Final Exam Study Guide
1. Define pharmacotherapy and pharmacokinetics. pharmacotherapy is what the drug
is treating and the effect it has on then condition. It is the application of drugs for the
purpose of disease prevention and treatment of suffering (pg4 ch1). pharmacokinetics
is the way the drug moves through the body and deals with absorption and
metabolism of the drug, it describes what the body does to the medication after it is
administered. Drugs face numerous obstacles to reach their target cells. For most
medications, the greatest barrier is crossing the many membranes that separate the
drug from its target cells. A drug taken by mouth, for example, must cross the plasma
membranes of the mucosal cells of the gastrointestinal tract and endothelial cells of
the capillaries to enter the bloodstream. To leave, it must again cross capillary cells,
travel through interstitial fluid, and perhaps enter target cells by passing through
their plasma membranes. (pgs 4 and pgs 27)
2. What is a placebo and how are they used in clinical trials? Phase 2. Several hundred
patients with the disease to be treated are given the drug. The primary focus of the
phase 2 trial is on effectiveness, although safety date continue to be recorded. In most
cases, the effectiveness of the new drug is compared to an inert substance, or placebo
(seems real but isn't), which serves as a control “nontreatment” group. In other
cases, the new drug is compared to a standard drug used for the same condition. If the
new drug is found to have the same effectiveness and safety profile compared to the
standard drug or placebo, the pharmaceutical company may stop the clinical trials.
This phase may take several years. (pg 19 ch 2)
3. What is simple diffusion, active transport, facilitated diffusion? Simple diffusion, or
passive transport, is the movement of a chemical from an area of high concentration
to low concentration. Ex., When first administered, a drug given by IV route is in high
concentration in the blood but has not yet entered the tissues. The drug will move
quickly by passive diffusion from its region or high concentration (blood) to a region
of low concentration (tissues) to produce its action. With time the drug will be
inactivated (metabolized) by the tissue and more doses of the drug may be
administered, creating a continual concentration gradient from blood to tissue.
Diffusion assumes that the chemical is able to freely cross the plasma membrane.
Drug molecules that are small, nonionized and lipid soluble will usually pass through
plasma membranes by simple diffusion and easily reach their target cells. drugs may
enter through open channels in the plasma membrane; however, the molecule must
be very small such as urea, alcohol, and water. Large molecules, ionized drugs, and
water-soluble agent have difficulty crossing plasma membranes by simple diffusion.
These agents may require carrier, or transport proteins to cross membranes. A drug
that moves into a cell along its concentration gradient utilizing a membrane carrier
protein is using the process of facilitated diffusion. This process does not require
energy expenditure from the cell but it does require that a specific carrier protein be
present on the plasma membrane. Transport proteins are selective and only carry
molecules that have specific structures. Some drugs cross membranes against their
gradient from LOW to HIGH concentration, through the process of active transport.
This requires expenditure of energy on the part of the cell and a carrier protein.
Carrier proteins that assist in active transport are sometimes called pumps. (pg 28
ch3)
4. What is potency and efficacy? tequila is more potent than beer (beer is more diluted
and has more solute than tequila). 2 beers = 1 shot this is efficacy (meaning which is
more effective) potency, is the amount of drug needed to produce a specified effect.
When compared to another drug in the same class, a drug that is more potent will
produce its therapeutic effect at lower doses. As an example, consider 2 calcium
channel blockers used for THN: amlodipine (Norvasc) and nifedipine (Procardia).
Amlodipine produces its decrease in blood pressure at a dose of 10mg/day and
nifedipine at 6mg/day. Amlodipine is clearly more potent than nifedipine because it
takes a lower dose (6 times less) to produce its antihypertensive effect.(pg 49)
efficacy, is defined as the maximum response that can be produced from a particular
drug. ex, acetaminophen 650mg and ibuprofen 200mg. both relieve headaches but
ibuprofen does it at a lower dose, making it more potent but both are equally as
effective giving them the same efficacy (pg49)
5. What is herbal therapy? Why is it important to assess the patient’s use of OTC meds
and supplements? Herbal therapy is the use of plant based substance with some useful
application as a medicine. It is important to assess the patient’s use of OTC meds and
supplements to determine if there may be interactions with other medications and
drug therapies and health conditions that it may be contraindicated for. Also, the FDA
does not have the same restrictions and testing procedures for Herbal medicines and
supplements so you really can not be sure of the dosage and formulation you are
taking. With herbal supplements the USP can verify( if a company pays for testing)
that the herb is in the ingredients but not necessarily the amounts.
