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N3540 Pharmacology > Exam 3 - Content Material > Flashcards

Exam 3 - Content Material Flashcards

1
Q

What is Lipohypertrophy?

A

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.

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2
Q

What does the Adrenal medulla secrete?

A

Secretes catecholamines (epi, NE)

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3
Q

What does the adrenal cortex secrete?

A

Secretes corticosteroids (glucocorticoids & mineralocorticoids)

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4
Q

What is the Zona reticularis?

A

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

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5
Q

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

A

Negative feedback

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6
Q

What classes of hormones does the adrenal cortex secrete?

A
  1. glucocorticoids
  2. mineralocorticoids
  3. adrenal androgens.
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7
Q

What factors cause the hypothalamus to release CRH?

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

NOTE THESE ARE ALL STRESS FACTORS

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8
Q

What effect does ACTH have on the adrenal cortex?

A

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

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9
Q

What should you consider when administering oral glucocorticoids?

A
  • —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
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10
Q

What are the symptoms of glucocorticoid withdraw?

A
  • Hypotension
  • hypoglycemia
  • myalgia
  • arthralgia
  • fatigue
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11
Q

What are some examples of glucocorticoid durgs?

A
  • cortisone
  • prednisone
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12
Q

What are some effects of glucocorticoids in general?

A
  • —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
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13
Q

What are some adverse reactions with high dose Glucocorticoids?

A
  • 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
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14
Q

What are low dose glucocorticoids used for?

A
  • Used to tx adrenocortical insufficiency
  • no toxic effects at physiologic doses
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15
Q

What are the effects of high dose glucocorticoids?

A
  • Used to tx nonendocrine disorders
  • Has high anti-inflammatory and immunosuppressive actions:
    • allergic rxns, asthma, inflammation, suppress immune response in organ transplant recipients & cancer
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16
Q

—Glucocorticoids increase blood glucose concentrations by what 5 methods?

A
  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
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17
Q

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

A
  • Main function
    • to suppress immune system and inflammation
  • Action:
    • —inhibiting chemical mediators such as prostaglandins, histamine , leukotrienes, lymphocytes, phagocytic cells, neutrophils & macrophage
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18
Q

What are the differences between —Glucocorticoids & NSAIDs?

A

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.
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19
Q

What are some short acting Glucocorticoids?

A
  • Cortisone
  • Hydrocortisone

8-12 min half life

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20
Q

What are some intermediate acting Glucocorticoids?

A
  • Prednisone
  • Prednisolone
  • Methylprednisolone
  • Triamcinoclone

18-36min half life

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21
Q

What are some long acting Glucocorticoids?

A
  • Bethmethasone
  • Deamethasone

36-54min half life

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22
Q

What are some uses for Glucocorticoids?

A
  • 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
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23
Q

How do high dose glucocorticoids cause Osteoporosis?

A
  • By inhibiting Ca++ absorption
  • Dec bone formation of osteoblast & accelerate the bone resorption of osteoclasts.
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24
Q

How do you prevent osteoporosis when giving high dose glucocorticoids?

A
  • 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)
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25
Q

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

A
  • 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
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26
Q

What is ketoacidosis?

A

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

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27
Q

What are the symptoms of Ketoacidosis?

A

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

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28
Q

What is —Cushing syndrome?

A

—adrenal hormone excess

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29
Q

What is addison’s disease?

A

Adrenal hormone deficiency

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30
Q

How would high doses of Glucocorticoids cause peptic ulcers?

A

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

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31
Q

What are the effects of Glucocorticoids on pregnant women?

A
  • —Crosses placenta (cleft palate, spontaneous abortion & low birth weight)
  • —Lactation – enter breast milk (doses > 5 mg/day prednisone) cause growth retardation
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32
Q

What are some drug interactions with Gluccocorticoids?

A
  • —Digoxin, thiazide & loop diuretics—
  • NSAID’s
  • —Insulin & oral hypoglycemics (may need insulin & hypoglycemic agents.—
  • Vaccines
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33
Q

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

A
  • 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.
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34
Q

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

A
  • 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
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35
Q

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

A
  • 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
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36
Q

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

A
  • —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
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37
Q

How are Glucocorticoids administered?

A
  • —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
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38
Q

What are tye metabolic effects of the glucocorticoids?

A

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

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39
Q

How are aldosterone levels controled?

A
  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
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40
Q

What does aldosterone do?

A
  • 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
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41
Q

Where are Mineralocorticoids produced?

A

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

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42
Q

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

A
  • Mineral corticosteroid
  • Has both high minealocorticoid and glucocotricoid activity
  • —Used for adrenocortical insufficiency (Addison dz)—and for tx of salt-losing adrenogenital syndrome
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43
Q

What are the pharmacokinetics of Fludrocortisone?

A
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44
Q

What is the MOA of fludrocortidone?

A
  • —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
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45
Q

What are some contraindications for mineralcorticoids?

A
  • —Systemic fungal infection—
  • Conditions not requiring mineralocorticoid activity
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46
Q

What are some adverse effects of Mineralcorticoids?

A
  • 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
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47
Q

What are some complications of Diabetes?

A
  • —HTN,
  • heart disease,
  • renal failure,
  • blindness,
  • neuropathy,
  • amputations,
  • impotence
  • stroke
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48
Q

When does Type I diabetes usually develop?

A
  • —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)
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49
Q

When does Type II diabetes usually develop?

A
  • —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
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50
Q

What are some characteristics of type I diabetes?

A
  • 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
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51
Q

What are some characteristics of type II diabetes?

A

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

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52
Q

What are some complications of Diabetes?

A
  • —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
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53
Q

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

A
  • ACEIs
  • ARBs
  • CCBs
  • low-dose diuretics
  • Insulin
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54
Q

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

A
  • —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
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55
Q

How is diabetes diagnosed?

A
  • —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%
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56
Q

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

A
  • Type I and Type II Diabtetes patients
  • This should be done before meals & hs.
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57
Q

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

A
  • systolic < 140 mm Hg
  • diastolic < 90 mm Hg
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58
Q

How would you prevent complications with type I diabetes?

