Download Pathology 122 Week 1-3 Concepts

Week 1: Introduction and Stress
Introduction
Pharmacology: study of medicine. How it works in the body.
Therapeutics: prevention of disease and suffering. Does not have to be related to drugs. For example,
massage is a therapeutic technique.
Pharmacotherapeutics: Use of drugs to prevent disease and suffering.
Drug Names
 Chemical: Name describing chemical structure
 Generic: Nonproprietary International Name
 Trade: Brand/Proprietary Name.
Chemical Name
Generic Name
Trade Name
N-acetyl-para-aminophenol
Acetaminophen
Tylenol
7-chloro-5-(o-chlorophenyl)-1,3- Lorazepam
Activan
dihydro-3-hydroxy-2H-1,4benzodiazepin-2-one
iso-butyl-propanoic-phenolic
Ibuprofen
Actiprofen
acid
Advil
Classification
 Therapeutic: Classification based on the overall effect of the drug.
 Pharmacological: Classification based on how a drug works in the body.
Prototype Drug: Model representative of a drug family/class. Other drugs of the same class are
compared to this one so similarities and differences in the drug group can be established.
Pharmacokinetics: The body’s influence on the drug.
 Absorption: Site of Administration  Blood(to distribution)/Target (to metabolism)
 Distribution: Blood  Target
 Metabolism: Usage of Drug/ Breakdown of drug or Construction from drug components
o First Pass Effect: If the drug passes the Liver, then a large portion of the drug may be
metabolized to become inactive. The drug may also become more active if metabolized
such as the cases with prodrugs.
 Prodrugs: Compounds without a therapeutic effect unless it is metabolized by
the Liver
 Explains why Lotensin and Cozaar (examples of prodrugs) are both in
tablet form.
 Excretion: Expulsion of Drug or what is left. Blood  Outside of Body/Kidney/Intestine
 Plasma Half Life: Time it takes for half of the drug to be used up (metabolism, excretion)
o Equilibrium: where drug is constantly in therapeutic range occurs in about four half lives
 Therapeutic Range: Drug concentration level where there is a therapeutic effect.
o Loading Dose: A large dose at the very beginning of treatment to increase the drug
concentration drastically into the therapeutic range. This is to shorten the time required
to plateau in the therapeutic range
o Maintenance Dose: Repeated dosage to keep drug concentrations in therapeutic range
Stress
Stress Response: Systematic response to change or demand on the body.
Stressor: Factor that creates significant change in the body or environment. Stressors are subjective.
General Adaptation Syndrome (GAS): Fight or Flight response.
 Alarm: Defenses are mobilized
 Resistance: Hormone levels are elevated. Operate at peak performance.
 Exhaustion: Cannot keep up with demands.
Factors in Coping with Stress
 Number, duration and intensity of stressors
 Past experiences
 Support systems available to the individual
 Personal qualities of the person
Significant Effects of the Stress Response:
 increase heart rate, blood pressure, blood glucose
 increase ventilation
 increase awareness and alertness
 decrease immune response.
Relationship between stress and disease.
 Stress Response will weaken your body: Thus higher chance of disease and illness
o Vasoconstriction
 Necrosis: not enough nutrients. Cells die.
 Inflammation: damage to cells or dying cells start inflammation response.
 Shut down of certain organs: Result of Necrosis
 Increase in blood pressure: physical stress on cardiovascular system
o Decreased immune system
 Higher chance of illness
 Cancer
Anxiety
Levels of anxiety
 1: Mild Anxiety
o Slight Arousal: Increased concentration and awareness
o Mild restlessness
 2: Moderate Anxiety
o Decreased concentration and perception.
o Nervous and Tense
 3: Severe Anxiety
o Decreased concentration and perception; unable to focus properly and may focus on
one detail at a time
o Nervous and Tense
 4: Panic
o Intense fear and altered perceptions (distorts events)
o Loses control
Anxiolytic Drugs
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Benzodiazepine: Enhances GABA which is an inhibitory neurotransmitter causing relaxation.
Barbiturate: Enhances GABA.
CNS Depressants: Depresses the central nervous system causing relaxation
The difference between stress and anxiety: Stress can be any change in your environment,
psychological or physical. It can be manifested from anger, joy, fear, etc. Anxiety on the other hand is
the feeling of helplessness and anticipated fear.
Week 2: Inflammation and Healing
Inflammation: A non-specific response to tissue injury. It is a defense mechanism in the body that tries
to remove the object causing injury.
