N212B - Exam #2 Study Guide

Anemia

• Reduction in the total number of erythrocytes in the circulating blood or in the quality/quantity of hemoglobin

• Could be caused by:

  • Impaired erythrocyte production

  • Acute/chronic blood loss

  • Inc. erythrocyte destruction

  • Combination of the above

• Classified by size and hemoglobin

  • Size → - cytic

    • Macrocytic, microcytic, and normocytic

  • Hemoglobin content → -chromic

    • Normochromic and hypochromic

Folate deficiency

• Anemias of diminished erythropoiesis

  • deficiencies in vitamin b12 or folate → results in defective DNA synthesis

• Folate deficiency anemia → a Macrocytic (megaloblastic) anemia

  • Humans are dependent on dietary intake of folate

  • Absorption of folate occurs in the upper small intestine

  • Not dependent on any other factor

  • Similar symptoms to pernicious anemia except neurologic manifestations are generally not seen

  • Treatment requires daily oral admin of folate until body levels are adequate

Anemia is a reduction in the number of red blood cells (RBCs), the amount of hemoglobin, or the hematocrit (percentage of packed RBCs per deciliter of blood). It can also be defined as a decrease in the quality or quantity of hemoglobin.

Important: Anemia is a clinical indicator, not a specific disease. It occurs with many health problems and is a pathophysiologic manifestation of various underlying disease states.

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Diagnostic Criteria

For adults:

• Men: Hemoglobin <14 g/dL (8.7 mmol/L)

• Women: Hemoglobin <12.0 g/dL (7.4 mmol/L)

Anemia refers to a true decrease in erythrocyte number, not a relative decrease from increased plasma volume (hemodilution)

• Definition and Pathophysiology

  Folate (folic acid) is an essential water-soluble vitamin required for RNA and DNA synthesis in maturing red blood cells. The daily adult requirement is 400 mcg, obtained entirely through diet—fruits, green leafy vegetables, liver, and fortified grains.

  Folate deficiency is more common than B12 deficiency, especially in individuals with alcoholism or chronic malnourishment. Deficient thymine production affects rapidly dividing cells in bone marrow, causing megaloblastic precursor cells and macrocytic anemia.

  Unlike B12, folate is absorbed from the upper small intestine and does not require intrinsic factor. After absorption, it circulates through and is stored in the liver.

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  High-Risk Groups

  • Females of childbearing age, non-Black Hispanic females, and older adults

  • Pregnant and lactating individuals (increased requirements; deficiency causes neural tube defects)

  • Individuals with alcoholism or chronic malnourishment

  • Inflammatory bowel disease (Crohn disease, ulcerative colitis) causing malabsorption

  • Those taking sulfasalazine (decreases folate absorption)

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  Clinical Manifestations

  Distinctive GI symptoms:

  • Cheilosis (scales/fissures of mouth)

  • Stomatitis and painful oral/tongue ulcerations (burning mouth syndrome)

  • Dysphagia, flatulence, watery diarrhea

  • GI histologic changes similar to celiac disease

  Blood findings: Macrocytic RBCs (high MCV)

  Key difference from B12 deficiency: Paresthesias do not occur because folate deficiency alone does not affect nerve function. If neurologic symptoms are present, consider thiamine deficiency, which often accompanies folate deficiency in malnourished individuals.

  Folate deficiency may suppress intestinal mucosa proliferation, worsening GI damage.

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  Diagnosis and Treatment

  Evaluation: Clinical manifestations, macrocytic RBCs (high MCV), and serum folate levels

  Treatment:

  • Oral folate preparations until adequate blood levels are achieved

  • Dietary adjustments: folate-rich foods

  • Manifestations disappear within 1-2 weeks

  • Long-term therapy unnecessary if diet is corrected

Leukemia Med Admin

Nursing implications:

• Assess baseline blood counts before administering antineoplastic drugs

• Follow specific administration guidelines for each antineoplastic drug

• Chemo-certified to give IV meds

• Remember that all rapidly dividing cells are affected by antineoplastic drugs

  • GI/Mucous membranes → stomatitis, altered bowel function w/ high risk for poor appetite, nausea, vomiting, diarrhea, and inflammation/ulcerations of GI mucosa

  • Hair follicles → alopecia

  • Bone marrow components → dangerously low (life-threatening) blood cell counts

• Monitor for effects/complications of these tissues

• Implement measures to monitor for and prevent infection in patients w/ neutropenia/leukopenia → hand hygiene, precautions

• Implement measures to monitor for and prevent bleeding in pts w/ thrombocytopenia and anemia

• Anticipate N/V, implement measures to reduce

  • Antiemetics work best when given 30-60 minutes before chemo is given

Safe Handling of Chemotherapy

All chemotherapy agents are designated hazardous drugs (HDs) and require strict safety protocols.

Key safety principles:

For IV chemotherapy:

• Nurses must undergo certification to administer IV chemotherapy

• Administer through a central line indwelling catheter device to minimize extravasation risk

• Check device patency before administration

• Monitor IV site constantly during infusion

For oral chemotherapy:

• Can be administered by any RN (no certification required)

• Never physically touch chemotherapy tablets—highly toxic to normal cells

• Same exposure risks as IV forms

• Toxicity causes DNA damage leading to cell death, cancer, birth defects, or immune dysfunction

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Extravasation Management

Extravasation (drug leakage into surrounding tissue) is a serious complication when vesicants (tissue-damaging chemicals) are involved.

If extravasation occurs:

1. Stop drug immediately but leave IV cannula in place (for possible antidote administration)

2. Follow institutional protocol (treatment is drug-specific)

3. Use of antidotes, hot/cold packs outlined in facility policy

4. Monitor hourly with documentation

5. May result in pain, infection, tissue loss, or need for reconstructive surgery

Prevention: Regular monitoring of blood return at access site during infusion

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Patient and Family Safety

Bodily fluid precautions: Patients excrete chemotherapy chemicals through urine, stool, vomit, sweat, and saliva. Families must be warned of exposure dangers when patients self-administer at home.

Key nursing considerations:

• Establish therapeutic relationship with trust and empathy

• Provide individualized education appropriate to patient's level

• Address fear and anxiety

• Coordinate with interdisciplinary team

• Monitor for toxicities affecting multiple body systems

Blood administration

Pretransfusion Phase

Preparation is critical to prevent transfusion reactions.

