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295 Cards in this Set

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1. What are the two major groups of drugs used to treat psychosis?
P. 311 conventional antipsychotics and atypical antipsychotics
2. Which of the above two groups has more extrapyramidal symptoms (EPS)?
P. 311 Conventional b/c they block receptors for dopamine in the CNS.
3. Differentiate between the negative and positive symptoms of schizophrenia.
P.311 Positive – exaggeration or distortion of normal function. Negative – loss or diminution of normal function.
4. What is the MOA of conventional antipsychotic drugs?
P. 315 Block receptors of dopamine, acetylcholine, histamine, norepinephrine. Block dopamine 2 receptors in the mesolimbic part of the brain.
5. How long does it take to reach a therapeutic response to antipsychotic drugs?
Initial 1-2 days. Substantial development 2-4 weeks. Full effects take several months.
acute dystonia
p. 315 severe spasms of muscles of tongue, face, neck or back. Oculogyric crisis (involuntary upward deviation of eyes) and opisthotonus (back cramps, hunched over with butt sticking out). Severe cramping can cause joint dislocation. Larangeal distonia, can impair respiration.
parkinsonism
p. 316 characterized by bradykinesia, mask-like facies, drooling, tremor, shuffling gait, rigidity, cogwheeling and stooped posture.
akathisia
3) p. 316 characterized by pacing and squirming brought on by an uncontrollable need to be in motion.
tardive dyskinesia
. 316 choreoathetoid (twitching, writhing, worm-like movements) of tongue and face. May also have lip smacking movements and tongue flicking in a “fly-catching” manner. For many S/E is irreversible.
neuroleptic malignant syndrome
p. 317 “lead-pipe” rigidity, sudden high fever, sweating, autonomic instability, manifested as dysrythmias and fluctuations in BP, LOC may rise and fall, pt may ppear confused or mute and seizures or coma may develop. Death can result from respiratory failure, cardiovascular collape, dysrhythmia.
Chlorpromazine (Thorazine) and haloperidol (Haldol) are examples of what type of antipsychotic agents?
P. 318-9 Conventional antipsychotics
Give an example of an atypical antipsychotic agent.
Clozapine, Risperdol, Abilify and Zyprexa
How do atypical antipsychotic agents differ from conventional agents?
320 have a greater effect on negative symptoms and cognitive dysfunction. Less EPS, higher in potency.
Why should anticholinergic agents be avoided when using low potency antipsychotics (conventional) such as chlorpromazine (Thorazine)?
Can intensify anti-cholinergic responses to CNS depressants and neuroleptics ?
State the anticholinergic effects experienced with Thorazine
11. . BUDCAT
When is Clozapine contraindicated
pt taking other drugs that can suppress bone marrow function (many anticancer drugs). Chemo=no clozapine
What is the monoamine hypothesis of depression?
P. 331 depression is caused by an insufficiency of monomine neurotransmitters (norepinephrine, serotonin or both)
Describe the MOA of tricyclic antidepressants (TCAs
). P. 332 block neuronal reuptake of 2 monoamine transmitters (NE and serotonin) Therefore TCA’s intensify effects on NE & Serotonin.
When would you expect to see a therapeutic response to treatment using a TCA?
P. 333 Initial 1-3 weeks. Maximum 1-2 months
Describe the adverse effects of TCAs.
. 333 Orthostatic hypotension, sedation, BUDCAT, most serious is cardiotoxicity, yawngasm, seizures.
What are the clinical manifestations of TCA toxicity?
P. 336 Dysrhythmias, hyperthermia, flushing, dry mouth, dilated pupils, confusion, agitation and hallucinations.
Monoamine oxidase inhibitors + TCA’s =
hypertensive crisis
Direct-acting sympathomimetics +TCA’s =
potentiated responses to NE and epinephrine
Indirect-acting sympathomimetics + TCA’s
= decreases responses to ephedrine and amphetamines.
Anticholinergic agents + TCA’s =
intensify effects of anticholinergic medication.
CNS depressants + TCA’s =
even more CNS depression
Why are depressed patients given no more than 1 week of TCAs at a time?
P. 336 to reduce the risk of death by suicide.
. What is the MOA of selective serotonin reuptake inhibitors (SSRIs)? P
provides selective inhibition of serotonin reuptake and thereby intensifies transmission and serotogenic synapses.
21. How long does it take to achieve therapeutic effect when using fluoxetine (Prozac)?
P. 337 Begin in 1-3 weeks (lecture 3-4 weeks) – one month
State the adverse effects of Prozac. P
338 Sexual dysfunction, Nausea, HA, nervousness, insomnia , anxiety, weight gain, serotonin syndrome, withdraw syndrome, neonatal withdraw symptom, extrapyramidal syndrome, bruxism, bleeding disorders, hyponatremia.
Why do SSRIs have a black box warning?
Suicide risk
Describe serotonin syndrome.
338 altered mental state (agitation, confusion, disorientation, anxiety, hallucinations, poor concentration), sweating, tremor and fever and death. Takes 2-72 hours after treatment for onset.
25. What is the problem encountered with use of St. John’s Wort and SSRIs?
Can lead to serotonin syndrome.
Should SSRIs be abruptly discontinued?
No. Can cause withdraw syndrome.
What happens if warfarin and Prozac are used together?
prozac can displace warfarin on plasma proteins.
