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BMS291 > W1 Pathophysiology, pharmacology, pharmacodynamics, Pharmacokinetics > Flashcards

W1 Pathophysiology, pharmacology, pharmacodynamics, Pharmacokinetics Flashcards

1
Q

Explain the term pathophysiology

A

Is the study of changes in physiology that occur as a result of a disease or disorder.
Explain: Homeostasis of cell function, by disruption of internal/external. Cell compensates to try and (repair) to reach new state = functioning at a subprime state.
Disruption of homeostasis → Aetiological agent (initial insult) → defective tissue/organ function → defective organ system → related systemic effects
↓ Manifests as signs and symptoms → diagnosis → therapy → prognosis

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2
Q

Define aetiology

A 
Aetiology is the cause of disease,
Biological eg. bacteria, viruses
Chemical: e.g poisons
Nutritional: e.g excess or deficit in diet
Physical: e.g trauma, burns UV
Genetic
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3
Q

Define nosocomial

A

Cause of disease that arise specifically because of exposure to a hospital or clinical care environment. The source must have been acquired while in clinical care

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4
Q

Define iatrogenic

A

Induced inadvertently by clinical practitioners

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5
Q

Define idiopathic

A

Cause of disease are unknown and disease appears to rise spontaneously .

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6
Q

Explain the term pathogenesis.

A

The progression of diseases even so when it does not cause abnormal physiology by themselves but is required for disease progression . All stages from initial exposure to the cause of disease to complete recovery (or not).

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7
Q

Describe the types of clinical

manifestations Signs and manifestations

A

Signs: changes that can be MEASURED by an observer eg swelling, temp, BP
Symptoms: OBSERVATION changes reported by a sufferer eg. pain, dizziness

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8
Q

Define diagnosis

A

A conclusion reached after assessing the signs and symptoms and interpreting the results of diagnostic tests

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9
Q

Define morphology

A

Structure of cells and tissues; alterations may occur as a result of disease. The cell structure is known as histology.

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10
Q

Define histology

A

Cell structure

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11
Q

Define epidemiology

A

The study of diease within population - occurrence, determinants, distributions, and control of disease within a population

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12
Q

Define sporadic

A

Disease that occurs occasionally at irregular intervals

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13
Q

Define endemic

A

Disease that is always present at low frequency within a population

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14
Q

Define hyperendemic

A

an increase level of endemic disease

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15
Q

Define epidemic

A

a sudden increase in a disease above an expected level

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16
Q

Define pandemic diseases

A

a sudden increase in a disease above expected levels over a very wide region or larger population (global)

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17
Q

Define outbreak

A

A sudden and unexpected occurrence of a disease (specific location)

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18
Q

Define index case

A

The first case in a epidemic

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19
Q

Define prevalence

A

Total number of cases, new and existing

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20
Q

Define morbidity

A

Number of ill people in a population per unit of population

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21
Q

Define mortality

A

death rate per units of population

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22
Q

Define drugs and the 3 ways of naming them

A

Drug: substances or products that are used or intended to b used to modify or explore physiological systems. ANy substances that brings about a change in biological function through chemical actions.
Pharmacology - study of interaction between drugs and living organisms.
Theerapeautics - drugs used to diagnosee, prevent and treeat disease or prevent pregnancy

Generic or Non-Propietary, Chemical name, Proprietary or brand/trade name

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23
Q

Explain how drugs are grouped and exemplify

A 
Uses: medicinal or recreational
effect: on the body
Source: synthetic or plant)
Legal status (legal/illegal)
Risk status (dangerous/safe)

HOT TIP:
azoles - antifungals
statins - anticholstrol drugs
mycin - antibacteria

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24
Q

Progression of pathogensis examples, small poxs + melanoma

A

Small pox:
Source → pathway of entry → transmission + retransmission (replication) → moves into organs → Incubation → widespread through organs → toxemic phase →death

