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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
Q

Example of receptor kinase activity

A

Insulin targets receptors in cell membrane

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26
Q

How does receptor for insulin function

A

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.

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27
Q

What are nuclear receptors

A

Ligand gated transcription factors

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28
Q

Signalling via steroid hormones

A

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

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29
Q

What involves drug elimination

A

Metabolism and excretion

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30
Q

What is involved in drug disposition

A

Absorption
Distribution
Metabolism
Excretion

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31
Q

General route of drug disposition

A

Ingestion - stomach - small intestine - excretion or liver (metabolism) - vascular compartment - kidney - excretion

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32
Q

What is partition coefficient of a drug

A

Ratio of drug concentration in the membrane and concentration in water at equilibrium

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33
Q

Ionised form of drug

A

A- and BH+, acids donate a proton, bases accept

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34
Q

When does pKa = pH

A

When 50% of drug is ionised and 50% isn’t

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35
Q

How to determine ionised and unionised drugs

A

Henderson-Hasselbach equation

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36
Q

Henderson-Hasselbach equation for acids

A

pKa-pH = log (AH/A-)

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37
Q

Henderson-Hasselbach equation for bases

A

pKa-pH=log(BH+/B)

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38
Q

Acidic drugs become less ionsed in what environment

A

Acidic drugs become less ionised in acidic environment

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39
Q

Basic drugs become less ionised in what environment

A

Basic drugs become less ionised in basic environment

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40
Q

Where are bases readily absorbed in the body

A

Small intestine, acid in stomach

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41
Q

Which are absorbed easier, weak acid/base or strong

A

Weak acid/base are absorbed easier than strong ones

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42
Q

What is oral availability of a drug

A

Fraction of drug that reaches systemic circulation after oral ingestion

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43
Q

What is systemic availability

A

Fraction of drug reaching systemic circulation after absorption. IV drugs have 100% systemic availability

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44
Q

What is enteral absorption

A

Via GI tract, Parenteral is not via GI tract

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45
Q

What is sublingual administration also known as

A

Buccal

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46
Q

What drug administration route is distasteful

A

Rectal

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47
Q

Disadvantage of IV administration

A

Sterile preparation required, risk of sepsis and embolism, high drug levels at heart

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48
Q

What type of drugs can move between compartments

A

Unbound drugs, unionised drugs move by diffusion

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49
Q

What is volume of distribution (Vd)

A

Apparent volume in which a drug is dissolved, for IV;

Vd = Dose(Total drug in body)/Plasma concentration

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50
Q

What does Vd < 10 L imply

A

Drug is largely retained in vascular compartment, if drugs largely bound to plasma protein (Warfarin, Aspirin) or too large to cross capillary wall (Heparin)

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51
Q

What does 10 L < Vd < 30 L suggest

A

Drug is largely restricted to extracellular water, low lipid solubility drug (Amoxicilin, Gentamicin)

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52
Q

What does Vd > 30 L indicate

A

Distribution of drugs throughout total body water or accumulation in certain tissues, lipid soluble drugs (Ethanol) or bind extensively to tissue protein (Digoxin)

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53
Q

Minimum Effective Concentration vs Maximum Tolerated Concentration

A

Critical concentration a drug must reach to achieve an effect - MEC
Concentration above which drug causes unwanted side effects - MTC

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54
Q

What is therapeutic ratio/index

A

TR = MTC/MEC, safe drugs have higher ratio

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55
Q

Why do IV drugs have no absorption rate (Kabs)

A

As IV drugs are absorbed 100%, hence it’s bypassed

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56
Q

What is first order kinetics of a drug

A

Rate of elimination is directly proportional to drug concentration

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57
Q

Relationship between plasma concentration and time

A

Exponential relation

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58
Q

What does does administered change first order kinetics

A

Changes plasma concentration directly but not elimination rate or half life

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59
Q

What is clearance of drug

A

Volume of plasma cleared of drug in unit time

Rate of elimination = Clearance * Plasma concentration

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60
Q

What is steady state of dosing

A

Rate of administration = Rate of elimination

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61
Q

How many half-lives to reach steady state Cp

A

Approx 5 half lives, also amount of half lives to eliminate

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62
Q

Steady state of oral vs IV

A

Oral administration fluctuates about an average steady state whereas IV is a single straight line