Process of Inflammation and Healing (Pathophysiology)
 Inflammation Phase
o Inflammation Response: Getting rid of the foreign/ harmful material.
 Injured mast cells send out chemical mediators (histamine, prostaglandins, etc)
 Chemical Mediators move to blood and nerves causing:
 Pain
 Vasodilation
 Increase in Capillary Permeability (+ osmosis  swelling/edema)
 White blood cell increase
 Permeability and white blood cells help with the healing process and dilution of
toxins.
o Exudate Production
 Removes Wastes (via lymphatic system) and helps isolate threats
 Proliferative Phase
o Blood clot
o Granulation Tissue forms in the gap: highly vascular, moist and pink/red. Contains new
capillary buds. Connective Tissue.
o Closing the gap: epithelial cell mitosis and scar tissue formation.
o Angiogenesis: production of new blood vessels in the vicinity.
 Maturation Phase
o Strong Scar: Cross linking and shortening of collagen fibers
o Disappearance of Redness: Capillaries in the inflamed area decrease.
Local Effects
 Redness: vasodilation
 Swelling/ Edema: increase capillary permeability
 Pain: direct damage, pressure and chemical mediators acting on nerves
 Loss of Cell Function: Malnourishment
Exudate: composed of fluid, dead cells and products from dead cells
 Serous: fluid + small amounts of protein and WBC (clear, serum w/o cells)
 Fibrinous: Thick and sticky. High cell and fibrin content. Increases scar tissue risk.
 Purulent (Pus): Thick, yellow-green. High WBC, cell debris and microbe content.

o Abscess: localized pocket of pus in a solid tissue.
Hemorrhagic/ Sanguinous: RBC in interstitial fluid. Indicates Blood vessel damage.
Diagnostic Tests
 Degree of Inflammation
o Leukocytosis (increase in WBC production)
o Increased Levels of C-Reactive Protein (CRP)
o Elevated Erythrocyte Sedimentation rate (ESR)
 Location of Inflammation
o Testing for Isoenzymes (Enzymes made by particular tissues)
Chronic Inflammation compared to Acute Inflammation
 Chronic Inflammation can be a result of Acute Inflammation if the damaging object is not dealt
with or infects the patient repeatedly.
 Immune system is stimulated when it is not necessary. The excessive amount of immune cells
circulating the body damage healthy cells which lead to further complications
 Less edema at inflamed site (swelling)
 More lymphocytes, macrophages and fibroblasts leading to scar tissue formation
 More tissue destruction occurs with chronic inflammation.
Anti-inflammatory Drugs
 NSAID: inhibits COX  inhibits prostaglandin formation. Inhibits pain, inflammation, blood
clotting and GI protection.
 Selective COX-2 Inhibitor: Inhibits COX-2  inhibits prostaglandin formation associated to pain
and inflammation.
 Systemic Glucocorticoids: Inhibits prostaglandin formation. Inhibit histamine release and
functions of WBC (which can release things like interleukins)
Healing
Types of Healing (Cellular Level)
 Resolution: Cells are slightly damaged but still alive and functioning. Healing occurs when they
recover and are at optimal conditions.
 Regeneration: Cells neighboring the wound undergo mitosis to fill in the gap.
 Replacement: Scar tissue formation. Although it is called “tissue”, these are not living cells so
they do not contain hair follicles and things like melanin (skin pigment).
Types of Healing (Systemic Level)
 Primary intention: clean wound. Tissue closed.
 Secondary intention: Considerable tissue loss. Extensive wound. Repair time is longer, scarring
greater and susceptibility to infection is greater
 Tertiary Intention (Delayed primary intention): Wound open for 3-5 days so edema and infection
resolve then wound is closed.
Factors affecting Healing
 Age
 Nutrition
 Hemoglobin count and Circulatory System status
 Wound Status/ First Aid
 Existing Complications and Medications
Complications in the Healing Process
 Loss of Function: Scar tissue replaces the wounded tissue. The scar tissue may not be able to
carry out the function of the replaced tissue if it is specialized.
 Contracture: Restriction of a joint because of scar tissue’s shrinkage.
 Obstructions: Occur when scar tissue shrinks causing surrounding structures to shorten or
narrow. Tubes and ducts may narrow causing objects to not be able to move through the
structures
 Adhesion: Bands of scar tissue joining two otherwise separate tissues.
 Hypertrophic Scar Tissue: Overgrowth of fibrous tissue. Causes hard ridges of scar tissue or
keloid formation. May cause contractures and pull tissue out of position.