Melanoma:
Exposure to UV light → Genetic damage to skin cells → damaged skin cellls, divide rapidly → growth of an abnormal cell mass → local tissue damage → movement of abnormal cells via vasculature → secondary melanoma → loss of organ function = death

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25
Q

Define Syndrome

A

Syndrome: a collection of signs and symptoms that occur together

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26
Q

Define complications

A

Complications: extention of disease or the result of treatment for a disease

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27
Q

Define sequelae

A

Sequelae: lesion or impairments that remain after a disease has been resolved

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28
Q

Outline and describe the phases of a disease’s clinical course (acute)

A

sudden onset but short term

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29
Q

Outline and describe the phases of a disease’s clinical course (chronic)

A

more slowly developing and longer lasting disease often relapsing/remitting

30
Q

Outline and describe the phases of a disease’s clinical course (pre-clinical or prodromal period)

A

Disease present but not yet developed specific symptoms. Vague symptoms

31
Q

Outline and describe the phases of a disease’s clinical course (subclinical)

A

Disease present but displays no symptoms

32
Q

Outline and describe the phases of a disease’s clinical course (Convalescent)

A

In process of recovering

33
Q

Describe Incidence

A

Number of new cases of a disease diagnosed within a particular period

34
Q

Define the process of drug absorption,

correlating with routes of administration

A 
[absorption]1. Oral: drug absorption is the movement of a drug into the blood stream after administration. 
Sublingual via vascular bed under the tongue
Stomach - not an important site
Small intestine - major site for absorption
Rectal suppository - absorption via vascular bed.
2. Topical place on the skin
3. Inhaled into the lungs
4. Parenteral (needle) - subcutaneous
Intramuscular
Intravenous
Intrathecal
Epidural
5. Others 
Intra-articular
Intra-osseous
Intra-peritoneal
Intrapleural
35
Q

Describe ways a drug can cross biological

membranes.

A

Oral: drug absorption is the movement of a dug into the blood stream after administration, primarily in the small intestine. They cross the cell membranes of epithelial cells in the gastrointestinal tract,

36
Q

Define mechanism of action and mode of action of drugs

A

Mechanism of action (MOA) : biochemical interaction through which a drug substance produces it pharmacological affect.

  1. drugs molecular target
  2. the ways drugs interact with that molecular target when bound to it.
37
Q

Define the mode of action of drugs

A

Mode of action (MoA): describes the functional or anatomical changes, at the cellular level resulting from the exposure of a living organism to a drug

38
Q

Outline the 4 typical molecular targets, explaining their cellular functions

A

The molecular target of a drug: molecule in the body usually a regulatory protein associated with a particular disease process. Regulatory proteins respond to endogenous substance: a chemical produced by the body, such as hormones and neurotransmitters → producing a therapeutic effect

  1. Transporter
  2. Enzyme
  3. Ion channel
  4. Receptor
39
Q

Exemplify drugs that do not interact with the typical protein targets.

A

Physiochemical action eg. some inhalant anaesthetics
Physical action: osmotic laxatives, activates charcoal
Some cancer chemotherapeutic and antimicrobial: e.g drugs bind to DNA
others: e.g sunscreens, spermacides

40
Q

Explain the concepts of drug specificity

A

Specificty: how successful a drug is in interacting with only one molecular target having one effect

41
Q

Outline molecular target RECEPTOR explaining their cellular functions

A 
Receptors are proteins that bind specific molecules (lock and key) activating a repsonse within a cell. They are translators of molecular signals from inside or outside a cell. Intracellular → cascade of protein activation or deactivation.
Extracellular receptors ↓
a. Protein G coupled receptor
b. Enzymes-linked receptor
c. Ligand-gated receptor

Intracellular receptors ↓: directly regulate gene expression.
a. steriod hormone receptors

42
Q

Outline molecular target ION CHANNELS explaining their cellular functions

A

Regulate flow of ions (Na+, K+, Ca+) through the plasma membrane. Channel blocker drugs “close the gate” to ions

43
Q

Outline molecular target TRANSPORTER/CARRIER explaining their cellular functions

A

Uses ATP energy (active transport) to move molecules that cannot cross the cell membranes by diffusion

44
Q

Outline molecular target ENZYMES explaining their cellular functions

A

Are biological catalysts that control biochemical reactions therefore physiological responses.

