is a stimulant**

Question 134

What are the clinical manifestations of having high thyroid levels?

Answer 134

* Eyes = prominent * Integumentary = fine, thin hair; hot, moist skin * Temperature = heat intolerant * Weight = \>appetite, \< weight * Emotional = nervous, irritable, insomnia * GI = diarrhea

Question 135

What are the clinical manifestations with low thyroid levels?

Answer 135

* Eyes = ptosis, edematous * Integumentary = dry, brittle hair; cold, dry skin * Temperature = cold intolerant * Weight = \< appetite, \> weight * Emotional = lethargic, depressed, \>sleep * GI = constipation

Question 136

What are some HypOthyroid Medications?

Answer 136

* desiccated thyroid (Armour Thyroid) * liothyronine (Cytomel) * levothyroxine, L-Thyroxine (Synthroid, Levoxyl, Levothroid) * liotrix (Thyrolar)

Question 137

What are some characteristics of Armour Thyroid?

Answer 137

* Natural Thyroid Extract --\> derived from pigs * —T3 & T4 * —Animal extract, desiccated thyroid (identical to natural hormone)— * Dispensed in mg and grains (15, 30, 60 90 & 120 grains)

Question 138

What are some characteristics of Levothyroxine, L-thyroxine?

Answer 138

* Synthroid, Levoxyl, Levothroid (names of the drugs in this class) * —T4 rapidly converted to T3, No real advantage of combing T3 & T4. (PO, injection)— * Low cost, synthetic (minimal allergic rxn), Long DOA— * Half-life approx 7 days, PO onset 3-5 days , IV 6-8 h. Take 4-8 wks b/4 full effects of dosage adjustments can be seen.

Question 139

What are some characteristics of Liothyronine?

Answer 139

* Drugs = —Cytomel & Triostat * —Available T3 & does NOT require conversion of T4 so has **faster onset of axn.—** * Synthetic (minimal allergic rxn), PO & injection— * **Better absorbed & more potent than levothyroxine** * —Long DOA 3 days shorter DOA than levothyroxine— * Can see effects of dosage adjustments in 1 to 2 wks.— * Serum T3 fluctuates so serum level high after admin & low at end of day, because of fluctuation not recommended for maintenance.— * **More cardiotoxic than levothyroxine**

Question 140

What are the characteristics of Liotrix?

Answer 140

* —Drug = Thyrolar * T4 & T3 (4:1 ratio by weight)— * Synthetic (minimal allergic rxn)

Question 141

Why causes Hypothyroidism?

Answer 141

mild deficiency of thyroid hormone in adults

Question 142

What causes Myxedema?

Answer 142

—severe deficiency of thyroid hormone

Question 143

What is Levothyroxine's MOA?

Answer 143

* T4 identical to the naturally occurring hormone. T4 will be converted to T3 * —Binds to rec throughout body to inc metabolic rate; stimulates protein synthesis; promotes cell growth

Question 144

What are some nursing implications of Levothyroxine?

Answer 144

* —Narrow therapeutic range, test TSH 6-8 wk after initiation of tx— * Take on empty stomach in the morning 30 min ac. * —Thyroid hormones inc cardiac responsiveness to catecholemines (epi, dopamine, dobutamine) * —Warfarin may need to be reduced if pt taking levothyroxine & warfarin

Question 145

What are the pharmacokinetics of Levothyroxine?

Answer 145

* —Variable absorption * metabolized liver * eliminated in bile/feces * slow onset with long DOA * half-life 6-7 days b/c protein bound * full effects in 2-3 wk * qd dosing

Question 146

What are the adverse effects of Levothyroxine?

Answer 146

* Thyrotoxicosis (too much thyroid hormone) leading to: * —Weight loss * palpitations * tachycardia * angina * CHF * tremors * nervousness * HA * insomnia * menstrual irregularities * impotence * \> bowel motility * hyperthermia * heat intolerance & sweating

Question 147

What are some drugs that decrease the absorption of levothyroxine?

Answer 147

* —Cholestyramine (Questran) * Colestipol (Colestid) * —Ca++ supplements (Tums, Os-Cal) * Sucralfate (Carafate) * Aluminum-containing antacids (Maalox, Mylanta) * Iron supplements (Ferrous sulfate)

Question 148

What are some drugs that accelerate the absorption of levothyroxine?

Answer 148

* —Phenytoin (Dilantin) * Carbamazepine (Tegretol, Carbatrol) * —Rifampin * Sertraline (Zoloft) * Phenobarbital

Question 149

What is the treatment for hyperthyroidism?

Answer 149

* —Antithyroid drugs (propylthiouracil (PTU), Methimazole) * beta blocker * exophthalmos use glucocorticoids * —Radiation or Surgery

Question 150

What is the MOA for Propylthiouracil (PTU)?

Answer 150

—Blocks thyroid synthesis by: 1) preventing oxidation of iodide by blocking peroxidase thus inhibiting iodine into tyrosine (thyroid gland) 2) Blocks conversion of T4 into T3 (peripheral tissue) **—PTU does NOT destroy pre-existing thyroid hormone so it may take 3-12 wk to produce euthyroid state**

Question 151

What is the prefered hyperthyroid treamtent medication to use during pregnancy?

Answer 151

* Propylthiouracil (PTU) * Is NOT as likely to cross placenta than methimazole.

Question 152

What are the pharmacokinetics of Propylthiouracil (PTU)?

Answer 152

* Quick onset of action 30 min to 1 h * half life 75 min so dosing throughout day * crosses placenta & can enter breast milk;

Question 153

What are some uses for Propylthiouracil (PTU)?

Answer 153

* —Graves disease * adjunct to radiation tx * suppresses thyroid hormone synthesis in preparation for thyroid surgery * thyrotoxic crisis

Question 154

What are some adverse effects of Propylthiouracil (PTU)?

Answer 154

* —Agranulocytosis (rare, develops quickly during 1st 2 months) * Sore throat * fever * ulcerations in mouth rectum & vagina * hypothyroidism

Question 155

What are some nursing implications of Propylthiouracil (PTU)?

Answer 155

* —Take with food— * If dose missed, take ASAP— * Store in light resistant container * —Ask pt to report the following symptoms: * weight gain * cold intolerance * depression * bruising * bleeding * fever * sore throat

Question 156

What is the role of calcium in the body?

Answer 156

—Critical to skeletal, muscular, nervous and CV system function

Question 157

What are some nursing implications for calcium?

Answer 157

* —Calcium reduces absorption of thyroid hormone-must give 1 hour apart * —Never give \>600 mg at one time to ensure proper absorption. * Thiazide diuretics decrease renal calcium excretion

Question 158

What are the symptoms for hypercalcemia?

Answer 158

* —N/V * constipation * polyuria * nephrolithiasis (kidney stones develop) * lethargy * depression * cardiac dysrhythmias

Question 159

Who is at risk for vitamin D deficiency?

Answer 159

* pregnant women * obese people * dark-skinned individuals

Question 160

What are the manifestations of vitamin D deficiency?

Answer 160

* —Rickets (children) * osteomalacia (adults) * both can be reversed

Question 161

What are the manifestations of vitamin D toxicity?

Answer 161

* —Early Response: Weakness, fatigue, nausea, vomiting, and constipation— * Later Presentation: polyuria, nocturia, and proteinuria —Toxicity is called hypervitaminosis D

Question 162

What is the treatment for vitamin D deficiency?

Answer 162

vitamin D

Question 163

What is the treatment for bone deterioration?

Answer 163

Calcium + Vitamin D They MUST be given together to work

Question 164

Which vitamin D supplement can be purchased OTC, and how large is the dose?

Answer 164

* Vitamin D3 (cholecalciferol) * 5.000 units once daily

Question 165

What type of vitamin D is produced naturally through sunlight?

Answer 165

Vitamin D3 (cholecalciferol)

Question 166

Which vitamin D supplement requires a prescription, and how large are the doses??

Answer 166

* —Vitamin D2 (ergocalciferol) * Dosed in 50,000 units once weekly * Produced through PLANTS.

Question 167

What are Bisphosphonates used for?

Answer 167

Prevents and treat osteoporosis in males and in postmenopausal females to help maintain bone strength and prevent bone loss

Question 168

What are some nursing implications of Bisphosphonates?

Answer 168

* Have pt. TAKE in the morning on empty stomach with a full glass of water. * Do NOT have pt. lie down OR take any other food or beverages for 30 minutes after taking a bisphosphonates

Question 169

What are some Adverse effects of Bisphosphonates?

Answer 169

Do NOT eat, lie down or give to patients who are immobilized for at least 30 minute after taking medication. This is to prevent esophagitis (erosion of the esophagus).

