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MRCS part A- Principles of surgery in general > Physiology for the MRCS part A > Flashcards

Physiology for the MRCS part A Flashcards

1
Q

What does P wave represent in normal ECG?

A

Atrial depolarisation:- Represents the wave of depolarisation that spreads from the SA node throughout the atria

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2
Q

What is the duration of the P wave in normal ECG?

A

Lasts 0.08 to 0.1 seconds(80-100 ms)

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3
Q

What does isoelectric period after the P wave represent in normal ECG?

A

Represents the time in which the impulse is travelling within the AV node

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4
Q

Define PR interval in normal ECG

A

Time from the onset of the P wave to the beginning of the QRS complex

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5
Q

What is the duration of the PR interval in normal ECG?

A

0.12-0.20 seconds

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6
Q

What does PR interval represent in normal ECG?

A

The time between the onset of atrial depolarisation and onset of ventricular depolarisation

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7
Q

What does QRS complex represent in normal ECG?

A

Ventricular depolarisation

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8
Q

What is the duration of QRS complex in normal ECG?

A

0.06-0.1 seconds

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9
Q

Discuss ST segment

A

(1) Isoelectric period following the QRS
(2) period which the entire ventricle is depolarised
(3) Plateau phase of the ventricular action potential

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10
Q

Define ST segment

A

Isoelectric period following the QRS

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11
Q

What does ST segment represent in normal ECG?

A

Represents period which the entire ventricle is depolarised

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12
Q

What does ST segment correspond to in normal ECG?

A

The plateau phase of the ventricular action potential

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13
Q

What does T wave represent in normal ECG?

A

Ventricular repolarisation

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14
Q

What is the duration of the T wave as a repolarisation compared to the depolarisation?

A

Longer in duration than depolarisation

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15
Q

What does small positive U wave represent in normal ECG?

A

(1) Follow the T wave
(2) Last remnants of ventricular repolarisation

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16
Q

What does QT interval represent in normal ECG?

A

Represents the following

(1) Both ventricular depolarisation and repolarisation
(2) Ventricular action potential

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17
Q

What is the duration of QT interval in normal ECG?

A

0.2-0.4 seconds depending upon heart rate

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18
Q

What is the effect of heart rate on QT interval in normal ECG?

A

At high rates,ventricular action potential shortens in duration,which decreases the Q-T interval

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19
Q

What is the duration of normal corrected QTc interval in normal ECG?

A

< 0.44 seconds

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20
Q

When bundle branch block is considered?

A

When QRS complex is wide

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21
Q

What are the ECG findings in left bundle branch block?

A

(1) Wide QRS complex
(2) W pattern or wave in V1-V2
(3) M pattern or wave in V3-V6

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22
Q

What findings do we see in leads V1-V2 in ECG of left bundle branch block?

A

W pattern or wave

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23
Q

In which leads does the W pattern or wave is seen in ECG of left bundle branch block?

A

V1-V2

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24
Q

What findings do we see in leads V3-V6 in ECG of left bundle branch block?

A

M pattern or wave

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25
Q

In which leads does the M pattern or wave is seen in ECG of left bundle branch block?

A

V3-V6

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26
Q

What are the ECG findings in right bundle branch block?

A

(1) Wide QRS complex
(2) M pattern in V1-V2
(3) W pattern in V3-V6

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27
Q

What findings do we see in leads V1-V2 in ECG of right bundle branch block?

A

M pattern or wave

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28
Q

in which leads does the M pattern or wave is seen in ECG of right bundle branch block?

A

V1-V2

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29
Q

What findings do we see in leads V3-V6 in ECG of right bundle branch block?

A

W pattern or wave

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30
Q

in which leads does the W pattern or wave is seen in ECG of right bundle branch block?

A

V3-V6

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31
Q

Picture illustrating ECG

A
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32
Q

What are the ECG features of hypokalaemia?

A

Mnemonic;Please U Sit Far

(1) Prolonged PR interval
(2) ST depression
(3) Flattened/inverted T
(4) U waves

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33
Q

What are the ECG features of hyperkalaemia?

A

Mnemonic;STW

(1) Small P
(2) Tall tented T wave
(3) Wide QRS complex

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34
Q

What are the ECG features of pulmonary embolism(PE)?

A

Mnemonic;P(TR)(IT)/STARRR

(1) P pulmonale(peaked P wave)
(2) Tall R in V1
(3) Inverted T in V1-V4
(4) S1-Q3-T3
(5) Tachycardia
(6) Atrial arrhythmia
(7) Right ventricular strain pattern
(8) RBBB
(9) Right axis deviation

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35
Q

What are the ECG features of hypocalcaemia?

A

(1) Short PR interval
(2) Long ST/ST depression
(3) Long QT
(4) Narrow QRS complex
(5) Flattened/inverted T wave
(6) Prominent U wave

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36
Q

What are the ECG features of hypercalcaemia?

A

Short QT

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37
Q

Illustrate push and pull effect of potassium on ECG

A
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38
Q

Picture illustrating ECG features of electrolytes disturbance

A

Picture

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39
Q

What are the causes of long QT in the ECG?

A

(1)Hypocalcaemia
(2)Hypothermia-J wave
(3)Pericarditis-concave upward ST
elevation(cave upward)
(4)MI-convex upward ST elevation
(5)WPW-δ wave
(6)Arterial line in situ
-On studying trace the incisura can be found
-the elastic recoil of the aorta is the
physiological event which causes this
process(V.IMP)

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40
Q

Picture illustrating treatment of hyperkalaemia

A
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41
Q

What are the causes (a )wave of jugular venous pressure(JVP)?

A

(A)trial contraction

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42
Q

What are the causes large(a )wave of jugular venous pressure(JVP)?

A

If atrial pressure.e.g.,:-

(1) Tricuspid stenosis
(2) Pulmonary stenosis
(3) Pulmonary hypertension

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43
Q

What are the causes canon (a )wave of jugular venous pressure(JVP)?

A

(1) atrial contractions against a closed tricuspid valve
(2) Complete heart block
(3) ventricular tachycardia
(4) nodal rhythm
(5) single chamber ventricular pacing

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44
Q

What are the causes (c )wave of jugular venous pressure(JVP)?

A

(1) ventricular (C)ontraction=(C)losure of tricuspid valve and it moves up
(2) Not normally visible

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45
Q

What are the causes (v)wave of jugular venous pressure(JVP)?

A

Atrial (V)enous filling=passive filling of blood into the atrium against a closed tricuspid valve

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46
Q

What are the causes prominent or giant(v)wave of jugular venous pressure(JVP)?

A

Tricuspid regurgitation

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47
Q

What are the causes (x) descent wave of jugular venous pressure(JVP)?

A

(1) atrium rela(X)es
(2) tricuspid valve moves up
(3) fall in atrial pressure during ventricular systole

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48
Q

What are the causes (y) descent wave of jugular venous pressure(JVP)?

A

(1) Opening of tricuspid valve
(2) Emptying of the right atrium
(2) Right ventricular filling

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49
Q

What are the causes slow (y)wave of jugular venous pressure(JVP)?

A

(1) tricuspid stenosis
(2) right atrial myxoma

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50
Q

What are the causes steep (y) descent wave of jugular venous pressure(JVP)?

A

Mnemonic;CRT

(1) Constrictive pericarditis
(2) Right ventricular failure
(3) Tricuspid regurgitation

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51
Q

What are the waves of jugular venous pressure(JVP)?

A
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52
Q

Enumerate acute phase proteins

A

Mnemonic;3CAT/2FISH/AP

(1) CRP
(2) Caeruloplasmin
(3) Complement
(4) Albumin
(5) Transferrin
(6) Ferritin
(7) Fibronigen
(8) Serum amyloid A

(9) Haptoglobin
(10) Alpha-1 antitrypsin
(11) Procalcitonin

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53
Q

Discuss acute phase response with regards to the acute phase proteins

A

Mnemonic;CART

During the acute phase response,the liver decreases the production of other proteins (sometimes referred to as negative acute phase proteins)

(1) Cortisol binding proteins
(2) Albumin
(3) Retinol binding proteins
(4) Transthyretin(formerly known as prealbumin)
(5) Transferrin

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54
Q

What is the other name for transthyretin?

A

Formerly known as prealbumin

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55
Q

Discuss C-reactive proteins

A

Definition
a protein synthesised in the liver

Function

(1) Binds to phosphocholine in bacterial cells
(2) On these cells undergoing apoptosis
(3) Activates the complement system

Causes of the increase

(1) Levels of CRP are commonly measured in acutely unwell patients
(2) Following surgery-levels > 150 at 48 hrs post operatively are suggestive of evolving complications

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56
Q

Define CRP

A

a protein synthesised in the liver

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57
Q

What is the function of CRP?

A

(1) Binds to phosphocholine in bacterial cells
(2) On these cells undergoing apoptosis
(3) In binding to these cells it is then able to activate the complement system

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58
Q

What are the causes of increasing CRP?

A

(1) Levels of CRP are commonly measured in acutely unwell patients
(2) Following surgery-levels > 150 at 48 hrs post operatively are suggestive of evolving complications

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59
Q

Discuss tumour necrosis factor(TNF)

A

+Definition
A pro-inflammatory cytokine with multiple roles in immune system

+Secreted by
Macrophages

+Functions(effect)
I)Paracrine effects
(1)Activates macrophages and neutrophils
(2)Co-stimulater for T-cell activation
(3)Mediates bodies response to gram negative septicaemia
(4)Similar properties to IL-1
(5)Anti-tumour effect(e.g.,phospholipase activation)
(6)TNF-alpha binds to both p55 and p75 receptors to induce apoptosis
(7)Activation of NFkB
II)Endothelial effects
(1)Increase expression of selectins
(2)Increase production of platelet activating factor,IL-1,prostaglandins
(3)TNF promotes the proliferation of fibroblasts and their enzymes production(protease and collagenase).It is thought
fragments of receptors act as binding points in serum
III)Systemic effects
(1)Pyrexia
(2)Increased acute phase proteins
(3)Disordered metabolism leading to cachexia
(4)TNF is important in the pathogenesis of rheumatoid arthritis-TNF blockers(e.g.,infliximab,etanercept)are licensed for treatment of severe rheumatoid as DMARDS(disease modifying anti rheumatoid disorders)

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60
Q

Define tumour necrosis factors(TNF)

A

A pro-inflammatory cytokine with multiple roles in immune system

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61
Q

What tumour necrosis factors(TNF) is secreted by?

