Pharmacology Flashcards

1
Q

Pharmacodynamics vs pharmacokinetics

A

Pharmacodynamics is what the drug does to the body

Pharmacokinetics is what the body does to the drug

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2
Q

Medicine vs drug

A

Used with the intention of a therapeutic effect

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3
Q

Affinity vs Efficacy

A

Binding step - Affinity, activation - Efficacy

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4
Q

Do antagonists have affinity or efficacy

A

Affinity

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5
Q

What shape is the curve of dose vs response

A

Hyperbolic

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6
Q

What is EC50 in a dose response relationship graph

A

EC50 is the agonist concentration that produces half the maximum response in a cell

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7
Q

What are full agonists

A

Agonists that can produce a 100% response

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8
Q

What is potency of agonist

A

Measure of concentration range over which agonist is effective

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9
Q

What is orthosteric binding

A

Binding of agonist and antagonist is at the same site

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10
Q

What shift is seen in response dose graph with a competitive antagonist

A

Parallel shift to the right with no depression of maximum respose

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11
Q

What happens in non-competitive antagonist

A

Receptor cells are blocked and maximum efficacy can’t be reached even with increasing agonist concentration

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12
Q

What is allosteric regulation

A

Regulation of enzyme by binding an effector molecule to a site other than its enzymes active site

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13
Q

Types of chemical signalling

A

Autocrine, paracrine (nearby) and endocrine (distant)

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14
Q

What are ion channels

A

Transmembrane pores formed by glycoproteins that span the membrane to create ion conducting pathway

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15
Q

What do pharmacologists consider true receptors

A

Ligand gated ion channels as they response to chemical signal

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16
Q

What is second messenger system

A

Receptor activation modulates activity of an effector that is generally an enzyme or ion channel

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17
Q

GPCR receptor structure

A

7 transmembrane spans, 3 extra and 3 intracellular loops

Integral membrane protein

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18
Q

What occupies Guanine Neucleotide Binding Site of alpa-subunit

A

GDP

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19
Q

What anchors G protein to membrane

A

Alpha and Gamma subunits have lipid chains attached

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20
Q

What two domains does alpha subunit have

A

Ras and AH, Ras - GTPase component

AH - Alpha helical element

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21
Q

What happens when GPCR is activated by agonist

A

Conformational change in alpha subunit -
Releases GDP and allows GTP to bind
Dissociates from beta-gamma dimer and receptor
GTP bound alpha and beta-gamma subunits are signalling units

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22
Q

How is GPCR signal turned off

A

Alpha subunit acts as a GTPase to hydrolyze GTP to GDP and Pi. This turns the signal off. G protein alpha and beta-gamma subunit recombine with receptor.

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23
Q

How is protein kinase regulated via GPCR

A

Adenyly cyclase can either be inhibited (Gi) or stimulated (Gs). Gs stimulates cAMP production from ATP. This intracellular signal transducer part of the cAMP-dependant pathway which stimulates Protein Kinase A (Serine/Thrombokinase) leading to cellular effects

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24
Q

What is the IP3/DAG pathway

A

Inositol triphosphate (IP3) and Diacylglycerol (DAG) is a secondary messenger molecule used in signal transuction. Ligand binding to GPCP activates Gq alpha subunit. This activates Phospholipase C (PLC) which converts PiP2 to IP3 and DAG. DAG remains in the membrane, activating Protein Kinase C; phosphorylating other cytosolic proteins. IP3 enters cytoplasm and activates IP3 receptors on smooth ER, causing Ca2+ influx and smooth muscle contraction

