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Pharm study guide review, Study Guides, Projects, Research of Pharmacology

Virginia State University (VSU)Pharmacology

Pharm study guide reviewPharm study guide review

Typology: Study Guides, Projects, Research

2023/2024

Available from 06/24/2024

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Pharm study guidereview
What you should master to move forward from pharmacology:
1. FDA process for drug approval (legal)
a. Phase 1: Activity
b. Phase 2: Dosage
c. Phase 3: Efficacy; clinical trial
d. Phase 4: Marketing (putting on shelf)
2. Patient rights and drug testing (ethics) FYI
a. HIPAA
b. Right dose
c. Right patient
d. Right drug
e. Right time
f. Right route
3. Scheduled drugs (controlled substances) and nurse’s role – (legal)
a. C-I : high abuse potential can only dispense with approved protocol.
b. C-II : high abuse potential, written prescription only, no prescription refills,
container must have warning lable
c. C-III : less than C-II abuse potential, written or oral prescription that expires 6
months, no more than 5 refills in 6 month period, container must have warning label
d. C-IV : less than C-III abuse potential, same dispensing restrictions as C-III
e. C-V : less than C-IV abuse potential, written prescription or OTC
4. Pharmacogenetics and pharmacogenomics
a. Pharmacogenetics : general term for the study of the genetics basis for variations in
the body’s response to drugs, with a focus on variations related to a single gene*
(genetic polymorphism)*
b. Pharmacogenomics : branch of pharmacogenetics that involves the survey of the
entire genome to detect multigenic determinants of drug response.
5. Medication safety and national patient safety goals related to medications
a. Medication reconciliation
i. Health care providers maintain an accurate and up-to-date list of medications
for all patients between all phase of health care delivery
b. LASA drugs
i. Look alike, sound alike
c. High alert drugs
i. Potentially toxic to nature require special care when prescribing,
dispensing, and/or administering
6. Differences between prescribed, OTC, and dietary supplements
a. Prescribed and OTC are approved by the FDA and dietary supplements are not*
i. *If drugs prescribed are FDA approved then they are said to be safe
and effective, but side effects still have to be reported*
b. Patient teaching issues
c. Number of active ingredients
i. OTC: >800 major active ingredients
d. Medication reconciliation
i. It is hard to know what a patient is taking OTC or dietary wise if you don’t ask
7. Difference between generic and trade
a. Generic:
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Partial preview of the text

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Pharm study guide review

What you should master to move forward from pharmacology:

  1. FDA process for drug approval (legal) a. Phase 1: Activity b. Phase 2: Dosage c. Phase 3: Efficacy; clinical trial d. Phase 4: Marketing (putting on shelf)
  2. Patient rights and drug testing (ethics) FYI a. HIPAA b. Right dose c. Right patient d. Right drug e. Right time f. Right route
  3. Scheduled drugs (controlled substances) and nurse’s role – (legal) a. C-I: high abuse potential can only dispense with approved protocol. b. C-II: high abuse potential, written prescription only, no prescription refills, container must have warning lable c. C-III: less than C-II abuse potential, written or oral prescription that expires 6 months, no more than 5 refills in 6 month period, container must have warning label d. C-IV: less than C-III abuse potential, same dispensing restrictions as C-III e. C-V: less than C-IV abuse potential, written prescription or OTC
  4. Pharmacogenetics and pharmacogenomics a. Pharmacogenetics: general term for the study of the genetics basis for variations in the body’s response to drugs, with a focus on variations related to a single gene* (genetic polymorphism)* b. Pharmacogenomics: branch of pharmacogenetics that involves the survey of the entire genome to detect multigenic determinants of drug response.
  5. Medication safety and national patient safety goals related to medications a. Medication reconciliation i. Health care providers maintain an accurate and up-to-date list of medications for all patients between all phase of health care delivery b. LASA drugs i. Look alike, sound alike c. High alert drugs i. Potentially toxic to nature require special care when prescribing, dispensing, and/or administering
  6. Differences between prescribed, OTC, and dietary supplements a. Prescribed and OTC are approved by the FDA and dietary supplements are not* i. If drugs prescribed are FDA approved then they are said to be safe and effective, but side effects still have to be reported b. Patient teaching issues c. Number of active ingredients i. OTC: >800 major active ingredients d. Medication reconciliation i. It is hard to know what a patient is taking OTC or dietary wise if you don’t ask
  7. Difference between generic and trade a. Generic:

i. Safest

a. Slows absorption* doesn’t necessarily change the extent of absorption b. Why do we tell pt to take drug with glass of water? Acts as a natural solvent*

