Endo

Unit 1: Blood

Aplastic Anemia + Hematopoietic Factors

What is Aplastic Anemia?

• Your bone marrow = factory that makes blood cells (red cells, white cells, platelets).

• In aplastic anemia, the factory shuts down. Not enough new cells get made.

• It can come on suddenly or slowly, and it can be mild or life-threatening.

• Causes:

  • Radiation, toxic chemicals, chemotherapy → damage bone marrow.

  • Autoimmune diseases → immune system attacks bone marrow.

  • Rarely inherited (from birth).

• Symptoms: tiredness, infections, bleeding/bruising (because you don’t have enough cells).

• Treatments:

  • Blood transfusions (give temporary new cells).

  • Bone marrow transplant (replace the factory).

  • Immune suppressive drugs (stop immune system from attacking marrow).

  • Hematopoietic factors (growth factor drugs that “wake up” blood cell production).

Hematopoietic Factors (Growth Factors)

• Fancy word for “drugs that tell your bone marrow to make more blood cells.”

• Your body naturally makes them, but we also make drug versions using recombinant DNA technology (genetic engineering).

• Clinically used for:

  • Aplastic anemia

  • Kidney failure (EPO)

  • Infections (to boost white cells)

  • During chemo or bone marrow transplant

Erythropoietin (EPO) → makes Red Blood Cells

• Normally made in the kidneys. If kidneys fail → anemia.

• Uses: anemia from kidney disease, AIDS, chemo, prematurity, inflammation.

• But you must also have enough iron, B12, and folate or the EPO won’t work.

• Drugs:

  • Epoetin (EPO) → given 3x/week.

  • Darbepoetin (Aranesp) → engineered with more sugar groups → longer half-life → given weekly.

  • Methoxy-PEG epoetin beta (Mircera) → PEG chain added → makes drug bigger, lasts longer → given every 2-4 weeks.

• Black Box Warnings: risk of heart attack, stroke, blood clots, tumor growth.

• Contraindications: uncontrolled high BP, allergic reactions, pure red cell aplasia.

Peginesatide (Omontys)

• A synthetic peptide (not related to EPO, but acts on the same receptor).

• Pegylated → longer half-life.

• Given monthly.

• Indication: anemia from chronic kidney disease (on dialysis).

• Risks: same black box warnings as EPO.

Myeloid Growth Factors (White Blood Cell Stimulators)

Help prevent infections when white cells (neutrophils) are too low.

• GM-CSF (Granulocyte-Macrophage Colony Stimulating Factor)

  • Drug: Sargramostim (Leukine).

  • Uses:

    • Increase neutrophils after chemo or transplant.

    • Collect stem cells for transplant.

    • Radiation exposure recovery.

  • Side effects: fever, nausea, diarrhea, swelling, rash, liver problems, lung issues.

  • No black box warning.

• G-CSF (Granulocyte Colony Stimulating Factor)

  • Drugs: Filgrastim (Neupogen), Pegfilgrastim (Neulasta).

  • Stimulates neutrophil production.

  • Uses: severe neutropenia, after chemo or transplant, before stem cell collection.

  • No black box warning.

Thrombopoietic Growth Factors (Platelet Stimulators)

Help make more platelets (for clotting).

• Romiplostim (Nplate)

  • Peptibody (protein + antibody piece).

  • Activates TPO receptor (normally turned on by natural thrombopoietin).

  • Use: immune thrombocytopenia not responding to other treatments.

  • Given weekly, adjusted based on platelet count.

  • No black box warning.

• Eltrombopag (Promacta)

  • Small molecule pill.

  • Uses:

    • Immune thrombocytopenia

    • Thrombocytopenia from Hepatitis C

    • Severe aplastic anemia

  • Black box warning: liver failure risk (especially in hepatitis patients).

Iron Deficiency Anemia

🩸 Iron = the raw material your body needs to build hemoglobin (the oxygen-carrying protein in red blood cells).

