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Norepinephrine-Adrenergic (adrenergic comes from the word adrenalin)
Alpha 1-all sympathetic target organs except the heart-constrict the blood vessels and dilation of pupils
Alpha 2-Presynaptic adrenergic nerve terminal-inhibits the release of norepinephrine
Beta 1-Heart and Kidneys (BETA 1-ONE HEART)-increased heart rate and force of contraction, release of renin
Beta 2-All sympathetic target organs-inhibits smooth muscle (BETA 2-TWO LUNGS)
Beta blockers/olol’s
Beta-Adrenergic Blockers
Metoprolol/Lopressor ENDING OLOL
Beta Blockers are use with heart failure, hypertension, angina and with myocardial infarctions.
Action = Blocks Beta-Receptors in the heart causing…
Decreases = HR, force of contraction, Rate of atrioventricular (AV) conduction
SE = Bradycardia, lethargy, GI disturbance, congestive heart failure, decrease BP, depressionThe beta blockers stop sympathetic nervous system stimulation of the heart. Does not allow the heart rate and blood pressure to rise with stress thus lowering the oxygen demand of the heart. It is very heart protective!
Will slow the heart rate and lower the blood pressure
Can have beta 2 blockage with larger doses-will constrict the bronchioles-watch for clients with known COPD, Asthma

Nursing Interventions
Check pulse-needs to be 60 or above
Check blood pressure-if hypotensive do not give (Systolic below 100 is a good rule of thumb I go by)
Monitor for sexual dysfunction-impotence for men-a good reason for non-compliance
Drowsiness/Fatigue-operating heavy machinery, driving could put client at risk
Contraindicated with Heart Blocks, Bradycardia, Worsening Heart Failure
Increases Hypoglycemic effect of Insulin-monitor blood sugars and for hypoglycemia, may need to lower insulin dosage
Beta Blockers have to be weaned slowly to prevent rebound hypertension and tachycardia-if a client wants to stop his beta-blocker they need to contract their physician

CCB,/calcium channel blockers

Nifedipine/Adalat/Procardia/Norvasc-controls blood vessels

Verapamil/Calan/Isoptin/Verelan-controls heart rate and blood vessels

Angina/Raynaud’s/Vasospastic Angina/Atrial Arrhythmia’s

Blocks calcium channels in the myocardial and vascular smooth muscles, decreases the contraction of smooth muscle-relaxes the arteries-vasodilation. Blocking of calcium channels in the SA and AV node-Slows conduction through the SA and AV node. Decreases the force of contraction slows heart rate

Grapefruit juice may increase absorption of nifedipine

Side Effects: Relaxes smooth muscle and cardiac muscle-
Dizziness-Take lying, sitting and standing B/P, educate client to sit and stand slowly
Peripheral edema-assess for edema, monitor for worsening (diuretic)
Reflex tachycardia-monitor for elevated heart rate (may need a BB)
Constipation-increase fibers and fluids (if not restricted) stool softener
Fatigue-Due to low heart rate-monitor EKG, pulse rate and rhythm
Weakness-Monitor B/P and Heart Rate
Impotence and sexual dysfunction-Discuss possibility with client-have client to call and not just to stop medications
Hepatotoxicity-ALT, AST, ALK PHOS, Bilirubin
MI-Monitor for chest pain, dyspnea, increases fatigue, weakness
CHF-Monitor for chest pain, dyspnea, edema, increasing weight, decreasing output, increasing HR and B/P
Angioedema-edema in face, throat, trouble swallowing, trouble breathing, thickened tongue
Grapefruit juice may increase absorption of nifedipine

Acute Toxicity
With an overdose or overmedicated
Gastric lavage
Monitor EKG-bradycardia-widening QRS, hypotension
Norepinephrine to treat hypotension and decreased cardiac contractility
Atropine or Isoproterenol-Bradycardia and Cardiac Blocks

Verapamil (Calan, Covera, Isoptin Verelan)
Class IV antidysrhythmic
Calcium channel blocker
Inhibits the flow of calcium ions both into the myocardia cells and the vascular smooth muscle, slow the conductions velocity and stabilizes dysrhythmias. Lowers the blood pressure, reduces cardiac workload and lowers the blood pressure. Dilates the coronary arteries-anti-anginal
Side Effects: Headache, constipation, hypotension, edema, bradycardia

Pril/ace inhibitors
PRIL-is the ending for ace’s
Reduces Angiotensin 2 and aldosterone levels
Prevents Angiotensin 1 from converting to Angiotensin 2 in the lungs-leaves the Angiotensin 1 hanging in the lungs-creates irritation-cough
Vasodilation-mostly arteriole (decreases afterload)
Excretion of sodium and water-retention of K (decreases preload)
Treats hypertension and heart failure
Do not take 2nd and 3rd Trimester of pregnancySE = Angioedema-allergic reaction-swelling of tongue, throat-stop taking and notify md
Hyperkalemia-monitor for widening and slowing of pulse/qrs, weakness, fatigue, avoid high K foods, AVOID SALT SUBSTITUTES-usually very high in K, avoid potassium sparing diuretics, sport drinks are high in K also
Orthostatic Hypotension-teach client to sit and stand slowly, enact fall precautions
Neutropenia/Agranulocytosis-monitor CBC-WBC count, reoccurring infections
Renal Insufficiency-Monitor weight, edema, I/O, BUN, Cr, and GFR
Hepatic Insufficiency-Monitor AST, ALT, ALK PHOS, Bilirubin
Cough-Cough lozenges, hard candy, increase fluid intake, sleep with HOB elevated, antihistamines

ACE Inhibitors

Discussed these medications with hypertension

Arb’s-Angiotensin receptor blockers, sartan’s
No Cough, same effects and side effects as Ace’s-just not as potent

Sartan’s/angiotension blockers/arb’s

Arb’s-Angiotensin receptor blockers, sartan’s
No Cough, same effects and side effects as Ace’s-just not as potent
Nitroglycerin/Nitrostat, Nitro-Bid, Nitro-Dur
Nitrates form nitric acid which is a relaxes smooth muscle and dilates venous and arterial blood vessels
Open veins-blood pools in the legs-not as much blood returning to the heart-reduces preload
Open arteries-heart does not have to work as hard to pump blood out of the heart-reduces afterload
Opens the coronary arteries and helps supply blood to the heart tissueCan be given sublingually, orally, topically, IV, buccal
Can be for acute or long term use
Nitroglycerin dilates any artery and vein-including yours if you touch it while administering it-WEAR GLOVES
Nitroglycerin IV needs a glass bottle and covered from light-some hospitals still use special tubing (nitro is absorbed in the tubing)
Short term-nitrostat-sublingually-1 tablet every 5 minutes x 3 for relief of chest pain-still having chest pain call 911/physician
Long-term nitro-dur will last for up to 14 hours in the body

Side Effects:
Headache-dilates the cerebral arteries-do not give with head trauma or increased intracranial pressure
Hypotension and reflex tachycardia-do not give with hypotension, monitor blood pressure and HR when administering
Hypotension-correct hypervolemia prior to giving nitroglycerin
DO NOT GIVE WITH VIAGRA, LEVITRA, OR CIALIS (nitroglycerin and Viagra increase nitric acid and relaxation of the smooth muscles-can kill a client with hypotension with a combination of these drugs)