  1. Blood flow and health status

a. Decreased bloodflow=hypotension

  1. Stomach pH

a. Acidic or alkaline

  1. Other drugs

b. Distribution i. Blood brain barrier (BBB)

  1. Tight junctions-small lipid soluble molecules can cross the BBB

a. Caffeine, alcohol, antidepressants, nicotine, seizure drugs

  1. Non ionized drugs pass through quicker*

ii. Placenta and breast milk

  1. Not a barrier, but a highway

iii. Protein binding (plasma protein binding = PPB)

  1. Low albumin (hypoalbuminemia) and highly PPB drug toxicity

a. Patient factors contributing to low albumin i. Liver dysfunction ii. Malnutrition (ex. Alcoholic)

  1. Bound versus free drug

a. Bound drug=inactive b. Free drug=active

  1. Equilibrium

a. Entry and exit rates are the same

  1. Protein binding competition (drug-drug interaction)

a. When more than one drug is trying to bind to albumin iv. Metabolism

  1. CYP450 inducers and inhibitors

a. Inducers i. Drugs that cause the liver to make more CYP enzymes. When a substrate drug is then given more of that drug will be metabolized leading to a lower blood lever b. Inhibitors i. Drugs that inhibit cause a decreased number of CYP enzymes to be produced. When a substrate drug is given there will be fewer enzymes to metabolize it and the level of free drug will then riseincreasing risk for toxicity c. Drug interactions i. Ex. Of Inducer

  1. Nicotine
  2. Theophylline

ii. Ex. Of Inhibitors

  1. Tagamet
    1. Grapefruit
  2. First pass effect

a. Drug goes through the liverblood level decreases as the body prepares to eliminate it.

  1. Excretion a. Serum creatinine and drug clearance i. Normal 0.8-1. ii. Decreased clearance=increased risk of toxicity iii. Increased clearance=decrease drug effect=decreased therapeutic effect b. Half life i. The time it takes for 50% of a drug dose to be eliminated from the body ii. Drug with short half life=more frequent dosing c. Steady state i. Physiologic state of equilibrium between absorption and elimination ii. Takes 4 half lives to reach steady state d. Loading dose c. Drug action versus effect i. Drug action: the cellular processes involved in the interaction between a drug and body cells; also called mechanism of action ii. Drug effect: the physiologic reactions of the body to a drug. They can be therapeutic or toxic and describe how the function of the body is affected as a whole by the drug. The terms onset, peak, and duration are used to describe drug effects. d. Therapeutic versus adverse response i. Therapeutic response: desired or intended effect of a particular medication ii. Adverse response: a general term for any undesirable effects that are a direct response to one or more drugs e. How drugs work (receptors, enzymes, or others) i. Dose of formulated drugadministrationdisintegration of dosage form, dissolution of drug in bodydrug available for absorptionabsorption, distribution, metabolism, excretiondrug available for actiondrug-receptor interactioneffect f. Specificity and affinity i. Specificity: being selective ii. Affinity: the degree to which a drug attaches to and binds with a receptor. g. Agonist versus antagonist i. Agonist: a drug that binds to and stimulates the activity of one or more receptors in the body. ii. Antagonist: a drug that binds to and inhibits the activity of one or more receptors in the body. Also call inhibitors. h. Efficacy versus potency i. Efficacy: Intrinsic activity (IA) or efficacy refers to the relative ability of a drug- receptor complex to produce a maximum functional response ii. Potency: a measure of drug activity expressed in terms of the amount required to produce an effect of given intensity i. Therapeutic index i. The ratio between the toxic and therapeutic concentrations of a drug. j. Adverse drug events

c. Patient teaching i. What do they need to stay safe when they go home?

