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Danielle's MD1 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

For any given volume of blood, the pressure depends on what 2 variables?

A

-compliance of the vessel wall (diastole) -active tension in the wall (systole)

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2
Q

Describe the term afterload

A

The load encountered by the ventricle as it commences contraction. (the amount of pressure the ventricle has to pump against.)

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3
Q

Describe the term preload.

A

The stretch on the myocyte fibres before they commence contraction. (amount of blood the heart has to pump. It indicates the efficiency of filling of the ventricles)

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4
Q

What is the formula for MAP?

A

MAP = CO X TPR

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5
Q

What is the formula for CO?

A

CO = HR X SV

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6
Q

What is the distribution (%) of blood in the systemic veins?

A

~65%

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7
Q

What is the distribution (%) of blood in the systemic arteries?

A

~13%

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8
Q

What is the distribution (%) of blood in the systemic capillaries?

A

~5%

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9
Q

What is the distribution (%) of blood in the lungs (pulmonary arteries, veins & capillaries)?

A

~10%

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10
Q

What is the distribution (%) of blood in the heart?

A

~7%

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11
Q

What has greater compliance, arteries or veins?

A

veins

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12
Q

What is more sensitive to changes in volume, arterial pressure or venous pressure?

A

arterial pressure

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13
Q

What is the mean circulatory filling pressure?

A

~7 mmHg

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14
Q

What does the vascular function curve describe?

A

It describes what happens to venous pressure when CO varies

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15
Q

What is central venous pressure? How is it assessed clinically?

A

-The pressure in the great veins (IVC, SVC) just outside the heart. -It is slightly higher than the right atrial pressure. -the filling pressure for the heart-It is assessed clinically by the JVP

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16
Q

What does the cardiac function curve describe?

A

It describes what happens to cardiac output when venous pressure varies

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17
Q

Nitric oxide is modulated by what factors?

A

-physical stimuli -hypoxia -circulating vasoactive factors -paracrine vasoactive factors

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18
Q

What substances do WBC release?

A

-NO -histamine -cytokines

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19
Q

What substances do platelets release?

A

-thrombin -ADP -thromboxane A2

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20
Q

What are the main types of non-competitive antagonists?

A

-allosteric inhibitors -pathway inhibitors -functional/physiological antagonists

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21
Q

What are the advantages of allosteric antagonists?

A

-substantial selectivity between receptor subtypes -incomplete antagonism is possible (toning down)

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22
Q

Describe Virchows Triad

A

Describes the 3 factors that contribute to thrombosis. The factors are: -the vessel wall -blood composition -bloow flow

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23
Q

What is the ‘starter motor’ for the coagulation system?

A

Tissue factor

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24
Q

What are the 3 summarised steps in the coagulation pathway?

A
  1. Initiation phase 2. Amplification phase 3. Propagation phase
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25
Q

List some global tests for bleeding

A

-ACT -APTT -PT/INR -Thrombin generation

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26
Q

List some specific assays for bleeding

A

-factor assays -vWF Ag -collagen binding assays -fibrinogen

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27
Q

What does the term pancytopenia mean?

A

Not enough cells (RBC, WBC, platelets)

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28
Q

What does the term anaemia mean?

A

Not enough RBCs

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29
Q

What does the term leukopenia mean?

A

Not enough general WBCs

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30
Q

What does the term neutropenia mean?

A

Not enough neutrophils

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31
Q

What does the term lymphopenia mean?

A

Not enough lymphocytes

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32
Q

What does the term thrombocytopenia mean?

A

Not enough platelets

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33
Q

What does the term polycythaemia mean?

A

Too many RBCs

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34
Q

What does the term leukocytosis mean?

A

Too many leukocytes

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35
Q

What does the term thrombocytosis mean?

A

Too many platelets

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36
Q

What does the term dyserythropoiesis mean?

A

RBCs aren’t working properly

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37
Q

What does the term white cell function defect mean?

A

WBCs don’t work properly

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38
Q

What does the term platelet function defect mean?

A

Platelets don’t work properly

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39
Q

What are the clinical signs of anaemia

A

-pale -lethargic -failure to thrive -hypoxic -ischaemia -tachycardia

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40
Q

What is the tissue oxygen delivery equation?