A

Macrophages

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62
Q

What are the functions(effect) of tumour necrosis factors(TNF)?

A

I)Paracrine effect
(1)Activates macrophages and neutrophils
(2)Co-stimulater for T-cell activation
(3)Mediates bodies response to gram negative septicaemia
(4)Similar properties to IL-1
(5)Anti-tumour effect(e.g.,phospholipase activation)
(6)TNF-alpha binds to both p55 and p75 receptors to induce apoptosis
(7)Activation of NFkB
II)Endothelial effect
(1)Increase expression of selectins
(2)Increase production of platelet activating factor,IL-1,prostaglandins
(3)TNF promotes the proliferation of fibroblasts and their enzymes production(protease and collagenase).It is thought
fragments of receptors act as binding points in serum
III)Systemic effects
(1)Pyrexia
(2)Increased acute phase proteins
(3)Disordered metabolism leading to cachexia
(4)TNF is important in the pathogenesis of rheumatoid arthritis-TNF blockers(e.g.,infliximab,etanercept)are licensed for
treatment of severe rheumatoid as DMARDS(disease modifying anti rheumatoid disorders)

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63
Q

What is the paracrine effect of tumour necrosis factors(TNF)?

A

(1) Activates macrophages and neutrophils
(2) Co-stimulater for T-cell activation
(3) Mediates bodies response to gram negative septicaemia
(4) Similar properties to IL-1
(5) Anti-tumour effect(e.g.,phospholipase activation)
(6) TNF-alpha binds to both p55 and p75 receptors to induce apoptosis
(7) Activation of NFkB

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64
Q

What are the endothelial functions(effects) of tumour necrosis factors(TNF)?

A

(1) Increase expression of selectins
(2) Increase production of platelet activating factor,IL-1,prostaglandins
(3) TNF promotes the proliferation of fibroblasts and their enzyme production(protease and collagenase).It is thought fragments of receptors act as binding points in serum

In conclusion:TNF affects the following
(1)Selectin

(2) Platelet activating factor
(3) IL-1
(4) Prostaglandins
(5) Fibroplasts
(6) Protease
(7) Collagenase
(8) Fragments of receptors

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65
Q

What are the systemic effects(functions) of tumour necrosis factors?

A

(1)Pyrexia
(2)Increased acute phase proteins
(3)Disordered metabolism leading to cachexia
(4)TNF is important in the pathogenesis of rheumatoid arthritis-TNF blockers(e.g.,infliximab,etanercept)are licensed for
treatment of severe rheumatoid as DMARDS(disease modifying anti rheumatoid disorders)

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66
Q

Define ultrasound in general

A

Ultrasound frequencies more than 20 kHz which is above the range detectable by the human ear

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67
Q

What are the ultrasound frequencies?

A

(1) Frequencies detectable by the human ears= > 20 kHz
(2) In medical imaging ultrasound frequencies range from 2 MHz to 15 MHz
(3) Trans-abdominal 3-3.5 MHz
(4) Trans-vaginal 5-7.5 MHz(post bladder void)
(5) Non-ionising radiation which utilises high frequency sound waves

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68
Q

What are the ultrasound frequencies detectable by the human ears?

A

> 20 kHz

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69
Q

What are the ultrasound frequencies in medical imaging?

A

2 MHz to 15 MHz

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70
Q

What is the frequency in trans-abdominal ultrasound?

A

3-3.5 MHz

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71
Q

What is the frequency in transvaginal ultrasound?

A

5-7.5 MHz(post bladder void)

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72
Q

What is the frequency of non-ionising radiation?

A

high frequency sound waves

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73
Q

How ultrasound is made in general?

A

(1) Produced by applying voltage across a piezoelectric crystal
(2) Crystal resonance produces sound waves which are then directed by the transducer

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74
Q

What are the types of radiotherapy?

A

I)According to DNA damage
(1)Direct-leading to cell death
(2)Indirect-leading to free radical formation
II)According to the place
(1)Locally placed(i.e.,Brachytherapy)
(2)External beam

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75
Q

What are the types of radiotherapy according to DNA damage?

A

(1) Direct-leading to cell death
(2) Indirect-leading to free radical formation

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76
Q

What are the types of radiotherapy according to the place?

A

(1) Locally placed(i.e.,Brachytherapy)
(2) External beam

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77
Q

How to reduce radiotherapy damage to normal tissue and shape?

A

*Technique-Multiple beams are used with a higher absorbed dose at the point of convergence
*Tools-[I]Radiosensitisers
+Definition:increase the effect of a given dose of radiation
+Types:(1)Oxygen
(2)Hypoxic cell sensitisers
(3)Halogenated pyrimidines
(4)Bioreductive agents
[II]Radioprotectors
+Definition:are agents that reduce the effects of radiation
+Role:their role is limited in clinical practice due to possible protection of tumours

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78
Q

What is the technique used to reduce radiotherapy damage to normal tissue and shape?

A

Multiple beams are used with a higher absorbed dose at the point of convergence

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79
Q

What are the tools used to reduce radiotherapy damage to normal tissue and shape?

A

[I]Radiosensitisers
+Definition:increase the effect of a given dose of radiation
+Types:(1)Oxygen
(2)Hypoxic cell sensitisers
(3)Halogenated pyrimidines
(4)Bioreductive agents
[II]Radioprotectors
+Definition:are agents that reduce the effects of radiation
+Role:their role is limited in clinical practice due to possible protection of tumours

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80
Q

Descuss radiosensitisers

A

+Definition:increase the effect of a given dose of radiation
+Types:(1)Oxygen
(2)Hypoxic cell sensitisers
(3)Halogenated pyrimidines
(4)Bioreductive agents
​[II]Radioprotectors
+Definition:are agents that reduce the effects of radiation
+Role:their role is limited in clinical practice due to possible protection of tumours

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81
Q

Define radiosensitisers

A

increase the effect of a given dose of radiation

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82
Q

What are the types of radiosensitisers?

A

(1) Oxygen
(2) Hypoxic cell sensitisers
(3) Halogenated pyrimidines
(4) Bioreductive agents

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83
Q

Define radioprotectors

A

are agents that reduce the effects of radiation

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84
Q

What is the role of radioprotectors?

A

their role is limited in clinical practice due to possible protection of tumours

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85
Q

Discuss radiotherapy dosing

A

+Unit(Discussed in part B osce)

(1) Gray(Gy)
(2) Columb
(3) Seivert
(4) Bacequrel

+Dependent factors
Total dose varies between tumour (1)type and (2)stage

+Amount
typical regimes involve 1.8 - 2.0 Gy fractions delivered over a number of weeks with total dose accumulation around 50 Gy

+Duration
Dilvered over a number of weeks

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86
Q

What are the units of radiotherapy?

A

+Unit(Discussed in part B osce)

(1) Gray(Gy)
(2) Columb
(3) Seivert
(4) Bacequrel

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87
Q

What are the dependent factors of radiotherapy dosing?

A

Total dose varies between tumour (1)type and (2)stage

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88
Q

What is the amount of radiotherapy dosing?

A

typical regimes involve 1.8 - 2.0 Gy fractions delivered over a number of weeks with total dose accumulation around 50 Gy

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89
Q

What is the duration of dilevering radiotherapy?

A

Dilvered over a number of weeks

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90
Q

What is amount of the accumulated dose of radiotherapy?

A

50 Gy

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91
Q

Discuss radiotherapy side effects

A

Usually vary significantly from site to site.Some side effects such as dry mouth may be acute or late.
(1)Moist skin desquamation
-is an acute side effect of radiotherapy
-epilation occurs in fields targeted by radiotherapy with cumulative dose of 45 Gy
(2)Myelodysplastic syndromes(MDS)
-Duration of radiotherapy required:develop years after radiotherapy
-Cause:10% of MDS are secondary,most often due to radiotherapy or chemotherapy for cancer
-Course:some MDS remain indolent whilst others transform to aggressive forms such as AML
(3)Fibrosis and lymphoedema
are late complications

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92
Q

Discuss dry mouth as a side effect of radiotherapy

A

Side effects of radiotherapy usually vary significantly from site to site.Some side effects such as dry mouth may be acute or late.

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93
Q

Discuss moist skin desquamation as a side effect of radiotherapy

A
  • is an acute side effect of radiotherapy
  • epilation occurs in fields targeted by radiotherapy with cumulative dose of 45 Gy
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94
Q

In what fields epilation occurs as a side effect of radiotherapy?

A

Occurs in fields targeted by radiotherapy

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95
Q

What is the dose of radiotherapy required to cause epilation as a side effect of radiotherapy?

A

Cumulative dose of 45 Gy

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96
Q

Discuss myelodysplastic syndromes(MDS) as a side effect of radiotherapy

A

-develop years after radiotherapy
-10% of MDS are secondary,most often due to radiotherapy or chemotherapy for cancer
-some MDS remain indolent whilst others transform to aggressive forms such as AML
(3)Fibrosis and lymphoedema
are late complications

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97
Q

What is the duration of radiotherapy required to cause myelodysplastic syndromes?

A

Develop years after radiotherapy

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98
Q

What is the cause of myelodysplastic syndromesMDS) as a side effect of radiotherapy?

A

10% of myelodysplastic syndromes(MDS) are secondary to radiotherapy or chemotherapy for cancer

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99
Q

What is the course of myelodysplastic syndromes(MDS) as a side effect of radiotherapy?