  1. Diet instructions related to drug
  2. Drug-drug interactions
  3. Medical alert identification tags
  4. Lab follow up
  5. Drug administration
  6. Side effects
  7. Prevention of harm
  8. Self Monitoring
  9. What do they do when they have side effects? 10. For every drug class, understand a.* How does this drug work? b. From this information, why would we use the drug? c. What side effects make sense related to the action of the drug? i. Which ones are most common? ii. Which ones are serious/life-threatening? iii. How will I recognize these side effects? iv. What will I do if they occur? v. What would I say to the healthcare provider? vi. Is there anything I can do to prevent these side effects (ie: check something before I give the drug ) d. What patient teaching do I need to do for this category of drug? e. Are there any drugs I need to know by name for this drug category? f. Are there any major drug interactions I need to know about? 11. ANS drugs a. Names that mean the same b. Muscarinic versus adrenergic receptors i. Muscarinic receptors: cholinergic receptors that are located post-synaptically in the effector organs such as smooth muscle, cardiac muscle, and glands supplied by parasympathetic fibers. ii. Adrenergic receptors: receptor sites for the sympathetic neurotransmitters norepinephrine and epinephrine c. Cholinergic drugs i. Direct acting
  10. Cholinergic agonists bind directly to cholinergic receptors and activate them ii. Indirect acting
  11. Cholinergic agonists stimulate postsynaptic nerve cell release of acetylcholine at the receptor site.
  12. Work by inhibiting the action of acetylcholinesterase iii. Antagonists
  13. Cholinergic-blocking drugs iv. Key points from cholinergic drugs
  14. cholinergic toxicity a. causes i. Systemic toxicity with topically applied cholinergics is seen most commonly with longer-acting drugs are given repeatedly over a long period of timeresult in

overstimulation of the parasympathetic nervous system and all the attendant responses. b. assessment findings i. SLUDGE

  1. Salivation
  2. Lacrimation
  3. Urinary incontinence
  4. Diarrhea
  5. GI cramps
  6. Emesis c. antidote to cholinergic toxicity i. Atropine
  7. prevention of injuries due to visual changes a. Provide a night light b. Monitor for visual changes
  8. assessment of heart and lungs v. Anticholinergic
  9. Drug name you have to know – atropine
  10. Key points a. Other drug classes have anticholinergic side effects i. Antihistamines (first generations) ii. Antipsychotics iii. Older antidepressants iv. Incontinence medications v. Parkinson’s drug Cogentin(FYI) b. Monitor Patient for i. Glaucoma
  11. Monitor for undiagnosed glaucoma in the elderly ii. CNS changes in the elderly iii. Toxicity
  12. Hot as a hare
  13. Dry as a bone
  14. Mad as a hatter
  15. Red as a beet vi. Sympathomimetics
  16. Epinephrine a. Effect of drug on beta 1, beta 2, and alpha 1 receptors b. Uses i. Alpha 1 receptor
  17. *Vasodilatation a. Venous and arterial dilatation- reduction preload and afterload b. Used for hypertension
  18. Reduces Urinary obstruction
  19. *Used for benign prostatic hypertrophy(BPH) ii. Alpha 2 agonist
  20. Used for hypertension, pain, opioid withdrawal iii. Beta 1 receptor
  21. Heart

12. Antihypertensives i. Beta blockers mask the signs of hyopglycemia a. Beta blockers and allergic reactions i. If going in for allergy testing come off beta blocker for 48-72 hours b. IV doses versus PO doses of beta blockers i. IV dose gives a lot of side effects ii. PO is the better route for administration c. Significant drug interactions (digoxin and calcium channel blockers) d. Decreases the BP

  1. Alpha 1 blockers (AKA alpha blockers) a. Orthostatic hypotension i. Patient teaching
  2. Move slowly ii. Safe care of these patients
  3. Alpha 2 agonists a. Goal of therapy i. Reduce the risk of mortality and cardiovascular and renal morbidity (stroke) b. CO and relationship to blood pressure i. Cardiac output is the volume of blood ejected by the left ventricle and affected by heart rate and stroke volume. ii. Blood pressure can be altered by cardiac output and systemic vascular resistance c. Beta blockers i. Cardio selective: block the B1 receptors on the heart and don’t block B2 at usual dosage. ii. Non-cardio selective: block B1 & B2, don’t give to someone with lung disease because it will bronchoconstrict and don’t give to someone with diabetes because it will mask the signs of hypoglycemia. iii. Common side effects: bradycardia, orthostatic hypotension, dizziness, fatigue, drowsiness, cold extremities iv. Serious side effects: CHF/MI, severe bradycardia, heart block, dysrythmias, bronchospasm, hypersensitivity reaction v. Drug Interactions: Alpha antagonist Clonidine (decreases BP), Cimetidine (Tagamet)-(increase blood level, toxic effects, CYP450 inhibitor), NSAIDS (can’t make prostaglandins which are important for bloodflow in kidneys, retention of fluids), Calcium Channel Blockers (decrease BP), Insulin and antidiabetic drugs (people won’t respond to hypoglycemia), caution in pts having an allergy test or cardiac stress test (come off beta blocker for 48- hrs and dr. will give something to substitute. Never come off beta blocker cold turkey it could cause stroke) d. Alpha 1 blockers i. Peripherally Acting Alpha Blockers ii. Mechanism of action: dilate arteries and veins, decreases peripheral vascular resistance, decreases systemic and pulmonary venous pressures, increases cardiac output. iii. Contraindications: peptic ulcer, colitis, severe depression iv. Get up slowly because it causes orthostatic hypotension, take at night* e. Alpha 2 agonists