Question 170

Which drug increases bone formation?

Answer 170

* —Teriparatide (Forteo) --\> form of PTH * —Administered subcutaneously * Used to also treat osteoporosis in postmenopausal women, in men and in glucocorticoid-induced osteoporosis

Question 171

What is Calcitonin-salmon used to treat?

Answer 171

Postmenopausal osteoporosis and should be taken with vitamin D.

Question 172

What do Selective Estrogen Receptor Modulators (SERMs) do?

Answer 172

Both block and activate estrogen receptors in various tissues which gives the benefits of estrogen by activating some receptors to protect against osteoporosis and decrease in LDL and by blocking some receptors giving protection against breast cancer, uterine cancer and thromboembolism. However it can sometimes produce hot flashes, increase risk of endometrial cancer.

Question 173

What are some Selective Estrogen Receptor Modulators (SERMs)?

Answer 173

* ralox**ifene** * tamox**ifen** * torem**ifene**

Question 174

What are some nursing implication of Selective Estrogen Receptor Modulators (SERMs)?

Answer 174

* SERM’s such as tamoxifen and toremifene treat breast cancer but raloxifene treats BOTH osteoporosis and breast cancer. * **Raloxifene is a PREGNANCY CATEGORY X drug.**

Question 175

What are the components that make up arterial pressure?

Answer 175

ARTERIAL PRESSURE = cardiac output (CO) X peripheral resistance

Question 176

CO is influenced by what 4 factors?

Answer 176

1. Heart rate (HR) 2. myocardial contractility (force of contraction) 3. blood volume 4. venous return of blood to the heart **An ↓ in these will cause a ↓ in CO & therefore an ↓ in BP**

Question 177

How is Arterial pressure regulated?

Question 178

High blood pressure is a major risk factor for what?

Answer 178

* Heart disease * Stroke * Kidney disease

Question 179

What are the characteristics of primary hypertension?

Answer 179

* No identifiable cause * Chronic progressive dz * Populations at higher risk: Elderly, African & Mexican American, postmenopausal, obese pts * Can lower BP but can’t “cure” the unknown cause * **Treatment is lifelong**

Question 180

What are the characteristics of Secondary hypertension?

Answer 180

* Identifiable cause * Fixing the underlying problem can lead to the condition being treated or “cured” * Chronic renal dz, renovascular dz, oral contraceptive induced, coarctation or the aorta, primary aldosteronism, Cushing syndrome, pheochromocytoma

Question 181

What causes secondary hypertension?

Answer 181

Can happen as a result of: * Chronic renal dz * renovascular dz * oral contraceptive induced * coarctation or the aorta * primary aldosteronism * Cushing syndrome * pheochromocytoma

Question 182

Untreated hypertension can lead to what?

Answer 182

* Left untx can lead to heart dz * Myocardial infarction (MI) * Heart failure (HF) * Angina pectoris * Renal failure * Cerebral hemorrhage (stroke)

Question 183

What is the goal BP for pts with diabetes or chronic kidney dz?

Answer 183

Systolic \< 140 mm Hg diastolic \< 90 mm Hg

Question 184

What are the 3 body systems that help regulate blood pressure?

Answer 184

1. SNS - Baroreceptor reflex 2. Renin-angiotensin-aldosterone system (RAAS) 3. Kidney

Question 185

What are the classes of antihypertensive drugs?

Answer 185

1. Diuretics 2. Drugs that suppress RAAS 3. Sympatholytics (antiadrenergic drugs) 4. Direct-acting vasodilators: hydralazine and minoxidil 5. Calcium channel blockers (CCBs)

Question 186

What are the major categories of diuretics?

Answer 186

* High-ceiling (loop) diuretics -- Furosemide * Thiazides & related diuretics -- Hydrochlorothiazide * Potassium-sparing diuretics * Aldosterone antagonists (blockers) – ex. spironolactone * Non-aldosterone antagonists – ex. Triamterene * Osmotic diuretics – ex. Mannitol * Carbonic anhydrase inhibitors

Question 187

What are some types of Drugs that suppress RAAS?

Answer 187

* ACE inhibitors * Angiotensin II receptor blockers * Aldosterone antagonists * spironolactone * eplerenone * Direct renin inhibitors - Aliskiren

Question 188

What are the types of Sympatholytics (antiadrenergic drugs)?

Question 189

Diuretics affect what four regoins of the kidney?

Answer 189

1. Glomerulus 2. Proximal convoluted tubule 3. Loop of Henle 4. Distal convoluted tubule (DCT)

Question 190

Diuretic drugs that produce the greatest diuresis act how?

Answer 190

Most diuretic drugs that act early in the nephron can block the greatest amount of solute reabsorption --- and produce the greatest diuresis

Question 191

What are the adverse effects of Diuretics in general?

Answer 191

* Hypovolemia * Acid-base imbalance * Electrolyte imbalances

Question 192

What is the MOA of Furosemide (Lasix)?

Answer 192

* Acts on ascending loop of Henle to block reabsorption of Na+ and Cl- * This also inhibits potassium recycling = ↓ in potassium * Loss of volume * Relaxation of venous smooth muscle

Question 193

What is Furosemide used for?

Answer 193

* ↓ Pulmonary edema r/t congestive heart failure (CHF) * Edematous states – of hepatic, cardiac, or renal origin that has been unresponsive to other diuretics * ↓ Hypertension not controlled by other diuretics – but can add a thiazide diuretic (no benefit to combining furosemide with another high-ceiling/loop agent)

Question 194

What are the adverse effects of Furosemide?

Answer 194

* Hyponatremia * hypochloremia * Hypocalcemia * hypomagnesemia * dehydration * Hypokalemia * If serum K+ falls below 3.5 mEq/L tx with K supplements or use K-sparing diuretic * Hypotension * Ototoxicity * Hyperglycemia * Hyperruricemia (a lot of peeing)

Question 195

What are the Drug interactions of Furosemide?

Answer 195

* Digoxin [hypokalemia from loops produces ↑ risk of dig-induced toxicity (ventricular dysrhythmias) * Ototoxic drugs * Lithium – in general, diuretics result in decreased renal lithium clearance = ↓ lithium excretion, so it can accumulate to toxic levels in the blood * Antihypertensive agents – lower BP already, now add loss of fluid volume and relaxation of venous smooth muscle * NSAIDs (Nonsteroidal anti-inflammatory drugs) – \*blunts efx of furosemide

Question 196

What is one important adverse effect of Ethacrynic acid?

Answer 196

Irreversible hearing loss

Question 197

In general what are the effects of Thiazides?

Answer 197

* Increase renal excretion of sodium, chloride, potassium, and water * Elevate levels of uric acid and glucose * Promote renal calcium retention * Loss of volume * Relaxation of venous smooth muscle

Question 198

When are Thiazides not effective?

Answer 198

Not effective when urine flow is low = GFR is \< 15-20 mL/min

Question 199

Where does Hydrochlorothiazide act?

Answer 199

early segment of the distal convoluted tubule

Question 200

What is Hydrochlorothiazide used for?

Answer 200

* **To treat essential hypertension – 1st line choice for most people** * **To treat edema** – preferred drug for mild to moderate HF and hepatic & renal edema * To treat diabetes insipidus – don’t know how it works * May protect from post menopausal osteoporosis

Question 201

What are the adverse effects of hydrocholorothiazide?

Answer 201

* Hyponatremia * Hypokalemia * If serum K+ falls below 3.5 mEq/L tx with K supplements (or eating K rich foods) or use K-sparing diuretic * Hypomagnesemia * hypochloremia * dehydration * Promotes renal calcium retention * **NO OTOTOXICITY** * Hyperuricemia * Hyperglycemia * usually only in DM pts...who may need larger doses of insulin or oral hypoglycemic drug * Impact on lipids - ↑ LDL, cholesterol, total cholesterol & trigs

Question 202

What are the drug interactions of Hydrochlorothiazide?

Answer 202

* Digoxin - If combined will further lower K+ lvls * NSAIDs may blunt diuretic effect * Lithium supplements - If combined can increase lithium levels due to retained lithium in kidneys * **Can be combined with ototoxic agents without increased risk of hearing loss**

Question 203

What are the classes of Potassium-Sparing Diuretics?

Answer 203

* Aldosterone antagonist (blocker) * Spironolactone * Nonaldosterone antagonists (blockers) * Triamterene * Amiloride

Question 204

What is the MOA of Spironolactone (Aldactone)?

Answer 204

* Blocks aldosterone in the distal nephron * Retention of potassium * (hyperkalemia \>5 mEq/L – mostly if used alone) * **Increased excretion of sodium & passive loss of water** * Slows myocardial remodeling & fibrosis * **Reduces Baroreceptor activatio**n * ​gynecomastia in men **NOTE: this is a Aldosterone antagonist **

Question 205

What is Spironolactone (Aldactone) used for?

