pp. 40- FINAL

  1. What is the peripheral nervous system?
    1. Everything but the brain

    2. Includes the AUTONOMIC NS and SOMATIC NS
  2. Autonomic Nervous System

    • 1) Cardiac and smooth muscle contraction
    • 2) Glandular secretion


    • 1) Sympathtic NS
    • 2) Parasympathetic NS
    • --> These two generally oppose each other
  3. Sympathetic Nervous System
    1) Catabolic (Expends energy)

    • 2) > HR, dilates bronchi, decreases secretions
    • "Speed up"

    3) When under stress, SNS predominates diverting energy to functions supporting "fight or flight"

    4) > tissue oxygenation and cardiac output
  4. What are the major neurotransmitters in the sympathetic NS?
    1) Dopamine --> Norepinephrine

    2) epiniphrine (adrenaline)
  5. Parasympathetic Nervous System
    1) Anabolic (conserves energy)

    • 2) < HR, stimulates GI function
    • "Slow Down" or "Poke Along"

    3) When in a resting state, PNS predominates

    4) Relative slowing of heart rate, adequate secretions, normal gut motility
  6. What are the major neurotransmitters in the parasympathetic NS?
  7. How is the autonomic NS pathway organized?
    2 neurons: presynaptic and postsynaptic
  8. Presynaptic neurons
    extend from the brain to autonomic ganglia where they transmit NS signals to postsynaptic neurons by releasing acetylcholine into the synaptic cleft
  9. Postsynaptic neurons
    transmit impulses to end organs (heart, gut, etc.) by releasing norepinephrine (NE) from sympathetic neurons or acetylcholine (ACh) from parasympathetic neurons
  10. What is the mechanism by which impulses are transmitted in the sympathetic division?
    NE and EPI (epinephrine) transmit most impulses of the SNS

    On release from the presynaptic neurons, NE diffuses across the synaptic cleft and binds to postsynaptic adrenergic receptors ( a1, a2, β1, β2 )
  11. a1 receptor location?**
    • 1) arterioles
    • 2) veins
    • 3) glands
    • 4) eye
    • 5) intestine
    • 6) myocardium
  12. a1 receptor effects when stimulated?**
    • 1) vasoconstriction
    • 2) decreased glandular secretion
    • 3) constriction of radial muscle
    • 4) decreased motility
  13. a2 receptor location?**
    • 1) CNS post and postynaptic terminals
    • 2) Beta islet cells in the pancreas
    • 3) larger vessels
    • 4) skin
    • 5) mucosa
    • 6) kidney
  14. a2 receptor effects when stimulated?**
    • 1) Decreased sympathetic outflow from brain
    • 2) Decreased NE release
    • 3) Decreased islet cell secretion
  15. β1 receptor location?**
    Heart: myocardial tissue and electrical conduction system

    1 Heart
  16. β1 receptor effects when stimulated?**
    • 1) > HR
    • + chronotropicity = increased HR
    • - chronotropicity = decreased HR

    • 2) > contractility (force of contraction)
    • + ionotropicity = increased cardiac output, strength of contraction
    • - Beta blockers can give cardiac effects)

    • 3) > conduction velocity
    • 4) > automaticity (ability to beat on its own)
  17. β2 receptor location?**
    • 1) Trachea
    • 2) Bronchioles
    • 3) Bronchi
    • 4) Uterus
    • 5) Arterioles (except brain and skin)
    • 6) Veins
    • 7) Vascular smooth muscle
    • 8) Liver

    2 Lungs
  18. β2 receptor effects when stimulated?**
    • 1) tracheal/bronchial relaxation
    • 2) uterine relaxation
    • 3) circulatory dilation
  19. During times of stress, the adrenal gland releases ___ and where? What is the action?
    EPI directly into the blood

    Like NE, circulating EPI is an agonist at adrenergic (sympathetic) receptors (A1, A2, B1, B2) --ALL receptors
  20. What is the mechanism by which impulses are transmitted in the parasympathetic division?
    ACh transmits all parasympathetic signals to end organs such as the heart and lungs by binding to muscarinic receptors.
  21. What does ACh do? (what type of impulses and where)
    1) Transmits both sympathetic and parasympathetic impulses from preganglionic neurons in brain and spinal cord to nicotinic ganglionic receptors on postganglioninc neurons of ANS

    2) occurs in sympathetic ganglia in the spinal cord and parasympathetic ganglia near end organs
  22. All ganglionic transmission is ______? Drugs which block ganglionic transmission does what?**