A

CO X Hb X %saturation X 1.34

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41
Q

What are the signs of increased RBC destruction?

A

-increased serum bilirubin –> jaundice -haptoglobins -LDH

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42
Q

What are the signs of increased RBC production?

A

-reticulocytes -polychromasia

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43
Q

RBCs are replaced every ______ days

A

120

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44
Q

WBCs are replaced every ________ days

A

3-4

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45
Q

Platelets are replaced every ________ days

A

10

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46
Q

List the cells that are found in the bone marrow stroma

A

-macrophages -fibroblasts -endothelial cells -fat cells -reticulum cells

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47
Q

List the components of the ECM within the bone marrow stroma?

A

-fibronectin -haemonectin -laminin -collagen -proteoglycan

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48
Q

During the first few weeks of fetal development where does haemopoiesis occur?

A

in the yolk sac

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49
Q

During 6weeks to 7 months of pregnancy, where does haemopoiesis occur?

A

in the liver and spleen

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50
Q

Name 3 haematinics

A

-Iron -Vitamin B12 -Folate

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51
Q

Hb carries respiratory carbon dioxide as what?

A

carbaminohaemoglobin

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52
Q

Hb makes up what % of RBC dry content?

A

97%

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53
Q

What are the 2 oxygen carrying proteins found in the blood?

A

Haemoglobin and myoglobin

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54
Q

What is the colour of aged blood?

A

dark brown

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55
Q

Oxygen binds to Fe at what angle? And why is this important?

A

At a 120 degree angle. This makes the oxygen easier to remove and therefore allows the O2 to be delivered to tissues

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56
Q

What is the general role for haemoglobin?

A

transports O2 in the blood

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57
Q

What is the general role of myoglobin?

A

stores O2 in muscle tissue

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58
Q

In the lungs how saturated is haemoglogin?

A

90% saturated. Therefore Hb has high affinity for O2.

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59
Q

In the venous blood how saturated is haemoglogin?

A

60% saturated

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60
Q

Describe the tertiary structure of myoglobin.

A

-monomeric -single polypeptide chain that is made up of 8 alpha helices (A-H) -Haeme binds in the pocket between helix F and H

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61
Q

Describe the quaternary structure of haemoglobin.

A

-tetrameric -2 alpha chains -2 beta chains -each subunit has a haem therefore there are 4 in total -affinity for O2 varies with pH, CO2 and 2,3-BPG

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62
Q

BPG is synthesised in what cell and via what metabolic pathway?

A

in RBCs via the glycolytic pathway

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63
Q

What is the main action of BPG?

A

When BPG binds to Hb it decreases Hb’s affinity for O2 because it locks out O2 from binding. It enables the release of O2 at the tissues

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64
Q

Describe the ways the body deals with/gets rid of CO2.

A

-Hb carries 15% of CO2 formed in the tissues to the lungs-the rest is converted to HCO3- by carbonic anhydrase. HCO3- is soluble in the plasma and is therefore excreted in the lungs&nb

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65
Q

Explain the Bohr effect

A

At low pHs Hb is more likely to give up O2 because binding of protons (from tissue acid production) lowers Hbs affinity for O2.

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66
Q

Describe sickle cell anaemia and its impact with malaria

A

-Normal HbA in position 6–> glutamate (acidic) -HbS a.a change–> valine (acidic and hydrophobic) -Hydrophobic Val binds to a hydrophobic pocket in deoxy-Hb –> sickle cell shape, cannot bind O2

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67
Q

Describe the actions of Botulinum toxin

A

-acts as a protease and cleaves SNARE proteins -prevents vesicles docking onto pre synaptic membrane -prevents fusion and release of Ach from the vesicle into the synaptic cleft

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68
Q

Name some therapeutic uses for botulinum toxin

A

-cosmetic -skeletal muscle dystonias e.g. blepharospasm (abnormal contraction of the eyelid)

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69
Q

Name a class of drugs that inhibits the degredation of acetylcholinesterase in the synaptic cleft.