A

Some myelodysplastic syndromes(MDS)remain indolent whilst others transform to aggressive forms such as AML

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100
Q

Discuss fibrosis and lymphoedema as a side effect of radiotherapy

A

Are late complications

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101
Q

Discuss LASER

A
  • LASER stands for Light Amplification by the Stimulated Emission of Radiation
  • There are multiple types
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102
Q

Define X-rays

A

Ionising electromagnetic radiation

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103
Q

What is the frequency value of the X-rays?

A

30 petahertz to 30 exahertz

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104
Q

What is the typical energy value of -rays?

A

100 eV to 100 keV

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105
Q

What is the severity of exposure to radiation in X-rays?

A

Chest X-rays equivalent to 2.4 days natural background radiation

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106
Q

What is the severity of exposure to radiation in CT?

A

CT abdomen by comparison is equivalent to 2.7 years natural background radiation

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107
Q

Define MRI

A

Non-ionising radiation that uses strong magnetic field causing protons to align with the field

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108
Q

What is the mechanism of the MRI?

A

(1) MRI uses strong magnetic fields that cause protons to align with the field
(2) Radiofrequency is then applied to disrupt the proton alignment
(3) Radiofrequency pulses then causes the proton to excite or spin
(4) When the radiofrequency is stopped,the protons relax back into alignment of the field
(5) Protons return to their axis of equilibrium
(6) Protons release energy in the process in the form of radio waves
(7) The radio waves are detected by the MRI sensors of the scanner
(8) Computers use the radio wave emissions to construct an image

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109
Q

Define the types of MRI images

A

(1) T1 weighted images-fluids appear dark
(2) T2 weighted images-fluids appear bright

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110
Q

What are the SI unit of of MRI?

A

(1) Tesla(T)-is SI unit for magnetic field
(2) Weber(Wb)-is SI unit of magnetic flux

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111
Q

What is the field value of MRI?

A

0.5 to 3 Tesla

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112
Q

What DEXA stands for?

A

Dual Emission X-rays Absorbtiometry

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113
Q

What is the use of DEXA scan?

A

For measurement of bone density to assess osteoporosis

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114
Q

What is the mechanism of DEXA scan?

A

(1) 2 low dose X-rays beams used at each site
(2) X-rays absorption measured by detectors
(3) Soft tissue absorption subtracted to give bone mineral density measurement(BMD measurement)
(4) T-score is standard deviation score when compared to a young healthy adult

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115
Q

What is the T-score that confirms osteoporosis in DEXA scan?

A

< _2.5

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116
Q

What is the mechanism of CT?

A

(1) Potential for high dose of ionising radiation
(2) Uses multiple X-rays analysed by computer to create 3D images

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117
Q

What is the equivalence of CT abdomen to chest X-rays?

A

A CT abdomen is equivalent to 400 chest X-rays or 2.7 years natural background radiation

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118
Q

What PET CT stands for?

A

Positron Emission Tomography CT

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119
Q

What is the mechanism of PET scan?

A

(1) Uses a radioactive tracer,usually fluorodeoxyglucose(FDG),an analogue of glucose
(2) FDG is given to the patient
(3) FDG is then taken up in areas of high metabolism(e.g., cancer mets)
(4) The tracer emits gamma rays which are detected by the scanner

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120
Q

What are the other names of diathermy?

A

(1) Surgical diathermy
(2) Electrosurgery

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121
Q

What is the mechanism of diathermy?

A

AC current is passed through a conductor with some energy appearing as heat

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122
Q

What are the types of diathermy?

A

(1) Monopolar current diathermy
(2) Bipolar current diathermy

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123
Q

Define monopolar current diathermy

A

Passed from small electrode held by surgeon and returned to a large area plate via patient’s tissues

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124
Q

What is the mechanism of monopolar current diathermy?

A

(1) The concentrated current at the electrode tip produces a lot of heat
(2) The current is dissipated over a large area at the plate
(3) It is important the plate is properly attached
(4) If the plate area(70 cm2) is reduced the current concentrates leads to tissue burns
(5) Better to be avoided in patients with prosthesis

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125
Q

What is the complications of monopolar current diathermy?

A

If the plate area(70 cm2) is reduced the current concentrates leads to tissue burns
​

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126
Q

What is the contraindicated of monopolar current diathermy?

A

Better to be avoided in patients with prosthesis

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127
Q

What is the use bipolar current diathermy?

A

Cutting

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128
Q

Define bipolar current diathermy

A

Passes between two electrodes held by the surgeon as forceps

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129
Q

What is the use of bipolar current diathermy?

A

Bipolar current diathermy is used to coagulate not cut

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130
Q

What is the mechanism of diathermy?

A

(1) In cutting(monopoly)the waveform can be varied
(2) A continuous single frequency sine wave is often used
(3) Pulsed waves can reduce local thermal tissue damage

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131
Q

What is the recommended frequency for bipolar current diathermy?

A

The recommended frequency-must be over 100 kHz,blow this electric shock or even electrocution could occur
Why-to prevent cell depolarisation (especially in cardiac tissue)

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132
Q

What is the the usual frequency of diathermy in surgical practice?

A

In surgical practice frequencies of around 500 KHz are used

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133
Q

What is the incidence of metabolic acidosis as acid base balance disorder?

A

The most common surgical acid base disorder

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134
Q

Define metabolic acidosis?

A

Reduction in plasma bicarbonate levels

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135
Q

What are the mechanisms of metabolic acidosis?

A

(1)Gain of strong acid(e.g.,diabetic ketoacidosis)

(2)Loss of base(e.g.,from bowel in diarrhoea)

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136
Q

Discuss anion gap and What is the equation of the anion gap?

A

(Na+k)-(Cl+HCO3)
If a question supplies the chloride,then this is often a clue that the anion gap should be calculated

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137
Q

What is the normal range of anion gap?

A

3-11 mmol/l or 4-12 mmol/l or 8-16 mmol/l or 10-18 mmol/l

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138
Q

What is the other name for normal anion gap acidosis?

A

Hyperchloraemic metabolic acidosis

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139
Q

What are the causes of normal anion gap metabolic acidosis?

A

Mnemonic;HARDUPS

(1) Hyperalimentation/hyperventilation
(2) Acetazolamide,Ammonium chloride injection,Addison’s disease
(3) Renal tubular acidosis
(4) Diarrhoea,fistula-causing gastrointestinal bicarbonate loss
(5) Ureteral diversion(uretrosigmoidostomy)-causing gastrointestinal bicarbonate loss
(6) Pancreatic fistula/Parentral saline (7)Spironolactone

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140
Q

What are the causes of increased anion gap metebolic acidosis?

A

Mnemonic;MUDPILES

(1) Methanol,Metformin(Renal failure),Mesentric ischaemia or infarction
(2) Uraemia,i.e.,urate(renal failure or CKD)
(3) Diabeti ketoacidosis,AKA,alcohol
(4) Propylene glycol/Paraldehyde/Phenformin,Paracetamol
(5) Isoniazide/Iron,Infections,Inborn errors of metabolism
(6) Lactic acidosis,i.e.,lactate(shock,hypoxia,burn,sepsis)
(7) Ethylene glycol,Ethanol
(8) Salycilates-Aspirin

N.B:Mesentric ischaemia or infarction is associated with lactic acidosis and metabolic acidosis late in its biochemical presentation

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141
Q

What are the causes of decreased anion gap mtabolic acidosis?

A

Mnemonic;HYP/HL

(1) Hypoalbuminaemia
(2) Hypercalcaemia
(3) Hypermagnesaemia
(4) Hyper γ-globulinaemia
(5) Hyperviscosity
(6) Halide(bromide or iodide)intoxication
(7) Lithium intoxication

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142
Q

What is the classification of metabolic acidosis secondary to high lactate levels?

A

(1) Lactic acidosis type A:Perfusion disorders e.g.,shock,hypoxia,burn
(2) Lactic acidosis type B:Metabolic e.g.,Metformin toxicity

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143
Q

Define metabolic alkalosis

A

Rise in plasma bicarbonate levels

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144
Q

What is the abnormal level of bicarbonate and what happens to it?

A

Rise of bicarbonate above 24 mmol/l will typically result in renal excretion of excess bicarbonate

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145
Q

What is the pathogenesis of metabolic alkalosis?

A

(1) Loss of hydrogen ions
(2) Gain of bicarbonate

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146
Q

What are the causes of metabolic alkalosis?

A

Mnemonic:VAD/PHCL/CBC

Problems of the kidney or gastrointestinal tract

(1) Vomiting/Aspiration(e.g., peptic ulcer leading to pyloric stenosis,nasogastric suction)
(2) Diuretics
(3) Primary hyperaldosteronism (4)Hypokalaemia
(5) Carbenoxolone,Liquorice
(6) Cushing syndrome
(7) Bartter’s syndrome
(8) Congenital adrenal hyperplasia

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147
Q

What is the mechanism of metabolic alkalosis?

A
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148
Q

How activation of renin angiotensin II aldosterone system(RAAS)contributes in metabolic alkalosis?

A

(1) Raises aldosterone levels causing reabsorption of Na in exchange for H in DCT
(2) Shift of H into cells to maintain neutrality

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149
Q

How vomiting or diuretics cause metabolic alkalosis?

A
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150
Q

How hypokalaemia cause metabolic alkalosis?

A
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151
Q

What is acid base balance of salycilate overdose?

A

Mixed respiratory alkalosis and metabolic acidosis

1st/Early salicylate overdose +Effect = Respiratory alkalosis

+Reason = Early stimulation of the respiratory centre

2nd/Late salicylate overdose

+Effect = Metabolic acidosis

+Reason = Direct acid effects of salicylate+Acute renal failure

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152
Q

What is acid base balance of early salycilate overdose?

A

+Effect = Respiratory alkalosis

+Reason = Early stimulation of the respiratory centre

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153
Q

What is acid base balance of late salycilate overdose?

