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MRCEM Primary Exam > Lyfjafræði > Flashcards

Lyfjafræði Flashcards

1
Q

Hver er munurinn á insúlín NPH (neutral protamine hagedron) og regular insúlín?

A

Regular insúlín er kombination prodúkt sem virkar hraðar en insúlín NPH eitt og sér.

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2
Q

Hvar örvar insúlín upptöku glúkósa?

A

Perifert, aðallega rákóttum vöðvum og fituvef.

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3
Q

Glycogenesis er…

A

…myndum glycogens úr glúkósa.

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4
Q

Glycolysis er…

A

…súrefnisháð (aerobic) ferli þar sem glúkósi er brotinn niður og myndar pýruvate ásamt myndum 2 ATP mólekúla.

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5
Q

Hvað er glycogenolysis?

A

Biochemical niðurbrot glycogen í glúkósa.

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6
Q

Gluconeogenesis er…

A

…ferli þar sem glúkósi er búinn til úr öðru en kolvetnum.

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7
Q

5 atriði sem hefta seyti insúlíns:

A
  • Hypoglycemia
  • Fasta
  • Somatostatin
  • Alfa-adrenergic activity
  • Leptin
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8
Q

10 atriði sem auka seyti insúlíns

A
  • Hyperglycemia
  • Aukning í fríum fitusýrum í blóði
  • Aukning í amínósýrum í blóði
  • Gastrointestinal hormónin (secretin, gastrin, CCK, GIP)
  • Glucagon, GH, Cortisol parasympathetic stimulation
  • Acetyl choline
  • Beta-adrenergic stimulation
  • Insulin resistance
  • Offita
  • Sulfonyl urea lyf (glyburide, tolbutamide)
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9
Q

2 dæmi um súlfonyl urea lyf.

A

Glyburide, tolbutamide

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10
Q

5 atriði sem valda því að sjúklingur þarf MEIRA insúlín en vanalega:

A
  • hiti
  • sýking
  • aðgerð
  • trauma
  • hyperthyroidismi
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11
Q

6 atriði sem valda því að sjúklingur þarf MINNA insúlín en vanalega:

A
  • niðurgangur
  • ógleði/uppköst
  • skert frásog næringar í GI
  • hypothyroidismi
  • nýrnabilun
  • lifrarbilun
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12
Q

Insúlín hindar/örvar framleiðslu glúkósa í lifur?

A

Hindrar.

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13
Q

Insúlín hindrar eða örvar prótínmyndun?

A

Örvar.

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14
Q

Insúlín hindrar eða örvar lipolysis og proteinolysis?

A

Hindrar.

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15
Q

6 aukaverkanir insúlíns.

A
  • hypoglycemia
  • insulin resistance
  • hypokalemia
  • ofnæmi
  • lipohypertrophy
  • lipodystrophy
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16
Q

Hvernig virkar glucagon?

A

Það er antagonisti, örvar cAMP synthesis.

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17
Q

Hvað gerir glucagon?

A

Hraðar á hepatic glycogenolysis og gluconeogenesis.

Slakar á sléttum vöðvum í meltingarvegi.

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18
Q

Ábendingar fyrir glucagon (3):

A
  • alvarleg hypoglycemia hjá sj. sem nota insúlín (notar 1mg á 20mín fresti, þarf svo að muna að gefa kolvetni til að replenisha glycogen birgðir í lifur!)
  • Fyrir myndgreiningu af meltingarvegi
  • Lyf gegn betablokker og calciumgangnablokker eitrun (gefur 3mg bolus og svo 3mg/klst dreypi ef þörf)
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19
Q

2 frábendingar fyrir notkun glucagons.

A

Insúlínoma og pheochromocytoma.

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20
Q

4 aukaverkanir glucagons:

A
  • ógleði/uppköst
  • útbrot
  • lágþrýstingur
  • tachycardia
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21
Q

Hvers vegna virkar glucagon ekki alltaf í hypoglycemiu?

A

Þarft að hafa glycogen birgðir í lifur - glucagon virkjar birgðirnar og breytir þeim í glúkósa en getur ekkert gert ef glycogen er ekki til staðar.

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22
Q

Hvað er levothyroxine og hvernig metaboliserast það?

A

T4 sem umbreytist ca 50% í T3 sem er virka formið.

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23
Q

Hversu mikið af levothyroxine er tekið upp í meltingarvegi?

A

40-80% ef tekið sem tafla per os

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24
Q

Hvað gerir T4?

A

Eykur grunnhraða metabolisma, eykur nýtingu glycogen birgða og örvar gluconeogenesis (framleiðslu glúkósa úr non-carbohydrate sources).

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25
Q

Hvenær næst hámarksvirkni levothyroxines per os vs iv?

A

Fyrsta svörun iv er eftir 6-8 klst og hámarksvirkni eftir 24 klst. Fyrsta svörun per os er eftir 3-5 daga og hámarksvirkni eftir nokkra daga.

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26
Q

Helmingunartími levothyroxine:

A

9-10 dagar ef hypothyroid manneskja, 6-7 dagar ef euthyroid.

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27
Q

Hvernig er levothyroxine skilið út?

A

Mestu leyti með þvagi en 20% í hægðum.

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28
Q

Hversu mikið calcium er í hartmann´s solution (lactated ringer)?

A

2mmól/l calcium

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29
Q

Hvernig virka barbituöt?

A

Barbiturates are thought to act primarily at synapses by depressing post-synaptic sensitivity to neurotransmitters and by impairing pre-synaptic neurotransmitter release

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30
Q

Hvernig lyf er thiopental sodium?

A

Barbiturate

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31
Q

Hvaða áhrif hefur thipental sodium á hjarta- og æðakerfið?

A

Thiopental sodium is negatively inotropic, decreases cardiac output by approximately 20%. It also decreases systemic vascular resistance sem veldur lágþrýstingi.

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32
Q

Hvaða áhrif hefur thiopental sodium á öndun?

A

It is potent respiratory depressant and a period of apnoea may occur after administration.

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33
Q

Hvaða áhrif hefur thiopental sodium á nýru?

A

Minnkar blóðflæði til þeirra OG eykur vasopressin seyti, sem allt saman veldur minnkuðu urine output.

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34
Q

8 aukaverkanir thiopental sodium:

A
  • Hypotension
  • Arrhythmias
  • Myocardial depression
  • Laryngeal spasm
  • Cough
  • Headache
  • Rash
  • Hypersensitivity reactions
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35
Q

Hver er intubation skammtur af suxa?

