Paper 1 Flashcards

1
Q

What is normal aortic pressure before the aortic valve will open?

A

80mmHg

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2
Q

Which pressure trace is the dicrotic notch seen in?

A

The aortic pressure trace as a result of elastic recoil of the aortic walls when the aortic valve closes.

It is not seen in the left ventricular pressure trace.

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3
Q

How do you calculate coronary perfusion pressure?

A

CPP = aortic-diastolic pressure - left ventricular end diastolic pressure

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4
Q

How much thicker is the left ventricular wall than the right?

A

3 x thicker

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5
Q

How long does diastole last for?

A

0.5 s (2/3 of cardiac cycle)

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6
Q

Where do the coronary arteries arise from?

A

The aorta immediately above the cusps of the aortic valve to recieve blood from the left ventricle.

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7
Q

How much of the circulating volume do the veins hold?

A

2/3rds

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8
Q

What are veins and venules collectively known as?

A

Capacitance vessels

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9
Q

Why are arterioles and arteries known as resistance vessels?

A

They can constrict and dilate in response to autonomic supply to control blood flow

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10
Q

What is the pressure/volume curve for veins like initially and why?

A

Very steep between 0-10 mmHg.

Due to the easily distensible walls - the volume increases relatively easily per unit rise in pressure.

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11
Q

What is the pressure of blood in the venules compared to larger veins?

A

Enters the venules at about 12-20 mmHg, in veins it falls to 10mmHg

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12
Q

Where does CVP measure the pressure from?

A

The superior vena cava

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13
Q

What is physiological dead space the sum of?

A

Anatomical dead space (normally 150ml) + alveolar dead space (normally 0ml)

It’s normally about 30% of tidal volume (Vd/Vt = 0.3) and calculated by the Bohr equation

Vd/Vt = PaCO2 - PeCO2/PaCO2

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14
Q

What are causes of increased anatomical dead space?

A
  • neck extension
  • jaw protrusion
  • increased tidal volumes
  • neonates/elderly
  • bronchodilation
  • anticholinergics
  • catecholamines
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15
Q

What are the causes of decreased anatomical dead space?

A
  • neck flexion
  • low tidal volumes
  • general anaesthesia
  • intubation
  • tracheostomy
  • 5HT
  • histamine
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16
Q

What are the causes of increased alveolar dead space?

A
  • pulmonary embolism
  • pulmonary disease
  • hypovolaemia
  • hypotension
  • general anaesthesia
  • intermittent positive pressure ventilation
  • positive end-expiratory pressure
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17
Q

Which area of lung has the best pulmonary blood flow in standing vs lateral positions? Why?

A

Standing - the base

Lateral - the lower lung

This is due to hydrostatic pressure where gravity increases perfusion pressure in the lungs by 1cm H2O for every cm in height below the level of the heart.

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18
Q

What is the Fick principle used to measure? What does it state?

A

Pulmonary blood flow.

This states that O2 consumption per unit time (VO2) is equal to the amount of O2 taken up by blood in the lungs per unit time (ie blood flow times the arterial O2 content CaO2 - venous oxygen content CvO2 difference)

VO2 = Q(CaO2-CvO2)

Q = VO2 / (CaO2 - CvO2)

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19
Q

What are the 3 zones of the lung?

A

Based on relationship between pulmonary arterial (Pa), pulmonary venous (Pv) and alveolar pressures (PA).

Zone 1 = PA > Pa > Pv (alveolar dead space)

Zone 2 = Pa > PA > Pv (blood flow determined by arterial-alveolar pressure difference)

Zone 3 = Pa > Pv > PA (blood flow determined by arterial-venous pressure difference)

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20
Q

How does hypoxic vasoconstriction work?

A

Hypoxic areas of lung undergo vasoconstriction to prevent blood flow to poorly ventilated alveoli. Reduces shunt.

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21
Q

What are the central controllers of respiration?

A
  • medullary respiratory centre
  • apneustic centre in lower pons
  • pneumotaxic centre in upper pons
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22
Q

What are the central chemoreceptors for respiration?

A
  • on the ventral medullary surface
  • stimulated by reduction in CSF pH (ie increase in H+ concentration) caused by metabolic acidosis or increased PCO2
    • NOT affected by PO2
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23
Q

Where are the peripheral chemoreceptors for respiration?

A
  • aortic bodies give vagal afferents and carotid bodies giving glossopharyngeal nerve afferents
  • stimulated by increased PCO2 in linear fashion, increase in H+ ions and a reduction in PO2 below 8-10 kPa
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24
Q

What lung receptors are there for control of respiration?

A
  • pulmonary stretch receptors
  • juxtaPULMONARY capillary receptors
  • irritant receptors
  • bronchial C fibres
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25
Q

What are the other receptors involved in control of breathing?

A
  • nose and upper airway receptors
  • arterial baroreceptors
  • joint and muscle receptors
  • higher centres: pain/temp/anxiety
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26
Q

What effect do the lungs have on angiontension?

A

The lungs convert angiotension I to angiotension II by ACE.

Then this is metabolised to angiotensin III in RBCs and vascular endothelium.

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27
Q

What are the lungs involved in the metabolism of?

A
  • bradykinin (80%)
  • 5-HT (serotonin)
  • noradrenaline
  • prostaglandins E2 and F
  • leucotrienes
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28
Q

What are the other functions of the lung?

A
  • metabolic processes (eg noradrenaline + leucotriene metabolism)
  • acid base balance
  • phospholipid synthesis (surfactant)
  • involvement in immune and coagulant function
  • reservoir of blood (500-900ml)
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29
Q

How many veins and arteries do the kidneys have?