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25
Example of receptor kinase activity
Insulin targets receptors in cell membrane
26
How does receptor for insulin function
Receptor kinases have two subunits. Alpha and beta. Insulin binds to the alpha subunit. This causes phosphorylation of the beta subunit. This attracts different signalling molecules towards them. This leads to cellular effects.
27
What are nuclear receptors
Ligand gated transcription factors
28
Signalling via steroid hormones
Steroid hormones are lipophilic, enter cytoplasm via diffusion. They combine with intracellular receptor producing dissociation of inhibitory HSP proteins. The receptor steroid complex moves into the nucleus to form a dimer. This binds to hormone response element in DNA. Hence, transcription is either switched on or off to alter mRNA, synthesis of protein
29
What involves drug elimination
Metabolism and excretion
30
What is involved in drug disposition
Absorption Distribution Metabolism Excretion
31
General route of drug disposition
Ingestion - stomach - small intestine - excretion or liver (metabolism) - vascular compartment - kidney - excretion
32
What is partition coefficient of a drug
Ratio of drug concentration in the membrane and concentration in water at equilibrium
33
Ionised form of drug
A- and BH+, acids donate a proton, bases accept
34
When does pKa = pH
When 50% of drug is ionised and 50% isn't
35
How to determine ionised and unionised drugs
Henderson-Hasselbach equation
36
Henderson-Hasselbach equation for acids
pKa-pH = log (AH/A-)
37
Henderson-Hasselbach equation for bases
pKa-pH=log(BH+/B)
38
Acidic drugs become less ionsed in what environment
Acidic drugs become less ionised in acidic environment
39
Basic drugs become less ionised in what environment
Basic drugs become less ionised in basic environment
40
Where are bases readily absorbed in the body
Small intestine, acid in stomach
41
Which are absorbed easier, weak acid/base or strong
Weak acid/base are absorbed easier than strong ones
42
What is oral availability of a drug
Fraction of drug that reaches systemic circulation after oral ingestion
43
What is systemic availability
Fraction of drug reaching systemic circulation after absorption. IV drugs have 100% systemic availability
44
What is enteral absorption
Via GI tract, Parenteral is not via GI tract
45
What is sublingual administration also known as
Buccal
46
What drug administration route is distasteful
Rectal
47
Disadvantage of IV administration
Sterile preparation required, risk of sepsis and embolism, high drug levels at heart
48
What type of drugs can move between compartments
Unbound drugs, unionised drugs move by diffusion
49
What is volume of distribution (Vd)
Apparent volume in which a drug is dissolved, for IV; | Vd = Dose(Total drug in body)/Plasma concentration
50
What does Vd < 10 L imply
Drug is largely retained in vascular compartment, if drugs largely bound to plasma protein (Warfarin, Aspirin) or too large to cross capillary wall (Heparin)
51
What does 10 L < Vd < 30 L suggest
Drug is largely restricted to extracellular water, low lipid solubility drug (Amoxicilin, Gentamicin)
52
What does Vd > 30 L indicate
Distribution of drugs throughout total body water or accumulation in certain tissues, lipid soluble drugs (Ethanol) or bind extensively to tissue protein (Digoxin)
53
Minimum Effective Concentration vs Maximum Tolerated Concentration
Critical concentration a drug must reach to achieve an effect - MEC Concentration above which drug causes unwanted side effects - MTC
54
What is therapeutic ratio/index
TR = MTC/MEC, safe drugs have higher ratio
55
Why do IV drugs have no absorption rate (Kabs)
As IV drugs are absorbed 100%, hence it's bypassed
56
What is first order kinetics of a drug
Rate of elimination is directly proportional to drug concentration
57
Relationship between plasma concentration and time
Exponential relation
58
What does does administered change first order kinetics
Changes plasma concentration directly but not elimination rate or half life
59
What is clearance of drug
Volume of plasma cleared of drug in unit time | Rate of elimination = Clearance * Plasma concentration
60
What is steady state of dosing
Rate of administration = Rate of elimination