Cardiac Glycoside
Digoxin/Digitek, Lanoxin, Lanoxicaps (Dig)
Increases the contractility of the heart muscle – Inotropic effect-
Increases cardiac output
Also Suppresses the SA node and slows conduction through the AV node
Half-life is 3-4 days
Great Drug-real side effects
Digoxin SE =
Toxicity 0.5-1.8 normal level
Signs of toxicity-halos around objects, Nausea/Vomiting/Anorexia, blurred vision, fatigue
Bradycardia-must take an apical pulse for one full minute, must be 60 or above to give digoxin
Give with caution with pediatric and geriatric patients due to inadequate renal or hepatic metabolic enzymes
Hyperkalemia can reduce effects of digoxin
Digoxin and Beta Blockers can really lower the pulse
Give with caution with renal failure-digoxin excreted via the kidneys
Decreases automaticity of the SA nose and slows conduction through the AV node
Atrial dysrhythmias
All the side effects and warnings are still important
Naturally found in the liver and lining of blood vessels
Prolong coagulation time
IV immediate onset, Sub Q 1 hour
Destroyed by gastric enzymes
Weight based
aPTT (PTT also, but in the hospital we use the aPTT)
Sub Q
Thrombocytopenia occurs in 30% of client
Protamine Sulfate is the antidote, 1 mg for every100 units of heparin, works for Lovenox also
Warfarin inhibits the action of Vitamin K, and without adequate Vitamin K the synthesis of clotting factors 2, 7, 9, and 10 is diminished
Warfarin takes 2-3 days to achieve therapeutic effect-99% of warfarin is bound to plasma proteins and unavailable to produce effects
Vitamin K is the antidote-green leafy veggies Aquamephyton-works within 6 hours
Normal INR therapeutic range is 2-3
Normal INR for everyone who is not taking an anticoagulant is around 1
Category X for pregnancy
Avoid alcohol, diuretics, SSRI’s, Antidepressants, Steroids, Antibiotics, Vaccines, Some Vitamins, Amiodarone-all can potentiate warfarin
Amiodarone (Cordarone/Pacerone)
Class III antidysrhythmic
Potassium channel blocker
Ventricular and Atrial Arrhythmias-especially with heart failure
IV onset or PO onset looks to be 2-3 days to 1-3 weeks
Half life can be greater than 100 days
Check K and MG levels prior to starting therapy
Side Effects: Fibrosis of lungs, destruction of thyroid, Photosensitivity-Smurfs, Liver destruction, N/V, Hypotension, Blindness, very hard on the stomach-GI Distress
Can increase serum digoxin levels by 70%, Increase warfarin levels, Increase phenytoion (Dilantin), Stop BB and CCB?
Statins (Lipitor)

HMG-CoA reductace inhibitor-(liver is where the cholesterol is made, it is where the HMG-CoA work)

LDL/Cholesterol is reduced
Give with food to reduce GI symptoms
Lipitor can be taken at anytime, most of the class of this medication needs to be taken at bedtime-cholesterol is made by the liver at night
Up to 30 days to achieve full affect

Side Effects:
GI-constipation, bloating, gas, nausea
Liver-monitor enzymes-alt, ast, alk phas, bilirubin, jaundice, enlarged liver-ascites
Rhabdomyolysis-muscle destruction-CK elevation-muscle pain-MD has to be notified.
Renal failure is very common with Rhabdomyolysis-need to make sure urine output is 30 ml or greater an hour
No grapefruit juice
The statins are hard on the liver-you need to make sure other drugs the client is on is not hard on the liver-Amiodarone and Nizoral are two drugs that come immediately to my mind

furosemide/lasix (-ide)
…Loop Diuretics-prevents Na/Cl reabsorption, thus Na leaves the body, water follows Na and K follows the water
Furosemide/Lasix, Bumex/Bumetanide, Torsemide/Demadex
Work on the entire Loop of Henle-large volumes of water, Na, and K are removed
Works in renal failure
Hypovolemic and hypokalemia very common
Nursing interventions
Know your potassium level prior to administration
Assess Lung Sounds, Weight, I/O, Edema, SaO2, RR, Blood Pressure, K Level prior to administration, assess all of these post administration, especially K Level and Lung Sounds, Sao2, I/O. If you urine bag is not twice as full 30 minutes post IV Lasix administration, check your IV site. If your client without a Foley has not called to urinate within an hour of giving po Lasix, check your client
Warn your client to get up slowly after taking Lasix, watch for orthostatic hypotension
Lasix does have sulfa as a base component
May not be used with anuria, hepatic coma
Use with extreme caution with electrolyte depletion
Low K with Digoxin can equal lethal Dysrhythmias, know your potassium level-has a digoxin level been ran
Anti-platelet drugs
ADP Receptor Blockers (Plavix, Ticlid, Effient)
Glycoprotein 2b./3a receptor antagonist (Repro, Integrillin, AggrastatADP receptor blockers

Irreversibly alter the plasma membrane of platelets, alters the ability of platelets to aggregate
Ticlid and Plavix are given orally
Ticlid can cause Agranulocytosis-only used when someone is allergic to Plavix
Glycoprotein is an enzyme necessary for platelet aggregation, IV only, Very expensive used with MI’s Strokes, and PTCA’s

Clopidogrel (Plavix) Antiplatelet drug
ADP receptor blocker
Inhibits ADP binding to its receptor’s-irreversible and will be with the platelet for their lifespan (5-7 days)
Used for MI’s, CVA’s, PAD/PVD, Unstable Angina, PTCA’s-first 6 months post ptca’s
Bleeding is a problem

