Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHYL2066 Content > Module 5 - Pharmacology > Flashcards

Module 5 - Pharmacology Flashcards

1
Q

Define Pharmacodynamics and outline its main components

A

= Pharmacodynamics = how drugs affect the body

  • receptors
  • enzyme targets
  • cell signalling
  • membrane channels
  • agonists and antagonists
  • drug interactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define Pharmacokinetics and outline its main components

A

= Pharmacokinetics = how the body affects drugs

  • absorption
  • distribution
  • metabolism
  • excretion
  • pharmacogenetics
  • clinical pharmacokinetics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define Agonist

A

= a substance that promotes a receptor-mediated biological response, often by competing with another substance at the same receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where do agonists bind on the receptor level?

A

= to receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Define Receptor

A

= a molecular (usually protein) structure or site on the surface or interior of a cell that binds with substances such as hormones, antigens, drugs or neurotransmitters with specificity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Define drug specificity

A
  • shape/physiochemical properties of the drug

- shape/physiochemical properties of the target molecule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe agonists at a relatively low concentration

A
  • agonist binds to its receptors, causing physiological changes in the targeted cell
  • obviously, if there are no receptors on cells and tissues, there is no effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe agonists at higher concentrations

A
  • many more of the receptors may be occupied at any given time, leading to a greater physiological effect
  • there will be a concentration range that results in the optimal effect for your patient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe Antagonists

A
  • drugs that are antagonists can also bind, but do not activate the receptor
  • notice that, in this case, the antagonist binds to the same area on the receptor as the agonist did earlier
  • this is called a “competitive antagonist” for the receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe how most drugs are antagonists

A
  • most drugs are antagonists, leading to reduction in the body’s response to a disease, injury etc
  • thus, for many drugs, there is competition between agonist and antagonist, modifying the resulting physiological response
  • by occupying the agonist’s receptor sites, the competitive antagonist physically blocks the sites, reducing the ability of the agonist to bind and cause a response
  • if concentration is sufficient, the agonist could “outcompete” the antagonist drug present
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe how few drugs are irreversible competitive antagonists

A
  • in which some of the receptors become permanently bound to receptors, at the same site as where the agonist binds
  • when the agonist is applied, the maximum number of receptors available is less than 100% as some of them are permanently occupied by the antagonist
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

List and Describe the 4 receptor types in the body

A
  1. Ligand-gated-ion channels (iontropic receptors)
    - Time scale = milliseconds
    - Examples = Nicotinic, ACh receptor
  2. G-protein-coupled receptors (metabotropic)
    - Time scale = seconds
    - Examples = muscarinic, ACh receptor
  3. Kinase-linked receptors
    - Time scale = hours
    - Examples = cytokine receptors
  4. Nuclear receptors
    - Time Scale = hours
    - Examples = oestrogen receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe Ionotropic receptors (ligand-gated-ion channels): Nicotinic Receptor

A
  • 5 transmembrane units
  • endogenous agonist is acetylcholine (ACh)
  • 2 molecules of ACh bind, opening Na+ channels
  • ions flow down concentration gradient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe G-protein-coupled receptors: beta-adrenoreceptor

A
  • 7 transmembrane units
  • largely composed of alpha helices
  • endogenous agonist is adrenaline
  • agonist binding activates G-proteins
  • extracellular domain interacts with agonist
  • intracellular domain interacts with G-protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do G-protein coupled receptors signal? (4 steps)

A
  1. Resting state
  2. Occupied recetor
  3. Activation of downstream targets
  4. GTP hydrolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

List the 7 step process of G-protein coupled receptor Adrenaline

A
  1. Signal molecule binds to G-protein coupled receptor
  2. It facilitates a G-protein to gain energy from a GTP molecule, converting it to GDP (via same process as ATP= ADP + Pi)
  3. The G-protein uses this energy to send a signal to adenyl cyclase
  4. Adenyl cyclase converts ATP to cyclic AMP (cAMP)
  5. Phosphodiesterase regulates the duration of activity of cAMP by converting it to its inactive form, AMP
  6. One of cAMP’s various activities is that it can activate protein kinase A (PKA)
  7. PKA can in turn produce cellular responses specific to the signal molecule (adrenaline in this case)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the Amplification of G-protein coupled receptor signalling (8 steps)