61
How many half-lives to reach steady state Cp
Approx 5 half lives, also amount of half lives to eliminate
62
Steady state of oral vs IV
Oral administration fluctuates about an average steady state whereas IV is a single straight line
63
What is a loading dose
Initial high dose of drug given at the beginning of a course of treatment before stepping down to a lower maintenance dose. Useful to decrease time to steady state for drugs with long half life
64
If dosing interval is same as half life, relation between loading and maintenance dose
Loading dose should be twice of maintenance dose
65
Loading dose for IV drugs
LD = Vd * Target plasma concentration | LD oral = Vd * CP / Oral bioavailability
66
What if half life of a drug (t 1/2)
Time for concentration of drug in plasma to halve | t 1/2 = 0.693 * Vd / Clearance
67
What is zero order kinetics
Drugs eliminated at a constant rate and not proportional to their plasma concentration, eg: Ethanol, Phenytoin
68
Elimination of zero order kinetics drugs
Generally constant rate converting to a first order at low concentration, ex: Alcohol dehydrogenase as enzyme becomes less saturated at low concentration
69
Main organ of drug metabolism
Liver but GI tract, lungs and plasma also have activity
70
Main aim for drug metabolism
Convert parent drug to more polar metabolites not readily reabsorbed by kidney allowing excretion Convert drugs to metabolites usually pharmacological less active than parent compound
71
Two common steps in drug metabolism
Addition of chemically reactive group to increase polarity (oxidation, reduction, hydrolysis) and Addition of endogenous compound further increasing polarity (conjugation) Some drugs can skip either or both steps
72
What are Cytochrome P450 family of monooxygenase
Haem proteins located in ER of liver hepatocytes mediating oxidation reactions of lipid soluble drugs
73
What is the Monooxygenase P450 cycle
Drug enters cycle as substrate RH Molecular oxygen (O2) provides two atoms of oxygen One atom combines with the drug RH to produce ROH Second atom combines with proton to form H2O
74
What is glucuronidation
``` Phase 2 reaction in the liver involving transfer of glucuronic acid to electron-rich atoms of substrate Endogenous substances (bilirubin, adrenal coricosteroids) are subject to glucuronidation ```
75
3 basic processes in renal excretion of drugs
Glomerular filtration Active tubular secretion Passive reabsorption by diffusion across tubular epitheli
76
Can glomerular filtration of drugs occur if bound to large plasma protein
No
77
When will plasma concentration of drug be more than glomerular filtrate
If drug binds appreciably to plasma proteins
78
Clearance of filtration (CLfil) is given by
CLfil = GFR * Fraction of drug unbound in plasma
79
Two transporter systems in epithelial cells of the proximal tubule that secrete drugs into lumen
Organic anion transporter (OAT) - Handles acidic drugs (Penicilin), endogenous acids (uric acid) and marker for renal plasma flow (PAH) Organic cation transporter (OCT) - Handles basic drugs (Morphine)
80
Most effective mechanism of drug elimination in kidney
Excretion by tubular secretion
81
How does tubular secretion in kidney secrete highly protein-bound drugs
Free drug concentration is reduced by secretion. This establishes new equilibrium between bound and free drugs. Free drug concentration further reduced by secretion causing additional drug to dissociate from protein
82
How can excretion of certain drugs from kidney be retarded
Drugs and other substances sharing same transport system compete with each other for secretion leading to interaction, eg: Probenecid has been used reduced Penicilin excretion Frusemide and thiazides reduce Uric acid excretion and precipitate gout
83
Why can thiazides and frusemide cause gout
Frusemide and thiazides may retard excretion of uric acid and precipitate gout
84
How does lipid solubility affect reabsorption in kidneys
Drugs with high lipid solubility will be extensively reabsorbed and excreted slowly
85
How does polarity affect reabsorption in kidneys
Highly polar drugs will be excreted without reabsorption
86
How does urinary flow rate affect reabsorption in kidneys
Diuresis decreases reabsorption
87