6. What are the priority nursing assessments when giving a medication to a pregnant
patient? What are the patient teachings for pregnant women regarding medication?
Priority nursing assessments when giving a medication to a pregnant patient are,
treatment for a preexisting condition, treatment of conditions unrelated to
pregnancy, treatment of complications related to pregnancy, Pregnancy category of
medications currently on and pregnancy categories of medications to prescribe, which
trimester of pregnancy the pt is in. potential for birth defects of medications,
potential for adverse reactions related to and unrelated to pregnancy. pregnancy risk
category the mother falls in before prescribing meds. plasma drug level in the mother,
solubility of the drug, molecular size of the drug such as alcohol to see what may pass
through the placenta, protein binding, drug ionization, blood flow to the placenta
(decreased uterine blood flow may cause drugs to remain trapped in the fetus for
extended periods, resulting in fetal adverse effects. (ch8)
Category A: Adequate and well-controlled studies have failed to demonstrate a risk to
the fetus in the first trimester of pregnancy
Category B: Animal reproduction studies have failed to demonstrate a risk to the fetus
and there are no adequate and well-controlled studies in pregnant women
Category C: Animal reproduction studies have shown an adverse effect on the fetus
and there are no adequate and well-controlled studies in humans, but potential
benefits may warrant use of the drug in pregnant women despite potential risks
Category D: There is positive evidence of human fetal risk based on adverse reaction
data from investigational or marketing experience or studies in humans, but potential
benefits may warrant use of the drug in pregnant women despite potential risks.
Category X: Studies in animals or humans have demonstrated fetal abnormalities and
there is positive evidence of human fetal risk based on adverse reaction data from
investigational or marketing experience, and the risks involved in use of the drug in
pregnant women clearly outweigh potential benefits
7. What are the additional considerations when administering meds to infants?
Children? Older adults? children-oral absorption of drugs consider they have an
increased pH and delayed gastric emptying. Low gastric acid production may enhance
the absorption of acid labile drugs such as ampicillin and penicillin and slow the
absorption of weak acids like phenobarbital. This is especially true for premature
infants and neonates. Gastric acid production may not reach adult levels until age 2 or
3. Slowed gastric motility in very young children will keep the drug in the stomach
longer . This will increase the absorption of drugs that are absorbed across the
stomach mucosa but slow the rate of drug absorption for drugs that rely on the
intestine for absorption. The rate of bile salt secretion is diminished in premature
infants and neonates which will delay the absorption of lipid soluble drugs and
vitamins. In the infants, relatively low blood flow to skeletal muscle leads to slow
and erratic absorption of drugs administered by the IM and subcu routes. Weak
muscle contractions may also contribute to the delayed absorption and distribution of
IM drugs. IM injections are generally avoided due to their unpredictable ab relatively
low blood flow to skeletal muscle leads to slow and erratic absorption of drugs
administered by the IM and subcu routes. Weak muscle contractions may also
contribute to the delayed absorption and distribution of IM drugs. IM injections are
generally avoided due to their unpredictable absorption rates and their associated
pain. The skin of infants is thin and highly permeable compared to adults, so topical
drugs are absorbed much more rapidly and can cause systemic effects. sorption rates
and their associated pain. The skin of infants is thin and highly permeable compared
to adults, so topical drugs are absorbed much more rapidly and can cause systemic
effects. Three main factors affecting drug distribution in children are the proportion
of water to fat, immature liver function, and the underdeveloped blood-brain
barrier. The rate at which drugs are metabolized in children is impacted by the
immaturity of the hepatic cytochrome P450 (CYP450) enzyme system. Metabolism is
significantly slower in children, leading to reduced clearance rates and extended half
lives for drugs extensively metabolized by the liver. Metabolic rate reaches adult levels
by age 3-5. Excretion, for children the ability to effectively excrete most drugs
depends on the kidneys function and maturity. pediatric doses can be given at approx
3 to 5 months of age. Pharmacotherapy of the infant is or neonate up to 28 days is
geared toward safety of the infant, proper dosing of prescribed drugs, and teaching
parents how to admin meds properly. The older adult should be started on the
smallest effective dose of medication and then be titrated upward. observe the older pt
for signs of drug accumulation about 3 to 5 days after new drug initiation. consider
any change in physical or emotional behavior as possible drug intoxication. monitor
hydration and nutritional status, especially among older pts, because dehydration and
low protein in the diet are primary causes of drug toxicity in this age group. half life of
drugs increases because kidney function declines. periodic serum creatinine tests
should be drawn and monitored. drugs will have extended duration of action because
of reduced metabolism from age related changes in the liver.
