Paper 2 Flashcards

1
Q

What is the equation for compliance?

A

Compliance = change in volume/change in pressure

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2
Q

What is specific compliance related to?

A

The FRC, not total lung capacity

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3
Q

What are the normal values for lung compliance vs total thoracic compliance?

A

85-100 ml/cmH2O Total thoracic compliance

200ml/cmH2O Lung compliance

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4
Q

Do children or adults have higher compliance?

A

Adults

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5
Q

What factors will increase compliance?

A
  • surfactant
  • emphysema
  • old age
  • acute asthma
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6
Q

What factors reduce compliance?

A
  • pulmonary fibrosis
  • pulmonary venous engorgement
  • pulmonary oedema
  • ARDS
  • neonates
  • extremes of lung volume
  • pneumonia
  • chronic bronchitis
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7
Q

What is closing capacity?

A

Lung volume at which airway closure occurs

= closing volume + residual volume

It is about 10% of vital capacity but increases gradually with age until it is about 40% of VC aged 65yrs

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8
Q

When does airway closure take place?

A

When closing capacity equals or exceeds the FRC

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9
Q

What factors increase closing capacity?

A
  • Asthma
  • Raised intrathoracic pressures
  • Smoking

CC may also encroach on FRC when FRC is reduced such as Pregnancy, Obesity, General anaesthesia

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10
Q

How do you measure closing capacity?

A

Fowler’s method - nitrogen or helium concentration analysis.

Phase 1 = dead space gas, no nitrogen/helium present

Phase 2 = Mix of dead space and alveolar gas with some marker gas

Phase 3 = Plateau of alveolar gas

Phase 4 = Closure of upper airways causing a rise in marker gas = closing volume

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11
Q

In dead space, what happens to the alveolar PCO2?

A

It will be approaching O kPa

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12
Q

In dead space, what happens to the end-capillary PCO2?

A

It approaches 0KPa

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13
Q

Where is a high V/Q ratio found in the lungs?

A

At the top of the lungs

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14
Q

What is the P50?

A

It is the partial pressure of O2 at which Hb is 50% saturated.

3.5 kPa normally

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15
Q

What will reduce the P50?

A

Left shift = increased O2 affinity (P50 <3.5 kPa)

  • reduced PaCO2
  • alkalosis
  • hypothermia
  • reduced 2,3, DPG
  • CO
  • MetHb
  • Fetal Hb
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16
Q

What will cause a right shift in the P50?

A

RIght shift = reduced O2 affinity = P50 >3.5kPa

  • elevated PaCo2
  • acidosis
  • hyperthermia
  • elevated 2,3 DPG
  • pregnancy
  • haemoglobin S
  • altitude
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17
Q

What is the Bohr effect?

A

The shift of the oxyHb curve to the right in response to a rise in PaCO2 or fall in pH

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18
Q

What is the haldane effect?

A

The phenomenon where deoxygenated Hb has a higher affinity for CO2 than oxygenated Hb

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19
Q

What does the x descent represent?

A

The fall in atrial pressure as the ventricle contracts - this lengthens the atria and causes a pressure drop

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20
Q

What is the y descent?

A

Once the mitral valve opens, blood flows into the ventricle from the left atrium, causing a pressure drop in the atrium

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21
Q

What is the Donnan effect?

A

This describes the phenomenon where charged particles that cannot diffuse across a membrane have an effect on the distribution of other charged particles.

Proteins and phosphates hold negatively charged molecules inside the cell, thus the inside is negative with respect to the outside and these cannot cross the cell membrane.

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22
Q

During exercise, how are the cardiovascular changes brought about?

A

By a change in autonomic nerve activity.

There is an increase in sympathetic drive and reduction in parasympathetic activity.

There is a rise in plasma catecholeamine levels but this contributes less to the overall cardiovascular changes.

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23
Q

What increases more in exercise, HR or SV?

A

Heart rate.

Because the stroke volume is limited by the size of the heart chambers and the time available for filling and ejection.

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24
Q

What is required to calculate capillary membrane permeability?

A
  • rate of solute transfer
  • membrane area
  • concentration difference across the wall
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25
Q

How can solute diffusion rate be measured?

A

Directly by optical methods (eg cannulated capillaries perfused with dyes).

Indirectly by the Fick Principle- calculates whole organ transfer of rapidly diffusing solutes across the whole microvascular bed.