EXAM 2 DRUGS!!!!!!!!!!!!
Vasopressin (pitressin)
The antidiuretic action of vasopressin is ascribed to increasing reabsorption of water by the renal tubules
40u IV
Adverse = cardiac ischemia/angina
DDAVP (desmopressin)
Prevents or controls thirst and frequent urination caused by diabetes insipidus and certain brain injuries.
Works on posterior pituitary….Treatment for: diabetes insipidus, bedwetting(nocturia), brain injuries, hemophilia A w/ some factor VIII production
nasally, IV, oral/subling tab
up to 20 hours
Treats hypothyroidism. Also treats an enlarged thyroid gland (goiter) and thyroid cancer.
Naturally occurring glucocorticoids (hydrocortisone and cortisone), which also have salt-retaining properties, are used as replacement therapy in adrenocortical deficiency states. Their synthetic analogs are primarily used for their potent anti-inflammatory effects in disorders of many organ systems. Glucocorticoids cause profound and varied metabolic effects. In addition, they modify the body’s immune responses to diverse stimuli.
Hydrocortisone belongs to the family of medications known as corticosteroids. It is used to treat many different conditions. It works by reducing swelling, inflammation, and irritation or as a replacement when the body does not make enough cortisol. Hydrocortisone is more commonly used to treat allergic reactions, some skin conditions, severe asthma, lupus, and arthritis.
It can also be used to treat steroid deficiency in the body, certain blood disorders, certain types of cancer, multiple sclerosis, and ulcerative colitis.
When people are under stress, levels of cortisol hormone rise. Chronic stress can result in chronically high levels of cortisol, which can lead to symptoms like weight gain, memory problems, high blood pressure, and other health problems. The stress release of cortisol is designed to enable the flight or fight response with a quick burst of energy, but when people are in a state of constant high stress, levels of the hormone never have a chance to fall back down to normal levels. This is one reason why treatments for chronic stress include exercises and activities that are designed to reduce stress levels, allowing production of this hormone to slow down.
Treats hyperthyroidism (too much thyroid hormone produced by the thyroid gland).
Treats Graves’ disease and hyperthyroidism (too much thyroid hormone from the thyroid gland) in patients who have already been treated with other medicines (such as methimazole) that did not work well.
H2 Blockers (-tidine)
PPI’s (-prazole)
30mL QID
This medication is used to treat the symptoms of too much stomach acid such as stomach upset, heartburn, and acid indigestion. Aluminum and magnesium antacids work quickly to lower the acid in the stomach. Liquid antacids usually work faster/better than tablets or capsules.
This medication works only on existing acid in the stomach. It does not prevent acid production. It may be used alone or with other medications that lower acid production (e.g., H2 blockers such as cimetidine/ranitidine and proton pump inhibitors such as omeprazole).
This medication can cause nausea, constipation, diarrhea, or headache
by mouth, usually after meals and at bedtimehis product may react with other medications (e.g., digoxin, iron, tetracycline antibiotics, quinolone antibiotics such as ciprofloxacin), preventing them from being fully absorbed by your body.
Bulk-Producing Laxative
*decrease* the *absorption* and *effects* of *Warfarin*, *Digoxin* and *Aspirin*. *Do not give* to patients with: *GI obstructions*, *fecal impaction* or *abdominal pain* and *N/V*
Monitor elevated serum glucose
Antidiarrheal, Anticholinergic
(dec blood sugar)
Is a polypeptide hormone that controls the storage and metabolism of carbohydrates, proteins, and fats. This activity occurs primarily in the liver, in muscle, ind in adipose tissues after binding of the insulin molecules to receptor sites on cellular plasma membranes
Logs –>fast acting
is a man-made insulin used to control high blood sugar in adults/children with DM.
Reg –>short acting
Humulin® R U-100 is a polypeptide hormone structurally identical to human insulin synthesized through rDNA technology in a special non-disease-producing laboratory strain of Escherichia coli bacteria
NPH –>intermediate-acting
Often used in combination with a shorter-acting insulin. NPH insulin is a man-made insulin product is the same as human insulin. It replaces the insulin that your body would normally make. It is an insulin (isophane). It starts to work more slowly but lasts longer than regular insulin. Helps blood sugar (glucose) get into cells so your body can use it for energy.
Lantas –>long-acting insulin
Treats diabetes mellitus. Insulin is a hormone that helps get sugar from the blood to the muscles, where it is used for energy. This type of insulin usually works longer than regular insulin.
Glucophage (metformin)
Used with diet and exercise to control blood sugar in patients with type 2 diabetes. May be used alone or with other medicines.
starting dose of GLUCOPHAGE (metformin hydrochloride) Tablets is 500 mg twice a day or 850 mg once a day, given with meals. Dosage increases should be made in increments of 500 mg weekly or 850 mg every 2 weeks, up to a total of 2000 mg per day.
The purpose of both insulin and metformin is to lower blood glucose levels. Insulin injections replace the insulin your body can no longer make when the cells in the pancreas cease to function. Metformin is an oral hypoglycemic, which lowers blood glucose levels by decreasing the liver’s output of glucose. Metformin also increases insulin sensitivity, and improves not only blood glucose levels but also lipid levels and often results in weight loss.
14% take insulin only
57% take oral medications only
14% take a combo of both.
Insulin VS Metformin Treatments? Mechanisms
Oral hypoglycemics are used only in Type 2 diabetes, because Type 1 diabetics make little or no insulin, so reducing the glucose levels produced by the liver won’t reduce blood glucose levels. Without insulin, glucose can’t enter cells and remains in the bloodstream. While all Type 1 diabetics take insulin, some Type 2 diabetics also need insulin in addition or instead of oral hypoglycemics such as metformin. Insulin, which must be injected, comes in several forms and doses, and can have rapid or slow onset.
Insulin VS Metformin Treatments?….Considerations
For Type 1 diabetics, insulin is the only medication choice. For Type 2 diabetics, medical practitioners generally start with an oral hypoglycemic such as metformin and add insulin only when oral hypoglycemics can’t stabilize blood glucose levels.
Insulin VS Metformin Treatments?….Benefits
Both metformin and insulin help to normalize blood glucose levels. Keeping blood glucose levels as close to normal levels as possible limits the damage high blood glucose imposes on every blood vessel and organ of the body. High blood glucose levels lead to poor circulation, heart problems, vision problems, nerve damage, susceptibility to infection and kidney damage. While damage occurs earlier in Type 1 diabetics, Type 2 diabetics can also experience complications.
Insulin VS Metformin Treatments?….Side Effects
Diarrhea, the most common side effect of metformin, improves if metformin is taken with food. Liver failure and increased acidity, acidosis, occur rarely, The Merck Manuals Online Medical Library states. Insulin must be carefully calibrated or blood glucose levels may drop too low, a condition called hypoglycemia. Taking insulin without eating or taking too much insulin for the amount of food eaten can cause hypoglycemia. Symptoms of hypoglycemia include weakness, shakiness, sweating, lightheadedness and confusion; coma and death can result in severe cases.
NSAIDS—->Ibuprofen (advil/motrin)
Work on Cox 1/Cox 2
Take with FOOD
Stop production of prostaglandins
Can cause –> kidney toxicity
NSAIDS = N/V, gi bleed, platelet aggregation, kidney toxicity possible)
NSAIDS (Ibuprofen)
Analgesic, anti-inflammatory, antipyretic, antiprostaglandin
Sodium based = may increase BP/heart failure, causes Ulcers
SE = N/V, GI bleeding, heartburn, epigastric pain, GI ulcer, renal impairment, bruising, blood in urine
Caution = with MI’s and bypass patient’s.
No more than 3,200 Mg/day (it can kill the kidneys/especially w/long term use)Nursing interventions = check GFR, platelets, bleeding times, liver enzymes.

Aspirin (ASA)
Blood thinner
Aspirin = binds to Cox 1/Cox 2 (stops platelet aggregation, gi upset, tinnitus, HA, sweating)
Aspirin (ASA)
Increased risk for GI bleeding (coffee ground emesis, black tarry stool)
Increase Prothrombin time (PT/INR) …stop a week before surgery due to platelet life of 7 days
Enteric coated = prevent GI bleed/upset
Toxicity = tinnitus, humming, dizzy, bad balance, nausea
Caution = with heparin, lovenox, coumadin, Nsaids
Tylenol (acetaminophen)
Acetaminophen (Tylenol/APAP)
Antipyretic/analgesic-Centrally acting Cox Inhibitor
Acts on hypothalamus—>dilates peripheral blood vessels
No Anti-inflammatory Property/Enhances opioids for pain relief
Side Effects:
Renal/Hepatic failure, N/V, Chills, abd. discomfort, Inhibits warfarin metabolism (can cause it to accumulate)
Acetylcystiene/Mucomyst—antidote for Tylenol OD
Baby Drops(babies)
Liquids (children)
Anti-pyretic–Analgesis—Centrally acting Cox Inhibitor
Acts on Hypothalamus –> dilates peripheral blood vessels
No inflammatory property
PCA pumps
4 hour dose limit
Set machine for how many mg/hour.
Encourage = use before activities
Assess client = LOC, RR, BP, HR
Educate = it’s very hard to OD on pumps
Nursing Intervention = check IV line patency, ask to change PCA to oral med if they’re feeling better
Nursing Prejudices = assess their pain, respirations must be 12+
Pain 1-4 = PO meds
Pain 5-10 = IV meds
Narcan (naloxone)
Opioid antagonist
Treats Overdose = competes w/opioid receptors
Don’t give with pregnancy
(Rebound resp depression, abstinence syndrome, titrate dosage, rapid infusion)
1/2 LIFE = 60-90 MINUTES
1/2 LIFE of opioid = 3-4 hours
Can lead to rebound respiratory depression
Respirations = Monitor for 4 hours after giving it
SE = tachycardia, tachypnea, ventricula arrhythmia, pulmonary edema
Abstinence syndrome = cramping, HTN, vomiting (by stopping morphine effect, we can induce withdrawal quickly)
Caution = history of heart failure/pulm edema (the HTN/teachycardia can induce heart failure by increasing workload of the heart)
Contraindicated = with opioid dependency (immediate withdrawal)
Titrate dosage = relieve pain, reverse respiratory depression (if you don’t titrate it can cause sudden onset of pain/withdrawal)
Rapid Infusion = HTN, tachycardia, N/V
Morphine (opioid)
Opioid agonist
TX of moderate/severe pain
Induces pleasure
Activates Mu receptors (analgesia, sedation, resp. depression, euphoria)
Activates Kappa Receptors (analgesia, sedation, decreased GI motility)
Attaches to receptors in CNS & alters perception & response to pain.
Complications = respiratory depression, constipation, orthostatic hypotenstion, urinary retention, cough supression (cough hourly), sedation, biliary colic (spasm of sphincter of Oddi–use meperidine), emesis
Overdose? Coma, respiratory depression, pinpoint pupils
Monitor –>Breath sounds, vitals, Narcan, mechanical ventilation

PO, SQ, IM, Rectal, IV epi, Intrathecal

Must have RR of 12 or higher!!!!
Don’t use = premature infants, demerol w/renal failure, with head injuries (LOC is too hard to access)
Precautions = asthma, emphasema, older, babies, respiratory depression, pregnancy, labor, obesity, IBD, enlarged prostate, liver/renal disease–prolonged accumulation of drug)
Anticholinergic agent–Benadryl, will increase effects of constipation/urinary retention
MAOI = high fever/coma
Anti-hypertensive meds = hypotensive effect
Nursing administration = assess pain, docoument, 1-10 scale
Oral = 45 – hr later
IV = 30 mintes later
Cancer? give fixed schedule, around the clock, PRN
Addicted? Taper off over 3 days!!!