8. What is angioedema? The sudden onset of edema (swelling) in the areas beneath the
skin or mucosa, particularly the mouth, lips, tongue, pharynx, larynx, and epiglottis.
Swelling occurs because of fluid accumulation. Although it may be hereditary,
angioedema is normally an allergic reaction and is highly associated with ACE
inhibitors. When ACE can no longer breakdown bradykinin, there is an excess amount
in circulation. Bradykinin is a vasodilator and increases vascular permeability - with
an increased amount of bradykinin, fluid builds up and can lead to angioedema.
Angioedema is more common in African Americans taking ACE inhibitors than any
other population; it typically occurs after the first dose of drug but can happen at
anytime.
9. What are enteral and parenteral feedings? When would it be appropriate to use
either? How are the nutrients delivered by both? Enteral Nutrition = nutritional
support used for patients with a functioning GI tract but who are unable to orally
ingest adequate amounts of nutrients to meet their metabolic needs...EN uses include
patients unable to swallow and those who are ordered NPO for more than 3 days.
Delivery can be a number or routes - PO is best when permitted; NG tube is for short
term use (less than 4 weeks); ND or NJ tubes can be used when the patient has low
gastric motility; PEG tubes are used for long term therapy (more than 4 weeks).
Contraindications for EN include peritonitis, intestinal obstruction, paralytic ileus, GI
ischemia, and uncontrolled vomiting/diarrhea. Parenteral Nutrition = the
administration of high-calorie nutrients via a central vein, such as the subclavian. PN
uses include patients who are unable to eat, have an inability to tolerate EN, or cannot
ingest an adequate intake for nutritional needs orally. Delivery method is through a
central venous catheter (subclavian/internal jugular veins)...PICC lines are used for
patients going home with TPN. PN is administered through an infusion pump; PPN
(partial parenteral nutrition) is given when there is no central vein access, and is
usually a temporary measure.
10. What are diarrhea and constipation? What are the causes? What are the
treatments? Understand each type of laxative and the teachings that go along with
each. Constipation = the infrequent passage of abnormally hard and dry stool. Causes
include dietary, GI disorders, lifestyle, medications, metabolic disorders, CNS
disorders, or pregnancy (table 60.1, page 1104). Treatment consists of laxatives, used
either as a treatment plan or prophylactically for certain patients (those with MI or
rectal pathology should not be straining, those using medications with a known side
effect of constipation, patients who are bedridden/unable to exercise, pregnant
women, older patients with weak abdominal/perineal muscles). Diarrhea = an
increase in the frequency and fluidity of bowel movements. Causes include infection,
malabsorption, food, medications, inflammation. Treatment is antidiarrheals
(Lomotil, Imodium, opium tincture, Pepto-Bismol, Kaopectate, octreotide,
telotristat).
7 types of Laxatives: Bulk-forming, saline (osmotic) cathartics, stimulant,
surfactant, herbal, opioid antagonists, miscellaneous.
Patient teachings: All laxatives ---> take with additional fluid & increase fluid intake
throughout the day/increase dietary fiber/exceeding the recommended dose (or
frequent use) decreases normal peristalsis and can lead to laxative dependency.
Bulk-forming ---> take other medications 1 hour before or 2 hours after laxative/
powders should be mixed with a full glass of liquid and taken immediately, followed
by another full glass of liquid.
Mineral oil (misc.) ---> should not be taken if pt is nauseas/should not be taken at
bedtime due to risk of aspiration.
11. What are meds for acid-blocking in GI? Proton pump inhibitors, H2-receptor
antagonists, Antacids. PPIs block the enzyme H+,K+ - ATPase which secrets
hydrochloric acid into the stomach. Meds = esomeprazole, lansoprazole, omeprazole,
pantoprazole, rabeprazole. H2-receptor antagonists block H2-receptors in the
parietal cells of the stomach which promote gastric acid secretion. Meds = cimetidine,
famotidine, nizatidine, ranitidine. Antacids neutralize gastric acid. Meds = aluminum
hydroxide, calcium carbonate, calcium carb with magnesium hydroxide, magnesium
hydroxide, mag hydroxide & aluminum hydroxide with simethicone, sodium bicarb
12. What is PUD? IBD? IBS? What are risk factors for each? Which treatments are
appropriate for each? What are the nursing priorities for these patients?