i. Centrally Acting Drugs

  1. Clonidine ii. Mechanism of action: alpha 2 agonists (presynaptic) and inhibits outflow of norepinephrine from CNS, also reduces activity of rennin iii. Dual Action Drugs: Carvedilol blocks alpha 1, beta 1 & 2, and calcium channel blockers. f. Ace inhibitors key points i. Potassium
  2. ACE inhibitors cause the retention of potassium ii. Orthostasis with first few doses iii. Cough*
  3. If you block ACE then you block the breakdown of bradykinin which causes the cough iv. Angioedema
  4. Lips and tongue is swollen-not an allergic reaction-tell pt. to call 911 v. Side effect
  5. Hyperkalemia* g. ARBs – how do they differ from ACE inhibitors? i. ARBs block the action of Angiotensin II and ACE inhibitors block the formation of Angiotensin II ii. Does not cause cough, but does cause angioedema and hyperkalemia* h. Calcium channel blockers i. Dihydropyridines versus nondihydropyidines ii. Dihydropyridines
  6. D=dilate iii. Nondihydropyridines
  7. N=Nodes but can also dilate iv. Uses
  8. Dihydros a. Act mainly on vascular smooth muscle b. Dilate arteries and arterioles
  9. Nondihydros a. Dilate vascular smooth muscle (arterioles)-hypotension b. Myocardium-decreases force of contraction c. Slows conduction-therefore slows H.R.*
  10. Overall use a. Angina-chronic stable b. Hypertension c. Dysrythmias d. Raynaud’s disease (peripheral vasoconstriction: hands & feet turn blue) v. Side effects
  11. Must know side effects that are particular to each subclass of calcium channel blockers a. Dihydros – dilate only, thus low BP, edema. b. Nondihydros dilate and affect node, so more cardiac side effects i. Nondihydros
  12. Constipation
  13. Gingival hyperplasia
  1. GI upset
  2. diarrhea
  3. gynecomastia in men*
  4. erectile dysfunction b. Triamterene i. Side effects:
  5. thrombocytopenia
  6. decreases folic acid
  7. can cause kidney stones
  8. megaloblastic anemia c. Common side effects: i. hypersensitivity anaphylaxis ii. jaundice iii. hyperkalemia iv. renal failure v. GI bleeding
  9. Potassium a. Potassium is retained (hyperkalemia)* 14. Digoxin a. Compensated versus decompensated heart failure i. Compensated: body can make up for the heart failure ii. Decompensated: body is unable to help the heart failure and you need meds* b. Action of digoxin and effects i. Contractility
  10. Increases force myocardial contraction and decreases the rate*
  11. Increases myocardial consumption ii. AV node conduction
  12. Prolongs refractory period
  13. Area between the SA node and the AV nodes iii. Effects
  14. Increases stroke volume
  15. Decreases venous blood pressure and venous engorgement
  16. Increases coronary circulation
  17. Promotes dieresis because of improved cardiac output
  18. Relieves exertional (exercise tolerance), and paroxysmal nocturnal dyspnea (waking up @ night SOB), cough and cyanosis (no fluid in the lungs) c. Uses i. Used in heart failure and to control the rate in arterial fibrillation or flutter d. Narrow TI drug i. Very narrow therapeutic window ii. Drug level much be monitored (0.5-2.0 np/ml)* iii. Low potassium levels increase toxicity (normal K levels are 3.5-5.5)* iv. Electrolyte levels must be monitored e. Bioavailability issue

i. Digoxin capsules have higher absorption and bioavailability f. Long half life* g. Digitalization (fyi) h. IV administration i. If given through an IV give it slowly and it CANNOT be pushed.* i. Drug interactions i. Don’t give with high fiber foods j. Symptomatic bradycardia which drug would you give to treat? i. Atropine* k. Potassium i. Low potassium levels could lead to toxicity* ii. If toxicity it could cause hyperkalemia >5 mEq/L l. Toxicity i. Recognition