A

Each kidney has 1 artery and 2 veins

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30
Q

What is the distribution of blood flow in the kidneys?

A

90% to the cortex

10% to medulla

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31
Q

Where do the vasa recta arise from?

A

Inner cortical efferent arterioles

(which also supply the peritubular capillaries)

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32
Q

What does the renal artery divide into?

A

Interlobular arteries which then divides into arcuate arteries then the afferent arterioles that go to the glomerulus.

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33
Q

Where is renin produced from and do?

A

This is a proteolytic enzyme produced by the JGA.

It acts on angiotensinogen (produced in the liver) to form angiotensin I. This is converted to angiotensin II by cleaving 2 amino acids.

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34
Q

What is the formula for calculating GFR?

A

GFR = UV/P

U - urine concentration of the indicator

V - urine flow rate

P - plasma concentration of indicator

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35
Q

What is the normal rate of GFR in an adult?

A

125ml/min

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36
Q

How much potassium is reabsorbed daily, and what % will be excreted in urine/faeces?

A

50 - 150 mmol reabsorbed

90% urine

10% faeces

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37
Q

What % of potassium storage is intracellular?

A

99% intracellular, mostly in muscle, but some liver/erythrocytes

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38
Q

What is the fasted method of moving extracellular K+ intracellularly?

A

Insulin.

Less fast - aldosterone, adrenaline, alkalosis

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39
Q

What % of potassium is reabsorbed at the PCT?

A

70%

Then 20% in LoH

Then the rest in DCT

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40
Q

What is normal cerebral blood flow? Where does the majority go?

A

15%

700ml/min

500ml/100g/min

Grey matter.

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41
Q

Where does the blood supply to the brain come from?

A

2/3 from internal carotids

1/3 from the 2 vertebral arteries

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42
Q

Where do the vertebral and carotid arteries join?

A

At the anterior and posterior communicating arteries to form the Circle of Willis

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43
Q

What range is CBF constant between?

A

MAP 80-150 mmHg

Above this there is a sharp increase in CBF

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44
Q

How does the Fick principle differ from the Fick law?

A

Principle - the uptake/release of a substance by an organ is the product of the blood flow through the organ and the arteriovenous difference in content.

Law- describes the rate of diffusion across a membrane being proportional to the concentration gradient

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45
Q

What is the total volume of CSF?

A

100-150ml (10% of intracranial volume)

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46
Q

What is the rate of production of CSF?

A

0.3L/min by the choroid plexuses in lateral, third and fourth ventricles

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47
Q

How much CSF is produced a day?

A

500ml

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48
Q

Is production of CSF dependent on ICP?

A

No, it’s independent.

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49
Q

What is the circulation of CSF?

A
  • lateral ventricles to 3rd ventricle via foramen of Munro
  • 3rd to 4th ventricle via aqueduct of Sylvius
  • 4th ventricle down the spinal cord/over cerebral hemispheres via midline foramen of Magendie or lateral foramen of Luschka
  • absorbed form dural venous sinuses via arachnoid villi
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50
Q

What electrolytes are greater in CSF than plasma?

A

Chloride and magnesium

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51
Q

What are the effects of parasympathetic stimulation?

A

Opthalmic

  • lacrimation, pupillary constriction

CVS

  • bradycardia, reduced contractility, vasodilation in skeletal muscle/coronary/pulmonary/renal/viscera

Pulmonary

  • bronchoconstriction, increased secretions

GI

  • increased motility and secretions
  • sphincteric relaxation

Metabolic

  • increased insulin + glucagon secretion

GU

  • detrusor muscle contraction
  • sphincteric relaxation
  • penile erection
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52
Q

What type of reflex is the withdrawal reflex?

A

Polysynaptic

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53
Q

What do muscle spindles respond to?

A

Changes in muscle length, rather than tension - so contraction of muscles causes shortening of spindles - to maintain posture.

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54
Q

What happens if muscle spindles are stretched?

A

They transmit impulses directly to effferent γ-motor neurones via type Ia or II fibres.

This is the monosynaptic stretch reflex.

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55
Q

What is responsible for sensing muscle tension?

A

Golgi tendon organs

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56
Q

What is the swallowing reflex?

A

Involuntary reflex which is a series of autonomic pharyngeal muscular contractions which takes 1-2 seconds.

  • soft palate is pulled upwards to close posterior nares to prevent food entering nasal passage
  • palatopharyngeal folds pulled medially to allow food to pass posteriorly into pharynx
  • larynx pulled upwards and anteriorly by the neck muscles
    • epiglottis covers the opening of the larynx to prevent food entering
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57
Q

Where is the most sensitive area of the pharynx for the initiaion of swallowing?

A

Around the pharyngeal opening - tonsillar pillars have greatest sensitivity

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58
Q

Where is calcitriol produced?

A

Active form of vit D that increases plasma calcium levels and is produced in cells of the proximal tubule of the renal nephron.

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59
Q

Where is calcitonin produced?

A

Thyroid parafollicular cells to reduce cerum calcium concentrations

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60
Q

Where is glucagon produced?

A

Peptide hormone produced by the alpha-cells of the pancreatic islets of Langerhands to increase blood glucose concentration

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61
Q

Where is cholecystokinin produced?

A

Peptide hormone produced in small intestinal and duodenal mucosa in response to fat and protein in chime.

It increases gastric transit time to allow further digestion of fats.