Required steps:

• Health care provider must discuss benefits/risks with patient

• Obtain physician prescription specifying component type, volume, and special conditions

• Obtain separate consent form per hospital policy

• Collect blood specimen for type and crossmatch to test donor/recipient compatibility

• Use blood filter (170 microns) to remove sediment

• Prime tubing with normal saline only—never Ringer's lactate or dextrose (causes clotting/hemolysis)

• Never add medications to blood (may cause clotting)

Critical safety check: Two registered nurses must verify:

• Patient identification (name, health record number, date of birth)

• ABO and Rh compatibility

• Expiration date

• Product appearance (no discoloration, gas bubbles, or cloudiness indicating bacterial growth)

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During Transfusion

Initial phase (first 15-30 minutes):

• Explain procedure to patient

• Assess baseline vital signs and temperature

• Start infusion slowly

• Stay with patient—severe reactions typically occur within first 50 mL

• Take vital signs at 15 minutes

• Ask patient to report chills, shortness of breath, hives, itching, or back pain

Continuation:

• If no reaction, increase rate to transfuse 1 unit over 2-4 hours (based on cardiac status)

• Monitor vital signs hourly throughout transfusion

• Blood products without large amounts of RBCs can infuse more quickly

• Older patients may require slower infusion rates

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Posttransfusion Phase

Completion steps:

• Discontinue infusion

• Dispose of bag/tubing per hazardous waste policy

• Obtain vital signs and compare to baseline

• Document: product type and number, volume infused, duration, vital signs, adverse reactions with interventions, patient tolerance

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Special Considerations: Platelet Transfusions

• Infuse immediately after bringing to room (platelets are fragile)

• Infuse over 15-30 minutes

• Use special transfusion set with smaller filter

• May premedicate with diphenhydramine and acetaminophen if patient has history of reactions

Platelet administration

Indications for Platelet Transfusions

When to give platelets:

• Platelet count <10,000/mm³ (10 × 10⁹/L)

• Patient with thrombocytopenia who is actively bleeding

• Patient scheduled for invasive procedure

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Product Types

Pooled platelets:

• Combined from up to 10 donors

• Volume: ~300 mL

• Do not need to match patient's blood type

Single-donor platelets:

• From one donor only

• Volume: ~200 mL

• Preferred for patients receiving HSCT or requiring multiple transfusions

• Reduces risk of allergic reactions1

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Administration Procedure

Equipment:

• Special transfusion set with smaller filter and shorter tubing

• Platelet filters remove WBCs for patients with history of febrile reactions or needing multiple transfusions

Timing and rate:

• Infuse immediately after bringing to patient's room (platelets are fragile)

• Infusion duration: 15-30 minutes

Vital signs:

• Before infusion starts

• 15 minutes after infusion starts

• At completion

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Preventing Reactions

Premedication for at-risk patients:

• Diphenhydramine (antihistamine)

• Acetaminophen (fever reducer)

• Given to patients with history of transfusion reactions to reduce fever and severe chills (rigors)

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Key Safety Points

• Platelets are fragile—handle gently and infuse promptly

• Never delay infusion once product arrives at bedside

• Monitor closely during first 15 minutes when reactions most likely occur

• Use appropriate filter to remove WBCs and prevent febrile reactions

Impaired hemostasis → Vitamin K deficiency

• Hemostasis is the arrest of bleeding by formation of blood clots at sites of vascular injury.

  • As a result of hemostasis, damaged blood vessels may maintain a relatively steady state of blood volume, pressure, and flow. Three equally important interactive components of hemostasis are the vasculature (endothelial cells and subendothelial matrix), platelets, and clotting factors. The general sequence of events in hemostasis is (1) transient arteriolar vasoconstriction to limit blood flow to the affected site; (2) formation of a platelet plug (primary hemostasis); and (3) coagulation and clot formation with aggregation of proteins synthesized by the liver, endothelial cells, and platelets (secondary hemostasis). The relative importance of the hemostatic mechanisms clearly varies with vessel size. Hemostasis in capillaries and smaller veins and arteries occurs with sealing of the injury. Damage to large vessels cannot easily be controlled by hemostasis but requires vascular contraction to decrease blood flow from the damaged vessels.

• Impaired hemostasis - inability of coagulation and stable fibrin clot

• Vitamin K is necessary for the synthesis and regulation of prothrombin and the procoagulant factors (VII, XI, and X) and proteins C and S

• Vitamin K's Role in Hemostasis

  Vitamin K is essential for hepatic biosynthesis of clotting factors II, VII, IX, and X. It also helps regulate prothrombin and anticoagulant factors (proteins C and S) within the liver. Without adequate vitamin K, these clotting factors cannot be properly synthesized, leading to coagulation disorders caused by hypoprothrombinemia.

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  Causes of Vitamin K Deficiency

  Primary sources of vitamin K:

  • Green leafy vegetables (dietary source)

  • Intestinal flora (synthesize sufficient amounts normally)

  Most common cause:

  • Parenteral nutrition combined with antibiotics that destroy normal gut flora

  Other causes:

  • Dietary deficiency (rare)

  • Bulimia (can suppress vitamin K–dependent activity)

  • Liver disease (cirrhosis, hepatocellular disease)—impairs production of vitamin K–dependent clotting factors

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  Clinical Manifestations

  Vitamin K deficiency results in impaired hemostasis with bleeding tendencies due to decreased levels of multiple clotting factors. The liver produces most factors involved in hemostasis, so vitamin K deficiency or liver damage causes:

  • Factor VII decreases first (rapid turnover)

  • Factor IX levels decrease with advanced liver destruction

  • Deficient clotting factor synthesis leads to coagulation disorders

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  Treatment

  Parenteral vitamin K administration:

  • Treatment of choice for vitamin K deficiency

  • Correction usually occurs within 8-12 hours

  Fresh-frozen plasma (FFP):

  • Reserved for life-threatening hemorrhages

  • Used when emergency surgery is required

  • Provides immediate clotting factors while waiting for vitamin K to work

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  Key Point

  Vitamin K deficiency is rare because intestinal flora normally synthesize adequate amounts. When deficiency develops, it can be corrected with supplementation. However, in patients on antibiotics with parenteral nutrition or those with severe liver disease, proactive monitoring and supplementation may be necessary to prevent bleeding complications

Chemotherapy

Care of pts receiving chemotherapy medications

Safe Handling and Administration

Protection requirements:

• Never physically touch chemotherapy tablets—highly toxic to normal cells

• Chemotherapy causes DNA damage leading to cell death, with potential injuries including cancer, birth defects, or immune dysfunction that may not appear for months or years

• Nurses must undergo certification to administer IV chemotherapy; oral chemotherapy can be administered by any RN

• Use proper protective techniques during unpacking, storage, handling, administration, and disposal

Patient excretion hazards:

• Patients excrete chemotherapy through urine, stool, vomit, sweat, and saliva

• Double-flush toilets during treatment and for 48 hours after discontinuing chemotherapy

• Warn families about exposure dangers, especially for children and pets

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Nursing Care During Treatment

Assessment priorities:

• Complete physical assessment including vital signs, height/weight

• Baseline hearing and vision testing

• Assess bowel/bladder patterns, neurologic status, heart sounds, breath sounds

• Evaluate skin and mucosa (turgor, hydration, color, temperature)

• Pain assessment using 0-10 intensity scale

• Monitor for chest pain, palpitations, dyspnea, numbness/tingling, bleeding signs

Critical monitoring during infusion:

• Monitor for reactions within first few minutes of infusion

• Watch for dyspnea, abdominal distention, lung crackles, dependent edema

• Assess for cutaneous reactions (rash on hands/feet) requiring immediate attention

• Ensure IV site patency—prevent extravasation of irritants/vesicants

• Follow facility protocol immediately if extravasation occurs

Preventing complications:

• Minimize tissue trauma (avoid IM injections, rectal temperatures if possible)

• Monitor blood counts closely with every treatment

• Address nausea/vomiting promptly to prevent dehydration and electrolyte disturbances

• Be aware of numerous IV incompatibilities

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Psychosocial Support

Reduce fear and anxiety:

• Establish therapeutic relationship with trust and empathy

• Provide individualized teaching appropriate to education level

• Encourage relaxation techniques (music, meditation, guided imagery)

• Connect with social services, spiritual guidance, financial assistance, and community resources

Chemotherapy and pregnancy

• Strict contraindication during 1st trimester but not complete contraindication during 2nd and 3rd trimesters

• Pregnancy Risk Classification

  Chemotherapy drugs are classified as pregnancy category D or X, indicating significant risk to the fetus. The decision to use chemotherapy during pregnancy is based on risk versus benefit analysis.