• Without enough iron → you make small, pale red blood cells → called microcytic, hypochromic anemia.

Causes

• Dietary deficiency (not eating enough iron)

• Blood loss (periods, ulcers, GI bleeding)

• Pregnancy (higher demand)

• Infants/children (growth spurts)

Symptoms

• Fatigue, weakness

• Pale skin

• Shortness of breath

• Craving weird things like dirt/ice (called pica)

Iron Supplements

Two main types:

1. Oral Iron (by mouth)

   • Cheap, effective.

   • Takes weeks–months to fix anemia.

   • Best absorbed on an empty stomach but often taken with food because it causes GI upset.

   • Side effects: constipation, nausea, black stools.

   • Examples: Ferrous sulfate, Ferrous gluconate.

2. Parenteral Iron (IV/IM)

   • Used when patient can’t take oral or needs rapid replacement.

   • Preparations: Iron dextran, Ferric gluconate, Iron sucrose.

   • Risks: allergic reactions (esp. iron dextran), low BP, joint/muscle pain.

Vitamin B12 Deficiency Anemia

📌 B12 = needed for DNA synthesis + myelin (nerve insulation).

• Without B12, red blood cells are big but fragile → called megaloblastic anemia.

Causes

• Pernicious anemia (autoimmune disease → body destroys intrinsic factor, a protein in stomach needed to absorb B12).

• GI surgery/disease (like gastric bypass, Crohn’s).

• Strict vegan diet (B12 only comes from animal products).

Symptoms

• Fatigue, pallor

• Neurological symptoms: numbness, tingling, memory loss, confusion (because of myelin damage).

Treatment

• Vitamin B12 replacement:

  • Oral (if mild, and gut absorption is ok).

  • IM injection (if intrinsic factor is missing).

  • Nasal spray also available.

• Works quickly for blood symptoms, but nerve damage may be permanent if untreated too long.

Folate (Folic Acid) Deficiency Anemia

📌 Folate = also needed for DNA synthesis.

• Without it, cells get stuck in growth phase → also megaloblastic anemia (like B12 deficiency).

Causes

• Poor diet (common in alcoholics).

• Pregnancy (higher need).

• Certain drugs (methotrexate, phenytoin, trimethoprim).

Symptoms

• Same as B12 anemia BUT no neurological problems.

Treatment

• Oral folic acid supplements.

• Preventive in pregnancy to avoid neural tube defects in baby (spina bifida).

✅ Comparison Chart

💡 Memory Trick:

• Iron → small red cells (think “low iron = shrunken cells”).

• B12 & Folate → big red cells (think “B vitamins = Big cells”).

• Neuro issues? Only B12!

🔑 Big Learning Goals

• Understand how calcium and phosphate are balanced in the body.

• Know the main “players”:

  • PTH (parathyroid hormone)

  • Vitamin D

  • FGF23 (fibroblast growth factor 23)

  • Calcitonin

• Learn how these hormones affect bones, kidneys, and intestines.

• Learn treatments for too much calcium (hypercalcemia) and too little calcium (hypocalcemia).

• Understand bone diseases like osteoporosis and the drugs used to treat them.

🧮 Calcium Basics

• Your body has 1.5 kg of calcium total.

• 98% of it is in your bones = your skeleton acts like a giant calcium bank.

• Calcium helps:

  • Keep bones hard

  • Muscles contract

  • Nerves send signals

• In blood, calcium is found in 3 forms:

  • Protein-bound (40%)

  • Complexed with anions (10%)

  • Free / ionized calcium (50%) → this is the active form.

• Normal blood calcium = 10 mg/dL (2.5 mM).

🍽 Calcium In & Out

• Food source: 75% comes from dairy.

• Daily needs:

  • Teens: 1300 mg

  • Adults: 1000 mg

  • Age 50+: 1200 mg

• Absorption:

  • Active transport (Vitamin D–dependent) = duodenum

  • Passive diffusion = rest of small intestine

• Drugs like glucocorticoids & phenytoin lower absorption.