A
  • this can lead to a rapid response as well as an increase in molecular products
    1. Reception: Binding of epinephrine to G-protein-linked receptor = 1 molecule
    2. Transduction: Inactive G-protein -> active G-protein = 10^2 molecules
    3. Inactive adenyl cyclase -> active adenyl cyclase = 10^2 molecules
    4. ATP -> cyclic AMP = 10^4 molecules
    5. Inactive protein kinase A -> active protein kinase = 10^4 molecules
    6. Inactive phosphorylase kinase -> active phosphorylase kinase = 10^5 molecules
    7. Inactive glycogen phosphorylase -> active glycogen phosphorylase = 10^6 molecules
    8. Response: Glycogen -> glucose-1-phosphate = 10^8 molecules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the 5 step process of Nuclear Receptors

A
  • receptors may also be present within the cells and on the DNA itself, leading to long-term changes due to protein synthesis
    1. The steroid hormone testosterone passes through the plasma membrane
    2. Testosterone binds to a receptor protein in the cytoplasm activating it
    3. The hormone-receptor complex enters the nucleus and binds to specific genes
    4. The bound protein stimulates the transcription of the gene into mRNA
    5. The mRNA is translated into a specific protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe how the binding of an agonist to its receptor(s) has structural specificity leading to affinity (attraction) and binding is mostly reversible

A
  • the binding of an agonist to its receptor(s) has structural specificity leading to affinity (attraction) and binding is mostly reversible, analogous to binding of an enzyme’s active site and substrate
  • factors such as charge, shape, hydrophobic/hydrophillic regions, etc, are crucial for binding to occur
  • in the case of a receptor, the binding of agonist causes small changes in the receptor’s shape, potentially leading to activation of a second messenger mechanism, such as ion movement or GPCR activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe agonist-receptor interaction and how they are concentration-dependent

A

[D] + [R] -> K1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe binding curves: measures of affinity

A
  • the Kd value can be thought of as the concentration at which 50% of the receptors are bound to the agonist/drug
  • we can see this physiological as the Effective Concentration for 50% response (EC50)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe the inverse relationship between Kd and affinity

A
  • the smaller the Kd value, the greater the affinity the drug has for its receptor site
  • conversely, the larger the Kd value for a drug, the lower the affinity it has for its receptor site
  • it is very important to remember that virtually all drugs lose their binding selectivity if their concentration increases, as binding may occur at other receptor types, resulting in undesired side effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe how binding the receptor is a key pharmacodynamic interaction

A
  • binding to receptor isn’t enough, the drug or agonist must also have intrinsic activity, the ability of a drug to induce changes in receptor structure leading to alterations in cellular activity. Often the exact cause of intrinsic activity is unknown
  • this is why not all drugs stimulate their receptors to the same extent, even if they are binding to the same sites, they may have different intrinsic activities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe how agonists are compared: Potency and Efficacy

A

Relative Potency of two Agonists:
- compare EC50 values

Relative Efficacy of two Agonists:
- compare fractional responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is an important thing to remember about antagonists

A

= receptor antagonists bind to receptors and do not cause a response themselves, instead they prevent or alter the binding of agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe Competitive antagonist on its own

A
  • the high affinity competitive antagonist binds to the receptor, but does not activate the effectors
  • notice that it binds to the same area on the receptor as the agonist did earlier
  • no concentration response curve is possible, as there is no response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe competitive antagonist + agonist

A
  • by occupying the agonists receptor sites, the competitive antagonist physically blocks the sites, reducing the ability of the agonist to bind and cause a response
  • this leads to a reduction in the effect of the agonist at each concentration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Describe agonists at high concentrations

A
  • at high concentration, the agonist can outcompete with the antagonist and eventually reach Emax
  • when the [full agonist] is high enough, it can compete effectively with the antagonist and thus bind enough receptors to produce a significant response
  • the odds of the antagonist binding to the receptor become virtually zero as there is so much agonist present
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe irreversible competitive antagonism

A
  • some of the receptors become permanently bound to receptors, at the same site as where the agonist binds
  • when the agonist is applied, the maximum number of receptors available is less than 100% as some of them are permanently occupied by the antagonist
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe non-competitive antagonism

A
  • non competitive antagonism can also occur and this involves an antagonist interfering in some way with either affecting the shape of the agonist’s binding site on the receptor or by interfering with the effector system used by the agonist
  • either at the level of the receptor itself, reversibly or irreversibly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Describe 3 other types of antagonism