Peptic Ulcer Disease (PUD): Lesion or erosion located in either the stomach or small
intestine. Patient risk includes infection w/ bacterium H.Pylori, family history, drug
usage (corticosteroids, NSAIDs, anti- platelet inhibitors such as aspirin and
clopidogrel), blood group O (intestinal epithelial cells bind to H.pylori more strongly
in these individuals), smoking, stress
treatment: PPI (omeprazole) H2-Receptor (Ranitidine)
risk factors: bleeding, perforation, penetratin, GI obstruction due to scaring
Inflammatory Bowel Disease (IBD): presence of ulcers in the intestinal tract. crohn’s
disease appear at the distal region of small intestine, most risk of acquiring GI cancer
symptoms: alternating periods of remission and exacerbation, abdominal cramping
w/ frequent bowel movements, weight loss, dehydration, fever, bloody diarrhea
Irritable Bowel Syndrome (IBS): disorder of the lower GI tract characterized w/
abdominal pain, visible bloating, excessive gas, and colicky cramping
bowel habits are altered, with diarrhea alternating with constipation and there may be
mucus in stool
treatment: dietary fiber and laxative
13. What are the patient's teachings regarding the drug Evista? Evista is a SERM
(antagonist on estrogen receptors in the breast). Patient teachings include: avoid
sitting for a prolonged period of time (risk for thromboembolic disorders; especially
in the first 4 months of use); may cause leg cramps and hot flashes, report S/S of CVA,
DVT, or PE; Do not use cholestyramine, colestipol, or estrogen in any form
(pill/patch/injection).
14. What are ways to maintain healthy levels of vitamin D and calcium in the body?
Vitamin D: food (fish and egg yolks; fortified milk, yogurt, OJ, cereal), supplements,
sunlight.
Calcium: food (dairy, salmon, leafy greens such as kale, cabbage, & broccoli;
nuts/seeds/oats), supplements (calcium compounds)
*15. Understand the clinical picture of the immune system. What causes each of the
signs and symptoms i.e. pain, fever, swelling, erythema etc.?
FEVER indicates infection, bacteria go to a break in the skin and wbc’s increase to put
out the fever
SWELLING indicates either trauma or introduction of bacteria and the body trying to
protect itself. it is a response by the body against a foreign invader or allergic reaction
caused by the capillaries leaking
PAIN indicates inflammation due to trauma, immune response, or infection.
ERETHRYMA (redness) indicates the body trying to compensate for injury or presence
of bacteria
16. What is the MOA of acetaminophen, ASA and NSAIDS? What are the patient
teachings for each?
Acetaminophen: MOA = acts centrally on the CNS by inhibiting COX. It also reduces
fever by having an effect on the heat-regulating center in the hypothalamus to
produce peripheral vasodilation, sweating, and heat dissipation.
Teaching= Do not exceed 4000mg/24 hours, many non-prescription combo drugs
contain acetaminophen, take with a full glass of water, do not consume alcohol, side
effects include GI hemorrhage, hepatotoxicity, nephrotoxicity.
ASA (Aspirin): MOA = reduced prostaglandin synthesis by inhibition of COX-1 and
COX-2 has an anti-inflammatory effect. Analgesic action occurs peripherally with
action in the CNS on the hypothalamus.
Teaching = report excessive/unusual bleeding, report GI ulceration or bleeding, avoid
other non-rx aspirin or NSAIDS, take a the same time daily with a full glass of water,
side effects include dyspepsia, agitation, confusion, dizziness, headache, lethargy,
Reye syndrome, seizure.
NSAIDs: MOA = inhibits COX-1 and COX-2 blocking prostaglandin synthesis and
modulating T-cell function.
Teaching = avoid use of multiple NSAIDs/Aspirin, avoid use in late pregnancy, in
patients with a cardiac hx - report S/S of MI or CVA, report S/S of serious GI events or
hepatotoxicity, report skin rash or blistering, take PO with food or milk, do not use
alcohol or tobacco, side effects may include fluid retention, abdominal pain,
constipation, diarrhea, dyspepsia, heartburn, nausea, vomiting, dizziness, headache,
hemorrhage.
17. What are patient teachings when on immunostimulants and
immunosuppressants? What are risk factors/side effects of and uses of? What
assessments are critical?
Immunostimulants increase the ability of immune system to fight infection/disease
(cancer, hepatitis). There are 4 classifications (interferons, interleukins, colonystimulating factors, & vaccines).
Risks of interferons include flu-like syndrome, neutropenia, depression/suicidal
ideation. Risks of interleukins are capillary leak syndrome, hypotension,
tachycardia/dysrhythmias.
Teachings = (interferons) avoid activities requiring mental alertness/coordination,
report depression/thoughts of suicide, report any visual disturbances, rotate injection
sites, call PCP if a dose is missed, pts with history of neuropsychiatric, autoimmune,
ischemic, infectious disorders should report disease exacerbation.