• Kidneys: filter 9 g/day but reabsorb 98% (mainly controlled by PTH).

🔄 Calcium Turnover

• In healthy adults:

  • Intake = output (no net bone loss).

  • 800 mg eaten → 150 mg absorbed → balanced by kidney excretion.

• The kidney is the main regulator of balance.

🧬 The Four Main Hormones

1. Parathyroid Hormone (PTH)

• Released when blood calcium is low.

• Effects:

  • Intestine → ↑ calcium absorption (via Vitamin D)

  • Kidney → ↓ calcium excretion, ↑ phosphate excretion

  • Bone →

    • Small bursts = bone formation

    • Long-term high levels = bone breakdown

• Drugs:

  • Teriparatide (Forteo) = PTH fragment (34 AA)

  • Abaloparatide (Tymlos) = engineered variant

  • Used for osteoporosis (daily injection)

  • ⚠ Risks: hypercalcemia, osteosarcoma (seen in rats)

2. Vitamin D (actually a hormone!)

• Vitamin D2 (ergocalciferol) = plant source

• Vitamin D3 (cholecalciferol) = skin (UV light + 7-dehydrocholesterol)

• Converted in:

  • Liver → calcidiol (25-OH D3)

  • Kidney → calcitriol (1,25-(OH)2D3, active form)

• Controlled by:

  • PTH (increases calcitriol)

  • FGF23 (decreases calcitriol)

• Effects:

  • Intestine → ↑ calcium & phosphate absorption

  • Kidney → ↓ calcium excretion

  • Bone → increases both bone formation & resorption

• Drugs:

  • Ergocalciferol (D2), Cholecalciferol (D3), Calcitriol (active form)

  • Uses: hypoparathyroidism, rickets, familial hypophosphatemia

  • ⚠ Overdose → hypercalcemia, kidney & soft tissue calcification

3. FGF23

• Secreted by bone cells.

• Requires Klotho as co-receptor.

• Effects:

  • ↓ intestinal calcium absorption

  • ↓ kidney calcitriol production

  • ↓ bone formation

  • ↓ serum phosphate (main effect)

• Drug: Burosumab (Crysvita) = anti-FGF23 antibody for X-linked hypophosphatemia.

4. Calcitonin

• Made by thyroid C-cells.

• Opposite of PTH.

• Effects:

  • Intestine → ↓ calcium absorption

  • Kidney → ↑ calcium excretion

  • Bone → stops bone breakdown

  • Net effect = ↓ serum calcium

• Drug: Salmon calcitonin (Miacalcin)

  • Longer half-life than human calcitonin

  • Admin: nasal spray or injection

  • Use: Osteoporosis (when others aren’t suitable), hypercalcemia

  • ⚠ Warnings: hypocalcemia, malignancy risk, antibodies

🧩 How They All Work Together

• PTH → ↑ Ca, ↓ phosphate

• Vitamin D → ↑ Ca & phosphate

• FGF23 → ↓ phosphate, neutral on Ca

• Calcitonin → ↓ Ca & phosphate

It’s like a team with push–pull regulation to keep calcium levels balanced.

⚠ Calcium Disorders

Hypercalcemia (too much Ca)

• Causes: hyperparathyroidism, cancer, Vitamin D overdose

• Symptoms: depression → coma

• Treatment:

  • Rehydration + diuretics

  • Calcitonin (fast but short-lived)

  • IV phosphate (dangerous but effective)

Hypocalcemia (too little Ca)

• Causes: hypoparathyroidism, Vitamin D deficiency, CKD

• Symptoms: muscle cramps, tetany, seizures

• Treatment:

  • IV calcium (slow infusion)

  • Oral calcium for mild cases

  • Vitamin D (calcitriol fastest)

🦴 Bone Remodeling

• Osteoclasts → chew up bone (resorption)

• Osteoblasts → build new bone (deposition)

• Whole cycle = ~6 months

• Balanced activity = strong bones

• Imbalance = osteoporosis

RANK / RANKL / OPG

• RANKL (from osteoblasts) → activates RANK → osteoclast formation

• OPG = decoy receptor that blocks RANKL → reduces osteoclast activity

• Low estrogen (menopause) → ↓ OPG → ↑ bone loss → osteoporosis

Sclerostin

• Protein that weakens bone.