A

+Effect = Metabolic acidosis

+Reason = Direct acid effects of salicylate+Acute renal failure

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154
Q

What is the mechanism of respiratory acidosis?

A

(1) Alveolar hypoventilation raises CO2
(2) Renal compensation causes compensated respiratory acidosis

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155
Q

What are the causes of respiratory acidosis?

A
  • COPD
  • Decompensation in other respiratory conditions e.g. Life-threatening asthma / pulmonary oedema
  • Sedative drugs: benzodiazepines, opiate overdose(e.g.,morphine)
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156
Q

What are the causes of respiratory alkalosis?

A

Mnemonic:CHEAP

(1) CNS stimulation:stroke,subarachnoid haemorrhage,encephalitis
(2) Hypoxia causing hyperventilation:High altitude,pulmonary embolism
(3) Early salycilate poisoning
(4) Psychogenic:Anxiety leading to hyperventilation (5)Pregnancy

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157
Q

Interpretation of acid base balance

A
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158
Q

What is the classification of body fluids compartment?

A
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159
Q

What is the fluid compartment volume in litres percentage of total volume?

A
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160
Q

What is the 60-40-20 rule of body fluids compartment?

A
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161
Q

Discuss measurement of body water volume

A
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162
Q

What is the definition of the cerebrospinal fluid(CSF)?

A
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163
Q

What is the amount of cerebrospinal fluid?

A
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164
Q

What are the cells that produces cerebrospinal fluid and in what amount?

A

Ependymal cells-produces 500 ml(70%)

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165
Q

What is the site of absorption of cerebrospinal fluid?

A

Reabsorbed into the venous system via the arachnoid granulations which project into the venous sinuses(superior sagital sinus)

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166
Q

Define the arachnoid granulations

A

Projections in the venous sinuses

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167
Q

Where do we find the ependymal cells?

A

In the

(1) choroid plexus(70%) which lies in all ventricles or
(2) blood vessels(30%)

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168
Q

Discuss the circulation of the cerebrospinal fluid

A
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169
Q

What is the composition of the cerebrospinal fluid?

A
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170
Q

What is the normal pressure of CSF?

A

10-15 mmHg

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171
Q

Define cerebral perfusion pressure

A

The net pressure gradient causing blood flow to the brain

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172
Q

What is the effect of cerebral perfusion pressure(CPP) change?

A

(1) Cerebral perfusion pressure(CPP) is tightly autoregulated to maximise cerebral perfusion
(2) A sharp rise in cerebral perfusion pressure(CPP) results in a rising ICP
(3) A fall in cerebral perfusion pressure(CPP) results in cerebral ischaemia
(4) Following trauma,the cerebral perfusion pressure(CPP) is carefully controlled and requires invasive ICP and mean arterial pressure(MAP)monitoring

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173
Q

What happens in case of increased CPP?

A

ICP rises

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174
Q

What happens in case of decreased CPP?

A

Cerebral ischaemia

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175
Q

How is the cerebral perfusion pressure(CPP)is calculated?

A

Cerebral perfusion pressure(CPP)=Mean arterial pressure(MAP) - Intracranial pressure(ICP)

CPP=MAP-ICP

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176
Q

How the mean arterial pressure(MAP) is calculated?

A

2 ways

(1) Mean arterial pressure(MAP) = Diastolic pressure + 1/3(systolic pressure - diastolic pressure)
(2) Mean arterial pressure(MAP)=DP+0.333(SP+DP)

where DP is diastolic pressure and SP is systolic pressure

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177
Q

What is the normal range of intracranial pressure(ICP)?

A

0-10 mmHg(lower in children)

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178
Q

What is the maximum value of ICP the brain can accommodate and

A

The brain can accommodate increases up to 24 mmHg,thereafter clinical features will become evident

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179
Q

What is the normal range of the MAP?

A

70-100mmHg

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180
Q

What are the factors affecting cerebral blood flow?

A
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181
Q

Define monro kelly doctorine reflex

A

It describes the relationship between the contents of the cranium and intracranial pressure.Alongside the brain tissue, the other major components found within the cranium are blood (mostly venous blood from within dural sinuses) and the cerebrospinal fluid (CSF). The volume of each of these components is restricted by the fixed space within the cranium.

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182
Q

What is the mechanism of Monroe-kelly-Doctrine?

A
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183
Q

What is the location of pituitary gland?

A

(1) Within the sella turcica
(2) Within the sphenoid bone
(3) In the middle cranial fossa

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184
Q

What is the covering of the pituitary gland?

A

Dural fold

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185
Q

What is the attachment of pituitary gland?

A

Attached to the hypothalamus by the infundibulum

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186
Q

What is the weight of the pituitary gland?

A

0.5g

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187
Q

Discuss the portal system of pituitary gland(pituitary portal system)?

A

I)Hypothalamus-pituitary portal system

(1) The anterior pituitary receives hormonal stimuli from the hypothalamus by way of hypothalamus-pituitary portal system
(2) It develops from a depression in the wall of the pharynx(Rathkes pouch)
(3) It is one of only few portal system of circulation that involves two capillary beds connected by venules rather than arterioles so it is called portal system

II)Hypothalamic-hypophyseal portal system

(1) Carries prolactin inhibitory hormone from the hypothalamus to the anterior pituitary gland
(2) In the absence of prolactin inhibitory hormone,prloctin increases 3 times the normal level

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188
Q

What are the anterior pituitary hormones?

A

Mnemonic;TAG/LMP

Anterior pituitary receives hormonal stimuli from hypothalamus by way of hypothalamic-pituitary portal system.

(1) Throid stimulating hormone
(2) ACTH

(3) Growth hormone(GH)
(4) LH and FSH
(5) Melanocyte releasing hormone(MRH)
(6) Prolactin

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189
Q

What are the posterior pituitary hormones?

A

Synthesised by hypothalamus

(1) Oxytocin
(2) Antidiuritic hormone(ADH)

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190
Q

Discuss Sheehan’s syndrome

A

Definition
Postpartum hypopituitarism

Aetiology
Necrosis due to haemorrhage and subsequent hypovolaemia during and after childbirth

Incidence
Rare complication during pregnancy

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191
Q

What are the types and location of the cardiac receptors?

A
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192
Q

Discuss receptor sites of action of inotropes

A
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193
Q

Discuss effects of receptor binding

A
194
Q

What is the effect of receptors on adenylate cyclase enzyme?

A
195
Q

Define inotropes

A

A class of vasoactive drugs that increases cardiac output

196
Q

What is the use of inotropes?

A

In patients with

(1) Inadequate circulating volume
(2) ongoing circulatory compromise

197
Q

a table illustrating inotropes

A
198
Q

table illustrating inotropes doses

A
199
Q

What is the very low dose of inotropes?

A

4 μg/kg/min

200
Q

What is the effect of the very low dose of inotropes?

A

1st/increases

(1) GFR
(2) Na excretion

2nd/Renal dose is an obsolete concept

201
Q

What is the action of the higher dose of inotropes?

A

β1agonist

202
Q

What is the effect of higher dose of inotropes?

A

increases

(1) Contractility
(2) HR

203
Q

What is the very high dose of inotropes?

A

>10 μg/kg/min

204
Q

What is the action of the very high dose of inotropes?

A

α1 agonist

205
Q

What is the effect of the very high dose of inotropes?

A

reduces

(1) GFR
(2) tissue perfusion

206
Q

Examples of commonly used inotropes

A
207
Q

Define vasoconstrictor agents

A

Used for peripheral vasodilation

208
Q

What is the difference between inotropes and vasoconstrictor agents?

A

*Inotropes:increase cardiac output
*Vasoconstrictor agents:used for peripheral vasodilation

209
Q

What is the physiological effect of catecholamines?

A

(1) Increase cAMP by adenylate cyclase activation
(2) This in turn increases intracellular calcium and thus force of contraction

210
Q

What is the physiological effect of adrenaline on receptors?

A

Mnemonic;BLAH

(1) At Lower doses-Beta adrenergic receptor agonist
(2) At Higher doses-Alpha adrenergic receptor agonist

211
Q

What is the physiological effect of noradrenaline on receptors?

A

(1) Predominately α receptor agonist
(2) Peripheral vasoconstrictor

212
Q

What is the physiological effect of dopamine on receptors?

A

[I]At higher doses dopamine activates the following:-
(1)dopamine receptor mediated renal and mesentric vascular dilatation
(2)β1 receptor agonism
(3)D1 and D2
[II]This causes +ve inotropic effect
[III]Results in increased cardiac output(CO)
[IV]Less myocardial ischaemia due to raised heart rate and blood pressure

213
Q

What is the physiological effect of dobutamine?

A

(1) predominantly β1 receptor agonist
(2) weak β2 and α receptor agonist

214
Q

table for the physiological effects of different inotropes

A
215
Q

What is the other name of the adrenal gland?

A

Suprarenal gland

216
Q

What is the location of the adrenal gland?

A

Superomedially to the upper pole of each kidney

217
Q

What are the relations of the adrenal glands?

A

[I]Right adrenal:(Mnemonic :PAIM-D/HB/K/V)

a) Posteriorly-Diaphragm
b) Anteriorly-(1)Hepatorenal(Morison) pouch (2)Bare area of the liver
c) Inferiorly-Kidney
d) Medially-Vena cava

[II]Left adrenal:(PAI-C/LS/PS)

a) Posteromedially-Crus of the diaphragm
b) Anteriorly-(1)Lesser sac and (2)Stomach
c) Inferiorly-(1)Pancreas (2) Splenic vessels

218
Q

What is the arterial blood supply of adrenal gland?

A

(1) Superior adrenal arteries-from inferior phrenic artery
(2) Middle adrenal arteries-from aorta
(3) Inferior adrenal arteries-from renal arteries

219
Q

What is the venous drainage of adrenal gland?

A

(1)Right adrenal-via one central vein directly into the IVC

(2)Left adrenal-via one central vein into the left renal vein(passes in front of the aorta)

220
Q

What are the hormones of the adrenal medulla?