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26
Q

What can radiolabelled albumin be used to measure?

A

Recording the extravascular accumulation of radiolabeled albumin after intravascular injection can assess capillary permeability to plasma macromolecules.

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27
Q

What transport method is used for water and solutes across capillary walls?

A

This is a passive process, down concentration gradients

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28
Q

What is autoregulation of the kidney affected by?

A
  • changes in resistance of the interlobular arteries as well as resistance in afferent and eferent arterioles of the cortical nephrons
  • not affected by changes in resistance of the larger interlobar arteries
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29
Q

What is the driving force for water reabsorption in the proximal tubule?

A

The main driving force is sodium reabsorption, followed by Cl and HCO3 reabsorption.

This creates a small osmotic gradient along which H2O passively diffuses out (isotonic reabsorption).

So the main drive in the proximal tubule is Na+ reabsorption.

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30
Q

What is the tonicity of fluid reaching the tubular fluid after the LoH?

A

Because the LoH ascending limb is relatively impermeable to water, the tubular fluid becomes HYPOTONIC (as NaCl is actively transported into medulary extracellular fluid)

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31
Q

Where is aldosterone produced?

A

In the adrenal cortex - zona glomerulosa

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32
Q

Which is the most important mineralocorticoid?

A

Aldosterone.

The main function of mineralocorticoids is to regulate transport of Na+ and K+ in the kidney and other organs such as the intestine, gallbladder and salivary glands.

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33
Q

What is cholesterol the precursor for?

A
  • synthesis of sex hormones (testosterone, progesterone, oestradiol)
  • glucocorticoids (cortisol)
  • mineralocorticoid aldosterone
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34
Q

When is aldosterone secretion highest and lowest?

A

Lowest in the evening and highest early in the morning. This diurnal variation applies to R-A-A as a whole and involves changes in posture, stress and melatonin secretion

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35
Q

What will stimulate release of aldosterone?

A
  • reduced blood volume
  • hyperkalaemia
  • hyponatraemia
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36
Q

How does a high protein diet cause a metabolic acidosis?

A

This will result in increased production of hydrochloric acid and sulphuric acids

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37
Q

What does incomplete oxidation of carbohydrate do?

A

This causes a metabolic acidosis, because it results in the anaerobic production of lactic acid

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38
Q

What does an increased metabolism of organic anions do?

A

Results in a metabolic alkalosis due to increased metabolism of organic anions such as lactate and citrate to CO2 and H2O

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39
Q

What does an increased intake of alkaline substances do to your acid-base balance?

A

It causes a metabolic alkalosis

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40
Q

What does a diet high in vegetable matter do?

A

Produces a large amount of HCO3-, which is excreted in the urine, making it alkaline

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41
Q

What does the mucosa of the stomach contain?

A
  • chief cells
  • parietal cells
  • endocrine cells
  • mucus producing cells
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42
Q

WHat is the rate of stomach emptying dependent on?

A
  • stomach signals from nervous stimulation caused by distension and the hormone gastrin, which is secreted by the antral mucosa - this increases pyloric pumping force and inhibits the pylorus - promoting stomach emptying
  • signals from the duodenum depress the pyloric pump and increase pyloric tone
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43
Q

What does gastrin do?

A

Causes secretion of acidic gastric juices by the stomach and has a stimulatory effect on motor functions of the stomach to enhance the activity of the pyloric pump and increase gastric emptying.

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44
Q

What bilirubin concentration does jaundice develop at?

A

Plasma bilirubin concentrations > 18micromol/L

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45
Q

What is pre-hepatic jaundice?

A

Increased production of bilirubin (eg due to excess haemolysis, when increased production far exceeds the liver’s capacity to conjugate bilirubin).

Therefore excess unconjugated bilirubin in plasma.

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46
Q

What can cause hepatic jaundice?

A
  • damaged hepatocytes
  • inflammation of liver cells (hepatitis)
  • deficiency of glucuronyl transferase (gilbert’s syndrome) - which is the enzyme responsible for conjugation of bilirubin for further metabolism
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47
Q

What forms of hepatic jaundice result in dark urine?

A
  • hepatocellular damage
  • Dubin-Johnson syndrome
  • all forms of post hepatic jaundice
    • the cause of dark urine is elevated levels of the conjugated, water soluble form of bilirubin
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48
Q

What causes post hepatic jaundice?