• Blocking it with anti-sclerostin antibodies (romosozumab) → stronger bones.

💊 Bone-Related Drugs

• Bisphosphonates (alendronate, risedronate, zoledronate)

  • Localize in bone

  • Kill osteoclasts by blocking FPPS enzyme

  • Long half-life (stay in bone)

  • Given carefully (upright after pill, take with water)

• Monoclonal antibodies

  • Denosumab (anti-RANKL) → blocks osteoclast formation

  • Romosozumab (anti-sclerostin) → increases bone formation

• PTH analogs → teriparatide, abaloparatide

• Calcitonin → less common

• Estrogen therapy → not first line (cancer/clot risks)

🦴 Osteoporosis

• Causes: age, low estrogen, chronic illness, certain meds (steroids, SSRIs, thyroid hormone)

• Prevention: diet (Ca + Vitamin D), exercise, no smoking, limit alcohol

• Treatments:

  • Bisphosphonates

  • Monoclonal antibodies (denosumab, romosozumab)

  • PTH analogs

  • Calcitonin (if others not tolerated)

Learning Goals:

• Know the types of diabetes.

• Know lab tests to check diabetes.

• Know units for blood sugar and HbA1C.

• Know what hormones the pancreas makes.

• Understand how food carbs turn into blood sugar.

• Know about glucose transporters and their role.

Types of Diabetes

Monitoring Diabetes

• Short-term: Blood sugar with glucose meter.

• Long-term: HbA1C (shows 3-month average sugar).

Tests:

• Fasting Glucose: After 10-hour fast → shows short-term sugar.

• Oral Glucose Tolerance Test: Drink sugar, check 2h later → shows how body handles sugar.

• HbA1C: Sugar sticks to hemoglobin → shows long-term average.

Pancreas & Islets of Langerhans

• Pancreas: Two jobs:

  1. Exocrine: Makes enzymes for digestion (lipase, amylase, proteases).

  2. Endocrine: Makes hormones for blood sugar (insulin, glucagon, amylin, somatostatin, pancreatic polypeptide, gastrin).

Islet Cells:

Glucose Intake & Uptake

• Food carbs → glucose → blood → liver, muscles, fat.

• Insulin:

  • Liver: stops making new sugar.

  • Muscle: stores sugar as glycogen.

  • Fat: makes fat from sugar.

• Incretins: Hormones from gut → tell pancreas to release insulin.

• Brain & RBCs take sugar without insulin.

Glucose Transporters (GLUTs)

• GLUT1: RBCs & brain, always works.

• GLUT2: Pancreas & liver, helps insulin release.

• GLUT3: Brain & placenta, always works.

• GLUT4: Muscle & fat, works when insulin is present.

• GLUT5: Gut, mainly moves fructose.

Significance: Different tissues need sugar differently, some rely on insulin, some don’t.

3.2 Oral Diabetes Drugs (Sept 10 & 12)

Learning Goals:

• How pancreatic β-cells release insulin.

• What hyperinsulinemia is.

• Drugs to treat high insulin.

How Insulin is Released

1. Glucose enters β-cells via GLUT2.

2. Glucose → ATP.

3. ATP closes K+ channels → cell depolarizes.

4. Ca++ channels open → Ca++ enters.

5. Ca++ triggers insulin vesicles to release insulin.

High blood sugar → more insulin released.