    - Drugs which block ganglionic transmission inhibits either sympathetic or parasympathetic signals, depending on which system is predominant at the moment
  23. When ACh is released from neurons, what is its mechanism of action?
    Causes muscle contraction by binding to nicotinic receptors on muscle cells, causing Ca++ influx
  24. Can ACh be considered as a neurotransmitter?
    Yes, acts as a nt in the brain

    Acts predominantly via muscarinic receptors
  25. How is NE synthesized? What broad category of nt is NE under?
    - NE is a catecholamine

    1) Synthesized from TYROSINE

    2) Tyrosine hydroxylated to dopa --> decarboxylated to dopamine in presynaptic neurons

    3) Dopamine diffuses into synaptic vesicles --> hydroxylated into NE

    4) When a nerve is stimulated --> Ca++ enters the presynaptic neuron --> vesicles fuse with plasma membrane and release NE into synaptic cleft
  26. NE can bind with what kind of receptors?**
    a1, B1, B2 adrenergic receptors

    - Direct sympathomimetic drugs such as EPI can bind to to these receptors as well, w/o interacting with the presynaptic neuron

    a2 adrenergic receptors on presynaptic neurons, when stimulated by NE, will inhibit subsequent NE release from the terminal
  27. What is an indirect sympathomimetic?
    Drugs that work by entering the presynaptic terminal and displacing NE
  28. What are adrenergic receptors?**
    - autonomic receptors

    • 1) Alpha receptors
    • 2) Beta receptors
  29. Alpha receptors**
    (For CV medications)

    - present in the neurons in the vascular smooth tissue

    - a1 receptors are found in the myocardium

    - a2 receptors are found in larger blood vessels (skin, mucosa, gut, kidney)

    - stimulation leads to arteriolar VASOCONSTRICTION
  30. Beta receptors**
    (For CV medications)

    • 1) B1 receptors
    • - located in myocardial tissue and in the cardiac conduction system
    • - Stimulation results in increased cardiac contractility and heart rate

    • 2) B2 receptors
    • - located in vascular smooth muscle tissue, bronchi, and liver
    • - stimulation leads to coronary and peripheral VASODILATION and BRONCHODILATION
  31. What are muscarinic receptors?
    - a cholinergic receptor

    - mediate postganglionic parasympathetic and CNS functions of ACh

    - can be M1, M2, or M3
  32. M3 Receptor
    - a muscarinic receptor

    • - Organs:
    • Glands, EYE

    • - Cholinergic Actions:
    • increases glandular secretions. In the eye, causes miosis and accommodation
  33. Nicotinic Receptors (won't be tested)
    located in the ganglia and at the neuromuscular junction

    N1: contraction of skeletal muscle

    N2: stimulation of ganglia

    N3: neurotransmission in CNS
  34. Mechanisms by which autonomic activities are decreased?
    • 5) Peripheral Receptor Blockade
    • - Can be Adrenergic or Cholinergic (details on other slides)
  35. Adrenergic Peripheral receptor blockade
    - a mechanism by which autonomic activities are decreased

    a: phenoxybenzamine, a1 - specific blockers such as prazosin and terazosin are available

    • β: beta adrenergic blockers such as propranolol and timolol
    • - β1 specific agents include metoprolol (Lopressor), esmolol, atenolol, betaxolol, etc are available.
    • - at high doses, β1 selectivity can be lost and some β2 effects can be seen
  36. Cholinergic Peripheral receptor blockade
    - Muscarinic: atropine

    - Nicotinic: atracurium, vecuronium and other similar neuromuscular blocking agents, and mecamylamine for severe hypertension
  37. Cholinergic stimulants are called ______.

    Cholinergic blocking agents are called ______.

  38. Autonomic Nicotinic Receptors
    - Parasympathomimetic (stimulant)

    1) Endogenous ACh (NOT exogenous)

    • 2) Nicotine
    • -used in decreasing amounts to overcome nicotine additcion. Adverse effects can include HTN. Nicotine overdose can result in respiratory arrest (due to ganglionic blockade) and seizures
  39. Muscarinic Receptors - Parasympathomimetic
    - Parasympathomimetic (stimulant)

    • - Direct Stimulants:
    • 1) ACh
    • 2) Pilocarpine
    • 3) Carbachol

    • - Cholinesterase Inhibitor:
    • 1) Pyridostigmine
    • 2) Ectothiophate
  40. Muscarinic Receptor: ACh
    Direct Stimulant

    • - used as a surgical miotic agent
    • - ADEs are rare but can cause complications in patients with PUD (peptic ulcer disease) (secondary to increase in acid/pepsin secretion), bronchial asthma, hyperthryroidism, Parkinson's disease, etc.
  41. Muscarinic Receptor: Pilocarpine
    Direct Stimulant

    - used for treating open angle glaucoma, causes miosis and changes aqueous outflow

    - common ADEs in the eye include local irritation/conjunctivitis, burning, ciliary spasm, lacrimation, etc.