Answer 205

* Pts w/ with Hypertension -- ↓ BP * Pts w/ with Edematous states -- ↓ BP * Pts w/ Heart failure -- decreases mortality in severe failure * Pts w/ primary hyperaldosteronism -- blocks aldosterone from being formed * **Potent antagonist of the androgen (testosterone) receptor as well as an inhibitor of androgen production **

Question 206

What are the adverse effects of Spironolactone (Aldactone)?

Answer 206

* Hyperkalemia -- possible fatal dysrhythmias; cell uptake of insulin could ↓ K+ levels by K+ uptake into cells * Endocrine effects – gynecomastia, menstrual irregularities, impotence, hirsutism, & deepening of the voice

Question 207

What are the drug interactions with Spironolactone (Aldactone)?

Answer 207

* Thiazide and loop diuretics – counteract K-wasting * Agents that raise potassium levels (because this drug ↑ K+ lvls), such as: * K supplements * Salt substitutes (KCl) * Or other K-sparing diuretic * ACE-inhibitors * ARBs * Direct renin inhibitors

Question 208

What is the MOA of Triamterene (Dyrenium)?

Answer 208

* Direct inhibitor of the exchange mechanism of Na ion transport\* * Disrupts sodium-potassium exchange in the distal nephron so works much faster than spironolactone (2-4 hrs. vs. 1-2 days) * Decreases sodium reuptake & reduces K secretion; Na+ excretion is increased, K is conserved * weak/mild diuresis

Question 209

What is Triamterene (Dyrenium) used for?

Answer 209

* Hypertension - decreases Blood volume, and rherefore BP * Edema - decreases fluids reducing edma * Counteracts the K-wasting efx of more powerful diuretics – most usual use * Usually given in combination with hydrochlorothiazide

Question 210

What are the adverse effects of Triamterene (Dyrenium)?

Answer 210

* Hyperkalemia * Leg cramps * Nausea * Vomiting * Dizziness * Blood dyscrasias (rare)

Question 211

What are some contraindications for Triamterene (Dyrenium)?

Answer 211

* Another K-sparing diuretic - Will result in hyperkalemia * K supplements - will result in hyperkalemia * Salt substitutes (KCl)

Question 212

What aare the two Nonaldosterone antagonists (blockers)?

Answer 212

* Triamterene * Amiloride

Question 213

What is the MOA of Amiloride (Midamor)?

Answer 213

* similar to triamterene * Blocks sodium exchange in the distal nephron

Question 214

What is Amiloride (Midamor) used for?

Answer 214

•To counteract potassium loss caused by more powerful diuretics

Question 215

What are the adverse effects of Amiloride (Midamor)?

Answer 215

Hyperkalemia – so don’t use w/ other K-sparing diuretics or K supplements

Question 216

What are the drug interactions of Amiloride (Midamor)?

Answer 216

* ACE inhibitors * ARBs * Direct renin inhibitor

Question 217

What type of drug is Mannitol (Osmitrol)?

Answer 217

Osmotic Diuretic

Question 218

What is the MOA of Mannitol?

Answer 218

* Promotes diuresis by creating osmotic force within lumen of the nephron\* * Freely filtered at glomerulus * Minimal tubular reabsorption * Minimal metabolism * Is pharmacologically inert (no biochem efx)

Question 219

What are some nursing implications for Mannitol?

Answer 219

* Drug must be given IV – cannot be transported across the GI epithelium/lining * Has NO effect on K or any other electrolytes * Works in 30-60 mins. for 6-8 hrs.

Question 220

What is Mannitol used for?

Answer 220

* Prophylaxis of renal failure\* * Reduction of intracranial pressure – osmotic force to draw water off

Question 221

What are some adverse effects of Mannitol?

Answer 221

* Edema – can leave the vascular system at all capillary beds EXCEPT the brain\* * Used w/ extreme caution in heart ds – can precipitate CHF and pulmonary edema * Must be d/ced if pts w/ heart failure or pulmonary edema develop renal failure\* * Headache * Nausea * Vomiting * Fluid and electrolyte imbalance

Question 222

What does Angiotensin II do?

Answer 222

* Vasoconstriction * Release of aldosterone * Alteration of cardiac and vascular structure

Question 223

Where is Angiotensin II produced?

Answer 223

* in blood, in individual tissues (local efx), and produced by pathways that do not involve ACE * so we can’t completely block angiotensin II

Question 224

What are some examples of ACE inhibitors?

Answer 224

* lisino**pril** * enala**pril** * capto**pril** All end in **PRIL**

Question 225

How do ACE Inhibitors work?

Answer 225

Prevents conversion of angiotension I, which causes: * suppression of SNS * kidney Na+Cl- excretion * K+ retention * suppression of aldosterone release * vasodilation * Suppression of ADH release

Question 226

What are ACE Inhibitors used to treat?

Answer 226

* HTN * HF * MI * DM & nonDM nephropathy * DM retinopathy prevention w/ T1 DM (enalapril) * To prevent adverse cardiovascular events: MI, stoke, & death due to CV events

Question 227

What are the adverse effects of ACE inhibitors?

Answer 227

* **Category X drug --\> No pregos!** * **Hyperkalemia** (K retention from aldosterone blocking efx) * Avoid K supplements, KCl salt substitutes * **Avoid K-sparing diuretics** * **Renal failure in pts. w/ renal artery stenosis** * **Kidney Na+Cl- excretion** * ​Suppression of aldosterone release ---\> no ADH release * **​Leads to Na+ and H20 loss** * **​​​**Vasodilation * Intensifies 1st dose hypotension * Dysgeusia (geusia = taste) & rash * Neutropenia = ↑ risk of infex (check WBC & diff q 2 wks during first 3 mos. Therapy) * **↑ bradykinin leads to Intractable cough **

Question 228

What are the drug interactions for ACE Inhibitors

Answer 228

1. Diuretics – may intensify 1st dose hypotension (so hold diuretics 1 wk before starting ACI-I 2. Other anti-HTN meds – synergistic effect 3. Drugs ↑ K levels such as: 1. K sparing diuretics 2. K supplements 4. Lithium – lithium toxicity (monitor frequently) 5. NSAIDs – may reduce anti-HTN efx

Question 229

How are ACE inhibitors administered?

Answer 229

* All ACE inhibitors are administered orally except for **enalaprilat** * All oral formulations may be administered without regard to meals except for **captopril** and **moexiprilr**

Question 230

What is the MOA of Angiotensin II Receptor Blockers (ARBs)?

Answer 230

* Block actions/access\* of angiotensin II * Cause dilation of arterioles and veins * Prevent angiotensin II from inducing pathologic changes in cardiac structure * Decrease release of aldosterone: * ↑ renal excretion of Na & water * Hyperkalemia – K retention (more from ARBs than ACE-I) * Increase renal excretion of sodium and water * Do not increase levels of bradykinin (no blocking of enzyme) * no cough

Question 231

What are Angiotensin II Receptor Blockers ARBs used for?

Answer 231

* Hypertension, **heart failure**, myocardial infarction, stoke & death * **improves LV ejection fraction, reduce HF symptoms, increase exercise tolerance** * ↓ bradykinin lvls -- no cough * Diabetic nephropathy - mitigates progression * If unable to tolerate ACE inhibitors: protection against MI, stroke, and death from cardiovascular (CV) causes in high-risk patients * Migraine headache – prophylactically (candesartan) * Slowed development of diabetic retinopathy (losartan)

Question 232

What are some adverse effects of Angiotensin II Receptor Blockers (ARBs)?

Answer 232

* Angioedema (lower than ACE-Is) * **Category X Drug** * Renal failure – w/ renal stenosis – same as ACE-Is

Question 233

What are some drug interactions with Angiotensin II Receptor Blockers (ARBs)?

Answer 233

Hypotensive efx with other anti-HTN meds (similar to ACI-Is)

Question 234

What's an exaample of a Direct Renin Inhibitor?

Answer 234

Aliskiren

Question 235

What is the MOA for Aliskiren?

Answer 235

* Binds tightly with renin and inhibits the cleavage of angiotensinogen to angiotensin I * Should shut down entire RAAS (works earlier than others but no proof that there are better clinical outcomes)

Question 236

What is Aliskiren used for?

Answer 236

only hypertension (still need to study outcomes – long term benefits not known)

Question 237

What is an example of a Selective Aldosterone Antagonist?

Answer 237

Eplerenone

Question 238

What is the MOA for Eplerenone?

Answer 238

Selective aldosterone receptor blocker (SARB)

Question 239

What is Eplerenone used for?