What occurs with simultaneous use of lithium and Prozac?
Elevates lithium levels.
What is the MOA of monoamine oxidase inhibitors (MAOIs)?
Cause irreversible inhibition of the enzyme MOA which is responsible for breaking down the monoamine neurotransmitters (NE, serotonin, dopamine). Therefore increasing levels.
State the adverse effects of MAOIs.
CNS stimulation (anxiety), orthostatic hypotension, hypertensive crisis from dietary tyramine.
Why are foods high in tyramine avoided when patients are taking MAOIs?
Can cause hypertensive crisis
List foods high in tyramine
. 345 Yeast extracts, most cheeses, fermented sausages (salami, pepperoni, bologne) and aged meat or fish.
35. Why are sympathomimetics and MAOIs incompatible
Can produce hypertensive crisis.
What are the clinical manifestations of bipolar disorder?
P. 354 Elevated mood to normal mood to depressed mood, repeated.
What is the drug of choice for bipolar disorder?
P. 354 Lithium – Mood stabilizer
What is considered a therapeutic plasma level of lithium?
P. 357 0.8-1.4 mEq/L for initial therapy and 0.4-1.0 mEq/L maintenance levels. (Below 1.5)
Describe the adverse effects that occur when lithium levels are excessive.
Convulsions, high output of dilute urine, blurred vision, clonic mvts, death. Table p. 33-3
Describe the adverse effects that occur when lithium levels are within therapeutic range
GI (nausea, diarrhea, bloating, anorexia), fatique, muscle weakness, HA, confusion and memory impairment (transient), plyuria and thirst occur in 30-50% of pt and may persist. Tremor, renal toxicity, goiter, hypothyroidism, teratogenesis.
What occurs when diuretics are used with lithium
Promote Na loss, decreasing lithium excretion and increasing lithium levels.
What occurs when sodium levels are low in patients taking lithium?
lithium toxicity
Why do patients taking lithium need to maintain hydration?
b/c polyuria is a SE
Why is diarrhea a problem in a patient taking lithium?
44. Dehydration
Is it advisable for pregnant women to take lithium?
P. 358 No. Category D – avoid during first trimester and through rest of pregnancy if risks outweigh benefits
Describe the MOA of benzodiazepines (BZDs)
Enhance GABA. GABA receptor has binding sites for BZD’s and barbiturates
State the therapeutic uses of BZDs
Anxiety, insomnia, seizure disorders, muscle spasms, alcohol withdraw, panic disorder, perioperative applications.
State the adverse effects of BZDs.
CNS depression, anterograde amnesia, paradoxical effects (used for anxiety but causes more anxiety or used for insomnia but keeps you awake), respiratory depression, abuse, Fetal harm.
List agents that should be avoided while taking BZDs
Alcohol and CNS depressants
Can BZDs lead to physical dependence
Yes
Describe the clinical manifestations of BZD toxicity
P. 367 Oral – drowsiness, confusion. IV – Profound hypotension, respiratory and cardiac arrest.
Which BZD has an increased potential for developing dependence
Alprazolam (Xanax, Niravam)
What is the name of the reversal agent used to treat BZD overdose?
Flumazenil (Romazicon)
How would you advise a pregnant mother regarding the use of a BZD?
warn about potential for fetal harm and instruct to discontinue.
Describe the pharmacologic effects of barbiturates?
CNS depression, cardiovascular effects, induction of hepatic drug-metabolizing enzymes.
What happens when barbiturates stimulate synthesis of hepatic microsomal enzymes?
P. 370 can accelerate their own metabolism and metabolism of other drugs.
What type of agent is zolpidem (Ambien)?
. P. 375 Benzodiazepine-like drugs; hypnotic
What warning is now given to patients taking agents similar to Ambien?
Sleep driving, dialing, cooking and daytime drowsiness. They can get hooked on it.
What are the principal drugs used to treat panic disorder?
Benzodiazepines, antidepressants (SSRI’s, TCA’s, MAOI’s)
What are the side effects of BZD’s?
p. 380 dizziness, HA, nausea, nervousness, lightheadedness, excitement.
Which TCA is approved to treat obsessive compulsive (OCD)?
Clomipramine
62. What are the CNS effects from use of amphetamines?
P. 387 At usual doses increases wakefulness and alertness, decreases fatigue, elevate mood and augment self-confidence and initiative. Euphoria, talkativeness and increased motor activity are likely.
63. State adverse effects from amphetamine use
P. 388 CNS stimulation, weight loss, cardiovascular effects, psychosis, tolerance, physical dependence, abuse.
64. How does methylphenidate help children with ADHD?
Reduce symptoms of ADHD by enhancing ability of pt to focus.
65. Why is methylphenidate a controlled substance?
P. 389 Same MOA as amphetamine – schedule II abuse liability
66. Why is it important to monitor height and weight in patients taking methylphenidate?
P. 393 B/c principle adverse effects are insomnia and growth suppression.
1. How is a myocardial infarction (MI) diagnosed?
1. P. 609 Presence of chest pain, characteristic ECG chnges and elevated serum levels of myocardial cellular components (troponin, creatine kinase)
1. What are the clinical signs of an MI?
1. p. 609 Chest pain – severe substernal pressure characterized as unbearable, crushing or constricting pain. Often radiates down arm and up to jaw. Lasts 20 minutes or longer and not relieved by nitroglycerin.