    - Caution in patients with Parkinson's dz, asthma, PUD, hyperthyroidism, abnormal blood pressure, epilepsy, tachycardia

    - usual dose for glaucoma is 1-2 drops up to 6 times a day, depending on concentration of solution use
  42. Muscarinic Receptor: Pyridostigmine
    Cholinesterase inhibitor

    - used for myasthenia gravis and reversal of non-depolarizing muscle relaxants

    - available in PO, IM, IV dosage forms

    (prob not on test)
  43. Muscarinic receptor: Echothiophate
    Cholinesterase inhibitor

    - Used for treatment of open-angle glaucoma

    - Occasionally used for accommodative esotropia in children

    - Possible ADEs include miosis, excessive salivation, rhinorrhea, Nausea/Vomiting/Diarrhea, convulsions, respiratory depression

    - Effects of the drug can be reversed with atropine or pralidoxime (2-PAM)
  44. Muscarinic Receptors - Parasympatholytic
    1) Atropine

    2) Scopolamine

    3) Homatropine

    Other medications in this class include oxybutinin, flavoxate, tolterodine, trihexyphenidyl, benztropine, etc.
  45. Muscarinic Receptor: Atropine**

    - Produces mydriasis and cyclopegia for examintion of the retina and optic disc, refraction

    - used for amblyopia, to treat anterior uveitis, and decrease secretions pre-operatively

    - also used in the treatment of GI spasms, symptomaitc bradycardia, pulseless electrical activity in the heart and asystole

    - used also in the treatment of organophosphate poisoning/overdose of cholinergic stimulants

    - ADEs can include excessive mydriasis,cycloplegia, facial flushing, xerostomia (dry mouth), confusion (irritation, delerium), urinary retention, tachycardia.

    - Contraindicated in narrow angle glaucoma
  46. Muscarinic Receptos: Scopolamine

    - Produces cyclopegia and mydriasis

    - used transdermally to prevent N/V associated with motion sickness

    - potential ADEs include xerotomia, confusion/disorientation, increased body temperature, facial flushing, urinary retention, tachycardia

    - contraindicated in narrow angle glaucoma
  47. Adrenergic stimulants are called ___________. Adrenergic blockers are called ___________.

  48. Sympathomimetic drugs acting on α1 adrenergic receptors
    • 1) Phenylephrine**
    • - used for eye exams
    • - includes mydriasis but not cycloplegia
    • - also used to produce mydirasis prior to ocular surgery
    • - Non-Rx strength available to relieve redness of the eye, but should not be used for longer than a 72 hour period
    • - caution if used within 21 days of an MAO-inhibitor
    • - many potential ADEs including increases in blood pressure, headache, dizziness, etc.
  49. Sympathomimetic drugs acting on α2 adrenergic receptors
    meds include those used for their ability to inhibit NE release in the CNS (ie clonidine, guanfacine and guanabenz) and those agents used for local vasoconstrictive effects (ie naphazoline and oxymetazolone)

    - also reviewed in the cardiac section and opiate withdrawal
  50. Propylthiouracil (PTU) and Methimazole
    Use: Hyperthyroidism

    Mechanism of Action: Inhibits synthesis of thyroid hormone within the thyroid gland

    Adverse Effects: Fever, blood dyscrasias, skin rash/itch, arthralgia (joint pain), peripheral neuropathy, dizziness, loss of taste, N/V, stomach pain, renal and hepatic complications, etc.

    Admin/PK: (won't ask bc we don't Rx) Usually given in divided doses every 8 hours. Doses will be lowered in elderly patients in PTU.

    Comments: No specific ocular side effects reported, but watch for bleeding episodes. Many possible DD interactions
  51. Levothyroxin**
    Use: HYPOthyroidism

    • Mechanism of Action: Supplemental thyroxine (T4)
    • - T4 is converted in the PERIPHERAL TISSUES to T3 (Tri-iodothyronine)

    Adverse Effects: usually dose related. Chest pain, diarrhea, leg cramps, apetitc changes, fast/irregular heart rate, termor, headache, irritiability, insomnia, change in sensitivity to heat, etc.

    • Admin/PK: Slow increasein dosage helps to prevent adverse effects
    • - Dosage will be reduced for elderly patients

    Comments: Preferred agent to use in the treatment of hypothyroidism. Effects more predictable because of standard hormone content. Effects of therapy may not be evident for months
  52. What factors are involved in good blood glucose control vs loss of control?
    • 1) Diet
    • 2) Exercise
    • 3) Drugs

    + Basic state of health/other stressors

    • Diet: compliance with recommendations
    • Physical Activity
    • Stress: physiological and psychological
    • Other meds
    • Physiologic hormonal changes (menstruation, puberty, pregnancy, etc)
    • Gastroparesis
    • Choice of/compliance with meds
  53. A pt complains of feeling dizzy, faint, hot, and nauseated. She shakes visibly and her menta; status rapidly declines. What do you do?