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63
Q

What is a loading dose

A

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

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64
Q

If dosing interval is same as half life, relation between loading and maintenance dose

A

Loading dose should be twice of maintenance dose

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65
Q

Loading dose for IV drugs

A

LD = Vd * Target plasma concentration

LD oral = Vd * CP / Oral bioavailability

66
Q

What if half life of a drug (t 1/2)

A

Time for concentration of drug in plasma to halve

t 1/2 = 0.693 * Vd / Clearance

67
Q

What is zero order kinetics

A

Drugs eliminated at a constant rate and not proportional to their plasma concentration, eg: Ethanol, Phenytoin

68
Q

Elimination of zero order kinetics drugs

A

Generally constant rate converting to a first order at low concentration, ex: Alcohol dehydrogenase as enzyme becomes less saturated at low concentration

69
Q

Main organ of drug metabolism

A

Liver but GI tract, lungs and plasma also have activity

70
Q

Main aim for drug metabolism

A

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
Q

Two common steps in drug metabolism

A

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
Q

What are Cytochrome P450 family of monooxygenase

A

Haem proteins located in ER of liver hepatocytes mediating oxidation reactions of lipid soluble drugs

73
Q

What is the Monooxygenase P450 cycle

A

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
Q

What is glucuronidation

A 
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
Q

3 basic processes in renal excretion of drugs

A

Glomerular filtration
Active tubular secretion
Passive reabsorption by diffusion across tubular epitheli

76
Q

Can glomerular filtration of drugs occur if bound to large plasma protein

A

No

77
Q

When will plasma concentration of drug be more than glomerular filtrate

A

If drug binds appreciably to plasma proteins

78
Q

Clearance of filtration (CLfil) is given by

A

CLfil = GFR * Fraction of drug unbound in plasma

79
Q

Two transporter systems in epithelial cells of the proximal tubule that secrete drugs into lumen

A

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
Q

Most effective mechanism of drug elimination in kidney

A

Excretion by tubular secretion

81
Q

How does tubular secretion in kidney secrete highly protein-bound drugs

A

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
Q

How can excretion of certain drugs from kidney be retarded

A

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
Q

Why can thiazides and frusemide cause gout

A

Frusemide and thiazides may retard excretion of uric acid and precipitate gout

84
Q

How does lipid solubility affect reabsorption in kidneys

A

Drugs with high lipid solubility will be extensively reabsorbed and excreted slowly

85
Q

How does polarity affect reabsorption in kidneys

A

Highly polar drugs will be excreted without reabsorption

86
Q

How does urinary flow rate affect reabsorption in kidneys

A

Diuresis decreases reabsorption

87
Q

How does urinary pH affect reabsorption in kidneys

A

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
Q

How can urinary pH be useful clinically

A

Urinary alkalinisation can be used to accelerate excretion of Aspirin (weak acids) in cases of overdose

89
Q

Depolarization vs Hyperpolarization

A

Depolarization - Membrane potential less negative

Hyperpolarization - Membrane potential more negative

90
Q

Why does Na flow into the cell via Na selective channels

A

Concentration and electrical gradient is inward

91
Q

Equilibrium potential for Na, Ena

A

Ena = + 60mV

92
Q

Why does K flow out of cell via K selective channels

A

Concentration gradient is outward and has energy greater than inward electrical gradient

93
Q

Equilibrium potential for K, Ek

A

Ek = -100mV

94
Q

Resting membrane potential

A

Vm = -80mV

95
Q

Driving force for Na and K

A

Membrane potential (Vm) - Equilibrium potential (Ena,Ek)
For Na = - 80 - 60 = -140mV (Inward movement)
For K = - 80 + 100 = +20mV (Outward movement)