A

Catecholamines which are(mnemonic;NAD):

(1) Noreadrenaline
(2) Adrenaline
(3) Dopamine

221
Q

What are the main cells of adrenal medulla?

A

Chromaffin cells

222
Q

What is the function of the main cells of adrenal medulla?

A

Chromaffin cells secrete catecholamines;noradrenaline,adrenaline,dopamine

223
Q

What is the main stimulant for the main cells of the adrenal medulla?

A

Acetylcholine-causing chromaffin cells to secret their contents by exocytosis

224
Q

What is the nerve supply of adrenal medulla?

A

Splanchnic nerves-the preganglionic sympathetic nerve fibres secret acetylcholine causing chromaffin cells contents by exocytosis

225
Q

What is the effect of acetylcholine on chromaffin cells of the adrenal medulla?

A

Causes chromaffin cells to secret their contents by exocytosis

226
Q

What is the name of the process in which chromaffin cells secrete their contents?

A

Exocytosis

227
Q

What is the clinical significance of chromaffin cells of the adrenal medulla?

A

Phaeochromocytomas are derived from these cells and will secrete both adrenaline and noradrenaline

228
Q

What are the histological zones of adrenal cortex and mention hormones of each zone?

A

Mnemonic;GFR-ACD

1st/Zona glomerulosa(outer zone)-mineralocorticocoids(mnemonic;A/CDC)
(1)Aldosterone-mainly
(2)Cortisone
(3)Deoxycorticosterone
(4)Corticosterone
2nd/Zona fasiculata(middle zone)-glucocorticoids(mnemonic;3Cs)
(1)Cortisol-mainly
(2)Cortisone
(3)Corticosterone
3rd/Zona reticularis(inner zone)-Androgens
Dehydroepiandrosterone(DHEA)-mainly

229
Q

What is the fate of glucocorticoids and aldosterone?

A

(1) Glucocorticoids and aldosterone are mostly bound to plasma proteins in the circulation
(2) Glucocorticoids are inactivated and excreted by the liver

230
Q

Discuss Beta-endorphin

A

Definition
a cleavage product of pro-opiomelanocortin(POMC)

Function
pro-opiomelanocortin(POMC)is a precursor hormone for ACTH

231
Q

What is the function of the pro-opiomelanocortin(POMC)?

A

A precursor of ACTH

232
Q

Discuss cortisol

A

(1) Is a glucorticoids
(2) Released by Zona fassiculata
(3) 90% protein bound + 10% active
(4) Shows circadian and diurnal rhythm:high in the morning
(5) Negative feedback via ACTH

233
Q

What is the action of cortisol?

A

(1) Glycogenlysis
(2) Glucaneogenesis
(3) Lipolysis (4)Protein catabolism
(5) Decrease protein in bones
(6) Increase gastric acid
(7) Stress response
(8) Anti-inflammatory response
(9) Increase all blood cells(neutrophils,platelets,RBCs)
(10) Inhibits fibroblastic activity

234
Q

What is the stress response of cortisol?

A
235
Q

Discuss metabolism of cortisol

A

Cortisol & adrenal androgens are synthesised from cholesterol.
The intermediary in the metabolism of cortisol and androgens is Pregnolone

236
Q

What is the source of cortisol and adrenal anrogens?

A

Cortisol & adrenal androgens are synthesised from cholesterol.

237
Q

What is the intermediary in the metabolism of cortisol and androgens?

A

Pregnolone

238
Q

What is pregnolone?

A

the intermediary in the metabolism of cortisol and androgens

239
Q

What are the causes of addisonian crisis?

A

Mnemonic;AS/ASS

(1) Autoimmune-the most common cause
(2) Steroid withdrawal
(3) Adrenal haemorrhage e.g.,Waterhouse Friderichsen syndrome(fulminant meningococaemia)
(4) Sepsis-causing an acute exacerbation of chronic insufficiency(Addison’s hypopituitarism)
(5) Surgery-causing an acute exacerbation of chronic insufficiency(Addison’s hypopituitarism)

240
Q

What is the most common causes of Addisonian crisis?

A

Autoimmune

241
Q

What is the other name for Waterhouse Friderichsen syndrome?

A

Fulminant meningococaemia

242
Q

What sepsis and surgery cause for a patient with Addisonian crisis?

A

Acute exacerbation of chronic adrenal insufficiency(Addison’s hypopituitarism)

243
Q

What sepsis causes for a patient with Addisonian crisis?

A

Acute exacerbation of chronic adrenal insufficiency(Addison’s hypopituitarism)

244
Q

What surgery causes for a patient with Addisonian crisis?

A

Acute exacerbation of chronic adrenal insufficiency(Addison’s hypopituitarism)

245
Q

What are the clinical features of Addisonian crisis?

A
246
Q

What is the management of Addisonian crisis?

A
247
Q

What is the drug of choice for Addisonian crisis?

A

Hydrocortisone

(1) 100 mg IM or IV 6 hourly
(2) Continued 6 hourly until the patient is stable

248
Q

How hydrocortisone is given to a patient with Addisonian crisis?

A

Hydrocortisone

(1) 100 mg IM or IV 6 hourly
(2) Continued 6 hourly until the patient is stable

249
Q

What is the dose of hydrocortisone given to a patient with Addisonian crisis?

A

100 mg

250
Q

What is the frequency of use of hydrocortisone for a patient with Addisonian crisis?

A

(1) 100 mg IM or IV 6 hourly
(2) Continued 6 hourly until the patient is stable

251
Q

What IV fluids to be given to a patient with Addisonian crisis?

A

normal saline

(1) 1 litre
(2) infused over 30-60 minutes or
(3) with dextrose if hypoglycaemic

252
Q

What is the amount of IV fluids to be given for a patient with Addisonian crisis?

A

normal saline

(1) 1 litre
(2) infused over 30-60 minutes or
(3) with dextrose if hypoglycaemic

253
Q

Is fludrocortisone required for the management of Addisonian crisis and why?

A

No fludrocortisone is required because high cortisol exerts weak mineralocorticoid action

254
Q

Why fludrocortisone is not required for the management of patient with Addisonian crisis?

A

Because high cortisol exerts weak mineralocorticoid action

255
Q

What is the way of using oral replacement therapy for management of patient with Addisonian crisis?

A

(1) Begin after 24 hours
(2) Reduced to maintenance over 3-4 days

256
Q

When do we start using oral replacement therapy for management of patient with Addisonian crisis?

A

after 24 hrs

257
Q

When do we reduce using oral replacement therapy to maintenance for management of patient with Addisonian crisis?

A

over 3-4 days

258
Q

What are the features of adrenaline?

A

(1) Fight or flight response
(2) Neurotransmitter and hormone
(3) Origin:catecholamine-from phenylalanine and tyrosine
(4) Released by adrenal medulla

259
Q

What is the nature of adrenaline?

A

Neurotransmitter and hormone

260
Q

What is the source(origin) of adrenaline?

A

Catecholamine-from phenylalanine and tyrosine

261
Q

From which organ adrenaline is released?

A

Adrenal medulla

262
Q

What is the action of noradrenaline?

A

acts as α agonist

263
Q

On which receptors the adrenaline act on and what is its effect?

A

1st/Acts on

(1) α1 and α2 receptors-main effect on α1 receptor
(2) β1 and β2 receptors

2nd/Effect

(1) Vasodilation
(2) Increase CO
(3) Increase total peripheral resistance
(4) This leads to vasconstriction in the skin and kidneys causing a narrow pulse pressure

264
Q

On which receptors the adrenaline act on?

A

(1) α1 and α2 receptors-main effect on α1 receptor on skeletal muscle
(2) β1 and β2 receptors

265
Q

What is the main receptor which adrenaline acts on?

A

α1 receptor on skeletal muscle

266
Q

What is the effect of adrenaline?

A

Main effect on α1 on skeletal muscle causing

(1) Vasodilation
(2) Increase CO
(3) Increase total peripheral resistance
(4) This leads to vasconstriction in the skin and kidneys causing a narrow pulse pressure

267
Q

What is the action of adrenaline?

A
268
Q

What is the action of adrenaline on α adrenergic receptors?

A

Mnemonic; IN/GLYCO

269
Q

What is the action of adrenaline on β adrenergic receptors?

A

Mnemonic: stimulates GAL

270
Q

Where does glycogenlysis occur in the body?

A

in the liver and muscles

271
Q

Where does glycolysis occur in the body?

A

in muscle

272
Q

Where does lipolysis occur in the body?

A

in adipose tissue

273
Q

What are the uses of adrenaline?

A

1st/Cardiac arrest

to convert non-shockable rhythm to shockable VF(i.e.,susceptible to shock)

2nd/Shock

(I)Circulatory shock:

1) raise BP
2) reduce renal blood flow

(II)Anaphylactic shock:

As a bronchodilator because it has the most bronchodilator effect amongst all

274
Q

What is the use of adrenaline in cardiac arrest?

A

to convert non-shockable rhythm to shockable VF(i.e.,susceptible to shock)

275
Q

What is the use of adrenaline in shock?

A

(I)Circulatory shock:

1) raise BP
2) reduce renal blood flow

(II)Anaphylactic shock:

As a bronchodilator because it has the most bronchodilator effect amongst all

276
Q

What is the use of adrenaline in circulatory shock?

A

1) raise BP
2) reduce renal blood flow

277
Q

What is the use of adrenaline in anaphylactic shock?

A

As a bronchodilator because it has the most bronchodilator effect amongst all

278
Q

What is noradrenaline?

A

A vasopressor

279
Q

What is the effect of noradrenaline?

A

little effect on cardiac output(CO)

280
Q

What is the action of dobamine?

A

acts as β1 agonist

281
Q

What is the effect of dopamine?

A

increases

(1) contractility
(2) heart rate

282
Q

What is the action of dobutamine?

A

Has both β1 and β2 effects

283
Q

What is the effect of dobuatamine?