Atrovent (ipratropium) —-> MDInhaler
Bronchodilator anti-cholinergic
Blocks parasympathetic NS
Onset = 5-15 minutes (2-3 minutes between squirts)
**little absorbed, peanut allergy, nasty taste
Inhaled anticholinergic work well on COPD/brochospasm allergen induced/exercise induced asthma
Very little absorbed from lungs, few systemic effects, dry nasal mucosa, dry mouth, hoarseness
Rinse mouth (for nasty taste), peanut allergy (don’t use)
Anticholinergic = dry mouth, urine retention (suck on candies/sip liquids)
Usually 2 puffs/doseDon’t use with ….GLAUCOMA OR ENLARGED PROSTATE

Afrin (oxymetazoline)

Nasal decongestant/sympathomimetic

Short-term = 3-5 days
Stimulates the Alpha adrenergic receptors
Arterioles constrict – dries mucous membranes

SE = use for 3-5 days only or could have Rebound congestion (worse than before), insomnia
Contraindicated = Heart disease, diabetes, HTN
Nursing Implications = Rebound congestion, taper use one nare @ a time.
CNS stimulation (nervous, uneasy, aggitated)
Vasoconstriction (avoid with CAD/HTN)
Administer = lay on side, lateral, head low on side
Effective? Breathe, sleep, no agitation, no HTN, no chest pain, no nasal congestion**Oral decongestants = work body wide, no rebound congestion, slower (SE = insomnia, anxiety)

Increase capillary permeability
Increase Blood
Increase runny nose
Brocho-constriction (try to keep out the allergens/dust)
Benadryl (diphenhydramine)
H1 receptor antagonist (1st Generation)
antihistamine/makes you sleepy
Treats: N/V, allergic reactions
Effects #1 = dry mouth
IM –> Z track, deep injection
Antihistamines = prevent release of histamine by blocking H1 receptor sites on the mast cells in nasal cavity.
SE = drowsy(excitation in kids)
anticholinergic(dry mouth, urinary retention, gi upset)
ACUTE toxicity (flushed face, fever, tachy, dry mouth, dilated pupils, mild hypotension)
Contraindicated–> BPH, glaucoma, 3rd trimester, breastfeeding, newborn, bowel obstruction, CNS depressants/alcohol INC effects
Toxicity = induce vomiting, remove anti-histamine, activated charcoal, tylenol for fever, ice packs, send them to ER
MAOI’s = hypertensive crisisEffectiveness? No Rhinitus (runny, itchy nose), no Uticaria (no itching, no allergic reactions)

Beclomethasone (Beconase) –> intranasal
Intranasal corticosteroid
Decrease inflammation of nasal passage
Few systemic effects unless swallowed in large amounts
Beconase (nasal)
SE = Nasal irritation, nosebleed, it masks signs of infections
Licorice = potentiate effects
Assess = signs of oral fungal infection, alternate nares, hoarseness, changes in voice
Interventions = blow nose before meds!!
Prednisone (ORAL glucocorticoid)
Anti-inflammatory corticosteroid
Glucocorticoids = inhibits making of prostaglandins, suppress histamine, stops some functions of phagocytes/lympocytes
Short-term use only/taper them off
auto-immune disease = long-term useFever = signs of inflammation/natural defense to neutralize foreign organisms
Prolonged fever in children = febrile seizures
Prolonged fever in adults = breakdown body tissue, delirium/coma
Obscure causes of fever –> SSRI (serotonin syndrome), Thorazie, Anesthetics (malignant hyperthermia), immunodilators, cytotoxic drugs, chemotherapy, neutropenic agents

Beclomethasone (Beconase) —> inhaled
Inhaled glucocorticoid/Dilates Bronchi
Anti-flammatory for Asthma/COPD
Allergic Rhinitus
Onset = 1-4weeks……1/2 life = 15 hours
Beconase (inhaled)
Supress inflammation, decrease mucous, promote Beta 2 response (dilation of the bronchi)
Anti-inflammatory for Asthma, COPD, allergic rhinitis, inhaled corticosteroid
SE = hoarse, dry mouth, changes in taste
MUST rinse mouth after/spit the water out –> Can cause Oral Candidiasis
Oral Candidiasis = fungal yeaste, look for white spots in the mouth.
Corticoidsteroids — glucocorticoids
Anti-inflammatory drugs
Must taper them off
Inhibits –> Making of prostaglandins, suppress histamines, stops some functions of phagocytes/lympocytes (so, when infection happens they’re aren’t enough WBC to fight off infection)
SE = suppress adrenal glands –> Addison’s crisis…hyperglycemia, mood changes, cataracts, PUD, electrolyte inbalance, osteoporosis, mask infections.
Long-term = Cushing’s syndromeGlucocorticoids = inhaled, oral, IV
End in -one
We give all 3 types for Asthma/COPD

Sickest = IV, then PO, then inhaled glucocorticoid

ORAL, IV systemic glucocorticoids
Suppresses the adrenal glands
Must taper them off the dose or…..
Can send them into Addison’s Crisis
Addison’s = Low BP, no energy, bone loss, increase blood sugar, muscle weakness, PUD (huge issue), take with food/no NSAIDS, sore throat.
Sodium Retention = hypokalemia (weak muscle/cramps)
Give Ca with Vitamin D
WATCH for edema, weight gain, HTN
Inflammation = Defense brought on by injury, toxic chemicals, heat, microorganisms, cell death, allergen response.
Sighs = swell, pain, warmth, redness
Acute = 1-2 weeks
Chronic = Lupus, RAWho responds to inflammation?
Mast cells, Bradykins, leukotrines, histamines, prostaglandins.

Beta 2 adrenergic agonists (Beta 2 – 2 lungs)
Activates SNS (relaxes smooth muscle/dilates bronchi)
**Relief of bronchospasm, histamine release stopped, increase ciliary motility.
Beta 2 adrenergic agonist
Quick-acting rescue inhaler (5 minutes)
Use before exercise to prevent Bronchoconstriction
Use beta 2 agonist inhaler before glucocorticoid
SE = HA, irritate throat, tremor, nervousness, tachycardia
Caution = HTN, cardiac, heart failure, seizures
Patients = keep log of attacks/frequency/what triggers them
Lungs = lotsa blood supply/large surface area, making them a quick onset (we don’t give PO)
Use = asthma control, prevent exercise induced asthma
Effective? Clear breath sounds–NO wheezing/rhonchi, respiratory rate @ baseline, SaO2 @ baseline 90%Note = Long-acting are combined w/corticosteroids. Get bronchi open and the corticosteroid can get in there easier when it’s dilated!

