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My year 2 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

branch block on ECG

A

prolonged QRS

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2
Q

branch block on ECG

A

prolonged QRS

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3
Q

Atrial fibrillation on ECG

A

absence of P wave

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4
Q

Define remodelling (heart)-

A

increase in myocardial mass

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5
Q

Mitral regurgitation murmur

A

pansystolic, at apex

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6
Q

Aortic stenosis murmur

A

midsystolic, Right 2nd intercostal space

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7
Q

Mitral stenosis murmur

A

diastolic murmur

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8
Q

Aortic regurgitation murmur

A

diastolic murmur

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9
Q

Orthopnea

A

SOB which occurs when lying flat, sign of pulmonary oedema

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10
Q

What’s the venous pressure in Pulmonary oedema?

A

25mmHg (15mmHg normal)

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11
Q

CXR signs of pulmonary oedema

A

Batwing sign, Kerley B line (lymphatic drainage), large cardiothoracic ratio (cardiomegaly)

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12
Q

Referred cardiac pain level

A

T1-T4, medial upper arm and neck/jaw

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13
Q

Infarct on inferior wall referred pain

A

T5-9, epigastrium (misinterpreted as indigestion)

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14
Q

J wave ECG cause

A

J wave ECG cause

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15
Q

ECG of first degree heart block

A

PR interval is a fixed constant duration >200ms, regular rate

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16
Q

Second degree heart block type 1

A

PR interval progressively gets longer, until skip beat

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17
Q

Second degree heart block type 2

A

AV node randomly fails to respond to some atrial pulses, rate is irregularly irregular

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18
Q

Third degree heart block

A

bradycardia, ventricular rhythm is independent to atrial rhythm

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19
Q

Junctional rhythm on ECG

A

(AVN takes over as pacemaker), bradycardia, inverted p wave (lead II) or absent p wave.

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20
Q

Supraventricular tachycardia (SVT) on ECG

A

rate 140-220 bpm, p wave absent or buried in T wave

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21
Q

Bundle branch block on ECG

A

prolonged QRS complex, notch on R wave or double R wave

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22
Q

What does depressed ST segment show?

A

coronary ischemia, hypokalaemia

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23
Q

Left axis deviation on ECG

A

positive lead I, negative aVF

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24
Q

Normal mean electrical axis on ECG

A

positive lead I and positive aVF (-30 to 90 degrees)

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25
Q

Right axis deviation on ECG

A

negative lead I and positive aVF

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26
Q

Definition of hypotension

A
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27
Q

Grade I hypertension

A

140-159/90-99 mmHg

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28
Q

Grade ii hypertension

A

160-179/ 100-109 mmHg

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29
Q

Grade III hypertension

A

180 />110 mmHg

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30
Q

What does hypertensive retinopathy show?

A

silver wire arteriole, cotton wool spots

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31
Q

Normal sodium level

A

135-145 mmol/L

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32
Q

Symptoms of hyponatremia

A

fatigue, confusion, muscle weakness, nausea & vomiting, headache, spasm, seizures, coma (due to brain swelling)

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33
Q

Optimal BP for diabetic

A
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34
Q

What is dextracardia?

A

anomaly where primitive heart tube folds to left in a mirror image of normal looping. Usually occurs in situs inversus

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35
Q

What is situs inversus?

A

all organ systems are reversed.

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36
Q

What molecule close ductus arteriosus?

A

bradykinin

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37
Q

What may reopen ductus arteriosus?

A

prostaglandin E2

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38
Q

Tetralogy of fallot 4 lesions

A

overriding aorta (above septal defect), ventricular septal defect, right ventricular hypertrophy, pulmonary stenosis

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39
Q

Persistent Truncus arteriosus, what is it and surgical repair for it

A

large VSD, truncus arteriosus supply both aorta and pulmonary artery. Rastelli repair.

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40
Q

Immediate procedure for transposition of the great vessel

A

catherisation of foramen ovale to allow mixing of blood.