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62
Q

Where are oxytocin and vasopressin produced?

A

They’re produced in the hypothalamus but released from the posterior pituitary

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63
Q

Where is aldosterone produced?

A

Adrenal cortex

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64
Q

Where is cortisol produced?

A

Adrenal cortex

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65
Q

Where are oestrogen and progesterone produced?

A

Ovaries

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66
Q

Where is adrenaline produced?

A

Adrenal medulla

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67
Q

Where is noradrenaline produced?

A

The adrenal medulla

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68
Q

Where is histamine produced?

A

Mast cells

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69
Q

Where is glucagon produced?

A

Pancreas

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70
Q

What hormones do the stomach and small intestine produce?

A
  • gastrin
  • secretin
  • cholecystokinin
  • gastric inhibitory peptide
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71
Q

What hormones does the anterior pituitary produce?

A
  • GH
  • prolactin
  • ACTH
  • melanocyte stimulating hormone
  • TSH
  • FSH
  • LH
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72
Q

What hormones does the hypothalamus produce?

A

Oxytocin, ADH

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73
Q

What state is the iron in Hb?

A

Ferrous (Fe2+) - can carry one O2 molecule and there are 4 per Hb

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74
Q

What is the Bohr effect?

A

High PCO2 reduces affinity of Hb for O2

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75
Q

What is the Haldane effect?

A

Deoxygenated Hb has a higher affinity for CO2

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76
Q

What is 1st pass metabolism?

A

Drugs absorbed from GI tract enter the portal vein and go to the liver where they undergo metabolism before reaching the systemic circulation.

This is minimised by SL or PR routes - which have higher bioavailibility than oral.

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77
Q

What does induction of hepatic enzymes do to 1st pass metabolism?

A

It increases 1st pass metabolism, thereby reducing bioavailibility.

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78
Q

To be given transdermally, what features must the drug exhibit?

A
  • lipophilic and hydrophilic
  • short half life
  • low melting point
  • low molecular weight (<500 Da)
  • high potency
  • unionised
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79
Q

Can GTN be given transdermally?

A

Yes

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80
Q

What methods can clonidine be given by?

A
  • oral
  • transdermal
  • IM
  • IV
  • intrathecal
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81
Q

What routes can alfentanil be given?

A

Only IV

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82
Q

What is the volume of distribution?

A

A theoretical volume in which a drug would have to disperse in order to achieve observed plasma concentrations.

Highly protein bound drugs also have a high VoD while highly polar/charged drugs don’t cross membranes easily and stay within the central compartment so have a small VoD.

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83
Q

How does the lipid solubility of fentanyl and morphine compare? How does this affect the VoD?

A

Fentantly is 600 times more lipid soluble than morphine.

VoD of fentanyl is 4L/kg whilst morphine is 3.5L/kg.

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84
Q

What is the VoD of non-depolarising neuromuscular blockers?

A

< 0.3 L/kg because they’re all highly polar

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85
Q

What drugs are excreted in the urine unchanged?

A

ACED LMNOP

Aminoglycosides

Cephalosporins

Ephedrine

Digoxin

Lithium

Milrinone/mannitol

Neostigmine

Oxytetracycline

Penicillins

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86
Q

What is the metabolism of adrenaline?

A

Metabolised in the liver by catechol-O-methyl transferase ti metadrenaline and metnoradrenaline

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87
Q

What properties would the ideal IV anaesthetic agent have?

A
  • highly lipid soluble
  • water soluble formulation
  • short half life
  • analgesic at low doses
  • pre-prepared solution
  • rapid recovery, no accumulation after infusion
  • minimal CVS/resp depression
  • antiemetic properties
  • painless on injection
  • no interaction with other drugs
  • no histamine release
  • long shelf life at room temp
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88
Q

What is thiopentone?

A

Sulphur analogue of the oxybarbiturate pentobarbitone.

Formulated as a sodium salt, sodium thiopentone and appears as a yellow power in a glass vial.

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89
Q

What is the pKa of thiopentone?

A

Weak acid with pKa of 7.6

When dissolved in water it forms an alkaline solution

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90
Q

How is free acid formation prevented in thiopentone?

A

Sodium thiopentone is stored in glass vials containing nitrogen, while sodium carbonate is added to react with water to produce hydroxide ions. This forms an alkaline solution to prevent accumulation of H+ ions and therefore the undissociated acid.

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91
Q

At physiological pH, how much thiopentone is available in the active form?

A

The active form is non-protein bound and unionised.

Only 12% of administered sodium thiopentone is available but it’s highly lipid soluble so the brain receives a relatively large dose.

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92
Q

What is Xenon?

A

An inert, odourless gas - makes up a tiny % of the atmosphere and is produced by fractional distillation of air.

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93
Q

What effects does Xenon have on the CVS?

A

It does not sensitise the myocardium to catecholamines.

It does not alter myocardial contractility.

It may cause a small reduction in HR and hence cardiac output.

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94
Q

What is the MAC of xenon?

A

71%

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95
Q

How dense/viscous is Xenon compared to Nitrous Oxide?

A

Xenon is 3 times denser

Twice as viscous

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96
Q

What is the molecular weight of Xenon?

A

131.2

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97
Q

What is the boiling point of Xenon?

A

-108C

It is non-flammable and does not support combustion.

It undergoes virtually no metabolism in the body.

98
Q

What is tolerance?

A

Occurs when larger doses of a drug are required to achieve a given response, often due to altered receptor sensitivity such as in chronic opioid use.

99
Q

What is tachyphylaxis?

