HPRS 2300 Unit 2 Exam Review: Nervous System and Drugs

Central Nervous System (CNS)

composed of brain and spinal cord; receives and interprets sensory info and initiates motor responses.

Peripheral Nervous System (PNS)

afferent nerves carry sensory impulses toward CNS; efferent nerves carry motor impulses away from CNS; includes cranial nerves (12 pairs) and spinal nerves (31 pairs).

Sympathetic Nervous System

increases heart rate and blood pressure, causes bronchodilation, decreases digestive activity, dilates pupils, and increases sweat production.

Preganglionic Neuron (Sympathetic)

Releases acetylcholine (ACH).

Postganglionic Neuron (Sympathetic)

Primarily releases norepinephrine (NE); exception for sweat glands where it releases acetylcholine (ACH).

Preganglionic Neuron (Parasympathetic)

Releases acetylcholine (ACH).

Postganglionic Neuron (Parasympathetic)

Releases acetylcholine (ACH).

Somatic Nervous System

Nerves branch from cranial and spinal motor nerves; innervates skeletal muscle; voluntary control by cerebral cortex.

Autonomic Nervous System (ANS)

Branches of cranial and spinal motor nerves innervate cardiac and smooth muscle of internal organs and glands; involuntary control regulated by the hypothalamus and medulla oblongata.

Autorhythmicity

Contraction without any stimulus.

Parasympathetic Nervous System Responses

Characterized as 'rest and digest' effects: decreased heart rate, decreased conduction, decreased contractility, decreased blood pressure, miosis, bronchoconstriction, increased digestion, increased GI secretions, increased defecation, urinary bladder contraction, urinary sphincter relaxation, increased urination, increased sweating.

Alpha-1 Adrenergic Receptor

Receptor located on smooth muscle that mediates smooth muscle contraction.

Alpha-2 Adrenergic Receptor

Receptor located on adrenergic nerve endings that reduces the release of norepinephrine (NE).

Sympatholytic Drugs

Block the effects of the sympathetic nervous system, leading to various actions depending on the specific receptors they target.

Alpha-1 Adrenergic Blocking Drugs

Block alpha-1 receptors, resulting in vasodilation and decreased blood pressure.

Cardiovascular System (Parasympathetic)

Decreased heart rate, decreased conduction, decreased contractility, decreased blood pressure.

Ocular System (Parasympathetic)

Miosis (pupillary constriction).

Respiratory System (Parasympathetic)

Bronchoconstriction (narrowing of airways).

Gastrointestinal (GI) System (Parasympathetic)

Increased digestion, increased GI secretions, increased defecation.

Urinary System (Parasympathetic)

Urinary bladder contraction, urinary sphincter relaxation, increased urination.

Glands (Parasympathetic)

Increased sweating (specifically through sympathetic cholinergic control of eccrine glands).

Sympathetic vs. Parasympathetic Effects

Sympathetic nervous system affects the whole body, while parasympathetic nervous system affects only one part.

Decreased Bladder Neck Obstruction

In conditions like benign prostatic hypertrophy (BPH), they can relax the smooth muscle in the bladder neck, improving urine flow.

Beta-Adrenergic Blocking Drugs

These drugs can be selective (targeting beta-1 receptors) or non-selective (targeting both beta-1 and beta-2 receptors).

Decreased Heart Rate (Negative Chronotropic Effect)

They slow the heart rate.

Decreased Force of Contraction (Negative Inotropic Effect)

They reduce the strength of heart muscle contractions.

Decreased Conduction (Negative Dromotropic Effect)

They slow the conduction of electrical impulses through the heart.

Decreased Cardiac Output and Blood Pressure

These are direct results of the heart-related effects.

Bronchoconstriction (Non-selective only)

Non-selective beta blockers can block beta-2 receptors in the lungs, leading to the narrowing of airways.

Beta-1 Receptors

Receptor located on the heart that increases heart rate and force of contraction.

Beta-2 Receptors

Receptor located on smooth muscle that relaxes smooth muscle when stimulated.

Indication of Dobutamine

Treatment of shock, increases blood pressure, and increases heart function with acute heart failure.

Chronic Bronchitis

Chronic inflammation and irritation of the respiratory tract, thickened mucous secretions, interference of gas exchange.

Asthma

Airway obstruction reversible spontaneously or with treatment, inflammation of the bronchioles causing bronchoconstriction.

Precipitating Factors of Asthma

Antigen or Allergen, URI, Exercise, Emotional Stress, Environmental Conditions (cold, fragrances, dust, chemicals), Drugs.