How does urinary pH affect reabsorption in kidneys
Degree of ionisation of weak acids and bases can strongly influence their absorption. Alkaline pH increases excretion of acids and acidic pH increases excretion of bases
88
How can urinary pH be useful clinically
Urinary alkalinisation can be used to accelerate excretion of Aspirin (weak acids) in cases of overdose
89
Depolarization vs Hyperpolarization
Depolarization - Membrane potential less negative | Hyperpolarization - Membrane potential more negative
90
Why does Na flow into the cell via Na selective channels
Concentration and electrical gradient is inward
91
Equilibrium potential for Na, Ena
Ena = + 60mV
92
Why does K flow out of cell via K selective channels
Concentration gradient is outward and has energy greater than inward electrical gradient
93
Equilibrium potential for K, Ek
Ek = -100mV
94
Resting membrane potential
Vm = -80mV
95
Driving force for Na and K
Membrane potential (Vm) - Equilibrium potential (Ena,Ek) For Na = - 80 - 60 = -140mV (Inward movement) For K = - 80 + 100 = +20mV (Outward movement)
96
What happens to membrane potential when Na and K channels are opened
Opening of Na channels cause depolarization whereas opening of K channels cause hyperpolarization
97
Which channels open first, Na or K in action potential
Na channels, K channels after a brief delay
98
Na or K channels function on positive feeback
Na channels are self-reinforcing, opening of a few channels causes further depolarization (positive feedback). Activation of K channels is self-limiting, outward movement of K cations cause repolarization
99
What states do Na channels enter
Close - Depolarization - Open - Main depolarization - Inactivated non-conducting - Repolarization - Close
100
Absolute vs relative refractory period
Absolute refractory period is when all Na channels are in the inactive non-conducting state. No stimulus however strong can elicit a second action potential Relative refractory period - Mixed population of inactive and closed Na channels. A stronger than normal stimulus can elicit a second action potential.
101
How does Rm/Ri ratio affect action potential speed
Distance over which current spreads depends on membrane resistance (Rm) and axial resistance (Ri) Increasing Rm/Ri increases length constant which increases current speed and AP velocity
102
How can passive current spread be increased
``` Decrease Ri (Axial resistance) - By increasing axon diameter Increase Rm (Membrane resistance) - Addition of insulating material such as Myelin ```
103
What produces Myelin in PNS and CNS
Schwaan cells - PNS | Oligodendrocytes - CNS
104
What is saltatory conduction in axons
Voltage activated Na channels cluster at the Node of Ranvier. Current flows along and axon with some loss at these nodes. This change in current causes a change in voltage, firing an action potential. This action potential jumps from one node to another. This is saltatory
105
When do absolute and relative refractory period occur
Absolute - Downstroke, Relative = Undershoot
106
Divisions of the autonomic nervous system
Enteric, Sympathetic and Parasympathetic
107
Simplistic description of sympathetic and parasympathetic
"Flight or fight" or "Rest and digest"
108
Transmitter of preganglionic neurones in ANS
Acetylcholine (ACh) via nicotinic cholinoceptors
109
Pre and postganglionic neurones in Sympathetic
Preganglionic neurone is short, transmits Acetylcholine. Postganglionic neurone is longer, transmits via Noradrenaline
110
Parasympathetic pre and postganglionic neurone
Preganglionic neurone is long and transmits via Acetylcholine. Postganglionic neurone is shorter and transmits via Acetylcholine (Muscarinic cholinoceptors)
111
Motor B vs C-fibres
Typically, parasympathetic and sympathetic preganglionic fibres are myelinated. These are called motor B fibres, white in appearance. Postganglionic fibres are largely unmyelinated and are called C-fibres
112
Length of sympathetic outflow
T1 to L2
113
How is sympathetic innervation of adrenal gland different
Preganglionic neurone synapse directly onto the adrenal gland (Chromaffin cells) and transmitter is via Acetylcholine, unlike sympathetic neurones
114
Where can sympathetics synapse