A
  • —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.
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59
Q

How would you prevent complications with type II diabetes?

A
  • —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
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60
Q

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

A

Metformin

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

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61
Q

What is Hemoglobin A1c?

A

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

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62
Q

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

A

HbA1c < 7%

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63
Q

Where is insulin synthesized and how is it secreted?

A
  • 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
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64
Q

What does insulin do?

A
  • —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
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65
Q

Insulin deficiency promotes hyperglycemia by what 3 ways?

A
  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)
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66
Q

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

A

—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

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67
Q

Severe insulin deficiency is manifested by?

A
  • —hyperglycemia
  • production of ketoacids
  • hemoconcentration
  • acidosis & coma
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68
Q

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

A
  • Pre-filled syringes store in vertical position in refrigerator.
  • Stable x1 week-max 2 wks
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69
Q

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

A
  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)
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70
Q

What are some Rapid acting/Short duration insulins?

A
  • —lispro (Humalog)
  • aspart (NovoLog)
  • glulisine (Apidra)
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71
Q

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

A
  • —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
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72
Q

What are some adverse effects of insulin?

A
  • —Hypoglycemia
  • edema
  • weight gain
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73
Q

What are some Slower acting/Short duration insulins?

A
  • Humulin R (regular human insulin)
  • Novolin R
  • Exubera
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74
Q

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

A
  • 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
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75
Q

What are some Intermediate duration insulins (NPH insulins)?

A
  • Humulin N
  • Novolin N
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76
Q

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

A
  • —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.
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77
Q

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

A
  • —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
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78
Q

What are some long duration insulins?

A

—Insulin Glargine (Lantus)

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79
Q

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

A
  • —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.
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80
Q

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

A

NPH insulins (Humulin N & Novolin N)

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81
Q

What are the SQ injection sights for insulin?

A
  • —upper arm, thigh (slowest) & abdomen(fastest)
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82
Q

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

A
  • —ONLY Regular insulin can be given IV.
  • Usually given for ketoacidosis or hyperkalemia
  • —Insulin is given to ALL pts. that have type I
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83
Q

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

A
  • —During infection
  • stress obesity
  • the adolescent growth spurt
  • pregnancy (after 1st trimester)
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84
Q

What drugs lower blood glucose when combined with insulin?

A
  • —sulfonylureas
  • meglitinides
  • beta blockers
  • alcohol
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85
Q

What drugs counteract the actions of insulin & produce hyperglycemia?

A
  • thiazide diuretics
  • glucocorticoids
  • sympathomimetics
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86
Q

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

A
  • Beta blockers
  • —(tachycardia, palpitations) & also cause further hypoglycemia by blocking glycogenolysis.
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87
Q

What causes hypoglycemia?

A
  • insulin overdose
  • reduced intake of food
  • vomiting/diarrhea
  • excess alcohol
  • unaccustomed exercise
  • childbirth
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88
Q

Hypoglycemia is defined by what blood glucose level?

A

< 50 mg/dl

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89
Q

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

A
  • —activation of the sympathetic nervous system leading to –>
  • tachycardia, palpitations, sweating, nervousness
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90
Q

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

A

—HA, confusion, drowsiness & fatigue

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91
Q

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

A
  • —Take fast acting sugar
  • glucose tablets, OJ, sugar cubes, honey, corn syrup, non diet soda
  • —If pt has severe hypoglycemia IV glucose is preferred
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92
Q

What produces glucagon and what are it’s effects?

A
  • —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.
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93
Q

How can glucagon be administered?

A

—IM, SQ & IV

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94
Q

What is the MOA for Sulfonylureas?

A

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

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95
Q

What are some nursing considerations for sulfonulureas?

A
  • —Only works in type 2 diabetes—
  • Can be used alone or in combo—
  • Avoid during pregnancy/nursing mothers
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96
Q

What are some side effects of sulfonylureas?

A
  • —Hypoglycemia (fatigue, excessive hunger, profuse sweating, palpitations)—
  • Weight gain
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97
Q

What are the Drug interactions for sulfonylureas?

A
  • —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
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98
Q

What are some 1st generation Sulfonylureas?

A
  • Tolbutamide
  • Acetoheamide
  • Tolazamide
  • Chloropamide
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99
Q

What are some 2nd generation Sulfonylureas?

A

Glipizide

Glyburide

Glime

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100
Q

What are some Metglitinides/Short-Acting Secretagogues?

A
  • —Repaglinide (Prandin)
  • nateglinide (Starlix)
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101
Q

What is the MOA for Metgilitinides/Short-acting Secretagogues

A
  • —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
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102
Q

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

A
  • —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
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103
Q

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

A
  • Side effects:
    • —Hypoglycemia (Less than with sulfonylureas), weight gain
  • ​​​Drug interactions
    • ​—Gemfibrizol (causes hypoglycemia)
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104
Q

What are the different types of Biguanides?

A

—Metformin (Glucophage, Fortamet, Glumetza, Riomet)

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105
Q

What is the MOA for metformin?

A
  • —Dec glucose production in the liver & enhances glucose uptake & utilization by muscle.
  • Does NOT promote insulin release
  • Dec LDL and triglyceride levels.
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106
Q

What are the nursing implications for metformin?

A
  • —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)
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107
Q

What are the contraindications for metformin?

A
  • —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
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108
Q

What are the side effects of metformin?

A
  • —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
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109
Q

What are some Type 2 Thiazolidinediones (Glitizones)?

A
  • —Rosiglitazone (Avandia)
  • Pioglitazone (Actos)
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110
Q

What is the MOA for Thiazolidinediones (Glitizones)?

A
  • —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.
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111
Q

What are some nursing implications for Thiazolidinediones (Glitizones)?

A
  • —Only approved for type 2— DM
  • Approved for monotx & for combo with metformin, sulfonylurea or insulin (carefully b/c insulin & glitizones cz edema).
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112
Q

What are some adverse effects of Thiazolidinediones (Glitizones)?

A
  • —Fluid retention (edema & wt gain), inc HDL, LDL and triglycerides
  • —Contraindicated in Class III or IV heart failure or hepatoxicity
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113
Q

What are the drug interactions for Thiazolidinediones (Glitizones)?

