Respiratory and Cardiovasicular Flashcards

(53 cards)

1
Q

What are the mechanisms of pulmonary ventilation

A

Lung expansion (ribs, diaphragm) and air movement (pleural pressure)

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2
Q

what and where is airway smooth muscle

A

from trachea to terminal bronchioles. contractions regulate airway diameter and airway resistance

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3
Q

what is smooth muscle influence by

A

parasympathetic and sympathetic factors

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4
Q

Thalidomide

A

A drug that was taken for morning sickness and was found to cause birth defects

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5
Q

what are advantages of pulmonary drug delivery

A

non-invasive, large surface area, rapid absorption,

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6
Q

what are the disadvantages of pulmonary drug delivery

A

accessibility- mucus, poor blood supply.

Method of delivery - MDI vs nebulizers

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7
Q

what conditions are treated with inhaled drugs

A

COPD, asthma, lung infections, diabetes melltius, growth hormone deficiency, pulmonary hypertension

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8
Q

what is COPD (chronic obstructive pulmonary disease) and affects

A

causes poor airflow, worsens over time, disease

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9
Q

what are used to treat COPD

A

glucocorticoids (anti-inflammatory)
bronchodilators
antitussives

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10
Q

What are broncodilators?

A

they are beta 2 adrenoceptor agonists. also can use xanthine drugs (coffee)

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11
Q

how do Beta 2 adrenoceptor agonists work

A

have a direct action on smooth muscle - causes to relax.

are antagonists of bronchoconstrictors. inhibit inflammatory mediator release. clear muscus

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12
Q

examples of beta-2-adrenoceptor agonists

A

salbutamol and terbutaline (inhaled as needed short acting) - 3 to 5 hours
clenbuterol (oral) inhaled twice daily last 8 - 12 hours

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13
Q

What are xanthines?

A

caffeine, theophylline, theobromine

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14
Q

what happens in the lungs due to asthma

A

the airways are inflammed with an increase amount of swelling and mucus. smooth muscle increase

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15
Q

what are used to treat asthma

A

bronchodilators and anti-inflammatories

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16
Q

what are glucocorticoids

A

as a natural occurring compound. act as anti-inflammatory

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17
Q

How do glucocorticoids work?

A

decrease formation of cytokines, inhibit vasodilator productions,

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18
Q

What are cardiomyocytes?

A

Heart muscle cells that make up a lot of the tissue in our hearts.

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19
Q

what are non-cardiomyocytes

A

pacemaker cells, cardiac fibroblasts

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20
Q

excitation-contraction coupling

A

events that link the action potentials inititated by Na influx into a cell, causes depolarises voltage gated Ca channels and causes Ca influx into cytosol. a small rise in Ca triggers Ca release from SR

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21
Q

Cardiac excitation-contraction coupling

A

the process by which an electrical event causes an increase in calcium - then translates into muscle contraction and pumping of blood

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22
Q

why is excitation contraction coupling important

A

mishandling of Ca by the myocyte is the main cause of cardiac contractile dysfunction and arrhythmias

23
Q

examples of types drugs that affect cardiac myocytes

A

anti-dysrhytmic drugs, cardiac glycosides, autonomic neurotransmitters, calcium antagonists

24
Q

what are cardiac dysrhythmias

A

abnormal rhythms of the heart’s electrical system that can affect its ability to effectively pump oxygenated blood throughout the body.

25
what cause cardiac dysrhythmias
delayed after depolarisation, re-entry, ectopic pacemaker activity, heart block
26
Anti-dysrhythmic Drugs
``` class I drugs: sodium channel blockers class II drugs: beta blockers class III drugs: potassium channel blockers class IV drugs: calcium channel blockers other ```
27
Class 1 anti dysrythmics MOA
bind the alpha subunit of Na channels. inhibits action potential propagation, reduces max depolarisation rate at phase 0
28
example of Class 1 antidysrhythmics
lidocaine, flecainide, ecnaidide, quinidine
29
Class 2 anti-dysrhythmics MOA
beta 1- adrenoceptor antagonists, (doesnt relax) prevents increased sympathetic activity, increases refractory period of a-v node.
30
what type of drug is propranolol and metoprolol
Class 2 anti-dysrhythmic, Beta 1- adrenoceptor antagonists (doesnt relax) propranolol is non selective and metoprolol is selective
31
Class IV antiarrhythmics
calcium channel blockers, specfically L-type channels, slow conduction in S-A and A-V nodes, reduce force of contraction
32
what type of drug is verapamil and diltiazem
calcium channel blocker, Class IV anti-dysrhytmia, affect Ca
33
what are calcium antagonists
block entry of Ca into the cell, cause AV block and slow heart rate
34
what are calcium antagonists used for
hypertension and preventing angina
35
drugs that increase myocardial contraction
cardiac glycosides
36
what are cardiac glycosides
drugs that effect pumping action of heart, slow conduction through AV node, increase force of contraction, inhibit the Na/K pump in cardiac myocytes, increase vagal outflow
37
what type of drug is digoxin
cardiac glycoside, affects pumping of the heart
38
what does digoxin do
slows conduction, increase contractility
39
sympathetic drive
acts on Beta 1 adrenoceptors, increase force of contraction, increase rate of contraction, increase automaticity, repolarisation, decreased cardiac efficeincy
40
parasympathetic drive
acts on M2-muscarinic receptors, no effect on contractility, decreased rate
41
parasympathetic nervous system increases heart rate (T/F)
false
42
drugs that affect cardiac function indirectly
calcium antagonists, vasodilators and vasoconstrictors, angiotensin-converting enzyme inhibitors, diuretics
43
What are vasoconstrictors?
Pharmacologic agents that cause blood vessels to constrict, reduce vessel volume and flow, increase blood pressure,
44
What are vasodilators?
agents that widen the blood vessels, increase vessel volume and flow, reduce blood pressure, calcium antagonists,
45
What are the RAAS inhibitors used for?
used for hypertension, congestive heart failure,
46
RAAS inhibitors
``` -ACE inhibitors reduce cardiac load and arterial BP -Angiotensin II receptor blockers reduce BP -Aldosterone antagonists Monitor K+ levels for hyperkalemia example is diuretics ```
47
ACE inhibitors
example is benazepril (prodrug), inhibit acction of angiotensin converting enzyme, reduce blood vessels and decrease blood volume
48
Diuretics
hypertension, oedema, inhibit Na resorption in the nephron, inhibit water resorption.
49
what are the different phases of asthma
acute and delayed phase
50
what occurs in the acute phase of asthma
triggered by interaction of allergen with mast cells. release of Ige causes mast cell degranulation\ release of mediators --> bronchoconstrictor and activation of inflammation
51
what occurs in the delayed phase of asthma
activation of TH2 lympocytes, promotes cytokine production.
52
why is the different phases of asthma important
depending on the type that people have drugs would need to be taken, eg salbutamol (short-acting) vs clenbuterol (long Acting)
53
MOA of xanthine and the side effects
MOA • Unclear - inhibits phosphodiesterase enzymes to relax smooth muscle (↑ cAMP) • Also adenosine receptor antagonist • May have some anti-inflammatory effect • Stimulate the CNS (useful in horses where expiration in active) Adverse effects • Narrow therapeutic window • Cardiac dysrhythmia, seizures, GIT upset, anxiety