A

Reversible, acute decrease in response to a given dose of drug after repeated administration and is synonymous with desensitisation (which takes place over a longer period ot time)

Underlying mechanisms include:

  • change of receptor structure
  • loss of receptors
  • reduction of mediators
  • increased breakdown of drug
  • physiological adaptation
100
Q

How are ester local anaesthetics metabolised?

A

They contain the CO-O linkage and undergo hydrolysis in the plasma

101
Q

How are amide local anaesthetics metabolised?

A

They have the NH-CO linkage and undergo hepatic metabolism

102
Q

Which route of giving local anaesthetic produces the highest systemic absorption?

A

Increasing systemic vascular absorption:

  1. Subcutaneous (least)
  2. Femoral
  3. Brachial plexus
  4. Epidural
  5. Caudal
  6. Intercostal (most)
103
Q

Do local anaesthetics cause vasodilation?

A

Most local anaesthetics cause vasodilation at low concentrations with vasoconstriction at higher doses.

However, cocaine is a pure vasoconstrictor.

104
Q

How does diazoxide work?

A

Structurally similar to bendroflumethiazide and acts as a vasodilator by modulating cAMP in arteriolar smooth muscle

105
Q

What are the Class I antiarrhymic drugs?

A

Class I

Local anaesthetic properties that exhibit membrane stabilising activity and affect conduction, refractoriness and the AP. They all slow phase 0 of the AP.

Ia - block Na+ channels, prolong refractory period (eg disopyramide, procainamide, quinidine)

Ib - block Na+ channels, shorten refractory period (eg lidocaine, mexiletine, phenytoin)

Ic - block Na+ channels, no effect on refractory period (flecaineide, propafenone)

106
Q

What are the Class II antiarrhythmic drugs?

A

Beta adrenoceptor blockers (eg atenolol, propranolol)

107
Q

What are the Class III antiarrhythmic drugs?

A

Potassium channel blockers (eg amiodarone, sotalol, bretylium)

108
Q

What are the Class IV antiarrhythmics?

A

Calcium channel blockade (diltiazem, verapamil)

109
Q

What antiarrhythmics do not fit any of the original classes?

A
  • adenosine
  • digoxin
  • magnesium sulphate
110
Q

Which antiarrhythmics work on the SA node?

A
  • beta blockers
  • class IV drugs
  • digoxin
111
Q

Which antiarrhythmics work at the AV node?

A

Class Ic and IV drugs

Beta blockers

Digoxin

Adenosine

112
Q

Which antiarrhythmics work at the ventricles?

A

Class III and I drugs

113
Q

What antiarhythmics work at the atria?

A

Class Ia and Ic drugs

Beta blockers

Class III drugs

114
Q

Which antiarhythmic drugs work at the accessory pathways?

A

Class Ia and III drugs

115
Q

What is the difference between dobutamine and dopamine?

A

Dobutamine is a synthetic analogue of dopamine (derivative of isoprenaline) and is a beta1-adrenoceptor stimulator. It is a positive inotrope. It does have beta2 efffects causing peripheral vasodilatation which can cause hypotension and reflex tachycardia.

Dopamine is a catecholamine-like agent used for treatment of severe heart failure and cardiogenic shock.

116
Q

What is the precursor of noradrenaline? How is it converted?

A

Dopamine.

The conversion of dopamine to noradrenaline occurs in granulated vesicles and is dependent on the enzyme dopamine beta hydroxylase.

117
Q

Which adrenergic receptors does dobutamine act on?

A

B1 > B2 > alpha.

No effect on dopaminergic receptors.

118
Q

What adrenoreceptors does dopamine act on?

A

Both beta and alpha-adrenergic reponses and causes vasodilatation through it’s action on dopaminergic receptors.

At high doses (>10 mcg/kg/min) it causes predominantly alpha effects with peripheral vasoconstriction, increased PVR and reduced renal blood flow.

119
Q

Which vessels do nitrates dilate peferentially?

A

Large coronary arteries and arterioles with diameters >100 micrometres

120
Q

How do nitrates reduce myocardial oxygen demand?

A
  • They redistribute blood flow from epicardial to endocardial regions
  • They relieve coronary spasm and dynamic stenosis
  • They increase the venous capacitance, causing pooling of blood in the peripheral veins and reduce venous return and ventricular volume. This reduces mechanical stress in the myocardial wall and myocardial O2 demand is reduced.
  • they cause a fall in aortic systolic pressure, which further reduces myocardial O2 demand
121
Q

How do nitrates work?

A

They are converted to nitrites followed by enzyme-mediated release of unstable nitric oxide. They vasodilate whether or not the endothelium is physically intact or functional.

The NO produced then stimulates the enzyme guanylate cyclase to produce cyclic guanosine monophosphate (cyclic GMP). This reduces calcium in the vascular monocyte and therefore vasodilation occurs.

122
Q

Are nitrates better at dilating veins or arterioles?

A

Venous

123
Q

What metabolises suxamethonium? Does it have active metabolites?

A

Hydrolyzed by plasma cholinesterase to choline and succinylmonocholine - so only 20% reaches the neuromuscular junction.

Succinylmonocholine is a weakly active ester of succinic acid with choline.

It’s rapidly metabolised - only 10% is excreted via the kidneys in the urine.

124
Q

What is the structure of suxamethonium?

A

2 acetylcholine molecules joined through acetyl groups.

125
Q

What are the monoquaternary and bisquaternary aminosteroids?