Answer 239

* Hypertension * Heart failure

Question 240

What are some adverse effects of Eplerenone?

Answer 240

* Hyperkalemia – don’t use with K+ sparing diuretics * Cautious use with ACE-Is and ARBS * Not for pts: w/ K \> 5.5 * Impaired renal fx * T2 DM w/ microalbuminuria

Question 241

What are some drug interactions with Elerenone?

Answer 241

* Inhibitors of P450 system: CYP3A4 * With drugs that increase K+ levels

Question 242

What are the categories of Sympatholytics (antiadrenergic drugs)?

Answer 242

1. Alpha1 blockers 2. Beta (1&2) blockers 3. Alpha/beta blockers 4. Centrally acting alpha2 agonists 5. Adrenergic neuron blockers

Question 243

How do Sympatholytics (antiadrenergic drugs) work?

Answer 243

* Cause direct blockade of adrenergic receptors --\> Suppress the influence of the sympathetic nervous system (SNS) on the heart, blood vessels, etc. * One exception, all produce reversible (competitive) blockade

Question 244

What are the two main categories of antiadrenergic drugs?

Answer 244

* Alpha-adrenergic blocking agents (α blockers) * Beta-adrenergic blocking agents (β blockers)

Question 245

What are some Alpha-blockers?

Answer 245

* Praz**osin** – for HTN (& BPH) * Teraz**osin** – for HTN (& BPH) * Doxaz**osin** – for HTN (& BPH) * Tamsul**osin** – only BPH * Alfuz**osin** - only BPH * Silod**osin** - only BPH All end in **OSIN**

Question 246

What are Alpha-blockers used for?

Answer 246

* Essential or primary hypertension * Not first line medication * Benign prostatic hyperplasia * Reduces contraction of smooth muscle in the bladder neck and prostatic capsule

Question 247

What is the MOA for Alpha-blockers?

Answer 247

Lowers blood pressure by blocking alpha1 receptors on arterioles (skin, viscera, & mucous membranes) and veins, causing vasodilation

Question 248

What are some adverse effects of Alpha-blockers?

Answer 248

* orthostatic hypotension – tell patients to take first dose at bedtime. (This is a result of the artierioles and veins being dialated --\> this reduces the BP) * **Reflex tachycardia** - reflex to increase heart rate via the ANS * Sodium retention & ↑ blood volume - usually combined with diuretic when used for hypertension * nasal congestion * inhibition of ejaculation

Question 249

What is Phenoxybenzamine and what does it do?

Answer 249

* Alpha 1 Blocker * Causes irreversible blockade used for pheochromocytoma (a tumor) * lasts several days until new receptors have been synthesized

Question 250

What are Beta-blockers used for?

Answer 250

To treat Pts w/ : * Angina * HTN * Cardiac dysrhythmias * MI * Heart failure * Hyperthyroidism * Migraine * Stage fright * Pheochromocytoma * Glaucoma All of these are due almost entirely to blocking β1 receptors

Question 251

What are the 3 generations of Beta-blockers?

Answer 251

* 1st gen: nonselective – block β1 & β2 (ex. propran**olol**) * 2nd gen: selective – block β1 (ex. metopr**olol**) * 3rd gen: * nonselective - β1&2, α1 (carvedi**lol** & labeta**lol**) * selective (β1) - nebiv**olol** **All end in "LOL"**

Question 252

What do 1st gen Beta-blockers do?

Answer 252

* They block β1 & β2, resulting in: * Reduced HR (β1) * Decreases the force of ventricular contraction (β1) * Slows impulse conduction through AV node (β1) * Suppresses secretion of renin (β1) * Bronchoconstriction - β2 blockade in the lung * Casoconstriction - β2 arteriole blockade in heart, lung, skeletal muscle * Reduces glycogenolysis (β2 blockade in skeletal muscle & liver)

Question 253

What are the adverse effects of 1st gen Beta-blockers?

Answer 253

* Bradycardia – can mask tachycardia from hypoglycemia * AV heart block * Heart failure * Rebound cardiac excitation * Bronchoconstriction * **Inhibition of glycogenolysis CNS effects – depression (rare but important**

Question 254

What are some drug interactions of Beta-blockers?

Answer 254

* Calcium channel blockers: identical efx to verapamil & diltiazem (reduction of HR, AV conduction & mycardial contractility) so combined may cause excessive cardiosuppression * Insulin

Question 255

What do 2nd gen Beta-blockers?

Answer 255

Block B1 receptors at normal doeses (B2 at high doses) resulting in: * reduced HR * decreased force of ventricular contraction * slowed impulse conduction through AV node * suppression of secretion of renin

Question 256

What are some adverse effects of 2nd gen Beta-blockers?

Answer 256

* Bradycardia – can mask tachycardia from hypoglycemia * AV heart block * Heart failure * Rebound cardiac excitation * **less CNS effects – depression (rare but important)** **no β2 bronchoconstriction or glycogenolysis unless REALLY HIGH doses**

Question 257

What do 3rd generation Beta-blockers do?

Answer 257

Blockers β1 & β2, and α1 receptors resulting in: * reduced HR (β1) * decreased force of ventricular contraction (β1) * slowed impulse conduction through AV node (β1) * suppressed secretion of renin (β1) * Bronchoconstriction (β2) * vasoconstriction (β2) * reduced glycogenolysis (β2) * dilated arterioles & veins (α1)

Question 258

What are the adverse effects of 3rd generation Beta-Blockers?

Answer 258

Same as 1st gen beta andrenergic antagonsts: * Bradycardia – can mask tachycardia from hypoglycemia * AV heart block * Heart failure * Rebound cardiac excitation * Bronchoconstriction * Inhibition of glycogenolysis * CNS effects – depression (rare but important

Question 259

Abrupt d/c of a Beta-blocker can cause what?

Answer 259

Rebound cardiac excitation

Question 260

What are some nursing interventions with Beta-Blockers?

Answer 260

* Teach pts to carry enough medication on away trips! * Teach pts s & sx of HF: * SOB, night coughs, edema of extremities * Nurse should assess for ↑ resp, ↑ BP, ↑ HR & auscultate lungs for crackles

Question 261

What are some examples of Centrally Acting Alpha2 Agonists?

Answer 261

* Clonidine: can cause rebound HTN if abruptly stopped. * Methyldopa: can cause hemolytic anemia & liver disorders

Question 262

How do Centrally Acting Alpha2 Agonists (sympatholitics) work?

Answer 262

Act within the brainstem to suppress sympathetic outflow to the heart & blood vessels thus vasodilation & reduced CO, HR, & myocardial contractility which dec BP

Question 263

What are some Adverse effects of Centrally Acting Alpha2 Agonists?

Answer 263

dry mouth sedation

Question 264

How do Adrenergic Neuron Blockers work?

Answer 264

* ganglionic blockade reduces sympathetic stimulation of the heart & blood vessels (dilation of arterioles & veins) * AE: deep depression * Drug: Reserpine

Question 265

What are some nursing interventions for Sympatholytics?

Answer 265

* ALWAYS assess HR before giving sympatholytic PO or IV * teach pts heart failure signs: SOB, night coughs, edematous extremities * Rebound cardiac excitation – teach pts to carry adequate supply of propranolol when traveling - especially dangerous for pre-existing cardiac ischemia * carefully assess for bronchoconstriction with COPD pts * teach pts that BB can mask tachy in hypoglycemia – can have s & sx w/o tachy alert - so teach other s & sx of hypoglycemia: sweating, hunger, fatigue, poor concentration

Question 266

How do Direct-Acting vasodilators do?

Answer 266

Selectivity of vasodilation efx: arterioles +/- veins * dilation of arterioles (resistance vessels) = **↓ cardiac afterload** * ​↓ cardiac work w/ ↑ CO and tissue perfusion * ​dilation of veins (capacitance vessels) = **↓ cardiac preload** * Reduce force of blood return to heart...reduces ventricular filling...decreases force of ventricular contraction = ↓ cardiac work w/ ↓ CO and tissue perfusion

Question 267

What are some examples of direct-acting vasodilators?

Answer 267

* Selective dilation of arterioles -- Hydralazine, Minoxodil * Selective dilation of veins -- Nitroglycerin * Dilate arterioles and veins -- Prazosin

Question 268

What are direct-acting vasodilators used to treat?

Answer 268

Uses: * Essential hypertension & hypertensive crisis * Angina pectoris & myocardial infarction * Heart failure * Pheochromocytoma * Peripheral vascular disease * Pulmonary arterial hypertension * Production of controlled hypotension during surgery

Question 269

What are some adverse effects of direct-acting vasodialators?