Week 3: Pain
Pain: Bad feeling or discomfort. Is subjective from person to person. Caused by the stimulation of
nociceptors from a mechanical, thermal or chemical source.
Types of Pain
 Somatic: Pain originating from Structural components of the body.
 Visceral: Pain originating from organs
 Neural: Damage to the neurons may cause neurons to fire irregularly or continuously.
Gate-Control Theory: Check Figure 13-2 in textbook.
Gate control theory is just a concept that the pain signal can be blocked off from the brain.
Open Gate: pain moves from the peripheral nerve to the synapse, convert the electrical signal to a
chemical signal in the form of “substance P”. The neurotransmitter “substance P” then moves to the
spinothalamic bundle. There the chemical signal is then reconverted to an electrical signal and sent to
the brain where it is processed. (Gould, 2006)
Closed Gate: substance P cannot get out from the synapse to the dorsal horn of the vertebra and thus to
the spinothalamic bundle. The pain signal is not reconverted electrically and does not reach the brain.
This occurs when the gate is closed and the opioid receptors are occupied. This can be done by afferent
impulses from the touch stimulus (the a β fiber; e.g cold pack), from the efferent impulses (from the
brain; e.g distractions) and using drugs. When the first two stimuli occur, the interneuron releases
enkephalins or endorphins which occupy the receptors and block off the gate. Opiates, when
administered, will bind the receptors and will block the gates themselves. (Gould, 2006)
Characteristics of Pain:
 Referred Pain: The phenomenon has to do with the fact that nerves branch out as you move
away from the spine. At the junction points, the brain has a difficult time differentiating which
branch the nerve impulse came from so it may think that pain is coming from one branch when
in fact the signal is coming from the other.
 Phantom Pain: Sensation or Pain still occurs in a lost limb following amputation. The brain thinks
the limb is present when there is a stimulus. This may be from a similar mechanism from the
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
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Referred Pain as stimuli to junction points may make the brain think the sensation is coming
from another place such as a missing limb.
Factors affecting pain perception
o Age
o Culture
o Prior Experience
o Anticipations
o Personality
o Anxiety/Fear/Stress
o Fatigue/ Hunger/ Complications
Pain Threshold: Point where a stimulus becomes discomforting or painful
Pain Tolerance: Amount of pain endured by the person before action is taken.
Acute vs. Chronic Pain
Pain
Onset
Cause
Affected area
Stress
Adverse Effects
Acute
Sudden, Severe, Short term
Tissue damage. Patient is aware
of it.
Local
Stress response occurs
Vomiting
High Anxiety
Chronic
Long Term
Not apparent to the patient.
May be internal injury
Generalized and hard to locate
Stress response burns out and
leads to fatigue
Depression
Sleep Disturbance
Hinders daily activities
Reduction in pain/illness/injury
tolerance
Analgesics and Related drugs
 Non opioid analgesics
o NSAID: COX inhibitor  inhibit prostaglandin formation.
o Acetaminophen: Centrally acting COX inhibitor  block prostaglandin formation in CNS
 Opiates: Binds to opioid receptors in the CNS and blocks Substance P from continuing the pain
signal.
 Opioid Antagonist: not an analgesic. Blocks Opiate actions to reverse their effects. Used during
opioid toxicity and addiction.
Compare and Contrast the Opioid Receptors and their Responses
Analgesia (Pain Killing)
Decreased GI Motility
Euphoria (High)
Miosis (Pupil constriction)
Dependence (Addiction)
Respiratory Depression
(Hypoventilation)
Sedation (Relaxation)
(Adams et al, 2011 )
Mu
Y
Y
Y
N
Y
Y
Kappa
Y
Y
N
Y
N
N
Y
Y
References
Adams, M., Holland, L. N., & Urban, C. Q. (2011). Pharmacology for nurses: a pathophysiologic approach
(3rd ed., pp. 3-4, 12-13,37-43,46-50,157-161,220-221,223,467-471). Upper Saddle River, N.J.: Pearson
Education.
Gould, B. E., & Buttle, G. (2006). Study guide for pathophysiology for the health professions (3rd ed., pp
20-34,218-233). Philadelphia: Saunders/Elsevier.
Kozier, B. (2010). Fundamentals of Canadian nursing: concepts, process and practice (2nd Canadian ed.,
pp 881-882, 934, 936-940, 1490-1948). Toronto: Prentice Hall.