A
  1. Chemical antagonism
    e. g. charcoal given in overdose
  2. Pharmacokinetic antagonism
    - competition for absorption
    - up-regulation of metabolic enzymes
  3. Physiological antagonism
    - activation of two pathways with opposing effects
    e. g. bronchoconstriction and bronchodilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

True or False: Some drugs can act without binding to a receptor

A

= false

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

True or False: Efficacy is the amount of drug needed to produce an effect

A

= false; concentration (x-axis) is the amount of drug, efficacy is the effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

True or False: Affinity is the attraction measured between two drug molecules

A

= false; affinity is between the receptor and the drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

True or False: Agonists are drugs which may bind to receptors to cause a physiological response

A

= true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

True or False: Partial agonists have affinity for receptors, but partial efficacy

A

= true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

True or False: GPCRs signal at a faster rate than receptors containing ion channels

A

= false

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

True or False: Antagonists have efficacy, but little to no affinity for receptors

A

= false; antagonists have no effect (no efficacy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

True or False: Pharmacodynamics is the study of absorption, destruction, metabolism and elimination of drug from the body

A

= false; ADME is pharmacokinetics not pharmacodynamics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How does the body deal with drugs that are taken?

A

Absorption: how a drug gets into the body
Distribution: how a drug moves around the body
Metabolism: how a drug is changed in the body
Excretion: how a drug is removed from the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Describe how crossing membranes is a major challenge of drugs

A
  • size is a factor, as smaller compounds can more easily cross the cell membrane
  • lipophillicity (uncharged non polar) is an advantage, charge is not
  • uncharged molecules cross membranes; pH may affect this - most drugs are weak acids or weak bases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Describe routes of administration

A
  • routes are optimised for delivery of required concentrations of drug, taking solubility and chemical factors, as well as adverse effects into account
  • Enteral: absorption through the GI tract: e.g. oral, rectal
  • Parenteral: all other routes: e.g. injection, sublingual, inhalation, topical
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

List advantages and disadvantages of oral administration

A

Advantages:

  • convenient
  • ~75% absorbed in 1-3 hours
  • slow release formulation

Disadvantages:

  • some drugs not well absorbed
  • irritation to gastric/intestinal mucosa
  • food can delay/affect absorption
  • much slower absorption than parental
  • inactivation by ‘first-pass’ metabolism by liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

List advantages and disadvantages of rectal administration

A

Advantages:

  • avoids ‘first-pass’ metabolism
  • reduces vomiting/nausea
  • good when patient is unconscious/seizures
  • local inflammation (e.g. haemorrhoids)

Disadvantages:

  • inconvenient
  • absorption often incomplete
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Describe metabolism by liver hepatocytes

A
  • drugs that are absorbed from the gut reach the liver via the hepatic portal vein before entering the systemic circulation. Some drugs may have low bioavailability/distribution due to this first-pass effect
  • some drugs can be given as pro-drugs, relying on the body’s metabolic processes to make an active metabolite
  • some metabolites are active, most are inactive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Describe oral availability

A
  • oral availability (F) is the fraction of drug that reaches the systemic circulation after oral ingestion. It is determined by ‘absorption’ and ‘first-pass’ metabolism
  • absorption refers to the ability of a drug to cross the gut wall into the portal vein
  • first pass metabolism describes presystemic drug elimination and can occur in the gut wall, portal vein or liver. The liver is usually the most important contributor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Define bioavailability

A

= fraction of oral dose that reaches systemic circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

List advantages and disadvantages of the 4 types of injections to avoid first-pass metabolism

A

Advantages:

  • rapid onset, compared to oral (intravenous>intramuscular>subcutaneous)
  • drugs are not broken down by acid/enzymes as in the gut
  • first pass metabolism in the liver is less of a problem

Disadvantages:

  • less convenient (needs a skilled person)
  • risk of infection
  • more toxic (higher peak blood levels)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Describe non-needled administration: Sublingual

A
  • dissolve tablet under the tongue
  • good vascularisation
  • rapid absorption into bloodstream
  • no first pass metabolism in the liver
  • e.g. anti-anginal drug nitroglycerin (vasodilator)
  • absorbed rapidly
  • straight to the heart
  • can’t be given orally
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Describe non-needled administration: Topical