Antidote for tylenol
Effectiveness?? Liver enzymes are normal/no enlargement)
Anticoagulant-low molecular weight heparin derivative.
Mechanism of action
Deactivates thrombin. Also prevents the conversion of fribrinogen and fribrin.
Used to inhibit clot formation in ACS including STEMI, NSTEMI, and unstable angina. Also used to prevent pulmonary embolism and DVT in patients predisposed to such problems.
Known hypersensitivity to the medication, pork products, or heparin.
Adverse reactions
CNS side effects include confusion and dizziness. Cardiovascular side effects include edema, chest pain, and irregular heartbeat. Irritation, pain, redness or bruising may occur at injection site. Bleeding, angioedema, rash, and hives.
Drug interactions
Interacts with NSAIDs, warfarin, and anti-platelet agents.
Dose and administration
*Adult: STEMI: single IV bolus of 30mg plus 1mg/kg SQ dose followed by 1mg/kg SQ every 12 hours (Max 100mg)
NSTEMI: 1mg/kg SQ every 12 hours in conjunction with oral aspirin therapy (100-325mg daily)
Ped: 1mg/kg SQ
Duration of action
onset: 3-5 hours
peak: 3-5 hours
duration: varies
Special considerations
Do not use in patients with active major bleeding or thrombocytopenia. Use with caution in the elderly or any patient with increased risk of bleeding.
Peptic Ulcer
a break in the lining of the stomach/duodenum
cause: IMBALANCE b/w protective/damaging factors
2 COMMON factors = H. pylori & NSAIDs
H. pylori
-gram negative, spiral, found in gastric antrum, orally transmitted
corkscrews through the gastric mucus layer
** H. Pylori = inflammation/epithelial cell damageincreased GASTRIN/dec SOMATOSTATIN

**its is able to live in such an acidic environment b/c of its production of UREASE
Urease = converts urea to ammonia (ammonia buffers the H+ & creates an alkaline cloud around the h.pylori)

Detecting H.pylori
-C-urea breath test (based on organisms production of urease)
*urease converts C-urea to CO2 that is detected in the breath
How do NSAID cause gastric epith cell damage?
they are weak acids…they become trapped….and cause damage
Zollinger-Ellison syndrome
Gastrin-secreting TUMOR of the non beta cells of the endocrine pancreas
Cigarette smoking & PUD
Impairs mucosal blood flow/healing and inhibits pancreatic bicarb production
4 H2 receptor antagonists -tidine
-cimetidine – inhibits many cytochrome P450 enzymes and thus can interfere w/ hepatic metabolism; not recommended during pregnancy or nursing. also has antiadrenergic effects –>gynecomastia
*reversibly and competitively inhibit the binding of HISTAMINE to H2 receptors, resulting in suppression of gastric acid secretion
*they also indirectly decrease gastrin and acetylcholine-induced gastric acid secretion
-peak plasma levels achieved w/in 1-3 hours
**benefits: CHEAPER, with the exception of cimetidine, safe for preg. and adverse effects better studied
PPI’s mechanism -prazole
-block the parietal cell H+/K+ ATPase (proton pump)
-superior to H2 receptor antagonist
*OMEPRAZOLE -prototype
also: esomeprazole, rabeprazole, lansoprazole, dexlansoprazole, pantoprazole
-all are PRODRUGS that require activation in an acidic env. –> converted to SULFENAMIDE (active form) which reacts with a cysteine residue on the H+/K+ ATPase–>irreversible inhibition of the proton pump
-for acid production to resume it takes ~18 hours before new H+/K+ ATPase can be produced
**there site of action is in the parietal cell canaliculus (this is why intravenous administration is useful to bypass the acidic stomach and duodenum)
Clinical indication of PPIs
-to tx H. pylori associated ulcers, hemorrhagic ulcers, AND to allow continued use of NSAIDs in a patient w/ a known peptic ulcer
**they also contribute to the eradication of the H. Pylori infection**-clot formation is impaired in acidic environments -so increasing pH allows for clotting of ulcers

Adverse effects of PPIs
-headache, nausea, disturbed bowel function, abdominal pain
-the large increase in gastrin secretion —> can induce ECL cells and parietal cells to hyperplasia –>carcinoid tumors ??? (not observed in humans)-may affect effectiveness of clopidogrel (anti-platelet agent) because CYP2C19 metabolizes PPIs as well as activates clopidogrel: this enzyme has various polymorphisms and is responsible for the variation in clearance rate of PPIs

The most widely used antacids are mixtures of ____ and ____
-aluminum hydroxide (can cause constipation)
-magnesium hydroxide (can cause diarrhea)
*so when taken together you can avoid those symptoms-OH combines w/ H+ to form water
-metals form salts with bicarbonate