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  Timing and Fetal Risk

  First trimester—HIGHEST RISK:

  • Greatest danger of drug-caused developmental defects extends from fertilization through the first trimester

  • Both radiation and chemotherapy can cause significant permanent fetal harm or death

  • Many women may not yet realize they are pregnant during this critical period

  Second and third trimesters:

  • Chemotherapy treatment is more likely to improve maternal outcome without significant fetal risk

  • Risk is reduced but not eliminated

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  Contraception Requirements

  During treatment:

  • Sexually active women of childbearing age must protect themselves against pregnancy due to risk of embryonic death

  • Use contraceptive measures throughout chemotherapy

  After treatment:

  • Continue contraception for up to 8 weeks after discontinuing therapy

  • Some antineoplastic drugs require contraception for up to 2 years after completion due to long-term risk of fetal genetic abnormalities

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  Reproductive Effects

  Antineoplastic drugs negatively impact the reproductive tract by:

  • Destroying germinal epithelium of testes

  • Damaging ovaries

  • Causing teratogenesis (fetal malformations)

  Male patients:

  • Risk of sterility, which may be irreversible

  • Discuss sperm banking before chemotherapy if appropriate

  Female patients:

  • Sterility

  • Amenorrhea

  • Premature menopausal symptoms (hot flashes, decreased vaginal secretions, mood changes, irritability)

  • Decreased libido or sexual dysfunction

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  Special Consideration: Prepubertal Patients

  Children who haven't reached puberty are more resilient and can have normal puberty and fertility after receiving chemotherapy

Diabetes Management

Insulin production

• Pancreas → located behind the stomach; both an endocrine and exocrine gland

  • Produces two hormones that are important in the regulation of glucose homeostasis: Insulin and glucagon

• Glycogen → excess glucose stored in the liver and skeletal tissue

• Glycogenolysis → conversion of glycogen into glucose when needed

• Insulin:

  • Direct effect on fat metabolism

  • Stimulates lipogenesis and inhibits lipolysis

  • Stimulates protein synthesis

  • Promotes intracellular shift of potassium and magnesium into the cells

  • Cortisol, epinephrine, and growth hormone work synergistically w/ glucagon to counter the effects of insulin

• Synthesis Process

  Precursor molecules: Insulin synthesis begins with preproinsulin, which is converted to proinsulin. Proinsulin is composed of:

  • A peptide

  • B peptide

  • C peptide (connecting the A and B peptides)

  • Two disulfide bonds

  Final formation: Proteolytic enzymes cleave the C peptide, leaving the bonded A and B peptides as the active insulin molecule. The mature insulin protein consists of 51 amino acids.

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  Location

  Insulin is synthesized by beta cells in the islets of Langerhans (pancreatic islets). The pancreas is located behind the stomach, between the spleen and duodenum.

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  Regulation of Secretion

  Stimulating factors:

  • Primary stimulus: Increased blood glucose levels

  • Parasympathetic nervous system (usually before eating)

  • Certain amino acids (leucine, arginine, lysine)

  • Gastrointestinal hormones (glucagon, gastrin, cholecystokinin, secretin)

  Inhibiting factors:

  • Low blood glucose (hypoglycemia)

  • High insulin levels (negative feedback to beta cells)

  • Sympathetic nervous system stimulation of beta cells

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  Circulation and Action

  Transport: Insulin circulates freely in the plasma and is not bound to a carrier protein.

  Target cells: Insulin binds to cell surface receptors found on cells throughout the body. This receptor activation initiates insulin signaling.

  Function: Insulin prevents hyperglycemia by allowing body cells to take up, use, and store carbohydrates, fat, and protein. It's called the "hormone of plenty" because it's secreted when food intake is high and works to move glucose from blood into cells.

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  Clinical Application: C-Peptide Measurement

  C-peptide level can be measured in the blood as an indirect measurement of serum insulin synthesis. This is useful clinically to evaluate β-cell destruction in diabetes, as C-peptide is released during insulin production

Diabetes management (oral and insulin)

• Insulin + Oral hypoglycemic drugs → both aim to produce normal blood glucose levels

• Non-insulin antidiabetic drugs:

  • Used for DM type 2

  • Effective treatment involves several elements:

    • Careful monitoring of blood sugar levels

    • Therapy w/ one or more drugs

    • Treatment of associated comorbid conditions like HTN and high cholesterol

• Biguanides (metformin)

  • MOA:

    • Decreases glucose production in liver

    • Decreases intestinal absorption of glucose

    • Increase uptake of glucose by tissues

    • Does not increase insulin secretion from the pancreas (doesn’t cause hypoglycemia)

  • Primarily affects GI tract: abdominal pain, bloating, nausea, cramping, diarrhea, feeling of fullness

  • May have metallic taste, reduced vitamin B12 levels

  • Lactic acidosis rare but life-threatening if it occurs

  • Contraindicated in renal/hepatic diseases

• Type 2 Diabetes Management First-Line Treatment

  Metformin is the first-line medication for new-onset type 2 diabetes, combined with lifestyle interventions. If A1C goals aren't achieved after 3-6 months with metformin at maximum tolerated dose and lifestyle modifications, add a second agent.