  1. Early signs: anorexia, nausea, vomiting, diarrhea*
  2. Severe signs: colored vision(seeing yellow, green, purple), halo vision, flicking lights*
  3. K level >5.0 mEq/L monitor dig-level and creatinine because if creatinine is high then it means kidneys aren’t functioning* ii. Suspect toxicity with loops
  4. Hearing loss iii. Management of toxicity
  5. Hold the dose and notify the prescriber
  6. Give Digibind m. Digibind i. Used in dig-toxicity n. Before administering drug i. Apical heart rate*
  7. Check the heart rate for 1 min.
  8. HR <60 hold dose and call prescriber ii. Creatinine
  9. Lab on creatinine levels to check kidney function* iii. Potassium
  10. Labs on potassium levels iv. Symptoms
  11. Don’t give if: hypokalemic, hepatic dysfunction, hypercalcemia, dysrythmias, hypothyroid disease, respiratory disease, renal disease,

o. Teaching i. Heart rate*

  1. If H.R. is <60 don’t take the drug and call the dr. ii. How do you know drug is working?
  2. Lungs: no more crackles
  3. Skin and temperature: improved
  4. Weight: lose pounds
  5. Urine output: increased
  6. Activity tolerance: increased iii. Diet
  7. Don’t eat high in fiber foods with the med. iv. Side effects

b. Long acting* i. Chewable ii. Oral capsules or tablets iii. Transdermal patches iv. Ointments v. Nitrate-free interval and tolerance

  1. Tolerance occurs when: Pt. taking nitrates around the clock or with long acting forms*
  2. Prevent tolerance by: a. Allowing a regular nitrate free interval to allow enzyme pathways to replenish b. Transdermal patch at bedtime to allow 8 hours free interval. Apply new patch in the morning vi. Sexual performance enhanced and dangers
  3. Associated use with erectile dysfunction drugs (Viagra, Cialis, Levitra)
  • could result in synergic or additive affects* vii. Treatment of acute chest pain at home*
  1. Sublingual, Buccal, and Translingual sprays viii. Treatment of acute chest pain in hospital
  2. I.V. solution ix. Wear gloves with ointment*
  3. If not you will get a headache x. Patient teaching
  4. Instruct pt in proper technique and guidelines for taking nitroglycerin for angina pain
  5. Don’t ever chew or swallow the sublingual form
  6. Tell the pt that the burning sensation felt with sublingual form indicates that the drug is still potent (potency lost after about 3 months once bottle is opened)*
  7. Store in an airtight dark glass bottle—metal cap & no cotton filler*
  8. Use proper technique for applying ointment (remove old ointment; wear gloves to apply; rotate site; don’t rub in)*
  9. Transdermal forms (rotate site; take off for 8 hrs at night; remove old patch)
  10. When taking for chest pain—stop activity and sit or lie down
  11. Take a sublingual nitro (may repeat every 5 min (total of 3 nitros))
  12. If no relief after the first nitro call 911 10.DO NOT DRIVE TO THE HOSPITAL 11.Turn positions slowly 12.Avoid alcohol, saunas, hot tubs—these may worsen hypotension 13.Keep a symptom diary

a. Number of attacks b. Precipitating events c. Number of nitro pills taken d. Therapeutic effects 14.Take nitro at first hint of angina pain* 15.If you’re having chest pain lay down to prevent fainting from hypotension 16.Therapeutic outcome* a. No chest pain 17.Headache will occur but will go away in time because body will build tolerance to it.* xi. IV nitrates – when and why?*

