Block A+B Flashcards

1
Q

what is a drug

A

a substance that modifies the activity of living tissue

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2
Q

what is physiology

A

the science of how living tissues function

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3
Q

what are therapeutics

A

the study of the use of pharmacological agents in disease states

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4
Q

what is pathology

A

the study of how the body goes wrong in disease states

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5
Q

what is an agonist

A

affinity- binding of agonist to its receptor
efficacy- ability of agonist to activate the receptor

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6
Q

what is an antagonist

A

when drugs counteract each other by acting on the same receptor type

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7
Q

what is irreversible-competitive antagonism

A

in some cases the bond between the antagonist and the receptor is so strong that even increasing concentrations of agonists cannot displace the antagonist. This is often due to covalent bonding

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8
Q

what is non-competitive antagonism

A

Antagonists which act at sites other than the agonist binding site are classified as non-competitive antagonists.

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9
Q

what is latrogenicity

A

the capacity to produce disease from the side effects or inappropriate prescribing of drugs

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10
Q

what is tetratogenicity

A

the capacity to produce abnormalities of the unborn child or foetus

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11
Q

what is PGE2

A

prostaglandin- involved in inflammation, mediated by COX-2

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12
Q

what is TXA2

A

another prostaglandin-like product and is involved in platelet aggregation during clotting, mediated by COX-1

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13
Q

what does ACE stand for

A

angiotensin converting enzyme

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14
Q

what does ACE do

A

converts angiotensin I to II

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15
Q

what is ACE inhibitors good as

A

blood pressure medication

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16
Q

what is statins good as

A

lowers cholesterol and prevents heart attacks

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17
Q

what is sildenafil (viagra) good for

A

inhibits the enzyme which breakdown cGMP- helps with erectile dysfunction

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18
Q

what is nevirapine good for

A

non-nucleoside reverse transcriptase inhibitor (NNRTI) of HIV-1 used to treat patients with HIV and AIDs

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19
Q

how does prozac work

A

an antidepressant that blocks the 5HT reuptake transporter its an SSRI (selective serotonin reuptake inhibitor)

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20
Q

what is serotonin

A

a neurotransmitter called 5-hydroxytryptamine (5-HT) released from nerve cells in the brain and affects other target nerve cells increasing activity. It interacts with 5-HT receptor on these target cells

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21
Q

salbutamol/adrenaline mechanism of action

A

interacts with Beta-2-receptor which activates Adenylyl cyclase receptor which increases intracellular cAMP. This inhibits calcium release, decreasing the amount of calcium in cytosol. Which promotes the release of smooth muscle relaxation which widens the airway making it easier to breathe

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22
Q

what are antihistamines

A

Histamine H1 antagonist

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23
Q

chemical antagonism

A

one drug antagonises the action of another drug by chemically combining with it

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24
Q

physiological antagonism

A

2 drugs counteract each other by producing opposing effects on different receptors

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25
Q

why do people have hypersensitivity to pollen

A

the overabundance of IgE, pollen binds to IgE which then binds to IgE receptors on the surface of mast cells which causes the release of histamine

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26
Q

what cells contain histamine

A

granules in mast cells

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27
Q

what does histamine cause

A

inflammation and swelling that leads to hay fever symptoms

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28
Q

what does histamine activating H1 receptor in noses cause

A

capillary widening- increased blood flow- heat and redness
increased permeability- fluid release into tissue- swelling
attraction of leukocytes- extraversion of leukocytes to site- swelling and tenderness
systematic response- fever and proliferation of leukocytes

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29
Q

what kind of inhibitor is aspirin

A

cyclo-oxygenase inhibitor

30
Q

aspirin mechanism of action

A

phospholipids–> arachidonic acid which interacts with catalytic site of cyclo-oxygenase which oxidises the acid and makes cyclical compound called PGH2. This gets rapidly converted to TXA2 by thromboxane synthetase or converted to PGE by prostaglandin synthetase. Aspirin acetylises serine residue in the enzymes active site which blocks catalytic site so arachidonic acid can’t be oxidised

31
Q

what happens when aspirin acetylises COX-1

A

it is completely inactivated

32
Q

what happens when aspirin acetylises COX-2 in same position

A

its ability to make prostaglandins is shut off but redirects enzyme activity to help make anti-inflammatory lipid products

33
Q

what converts angiotensin I to II

A

ACE

34
Q

what are the ACE inhibitors

A

captopril, enalopril, lisinopril

35
Q

what is depression caused by

A

lack of serotonin

36
Q

what does proton pump transport

A

hydrogen ions from the cytoplasm to extracellular fluid. It’s an active pump so requires ATP and an anti-porter so potassium ions go in the opposite direction

37
Q

what are ion channels

A

pores in the membrane made up of proteins

38
Q

ligand-gated channel

A

when a neurotransmitter binds to ion channel via receptor, when bonded ion channel opens

39
Q

mechanically-gated channel

A

pressure on cell opens the ion channel

40
Q

voltage-gated channel

A

polarity changing opens the ion channel

41
Q

what do CA2+ channels in the vascular smooth muscle do

A

mediates contraction

42
Q

what do sensory nerves do

A

pick up changes in different parts of the body and send afferent neurons to the brain. Once that info has been integrated into the CNS, impulses are sent down the spinal cord out through efferent neurons to skeletal muscles (somatic system)

43
Q

autonomic system

A

regulates multiple functions within the body, particularly glands and muscles. Rises from CNS, sending impulses down the efferent neurons, sending impulses to end organs. eg glands and cardiac muscle.