  Metformin mechanism:

  • Decreases glucose production by the liver

  • May decrease intestinal glucose absorption

  • Improves insulin receptor sensitivity

  • Increases peripheral glucose uptake

  • Decreases hepatic triglyceride and cholesterol production

  • Does NOT stimulate insulin secretion—no significant hypoglycemia or weight gain when used alone

  Additional Oral/Injectable Agents

  GLP-1 agonists:

  • Dulaglutide, exenatide, liraglutide, lixisenatide, semaglutide

  • Work like natural gut hormones released after food intake

  • Taken subcutaneously (daily or weekly); semaglutide available orally or subcutaneously

  SGLT2 inhibitors:

  • Prevent kidney reabsorption of filtered glucose

  • Excess glucose is excreted in urine

  When to Add Insulin

  Indications for insulin in Type 2 DM:

  • Target glucose levels not met with 2-3 different antidiabetic agents (including GLP-1 agonists)

  • A1C above 10% with diabetes symptoms at presentation

  • Beta cell function declines over time—some patients eventually require insulin alone or with other drugs

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  Insulin Regimens

  Basal coverage:

  • Intermediate-acting (NPH), long-acting (glargine, detemir), or ultra-long-acting (degludec)

  • Single daily injection for basal coverage, often combined with oral agents or GLP-1 for bolus stimulation

  • Effectiveness assessed by fasting blood glucose

  Multiple daily injections (MDI):

  • Basal dose (intermediate/long/ultra-long-acting)

  • Mealtime bolus (short/rapid-acting) to bring glucose into target range

  • Correction doses for elevations above target

  Combination therapy:

  • Two-thirds daily dose before breakfast, one-third before evening meal

  • Bedtime snack may prevent nocturnal hypoglycemia with NPH

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  Treatment Selection Factors

  Consider:

  • Efficacy, cost, side effects

  • Comorbidities, weight effects, hypoglycemia risk

  • Patient preference and ability to manage multiple dosages

  • Once-daily or once-weekly dosing improves adherence

  • Always combine with balanced eating and regular physical activity

• GLP-1s → Mimic naturally secreted incretin hormones

  • Incretin hormones increase insulin synthesis and lower glucagon secretions

  • Incretins increase insulin synthesis and lowers glucagon secretion

Non-insulin Antidiabetic drugs

• Metformin (Glucophage)

  • 1st-line drug and most commonly used oral med for treatment of DM type 2

  • Not used for DM type 1

• Sulfonylureas

  • 2nd gen → glimepiride (Amaryl), glipizide (Glucotrol), glyburide (DiaBeta)

  • Stimulate insulin secretion from the beta cells of the pancreas, increasing insulin levels

  • Beta cell function must be present

  • Improves sensitivity to insulin in tissues

  • Lowers blood glucose level

  • Adverse effects: hypoglycemia, hematologic effects, nausea, epigastric fullness, heartburn, and others

• Glinides:

  • Repaglinide (Prandin), nateglinide (Starlix)

  • Used for type 2

  • MOA is similar to Sulfonylureas

  • Increases insulin secretion from the pancreas

  • Adverse effects: hypoglycemia and weight gain

• Thiazolidinediones (glitazones)

  • Pioglitazone (Actos)

  • Rosiglitazone (Avandia) → only available through specialized manufacturer programs

  • “Insulin-sensitizing drugs”

  • Used for type 2

  • MOA: Decreases insulin resistance, increases glucose uptake and use in skeletal muscle, inhibits glucose and triglyceride production in the liver

  • Contraindications: HF; can exacerbate or cause HF→ peripheral edema, weight gain and decreased bone marrow density

Incretin Mimetics

• Mimic naturally secreted incretin hormones

  • Incretin hormones increase insulin synthesis and lower glucagon secretions

  • Incretins increase insulin synthesis and lower glucagon secretion

  • Oral + injectable

• Dipeptidyl peptidase IV inhibitors (DPP-IV)

  • “gliptins”

  • Sitagliptin (Januvia)

  • Saxagliptin (Onglyza)

  • Improve glycemic control in type 2

  • Used as an adjunct w/ diet and exercise

  • Adverse effects: upper respiratory tract infections, H/A, and diarrhea, possible pancreatitis

• Glucagon-like peptide-1 (GLP-1) receptor agonists

  • Semaglutide (Ozempic)

  • Exenatide (Byetta, Bydureon)

  • Liraglutide (Victoza)

  • Enhance glucose-dependent insulin secretion

  • Slows gastric emptying

  • Inc. 1st and 2nd phase insulin secretion

  • Indicated for pts w/ type 2 who have not been able to achieve blood glucose control w/ metformin, a sulfonylurea and/or a glitazone

  • Adverse effects:

    • Black box warning → risk of developing thyroid C-cell tumors

    • N/V

    • Diarrhea

    • Rare - hemorrhagic or necrotizing pancreatitis

    • Pts may experience weight loss of 5-10 pounds

GLP-1s

Mechanism of Action

GLP-1 agonists mimic natural incretin hormones released by the GI tract in response to food. They work by:

• Enhancing glucose-dependent insulin secretion

• Suppressing elevated glucagon secretion

• Slowing gastric emptying

• Increasing satiety

• Improving first- and second-phase insulin secretion

Natural incretins are rapidly broken down by the enzyme DPP-IV, but GLP-1 agonists resist this degradation.

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Available Medications

Injectable GLP-1s:

• Exenatide (Byetta, Bydureon)—twice daily or once weekly

• Dulaglutide (Trulicity)—once weekly

• Liraglutide (Victoza)—once daily

• Albiglutide (Tanzeum)—once weekly

• Lixisenatide (Adlyxin)

• Semaglutide (Ozempic)—once weekly

Oral option:

• Semaglutide (Rybelsus)—once daily

Combination products:

• Soliqua (insulin glargine + lixisenatide)

• Xultophy (insulin degludec + liraglutide)

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Clinical Use

Indications:

• Type 2 diabetes patients unable to achieve glucose control with metformin, sulfonylureas, and/or glitazones

• Added when lifestyle modifications and maximum metformin dose don't achieve A1C goals after 3-6 months

Administration:

• Best given 60 minutes before a meal

• Subcutaneous injection (except oral semaglutide)

Cardiovascular benefits:

• GLP-1s directly improve cardiovascular outcomes according to 2020 American College of Cardiology consensus

• Reduce risk for renal and heart disease, even in obese individuals without diabetes

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Additional Benefits

Weight management:

• GLP-1 receptor agonists cause significant weight loss4

• Helps control postprandial glucose by promoting glucose-dependent insulin secretion

• Lower HgA1C effectively

Safety note:

• All GLP-1s are pregnancy category C

Gestational diabetes

• Hyperglycemia that develops during pregnancy

• Insulin must be given to prevent birth defects

• Usually subsides after delivery

• 30% of patients may develop DM type 2 within 10-15 years

Definition

Gestational Diabetes Mellitus (GDM) is carbohydrate intolerance that develops during pregnancy, regardless of whether management includes medication (insulin or oral hypoglycemic agents) or only dietary changes. The American Diabetes Association defines GDM as diabetes diagnosed during pregnancy that is clearly not preexisting (overt) diabetes.

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Pathophysiology

GDM develops during the second or third trimester when:

• Fetal nutrient demands increase

• Maternal insulin resistance rises due to placental hormones, cortisol, and insulinase

• Maternal insulin demands increase as much as threefold

• The pancreas cannot produce sufficient insulin or insulin isn't used effectively

Most pregnant women compensate by increasing insulin production, but those who cannot develop GDM.