Symptoms of Asthma

Wheezing, chest tightness, coughing, tachypnea (rapid breathing), dyspnea (shortness of breath), tachycardia, respiratory weakness (fatigue)/shortness of breath.

Treatment for Asthma

Treat with bronchodilators, steroids, and possibly allergy meds.

COPD

Chronic Obstructive Pulmonary Disease, a group of progressive lung diseases that block airflow and make it difficult to breathe.

Emphysema

Condition involving the destruction of alveoli and the enlargement of air spaces, leading to trapped expiratory air and reduced respiratory exchange.

Treatment for COPD

COPD is often treated with steroids and bronchodilators.

Ipratropium Bromide (Atrovent®)

An anticholinergic bronchodilator that works by blocking muscarinic receptors and the actions of acetylcholine (ACH), resulting in bronchodilation.

Common Side Effect of Ipratropium

Drying of mucous membranes.

Administration of Ipratropium

Ipratropium is administered by oral inhalation.

Onset and Duration of Ipratropium

It has a slow onset but prolonged duration of action (6 hours).

Generation 1 and 2 Antihistamines

Differences between generation 1 and 2 antihistamines.

Generation 1 antihistamines

Sedating.

Generation 2 antihistamines

Non-sedating.

Indications of alpha-1 adrenergic agonists

Increasing circulation of vital organs, increasing blood pressure, promoting decongestion by causing vasoconstriction of blood vessels in nasal passages, which shrinks swollen mucous membranes.

Indications of beta-2 agonists

Asthma, respiratory illness/disease, preterm labor.

Effects of beta-1 adrenergic agonists at low dose

Stimulates dopaminergic (d-1) receptors in kidneys causing vasodilation and increased renal blood flow.

Effects of beta-1 adrenergic agonists at moderate dose

Stimulates beta 1 receptors-heart, increases force of contraction and cardiac output.

Effects of beta-1 adrenergic agonists at high dose

Stimulates alpha-1 receptors causing vasoconstriction → increase in blood pressure.

Effects of beta-1 adrenergic blockers

Decreases force of contraction (negative inotropic), decreases cardiac output, decreases HR (negative chronotropic), decreases conduction (negative dromotropic), decrease in cardiac output also decreases BP.

Drug classifications used for bronchodilation

Beta-2 Adrenergic Agonists, Anticholinergics/Parasympatholytics, Bronchodilators (general classification).

Beta-2 Adrenergic Agonists

Stimulate beta-2 receptors, leading to the relaxation of smooth muscle in the lungs. Examples include albuterol, terbutaline, formoterol, and salmeterol.

Anticholinergics/Parasympatholytics

Cause bronchodilation by blocking muscarinic receptors and the actions of acetylcholine.

Classification that decreases GI secretions

Anticholinergics/Parasympatholytics.

Classification of atropine

Anticholinergics/Parasympatholytics.

Therapeutic effects of atropine

Increases HR; decreases vagus nerve activity (parasympathetic response); pre-op med slows digestion and urination; mydriasis.

Effects of parasympathomimetics

Mimic the effects of acetylcholine (ACH) and the parasympathetic nervous system, leading to decreased heart rate, decreased conduction, decreased contractility, decreased blood pressure, miosis, bronchoconstriction, increased digestion, increased GI secretions, urinary bladder contraction, urinary sphincter relaxation, increased urination, increased defecation, and increased sweating.

Dicyclomine (Bentyl®) usage

GI disorders (ulcers, colitis, IBS).

Side effects of dicyclomine (Bentyl®)

Dry mouth, visual disturbances, urinary retention, constipation, tachycardia.

Vision changes from adrenergics and cholinergics

Both can cause vision changes due to their opposing effects on the eyes, primarily affecting pupil size and intraocular pressure.

Effects of adrenergics on eyes

Cause mydriasis (pupil dilation) due to stimulation of alpha-1 receptors.

Effects of cholinergics on eyes

Cause miosis (pupil constriction) and can lead to blurred vision as a side effect.

Beta-1 Blockers

These drugs specifically block beta-1 receptors, which are primarily located in the heart. This action leads to a decrease in heart rate (negative chronotropic effect), force of contraction (negative inotropic effect), and conduction (negative dromotropic effect). Consequently, cardiac output and blood pressure are decreased.

Examples of Selective Beta-1 Blockers

Atenolol (Tenormin®) and metoprolol (Lopressor®).

