Sapna Gupta, Associate Professor
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Final Exam Review 
In general for all treatments, study
  • the disease
  • at least two treatments or drug type
  • adverse effects of each of the treatment
  • concerns for the Physical Therapist
CNS SYSTEM

SEDATIVE DRUGS

ANESTHETICS

Skeletal Muscle Relaxants

ANALGESICS AND ANTI-INFLAMMATORY DRUGS

AUTONOMIC NERVOUS SYSTEM

Antihypertensive Drugs

Angina Pectoris

Cardiac Arrhythmias

Congestive Heart Failure

Coagulation Disorders and Hyperlipidia

Endocrine Pharmacology

Male and Female Hormones

DIABETES

THYROID AND PARATHYROID HORMONES

OTC AND TOXICITY

CNS SYSTEM

CNS neurotransmitter: a chemical interacts with the synaptic membrane receptors e.g. Acetylcholine, dopamine, norepinephrine, serotonin, GABA, glutamic acid, glycine.

Concepts:

1) targets of CNS drug action 

a) receptor, 

b) ion channel

SEDATIVE DRUGS 

e.g. benzodiazepines, barbiturates, cyclic ethers. 

Know the following terms: sedation, hypnosis, tolerance, physical dependence, anesthesia, coma, psychological dependence. 

Pharmacokinetics: most drugs are lipid soluble, are well absorbed and have good distribution in the brain. Drugs are metabolized in the liver and some drugs have active metabolites which cause side effects in prolong use. 

Degree of effect: sedation ---> hypnosis----> anesthesia ---> anticonvulsant actions----> muscle relaxation ----> medullary depression (respiratory and cardiac arrest) ---> coma.

Toxicity:

ANESTHETICS

Common drugs used: chloroform and ether (old drugs).  New drugs : dinitrogen oxide, halothane are the gases used.  Intravenous e.g.. Thiobarbiturates, narcotics (morphine)

Stages of anesthesia : analgesia , excitement, surgical anesthesia, medullary depression, coma

Pharmacokinetics in general for both inhaled and intravenous anesthetics. 

Toxicity

Local anesthetics

block the sodium ion channel thus prevent sensation.

Properties of local anesthetic agents

Pharmacokinetics and pharmacodynamics.

SKELETAL MUSCLE RELAXANTS

Spasticity: exaggerated muscle excitability, due to cerebral accident, traumatic lesions or multiple sclerosis.

Spasms: increased tension, voluntary

Therapy: Muscle relaxants: Baclofen, Diazepam; Direct Acting Drugs: Dantrium

  ANALGESICS AND ANTI-INFLAMMATORY DRUGS

Pharmacokinetics

Opioid drugs: effect of narcotic analgesics, adverse effects 

NSAIDS: aspirin, benefits and side effects of aspirin and aspirin like drugs.

Patient controlled analgesics: different routes, side effects

 AUTONOMIC NERVOUS SYSTEM

Know the following terms:

Parasympathetic: the part of the autonomic nervous system hat originated in the cranial nerves and the sacral part of the spinal cord andergenic: a synapse in which norepinephrine is the primary transmitter in the parasym. NS

Sympathetic: the part of ANS that originates in th throacid and lumbar parts of the spinal cord.

Epinephrine: increases cardiac function and cellular metabolism.

Cholinergic: a nerve receptor that releases acetylcholine as the primary transmitter. Have muscarinic and nicotinic receptors.

Andrenergic: a nerve receptor that releases norepinephrine as the primary transmitter. Has alpha and beta receptors for amphetamines, ephedrine etc.

Pre and post synaptic receptors: the receptors that modulate release and effector of the neurotransmitter respectively

Somatic : voluntary motion e.g. the skeletal muscle

HYPERTENSION

What is hypertension?

What causes hypertension?

Therapy

1) diuretics e.g. Hydrochlorothiazide 

2) sympatholytics (e.g. beta blockers) e.g. Veratrum alkaloids, reserpine

3) vasodialators e.g. Hydralazine  e.g. calcium blockers

4) ACE inhibitors: e.g. Captopril  angiotensin converting enzyme inhibitors. They prevent synthesis of angiotensin thus increasing vasodilatation. 

