Quiz
Medicine Management
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Questions in this quiz (176)
1What is pharmacology?
- AThe branch of medicine concerned with the users, effects and modes of action of drugs
- BThe branch of medicine concerned with the uses and doses of drugs
- CThe branch of medicine concerned with the amounts of drugs people can legally take
- DThe study of the human mind
2Pharmacology. Match the names to the description.
[blank_start]Pharmacokinetics[blank_end] - What the body does to the drug
[blank_start]Pharmacodynamics[blank_end] - What the drug does to the body -- APharmacokinetics
- BPharmacodynamics
3PHARMACOKINETICS
To exert a benifical pharmacological effect, a drug must be: (select all that apply)- AIn the right place
- BAt the right concentration
- CPresent for the right amount of time
- DStrong
4Complete the below for the processess involved in Pharmacokinetics
A - [blank_start]Absorption[blank_end]
B - [blank_start]Distribution[blank_end]
M - [blank_start]Metabolism[blank_end]
E - [blank_start]Excretion[blank_end]- AAbsorption
- BDistribution
- CMetabolism
- DExcretion
5ABSORPTION
To exert an effect on the body, the drug must first enter the body. How?
Select all that apply- AOral
- BRectal
- CSubcutaneous Injection
- DInhalation
- ETranscutaneous
- FBuccal
- GIntravenous
- HIntraosseous
- IMuscular Injection
- JBucces
6PARENTAL
Intravenous , Transcutaneous , Intraosseous Injection, Buccal, [blank_start]Muscular[blank_end] Injection, Subcutaneious Injection, [blank_start]Inhalation[blank_end]
ENTERAL
Oral, [blank_start]Rectal[blank_end]- ARectal
- BOral
- CIntravenous
- DInhalation
- EOral
- FRectal
- GMuscular
- HTranscutaneous
- IOral
7To be useful inside the body, the drug must what?
- ADissolve
- BBe strong enough
- CDiggest
8Rate of dissolution can control duration of drug effects?
- ATrue
- BFalse
9To be useful inside the body, the drug must dissolve.
* Rate of dissolution can control duration of drug effects
* May result in different dosages for different [blank_start]presentations[blank_end]- Apresentations
- Bpurposes
10To be useful inside the body, the drug must dissolve and what?
- ABe aborbed into the blood stream
- BDigest
- CDilute
11By what methods is the drug absorbed into the blood stream? (Select 2)
- APassive
- BFacillitated
- CAbsorb
- DIntragrate
12PASSIVE DIFFUSION
What is passive diffusion?- APassive diffusion is where the drug moves from an area of high concentration to an area of low concentraction
- BPassive diffusion is where the drug moves from an area of low concentration to an area of high concentraction
13In passive diffusion no energy is required (no energy expenditure)
- ATrue
- BFalse
14PASSIVE DIFFUSION
Drug moves from area of high concentration to area of low concentration. Which kind of drugs use this kind of diffusion? (select 2)- AWater-soluble drugs
- BLipid-soluble drugs
- Call soluble drugs
15Water-solable drugs.....
- Acannot cross hydrophobic tail region
- Bare able to cross the hydrophobic tail region
16How do water soluable drugs cross?
- AWater soluble drugs must cross using membrane pores
- BWater soluable drugs must cross by being absorbed in the cytoplasm
17Lipid-soluable drugs
- ACan dissolve directly through the lipid layer
- BCross by using the membrane pores
- CCross by active transport
18The majority of drugs can be absorbed via passive diffusion.
- ATrue
- BFalse
19FACILITATED DIFFUSION
If a drug molecule is too [blank_start]large[blank_end] to diffuse across the membrane directly / via a pore, it can be moved using a '[blank_start]transport / carrier protein'[blank_end].- Alarge
- Bsmall
- Ctransport / carrier protein'
- Dlipid layer
- EHydrophobic Tail
20Facilitated Diffusion
If the drug molecule is too large to diffuse across the membrane directly / via a pore, it can be moved using a transport / carrier protein.- AThe drug moves from high concentration to low concentration
- BNo energy expenditure
- CCarrier protein undergoes conformational change
- DEnergy is required to move the drug from high concentration to low concentration
21Active Transport
This proces is very similar to facilitated diffusion - using carrier proteins to move molecules across the membrane.- ATrue
- BFalse
22Active transport does not require energy to transport the drug
- ATrue
- BFalse
23Via Active transport, the drug is able to move from low consentration to high. It also does the following:
- ARequires energy expenditure (ATP->ADP)
- BDrugs mimicking naturally occuring substances ofter utilse this method
- CCompetitive - carriers can become saturated
- DDoes not required energy to move from low consentration to high concentration
- EIs not competitive. Instead it lies dormant in the system until required
24Endocytosis / Exocytosis is ....
- AUtilised for transporting very large drug molecules
- BUtilised for transporting very small drug molecules
- CUtilised for energy which is required for active transport
25Endocytosis
- ACell mebrane engulfs the drug molecule and pulls it into the cell - 'pinching' off the drug-filled vesicle.
- BOpposite to exocytosis - the vesicle is expelled from the cell
- CUsed in the production of new bone marrow
26Exocytosis
- ACell membrane engulfs the drug molecule and pulls it into the cell - 'pinching' off the drug filled vesicle.
- BOpposite of endocytosis - the vesicle is expelled from the cell.
27Factors which affect drug absorption include:
Blood flow to area, GI motility / malabsorption syndromes, Blood Ph (acidosis / alkalosis), Lack of specific receptor or absorption counterpart (Vit D & calcium, Inactivation of drug by acidity / enzymes, Drug interations, and what else?- AFood / Stomach acidity (enhance / impair)
- BFormation / preparation (enteric coated, slow release)
- CRoute of administration (oral vs IV)
- DSite of absorption (stomach, lungs, intestine)
28Bioavailability
What does bioavailability mean?- AHow much unchanged drug reaches systemic circulation
- BHow much is available for administration
- CHow much drug reaches the liver
- DThe bioavailability pre adminisitration
29How is bioavailility usually expressed?