A

Anticholinesterases

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70
Q

Name a short acting anticholinesterase

A

edrophonium

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71
Q

Name a medium acting anticholinesterase

A

neostigmine/pyridostigmine

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72
Q

Name an anticholinesterase that is used in the diasgnosis of myasthenia gravis

A

edrophonium

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73
Q

Name an anticholinesterase that is used in the treatment of myasthenia gravis

A

neostigmine/ pyridostigmine

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74
Q

Name an anticholinesterase that is used in the treatment of Alzheimers disease

A

donepezil because it enters the CNS well

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75
Q

Describe myasthenia gravis and how anticholinesterases can be used to help treat the disease.

A

-Myasthenia gravis is an autoimmune disease where you have Abs to nicotinic cholinergic receptors on skeletal muscle. Abs bind to receptors–> complement activation or cross linking of 1 ab to more than 1 receptor –> loss of integrity of post junctional membrane and loss of receptors via receptor internalisation. -Anticholinesterases can block the degredation of Ach by AchE in the synaptic cleft thereby increasing the levels of Ach in the synapse that can bind to the remaining few nicotinic receptors. NOTE: anticholinesterases only treat the symptoms.

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76
Q

What is another name for the test used to diagnose myasthenia gravis

A

Tensilon test (using edrophonium)

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77
Q

Which receptors do nicotine and varenicline act on and what are their therapeutic uses?

A

They are agonists at nicotinic receptors, and are used in smoking cessation

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78
Q

Name 3 nicotnic receptor antagonists

A

-tubocurarine -vecuronium -hexamethonium

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79
Q

What is the therapeutic use of tubocurarine and vecuronium?

A

used for pre-surgical skeletal muscle relaxation

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80
Q

What is the therapeutic use of hexamethonium

A

ganglion nicotinic receptor blocker

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81
Q

Where does pilocarpine act and what is a the therapeutic use of the drug?

A

Pilocarpine is an agonist at muscarinic receptors. It is used in glaucoma

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82
Q

Agonists at muscarinic receptors cause what effects?

A

-Anti- SLUD -sweating -bradycardia -bronchoconstriction -vasodilation

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83
Q

Name 3 anti-muscarinics and their therapeutic uses

A

Atropine -reduce secretions and produce bronchodilation in anaesthesia -for bradycardia -pupil dilation for an eye exam -AChE- inhibitor poisoning (organophosphates) Hyoscine -motion sickness Ipratropium -COPD

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84
Q

Name 2 drugs that block NA uptake 1

A

-cocaine

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85
Q

Name a class of drugs that block the degredation of NA

A

MAO-inhibitors

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86
Q

Name a class of drugs that indirectly increase the levels of NA in the synaptic cleft. Name some examples of drugs in this group.

A

Indirectly acting sympathomimetics. They are taken up into the pre-synaptic neuron via uptake 1 where they displace NA from vesicles which can then be either degraded by MAO or be released passively into the synapse. NOTE: this process is exocytotis and calcium independent-amphetamine-ephedrine-tyramine

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87
Q

Name a selective alpha-adrenoceptor agonist

A

Phenylephrine

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88
Q

Name a selective beta-adrenoceptor agonist

A

Isoprenaline

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89
Q

Name a non-selective adrenoceptor agonist

A

Adrenaline

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90
Q

Name a beta-1 adrenoceptor agonist and name its therapeutic use

A

dobutamine (useful in heart failure)

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91
Q

Name a beta-1 adrenoceptor antagonist and name its therapeutic use

A

atenolol (useful in hypertension)

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92
Q

Name a beta-2 adrenoceptor agonist and name its therapeutic use

A

salbutamol (useful in asthma)

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93
Q

Name an alpha-1 adrenoceptor agonist and name its therapeutic use

A

phenylephrine (useful as a nasal decongestant)

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94
Q

Name an alpha-1 adrenoceptor antagonist and name its therapeutic use

A

prazosin (useful in hypertension)

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95
Q

Where are alpha 2 adrenoceptors commonly found and what are their functions?

A

on pre-junctional receptors. they act as auto-inhibitory receptors

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96
Q

Histamine is stored and released from what cells?

A

-mast cells -basophils -enterochromaffin like cells -periperal and central histaminergic neurons

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97
Q

List some stimuli that cause histamine release.