1. How does the pain of an MI differ from angina
Angina is relieved by nitro
1. Why are thrombolytic drugs considered standard treatment for early MI?
1. Opens occluded artery in 80% of pt if given soon enough.
1. What is the major complication of thrombolytic therapy?
1. bleeding
MI- Morphine
p. 611 promotes venodilation reducing cardiac preload and modest arterial dilation causes some reduction in afterload. Lowers oxygen demand thereby preserving ischemic myocardium.
MI-ASA
– suppresses platelet aggregation
MI-Nitroglycerin
– reduces preload which reduces oxygen demand, ncreases blood flow to the ischemic part of the heart, controls htn, improved fx of left ventrical.
MI- Beta-blockers
p. 611 Reduce cardiac pain, infarct size and short-term mortality.
MI-ACE inhibitors
– reduce preload and afterload and promote water loss.
What are the most severe complications of MI?
p. 613 ventricular dysrythmias, cardiogenic shock, heart failure, cardiac rupture.
. Why are iron requirements increased during pregnancy?
Expansion of maternal blood volume, production of RBC’s by fetus.
What are the most common causes of iron deficiency anemia (IDA)?
9. Blood volume expansion during pregnancy coupled w/ RBC production by fetus and Blood volume expansion during infancy and early childhood, chronic blood loss, usually of GI or uterine origin. Rarely occurs from reduce iron uptake unless gastrectomy and sprue.
How can adverse effects and staining of the teeth be avoided in patients receiving liquid iron replacement therapy?
P. 626 Dilute with water or juice, administer w/ droper or through a straw, rinse mouth after admin.
11. What is the typical daily dose for an adult being treated for IDA?
65mg 3X’s day ~200mg/day.
Why are iron dosages spaced evenly throughout the day
provides bone marrow w/ a continuous iron supply thereby maximizing RBC production
DNA synthesis requires the presence of which vitamins?
B12
. What is pernicious anemia
Vit B12 deficiency caused by an absence of intrinsic factor.
Why are patients with pernicious anemia given B12 parenterally?
Due to lack of intrinsic factor Oral B-12 will not be absorbed
Why are B12 and folic acid given together?
. P. 631 Folic acid can reverse hematologic effects of B12 deficiency but will not alleviate neurologic effects – Can mask B12 deficiency.
What electrolyte imbalance is associated with cyanocobalamin (B12) therapy?
Hypokalemia
Is cyanocobalamin ever given intravenously?
No
Giving folic acid will correct the anemia but may mask the B12 deficiency. Why is this problematic
Can lead to under-treatment w/ B12, creating permanent neurologic impairments.
. What is the function of erythropoietin and where is it produced?
stimulates production of RBC’s produced in peritubular cells in the proximal tubules of the kidney.
Why do patients with renal failure benefit from epoetin alpha?
P. 638 Reverses anemia associated w/ CRF – eliminates need for transfusions.
What is the major adverse effect when using epoetin alpha
HTN
How should a vial of epoetin alpha be handled?
Do not re-enter single-use vials, don’t agitate, don’t mix w/ other drugs, store @ 2-8 degrees C, don’t freeze
What are the principal uses of filgrastim (Neupogen)?
. P. 639-40 Reduce the risk of infection in chemotherapy patients. Treatment for congenital neutropenia (Kostmann’s syndrome), a condition characterized by pronounced neutropenia and frequent, severe infections. Also used for idiopathic and cyclic neutropenia.
. Why are WBCs measured weekly on patients receiving Neupogen?
to determine if WBC’s are above 100,000 and reducing the dosage if this occurs.
is Neupogen not used in patients with cancers that originate in the bone marrow (myeloid tissues)?
Because it stimulates proliferation of bone marrow cells.
What are the clinical signs of diabetes mellitus (DM)?
647 Sustained hyperglycemia, Polyuria, polydipsia, polyphagia, weight loss and ketonuria for Type I. Type II may be asymptomatic.
How is DM diagnosed?
Type I – Insulin antibodies (IAA), Islet cell antibodies (ICA), Glutamic acid decarboxylase (GAD). Excessive plasma glucose is diagnostic. Fasting plasma glucose (FPG) >126, a casual plasma glucose test >200, and an oral glucose tolerance test (OGTT) >200, Impaired fasting glucose >100, Impaired glucose tolerance >140 and <200.
P. 649 and notes
30. What is glycosylated hemoglobin (HbgA1c)?
P. 650 provides an index of average glucose levels over the prior 2-3 months. Shows long-term glycemic control.
. What is the target value HbgA1c for diabetics?
<6.5%
Why are C-peptide levels measured in patients with diabetes?
P. 651 It is a way to assess residual capacity for insulin synthesis, the presence of C-peptide indicates the pancreas is still producing some insulin.
. If a patient was taking regular insulin before breakfast at 7:30 a.m., when would they be at greatest risk for hypoglycemia?
Peaks at 1-5hrs for Humulin R and Novolin R and 0.5-1.5 for Exubera.
Which types of insulin are cloudy?
P. 655 Long acting.
How do you disperse the particles in suspension prior to administration in order to prevent frothing that can make dosing of NPH insulin inaccurate?
Rolling the vial between the palms of the hands.
Why is regular insulin always drawn up first when combinations of insulin are used?