- AAs a percentage
- BAs a decimal
- CAs a fraction
30Bioavailability
First- pass metabolism
* Oral drugs usually absorbed from [blank_start]small[blank_end] intestines into [blank_start]hepatice portal system[blank_end]
* Transported via the [blank_start]liver[blank_end] before reaching 'systemic circulation'.
* [blank_start]Liver[blank_end] has great metabolic capacity - [blank_start]large[blank_end] amount of the drug never reaches systemic circulation
* [blank_start]Enteral[blank_end] doses higher than [blank_start]parental[blank_end]- Asmall
- Blarge
- Chepatice portal system
- Dcentral nervous system
- Ehepatic portal system
- Fliver
- Gkidney
- Hlungs
- ILiver
- JThe kidneys
- Klarge
- Lsmall
- MEnteral
- NParental
- Oparental
- Penteral
31Distribution
Once the drug reaches the systemic circulation, it can be transported to where it needs to be (body tissue). What factors can affect this?- AAdequate tissue perfusion
- BWhether drug molecule is positively or negatively charged
- CVasocontriction / dillation
- DCirculating blood volumme / pressure
- EEffectiveness of circulation (e.g. heart problems)
- FConcentration of plasma proteins (e.g. albumin)
- GProtein binding
- HRoute of administration
32Many drugs bind to what in the blood?
- Acirculating plasma proteins
- Bcirculating red blood cells
- Ccirculating white blood cells
- Danything within the blood stream which will uptake the drug
33Binding is usually reversible --> Equilibrium exists
- ATrue
- BFalse
- CDepending on the patient
- DDepending on the blood type of the patient
34Protein binding may be tightly bound or loosely bound. How will this affect the drug?
- ADiffering release times
- BDillutes the drug through absorption
35Bound : unbound drug concentrations are not changeable.
- ATrue
- BFalse
36Only 'free' drug can have an effect on the body. What does this mean?
- AProtein / drug complex is pharmacologically inactive
- BIf the drug is free to the patient
- CIf the drug contains water
37What is the difference between an unbound and bound drug?
- AAn unbound drug can be excreted by the kidneys - bound drug is not
- BA bound drug can be excreted by the kidneys - unbound drug is not
- CThey are different shapes
- DThe only difference is the release times
38Unbound drugs can be excreted by the kidneys - bound drugs can not. Why?
- AAs unbound drug is metabolised and excreted - bound drug will release to maintain equilibrium
- Bunbound drugs carry different proteins which are excreted by the kidneys
- Cunbound drugs are extreted due to the components within the binding
39Drugs may compete for binding sites (drug interations)
- ATrue
- BFalse
40Metabolism
Where is the main site for metabolism?
although can be metabolised in other organs too.- ALiver
- BKidneys
- CLungs
- DSmall intestine
41What can affect metabolim?
- ACan be affected by hepatic blood flow and function
- BCan be affected by age of patient
- CCan be affected by diet of patient
42What is Hepatic extraction radio?
- AExtent to which the liver removes a drug from incoming blood
- BExtent to which how much drug enters the liver
43Hepatic Extraction Ratio
Drugs with a high hepatic extraction ratio either cannot be given orally or must be given in higher oral dosages.
Tick the drugs below which have high hepatic extration ratio?- AGTN - cannot be given orally to avoid first pass metabolism
- BMorphine
- CLignocaine
- DParacetamol
44What does lipophilic mean?
- ABetter ability to cross phospholipid layer
- BFull of lipohilic
- CCan not cross the phospholipid layer
45PHARMACODYNAMICS
What is a receptor?- AProtein which offers a binding site for a molecule (acts as a lock)
- BAny molecule which attaches to a ligand ('key' which fits a 'lock')
46What is a Ligand?
- AProtein which offers a binding site for a molecule (acts as a 'lock')
- BAny molecule which attaches to a receptors
47Receptor is usually linked to an 'integral membrane protein' which allows molecules on one side of the cell to have an effect of the other. What is and Endogenous Ligand?
- AThe body's natural chemical which activates the receptor
- BThe body's natural chemical which deactivates the receptor
48What is an agonist?
- Amolecule which activates the receptor (lock)
- Ba type of ligand which attaches to the receptor
- Ca type of protein
49Agonists have a receptor binding site which is similar to _______ , allowing them to bind to the receptor and elicit a response.
- Athe endogenous ligand
- Bprotein molecules
- Cnothing
50Full / Partial Agonist
What is a full agonist?- AWhen full agonists bind, they fit the receptor perfectly, touching all of the necessary surfaces and the full response is elicited
- BOnly activates some of the receptor surface, therefore causing only a partial response
- CA receptor binding site which is full
51What is a partial agonist?
- AA partial agonist fits the receptor to varying degrees & only activates some of the receptor surface, therefore only causing a partial response.
- BA partial agonist is part receptor binding site and part protein.
- CA partial agonist fits the receptor, touching all the necessary surfaces but only part of the response is elicited
52What is an Antagonist?
- Aa molecule which competitively blocks the receptor ('lock') to stop agonist from activating it.
- Ba receptor binding site which is similar to the endogenous ligand, allowing them to bind to the receptors and elicit a response.
- Ca blocked receptor binding site
- Da large receptor binding site which is similar to the endogenous ligand, allowing them to bind to the receptor and elicit a larger response.
53Antagonists are shaped [blank_start]similarly enough[blank_end] to the endogenous ligand to allow them to fit into the [blank_start]receptor site[blank_end], but don't fit well enough to elicit a response from the cell.
They compete for & block the receptor site, stopping endogenous ligands from binding & therefore [blank_start]blocking the response[blank_end] they would usually elicit.- Asimilarly enough
- Bexactly
- Creceptor site
- Dligand
- Eblocking the response
- Fmimic the response
54What is a neurotramitter?
- AChemical which conveys messages (chemical messages)
- BA type of neuron
- CA type of protein
55Neurotransmitters carry messages between nerve cells, across synapses.