96
Q

What happens to membrane potential when Na and K channels are opened

A

Opening of Na channels cause depolarization whereas opening of K channels cause hyperpolarization

97
Q

Which channels open first, Na or K in action potential

A

Na channels, K channels after a brief delay

98
Q

Na or K channels function on positive feeback

A

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
Q

What states do Na channels enter

A

Close - Depolarization - Open - Main depolarization - Inactivated non-conducting - Repolarization - Close

100
Q

Absolute vs relative refractory period

A

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
Q

How does Rm/Ri ratio affect action potential speed

A

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
Q

How can passive current spread be increased

A 
Decrease Ri (Axial resistance) - By increasing axon diameter
Increase Rm (Membrane resistance) - Addition of insulating material such as Myelin
103
Q

What produces Myelin in PNS and CNS

A

Schwaan cells - PNS

Oligodendrocytes - CNS

104
Q

What is saltatory conduction in axons

A

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
Q

When do absolute and relative refractory period occur

A

Absolute - Downstroke, Relative = Undershoot

106
Q

Divisions of the autonomic nervous system

A

Enteric, Sympathetic and Parasympathetic

107
Q

Simplistic description of sympathetic and parasympathetic

A

“Flight or fight” or “Rest and digest”

108
Q

Transmitter of preganglionic neurones in ANS

A

Acetylcholine (ACh) via nicotinic cholinoceptors

109
Q

Pre and postganglionic neurones in Sympathetic

A

Preganglionic neurone is short, transmits Acetylcholine. Postganglionic neurone is longer, transmits via Noradrenaline

110
Q

Parasympathetic pre and postganglionic neurone

A

Preganglionic neurone is long and transmits via Acetylcholine. Postganglionic neurone is shorter and transmits via Acetylcholine (Muscarinic cholinoceptors)

111
Q

Motor B vs C-fibres

A

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
Q

Length of sympathetic outflow

A

T1 to L2

113
Q

How is sympathetic innervation of adrenal gland different

A

Preganglionic neurone synapse directly onto the adrenal gland (Chromaffin cells) and transmitter is via Acetylcholine, unlike sympathetic neurones

114
Q

Where can sympathetics synapse

A

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
Q

Postganglionic fibres innervating thermoregulatory sweat glands and few blood vessels secrete?

A

Sudomotor fibres innervating eccrine (thermoregulatory) sweat glands are cholinergic (Acetylcholine). Receptors are muscarinic cholinoceptors. Sudomotor neurones to (apocrine) stress sweat glands are adrenergic

116
Q

Other transmitters of parasympathetic neurones

A

Adenosine Triphoshate (ATP) and Neuropeptide Y (NYP)

117
Q

Nerve involved in parasympathetic innervation

A

CN III (Occulomotor), VII (Facial), IX (Glossopharyngeal) and X (Vagus) and S2 to S4, Craniosacral outflow

118
Q

Synapses of parasympathetic

A

III - Ciliary ganglia - Eye
VII - Pterygopalatine, Submandibular
IX - Otic (Parotid salivary gland), vagus has many ganglia

119
Q

What is Nervi eringentes

A

Pelvic splanchnic nerves arising from S2-S4 and supplying hindgut

120
Q

Other transmitters in parasympathetics

A

Nitric oxide and Vasoactive Intestinal Peptide (VIP)

121
Q

Chemical transmission in Sympathetic ANS

A

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
Q

What receptor is present at presynaptic sympathetic and parasympathetic terminals

A

Nicotinic Acetylecholine Receptors

123
Q

Chemical transmission in Parasympathetic ANS

A

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
Q

What is NANC transmission

A

Non-adrenergic non-cholinergic transmision is when neither NA nor ACh are the transmitters

125
Q

Response time of neurotransmitters in ANS

A 
Parasympathetic - 
Fast - ACh
Medorate - NO
Slow - VIP (Vasoactive Intestinal Peptide)
Sympathetic -
Fast - ATP
Moderate - NA
Slow - Neuropeptide Y (NPY)
126
Q