  1. When: hospital
  2. Why: CHF and the 3 sublingual nitrates didn’t work d. Beta blockers e. Calcium channel blockers 16. Lipid-lowering drugs a. LDL, HDL, and triglycerides b. Which drug classes work best on each of the above? i. LDL:
  3. Niacin
  4. Bile acid sequestrates
  5. Statins* ii. HDL:
  6. Fibric acid derivatives (fibrates)
  7. Niacin iii. Triglycerides:
  8. Fibric acid derivatives (fibrates)*
  9. Niacin c. Statins main drug class for LDL reduction i. Myalgias versus myositis
  10. Myalgias: muscle pain, can occur up to 3 years after starting a statin* can see myoglobulin in the urine*
  11. Myositis: inflammation of skeletal muscles (voluntary muscles) ii. Drug interactions with grapefruit
  12. Grapefruit is a CYP450 inhibitor and can cause toxicity of statin which can cause renal failure* iii. Therapeutic effects
  13. Lower the blood cholesterol level by decreasing the rate of cholesterol production iv. Pertinent labs (LDL, CPK)
  14. LDL: <
  15. CPK: 60- 400 d. (Fibric acid derivatives)Fibrates – triglycerides* e. Niacin – mixed hyperlipidemia* i. Flushing, burning, and itching prevented with aspirin 30 minutes before f. Bile acid sequestrants i. Local effect only

b. Depressants i. Alcohol i. Depression, suicidal thoughts and behavior, paranoid delusions

  1. Metabolism and acute versus chronic alcohol ingestion a. Chronic alcohol ingestion i. Nutritional and vitamin deficiencies (especially B vitamins) 1. Wernicke’s encephalopathy(can’t understand what you’re saying 2. Korsakoff’s psychosis (agitated) 3. Polyneuritis 4. Nicotinic acid deficiency encephalopathy ii. Seizures iii. Alcoholic hepatitis, progressing to cirrhosis iv. Chronic ingestion
  2. Cardiomyopathy (disease of heart muscle) v. Fetal Alcohol Syndrome (FAS)
  3. Craniofacial abnormalities
  4. CNS dysfunction
  5. Prenatal and postnatal growth retardation
  6. Withdrawal a. Signs i. Increased psychomotor activity; agitation; muscular weakness; diaphoresis; delirium; convulsions; elevated BP, pulse, and temperature; tremors (eyelids, hands, tongue) b. Symptoms i. Anxiety, depression, euphoria, incoherent thoughts, hostility, disorientation, hallucinations, suicidal thoughts, others c. Mild Withdrawal i. BP greater than 150/ ii. Haven’t had a drink in 24 hours iii. Temp greater than 100 iv. Pulse greater than 110 beats/minute v. Insomnia vi. Tremors vii. Agitation d. Moderate Withdrawal i. BP greater than 150/ ii. Haven’t have a drink in 24-36 hours iii. Temp 100- 101 iv. Pulse 110-140 beats/minute v. Insomnia vi. Tremors vii. Agitation e. Severe Withdrawal ( Delirium Tremors )* i. BP greater than 200/

19. Anemia ii. Haven’t had a drink in over 48 hours * iii. Temp greater than 101 iv. Pulse greater than 140 beats/minute v. Insomnia vi. Tremors vii. Agitation viii. Cardiac arrest-dysrythmias often due to hypomagnesaemia ii. Combining CNS depressant drugs

  1. Flunitrazepam (Rohypnol) a. AKA “roofies” b. Used with alcohol produces disinhibition and amnesia a. Iron deficiency i. Patient teaching
  2. Administration of iron PO a. Preparations are available as ferrous salts b. If someone cannot take iron PO then IV form is available c. Take with juice and NOT with milk* i. Vitamin C increases absorption of iron* d. Taking it with food can decrease the effectiveness, but may needed to be taken with food to prevent GI upset
  3. Side effects of iron therapy a. Nausea, vomiting, diarrhea, constipation, stomach cramps, and stomach pain* (GI) ii. Monitoring
  4. Can have black stools but it doesn’t mean GI bleeding* b. B12 deficiency versus folate deficiency i. B12 deficiency: due to failure of the stomach lining to produce intrinsic factor ii. Folate deficiency: malabsorption syndromes are the most common cause, usually occurs during pregnancy. 20. Thyroid drugs a. Drug for hypothyroidism i. Most common drug prescribed 1. Levothyroxine (Synthroid)* ii. What happens with hypothyroidism?
  5. Fatigue, weight gain, constipated, hair falling out* iii. Side effects
  6. Cardiac dysrythmias with the risk for life-threatening or fatal irregularities iv. Outcomes
  7. Replaces what the thyroid gland itself cannot produce to achieve normal thyroid hormone levels. b. Antithyroid drugs (FYI) i. Agranulocytosis 1. Bone marrow toxicity c. Iodides (FYI) i. Administration and teaching 1. Take with meals to decrease stomach upset