A

-Ag binding via IgE-complement (C3a/C5a)= anaphylatoxin -neuropeptides -cytokines and chemokines -bacterial components -physical trauma

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98
Q

Describe the general features of histamine receptors

A

-4 main receptors (H1, H2, H3, H4) -all are GPCR

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99
Q

What response does histamine typically cause?

A

The triple response -Reddening: vasodilation -Wheal: increase in vascular permeability -Flare: spreading response through sensory fibres

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100
Q

At what receptor does anti-histamines usually work at?

A

H1 receptors

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101
Q

Name 2 first generation H1 anti-histamines and their major side effects.

A

-chlorpheniramine -promethazine Major side effect= sedation

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102
Q

Name 2 later generation H1 anti-histamines that are associated with no sedation, and name their major side effects.

A

-terfenadine -astemizole Better than 1st generation antihistamines because there is no sedation since there is poor entry into the CNS, and they lack anti-muscarinic activity and GIT effects.Majo

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103
Q

Name 2 newer generation H1 anti-histamines and their benefits over the older generation antihistamines

A

-cetirizine -loratidine Note: they have a reduced risk of unwanted cardiac effects

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104
Q

Name 2 H2 anti-histamines(receptor antagonists) and their major use.

A

-cimetidine -ranitidine used in the treatment of peptic ulcers

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105
Q

Why are H2 receptor antagonists useful in treating peptic ulcers?

A

-they block H2 receptors on the parietal cell -histamine can’t act on the H2 receptors on the parietal cells therefore no increase in cAMP occurs so H+ ions are not pumped out into the lumen into the stomach

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106
Q

What are the main roles of bradykinin?

A

-local peptide mediator in pain and inflammation

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107
Q

Describe how bradykinin is made

A

-Prekallikrein is converted to Kallikrein by activated Hageman factor (Factor XII) -Kallikrein then converts high molecular weight kininogen to bradykinin

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108
Q

How is bradykinin degraded?

A

by Kinase I and kinase II note: Kinase II=ACE

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109
Q

What are the actions of bradykinin?

A

Vascular actions -dilates arterioles and venules-increases vascular permeability Neural -simulates sensory nerve endings–> pain Contracts uterus, airways and gut Epithelial secretions in airways and gut

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110
Q

Describe the receptors for bradykinin

A

-B1 and B2 -both are GPCR

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111
Q

Name a selective B2 receptor antagonist and is clinical use

A

icatibant -used in hereditary angioedema (C1esterase inhibitor deficiency) -C1esterase normally inhibits proteases such as kallikrein so a deficiency in this inhibitor means the kallikrein pathway is over active and results in lots of bradykinin being produced

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112
Q

Describe the conundrum with acetylcholine

A

-in vivo Ach is a vasodilator (endothelium is intact because they used a transverse ring) -in vitro Ach is a vasoconstrictor (endothelium is removed because they used a helical strip) When Ach comes into contact with intact e

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113
Q

What are the 3 isoforms of NOS?

A

-nNOS (nerves, epithelial cells) -iNOS (inducible in macrophages, smooth muscle) -eNOS (endothelial cells)

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114
Q

Name a substance that blocks NOS and its actions

A

L-NAME -produces vasoconstriction and hypertension

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115
Q

What are the 3 main roles of NO?

A

-flow dependent vasodilation -inhibits platelet adhesion and aggregation -neurotransmitter

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116
Q

List some features of a non-longitudinal study, and name an example.

A

-no follow up of subjects -information is collected from 1 encounter e.g. ecological, cross sectional, case control studies

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117
Q

List some features of longitudinal studies and name an example.

A

-involves follow up -information is collected over multiple encounters over a period of time e.g. cohort studies, clinical trials

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118
Q

What does the term prevalence mean? How is prevalence expressed?

A

-the number of existing cases of an outcome in a defined population at one point or time period -as a proportion or percentage

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119
Q

What does the term incidence mean? And how is it expressed?