Answer 269

* Postural hypotension * Reflex tachycardia * Expansion of blood volume

Question 270

What is the MOA for hydralazine and what is it used for?

Answer 270

MOA: * Selective dilation of arterioles – acts on vascular smooth muscle (VSM) Uses: * Essential hypertension * Hypertensive crisis – drug given in small incremental doses * Heart failure – with prolonged therapy, tolerance develops

Question 271

What are the adverse effects of hydralazine?

Answer 271

* Reflex tachycardia – beating faster is burden on heart **(use of beta blocker to counteract)** * Increased blood volume – after prolonged use body tries to restore BP to pretreatment levels with Na and water retention **(use of diuretic to counteract)**

Question 272

What are the Drug interactions hydralazine?

Answer 272

* Other antihypertensive agents – avoid excessive hypotension * Combined with beta blocker to protect against reflex tachycardia and diuretics to prevent sodium and water retention and expansion of blood volume * Combined with isosorbide dinitrate (venous dilator) for HF

Question 273

What is Minoxodil used for?

Answer 273

* Selective dilation of arterioles * Used for severe hypertension * Same adverse effects of hydralazine

Question 274

What is Sodium Nitroprusside, what does it do, what is it used for, how is it administered, and how fast does it work?

Answer 274

* IS: Fastest-acting antihypertensive agent * DO: causes venous and arteriolar dilation * Used 4: hypertensive emergencies – must be monitored continuously. * Admin: It is administered via IV * **Onset: immediate** (BP returns to pretreatment level in minutes when stopped)

Question 275

What are the adverse effects of sodium nitroprusside?

Answer 275

* Excessive hypotension * \*Cyanide poisoning – rarely, but can in liver ds pts and low thiosulfate (cofactor needed for cyanide detoxification), so admin thiosulfate * Thiocyanate toxicity – after several days may accumulate so monitor CNS for efx (disorientation, psychotic behavior, delirium) and monitor for plasma thiocyante levels

Question 276

How do Calcium Channel Blockers work?

Answer 276

* Drugs that prevent calcium ions from entering cells * Also known as calcium antagonists and slow channel blockers

Question 277

What are calcium channel blockers used to treat?

Answer 277

Used to treat: 1. Hypertension 2. angina pectoris 3. cardiac dysrhythmias

Question 278

What are some types of Calcium Channel blockers?

Answer 278

Non-dihypropyridines: * Verapamil and diltiazem -- agents that act on vascular smooth muscle and the heart Dihydropyridines: * Nifedi**pine**, Nicardi**pine**, amlodi**pine**, etc-- agents that act mainly on vascular smooth muscle of the heart

Question 279

What are the effects of blocking or unblocking calcium channels in the vascular smooth muscle?

Answer 279

* When calcium channels are open = Contractile process (VSM contracts) * When calcium channels are blocked = Vasoconstriction of VSM **No significant effect on veins**

Question 280

In general what 3 areas do CCB's work on in the heart and what happens at each?

Answer 280

1. Myocardium * ↓ contractility in atrial and ventricular muscle 2. Sinoatrial (SA) node * ↓ pacemaker activity = ↓ HR 3. Atrioventricular (AV) node * ↓ contraction of the ventricles **_In the heart cardiac calcium channels are coupled to β1 receptors so CCBs and β1 blockers have SAME EFX_**

Question 281

What are Verapamil and Diltiazem (non-dihydropyridines) used to treat?

Answer 281

* Essential HTN * First-line agent on some * Angina (“angina pectoris”) -- inadequate blood going to heart * vasodilation * Cardiac dysrhymias (Atrial flutter, atrial fib, paroxysmal SVT) * slows ventricular rate by suppressing impulse conduction through AV node * IV verapamil is used, **BUT NOT Diltiazem** * **​ Blood pressure and ECG should be monitored with resuscitation equipment immediately available** * Migraine * Reduces pressure in blood

Question 282

What are the 5 Hemodynamic Effects of Verapamil and Diltiazem?

Answer 282

1. Blockade at peripheral arterioles * Reduces arterial pressure 2. Blockade at arteries and arterioles of heart * Increases coronary perfusion 3. Blockade at SA node * Reduces heart rate 4. Blockade at AV node (most important) * Decreases AV nodal conduction 5. Blockade in the myocardium * Decreases force of contraction

Question 283

What are some adverse effects of Verapamil and Diltiazem?

Answer 283

* Baroreceptor reflex * Release of NE to ↑ HR, force of contraction, & AV conduction because it has gone to low. * **Constipation** - from blockade of calcium channels in smooth muscle of the intestine * Most common complaint * ** Diltiazem has less constipation** * Dizziness * Facial flushing * **Edema of ankles and feet** * HA

Question 284

What are the drug interactions of of Verapamil and Diltiazem?

Answer 284

* Digoxin - Has opposite effects * β blockers - Will further decrease heart rate, BP, etc * Grapefruit juice

Question 285

What are some toxic effects of Verapamil and Diltiazem?

Answer 285

* Severe hypotension * Bradycardia and AV block * Ventricular tachydysrhythmias

Question 286

How does Nifedipine (a Dihydropyridine) work?

Answer 286

They cause vasodilation by blocking calcium channels in peripheral arterioles' vascular smooth muscle

Question 287

What is Nifedipine (a Dihydropyridine) used to treat?

Answer 287

* Essential hypertension * Angina * **Cannot be used to treat dysrhythmias** **_fast-acting formulation: efx begin almost immediately_**

Question 288

What are some effects of Nifedipine (a Dihydropyridine)?

Answer 288

* Lowers blood pressure * by dialating vascular smooth muscle in peripheral arterioles

Question 289

What are some adverse effects of Nifedipine (a Dihydropyridine)?

Answer 289

* Flushing * Dizziness * Peripheral edema * Very little constipation * due to slight blocking for Ca++ channels in intestines * **Baroreflex**

Question 290

How are all Dihydropyridine's identified?

Answer 290

They all end in "**i****pine**" Nicard**ipine**, amlod**ipine**, israd**ipine**, felod**ipine, etc**

Question 291

african american's with hypertension should be treated with what types of medications?

Answer 291

* diuretics (thiazide first line) * CCB’s & * α/β blockers work best

Question 292

White people with hypertension with what types of medications?

Answer 292

β blockers or ACEIs

Question 293

What is the DOC for Hypertensive Emergencies (diastolic above 120)?

Answer 293

Sodium nitroprusside

Question 294

What are the effects of Sodium nitroprusside?

Answer 294

* dilates arterioles & veins * **immediate efx – continuous IV infusion** * don’t infuse longer than 72 hr. - ↑ risk of toxicity

Question 295

What hypertensive drugs are contraindicated during pregnancy?

Answer 295

ACE inhibitors, ARBs, and DRIs

Question 296

What is the hypertensive DOC during pregnancy?

Answer 296

Methyldopa, and it is used only during pregnancy as a maintenance medication

Question 297

What happens during Heart Failure?

Answer 297

* ↓ CO * insufficient tissue perfusion (fatigue, SOB, exercise intolerance) * signs of fluid retention (peripheral edema & SOB, venous distention) **HEART FAILURE IS A CARDIAC OUTPUT PROBLEM -- Everything goes wrong because of this**

Question 298

What are the major underlying causes of Heart failure?

Answer 298

* **Chronic hypertension** * The increase in pressure on the heart causes it to not pump normally * **Myocardial infarction** * Valvular heart disease * Coronary artery disease * Congenital heart disease * Dysrhythmias * Aging of the myocardium

Question 299

What leads to cardiac remodeling?

Answer 299

* Dilated ventricles * Hypertrophy of heart * increase in heart wall thickness * Heart becomes more spherical (less cylindrical) * Results in ↓ Cardiac output

Question 300

What are the signs and symptoms of heart failure?

Answer 300

* Reduced exercise tolerance - because of ↓ Tissue perfusion * Fatigue - because of ↓ Tissue perfusion * SOB (also from pulm edema) - because of ↓ Tissue perfusion * Tachycardia – from ↑ SNS tone * Cardiomegaly (↑ heart size) – from ↑ vent filling, ↓ systolic ejection, myocardial hypertrophy * Pulm edema - ↑ venous tone & blood volume * Peripheral edema - ↑ venous tone & blood volume * Hepatomegaly - ↑ venous tone & blood volume * Distention of jugular veins - ↑ venous tone & blood volume

Question 301

What are some drugs used for heart failure?

Answer 301

* **Diuretics** * RAAS inhibitors * **ACE inhibitors** * **Angiotensin II receptor blockers** * Aldosterone antagonists * Direct renin inhibitors * **Beta blockers** * Digoxin and other cardiac glycosides

Question 302

What are the first line agents to treat volume overload in the heart?