Hyperinsulinemia

• Too much insulin in blood. Causes:

  • Obesity/metabolic syndrome

  • Pancreas tumors

  • Genetic defects (rare, mostly in infants)

  • Babies of diabetic moms may have temporary high insulin

Non-drug treatments:

• Lifestyle changes (diet, exercise)

• Surgery for tumors

Drug treatments:

Monitor: Blood sugar to avoid too high sugar (hyperglycemia).

Major Learning Objectives

• Name main classes of oral diabetes drugs

• Give examples (generic + brand)

• Explain mechanisms of action

• Know risks and contraindications

1. Main Classes of Oral Diabetes Drugs

2. Biguanides – Metformin (GLUCOPHAGE)

• Mechanism: ↓ hepatic gluconeogenesis (main), minor ↑ insulin sensitivity

• Extras: Activates AMPK, stimulates FA oxidation, reduces lipogenesis

• Effects: Anti-hyperglycemic, rarely causes hypoglycemia, may cause mild weight loss

• Use: First-line therapy; can be monotherapy or in combination

• Pharmacokinetics: Not protein bound, excreted unchanged in urine

• Dosage (adult example): Start 500 mg once daily; max 2,000 mg/day

• Contraindications: Renal impairment, acidosis

• Warnings: Lactic acidosis, B12 deficiency, hypoglycemia with insulin or secretagogues

3. Sulfonylureas

• Mechanism: Bind ATP-sensitive K⁺ channel in β-cells → depolarization → Ca²⁺ influx → ↑ insulin release

• First Gen: Tolbutamide, Tolazamide, Chlorpropamide (rarely used)

• Second Gen: Glipizide, Glyburide, Glimepiride (100x more potent, longer duration)

• PK: Highly protein-bound (90–99%), metabolized in liver, excreted in urine

• Risks: Hypoglycemia, CV mortality, interactions with other drugs

• Contraindications: T1DM, hepatic/renal impairment

4. Meglitinides (Glitinides)

• Mechanism: Same target as sulfonylureas (SUR1 subunit), fast-acting → short insulin release

• Examples: Repaglinide (PRANDIN), Nateglinide (STARLIX)

• PK: Hepatic metabolism (CYP3A4 ± CYP2C8), rapid onset (~1h), short duration (4–8h)

• Use: Take before meals, mono or combo therapy

• Risks: Hypoglycemia if meal skipped, drug interactions

5. Thiazolidinediones (TZDs)

• Mechanism: PPARγ agonists → ↑ transcription of insulin-responsive genes → ↑ insulin sensitivity (adipose, muscle, liver)

• Examples & Dose: Pioglitazone 15–45 mg/day, Rosiglitazone 4–8 mg/day

• PK: Hepatic metabolism (CYP2C8 ± CYP2C9/3A4)

• Time to Effect: 6–12 weeks

• Risks: CHF, hypoglycemia if combined with secretagogues

6. DPP-4 Inhibitors

• Mechanism: Inhibit DPP-4 → ↑ incretins (GLP-1, GIP) → ↑ glucose-dependent insulin secretion

• Examples: Sitagliptin, Saxagliptin, Linagliptin, Alogliptin

• Use: Adjunct to diet/exercise

• PK: Mostly renal excretion (Sitagliptin), some CYP metabolism

• Risks: Pancreatitis, renal failure, joint pain

7. α-Glucosidase Inhibitors

• Mechanism: Inhibit GI enzymes → ↓ postprandial glucose

• Examples: Acarbose (PRECOSE), Miglitol (GLYSET)

• Use: Type 2 DM, elderly, postprandial hyperglycemia

• Risks: GI side effects (fermentation, gas, diarrhea), contraindicated in intestinal disorders

• No hypoglycemia alone

8. SGLT2 Inhibitors

• Mechanism: Inhibit renal glucose reabsorption → ↑ urinary glucose excretion

• Examples: Canagliflozin (INVOKANA), Dapagliflozin (FARXIGA), Empagliflozin (JARDIANCE)