A

-the number of new cases of an outcome arising from a defined population during a time interval -it is expressed as a rate (so the denominator includes a time component) -only drawn from longitudinal studies

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120
Q

Define the term risk

A

the probability of a disease occurring in a disease free population during a specific time period risk =number of new cases/ population at risk

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121
Q

Define the term rate

A

the probability of a disease occurring in a disease free population during the sum of individual follow up periods rate= number of new cases in a defined period/ total person time of follow up

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122
Q

Define the term hazard

A

a specific type of rate that is continuously updated as a longitudinal study progresses (but it is always a measure of the rate in that particular point of time) IT IS INSTANTANEOUS-derived from longitudinal studies

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123
Q

Associations in epidemiology are made to make inferences about what two things?

A

-case and effect -correlation

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124
Q

Define the term absolute risk and absolute rate

A

-its an isolated measurement of risk or rate -it gives no indication of association with exposure

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125
Q

Define the term relative risk and attributable risk

A

-provides an indication of association and cause and effect relationship -each relies on comparing 2 absolute risk or rate measurements(i.e. comparing Re with Ru)

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126
Q

What is a relative risk?

A

aka risk ratio-indicates the relative magnitude of change in risk of outcome associated with exposure RR= Re/Ru

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127
Q

What is an attributable risk?

A

aka risk difference -indicates the absolute magnitude of a change in risk of outcome, associated with exposure AR= Re- Ru

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128
Q

What is an attributable risk percent?

A

-the proprotion of the disease among exposed people that is due to the exposure AR%= [(Re-Ru)/Re] X 100

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129
Q

What is a population attributable risk?

A

-it indiccates the additional risk or excess risk of the outcome in the population, that is due to the exposure PAR= Rt - Ru

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130
Q

What is the population attributable risk percent?

A

-proportion of the disease among the whole population that is due to the exposure -aka preventable fraction PAR%= [(Rt-Ru)/Rt] X 100

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131
Q

What are the main types of drugs used to stable angina?

A

-Nitrates -Ca2+ channel blockers -beta adrenoceptor antagonists -ivabradine

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132
Q

List some drug treatments for unstable angina.

A

-same drugs as for stable angina but include asprin as well to prevent thrombosis

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133
Q

The oxygen supply to the heart depends on what?

A

-coronary artery flow

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134
Q

How can you increase blood flow to the heart muscle?

A

-dilate coronary arteries -decrease heart rate =increased O2 supply -decrease CO -decrease preload -decrease afterload =decreased O2 demand

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135
Q

What is angina pectoris?

A

chest pain due to -imbalance between O2 supply and demand -therefore there is insufficient O2 to meet cardiac demand -ultimately causing reduced perfusion NB: ischaemic heart disease can cause angina

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136
Q

What are the 3 main types of angina? And briefly explain each.

A

Stable angina -chest pain with exertion and stress -associated with coronary artery disease Variant angina -coronary vasospasm at rest Unstable angina -chest pain at rest and with exertion -potential for thrombi formation

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137
Q

Describe the mechanism of action of nitrates used in stable angina?

A

-nitrate= prodrug -undergoes biotransformation -releases NO from endothelium and diffuses into vascular smooth muscle -stimulates guanylate cyclase-GTP–> cGMP -cGMP dephosphorylates myosin light chain

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138
Q

Name 2 nitrates that are used in angina

A

-GTN (glyceryl trinitrate) -isosorbide dinitrate which is converted into isosorbide-5-mononitrate

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139
Q

What are some adverse effects of nitrates in angina?

A

-brief relaxation of gut and airways -postural hypotension -headache, flushing -reflex tachycardia

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140
Q

Describe how one developes tolerance to nitrates

A

tolerance develops due to -depletion of tissue thiols (required for NO production from GTN) -increased release/sensitivity to constrictors -increased endothelial scavenging of NO e.g. via free radical production -reduced activity of ALDH2 (decreased NO production)

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141
Q

Name 3 calcium channel blockers and describe their selectivity.