Answer 302

Diuretics: * Potassium-sparing diuretics * Thiazide diuretics * High-ceiling (loop) diuretics

Question 303

How do ACE inhibitors help pts w/ Heart failure?

Answer 303

They prolong life so they are expected to be used with **all HF pts**

Question 304

What does Dopamine activate and what does the activation cause?

Answer 304

Activates Beta 1 receptors in the heart, kidney, and blood vessels: * ↑ heart contractility * ↑ HR -- risk of tachycardia * Dilates renal blood vessels – increases renal blood flow & urine output Activates Alpha 1 receptors **(In high doses)**: * constricts arterioles & veins – increases vascular resistance (afterload) - ↓ CO

Question 305

What does Dobutamine activate and what does the activation cause?

Answer 305

Activates Beta 1 receptors in the heart, kidney, and blood vessels: * ↑ heart contractility * ↑ HR -- risk of tachycardia * Dilates renal blood vessels – increases renal blood flow & urine output. preferred to dopamine

Question 306

What are the effects of Digoxin?

Answer 306

* Increases myocardial contractility = ↑ CO * Increased cardiac output * reduce HF symptoms * increase exercise intolerance * decrease hospitalizations * Decreased sympathetic tone * Increased urine production * Decreased renin release --\> ↓ aldosterone --\> ↓ angiotensin II: **Potassium levels must be kept in normal physiologic range** * **If K+ are too low, digoxin can be toxic** * **if K+ levels are too high digoxin won't work as well**

Question 307

What are the adverse effects of digoxin?

Answer 307

* **Can cause severe dysrhythmias** * ​most common: AV block with escape beats * most dangerous: v flutter & v fib * Anorexia, nausea, vomiting (GI) * Fatigue (CNS) * Visual disturbances: blurred vision, yellow tinge to vision, halos around objects * Does NOT prolong life * May shorten life in women - ↑ mortality

Question 308

Describe the↓ sympathetic tone when taking Digoxin and its effects

Answer 308

Since digoxin ↑ ↑ contractile force & CO of the heart, arterial pressure is increased leading to a ↓ sympathetic tone = ↓ baroreceptor reflex, which leads to: * ↓ HR (allows more complete vent filling) * afterload is reduced (b/c of ↓ arteriolar constriction) so more complete emptying * venous pressure is reduced (b/c of ↓ venous constriction) thus reducing cardiac distention, pulmonary congestion & peripheral edema.

Question 309

Describe the effects of ↑ urine production due to dijoxin?

Answer 309

1. ↑ urine production due to dijoxin causes ↑ CO 2. This causes ↑ renal blood flow 3. which reduces blood vol 4. which reduces cardiac distention, pulm cong, & peripheral edema

Question 310

Why is there a ↓ renin release when taking digoxin?

Answer 310

* Because digoin ↑ arterial pressure (from ↑ urine production, ↑ contractile force & CO), renin release declines causing aldosterone & angiotensin II to decline also

Question 311

What occurs when there is a ↓ in aldosterone?

Answer 311

Reduces retention of Na+ & H2O which reduces blood vol, which reduces venous pressure

Question 312

What occurs when there is a ↓ in angiotensin II?

Answer 312

↓ vasoconstriction reducing afterload & venous pressure

Question 313

What can cause Digoxin related dysrhythmias?

Answer 313

* Hypokalemia (from diuretics...also v/d) * elevated digoxin level = too much cardiac suppression * Heart disease may cause extra issues with dysrhythmias

Question 314

How do you manage digoxin-induced dysrhythmias?

Answer 314

* Withdraw digon and /or K+ wasting diuretics * Low serum K+ - admin K+ * Antidysrhythmic drugs (phenytoin & lidocaine) * brady or AV block – atropine (blocks vagal influence) or use pacing

Question 315

What are some drug interactions with Digoxin?

Answer 315

* Diuretics - because they cause **K+ loss**, monitor K+ levels * ACEIs and ARBs - Because these **increase K+ levels** * Dopamine & Dobutamine - ↑ in HR may ↑ risk of tachydysrythmia * Quinidine – displaces dig & reduces renal excretion of dig...so can promote dig toxicity * Verapamil (CCB)– causes ↑ levels of dig & suppresses cardiac contractility

Question 316

What are the Pharmacokinetics of Digoxin?

Answer 316

* Taken with meals decreases absorption * Narrow Theraputic range: 0.5-0.8 ng/mL * Distributed widely and crosses the placenta

Question 317

What are some nursing implications for Digoxin?

Answer 317

* When administering orally: **OBTAIN HR & RHYTHM BEFORE ADMIN (check apical HR x 1 minute)** * IF \< 60 bpm or Δ in rhythm – withhold dig & notify HCP * When administering via IV: **monitor cardiac status closely for 1-2 hrs after IV injection** * assess for orthhopnea, dyspnea, JVD, edema, rales, sleep, participation in activities * withhold dig if significant Δ in HR or rhythm * assess for N&V, anorexia, fatigue, visual disturbances (blurred or yellow vision) * monitor K+

Question 318

What are some characteristics of stage A heart failure?

Answer 318

* No symptoms of HF * No structural or functional cardiac abnormalities * Pt. may have Hypertension, CAD, diabetes, family history of cardiomyopathy, personal history of alcohol abuse, rheumatic fever, or treatment with a cardiotoxic drug (eg, doxorubicin, trastuzumab) * Management directed at reducing risk: smoking, ETOH

Question 319

What are some characteristics of stage B heart failure?

Answer 319

* No signs and symptoms of HF * Goal of is to prevent development of symptomatic HF

Question 320

What are the treatment options for Stage B heart failure?

Answer 320

ACE inhibitor or and ARB are DOC for HF. Will stop remodoling process **a beta blocker will be added for people with reduced injection fraction**

Question 321

What are some characteristics of stage C heart failure?

Answer 321

* Symptoms of HF * Structural heart disease. * They might start having some edema * Four major goals: 1. Relieve pulmonary and peripheral congestive symptoms 2. Improve functional capacity and quality of life 3. Slow cardiac remodeling and progression of LV dysfunction 4. Prolong life

Question 322

What are the treatment options for Stage C heart failure?

Answer 322

First line therapy: * Diuretics * ACEI/ARBs * Beta blockers * Aldosterone antagonists * Digoxin Other: * Device therapy * Implanted cardioverter-defibrillators (ICDs) * Cardiac resynchronization – biventricular pacemaker * Exercise training – for stable pts

Question 323

What are some drugs to avoid in the treatment of stage C heart failure?

Answer 323

* Antidysrhythmic agents – cardiosuppressant & prodysrthythmic * Because these can cause arythmias * Calcium channel blockers * NSAIDs – Na+ retention & peripheral vasoconstriction

Question 324

What are some characteristics of stage D heart failure?

Answer 324

* Marked symptoms of HF * Advanced structural heart disease * Repeated hospitalizations

Question 325

What are the treatment options for stage D heart failure?

Answer 325

* Best solution is a heart transplant * LV mechanical assist device (LVAD) used until heart is available * Management ÐControl of fluid retention ×Loop diuretic, thiazide diuretic ×Dopamine, dobutamine ÐBeta blockers pose high risk for worsening HF

Question 326

What are the two types of dysrhythmias?

Answer 326

* Supraventricular dysrhythmias * Ventricular dysrhythmias

Question 327

What are the two fundamental causes of dysrhythmias?

Answer 327

* Disturbances of automaticity * produce tachycardia (\> 100 bpm) * bradycardia (\< 60 bpm) * normal (60-100 bpm) * Disturbances of conduction * Degrees of AV block: 1. first degree – impulse delayed 2. second degree – some impulses pass through 3. third degree – no impulses pass through

Question 328

What are the different classifications of Antidysrhythmic Drugs?

Answer 328

* Class I - sodium channel blockers * Class II - beta blockers * Class III - potassium channel blockers * Class IV - calcium channel blockers * adenosine & digoxin

Question 329

In general how do class I Antidysrhythmic Drugs work?

Answer 329

sodium channel blockers slow impulse conduction in all 3 electrical areas (atria, ventricles, & His-Purkinje system) of the heart.

Question 330

In general how do class II Antidysrhythmic Drugs work?

Answer 330

Beta blockers work on two different areas of the heart: 1. SA node - reduce automaticity 2. AV node – slow conduction; in both atria & ventricles they reduce contractility

Question 331

In general how do class III Antidysrhythmic Drugs work?

Answer 331

Potassium channel blockers delay repolarization in the heart; this prolongs both the action potential duration and the effective refractory period

Question 332

In general how do class IV Antidysrhythmic Drugs work?