P.655 Short-acting (Humulin R, Novolin R, Exubera) insulin should be drawn into the syringe first to avoid contaminating the stock vial with NPH insulin.
Insulin U100 means that each ml contains_______units of insulin?
100
What is the major complication from insulin treatment?
Hypoglycemia
What are the clinical signs of hypoglycemia?
Palpitations, Tremor/shaking, tingling, heavy breathing, slowed thinking, blurred vision, incoordination, numbness, trouble concentrating, dizziness, hunger, seizure, loss of consciousness.
What happens to signs of hypoglycemia if the patient is receiving a beta-blocker
delay awareness of insulin-induced hypoglycemia.
Name three drug classes that increase blood sugar
Thiazide diuretics, Glycocorticoids,, and Sympathomimetics.
Sulfonylureas stimulate the release of insulin from the pancreas and are used in patients with type 2 diabetes. State the major adverse effect from these oral hypoglycemics.
P. 661 Hypoglycemia, cardiovascular toxicity, teratogenesis when used in pregnancy and lactation.
Can oral hypoglycemics be used during pregnancy?
no
Repaglinide (Prandin) also stimulates the release of insulin from the pancreas and can lead to hypoglycemia. The difference is that it must be given in association with _________?
food
. Metformin (Glucophage) does not promote insulin secretion or cause hypoglycemia. How does metformin lower blood sugar in diabetic patients?
P. 663 Decreases production of glucose in the liver. Appears to suppress glucogeogenesis. Also enhances glucose uptake and utilization by muscle.
Metformin can cause decreased appetite, nausea and diarrhea. What is the most important rare side effect associated with use of metformin?
. 663 Lactic acidosis.
What problems may cause a patient taking metformin to be more prone to lactic acidosis?
Renal insufficiency, liver dz, severe infection, history of lactic acidosis, patients who consume alcohol to excess and patients with shock and other conditions that can result in hypoxemia and Heart failure, iodinated contrast media
What are the clinical signs of lactic acidosis?
hyperventilation, myalgia, malaise, and unusual somnolence.
Why is metformin usually held prior to diagnostic tests using dyes and prior to surgery?
Can cause lactic acidosis.
There are two drugs that lower blood sugar by inhibiting digestion and absorption of dietary carbohydrates thereby reducing the rise in blood sugar that occurs after meals. These two drugs (Precose and Glyset) are called______________inhibitors.
Alpha-Glucosidase Inhibitors.
Thiazolidinediones (TZDs) such as rosiglitazone (Avandia) and pioglitazone (Actos) reduce blood sugar by increasing insulin________________?
Reduce glucose levels by decreasing insulin resistance.
TZDs are contraindicated in patients with____________?
P. 664 Severe heart failure
How is diabetic ketoacidosis treated?
ABGs, bicarb, lucose, serum acetone, Cr/BUN, CBC.
Glucagon is used to treat_____________________?
Insulin overdose.
State the clinical signs and symptoms of hypothyroidism
P. 676 Moderate to Severe – Face is pale, puffy, and expressionless. Skin is cold and dry. Hair is brittle, and hair loss occurs. Heart rate and temperature are lowered. Pt. may complain of lethargy, fatigue and intolerance to cold. Mentality may be impaired. Thyroid enlargement (goiter) may occur if reduced levels of T3 and T4 promote excessive release of TSH.
In a patient with hypothyroidism, the TSH would be (elevated or depressed)?
Elevated
Hashimoto’s thyroiditis is associated with (hypothyroidism or hyperthyroidism)?
Hypothyroidism
Graves’ disease results from excessive levels of thyroid hormone. A patient with Graves’ disease has (hypothyroidism or hyperthyroidism)?
Hyperthyroidism
What are the clinical signs of Graves’ disease?
P. 677 heartbeat is rapid and strong, and dysrhythmias and angina may develop. Nervousness, insomnia, rapid thought flow and rapid speech due to CNS stimulation. Skeletal muscles may weaken and atrophy. Metabolic rate is raised resulting in increased heat production, increased body temp, intolerance to heat, and skin that is warm and moist. Appetite in increased. Weight loss occurs. Exopthalmos.
In a patient with Graves’ disease, the TSH would be (elevated or depressed)?
depressed
How is hypothyroidism treated?
Replacement with thyroid hormones, Levothyroxine (T4), Liothyronine (T3)
How should oral levothyroxine be administered?
Take on an empty stomach and don’t take with calcium or ferrous sulfate.
How long does it take for levothyroxine to reach plateau?
Half-life 7 days. Plateau?
How is Graves’ disease treated?
P. 678 Directed at decreasing the production of thyroid hormones. 3 modalities used 1. Surgical removalof thyroid tissue. 2. Destruction of thyroid tissue with radioactive iodine, and 3. Suppression of thyroid hormone synthesis with antithyroid drugs (propylthiouracil, methimazole)
Propylthiouracil (PTU), methimazole (Tapazole) and radioactive iodine-131 are used to treat (hypothyroidism or hyperthyroidism).
hyperthyroidism
How does propranolol help in the treatment of hyperthyroidism?
. P. 682 Suppress tachycardia and other symptoms of grave’s dz
Give an example of a patient that would be inappropriate for treatment with radioactive iodine.
Pregnant or lactating pt.
Name the disorder associated with excessive growth hormone
Gigantism – prior to puberty and Acromegal – during adulthood.