A

The ‘intubating’ dose of suxamethonium is 0.5-2 mg/kg and the usual single dose for an adult is between 50-100 mg intravenously. Infants and younger children are relatively resistant to suxamethonium and usually require a dose of 1-2 mg/kg.

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36
Q

Hver er hámarksskammtur lidocain per kíló?

A

The maximum safe dose of plain lidocaine is 3 mg/kg (maximum 200 mg). When administered with adrenaline 1:200,000 the maximum safe dose is 7 mg/kg (maximum 500 mg).

In this case the patient weighs 70 kg and the maximum safe dose is 70 x 3 mg, which equals 210 mg lidocaine hydrochloride, the maximum dose for local infiltration according to the BNF(link is external), however, is 200 mg.

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37
Q

7 aukaverkanir própófóls

A
  • Pain on injection (in up to 30%)
  • Hypotension
  • Transient apnea
  • Hyperventilation
  • Coughing and hiccough
  • Headache
  • Thrombosis and phlebitis
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38
Q

Hvernig virkar própófól?

A

Its mechanism of action is unclear but is thought to act by potentiating the inhibitory neurotransmitters GABA and glycine, which enhances spinal inhibition during anaesthesia.

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39
Q

7 atriði sem lengja virkni atracurium og annarra non-depolariserandi neuromuscular blokkandi lyfja:

A
  • Hypokalaemia
  • Hypocalcaemia
  • Hypermagnesaemia
  • Hypoproteinaemia
  • Dehydration
  • Acidosis
  • Hypercapnia
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40
Q

Hvernig virkar atracurium? (sem er non-dep neuromuscular blokker)

A

Atracurium competes with acetylcholine for nicotinic (N2) receptor binding sites at the post-synaptic membrane of the neruomuscular junction. This prevents acetylcholine from stimulating the receptors. Because the blockade is competitive muscle paralysis occurs gradually

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41
Q

Hvað gerist ef maður gefur meira en 600 microg per kíló af atracurium? Hver eru þá einkennin?

A

Histamine release may occur if doses >600 μg/kg are used. This can result in:

  • cutaneous flushing
  • hypotension
  • bronchospasm
  • Bradycardia has also been reported
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42
Q

Hver er intubations skammtur af atracurium?

A

The ‘intubating’ dose of atracurium is 0.3-0.6 mg/kg and subsequent doses are one-third of this amount. Satisfactory intubating conditions are produced within 90 seconds of administration. There is a linear relationship between the dose and the duration of action and atracurium is non-cumulative with repeated administration.

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43
Q

Hvers vegna veldur lidoccain vasodilation?

A

This is believed to be due mainly to the inhibition of action potentials via sodium channel blocking in vasoconstrictor sympathetic nerves.

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44
Q

Hvernig virkar lidocain?

A

Lidocaine works as a local anaesthetic by diffusing in its uncharged base form through neural sheaths and the axonal membrane to the internal surface of the cell membrane sodium channels. Here it alters signal conduction by blocking the fast voltage-gated sodium channels. With sufficient blockage, the membrane of the postsynaptic neuron will not depolarize and will be unable to transmit an action potential, thereby preventing transmission of pain signals.

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45
Q

Hver er helmingunartími lidocains?

A

1,5 til 2 klst! Virkar hins vegar bara 30-60 mín nægjanlega til verkjastillingar fyrir inngrip.

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46
Q

7 aukaverkanir suxa:

A
  • Bradycardia
  • Hyperkalaemia
  • Raised intracranial pressure
  • Raised intraocular pressure
  • Prolonged paralysis
  • Anaphylaxis
  • Malignant hyperthermia
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47
Q

Hvað getur gerst ef þú notar theophylline og citalopram saman og hvers vegna?

A

Citalopram can result in hypokalaemia, potentially increasing the risk of torsades de pointes when prescribed together with theophylline. Co-prescription with theophylline should, therefore, be avoided.

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48
Q

Acetaminophen er…

A

…paracetamól!

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49
Q

Hvernig virkar paracetamól?

A

Paracetamol is thought to work by selectively inhibiting cyclo-oxygenase 3 (COX-3) receptors in the brain and spinal cord. COX-3 is responsible for the production of prostaglandins in these areas, which sensitizes free nerve endings to the chemical mediators of pain. Therefore by selectively inhibiting COX-3 paracetamol effectively reduces pain sensation.

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50
Q

Hvernig er paracetamól skilið út?

A

It is metabolized in the liver and excreted renally.

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51
Q

Hvaða pathways eru notaðir í lifur til að skilja paracetamól út?

A
  • Glucuronidation (40-60%)
  • Sulfate conjugation (20-40%)
  • N-hydroxyloxation via the hepatic cytochrome p450 enzyme system (10-15%)
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52
Q

Hvers vegna getur paracetamól valdið eitrun?

A

N-hydroxylation via the hepatic cytochrome p450 enzyme system is responsible for the production of NAPQI (N-acetyl-p-benzo-quinone imine). NAPQI is primarily responsible for the toxic effects of paracetamol. NAPQI is an intermediate product and is subsequently irreversibly conjugated with the antioxidant glutathione to produce an inactive, non-toxic, metabolite.

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53
Q

Fyrir hvað stendur ABCDE í verkjameðhöndlun?

A
  • A - Ask about pain regularly. Assess pain systematically.
  • B - Believe the patient and family in their reports of pain and what relieves it.
  • C - Choose pain control options appropriate for the patient, family, and setting.
  • D - Deliver interventions in a timely, logical, coordinated fashion.
  • E - Empower patients and their families. Enable patients to control their course to the greatest extent possible.
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54
Q

Dæmi um skala til að meta verki hjá börnum.

A
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55
Q

Hvaða verkjalyf skal nota fyrir börn með væga, miðlungs eða slæma verki?

A
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56
Q

Áhætta ACE inhibitors e.g. ramipril á meðgöngu?

A

If given in 2ndand 3rd trimester can cause hypoperfusion, renal failure and the oligohydramnios sequence.

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57
Q

Áhætta Aminoglycosides eins og gentamicin á meðgöngu?

A

Ototoxicity

Deafness

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58
Q

Áhætta aspirins á meðgöngu?