• Risks: UTIs, genital infections, hypoglycemia if combined with insulin/secretagogues

• Contraindications: Severe renal impairment, dialysis

9. Bile Acid Sequestrant

• Example: Colesevelam (WELCHOL)

• Mechanism: Unknown for glucose lowering, binds bile acids for LDL reduction

• PK: Not metabolized, excreted fecally

• Risks: Reduces absorption of some drugs

10. Dopamine Agonist

• Example: Bromocriptine (CYCLOSET)

• Mechanism: Unknown, does not ↑ insulin

• Use: Adjunct to diet/exercise

• Risks: Contraindicated in nursing women, syncopal migraines

Learning Objectives

1. Explain GLP-1 and its analogs’ mechanism.

2. Describe how GLP-1 drugs treat diabetes.

3. Explain why GLP-1 analogs have different dosing.

4. Explain engineered GIP mechanism.

5. Explain amylin and analogs’ mechanism.

6. Describe amylin-based drugs for diabetes.

7. Know different insulin types, engineered variants, and use.

8. Understand glucagon mechanism and clinical use.

Injection Diabetes Drugs Overview

GLP-1 (Glucagon-like peptide 1)

• Peptide of 30–31 residues, from proglucagon.

• Made in gut cells and certain brain neurons (not pancreas α-cells).

• Released after carbs (food).

• Functions:

  • Stimulates insulin → lowers blood sugar.

  • May increase β-cell mass.

  • Reduces glucagon release.

  • Slows gastric emptying.

  • Reduces appetite.

• Half-life: ~5 min (short) → engineered analogs last longer.

Engineering Strategies

1. Amino acid changes → resist proteases/DPP4.

2. Fuse to IgG Fc → bigger, slower clearance.

3. Fuse to albumin → bigger, slower clearance.

4. Add long fatty acid → self-aggregation or albumin binding.

GLP-1 Analogs & Half-life

Black Box Warning: Most GLP-1 analogs → thyroid C-cell tumor (except BYETTA and ADLYXIN).

GIP (Glucose-dependent insulinotropic peptide)

• Similar to GLP-1; 42 amino acids.

• Made in intestinal K-cells, released after carbs.

• Effects:

  • Stimulates insulin, may increase β-cell mass.

  • Increases glucagon (unlike GLP-1).

  • Reduces gastric acid, slows gastric emptying.

  • Affects bone and fat tissue.

• Half-life: ~2 min → engineered analogs last longer.

Tirzepatide (MOUNJARO)

• GIP + GLP-1 dual agonist.

• Hydrophobic anchor binds albumin → longer half-life.

• Approved 2022 for type 2 diabetes.

• Warning: Thyroid C-cell tumors.

• Can delay gastric emptying, affecting absorption of other oral meds.

Amylin & Analogs

• Amylin: 37-residue peptide, co-secreted with insulin.

• Effects:

  1. Moderates appetite

  2. Slows gastric emptying

  3. Suppresses glucagon

  4. Lowers postprandial glucose

• Pramlintide (SYMLIN):

  • Engineered analog, slightly more stable (~48 min vs 15–20 min).

  • Used with mealtime insulin in T1D/T2D patients.

  • Start low, titrate dose, reduce insulin by 50% at start.

  • Contraindications: Gastroparesis, hypoglycemia unawareness.

  • Boxed Warning: Severe hypoglycemia.

Insulin Types

• Short-acting: Regular (HUMULIN R / NOVOLIN R)

• Rapid-acting (engineered): Lispro, Aspart, Glulisine

• Intermediate-acting: NPH (protamine + zinc)

• Long-acting (engineered): Glargine, Detemir, Degludec

• Inhaled rapid: AFREZZA (native human sequence)

Engineering Principles

• Rapid-acting: Amino acid changes → break hexamers → fast absorption.

• Intermediate: Protamine → slow release.