Paravertebral sympathetic ganglia - Postganglionic fibres join peripheral nerve fibres via grey rami communicantes to target organ Prevertebral sympathetic ganglia - In the abdomen via paravertebral ganglia and onwards in Splanchnic nerves to internal organs
115
Postganglionic fibres innervating thermoregulatory sweat glands and few blood vessels secrete?
Sudomotor fibres innervating eccrine (thermoregulatory) sweat glands are cholinergic (Acetylcholine). Receptors are muscarinic cholinoceptors. Sudomotor neurones to (apocrine) stress sweat glands are adrenergic
116
Other transmitters of parasympathetic neurones
Adenosine Triphoshate (ATP) and Neuropeptide Y (NYP)
117
Nerve involved in parasympathetic innervation
CN III (Occulomotor), VII (Facial), IX (Glossopharyngeal) and X (Vagus) and S2 to S4, Craniosacral outflow
118
Synapses of parasympathetic
III - Ciliary ganglia - Eye VII - Pterygopalatine, Submandibular IX - Otic (Parotid salivary gland), vagus has many ganglia
119
What is Nervi eringentes
Pelvic splanchnic nerves arising from S2-S4 and supplying hindgut
120
Other transmitters in parasympathetics
Nitric oxide and Vasoactive Intestinal Peptide (VIP)
121
Chemical transmission in Sympathetic ANS
AP originates in the CNS. This reaches the presynaptic terminal triggering Ca2+ entry through voltage-gated Ca2+ selective ion channels and releases ACh by exocytosis. ACh bind to ligand-gated ion channels (Nicotinic ACh receptors) in postganglionic neurone causing depolarization and initiation of action potential. This propagates to postsynaptic terminal, triggering Ca2+ entry and release of noradrenaline (usually), ATP or neuropeptide. This activated GPCR in effector cell membrane causing cellular response.
122
What receptor is present at presynaptic sympathetic and parasympathetic terminals
Nicotinic Acetylecholine Receptors
123
Chemical transmission in Parasympathetic ANS
AP originates in CNS. This travels along the neurone and reaches the presynaptic terminal. Entry of Ca2+ via voltage-activated Ca2+ selective channels and release of Acetlycholine by exocytosis. This Acetylcholine binds to ligand-gated ion channels (Nicotinic ACh receptors) causing depolarization and generation of an action potential. This AP reaches the postsynaptic terminal where entry of Ca2+ triggers release of Acetylcholine (usually), nitric oxide or vasoactive intestinal peptide onto Muscarinic ACh receptors. This causes cell effect
124
What is NANC transmission
Non-adrenergic non-cholinergic transmision is when neither NA nor ACh are the transmitters
125
Response time of neurotransmitters in ANS
``` Parasympathetic - Fast - ACh Medorate - NO Slow - VIP (Vasoactive Intestinal Peptide) Sympathetic - Fast - ATP Moderate - NA Slow - Neuropeptide Y (NPY) ```
126
Eendogenous agonist of cholinergic receptors
Acetlycholine
127
Types of cholinoceptors
Nicotinic: Ligand-gated ion channel Muscarinic: GPCR
128
Most important muscarinic cholinoceptor type ANS
M1 to M3
129
Endogenous agonist of adrenoceptors
Noradrenaline/Adrenaline
130
What can adrenoceptors be classed into
Alpha 1 and 2, Beta 1,2 and 3
131
How do sympathetics affect following organs: | Heart, Lungs, GI tract, Adrenal Gland, Penis
Heart (B1) - Increase rate and force of contraction Lung (B2) - Bronchodilation and less mucus production GI (A1,2,B2) - Less motility, constrict sphincters Vasculature (A1) - Vasoconstriction Adrenal medulla (Nicotinic AChR) - Release NA/A Bladder - Relaxes walls (B2,B3), constrict internal urethral sphicter (A1) Penis (A1) - Ejaculation
132
How do parasympathetics affect following organs: | Heart, Lungs, GI tract, Adrenal Gland, Penis
Heart (M2) - Less heart rate and force in atria Lungs (M3) - Bronchoconstriction, more mucous GI (M3) - Increase intestinal motility, relax sphincter (NO) Vasculature (M3) - Relax in penis, salivary glands, pancreas Bladder (M3) - Contract wall, relax internal urethral sphincter (NO) Penis (M3) - Erection (NO)
133
What organ used Beta3 adrenoceptors
Bladder for micturition
134
Describe coordinated activity of ANS in micturition
During filling, sympathetic activity dominates. The detrusor (smooth muscle wall) is relaxed by release of NA activating B2,B3 adrenoceptors. NA acts on A1 adrenoceptors to constrict the internal urinary sphicter. During voiding, parasympathetics dominate. Detrusor is contracted by ACh acting on M3 muscarinic receptors. NO stimulates release of cGMP in smooth muscle cells that relaxes internal urinary sphincter.