They are important in conveying messages to and from the [blank_start]brain[blank_end].
These neurotramitters are packaged into [blank_start]vesticles[blank_end] in the nerve endings, and are released into the [blank_start]synapse[blank_end] when the impulse is received. They travel across the synapse and bind to their [blank_start]allocated receptor[blank_end], allowing the message to be carried further.- Abrain
- Bliver
- Ckidneys
- Dmuscles
- Evesticles
- Fbundles
- Gprotein molecules
- Hsynapse
- Iliver
- Jallocated receptor
- Kallocated protein
56There are a variety of different neurotransmitters, all with different purposes:
Adrenaline - [blank_start]fight or flight[blank_end] neurotransmitter
Dopamine - [blank_start]Pleasure[blank_end] neurotransmitter
GABA - [blank_start]Calming[blank_end] neurotransmitter
Glutamate - [blank_start]Memory[blank_end] neurotransmitter
noradrenaline - [blank_start]Concentration[blank_end] neurotransmitter
Serotonin - [blank_start]mood[blank_end] neurotransmitter
Acetylcholine - [blank_start]learning[blank_end] neurotransmitter
Endorphine - [blank_start]Euphoria[blank_end] neurotransmitter- Afight or flight
- Bpleasure
- Ccalming
- Dmood
- EPleasure
- Ffight or flight
- Geuphoria
- HCalming
- Ipleasure
- JMemory
- Kmood
- LConcentration
- Mmemory
- Nmood
- Opleasure
- Plearning
- Qcalming
- REuphoria
- Spleasure
57Theories of drug action
There are four main methods by which drugs have an effect on the body:- ABinding to receptor sites
- BAltering a normal metabolic pathway
- CChanging the physical properties (osmotic balance) of cells
- DChemically combining with other proteins / chemicals
- EChaning proteins / chemicals within the body
58Adrenergic Receptors
How many adrenergic receptors are there?- A5
- B6
- C7
59a1 adrenergic receptor :
- ALocated mainly in smooth muscle (mainly arteries & veins). When activated they stimulate vasoconstriction, increase blood pressure, dilate pupils (mydriasis) - Activated by adrenaline & noradrenaline
- BFound in pre-synaptic nerve endings when activated, they inhibit release of noradrenaline, acetylcholine and insulin. - Activated by adrenaline & noradrenaline
- CLocated mainly in cardiac muscle when activated, they increase heart rate & cardiac contractility, stimulate fat breakdown & increase renin release - Activated by adrenaline & noradrenaline
- DFound mainly in smooth muslce of the bronchi & vein. When activated, they stimulate relaxation of the smooth muscles (bronchodilation & vasodilation), increase sugar availability (glycogenolysis) & relax uterine smooth muscle.
- EFound mainly in cardiac muscle & fat tissue. Not well understood at present. Thought to be involved in pathophysiology of heart failure.- Thought to be activated by adrenaline and noradrenaline.
60a2 adrenergic receptor:
- AFound in pre-synaptic nerve endings. When activated, they inhibit release of noradrenalilne, acetylcholine & insulin.
- BLocated mainly in cardiac muscle. When activated, they increase heart rate & cardiac contractility, stimulate fat breakdown and increase renin release.
- CFound mainly in smooth muscle of the bronchi and veins.
- DLocated in smooth muscle (mainly arteries and veins) When activated, they stimulate vasoconstriction, increase blood pressure, dilate pupils (mydriasis)
61b1:
- ALocated mainly in cardiac muscle. When activated, they increase heart rate and cardiac contractility, stimulate fat breakdown and increase renin release.
- BLocated mainly in smooth muscle (mainly arteries and veins) When activated, they stimulate vasoconstriction, increase blood pressure, dilate pupils (mydriasis)
- CFound mainly in smooth muscle of the bronchi and veins. When activated, they stimulate relaxation of the bronchi and veins.
62b2:
- AFound mainly in smooth muscle of the bronchi and veins. When activated they stimulate relaxation of the smooth muscles (bronchodilation and vasodilation), increase sugar availability (glycogenolysis) and relax uterine smooth muscle.
- BLocated mainly in smooth muscle (mainly arteries and veins) When activated, they stimulate vasoconstriction, increase blood pressure, dilate pupils.
- CFound in pre-synaptic nerve endings. When activated, they inhibit release of noradrenaline, acetylcholine and insulin
63b3:
- AFound mainly in cardiac muscle and fat tissue. Not well understood at present.
- BFound in pre-synaptic nerve endings when activated, they inhibit release of noradrenaline, acetylcholine and insulin
- CFound mainly in smooth muscle of bronchi and veins. When activated, they stimulate relaxation of the smooth muscles (bronchodilation and vasodilation), increase sugar availability (glycogenolysis) and relax uterine smooth muscle.
64What is released by the adrenal gland in adrenergic stimulation?
- AEpinephrine
- BAdrenaline
- CDopamine
65Which receptors cause excitation?
- Aa1 & b1
- Ba2 & b2
66Which receptors cause inhibition?
- Aa2 & b2
- Ba1 & b1
67Cholinergic Receptors
2 different types, both activated by what?- Aacetylcholine
- Badrenaline
68What are the 2 different types of cholinergic receptors?
- ANicotinic & Muscarinic receptors
- BNicotonic & Muscareane receptors
69Nicotonic receptors: usually found in the ____________
- Apost synaptic neurones
- Bcentral nervous systems
- Cliver
70Muscarinic receptors are usually found in _________
- Atarget tissue
- Bpost synaptic neurones
- Cspinal cord
- Dbrain
71Muscarinic receptors: Usaully found in the target tissue
m1 receptors: [blank_start]CNS[blank_end]
m2 receptors: [blank_start]Heart[blank_end]
m3 receptors: [blank_start]Smooth muscle[blank_end] (bronchi, exocrine glands, bladder)
m4 receptors: [blank_start]CNS[blank_end]
m5 receptors: [blank_start]CNS[blank_end]- ACNS
- BHeart
- CLiver
- DHeart
- ELiver
- FCNS
- GSmooth muscle
- HSoft muscle
- ICNS
- JHeart
- KCNS
- LHeart
72Adrenergic Receptors
a1: Located mainly in [blank_start]smooth muscle[blank_end] (mainly arteries and veins). When activated, they stimulate [blank_start]vasoconstriction[blank_end], increase blood pressure, dilate pupils ([blank_start]mydriasis[blank_end])- Asmooth muscle
- Bcardiac muscle
- Cvasoconstriction
- Dadrenaline
- Emydriasis
- Fmidriasis
73a2: Found in [blank_start]pre-synapitic nerve endings[blank_end]. When activated, they inhibit release of [blank_start]noradrenaline, acetylcholine and insulin[blank_end].
