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Phase 2 - CVR > Week 4 > Flashcards

Week 4 Flashcards

(101 cards)

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1
Q

What is pulmonary fibrosis

A

Scarring of the lung tissue leading to thickening of alveolar walls. Reduction in surface area for gas exchange

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2
Q

What is emphysema

A

Walls between alveoli are breaking down and the air sacs converge into one big space. Reduction in surface area for gas exchange

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3
Q

what is contained in the conducting portion

A

nasal cavities to terminal bronchioles

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4
Q

what is contained in he respiratory portion

A

respiratory bronchioles to alveoli

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5
Q

describe respiratory epithelium

A

ciliated pseudostratified columnar epithelium with goblet cells.

warms, humidifies and filters incoming cells

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6
Q

what is the mucociliary escalator system

A

movement of particles by cilia up the throat to the pharynx where it is taken up by mucous and swallowed

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7
Q

Discuss the correlation between the trachealis muscle and air speed

A

The trachealis (smooth) muscles joins the two ends of the C-shaped cartilage of the trachea posteriorly. It is what contracts and relaxes to change the diameter of the lumen. WHen it contracts, ie when coughing, this increases the speed of air flow and helps to expel any debris.

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8
Q

What else (not goblet cells) produces mucous

A

Seromucous glands found in the submucosa

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9
Q

Describe the structure of bronchioles

A

Do not posess cartilage or submucosal walls

Smooth muscle

Simple ciliated columnar epithelium

As bronchioles decrease in size, epithelium becomes simple cuboidal, few cilia, more club cells

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10
Q

function of club cells

A

secrete anti-inflammatory, anti-microbial and immune-regulating proteins

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11
Q

Describe type 1 pneumocytes

A

Flattened (squamous) with flat, dark, oval nuclei and very thin cytoplasm

Primarily involved in gas exchange

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12
Q

Describe type 2 pneumocytes

A

Cuboidal cells that bulge into the alveolar space
Produce surfactant

Progenitor cells that can proliferate to replace both types of pneumocytes

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13
Q

Describe the tunica intima

A

Endothelium + subendothelial connective tissue

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14
Q

Describe the tunica media

A

Contains muscle tissue

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15
Q

Describe the tunica adventitia

A

Collagen and elastic fibres in connective tissue
Vasa vasorum

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16
Q

Describe epicardium

A

Mesothelium + thick connective tissue layer

Mesothelial cells = visceral layer of serous pericardium

Contains abundant adipose tissue, which surrounds larger vessels

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17
Q

Describe myocardium

A

Thickest and middle layer of heart wall

Cardiac muscle (striated and branching with a central nucleus), connective tissue and abundant capillaries

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18
Q

Describe endocardium

A

Endothelium (simple squamous epithelium) + thin connective tissue layer

Connective tissue contains purkinje fibres and small blood vessels

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19
Q

What do intercalated discs of cardiac muscle contain

A

Gap junctions which help synchronise contractions of cardiac muscle cells

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20
Q

Appearance of purkinje fibre histology

A

Specialised cardiomyocytes

Appear paler than cardiomyocytes due to having fewer myofibrils

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21
Q

Describe elastic arteries

A

Conduct high pressure blood flow out of the heart (pulmonary artery, aorta, common carotid)

Characterised by numerous bundles of elastic fibres in tunica media

Enable the walls to resist pressure and recoil to maintain arterial pressure during diastole