Drugs can interact with enzymes in a number of ways

45
Q

Explain the concepts of drug specificity

A

Specificty: how successful a drug is in interacting with only one molecular target having one effect

46
Q

Outline molecular target ENZYMES explaining their cellular functions

A

Are biological catalysts that control biochemical reactions therefore physiological responses.

Drugs can interact with enzymes in a number of ways

47
Q

Explain the concepts of drug selectivity

A

Drugs favor and bind to one receptor over another

48
Q

Describe ways a drug can interact with molecular targets (possible effects).

A

Agonists: drugs that occupy receptors and activates them → produces a biological responses in the same way that endogenous agonist (naturally made by body). Mimics the natural receptor to bind ‘lock and key’ .
Effects:

Antagonists: Drugs that occupy receptors but do not activate them. Antagonists block receptor activation by agonists → bind by produce no functional response.
Effects: Agonist / Orthostetic agonist - occupies that same binding site as the endogenous agonists. → Produces a response.
Allosteric agonist: Occupies a distinct binding site as the endogenous agonists. ↑ the response in the presence of the endogenous agonist.

Competitive reversible antagonist: compete for binding site. Binds with low affinity so it can bounce off the receptor. Effect can be overcome by ↑ concentration of the receptor agonist.
Competitive irrevrsible antagonist: receptor becomes permanently blocked, The affinity between antagonist and binding site is hight.
Non-competitive antagonist: share the binding site with the agonist. ↓ response.
Allosteric modulator: occupies a different binding site (not the agonists binding site). Modulates (regulates) response (m may ↑or↓)

49
Q

Explain the drug concentration-response relationship, contrasting potency and efficacy.

A

Relationship between the concentration of a drug at a receptor site and the magnitude of the response. EC50 effective concentration is the concentration at which the drug produces 50% of the maximal response.
Maximal efficacy Emax when all the receptors are occupied by the drug.

Potency: how strong the drug is
- Correlated with affinity of the drug for it’s target.
Efficacy: how well the drug does it’s job; the ability of the drug to elicit a response once bound to the receptor

50
Q

Define toxic dose, effective dose, and therapeutic index.

A

Toxic does: Keep giving drug until 50% of people DIE, can damage an organisim
Effective dose: Persons whom have responded to does
Therapeutic index: is a quantitative measurement of the relative safety of a drug. It is a comparison of the amount of a therapeutic agent that causes the therapeutic effect to the amount that causes toxicity.

51
Q
  1. Explain the relevance of knowing the therapeutic index of a drug.
A

Therapeutic index: is a quantitative measurement of the relative safety of a drug. It is a comparison of the amount of a therapeutic agent that causes the therapeutic effect to the amount that causes toxicity.

52
Q

Compare adverse drug reaction, adverse drug event and adverse effects.

A

Adverse effects: unwanted effect that results from activation of a secondary molecular target. May or may not be dose related.

Adverse drug reaction: any response to a drug that is noxious, unintended, and occurs at doses normally and appropriately used in man for prophylaxis, diagnosis, therapy of a disease.

Adverse drug event: Inury resulting from medical intervention related to a drug. Occurs while taking the drug but may not be directly due to the drug, eg operator

53
Q

Explain and contrast drug tolerance from tachyphylaxis.

A

Drug tolerance: When the repeated use of a drug leads to a ↓ in drug effect for same does. May be due to an ↓ in drug metabolism or receptor downre gulation.

Tachyphylaxis (short term, acute, sudden): ↑ doses are ineffective! Sudden irresponsiveness

54
Q

Define drug dependence and withdrawal.

A

The need to use a drug to function normally. may exist when the body has a deficienxy and a drug is needed for survival.. May develop fron continual exposure, leading to body adaptation.