A

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

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114
Q

What are some Alpha-glucosidase inhibitors?

A
  • —Acarbose (Precose)
  • Miglitol (Glyset)
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115
Q

What is the MOA for Alpha-glucosidase inhibitors?

A

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

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116
Q

What are the nursing implications for Alpha-glucosidase inhibitors?

A

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

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117
Q

What are the Adverse effects for Alpha-glucosidase inhibitors?

A
  • —Flatulence, cramps, abdominal distention, borborygmus (rumbling bowel sounds) & diarrhea—
  • Dec absorption of iron (anemia), liver dysfunction
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118
Q

What are some Amylin Mimetics drugs?

A

—Pramlintide (Symlin)

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119
Q

What is the MOA for Amylin Mimetics?

A

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

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120
Q

What are some nursing implications for Amylin Mimetics?

A
  • —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
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121
Q

What are some adverse effects of Amylin Mimetics?

A
  • —Hypoglycemia (esp. when used in combo with insulin & usually develops within 3 h)
  • Nausea, Injections site rxn’s
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122
Q

What are some drung interactions of Amulin Mimetics?

A
  • —PO drugs should be taken 1 h before injecting Pramlintide
  • drugs that slow motility (anticholinergics)
  • drugs that slow absorption of nutrients (acarbose, miglitol)
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123
Q

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

A

—Exenatide (Byetta)

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124
Q

What is the MOA of Exenatide (Byetta)?

A
  • —Slows gastric emptying
  • stimulates glucose-dependent release of insulin
  • inhibits postprandial release of glucagon & suppresses appetite
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125
Q

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

A
  • —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.
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126
Q

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

A

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

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127
Q

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

A

—Oral contraceptives & antibiotics

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128
Q

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

A

Injectables

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129
Q

What are the 5 —principle actions of Thyroid hormones?

A

—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

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130
Q

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

A
  • Educate to take only as directed
  • That replacement therapy is for life
  • Never discontinue without talking to provider first!
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131
Q

What are some characteristics of thyroid hormones?

A
  • 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
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132
Q

When is thyroid hormone usually given?

A

In the morning

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133
Q

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

A
  • —irritability
  • insomnia
  • tachycardia
  • arrhythmias
  • inc. blood pressure
  • anxiety
  • wt. loss

Thyroid hormone is a stimulant

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134
Q

What are the clinical manifestations of having high thyroid levels?

A
  • Eyes = prominent
  • Integumentary = fine, thin hair; hot, moist skin
  • Temperature = heat intolerant
  • Weight = >appetite, < weight
  • Emotional = nervous, irritable, insomnia
  • GI = diarrhea
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135
Q

What are the clinical manifestations with low thyroid levels?

A
  • Eyes = ptosis, edematous
  • Integumentary = dry, brittle hair; cold, dry skin
  • Temperature = cold intolerant
  • Weight = < appetite, > weight
  • Emotional = lethargic, depressed, >sleep
  • GI = constipation
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136
Q

What are some HypOthyroid Medications?

A
  • desiccated thyroid (Armour Thyroid)
  • liothyronine (Cytomel)
  • levothyroxine, L-Thyroxine (Synthroid, Levoxyl, Levothroid)
  • liotrix (Thyrolar)
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137
Q

What are some characteristics of Armour Thyroid?

A
  • 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)
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138
Q

What are some characteristics of Levothyroxine, L-thyroxine?

A
  • 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.
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139
Q

What are some characteristics of Liothyronine?

A
  • 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
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140
Q

What are the characteristics of Liotrix?

A
  • —Drug = Thyrolar
  • T4 & T3 (4:1 ratio by weight)—
  • Synthetic (minimal allergic rxn)
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141
Q

Why causes Hypothyroidism?

A

mild deficiency of thyroid hormone in adults

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142
Q

What causes Myxedema?

A

—severe deficiency of thyroid hormone

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143
Q

What is Levothyroxine’s MOA?

A
  • 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
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144
Q

What are some nursing implications of Levothyroxine?

A
  • —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
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145
Q

What are the pharmacokinetics of Levothyroxine?

A
  • —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
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146
Q

What are the adverse effects of Levothyroxine?

A
  • 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
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147
Q

What are some drugs that decrease the absorption of levothyroxine?

A
  • —Cholestyramine (Questran)
  • Colestipol (Colestid)
  • —Ca++ supplements (Tums, Os-Cal)
  • Sucralfate (Carafate)
  • Aluminum-containing antacids (Maalox, Mylanta)
  • Iron supplements (Ferrous sulfate)
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148
Q

What are some drugs that accelerate the absorption of levothyroxine?

A
  • —Phenytoin (Dilantin)
  • Carbamazepine (Tegretol, Carbatrol)
  • —Rifampin
  • Sertraline (Zoloft)
  • Phenobarbital
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149
Q

What is the treatment for hyperthyroidism?

A
  • —Antithyroid drugs (propylthiouracil (PTU), Methimazole)
  • beta blocker
  • exophthalmos use glucocorticoids
  • —Radiation or Surgery
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150
Q

What is the MOA for Propylthiouracil (PTU)?

A

—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

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151
Q

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

A
  • Propylthiouracil (PTU)
  • Is NOT as likely to cross placenta than methimazole.
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152
Q

What are the pharmacokinetics of Propylthiouracil (PTU)?

A
  • Quick onset of action 30 min to 1 h
  • half life 75 min so dosing throughout day
  • crosses placenta & can enter breast milk;
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153
Q

What are some uses for Propylthiouracil (PTU)?

A
  • —Graves disease
  • adjunct to radiation tx
  • suppresses thyroid hormone synthesis in preparation for thyroid surgery
  • thyrotoxic crisis
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154
Q

What are some adverse effects of Propylthiouracil (PTU)?

A
  • —Agranulocytosis (rare, develops quickly during 1st 2 months)
  • Sore throat
  • fever
  • ulcerations in mouth rectum & vagina
  • hypothyroidism
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155
Q

What are some nursing implications of Propylthiouracil (PTU)?

