Pathophysiology and Pharmacology Unit 1

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What is Pathophysiology?
a science that provides understanding of disease mechanism and how/why physiology changes in body structure and function lead to clinical manifestations of disease.

study of disease

study of functions of living organism

Prevention: Primary
health promotion and protection to reduce/prevent incidence of disease
ei: immunization, diet, exercise

Prevention: Secondary
early detection of disease to alter outcome
ei: screening-cholesterol, education, breast exam

Prevention: Tertiary
treatment and rehab of illness to avoid/postphone complications, sequelae
ei: stroke rehab, diabetes management



science of the origin, nature, effect, chemistry, and uses of drugs

the study of

the study of drugs and their interactions with living systems

Ideal Properties: Effectiveness
the desire reponse acheive

Ideal Properties: Safety
the drug dosen’t produce harmful effect even at high dose

Ideal Properties: Selectivity
only achieve a response at it given, no side effects
ei: antihistamine causes drowsiness

Intensity of Responses



the actions of the body on a drug

Determine drug concentration at site of action:

Pharmacokinetics: Absorption
movement of drug from its site of administration to the blood

Pharmacokinetics: Absorption
Affected by:
Affected by:
-Rated of Dissolution
-Surface Area (Larger=better)
-Blood flow(^flow=flows faster)
-Lipid Solubility(easily to cross membrane)
-pH Partitioning

Pharmacokinetics: Absorption

Infuenced by routes of administration

-Via. Gl tract (anything in side GI tract)
-Oral, mouth, GI Tube, PO
-outside the GL tract
-“by injection”

Pharmacokinetics: Distributions
-movement of the drug thoughout the body

Pharmacokinetics: Distributions
Determined by:
Determined by:
-blood flow to tissues
-ability to exit vascular system
-ability of drug to enter cells

Pharmacokinetics: Distributions
-Blood flow to tissues
-Blood brain barrier: might block the drug from entering the brain
-Placental drug transfer: lipid-solubility can transfer material to baby
-Protein binding: drugs form reversible bond with protein

Pharmacokinetics: Metabolism
-Biotransfermation (metabolizing)
-Hepatic Drug: Metabolizing Enzymes

Pharmacokinetics: Metabolism
-Factors affecting Drug Metabolism
-First Pass effect
-Individual response
Factors affecting Drug Metabolism
-Prodrug: become active when in the body but inactive outside the body
-First Pass effect: rapid inactivation of a drug when the drug is absorb in the GI Tract
-Individual response: every1 is different

Pharmacokinetics: Excretion
removal of the drug from the body

Pharmacokinetics: Excretion
Renal System:
1) Glomerular Filtration
2) Passive Tubular Reabsorption
3) Active Tubular Secrection
Renal System:
1) Glomerular Filtration: blood to tubular to urine
2) Passive Tubular Reabsorption: from tubular back to the blood
3) Active Tubular Secrection: active transfer pump from the blood to the tubular, some urine gets reabsorbed

Pharmacokinetics: Time Course of Drug Responses
-Minimum Effective Concentration
-Toxic Concentration
-Therapeutic range
-Minimum Effective Concentration: when response occur
-Toxic Concentration: when levels are too high
-Therapeutic range: eough of the drug present to have theri therapeutic response

Pharmacokinetics: Time Course of Drug Responses
-Plateau Drug Levels
-Loading dose
-Maintenance dose
-Decline from Plateau
-Plateau Drug Levels: steady dose /remaining constant (average drug level)
-Loading dose: large, initial dose make the plateau dose more effective
-Maintenance dose: smaller dose use to maintance the plateau dose
-Decline from Plateau- most drug takes 4 half live to get it out of the system

Pharmacokinetics: Role of the cell membrane
Phospholipid Molecule:
Hydrophilic head: water loving head

Hydrophobic tail: water hating tails

Pharmacokinetics: Movement across cell membrane
-Transport systems
-Directly crossing membrane
-Channels/Pores: small comound can escape
-Transport systems: move stuffs from one side to another
-Directly crossing membrane: direct cross the membrane( must be lipid

Definition: the process by which drugs influence cell physiology to achieve desired result
-how a drug changes the body

-what drug do to the body and how they do it

-Maximal efficacy
-Relative Potency
-Drug Receptors
-Maximal efficacy: largest effect that the drug can produces
-Relative Potency: amount of drug that must given to get an effect
-Drug Receptors: any fuction marcomolecule to which a drug is to bing to be effective

Receptor Theory
-drugs generally attach to cell receptors to elicit celluar response(it can block or make it work)
-2nd messager response
-drug-> receptor-> cellular response

-activate receptors, mimic(ei: nervous transmitter)

partial agonist
-moderate agonist activity (not a complete mimic)

-prevent receptor activity (blocking it)