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41
Q

Types of atrial septal defect

A

– primum atrial septal defect (ostium primum is patent as septum primum has not fused with the endocardial cushions), secundum atrial septal defect (short septum primum doesn’t overlap foramen ovale), patent foramen ovale

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42
Q

Cyanotic heart defects

A

tetralogy of Fallot, persistent truncus arteriosus, transposition of great vessels, tricuspid atresia

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43
Q

What does ductus arteriosus become after birth?

A

ligmentum arteriosum

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44
Q

Treatment for patent ductus arteriosus

A

prostaglandin inhibitor (ibuprofen), if fails to work surgical slip.

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45
Q

Acyanotic heart defects

A

ASD, VSD, PDA (may due to pulmonary/aortic valve atresia), coarctation of aorta (pre-ductal type)

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46
Q

Site of erythropoietin at 3rd week

A

yolk sac, mesothelial layer of placenta

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47
Q

Site of erythropoietin at 6 week

A

liver and spleen

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48
Q

Which part of the bone marrow does erythropoiesis occur?

A

yellow bone marrow

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49
Q

the process by which RBC pass from bone marrow into the blood capillaries

A

diapedesis (squeezing through the pores of the capillary membrane)

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50
Q

site of EPO production

A

fibroblast in proximal tubule (kidney), type 1 cell of carotid body. These sites are not subject to variation during exercise. Are sensitive to hypoxia

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51
Q

what does raised ESR indicate

A

-specific marker for infection in blood

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52
Q

how does RBC make ATP and NADPH?

A

Anaerobic glycolysis for ATP. Pentose phosphate pathway for NADPH.

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53
Q

How is old RBC in spleen recognised for break down?

A

old RBC contain different surface antigens (rise in level of methaemoglobin), lack of deformability of old RBC so become trapped in spleen

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54
Q

Process of RBC break down

A

splenic macrophage break RBC by osmotic lysis. Haem group is removed and broken down by haem-oxygenase, iron is removed for reused, left with biliverdin. Biliverdin is converted to bilirubin by biliverdin reductase.

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55
Q

Enzyme for unconjugated bilirubin ->unconjugated bilirubin

A

glucuronic transferase (unconjugated bilirubin is combined with glucuronic acid)

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56
Q

Diagnosis criteria for MI

A

rise/fall of troponin & either symptoms of ischaemia OR ECG changes

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57
Q

STEMI reperfusion therapy

A

Aspirin and clopidogrel (ticagrelor), GP IIb/IIIa inhibitor, PCI

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58
Q

Prevention for STEMI

A

aspirin, clopidogrel (ticagrelor), statin, beta-blocker, ACE-I

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59
Q

Atrial fibrillation on ECG

A

absence of P wave

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60
Q

Define remodelling (heart)-

A

increase in myocardial mass

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61
Q

Mitral regurgitation murmur

A

pansystolic, at apex

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62
Q

Aortic stenosis murmur

A

midsystolic, Right 2nd intercostal space

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63
Q

Mitral stenosis murmur

A

diastolic murmur

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64
Q

Aortic regurgitation murmur

A

diastolic murmur

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65
Q

Orthopnea

A

SOB which occurs when lying flat, sign of pulmonary oedema

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66
Q

What’s the venous pressure in Pulmonary oedema?

A

25mmHg (15mmHg normal)

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67
Q

CXR signs of pulmonary oedema

A

Batwing sign, Kerley B line (lymphatic drainage), large cardiothoracic ratio (cardiomegaly)

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2
3
4
5
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68
Q

Referred cardiac pain level

A

T1-T4, medial upper arm and neck/jaw

How well did you know this?
1
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2
3
4
5
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69
Q

Infarct on inferior wall referred pain

A

T5-9, epigastrium (misinterpreted as indigestion)

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3
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70
Q

J wave ECG cause

A

J wave ECG cause

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71
Q

ECG of first degree heart block

A

PR interval is a fixed constant duration >200ms, regular rate

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3
4
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72
Q

Second degree heart block type 1

A

PR interval progressively gets longer, until skip beat

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73
Q

Second degree heart block type 2

A

AV node randomly fails to respond to some atrial pulses, rate is irregularly irregular

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74
Q

Third degree heart block

A

bradycardia, ventricular rhythm is independent to atrial rhythm

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75
Q

Junctional rhythm on ECG

A

(AVN takes over as pacemaker), bradycardia, inverted p wave (lead II) or absent p wave.