(interleukins) pts with history of cardiac/pulmonary disease should report
exacerbation of the disease, side effects may include hypotension, stomatitis, anuria,
oliguria, flu-like illness. Immunosuppressants inhibit the immune response or
dampen hyperactive immune response.
Teachings = (calcineurin inhibitors)
18. What is selective toxicity? the ability of a drug to selectively kill/inhibit the growth
of microbial targets while causing minimal or no harm to the host
19. How does a bacteria develop resistance?
The bacteria can produce an enzyme that destroys or deactivates the drug
Prevention of drug entry into the pathogens. Some bacteria have developed enzymes
that inactivate the drug as it crosses the cell wall. Others have changed the structure of
the channels or pores that the antibiotic normally uses to enter the cell.
Removal of resistance pumps. Some bacteria have developed a system that rapidly
pumps the antibiotic out of the bacterial cell before it can reach intracellular targets
such as ribosomes. resistant bacteria have developed several types of pumps, each of
which is used to remove different antibiotics.
Alteration of the drugs target site. Most antibiotics bind to a specific receptor that is
located on the cell surface or inside the bacteria. Certain bacteria have changed the
shape of these receptors so they no longer bind the drug.
Development of alternative metabolic pathways. Some antibiotics act by depleting the
pathogens of an essential substance necessary for growth. Some resistant organisms
have survived antibiotic application by synthesizing larger amounts of the essential
substance or by finding alternative means of obtaining it from the environment
20. What are patient teachings regarding the administration of antibiotics? take as
prescribed, …… Complete the entire course of therapy, Do not share with other family
members, Do not stop taking when starting to feel better, Take medication as evenly
spaced throughout each day as feasible, increase overall fluid intake while taking
antibacterial drug, Discard outdated medications or those no longer in use
21. What is the nurse’s priority assessment when administering an antibacterial?
Assess for adverse effects: nausea, vomiting, abdominal cramping, diarrhea,
drowsiness, tinnitus, or dizziness. Severe diarrhea, especially that containing mucus,
blood or pus, yellowing of the sclera or skin, decreased urine output or darkened urine
should be reported immediately.pg.882
22. What are the side effects and patient teachings for vancomycin? Side effects =
(common) hypokalemia, abdominal pain, diarrhea, nausea, vomiting; (serious)
cardiac arrest, hypotension, C.diff diarrhea, neutropenia, thrombocytopenia,
agranulocytosis, anaphylaxis, ototoxicity, nephrotoxicity. Teachings = complete the
entire course of therapy, avoid/eliminate alcohol, take with food or milk (avoid
acidic/carbonated beverages), increase fluid intake, take the medication as evenly
spaced out as possible. *RED MAN SYNDROME adverse effect*
23. What are the patient teachings and side effects when administering a tetracycline?
Side effects: superinfections, nausea, vomiting, diarrhea, epigastric burning,
discoloration of the teeth, photosensitivity, can worsen pre existing kidney
impairment, anaphylaxis, fatty degeneration of the liver, and exfoliative dermatitis.
Patient teachings: drink with a full glass of water on an empty stomach, do not take
before sleeping, report sudden onset of pain or dysphagia, report oliguria and any
changes in urine appearance. Report severe headache or visual disturbances.
24. Why does an antibacterial that disrupts a bacteria DNA not affect human DNA?
Human ribosomes are larger and denser than bacterial ribosomes. This is why
antibiotics that inhibit bacterial protein synthesis do not kill human ribosomes.
●
25. What are the signs and symptoms of cystitis, prostatitis and pyelonephritis?
pyelonephritis= flank back pain, cystitis, frequent urge to urinate burn with
urinatiin, prostatitis, urge to urinate but cant & urinary retention
26. What are patient teachings regarding the use of trimethoprim-sulfamethoxazole
(TMP-SMZ)? Sulfonamide-broad spectrum for gram - and +.
Side effects: may cause crystalluria (crystals that form in the urine and potentially
obstruct the kidneys or ureters) The risk is higher in dehydrated patients and when
urine pH is abnormally low. Drinking 3L a day to achieve urinary output of
1500mL/24hr should be encouraged.
stay out of the sun PHOTOSENSITIVITY
27. What is the primary reason for failure of treatment with TB infections?
NONADHERENCE NONCOMPLIANCE
Pharmacotherapy must continue for 6 to 12 months
Critical that therapy be continued for the entire period
Pts who develop multi-drug resistant infections may require therapy for as long as 2
yrs
In high-risk pts, directly observed therapy (DOT) is necessary - swallowing pills,
whether in hospital, office, or home care setting
28. What is the reason so many medications are used at the same time to treat TB? (ch.
51 pg. 918) Combination drug therapy is necessary because mycobacteria grow slowly
and often develop resistance during the course of treatment.