• Long-acting: Amino acid changes + fatty acid tail → slow release, albumin binding.

• Inhaled: Formulation + route → rapid action.

Therapeutic Use

• Type 1 diabetes: mainstay.

• Type 2: when oral meds fail.

• Pregnancy/gestational diabetes: insulin preferred.

• Emergency: DKA, HHS.

Adverse Effects

• Hypoglycemia (most common, can be severe).

• Warning signs: sweating, hunger, palpitations, tremor, confusion, blurred vision, loss of consciousness.

Glucagon

• 29-amino acid peptide from preproglucagon.

• Made in pancreatic α-cells.

• Counteracts insulin:

  • Increases blood glucose via glycogen breakdown.

• Regulation: Stimulated by low glucose, amino acids; inhibited by somatostatin, fatty acids, ketones.

• Clinical use: Treat severe hypoglycemia.

• Forms:

  • GlucaGen injection or nasal powder (Baqsimi)

• Contraindications: Insulinoma, pheochromocytoma.

Summary Tables: Drugs to Know

Non-Insulin Injectable Drugs

Insulin Drugs

Exam 2 drugs

1. Muscarinic agonists

• Bethanechol

  • urinary retention

• Pilocarpine

  • xerostomia

• Adverse Effects/ Contraindications
  - Adverse Effects: eyes; salivary glands; cardiovascular; lungs; GI; ; sweat
  glands
  - Contraindications: Asthma/COPD ; Peptic ulcer disease; Urinary or GI
  obstruction ; heart disease. Also: plants ; mushrooms

2. Muscarinic antagonists

• atropine

  • Bradycardia, pre-op for secretions, antidote for muscarinic intoxication

• scopolamine

  • Motion sickness (CNS effect)

• ipratropium

  • COPD and asthma

• tiotropium

  • COPD and asthma

• oxybutynin

  • overactive bladder, urinary incontinence

• tolterodine

  • overactive bladder, urinary incontinence

• dicyclomine

  • GI hypermotility (e.g. IBS)

• Adverse Effects

  • Visual (Cyclopegia- blurred vision, Mydriasis-photophobia) ; Xerostomia ; Constipation ; Urinary retention ; Tachycardia ; drowsiness

• Contraindications

  • Glaucoma ; Urinary retention ; GI retention ; Elderly (caution in elderly men and avoid if history of prostatic hyperplasia)

3. Adrenergic Agonists

• epinephrine

  • cardiac arrest, anaphylaxis, vasoconstriction

• norepinephrine

  • acute hypotension

• phenylephrine

  • acute hypotension, nasal decongestant, mydriasis

• clonidine

  • hypertension

• brimonidine

  • glaucoma

• isoproterenol

  • heart block

• dobutamine

  • cardiogenic, acute heart failure

• albuterol

  • asthma, COPD

• formoterol

  • asthma, COPD

• salmeterol

  • asthma, COPD

• mirabegron

  • urinary incontinence, overactive bladder

• Adverse Effects:
  - Cardiovascular: Cardiac arrythmias, increased cardiac workload,
  increased blood pressure, stroke, myocardial infarction (MI)
  - CNS: Headache, restlessness, insomnia, tremor, seizures

• Contraindications:
  - Heart disease, hyperthyroidism, benign prostatic hyperplasia, hypertension
  - Drug interactions: MAO or COMT inhibitors are contraindicated especially
  with other indirect acting sympathomimetics

4. adrenergic antagonists

• metoclopramide

  • impaired gastric emptying, GERD, nonulcer dyspepsia, prevent vomiting

  • adverse effects

    • restlessness, drowsiness, insomnia, anxiety, agitation

  • contraindications

    • situations where increased gastric motility could be dangerous, seizure disorders

• ondansetron

  • inhibits nausea and vomiting. Anti-emeitc

  • adverse effects: ECG changes

  • contraindications: drugs/conditions that have prolonged QT interval