Eendogenous agonist of cholinergic receptors

A

Acetlycholine

127
Q

Types of cholinoceptors

A

Nicotinic: Ligand-gated ion channel
Muscarinic: GPCR

128
Q

Most important muscarinic cholinoceptor type ANS

A

M1 to M3

129
Q

Endogenous agonist of adrenoceptors

A

Noradrenaline/Adrenaline

130
Q

What can adrenoceptors be classed into

A

Alpha 1 and 2, Beta 1,2 and 3

131
Q

How do sympathetics affect following organs:

Heart, Lungs, GI tract, Adrenal Gland, Penis

A

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
Q

How do parasympathetics affect following organs:

Heart, Lungs, GI tract, Adrenal Gland, Penis

A

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
Q

What organ used Beta3 adrenoceptors

A

Bladder for micturition

134
Q

Describe coordinated activity of ANS in micturition

A

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
Q

Tonic activity of sympathetic

A

Skin, muscle, gut vasoconstriction
Inhibition of gut motility, gut secretions
Detrusor relaxation, internal urinary sphincter contract

136
Q

What type of receptors are Alpha and Beta

A

G-Protein Coupled Receptors

137
Q

End result of cholinergic transmission

A

Enzyme-mediated inactivation of transmitter

138
Q

End result of adrenergic transmission

A

Reuptake of transmitter

139
Q

Overview of neurochemical transmission in ANS

A

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
Q

Cholinergic transmission at ganglia

A

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
Q

What can block sympathetic and parasympathetic trans

A

Hexamethonium, open channel block (non-compete)

142
Q

What causes degradation of ACh at receptor junction

A

Acetylcholinesterase, ACh to Choline and Acetate

143
Q

What reuptakes NA at noradrenergic junctions

A

Uptake 1 - Back to preganglionic neurone

Uptake 2 - Towards postganglionic neurone

144
Q

What are autoreceptors

A

Type of receptor located on membranes of presynaptic nerve cells. Sensitive to neurotransmitter released from same neurone and is involved in negative feedback.

145
Q

How do autoreceptors help with negative feedback

A

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
Q

How does Cocaine affect the ANS

A

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
Q

Effect of Amphetamine on ANS

A

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
Q

Action of Prazosin in ANS

A

A1 antagonist. Vasodilation used as anti-hypertensive

149
Q

Action of Atenolol in ANS

A

B1 antagonist. Anti-anginal and anti-hypertensive

150
Q

Action of Salbutamol in ANS

A

B2 agonist, bronchodilator in asthma

151
Q

Action of Atropine in ANS

A

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
Q

How do platelets adhere to von Willebrand factor

A

Via Glycoprotein 1b

153
Q

How do platelets adhere to each other

A

Via Glycoprotein 2b3a

154
Q

What stimulates further platelet activation

A

Thromboxane A2 and ADP

155
Q

Primary haemostasis vs secondary haemostasis

A

Formation of platelet plug - Primary haemostasis

Formation of fibrin clot - Secondary haemostasis

156
Q

Drug with Thromboxane inhibitor function

A

Aspiring

157
Q

ADP-receptor antagonist drug

A

Clopidogrel, Prasugrel

158
Q

Drugs that are glycoprotein 2b/3a inhibitors

A

Eptifibatide

159
Q

Treatment directed against venous thrombosis

A

Inhibition of clot formation such as inhibiting Thrombin and factor Xa. Heparin/ Warfarin used

160
Q

What factors does Warfarin block

A

Factors VIIA, IXa and Xa as well as Prothrombin. All of these require vitamin K.

161
Q

How does Fibrinolysis work

A

Fibrin is converted to FIbrin Degradation Products via Plasmin which is made from Plasminogen via tissue Plasminogen Activator (tPA)

162
Q

How does Heparin function

A

Heparin binds to Anti-Thrombin 2. This causes a conformational change and increases adherence to proteins such as factors VIIa, IXa, Xa and Thrombin

Principles (14 decks)

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