Children who are candidates for GH replacement have (decreased or excess) serum levels of growth hormone
decreased
Treatment with GH can lead to (hyperglycemia or hypoglycemia
hyperglycemia
Is GH used once epiphyseal closure has occurred
no
Galactorrhea is the abnormal production of breast milk. Pituitary tumors can cause excessive levels
of prolactin that stimulate production of breast milk. Name a drug used to inhibit excessive production of prolactin (hyperprolactinemia).
Cabergoline (Dostinex) a dopamine agonist. Dopamine and prolactin have an inverse relationship.
Diabetes insipidus is the result of (excess or decreased) levels of ADH?
decreased
How is diabetes insipidus treated?
Replacement therapy w/ ADH
Why is vasopressin used with caution in patients with coronary artery disease or hypertension?
P. 692 It is a powerful vasonconstrictor and constricts arteries of the heart causing angina pectoris and even myocardial infaction, especially in patient’s w/coronary insufficiency. Reduceses cardiac perfusion and decreases blood flow in the periphery that may cause gangrene.
Where are glucocorticoids produced?
Adrenal cortex.
Cushing’s syndrome results in (excess or decreased) levels of glucocorticoids?
excess
What are the causes of Cushing’s syndrome
Excess levels of circulating glucocorticoids principally by 1. Hypersecretion of ACTH by pituitary adenomas (Cushing’s disease) 2. Hypersecretion of glucocorticoids by adrenal adenomas and carcinomas, and 3. Administering glucocorticoids in the large doses used to treat arthritis and other nonendocrine disorders.
Describe the clinical signs of Cushing’s syndrome.
P. 698 Obesity, hyperglycemia, glycosuria, hypertension, fluid and electrolyte disturbances, osteoporosis, muscle weakness, myopathy, hirsutism, menstrual irregularities, and decreased resistance to infection. The skin is weakened, resulting in striae (stretch marks) and increased susceptibility to injury. Fat undergoes redistribution to the abdomen, face, and upper back, giving the patient a characteristic potbelly, “moon face” and “buffalo hump”. Psychiatric changes are common.
Addison’s disease is due to a deficiency of_________________?
deficiency of glucocorticoids and mineralocorticoids that occurs secondary to adrenal atrophy. Causes can include carcinoma, infection and autoimmune disease.
What is the treatment of Addison’s disease?
replacement therapy w/ adrenocorticoids. Hydrocortisone, which has both glucocorticoid and mineralocorticoid activity, is a drug of choice.
During times of stress, patients with adrenal insufficiency need (increased or decreased) doses of glucocorticoids
increased-Failure to increase dosage can be fatal. (surgery, infection, trauma)
What are the adverse effects of sildenafil?
Hypotension, priapism, HA, flushing, dyspepsia, nasal congestion, diarrhea, rash, mild transient visual disturbances (blue color tinge, increased sensitivity to light, blurring).
3. _________________ is a painful erection lasting longer than 6 hours.
Priapism
4. Sildenafil is absolutely contraindicated for patients taking _______________.
nitrates
What other type of antihypertensive can cause excessive hypotension when used with PDE5 inhibitors
Alpha blockers
Benign prostatic hyperplasia (BPH) is a __________________ prostate enlargement caused by excessive growth of epithelial cells and smooth muscle cells.
nonmalignant
6. BPH can be treated with two classes of drugs: ________________________________ and _____________________________.
alpha-reductase inhibitors and alpha1-adrenergic antagonists.
How do alpha1 blockers relieve BPH symptoms?
Relaxes smooth muscle in the bladder neck (trigone and sphincter), prostate capsule, prastatic urethra, thereby reducing dynamic obstruction of the urethra.
7. _________________________ is an herbal preparation that can reduce symptoms of BPH
Saw palmetto
Vaccination produces (active or passive) immunity?
active
giving immunoglobulin for exposure to hepatitis is an example of (active or passive) immunity?
passive
What are the severe adverse effects of the MMR vaccine?
Transient thrombocytompenia
What are the severe adverse effects of the DTaP vaccine?
Encephalopathy
. Why are live vaccines generally avoided in children with HIV or lymphoma?
781 b/c they are immunosuppressed
Should children born prematurely be immunized?
Yes, same dosage and timing as full-term
When are vaccines contraindicated?
Anaphylacitic reaction to vaccine or vaccine component or moderate to severe illnesses with or without fever.
Should a child with a cough or mild fever receive a vaccine?
yes
Should a child receiving antibiotics receive a vaccine?
yes
What is the VAERS?
Vaccine adverse event reporting system. , est by national childhood vaccine injury act of 1986.
What is the purpose of the National Vaccine Injury Compensation Program?
P. 781 provide compensation for injury or death resulting from vaccination. Intended as an alternative to civil litigation in that negligence need not be provided.
. What information needs to be recorded in the patient’s record for each vaccination?
Date of vaccination, route and site, vaccine type, manufacturer, lot# and expiration date, name, address and title of person administering.
What are the clinical signs of tetanus?
Stiffness in the jaw, stiff neck, difficulty swallowing, restlessness, HA, irritability, fear, chills, fever and convulsions.
what are the most common complications of varicella disease in children and adults?
P.783 bacterial superinfection, acute cerebellar ataxia; reye’s syndrome and encephalitis.