How well did you know this?
1
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2
3
4
5
Perfectly
76
Q

Supraventricular tachycardia (SVT) on ECG

A

rate 140-220 bpm, p wave absent or buried in T wave

How well did you know this?
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2
3
4
5
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77
Q

Bundle branch block on ECG

A

prolonged QRS complex, notch on R wave or double R wave

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78
Q

What does depressed ST segment show?

A

coronary ischemia, hypokalaemia

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79
Q

Left axis deviation on ECG

A

positive lead I, negative aVF

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80
Q

Normal mean electrical axis on ECG

A

positive lead I and positive aVF (-30 to 90 degrees)

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81
Q

Right axis deviation on ECG

A

negative lead I and positive aVF

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82
Q

Definition of hypotension

A
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83
Q

Grade I hypertension

A

140-159/90-99 mmHg

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84
Q

Grade ii hypertension

A

160-179/ 100-109 mmHg

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85
Q

Grade III hypertension

A

180 />110 mmHg

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86
Q

What does hypertensive retinopathy show?

A

silver wire arteriole, cotton wool spots

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87
Q

Normal sodium level

A

135-145 mmol/L

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3
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5
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88
Q

Symptoms of hyponatremia

A

fatigue, confusion, muscle weakness, nausea & vomiting, headache, spasm, seizures, coma (due to brain swelling)

How well did you know this?
1
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2
3
4
5
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89
Q

Optimal BP for diabetic

A
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90
Q

What is dextracardia?

A

anomaly where primitive heart tube folds to left in a mirror image of normal looping. Usually occurs in situs inversus

How well did you know this?
1
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2
3
4
5
Perfectly
91
Q

What is situs inversus?

A

all organ systems are reversed.

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92
Q

What molecule close ductus arteriosus?

A

bradykinin

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93
Q

What may reopen ductus arteriosus?

A

prostaglandin E2

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94
Q

Tetralogy of fallot 4 lesions

A

overriding aorta (above septal defect), ventricular septal defect, right ventricular hypertrophy, pulmonary stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Persistent Truncus arteriosus, what is it and surgical repair for it

A

large VSD, truncus arteriosus supply both aorta and pulmonary artery. Rastelli repair.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Immediate procedure for transposition of the great vessel

A

catherisation of foramen ovale to allow mixing of blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Types of atrial septal defect

A

– primum atrial septal defect (ostium primum is patent as septum primum has not fused with the endocardial cushions), secundum atrial septal defect (short septum primum doesn’t overlap foramen ovale), patent foramen ovale

How well did you know this?
1
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2
3
4
5
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98
Q

Cyanotic heart defects

A

tetralogy of Fallot, persistent truncus arteriosus, transposition of great vessels, tricuspid atresia

How well did you know this?
1
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2
3
4
5
Perfectly
99
Q

What does ductus arteriosus become after birth?

A

ligmentum arteriosum

How well did you know this?
1
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2
3
4
5
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100
Q

Treatment for patent ductus arteriosus

A

prostaglandin inhibitor (ibuprofen), if fails to work surgical slip.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Acyanotic heart defects

A

ASD, VSD, PDA (may due to pulmonary/aortic valve atresia), coarctation of aorta (pre-ductal type)

How well did you know this?
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2
3
4
5
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102
Q

Site of erythropoietin at 3rd week

A

yolk sac, mesothelial layer of placenta

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103
Q

Site of erythropoietin at 6 week

A

liver and spleen

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104
Q

Which part of the bone marrow does erythropoiesis occur?

A

yellow bone marrow

How well did you know this?
1
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2
3
4
5
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105
Q

the process by which RBC pass from bone marrow into the blood capillaries

A

diapedesis (squeezing through the pores of the capillary membrane)

106
Q

site of EPO production

A

fibroblast in proximal tubule (kidney), type 1 cell of carotid body. These sites are not subject to variation during exercise. Are sensitive to hypoxia

107
Q

what does raised ESR indicate

A

-specific marker for infection in blood

108
Q

how does RBC make ATP and NADPH?