- Apre-synapitic nerve endings
- Bcardiac muscle
- Cnoradrenaline, acetylcholine and insulin
- Dadrenaline, renin and insulin
74b1: Located mainly in [blank_start]cardiac muscle[blank_end]. When activated, they increase [blank_start]heart rate and cardiac contractility[blank_end], stimulate fat breakdown and increase [blank_start]renin[blank_end] release.
- Acardiac muscle
- Bsmooth muscle
- Cheart rate and cardiac contractility
- Dblood pressure
- Erenin
- Fvasoconstriction
75b2: Found mainly in [blank_start]smooth muscle[blank_end] of the [blank_start]bronchi and veins[blank_end]. When activated, they stimulate relaxation of the smooth muscles ([blank_start]brochodilation and vasodilation[blank_end]), increase sugar availability (glycogenolysis) and relax [blank_start]uterine smooth muscle[blank_end].
- Asmooth muscle
- Bcardiac muscle
- Cbronchi and veins
- Darteries and veins
- Ebrochodilation and vasodilation
- Fincrease blood pressure
- Guterine smooth muscle
- Hthe heart muscle
76What is first pass metabolism?
- ARemoval / inactivation of drugs before reaching the systemic circulation by the liver
- BRemoval / inactivation of drugs after reaching the liver
- CRemoval / activation of drugs before reaching the systemic circulation by the liver
77What organ is responsible for excretion?
- ALiver
- BKidneys
- CLungs
78Paracetamol is an:
- AAnalgestic & Antipyretic
- BAnalgestic only
- CAntipyretic only
79Ibuprofen is an NSAID:
- AAnalgestic, Anytpyretic and Anti-inflammatory
- BAnalgestic & Anytpyretic
- CAnalgestic and Anti-inflammatory
80Pain is detected by what?
- Anociceptors
- Breceptors
- Cneurons
81What are nociceptors?
- ASpecialised cells which detect unpleasant (noxious) stimuli
- BSpecialised neurons which detect unpleasant (noxious) stimuli
- CSpecialised cells which attach to protein
82NOCICEPTORS
These stimili are converted into [blank_start]electrical signals[blank_end] and transported to the brain, to inform it that the body has suffered an [blank_start]insult.[blank_end]- Aelectrical signals
- Belectric shocks
- Cinsult.
- Da shock
83When tissue is damaged, inflammatory mediaters are released. Name proteins called ____?
- AProstaglandins, cytokines & leukotrienes
- BPrestoglodins, cyteekines & lukotrients
84Although not full understood, it is believed that both paracetamol & NSAIDs such as ibuprofen have an inhibitory effect on the production of prostaglandins. Ibuprofen is known as a __________?
- ACOX inhibitor
- BCIX inhibitor
- CCON inhibitor
85Both paracetamol & ibuprofen are also known to have an anti-pyretic effect. So can be used to reduce ______.
- AFever
- BNausea
86Entonex
50/50 misxture of oxygen & ______.- ANitrous oxide (N2O)
- BNitrous dioxide
- CCarbon dioxide
87Entonox appears to stimulate the release of [blank_start]endogenous opiod molecules[blank_end], stimulating opioid receptors in the CNS.
Entonox also appears to have an [blank_start]anxiolytic[blank_end] effect - though to be from binding to the [blank_start]benzodiazepine[blank_end] binding site on GAGAa receptors.
Most contraindications and cautions are due to the potential dangers of [blank_start]nitrogen[blank_end] build-up in the body.- Aendogenous opiod molecules
- Bandogenous opiod molecules
- Cindogenous opiod molecules
- Danxiolytic
- Eantixiolytic
- Famiotic
- Gbenzodiazepine
- Hpenzodiazepine
- Imenzodiazepine
- Jnitrogen
- Koxygen
- Lcarbon dioxide
88Salbutoamol
Salbutamol is a highly selective _______ agonist.- AB2
- BB1
- CA1
89Salbutamol is a highly selective B2 agonist. This means ________
- AIts structure has been manipulated so that it predominatly activates the B2 adrenoceptors rather that all adrenoceptors
- BThis allows bronchodilation and eases the spasms in the smooth muscle during an asthma attack.
- Cappears to stimulated the release of endogenous opiod molecules, stimulating opiod receptors in the CNS
90Salbutamol
Although highly selective for B2 adrenoceptors, salbutamol does still have a slight effect on B1 receptors.- AHypertension: Renin release activates the renin-angiotensin - aldosterone system which raises blood pressure
- BAngina: Increase HR & cardiac contractility can put undue pressure on the heart
- COveractive thyroid: Suffers already have an elevated metabolic rate. Lipolysis can worsen this.
- DLate pregnacy: Relaxation of the smmoth muscle (an effect of B2 adrenoceptor stimulation.
- EPotential for severe hypertension in conjuntion with beta-blockers:B- agonist & antagonist competing for same receptor.
91What are the side effects of salbutamol
- ATachycardia
- BPalpitations
- CHeadache
- DFelling of tension
- EPeripheral vascodilation
92Ipratropium is an
- Aantagonist at muscarinic receptors
- Bagonist at the muscarinic receptors
93Therefore Ipratropium Bromide_____
- Ais an anti-muscarinic bronchodilator (anti-cholingergic drug)
- Bis a muscarinic bronchodilator (anti-cholingergic drug)
94Ipratropium usually blocks __________ from binding to its M3 muscarinic receptors
- Aacetylcholine
- Batrenaline
- Cdopamine
- Dacychorine
95Ipratropium bromide blocks acetylcholine from binding to its M3 muscarinic receptors in the smooth muscle of the bronchi.