29. What is the length of time a patient will be taking TB drugs? (ch. 51 pg. 918)
For the drugs to reach the mycobacteria isolated in the tubercles and inside
macrophages, pharmacotherapy must continue for 6-12 months . Patients who
develop multidrug-resistant infections may require therapy for as long as 2 years.
30. How is peripheral neuropathy treated when taking anti-TB drugs?
Gabapentin
31. Why does a patient take antifungal drugs for so long? Fungi are much more
complex than bacteria and require a different medication approach. Fungi grow slowly
and infections may progress for many months before symptoms develop. Fungal
infections takes a long time to clear up , so it may be necessary to take the medication
for several months, or even for a year or longer.
32. What is a systemic fungal infection vs a superficial infection and how would we
treat each? (PO, topical parenteral or both).
Superficial
● affect the scalp, skin, nails, mucous, oral cavity, and vagina
● usually treated with topical agents but sometimes are treated P0 and topical
● common topical med is nystatin
Systemic
● mostly PO meds
● affect internal organs: lungs, brain, and digestive organs
● amphotericin B deoxycholate (Fungizone)
● fluconazole (diflucan)
○ largest and most versatile antifungal
○ can be administered PO
33. Where would the following fungal infections reside? Tinea corporis, Tinea pedia,
Tinea cruris face, trunk, and extremities. Tinea corporis is a dermatophytosis that
causes pink-to-red annular (O-shaped) patches and plaques with raised scaly borders
that expand peripherally and tend to clear centrally AKA ringworm. soles of the feet
and the interdigital spaces. Tinea pedis is most commonly caused by Trichophyton
rubrum AKA Athlete’s foot. genitals, inner thighs and buttocks. Jock itch causes an
itchy, red, often ring-shaped rash in these warm, moist areas of your body.
34. What vessels supply the heart muscle with blood? CORONARY ARTERIES!!!
Left and Right coronary arteries. pg.480
35. Explain the electrical conduction through the heart. (Ch.21 pg.481)
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●
●
●
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The SA node fires a stimulus across the walls of both the left and right atria
causing them to contract
The stimulus arrives at the AV node.
The stimulus is directed to follow the AV bundle (Bundle of His).
The stimulus now travels through the apex of the heart through the bundle
branches.
The purkinje fibers distribute the stimulus across both ventricles causing
ventricular contraction.
36. Define cardiac output, stroke volume, peripheral vascular resistance, preload,
afterload. (ch.21 pg.481-482)
Cardiac output (CO): the amount of blood pumped by each ventricle per minute,
Stroke volume X Heart rate=CO
Stroke Volume: The amount of blood pumped by a ventricle in a single contraction.
Preload: The degree to which the ventricles are filled with blood and the myocardial
fibers are stretched just prior to contraction.
Afterload: The systolic pressure in the aorta that must overcome for blood to be
ejected from the left ventricle.
Peripheral vascular resistance: The friction that blood encounters in the arteries.
37. Know the types of cholesterol and the lab values associated with hyperlipidemia.
LDL (lousy cholesterol or low density lipoproteins) these are the bad guys mainly
responsible for CAD, Triglycerides, the most common type are neutral fats, which
consists of three fatty acids attached to a chemical backbone of glycerol. Triglycerides
are the major storage form of fat in the body and only type of lipid that serves as an
important energy source. They account for 90% of the total lipid in the body. , HDL
(happy cholesterol or high density lipoproteins) these are responsible for helping
control the bad guys, contains the most apoprotein, VLDL (very low density
lipoproteins) these are like part strength versions of the really bad guys because it
gets reduced in size to become LDL and VLDL is the primary carrier for triglycerides in
the blood. Hyperlipidemia can be elevated cholesterol, triglycerides, or phospholipids.
TOTAL CHOLESTEROL (STILL WORKING ON THIS ONE. NEED TO ADD LAB VALUES,
ETC)
38. What are the nursing considerations, adverse effects and contraindications of
statins, fibric acid agents, niacin and bile acid sequestrants?
Statins: Rhabdomyolysis, avoid Macrolide antibiotics, if creatine kinase(CK) levels
increase discontinue immediately, Pregnancy test its category X, can damage liver
monitor liver enzyme test, avoid grapefruit/juice.Should be taken at night.