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Screening

Timing: 24-28 weeks of gestation

Two-step method (ACOG recommended):

1. Step 1: 50-g oral glucose load (no fasting required), plasma glucose measured at 1 hour

   • Positive screen: 130-140 mg/dL or higher

2. Step 2: 3-hour (100-g) oral glucose tolerance test (OGTT) on another day if step 1 positive

   • Requires overnight fast and at least 3 days of unrestricted diet (≥150 g carbohydrates)

   • Avoid caffeine and smoking for 12 hours before test

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Maternal and Fetal Risks

Pregnancy complications:

• Infant macrosomia (extra-large baby)

• Neonatal hypoglycemia

• Preeclampsia

• Cesarean delivery

Long-term maternal risks:

• Up to one-third will have diabetes or impaired glucose metabolism postpartum

• High risk for recurrent GDM in future pregnancies

• Up to 70% chance of developing type 2 diabetes within 10-20 years

Child health risks:

• Increased risk for obesity and type 2 diabetes later in life

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Management

CDC recommendations:

1. Eat healthy foods

2. Exercise regularly

3. Monitor blood sugar often

4. Take insulin if needed

5. Get tested for diabetes after pregnancy

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Postpartum Follow-up

Immediate screening:

• 75-g, 2-hour OGTT or fasting plasma glucose at 6-12 weeks postpartum

Lifelong monitoring:

• Repeat screening at least every 3 years with normal postpartum results

• Use hemoglobin A1c, fasting plasma glucose, or 75-g 2-hour OGTT

Diabetes medications and contraindications/contrast

• Metformin will need to be discontinued if the patient is to undergo studies w/ contrast dye because of possible renal effects → check w/ prescriber

Diabetes medications and NPO status

• If a pt is NPO for a test or procedure, consult the PCP to clarify orders for antidiabetic drug therapy

• General Principles

  When a patient is NPO, it's crucial to follow the prescriber's orders regarding diabetes medication administration. If there are no written orders about NPO status and diabetes medications, contact the prescriber for further instructions.

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  Oral Diabetes Medications

  Timing is critical:

  • Ensure food will be or is being tolerated before the dose is given

  • If oral medication is taken without a meal or the meal is delayed, hypoglycemia may result and cause negative health consequences, even unconsciousness

  Preoperative management:

  • Sulfonylureas: Discontinued 1 day before surgery

  • Metformin: Stopped at least 24 hours before surgery; restarted only after kidney function documented as normal

  • All other oral drugs: Stopped the day of surgery

  SGLT2 inhibitors:

  • Usually given in the morning before the first meal

  • Follow prescriber's orders if patient is NPO

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  Insulin Management

  Rapid-acting and short-acting insulin:

  • Will cause hypoglycemia if patient is not eating

  • Should NOT be given when NPO

  Amylin and incretin mimetics:

  • Also cause hypoglycemia if patient is not eating

  • Should NOT be given when NPO

  Basal insulin (intermediate or long-acting):

  • Should be given when patient is NPO (often at a reduced dose)

  • Controls baseline glucose levels independent of food intake

  Special consideration: If patient is NPO but receiving IV dextrose solution, the prescriber may still order insulin—always clarify the order

  Preoperative insulin adjustments:

  • Long-acting insulin may need to be switched to intermediate-acting forms 1-2 days before surgery

  • Target preoperative blood glucose: <200 mg/dL

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  Inpatient Insulin Management

  Hospitalized patients:

  • Continuous IV insulin (insulin drip): Most effective for critically ill patients

  • Scheduled subcutaneous injections: Basal, meal, and correction doses for non-critically ill patients

Rapid-acting insulin (Peak and Duration)

• Most rapid onset of action → 5-15 minutes

• Peak: 1 to 2 hours

• Duration: 3 to 5 hours

• Pt must eat a meal after injection

• Don’t LAG -

  • lispro (Humalog)

  • aspart (Novolog)

  • glulisine (apidra)

• Given SUBQ or via continuous SUBQ infusion pump, NOT IV

Short-acting insulin (Peak and Duration)

• Humulin R

• Routes: IV bolus, IV infusion, IM, and SUBQ

• SUBQ route -

  • Onset: 30 to 60 minutes

  • Peak: 2.5 hours

  • Duration: 6 - 10 hours

• IV route -

  • Immediate onset

  • Duration: 2 to 6 hours

Intermediate acting insulin (Peak and Duration)

• Insulin isophane suspension (NPH) *cloudy

• Clear (regular) → cloudy (NPH) when mixing

• Onset: 1 to 2 hours

• Peak: 4 to 8 hours

• Duration: 10 to 18 hours

Long-acting insulin (Peak and Duration)

• Insulin glargine (Lantus) or “basal insulin”

  • Clear and colorless, constant level of insulin in the body, usually dosed once daily but can be dosed every 12 hours

  • Onset: 1 to 2 hours

  • Peak: None

  • Duration: 24 hours

• Detemir (Levemir)

  • Duration of action is dose dependent

• Degludec (Tresiba)

  • Ultra-long-acting

  • Once daily

GLP-1 Effects

• Adverse effects:

  • Black box warning → risk of developing thyroid C-cell tumors

  • N/V

  • Diarrhea

  • Rare - hemorrhagic or necrotizing pancreatitis

  • Pts may experience weight loss of 5-10 pounds

• Physiological Effects

  Insulin and glucagon regulation:

  • Enhance glucose-dependent insulin secretion

  • Suppress elevated glucagon production

  • Improve first- and second-phase insulin secretion

  Gastrointestinal effects:

  • Slow gastric emptying

  • Increase satiety (feeling of fullness)

  Background: GLP-1 is an endogenous incretin hormone naturally released by the GI tract in response to food intake. In type 2 diabetes, β-cell responsiveness to GLP-1 is decreased, reducing insulin secretion after meals.

  ---

  Clinical Benefits

  Glucose control:

  • Help control postprandial glucose levels by promoting glucose-dependent insulin secretion

  • Lower HgA1C effectively

  Weight management:

  • Cause significant weight loss

  • Improve weight management for individuals with type 2 diabetes

  Cardiovascular and renal protection:

  • Reduce risk for renal and heart disease, even in obese individuals without type 2 diabetes

  • Directly improve cardiovascular outcomes

  ---

  How They Work

  Natural incretin hormones like GLP-1 are rapidly broken down by the enzyme DPP-IV. GLP-1 agonist medications resist this degradation, allowing prolonged therapeutic effects.

  Effect is glucose-dependent: GLP-1s stimulate insulin secretion primarily when blood glucose is elevated, which reduces the risk of hypoglycemia compared to some other diabetes medications.