    • Want to give pt:
    • High carbs
    • Low fat
    • some proteins

    GOOD: tomato juice, skittles, cheese and crackers, juice, nonfat milk, raisins

    Advise pt to report to PCP, to carry a glucose source, pt ed on hypoglycemia
  54. Current recommendations for fasting/postprandial blood glucose and hemoglobin A1C levels
    • HbA1c: 6.5% or below
    • Fasting BG: 110 mg/dL or less
    • Postprandial BG: 140 mg/dL or below

    HbA1c measures % of HbA that has been irreversibly glycolsylated

    RBC lives up to 120 days, HbA1C indicates glycemic control over preceding 2-3 mos.
  55. Insulins: MOA, Uses, ADE, DD Interactions
    MOA: Hormone that controls the storage and metabolism of carbohydrates, proteins, and fats. Substitutes for endogenous insulin in patients with Type I DM.

    Uses: Type 1 DM, possible Type 2 DM

    ADE: Hypoglycemia, weight gain, and (rarely) edema and lipohypertrophy

    Possible Drug Interactions: Ethanol (increases potential for hypoglycemia), Beta adrenergic blocking agents--including opthalmic formulations (may modify carbohydrate metabolism and lead to hyperglycemia, but may also cause hypoglycemia and block physiologic responses to hypoglycemia). Corticosteroids antagonize insulin effects
  56. Rapid Acting Insulin includes:**
    • LAGR
    • 1) Insulin Aspart*
    • 2) Insulin Lispro*
    • 3) Insulin Glulisine*
    • 4) Regular

  57. Intermediate-acting Insulin includes:**
  58. Long-acting Insulin includes:**
    • 1) Insulin Glargine
    • 2) Insulin Detemir
  59. The only insulin that can be givne intravenously is...

    no insulin should ever be given IM
  60. Glipizide
    Use: Type 2 Diabetes

    ADE: Hypoglycemia, weight gain, hepatic and renal complications, blood dyscrasias, GI disturbances, headache, increased cardiac risk in those with CV disease

    • Admin/PK: Patient monitored for hepatic and renal function
    • - doses are reduced in elderly patients

    blurred vision and changes in accommodation

    D:D interaction with some SOP meds
  61. Glimepiride
    Use: Type 2 Diabetes

    ADE: Hypoglycemia, weight gain, hepatic and renal complications, blood dyscrasias, GI disturbances, headache, increased cardiac risk in those with CV disease

    • Admin/PK: Patient monitored for hepatic and renal function
    • - doses are reduced in elderly patients

    Comments: ocular side effects include blurred vision and changes in accommodation

    - D:D interaction with some SOP meds
  62. Glyburide
    Use: Type 2 Diabetes

    ADE: Hypoglycemia, weight gain, hepatic and renal complications, blood dyscrasias, GI disturbances, headache, increased cardiac risk in those with CV disease

    • Admin/PK: Patient monitored for hepatic and renal function
    • - doses are reduced in elderly patients

    Comments: ocular side effects include blurred vision and changes in accommodation

    - D:D interaction with some SOP meds
  63. Acarbose
    • Use: Type 2 Diabetes
    • ADE: Flatulence, diarrhea, abdominal pain.
    • - Should not cause hypoglycemia when used as monotherapy
    • - if occurs, treat with oral glucose instead of table sugar (sucrose)

    Admin/PK: caution is used when the drug is administered with other meds that lower blood glucose due to increased risk of hypoglycemia

    • Comments: Best effect as an adjunct is approx 0.5-0.8% recution in A1c.
    • - Not used as montherapy

    - Renal function should be monitored in MIGLITOL
  64. Metformin**
    • Use: Type 2 diabetes
    • ADE: N/V/D, flatulence, rash, weakness, HA, hypoglycemia, lactic acidosis, myalgia, blood dyscrasias, chest discomfort, etc.

    Admin/PK: Caution is used when the drug is administered with other meds that lower blood glucose due to increased risk of hypoglycemia.

    • Comments: renal function should be monitored. The drug may be discontinued in renal dysfunction.
    • - Medication is held before surgeries and use of contrast media.
    • - Best effect is 1-2% reduction in A1c
    • - D:D interactions with some SOP meds (ie Trimethoprim and oral fluoroquinolones)
Card Set
pp. 40- FINAL
Final exam