A

Anaerobic glycolysis for ATP. Pentose phosphate pathway for NADPH.

109
Q

How is old RBC in spleen recognised for break down?

A

old RBC contain different surface antigens (rise in level of methaemoglobin), lack of deformability of old RBC so become trapped in spleen

110
Q

Process of RBC break down

A

splenic macrophage break RBC by osmotic lysis. Haem group is removed and broken down by haem-oxygenase, iron is removed for reused, left with biliverdin. Biliverdin is converted to bilirubin by biliverdin reductase.

111
Q

Enzyme for unconjugated bilirubin ->unconjugated bilirubin

A

glucuronic transferase (unconjugated bilirubin is combined with glucuronic acid)

112
Q

Diagnosis criteria for MI

A

rise/fall of troponin & either symptoms of ischaemia OR ECG changes

113
Q

STEMI reperfusion therapy

A

Aspirin and clopidogrel (ticagrelor), GP IIb/IIIa inhibitor, PCI

114
Q

Prevention for STEMI

A

aspirin, clopidogrel (ticagrelor), statin, beta-blocker, ACE-I

115
Q

What artery supplying the brain is most prone to blockage by emboli and what do they supply

A

lenticulo-striate artery which leave MCA at 90 degrees. Supply basal ganglia and internal capsule (motor commands)

116
Q

What is penumbra

A

area surrounding an ischemic event such thrombotic or embolic stroke. Treatment target survival of neurones in penumbra.

117
Q

What controls Cardiac output?

A

preload and heart rate, NOT afterload (which controls blood pressure).

118
Q

What controls blood pressure?

A

CO and systemic vascular resistance

119
Q

What local factors affect arteriole constriction/ dilation?

A

– Endothelin act on ETA Receptors cause vasoconstriction. Endothelin act on ETB Receptors to release NO, cause vasodilation. Prostacyclin (from arachidonic acid) cause vasodilation. Noradrenaline and angiotensin II cause vasoconstriction (not local factor)

120
Q

What is shock?

A

inadequate tissue perfusion resulting in cellular hypoxia. Either caused by inadequate blood pressure or systemic vascular resistance.

121
Q

Meaning of diaphoresis

A

sweating

122
Q

How much blood loss is life-threatening?

A

How much blood loss is life-threatening?

123
Q

Most common cause of haemolytic disease of the new born?

A

– Rh–ve mother with first pregnancy carrying Rh+ve child, the immune system is sensitised to D antigen. Second Rh+ve child, anti-D stimulated and cross placenta and destroy foetal red blood cells.

124
Q

Treatment for HDN?

A

anti-D immunoglobulin prophylaxis

125
Q

When to stop transfusion immediately?

A

temperature spike >40 degrees, suggest intravascular haemolysis

126
Q

Treament for an acute transfusion reaction

A

stop transfusion, IV saline (hypotension), Frusemide (maintain renal perfusion), treat DIC

127
Q

Definition of haematoma

A

blood clot outside of blood vessel (in tissues)

128
Q

What’s Virchow’s triad

A

reduced blood flow (stasis), vessel wall disorder, hypercoagulability

129
Q

DVT confirmation of diagnosis

A

pretest probability score, D-dimer (blood test for fibrin), compression ultrasound, venography (gold standard)

130
Q

What does ECG show for pulmonary embolism

A

sinus tachycardia, right heart strain, T-wave inversion anterior leads, S1Q3T3 pattern

131
Q

Diagnostic test for PE

A

– CTPA (CT pulmonary angiogram), isotope lung scan (V/Q scan)

132
Q

Two types of heparin

A

unfractionated heparin (UFH- immediate onset, short half life, IV), low molecular weight heparin (LMWH, longer half life, subcutaneous administration)

133
Q

Heparin antagonist

A

Heparin antagonist

134
Q

How does warfarin work

A

vitamin K antagonist (factors II, VII, IX, X, protein C & S)

135
Q

What is antiphospholipid syndrome

A

acquired form of thrombophilia

136
Q

Treatment for DVT/ PE

A

heparin then warfarin

137
Q

What pathogen cause Rheumatic fever

A

group A streptococcus pyogenes

138
Q

Heart failure what does the chest X-ray show?