A

(1) increase CO
(2) decrease systemic vascular resistace

284
Q

What is milrinone?

A

a phosphodiesterase inhibitor

285
Q

What is the feature of milrinone?

A

It has a short half life= 1-2 hours

286
Q

What is the half life of milrinone?

A

It has a short half life= 1-2 hours

287
Q

What is the effect of milrinone?

A

(1) Positive inotropic effect
(2) Vasopressors often co-administered as it is a vasodilator

288
Q

What causes release of aldosterone?

A

Mnemonic;AKA

Raised

(1) Angiotensin II
(2) K
(3) ACTH

289
Q

What are the factors that regulate aldosterone secretion?

A

(1) Renin angiotensin system(RAS)
(2) Plasma levels of Na and K

290
Q

What is the action of aldosterone?

A

responsible for regulating ion exchange in salivary gland

291
Q

What is the effect of aldosterone?

A
292
Q

What are consequences of lack of aldosterone?

A

(1) Hyperkalaemia
(2) Hyponatraemia

293
Q

From which organ the renin is released?

A

Juxtaglomerular apparatus(JGA)cells in the kidney

294
Q

What causes renin release?

A

Reduced

(1) renal prefusion
(2) sodium

295
Q

What is the function of renin?

A

Hydrolyses angiotensinogen to angiotensin I

296
Q

What are the factors affecting renin release?

A
297
Q

What are the factors stimulating renin secretion?

A
298
Q

What are the factors reducing renin secretion?

A

ANP

released in response to high BP and in turns inhibits the release of renin.This acts to reduce BP,as downstream effects of activation of RAAS all lead to the increase of BP.

299
Q

What are the functions of angiotensin?

A
300
Q

Define Bainbridge reflex

A

release aldosterone to increase heart rate mediated by atrial stretch receptors that occurs following rapid blood infusion

301
Q

A summary of hormonal changes associated with the stress response

A
302
Q

What are the hormones increased with stress?

A

Mnemonic;CAAR/GGAP

303
Q

What are the hormones that don’t change with stress?

A

Mnemonic;TLF

304
Q

What are the hormones decreased with stress?

A

Mnemonic;ITO

305
Q

Discuss hormones released from the islets of Lanagerhans

A

Mnemonic;BAD FEG/IGSPGG

306
Q

What is the most common hormone released from pancreatic islets of langerhans and from which cells and in what percentage?

A
  • Hormone:Insulin
  • Secreting cells:Beta(β)cells
  • Percentage:70% of total secretions
307
Q

What is the hormone released from Beta(β) cells of islets of Langerhans?

A

Insulin(70% of total secretions)

308
Q

What is the hormone released from Alpha(α) cells of islets of Langerhans?

A

Glucagon

309
Q

What is the other name of delta(δ) cells of islets of langerhans?

A

D-cells

310
Q

What is the hormone released from Delta(δ) or D cells of islets of Langerhans?

A

Somatostatin

311
Q

What are the sites of secretion of somatostatin?

A

Mnemonic;HIP

(1) Hypothalamus-causing negative feedback on growth hormone(GH)
(2) Intestinal enterochromaffin cells
(3) Pancreatic delta(D) cells

312
Q

What is the cause of secretion of somatostatin?

A

The substances that stimulate insulin release will also induce somatostatin secretion

313
Q

What is the function of somatostatin?

A

(1) Decrease the volume of secretions pancreatic juice
(2) Partially supresses insulin and glucagon secretion
(3) Inhibits growth hormone(GH) and TSH from pituitary gland
(4) Delays gastric emptying
(5) Reduces gastric secretion
(6) Reduces pancreatic exocrine secretions
(7) treatment of pancreatic fistula

314
Q

Give an example for somatostatin

A

Octreotide

315
Q

What is the mode of action of octreotide?

A

(1) Decrease the volume of secretions pancreatic juice
(2) Partially supresses insulin and glucagon secretion
(3) Inhibits growth hormone(GH) and TSH from pituitary gland
(4) Delays gastric emptying
(5) Reduces gastric secretion
(6) Reduces pancreatic exocrine secretions
(7) treatment of high output pancreatic fistula

316
Q

What are the uses of octreotide?

A

(1) High output pancreatic fistula-because it reduces pancreatic exocrine secretions
(2) Acromegaly
(3) Variceal bleeding

317
Q

What is the other name for F cells of ielts of Langerhans?

A

(1) Pancreatic polypeptide(PP)cells
(2) Gamma cells

318
Q

What is the hormone released from F(PP) cells of islets of Langerhans?

A

Pancreatic polypeptide

319
Q

What is the function of pancreatic polypeptide?

A

Inhibit gall bladder(GB)contraction

320
Q

What is the site of Epsilon cells?

A

(1) Stomach(mainly)
(2) Pancreatic islets of Langerhans

321
Q

What is the hormone released from Epsilon cells of ielts of Langerhans?

A

Gherlin mainly from the stomach

322
Q

What is the site of release of Gherlin?

A

From Epsilon cells in

(1) Stomach(mainly)
(2) Pancreatic islets of Langerhans

323
Q

What is the function of Gherlin?

A

Hunger hormone = stimulates appetite

324
Q

What is hunger hormone?

A

Gherlin

325
Q

What is the function of hunger hormone?

A

Gherlin-Stimulates appetite

326
Q

What is the site of G cells?

A

(1) Duodenum(mainly)
(2) Pancreatic islets of Langerhans

327
Q

What hormone released from pancreatic G cells?

A

Gastrin mainly from duodenum

328
Q

What is the site of release of Gastrin?

A

G cells in

(1) Duodenum(mainly)
(2) Pancreatic islets of Langerhans

329
Q

Table for pancreatic hormones and its functions

A
330
Q

Discuss functions of very important pancreatic hormones

A
331
Q

What is the innervation of somatic pain?

A
332
Q

What are the types of peripheral nociceptors?

A

1st/According to nerve fibres

(1) A delta fibres-small+myelinated
(2) C fibres-unmyelinated

2nd/According to function

(1) Mechanical
(2) Thermal
(3) Chemical
(4) Polymodal

333
Q

What is the intensity of somatic pain?

A

(1) A-gamma(γ)-high intensity mechanical stimuli+motor proprioception
(2) C-fibres-slow transmission of high intensity mechanothermal stimuli

334
Q

How fast is the transmission by C- nerve fibres?

A

slow

335
Q

Discuss transmission of somatic pain?

A

(1) C-fibres-slow transmission of high intensity mechanothermal stimuli
(2) A-alpha(α)-motor proprioception
(3) A-gamma(γ)-high intensity mechanical stimuli+motor proprioception
(4) A-delta(δ) fibres-small myelinated
(5) A-β fibres-touch and pressure
(6) B-fibres-autonomic(sympathetic and parasympathetic)fibres

336
Q

What are the types of nerve fibres and their functions?

A

(1) C-fibres-slow transmission of high intensity mechanothermal stimuli
(2) A-alpha(α)-motor proprioception
(3) A-gamma(γ)-high intensity mechanical stimuli+motor proprioception
(4) A-delta(δ) fibres-small myelinated
(5) A-β fibres-touch and pressure
(6) B-fibres-autonomic(sympathetic and parasympathetic)fibres

337
Q

Discuss classification of nerve fibres

A
338
Q

What is the primary method for CNS blood supply autoregulation?

A
339
Q

What are the affecting factors of CNS blood supply autiregulation?

A
340
Q

What is the other name of lidocaine?

A

Lignocaine

341
Q

What is the nature of lidocaine?

A

An amid

342
Q

What are the uses of lidocaine?

A
343
Q

Why lidocaine is less commonly used as antiarrhythmic?

A

Lidocaine blocks Na channels in axons,this will typically be activated first hence the pain experienced by some patients

344
Q

Discuss metabolism of lidocaine

A

Mnemonic:HPR

345
Q

Discuss the toxicity of lidocaine?

A
346
Q

What are the causes of lidocaine toxicity?

A
347
Q

What is the treatment of lidocaine toxicity?

A

Intralipid 20%

348
Q

What are the features of toxicity of lidocaine?

A

(1) Initial CNS overactivity then deprsession: Lidocaine initially blocks inhibitory pathways then blocks both inhibitory and activating pathways
(2) Cardiac arrhythmia

349
Q

Why lidocaine induces CNS activity first then depression?

A

Lidocaine initially blocks inhibitory pathways then blocks both inhibitory and activating pathways

350
Q

What are the side effects of lidocaine?

A
351
Q

What is the effect of acidosis on lidocaine?

A

Acidosis detaches lidocaine from protein

352
Q

What is the effect of adrenaline on lidocaine?

A

Increased dose may be combined with adrenaline to limit systemic absorption

353
Q

What are the drug interactions of lidocaine?

A

(1) Beta blockers
(2) Ciprofloxacin
(3) Phenytoin
(4) Adrenaline-increased dose may be combined with adrenaline to limit systemic absorption

354
Q

What is the nature of cocaine?

A
355
Q

What is the chemical composition of cocaine?

A

pure cocaine is salt,usually cocaine hydrochloride

356
Q

What is the effect of cocaine on blood brain barrier(BBB)?

A

It is lipophilic and can easily cross blood brain barrier(BBB)

357
Q

What are the advantages of cocaine?

A
358
Q

What are the modes of administration of cocaine

A

Mnemonic;PCT

359
Q

What are the side effects of cocaine?

A
360
Q

What is the mode of action of bupivacaine?

A
361
Q

What is the use of bupivacaine?

A
362
Q

What are the contraindications of bupivacaine?

A
363
Q

What happens if bupivacaine coadministered with adrenaline?

A

The coadministration of adrenaline

(1) concentrates it at the site of action
(2) allows the use of higher dose
(3) does not permit increases in the total dose of bupivacaine,in contrast to lignocaine

364
Q

What is the cause of bupivacaine toxicity?

A

Protein binding

365
Q

What is the alternative for bupivacaine?

