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49 Cards in this Set

  • Front
  • Back
Adrenergics
-stimulate SNS

-also called
Adrenergic Agonists, Sympathomimietics
Catecholamines
substances that can produce a sympathomimetic response

- NE, EP, DA, synthetic
Alpha Receptors
produce excitatory response (except GI)
Alpha 1
POSTsynaptic
- vasoconstriction
- uterus & bladder contraction
- mydriasis (dilation)
- ejaculation
- GI relaxation
Alpha 2
- control release of NT
Alpha Side Effects
- HTN
- Tachycardi, palpations, dysrythmias
- dry mouth, N & V
- anorexia
Beta Receptors
produce inhibitory response (except in heart cells)
Beta 1
- located on heart (SA & AV nodes)

- positice inotropic, chronotropic, and dromotropic effects
Beta 2
- located on bronchioles, arterioles, visceral organs
- bronchodilation
- vasodilation
- relax uterus & GI
- increase glycogenolysis
- increase renin secretion
Beta Side Effects
- tremors, headache, nervous
- tachycardia, palpations
Dopaminergenic Receptors
- stimulated by dopamine only
- vasodilation in renal, mesenteric, coranary, cerebral
Respiratory Indications
Beta 2 (bronchiodilators)
Topical Nasal Decongestants
Alpha 1 (vasoconstrictors)
Opthalmic Indications
Alpha 1 (vasoconstrictors)

Beta 2 (vasodilators)
Vasoactive (Cardiac) Indications
Beta 1 :Dobutamine, DA, EP
Adrenergic Antagonists

Blockers
block SNS stimulation by binding to androgenic receptors

- sympatholytics
Alpha Blockers
- vasodilation
- miosis (constrict)
- supress ejaculation
Alpha Blocker Drugs
Ergotamines: vasoconstriction for migraines

Oxytocies: increase uterine contractions

Prazosin: vasodilator to treat HTN
Beta 1 Blockers
(cardioselective)
- decrease HR
- slows conduction
- decrease force of contraction

to treat angina, HTN, dysrythmia
Beta 2 Blockers
(nonselective)
also affects:
- constrict broncholes (SOB)
- vasoconstriction (HTN)
Beta BLocker Drug Interactions
1. Antacids: decrease absorption
2. Anticholonergics: decrease effect
3. Diuretics / CV drugs: cause hypotension
Beta Blocker Drugs
Atenolol & Metopranolol: cardioselective

Carvedilol & Propranolol: nonselective
Cholinergics
- stimulate the PSNS (oppose SNS)

- ACh
Muscarinic Receptors
- increase bronchi secretions, constriction
- vasodilation
- miosis
- increase GI tone & contractility
- relax sphincter
- increase gland secretion
- salavary, lacrimal, sweat
Nicotinic Receptors
- vasoconstriction
- miosis
- increase GI tone & contractility
- increase skeletal muscle contraction
Cholinergic Uses
- weak bladder conditions
- GI disorders
- eye pressure
- mysthenia gravis
- alzheimers
Cholinergic Antedote
Atropine
Cholinergic Blockers
- peptic ulcers, gastritis
- antispasmic for urinary inc.
- mydriasis (dilation)
- hypotension
- Parkinson's (decrease salvation, spastic muscles)
Diabetes Mellitus
- defficency in insulin, resistance to insulin, or both
- causes impaired metabolism and hyperglycemia
Type I DM
- insulin dependant
- autoimmune disorder
- Beta cells destroyed and don't produce insulin
Type II DM
- non insulin dependant
- major cause - obesity
- increase in glucose, body doesn't make enough insulin to maintain metabolism
Insulin
- glycogen synthesis: glucose storeage in liver
- decreased proteinolysis, lipolysis
- decreased gluconeogenisis
Insulin Preperations
Animal - not used

Human Analog: recombanant DNA, same as human insulin with the reversal of lysine & proline
Rapid Acting Insulin
1. Humaog (lispro)
2. NovoRapid (aspart)

starts in 10-15 min
peaks in 1 - 1.5 hous
duration 4 - 5 hours
Fast Acting Insulin
1. Humalin - R
2. Novolin - Toronto

starts in 30-60 min
peaks in 2 - 4 hours
duration 5 - 8 hours
Intermediate Acting Insulin
1. Humalin - N
2. Humalin - L
3. Novalin - NPH

starts in 1 - 3 hours
peaks in 5 - 8 hours
duration up to 18 hours
Long Acting Insulin

* watch for hyoglycemia at night
1. Humalin - U

starts in 3 - 4 hours
Peaks in 8 - 15 hours
duration 22 - 26 hours
Extended Long Acting Insulin

*no peak (can't mix)
1. Lantus

starts in 90 min
duration 24 hours
Premixed

*ratio of Fast Acting and Inermediate Acting
1. Humalog
2. Humulin 20/80, 30/70
3. Novolin 10/90, 20/80, 30/70...

starts in 5 - 15 min
peaks in .75 - 2.5 hours
duration 18 - 24 hours
Lipodystrophy
atrophy or hypertrophy of fat tissue at injection site

d/t overused site, cold meds
Hot & Dry....

Sugar High
Cold & Clammy...

need some candy
Oral Hyperglycemic Agents
- for Type II DM

1. Sulphonylureas
2. Non-Sulphonylureas
Sulphonylureas
- stimulates B-cells to secrete insulin
- increase sensetivity to insulin
- decrease glucose production
Sulphonylureas Contraindications
- must have functioning B-cells
- no allergies to sulpha
- not pregnant
- Alcohol, ACE inh, NSAIDs, MAO's, steroids increase effects
Second Generation Sulphonylureas
DiaBeta (glyburide)

onset 1-4 hours
peak 2-4 hours
duration 24 hours
Alpha Glucosidase Inhibitors
1. Precose (acarbose)
2. Glyset (miglitol)

- inhibits enzymes sucrase, maltase, amylase (decrease glucose digestion)

- anti flatus drugs counteract them

- if hypo take dextrose (not table sugar)
Biguanide
1. metformin

- increase use of glucose
- decrease gluscose production
- decrease GI absorp of gluc.

- digoxen increases effect (anticoag)
Glitazones (thiazolidenediones)
- increase sensitivity of insulin receptors
- decrease gluconeogenisis

- may take 6wks to effect blood sugar

- fluid retention (CHF)
Meglitinides (CMBA's)
1. Prandin (repaglinide)

- stimulate insulin secretion
-peak & 1/2 life quick