This blocks what?- AThe bronchoconstrictive effects of acetylcholine creates
- BThe bronchodilation effects of acetylcholine creates
- CThe receptror site for B2
96Cautions in Ipratropium Bromide use
Cholinergic activation usually results in : [blank_start]increased[blank_end] sweating, [blank_start]increased[blank_end] digestive secretions; [blank_start]decreased[blank_end] pulserate; [blank_start]constriction[blank_end] of the pupils; [blank_start]contraction[blank_end] of smooth muscle in the lungs, bladder and digestive tract.- Aincreased
- Bdecreased
- Cincreased
- Ddecreased
- Edecreased
- Fincreased
- Gconstriction
- Hdilation
- Icontraction
- Jrelaxation
97Name the cautions of Impratropium bromide
- AGlaucoma, pregnancy, breastfeeding and prostatic hyperplasia
- BPregnancy and breast feeding
- CAsthma
- DMental capacity
98Glaucoma: Ipratropium bromide blocks the [blank_start]muscarinic receptors[blank_end] controlling the constriction of the pupils. This can block the drainage of the fluid around the lens and can raise [blank_start]intra-ocular pressure[blank_end]
- Amuscarinic receptors
- Badrenic receptors
- Cintra-ocular pressure
- Douter-ocular pressure
99Pregnancy: Ipratropium bromide blocks the muscarinic receptors in the [blank_start]smooth muscle of the uterine wall[blank_end] - may cause the [blank_start]relaxation[blank_end] of the uterus.
Breast feeding: many drugs are excreted in [blank_start]breast milk[blank_end] - caution advised.
Prostatic hyperplasia - prone to uring retension- Asmooth muscle of the uterine wall
- Bcardiac muscle of the uterine wall
- Crelaxation
- Dconstriction
- Ebreast milk
- Furine
100Side effects of Ipratropium bromide use.
Cholinergic activation usually results in; increase sweating; increased digestive secretions; decreased pulse rate; constriction of the pupils; contraction of the smooth muscle in the lungs, bladder and digestive tract.
What are the side effects?- ANausea: Potentially as a result of decreased digestive secretions and relaxation of the digestive tract
- BDry mouth: Decrease digestive secretion
- CTachycardia: Ipratropium blocks the parasympathetic action of acetylcholine on the heart, speeding up the P.R
- DParoxysmal tighness of the chest
- EHeadache and feeling of tension
101ADRENALINE 1:1000
Adrenaline stimulates which adrenoceptor (s) ?- Aboth alpha and beta
- Balpha
- Cbeta
102What is adrenaline 1:1000 given for:
- ARespiratory problems and anaphalysis
- BBrady cardia
- CHypertension
103What action do we want with Adrenaline 1:1000?
- AThe action we want in this case is with the B2 receptors in the lungs, to aid brochodilation
- BThe action we want in this case is with the B1 receptors in the lungs, to aid brochodilation
- CThe action we want in this case is with the A1receptors in the lungs, to aid brochodilation
- DThe action we want in this case is with the A2 receptors in the lungs, to aid brochodilation
104Adrenaline is non-selective, so it will also produce reactions associated with the outer adrenoceptors
- ATrue
- BFalse
105What are the contraindications of Adrenaline 1:1000?
- AHypothermia
- BHyperthermia
- CHypertension
- DHypotension
106What are the cautions for Adrenaline 1:1000?
- APatients on beta-blockers (may cause severe hypertension)
- BPatients on anitbiotics (may cause severe hypertension)
- CPatients already in distress (may cause severe hypertension)
- DPatients on warfarin (may cause severe hypertension)
107What is Hydrocortisone?
- AA glucocorticoid drug which reduces inflammation and suppresses immune response
- BA drug which caused vasodillation
- CA drug which caused vasoconstriction
- DA histomine
108HYDROCORTISONE
By binding to [blank_start]glycocorticoid[blank_end] receptors, hydrocortisone causes the new drug / receptor complex to be relocated to the cell [blank_start]nucleus[blank_end], where it alters the expression of certain proteins.
Secondly, it stimulates the cell to produce a protein called [blank_start]lipocortin-1[blank_end]. This migrates out of the cell and attaches itself to receptors on the [blank_start]leukocyte membrane[blank_end].
This stops them from reacting to the inflammation and releasing more [blank_start]inflammatory proteins[blank_end] (such as [blank_start]cytokines[blank_end], histamine, leukotrienes).
Histamines cause vaso[blank_start]dilation[blank_end], increased vascular permeability, bronchospasm and stimulate [blank_start]mucus[blank_end] production.
[blank_start]Leukotrienes[blank_end] cause bronchial smooth muscle contraction, vascular permeability and increased mucus secretion.- Aglycocorticoid
- Bglycogen
- Chydrocortisone
- Dnucleus
- Emembrane
- Flipocortin-1
- Gmuscarinic m3
- Hlipocoatine - 2
- Ileukocyte membrane
- Jglycocorticoid membrane
- Kinflammatory proteins
- Ldopamine
- Mcytokines
- Nadrenaline
- Odilation
- Pconstriction
- Qmucus
- Rmuscle
- SLeukotrienes
- Tcytokines
109DIAZEPAM / DIAZEMULS AND MIDAZOLAM
Diazepam and midazolum are both __________?- ABenzodiazepines
- BTypes of adrenaline
- CTypes of nerve cells
- DGlucocorticord drugs
110When a seizure occurs, what is happening within the body?