A
  • direct application to diseased or injure site
  • require lower overall doses
  • reduced systemic toxicity
  • skin: few drugs penetrate skin readily
  • patches work well: nicotine, scopolamine, fentanyl
  • eyes, ears, nose, vagina
  • local effect required (e.g. corticosteroids)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

List 3 sites of absorption

A
  • GI tract
  • lungs
  • skin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Describe absorption across membranes

A
  • GI tract
  • blood brain barrier
  • cell membrane
  1. Passive diffusion: passage along concentration gradient
  2. Facilitated transport: involves carriers or transporters
53
Q

Describe Passive Diffusion (most important mechanisms for most drugs)

A
  • passive diffusion is the movement of substances across cell membranes without any energy needed
  • sufficient concentration and time are needed if the drug molecules can pass through the membrane
54
Q

Describe how the distribution of drugs requires crossing of barriers

A
  • principles same as those for absorption:
  • drugs are delivered from site of injection/absorption to site of action via the blood
  • drugs generally diffuse into peripheral tissues depending on their physicochemical characteristics
  • only free (unbound) drugs can diffuse out of the blood circulation into peripheral tissues
  • tissues which receive the greatest amount of blood may receive the greatest amount of drug over time
55
Q

Describe Metabolism

A
  • drugs (mostly) are foreign compounds (xenobiotics)
  • the purpose of metabolism of xenobiotics to:
    1. Increase the rate of excretion
    2. Decrease likely toxicity
  • drug molecules are enzymatically processed using the same pathways as “natural” compounds
  • a drug may have its actions increased or decreased
  • individual variation, genetically determined, can be significant
  • may be multiple routes of metabolism
  • may not terminate drug action initially
  • may take place in various places, BUT liver is prime site
  • not constant: can be changed by other drugs, making a drug interaction
  • metabolism is what the body does to a drug
56
Q

What are the two major types of enzymatic reactions?

A
  1. Phase 1 reactions
    - oxidations (cytochrome P450)
    - reduction (reductases)
    - hydrolysis (esterase’s)
  2. Phase 11 reactions
    - add water soluble moiety to drug
    * glucuronide
    * glutathione
    * sulfate
    * acetate
57
Q

Describe Phase 1 Reaction: Oxidation (cytochrome p450s)

A
  • more than 50 different forms of cytochrome p450 enzymes exist, with different substrate specificities and mechanisms
  • most lipophilic drugs and environmental chemicals are substrates for one or more forms of p450
58
Q

Describe Phase 1 Reaction: Reduction and hydrolytic reactions (reductases and esterase’s)

A
  • each reaction, whether oxidation, reduction or hydrolysis, increase the water solubility of the resulting metabolite
59
Q

Describe Phase 11 reactions

A
  • glucuronidation
  • sulfation
  • acetylation
  • glutathione conjugation
  • methylation

*Addition of a water-soluble moiety (therefore, involves a co-factor)

60
Q

Describe Phase 11 metabolites in general

A
  • more highly ionised
  • more water soluble
  • more likely to be excreted by the liver and kidneys
  • less pharmacologically active
  • less toxic
61
Q

List some factors affecting drug metabolism

A
  • genetics: e.g. metabolism of codeine to morphine
  • age: aged patients and children may metabolise at different rates compared to adults
  • gender: e.g. women are slower ethanol metabolisers
  • other drugs being taken: induction or inhibition of P450s
  • food: charcoal grill ++ CYPIA2 or grapefruit juice – CYP3A4
62
Q

Describe how many drugs can affect the metabolism of other drugs by inhibiting or reducing CYP enzyme activity

A
  • this is a potential problem when drugs are given at the same time which are both metabolised by the same enzymes (cytochrome p450s)
  • other drugs may induce or stimulate CYP function, which may stimulate breakdown of medications
    i. e. grapefruit juice slows the breakdown of multiple drugs by inhibiting cytochrome CYP3A4, potentially leading to adverse effects
63
Q

Describe dose adjustment

A
  • liver metabolism and kidney clearance of most drugs is crucial to avoid toxicity
  • drugs are eliminated by excretion unchanged through the kidneys, or by metabolism to an inactive product usually in the liver
  • the fraction excreted unchanged (fu) defines the renal elimination, while (1-fu) describes the metabolic elimination
64
Q