Quadruple therapy for H. pylori
*both broad spectrum antibiotics
-bismuth (for coating and eradication)
Triple therapy for H. pylori
TSH is the best screening test for?
Primary thyroid dysfunction (usually outpatient)
Hashimoto’s disease
Autoimmune disease = thyroid gland is attacked
Similar to–>Type 1 Diabetes
Thyroid Replacement….1st step
1-2 mcg/kg
T4 for full replacement
Children generally need more
Thyroid Replacement in Elderly?
Start SLOW
25 mcg/day (if 50+/cardio risks)
50 mcg/day otherwise
Lab monitoring in stable patients?
Follow up: 6-12 mo
Need for hormone decreases with age
Drug Interactions: Protein binding
Anticonvulsants, Estrogen, increases Warfarin
Warfarin interaction
hyperthyroid = decrease warfarin
hypothyroid = increase warfarin
Hypothyroid pregnancy?
increase dose
1/2 life of T4 is…
a week
PO dose —> IV?
cut in 1/2
Myxedema Coma
SEVERE HypOthyroidism
= mental, cold, low HR
Myxedema TX? (mistaken for adrenal dysfunction at times)
1. Synthroid by IV
2. Glucocorticoids (dec stress on body when metabolism goes up)
3. Management/treat causative factors
Toxic diffuse goiter (Graves’ disease)
Antibodies stimulate TSH receptors
Not TSH but acts like it
Toxic adenoma?
benign tumors releasing TH
Painful subacute thyroiditis
Acute = thyroid is destroyed in Hashimotos
Acute then goes down to hypOthyroidism
• Performed w/radioactive iodine (131)
• Initially increase symptoms
• Results in chronic hypOthyroidism
• Lifelong TH supplement
(PTU) drug for hyperthyroid
stop TH synthesis
agranulocytosis, GI upset, Iiver Damage (especially PTU), Rashes
Hyperthyroidism: During pregnancy?
PTU preferred in first trimester/Tapazole later in pregnancy
Hyperthyroidism: Monitoring?
Follow-up 4-12 week intervals initially (3-4 mo when stable)
Labs: Symptoms, wt., pulse, Free T4, TSH, CDC Tests
Subclinical disease
Low TSH = T4 oversupplementation
Thyrotoxicosis –> THYROID STORM!!!!
Exaggerated signs/symptoms of HYPERTHYROIDISM
Fever, mental, precipitated by illness
Management? (Tapazole & PTU)
Potassium Iodide, KI = stops release of thyroid hormone
Propranolol = treat peripheral effects (lowers BP, angina, irregular Hbeat, migraines, tremors)
types of antacids (MC)
1) Ca*
2) sodium bicarbonate
3) aluminum
4) magnesium
5) combinations
indications…when to use?
1) hyperacidity
2) aluminum-hyperhosphatemia
3) magnesium-magnesium deficiency, malnutrition
unlabeled uses
1) GERD (immediate relief of intermittent heartburn)
2) osteoporosis
how do they work
-weak bases that neutralize HCl acid
-raise pH which inactivates pepsin
-increase Lower Esophageal Sphincter tone, which decreases reflux
-does NOT coat stomach lining
goal of antacid
1) symptom relief
2) lifestyle modification needed
-raise head of bed
-limit caffeine
-stop smoking
-weight loss
-diet (increase fiber)
duration of action
2 hours
what to use if signs/symptoms >2 hours or occur at bedtime
H2 blockers
H2 blockers-how long to work?
30 min.
H2 use in what severity?
moderate s/s are…
s/s several times a week or daily
tx (treatment)?
H2 blockers BID for 8-12 wks
Treatment (tx) in severe or erosive dz
PPI q daily
if PPI is uneffective q daily?
PPI BID for 8-12 wks
what’s common when stop taking meds?
relapse (80%)
what if that happens
maintenance tx needed (use lower dose than initial tx)
caffeine effect?
1) decrease LES pressure
2) increase acidity
3) makes GABA less effective
AA w/ highest acid-neutralizing capacity (ex.)
1) sodium bicarb (alka-seltzer)
2) calcium bicarb (tums & rolaids)
why should you try not to use sodium bicarbonate??
It increases Na = bad for fluid retention & CHF
Which formulation has highest acid-neutralizing capacity?
1) gels
2) suspensions
pt. education with tablets?
chew & take w/ full glass of water
when to take
1 hour after meals
when to take to avoid interaction w/ other meds?
1 hour before/2 hours after other meds
Calcium & aluminum AA side effects?
1) constipation
2) precipitate stone (Ca ones)
Magnesium AA Side effect?
What can help balance the side effects?
give them together
What AA to give pt. w/ a renal insufficiency?
magnesium AA
check electrolytes periodically
prego cat
What can happen when AA are stopped?
acid rebound
Chronic Ca carbonate or sodium bicarbonate AA use (can lead to) risk for:
-milk-alkali syndrome
1) alkalosis
2) increase Ca
3) renal impairment
1) Headache
2) nausea
3) irritability
4) weakness
max. effect occurs?
taken 1 hour after meals
How soon when taken on empty stomach
20-40 min.
tums/rolaid dose
amphojel dose
600mg po TID or QID
maalox dose
30 mL—QID
MOM (milk of mag) dose
15-30 mL—QID
what AA have more SE
Na bicarbonate
H2 blockers uses…(-tidine)
2) PUD
3) hypersecretory conditions (ZE)
PPI uses… (-prazole)
2) PUD
3) hypersecretory conditions
4) H. pylori
decrease amount of acid produced by stomach
which are more powerful (how)
PPI (decrease acid to greater extent)
1) balanced meals at regular intervals
2) avoid foods that exacerbate sx
3) high fiber diet
4) avoid caffeine & alcohol
5) stop smoking
goal of tx w/ H2 & PPI
relieve sx & heal ulcers
1st line tx in mild-mod dz
H2 blockers
Treatment (tx) for severe PUD?
What if NO improvement in a week with H2 blockers??
increase dose or change to PPI
length of tx for hypersecretory or erosive conditions
Longer treatment with H2 or PPI?
H2 blockers
tx h. pylori
H2 or PPI + antibiotics & sometimes Bismuth
SE of bismuth
dark stool (When Helicobacter pylori is implicated, bismuth acts as an antimicrobial agent, suppressing the organism but not eliminating it. In recent studies, bismuth compounds have been used with conventional antibiotics, producing elimination of the organism, histological improvement)
When are H2 blockers given?
early evening or after meals
When to take PPI’s?
30 min. BEFORE meal
Should you use PPI & H2 together?
Nursing Interventions?
1) check stools/vomit for blood
2) LFT (Liver enzyme tests, formerly called liver function tests (LFTs), are a group of blood tests that detect inflammation and damage to the liver. They can also check how well the liver is working. Liver enzyme testing includes ALT, AST, alkaline phosphatase; true liver function tests (LFTs) include PT, INR, albumin, and bilirubin)
3) BUN/crea
4) don’t crush or chew PPI’s
how long does it take for blood to clear tract
72 hours
H2 blocker—Prototype Drug?
why are there less SE w/ axid (H2)
doesn’t start the P450 system (P450=the major enzymes involved in drug metabolism and bioactivation, accounting for about 75% of the total number of different metabolic reactions.)
Which H2 blocker has lots of SE & drug interactions?
cimetidine (Tagamet)
PPI ….1/2 life?
LONG = (72 hours)
MORE side effects: H2 or PPI?
Drugs that PPI interfere with?
drugs that need acid environ. for absorption (ex. iron)
cheapest PPI?
rabeprazole (Aciphex) & pantoprazole (Protonix)
PPI with longer 1/2 life?
Nexium (esomeprazole)
Zantac (ranitidine) dose?
Prototype H2 Blocker….150 mg BID/300 mg @ night
pepcid dose
20mg BID or 40mg po Q HS
Axid (nizatidine) dose
150mg BID or 300 mg Q HS
Prilosec (omeprazole) dose
PPI –20 mg q daily or 20 mg BID
Prilosec (omeprazole) tx w/ h. pylori
-40 mg q daily x 2 weeks
-then 20 mg w daily x 2 weeks + antibiotic
Prevacid (lansoprazole) dose
PPI—15 mg q daily x 8 weeks
Prevacid (lansoprazole) in h. pylori?
30 mg BID x 2weeks + 2 antibiotics
Aciphex (rabeprazole) dose?
PPI—-20mg po q daily
Nexium (esomeprazole) dose?
PPI—20-40mg po q daily
Protonix (pantoprazole) dose
40 mg po q daily x 8-16 weeks
Dexilan (dexlansoprazole) dose?
PPI…….-30 mg q daily
-60 mg q daily if more erosive
Nurse can increase gastrin level while on PPI to around what range
How long once PPI’s are stopped to return to normal gastric level??
3-5 days
PPI’ s heal 90% gastric ulcers w/in :
6 – 8 weeks
PPI’s heal 90% of duodenal ulcers w/in:
4 weeks
PPI’s usually taken?
during the day
Benefits of PPI last:
3 – 5 days after therapy is stopped
PPI’s are used for:
short term control, PUD, GERD
Adverse effects of PPI’s are:
not common
Most commonly reported adverse effects of PPI’s are:
– headache
– abd pain
– diarrhea
– N/V
PPI’s are effective at:
reducing gastric acid secretions
Nexium (esomerprazole):
PUD, GERD, PO; 20-40mg/day
Prevacid (lansoprazole):
– combo w/antibiotics for H. Pylori
* PO; 15-60mg/day
— Prevacid combines (lansoprazole) w/amoxicillin/clarithromycin
Prilosec (omeprazole):
– often used in combo w/
– antibiotics for H. Pylori
* 20-60mg 1 -2 daily
Protonix (pantoprazole):
– mainly for GERD
– IV form avail
* PO; 40mg/day
AcipHex (rabeprazole):
* PO; 20mg/day
H1 distribution
Smooth muscle
H2 distribution
Gastric mucosa
Cardiac muscle
Vascular SM
GI Tract
H2 activation of parietal cells –> gastric acid secretion
H1 activation –> contraction of GI Submuc
Role of H2 receptor in acid secretion
ECL cell stimulation by gastrin or Ach –> histamine release –> H2 receptor activation on parietal cells –> AC activation –> cAMP production –> protein kinase activation –> acid secretion by proton pump (K in; H out)
H2 receptor antag- MOA (mechanism of action)
Reduce gastric acid secretion
H2 receptor antag – therapeutic use?
Peptic ulcer disease PUD
Gastric acid hypersecretion
Inhibit stimulated acid secretion
Nocturnal acidity (useful when added to proton pump therapy to control “nocturnal acid breakthrough”)**
H2 receptor antagonists – drug names
RanitidineNote: these drugs have different structures and therefore different side effects