Explain how shingles occurs.
Reactivation of varicella virus virus, blister-like lesions develop.
Which vaccines are considered “live viruses”? Which individuals should not receive live virus vaccines?
Measles, mumps, and rubella virus vaccine MMR (MMR II), Measles, mumps, and rebulla, and varicella virus vaccine (proquad), Varicella virus vaccine (varivax), Influenze vaccine -live (flumist), Rotavirus vaccine (RotaTeq)
Being allergic to egg was at one time a contraindication for receiving which vaccine?
Influenza
When is MMR contraindicated?
Pregnancy
When is DTaP contraindicated?
If prior vaccination produced and immediate anaphylactic reaction or encephalopathy w/in 7 days of vaccination.
What is the difference between IPV and OPV polio vaccines?
IVP – devoid of serious adverse effects. OPV – has caused vaccine-associated pralytic poliomyelitis (VAPP) – can be fatal in immunocompromised.
Which polio vaccine is used in this country?
IVP
At what age is the varicella vaccine given?
Preferred age 12-18 months
A child over 13 years old with no prior vaccination needs_________doses of varicella vaccine administered at least_______ weeks apart?
2, 4
Can varicella vaccine be administered to a pregnant woman?
no
When is the third dose of HBV given?
No sooner than 6 months after 2nd dose.
What are the differences between the 2 influenza vaccine preparations (LAIV and TIV). State contraindications for each.
Contraindications for both: Anaphylactic reaction to vaccine, any of its components or eggs.
LAIV – Live attenuated influenza vaccine – given intranasally. Contraindications: Prenncy, asthma, reactive airway dz or other chronic disorder of the pulmonary or cardiovascular system; an underlying medical condition, including metabolic dz such as diabetes, renal dysfunction, hemoglobinopathy; a known or suspected immune deficiency disease or current receipt of immunosuppressive therapy; history of GBS.
TIV – Trivalent inactivated influenza vaccine – given IM.
What are the effects of H1 (histamine) receptor stimulation on Blood vessels and capillaries
vasodilation of arterioles and venules, prominent in the skin and face of the upper body. Increased capillary refill.
What are the effects of H1 (histamine) receptor stimulation on Bronchi:
Bronchoconstriction – caution w/ asthma
What is the effect of histamine2 receptor stimulation?
secretion of gastric acid.
What is the major difference between first generation and second generation antihistamines
First generation – highly sedating. Second generation – non-sedating.
Name two of the first generation antihistamines possessing the highest anticholinergic and sedating effects.
Clemastine, Diphenhydramine
What benefits do antihistamines have in the treatment of the common cold?
None – may moderately decrease rhinorrhea due to anticholinergic properties.
Name the antihistamine that is delivered via nasal spray.
astelin
The enzyme cyclooxygenase (COX) (decreases or increases) prostaglandins.
increases
Prostaglandins (protect or destroy) gastric mucosa?
protect
COX one inhibitors have the following effect on:gastric mucosa
erosion and ulceration
COX one inhibitors have the following effect on:kidney
renal impairment
COX one inhibitors have the following effect on:brain
protect vs stroke
COX one inhibitors have the following effect on:uterus
bleeding
What is the purpose of low-dose aspirin following an MI?
decreased risk of vascular mortality for acute MI, decreased combined risk of death and nonfatal MI for previous MI. Prevent embolism, by suppression of platelet aggregation.
What is the primary difference between COX-1 and COX-2 inhibitors?
809 COX-1 – mediates beneficial responses. COX-2 – mediates harmful processes, tissue injury - harmful
When should patients be advised to discontinue ASA and NSAIDs prior to surgery?
at least 1 weak prior.
Why should children and teenagers avoid ASA if suspected of having influenza or chickenpox
Reye’s syndrome
Is acetaminophen used for its antiinflammatory actions?
No, analgesic and antipyretic
Give an example of a COX-2 inhibitor that is considered safer than NSAIDs in the causation of gastric ulcers
Celecoxib
Tylenol overdose may lead to damage of what organ?
Liver
Which COX-2 inhibitor contains sulfa and should not be taken by patients with sulfonamide allergy?
P. 820 Celecoxib
Do COX-2 inhibitors prolong bleeding time?
P. 820 no, but may increase anticoagulent effects of warfarin
What are the mechanisms by which glucocorticoids interrupt the inflammatory response?
Can inhibit synthesis of chemical mediators (prostaglandins, leukotrienes, histamine) and therby reduce swelling, warmth, redness, and pain. In addition, they suppress infiltration of phagocytes. Hence, damage from lyssomal enzymes is averted. Lastly, they suppress proliferation of lymphocytes, and thereby reduce the immune component of inflammation. Because they act by several mechanisms they have a greater anti-inflammatory effects thand do NSAID’s that only work by inhibiting prostaglandins.
State a few disorders in which glucocorticoids are used.
Rheumatoid arthritis, SLE, IBD, misc. inflammatory disorders, allergic conditions, asthma, dermatologic disorders, neoplasms, suppression of allograft rejection, prevention of respiratory distress syndrome in pre-term infants
How do glucocorticoids cause bone loss?
suppress bone formation by osteoblasts; accelerate bone resorption by osteoclasts.