A
  • —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
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156
Q

What is the role of calcium in the body?

A

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

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157
Q

What are some nursing implications for calcium?

A
  • —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
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158
Q

What are the symptoms for hypercalcemia?

A
  • —N/V
  • constipation
  • polyuria
  • nephrolithiasis (kidney stones develop)
  • lethargy
  • depression
  • cardiac dysrhythmias
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159
Q

Who is at risk for vitamin D deficiency?

A
  • pregnant women
  • obese people
  • dark-skinned individuals
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160
Q

What are the manifestations of vitamin D deficiency?

A
  • —Rickets (children)
  • osteomalacia (adults)
  • both can be reversed
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161
Q

What are the manifestations of vitamin D toxicity?

A
  • —Early Response: Weakness, fatigue, nausea, vomiting, and constipation—
  • Later Presentation: polyuria, nocturia, and proteinuria

—Toxicity is called hypervitaminosis D

162
Q

What is the treatment for vitamin D deficiency?

A

vitamin D

163
Q

What is the treatment for bone deterioration?

A

Calcium + Vitamin D

They MUST be given together to work

164
Q

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

A
  • Vitamin D3 (cholecalciferol)
  • 5.000 units once daily
165
Q

What type of vitamin D is produced naturally through sunlight?

A

Vitamin D3 (cholecalciferol)

166
Q

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

A
  • —Vitamin D2 (ergocalciferol)
  • Dosed in 50,000 units once weekly
  • Produced through PLANTS.
167
Q

What are Bisphosphonates used for?

A

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

168
Q

What are some nursing implications of Bisphosphonates?

A
  • 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
169
Q

What are some Adverse effects of Bisphosphonates?

A

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).

170
Q

Which drug increases bone formation?

A
  • —Teriparatide (Forteo) –> form of PTH
  • —Administered subcutaneously
  • Used to also treat osteoporosis in postmenopausal women, in men and in glucocorticoid-induced osteoporosis
171
Q

What is Calcitonin-salmon used to treat?

A

Postmenopausal osteoporosis and should be taken with vitamin D.

172
Q

What do Selective Estrogen Receptor Modulators (SERMs) do?

A

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.

173
Q

What are some Selective Estrogen Receptor Modulators (SERMs)?

A
  • raloxifene
  • tamoxifen
  • toremifene
174
Q

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

A
  • 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.
175
Q

What are the components that make up arterial pressure?

A

ARTERIAL PRESSURE = cardiac output (CO) X peripheral resistance

176
Q

CO is influenced by what 4 factors?

A
  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

177
Q

How is Arterial pressure regulated?

A
178
Q

High blood pressure is a major risk factor for what?

A
  • Heart disease
  • Stroke
  • Kidney disease
179
Q

What are the characteristics of primary hypertension?

A
  • 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
180
Q

What are the characteristics of Secondary hypertension?

A
  • 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
181
Q

What causes secondary hypertension?

A

Can happen as a result of:

  • Chronic renal dz
  • renovascular dz
  • oral contraceptive induced
  • coarctation or the aorta
  • primary aldosteronism
  • Cushing syndrome
  • pheochromocytoma
182
Q

Untreated hypertension can lead to what?

A
  • Left untx can lead to heart dz
  • Myocardial infarction (MI)
  • Heart failure (HF)
  • Angina pectoris
  • Renal failure
  • Cerebral hemorrhage (stroke)
183
Q

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

A

Systolic < 140 mm Hg

diastolic < 90 mm Hg

184
Q

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

A
  1. SNS - Baroreceptor reflex
  2. Renin-angiotensin-aldosterone system (RAAS)
  3. Kidney
185
Q

What are the classes of antihypertensive drugs?

A
  1. Diuretics
  2. Drugs that suppress RAAS
  3. Sympatholytics (antiadrenergic drugs)
  4. Direct-acting vasodilators: hydralazine and minoxidil
  5. Calcium channel blockers (CCBs)
186
Q

What are the major categories of diuretics?

A
  • 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
187
Q

What are some types of Drugs that suppress RAAS?

A
  • ACE inhibitors
  • Angiotensin II receptor blockers
  • Aldosterone antagonists
    • spironolactone
    • eplerenone
  • Direct renin inhibitors - Aliskiren
188
Q

What are the types of Sympatholytics (antiadrenergic drugs)?

A
189
Q

Diuretics affect what four regoins of the kidney?

A
  1. Glomerulus
  2. Proximal convoluted tubule
  3. Loop of Henle
  4. Distal convoluted tubule (DCT)
190
Q

Diuretic drugs that produce the greatest diuresis act how?

A

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

191
Q

What are the adverse effects of Diuretics in general?

A
  • Hypovolemia
  • Acid-base imbalance
  • Electrolyte imbalances
192
Q

What is the MOA of Furosemide (Lasix)?

A
  • 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
193
Q

What is Furosemide used for?

A
  • ↓ 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)
194
Q

What are the adverse effects of Furosemide?

A
  • 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)
195
Q

What are the Drug interactions of Furosemide?

A
  • 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
196
Q

What is one important adverse effect of Ethacrynic acid?

A

Irreversible hearing loss

197
Q

In general what are the effects of Thiazides?

A
  • 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
198
Q

When are Thiazides not effective?

A

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

199
Q

Where does Hydrochlorothiazide act?

A

early segment of the distal convoluted tubule

200
Q

What is Hydrochlorothiazide used for?

A
  • 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
201
Q

What are the adverse effects of hydrocholorothiazide?

A
  • 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
202
Q

What are the drug interactions of Hydrochlorothiazide?

A
  • 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
203
Q

What are the classes of Potassium-Sparing Diuretics?

A
  • Aldosterone antagonist (blocker)
    • Spironolactone
  • Nonaldosterone antagonists (blockers)
    • Triamterene
    • Amiloride
204
Q

What is the MOA of Spironolactone (Aldactone)?

A
  • 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 activation
  • ​gynecomastia in men

**NOTE: this is a Aldosterone antagonist **

205
Q

What is Spironolactone (Aldactone) used for?