135
Tonic activity of sympathetic
Skin, muscle, gut vasoconstriction Inhibition of gut motility, gut secretions Detrusor relaxation, internal urinary sphincter contract
136
What type of receptors are Alpha and Beta
G-Protein Coupled Receptors
137
End result of cholinergic transmission
Enzyme-mediated inactivation of transmitter
138
End result of adrenergic transmission
Reuptake of transmitter
139
Overview of neurochemical transmission in ANS
Uptake of precursor, synthesis of transmitter, storage of transmitter. Depolarization by action potential leads to Ca2+ entry, inducing exocytosis of neurotransmitter. Receptor is activated leading to either enzyme mediated inactivation (cholinergic) or reuptake (adrenergic)
140
Cholinergic transmission at ganglia
Acetylcholine release from preganglionic neurones activates cation-selective nicotinic receptors of postganglionic neurone cell body. This elicits a rapid excitatory postsynaptic potential (epsp) triggering an action potential
141
What can block sympathetic and parasympathetic trans
Hexamethonium, open channel block (non-compete)
142
What causes degradation of ACh at receptor junction
Acetylcholinesterase, ACh to Choline and Acetate
143
What reuptakes NA at noradrenergic junctions
Uptake 1 - Back to preganglionic neurone | Uptake 2 - Towards postganglionic neurone
144
What are autoreceptors
Type of receptor located on membranes of presynaptic nerve cells. Sensitive to neurotransmitter released from same neurone and is involved in negative feedback.
145
How do autoreceptors help with negative feedback
Neurotransmitters released from neurones can act on presynaptic autoreceptors. This reduces the amount of Calcim entering the cell. Hence, activation of autoreceptors decreases the amount of neurotransmitter released. Agonists (neurotransmitter) decreases release whereas antagonist increase release
146
How does Cocaine affect the ANS
Cocaine blocks U1, increasing levels of noradrenaline in the synaptic cleft. This increases adrenoceptor stimulation. Peripheral actions include vasoconstriction (A1) and cardiac arrhythmia (B1)
147
Effect of Amphetamine on ANS
Amphetamine is a substrate for U1. Enters noradrenergic terminal, inhibits Monoamine oxidase (MAO), and enters synaptic vesicle. This displaces Noradrenaline into the cytoplasm. This NA then runs back on U1 enters synaptic cleft causing increased adrenoceptor stimulation Peripheral actions are vasoconstriction (A1) and cardiac arrhythmia (B1)
148
Action of Prazosin in ANS
A1 antagonist. Vasodilation used as anti-hypertensive
149
Action of Atenolol in ANS
B1 antagonist. Anti-anginal and anti-hypertensive
150
Action of Salbutamol in ANS
B2 agonist, bronchodilator in asthma
151
Action of Atropine in ANS
Muscarinic ACh receptor antagonist, blocks all (M1, 2 and 3) with equal affinity. Blocks parasympathetic and widespread body effect such as increasing heart rate following MI and anticholinesterase poisoning
152
How do platelets adhere to von Willebrand factor
Via Glycoprotein 1b
153
How do platelets adhere to each other
Via Glycoprotein 2b3a
154
What stimulates further platelet activation
Thromboxane A2 and ADP
155
Primary haemostasis vs secondary haemostasis
Formation of platelet plug - Primary haemostasis | Formation of fibrin clot - Secondary haemostasis
156
Drug with Thromboxane inhibitor function
Aspiring
157
ADP-receptor antagonist drug
Clopidogrel, Prasugrel
158
Drugs that are glycoprotein 2b/3a inhibitors
Eptifibatide
159
Treatment directed against venous thrombosis
Inhibition of clot formation such as inhibiting Thrombin and factor Xa. Heparin/ Warfarin used
160
What factors does Warfarin block
Factors VIIA, IXa and Xa as well as Prothrombin. All of these require vitamin K.
161
How does Fibrinolysis work
Fibrin is converted to FIbrin Degradation Products via Plasmin which is made from Plasminogen via tissue Plasminogen Activator (tPA)
162
How does Heparin function
Heparin binds to Anti-Thrombin 2. This causes a conformational change and increases adherence to proteins such as factors VIIa, IXa, Xa and Thrombin