A 
High doses can cause 1st trimester abortions, delayed onset labour, premature closure of the fetal ductus arteriosus and fetal kernicterus.
Low doses (e.g. 75 mg) have no significant associated risk.
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59
Q

Áhætta Benzodiazepines

e.g. diazepam á meðgöngu?

A

When given late in pregnancy respiratory depression and a neonatal withdrawal syndrome can occur.

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60
Q

Áhætta Calcium-channel blockers á meðgöngu?

A

If given in 1st trimester can cause phalangeal abnormalities.
If given in the 2nd and 3rd trimester can cause fetal growth retardation.

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61
Q

Áhætta Carbemazepine á meðgöngu?

A

Haemorrhagic disease of the newborn

Neural tube defects

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62
Q

Áhætta Chloramphenicol á meðgöngu?

A

Grey baby syndrome

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63
Q

Áhætta corticosteroids a meðgöngu?

A

If given in the 1st trimester may cause orofacial clefts

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64
Q

Áhætta danazol á meðgöngu?

A

If given in the 1st trimester can cause masculinisation of female fetus’s genitals.

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65
Q

Áhætta finasteride á meðgöngu?

A

Finasteride should not be even handled by a pregnant woman. Crushed or broken tablets can be absorbed through the skin and can affect male sex organ development.

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66
Q

Áhætta haldóls á meðgöngu?

A

If given in the 1st trimester may cause limb malformations.

If given in the 3rd trimester increased risk of extrapyramidal symptoms in neonate.

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67
Q

Áhætta heparíns á meðgöngu?

A

Maternal bleeding

Thrombocytopaenia

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68
Q

Áhætta isoniazid á meðgöngu?

A

Maternal liver damage.

Neuropathy and seizures in the neonate.

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69
Q

Áhætta isotretinoin á meðgöngu?

A

High risk of teratogenicity (e.g. multiple congenital malformations, spontaneous abortion, and intellectual disability.

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70
Q

Áhætta lithiums á meðgöngu?

A

If given in 1st trimester risk of fetal cardiac malformations.
If given in 2nd and 3rd trimesters risk of hypotonia, lethargy, feeding problems, hypothyroidism, goitre and nephrogenic diabetes insipidus in neonate.

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71
Q

Áhætta metformíns á meðgöngu?

A

Risk of neonatal hypoglycaemia.

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72
Q

Áhætta methadons á meðgöngu?

A

Risk of neonatal opioid withdrawal syndrome.

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73
Q

Áhætta methotrexate á meðgöngu?

A

Risk of numerous congenital malformations e.g. fetal growth retardation, mandibular hypoplasia, cleft palate, spinal defects, ear defects and club foot.

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74
Q

Áhætta misoprostols á meðgöngu?

A

Can cause miscarriage

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75
Q

Áhætta NSAIDS á meðgöngu?

A

If given in 1st trimester can cause miscarriage, delayed onset labour, premature closure of the fetal ductus arteriosus and fetal kernicterus.

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76
Q

Áhætta estrodiols á meðgöngu?

A

Increased risk of urogenital abnormalities.

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77
Q

Áhætta phenobarbitone á meðgöngu?

A

Haemorrhagic disease of the newborn.

Some risk of congenital malformation.

78
Q

Áhætta phenytoin á meðgöngu?

A

Haemorrhagic disease of the newborn.

Risk of congenital malformations e.g. cleft lip, hypospadias and cardiovascular defects.

79
Q

Áhætta sodium valproate á meðgöngu?

A

Risk of major congenital malformations e.g. neural tube, cardiac, craniofacial and limb defects.

80
Q

Áhætta SSRIs

e.g. sertraline, fluoxetine á meðgöngu?

A

If given in 3rd trimester is associated with discontinuation syndrome and persistent pulmonary hypertension of the newborn.

81
Q

Áhætta Statins

e.g. simvastatin, atorvastatin á meðgöngu?

A

Cholesterol is required for fetal growth and its reduction by statins may affect fetal development.

82
Q

Áhætta tetracycline á meðgöngu?

A

Slowed bone growth, enamel hypoplasia, permanent yellowing of teeth and increased susceptibility to cavities in offspring.
Occasionally causes liver failure in pregnant women.

83
Q

Áhætta trimetoprim á meðgöngu?

A

If given in 1st trimester increased risk of neural tube defects due to folate antagonism.

84
Q

Áhætta warfarins á meðgöngu?

A

If given in 1st trimester may cause fetal warfarin syndrome (nasal hypoplasia, bone stippling, bilateral optic atrophy and intellectual disability)
If given in 2nd or 3rd trimester can cause optic atrophy, cataracts, microcephaly, microphthalmia, intellectual disability and fetal and/or maternal haemorrhage.

85
Q

Hvaða verkjalyf á að gefa börnum með milda verki?

A
  • Oral/rectal paracetamól 20mg/kg loading dose, svo 15mg/kg á 4-6 klst fresti
    EÐA
  • Oral ibuprofen 10mg/kg á 6-8 klst fresti
86
Q

Hvaða verkjalyf á að gefa börnum með miðlungs verki?

A

Oral/rectal paracetamól eða ibufen eins og börnum með milda verki en til viðbótar við það:
- oral/rectal diclofenac 1mg/kg á 8 klst fresti (ef þau fengu ekki ibufen í fyrstu)
EÐA
- oral codeine phosphate 1mg/kg á 4-6 klst fresti ef yfir 12 ára
EÐA
- oral morfín 0,2-0,5mg/kg stat

87
Q

Hvaða verkjalyf á að gefa börnum með mikla verki?

A
  • íhuga hláturgas til að byrja með (entonox)
  • intranasal diamorphine 0,1mg/kg
    OG/EÐA
  • iv morfín 0,1-0,2mg/kg
88
Q

Hver er mekanisminn bak við vancomycin?

A

Vancomycin is a bactericidal antibiotic that acts by inhibiting cell wall synthesis in Gram-positive bacteria. It prevents N-acetylmuramic acid (NAM)- and N-acetylglucosamine (NAG)-peptide subunits from being incorporated into the peptidoglycan matrix; which forms the major structural component of Gram-positive cell walls. The large hydrophilic molecule is able to form hydrogen bond interactions with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides. This binding of vancomycin to the D-Ala-D-Ala prevents the incorporation of the NAM/NAG-peptide subunits into the peptidoglycan matrix.

89
Q

Hvort virkar vancomycin gegn gram pos eða neg bakteríum?