A
  • 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 **
206
Q

What are the adverse effects of Spironolactone (Aldactone)?

A
  • 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
207
Q

What are the drug interactions with Spironolactone (Aldactone)?

A
  • 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
208
Q

What is the MOA of Triamterene (Dyrenium)?

A
  • 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
209
Q

What is Triamterene (Dyrenium) used for?

A
  • 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
210
Q

What are the adverse effects of Triamterene (Dyrenium)?

A
  • Hyperkalemia
  • Leg cramps
  • Nausea
  • Vomiting
  • Dizziness
  • Blood dyscrasias (rare)
211
Q

What are some contraindications for Triamterene (Dyrenium)?

A
  • Another K-sparing diuretic - Will result in hyperkalemia
  • K supplements - will result in hyperkalemia
  • Salt substitutes (KCl)
212
Q

What aare the two Nonaldosterone antagonists (blockers)?

A
  • Triamterene
  • Amiloride
213
Q

What is the MOA of Amiloride (Midamor)?

A
  • similar to triamterene
  • Blocks sodium exchange in the distal nephron
214
Q

What is Amiloride (Midamor) used for?

A

•To counteract potassium loss caused by more powerful diuretics

215
Q

What are the adverse effects of Amiloride (Midamor)?

A

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

216
Q

What are the drug interactions of Amiloride (Midamor)?

A
  • ACE inhibitors
  • ARBs
  • Direct renin inhibitor
217
Q

What type of drug is Mannitol (Osmitrol)?

A

Osmotic Diuretic

218
Q

What is the MOA of Mannitol?

A
  • 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)
219
Q

What are some nursing implications for Mannitol?

A
  • 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.
220
Q

What is Mannitol used for?

A
  • Prophylaxis of renal failure*
  • Reduction of intracranial pressure – osmotic force to draw water off
221
Q

What are some adverse effects of Mannitol?

A
  • 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
222
Q

What does Angiotensin II do?

A
  • Vasoconstriction
  • Release of aldosterone
  • Alteration of cardiac and vascular structure
223
Q

Where is Angiotensin II produced?

A
  • in blood, in individual tissues (local efx), and produced by pathways that do not involve ACE
  • so we can’t completely block angiotensin II
224
Q

What are some examples of ACE inhibitors?

A
  • lisinopril
  • enalapril
  • captopril

All end in PRIL

225
Q

How do ACE Inhibitors work?

A

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
226
Q

What are ACE Inhibitors used to treat?

A
  • 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
227
Q

What are the adverse effects of ACE inhibitors?

A
  • 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 **
228
Q

What are the drug interactions for ACE Inhibitors

A
  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:
  4. K sparing diuretics
  5. K supplements
  6. Lithium – lithium toxicity (monitor frequently)
  7. NSAIDs – may reduce anti-HTN efx
229
Q

How are ACE inhibitors administered?

A
  • All ACE inhibitors are administered orally except for enalaprilat
  • All oral formulations may be administered without regard to meals except for captopril and moexiprilr
230
Q

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

A
  • 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
231
Q

What are Angiotensin II Receptor Blockers
ARBs used for?

A
  • 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)
232
Q

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

A
  • Angioedema (lower than ACE-Is)
  • Category X Drug
  • Renal failure – w/ renal stenosis – same as ACE-Is
233
Q

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

A

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

234
Q

What’s an exaample of a Direct Renin Inhibitor?

A

Aliskiren

235
Q

What is the MOA for Aliskiren?

A
  • 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)

236
Q

What is Aliskiren used for?

A

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

237
Q

What is an example of a Selective Aldosterone Antagonist?

A

Eplerenone

238
Q

What is the MOA for Eplerenone?

A

Selective aldosterone receptor blocker (SARB)

239
Q

What is Eplerenone used for?

A
  • Hypertension
  • Heart failure
240
Q

What are some adverse effects of Eplerenone?

A
  • 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
241
Q

What are some drug interactions with Elerenone?

A
  • Inhibitors of P450 system: CYP3A4
  • With drugs that increase K+ levels
242
Q

What are the categories of Sympatholytics
(antiadrenergic drugs)?

A
  1. Alpha1 blockers
  2. Beta (1&2) blockers
  3. Alpha/beta blockers
  4. Centrally acting alpha2 agonists
  5. Adrenergic neuron blockers
243
Q

How do Sympatholytics
(antiadrenergic drugs) work?

A
  • 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
244
Q

What are the two main categories of antiadrenergic drugs?

A
  • Alpha-adrenergic blocking agents (α blockers)
  • Beta-adrenergic blocking agents (β blockers)
245
Q

What are some Alpha-blockers?

A
  • Prazosin – for HTN (& BPH)
  • Terazosin – for HTN (& BPH)
  • Doxazosin – for HTN (& BPH)
  • Tamsulosin – only BPH
  • Alfuzosin - only BPH
  • Silodosin - only BPH

All end in OSIN

246
Q

What are Alpha-blockers used for?

A
  • Essential or primary hypertension
    • Not first line medication
  • Benign prostatic hyperplasia
    • Reduces contraction of smooth muscle in the bladder neck and prostatic capsule
247
Q

What is the MOA for Alpha-blockers?

A

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

248
Q

What are some adverse effects of Alpha-blockers?

A
  • 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
249
Q

What is Phenoxybenzamine and what does it do?

A
  • Alpha 1 Blocker
  • Causes irreversible blockade used for pheochromocytoma (a tumor)
    • lasts several days until new receptors have been synthesized
250
Q

What are Beta-blockers used for?

A

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

251
Q

What are the 3 generations of Beta-blockers?

A
  • 1st gen: nonselective – block β1 & β2 (ex. propranolol)
  • 2nd gen: selective – block β1 (ex. metoprolol)
  • 3rd gen:
    • nonselective - β1&2, α1 (carvedilol & labetalol)
    • selective (β1) - nebivolol

All end in “LOL”

252
Q

What do 1st gen Beta-blockers do?