  ---

  Summary of Key Effects

  ✓ Stimulate insulin release (when glucose is elevated)
  ✓ Reduce glucagon secretion
  ✓ Slow stomach emptying
  ✓ Increase fullness after eating
  ✓ Promote weight loss
  ✓ Protect heart and kidneys
  ✓ Lower A1C levels

Treatment of Hypoglycemia

• Hypoglycemia → abnormally low blood glucose level (below 70 mg/dL)

  • Mild cases can be treated w/ diet → higher protein intake and lower carbohydrate intake to prevent rebound hypoglycemia

• Glucose-elevating drugs:

  • Oral forms of concentrated glucose → buccal tablets and semisolid gel

  • IV → 50% dextrose in water (D50W)

  • SUBQ → glucagon

• Recognition of Hypoglycemia

  Definition: Blood glucose below 70 mg/dL (3.9 mmol/L)

  Early warning symptoms (autonomic):

  • Sweating, irritability, tremors

  • Anxiety, tachycardia, hunger

  Advanced symptoms (neuroglycopenic):

  • Confusion, paralysis

  • Seizures, coma

  ---

  The 15-15 Rule (Hospital Protocol)

  Step 1: Give fast-acting carbohydrate

  • 15 g of carbohydrate if blood glucose <70 mg/dL (3.9 mmol/L)

  • 30 g of carbohydrate if blood glucose <50 mg/dL

  • Preferred: Liquid form (if patient can swallow)

  • Avoid: High-potassium options like orange juice; chocolate and concentrated sweets (fat slows absorption)

  Step 2: Recheck in 15 minutes

  • If still low: Repeat same treatment

  • If above hypoglycemic range: Follow with complex carbohydrate (crackers with nut butter)

  Why complex carbs matter: They help prevent subsequent hypoglycemia after initial treatment

  ---

  When Patient Cannot Swallow

  Drug options:

  • IV concentrated dextrose (hospital setting)

  • IM or nasal glucagon (first-line therapy for severe hypoglycemia)

  Glucagon precautions:

  • Can induce vomiting

  • Position patient on side to prevent aspiration

  IV dextrose precautions:

  • Give carefully to avoid extravasation (hyperosmolar solution can damage tissue)

  ---

  Monitoring After Treatment

  Short-term:

  • Monitor blood glucose every 15 minutes until hypoglycemia resolves

  • Continue monitoring for several hours (effects of glucagon and dextrose are temporary)

  Target glucose level: 70-110 mg/dL (3.9-6.2 mmol/L)

  Additional treatment may be needed if initial response is inadequate

  ---

  Best Treatment Approach

  Most effective: Glucose or glucose-containing foods, NOT complex carbohydrates initially

  Treatment sequence:

  1. Fast-acting simple carbohydrate (glucose tablets, gel, juice, non-diet soda)

  2. Recheck blood glucose

  3. Follow with complex carbohydrate once resolved

Endocrine and Thyroid Disease

Treatment of Diabetes Insipidus (DI)

• Diabetes insipidus → insufficiency of ADH causing loss of too much water in the urine (3-5L/day)

  • Two forms:

    • Neurogenic (central) - insufficient secretion of ADH

      • doesn’t release enough vasopressin

    • Nephrogenic - inadequate response to ADH

      • vasopressin is present but doesn’t respond properly

  • Symptoms:

    • Polyuria

    • Nocturia

    • Continuous thirst

• Treatment:

  • Desmopressin (DDAVP) → replaces the missing hormone vasopressin

  • Nephrogenic: also uses a thiazide diuretic (HCTZ)

Diabetes insipidus (DI) presents as excessive thirst (polydipsia), excessive urination (polyuria), and dehydration due to deficiency or resistance to antidiuretic hormone (ADH/vasopressin).

Two main types:

• AVP-D (Arginine Vasopressin Deficiency): Insufficient ADH production

• AVP-R (Arginine Vasopressin Resistance): Kidneys don't respond to ADH

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Drug Therapy for AVP-D

Primary medication: Desmopressin (DDAVP)

• Synthetic replacement for natural vasopressin (ADH)

• Routes available: Oral, sublingual "melt," subcutaneous, intranasal metered spray

• Dosing frequency: Varies with individual patient response

Alternative: Vasopressin (Pitressin)

• Available as nasal spray or injection (IM/IV)

• Used to prevent or control polydipsia, polyuria, and dehydration in DI

Route selection considerations:

• Intranasal preparations may cause mucosal ulceration, allergy, chest tightness, or lung inhalation

• Intranasal changes can lead to unpredictable drug absorption

• If side effects occur or patient has upper respiratory infection, switch to oral or subcutaneous route

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Treatment of AVP-R

Non-drug approaches:

• Low-salt diet: <2.3 g sodium/day

• Low-to-normal protein: <1.0 mg/kg daily

• Thiazide diuretics: Induce mild volume depletion; even 1-1.5 kg weight loss significantly reduces urine output

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Key Nursing Monitoring

Risk: Fluid overload/water toxicity

• Drug therapy induces water retention

• Daily weights: Same scale, time, clothing

• Warning signs: Weight gain >2.2 lb (1 kg), persistent headache, confusion, nausea, vomiting

• Action: Go to ED or call 911 immediately

Hospitalized patients:

• Accurately measure I&O

• Check urine specific gravity

• Daily weights

• Ensure fluid intake equals urine output

Missed doses: Can cause severe electrolyte abnormalities leading to significant harm or death

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Patient Education

✓ Wear medical alert bracelet
✓ Recognize polyuria/polydipsia as signs needing another dose
✓ May require lifelong therapy
✓ Children need unrestricted water/bathroom access at school

Administration of thyroid medication

• Hypothyroidism is treated w/ levothyroxine (Synthroid) (T4), which replaces the hormone the thyroid isn’t making enough of

  • Take on an empty stomach 30-60 minutes before food intake

  • Meds and supplements can interfere w/ absorption

  • Do not stop taking thyroid medication abruptly

  • TSH level checked 6-8 weeks after change of dose

Timing and Food Interactions

Take on an empty stomach

• 30 to 60 minutes before breakfast

• Tube feedings can impair absorption

Why timing matters: Food interferes with medication absorption, reducing effectiveness

---

Consistency is Critical

Same brand throughout treatment

• Switching between brands can destabilize treatment

• If brand change occurs, monitor thyroid function tests more carefully

Daily routine:

• Take consistently every morning

• Helps maintain stable hormone levels

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Dosing Precautions

Common medication error:

• Levothyroxine is dosed in micrograms (mcg), NOT milligrams (mg)

• Writing dose in milligrams results in 1000-fold overdose

• Doses higher than 200 mcg need to be questioned

Starting therapy safely:

• Start at lowest dose for:

  • Older adults

  • Patients with cardiac disease

  • Severe hypothyroidism

  • Unknown degree of hypothyroidism

• Dose gradually increased over weeks if needed

• Too high or too rapid increases can cause abnormal heart rhythms, heart failure, or myocardial infarction

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Special Situations

Myxedema coma:

• May require IV administration due to severely reduced GI motility and absorption

Before thyroid scans:

• Usually discontinued 4 weeks before radioactive iodine studies (as prescribed)

Older adults (≥60 years):

• May require 25% dose reduction

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Drug Interactions to Avoid

Fiber supplements:

• May interfere with thyroid hormone absorption

Over-the-counter medications:

• Do not take without consulting provider—thyroid hormones interact with many drugs and supplements

---

Monitoring Effectiveness

Two easiest self-monitoring parameters:

1. Sleep requirements (need for more sleep may indicate low levels)

2. Bowel elimination (constipation may indicate low levels)

If these worsen: Contact provider for potential dose adjustment

Digestive Health

Treatment of Diarrhea

• Diarrhea: Presence of loose, watery stools, acute or persistent

  • Large-volume diarrhea → Caused by excessive amounts of water or secretions, or both, in the intestines

  • Small-volume diarrhea → Volume of feces is not increased; usually results from excessive intestinal motility