A

gram pos

90
Q

Af hverju virkar vancomycin ekki gegn gram neg bakteríum?

A

Due to the different mechanisms by which Gram-negative bacteria produce their cell walls and the various factors related to entering the outer membrane of Gram-negative bacteria, it is not active against Gram-negative bacteria.

91
Q

Hvernig frásogast vancomycin og hvernig er það skilið út?

A

Vancomycin is not absorbed orally and is excreted unchanged renally.

92
Q

Helmingunartími vancomycins?

A

It has a biological half-life in adults of 4 to 11 hours in an adult with normal renal function but this can increase to as long as 10 days in patients with impaired renal function.

93
Q

2 algengar aukaverkanir vancomycins og óalgengari?

A

Algengar:

  • Localised pain at injection site
  • Thrombophlebitis

Óalgengar:

  • Renal failure (nephrotoxicity)
  • Hearing loss (ototoxicity)
  • Toxic epridermal necrolysis
  • Erythema multiforme
  • Red man syndrome
  • Blood dyscrasias
94
Q

2 atriði sem vancomycin er sérstaklega mikilvægt fyrir:

A

It is important for the treatment of patients with septicaemia or endocarditis caused by methicillin-resistant strains of Staphlyococcus aureus. It can also be given orally for the treatment of antibiotic-associated pseudomembranous colitis (C.difficile infection)

95
Q

6 algengar aukaverkanir bendroflumethiazide:

A
  • Postural hypotension
  • Electrolyte disturbance (hypokalaemia, hyponatraemia, hypercalcaemia)
  • Impaired glucose tolerance
  • Gout
  • Impotence
  • Fatigue
96
Q

5 sjaldgæfar aukaverkanir bendroflumethiazide:

A
  • Thrombocytopenia
  • Agranulocytosis
  • Photosensitive rash
  • Pancreatitis
  • Renal failure
97
Q

Hvað er bumetanide og hvernig virkar það? Hvaða sj. myndi maður helst velja fyrir það?

A

Bumetanide is a loop diuretic that acts on the Na.K.2Cl co-transporter in the ascending loop of Henlé to inhibit sodium, chloride and potassium reabsorption. This prevents the generation of a hypertonic renal medulla and reduces the osmotic gradient that forces water to leave the collecting duct system. This has a powerful diuretic effect.
Velur sjúklinga sem hafa ekki svarað

98
Q

Hver er munurinn á furosemide og bumetanide?

A

The main difference between bumetanide and furosemide is in bioavailability and pharmacodynamic potency. Furosemide is incompletely absorbed in the intestine and has a bioavailability of 40-50%. In contrast bumetanide is almost completely absorbed in the intestine and has a bioavailability of approximately 80%. Bumetanide is 40 times more potent than furosemide and a dose of 1 mg is roughly equivalent to 40mg of furosemide.

99
Q

Hvaða virkni hefur bumetanide gegn flogum?

A

Bumetanide decreases neuronal chloride concentration making the action of GABA more depolarizing. It is currently under evaluation as an antiepileptic in the neonatal period

100
Q

Hvaða áhrif hafa thiazide þvagræsilyf á kalkbúskap?

A

Thiazide diuretics, such as bendroflumethiazide, are calcium sparing and result in a low rate of excretion of calcium.

101
Q

Hvernig þvagræsilyf er mannitol og hvað gera nýrun við það?

A

Mannitol is an osmotic diuretic, which is filtered at the glomerulus but cannot be reabsorbed.

102
Q

Hvernig virka Loop diuretics e.g. furosemide, bumetanide?

A

Act on the Na.K.2Cl co-transporters in the ascending loop of Henlé to inhibit sodium, chloride and potassium reabsorption.

103
Q

Hvernig virka thiazide diuretics e.g. bendroflumethiazide, hydrochlorothiazide?

A

Act on the Na.Cl co-transporter in the distal convoluted tubule to inhibit sodium and chloride reabsorption.

104
Q

Hvernig virka Osmotic diuretics e.g. mannitol?

A

Increases the osmolality of the glomerular filtrate and tubular fluid, increasing urinary volume by an osmotic effect.

105
Q

Hvernig virka Aldosterone antagonists e.g. spironolactone?

A

Acts in the distal convoluted tubule as a competitive aldosterone antagonist resulting in inhibition of sodium reabsorption and increasing potassium reabsorption.

106
Q

Hvernig virka Carbonic anhydrase inhibitors e.g. acetazolamide? (þvagræsilyf)

A

Inhibits the enzyme carbonic anhydrase preventing the conversion of bicarbonate and hydrogen ions into carbonic acid. This reduces the availability of hydrogen ions and causes sodium and bicarbonate to remain in the renal tubule resulting in diuresis.

107
Q

Hvað er og hvernig gerist torsades de pointe?

A

Torsades de pointes is a specific form of polymorphic ventricular tachycardia that occurs in the presence of prolongation of the QT interval. It has a very characteristic appearance in which the QRS complex appears to twist around the isoelectric baseline.
A prolonged QT interval reflects prolonged myocyte repolarisation due to ion channel malfunction and also gives rise to early after-depolarisations (EADs). EADs can manifest as tall U waves, which can cause premature ventricular contractions (PVCs). Torsade de pointes is initiated when a PVC occurs during the preceding T wave (‘R on T’ phenomenon)

108
Q

4 atriði sem geta orsakað torsades de pointes:

A
  • Myocardial infarction
  • Electrolyte disturbance, e.g. hypokalaemia, hypomagnesaemia and hypocalcaemia
  • Congenital, e.g. Romano-ward syndrome and Lange-Nielson syndrome
  • Drugs, e.g. disopyramide, amiodarone, sotalol, terfenadine
109
Q

Meðferð torsades de pointes:

A

The drug treatment of choice for torsade de pointes is IV magnesium sulphate. Magnesium sulphate acts by decreasing the influx of calcium and lowering the amplitude of EADs.

DC cardioversion is usually kept as a last resort in a haemodynamically stable patient because of the paroxysmal and recurrent nature of torsade de pointes.

110
Q

Hver er fyrsta meðferð gout?

A

NSAIDS, nema ef háþrýstingur. Þá t.d. colchicine (allopurinol er ekki notað í akút fasanum því það getur lengt hann).

111
Q

Hvaða tveir calcium gangna blokkerar eru lífshættulegastir í overdose? Hvernig virka þessi tvö lyf?