H2 receptor antag- pharmacokinetics
Absorption: well absorbed after oral administration
Peak plasma concentrations reached in 1-2 hours
T1/2: 1-3 hours
Some hepatic biotransformation (cimetidine has the greatest)
Mostly excreted unchanged by the kidney
H2 receptor antag that can cause: gynecomastia (male breasts)/galactorrhea (milk leakage)
Due to decreased estrogen metabolism (cyt p450 inhibition)
PPIs – MOA (mech of action)
Irreversibly inhibit the gastric parietal cell proton pump H/K ATPase (Note: the prolonged duration of action reflects the covalent modification of the pump, rather than prolonged serum half life)**
A single daily dose can effectively inhibit 95% of gastric acid secretion
Prodrugs – activated in an acidic environment
PPIs – Drug of choice (DOC) for…
Zollinger-Ellison syndrome (g acid secreting tumor)
GERD (Gastricesophageal Reflux Disease)
PPIs – use with H2 antagonists?
Should not be given simultaneously because the H2 antagonist reduces the efficacy of the PPI
Usually the PPI is taken during the day and the H2 antagonist is taken at night
PPIs – drug interactions
Decrease the metabolism and clearance of:
–PhenytoinReduce absorption of:

Increase the absorption of:

PPIs – drug names
Omeprazole (children, GERD)
Lansoprazole (NSAID ulcers)
PPIs- adverse reactions

Few and generally mild

Muscle pain

Mucosal protective agents – drug names
Colloidal bismuth (Pepto-Bismol)
coats stomach ulcer, helping it to heal
H. pylori – risk
recurrent ulcer (60-85% vs 5-10% if cured)
H. pylori – treatment**
PPI + 2 of the following antibiotics
–AmoxicillinOne week treatment: 90% cure rate

Two weeks of PPI + 1 antibiotic (typically clarithromycin): 10-20% lower cure rate

MHD notes:
–Tetracycline can be 1 of the 2 antibiotics
–Bismuth salts, doxycycline, and metronidazole for 14 days is cheap and effective

Other drugs – Pirezepine
Blocks binding of Ach to M3 receptors –> decreased acid secretion
Other drugs – Misoprostol
Blocks binding of prostaglandins to parietal cell receptor –> decreased acid secretion
Insulin (never given PO)
Available in 1922 (1922-1980’s Insulin from Pork or Beef pancreas)
Insulin must be available when glucose is in the blood
Control of Diet-when and what is eaten
Control of Exercise
During Illness
Never PO-GI Juices destroys the insulin
Vial in use @ room temp (extra vial in refrigerator)Recombinant DNA (rDNA) now is used almost exclusively
Most effective, fewer allergies, lower incidence of resistance

LOG’s –Rapid Acting
Onset 5-15 minutes
Peak 1-3 hours
Duration 3-5 hoursThese have to be given with the meal in front of the client
Humalog/Lispro Insulin
Novalog/Insulin Aspart
Apidra/Insulin Glulisine

Regular Insulin = Fast Acting
Humulin R, Novolin R/Insulin Regular
Onset 30-60 minutes
Peak 2-6 hours
Duration 6-10 hours
THIS IS THE ONLY Insulin That Can Be Given IV
Intermediate Acting = NPH
Humulin N
Onset 1-2 hours
Peak 6-14 hours
Duration 16-24 hours
Long Acting = Lantus
Lantus/Insulin Glargine
Onset-gradual-1 hour
Peak-No Peak
Duration-24 hoursOnce/day @ night

Specially calibrated syringes for insulin.
NOTE: NEVER put anything but INSULIN in these syringes
Blood sugar is low, usually below 70 (70-110 is considered normal range)
The brain is not getting sugar, it needs sugar to keep functioning
First signs are neuro in nature
Blurred vision
Diaphoretic (sweating)
Decreased LOC
And whatever else your patient states is a sign of their hypoglycemia. If your patient states they are hypoglycemic, believe them
Tx for HYPOglycemia (or brain cells will die)
High sugar = coke, OJ, candy.
Complex carb = peanut butter/crackers. (will stabilize sugar from falling after the high sugar snack)
Unconscious? D50, sugar in the buccal area, or glucagon in a tube in buccal area
In the hospital? get accu check 1st, then get sugar asap!
Polyuria-frequent urination
Polydipsia- thirst
Glycosuria-high sugar in the urine
Weight loss-even though their sugar is high, they aren’t getting nutrients into the cell
Ketones- in the urine/breath–gives off ketones (fruity Smell to the breath)
No nutrients to the cell, burning fat for energy
Rapid, Deep Respirations (blowing off the ketones)
Dry Skin (Dehydrated from peeing too much)
Tx for HYPERglycemia
1. check sugar
2. ketones in pee?
3. give insulin
Adrenal Glands
Sit on top of the kidneys.
Inner Medulla- Epi/Norepinephrine
Outer Cortex – Glucocorticoids (sugars), Mineralocorticoids (salts), gonadocorticoids (sex)
Aldosterone-95% of the mineralocorticoids secreted by the adrenals
Aldosterone regulates plasma volume: Na REABSORPTION & K EXCRETION by the tubules.
1. Plasma volume falls
2. Kidney senses this and release renin
3. Renin allows angiotensin 1 –>angiotensin 2.
4. Angiotensin 2 causes aldosterone secretion
5. Allowing sodium reabsorption/potassium depletion (remember, WATER follows salt!)
2 Ways of increasing FLUID volume?

ADH/Aldosterone are 2 ways our body maintains homeostasis in fluid volume.

ADH-sent by pituitary to make kidneys reabsorb H20 in the collecting ducts
Aldosterone-sensed by the kidneys-release of renin-converts angiotensin 1 to 2-angiotensin 2 allows aldosterone to act on the kidneys to increase Na reabsorption and K depletion

What are glucocorticoids?
1. Hypothalamus senses low glucocorticoid levels in the blood-
2. Releases CRF (corticotropin releasing factor) to pituitary gland
3. Pituitary releases ACTH (Adrenocorticotropic hormone)
4. ACTH travels to adrenal cortex and tells it to release glucocorticoids
5. Glucocorticoids support BP, GI functions, Mental Functions, Help control the immune response mechanisms
Use of Glucocorticoids
Adrenal Insufficiency
Inflammatory Bowel Disease (Crohn’s/Ulcerative Colitis
Transplant Rejection Prophylaxis
Rheumatic Disorders
Skin Disorders
Glucocorticoids (-sone)
Prototype Drug: Hydrocortisone/Cortef
Contra Ind: diabetes, osteoporosis, psychoses, liver disease, hypothyroidism
Cortef (hydrocortisone) side effects
Immune –> susceptible to infection and signs of infection will be masked
PUD-Give w/food, Give prophylactic H2 or PPI
do NOT give with NSAIDS
Monitor: abd pain, coffee ground emesis, tarry stools, fever
Osteoporosis-Have client take Ca/vit D, walk
Psychoses-monitor for irritability, nervousness, mood changes before increasing to hallucinations/suicidal ideation,
Cortef (side effects/monitor?)
Cataracts/glaucoma (yearly exams, trouble reading?)
Na/H2O Retention (BP, wt., I/O, breath sounds, Na/K levels)
Metabolic Changes (high sugar, hyperlipidemia, abnormal fat deposits/wt. gain)
Myopathy (muscle wasting, hyperkalemia, fatigue/weak, respiratory muscles & eyes)
Interaction w/Cortef (other corticosteroids)
NSAID’s/alcohol-may increase chance of GI Bleed
Oral Anticoagulants may inc/dec anticoagulation
Use with diuretic, increase K depletion
Monitor? EKG/K levels
Vaccines? May reduce the antibody response to vaccine
Too much cortisol? (Cushing’s syndrome)
Body is exposed to high levels of the hormone cortisol for a long time. The most common cause of Cushing syndrome, sometimes called hypercortisolism, is the use of oral corticosteroid medication. The condition can also occur when your body makes too much cortisol.
Causes? pituitary adenoma, tumor: lungs, pancreas, thyroid or thymus gland.
Signs: Adrenal atrophy, osteoporosis, hypertension, increased risk of infections, delayed wound healing, acne, peptic ulcers, general obesity, redistribution of fat around the face-Moon Face-shoulders, and neck-Buffalo Hump.
Mood/personality changed
High mortality rate from the complications such as hypertension from sodium and water retention
Too little cortisol? (Addison’s disease)
What Causes Addison’s Disease?
Result from a problem with the adrenal glands themselves (primary adrenal insufficiency). Autoimmune disease accounts for 70% of Addison’s disease.
This occurs when the body’s immune system mistakenly attacks the adrenal glands. This autoimmune assault destroys the outer layer of the glands.
When glucocorticoids are in use, especially in higher dose and long term therapy-the adrenal glands shrink/atrophy
If we taper clients off glucocorticoids, then adrenal glands return to normal function.
If we suddenly stop the glucocorticoids, we have Addison’s Crisis, the client will start losing there blood pressure, have renal failure, be very tired and lethargic, have nausea and vomiting, asthenia (lack of strength), they will die without getting a dose of glucocorticoids
Corticosteroids produced in the adrenal cortex.
Corticosteroids: stress response, immune response, regulation of inflammation, carbohydrate metabolism, protein catabolism, blood electrolyte levels, behavior.Glucocorticoids: Cortisol. Control carbohydrate, fat protein metabolism, anti-inflammatory by preventing phospholipid release, decreasing eosinophil action and a number of other mechanisms.
Mineralocorticoids: Aldosterone. Control electrolyte/water levels, mainly by promoting sodium retention in the kidney.