A

Monoquaternary (contain a single N+ -CH3 group)

  • vecuronium
  • rocuronium

Bisquaternary (contain 2 N+ -CH3 groups)

  • pancuronium (more potent analogue of vecuronium)
126
Q

What % of aspirin is bound to plasma proteins? How analgesic/antipyretic/anti-inflammatory is it?

A

85%

Analgesic + antipyretic +++

Anti-inflammatory ++

127
Q

What % of diclofenac is bound to plasma proteins? How analgesic/antipyretic/anti-inflammatory is it?

A

99%

Analgesic and antipyretic +

Antiinflammatory +++

128
Q

What % of ibuprofen is bound to plasma proteins? How analgesic/antipyretic/anti-inflammatory is it?

A

99%

Analgesic + antipyretic +

Anti-inflammatory +

129
Q

What % of ketorolac is bound to plasma proteins? How analgesic/antipyretic/anti-inflammatory is it?

A

99%

Analgesic/antipyretic ++

Anti-inflammatory +

130
Q

What % of paracetamol is bound to plasma proteins? How analgesic/antipyretic/anti-inflammatory is it?

A

10%

Analgesic/antipyretic +++

Anti-inflammatory ++

131
Q

What is the structure of morphine?

A

Naturally occuring opiate with a phenanrene structure comprising 3 fused benzene rings

132
Q

How does morphine affect the gut and bowel?

A

Constricts gut sphincters - causes immobility of bowel resulting in constipation.

Causes contraction of the sphincter of Oddi, causing an increase in intraluminal pressure within the biliary tree.

133
Q

Why does morphine cause nausea?

A

It stimulates the chemoreceptor trigger zone via 5HT3 and dopaminergic receptors.

Muscarinic receptors are NOT activated by morphine.

134
Q

How does morphine and other opioids cause chest wall rigidity?

A

As a result of dopaminergic and GABA pathways in the substantia nigra interacting with the opioid receptors.

135
Q

What hormones does morphine inhibit the release of? Which ones does it increase secretion of?

A

Inhibits:

  • adrenocorticotropic hormone
  • prolactin
  • gonadotrophic hormones

Increases:

  • vasopressin - can cause water retention and hyponatraemia
136
Q

How do benzodiazepines work?

A

Hypnotic drugs that act on the alpha-subunit of GABAA receptors to open the ligand gated chloride channel causing hyperpolarisation of post synaptic neuronal membranes.

They do not act via second messenger systems.

137
Q

How protein bound are benzodiazepines?

A

Highly protein bound and usually have active metabolites - however lorazepam is glucuronated to inactive metabolites.

138
Q

How does zopiclone work?

A

It’s a non-benzodiazepine “Z-drug” that lacks the benzodiazepine structure but binds to GABAA receptors in a similar fashion.

139
Q

What are the biochemical effects of furosemide?

A
  • hyponatraemia
  • hypokalaemia
  • hypochloraemic alkalosis
  • hypomagnesaemia
  • hyperuricaemia
  • hypocalcaemia - by increasing Ca2+ excretion
140
Q

What effects on calcium does bendroflumethiazide have?

A

Causes hypercalcaemia through reducing renal excretion

141
Q

What biochemical effects does spironolactone have?

A
  • competitive aldosterone antagonist
  • reduces excretion of K+
    • hyperkalaemia
  • increases excretion of Na+ and H2O
  • used to treat ascites, Conn’s syndrome (primary hyperaldosteronism) and nephrotic syndrome
142
Q

How does mannitol affect preload and cardiac output?

A

It’s usually given as a loading dose for treatment of raised ICP at a dose of 1g/kg then an infusion.

Due to the large infusion volumes - the initial circulating volume is increased which increases preload and cardiac output.

143
Q

What are the haematological effects of bendroflumethiazide?

A

Haemolytic anaemia

Aplastic anaemia

Leucopaenia

Thrombocytopenia

Agranulocytosis

144
Q

How can the flow of electrons pass from one atom to another?

A

Electricity is the flow of electrons from one atom to another under the influence of a potential difference or under the influence of a changing magnetic field.

145
Q

Are body fluids conductors or insulators?

A

They’re conductors because they contain positive and negative ions, which can move when a potential difference is applied to them - conducting electricity.

Electrons in a conductor are loosely bound, so can readily move when influenced by a potential difference.

146
Q

What are diodes, thermistors and transistors in terms of conductors/insulators?

A

Semiconductors

147
Q

What is the frequency of surgical diathermy?

A

1 MHz

148
Q

What is more likely to cause VF, high or low frequency currents?

A

Low frequency AC or direct current is more likely to cause VF than surgical diathermy at high frequency.

149
Q

How many connections to the patient do monopolar and bipolar diathermy require?

A

Monopolar - 2 connections, one the patient plate (neutral) and one the active/cutting electrode

Bipolar - 2 connections but both are the ends of the forceps, diathermy plate not required

150
Q

Which uses lower power, bipolar or monopolar?

A

Bipolar

151
Q

Does diathermy contain capacitors?

A

Yes, isolating capacitors are placed within the diathermy apparatus to increase the safety and reduce the risk of burns to the patient in the event of the diathermy pad becoming detached

152
Q

Does MRI involve ionising radiation?

A

No

153
Q

Can MRI cause involuntary muscle contractions?

A

Yes - when the magnetic field gradient is switched, eddy currents can be induced and this can induce small currents in biological conductors- especially nerve fibres, which can cause involuntary muscle contraction.

There is also a small risk of breathing difficulties and VF.

154
Q

What side effects can strong magnetic fields cause?