A

Verapamil and diltiazem
These act by binding alpha-1 subunit of L-type calcium channels, thereby preventing the intracellular influx of calcium. These channels are functionally important in cardiac myocytes, vascular smooth muscle cells, and islet beta-cells.

112
Q

8 skref fyrir fyrstu viðbrögð í alvarlegri calcium gangnablokker-eitrun (fyrir utan ABC fyrst)

A
  1. Fluid resuscitation:
    Give up to 20 mL/kg of crystalloid
  2. Calcium administration
    This can be a useful temporising measure to increase blood pressure and heart rate.
    10% calcium gluconate 60 mL IV (0.6-1.0 mL/kg in children), or;
    10% calcium chloride 20 mL IV (0.2 mL/kg in children) via central venous access
    Repeat boluses can be given up to 3 times
    Consider calcium infusion to keep serum calcium >2.0 mEq/L
  3. Atropine:
  4. 6 mg every 2 min up to 1.8 mg can be considered but is frequently ineffective
  5. High dose insulin – euglycaemic therapy (HIET):
    The place of HIET in the step-wise approach to managing cardiovascular toxicity has evolved
    This used to be considered a last-ditch measure, but early use is now being increasingly advocated
    Short-acting insulin 1 U/kg bolus plus 50 mL of 50% glucose IV bolus (unless marked hyperglycaemia present)
    Continue therapy with short-acting insulin/dextrose infusion
    Monitor glucose every 20 minutes for the first hour and then hourly
    Monitor potassium levels regularly and replace if < 2.5 mmol/L
  6. Vasoactive infusions:
    Titrate catecholamines to effect (inotropy and chronotropy); options include dopamine, adrenaline and/ or noradrenaline
  7. Sodium bicarbonate:
    Consider using in cases where a severe metabolic acidosis develops
    50-100 mEq sodium bicarbonate (0.5-1.0 mEq/kg in children)
  8. Cardiac pacing:
    Electrical capture can be challenging to achieve and may not improve overall perfusion
    Use ventricular pacing to bypass AV blockade, typical with rates not in excess of 60/min
  9. Intralipid
    Consider using in refractory cases, as calcium channel blockers are lipid-soluble agents
113
Q

Hvaða ppi lyf er drug of choice sem fyrirbyggjandi með NSAIDS og í hvaða skammti?

A

omeprazol 20mg

114
Q

Hvaða 4 typur af lyfjum geta aukið GI blæðingahættu samhliða notkun á NSAIDS og ætti þá að nota PPI lyf með?

A

Low dose aspirin
Anticoagulants
Corticosteroids
Anti-depressants including SSRIs and SNRIs

115
Q

4 dæmi um 1. kynslóðar antipsychotica lyf:

A

Chlopromazine
Haloperidol
Fluphenazine
Trifluoperazine

116
Q

5 dæmi um 2. kynslóðar antipsychotica:

A 
Clozapine
Olanzapine
Quetiapine
Risperidone
Aripiprazole
117
Q

Hvers konar lyf eru 1. kynslóðar antipsychotica?

A

Sterkir D2 antagonistar.

118
Q

Hverjar eru aukaverkanir 1. kynslóðar antipsychotica?

A

First-generation antipsychotics have a high rate of extrapyramidal side effects, including rigidity, bradykinesia, dystonias, tremor, and akathisia. Tardive dyskinesia, which is involuntary movements in the face and extremities, is another adverse effect that can occur with first-generation antipsychotics. Neuroleptic malignant syndrome (NMS) can also occur with these agents.

119
Q

Hverjar eru aukaverkanir 2. kynslóðar antipsychotica?

A

Second-generation (novel or atypical) antipsychotics, with the exception of aripiprazole, are dopamine D2 antagonists, but are associated with lower rates of extrapyramidal adverse effects and TD than the first-generation antipsychotics. However, they have higher rates of metabolic adverse effects and weight gain.

120
Q

Öll 2. kynslóðar antipsychotica eru D2 antagonistar NEMA eitt…

A

…aripiprazole

121
Q

Hvernig lyf er ipratropium bromide, hvenær er þa notað og hvaða lyf myndi maður nota frekar?

A

Ipratropium bromide is an anti-muscarinic drug used in the management of acute asthma and COPD. It can provide short-term relief in chronic asthma, but short-acting β2 agonists act more quickly and are preferred.
The BTS guidelines recommend that nebulised ipratropium bromide (0.5 mg 4-6 hourly) can be added to β2 agonist treatment for patients with acute severe or life-threatening asthma or those with a poor initial response to β2 agonist therapy.

122
Q

Hversu hratt virkar ipratropium bromide?

A

Its maximum effect occurs 30-60 minutes after use; its duration of action is 3-6 hours and bronchodilation can usually be maintained with treatment 3 times per day.

123
Q

Hver er helsta aukaverkun ipratropium bromide?

A

The commonest side effect of ipratropium bromide is dry mouth. It can also cause constipation, cough, paroxysmal bronchospasm, headache, nausea and palpitations. It can cause urinary retention in patients with prostatic hyperplasia and bladder outflow obstruction. It can also trigger acute closed angle glaucoma in susceptible patients.

124
Q

Hvernig eru QRS komplexarnir vanalega í VT og hvaða lyf notum við?

A

The QRS complexes are also typically very broad (>160 ms).
Stuða fyrst 3x. Ef ekki virkar þá:
Amiodarone 300mg á 10-20 mín.
Ef ekki virkar þá stuða aftur.
Ef ekki virkar þá amiodarone 900mg á 24klst.
Hægt að nota lidocaine sem alternative.

125
Q

Hvernig eru anaphylaxa lyfjaskammtar fyrir börn vs fullorðna?

A

Child under 6 years: 150 mcg (0.15 mL of 1:1000)
Child 6-12 years: 300 mcg (0.3 mL of 1:1000)
Child over 12: 500 mcg (0.5 mL of 1:1000)
Adult: 500 mcg (0.5 mL of 1:1000)

126
Q

Hvernig virkar adenosine?

A

It acts by stimulating A1-adenosine receptors and opening acetylcholine-sensitive potassium channels. This hyperpolarizes the cell membrane in the atrio-ventricular (AV) node and, by inhibiting the calcium channels, slows conduction in the AV node.

127
Q

Adenosine skammtar

A

The initial adult dose is 6 mg, followed if necessary by a 12 mg, and then a further 12 mg bolus at 1-2 minute intervals until an effect is observed.