A

Obstruction to the bile ducts by stones or tumour - causes increased levels of conjugated bilirubin in the blood.

There is very little bilirubin that enters into the intestine in post-hepatic jaundice. The intestine is where bilirubin is broken down by bacteria to stercobilinogen, which is then oxidised to stercobilin.

Stercobilin = brown colour of faeces (low levels therefore = pale stools)

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49
Q

What factors increase blood flow to the liver?

A
  • food
  • acute hepatitis
  • supine posture
  • enyzme inducing drugs
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50
Q

What factors decrease blood flow to the liver?

A
  • positive pressure ventilation
  • hypoxia
  • hypercarbia
  • abdominal surgery
  • ganglion blocking drugs
  • vasopressin
  • volatile anaesthetics
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51
Q

What is fever?

A

Fever is an abnormally high body temperature and the most frequent cause is infection by bacteria or viruses.

Prostaglandins released by phagocytes reset the hypothalamic thermostat to a higher temperature. Temperature regulating reflex mechanisms then bring the body temp up to the new setting, therefore causing a high temp.

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52
Q

What is heat exhaustion?

A
  • normal body temp
  • profuse perspiration
  • cool and clammy skin
  • symptoms
    • dizziness
    • muscle cramps
    • vomiting
    • fainting
      • due to loss of fluids and electrolytes
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53
Q

What is heatstroke?

A

Occurs when temperature and relative humidity are high, making it difficult for the body to lose heat by radiation, conduction or evaporation.

Blood flow to skin is decreased and perspiration is reduced resulting in body temp increasing.

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54
Q

Why are the elderly more prone to hypothermia?

A

They have reduced metabolic response to lower temperatures and a reduced perception of cold as well as hot temperatures.

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55
Q

How do macrophages cause fever?

A

They release interleukins 1 and 6 (IL1 and IL6) once they become active during inflammation and infection.

These promote synthesis of proteins in the liver that act as pyrogens to generate fever.

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56
Q

What does insulin do?

A

Main action is to decrease blood glucose levels by:

  • increasing transport of glucose from blood into cells
  • increasing glycogenesis (glucose into glycogen)
  • increasing lipogenesis (glucose into fat)
  • decreasing glycogenolysis (glycogen into glucose and glucose 1 phosphate)
  • reducing gluconeogenesis (formation of glucose from non-carbohydrate substances such as lactate)
  • increasing protein synthesis
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57
Q

What causes insulin secretion?

A
  • high blood glucose
  • increased blood levels of amino acids
  • hGH raises glucose concentration which then stimulates insulin
  • ACTH increases plasma glucose concentrations which then stimulates insulin release
  • somatostatin inhibits insulin release
  • increased parasympathetic activity stimulates insulin release
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58
Q

How does body temperature affect cerebral blood flow?

A

For each degree celcius decrease in body temp there is a 5% decrease in CBF

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59
Q

How do volatile anaesthetics affect cerebral blood flow?

A

They increase CBF via a vasodilatory effect

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60
Q

How does pCO2 affect cerebral blood flow?

A

Between a PaCo2 of 2.7 - 10.7 kPa there is a linear increase in CBF by approximately 2-4% for each 0.13 kPa (1mmHg) in PaCO2.

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61
Q

What what PaO2 would cerebral blood flow increase?

A

PaO2 < 6.7 mmHg

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62
Q

What drugs will affect cerebral blood flow?

A

Opioids - no effect

Thio/propofol/benzodiazepines/etominate - decrease

Ketamine - increases

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63
Q

What affects hepatic extraction ratio?

A
  • hepatic blood flow (drug delivery)
  • free or unbound drug fraction (fraction of drug that can interact with hepatic enzmes)
  • intrinsic metabolic capacity of enzymes represented by Michaelis-Menton constants, accounting for the intrinsic ability of liver enzymes to metabolise individual substances in the absence of flow or protein binding restrictions
    • pKa and lipid solubility have no direct effects on hepatic extraction ratio
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64
Q

What does a high hepatic extraction ratio mean?

A

High HER (>0.7) is “flow dependent clearance” - high metabolic capacity for a drug causes rapid removal of free drug from the circulation.

This clearance is independent of protein binding, but highly dependent on hepatic blood flow.