Interpatient Variablity
-LD 50
-ED 50
-Therapeutic Index
-LD 50: dose lethal in 50% animals( dose that casues 50/100 animal to die)
-ED 50: average effective dose(dose that have effecet in 50% of the popluation)
-Therapeutic Index: ratio of average lethal(LD 50) dose to effective dose (ED 50)

Variation in Patient Response
-Individual Characteristics: age, race, body composition, diet, compliance
-abnormal physiology
-drug formulation

the study of how gentic indivdual effects to the drug

Genetics: Pharmacogenomics
-can alter:
-Drug Targets
-Immune response

Benefits of Pharmacogenomics
-can increase efficacy and safety of drugs
-create better drugs
-increase quality of care
-better disease management
-decrease cost of health care

Cellular Adaption

Cellular Adaptation: Atrophy
-decrease of size of cells
ei:thymus gland gest small in child,
adnormal= smaller cell size in the heart due to workload

Cellular Adaptation: Atrophy
-Physiology: ei: thymus gland gets smaller as child grows
-Pathologic: blood supply, nutrition
-Disuse: individual can’t move or in bed(immobilize)

Cellular Adaptation: Hypertrophy
-increase in the side of cells
ei: the heart

-Mechanical:stressing of muscle
-Trophic: growing factors

Cellular Adaptation: Hyperplasia
-Increase amount of cells

-Compensatory: regrow of cells
-Hormonal:estrogen, ei:when the girl get pregnant
-Pathologic:increase cells related to disease

Cellular Adaptation: Maladaption


-trait that is (or has become) more harmful than helpful

-Neoplasia:abnormal pattern of growth/abnormal proliferation of cells

Cellular Adaptation:Metaplasia
-replacement of one mature cell type with another
-reprogramming of stem cells due to noxious stimulus
-if cells has injury the cells can regrow

Cellular Adaptation:Dysplasia(atypical hyperplasia)
-Abnormal size, shape, organization of mature cells
-low to high grade
-remove dysplastic tissue/ remove stimulus
-common in the urine due to inflammation

Cellular Injury
-most diseases start with cell injury
-cell unable to maintain homeostasis or adapt
-injured cells have capacity to recover(reversible injury/recover), or die (irreversible/ possible for cellular death)

Casues of Cellular Injury
-Free radicals
-Chemical agents

Hypoxic Injury
Hypoxia- insufficient to tissues (most common cause of cellular injury)

Ischemia (reduced blood supply) most common cause of hypoxia

Anoxia-lack of oxygen to tissues(no oxygen)

ei: heart failure

Hypoxic Cellular Injury
1) ischemia-> decrease in oxygen in mitochondria-> decrease ATP
2)decrease ATP-> alters NA/K pump and NA/CA exchange (altered membrane permeability)
3) increase intracellular NA and CA -> K moves out of the cell
4) water enters cell -> swelling and ER dilation
5) ribosomes detach with decrease protein synthesis
6) vacuolation
7) cell membrane damage

if oxygen is restored-reversible/recover
if not restored- irreversible cell injury/ not recover

Reperfusion injury/ Oxidative injury

can occur with restoration of blood flow and oxygenation

-free radicals generated leading to additional cellular damage
– unstable atom group steals electron
-bond formations-injurious
-target mitochondria

other sources of oxidation injury
-extreme energy expose (uv, radiation)
-endogenous reactions
-chemical exposure

Damage Cause by Free Radicals
1)Lipid peroxidation
2)alters ion pumps/ transport mechanisms
3)fragments DNA
4) mitochondrial damage
1)Lipid peroxidation: the lipid bilayer went bad
2)alters ion pumps/ transport mechanisms: damage the pump
3)fragments DNA: decrease protein sythesis
4) mitochondrial damage: Ca is release cause membrane break down

Mechanisms of Chemical Injury
-exaggerated response
-biologic activation
-rare toxicites

Examples of Chemical Agents(cause chemical injury)
-carbon monoxide
-social “street drug”
-OTC, prescription drugs
-chronic air pollution exposure

Outcomes of Cellular Injury


-Necrosis: cells are not longer able to function
-Apoptosis: self destruction (ei: cancer, DNA damage)
-Autophagy: cell self eating itself (ei: cell is starving or lack of nutrition)

-Tumor/ abnormal cell growth/ new growth

-“new growth”
-carcionma in situ

Benign Tumor
-well organized
-encapsulated( surrounded by capsule)
-normal cell structure
-well differentiated (easily find)
-non invasive
-slow growing
– -oma

Malignant Tumor
-grow rapidly; high mitotic rate
-loss of differentiation; Anaplasia
-disorganized tissue
-not encapsulated
-named for tissue of origin
-less specialize

Tumor Nomenclature: Malignant
-Carcinoma: epithelial tissue
-Adenocarcinoma: ducts or glangs
-Sarcome: connective tissue
-Lymphoma: lymph
-Leukemia: blood forming cells

Classification of Tumors
-Appearance of tissue
-Genetic analysis
-Molecular analysis

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