128
Q

5 aukaverkanir adenosine:

A 
Sense of ‘impending doom’
Facial flushing
Dyspnoea
Chest discomfort
Metallic taste
129
Q

7 contraindicationir fyrir adenosine

A
  • 2nd or 3rd degree AV block
  • Sick sinus syndrome
  • Long QT syndrome
  • Severe hypotension
  • Decompensated heart failure
  • Chronic obstructive lung disease
  • Asthma
130
Q

Dæmi um tvennt sem veldur því að sj. þarf minni skammta af adenosine:

A

Nýlegt hjartatransplant og lyfið dipyrimadole.

skammtar þá 3-6-12

131
Q

Hvernig virkar ketamín?

A

Ketamine acts by non-competitive antagonism of the NMDA receptor Ca2+ channel pore and also inhibits NMDA receptor activity by interaction with the phenylcyclidine binding site.

132
Q

5 aðalaukaverkanir ketamíns

A
  • Nausea and vomiting
  • Hypertension
  • Nystagmus
  • Diplopia
  • Rash
133
Q

Skammtastærðir, hraði á virkni og gjafaleiðir fyrir ketamín.

A

Ketamine can be used intravenously and intramuscularly. The intramuscular dose is 10 mg/kg and when used by this route it acts within 2-8 minutes and has a duration of action of 10-20 minutes. The intravenous dose is 1.5-2 mg/kg administered over a period of 60 seconds. When used intravenously it acts within 30 seconds and has a duration of action of 5-10 minutes. Ketamine is also effective when administered orally, rectally, and nasally.

134
Q

Hvaða áhrif hefur ketamín á hjarta- og æðakerfi?

A

Ketamine causes

  • tachycardia
  • an increase in blood pressure
  • increased central venous pressure
  • increased cardiac output, secondary to an increase in sympathetic tone.
  • Baroreceptor function is well maintained and arrhythmias are uncommon.
135
Q

Skilgreiningin á SIADH:

A

The syndrome of inappropriate antidiuretic hormone (ADH) secretion (SIADH) is defined as the presence of hyponatremia and hypo-osmolality resulting from inappropriate, continued secretion or action of the hormone despite normal or increased plasma volume, which results in impaired water excretion.

136
Q

Sýklalyf sem stundum er notað til að meðhöndla SIADH og hvernig virkar það?

A

Demeclocycline is a tetracycline antibiotic that reduces the sensitivity of ADH receptors in the distal convoluted tubules. It is sometimes used in the management of SIADH that has responded to fluid restriction alone.

137
Q

5 flokkar af ástæðum fyrir SIADH?

A
  • CNS damage: meningitis, subarachnoid haemorrhage
  • Malignancy: small-cell lung cancer
  • Drugs: carbamazepine, SSRIs, amitryptline, morphine
  • Infection: pneumonia, lung abscess, brain abscess
  • Endocrine: hypothyroidism
138
Q

Hvernig virka Penicillins, Cephalosporins og Vancomycin?

A

Inhibition of cell wall synthesis

139
Q

Hvernig virka Polymyxins, Nystatin og Amphotericin B?

A

Disruption of cell membrane function

140
Q

Hvernig virka Macrolides, Aminoglycosides, Tetracyclines, Chloramphenicol?

A

Inhibition of protein synthesis

141
Q

Hvernig virka Quinolones, Trimethoprim, 5-nitroimidazoles og Rifampicin?

A

Inhibition of nucleic acid synthesis

142
Q

Hvernig virka Sulfonamides og Isoniazid?

A

Anti-metabolic activity

143
Q

Hvernig virkar cefuroxime?

A

Cefuroxime and the other cephalosporin antibiotics are ß-lactam antibiotics and are bactericidal. Like the penicillins they produce their antimicrobial action by preventing cross-linkage between the linear peptidoglycan polymer chains that make up the bacterial cell wall. They therefore inhibit cell wall synthesis.

144
Q

Hvernig lyf er amló?

A

Calcium-channel blokker

145
Q

Hvaða skammt gefur maður af dexametasón í croup?

A

No definite standard dose for the use of dexamethasone has currently been agreed in the UK. The APLS guidelines, however, recommend a dose of 150 mcg/kg, with a suggested maximum single dose of 12 mg

146
Q

Hvenær á að gefa atrópín?

A

Atropine is indicated for sinus, atrial, or nodal bradycardia or AV block, when the haemodynamic condition of the patient is unstable because of the bradycardia. Virkar oft illa á Mobitz II.

147
Q

Hvenær mælir ALS algorythminn með 500mcg atropin iv?

A

Bradycardia + eitthvað af þessu:

  • Shock
  • Syncope
  • Myocardial ischaemia
  • Heart failure
148
Q

Með hverju mælir ALS ef atrópín klikkar í bradycardiu (gefa 500mcg á 3-5 mín fresti upp í 3mg, þá þetta):

A
  • Transcutaneous pacing
  • Isoprenaline infusion 5 mcg/min
  • Adrenaline infusion 2-10 mcg/minutes
  • Alternative drugs (aminophylline, dopamine, glucagon, glycopyrrolate)
149
Q

Hvað gerir Protamine sulphate?

A

Antidote fyrir heparine. Gefið hægt iv og er sterkur basi (heparín er sýra). Gefið 1mg protamin fyrir hverjar 100 einingar af heparíni.

150
Q

Protamine sulphate getur haft örlitla anticoagulant virkni. Hvernig virkar það?

A

Protamine sulphate also has its own, weak intrinsic anticoagulant effect. This is thought to be due to the inhibition of the formation and activity of thromboplastin.

151
Q

Aukaverkanir protamine sulphate?

A
  • Protamine sulphate is a myocardial depressant

- may cause bradycardia and hypotension secondary to complement activation and leukotriene release.

152
Q

Hvernig eru leiðbeiningar fyrir meðhöndlun astma hjá börnum yfir 1 árs aldri? 3 skref.