Eg propofol, ketamine, morphine and lidocaine

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65
Q

What is low hepatic extraction ratio?

A

Low HER (<0.3) - capacity limited clearance - low metabolic capacity means even if there is low protein binding, enzymes saturate rapidly and a concentration gradient between plasma and hepatocytes is eliminated rapidly.

Clearance is independent of hepatic blood flow.

Eg warfarin, phenytoin, diazepam

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66
Q

What is an intermediate hepatic extraction ratio?

A

Intermediate HER (0.3 - 0.7) - clearance is affected by changes in protein binding metabolic capacity and hepatic perfusion.

Examples include aspirin and codeine.

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67
Q

What is the time constant inversely proportional to?

A

The rate constant (k) and clearance (Cl). It’s directly proportional to the volume of distribution.

time constant = Vd/Cl

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68
Q

Which drugs undergo zero order kinetics?

A
  • Phenytoin
  • Ethanol
  • Salicylates
  • Thiopentone
  • Theophylline
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69
Q

Which drugs bind to albumin?

A

Albumin is a basic protein and binds acidic and neutral drugs

  • warfarin
  • NSAIDS
  • phenytoin
  • diazepam
  • thiopentone
  • propofol
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70
Q

Which drugs bind to alpha1 glycoprotein?

A

Alpha 1 glycoprotein is acidic therefore mainly binds basic drugs such as morphine, fentanyl, lidocaine and quinine.

71
Q

Which is more lipid soluble, thiobarbiturates or oxybarbiturates?

A

Thiobarbiturates.

These are generally very lipid soluble, highly protein bound and metabolised in the liver.

Wherease oxybarbiturates are less lipid soluble, less protein bound and can be excreted unchanged in urine.

72
Q

What is the protein binding of thiopentone compared to other barbiturates?

A

Thiopentone is a highly lipid soluble and protein bound barbiturate. It is 80% protein bound (one of the most highly protein bound barbiturates)

73
Q

What is the MOA of barbiturates?

A

They increase the duration of opening of GABA dependent chloride channels in the CNS, increasing chloride conductance and resulting in hyperpolarisation of the channels and subsequent neuronal inhibition.

The thiobarbiturates ONLY act on the beta subunit of GABAA receptors.

74
Q

Is thiopentone a sulphur analogue of pentobarbitone?

A

Yes

75
Q

What are barbiturates derived from?

A

Barbituric acid, which is the condensation product of urea and malonic acid

76
Q

What is ketamine?

A

A phencyclidine derivative

77
Q

How does ketamine work?

A

It causes dissociation between the thalamocortical and limbic systems. It acts as a potent analgesic and has amnesiac properties.

SEs like hallucinations are less common in extremes of age and if opioids/benzodiazepines are used concurrently.

78
Q

What are the CVS SEs of ketamine?

A

It is a sympathetic stimulant, opposite to all the other induction agents.

This increases the plasma levels of noradrenaline and adrenaline - causing increased HR, CO and BP. This results in increased myocardial O2 demand.

79
Q

How does ketamine affect cerebral blood flow and ICP?

A

It increases both

80
Q

Does ketamine affect PONV?

A

Nausea and vomiting occur more frequently than with the admin of other IV induction agents.

81
Q

What is paracetamol classed as?

A

An NSAID. It doesn’t have an effect on COX but has moderate analgesic and anti-pyretic properties.

82
Q

How does paracetamol exert it’s anti-pyretic effect?

A

No effecct on leukotrienes. It is thought to inhibit prostglandin synthesis in the CNS.

83
Q

How is paracetamol metabolised?

A

It’s well absorbed from the gut and has an oral bioavailability of 80%.

Metabolised by the liver to glucuronide, sulphate and cysteine conjugates.

The main metabolites are the glucuronide conjugates that are actively excreted in the urine.

One of the metabolites, N-acetyl-p-amino-benzoquinoeimine, is highly hepatotoxic but rapidly conjugated then excreted.

84
Q

What is an opioid vs opiate?

A

Opioid - substance that includes naturally occurring and synthetic substances that have an affinity for opioid receptors.

Opiates - naturally occuring substances with morphine-like properties.

85
Q

What are the subtypes of opioid receptors?