Fibric acid agents-can cause biliary disease, Contradicted with pre-existing
gallbladder disease or serious liver impairment used with Statins increases the risk of
myositis rhabdomyolysis, CK levels need to be monitored, risk of bleeding is increased
with patients on anticoagulants..
Niacin & bile acids-may increase triglyceride levels, mix with noncarbonated fluid to
prevent esophageal irritation(to small amount of fluid can cause obstruction).GIobstruction,hyperchloremic acidosis, increase bleeding asso. with vitamin K
deficiency.pg496&501
39. What is the role of calcium in the blood vessels and cardiac system?
The influx of calcium ions are essential for maintaining the tone of smooth muscle
and contraction
40. What are the contraindications to prescribing a non dihydro CCB to a patient?
p.517 - 518
Non-dihydropyridines have a greater effect in slowing down cardiac contractility and
conduction, resulting in a slower heart rate. Verapamil and diltiazem block calcium
channels in the myocardium, causing a negative inotropic effect.
Contraindications include patients with AV heart block, severe hypotension, sick sinus
syndrome, bleeding aneurysm and those undergoing intracranial surgery. Patients
with HF should be carefully monitored, especially when the drug is administered IV
41. What are the side effects of CCB’s? CH.30
Flushed skin, Headache,Dizziness, Lightheadedness, Peripheral edema,
Hepatotoxicity, MI, CHF, confusion
42. Understand the RAAS system and it’s triggers. p.504
(RAAS) Renin-angiotensin-aldosterone System:
○
manages BP, especially when ↓
Blood pressure drops → Sympathetic Nervous System stimulates →
Kidneys release renin → Activate Angiotensinogen → Creates
Angiotensin 1, ACE → Angiotensin II and constrict blood vessels
→ Kidneys, Adrenal Cortex and pituitary gland are stimulated
○
○
○
Kidneys - Conserve Na+ H20
Adrenal Cortex - Aldosterone: Na+ H20, K+ is excreted
Pituitary gland - ADH: Keep H20
Renin: synthesized, stored, and secreted by special cells in the kidney
known as juxtaglomerular cells
ACE: decreases blood pressure, found on the surface of lung because the lung have the
most blood vessels
○ Inactivate bradykinin by breaking it down
■ Bradykinin increases arteriolar vasodilation and vascular
permeability
○
43. What are the nursing considerations, adverse effects and contraindications of ACE
inhibitors, Beta blockers and diuretics?
ACE Inhibitors- lisinopril (Prinivil, Zestril)
● Adverse Effects: Headache, Dizziness, Orthostatic hypotension, allows for
accumulation of
● bradykinin!!
● Serious Adverse Effects: Angioedema. Agranulocytosis, Hepatotoxicity, *Cough
● Nursing Responsibilities: Monitor BP before administration and 30 minutes to 1 hour
after
Beta Blockers- atenolol (Tenormin)
● Adverse effects: Fatigue, lethargy, depression, SOB, respiratory distress
● Nursing Responsibilities: Assess BP and HR before administration, monitor apical
pulse and vital signs throughout dosage adjustment, assess pulmonary status
● May cause bradycardia if overdose or mixed with other antihypertensive medications
Diuretics-Furosemide (Lasix)
● Adverse Effects: Hypovolemia, Orthostatic hypotension, syncope (dizziness,
fainting), tachycardia, dysrhythmias nausea, vomiting, ototoxicity,
hyperuricemia,metabolic alkalosis
● Nursing Responsibilities: Monitor vital signs and BP frequently, Establish safety
precautions (orthostatic hypotension), observe older adults carefully, ensure ready
access to bathroom, administer early in day, drug interactions
Hydrochlorothiazide (Microzide)
● Nursing responsibilities: Baseline and periodic determination of serum electrolytes,
Measure BP before therapy and at regular intervals, Monitor l1&0
Spironolactone (Aldactone)
● Adverse effects: Muscle weakness, Paresthesia, Flaccid paralysis, fatigue,
bradycardia,
●
●
●
decreased fertility
Serious Adverse Effects: Life-threatening dysrhythmias", Shock
Nursing responsibilities: Baseline and periodic determination of serum electrolytes.
measure BP before therapy and at regular intervals, assess for signs of
fluid/electrolyte retention
44. What is the significance of protein in the urine?
sign of kidney disease. htn check microalbumin for kidney damage
45. What is the goal of treatment when administering fluids to a patient? maintain
homeostasis and replace any loss of fluids.