A

bat-wing (pulmonary oedema), cardiomegaly, upper zone vessel enlargement (pulmonary venous hypertension), Kerley B lines, pleural effusion

139
Q

Test for heart failure

A

– brain natriuretic peptide (secreted by myocardial cells due to overstretching, promotes natriuresis & vasodilation, inhibit ADH and aldosterone release), Doppler echo

140
Q

Heart failure treatment

A

diuretics, ACE-I, ARB, Beta-bloker, spironolactone (NYHA grade III and IV, LVEF5.0)

141
Q

Causes of aortic stenosis

A

rheumatic disease, calcific disease, congenital bicuspid valve

142
Q

Lipid target

A

total cholesterol

143
Q

Management of MI

A

– give O2, morphine (with antiemetic- metoclopramide), aspirin + clopidogrel, PCI

144
Q

Clopidogrel mechanism of action

A

block platelet aggregation by stopping ADP binding, so prevent activation of GpIIb-IIIa receptor complex for fibrinogen

145
Q

Fibrinogen binding site on platelet

A

GpIIb/IIIa receptor

146
Q

Thrombolysis specific agents (2)

A

rTPA/tenecteplase, streptokinase

147
Q

CVD (MI) prevention

A

lifestyle changes, blood pressure control/medication, ACE-I (ARB), beta-blocker, aspirin, simvastatin (cholesterol >5.0) = polypill

148
Q

Muscle for deep inspiration

A

accessory muscle- scalene, SCM, pectoralis minor, serratus posterior superior

149
Q

Muscle for quite inspiration

A

diaphragm, external intercostal m, interchondral part of internal intercostal

150
Q

Muscles for deep expiration

A

interosseous part of internal intercostal m, abdominal muscles, serratus posterior inferior

151
Q

Where to put needle for mid-axillary thoracocentesis? –

A

– mid-axillary line, 9th intercostal space (costodiaphragmatic recess), needle angled up (to avoid liver)

152
Q

Where to put thoracostomy (chest drain)

A

5/6 intercostal space

153
Q

Blood supply to lung

A

pulmonary artery, bronchial (enter at hilum and supply all tissues except alveoli)

154
Q

Tumour to sympathetic chain in apex of thorax (stellate ganglion), what would this cause?

A

– Horner’s syndrome= pupil constriction, drooping of eyelid, sunken eye

155
Q

Tumour to thoracic duct, what would this cause

A

chylothorax, effusion of lymph into pleural cavity

156
Q

What is upper respiratory tract?

A

nasocavity, larynx, pharynx

157
Q

Commonest bacterial cause of pneumonia

A

streptococcus pneumoniae

158
Q

Identification of streptococcus pneumoniae

A

catalase negative, alpha haemolytic

159
Q

Causes of atypical pneumonia

A

Mycoplasma pneumoniae, chlamydia pneumoniae, legionella pneumophilia, coxiella burnetil (Q fever)

160
Q

Pneumonia treatment

A

beta-lactams (amoxicillin), not effective against Mycoplasma pneumoniae

161
Q

What organisms cause TB?

A

mycobacterium tuberculosis, m. bovis, m. africanum, m. microti (aerobic, lipid rich cell wall)

162
Q

Stain for TB

A

Ziehl-Neelsen stain, auramine (fluoroscopy)

163
Q

What stain is BCG vaccine made from

A

M. bovis

164
Q

Common infections of upper respiratory tract

A

colds, pharyngitis (sore throat), tonsillitis, sinusitis, otitis media

165
Q

Common cause of pharyngitis (sore throat)

A

group A streptococcus (beta-haemalytic)

166
Q

Cause of common cold

A

rhinovirus

167
Q

Complication of group A streptococcus

A

rheumatic fever, glomerulonephritis

168
Q

Whooping cough cause

A

Bordetella pertussis

169
Q

Stages of whooping cough

A

catarrhal phase (week 1), paroxysmal stage (2-4 weeks, whooping cough & haemorrhage)

170
Q

Cause of diphtheria

A

Corynebacterium diphtheria

171
Q

What does Epstein Barr virus cause

A

glandular fever

172
Q

Neuraminidase inhibitor (influenza treatment)

A

zanamavir

173
Q

Cause of acute respiratory bronchiolitis

A

respiratory syncytial virus (RSV)

174
Q

What immunoglobulin activate mast cell?

A

IgE

175
Q

How does innate immune cells bind to antibody (e.g. IgG)

A

Fc receptor

176
Q

What is atopy?

A

inherited disposition to make IgE to common environmental antigens (hypersensitivity)

177
Q

What is type 1 hypersensitivity?

A

mast cell activation, release histamine (increase permeability of venule), leukotriene (increase permeability), prostaglandin

178
Q

Clinical manifestation of type 1 hypersensitivity

A

local (asthma, allergic rhinitis, atopic eczema), systemic= ANAPHYLACTIC SHOCK

179
Q

Symptoms of anaphylactic shock

A

hypotension (dilation of great vein, fluid lead into ISF), angioedema, urticaria (hives), bronchoconstriction…

180
Q

Acute treatment of anaphylactic shock

A

IM adrenaline (Epipen), oxygen, IV fluid, antihistamine (chlorpheniramine), glucocorticosteroids (hydrocortisone)

181
Q

What’s the difference between anaphylactic and anaphylactoid shock?

A

anaphylactoid shock doesn’t involve IgE

182
Q

What activate mast cells & basophils?

A

IgE, complement C3a&C5a, substance P (axon reflex of sensory nerves), direct contact with pathogen

183
Q

What medication for hereditary angioedema

A

C1 esterase inhibitor (doesn’t respond to adrenaline)

184
Q

Definition of respiratory failure

A

PaO2 6.7kPa (50mmHg)

185
Q

Type 1 respiratory failure

A

hypoxic (with/without low PCO2), PaO2

186
Q

Causes of type 1 respiratory failure

A

reduced perfusion (emphysema, pulmonary emboli, pulmonary arterial hypertension), reduced ventilation (pneumonia, obstructed airway, pleural effusion, atelectasis, muscle weakness)

187
Q

Treatment of type 1 respiratory failure

A

give oxygen

188
Q

How does peripheral chemo-sensitive area react to hypoxia

A

carotid and aortic bodies have oxygen sensitive K+ channels and haem based mitochondrial cytochrome enzymes responsive to local PO2 concentration. When PO2 increase ventilation.

189
Q

Type 2 respiratory failure

A

Raised PaCO2 (with/without hypoxia), PaCO2 > 6.7kPa (50mmHg)

190
Q

Definition of atelectasis

A

partial collapse or incomplete inflation of the lung.

191
Q

How does chemo-sensitive area react to increase PCO2?

A

– effect via central chemo-sensitive area. Increase in arterial PCO2 increase CSF PCO2, lead to increase H+ ion and CSF acidosis -> increase rate and volume of breathing.

192
Q

Causes of type 2 respiratory failure

A

decreased ventilation due to loss of lung ventilator capacity (consolidation, PE, COPD), loss of chest wall ability to ventilate, failure of central control of respiration (head/brain stem injury, acclimatisation to high PaCO2, sleep)

193
Q

Treatment of type 2 respiratory failure

A

controlled oxygen therapy, ventilator support- drugs (doxapram, acetazolamide, progesterone) or CPAP, BIPAP or intubation

194
Q

What oxygen saturation is aimed for people with hypercapnia respiratory failure?

A

88-92% e.g. in COPD

195
Q

FEV1/VC of obstructive defect

A
196
Q

Examples of obstructive defects

A

asthma, COPD, upper airway obstruction

197
Q

FEV1/VC of restrictive defect

A

> 75%

198
Q

Examples of restrictive defects

A

lung fibrosis, reduced chest wall movement and muscle disease

199
Q

Diagnosis of asthma with peak flow

A

> 20% diurnal variation for 3days/week for 2 weeks on PEFR diary

200
Q

Asthma response to bronchodilator

A

FEV1 > 15% and 200ml

201
Q

How is TLC measured

A

dilution of helium

202
Q

How is gas transfer in the lung measured

A

TLCO= KCO x Va, single breath of air + CO + He. Calculate total CO transfer TLCO.

203
Q

What factors affect gaseous exchange?

A

Fick Principle – volume of gas, surface area of alveoli, thickness, difference in pressure, permeability (Graham’s Law- molecular weight)

204
Q

How does emphysema and fibrosis change compliance of lung

A

emphysema increase compliance, fibrosis decrease compliance

205
Q

What’s airway resistance

A

pressure difference between alveolae and mouth

206
Q

What’s the maximum altitude people can stay at (death zone)

A

7500m

207
Q

Response to rapid ascend

A

low PaO2, increase sympathetic activity (HR, BP), increase pulmonary vasoconstriction, cause pulmonary arterial hypertension

208
Q

Mechanism of acclimatisation

A

metabolic acidosis (increase excretion of HCO3-, decrease excretion of H+, activate central and peripheral chemoreceptors to increase ventilation), increase kidney EPO secretion & increase haematocrit, pulmonary vascular resistance fall (reduced hypoxic vasoconstriction response)

209
Q

How does acute mountain sickness occur

A

hypoxia-driven hyperventilation response (chemoreceptor in carotid body) inhibited by respiratory alkalosis (hyperventilation and hypocapnea), cause hypoxemia.

210
Q

Acute mountain sickness treatment

A

descend, oxygen, acetazolamide (Diamox- carbonic anhydrase inhibitor cause metabolic acidosis), dexamethasone

211
Q

Acute mountain sickness symptoms

A

headache, poor sleep, tiredness, loss of appetite, vomiting, nausea, dizziness

212
Q

Pathophysiology of HACE (high altitude cerebral oedema)

A

hypoxaemia, lack supply of ATP to brain cell, Na+ pump not working, Na+ leak into nerve cell and pull water in cause brain cells to swell. Raise intracranial pressure and block cerebral veins

213
Q

Treatment Of HACE

A

descend, acetazolamide. Oxygen, dexamethasone, hyperbaric chamber

214
Q

Symptoms of HACE

A

ataxia, nausea/vomiting, hallucination/disorientation, confusion, soma

215
Q

Symptoms of HAPE (pulmonary oedema)

A

dyspnoea, reduced exercise tolerance, dry cough, blood stained sputum, crackles

216
Q

Pathophysiology of HAPE

A

hypoxia induce pulmonary vasoconstriction, cause pulmonary arterial hypertension, fluid leave blood and enter alveoli.

217
Q

Treatment of HAPE

A

descend, sit upright, nifedipine (Calcium channel blocker- block constriction of pulmonary arteries), hyperbaric chamber, Viagra (slow down breakdown of cyclic GMP= vasodilator produced by nitric oxide, cause pulmonary artery relaxation)

218
Q

Meaning of epistaxis

A

noseblood

219
Q

4 sinuses

A

frontal, ethmoid air sinus, sphenoid, maxillary

220
Q

4 tonsils

A

adenoid, tubal, palatine, lingual tonsil

221
Q

Where does palatine tonsil lay

A

between palatoglossal and palatopharyngeus, in tonsillar bed

222
Q

Where could foreign body lodge in pharynx

A

tonsil, base of tongue, vallecular, pyriform fossa

223
Q

Where is oesophagus likely to have strictures

A

cricopharyngeus, left main bronchus cross oesophagus, cardia

224
Q

Level of hyoid

A

C3

225
Q

Level of cricoid cartilage

A

C6

226
Q

Position of thyroid isthmus

A

2/3rd tracheal ring

227
Q

Damage of what nerve cause voice hoarseness

A

recurrent laryngeal nerve

228
Q

Damage to what nerve cause absent of choking reflex

A

superior (internal) laryngeal nerve

229
Q

What nerve supply cricothyroid muscle

A

superior (external) laryngeal nerve

230
Q

Types of exercise

A

dynamic (rhythmical contraction), static (maintained contraction, e.g. lifting)

231
Q

What is VO2 max

A

highest oxygen uptake during dynamic exercise. Reflect aerobic physical fitness of a person.

232
Q

Redistribution of blood flow during exercise mechanism

A

increase sympathetic activity, local control (nitric oxide, tissue factors- adenosine, inorganic phosphate, carbon dioxide, H+, K+ released from muscle)

233
Q

What is excess post-exercise oxygen consumption

A

eliminate oxygen debt, ATP and creatinine phosphate resynthesized, lactate -> glucose and glycogen

234
Q

How does macrophage uptake LDL

A

apolipoprotein B100, LDL receptor mediated endocytosis (negative feedback), modified LDL through scavenger receptor (no negative feedback)

235
Q

2 types of smooth muscle

A

resting (contractile), proliferating (secrete ECM)

236
Q

Desirable level of blood cholesterol

A

Total cholesterol

237
Q

Genetic risk factor to arteriosclerosis

A

homocysteinaemia, lipoprotein a

238
Q

What chromosome is gene coding for alpha subunit of haemoglobin on

A

16

239
Q

What chromosome is gene coding for beta subunit of haemoglobin on

A

11

240
Q

Definition of anaemia (adult)

A
241
Q

Definition of anaemia (6months- 6years)

A
242
Q

Definition of anaemia (6yrs -14yrs)

A
243
Q

Normal MCV

A

76-96fl

244
Q

Causes of microcytic anaemia

A

deficiency, thalassaemia

245
Q

Causes of normocytic anaemia

A

acute blood loss, cancer, chronic disease (e.g. rheumatoid arthritis, renal disease-EPO), haemolytic anaemia

246
Q

Causes of macrocytic anaemia

A

B12/folate deficiency, alcohol/liver disease, myelodysplasia, bone marrow failure (aplastic anaemia), drugs (anticonvulsants, chemotherapy)

247
Q

Feature on blood film of b12/folate deficiency

A

macrocytic anaemia, hypersegmented neutrophils, oval macrocyte, (bone marrow- megaloblastic marrow)

248
Q

Who are more likely to get pernicious anaemia

A

fair hair, blue eyes, blood group A

249
Q

Pathophysiology of pernicious anaemia

A

autoimmune – autoantibodies against gastric mucosa (parietal cells) and intrinsic factor, lead to gastric atrophy, achlorhydria (lack of acid production). IF is needed for B12 absorption in ileum.

250
Q

Difference between symptoms of B12 & folate deficiency

A

B12 deficiency causes neuropathy. (same symptoms include- anaemia, glossitis, jaundice_

251
Q

Feature on blood film of haemolytic anaemia

A

spherocytosis, polychromatic (reticulocyte)

252
Q

Extravascular causes of haemolytic anaemia

A

sickle cell, Thalassaemia, antibody-induced, Rh mismatch, hereditary spherocytosis

253
Q

Intravascular causes of haemolytic anaemia

A

ABO mismatch, snake bite, infection, G6PD deficiency

254
Q

Clinical features of G6PD deficiency

A

neonatal jaundice, acute haemolysis with oxidant drugs/ fava beans (G6PD reverses oxidation of Hb)

255
Q

Life span of platelet

A

8-14days

256
Q

Cell membrane of platelet

A

glycoprotein molecule (GpIIb/IIIa, receptor for coagulation factors, platelets etc), phospholipid (prostaglandin synthesis)

257
Q

Organelle of platelet

A

dense body, alpha-granules (VWF, fibrinogen, platelet factor 4, β-thromboglubulin)

258
Q

What is haemarthroses?

A

joint bleeding

259
Q

Feature on blood film of iron deficiency anaemia

A

microcytic anaemia, pencil cell

260
Q

What is chyle

A

fat lymph

261
Q

Left and right Lymph drainage

A

right quadrant= right lymphatic duct -> right venous angle, left= cisterna chyle -> thoracic duct -> left venous angle

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