A

μ1 receptors produce analgesia

μ2 receptors produce respiratory depression, inhibit gut motility, cause miosis and euphoria and can cause bradycardia

κ receptors cause analgesia, sedation and miosis

δ cause analgesia and respiratory depression

86
Q

How many types of each subtype of opioid receptor are there?

A

3 μ

2 δ

3 κ (κ1, κ2, κ3) act on G-protein coupled receptors

87
Q

Where are opioid receptors located?

A

Located presynaptically and activate the inhibitory G-protein-coupled receptors leading to cell membrane hyperpolarisation

88
Q

Which opioid receptor subtype does naloxone have the highest affinity for?

A

They reverse the opioid effects of μ, δ and κ receptors.

They have highest affinity for μ receptors.

89
Q

What is quinidine?

A

Class Ia agent. Active against both atrial and ventricular arrhythmias.

It slows phase 0 of the action potential and leaves the resting potential unaltered.

Conduction through atrial, ventricular and Purkinje fibres are slowed, but AV nodal conduction may accelerate due to it’s vagolytic effects.

90
Q

What is flecainide?

A

Fluorinated aromatic hydrocarbon.

Class Ic agent,

Supresses ventricular arrhythmias.

91
Q

What is the 1st line antiarrhythmic for ventricular arrhythmias?

A

Lidocaine

92
Q

What is disopyramide?

A

Class Ia antiarrhythmic

Has electrophysical properties similar to quinidine but with added class III activity.

Active against atrial and ventricular ectopics.

93
Q

What are beta blockers?

A

Class II agents.

Used in prevention and treatment of supraventricular arrhythmias, especially those due to WPW syndrome.

94
Q

What is sotalol and what class is it?

A

A non-selective beta adrenoceptor antagonist.

Prolongs cardiac repolarisation.

Demonstrates both class II and class III properties.

95
Q

What class antiarrhythmic is amiodarone?

A

Class III

Also has powerful class I and ancillary class II and IV activity.

It blocks sodium and calcium channels, and repolarises potassium channels.

96
Q

How does amiodarone work in AF?

A
  • it has actions on the superior pulmonary veins and AV node
  • it prolongs the refractory period of the superior pulmonary veins and inhibits the AV node.
  • it also non-competitively blocks alpha and beta adrenergic receptors (Class II).
  • the class IV (calcium antagonist) effect may explain bradycardia and AV nodal inhibition and the low incidence of Torsades de Pointes
97
Q

Why does amiodarone require a large oral loading dose?

A

Because it has a slow onset of action when given orally. It has a low GI absorption of up to 50% bioavailibility and is slowly eliminated with a long half life of up to 6 months.

98
Q

What is the metabolism of amiodarone?

A

Hepatic metabolism.

Excretion is largely via the biliary tract and skin.

99
Q

How protein bound is amiodarone?|

A

95%

100
Q

What is IV amiodarone indicated for?

A

For treatment and prophylaxis of frequently recurring VF or destabilising VT and in those refractory to other treatments. It can cause hypotension.

101
Q

What are the SEs of amiodarone?

A
  • sinus bradycardia (esp in elderly)
  • optic neuritis/neuropathy
  • skin discolouration
  • photosensitivity
  • hypothyroidism
  • hyperthyroidism
  • pulmonary fibrosis
  • peripheral neuropathy
  • hepatotoxicity
102
Q

What is an inodilator?

A

An agent which has both inotropic and vasodilator properties.

They are able to reduce afterload and preload whilst increasing myocardial contractility.

103
Q

Which drugs are inodilators?

A

Low dose:

  • dopamine
  • milrinone
  • dobutamine
104
Q

How do the effects of dopamine differ at low vs high dose?

A

Low dose - acts on dopaminergic receptors peripherally which inhibits noradrenaline release and this causes vasodilatation, and also has inotropic effects by acting on the beta-adrenoceptors in the heart

High doses - dopamine causes alpha adrenoceptor stimulation with peripheral vasoconstriction

105
Q

What are phosphodiesterase inhibitors used for?

A

They are inodilators.

They are reserved for very serious haemodynamic compromise such as in acute left ventricular failure with low cardiac output despite adequate LV filling.

106
Q

What is milrinone?

A

It is a PDE inhibitor which inhibits the breakdown of cAMP in cardiac and peripheral vascular smooth muscle, resulting in augmented myocardial contractility and peripheral arterial and venous dilatation.