- AThe neurons fire too rapidly and the brain becomes over-stimulated
- BThe neurons fire too slowly and the brain becomes under-stimulated
- CThe neurons fire too rapidly and the brain becomes under-stimulated
- DThe neurons fire too slowly and the brain becomes over-stimulated
111Benzopdiazepines are [blank_start]GABA-A[blank_end] (gamma- Aminobutyric Acid) [blank_start]Agonists[blank_end]. They act of the GABA-A receptors. These are ligand - gated chloride channels, located in the [blank_start]neuron[blank_end] synapses.
GABA-A receptors have binding sites for [blank_start]endogenous[blank_end] GABA, but have a seperate site for [blank_start]benzopdiazepine[blank_end] binding.
When a benzodiazepine binds, it enhances the effects of the endogenous GABA ligand, casuing the ion channels to [blank_start]open[blank_end] more [blank_start]ofte[blank_end].
GABA-A: Ligand -gated ion channel
Binding sites for a variety of drugs with [blank_start]anziolytic[blank_end], anticonvulsant, sedative and muscle relaxant properties.- AGABA-A
- BGABA-B
- CGABA-C
- DAgonists
- EAntagonists
- Fneuron
- Ghepatic
- Hendogenous
- Iundogenous
- Jbenzopdiazepine
- Kprotein
- Lantagonist
- Mopen
- Nclose
- Ooften
- Pwidely
- Qanziolytic
- Rantiziolytic
112HYPERPOLARISATION
Our nerve cells are usually negative on the inside and positive on the outside. This is usally held stable - 'resting potential'- ATrue
- BFalse
113For a neuron to 'fire' what does it need?
- AFor a neuron to fire it needs to create an 'action potential' by deplorising.
- BFor a neuron to fire it needs to create ATP
- CFor a neuron to fire it needs receive a neurologically message from the cells.
114For a neuron to 'fire' it needs to create an 'action potential' by depolarising. This happens via ion exchange which _____
- Amakes the inside of the cell less negative, allowing the charges to swop for a fraction of a second
- Bmakes the inside of the cell posivtely charged, allowing the charges to swop for a fraction of a second
- Cmakes the inside of the cell less aggressive, allowing the charges to swop for a fraction of a second
- Dmakes the inside of the cell less negative, which disallows the charges to swop, even for a fraction of a second
115For a neuron to fire it needs to create an action potential by deploarising. This happens via ion exchange, making the inside of the cell less negative and allowing the charges to swop for a fraction of a second. When this happens too rapidly, for example in a seizure state.......
- Athe influx of negatively charged CI- ions INTO the cell, via the GABA-A gated chloride channel, causes the interior of the cell to become more negative.
- Bthe influx of negatively charged CI- ions INTO the cell, via the GABA-b gated chloride channel, causes the interior of the cell to become more positive.
- Cthe influx of positively charged CI- ions INTO the cell, via the GABA-A gated chloride channel, causes the interior of the cell to become more negative.
116For a neuron to fire it needs to create an action potential by deploarising. This happens via ion exchange, making the inside of the cell less negative and allowing the charges to swop for a fraction of a second. When this happens too rapidly, for example in a seizure state, the influx of negatively charged CI- ions INTO the cell, via the GABA-A gated chloride channel, causes the interior of the cell to become more negative 'hyperpolarisation'
- AThis makes it much more difficult for the excitatory neurotransmitters to depolarise the neuron, therefore no action potential is created and these impulses are not carried along the neurons, the message is stopped.
- BThis makes it easier for the excitatory neurotransmitters to depolarise the neuron, therefore action potential is created and these impulses are carried along the neurons, the message is received.
117Side effects of Benxodiazepines.
[blank_start]Resp. depresson, Drowsiness,[blank_end] light- headedness, confusion, unsteadiness and amnesia.
Benzodiazepines have a general systemic effect - all caused by various impulses being [blank_start]blocked[blank_end] as a result of hyperpolarisaton.- AResp. depresson, Drowsiness,
- BHypertension, Tackycardia,
- Cblocked
- Dopened
118MORPHINE SULPHATE
- AMorphine is a strong opioid analgestic
- BIt crosses the blood-brain barrier and acts directly on the CNS
- CIt acts upon opioid receptors, found mainly in the CNS and digestive system
- DIt mimics the effects of endorphins (short for endogenous morphine)
- EMorphine is a benzodiazepine
- FMorphine stimulates both alpha and beta receptors
119Morphine Sulphate has a large number of opioid receptors. Which are the main three?
- AU-, 6- AND K-
- BK- AND CO-
120Morphine Sulphate
U- receptors have a variety of subtypes
* U1: [blank_start]Analgesia & dependance[blank_end]
* U2: [blank_start]Resp. Depression, myosis, euphoria,[blank_end] reduced GI motility, depednace
* U3 - Unknown.- AAnalgesia & dependance
- BResp. Depression
- CUnknown.
- DResp. Depression, myosis, euphoria,
121Morphine is a specific U- receptor
- Aagonist
- Bantagonist
122Morphine is a __________
- Ahydrophilic (water-loving) molecule which results in a slow passage across the blood-brain barrier
- Bhydrophilic (water-loving) molecule which results in a fast passage across the blood-brain barrier
- Chydrophobic (water-hating) molecule which results in a slow passage across the blood-brain barrier
123Morphine acts in a very similar way to benxodiazepines, but
- Astops nociceptors from producing pain - signals to send to the brain.
- Bproduces nociceptors pain - signals & sends them to the brain.
- Cstops nociceptors from producing protein signals to send to the brain.
124Morphine inhibits a number of ____________ channels from opening, stopping positively charged calcium ions from entering the neuron.
It also activates pumps which push _______ ioncs out of the cell. Making the inside of the cell MORE negative, hyperpolarisation. This makes the cell more difficult to depolarise. Action potiential can not be produced and therefore the pain message cannot be transmitted.- ACa2, K+
- BCO2, K+
- CCa2, K-
- DCOX , O2
125What are the contraindications of morphine sulphate?
- AChildren under 1: increased permeability of the blood-brain barrier in young children.