• Treatment:

  • Fluid restoration, antimotility, or water-absorbent medications, and treatment of causal factors

  • Oral rehydration if tolerated

  • BRAT diet

  • Imodium (loperamide) → if there is no blood in the stool, “don’t love” as overuse can cause constipation

  • Pepto-Bismol → avoid if allergic to ASA or taking blood thinners

• Antidiarrhea Drug Classes:

  • Antimotility/anticholinergics → Imodium (loperamide)

    • Decrease intestinal muscle tone and peristalsis of the GI tract, slowing the movement of fecal matter; reduce peristalsis and gastric secretions

  • Absorbents → Pepto-Bismol

    • Coat the walls of the GI tract and bind to the causative bacteria or toxin, which is then eliminated through the stool; avoid if allergic to ASA or taking blood thinners

  • Probiotics → Lactobacillus acidophilus (Bacid)

    • AKA intestinal flora modifiers and bacterial replacement drugs; Lactobacillus supplies missing bacteria and suppresses growth of diarrhea-causing bacteria

• Anticholinergics and opiates used for more serious cases

Primary objectives:

• Stop stool frequency and alleviate abdominal cramps

• Replenish fluids and electrolytes

• Prevent weight loss and nutritional deficits from malabsorption

Often fluid replacement is the only treatment needed

---

Oral Rehydration Therapy (ORT)

First-line treatment for acute diarrhea with dehydration

Why ORT is preferred:

• More effective, safer, less painful, and less costly than IV rehydration

• Recommended by American Academy of Pediatrics, WHO, and CDC

Oral rehydration solutions (ORS):

• Enhance and promote reabsorption of sodium and water

• Greatly reduce vomiting, illness duration, and need for IV fluids

• Available as commercially prepared solutions in the U.S.

Administration:

• Give in small quantities at frequent intervals4

• Vomiting is NOT a contraindication unless severe

After rehydration:

• Alternate ORS with low-sodium fluids (breast milk, lactose-free formula, or half-strength lactose-containing formula) during maintenance therapy

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Antidiarrheal Medications

Three main categories:

1. Adsorbents

2. Antimotility drugs (anticholinergics and opiates)

3. Probiotics (intestinal flora modifiers)

Bismuth subsalicylate (specific example):

• Turns stool black or gray

• Chewable tablets: chew thoroughly with ≥6 oz water

• Non-chewable tablets: take with 6-8 oz water

• Do NOT combine with other salicylates (risk of toxicity)

• Avoid in children/teens with viral infections (chickenpox, influenza) due to Reye's syndrome risk

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Dietary Management

Reintroduce normal diet after rehydration

• Slightly higher stool output initially is expected

• Benefits of continuing normal diet: Better nutritional outcomes, fewer complications, shorter illness duration

• These benefits outweigh temporary stool frequency increase

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When to Seek Medical Attention

Contact provider if:

• Symptoms persist despite treatment

• Signs of dehydration worsen

Hospitalization may require:

• NPO status for 12-48 hours

• Parenteral fluid therapy

Treatment of constipation – medication actions

Laxatives

• Bulk forming

• Hyperosmotic

• Stimulant

• Emollient (stool softeners, lubricant laxatives)

• Saline

Laxatives: Bulk Forming

• Examples:

  • Psyllium (Metamucil)

  • Methylcellulose (Citrucel)

• MOA:

  • High fiber

  • Absorbs water to increase bulk

  • Distends the bowel to initiate reflex bowel activity

• Indications:

  • Acute and chronic constipation

  • IBS

  • Diverticulosis

Bulk-forming laxatives

• Absorb water into the intestine, increasing bulk and distending the bowel

• Trigger reflex bowel activity promoting movement

• Produce normal, formed stools

• Safest for long-term use

• Must take with liberal amounts of water to prevent esophageal obstruction or fecal impaction

• Examples: psyllium (natural), methylcellulose (synthetic)

Laxatives: Emollient

• Examples:

  • Docusate salts (Colace, Surfak) → stool softeners

  • Mineral oil → lubricant

• MOA:

  • Stool softeners and lubricants

  • Promote more water and fat in the stools

  • Lubricate the fecal material and intestinal walls

• Indications:

  • Acute and chronic constipation

  • Fecal impaction

  • Facilitation of bowel movements in anorectal conditions

Emollient laxatives (stool softeners and lubricants)

• Docusate salts: Lower surface tension of GI fluids so more water and fat absorb into stool

  • Facilitate passage of water and lipids into fecal mass

  • Do NOT cause defecation—only soften stool to ease passage

• Mineral oil: Lubricates fecal material and intestinal wall, preventing water absorption

  • Water remains in bowel to soften and expand stool

  • Promotes bowel distention and reflex peristalsis

Laxatives: Hyperosmotic

• Examples:

  • Polyethylene glycol (PEG)

  • Sorbitol, lactitol, glycerin

  • Lactulose (also used to reduce serum ammonia levels)

• MOA:

  • Increased fecal water content

  • Results in bowel distention, increased peristalsis, and evacuation

• Indications:

  • Chronic constipation

  • Diagnostic and surgical preps

Hyperosmotic laxatives

• Increase fecal water content, causing distention

• Result: increased peristalsis and evacuation

• Action limited to large intestine

Laxatives: Saline

• Examples:

  • Magnesium hydroxide (Milk of Magnesia)

  • Magnesium citrate

• MOA:

  • Increases osmotic pressure within the intestinal tract, causing more water to enter the intestines

  • Results in bowel distention, increased peristalsis, and evacuation

  • “works from above” → pushes down

• Indications:

  • Constipation

  • Diagnostic and surgical preps

Saline laxatives

• Increase osmotic pressure in small intestine

• Inhibit water absorption

• Increase water and electrolyte secretions from bowel wall into bowel lumen

• Produce watery stool

• Increased distention promotes peristalsis and evacuation

• Rectal enemas: produce defecation in 2-5 minutes

Laxatives: Stimulant

• Examples:

  • Senna (Senokot)

  • Bisacodyl (Dulcolax)

• MOA:

  • Increases peristalsis via intestinal nerve stimulation

• Common after surgery

  • Anesthesia slows smooth muscle activity

• Indications:

  • Acute constipation

  • Diagnostic and surgical preps

• Stimulant laxatives

  • Stimulate nerves that innervate the intestines

  • Result: increased peristalsis

  • Also increase fluid in the colon, increasing bulk and softening stool

Renal

Adrenergic Blockers

• Drugs that stimulate the sympathetic nervous system (SNS)

• Fight-or-flight

  • Run faster → Increases HR

  • Breathe better → widens airway

  • Pumps harder → more blood to muscles

• Catecholamines: are the “emergency drugs” that activate the adrenergic and dopaminergic receptors, fight-or-flight chemicals

  • Norepinephrine (NE)

  • Epinephrine (EPI)

  • Dopamine

• Located throughout the body, there are receptors for the sympathetic neurotransmitters