The dilator effect helpts to conserve myocardial oxygen consumption.

107
Q

How does sodium nitroprusside work?

A

It is a donor of nitric acid that vasodilates by formation of cyclic guanosine monophosphate (cGMP) in vascular tissue.

No inotropic action.

108
Q

In local anaesthetics, what determines the potency?

A

Lipid solublility - the more lipid soluble they are, the more potent.

109
Q

In local anaesthetics, if the drug is highly protein bound, does this make it longer duration or shorter?

A

The higher protein bound the longer lasting it is, because the protein bound form represents a store of drug.

110
Q

For weak bases, are they more or less ionised below their pKa?

A

Weak bases are more ionised below their pKa.

Therefore, the higher the pKa, the more ionised a drug will be at physiological pH. Because it is the unioinised form that is active - the lower the pKa the faster the speed of onset.

111
Q

What is prilocaine in EMLA broken down to and what is it’s significance?

A

O-toluidine - which can lead to metHb-aemia

112
Q

Which anticholinesterases are quaternary amines?

A

Edrophonium

Neostigmine

Pyridostigmine

113
Q

What are the first generation cephalosporins?

A
  • cefalexin
  • cephradine
  • cefuroxime
114
Q

What are the 2nd gen cephalosporins?

A

Cefaclor

Cefotaxmine

115
Q

What are the 3rd gen cephalosporins?

A

Ceftazidime

116
Q

What are the beta lactams?

A

Meropenam

Imipenem

117
Q

What are the 4-quinolones?

A

Ciprofloxacin

Nalidixic Acid

118
Q

What receptor does midazolam act on?

A

GABAA - demonstating it’s physical property of tautomerism.

In a solution of pH 3.5 it is ionised with an open 7-membered diazepine ring, making it water soluble.

When pH is >4, the ring closes and the midazolam is no longer ionised, making it more lipid soluble.

119
Q

What is the oral bioavailibility of midazolam?

A

< 45%

120
Q

What is the VoD of midazolam?

A

1 L/kg

121
Q

Is midazolam highly protein bound?

A

Yes, 95%

122
Q

What is midazolam metabolised to?

A

1-alpha-hydroxymidazolam - which has weak activity, followed by conjugation, then urinary excretion.

123
Q

What are imipramine, amitriptyline and nortriptyline?

A

Tricyclic antidepressants

124
Q

How do tricyclic antidepressants work?

A

They prevent noradrenaline and serotonin reuptake into nerve terminals of monoaminergic neurones by competitively inhibiting uptake 1.

Some might also inhibit presynaptic alpha2 receptors to increase noradrenaline release.

They also have antimuscarinic, antihistaminergic (H1 receptors) and antiadrenergic (alpha1-adrenoceptors) effects.

125
Q

What SEs do tricyclic antidepressants have?

A
  • sedation
  • fatigue
  • proconvulsant
  • antimuscarinic
    • constipation
    • urinary retention
    • dry mouth
    • blurred vision
  • postural hypotension
  • arrhythmias (prolonged PR and QT intervals with amitriptyline)
126
Q

What is phenelzine?

A

MAOI

127
Q

What are the classes of diuretics and where do they act on the nephron?

A

Aldosterone antagonists (eg spironolactone, eplerenone)

  • DCT + early collecting duct

Carbonic anhydrase inhibitors (eg acetazolamide)

  • PCT

Loop diuretics (eg furosemide)

  • ascending LoH

Osmotic diuretics (eg mannitol)

  • ascending LoH

Potassium sparing diuretics (eg amiloride)

  • DCT

Thiazide diuretics (eg bendoflumethiazide)

  • DCT
128
Q

What is magnetism?

A

Two conductors with a current flowing through them will exert a force on each other and the region through which this force is exerted is the magnetic field.

129
Q

How does a magnetic field produce an electric current?

A

When a magnetic field changes direction, there is a flow of electrons induced

130
Q

What is the magnetic field strength defined as?

A

The power of the magnetic field in a vacuum

131
Q

What is the magnetic flux?

A

Used to describe the magnetic field present in a material.

Diamagnetic materials decrease the magnetic flux, while ferromagnetic and paramgnetic increase it.

132
Q

What is the unit of magnetic flux and magnetic flux density?

A

The Weber (wb) = flux

The Tesla (T) = flux density

133
Q

What happens if you combine AC and DC current?