A

Levobupivacaine(chirocaine)

(1) less cardiotoxic
(2) causes less vasodilation

366
Q

Why levobupivacaine is the alternative for bupivacaine?

A

(1) less cardiotoxic
(2) causes less vasodilation

367
Q

What is the other name for levobupivacaine?

A

chirocaine

368
Q

What are the advantages of levobupicaine?

A

(1) less cardiotoxic
(2) causes less vasodilation

369
Q

What is the mechanism of action of prilocaine?

A

similar to other local anaesthetics

370
Q

What are the advantages of prilocaine?

A

Far less cardiotoxic and is therefore the agent of choice for IV regional anaesthesia e.g.,Biers block

371
Q

What is the cause of therapeutic effect of local anaesthetics?

A
372
Q

Examples of doses of different local anaesthetics?

A
373
Q

What are the factors affecting the actual doses of local anaesthetics?

A

Mnemonic;STC

(1) Site of administration
(2) Tissue vascularity
(3) Comorbidities

374
Q

What is the factor affecting the maximum dose of local anaesthetics?

A

Ideal body weight

375
Q

What is the effect of coadministration of adrenaline with a local anaesthetic?

A

(1) Prolongs the duration of action at the site of injection
(2) Permits the use of higher doses

376
Q

What is the contraindications of adrenaline use?

A

Patients taking

(1) MAOIs
(2) Tricyclic antidepressants

377
Q

What are the locations of opiate receptors?

A

Mnemonic;PLS

(1) Periaquiductal grey matter
(2) Limbic system
(3) Substantia gelatinosa

378
Q

What are the opiod receptors?

A

morphin attaches to Mu1

379
Q

Define morphine

A

A prototype narcotic drug

380
Q

What is the feature of morphine?

A

strong opiate analgesic

381
Q

What is the mode of action of morphine?

A

Its affects are mediated bt 4 types of opioid receptors within

(1) CNS
(2) GIT

382
Q

What are the route of administration of morphine?

A

(1) Orally
(2) IV

383
Q

What are the side effects of morphine?

A

Mnemonic;N/CAR

(1) Nausea
(2) Constipation
(3) Addiction-in long term use
(4) Respiratory depression

384
Q

What is the treatment of morphine toxicity?

A

Naloxone

385
Q

What is the cause of Cheyne strokes breathing

A

Compression of respiratory centre

386
Q

What is the triad of Wernickes encephalopathy?

A
387
Q

What are the causes of Wernickes encephalopathy?

A

(1) Chronic alcoholism
(2) Post-bariatric surgery or
(3) Malnutritiion-post recieving a carbohydrate rich diet without any thiamine or vitamin B co-strong replacement

388
Q

Define refeeding syndrome

A

the metabolic abnormalities after feeding following a period of starvation

389
Q

What are the clinical features of refeeding syndrome?

A

the metabolic consequences are (1)hypokalaemia

(2) hypoposphataemia
(3) hypomagnesaemia
(4) abnormal fluid balance

these abnormalities lead to organ failure

390
Q

What are the metabolic consequences of refeeding syndrome?

A

the metabolic consequences are (1)hypokalaemia

(2) hypoposphataemia
(3) hypomagnesaemia
(4) abnormal fluid balance

these abnormalities lead to organ failure

391
Q

What is the complication of refeeding syndrome?

A

the metabolic consequences lead to oran failure

392
Q

Discuss high risk features of refeeding syndrome

A

If one or more of the following:

(1) BMI < 16 kg/m2
(2) Unintentional weight loss >15% over 3-6 months
(3) Little nutritional intake > 10 days
(4) Hypokalaemia, Hypophosphataemia or hypomagnesaemia prior to feeding (unless high)

If two or more of the following:

(1) BMI < 18.5 kg/m2
(2) Unintentional weight loss > 10% over 3-6 months
(3) Little nutritional intake > 5 days
(4) History of: alcohol abuse, drug therapy including insulin, chemotherapy, diuretics and antacids

393
Q

What are the criteria for diagnosis of refeeding syndrome?

A

If one or more of the following:

(1) BMI < 16 kg/m2
(2) Unintentional weight loss >15% over 3-6 months
(3) Little nutritional intake > 10 days
(4) Hypokalaemia, Hypophosphataemia or hypomagnesaemia prior to feeding (unless high)

If two or more of the following:

(1) BMI < 18.5 kg/m2
(2) Unintentional weight loss > 10% over 3-6 months
(3) Little nutritional intake > 5 days
(4) History of: alcohol abuse, drug therapy including insulin, chemotherapy, diuretics and antacids

394
Q

What is the treatment of refeeding syndrome?

A
395
Q

What are the types of traumatic brain injuries?

A

(A)PRIMARY TRAUMATIC BRAIN INJURY

1st/Focal or intracranial (contusion/haematoma) injury

I)Haematoma (1)Extradural heamatoma (2)Subdural haematoma (3)Subarachnoid(intracerebral) haemorrhage

II)Contusion (1)Coup-adjacent to the side of impact (2)Counter coup-contralateral to the side of impact

2nd/Diffuse axonal injury (1)Occurs as a result of mechanical shearing following deceleration (2)Causes disruption and tearing of axons

(B)SECONDARY TRAUMATIC BRAIN INJURY

Occurs when the following exacerbates the original injury (1)Cerebral oedema (2)Ischaemia (3)Infection (4)Tonsillar herniation (5)Tentorial herniation

396
Q

Define extradural heamatoma

A

Bleeding into the space between the dura matter and the skull

397
Q

What is the aetiology of extradural haematoma?

A

(1) Acceleration deceleration injury
(2) Blow to the side of the head

398
Q

What is the site of occurrence of extradural haematoma?

A

Temporal region where skull fractures rupture the middle meningeal artery

399
Q

What are the clinical features of extradural haematoma?

A

(1) Raised ICP
(2) Lucid interval

400
Q

Define subdural haematoma?

A

Bleeding into the outermost meningeal layer

401
Q

What is the site of occurrance of subdural haematoma?

A

Frontal and parietal lobes

402
Q

What are the types of subdural haematoma?

A

Acute or chronic

403
Q

What are the risk factors of subdural haematoma?

A

(1) Old age
(2) Alcoholism

404
Q

What is the clinical picture of subdural haematoma?

A

Slower onset of symptoms than extradural haematoma

405
Q

What is the aetiology of subarachnoid haemorrhage?

A

(1) Spontaneous-due to ruptured cerebral aneurysm
(2) In association with other traumatic brain injuries

406
Q

Discuss clinical picture of traumatic brain injury

A

(1)The normal cerebral auto regulatory processes are disrupted following trauma rendering the brain more susceptible to blood flow changes and hypoxia

(2)The Cushing reflex (hypertension,bradycardia and altered respiratory pattern) often occurs late and is usually a preterminal event (Monro Kelly Doctrine reflex)

407
Q

Discuss investigations of head injury?

A
408
Q

Interpretation of pupillary findings in head injuries

A
409
Q

Discuss management of head injury

A

1st/Medical management-IV mannitol/frusemide indications

(1) Life threatening raised ICP
(2) Theatre is prepared
(3) Transfer is arranged

2nd/Surgical

(1) Decompressive craniotomy-for diffuse cerebral oedema
(2) Exploratory Burr Hole
- Have little management in modern practice except where scanning may be unavailable and
- to thus facilitate creation of formal craniotomy flab
(3) Skull fractures
- Formal open reduction and debridement-for depressed skull fractures
- Non operative-for closed injuries with minimal displacement

410
Q

Discuss medical management of head injury

A

IV mannitol/frusemide indications

(1) Life threatening raised ICP
(2) Theatre is prepared
(3) Transfer is arranged

411
Q

What is the surgical management of head injury

A

(1) Decompressive craniotomy-for diffuse cerebral oedema
(2) Exploratory Burr Hole
- Have little management in modern practice except where scanning may be unavailable and
- to thus facilitate creation of formal craniotomy flab
(3) Skull fractures
- Formal open reduction and debridement-for depressed skull fractures
- Non operative-for closed injuries with minimal displacement

412
Q

What is the indication of IV mannitol/frusemide in head injury?

A

IV mannitol/frusemide indications

(1) Life threatening raised ICP
(2) Theatre is prepared
(3) Transfer is arranged

413
Q

What is the indication of decompressive craniotomy in head injury?

A

for diffuse cerebral oedema

414
Q

What is the indication of exploratory Burr Hole in head injury?

A
  • Have little management in modern practice except where scanning may be unavailable and
  • to thus facilitate creation of formal craniotomy flab
415
Q

What is the indication of formal open reduction and debridment in head injury?

A

for depressed skull fracture

416
Q

What is the indication of non operative management in skull fracture in head injury?

A

for closed injuries with minimal displacement

417
Q

Compare sympathetic and parasympathetic nervous system

A
418
Q

Define shock

A

Insufficient tissue perfusion

419
Q

What are the types(causes)of shock?

A

Mnemonic;DOCH

(1)Distributive-Mnemonic;SANADT

  • Septic
  • Anaphylactic
  • Neurogenic
  • Addison’s crisis
  • D***_rugs/T_***oxins

(2)Obstructive

  • Tension pneumothorax
  • Tamponade
  • PE

(3)Cardiogenic-Mnemonic;CAM/VAP

  • Cardiomyopathy
  • AMI
  • Direct myocardial trauma or contusion-the main cause in trauma cases
  • Valve failure
  • Arrhythmia
  • PE

(4)Hypovolaemic

  • Haemorrhagic
  • Non haemorrhagic
  • Fluid loss: 1.Vomiting 2.Diarhoea 3.Dehydration 4.3rd space loss during major operations
420
Q

Comparison of different types of shock

A
421
Q

Define hypovolaemic shock

A

Blood volume depletion

422
Q

What are the causes of hypovolaemic shock?

A

(1) Haemorragic
(2) Non haemorrhagic
(3) Fluid loss

  • Vomiting
  • Diarrhoea
  • Dehydration
  • 3rd space loss during major operations
423
Q

What are the features of hypovolaemic shock?