Describe renal function

A
  • poorly developed in neonates and tends to decrease in the elderly
  • this may prolong the time course and efficiency of excretion
  • also, when a patient has chronic renal failure, excretion of drugs is almost non-existent and in patients with cardiac failure, reduced blood flow to the kidneys may decrease renal excretion of unchanged drugs and metabolites
  • monitoring of patients is a must in these situations
65
Q

Describe factors impacting oral dosing of medication

A
  • one dose of drug will give you a time-contraction curve
  • this means that you know the time the drugs needs for ADMA, and that you know the therapeutic drug concentration required as well
  • but you want to keep the drug concentration in the therapeutic range to treat the disease
66
Q

Describe therapeutic range/steady state

A
  • medications need to be taken on time per instructions
  • this helps with maintaining the steady-state concentration of drugs in your body, while the drug is going through ADMA the balance between dose and timing is structured so that plasma concentrations are, on average, constant during treatment
67
Q

True or False: Intramuscular injection of drugs is much faster for patient treatment than intravenous injection

A

= false; intravenous is faster than intramuscular
- intravenous travels directly through bloodstream, whereas, intramuscularly creates a ‘depot’ where drug can be released more slowly over time

68
Q

True or False: Active transport mechanisms are responsible for most aspects of drug distribution in the body

A

= false; passive diffusion is the main mechanism

69
Q

True or False: Oxidation of drugs in the body is usually carried out by hepatic microsomal enzymes

A

= true; oxidation occurs via hepatic microsomal enzymes (also called cytochrome P450s)

70
Q

True or False: Drug metabolism occurs predominantly in the liver

A

= true

71
Q

True or False: Phase 1 reactions include hydrolysis and oxidation

A

= true; Phase 1 reactions includes oxidation, reduction and hydrolysis

72
Q

True or False: Phase 11 reactions includes hydrolysis and oxidation

A

= false; Phase 11 reactions include glucuronidation, sulfation, acetylation, glutathione conjugation, methylation

73
Q

True or False: It is important to know what other medications a patient may be taking when adding new drugs to their treatment

A

= true

74
Q

True or False: If you miss a dose in treatment, it is 100% fine if you simply double the dose when you remember

A

= false; this can lead to toxic dosages

75
Q

How might dosages of medications be modified if a patient has liver issues?

A

= if patient has liver issues, metabolism (phase 1 and 11) may not be occurring properly. Normal levels of drugs may be toxic due to the fact that there is a breakdown in metabolism. In this case, a patient should be given a LOWER dosage to mitigate possible toxicity

76
Q

Define High Blood Pressure (HBP)

A

= blood pressure over 140/90 mmHg, with emphasis on the diastolic pressure being greater than 90mmHg

77
Q

Describe Antihypertensives

A

= a very large range of diverse drugs can be used to assist and usually a combination of drugs is the best approach:

  • diuretics
  • directly acting vasodilators
  • calcium channel blockers
  • sympathetic antagonists (peripheral and central)
  • beta blockers
78
Q

Describe Calcium Channel Blockers (e.g. Nifedipine and Verapamil)

A
  • inhibit Ca ion movement into vascular and cardiac muscle
  • interferes with inwards movement of calcium ions
  • affects depolarisation and contraction processes
  • relaxant effects mainly on arteriole smooth muscle
  • results?
  • peripheral and coronary vasodilation
  • decrease heart rate and contractility
79
Q

Describe Beta Blockers

A
  • the beta drugs act predominantly on the heart tissue, if they are selective for antagonists for beta-1 adrenergic receptors
  • results?
  • reduce heart rate
  • reduce ventricular contractility
80
Q

Describe Myocardial Ischaemia

A
  • reduced blood flow through coronary arteries
  • leading to inadequate oxygenation of heart myocytes
  • leading to chest pain (short term) and to myocyte cell death (long term)
81
Q

Describe Coronary Artery Disease

A
  • atherosclerosis
82
Q

Define Stable Angina and describe how it can be treated

A

stable angina= predictable chest pain experienced with exertion due to underlying narrowing of the coronary vessels by atheroma (accumulated fatty deposits and scar tissue)

Treat by targeting cardiac work and blood supply (organic nitrates, vasodilators, beta blockers); underlying atheroscelorosis (statins); anti-thrombotic therapy (aspirin)

83
Q

Define Unstable Angina and describe how it can be treated

A

unstable angina= pain occurring with reduced exertion, culminating in pain at rest. Similar pathology to a myocardial infarction