Stepped care in Hypertension: the above are given step by step if the previous does not work, in addition to the previous one

ANGINA 

Arteriosclerosis is the most common one, in which there is obstruction of flow of blood thus resulting in acidic metabolites thus causing pain.

Therapy

1)nitrates (nitroglycerin most common): there is a general dilation of muscles with the nitrates.

2)calcium channel blockers: e.g. Nifedipine, Diltiazem; block the calcium channel thus decreasing the action potential of the membrane thus reducing the contractility of the muscle.

3)Beta Blockers: e.g. Propranolol; block the beta receptor of the andergenic receptors thus preventing the contraction of the vessels. E.g. Metoprolol

 CARDIAC ARRHYTHMIAS

Deviation from normal heart beat. Can be fatal. Caused usually by abnormality in the electric potential of the cell membrane (which is responsible for normal heartbeat). There can be either abnormal generation or conductance.

Therapy:

1) sodium channel blockers (class A, B and C): inhibit sodium channel from opening

2) beta blockers: slow down heart rate thus conduction.

3) drugs that prolong repolarization: delay repolarization.

4) calcium channel blockers: inhibit calcium ion influx.

Adverse effects

 CONGESTIVE HEART FAILURE

condition where cardiac output is insufficient for the needs of the body. It is a four step cyclic process:

1) Decreased cardiac performance: due to high BP or other diseases.

2) Neurohormonal compensation: sympathetic system sends out hormones to elevate heart beat (also increased sympathetic tone)

3) Increased cardiac workload because of increased sympathetic flow

4) Changes in the myocardial cell - damage to heart cells thus going back to 1)

Therapy:

1) Digitalis glycosides: e.g. Digoxin; it inhibits the sodium channel which results in less calcium removed from cell thus increases cell contractility. Caution: drug has to be monitored closely as there are severe side effects especially arrhythmias.

2) ACE inhibitors

3) diuretics

COAGULATION AND HYPERLIPIDIA

Homeostasis is regulation of blood factors in order to prevent blood loss during bleeding.

Clot formation process.

Overclotting:

1) Anticoagulants: e.g. heparin and warfarin

2) Antithrombotics

3) Thrombolytics

Adverse effects

Clotting deficiencies:

1) hemophilia: genetic disorder, unable to synthesize clotting factors; usually given from human blood.

2) deficiency of vitamin K: given orally through diet or supplements.

3) antifibrinolytics: excessive bleeding after surgery.

Hyperlipidia

Causes: poor diet and lifestyle etc.

Therapy: HMG-CoA inhibitors, Fibric Acids etc.

HORMONES

function of hormones

mechanism of action of hormones

MALE AND FEMALE HORMONES

Androgens and anabolic steroids: physiological effects, clinical/pharmacological uses, adverse effects

Anabolic steroid use in sports: how anabolic steroids work, major effects of steroid use, side effects.

Estrogen and progesterone: physiological effects, clinical/pharmacological uses, adverse effects

DIABETES

causes and treatment of both Type I and Type II diabetes mellitus

caution, concerns, adverse effects of insulin therapy

THYROID AND PARATHYROID HORMONES

THYROID

Functions: thermogenesis, growth and development, cardiovascular, metabolic effect

Disorders: hyper and hypothyroidism

Therapy for Hyperthyroidism: antithyroid agents, iodide, radioactive iodine and beta andrenergic blockers.

PARATHYROID

Functions: calcium ion homeostasis (functions of Calcium ion). How does the hormone work?

How does calcium homeostasis work? What are the factors involved?

Calcium imbalance: Causes eg hypoparathyroidism, hyperparathyroidism, oesteoporosis, rickets etc.  Their causes and treatments. (know at least four)

Therapy of hypocalcemia: vitamin D, diphosphonates, calcitonin, estrogen therapy.

OVER THE COUNTER DRUGS

e.g. analgesics different forms, types, strength etc.

Problems encountered

TOXICOLOGY

approach to poisoned patient

the physical exam

Lab procedures

Decontamination


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