Answer 332

calcium channel blockers (verapamil & diltiazem) are only antidysrhythmics -- they work the same as BBs

Question 333

In general how do adenosine & digoxin work?

Answer 333

suppress dysrhythmias by ↓ conduction through AV node & ↓ automaticity in SA node

Question 334

What are some characteristics of Supraventricular dysrhythmias?

Answer 334

* generally less harmful (dysrhythmic activity in atria usually doesn’t reduce CO) * Impulse arises above the ventricle – in atria, SA node, AV node * **Atrial fibrillation – (**HR up to 600 bpm); clot formation 5X greater risk of stroke than someone without. * Tx w/ long-term oral anticoags or radiofrequency (RF) ablation * **Atrial flutter –** (HR 250-350 bpm) – risk of stroke * Long-term: tx w/ cardioversion, RF ablation or control ventricular rate w/ drugs

Question 335

What are some characteristics of Ventricular dysrhythmias?

Answer 335

* can cause significant disruption of cardiac pumping = more dangerous * cardioversion usually 1st tx * Sustained ventricular tachycardia * tx: cardiovert 1st, then drugs or implantable cardioverter-defibrillator (ICD) * Ventricular fibrillation – then drugs or ICD * Ventricular premature beats - tx: Beta blockers * Digoxin-induced ventricular dysrhythmias – can mimic everything * tx: Treatment is lidocaine and phenytoin * Torsades de pointes – from prolongation of QT interval from Clas IA and class III antidysrhythmia durgs * tx: IV magnesium cardiocnversion

Question 336

What are the different types of Class I Antidysrhythmic Drugs (sodium channel blockers?)

Answer 336

* Class IA agents - delay repolarization * Class IB agents - accelerate repolarization * Class IC agents - pronounced prodysrhythmic actions

Question 337

What are some examples of Class IA Sodium Channel Blockers?

Answer 337

Quinidine, Procainamide, Disopyramide

Question 338

What is the MOA of Quinidine?

Answer 338

* Slows impulse conduction in the atria, vent, His-Purkinje system & delays repolarization * Strong anticholinergic * **ECG:** widens the QRS complex (by slowing depolarization of the vent), & prolongs the QT interval (by delaying vent repolarization)

Question 339

What is Quinidine used for?

Answer 339

* Used for supraventricular & vent dysrhythmias * Give w/ digoxin, verapamil, beta blocker with quinidine to ↓ vent rate

Question 340

What are the adverse effects of quinidine?

Answer 340

Diarrhea, cinchonism **(tinnitus, HA, nausea, vertigo, blurred vision),** Cardiotoxicity, Arterial embolism (thrombi in the atria), hypotension

Question 341

What are some examples of Class IB Sodium Channel Blockers and the MOA for these kinds of drugs?

Answer 341

Lidocaine, Mexiletine, Phenytoin **All these drugs Accelerate repolarization & little effect on ECG**

Question 342

What are the effects of Lidocaine?

Answer 342

1. Slows conduction in the atria, vent & His-Purkinje system 2. Reduces automaticity in vent & His-Purkinje 3. Accelerates repolarization (shortens axn potential)

Question 343

What some nursing considerations of lidocaine?

Answer 343

* IV, used ONLY for vent dysrhythmias NOT used for supraventricular dysrhythmias * **Whenever lidocaine is used equipment for resuscitation must be available**

Question 344

What are the adverse effects of lidocaine?

Answer 344

* CNS (paresthesias, drowsiness) * Convulsions * resp arrest

Question 345

What are some examples of Class IC Sodium Channel Blockers and the MOA for these kinds of drugs?

Answer 345

Flecainide, Propafenon, Moricizine **Reduce conduction velocity in the atria, vent & His-Purkinje system. Also, delay vent repolarization, causing small ↑ in refractory period**

Question 346

What are Flecainide &Propafenone used for?

Answer 346

Maintenance tx of supraventricular dysrhythmias

Question 347

What is Moricizine used for?

Answer 347

**Life-threatening** ventricular dysrhythmias

Question 348

What are some examples of Class II Antidysrhythmic Drugs (Beta Blockers)?

Answer 348

**Non-Selective:** * Propranolol * Acebutolol **Selective:** * Esmolol (IV) * Sotalol (selective beta 1 & also blocks K+ channels)

Question 349

What are the effects of Beta Blockers on the heart?

Answer 349

1. ↓ automaticity of the SA node 2. ↓ velocity of conduction through the AV node which prolongs PR interval 3. ↓ myocardial contractility

Question 350

What are Beta Blockers used for?

Answer 350

* Dysrhythmias caused by excessive sympathetic stimulation. * Control of vent rate in pts with supravent tachydysrhythmias

Question 351

What are some examples of Class III Antidysrhythmic Drugs (K+ Channel Blockers)?

Answer 351

* Amiodarone * Bretyllium (IV) * Ibutilide (IV) * Dofetilide * Sotalol (IV) **A BIDs**

Question 352

What is the MOA for K+ Channel Blockers?

Answer 352

All delay repolarization of fast axn potentials thus prolong potential duration & prolong QT interval

Question 353

What type of drug is Amiodarone, and what are some drug interactions with this drug?

Answer 353

1. K+ Channel Blockers 2. Interacts with** **P450 – CYP3A4 causing: * ↑ the levels of quinidine, procainamide, phenytoin, digoxin, diltiazem, warfarin, cyclosporine, lovastatin, simvastatin, atorvastatin * Lvls of Amiodarone are ↑ by drinking grapefruit juice * Lvls of Amiodarone are ↓ by cholestyramine, St. John’s wort, rifampin Combo with diuretics can cause severe dysrhythmia Combo with beta blocker, verapamil or diltiazem can lead to excessive slowing of HR

Question 354

What class of Antidysrhythmic Drug is **Sotalol**, and what is it used for?

Answer 354

1. Class III: K+ Channel Blockers 2. **Used for life-threatening ventricular dysrythmias**

Question 355

What type of durg is Bretylium, what is it used for, and what are some adverse effects of this drug?

Answer 355

1. Class III: K+ Channel Blockers 2. Used ONLY for short-term tx of severe vent dysrhythmias **-- Given IV** 3. Profound hypotension (very common so monitor)

Question 356

What type of durg is amiodarone, what is it used for, and what are some adverse effects of this drug?

Answer 356

1. Class III: K+ Channel Blockers 2. **Used ONLY for life-threatening vent dysrythmias but now can be used also for atrial dysrhythmias** 3. Pulmonary (lung damage), Cardiotoxicity, **Avoid during pregnancy** & breast feeding for several months, optic neuropathy, blue-gray discoloration of skin

Question 357

What are some examples of Class IV Antidysrhythmic Drugs (Ca++ Channel Blockers)?

Answer 357

Verapamil & Diltiazem are the o nly 2 CCBs able to block Ca+ channels in heart

Question 358

\What is the MOA for Ca++ Channel Blockers?

Answer 358

1. Slow SA node automaticity 2. Delay AV node conduction 3. Reduction of myocardial contractility * All 3 are identical to efx of BBs b/c BBs also promote Ca+ channel closure in heart

Question 359

What are Verapamil & Diltiazem used for?

Answer 359

Control vent rate in pts with supravent tachydysrhythmias

Question 360

What are the adverse effects of Verapamil & Diltiazem?

Answer 360

* **Bradycardia, AV block, HF**, hypotension, peripheral edema, constipation * Drug interactions: elevate digoxin levels; don’t combine w/ beta blockers b/c of ↑ bradycardia

Question 361

What is Adenosine** **used for?

Answer 361

* Decreases automaticity in the SA node * Slows conduction through the AV node * Prolongation of PR interval * **DOC for termination of paroxysmal SVT**

Question 362

What are the two stages of hemostasis?

Answer 362

Stage 1: formation of platelet plug Stage 2: coagulation

Question 363

Describe the formation of a platelet plug?

Answer 363

Platelet plug forms when platelets come in contact with damaged blood vessel collagen - platelets are activated & form bridges via glycoprotein IIb/IIIa receptors & also upon activation by thromboxane A2 (TXA2), thrombin, collagen, platelet activation factor (PAF) & ADP - binds to fibrinogen & forms platelet plug

Question 364

Describe coagulation?

Answer 364

* The plug must then be reinforced with fibrin that is formed from a cascade of events from both the intrinsic & extrinsic coagulation pathways. * Some coagulation factors (VII, IX & X) * **require vitamin K** for their synthesis

Question 365

What is an Arterial thrombosis?

Answer 365

Adhesion of platelets to the arterial wall due to rupture or atherosclerotic plaque. Platelets then release ADP or TXA2 converging additional platelets. The plug is then reinforced with fibrin (localized clot)

Question 366

What is an Venous thrombosis?