Non-selective Beta Blockers

These drugs block both beta-1 and beta-2 receptors. Blocking beta-1 receptors results in decreased heart rate, force of contraction, and conduction, leading to decreased cardiac output and blood pressure. However, by blocking beta-2 receptors, which are found in the lungs, they can also cause bronchoconstriction.

Examples of Non-selective Beta Blockers

Nadolol (Corgard®), propranolol (Inderal®), and timolol (Blocadren®).

Contraindication of Non-selective Beta Blockers

Due to their effect on beta-2 receptors, non-selective beta blockers are contraindicated in patients with asthma and respiratory diseases, as they can trigger respiratory distress.

Excessive Dosing of Beta-1 Blockers

Can lead to significant bradycardia, hypotension, CNS depression, GI upset, and other potential effects like fatigue and electrolyte imbalances.

Significant Bradycardia

A dangerously slow heart rate due to pronounced negative chronotropic effects.

Hypotension

A substantial drop in blood pressure resulting from decreased cardiac output and force of contraction.

CNS Depression

Increased drowsiness and mental depression.

GI Upset

Digestive disturbances.

Antidote for Succinylcholine

No antidote; support respirations until drug is metabolized by cholinesterase in the body.

N2 Receptors

Also known as Nicotinic 2 (Nm) receptors, are a type of cholinergic receptor found primarily at the neuromuscular junction of skeletal muscles.

Location of N2 Receptors

They are primarily located at the neuromuscular junction of skeletal muscles, where somatic motor neurons connect with skeletal muscle fibers.

Muscarinic Receptors

A type of cholinergic receptor found in various locations throughout the body.

Location of Muscarinic Receptors

They are located on cardiac muscle, smooth muscle, and glands, specifically at the parasympathetic postganglionic nerve endings.

Effects of Muscarinic Receptors When Stimulated

Decreased heart rate, bronchoconstriction, increased digestion, increased gastrointestinal (GI) secretions, increased urination, and pupillary constriction.

Stimulus for N2 Receptors

Acetylcholine (ACH).

Stimulus for Muscarinic Receptors

Acetylcholine (ACH).

Drug Classification Ending in 'azosin'

Refers to a class of medications used primarily for hypertension and benign prostatic hyperplasia.

Alpha 1 Adrenergic Blocking Drugs

The drug classification that commonly ends in 'azosin' for the generics.

Examples of Alpha 1 Adrenergic Blocking Drugs

Prazosin (Minipress®), doxazosin (Cardura®), and terazosin (Hytrin®).

What do alpha-1 adrenergic antagonists treat?

Hypertension, Benign Prostatic Hyperplasia.

What is BPH?

An enlarged prostate or benign prostatic hypertrophy is a non-cancerous condition in which the prostate gland becomes larger than normal.

What drug classification treats BPH?

Alpha-1 Adrenergic Blocking Drugs.

Risk factors for asthma attacks

Antigen or Allergen, URI, Exercise, Emotional Stress, Environmental Conditions (cold, fragrances, dust, chemicals), Drugs.

Functions of the respiratory system

Gas exchange, O2 in, CO2 out, Smooth muscle in respiratory passages, Sympathetic stimulation, beta-2 receptors, bronchodilation, Parasympathetic stimulation, muscarinic receptors, bronchoconstriction.

Indications for nasal steroids

Asthma, allergic rhinitis, URI, cold, bronchitis.

What are alveoli?

Alveoli are tiny, air-filled sacs located at the end of the bronchioles within the lungs. They are considered the fundamental units of the respiratory system, often appearing in clusters resembling small bunches of grapes.

Functions of alveoli

The primary function of alveoli is gas exchange, facilitating oxygen uptake and carbon dioxide release.

Oxygen uptake process in alveoli

Oxygen from the inhaled air diffuses across the extremely thin walls of the alveoli and into the capillaries surrounding them, where it is then transported into the bloodstream.

Carbon dioxide release process in alveoli

Carbon dioxide, a waste product from the body's metabolism, diffuses from the bloodstream (in the capillaries) into the alveoli, from where it is exhaled.

Important information about xanthines

Xanthines have a narrow therapeutic range, meaning there is a small difference between the effective dose and a dose that can cause toxicity.

Monitoring blood levels of xanthines

It is crucial to monitor blood levels of xanthines to ensure they are within the therapeutic window.

Example of a xanthine drug

Theophylline (Theo-dur®), aminophylline (Paladron®).

Effects of long-term corticosteroid use

Changes in BP and blood sugars, osteoporosis, weight gain, difficulty sleeping, increased risk for infection, skin breakdown.