Why are doses of glucocorticoids discontinued with a drug taper
Due to adrenal suppression and to prevent withdraw symptoms. Symptoms include hypotension, hypoglycemia, myalgia, arthralgia, and fatique. In certain disorders this can be seen as a return of the disease. W/D discomfort can be minimized by gradual dosage reduction and concurrent tx w/ NSAIDs
Glucocorticoids cause (hyperglycemia or hypoglycemia)?
hyperglycemia
Why are patients taking glucocorticoids more susceptible to infection?
Suppress host defenses (immune responses and phagocytic activity of neutrophils and macrophages)
Should live virus vaccines be given to patients taking glucocorticoids
No b/c they are immunosuppressed.
What is the best time of day to administer prednisone?
Prior to 9:00am to alow maximum recovery of endocrine function.
In rheumatoid arthritis (RA) joint destruction is caused by an autoimmune process. What are the goals of treatment?
Relieve symptoms (pn, inflammation and stiffness), 2. Maintaining joint function and range of motion, 3. Minimizing systemic involvement, 4. Delaying dz progression.
Which class of drugs used to treat RA slows disease progression and delays joint injury? P
DMARDS – Disease modifying antirheumatic drugs
Do disease-modifying antirheumatic drugs (DMARDs) have an immediate effect
No, 3-5 months.
What are the adverse effects of DMARDs?
Injection site reactions (itching erythema, swelling, pn), increased risk of serious infection (tuberculosis), entenercept may pose risk of heart failure, CNS demyelinating disorder (MS, myelitis, optic neuritis ) and hematologic disorders, including fatal cases of aplastic anemia.
Give an example of a DMARD used to treat RA that is contraindicated in pregnancy.
Leflunomide
What is the role of glucocorticoids in the treatment of RA
Relieve symptoms of RA and may retard dz. Oral tx of generalized dz. Intra-artricular injections if only 1 or 2 joints are affected.
Colchicine is an antiinflammatory drug used to treat an acute attack of gout. What are the adverse effects of this drug?
P. 844 N/V, diahrea, abd pn – may injure rapidly proliferating GI cells. IV – bone marrow suppression, renal failure, heapatic necrosis, seizures and death.
Allopurinol (increases or decreases) uric acid levels?
decreases
. What is the name of the gland that regulates calcium balance in the body?
Parathyroid
. Rickets and osteomalacia are associated with deficits is vitamin________?
D
What is the recommended daily intake of calcium for adults 19-50 years old?
1,000-2,500 mg/day
How many mg of calcium in one 8-ounce glass of milk?
300 mg.
How would you advise a patient to take alendronate (Fosamax)? P
On an empty stomach, w/ full glass of water and maintain upright position for ½ hr.
What are the adverse effects of Fosamax?
musculoskeletal pn, ocular inflammation, osteonecrosis of the jaw and rarely esophagitis resulting in ulceration.
Selective estrogen receptor modulators (SERMs) such as Evista are used to treat ___________________?
Potmenopausal osteoporosis, Breast CA, cardiovascular dz
State the adverse effects of SERMs
Venous thromboembolism, fetal harm, hot flushes.
State lifestyle measures that promote bone health.
performing weight bearing exercises (walking, jogging, dancing, racquet sports, team sports, stairclimbint), avoid excessive alcohol and smoking.
When do women experience accelerated bone loss?
after menopause
How is osteoporosis diagnosed?
By measuring bone mineral density, most often by Duel-energy x-ray absorptiometry (DEXA)
What is the difference between MDIs and DPIs?
MDI – metered dose inhaler – use propellant to deliver measured dose. DPI – dry powder inhaler – no propellant, breath activated. Don’t require hand-lung coordination, therefore easier to use. DPI’s deliver more rug to the lungs.
What is the purpose of using a spacer?
increase delivery to the drug to the lungs and decrease deposition of drug on oroharangeal mucosa. Oneway valves reduce need for hand-lung coordination.
What is the MOA of beta-2 adrenergic agonists
Selective activation of B2-adrenergic receptors. Promote bronchodilation. Seuppress histamine release in lung and increase ciliary motility.
Name two beta-2 agonists that are long acting.
Slameterol (Severent Diskus) and Formoterol (Foradil Aerolizer)
Why is salmeterol (Serevent) never used as a “rescue” medication?
takes 10-30 minutes for bronchodilation to occur.
What is the most common adverse effect of inhaled glucocorticoids (ICSs)?
Oropharyngeal candidiasis (rinse mouth after to prevent) and dysphonia (hoarsness and difficulty speaking.
Why are glucocorticoids used to treat asthma?
decrease inflammation, therefore decrease bronchial hyperreactivity. Used for prophylaxis of chronic asthma. Also decreases mucous production and increases number of bronchial B2 receptors as well as their response to B2 agonists.
What is the advantage of using inhaled glucocorticoids rather than oral glucocorticoids in the treatment of asthma?
Safer. Oral increase risk of toxicity with duration of use.
Are ICSs used as rescue medications?
no. beneficial effects develop slowly.
When are oral glucocorticoids used in the treatment of asthma?
pt w/ severe asthma
What are the components that make up Advair?
Fluticasone and salmeterol
What is the normal plasma level of theophylline?
10-20 micrograms/ml
What are the major drug reactions with the use of theophylline? Notes
Increase ciprofloxacin levels
How does montelukast (Singulair) help treat asthma symptoms?
leukotriene receptor blocker
Why are asthmatics asked to monitor their peak expiratory flow rates?
if peak value is <80% of their personal best, more frequent monitoring should be done.
