Block A+B Flashcards
what is a drug
a substance that modifies the activity of living tissue
what is physiology
the science of how living tissues function
what are therapeutics
the study of the use of pharmacological agents in disease states
what is pathology
the study of how the body goes wrong in disease states
what is an agonist
affinity- binding of agonist to its receptor
efficacy- ability of agonist to activate the receptor
what is an antagonist
when drugs counteract each other by acting on the same receptor type
what is irreversible-competitive antagonism
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
what is non-competitive antagonism
Antagonists which act at sites other than the agonist binding site are classified as non-competitive antagonists.
what is latrogenicity
the capacity to produce disease from the side effects or inappropriate prescribing of drugs
what is tetratogenicity
the capacity to produce abnormalities of the unborn child or foetus
what is PGE2
prostaglandin- involved in inflammation, mediated by COX-2
what is TXA2
another prostaglandin-like product and is involved in platelet aggregation during clotting, mediated by COX-1
what does ACE stand for
angiotensin converting enzyme
what does ACE do
converts angiotensin I to II
what is ACE inhibitors good as
blood pressure medication
what is statins good as
lowers cholesterol and prevents heart attacks
what is sildenafil (viagra) good for
inhibits the enzyme which breakdown cGMP- helps with erectile dysfunction
what is nevirapine good for
non-nucleoside reverse transcriptase inhibitor (NNRTI) of HIV-1 used to treat patients with HIV and AIDs
how does prozac work
an antidepressant that blocks the 5HT reuptake transporter its an SSRI (selective serotonin reuptake inhibitor)
what is serotonin
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
salbutamol/adrenaline mechanism of action
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
what are antihistamines
Histamine H1 antagonist
chemical antagonism
one drug antagonises the action of another drug by chemically combining with it
physiological antagonism
2 drugs counteract each other by producing opposing effects on different receptors
why do people have hypersensitivity to pollen
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
what cells contain histamine
granules in mast cells
what does histamine cause
inflammation and swelling that leads to hay fever symptoms
what does histamine activating H1 receptor in noses cause
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
what kind of inhibitor is aspirin
cyclo-oxygenase inhibitor
aspirin mechanism of action
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
what happens when aspirin acetylises COX-1
it is completely inactivated
what happens when aspirin acetylises COX-2 in same position
its ability to make prostaglandins is shut off but redirects enzyme activity to help make anti-inflammatory lipid products
what converts angiotensin I to II
ACE
what are the ACE inhibitors
captopril, enalopril, lisinopril
what is depression caused by
lack of serotonin
what does proton pump transport
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
what are ion channels
pores in the membrane made up of proteins
ligand-gated channel
when a neurotransmitter binds to ion channel via receptor, when bonded ion channel opens
mechanically-gated channel
pressure on cell opens the ion channel
voltage-gated channel
polarity changing opens the ion channel
what do CA2+ channels in the vascular smooth muscle do
mediates contraction
what do sensory nerves do
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)
autonomic system
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.
what is the autonomic system staging post called
ganglia
what is the sympathetic nervous system known as
‘fight or flight’ reaction
what is the parasympathetic system known as
‘rest and repair’ system
parasympathetic system
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
sympathetic adrenergic
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
sympathetic cholinergic
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
sympathetic dopaminergic
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
G-protein-coupled receptors (metabotropic)
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
what do B2-agonists treat
asthma by causing bronchial dilation
what are B1-agonists used for
to stimulate the force of heart contractions
what do alpha-1-agonists treat
blocked nose/sinuses
what are alpha-2-agonists
centrally acting hypotensive drugs
cardiovascular system functions
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
blood flow from heart to lungs
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.
blood flow from lungs to body
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
what are the walls of the heart composed of
cardiac muscle cells- myocardium
what is endocardium
inner surface of walls that are in contact with blood
what is epicardium
inner lining of the pericardium is continuous with the covering of the heart itself
what is pericardium
fluid-filled membranous sac where the heart is located within
what are cardiac muscles joined together by
gap junctions, which allow for spread of excitation from one cell to another
what are the events leading to cardiac construction
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
sympathetic fibres
noradrenaline beta receptors increase permeability of the nodal cell plasma membrane to sodium and calcium ions
parasympathetic fibres
Acetylcholine- m2 receptors increase permeability to potassium ions and decrease sodium + calcium ions permeability
cardiac output calculation
stroke volume - heart rate
gas exchange from alveoli to tissue
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
what is ventilation
exchange of air between atmosphere and alveoli by bulk flow
what happens during exercise
increase in skeletal muscle and skin blood flow
increased cardiac output (increase sympathetic, decrease parasympathetic control)
increase respiratory output
what happens during endurance training
increase VO2 max/mitochonria/muscle capillaries
what happens during strength training
increase glycolytic fibre size/glycolytic enzymes/stores