A
  • 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)
253
Q

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

A
  • Bradycardia – can mask tachycardia from hypoglycemia
  • AV heart block
  • Heart failure
  • Rebound cardiac excitation
  • Bronchoconstriction
  • Inhibition of glycogenolysis CNS effects – depression (rare but important
254
Q

What are some drug interactions of Beta-blockers?

A
  • Calcium channel blockers: identical efx to verapamil & diltiazem (reduction of HR, AV conduction & mycardial contractility) so combined may cause excessive cardiosuppression
  • Insulin
255
Q

What do 2nd gen Beta-blockers?

A

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
256
Q

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

A
  • 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

257
Q

What do 3rd generation Beta-blockers do?

A

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)
258
Q

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

A

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
259
Q

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

A

Rebound cardiac excitation

260
Q

What are some nursing interventions with Beta-Blockers?

A
  • 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
261
Q

What are some examples of Centrally Acting Alpha2 Agonists?

A
  • Clonidine: can cause rebound HTN if abruptly stopped.
  • Methyldopa: can cause hemolytic anemia & liver disorders
262
Q

How do Centrally Acting Alpha2 Agonists (sympatholitics) work?

A

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

263
Q

What are some Adverse effects of Centrally Acting Alpha2 Agonists?

A

dry mouth sedation

264
Q

How do Adrenergic Neuron Blockers work?

A
  • ganglionic blockade reduces sympathetic stimulation of the heart & blood vessels (dilation of arterioles & veins)
  • AE: deep depression
  • Drug: Reserpine
265
Q

What are some nursing interventions for Sympatholytics?

A
  • 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
266
Q

How do Direct-Acting vasodilators do?

A

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
267
Q

What are some examples of direct-acting vasodilators?

A
  • Selective dilation of arterioles – Hydralazine, Minoxodil
  • Selective dilation of veins – Nitroglycerin
  • Dilate arterioles and veins – Prazosin
268
Q

What are direct-acting vasodilators used to treat?

A

Uses:

  • Essential hypertension & hypertensive crisis
  • Angina pectoris & myocardial infarction
  • Heart failure
  • Pheochromocytoma
  • Peripheral vascular disease
  • Pulmonary arterial hypertension
  • Production of controlled hypotension during surgery
269
Q

What are some adverse effects of direct-acting vasodialators?

A
  • Postural hypotension
  • Reflex tachycardia
  • Expansion of blood volume
270
Q

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

A

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
271
Q

What are the adverse effects of hydralazine?

A
  • 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)
272
Q

What are the Drug interactions hydralazine?

A
  • 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
273
Q

What is Minoxodil used for?

A
  • Selective dilation of arterioles
  • Used for severe hypertension
  • Same adverse effects of hydralazine
274
Q

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

A
  • 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)
275
Q

What are the adverse effects of sodium nitroprusside?

A
  • 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
276
Q

How do Calcium Channel Blockers work?

A
  • Drugs that prevent calcium ions from entering cells
  • Also known as calcium antagonists and slow channel blockers
277
Q

What are calcium channel blockers used to treat?

A

Used to treat:

  1. Hypertension
  2. angina pectoris
  3. cardiac dysrhythmias
278
Q

What are some types of Calcium Channel blockers?

A

Non-dihypropyridines:

  • Verapamil and diltiazem – agents that act on vascular smooth muscle and the heart

Dihydropyridines:

  • Nifedipine, Nicardipine, amlodipine, etc– agents that act mainly on vascular smooth muscle of the heart
279
Q

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

A
  • When calcium channels are open = Contractile process (VSM contracts)
  • When calcium channels are blocked = Vasoconstriction of VSM

No significant effect on veins

280
Q

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

A
  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

281
Q

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

A
  • 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
282
Q

What are the 5 Hemodynamic Effects of Verapamil and Diltiazem?

A
  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
283
Q

What are some adverse effects of Verapamil and Diltiazem?

A
  • 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
284
Q

What are the drug interactions of of Verapamil and Diltiazem?

A
  • Digoxin - Has opposite effects
  • β blockers - Will further decrease heart rate, BP, etc
  • Grapefruit juice
285
Q

What are some toxic effects of Verapamil and Diltiazem?

A
  • Severe hypotension
  • Bradycardia and AV block
  • Ventricular tachydysrhythmias
286
Q

How does Nifedipine (a Dihydropyridine) work?

A

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

287
Q

What is Nifedipine (a Dihydropyridine) used to treat?

A
  • Essential hypertension
  • Angina
  • Cannot be used to treat dysrhythmias

fast-acting formulation: efx begin almost immediately

288
Q

What are some effects of Nifedipine (a Dihydropyridine)?

A
  • Lowers blood pressure
    • by dialating vascular smooth muscle in peripheral arterioles
289
Q

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

A
  • Flushing
  • Dizziness
  • Peripheral edema
  • Very little constipation
    • due to slight blocking for Ca++ channels in intestines
  • Baroreflex
290
Q

How are all Dihydropyridine’s identified?

A

They all end in “ipine”

Nicardipine, amlodipine, isradipine, felodipine, etc

291
Q

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

A
  • diuretics (thiazide first line)
  • CCB’s &
  • α/β blockers work best
292
Q

White people with hypertension with what types of medications?

A

β blockers or ACEIs

293
Q

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

A

Sodium nitroprusside

294
Q

What are the effects of Sodium nitroprusside?

A
  • dilates arterioles & veins
  • immediate efx – continuous IV infusion
  • don’t infuse longer than 72 hr. - ↑ risk of toxicity
295
Q

What hypertensive drugs are contraindicated during pregnancy?

A

ACE inhibitors, ARBs, and DRIs

296
Q

What is the hypertensive DOC during pregnancy?

A

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

297
Q

What happens during Heart Failure?

A
  • ↓ 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

298
Q

What are the major underlying causes of Heart failure?

A
  • 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
299
Q

What leads to cardiac remodeling?

A
  • Dilated ventricles
  • Hypertrophy of heart
    • increase in heart wall thickness
  • Heart becomes more spherical (less cylindrical)
    • Results in ↓ Cardiac output
300
Q

What are the signs and symptoms of heart failure?

A
  • 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
301
Q

What are some drugs used for heart failure?