Treat with anti platelet drugs, organic nitrates

84
Q

Define Myocardial Infarction and describe how it can be treated

A

myocardial infarction= sudden occlusion of a coronary vessel leading to death of cardiac tissue due to oxygen deprivation. The location and size of the block determines the extent of the dame

Treatment: restore myocardial flow by physical and pharmacological means

85
Q

List a pro and con for Stents

A

Pro: best treatment if emergency
Con: facilities and personnel are needed

86
Q

Describe Coronary Artery Bypass Grafting

A
  • surgical procedure performed to relieve angina and reduce risk of death
  • arteries or veins from elsewhere in the body are grafted to coronary arteries to bypass atherosclerotic narrowing and improve blood supply to the coronary circulation to the myocardium
87
Q

Describe Congestive Heart Failure

A
  • the inability of the heart to supply adequate nutrients to the metabolising tissues of the body; it simply cannot pump effectively or efficiently
  • lethal disease with a 5 year survival rate for 25% of patients after first hospitalisation
  • very complex disease
88
Q

Describe Left Heart Failure

A
  • blood accumulates in pulmonary circulation, leading to pulmonary congestion and fluid in the lungs
89
Q

Describe Right Heart Failure

A
  • accumulates in venous circulation causing organ congestion and peripheral oedema
90
Q

Describe the pathophysiology of heart failure

A
  • cardiac output (CO) decreases in heart failure
  • one strategy would be to increase heart function by increasing adrenaline
  • long term, though, this is not a good idea as vasoconstriction is increased along with CO and the workload on the heart is increased
  • activation of adrenal medulla leads to activation of reninangiotensin system (RAS)
  • long term, this is not good either as RAS leads to retention of salt and water, leading to congestion and oedema
91
Q

Describe treatment of heart failure

A
  • improve the ability of the heart muscle to contract
  • decrease the workload of the heart (vasodilators and diuretics)
  • the most successful treatments, defined as improved survival, all reduce cardiac workload
  • this usually involves a mixture of medications
92
Q

List drugs used in Heart Failure

A
  • positive inotropic agents: digoxin
  • vasodilators: ACE inhibitors, nitrates
  • diuretics
  • beta blockers
93
Q

Describe Positive Inotropic Agents: Digoxin/Digitalis

A
  • inhibition of the Na-K pump impairs exchange between sodium and calcium ions indirectly; elevated calcium ions increase the force of myocyte contraction;
    stronger myocardial contract - improved cardiac efficiency = increased cardiac output
94
Q

Describe ACE inhibitors

A
  • lower blood pressure and increase blood to heart
  • dilated artery = lower blood pressure
  • opens coronary arteries
  • ACE inhibitors stop angiotensin production
95
Q

Describe Diuretics

A
  • the use of diuretics improves kidney function such that oedema is relieved
  • by reducing swelling in the organs and limbs, the work of the heart is reduced significantly
  • diuretics are often combined with all other forms of heart failure treatment
96
Q

Describe the use of beta-blockers in heart failure

A
  • uncertain evidence, but it has been suggested use of beta blockers may somehow protect the heart from harmful stimulatory effects of noradrenaline and adrenaline
97
Q

Describe the 4 classes of the New York Heart Association and Heart Failure Management

A

Class 1: Cardiac disease, but no symptoms and no limitation in ordinary physical activity (e.g. shortness of breath when walking, climbing stares)
Treatment/management = educate

Class 2: Mild symptoms (mild shortness of breath and/or angina) and slight limitation during ordinary activity
Treatment/management=
- ACE inhibitors
- beta blockers

Class 3: Marked limitation in activity due to symptoms, even during less than ordinary activity (e.g. walking short distances [20-100m]). Comfortable only at rest
Treatment/ management= 
- ACE inhibitors
- Diuretic
- Digoxin
- beta blockers
- rest

Class 4: Severe limitations. Experience symptoms even while at rest. Mostly bed bound patients.
Treatment/management=
- Phase 111 drugs + add diuretics or increase dose NG also Hydral, Amlod or Nitroprusside, Oxygen Dobutamine, Centesis

98
Q

List the drugs used in Hypertension

A
  • beta blockers

- calcium blockers

99
Q

List the drugs used in Angina

A
  • beta blockers
  • calcium blockers
  • nitrates
100
Q

List the drugs used in Heart Failure

A
  • vasodilators
  • diuretics
  • beta blockers
  • positive inotropic agents
  • ACE inhibitors
101
Q