A

Flashing lights and various taste sensations

155
Q

What is power?

A

Rate of work (watts)

1 W = 1 J/sec

156
Q

What happens if the point of application of a force moves in the direction of the force?

A

Energy is expended and work is done

It’s measured in joules.

The energy expended when applying a force of 1 N through a distance of 1 metre.

157
Q

How can the power of breathing be calculated?

A

The area under the pressure/volume curve = work done

Power is the rate of work done

So for power of breathing, divide the work done (AUC) by time.

158
Q

What happens to the chemical energy created by respiratory muscles?

A

Converted to heat energy, only a small proportion is converted to mechanical energy.

159
Q

What does the wet and dry bulb hygrometer measure?

A

Measures ambient humidity, while relative humidity is obtained from a set of tables and is not directly measured.

160
Q

What is absolute humidity expressed in?

A

mg H2O/litre of gas

161
Q

What is relative humidity?

A

The amount of water vapour at a particular temperature, expressed as a % of the amount that would be held if the gas were fully saturated.

162
Q

What happens to the absolute and relative humidity if a gas saturated with water vapour is cooled?

A

The water vapour will condense out.

The amount of condensed water vapour will be the amount held at the original temperature minus the amount it can hold at the lower temperature.

The absolute humidity will therfore fall, but relative humidity remains at 100%.

163
Q

What is heat?

A

The energy that can be transferred from a hotter object to a coller object down it’s temperature gradient.

164
Q

What is temperature?

A

A measure of the tendency of an object to gain or lose heat.

165
Q

What is the triple point of water?

A

The temp at which it exists as a solid, liquid and gas simultaneously.

273.16K or 0.01°C

166
Q

What form is CO2 stored in cylinders as?

A

Liquid

167
Q

What is a fluid?

A

A form of matter that changes shape under shear forces and can either be liquids or gases.

168
Q

What is the velocity profile in laminar flow?

A

Across the pipe during laminar flow is parabolic, with the highest flow in the centre. The peak velocity in the centre is twice the average across the pipe at equilibrium.

169
Q

What kind of energy is ultrasound?

A

Mechanical.

In the form of high frequency vibrations.

170
Q

How is the wavelength of US related to the frequency?

A

Wavelength is the reciprocal of the frequency.

171
Q

Under single fault conditions, type 1 CF equipment should have what leakage currents?

A

50 microamps

172
Q

What are the safety classes of equipment?

A

Class I

  • any accessible conducting part of the equipment is connected to an earth wire
  • live, neutral and earth wires never come in contact with each other

Class II

  • double-insulated
  • all accessible parts have 2 layers of insulation
  • power cables contain live and neutral conductors with a single fuse

Class III

  • can’t have electrical supply >50V DC or 24V AC
  • “safety extra low voltage”
  • still provides theoretical risk of microshock
173
Q

What are the max leakage currents for Type B, BF and CF?

A

Type B

  • safe for external patient connection
  • class I = 500mA
  • class II = 100mA

Type BF

  • same as type B
  • but the part connected to the patient is isolated “floating”

Type CF

  • safe for direct connection to the heart with isolated circuits
  • class I = 50mA
  • class II = 10mA
174
Q

What is a current operated earth leakage circuit breaker?

A

Consists of a live wire and neutral wire attached to a relay circuit breaker.

Faulty currents (eg high leakage current) lead to magnetic field between the live and neutral wires that induces the relay to break the circuit.

There is no fuse.

175
Q

What colour cylinder is nitrous oxide stored in?

A

French blue bodies and shoulders

176
Q

What is entonox stored in?

A

Cylinders with white and blue quartered shoulders

177
Q

What is the pressure in nitrous oxide cylinders?

A

4400 kPa

44 bar

178
Q

What happens to the pressure in nitrous oxide cylinder as it is used up?

A

It decreases slowly until all the liquid is utilised with only vapour remaining at which point the pressure decreases rapidly.

The slow decrease is due to the latent heat of vaporisation cooling the cylinder, thereby reducing vapour pressure, Therefore, cylinder pressures do not decrease in a linear manner.

179
Q

What is the capacity of size E cylinders for nitrous oxide?

A

1800 L

180
Q

What is the capacity of nitrous oxide in size J cylinders?

A

18000 L

181
Q

What temperature and pressure is O2 stored in the VIE at?

A

-160°C

7 bar /700kPa

182
Q

How is the temperature/pressure within the VIE maintained?

A

With reduced use of O2, the temperature rises (less latent heat of vaporisation).

Internal pressure rises, if this exceeds 17 bar then a safety valve opens.

Vapourised O2 escapes. This leads to further vaporisation, reducing the temperature once more.

183
Q

How does the rotameter vary depending on flow rates?

A

At low flow - orifice is long and narrow, so flow is laminar depending on gas viscosity.

At high flow - orifice is wider, so flow is turbulent, depending on gas density.

184
Q

How accurate are flowmeters?

A

2.5%

185
Q

What can reduce accuracy of the flowmeters?

A
  • dirt in the flowmeter tubes
  • static electricity build up (35% inaccurate)
  • back pressure from the common gas outlet of up to 10%
186
Q

What are the maximally accepted 8hr time weighted average concentrations for the UK for enflurane, halothane, isoflurane and nitrous oxide?

A

Halothane - 10 ppm

Enflurane - 50 ppm

Isoflurane - 50 ppm

Nitrous oxide - 100 ppm

187
Q

What is the Lack system?