A
  • Diuretics
  • RAAS inhibitors
  • ACE inhibitors
  • Angiotensin II receptor blockers
  • Aldosterone antagonists
  • Direct renin inhibitors
  • Beta blockers
  • Digoxin and other cardiac glycosides
302
Q

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

A

Diuretics:

  • Potassium-sparing diuretics
  • Thiazide diuretics
  • High-ceiling (loop) diuretics
303
Q

How do ACE inhibitors help pts w/ Heart failure?

A

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

304
Q

What does Dopamine activate and what does the activation cause?

A

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
305
Q

What does Dobutamine activate and what does the activation cause?

A

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

306
Q

What are the effects of Digoxin?

A
  • 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
307
Q

What are the adverse effects of digoxin?

A
  • 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
308
Q

Describe the↓ sympathetic tone when taking Digoxin and its effects

A

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.
309
Q

Describe the effects of ↑ urine production due to dijoxin?

A
  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
310
Q

Why is there a ↓ renin release when taking digoxin?

A
  • Because digoin ↑ arterial pressure (from ↑ urine production, ↑ contractile force & CO), renin release declines causing aldosterone & angiotensin II to decline also
311
Q

What occurs when there is a ↓ in aldosterone?

A

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

312
Q

What occurs when there is a ↓ in angiotensin II?

A

↓ vasoconstriction reducing afterload & venous pressure

313
Q

What can cause Digoxin related dysrhythmias?

A
  • Hypokalemia (from diuretics…also v/d)
  • elevated digoxin level = too much cardiac suppression
  • Heart disease may cause extra issues with dysrhythmias
314
Q

How do you manage digoxin-induced dysrhythmias?

A
  • 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
315
Q

What are some drug interactions with Digoxin?

A
  • 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
316
Q

What are the Pharmacokinetics of Digoxin?

A
  • Taken with meals decreases absorption
  • Narrow Theraputic range: 0.5-0.8 ng/mL
  • Distributed widely and crosses the placenta
317
Q

What are some nursing implications for Digoxin?

A
  • 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+
318
Q

What are some characteristics of stage A heart failure?

A
  • 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
319
Q

What are some characteristics of stage B heart failure?

A
  • No signs and symptoms of HF
  • Goal of is to prevent development of symptomatic HF
320
Q

What are the treatment options for Stage B heart failure?

A

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

321
Q

What are some characteristics of stage C heart failure?

A
  • 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
322
Q

What are the treatment options for Stage C heart failure?

A

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
323
Q

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

A
  • Antidysrhythmic agents – cardiosuppressant & prodysrthythmic
    • Because these can cause arythmias
  • Calcium channel blockers
  • NSAIDs – Na+ retention & peripheral vasoconstriction
324
Q

What are some characteristics of stage D heart failure?

A
  • Marked symptoms of HF
  • Advanced structural heart disease
  • Repeated hospitalizations
325
Q

What are the treatment options for stage D heart failure?

A
  • 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
326
Q

What are the two types of dysrhythmias?

A
  • Supraventricular dysrhythmias
  • Ventricular dysrhythmias
327
Q

What are the two fundamental causes of dysrhythmias?

A
  • 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
328
Q

What are the different classifications of
Antidysrhythmic Drugs?

A
  • Class I - sodium channel blockers
  • Class II - beta blockers
  • Class III - potassium channel blockers
  • Class IV - calcium channel blockers
  • adenosine & digoxin
329
Q

In general how do class I Antidysrhythmic Drugs work?

A

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

330
Q

In general how do class II Antidysrhythmic Drugs work?

A

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
331
Q

In general how do class III Antidysrhythmic Drugs work?

A

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

332
Q

In general how do class IV Antidysrhythmic Drugs work?

A

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

333
Q

In general how do adenosine & digoxin work?

A

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

334
Q

What are some characteristics of Supraventricular dysrhythmias?

A
  • 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
335
Q

What are some characteristics of Ventricular dysrhythmias?

A
  • 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
336
Q

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

A
  • Class IA agents - delay repolarization
  • Class IB agents - accelerate repolarization
  • Class IC agents - pronounced prodysrhythmic actions
337
Q

What are some examples of Class IA Sodium Channel Blockers?

A

Quinidine, Procainamide, Disopyramide

338
Q

What is the MOA of Quinidine?

A
  • 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)
339
Q

What is Quinidine used for?

A
  • Used for supraventricular & vent dysrhythmias
  • Give w/ digoxin, verapamil, beta blocker with quinidine to ↓ vent rate
340
Q

What are the adverse effects of quinidine?

A

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

341
Q

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

A

Lidocaine, Mexiletine, Phenytoin

All these drugs Accelerate repolarization & little effect on ECG

342
Q

What are the effects of Lidocaine?

A
  1. Slows conduction in the atria, vent & His-Purkinje system
  2. Reduces automaticity in vent & His-Purkinje
  3. Accelerates repolarization (shortens axn potential)
343
Q

What some nursing considerations of lidocaine?

A
  • IV, used ONLY for vent dysrhythmias NOT used for supraventricular dysrhythmias
  • Whenever lidocaine is used equipment for resuscitation must be available
344
Q

What are the adverse effects of lidocaine?

A
  • CNS (paresthesias, drowsiness)
  • Convulsions
  • resp arrest
345
Q

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

A

Flecainide, Propafenon, Moricizine

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

346
Q

What are Flecainide &Propafenone used for?

A

Maintenance tx of supraventricular dysrhythmias

347
Q

What is Moricizine used for?

A

Life-threatening ventricular dysrhythmias

348
Q

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

A

Non-Selective:

  • Propranolol
  • Acebutolol

Selective:

  • Esmolol (IV)
  • Sotalol (selective beta 1 & also blocks K+ channels)
349
Q

What are the effects of Beta Blockers on the heart?

A
  1. ↓ automaticity of the SA node
  2. ↓ velocity of conduction through the AV node which prolongs PR interval
  3. ↓ myocardial contractility
350
Q

What are Beta Blockers used for?