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22
Q

Describe muscular arteries

A

Distribute blood to small arteries in the organs of the body

Thick tunica media dominated by smooth muscle, little elastic tissue

Enables them to contract to maintain bp away from heart

IEL and EEL

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23
Q

Describe Internal elastic lamina

A

IEL forms a clear boundary between the tunica intima and tunica media

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24
Q

Describe external elastic lamina

A

EEL forms a boundary between the tunica media and tunica adventitia

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25
Describe the histology of veins
Veins have a tunica intima, media and adventitia however these layers are less obvious compared to arteries In general, the tunica media of veins is thinner than adventitia and the smooth muscle cells are not as well organised as in arteries Valves
26
What is Pharmacokinetics and list its four aspects
"What the body does to the drug" following administration -Absorption -Distribution -Metabolism -Excretion
27
3 factors determining the route of drug administration
Properties of the drug Patient factors Therapeutic objectives
28
Describe the enteral route of drug delivery
Delivery of the drug via the GI tract with a system wide effect - Oral - Rectal - NasoGastric - Buccal
29
Describe the parental route for drug delivery
Delivery of the drug directly into the systemic circulation with a system-wide effect Drugs that are poorly absorbed or unstable in GI tract - Intravenous - Intramuscular - Subcutaneous - Inhalation
30
Describe the Topical route of drug delivery
Deliver drugs to specific tissues with local effect - Cutaneous - Ocular - Respiratory - Luminal
31
Advantages of oral administration
Route convenient, safe and economical Self-administration Suitable for prolonged administration Toxicities/Overdose may be overcome
32
Disadvantages of oral administration
Absorption: Variable affected by stomach enzymes, contents & motility. Susceptible to first-pass metabolism Onset of action is delayed Patient compliance is necessary
33
Describe passive diffusion
Drugs pass directly through the lipid bilayer ie, Small/lipophilic drugs, such as alcohol
34
Describe facilitated diffusion
Drugs move via solute carrier/membrane transporter proteins ie, large/hydrophilic drugs, such as certain steroids/chemotherapy agents
35
Describe active transport
Drug is transported against a concentration gradient (low to high) and requires energy expenditure ie, large/hydrophilic drugs such as levodopa
36
Describe endocytosis
Drug binds to a receptor on the cell membrane and is engulfed by the cell into a vesicle and is then exocytosed into the bloodstream ie, Insulin
37
Drug factors influencing absorption
Molecular size Lipid solubility pKa and pH
38
Describe the Henderson-Hasselbach equation for weak acids
HA <-----> H+ + A+ Increasing acidity in the environment shifts the reaction in favour of the unionised form. This is important as only the unionised form of the drug is lipid soluble. Therefore, weak acidic drugs are more favourably absorbed in highly acidic environments such as the stomach.
39
Describe the henderson-hasselbach equation for weak bases
BH+ <----> B + H+ ionised Decreasing acidity shifts the reaction in favour of the unionised than the ionised form. Therefore weak basic drugs are more readily absorbed in highly alkaline environments of the intestine
40
Define first-pass metabolism
Process in which a drug administered by mouth has to pass through three organs - stomach, intestine and liver. It must avoid interaction and degradation by stomach acid and digestive enzymes in the GI tract and liver in order to reach systemic circulation and have a therapeutic effect.
41
Define bioavailability
The fraction of an administered drug that reaches the systemic blood stream intact. It is determined from the area under the curve for plasma drug concentration versus time following oral and intravenous administration.
42
Equation for bioavailability
Bioavailability (F) = amount of drug in the circulation after an oral dose x 100 / amount of drug in the circulation after an Iv dose
43
What are the four functionally distinct compartments of body water
Plasma water (3L) Interstitial water (11L) Intracellular water (28L) Transcellular water
44
Factors that influence drug distribution
Increase in blood flow Decrease in protein binding Increase in lipid solubility
45
Due to which 2 processes do plasma concentrations of drugs decrease once they reach the blood circulation
1. Distribution to other tissues 2. Elimination by metabolism & Secretion
46
What is volume of dristribution
An estimation of drug distribution and can be defined as the volume of plasma that would be necessary to account for the total amount of drug in the patients body
47
How to calculate volume distribution
Vd (L) = Q dose administered (mg) / Cp Plasma concentration (mg/L) this is usually further divided by body weight and expressed in terms of litres/kg
48
If the Vd is low (<10L) where will the drug occupy
Plasma
49
If the Vd is medium (<15L) where will the drug occupy
Plasma Interstitial fluid
50
If the Vd is high (>15L) where will the drug occupy
Plasma Interstitial fluid Intracellular fluid Transcellular fluid Tissue Binding All compartments!
51
What is the mechanism of action of Gentamicin
Inhibition of mRNA translation at the ribosome Aminoglycoside used against gram-negative bacilli
52
What does a Phase 1 reaction in drug metabolism involve
Creating a functional reactive group, which will make the drug more polar and reduce reabsorption
53
What does a Phase 2 reaction in drug metabolism involve
Conjugation (attachment) and result in an inactive product that aids excretion
54
3 main roles of the liver in drug metabolism
1) Detoxify toxins and carcinogens by converting them in to a nontoxic metabolite 2) Activate prodrugs by converting the inactive precursor to an active drug 3) Inactivate a drug by converting the active drug into an inactive form
55
What are phase 1 drug metabolism reactions catalysed by