Drung withdrawal: Group of symptoms that occur upon the abrupt discontinuation of ↓ in intake of medications or recreational drugs to which the body was dependent.

55
Q

Explain the concepts of drug affinity.

A

Strength of the bond between a drug and its molecular target. Bonds well to it’s binding site.

Eg. ionic, covalent, or hydron bonding, hydrophobic interactions

56
Q

Explain the concepts of drug affinity.

A

Strength of the bond between a drug and its molecular target. Bonds well to it’s binding site.

Eg. ionic, covalent, or hydron bonding, hydrophobic interactions

57
Q

Outline the 4 processes described by pharmacokinetics.

A

Is the branch of pharmacology concerned with how the body affects a specific drug after administration. Movement of drugs inside the body and the physiological process that acts on the drug once it enters the body
Absorption: how the drug enters the blood
Distribution: where the drug goes in the body
Metabolisim: how the body processes the drug
Excretion: eventually the body gets rid of the drug

58
Q

Describe ways a drug can cross biological membranes.

A

Transporter proteins and channels
move charged or polar molecules
across membranes through pores
lined with hydrophilic domains

59
Q

Discuss factors that may impact drug absorption.

A
  1. Surface for absorption – area of the GIT wall
  2. Blood flow – increased blood supply improves absorption
  3. Formulation – e.g. the type of drug coating
  4. Molecule size – most drugs are small. It’s harder to absorb larger
    molecules such as peptides (like hormones).
  5. Drug concentration gradient – the larger the dose, quicker is
    absorption
  6. Solubility of the drug – non-polar molecules move across
    membranes more rapidly than polar ones.
  7. Ionisation – unionised molecules can cross membranes
    – ionised drugs use transport systems to move drugs from gut to
    blood and from blood to urine
60
Q

Define drug metabolism, explaining roles of phase I and phase II metabolic reactions.

A

Drug metabolism is the term used to describe the biotransformation of
pharmaceutical substances in the body so that they can be more easily
eliminated
• Occurs predominantly in the liver.

Phase I – catabolic reactions
• Tends to make more chemically reactive products
• Uses cytochrome (CYP) P450 family of enzymes
Phase II – anabolic (synthetic) reactions
• Conjugation reactions that tend to result in inactive products.

1. makes the drug more water soluble to increase renal excretion
– pentobarbital → hydroxypentobarbital
2. Inactivates the drug
– procaine → PABA
3. Increase or change the action
– codeine → morphine
4. Activate a prodrug
– Levodopa → dopamine
5. Alter toxicity
– paracetamol → hepatotoxic compound
PHASE 1
Functionalisation
Enzymes make drug
more polar, adding a
functional group
PHASE 2
Conjugation
Different enzymes bind
that functional group to
a polar molecule
61
Q

Explain the role of the P450 enzyme group in drug metabolism.

A

Phase I: functional group added, oxygen, hydrogen, water. ↑ water solubility
Involves; cytochrome (CYP) p450 enzyme family. Main role is to generate a reactive site. Eg, asprin, heroin .
ConjugationL joins modified compind to a polar moleecule. Increases water solubility even more enhancing renal excretion

62
Q

Define bioavailability and hepatic first-pass effect, discussing their relationship.

A

Bioavaliablity: Amount % of the drug that is available to the body to produce a therapeutic effect. The amount of a drug reaching the systemic circulation is dependent on:
1. The amount of drug not actually absorbed.
2. The amount drug inactivated the first time it passed through the liver.
Hepatic first-pass effect: The amount of drug inactivated after passing through the liver for the first time after absorption. Eg loss of active drug molecules.

63
Q

Discuss how chemical substances may interfere with metabolic enzymes

A

Enzyme induction: enzymes and transporters are proteins an ↑ in a proteins expression ↑ it activity. ↓ bioactivaliablity

Induction ↑ expression of enzyme.

Inhibition: result of competition for the active site of an enzyme. ↓ metabolisim of atleast. this affects bioavaliablity by ↑ it

64
Q

Explain how genes influence drug metabolism.