A

It results in a current which does not have a steady value but whose electrons move in one direction

134
Q

What is one ampere?

A

The flow of 6.24 x 1018 electrons per second past a point and is defined as the electromagnetic force associated with an electric current.

135
Q

What is a galvanometer?

A

A current, which is being measured, is passed through a coil of wire that is suspended in a magnetic field.

As the current flow, the coil rotates due to the magnetic field, and the rotational force is proportional to the strength of the current.

136
Q

Where is the magnetic field strongest when a coil of wire has a current passed through it?

A

In the core of the coil

137
Q

What is the potential difference across a conductor based on?

A

Energy production and current flow.

The unit of potential difference is the volt (potential difference that produces a current of 1 amp when the rate of energy dissipated is 1 watt).

138
Q

How is the high voltage electricity from power stations reduced?

A

At substations using transformers

139
Q

How is electricity transported to the hospital from the substation?

A

Via 2 wires, live and neutral - neutral is earthed at the substation but the live wire is not.

At the hospital - the mains sockets have live, neutral and earth conductors.

140
Q

Is the impedence of skin/tissues low or high?

A

It’s relatively small but antistatic shoes provide a high impedance to protect against electric shock and allow safe dissipation of electrostatic charges that build up on clothing.

Their impedance will be up to 10MΩ

141
Q

What kind of process is a wash-in curve an example of?

A

Exponential

142
Q

What is a build up exponential curve?

A

It is an inverted negative exponential.

Eg curve generated by a constant pressure generator ventilator.

Similar to a wash-in curve.

143
Q

What is the graph like for a constant flow generator if you plot volume against time for inspiration?

A

It is a linear relationship as the rate of filling of the lungs is constant due to the constant flow.

This is a linear, non-exponential process.

144
Q

What kind of curve does expiration of gases from the lungs produce?

A

A wash-out curve which is a negative exponential.

The rate of emptying is initially fast then slows down.

145
Q

What is the curve seen for the plot of dye concentration against time for the dye dilution technique of measuring cardiac output?

A

It is an exponential curve but there is recirculation of dye so there is a second curve.

146
Q

What does a plot of temperature against time look like for the thermodilution technique?

A

It is an exponential wash out curve without a second curve.

147
Q

What are the SI units?

A
  • meters (length)
  • kilograms (mass)
  • seconds (time)
  • amperes (current)
  • moles (amount of substance)
  • kelvins (temperature)
  • candela (luminous intensity)
148
Q

What are the derived SI units?

A
  • Hertz (frequency)
  • Newton (force)
  • Pascal (pressure)
  • Joules (energy/work)
  • Watts (power)
  • Coulombs (charge)
  • Volts (electric potential)
  • Grays (absorbed dose)
  • Degrees Celcius (temp)
149
Q

How is body temperature controlled?

A

The anterior hypothalamic nucleus is responsible for themroregulation in humans.

The central core is maintained at a constant temperature (37C) whilst the surface layer is variable (32 to 35C) to ensure optimal enzymatic activity throughout core compartments.

Core compartment organs - brain, thorax, abdominal organs, deep tissues of limbs. These contribute 75% of thermal input to thermoregulatory system.

150
Q

What is the relative humidity by the time the gases reach the alveoli?

A

100% RH

151
Q

What are heat and moisture exchangers?

A

Disposable devices that can have a hydrophobic/hygroscopic membrane incorporated.

Hydrophobic membrane has a large surface area and offers low resistance to flow of gas. The membrane has a low thermal conductivity that can generate a temperature gradient, allowing water vapour from expired gases to condensate on the surface. Breath is then humidified and heated by this condensed water vapour.

Hygroscopic filters are made of a hygroscopic layer plus polarised fibre membrane. They work similarly but are more efficient.

152
Q

Do heated breathing tubes increase the humidity of inspired gases?

A

Yes

153
Q

Can both ultrasonic and pneumatic nebulisers be heated?

A

Yes.

Pneumatic ones require a jet of high pressure gas, ultrasonic ones don’t need a driving gas.

Ultrasonic nebs create smaller, finer droplets compared with pneumatic nebulisers.

154
Q

What is the formula to calculate Reynold’s number?

A

Re = pvd / π

p = fluid density

v = mean flow velocity

d = diameter

π = viscosity

155
Q

What current is required when applied to the body to cause VF?