A

1st/Clinical features

(1) Tachycardia
(2) Weak thready pulse
(3) Cool,pale,moist skin
(4) Hypotension
(5) U/O decreased

2nd/Pathophysiological features

+Increased

(1) SVR
(2) HR(tachycardia)

+Decreased

(1) Cardiac output(CO)
(2) BP(hypotension)

424
Q

What are the clinical features of hypovolaemic shock?

A

(1) Tachycardia
(2) Weak thready pulse
(3) Cool,pale,moist skin
(4) Hypotension
(5) U/O decreased

425
Q

What are the pathophysiological features of hypovolaemic shock?

A

+Increased

(1) SVR
(2) HR(tachycardia)

+Decreased

(1) Cardiac output(CO)
(2) BP(hypotension)

426
Q

Discuss pathogenesis of haemorrhagic shock

A

(1) ⇣BP
(2) Organ hypoperfusion
(3) Myocardial ischaemia

427
Q

What is the value of cardiac index for haemorrhagic shock?

A

Cardiac index= CO/Body surface area

428
Q

What are the commonest causes of shock in a patient with trauma?

A
429
Q

Define septic shock

A

Peripheral vascular dilatation causing a fall in SVR

430
Q

What are the components defining septic shock?

A

(1) Peripheral vascular dilatation
(2) SVR

431
Q

What are the commonest causes of septic shock?

A

(1) Abdominal infection
(2) Kidney infection
(3) Pneumonia
(4) Bactraemia(blood infection)

432
Q

What is the differential diagnosis of septic shock?

A

(1) Anaphylactic
(2) Neurogenic

433
Q

What are the features of septic shock?

A

1st/Clinical features

(1) Tachycardia
(2) Full pounding pulse
(4) Warm,pink,flushed skin
(5) Fever
(6) U/O decreased

2nd/Pathophysiological-Mnemonic ;R/INR

(1) Reduced SVR
(2) Increased HR
(3) Normal/Increased CO
(4) Reduced BP

434
Q

What are the clinical features of septic shock?

A

(1) Tachycardia
(2) Full pounding pulse
(4) Warm,pink,flushed skin
(5) Fever
(6) U/O decreased

435
Q

What is the mortality rate of septic shock?

A

(1) Severe sepsis patients’ mortality rate > 40%
(2) Patients admitted to the ICU mortaliy rate
- with no organ failure = 6%
- with 4 organ failure = 65%

436
Q

Define sepsis

A

Infection with systemic inflammatory response syndrome (SIRS)

437
Q

What are the characteristics of systemic inflammatory response syndrome (SIRS)?

A
438
Q

Diagram shows sepsis and SIRS

A
439
Q

What is the clinical definition of severe sepsis?

A

Sepsis associated with

(1) end organ dysfunction
(2) hypoperfusion
(3) hypotension

440
Q

Discuss pathology of septic shock

A

(1) Bacterial toxins
(2) Excessive cytokines release
(3) Endothelial cell damage + Neutrophil adhesion
(4) Excessive inflammation + coagulation + fibrinolytic suppression

441
Q

What is the name for sepsis guidlines?

A

Surviving sepsis campaign (2012)

442
Q

What are the surviving sepsis campaign guidlines?

A
443
Q

What are the guidelines for management of sepsis?

A

(1) Fluids
(2) Antibiotics
(3) Vasopressors
(4) Surviving sepsis campaign guidlines(2012)

444
Q

How to haemodynamically stabilise septic patients?

A
445
Q

How modulation of septic response is done?

A

(1) Counteract changes
(2) Tight glycaemic control
(3) use of activated protein C
(4) IV steroids- not advised

446
Q

What is the value of cardiac index in sepsis?

A

Cardiac index= CO/Body surface area

447
Q

What are the risk factors for sepsis for surgical patients?

A

(1) Anastomotic leak
(2) Abscesses
(3) Extensive superficial infections,e.g.,necrotising fasciitis

448
Q

What is the aim of surgery in septic shock?

A
449
Q

What is the main cause of neurogenic shock?

A

Spinal cord transection,usually at a high level,resulting in interruption of the autonomic nervous system

450
Q

What are the features of neurogenic shock?

A

1st/Clinical features

(1) Bradycardia
(2) Warm dry skin
(3) Hypotesion

2nd/Pathophysiological features

451
Q

What are the clinical features of neurogenic shock?

A

(1) Bradycardia
(2) Warm dry skin
(3) Hypotension

452
Q

What are the pathophysiological features of neurogenic shock?

A
453
Q

What is the management of neurogenic shock?

A

Mnemonic;VIP

(1) IV fluids
(2) Peripheral vasoconstrictors-to return vascular tone to normal
(3) Vasopressors

454
Q

Why peripheral vascular vasoconstrictors are used for the management of neurogenic shock?

A

To return vascular tone to normal

455
Q

What are the causes of cardiogenic shock?

A

Mnemonic;CAM/VAP

  • Cardiomyopathy
  • AMI-ishaemic heart diseases are the main cause in medical cases
  • Direct myocardial trauma or contusion-the main cause in trauma cases
  • Valve failure
  • Arrhythmia
  • PE
456
Q

What are the features of cardiogenic shock?

A

1st/Clinical features

(1) Tachycardia
(2) Weak thready pulse
(3) Cool,pale moist skin
(4) Tachypnoea,crackles
(5) Hypotension
(6) U/O < 30 ml/hr

2nd/Pathophysiological features

(1) Increased SVR
(2) Decreased CO

457
Q

What are the investigation of cardiogenic shock?

A

(1) ECG changes-with sternal fractures or contusions raise the suspicion of injury
(2) Transthoracic echocardiography to show

  • pericardial fluid
  • direct myocardial injury

(3)Troponin in trauma-less useful in showing extent of myocardial trauma than following MI

458
Q

What is the most common site of injury in blunt cardiac injury with cardiogenic shock?

A

In blunt cardiac injury with cardiogenic shock,the right side of heart is the most likely affected with chamber and or valve rupture. These patients require surgery to repair these defects.

459
Q

What is the surgical management of cardiogenic shock?

A

(1) Cardiopulmonary bypass-as in blunt cardiac injury with cardiogenic shock,the right side of heart is the most likely affected with chamber and or valve rupture. These patients require surgery to repair these defects.
(2) Intra-aortic ballon pump counterpulsation-as a bridge to surgery

460
Q

Define anaphylaxis

A

Hypersensitivity reaction

(1) Generalised or systemic
(2) Severe
(3) Life threatening

461
Q

What is the significance of anaphylaxis?

A

Anaphylaxis is one of the few times when you would not have time to look up the dose of a medication

462
Q

What is the cause of anaphylaxis?

A

+In general-food(e.g.,nuts)

+In children-drugs,venom(e0g.,wasp sting)

463
Q

What are the clinical features of anaphylactic shock?

A

(1) Pruritus
(2) Urticaria
(3) Cough
(4) Dyspnoea
(5) Restlessness
(6) Tachycardia
(7) Hypotension
(8) Decreased level of consciousness(LOC)

464
Q

What is the treatment of anaphylaxis ?

A
465
Q

Summary of all types of shock

A
466
Q

Define priapism?

A

Erection

(1) Prolonged
(2) Unwanted
(3) In the absence of sexual desire
(4) Lasting more than 4 hours

467
Q

What are the types of priapism?

A

(1)Low flow priapism

  • due to high veno-oclusion(high intracavernosal pressure)
  • often low cavernosal flow
  • most common type
  • often painful
  • if present > 4 hours requires emergency treatment

(2)High flow priapism

  • due to unregulated arterial blood flow
  • usually pesents as semirigid painless erection

(3)Recurrent priapism

  • due to sickle cell disease
  • most commonly of high flow type
468
Q

Discuss low flow priapism

A
  • due to high veno-oclusion(high intracavernosal pressure)
  • often low cavernosal flow
  • most common type
  • often painful
  • if present > 4 hours requires emergency treatment
469
Q

Discuss high flow priapism

A
  • due to unregulated arterial blood flow
  • usually pesents as semirigid painless erection
470
Q

Discuss recurrent priapism

A
  • due to sickle cell disease
  • most commonly of high flow type
471
Q

What are the causes of priapism?

A

Mnemonic;BINT

(1) Blood disorders such as leukaemia and sickle cell disease
(2) Intracavernosal drug therapy(e.g.,for erectile dysfunction)
(3) Neurogenic disorders such as spinal cord transection
(4) Trauma to penis resulting in arteriovenous malformation

472
Q

What are the tests for priapism?

A

(1) Exclude leukaemia and sickle cell disease 🦠
(2) Blood sampling from cavernosa to determine whether high or low flow(low flow is often hypoxic)

473
Q

What is pathophysiology of priapism?

A
474
Q

complete the blanks

(1) Ejaculation is a ———— function
(2) Erection is a ——— function

A

(1) sympathetic
(2) parasympathetic

475
Q

Define onufs nucleus

A
  • In AHC of S2 for external urethral sphincter
  • If affected⇒incontinence
476
Q

Define Hartmans solution

A

the most electrolyte rich

477
Q

Complete the blanks

both pentastarch and gelofusin have more——-

A

Macromolecules

478
Q

Complete the blanks

both ——- and ——– have more macromolecules

A

pentastarch and gelofusin

479
Q

What are the indications of intraoperative fluid management?

A

(1) To optimise cardiac stroke volume
(2) non elective orthopaedic or abdominal surgery

  • should receive IV fluids for the first 8 hours post-operatively
  • supplemented by a low dose dopexamine infusion in selected cases
480
Q

What is the composition of commonly used IV fluids?

A
481
Q

Discuss the latest intra-operative fluids NICE guidelines 2013

A

the guidelines didn’t adress the specific requirements of intraoperative fluid administration as there is no rigid algorithms

482
Q

Discuss myocardial or cardiac action potential

A

MRCS part A- Principles of surgery in general (5 decks)

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