A
  1. Bronchodilator therapy
    Inhaled β agonists are the first line treatment for acute asthma.
    Discontinue long-acting β2 agonists when short-acting β2 agonists are required more often than four hourly.
    A pmDI + spacer is the preferred option in children with mild to moderate asthma.
    Individualise drug dosing according to severity and adjust according to the patient’s response.
    If symptoms are refractory to initial β agonist treatment, add ipratropium bromide (250 micrograms/dose mixed with the nebulised β2 agonist solution).
    Repeated doses of ipratropium bromide should be given early to treat children who are poorly responsive to β2 agonists.
    Consider adding 150 mg magnesium sulphate to each nebulised salbutamol and ipratropium in the first hour in children with a short duration of acute severe asthma symptoms presenting with an oxygen saturation less than 92%.
  2. Steroid therapy
    Give oral steroids early in the treatment of acute asthma attacks.
    Use a dose of 10 mg prednisolone for children under 2 years of age, 20 mg for children aged 2–5 years and a dose of 30–40 mg for children >5 years. Those already receiving maintenance steroid tablets should receive 2 mg/kg prednisolone up to a maximum dose of 60 mg.
    Repeat the dose of prednisolone in children who vomit and consider intravenous steroids in those who are unable to retain orally ingested medication.
    Treatment for up to three days is usually sufficient, but the length of course should be tailored to the number of days necessary to bring about recovery. Tapering is unnecessary unless the course of steroids exceeds 14 days.
  3. Second-Line Treatment of Acute Asthma
    Consider early addition of a single bolus dose of intravenous salbutamol (15 micrograms/kg over 10 minutes) in a severe asthma attack where the patient has not responded to initial inhaled therapy.
    Aminophylline is not recommended in children with mild to moderate acute asthma.
    Consider aminophylline for children with severe or life-threatening asthma unresponsive to maximal doses of bronchodilators and steroids.
    In children who respond poorly to first-line treatments, consider the addition of intravenous magnesium sulphate as first-line intravenous treatment (40 mg/kg/day)
153
Q

Hvað er DigiFab?

A

Digoxin-specific antibody

154
Q

Hvernig er DigiFab búið til?

A

Digoxin-specific antibody (DigiFab) is an antidote used for overdose of digoxin. It is a sterile, purified, lyophilized preparation of digoxin-immune ovine Fab immunoglobulin fragments. These fragments are obtained from the blood of healthy sheep immunised with a digoxin derivative, digoxin- dicarboxymethoxylamine (DDMA), a digoxin analogue which contains the functionally essential cyclopentaperhydrophenanthrene:lactone ring moiety coupled to keyhole limpet hemocyanin (KLH).

155
Q

Hvernig virkar DigiFab?

A

DigiFab has an affinity for digoxin that is greater than the affinity of digoxin for its sodium pump receptor, the presumed receptor for its therapeutic and toxic effects. When administered to the intoxicated patient, DigiFab binds to molecules of digoxin reducing free digoxin levels, which results in a shift in the equilibrium away from binding to the receptors, thereby reducing cardio-toxic effects. Fab-digoxin complexes are then cleared by the kidney and reticuloendothelial system.

156
Q

Indikasjónir fyrir notkun DigiFab í akút digoxin eitrun (6):

A
  • Cardiac arrest
  • Life-threatening arrhythmia
  • Potassium level > 5 mmol/l
  • > 10 mg digoxin ingested (adult)
  • > 4 mg digoxin ingested (child)
  • Digoxin level > 12 ng/ml
157
Q

4 indikasjónir fyrir notkun digoxins í krónískri digoxin eitrun:

A
  • Cardiac arrest
  • Life-threatening arrhythmia
  • Significant gastrointestinal symptoms
  • Symptoms of digoxin toxicity and coexistent renal failure
158
Q

Hvernig virkar abciximab? (ReoPro)

A

Abciximab (ReoPro) is a chimeric monoclonal antibody that is a glycoprotein IIb/IIIa receptor antagonist. It inhibits platelet aggregation and is mainly used during and after coronary artery procedures such as angioplasty.

159
Q

Þegar sj. á warfarin er með major blæðingu, hvert þarf INR að vera til að við snúum warfarininu við?

A

Skiptir ekki máli, snúum því við regardless ef sjúklingurinn er í lífshættu.

160
Q

Sj. á warfarin með major akút blæðingu sem ekki tekst að stoppa. Hvað á að gera, 4 skref:

A
  • Stop warfarin
  • Administer 5 mg IV vitamin K (phytomenadione)
  • Administer dried prothrombin complex concentrate (factors II, VII, IX and X)
  • Or administer fresh frozen plasma 15 ml/kg if dried prothrombin complex is unavailable
161
Q

Sj. á warfarin með minor blæðingu og INR yfir 8, hvað á að gera, 4 skref:

A
  • Stop warfarin
  • Administer 1-3 mg vitamin K (phytomenadione) by slow injection
  • The dose may be repeated after 24 hours if INR remains high
  • Restart warfarin when INR is less than 5.0
162
Q

Sj. á warfarin og INR er yfir 8 (engin blæðing). Hvað á að gera í 4 skrefum:

A
  • Stop warfarin
  • Administer 1-5 mg vitamin K (phytomenadione) orally
  • The dose may be repeated after 24 hours if INR remains high
  • Restart warfarin when INR is less than 5.0
163
Q

Sj. á warfarin með minor blæðingu og INR milli 5 og 8. Hvað á að gera?

A
  • Stop warfarin
  • Administer 1-3 mg vitamin K (phytomenadione) by slow injection
  • Restart warfarin when INR is less than 5.0
164
Q

Sj. á warfarin með INR milli 5 og 8 með enga blæðingu, hvað á að gera?

A
  • Withhold 1 or 2 doses of warfarin

- Reduce subsequent maintenance dose

165
Q

Hvernig virkar metoclopramide?

A

Metoclopramide exerts its anti-emetic action via dopamine D2-receptor antagonist. At high doses it is also thought to have 5-HT3 antagonist activity.

166
Q

Hvernig virka Cyclizine, Promethazine og Cinnarizine?

A

Anti-histamines

167
Q

Hvernig virka Domperidone, Metoclopramide og Prochlorperazine?

A

Dopamine receptor antagonists

168
Q

Hvernig virkar Hyoscine?

A

Anti-muscarinics

169
Q

Hvernig virkar Ondansetron og Granisetron?

A

5-HT3 receptor antagonists

170
Q

Hvernig virkar Aprepitant?

A

Neurokinin receptor antagonists

171
Q

Hvernig virkar thiopental sodium?

A

Barbiturates are thought to act primarily at synapses by depressing post-synaptic sensitivity to neurotransmitters and by impairing pre-synaptic neurotransmitter release.