A

Genetic differences between people can influence absorption time, hepatic drug metabolism, clearance and drug effects.

65
Q

Describe how plasma protein binding of a drug affects drug distribution and action.

A

Distribution: Some drugs are carried around the body by plasma proteins. Only free (unbound) drug can exert a therapeutic effect,

  • This may depend on drug/plasma protein affinity.
  • The amount of free drug tends to be constant.
66
Q

Explain the factors affecting drug distribution.

A

Factors that impact on binding:

  1. Number of binding sites
  2. Abnormal plasma protein
  3. drug concerntration
  • Blood supply to tissue
  • Lipid soluable drugs cross membranes
  • Affinity for plasma protein binding
  • Presence of drug transporters

DRUGS WILL NOT GO:
The brain (blood brianbarrier.
The placenta.

Only lipid soluable drugs will pass through thse tissues

67
Q

Explain the factors affecting drug distribution.

A

Factors that impact on binding:

  1. Number of binding sites
  2. Abnormal plasma protein
  3. drug concerntration
  • Blood supply to tissue
  • Lipid soluable drugs cross membranes
  • Affinity for plasma protein binding
  • Presence of drug transporters

DRUGS WILL NOT GO:
The brain (blood brain barrier.
The placenta.

Only lipid soluable drugs will pass through these tissues

68
Q

Define drug clearance and explain why it is it is clinically relevant.

A

Clearance: a measurement of how quickly a drug is eliminated by the body - useful to determine dosage regime
CL = CL hepatic + CL rental + Cl other

69
Q

Define the half-life of a drug and explain why it is clinically relevant.

A

Half-life is the time rquired to reduce th plasma concerntration of the drug to 50% of the original value. Used to determin dosing requirements to reach a steady state. (steady state → the amount of drug administrated = amount od drug eliminated within one dosing interval resulting in a plateau or constant serum level

When a drug is ingested: plasma drug concentration will ↑ until the drug is fully absorbed then ↓ while it is eliminated.
( The area under the curve reflects the time body is exposed to drug aftere dose administration.
Drugs administered intravenously reach a peak concentration sooner. Drugs administered orally take longer to have an effect but stay longer in the system

70
Q

Discuss how renal failure can impact on drug half-life and the risk for drug toxicity.

A

Renal failure results in not being able to eliminate the drug, Therefore remains in blood longer, thus increasing in the blood. The dose should be decreased

71
Q

Discuss how age interferes with drug therapy.

A

Organ fucntion may be comprimised by
OLDER
age = ↑ risk of toxicity.
Absorption: slower gastric emptying.
Distribution: ↓ body water. ↓ increased body fat. ↓ reduced plasama protein. blood-brain barrier more permeable.
Metabolism: ↓ hepatic blood flow,’↓Reduced enzymatic activity.
Excretion: ↓ renal blood flow, ↓atrophic renal tissue.

NEONATES: less than one month old.
- ↓ protective mechanisims
↓ skin is thin and permeable
↓ body fat
↓ stomach lacks acid 
↓ renal excretion is less efficient
↓ regulate temp poorly 
↓ becomes easily dehydrated
↓ delayed maturation of hepatic drug metabolsim enzymes which can lead to drug toxicity
72
Q

Define drug distribution and describe interactions with different body tissues.

A

Distrubution through the blood stream → exits the blood stream through capillary walls. → enters ECF, diffuses to cells → binds to target on cell → (1) DRUG ACTION or enters cell → (2) drug action.

DRUGS WILL NOT GO:
The brain (blood brainbarrier.
The placenta.

Only lipid soluable drugs will pass through these tissues.

Drugs maybe stored in adipose tissue (fat). It has a ↑ affinity for lipid soluable drugs. Acts as a stable reservoir of the drug .

Bone affinity: tetracycline antibiotics absorbed by bone crystal matrix acting as a storage site for teeth: this causes discolouration.
- Bisphosphonates: uses to stablise bone matrix in osteoporosis

BMS291 (9 decks)

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