P450 enzyme To reach these enzymes (found in most cells, primarily liver and GI) a drug must cross the plasma membrane
56
Factors affecting Phase 1 metabolism
Patient polymorphism Increases in patient metabolism decreases in patient metabolism Polypharmacy (CYP450 inducers/inhibitors) Liver disease
57
In what 4 ways can drugs be excreted
Kidneys in Urine Hepatobiliary system in bile Lungs in exhaled gases GI tract in faeces
58
Define drug clearance (CLtotal)
The volume of plasma which is cleared of the total amount of drug per unit of time (ml/min) or (L/h). It is the sum of all organ clearance rates involved in removing a drug, such as the liver, kidneys, lungs
59
equation for drug clearance
CLtotal (ml/min) = rate of drug elimination / concentration of drug in plasma CLtotal = volume of distribution x 0.693 / half life
60
what is the rate of drug elimination dependent on
Drug metabolism and excretion
61
equation for half-life of a drug
volume of distribution x 0.693 / drug clearance
62
describe first-order enzymatic kinetics
as the plasma concentration of the drug increases so does the rate of drug metabolism because the number of enzymes actively involved in processing the drug increases proportionally.
63
describe zero order enzymatic kinetics
if a drug functions under zero order kinetics then all available enzymes are actively processing the drug and they are saturated. Therefore as the drug concentration increases there are no additional enzymes to process the drug to its inactive metabolite
64
describe the graph trends for first order metabolism
Increase drug concentration = increase rate of metabolism Rate of metabolism is dependent on drug concentration and is proportional Half life is constant
65
describe the graph trends for zero order metabolism
increase in drug concentration no longer = an increase in rate of metabolism rate of metabolism becomes independent of drug concentration and is constant half life is variable
66
describe first order elimination
constant proportion of the drug is eliminated over time ie, 50% of the drug is removed every hour, therefore the graph is exponential
67
describe zero order elimination
constant amount of the drug is eliminated over time ie, 25mg of drugs is removed every hour, therefore the graph is linear
68
define steady-state concentration
the time during which the concentration of a drug remains stable or consistent when it is administered repeatedly (repeat dosing) or continuously (IV infusion)
69
what is the equation for steady-state plasma concentration
Css = rate of drug administration / drug clearance
70
loading dose equation for IV drugs
desired initial plasma concentration x volume of distribution
71
loading dose equation for non IV drugs
desired intial plasma concentration x volume of distribution
72
Action of cholinergic system in lungs
Bronchoconstriction and hypersecretion
73
Action of adrenergic system in lungs
Bronchodilation
74
4 types of bronchidilators
B2 adrenoceptor agonists Anticholinergic agents Leukotriene antagonists Xanthines
75
examples of long acting B2 adrenoceptor agonists
Salmeterol, Formoterol
76
examples of short acting adrenoceptor agonists
Salbutamol, Terbutaline
77
Examples of anticholinergic agents
Ipratropium - Short acting Tiotropium - Long acting
78
Examples of leukotriene
Montelukast, Zafirlukast
79
Describe xanthines
Bronchodilators, Weak-anti inflammatory action oral or intravenous Theophylline, Aminophylline
80
Side effects of Xanthines
Cardiac dysrhythmias Seizures GI intolerance
81
examples of anti-inflammatory agents
Glucocorticoids Cromoglycate/Nedocromil Anti IgE antibodies
82
Function of glucocorticoids
Decrease Th2 cytokines Intracellular receptor, Intranuclear action
83
New asthma therapies
Novel scheduling - SMART Anti-Interleukins - Mepolizumab, Benralizumab
84
Why is MRI the best imaging form for Pancoasts tumour
Magnetic properties of hydrogen Easier to generate images in other planes Lower resolution Better at determining invasion of chest wall or mediastinum by cancer
85
Tests to examine pulmonary function
Spirometry Arterial blood gases Progressive exercise tests Sleep studies
86
Things to consider when choosing an investigation
Anxiety, Pain, discomfort complications Sensitive, specific, reliable, repeatable Ease, time, cost
87
What is spirometry
Breathing test that measures volume of air inhaled and exhaled along with speed of breath.
88
Bronchoscopy
Examination of the trachea and bronchus involving a thin tube inserted via the mouth or nose.
89
What is an ABG test
Blood is taken and tested for oxygen, CO2 and blood pH
90
Arterial blood gases of Type 1 respiratory failure
Low O2. <8kPa
91
Arterial blood gases of Type 2 respiratory failure
Low O2. <8kPa High CO2. >6kPa
92
What is a CTPA
A CT pulmonary angiogram (CTPA), also known as a CT scan of the pulmonary arteries, is a medical imaging technique used to visualize the blood vessels in the lungs, primarily to detect and diagnose pulmonary embolism (blood clots in the lungs).
93
How to assess severity of Pulmonary Embolic disease
Clinical: Haemodynamic stability (HR and BP), Respiratory rate Investigations: Troponin, Echo, RV dysfunction on CTPA
94
Treatment options for Pulmonary embolic disease
S/C fractionated heparin Oral anticoagulants IV thrombolytics Mechanical Intervention
95
what are cytochrome CYP450 enzymes
superfamily of enzymes that are haem proteins that catalyse the addition of one atom of oxygen to the drug to form a hydroxyl group
96
patient factors that affect drug metabolism
patient polymorphism polypharmacy age disease
97
define patient polymorphism
the presence of two or more variant forms of a specific DNA sequence that can occur among different individuals
98
effect of polypharmacy on CYP inducers
decrease in active drug in blood increase in inactive drug in kidney
99
effect of polypharmacy CYP inhibitors
increase active drug in blood decrease inactive drug in kidney
100
how to calculate time to 95% Css (Steady state concentration)
4.3 x half-life
101

Phase 2 - CVR (5 decks)

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