- BRespiratory depression: (Less than 10/min): U receptors stimulate resp. depression
- CHypotensions: morphine can cause vasodilation and reduce baroreceptors reflexes, allowing the blood pressure to drop. Vasodilation occurs because morphine causes local histamine-modulated nitric oxide release, but mechanism is not fully understood.
- DHypertensions: morphine can cause vasodilation and reduce baroreceptors reflexes, allowing the blood pressure to drop. Vasodilation occurs because morphine causes local histamine-modulated nitric oxide release, but mechanism is not fully understood.
- EBradycardia
- FHypotensions: morphine can cause vasoconstriction and reduce baroreceptors reflexes, allowing the blood pressure to drop. Vasoconstriction occurs because morphine causes local histamine-modulated nitric oxide release, but mechanism is not fully understood.
- GHead injury with significantly impaired level of consciousness and Headach: Pre-existing raised ICP can enhance the resp. depression effects of morphine and further elevate cerebrospinal fluid pressure through vasodilation (monroe-kellie hypothesis)
126What is Atropine used for ?
- ABradycardia
- BTackycardia
- CHypertension
- DTo increase resp. rate
127Atropine is a Anticholinergic drug which means what?
- AIt is an antagonist at the muscarinic receptor
- BIt is an angonist at the muscarinic receptor
- CIt affects both the nicatinic and muscaric receptors
128Vagus (parasyspathetic) nerves that innervate the heart release what as thier primary neurotransmitter?
- Aacetylcholine
- Badrenaline
- Cadrenic
- Dacetonin
- ERenin
129ACh binds to which receptors which are found mainly in the SA and AV nodes?
- AMuscarinic receptors (M2)
- BNicotrinic receptors
- CMuscarinic receptors (M3)
- DMuscarinic receptors (M4)
130Atropine
Increases vagal activity to the SA node - decreases the firing rate of the pacemaker cells which does what?- ADecreases the heart rate
- BIncreases the heart rate
- CCauses hypertension
- DCauses hypotension
131Atropine [blank_start]antagonises[blank_end] effect - reverses [blank_start]bradycardia[blank_end]
- Aantagonises
- Bagonises
- Cbradycardia
- Dtackycardia
132What is the contraindication of Atropine?
- Abradycardia related hypothermia
- Btackycardia related hyperthermia
- CPregnancy
- DElderly and children
133What are the side effects of Atropine?
- ADry mouth, visual blurring, dilated pupils ( cholinergic response (ACh mediated) being antagonised)
- BConfusion / occasional hallucinations
Can cross the BBB and act directly on the M1/M4/M5 receptors of the CNS - CRetention of urine (elderly)
Bladder relaxation (M3- smooth muscle) - inability to empy bladder effectively. - DHeadache and feeling of tension
- EResp. depression
- FConfusion
134Atropine
MI-related bradycardia
Use atropine cautiously in the presence of actue MI or ischaemia. Why?- AIncreases the heart rate - which increases the workload of the heard - increase myocardial oxygen demand (worsen ischaemia)
- BAtropine will not reach all areas of the heart; causing toxic buildup
135DRUG ADMINISTRATION
Routes of administration
Percutaneous:- AAbsorbed through the skin or mucous membrane
- BAborbed via the alimentry canal
- CAbosrbed via any other route
136Enteral:
- AAbsorbed through the skin or mucous membrane
- BAbsorbed via the alimentry canal
- CAbsobed via any other route
137Parenteral:
- AAbosorbed through the skin or mucous membrane
- BAbsorbed via the alimentry canal
- CAbsorbed via any other route
138Absorption:
Buccal and sublingual- Amoderate / fast absoption: 3-10 minutes
- Bfast absoption: 60 seconds
- Cslow absorption: 30-60 minutes
139Inhaled drugs.
- AModerate / Fast acting - 3 minutes
- BModerate / Fast acting - 3 - 15 minutes
- CFast acting - 60 seconds
140Oral drugs:
- ASlow rate of absorption : 30-90 minutes
- BModerate / fast absorption: 3 minutes
- CModerate / fast absorption: 3 - 10 minutes
- DFast absorption - 60 seconds
141Rectal drugs:
- Amoderate / fast absorption : 5-30 minutes
- Bmoderate / fast absorption : 3-10 minutes
- Cslow absorption :30-90 minutes
- Dfast absorption: 60 seconds
142Parental Drug Routes
Subcutaneous and Intramuscular injections are both given via injections.
[blank_start]Subcutaneous[blank_end]: Injection into the fat or connetive tissue beneath the skin
[blank_start]Intramuscula[blank_end]r: Injection into the underlying muscle- ASubcutaneous
- BIntramuscula
143What is the largest amount which can be injected subcutaneously?
- ALess than 2ml
- B5ml
- C1ml
- D10 ml
144How long does a drug which has been given subcutaneously take to reach peak drug effect?
- A30 minutes
- B5 minutes
- C60 seconds
- D90 minutes
145What size needle is normally used when giving a subcutaneous injection?
- A25G
- B20G
- C18G
- D16G
146What is the absorption rate for an Intramuscular injection?
- A10-20 Minutes
- B30 minutes
- C60 seconds
- D45-90 minutes
147Intramuscular injections are giving using a [blank_start]hypodermic[blank_end] needle.
Usually limited to [blank_start]1-2ml[blank_end] injections (although can give up to 5mls in larger muscles)
Green: [blank_start]21G[blank_end]
Blue : [blank_start]23G[blank_end]
Orange: [blank_start]25G[blank_end]- Ahypodermic
- Bcannula
- Chyperdermic
- D1-2ml
- E3ml
- F2.5ml
- G21G
- H32G
- I52G
- J23G
- K56
- L25G
- M52G
- N29G
148Intravenous is where the cannula is inserted where?
- AVein
- BBone
- CMuscle
- DFat tissue
149Intravenous Injection requires a cannula to be placed in a peripheral [blank_start]vein[blank_end].