A
  • Dysrhythmias caused by excessive sympathetic stimulation.
  • Control of vent rate in pts with supravent tachydysrhythmias
351
Q

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

A
  • Amiodarone
  • Bretyllium (IV)
  • Ibutilide (IV)
  • Dofetilide
  • Sotalol (IV)

A BIDs

352
Q

What is the MOA for K+ Channel Blockers?

A

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

353
Q

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

A
  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

354
Q

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

A
  1. Class III: K+ Channel Blockers
  2. Used for life-threatening ventricular dysrythmias
355
Q

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

A
  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)
356
Q

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

A
  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
357
Q

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

A

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

358
Q

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

A
  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
359
Q

What are Verapamil & Diltiazem used for?

A

Control vent rate in pts with supravent tachydysrhythmias

360
Q

What are the adverse effects of Verapamil & Diltiazem?

A
  • Bradycardia, AV block, HF, hypotension, peripheral edema, constipation
  • Drug interactions: elevate digoxin levels; don’t combine w/ beta blockers b/c of ↑ bradycardia
361
Q

What is Adenosine** **used for?

A
  • Decreases automaticity in the SA node
  • Slows conduction through the AV node
  • Prolongation of PR interval
  • DOC for termination of paroxysmal SVT
362
Q

What are the two stages of hemostasis?

A

Stage 1: formation of platelet plug

Stage 2: coagulation

363
Q

Describe the formation of a platelet plug?

A

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

364
Q

Describe coagulation?

A
  • 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
365
Q

What is an Arterial thrombosis?

A

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)

366
Q

What is an Venous thrombosis?

A

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.

367
Q

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

A
  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
368
Q

What are the 3 groups of Antiplatelet Drugs?

A
  1. Aspirin
  2. ADP receptor antagonists
  3. GP IIb/IIIa receptor antagonists
369
Q

What is the MOA of Aspirin?

A
  • 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
370
Q

What is asprin used for?

A

Prevention of MI, TIA, stroke, chronic stable & unstable angina, coronary stenting, previous MI, primary prevention of MI

Dose: chronic therapy - 81 mg/d; acute event – 325 mg/d

371
Q

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

A
  • Clopidogrel
  • prasugrel
  • ticlopidine
  • ticagrelor
372
Q

What is the MOA of ADP Receptor Antagonists?

A

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

373
Q

What are some uses of ADP Receptor Antagonists?

A

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

374
Q

What are some adverse effects of ADP Receptor Antagonists?

A
  • Potential fatal hematologic effects;
  • risk is much higher with ticlopidine: neutropenia/agranulocytosis, thrombotic thrombocytopenic pupura
375
Q

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

A
  • Abciximab
  • Tirofiban
  • Eptifibatide
376
Q

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

A
  • Most effective antiplatelet drugs on the market
  • Administered IV in combo usually with aspirin or heparin
  • VERY EXPENSIVE
377
Q

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

A

REVERSIBLE blockade of platelet GP IIb/IIIa rec which inhibits final step in aggregation by all factors

AE = bleeding

378
Q

What are Glycoprotein IIb/IIIa Receptor Antagonists used for?

A

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

379
Q

What are some examples of Anticoagulant drugs?

A
  • Heparins & fondaparinux
  • Warfarin
  • Direct thrombin inhibitors
    • dabigatran etexilate
    • hirudin analogs
    • argatroban
  • Direct factor Xa inhibitor (Rivaroxaban)
  • Antithrombin
380
Q

What is the MOA of Anticoagulant drugs?

A
  • 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
381
Q

What are the 3 different types of heparins?

A
  1. (unfractionated) heparin
  2. low-molecular-weight (LMW) heparins
  3. fondaparinux
382
Q

What are some nursing considerations of (Unfractionated) Heparin?

A
  • 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)
383
Q

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

A
  • 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
384
Q

What is (Unfractionated) Heparin used for?

A
  • Prophylaxis of venous thrombosis (acts immediately)
  • pulmonary embolism
  • evolving stroke
  • massive deep vein thrombosis (DVT)
  • open heart surgery
  • pregnancy
  • acute MI
385
Q

What are the adverse effects of (Unfractionated) Heparin?

A
  • 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)
386
Q

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

A
  • Enoxaparin
  • Dalteparin
  • Tinzaparin
387
Q

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

A
  • 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
388
Q

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

A

protamine sulfate

389
Q

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

A
  • Bleeding (but less than with unfractionated heparin)
  • HIT (10x less than heparin)
390
Q

What are some characteristics of Fondaparinux?

A
  • An Anticoagulant drugs that only inhibits factor Xa – reduces thrombin
  • no effect on platelets
  • Administered Sub Q
  • Can’t reverse with protamine sulfate
391
Q

What is the MOA of Warfarin?

A
  • 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
392
Q

What are some nursing considerations of Warfarin?

A
  • 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
393
Q

What is Warfarin used for?

A

Prevention of venous thrombosis & PE

  • & in pts with prosthetic heart valves
  • ** during atrial fibrillation**
394
Q

What is the treatment for a Warfarin overdose?

A
  • 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
395
Q

What are the adverse effects of Warfarin?

A
  • Hemorrhage
  • Category X (if need anticoag during pregnancy give heparin)
  • Do not use during breast feeding
396
Q

What are the drug interactions with Warfarin?

A
  • Drugs that promote bleeding
  • Drugs that ↑ anticoag effects
  • Drugs that ↓ anticoag effects
397
Q

What are some drugs that promote bleeding when taking warfarin?

A
  • Heparin
  • Asprin
  • Acetaminophen
  • non-ASA (clopidogrel, dypyridamole, ticlopidine, abciximab)
398
Q

What are some Drugs that ↑ anticoag effectswhen taking warfarin?

A
  • miconazole (oral & intravaginal)
  • cimetidine
  • disulfiram (anti-ETOH drug)
  • sulfonamides
399
Q

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

A
  • Vit K (and in food)
  • phenobarbital
  • carbamazepine
  • rifampin
400
Q

What are some contraindications with Warfarin?

A
  • Vit K deficiency
  • liver ds
  • alcoholism

N3540 Pharmacology (5 decks)

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