Receptors
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 norepineph
EXAM 1 DRUGS!!!!
...........
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
CCB,/calcium channel blockers
Nifedipine/Adalat/Procardia/Norvasc-controls blood vessels
Diltiazem/Cardizem
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 vascu
Pril/ace inhibitors
Enalapril/Vasotec
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 art
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
Nitrates
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 arterie
Digoxin
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
Heparin
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 clien
Coumadin
Warfarin/Coumadin
Warfarin inhibits the action of Vitamin K, and without adequate Vitamin K the synthesis of clotting factors 2, 7, 9, and 10 is diminished
INR/PT
Warfarin takes 2-3 days to achieve therapeutic effect-99% of warfarin is bound to plasma pro
Amiodarone
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
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 b
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
plavix
Anti-platelet drugs
ASA
Persantine
ADP Receptor Blockers (Plavix, Ticlid, Effient)
Glycoprotein 2b./3a receptor antagonist (Repro, Integrillin, Aggrastat
ADP receptor blockers
Irreversibly alter the plasma membrane of platelets, alters the ability of plat
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 productio
Synthroid
Treats hypothyroidism. Also treats an enlarged thyroid gland (goiter) and thyroid cancer.
Cortef
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-inflammato
Hydrocortisone
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. Hydro
Cortisol
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 relea
Tapazole
Treats hyperthyroidism (too much thyroid hormone produced by the thyroid gland).
PTU
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)
Ranitidine
PPI's (-prazole)
Omeprazole
Antacids
...
Maalox
30mL QID
Mylanta
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 t
Mylanta
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
Bulk-Producing Laxative
Metamucil
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
Lomotil
Antidiarrheal, Anticholinergic
Insulins
(dec blood sugar)
Insulin
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 pla
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 las
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. Dos
Diabetics:
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
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
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 gluco
EXAM 3 DRUGS
.......
NSAIDS---->Ibuprofen (advil/motrin)
Antipyretic
Analgesis
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
Aspirin (ASA)
Non-opioid
non-steroidal
anti-inflammatory
antipyretic
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 balan
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
Hepatotoxic ....NO MORE THAN 4 GRAMS/DAILY
Side Effec
Tylenol
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 be
Narcan (naloxone)
Opioid antagonist
Treats Overdose = competes w/opioid receptors
Don't give with pregnancy
(Rebound resp depression, abstinence syndrome, titrate dosage, rapid infusion)
IV, IM, SQ, NOT ORALLY
1/2 LIFE = 60-90 MINUTES
1/2 LIFE of opioid = 3-4 hours
Can lea
Narcan
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 induc
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 & r
Morphine
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, pregnan
Atrovent (ipratropium) ----> MDInhaler
Bronchodilator anti-cholinergic
Blocks parasympathetic NS
TX ---> COPD/ASTHMA
Onset = 5-15 minutes (2-3 minutes between squirts)
**little absorbed, peanut allergy, nasty taste
Atrovent
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)
Anticho
Afrin (oxymetazoline)
Nasal decongestant/sympathomimetic
Short-term = 3-5 days
Stimulates the Alpha adrenergic receptors
Arterioles constrict - dries mucous membranes
Afrin
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)
V
Histamines
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 n
Benadryl
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
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 use
Fever = signs of inflammation/na
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 --> C
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 gland
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 Retenti
Bronchodilators
Beta 2 adrenergic agonists (Beta 2 - 2 lungs)
Activates SNS (relaxes smooth muscle/dilates bronchi)
**Relief of bronchospasm, histamine release stopped, increase ciliary motility.
Proventil
Beta 2 adrenergic agonist
Brochodilator
Quick-acting rescue inhaler (5 minutes)
Use before exercise to prevent Bronchoconstriction
Use beta 2 agonist inhaler before glucocorticoid
Proventil
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
Mucomyst
Antidote for tylenol
Effectiveness?? Liver enzymes are normal/no enlargement)
Lovenox....
Anticoagulant-low molecular weight heparin derivative.
Mechanism of action
Deactivates thrombin. Also prevents the conversion of fribrinogen and fribrin.
Indications
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.
Contraindications
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 damage
increased GASTRIN/dec SOMATOSTATIN
**its is able to live in such an acidic environment b/c of
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
-ranitidine
-famotidine
-nizatidine
*reversibly and competitivel
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. --> con
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
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 (ant
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
-tetracycline
-metronidazole
*both broad spectrum antibiotics
-PPI
-bismuth (for coating and eradication)
Triple therapy for H. pylori
-amoxicillin
-clarithromycin
-PPI
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
Adults
1-2 mcg/kg
T4 for full replacement
Children generally need more
Thyroid Replacement in Elderly?