A
  • Mapleson A (Magill) breathing system that can also be arranged in parallel.
  • 14mm inner tube attached to an APL valve for exhaled gases and a 30mm outer tube supplying the FGF
  • efficient for spontaneous ventilation - requires 70ml/kg/min FGF
  • inefficient for controlled ventilation - requiring a FGF 2-3x minute ventilation
188
Q

What is the most efficient Mapleson system for controlled ventilation?

A

Mapleson D - the Bain.

189
Q

What is the electrical potential generated by the heart?

A

90mV but this is reduced as it passes through the tissues until it leaves a signal output of 1-2 mV

190
Q

How does an ECG work?

A

The initial signal is increased by a differential amplifier that may be set at a monitoring mode (freq 0.5 - 40Hz) or diagnostic mode (0.05 - 100Hz).

The differential amplifier minimises noise and signal interference using common mode rejection - where interference that is the same in 2 leads is eliminated.

Signal output - displayed via oscilloscope or on paper running at 25mm/s with a signal of 1mV/cm

191
Q

How many bipolar and unipolar leads are there in the ECG?

A

Bipolar: I, II, III, aVR, aVL, aVF

Unipolar: V1-V6

192
Q

What does the null hypothesis mean?

A

That no difference exists between 2 sample groups. It must be set before any clinical trial, and if a difference between the 2 samples is detected, the null hypothesis must be rejected.

193
Q

What is a type I error?

A

Alpha error / false positive.

A difference is found where one does not truly exist causing incorrect rejection of the null hypothesis.

Most commonly due to a high p-value or small sample size.

194
Q

What is a type II error?

A

Beta error/ false negative.

No difference is found when one does exist causing incorrect acceptance of the null hypothesis.

Most commonly due to small sample sizes.

195
Q

What is the power of a study?

A

It indicates what size of sample is required. It measures the probability of a difference being detected when one exists and is calculated as 1 - ß.

A power of >80% (ie ß <20%) is sufficient for a study to be adequately powered.

196
Q

What is standard deviation?

A

A measure of spread around central tendancy.

197
Q

How do differential pressure transducers work?

A

By detecting a difference in pressure between two sides of a given sensor. It compares a measurement sample with a reference sample to give a pressure difference, which can be analyzed and interpreted.

198
Q

Is there a differential pressure transducer in the VIE?

A

Yes - it measures the pressure difference between the top and bottom of a cylinder to calculate the liquid O2 remaining

199
Q

Do paramagnetic analyzers use differential pressure transducers?

A

A reference gas of 21% oxygen is compared with a measured gas with a set concentration of oxygen.

When exposed to a magnetic field the paramagnetic properties of oxygen cause it to be attracted to the field, leading to a difference in pressure between both chambers that is proportional to the partial pressure of O2.

200
Q

Do end tidal CO2 analyzers incorporate a differential pressure transducer?

A

No

201
Q

Does the Tec 6 desflurane vapouriser contain a differential pressure transducer?

A

Yes - between the FGF channel and vapourising channel, which is then interpreted and electronically alters the gas flow accordingly.

202
Q

What is the Pitot tube design?

A

Some pneumotachographs use this design.

One tube faces the direction of FGF, while the other faces the opposite direction, being the reference tube.

The pressure difference between the 2 tubes is proportional to the flow rate squared.

203
Q

In cardiac output, what would the end tidal CO2 be?

A

0.4 kPa

There is no cardiac output, no perfusion of the lungs - this is extreme dead space.

Arterial CO2 will be elevated but end tidal will be low if there is effective CPR or zero if ineffective.

204
Q

What factors will increase lung compliance?

A
  • surfactant
  • emphysema
  • old age
  • acute asthma
205
Q

What factors will decrease lung compliance?

A
  • pulmonary fibrosis
  • pulmonary venous engorgement
  • pulmonary oedema
  • ARDS
  • pneumonia
  • neonates
  • extremes of lung volume
  • chronic bronchitis (dynamic)
206
Q

How much will cerebral blood flow reduce by for each 0.13 kPa reduction in PaCO2?

A

2-4%

207
Q

What anaesthetic drugs increase ICP?

A
  • ketamine
  • volatiles
  • suxamethonium (transiently)
208
Q

What anaesthetic drugs decrease ICP?

A
  • barbiturates
  • etomidate
  • propofol
  • opioids
209
Q

What nerves does an ankle block block?

Which one is the only one with a motor component and what movement does this cause?

A
  • sural
  • deep and superficial peroneal nerves
  • saphenous nerve
  • tibial nerve

Tibial is the only one with a motor component beyond the block site, so is the only one that can be blocked using a nerve stimulator.

This leads to plantar flexing of the toes via contraction of flexor digitorum longus and flexor hallicus longus.

It supplies sensory supply to the medial aspect of the ankle and foot.

210
Q

What is the calculation for paeds ETT size internal diameter?

A

(Age/4) + 4

211
Q

What is the calculation for paeds ETT length (oral) at the lips?

A

Age/2 + 12

212
Q

What is the calculation for paeds ETT length (nasal) at the lips?

A

Age/2 +15

213
Q

What size LMA corresponds to weight? (children and adults)

A

SIZE WEIGHT

1 <5 kg

1.5 5 - 10 kg

2 10 - 20 kg

2.5 20 - 30kg

3 30 - 50 kg

214
Q

What are the paediatric doses for:

  • Paracetamol
  • Ibuprofen
  • Diclofenac
  • Codeine
  • Fentanyl
  • Morhpine
  • Dexamethasone
  • Ondansetron
A
  • Paracetamol = 15mg/kg IV
  • Ibuprofen = 10mg/kg
  • Diclofenac = 1mg/kg
  • Codeine = 0.5mg/kg
  • Fentanyl = 1mcg/kg
  • Morphine = 0.1 - 0.2mg/kg
  • Dexamethasone = 0.1 - 0.2 mg/kg
  • Ondansetron = 0.1 - 0.2 mg/kg
215
Q

What drugs are the most likely cause of anaphylaxis in an anaesthetic setting?