46. How would hypertonic and hypotonic fluids shift fluids or solutes?
hypertonic: water follows salt. fluid goes into cells and back out pulling excess fluid
hypertonic, water will move by osmosis towards the hypertonic solution. If the blood
is hypertonic to the surrounding tissue, then water will move from the surrounding
tissue into the blood. increasing BP
hypotonic: goes into cells and sticks there
hypotonic, water will always leave a hypotonic solution. if the blood is hypotonic to
the surrounding tissue, then the water will leave the blood and enter the tissue.
decreasing blood volume and BP
47. How would the nurse address prehypertension with a patient? Chapter 34 p.584
Encourage patient to have positive lifestyle changes so it does not progress to
Hypertension and to avoid the use of pharmacotherapy.
Limit Alcohol.
Restrict sodium consumption and increase potassium intake.
Reduce Intake of saturated fat and cholesterol, and increase consumption of fruits and
vegetables.
Increase aerobic physical activity.
Discontinue use of all tobacco products
Explore measures for dealing with excessive stress.
Maintain optimal weight.
48. What systems in the body can be damaged by hypertension? Chapter 34 p.583, 584
Heart - Heart Failure, Myocardial Infarction
Eyes - subtle vision changes to blindness
Kidneys - Kidney Failure and End Stage Kidney disease
Brain - stroke, transient ischemic attacks
49. Why do we give patients who have suffered an MI thrombolytics? Thrombolytics
dissolve clots
50. What is angina ,its causes and how is it treated? Acute chest pain caused by
myocardial ischemia. caused by physical exertion- emotional excitement events
associated with increased myocardial oxygen demand. Angina is acute chest pain
caused by myocardial ischemia. Causes are events associated with increased
myocardial oxygen demand (physical exertion or emotional excitement). Treatment =
nitroglycerin. (pg 604-605)
51. What are signs and symptoms of left sided and right sided heart failure? left sided
heart failure signs are lowered EF and SOB, dyspnea, pulmonary edema, cough,
crackles, wheezes, orthopnea, tachypnea. Right sided, JVD, peripheral edema,
preserved EF, weight gain, ascites
52. What is heart failure and how would the patient present in terms of symptoms and
vital signs?
left sided (High BP, tachypnea,
rapid pulse rate)
D=dyspnea
R=rales
O=orthopnea
W=wheezes
N=nocturnal dyspnea
paroxysmal
I=increased hr
N=nagging cough
G=gaining weight
right sided (low BP possible)
S= swelling of legs n hands
W=weight gain
E=edema
L= large neck vein jvd
L= lethargic
I=irregular heart beat
N= nocturia
G=girth ascites
how many pillows do you sleep with at night
53. What is the concern when putting a patient with CHF on a beta blocker? Beta
blockers may increase contractility of the heart. Can increase vasoconstriction.
Potential adverse effects: tachycardia, dysrhythmias.
54. What are the adverse effects of amiodarone and how would we monitor for them?
CHAPTER 37 Dysrhythmias pg.653 Amiodarone is a Potassium Channel Blocker, it
prolongs the refractory period of the heart. Adverse Effects are: Nausea, Vo miting,
Anorexia, Fatigue, Dizziness, Hypotension, Blurred Vision, Photosensitivity, Rashes.
ARDS - Adult Respiratory Distress Syndrome. Signs and symptoms are dyspnea,
tachypnea, rales / crackles. Chest Xray would show Bilateral, diffuse pulmonary
infiltrates. Monitor for pulmonary toxicity and cardiac arrest
55. Which patients are at greatest risk of a DVT? Surgical and bed bound, long flight,
DM, Immobility of any kind, clotting disorder
56. What are patient teachings regarding taking Coumadin? Advise pt to report
symptoms of bleeding immediately. Have pt report a fall if it occurs (falls may
increase the risk of complications). Tell pt to report serious illness such as diarrhea,
fever, infection, etc. (side effects may include nausea, vomiting, abdominal pain, rash,
pruritus, dermatitis, chills). Avoid OTC salicylates like aspirin or topical analgesics.
Instruct pt to take a missed dose ASAP on the daysame - if an entire day has passed
skip the missed dose and resume normal schedule.
57. What lab values do you monitor for Coumadin and heparin?
Coumadin = INR ( therapeutic range 2-3) & PTT INR, stroke from Afib, monitor lab
values
heparin =iv heparin monitor PTT( therapeutic range 60,70,80 is around
normal,)short term (can destroy platelets), don’t have to monitor labs
58. MATH
Drip factor
household measurements
1tb=15 mL
1tsp = 5mL
30mL = 1 oz
2.2 kg=1 lbs
2.54 cm= 1 inch
Good luck