Anti-Diuretic Hormone Drugs
Vassopressin (pitressin) Half-life 2-8 hours
Desmopressin (DDAVP) Half-life 20 hours
Promotes water reabsorption by the kidneys, vasoconstriction, and increased clotting factor VIII-used with hemophilia and von Willebrand’s Disease, off label use-bedwetting in children
Side Effects: Fluid Overload (reabsorbed too much water)-monitor for edema, hypertension, pounding headache, sleepiness. Myocardial Ischemia from vasoconstriction
monitor: EKG and blood pressure, chest pain, dyspnea, diaphoresis
Category X for Pregnancy
Do not use in clients with CAD, Decreased Peripheral Circulation, and Chronic Nephritis
Nursing considerations for ADH meds
Monitor vital signs, I/O, specific gravity, daily weights, Electrolytes,
Nursing considerations 2
Monitor for signs of water intoxication-headache, confusion, pounding headache, edema, hypertension, sleepiness
Nursing considerations 3
Extravasation of IV vasopression can lead to Gangrene
Nursing considerations 4
Effectiveness-normal urine output, without signs of fluid overload
Diabetes Insipidus (DI)
No Antidiuretic Hormone = large amt of fluid lost. You will see DI = w/head injuries & lung cancer.
ADH = maintain fluid balance, control BP, and cardiac output in your body.
Antidiuretic – holds fluids
Diuretics allow fluids to be lost through the kidneysHypothalamus sense if the plasma volume has decreased, if the Na
level has risen (or the osmolality of the blood) and will send ADH to increase the amount of fluid retained by the kidneys.

When glucocorticoids are in use, especially in higher dose and long term therapy-the adrenal glands shrink/atrophy
If we taper clients off glucocorticoids, then adrenal glands return to normal function.
If we suddenly stop the glucocorticoids, we have Addison’s Crisis, the client will start losing there blood pressure, have renal failure, be very tired and lethargic, have nausea and vomiting, asthenia (lack of strength), they will die without getting a dose of glucocorticoids
Too much glucocorticoids for a long time
Signs Adrenal atrophy, osteoporosis, hypertension, increased risk of infections, delayed wound healing, acne, peptic ulcers, general obesity, redistribution of fat around the face-Moon Face-shoulders, and neck-Buffalo Hump. Mood and personality changed
High mortality rate from the complications such as hypertension from sodium and water retention
Med interactions w/glucocorticoids
NSAID’s and Alcohol-may increase chance of GI Bleed
Oral Anticoagulants may increase or decease anticoagulation
Use with diuretic, may increase K depletion-monitor EKG and K levels
Vaccines-may reduce the antibody response to vaccine
Synthroid (treats hypothyroid ^tsh low t3/t4)
generic name: levothyroxine
Synthroid–>#1 adverse reaction?
Nervousness :-/
What will prevent complete absorption of Synthroid?
Ca, Fe, Mg, Zinc
Why do you need thyroid med?
to replace/substitute diminished or absent thyroid function
Synthroid is contraindicated with?
hypersensitivity, recent MI, hypothyroidism (untreated low TSH level but normal T3/T4 levels)
Side effects of Synthroid
Insomnia, irritable, nervous, arrhythmia, tachycardia, wt loss, cardiovascular collapse.
Monitor blood/urine glucose in what kind of patient’s taking Synthroid?
When to take Synthroid?
MORNING/same time every day
Nursing Assessments w/Synthroid?
Apical pulse, BP, tachyarrthymias, chest pain
Initial dose of geriatric/cardiac pt. taking synthroid?
5-10 mL
Give synthroid before breakfast to prevent____.
Deficient knowledge R/T medication regimen
Potential nursing diagnoses for pt. taking Synthroid?
75-125 mcg/day
Maintenance dose for levothyroxine?
Monitor: Ht., wt, psychomotor development.
When a child is taking Synthroid.
Synthroid toxicity/overdose
100 mcg/over 1 MIN
IV administration of Synthroid
Take Synthroid with:
Test given yearly to pt’s on Synthroid?
Thyroid Function Test
Thyroid Therapy
Partial hair loss may be experienced in kids taking __ ___.
Treatment: Synthroid overdose?
Stop dose for 2-6 days
Treatment: Acute Synthroid overdose
Stomach pump(puke) + activated Charcoal (treat poisonings)
Synthroid Routes?
Synthroid metabolic adverse reactions?
Heat intolerance & weight loss
Treats hypothryroidism. Know for pharm exam 2.
IV/PO dose
IV = 200, 500 mcg vial
Tab = 25-300 mcg
Desmopressin acetate (DDAVP): is
an antidiuretic hormone, works by limiting the amount of water that is eliminated in the urine.
Desmopressin acetate (DDAVP): duration of action
up to 20 hours
Desmopressin acetate (DDAVP): available as
nasally, IV, oral/subling tab
Desmopressin acetate (DDAVP): works on the
posterior pituitary
Desmopressin (DDAVP): used for
Treatment for: diabetes insipidus, bedwetting(nocturia), brain injuries, hemophilia A w/ some factor VIII production

We use cookies to give you the best experience possible. By continuing we’ll assume you’re on board with our cookie policy Lipoprotein the combination of triglyceride or cholesterol with apolipoprotein Very low density lipoprotein produced by the liver, transports endogenous …

We use cookies to give you the best experience possible. By continuing we’ll assume you’re on board with our cookie policy heart failure What is the heart’s inability to pump enough blood to meet the needs of the body (oxygen …

We use cookies to give you the best experience possible. By continuing we’ll assume you’re on board with our cookie policy Antiulcer Drugs: Include antacids, Histamine Antagonists, Antacids: Neutralize gastric acid WE WILL WRITE A CUSTOM ESSAY SAMPLE ON ANY …

We use cookies to give you the best experience possible. By continuing we’ll assume you’re on board with our cookie policy Alpha Blockers (central acting) Purpose: decrease cerebral sympathetic blood flow, lower BP, treats hypertensive crisis Drugs: Clonidine, Methyldopa Alpha …

We use cookies to give you the best experience possible. By continuing we’ll assume you’re on board with our cookie policy 1 Identify antineoplastic drugs, and understand their different modes of action. 2 Explain the use of antineoplastic drugs in …

We use cookies to give you the best experience possible. By continuing we’ll assume you’re on board with our cookie policy Glycosides Digoxin, Amrinone Inotrope, chronotrope, dromotope Control contraction and rate Vasodilators Nitrates Decrease preload WE WILL WRITE A CUSTOM …

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