A

Verapamil - non selective Diltiazem - vascular selective Nifedipine - extremely vascular selective

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142
Q

Describe the mechanism of action of calcium channel blockers used in angina

A

block Ca2+ entry into heart through L-type channels -decreased HR, increased O2 supply -decreased HR,SV,CO, reduced O2 demand e.g. verapamil, diltiazem block Ca2+ entry into vessels through L-type channels and receptor operated channels -arterial dilation, reduced afterload, reduced O2 demand e.g. nifedipine, felodipine

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143
Q

Describe the adverse effects of using calcium channel blockers in angina

A

-all cause flushing, headache and oedema but the cardioselective drugs cause -bradycardia, AV block and the vascular selective drugs cause -hypotension -reflex tachycardia

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144
Q

Describe the mechanism of action of beta blockers in angina

A

-blocks B1 adrenoceptors

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145
Q

List some beta blockers used in angina

A

-atenolol (cardiac beta 1 selective) therefore its more widely used than propranolol -propranolol (beta1 and beta2)

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146
Q

Describe the mechanism of action of ivabradine used in angina

A

-selectively inhibits the sodium-potassium Ifunny current in the SA node -slowing of depolarisation (Na inward current is inhibited) -reduces steepness of slope -takes longer to get to threshold -therefore decreases HR

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147
Q

What are some adverse effects of ivabradine?

A

-retinal effects (brightness in visual field) -conduction abnormalities

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148
Q

Name some drug treatments for variant angina

A

-short acting nitrates to relieve coronary spasm -calcium channel blockers for prophylaxis treatment

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149
Q

list the general considerations used when choosing an antibiotic

A

-clinical diagnosis -microbiological diagnosis -susceptibility -host factors -properties of the antibiotic

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150
Q

Name 2 ways bacteria is tested for antimicrobial susceptiblity

A

-dilution methods with tubes with doubling dilutions of AB -diffusion methods with antibiotic discs being placed on a growth of bac on agar

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151
Q

What does the term susceptibility S mean?

A

the bacteria is susceptible to the antibiotic of interest

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152
Q

What does the term susceptibility I mean?

A

the bacteria is intermediately resistant to the antibiotic of interest

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153
Q

What does the term susceptibility R mean?

A

the bacteria is resistant to the antibiotic of interest

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154
Q

What is an E test strip used for?

A

-to measure the MIC directly without a graph of zone diameter vs MIC -they are directly placed on the agar plate with bac already cultured on there -the strip contains an exponential antibiotic gradient and a reading scale

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155
Q

List the specific considerations regarding the choice of antimicrobial agents

A

-antimicrobial spectrum (anaerobic, aerobic?) -clinical efficacy -route of administration -route of excretion -pharmacokinetics/dynamics -availability -cost

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156
Q

List some reasons why antibiotic comibinations would be used

A

-as a temporary measure in an ill patient -to delay the emergence of resistance -to treat mixed infections -to reduced toxicity e.g. when you treat TB you used 4 diff ABs because the TB may be already resistant to 2 of the ABs, and for the TB to become resistant to the 2 ABs its not resistant to is unlikely -to achieve a synergistic effect

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157
Q

What are the 3 classifications of effects of antibiotic combinations and describe them.

A

-indifference/additive A+B produces a greater effect than them each alone (adds the two effects together) -antagonism A+B is worse than A or B alone -synergy A+B is more effecti

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158
Q

What are the mechanisms that enable synergy of 2 Antibiotics?

A

-block sequential steps of a metabolic pathway -inhibit enzymatic degradation e.g. co-amoxyclav -enhance antimicrobial uptake by the bacterial cell e.g. aminoglycosides and beta-lactams (beta lactams enable aminoglycosides which normally cant get into a cell, in)

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159
Q

What are the mechanisms that enable antagonism of 2 Antibiotics?

A

-inhibition of bactericidal activity by a bacteriostatic agent e.g. tetracycline and penicillin G in meningitis -induction of enzymatic degradation e.g. ampicillin and piperacillin -competition for binding to the same target e.g. lincosamide and macrolide -inhibition of target e.g. polyene and imidazole

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160
Q

What are Jawetz’s laws?

A

-bacteriostatic and bacteriostatic–> additive/indifferent action -bacteriostatic and bacteriocidal–> antagonistic action -bacteriocidal and bacteriocidal–> synergistic

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161
Q

What are some risk factors for CVD?