44
Q

what is the autonomic system staging post called

A

ganglia

45
Q

what is the sympathetic nervous system known as

A

‘fight or flight’ reaction

46
Q

what is the parasympathetic system known as

A

‘rest and repair’ system

47
Q

parasympathetic system

A

action potential comes along the system from CNS to the ganglia where acetylcholine is released and interacts with the nicotine acetylcholine receptor which helps reestablish the action potential which keeps going down to the end organ. Acetylcholine is released and interacts with muscarinic receptors in the heart and some blood vessels

48
Q

sympathetic adrenergic

A

action potential comes along the system from CNS to the ganglia where acetylcholine is released and interacts with the nicotine acetylcholine receptor which helps reestablish the action potential which keeps going down to the end organ. Once hits end organ it causes release of noradrenaline which interacts with alpha and beta receptors

49
Q

sympathetic cholinergic

A

action potential comes along the system from CNS to the ganglia where acetylcholine is released and interacts with the nicotine acetylcholine receptor which helps reestablish the action potential which keeps going down to the end organ. Acetylcholine is released at end organ in sweat glands

50
Q

sympathetic dopaminergic

A

action potential comes along the system from CNS to the ganglia where acetylcholine is released and interacts with the nicotine acetylcholine receptor which helps reestablish the action potential which keeps going down to the end organ. Dopamine is released and interacts with dopamine receptors to regulate renal vessels

51
Q

G-protein-coupled receptors (metabotropic)

A

on the plasma membrane, once activated by agonists they interact with a G-protein. Once activated they activate an effector enzyme which can generate a second messenger which goes on to initiate a cascade of activity which results in a cellular response

52
Q

what do B2-agonists treat

A

asthma by causing bronchial dilation

53
Q

what are B1-agonists used for

A

to stimulate the force of heart contractions

54
Q

what do alpha-1-agonists treat

A

blocked nose/sinuses

55
Q

what are alpha-2-agonists

A

centrally acting hypotensive drugs

56
Q

cardiovascular system functions

A

Rapid transport of nutrients
Remove waste products of metabolism
Hormonal control by transporting hormones to their target organs and by secreting their own hormones
Temperature regulation
Host defence

57
Q

blood flow from heart to lungs

A

Deoxygenated blood from vena cava comes in at right atrium, as it fills puts pressure on valves to open to allow movement of blood. Tricuspid valve opens allowing blood from right atrium to right ventricle, once filled opens semi-lunar valve then blood flows to lungs via pulmonary artery.

58
Q

blood flow from lungs to body

A

Blood gets oxygenated in lungs and flows into left atrium via pulmonary vein, filling allows bicuspid-mitral valve to open. Blood goes to left ventricle, aortic semi-lunar valves open and blood flows to aorta and is pumped around the body

59
Q

what are the walls of the heart composed of

A

cardiac muscle cells- myocardium

60
Q

what is endocardium

A

inner surface of walls that are in contact with blood

61
Q

what is epicardium

A

inner lining of the pericardium is continuous with the covering of the heart itself

62
Q

what is pericardium

A

fluid-filled membranous sac where the heart is located within

63
Q

what are cardiac muscles joined together by

A

gap junctions, which allow for spread of excitation from one cell to another

64
Q

what are the events leading to cardiac construction

A

depolarisation of plasma membrane which opens voltage-sensitive Ca2+ channels. calcium ions then flow into cell and are released from sarcoplasmic reticulum. rise in cytosolic calcium ion concentration leads to contraction

65
Q

sympathetic fibres

A

noradrenaline beta receptors increase permeability of the nodal cell plasma membrane to sodium and calcium ions

66
Q

parasympathetic fibres

A

Acetylcholine- m2 receptors increase permeability to potassium ions and decrease sodium + calcium ions permeability

67
Q

cardiac output calculation

A

stroke volume - heart rate

68
Q

gas exchange from alveoli to tissue

A

Exchange of oxygen and carbon dioxide between alveolar air and blood in lung capillaries by diffusion
Transport of oxygen and carbon dioxide through pulmonary and systematic circulation by bulk flow
Exchange of oxygen and carbon dioxide between blood in tissue capillaries and cells in tissue by diffusion
Cellular utilisation of oxygen and production of carbon dioxide

69
Q

what is ventilation

A

exchange of air between atmosphere and alveoli by bulk flow

70
Q

what happens during exercise

A

increase in skeletal muscle and skin blood flow
increased cardiac output (increase sympathetic, decrease parasympathetic control)
increase respiratory output

71
Q

what happens during endurance training

A

increase VO2 max/mitochonria/muscle capillaries

72
Q

what happens during strength training

A

increase glycolytic fibre size/glycolytic enzymes/stores