TRUE OR FALSE: Hypertension is generally classified as having a diastolic value greater than 90 mmHg

A

= true

102
Q

TRUE OR FALSE: Hypertension may be treated by beta agonists to maximise heart function and cardiac output

A

= false; beta agonists promote greater hypertension in the heart

103
Q

TRUE OR FALSE: Angina is commonly caused by inadequate oxygenation of heart muscle, resulting in pain

A

= true

104
Q

TRUE OR FALSE: Vasodilators decrease workload on the heart muscle

A

= true; by reducing peripheral resistance

105
Q

TRUE OR FALSE: beta receptor agonists cause an increase in heart rate by working through beta-one receptors

A

= true

106
Q

TRUE OR FALSE: Digitalis works by blocking the Na-Ca exchange in the cardiomyocyte membrane

A

= false; digitalis blocks Na-K pump which impairs Ca ion transfer out of membrane
Increased build-up of Ca ions leads to a stronger, full, less erratic heart beat

107
Q

Describe Asthma

A
  • the inside lining of the airways becomes red and swollen (inflammation)
  • extra mucous may be produced
  • the smooth muscles around the airways tighten (bronchoconstriction)
  • intermittent attacks of wheezing, shortness of breath and regular coughing events
  • these lead to an increase in residual volume and a reduction in forced expiratory volume
108
Q

What factors may trigger an asthma attack?

A
  • allergens: moulds, dust, animal dander, pollen, food, pests (dust mites, cockroaches)
  • irritants: secondhand smoke, strong doors, ozone, chemicals, perfume
  • exercise: cold and dry air
  • viral infections
  • some causes are unknown and are non-allergic
  • genetic factors also play a role in our response to potential allergens
  • one of the best methods of allergic asthma management is simply minimising exposure to allergens
109
Q

Describe the pathogenesis of Early Phase Asthma

A
  • bronchoconstriction
110
Q

Describe the pathogenesis of Late Phase Asthma

A
  • inflammation
  • mucous hypersecretion
  • eosinophilic infiltration
  • elevated IgE levels
  • subepithelial fibrosis
  • airway hyper-responsiveness
111
Q

Describe pharmacokinetics of inhaled medications

A
  • delivery of medication “topically” to the lungs via several tools, such as inhalers
  • many of the medications for asthma treatment would have serious side effects if delivered systemically (e.g. inhaled corticosteroids, First pass metabolism also reduces side effects)
  • maximum delivery of drugs to site of action (10-20%) [with spacer this can be doubled]
  • rapid onset of action as absorption/distribution avoided. Lower drug needed to reach desired concentration in the lungs than if given systemically
  • particle size is also a critical factor - the larger the particles, the more likely that they will settle in upper airways. Smaller particles may remain suspended and then exhaled
112
Q

Describe the Pressurised Metred-Dose Inhaler (pMDIs) method of delivery

A
  • propellant gas is likely to be HFA (ozone compliant)
113
Q

Describe the Nebuliser method of delivery

A
  • drug is inhaled during tidal breathing and higher doses can be given
  • good in case of attacks
114
Q

Describe the Spacer method of delivery

A
  • used between the inhaler and the patient, allows of inhaled particles to slow in speed and for propellant to dry, rendering the medication smaller in volume
    This combined effect reduces the swallowing of drug and increases the depth of the airways reaches. Helps with young patients as well
115
Q

Describe the Dry Powder Inhaler (DPI) method of delivery

A
  • tablet is crushed and inhaled
116
Q

List 4 Reliever medications of asthma

A
  1. Short acting beta-agonists
  2. Long acting beta agonists
  3. Methylxanthines
  4. Muscarinic Receptor Antagonists
117
Q

List 3 Preventer medications of asthma

A
  1. Leukotriene receptor antagonists
  2. Glucocorticoids
  3. Anti-IgE antibodies
118
Q

Describe SABAs including:

a) agonist or antagonist ?
b) mechanism of action
c) duration of action
d) what does it do?
e) possible side effects
f) active drug component

A

Short Acting Beta-2 Agonists (SABAs)

a) Agonist
b) Short term stimulation of beta-2 receptors on smooth muscle lining of the bronchioles. Effective in early phase asthma
c) 3 – 5 hours. With 1 – 5 minutes onset of action
d) Symptomatic relief of bronchospasms and constriction
e) Increased heart rate, muscle tremors, feeling light-headed or shaky, headache
f) Salbutamol