Orange / Brown - 14G
Grey: [blank_start]16G[blank_end]
Green: [blank_start]18G[blank_end]
Pink: [blank_start]20G[blank_end]
Blue: [blank_start]22G[blank_end]
Yellow: [blank_start]24G[blank_end]- Avein
- Bartery
- C16G
- D24G
- E18G
- F16G
- G20G
- H25
- I22G
- J24G
- K24G
- L16G
150What is the absorption time for a drug which has been given via IV?
- A30-60 seconds
- B5 minutes
- C1-2 minutes
- D90 minutes
151DRUG CALCULATIONS.
What does the formula WIG Stand for?- AWhat does do we WANT, What volume it is IN, What dose we have already GOT
- BWHAT have we got, What volume it is IN, What do we Want
- CWeight, Inches, Grams
152WETFLAAG
Paediatric ALS calculations can be difficult to remember. Wetflag is used to help.
W[blank_start]eight[blank_end]
E[blank_start]nergy[blank_end]
T[blank_start]ube[blank_end]
F[blank_start]luid[blank_end]
L
A[blank_start]drenaline[blank_end]
A[blank_start]miodarone[blank_end]
G[blank_start]lucose[blank_end]- Aeight
- Bnergy
- Cube
- Dluid
- Edrenaline
- Fmiodarone
- Glucose
153Cardiac Arrest Drugs
Adrenaline (1:[blank_start]10,000[blank_end])
[blank_start]1mg[blank_end] in 10 mls
Stimulates alpha and beta adrenergic receptors
Vasco[blank_start]constriction[blank_end] effects: adrenaline binds directly to alpha-1 adrenergic receptors of the blood vessels causing direct vasoconstriction = elevated [blank_start]blood pressure[blank_end].
Cardiac outputs: adrenaline also binds to beta-1 adrenergic receptors of the heart. This indirectly improves [blank_start]cardiac[blank_end] output by:
Increasing h[blank_start]eart[blank_end] r[blank_start]ate[blank_end]
Increasing heart muscle [blank_start]contract[blank_end]ility
Increasing [blank_start]conduct[blank_end]ivity through AV node.- A10,000
- B1mg
- Cconstriction
- Dblood pressure
- Ecardiac
- Feart
- Gate
- Hcontract
- Iconduct
154Cardiac Arrest Drugs
Amiodarone
[blank_start]300[blank_end]mg in 10 mls
Anti-arrhythmic: lenghens cardiac action potential & therefore promotes effective refratory period
Blocks [blank_start]sodium[blank_end] and potassium channels
Acts to stabilise and r[blank_start]educe[blank_end] electrical irritability
Given after 3rd shock and fith shock (150mg given)
Given only in pulseless [blank_start]VT[blank_end] and [blank_start]VF[blank_end].- A300
- Bsodium
- Ceduce
- DVT
- EVF
155Intravenous Fluids
What types are there?- ACrystalloids
- BColloids
156How many units of fluid do we give to 1 unit of blood loss?
- A3
- B1
- C5
157Intravenous Fluids only function is to expand the intravascular compartment in an attempt to increase blood pressure and support organ perfusion (isotonic)
- ATrue
- BFalse
158Sodium Chloride 0.9%
- AStays within the intravascular compartment (and so good at supporting blood pressure, albeit intially)
- BDoes not create a fluid shift to other compartments
- CCan cause circulatory overload
- DCan not cause circulatory overload
- ECan overload vascular compartment
- FCan not overload vascular compartment
- GHas no oxygen carrying capacity
159Digoxin is used for the treatment of post myocardial infarction by reducing the conductivity at the AV node.
- ATrue
- BFalse
160Statins are prescribed for patients who may be at risk of atherosclerosis and for conditions such as heart disease and angine.
- ATrue
- BFalse
161Statins help to reduce cholesterol (HDL)
- ATrue
- BFalse
162Which of the following is a commonly prescibed statin? (only one answer is correct)
- APropranolol
- BAmlodipine
- CSivastatin
163ACE stands for
- AAngiotensin Converting Enzyme
- BAngiogram Confessing Enzyme
- CAngio Converting Enzyme
164The role of ACE inhibitors is to primarily:
- AIncrease water and sodium reabsorption
- BCause vasodilation and reduce water reabsotption
- CReduce heart rate
165Calcium channel blockers such as amlodipine, reduce myocardial contractility, supress electrical activity and are useful for treating hypertension.
- ATrue
- BFalse
166What classification of drug is isosorbide monohydrate?
- ANitrate
- BBeta-blocker
- CVasoconstrictor
167What is the primary action of isosorbide monohydrate?
- ATo cause vasoconstriction, to increase ventricular pre-load and to increase blood pressure
- BTo cause vasodilation, to decrease ventricular pre-load and reduce blood pressure
168What is the drug bendroflumethiazide typically presribed for?
- ACoagulation problems
- BPain relief
- CHpertension
169Atrovent is the trade name for which drug?
- ASalbutamol
- BIpratropium Bromide
170Predisolone is a corticosteroid. What is the primary function of such a drug?
- APain relief
- BTo help build new tissue
- CReduce inflammation
171Aspirin is a NSAID and is useful for arthritis
- ATrue
- BFalse
172Which of the following will assist with pain management?
- ANaproxen
- BDiclofenac
- CAspirin
- DAll of the above
173Which drug classification am I? I have an enhanced response to the inhibitory neurotransmitter GABA and if too much of me is administered, I am very good at causing respiratory depression (tee-hee)
- ABenzodiazepines
- BBeta-Blocker
174Which of the following is a drug that is commonly administered for patients with a stomach ulcer?
- AMetoclopramide
- BLansoprazole
- CCyclizine
175Which drug classification do Sertraline and Amitriptyline belong to?
- AAnti-arrythimics
- BAnti-coagulants
- CAnti-depressants
176Which drug classification am I? I am used for the managment of hypertension and anxiety by a reductionin resting heart rate, cardiac output, systolic and diastolic blood pressure.
- ABeta-Blocker
- BBenzodiazipoid
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- Paramedic Practice Quiz on Medicine Management, created by Vicki Walker on 30/03/2017.
- Author
- Vicki Walker
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- English
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