A

100mA

156
Q

Which requires a lower current to cause VF, AC or DC?

A

AC

157
Q

If the frequency of a current applied to a patient is increased, is this higher or lower shock risk to the patient?

A

The higher the frequency, the less risk for the patient.

Mains current (50hz most dangerous).

158
Q

What do the cylinders that oxygen is stored in look like?

A

Black body with white shoulders at a pressure of 137 bar.

Pins 2 and 5 positions.

In a cylinder bank, size J are used with a capacity of 6800L.

Size E used on anaesthetic machines - 680L.

The decrease in pressure is a linear one with progressive use of O2.

159
Q

What is entonox stored in?

A

French blue bodied cylinders with white and blue quartered shoulders.

At 13700 kPa.

160
Q

What is the pseudocritical temperature of entonox?

A

That is the temperature which a gas mix may separate into its constituent components = -5.5C.

This is called the Poynting effect. The cylinder will then contain a liquid mix of N2O and gas of predominantly O2 above it. Therefore there will be an initial high concentration of O2 which is used up first followed by a hypoxic mix of N2O.

161
Q

What is the name of the 2 stage pressure demand regulator valve used for entonox?

A

The carnet demand valve.

1st stage contains 2 chambers to reduce the inlet pressure, 2nd stage chamber delivers the gas on inspiration by the patient at ambient pressure.

162
Q

What are the methods used to measure flow?

A
  • rotameters
  • pneumotachographs
  • pitot tubes
  • electromagnetic flowmeter (change in temp of thermistors proportional to gas flow)
  • wright respirometer
  • Bourdon gauge
  • Ultrasonic flowmeters
  • Fick principle
  • Benedict roth spirometers
163
Q

What does the Tec 6 do to desflurane?

A

It heats it to 39C at a pressure of 195kPa (almost 2 atm), after which the gas is directly added to the FGF.

The amount of vapour added to the FGF must be proportional to the FGF rate which is achieved using the flow restrictor to the FGF causing increased back pressure that is detected by differential pressure transducers altering vapour delivery.

164
Q

What do passive scavenging systems consist of?

A
  • require no external energy supply
  • have a collecting and transfer system
    • 30mm connectors
    • collecting tubing is attached to expiratory valves or APL valves and driven by patient expiration or the ventilator
  • a receiving system
    • may use reservoir bags
    • these contain pressure relief valves to avoid positive pressure over 1kPa and negative pressures of < -50 Pa
  • disposal system
    • comprises wide bore tubing to the roof of the building or theatre ventilation system
    • uses wind to entrain expired gases
      • excessive pressures caused by wind can reverse the flow
165
Q

What type of breathing is the Bain circuit efficient for?

A

Controlled (most efficient system for this) - and this is not affected by length of tubing.

166
Q

Is the Bain bulky at the patient end?

A

No, it is compact

167
Q

What is the internal volume of the Bain?

A

>500ml

168
Q

What is the Pethnik test?

A

This is to check the patency of the internal tubing of the Bain.

The end of the circuit is occluded and filled with O2 from the emergency oxygen flush with the APL valve closed.

Then releasing the occlusion and pressing the emergency flush again. Because of the venturi effect, a patent inner tube will cause the reservoir bag to collapse as the air within the large tube becomes entrained.

169
Q

What principles does pulse oximetry use?

A

Spectrophotometric principles of absorption of radiation through a sample.

Beer’s Law relates the absorption of radiation through a solution to it’s concentration, while Lambert’s Law relates the absorption of radiation to the thickness of the layers it passes through.

170
Q

What wavelength light better absorbs dexyHb?

A

Red light at 660nm

171
Q

What wavelength light better absorbs oxyHb?

A

Infrared wavelengths of 940nm

172
Q

What does a Severinghaus electrode contain?

A

Modification of a pH electrode to measure partial pressure of CO2. It is slow (2-3mins). Must be temp controlled at 37C and regularly calibrated.

  • contains a Co2 permeable membrane separating the sample and a thin film of sodium bicarbonate solution in contact with hydrogen ion sensitive glass
  • as the CO2 diffuses into solution, it then reacts with water to generate H+ ions sensed by the glass
  • also a silver/silver chloride reference electrode in contact with the electrolyte solution
173
Q
A
174
Q
A