What are environmental control measures that help decrease asthma symptoms?
Wash pets; decrease dust mite exposure through sheets impermeable to allergens, wash bedding and stuffed animals weekly, remove carpeting and rugs and avoid sleeping or lying on upholstered furniture. Keep indoor humidity below 80%.
What is the problem with using B2 agonists on a daily basis?
Tachycardia
Why does Serevent have a Black Box Warning
Death
Do nasal corticosteroids reduce congestion immediately?
No, 1 week or more
What is the problem with using topical sympathomimetic nasal decongestants like Afrin?
Abuse is common. Rebound congestion, Rhinitis medicamentosa.
Oral sympathomimetics like pseudoephedrine (Sudafed) cause vasoconstriction and should not be used in patients with_________________________?
stroke
What is the name of the non-opioid preparation that decreases cough?
Dextromethorphan & Diphenhydramine
Guaifenesin is an expectorant that makes secretions (easier or more difficult) to expel?
easier
What is the gram-negative organism is associated with peptic ulcer disease (PUD)?
Helicobactor Pylori
State other factors that may lead to PUD.
Imbalance b/tw mucosal barriers, NSAIDS, smoking, increased acid secretion nd decreased bicarbonate production.
How long is treatment given for H-pylori eradication?
14 days – eradication rates are consistently higher
How do H2 receptor blockers promote ulcer healing
suppress secreation of gastric acid
What are the antiandrogenic effects of cimetidine?
Gynecomastia, decreased libido, impotence.
How do proton pump inhibitors (PPIs) promote ulcer healing?
Causes irreversible inhibition of H+, K+ ATPase, the enzyme that generates gastric acid.
Describe how sucralfate (Carafate) promotes ulcer healing.
Undergoes polymerization and cross-linking reactions. Result is viscid and sticky gel that adheres t the ulcer crater, creating a barrier to back-diffusion of hydrogen ions, pepsin, and bile salts. Lasts 6 hours.
What are the therapeutic uses of misoprostol (Cytotec)?
Prevention of gastric ulcers caused by longterm therapy with NSAIDS approved in US. Other countries approved for use of PUD not related to NSAIDS. Also used for cervical ripening.
What type of antacids cause diarrhea?
Magnesium hydroxide.
What types of antacids cause constipation?
Aluminum hydroxide.
What is the principle cause of constipation
poor diet (lack of fiber and fluid)
Which type of laxative can lead to esophageal obstruction?
Bulk-forming laxatives
When are laxatives contraindicated?
disorder of bowel, abdominal pain, nausea, vomiting, cramps, symptoms of appendicitis, regional enteritis, diverticulitis, ulcerative colitis, acute surgical abdomen, fecal impaction or bowel obstruction, laxative abuse, Caution in pregnancy and lactation.
Docusate sodium (Colace) is an example of what type of laxative
Surfactant
Give a few examples of stimulant laxatives.
Bisacodyl (correctol, dulcolax, fenn-a-mint, fleet) & Senna (Ex-lax, senokot)
What are the consequences of chronic exposure to laxatives?
decreased defecatory reflexes, electrolyte imbalance, dehydration colitis.
What non drug measures relieve constipation?
Bowel training, fluids, fiber, exercise, heed the defecatory reflex.
Metoclopramide (Reglan) is a prokinetic drug. What are the therapeutic uses for this drug?
suppress post-operative nausea, vomiting as well as emesis caused by anti-cancer drugs, opiods, toxin and radiation therapy.
How does ondansetron (Zofran) help patients undergoing chemotherapy
Suppresses nausea and vomiting. Blocks type 3 serotonin receptors in the CTZ on afferent vagal neurons in the GI tract.
Prochlorperazine (Compazine) and promethazine (Phenergan) suppress emesis by blocking dopamine2 receptors in the chemoreceptor trigger zone (CTZ). What are the major side effects of these two drugs
EPS, anticholinergic effects, hypotension and sedation
Name two drugs that decrease motion sickness.
Scopolamine and antihistamines (Dramamine, antivert, marezine)
Diphenoxylate in combination with atropine (Lomotil) and loperamide (Imodium) are used to treat (diarrhea or constipation)?
diarrhea
Which vitamin is teratogenic in excessive amounts?
Vitamin A
Which vitamin has been shown to decrease congenital malformations such as spina bifida
Folic Acid/B12
Which vitamin is used as an antidote for warfarin (Coumadin) overdose)?
Vitamin K
Which vitamin is used to lower cholesterol levels?
Nicotinic acid
When a patient is receiving total parenteral nutrition (TPN) what may occur to the blood sugar if the infusion is disrupted? Why does this occur?
Hypoglycemia – continuous release of endogenous insulin therefore supplement with 10% dextrose.
Why are patients receiving TPN at risk for infection?
no aseptic technique during administration or preparation or catheter insertion.
Patients with body mass index (BMI) of___________are considered overweight?
25 to 29.9
Patients with BMI of ____________are considered obese?
30
Sibutramine (Meridia) can (increase or decrease) blood pressure?
increase
What are the adverse effects of orlistat (Xenical)?
Oily spotting, flatulence w/ discharge, fecal urgency, fatty or oily stools, oily evacuation, increased defecation and fecal incontinence.