  • Alpha-adrenergic receptors

  • Beta-adrenergic receptors

  • Dopaminergic receptors → only respond only to dopamine

    • Receptors determine where these effects occur

The Adrenergic Receptors

• Alpha-1 adrenergic receptors are located on postsynaptic effector cells (the cell, muscle, or organ that the nerve stimulates)

• α1 = constricts blood vessels

  • Vasoconstriction

  • Increased BP

  • Pupil dilation

  • Urinary retention

    • e.g. → phenylephrine

• Alpha-2 adrenergic receptors are located in the brain (the nerve that stimulates the effector cells)

  • α2 stimulation = BP decreases

• α2 = shuts down norepinephrine release

  • Decreases sympathetic activity

  • Lowers BP

  • Slows HR

    • e.g. → clonidine

• Beta-Adrenergic Receptors → all located on postsynaptic effector cells

  • Beta-1 adrenergic receptors are located primarily in the heart

  • B1 = One heart

  • Effects:

    • Increased HR

    • Increased contractility

    • Increased cardiac output

      • e.g. → dobutamine

• Beta- 2 adrenergic receptors are located in the cmooth muscle of the bronchioles, arterioles, and visceral organs

  • B2 = Two lungs

  • Effects:

    • Bronchodialation

    • Vasodialation

    • Relaxed uterus

      • e.g. → albuterol and terbutaline

Dopaminergic Receptors

• D1 = “Dilate and Diurese”

  • Causes dilation of the following blood vessels, resulting in increased blood flow

    • Renal

    • Mesenteric

    • Coronary

    • Cerebral

• D2 = Don’t release dopamine

  • Effects:

    • Inhibits dopamine release

    • Affects movement, mood, and nausea

    • Example → Tetrabenazine, lowers the amount of dopamine released to decrease involuntary movements

  • Clinical correlation:

    • Antipsychotics block D2 receptors

    • Metoclopramide blocks D2 receptors to reduce nausea

    • Parkinsons meds

Epinephrine

• Epinephrine = The Superhero

  • “Works everywhere”

• Stimulates:

  • a1

  • B1

  • B2

• Effects:

  • Increases HR

  • Increases contractility

  • Increases bronchodilation

  • Increases BP

• Uses:

  • Anaphylaxis

  • Cardiac arrest

  • Severe asthma reactions

• If the pt can’t breathe and their BP is crashing, think → epinephrine

Norepinephrine

• Norepinephrine = The Pressure Drug

  • “Squeeze the vessels”

• Stimulates:

  • a1 strongly

  • B1 somewhat

• Effects:

  • Vasoconstriction

  • Increased SVR

  • Increased BP

• Uses:

  • Septic shock

  • Vasodilatory shock

  • “any kind of BP support”

Dopamine

• Dopamine = The Dose Drug

• Dopamine is a dopaminergic drug that becomes an adrenergic drug as the dose rises

  • Effects change w/ the dose

    • Low → kidneys

    • Medium → heart

    • High → blood vessels

• Receptors

  • D1

  • B1

  • a1

Low-dose dopamine

• Low-dose dopamine (0.5 - 2 mcg/kg/min)

• Simulates D1 receptors → D for diuresis

• Effects:

  • Increases kidney perfusion

  • Increases urine output

    • “Kick to the kidneys to work”

Medium-dose dopamine

• Medium-dose dopamine (2 - 10 mcg/kg/min)

• Stimulates B1 receptors → works more on the heart

• Effects:

  • Increases HR

  • Increases contractility

  • Increases cardiac output

• “Dopamine wakes up the heart”

  • Used as opposed to open heart surgery

High-dose dopamine

• High-dose dopamine (>10 mcg/kg/min)

• Activates a1 receptors

• Effects:

  • Vasoconstriction

  • Increases BP

• “Dopamine starts squeezing vessels”

Medication and administration of the patient with hypotension

Vasoactive Adrenergic Medications

Primary drugs for hypotension/shock:

• Norepinephrine (Levophed)

• Dopamine

• Epinephrine

• Phenylephrine (Neo-Synephrine)

• Ephedrine

• Dobutamine

• Midodrine

• Fenoldopam

Also available: Angiotensin II (Giapreza) - not an adrenergic but used as vasoactive agent for septic or other shock

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Administration Guidelines

Route: IV infusion only (except midodrine)

• Use continuous IV infusion

• Only use clear solutions

• Administer with IV infusion pump

• Follow manufacturer's instructions and suggested infusion rates

Dosing:

• Titrated to desired physiologic response

• Very potent and quick-acting

• Effects cease quickly when stopped

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Critical Nursing Monitoring

IV site assessment:

• Check every hour for infiltration

• Infiltration causes tissue necrosis from excessive vasoconstriction

• Phentolamine used to treat infiltration

Cardiac monitoring:

• Continuous vital signs

• Heart sounds

• ECG monitoring

Dangers of improper administration:

• Too rapid infusion causes precipitous, dangerously high blood pressure2

• Elevated pulse rate with subsequent complications

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Important Safety Alerts

Medication error risk:

• Norepinephrine (Levophed) vs. Phenylephrine (Neo-Synephrine) sound alike

• Both may be ordered simultaneously

• Wrong drug administration possible—verify carefully

• Epinephrine concentration:

• Now labeled in mg/mL (no longer ratios)

• Available in two strengths for IV use

• Carefully check correct concentration against order

---

Specific Drug: Dopamine

Unique renal benefit:

• Lacks renal vasculature vasoconstriction

• Improves perfusion through kidneys

• Salvages kidney function while increasing blood pressure

---

Oral Option for Chronic Hypotension

Droxidopa (Northera):

• For neurogenic orthostatic hypotension

• Converted to norepinephrine in the body

• Black box warning: Supine hypertension risk

• Sleep with head/upper body elevated

• Last dose ≥3 hours before bedtime

Overactive Bladder - treatment

Overactive Bladder - treatment cont.

Lifestyle modifications:

• Pelvic floor (Kegel) exercises—muscle contraction inhibits detrusor contraction, providing time to reach toilet

• Bladder training with timed voiding

• Managing fluid intake, caffeine, and alcohol

• Managing constipation

• Biofeedback techniques

Beta₃-Adrenergic Agonists

Medications:

• Mirabegron (Myrbetriq)

• Vibegron (Gemtesa)

Mechanism:

• Stimulates beta₃ receptors in urothelium and detrusor muscles

• Relaxes detrusor muscle during storage phase

• Increases bladder capacity

Adverse effects (different from antimuscarinics):

• Hypertension—monitor blood pressure

• Urinary tract infection

• Headache

• Nasopharyngitis

• Nausea and dizziness

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Advanced Therapies (Neuromodulation)

When behavioral/pharmacologic therapy insufficient:

• Intradetrusor botulinum toxin A (Botox) injections—inhibits acetylcholine release

• Peripheral tibial nerve stimulation

• Sacral neuromodulation

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Nursing Monitoring

When starting antimuscarinics:

• Use bladder diary to track effectiveness

• Monitor for decreased urgency, frequency, and incontinence episodes

• Regularly assess for constipation via bowel movement record

For mirabegron: Monitor blood pressure regularly