Thiopental sodium binds at a distinct binding site associated with a chloride ionopore at the gamma-aminobutyric acid type A (GABAA) receptor, increasing the duration of time for which the chloride ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.

172
Q

Hvað er bivalirudin?

A

Bivalirudin is a specific and reversible direct thrombin inhibitor (DTI). NICE recommends it as a possible treatment for adults with STEMI who are having percutaneous coronary intervention.

173
Q

Hvenær á að gefa NSTEMI sj. lmw heparin vs fondaparinux?

A

Fondaparinux should be administered to patients who do not have a high bleeding risk, unless coronary angiography is planned within 24 hours of admission.

Offer unfractionated heparin as an alternative to fondaparinux to patients who are likely to undergo coronary angiography within 24 hours of admission. Unfractionated heparin should also be considered, with dose adjustment guided by monitoring of clotting function, as an alternative to fondaparinux for patients with significant renal impairment (creatinine above 265 micromoles per litre).

174
Q

IV skammtur af lorazepam fyrir barn í flogi?

A

The dose of IV lorazepam advised in the treatment of the convulsing child is 0.1 mg/kg.

175
Q

Fyrsta val í sýklalyfjum fyrir kvk yfir 16 ára aldri ekki óléttar með UTI:

A
  • Nitrofurantoin 100 mg modified-release PO BD for 3 days – if eGFR >45 ml/minute
  • Trimethoprim 200 mg PO BD for 3 days – (if low risk of resistance*)
176
Q

Annað val fyrir kvk yfir 16 ára með UTI ekki óléttar ef fyrri meðferð skilaði ekki árangri á 48 klst, 3 lyf:

A
  • Nitrofurantoin 100 mg modified-release PO BD for 3 days – if eGFR >45 ml/minute
  • Pivmecillinam 400 mg PO initial dose, then 200 mg PO TDS for 3 days
  • Fosfomycin 3 g single sachet dose
177
Q

Hvað er grey baby syndrome og hver eru 10 aðaleinkennin?

A

‘Grey baby syndrome’ is a rare but serious side effect that occurs in neonates (especially premature babies) as a consequence of the accumulation of the antibiotic chloramphenicol.

The principal features of ‘grey baby syndrome’ are:

  • Ashen grey colour of skin
  • Poor feeding
  • Vomiting
  • Cyanosis
  • Hypotension
  • Hypothermia
  • Hypotonia
  • Cardiovascular collapse
  • Abdominal distension
  • Respiratory difficulties
178
Q

Hversu mikill á styrkur theophylline að vera, hvenær getur maður fengið aukaverkanir og hvenær þarf að mæla styrkinn? (notað í astma)

A

In most individuals, a plasma theophylline concentration of 10-20 mg/litre (55-110 micromol/litre) is required for satisfactory bronchodilation, although a lower plasma-theophylline concentration may be effective. Adverse effects can occur within the range 10-20 mg/litre and both the frequency and severity increase at concentrations above 20 mg/litre.

Plasma theophylline concentration is measured 5 days after starting oral treatment and at least 3 days after any dose adjustment. A blood sample should usually be taken 4-6 hours after an oral dose of a modified-release preparation (sampling times may vary - consult local guidelines). If aminophylline is given intravenously, a blood sample should be taken 4-6 hours after starting treatment.

179
Q

Hvernig virkar ciprofloxacin?

A

Ciprofloxacin and the other quinolone antibiotics act by inhibiting DNA gyrase, an enzyme that compresses bacterial DNA into supercoils, and a type II topoisomerase, that is necessary to separate bacterial DNA. They therefore inhibit nucleic acid synthesis.

180
Q

Hvað er mikið Na og HCO3- (bicarbonat) í 1,26% sodium bicarbonat lausn?

A

150mL/L af hvoru tveggja

181
Q

Magn Na, K, bíkarbónats, Cl og Ca í normal plasma í mmól/L:

A 
Na+  142
K+  4,5
HCO3-  26
Cl-  103
Ca++  2,5
182
Q

Magn Na, K, bíkarbónats, Cl og Ca í 0,9% sodium chloride lausn í mmól/L:

A 
Na+  150
K+  
HCO3- 
Cl-  150
Ca++
183
Q

Magn Na, K, bíkarbónats, Cl og Ca í Compound Sodium Lactate (Hartmann’s) lausn í mmól/L:

A 
Na+  131
K+  5
HCO3-  29
Cl-  111
Ca++  2
184
Q

Magn Na, K, bíkarbónats, Cl og Ca í 5% Glucose (1 L contains 50 g of dextrose) lausn í mmól/L:

A

Allt saman núll.

185
Q

Magn Na, K, bíkarbónats, Cl og Ca í 0.3% Potassium Chloride and 5% Glucose lausn í mmól/L:

A

K+ 40

Cl- 40

186
Q

Magn Na, K, bíkarbónats, Cl og Ca í 0.3% Potassium Chloride and 0.9% Sodium Chloride lausn í mmól/L

A 
Na+  150
K+  40
HCO3-  núll
Cl-  190
Ca++ núll
187
Q

Magn Na, K, bíkarbónats, Cl og Ca í 1.26% Sodium Bicarbonate lausn í mmól/L

A 
Na+  150
K+  
HCO3-  150
Cl- 
Ca++
188
Q

Magn Na, K, bíkarbónats, Cl og Ca í 4.5% Albumin (1 L contains 40-50 g of albumin) lausn í mmól/L

A 
Na+  undir 160
K+  undir 2
HCO3-  núll
Cl- 136
Ca++  núll
189
Q

Magn Na, K, bíkarbónats, Cl og Ca í 4.5% Albumin (1 L contains 40-50 g of albumin) lausn í mmól/L

A 
Na+  undir 160
K+  undir 2
HCO3-  núll
Cl- 136
Ca++  núll
190
Q

Magn Na, K, bíkarbónats, Cl og Ca í 4% Gelatin (Gelofusine) lausn í mmól/L

A 
Na+  154
K+  undir 0,4
HCO3-  núll
Cl- 120
Ca++  undir 0,4
191
Q

Hvers vegna má ekki taka furix og SSRI lyf saman?

A

There is an increased risk of hyponatraemia when furosemide and SSRI drugs are prescribed together. There is also an increased risk of hypokalaemia, potentially increasing the risk of torsades de pointes when furosemide and SSRI drugs are prescribed together. Co-prescription with citalopram should, therefore, be avoided.

MRCEM Primary Exam (21 decks)

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