A

Neuromuscular blocking drugs (60% -mostly sux, rocuronium)

Latex (20%)

Antibiotics (15% - penicillins and cephalosporins account for 70% of these)

Rare - colloids, opioids, LAs, anaesthetic agents (propofol/thio)

216
Q

What is the most common complication of an interscalene block?

A

Nearly 100% of patients have a phrenic nerve block.

Other complications :

  • stellate canglion block causing Horner’s syndrome in up to 25% of patients
  • recurrent laryngeal nerve palsy (10%) + vagal nerve damage
  • vertebral artery and other vessel puncture may occur, and intrathecal/epidural injection may take place
  • pneumothorax is rare but more common in COPD patients
217
Q

What is the treatment for hypoxia in ARDS in ventilated patients?

A
  • best achieved with alveolar recruitment
    • increase mean airway pressures, either by increasing the PEEP or prolonging inspiratory time
  • use pressure controlled ventilation
  • aim for tidal volumes 6mg/kg
  • plateau pressure of <30cm H2O
  • PEEP 10-12cm H2O
  • titrate FiO2 to a PaO2 of 8kPa
  • permissive hypercapnia of 8kPa, increasing RR to reduce PaCO2
218
Q

What are the pin positions for nitrous oxide?

A

3 and 5

219
Q

What are the pin positions for oxygen?

A

2 and 5

220
Q

What is the pin positions for air?

A

1 and 5

221
Q

What is the pin position for CO2?

A

1 and 6

222
Q

What is the pin position for entonox?

A

7

223
Q

Why does the pulse oximeter over-read in the presence of carboxyhaemoglobin?

A

Because the absorption coefficient is so similar to that of oxyHb.

224
Q

Where does the pulmonary capillary wedge pressure measure the pressure of?

A

Left atrium

225
Q

Which Mapleson breathing system would be most efficient for a gas induction?

A

Mapleson A - most efficient for spontaneous ventilation and FGF required are equal to alveolar minute ventilation.

This system is not efficient for controlled ventilation (needs FGF 3x minute ventilation).

Mapleson B + C are not efficient for spontaneous/controlled ventilation.

B is more efficient than A or C for controlled ventilation.

The Bain (coaxial D) is not efficient for spontaneous ventilation (FGF required 2x min ventilation) but is efficient during controlled ventilation.

226
Q

What is decontamination?

A

Process of removing contaminants such that they are unable to reach a site in sufficient quantities to initiate an infection or other harmful reaction. The process always starts with clearning and is followed by sterilisation or disinfection.

Fibroscopes are classed as intermediate risk equipment (don’t penetrate skin/enter sterile cavities) so decontamination by cleaning followed by disinfection is an acceptable method of cleaning this type of equipment.

227
Q

What is cleaning?

A

Process of physically removing foreign material from an object without necessarily destroying any infective material.

An example of manual cleaning is washing, automated cleaning is performed using an ultrasonic bath or low temp steam.

228
Q

What is disinfection?

A

Process of rending an object free from all pathological organisms except bcaterial spores.

Chemicals used for disinfection are glutaraldehyde 2%, alcohol 60-80%, chlorhexidine 0.5-5% and hydrogen peroxide.

229
Q

What is pastuerization?

A

Process of using heat to destroy pathogenic organisms without destroying bacterial spores. It’s an alternative to chemical disinfection.

230
Q

What is sterilisation?

A

Process of rendering an object completely free of all visible infectious agents including bacterial spores. This can be done using chemicals such as ethylene oxide and glutaraldehyde 2%, using radiation like gamma irradiation using heat such as the autoclave.

231
Q

What does the a wave, c wave, x descent, v wave and y descent represent?

A
  • a wave - atrial contraction
  • c wave - bulging of closed tricuspid at the start of isovolumetric ventricular contraction
  • x descent - atrial relaxation
  • v wave - venous return against a closed tricuspid valve
  • y descent - atrial relaxation while emptying into the right ventricle
232
Q

What would an elevated JVP with absent waveforms indicate?

A

Superior vena cava obstruction

233
Q

What do large V waves mean on the JVP waveform?

A

Tricuspid regurg

234
Q

What does an elevated JVP with deep x and y descents indicate?

A

Constrictive pericarditis

235
Q

What is the effect of delaying analysis of an ABG sample?

A
  • reduced pH
  • reduced PaO2
  • increased PaCO2
  • reduced glucose
  • increased lactate
236
Q

What effect does clotting of an ABG sample have?

A

Increases potassium

237
Q

What do air bubbles in an ABG syringe cause?

A

Increased PaO2 and increased pH

238
Q

What are the features of a fat embolism?

A

This occurs when fat from bone marrow enters the circulation and restricts right ventricular outflow by increasing pulmonary artery pressures.

RS: tachypnoea, dyspnoea, pulmonary oedema, hypoxia

Neuro: confusion, drowsiness

Petechial rash: usually on chest wall, axilla or conjunctiva

Treatment is supportive.

239
Q

How much oxygen does a size E contain?

A

680L of O2

240
Q
A