119
Q

Describe LABAs including:

a) agonist or antagonist ?
b) mechanism of action
c) duration of action
d) what does it do?
e) possible side effects
f) active drug component

A

Long Acting Beta-2 Agonists (LABAs)

a) Agonist
b) Long term stimulation of beta-2 receptor on smooth muscle lining of the bronchioles
c) 12+ hours. With 30 – 45 minutes onset of action
d) Used prophylactically for asthma treatment
e) Increased heart rate, muscle tremors, feeling light-headed or shaky, headache
f) Salmeterol

120
Q

Why choose long-acting relievers ?

A

= generally these are prescribed for individuals whose asthma is poorly controlled and who have been on inhaled corticosteroids for more than 3 months

121
Q

Describe Methylxanthines including:

a) agonist or antagonist ?
b) mechanism of action
c) duration of action
d) what does it do?
e) possible side effects
f) active drug component

A

Methylxanthines

a) Antagonist
b) Inhibits phosphodiesterase (PDE), may reduce transcription of inflammatory genes. Stimulates the CNS and increases breathing rate
c) 12+ hours
d) Increases cAMP (cyclic AMP) and promotes bronchodilation
e) Cardiac dysrhythmia, GI disturbances, seizures, narrow therapeutic window, P450 metabolism
f) Theophylline

122
Q

Describe Muscarinic Antagonists including:

a) agonist or antagonist ?
b) mechanism of action
c) duration of action
d) what does it do?
e) possible side effects
f) active drug component

A

Muscarinic Antagonists
a) Antagonist
b) Blocks M3 receptors, preventing parasympathetic contraction of smooth muscle. Used with beta-2 agonists or steroids in acute severe asthma
c) 2 – 3 hours
d) Short acting bronchodilator
Inhibits bronchoconstriction and mucous secretion
e) Limited side effects, as not permeable into systemic circulation. Bitter in taste. Nebulised patients of age may develop glaucoma if using face mask
f) Ipratropium

123
Q

Describe Leukotriene Receptor Antagonist (LTRAs) including:

a) agonist or antagonist ?
b) mechanism of action
c) duration of action
d) what does it do?
e) possible side effects
f) active drug component

A

Leukotriene Receptor Antagonist (LTRAs)

a) Antagonist
b) Taken orally to reduce leukotriene activity. Relaxation of smooth muscle. No effect on inflammation
c) 12+ hours
d) Relaxes airways
e) GI irritation
f) Montelukast

124
Q

Describe Inhaled Corticosteroids (ICS) including:

a) agonist or antagonist ?
b) mechanism of action
c) duration of action
d) what does it do?
e) possible side effects
f) active drug component

A

Inhaled Corticosteroids (ICS)
a) Antagonist
b) Inhibition of release of immune mediators from macrophages, T-cells and eosinophils. Reduction of mucous secretion and reduced inflammation
c) 18 – 36 hours
d) Reduces mucous secretion and inflammation
e) Oral thrush, cataract risk, reduced bone density, glaucoma, reduced growth rate in children
f) Beclomethasone
Fluticasone
Prednisone

125
Q

Describe Anti-IgE Antibodies including:

a) agonist or antagonist ?
b) mechanism of action
c) duration of action
d) what does it do?
e) possible side effects
f) active drug component

A

Anti-IgE Antibodies

a) Antagonist
b) Reduces stimulation of mast cells and releases anti-inflammatory mediators
c) 2 – 4 weeks
d) Controls/reduces inflammation
e) Rash, itching, joint pain, nausea, dizziness, cold-like symptoms
f) Omalizumab

126
Q

TRUE OR FALSE: The early phase of an asthma attack is caused by smooth muscle constriction of the airways

A

= true

127
Q

TRUE OR FALSE: Early phase treatment is best done using relievers, which are glucocorticoid based treatments

A

= false; early phase is best treated using relievers, but should be beta-2 based receptor agonists

128
Q

TRUE OR FALSE: Late phase asthma attacks are effectively managed with beta-2 receptor agonists

A

= false; preventers should be used as they are anti-inflammatory

129
Q

TRUE OR FALSE: A spacer may be used by asthmatics to improve inhalation of the drug at a constant rate and reducing loss on tongue, mouth and throat

A

= true

PHYL2066 Content (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions