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Medicine Phase One > Cardio-Respiraoty Week Two > Flashcards

Cardio-Respiraoty Week Two Flashcards

1
Q

What is the tunica externa (adventitia) composed of?

A

This is the outer layer with thick loose connective tissue. Collagen and elastin are arranged longitudinally. There is the vasa vasorum present.

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2
Q

What is the tunica media composed of?

A

There is concentric layers of smooth muslces and layers of elastic fibres. There is type one collagen and proteoglycans.

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3
Q

What is the external elastic lamina?

A

This is part of the tunica media and separates this layer from the tunica externa.

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4
Q

What is the tunica intima composed of?

A

This has a single layer of endothelium in contact with the blood. There is then a basement membrane with a collagen framework for strength. The outer layer has the internal elastic lamina which has openings to allow diffusion from tunica media.

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5
Q

What are the two main types of arteries called?

A

Elastic and Muscular

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6
Q

What are some examples of elastic arteries?

A

Pulmonary, Aorta, Subclavian and Common iliac

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7
Q

What are the characteristics of elastic arteries?

A

There is a well defined intima with supporting collagen. The tunica media has a high elastin concentration and it is arranged as lamellae. The elastin will hold mechanical energy and then recoil allow blood to flow. There tunica externa is thinner than the media.

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8
Q

How is elastin arranged in elastic arteries?

A

Lamellae

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9
Q

What are some examples of muscular arteries?

A

Cerebra, Popliteal, Brachial

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10
Q

What are the characteristics of muscular arteries?

A

Their tunica media has a higher proportion of smooth muslce than elastin. Their media is thicker than the lumen which means there are resistant to collapsing. Their externa is thicker than their media. Their external elastic lamina is thin.

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11
Q

What are the characteristics of arterioles?

A

Their interna is very thin and is fenestrated. Their media has 1-2 layers of circular smooth muslce and the distal end forms a pre-capillary sphincter. Their externa is loose connective collagenous tissue. The terminal end is called a metateriole.

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12
Q

What are the main features of capillaries?

A

Their intima only has endothelium and basement membrane. There is no externa or media.
They are surrounded by pericytes which are involved in contraction.

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13
Q

What are the three types of capillaries?

A

Continuous, Fenestrated and Sinusoids.

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14
Q

What are the characteristics of continuous capillaries?

A

The walls have continuous endothelial layer with narrow clefts between cells.

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15
Q

What are the characteristics of fenestrated capillaries?

A

These are mainly found in tissues specialised for bulk fluid exchange eg exocrine glands and kidneys. Their endothelial cells have fenestrations for free passage of molecules (water and salt0.

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16
Q

What are the characteristics of Sinusoids (discontinuous)?

A

These are found in liver, spleen and bone marrow. They are have large gaps big enough for red blood cells and plasma.

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17
Q

What layers do metaterioles have?

A

Intima: endothelium and BM
No media
Sparse externa

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18
Q

What are the characteristics of venules?

A

They have a defined tunica interna and 1-2 layers of circular muslce. The externa is sparse.

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19
Q

What are the characteristics of veins?

A

The tunica externa is the thickest. There is no internal or external lamina. The tunica intima folds to form valves/

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20
Q

What type of muscle do pulmonary veins have?

A

Cardiac

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21
Q

What are anterio-venous shunt vessels?

A

They are specialized connections between venules and metaterioles. and they can avoid capillaries.

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22
Q

What are end arteries?

A

An Artery that is the only supply of oxygenated blood to a portion of tissue.

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23
Q

What is the difference between systolic BP and diastolic BP?

A

Systolic: highest pressure attained in arteries during systole
Diastolic: lowest arterial pressure during diastole

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24
Q

What is the Blood pressure in capillaries?

A

35mmHg

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25
Q

How is MAP calculated?

A 
MAP = diastolic BP + 1/3 ( systolic - diastolic)
MAP = CO x TPR
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26
Q

How does blood volume affect blood pressure?

A

An increase in blood volume ( for example from water retention) will increase blood pressure.
A decrease of blood volume above 10% of total volume with no homeostatic mechanisms will decrease blood pressure.

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27
Q

What three factors does vascular resistance include?

A
  • Lumen size
  • Blood viscosity
  • Blood vessel length
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28
Q

How does lumen size affect blood pressure?

A

The small the lumen, the greater the resistance and the greater the blood pressure. Vasoconstriction narrows the lumen.

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29
Q

What is vascular resistance?

A

This is the opposition to blood flow

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30
Q

How does blood viscosity affect blood pressure?

A

The higher the viscosity, the higher the resistance and the higher the blood pressure.
Conditions increasing blood viscosity include dehydration and polycythaemia.
Conditions that decrease blood viscosity include anaemia or haemorrhage.

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31
Q

How does blood vessel length affect blood pressure?

A

The longer the vessel, the greater the resistance.

Obese people will have a high BP due to additional blood vessels in adipose tissue.

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32
Q

What is venous return?

A

This is the volume of blood returning back to the heart. The pressure difference of venules compared to right ventricle is 16mmHg to 0mmHg.

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33
Q

What is the skeletal muscle pump?

A

This promotes venous return during normal locomotory activity. When moving upright, blood volume will generally flow to peripheral areas. To combat this, muslces involved in standing will contract and help VS to the heart.

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34
Q

How does velocity of blood flow affect blood pressure?

A

Blood velocity is inversely related to cross-sectional area.
Each time an artery branches, the cross-sectional area increase and hence the blood velocity decrease as it flows away from the heart. The pressure decreases as velocity decreases.

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35
Q

What is blood velocity inversely related to?

A

Cross-sectional area. The flow is slowest when area is greatest.

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36
Q

Where is the cardiovascular centre located?

A

Medulla oblongata

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37
Q

What is the role of Baroreceptors?

A

These are mechanoreceptors located in carotid sinus and aortic arch. They detect wall stretch from pressure changes. The less stretched, the less impulses fired through glossopharyngeal (carotid sinus) and Vagus nerve (aortic arch).

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38
Q

Which baroreceptors are the Vagus and Glossopharyngeal nerve attached to?

A

Vagus: Aortic arch
Glossopharyngeal: Carotid sinus

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39
Q

What is the role of Proprioceptors?

A

These monitor the limb position. They provide input during physical activity. Their activity accounts for rapid increase in heart rate during exercise.

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40
Q

What is the role of chemoreceptors?

A

These are close to the baroreceptors and they monitor concentrations of oxygen, carbon dioxide and pH.

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41
Q

What is the role of ADH in blood pressure regulation?

A

This is made in hypothalamus and secreted/stored in posterior pituitary.
When Osmo recepotrs in hypothalamus detect low BP, ADH is released. They act on the collecting ducts to promote water retention. This increases blood volume and decreases urine production. This therefore decreases blood pressure

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42
Q

What is the role of Aldosterone in blood pressure regulation?

A

This is secreted by adrenal cortex when there is low blood pressure. This acts on the DCT and CD to promote sodium retention and potassium secretion. This increases blood volume and blood pressure.

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43
Q

What is the role of Angiotensin II in blood pressure regulation?

A

This is formed when there is low Blood pressure, low blood volume or blood flow to kidney decreases.
Angiotensin II is a vasoconstrictor and raises BP by increases systemic vascualr resistance. It also stimulates aldosterone releases and the thirst sensor.

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44
Q

What is the role of ANP in blood pressure regulation?

A

This is released from right atrium when there is excessive stretching during diastole. It promotes sodium/water loss and results in decreased blood volume, hence reducing blood pressure. It blocks the release of ADH, NA and aldosterone and renin.

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45
Q

What is the role of Adrenaline and Noradrenaline in blood pressure regulation?

A

The adrenal medulla secrets these in response to sympathetic response. They act on alpha-one receptor on blood vessels and causes vasoconstriction. They increase heart rate by acting on beta-one receptors. They increase blood pressure.

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46
Q

What is the role of erythropoietin in blood pressure regulation?

A

This is secreted by the kidney and increased the oxygen capacity of the blood.

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47
Q

What are the stages of Hypertension?

A

Stage one: clinic BP is 140/90mmHg or higher and ABPM is 135/85mmHg or higher.
Stage two: clinic BP is 160/100mmHg or higher and ABPM is 150/95mmHg or higher.
Severe: the systolic is 180mmHg or higher or diastolic is 110mmHg or higher.

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48
Q

What is the difference between primary and secondary hypertension?

A

Primary: this is 90% of cases and is due to risk factors
Secondary: this is 10% of cases and is a result of another condition. This can be pregnancy, endocrine, renal damage, pheochromocytoma

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49
Q

What is pheochromocytoma?

A

Tumour in adrenal glands causing high amounts of catecholamines, mostly norepinephrine, plus epinephrine to a lesser extent.

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50
Q

What are some of the clinical patterns associated with hypertension?

A
  • increased heart workload causes left ventricular hypertrophy. The increased muscle mass will have a higher oxygen demand and this may lead to MI or ischaemia.
  • increased blood pressure will place physical stress on blood vessel walls and this may cause arteriosclerosis, haemorrhages and aneurysms.
  • renal or heart failure
  • retinopathy (vessels supplying retina often affected)
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51
Q

What are some examples of ACE inhibitors?

A

These drugs end in ‘pril’.

Captopril, Enalaprill, Ramipril, Lisinopril

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52
Q

What is the mechanism of action of ACE inhibitors?

A

This inhibits the enzyme responsible for converting angiotensin I to angiotensin II.
This causes:
- decreased peripheral resistance
- decreased aldosterone causing decreased sodium/water retention
- dilation of arteries
- sympathetic activity decrease

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53
Q

What are some side effects of ACE inhibitors?

A
  • There is reduced bradykinin breakdown, peptide which activates sensory nerves in the lung, and hence this causes a dry cough
  • Sudden fall of blood pressure on first dose
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54
Q

What at some examples of Angiotensin receptor blockers?

A

These end in ‘Sartan’

Candesartan, Losartan

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55
Q

What is the mechanism of action of Angiotensin receptor blockers?

A

These block the Angiotensin receptor (which mediates the vasoconstriction and aldosterone released actions of angiotensin II).

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56
Q

What are some side effects of Angiotensin receptor blockers?

A

They do not inhibit bradykinin breakdown and hence there is no dry cough.
Side effects include headache, dizziness, back pain and diarrhoea.

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57
Q

What are some examples of alpha-one receptor blockers?

A

These end in ‘zosin’.

Prazosin, doxazosin, terozosin

58
Q

What is the mechanism of action of alpha-one receptor blockers?

A

Smooth muslce on blood vessels have alpha-one recepotrs and when noradrenaline/ adrenaline bind, the cause contraction and hence blood pressure increase.

59
Q

What are some side effects from alpha-one receptor blockers?

A

Postural hypotension (loss of sympathetic vasoconstriction)
Reflex tachycardia
Dizziness

60
Q

What are some examples of beta-blockers?

A

These end in ‘lol’

Atenolol, bisoprolol, propranolol

61
Q

What is the mechanism of action of beta-blockers?

A

The heart has beta-one recepotrs and activation caused increased HR, contractility and conduction.
The blood vessels have beta-two and binding causes relaxation.
The effects include decreased CO, decreased sympathetic activity on CNS and decreased renin release.

62
Q

What is the difference between non-selective and selective beta-blockers?

A

Selective work on heart eg atenolol.

Non-selective work on heart and peripheral eg propranolol.

63
Q

What are some side effects from beta-blockers?

A
  • cold extremities (loos of beta-two vasodilation)
  • fatigue (reduced CO and muscle perfusion)
  • bradycardia
  • hypotension
  • bronchoconstriction
  • hypoglycaemia
64
Q

What is the mechanism of action of calcium channel blockers?

A

These drugs block L-type voltage gated calcium channels. These channels open upon membrane depolarization and allow calcium enter into cardiac and vascular smooth muscle. The drugs will block the receptor and hence reduce calcium entry. There will be reduced peripheral resistance and reduced cardiac output.
L-type channels are found in vascualr smooth muslce, cardiac myocytes and cardiac nodal tissue.

65
Q

What are the two main types of channel blocks done by calcium channel blockers?

A

Open channel blocks: the drug binds to pore where calcium flows through eg verapamil, diltiazem.
Allosteric modulation: drugs bins to allosteric side and cause shape change which limits opening eg amlodipine and nifedipine.

66
Q

Which of the following drugs is best for smooth muslce and which for cardiac muscle? Nifedipine, verapamil, diltiazem

A

Smooth muslce: Nifedipine > diltiazem > verapamil

Cardiac muslce: Verapamil > diltiazem > nifedipine

67
Q

What are some side effects from calcium channel blockers?

A

Headache, constipation, palpations

68
Q

What is the mechanism of action of loop diuretics?

A 
They inhibit calcium, sodium and water reabsorption in the loop of Henle. 
Bumetanide (Bumex)
Ethacrynic acid (Edecrin)
Furosemide (Lasix)
Torsemide (Demadex)
69
Q

What is the mechanism of action of thiazides?

A

These prevent sodium reabsorption in the DCT. Bendroflumethaizide.

70
Q

What is the mechanism of action of potassium sparing diuretics?

A

These inhibit the transporter in the collecting duct involved in secreting potassium and absorbing sodium.

71
Q

What are some side effects of diuretics?

A
  • hypokalaemia

- hypotension

72
Q

What is the mechanism of action of endothelium receptor antagonists?

A

Smooth muscle cells have endothelium-one receptors on them and will contract when bound to ET-1. Examples include basentan, ambisentan.
Side effects include headache, peripheral oedema, and palpations

73
Q

Explain the baroreceptor reflex

A

The receptors detect a low Blood pressure and they decrease the firing rate in response to reduced blood volume. This increases he sympathetic response and hence HR and contractility increases.
Peripheral vasoconstriction increases the total peripheral resistance, which helps restore BP.

74
Q

How many fatty acids to they following fats have: triacylglycerol , phospholipid and cholesterol?

A

Triacylglycerol: 3 fatty acids
Phospholipids: 2 fatty acids
Cholesterol: 1 fatty acid

75
Q

What is the difference between cis and trans unsaturated fats?

A

Cis: hydrogen is one same side as double bond fat is liquid
Trans: hydrogen is on opposite side and fat is liquid

76
Q

Describe Chylomicrons?

A

These carry dietary facts from gut to fat and muslce. The major apoprotein is B48

77
Q

Describe VLDL?

A

This carries TAG from liver to muslce. The major apoprotein is B100.

78
Q

Describe LDL?

A

This carries cholesterol from liver to tissues. The major apoprotein is B100.

79
Q

Describe HDL?

A

This carries cholesterol form tissues to liver. The major apoprotein is A1 and A2.

80
Q

What artery determines the dominance of the coronary blood supply?

A

Posterior interventricular

81
Q

In the foetal circulation, what is the function of the ductus venosus?

A

Blood flows from the umbilical vein and through this in-order to avoid the liver

82
Q

In the foetal circulation, what is the function of the foramen ovale?

A

Blood flows from the right atrium and into this. This allows blood to flow into the left atrium, bypassing the lungs.

83
Q

In the foetal circulation, what is the function of the ductus arterioisus?

A

This connects the pulmonary trunk and the descending aorta. This allows blood to bypass the lung

84
Q

When entering the hilum of the lung, is the artery superior or inferior to the vein?

A

The artery is superior and the vein is inferior

85
Q

What is atelectasis?

A

Lung collapse

86
Q

When entering the hilum of the lung, is the bronchi anterior or posterior to the vessels?

A

Posterior

87
Q

How many centimetres does the pleura cavity extend over the clavicle?

A

2-3cm

88
Q

What is a pneumothorax?

A

Collection of air

89
Q

What is a haemothorax?

A

Collection of blood

90
Q

What is a chylothorax?

A

Collection of chyle

91
Q

What is a empyema?

A

Collection of pus

92
Q

What is the costodiaphragmatic recess?

A

This is a potential space in the pleural cavity. The lungs expand and fill this recess during forced inspiration. During expiration, it is full of pericardial fluid. It goes from the 8-10th rib along mid-axillary line.

93
Q

Where is an inhaled object more likely to get stuck?

A

The right bronchus as it is shorter, wider and more vertical.

94
Q

In the thorax, which Vagus nerve, left or right, forms the anterior and posterior Vagal trunk?

A

The right forms the posterior and the left forms the anterior.

95
Q

Where do the left and right recurrent laryngeal nerves arise?

A

Right: in the base of the neck
Left: in the thorax

96
Q

Which vessels does the right Vagus nerve travel between?

A

It goes posterior to the brachiocephalic vein and anterior to the brachiocephalic artery.

97
Q

What makes up the right border of the heart?

A

Right atrium

98
Q

What makes up the inferior border of the heart?

A

Left and right ventricle

99
Q

What makes up the left border of the heart?

A

Left ventricle

100
Q

What makes up the superior border of the heart?

A

The left and right atrium and great vessels

101
Q

What is pericardial effusion?

A

Excess fluid in the pericardial cavity

102
Q

What is pericardial tamponade?

A

Compression of the heart due to excess fluid

103
Q

What is the remnant of the ductus arteriosus?

A

Ligamentum arteriosum

104
Q

What three vessels from the superior vena cava?

A
  • internal jugular
  • subclavian
  • brachiocephalic
105
Q

Where do the left and right bronchi enter?

A

Left: T6
Right: T5

106
Q

Which opening in the diaphragm does the Vagul trunk enter?

A

Oesophageal

107
Q

What is cardiomyopathy?

A

A disease of the heart that interferes with the ability to pump blood

108
Q

What is cardiac output?

A

This is the measure of the amount of blood pumped out by the heart per minute.

109
Q

How do you calculate cardiac output?

A

CO= HR x SV

110
Q

Which Vagus nerve innervates the SA node and which innervates the AV node?

A 
SA = right Vagus
AV = left Vagus
111
Q

Explain the respiratory pump

A

This is dependent on pressure. During inspiration, pressure decreases in the thoracic cavity and increases the abdominal pressure. This creates a ‘sucking’ effect that brings the blood up to the heart.

112
Q

With referred pain, what would be indicated by a sore right shoulder?

A

Damage to the diaphragm.

113
Q

Which blood circuits have no autonomic innervation?

A

The pulmonary and coronary circuits

114
Q

What is resistance to flow directionally proportional and inversely proportional to?

A

Directionally proportional: vessel length and viscosity

Inversely proportional: radius

115
Q

What is Conn’s syndrome?

A

An aldosterone producing tumour. The side effects include hypokalaemia, hypernatremia and hypertension.

116
Q

What is the role of aldosterone?

A

Increases sodium and water reabsorption in the collecting duct and distal convoluted tubule. It also promotes potassium secretion.

117
Q

What is hypernatremia?

A

High serum sodium

118
Q

What is the role of Alpha-one receptors?

A

These are present on vascualr smooth muslce and are stimulatory. When activated by norepinephrine and adrenaline, they cause vasoconstriction.

119
Q

What is the role of Alpha-two receptors?

A

These are present on post-synaptic terminals at the end of neurons innervating blood vessels of nasal mucosa and skin. They are inhibitory and function to dampen vasoconstriction. They act as negative feedbacks as they prevent norepinephrine release.

120
Q

What is the role of Beta-one receptors?

A

These are in the heart and are activated by norepinephrine an epinephrine, causing increased heart rate and contractility. Activation causes activated cAMP and then P-KA which phosphorylates L-calcium channels and increases calcium

121
Q

What is the role of Beta-two receptors?

A

These are on vascular smooth muscle and they mainly bind to adrenaline. They increase cAMP in vessels and cause relaxation. Activation of these receptors in the lungs cause bronchodilation.

122
Q

What are the contents of the posterior mediastinum (DATES)?

A 
D: descending aorta
A: Azygous and Hemiazygous vein
T: Thoracic duct
E: Oesophagus 
S: Sympathetic trunk
123
Q

What are the contents of the anterior mediastinum?

A

Thymus, Internal thoracic artery and fat

124
Q

What is the direction of the innermost intercostal muslces?

A

Straight down

125
Q

What is the superior aperture?

A

Their superior opening of the thoracic cavity

126
Q

What cells does ADH add aquaporin-2 channels to?

A

Principle cells of the Collecting Duct

127
Q

What are tight junctions made up of?

A

Claudins

128
Q

What does the apical surface face and what does the basal surface face?

A

Apical: Lumen or External environment
Basal: Basement membrane

129
Q

What are the steps in rational prescribing?

A
  • Diagnosis
  • Prognosis
  • Goals of treatment
  • Treatment selection
  • Monitoring
130
Q

During rational prescribing, what is involved in the diagnosis of the treatment?

A

This is based on the primary and secondary diagnosis. This is made of confirmed by the prescriber.

131
Q

What affect on primary disease treatment will a secondary disease with poor prognosis have?

A

Limit benefits of treatment

132
Q

What are some examples of goals of a treatment?

A
  • cure disease
  • relieving symptoms
  • combing two outcomes
  • long term prevention
  • replace deficiencies
  • therapeutic trials to aid diagnosis
133
Q

What is involved in monitoring of a patient treatment?

A
  • monitor effects
  • evaluate harm-benefit balance
  • patient satisfaction is key
134
Q

Is a high therapeutic index good or bad?

A

Good (this is the ratio between dose required to cause adverse effects and that required for efficacy)

135
Q

Why is partnership with patients important in rational prescribing?

A
  • make contributions
  • beliefs and expectations
  • monitoring
  • clear communication
  • compliance
136
Q

Why is rational prescribing carried out?

A
  • maximise clinical effectiveness
  • minimise harm
  • avoid wasting resources
  • respect patient care
137
Q

Where is the aortic valve heard?

A

Right 2nd intercostal space

138
Q

Where is the pulmonary valve heard?

A

Left 2nd intercostal space

139
Q

Where is the tricuspid valve heard?

A

Lower left sternal border at the 4th intercostal space

140
Q

Where is the mitral valve heard?

A

Left 5th intercostal space medial to the midclavicular line. This is the apex beat.

Medicine Phase One (44 decks)

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