Start SLOW
Synthroid
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
Ablation
� 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
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?
mild
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?
diarrhea
What can help balance the side effects?
give them together
What AA to give pt. w/ a renal insufficiency?
magnesium AA
monitor
check electrolytes periodically
prego cat
none
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
s/s
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
PRN
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)
1) GERD
2) PUD
3) hypersecretory conditions (ZE)
PPI uses... (-prazole)
1) GERD
2) PUD
3) hypersecretory conditions
4) H. pylori
actions
decrease amount of acid produced by stomach
which are more powerful (how)
PPI (decrease acid to greater extent)
nonpharms
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?
PPI
What if NO improvement in a week with H2 blockers??
increase dose or change to PPI
length of tx for hypersecretory or erosive conditions
long-term
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 or
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?
NO
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 i
how long does it take for blood to clear tract
72 hours
H2 blocker---Prototype Drug?
Zantac
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?
H2
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
200-300
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):
- PUD
- combo w/antibiotics for H. Pylori
* PO; 15-60mg/day
-- Prevacid combines (lansoprazole) w/amoxicillin/clarithromycin
Prilosec (omeprazole):
- PUD/GERD
- 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):
_ PUD/GERD
* PO; 20mg/day
H1 distribution
Smooth muscle
Endothelium
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
Climetidine
Famotidine
Nizatidine
Ranitidine
Note: 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)
Cimetidine
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 gastr
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:
--Bendodiazepines
--Warfarin
--Phenytoin
Reduce absorption of:
--Ketoconazole
Increase the absorption of:
--Digoxin
PPIs - drug names
Omeprazole (children, GERD)
Lansoprazole (NSAID ulcers)
Rabeprazole
Pantoprazole
Esomeprazole
PPIs- adverse reactions
Few and generally mild
Diarrhea
Headache
Drowsiness
Muscle pain
Constipation
Mucosal protective agents - drug names
Sucralfate
Colloidal bismuth (Pepto-Bismol)
Sucralfate
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
--Clarithromycin
--Metronidazole
--Amoxicillin
One 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 antibiotic
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
LOG's --Rapid Acting
Onset 5-15 minutes
Peak 1-3 hours
Duration 3-5 hours
These 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
NPH
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 hours
Once/day @ night
CAN'T MIX WITH ANY OTHER INSULIN!!!!
Syringes
Specially calibrated syringes for insulin.
NOTE: NEVER put anything but INSULIN in these syringes
HYPOglycemia
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
Sweating
Tremors
Irritability
Blurred vision
Diaphoretic (sweating)
Headache
Lighth
Tx for HYPOglycemia (or brain cells will die)
(HIGH SUGAR SNACK, THEN COMPLEX CARB)
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 t
HYPERglycemia
3-P's
Polyuria-frequent urination
Polyphagia-hunger
Polydipsia- thirst
Glycosuria-high sugar in the urine
Weight loss-even though their sugar is high, they aren't getting nutrients into the cell
Fatigue
Ketones- in the urine/breath--gives off ketones (fru
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)
Mineralocorticoids
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 -->angiotens
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 aldos
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 glucocort
Use of Glucocorticoids
Adrenal Insufficiency
Allergies
Asthma
Inflammatory Bowel Disease (Crohn's/Ulcerative Colitis
Cancer-Hodgkin's/Leukemia's/Lymphoma's
Transplant Rejection Prophylaxis
Rheumatic Disorders
Shock
Skin Disorders
Glucocorticoids (-sone)
PO, IV, IM
Prototype Drug: Hydrocortisone/Cortef
w/food
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
Psycho
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, respirator
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
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 gla
Corticosteroids
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
Anti-Diuretic Hormone Drugs
ADH
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-bedw
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.
WHAT is ADH?
ADH = maintain fluid balance, control BP, and cardiac output in your body.
Antidiuretic - holds fluids
Diuretics allow fluids to be lost through the kidneys
Hypothalamus sense if the plasma volume has decreased, if the Na
level has risen (or the osmolalit
Addison's
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 Add
Cushing
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-Buff
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?
Diabetic
When to take Synthroid?
MORNING/same time every day
Nursing Assessments w/Synthroid?
Apical pulse, BP, tachyarrthymias, chest pain
LOW
Initial dose of geriatric/cardiac pt. taking synthroid?
5-10 mL
LEVOTHYROXINE SHOULD BE CRUSHED FOR PATIENTS WITH DIFFICULTY SWALLOWING AND PLACE IN HOW MANY ML OF WATER?
Insomnia
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.
HYPERthyroidism?
Synthroid toxicity/overdose
100 mcg/over 1 MIN
IV administration of Synthroid
Take Synthroid with:
WATER
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)
IV/PO
Synthroid Routes?
Synthroid metabolic adverse reactions?
Heat intolerance & weight loss
Synthroid
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