Answer 366

A clot that develops where blood is slow. Same cascade of events as with arterial thrombus but in the veins the tail of the thrombus breaks off (embolus) & travels the vascular system until it gets lodged in a secondary site.

Question 367

What are the 3 major groups of drugs used for thromboembolic Disorders?

Answer 367

1. Antiplatelet drugs (ASA, ADP blockers, etc.) * inhibit platelet aggregation. * Prevents arterial thrombosis 2. Anticoagulants (warfarin, heparins, direct thrombin inhibitors, etc.) * suppress production of fibrin. * Most effective against venous thrombosis 3. Thrombolytic drugs (alteplase, streptokinase, etc.) * promote lysis of fibrin

Question 368

What are the 3 groups of Antiplatelet Drugs?

Answer 368

1. Aspirin 2. ADP receptor antagonists 3. GP IIb/IIIa receptor antagonists

Question 369

What is the MOA of Aspirin?

Answer 369

* causes **IRREVERSIBLE** inhibition of cycloxygenase (COX) which is needed to synthesize thromboxane A2 (TXA2) so the effect of aspirin lasts for the life of the platelet (7-10 d) * TXA2 promotes platelet aggregation & vasoconstriction (promoting hemostasis) – so blocking it reduces risk of thrombosis with vaso-relaxation * inhibits synthesis of prostacyclin by blood vessel wall (prostacyclin suppresses platelet aggregation) * •if keep dose low (325/d or less) can minimize prostacyclin inhibition while maintaining inhibition of TXA2

Question 370

What is asprin used for?

Answer 370

Prevention of MI, TIA, stroke, chronic stable & unstable angina, coronary stenting, previous MI, primary prevention of MI ## Footnote **Dose: chronic therapy - 81 mg/d; acute event – 325 mg/d**

Question 371

What are some examples of Adenosine Diphosphate (ADP) Receptor Antagonists?

Answer 371

* Clopidogrel * prasugrel * ticlopidine * ticagrelor

Question 372

What is the MOA of ADP Receptor Antagonists?

Answer 372

Causes **IRREVERSIBLE ** (except ticagrelor) blockade of ADP receptors on the platelet surface thereby preventing aggregation

Question 373

What are some uses of ADP Receptor Antagonists?

Answer 373

Both are used for stroke & only clopidogrel is used for MI

Question 374

What are some adverse effects of ADP Receptor Antagonists?

Answer 374

* Potential fatal hematologic effects; * risk is much higher with **ticlopidine**: neutropenia/agranulocytosis, thrombotic thrombocytopenic pupura

Question 375

What are some examples of Glycoprotein IIb/IIIa Receptor Antagonists? (aka Super asprins)

Answer 375

* Abciximab * Tirofiban * Eptifibatide

Question 376

What are some nursing implications of Glycoprotein IIb/IIIa Receptor Antagonists?

Answer 376

* Most effective antiplatelet drugs on the market * Administered IV in combo usually with aspirin or heparin * VERY EXPENSIVE

Question 377

What is the MOA of Glycoprotein IIb/IIIa Receptor Antagonists and what are some AE?

Answer 377

**_REVERSIBLE_** blockade of platelet GP IIb/IIIa rec which inhibits final step in aggregation by all factors AE = bleeding

Question 378

What are Glycoprotein IIb/IIIa Receptor Antagonists used for?

Answer 378

Short term to prevent ischemic events in pts with acute coronary syndromes & those undergoing percutaneous coronary intervention

Question 379

What are some examples of Anticoagulant drugs?

Answer 379

* Heparins & fondaparinux * Warfarin * Direct thrombin inhibitors * dabigatran etexilate * hirudin analogs * argatroban * Direct factor Xa inhibitor (Rivaroxaban) * Antithrombin

Question 380

What is the MOA of Anticoagulant drugs?

Answer 380

* Reduce the formation of fibrin * Two mechanisms of action: * Inhibit the synthesis of clotting factors - warfarin * Inhibit the activity of clotting factors – all the rest

Question 381

What are the 3 different types of heparins?

Answer 381

1. (unfractionated) heparin 2. low-molecular-weight (LMW) heparins 3. fondaparinux

Question 382

What are some nursing considerations of (Unfractionated) Heparin?

Answer 382

* Made from the lungs of cattle & intestines of pigs (may have antigens – allergy) * Only given •IV, SQ -- **NO PO** * Monitor dose closely so that aPTT does not exceed 2 times the control value; **aPTT should be 60-80 secs** (normal 40 secs) * Avoid antiplatelet drugs (aspirin, NSAID’s)

Question 383

What would you give for an overdose of (Unfractionated) Heparin?

Answer 383

* Use protamine sulfate – by slow IV injection (20 mg/min or 50 mg/10 mins); 1 mg neutralizes 100 units of heparin * IV effects are immediate & last for 2 hours

Question 384

What is (Unfractionated) Heparin used for?

Answer 384

* Prophylaxis of venous thrombosis (acts immediately) * pulmonary embolism * evolving stroke * massive deep vein thrombosis (DVT) * open heart surgery * pregnancy * acute MI

Question 385

What are the adverse effects of (Unfractionated) Heparin?

Answer 385

* Hemorrhage: can be fatal * Blood loss (reduced blood pressure, ↑ HR, bruising, red/black tarry stools, cloudy or discolored urine, pelvic pain * **Heparin-induced Thrombocytopenia (HIT): reduced platelet count** * Hypersensitivity reactions – animal antigens (give small test dose before running heparin)

Question 386

What are some examples of Low-Molecular Weight (LMW) Heparin?

Answer 386

* Enoxa**parin** * Dalte**parin** * Tinza**parin**

Question 387

What are some nursing implications of Low-Molecular Weight (LMW) Heparin?

Answer 387

* As effective as heparin (higher bioavailability) * Given sub Q * can be given at a fixed dose – plasma levels predictable * does not require aPTT monitoring - given at home (qd or bid) * based on body weight * less likely to cause thrombocytopenia * **Costs more than heparin** * **1st line tx in Deep Venous Thrombosis**

Question 388

What would you give for an Low-Molecular Weight (LMW) Heparin overdose?

Answer 388

protamine sulfate

Question 389

What are some adverse effects of Low-Molecular Weight (LMW) Heparin?

Answer 389

* Bleeding (but less than with unfractionated heparin) * HIT (10x less than heparin)

Question 390

What are some characteristics of Fondaparinux?

Answer 390

* An Anticoagulant drugs that only inhibits factor Xa – reduces thrombin * no effect on platelets * Administered Sub Q * **Can’t reverse with protamine sulfate**

Question 391

What is the MOA of Warfarin?

Answer 391

* Antagonist of vitamin K (needed for factors VII, IX, X & prothrombin) * **Anti-clotting action delayed b/c it has no effect on clotting factors already in circulation**

Question 392

What are some nursing considerations of Warfarin?

Answer 392

* Initial response 8-12 h & several days for peak * **INR range should be kept between 2 - 4.5** * If using warfarin with heparin, monitor levels (blood draw) **no sooner than 5 h after IV or no sooner than 24 h after SQ inj**

Question 393

What is Warfarin used for?

Answer 393

Prevention of venous thrombosis & PE * & in pts with prosthetic heart valves * ** during atrial fibrillation**

Question 394

What is the treatment for a Warfarin overdose?

Answer 394

* Tx with **vitamin K1** (phytonadione) PO, IV (avoid SQ), infuse slowly * If vit K1 does not work, use whole blood or fresh-frozen plasma * food w/ Vit K can reduce efx: mayonnaise, canola oil, soybean oil, green leafy veggies – keep intake of these constant when testing

Question 395

What are the adverse effects of Warfarin?

Answer 395

* Hemorrhage * Category X (if need anticoag during pregnancy give heparin) * Do not use during breast feeding

Question 396

What are the drug interactions with Warfarin?

Answer 396

* Drugs that promote bleeding * Drugs that ↑ anticoag effects * Drugs that ↓ anticoag effects

Question 397

What are some drugs that promote bleeding when taking warfarin?

Answer 397

* Heparin * Asprin * Acetaminophen * non-ASA (clopidogrel, dypyridamole, ticlopidine, abciximab)

Question 398

What are some Drugs that ↑ anticoag effectswhen taking warfarin?

Answer 398

* miconazole (oral & intravaginal) * cimetidine * disulfiram (anti-ETOH drug) * **sulfonamides**

Question 399

What are some Drugs that ↓ anticoag effects when taking warfarin?

Answer 399

* Vit K (and in food) * phenobarbital * carbamazepine * rifampin

Question 400

What are some contraindications with Warfarin?

Answer 400

* Vit K deficiency * liver ds * alcoholism