A

-smoking -HT -diabetes -hypercholesteraemia -family history -age -male gender -alcohol -stress

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162
Q

Describe the whitehall I study

A

-18000 males in the british civil service - 20-67 y/o -graded according to work hierarchy -found that those lower in the hierarchy have increased probability of death from CHD than those higher in the hierarchy -this is associated with: obesity, smoking, reduced leisure time, lower levels of physical activity, more underlying illness, higher BP, shorter height, increased work load BUT these differences only accounted for 40% of the difference between the lower and higher grades of hierarchy. The other 60% was due to stress!

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163
Q

Briefly describe the biology of chronic stress

A

-impaired memory -increased risk of depression -deteriorated imm response -elevated BP -increased risk of CVD -high hormone levels -higher risk of infertility and spontaneous miscarriage

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164
Q

Briefly describe the Whitehall 2 study

A

-10,308 women and men in british civil service -similar gradient in morbidity for men and women -people who had lower levels of trust, weaker community life and had more concern with status experienced increased levels of mental illlnesses

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165
Q

The visceral pleura covers what?

A

it covers the lungs

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166
Q

The parietal pleura covers what?

A

lies on top of the visceral pleura and it lines the cavity that contains the lungs

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167
Q

What is the pleural cavity?

A

-the potential space between visceral and parietal pleura -contains a few mls of serous fluid–> provides a frictionless surface for the lungs to expand against -you only fill the space on full inspiration (not during quiet breathing)

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168
Q

What are the main divisions of parietal pleura?

A

-cervical pleura -mediastinal pleura -costal pleura -diaphragmatic pleura

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169
Q

What is the pulmonary ligament? And what is its function

A

-a double fold of pleura -it allows the structures to expand and not be constricted by a tight sleeve of pleura

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170
Q

Describe the nerve supply to the visceral pleura and the sensation of pain from the visceral pleura

A

-visceral(autonomic) nerve supply -therefore pain is dull and poorly localised

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171
Q

Describe the nerve supply to the parietal pleura and the sensation of pain from the parietal pleura

A

-somatic nerve supply -pain is excruciating, sharp, severe and well localised

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172
Q

At what level does the trachea begin at?

A

begins in the neck at C6

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173
Q

At what level does the trachea divide into the right and left main bronchi?

A

At T4/5

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174
Q

Describe the differences between the left and right main bronchi

A

the right main bronchi is: -shorter -wider -more vertical therefore it is easier for foreign bodies to be stuck there

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175
Q

Describe the structure of the trachea

A

-composed of U shaped cartilage discs -posteriorly it is closed by the trachealis muscle

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176
Q

Describe the generations/divisions of the bronchi tree

A

L/R main bronchi–> L/R lobar bronchi–> L/R segmental bronchi

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177
Q

Describe what a bronchopulmonary segment is?

A

-pyramid shaped sections of the lung with its apex directed towards the hilum and the base on the surface -they are functionally distinct regions of lung tissue -each segment is supplied by its own segmental bronchi, artery and vein

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178
Q

In what section of the respiratory system does fluid normally collect in?

A

the apical segment of the right lower lobe

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179
Q

Describe the lobes of the lungs

A

Right lung -3 lobes: upper, middle and lower -2 fissues: olblique fissure, horizontal fissure Left lung -2 lobes: upper and middle -1 fissure: oblique fissure

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180
Q

What is the bronchus intermedius?

A

The continuation of the right main bronchus into the lung (because the right main bronchi divides into 2 before it enters the hilum of the lung to supply the upper lobe)

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181
Q

What structures cause imprints on the right lung?

A

-SVC -arch of the azygous -right atrium

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182
Q

What structures cause imprints on the left lung?

A

-aorta -left ventricle NB: these imprints are larger/deeper than the imprints on the right lung because the imprints are from arteries which are pulsatile structures

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183
Q

Describe the systems of lymphatics associated with the lungs

A

2 systems -superficial network: located on the lung surface -deep: follow the airways and blood vesselsboth meet at the hilum and drain into the hila LN–> lymphatic channels that head to the thoracic duct on the left and the right lymphatic duct on the right–> venous system

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184
Q

Describe the nerve supply to the lungs

A

-sympathetic nerves come from the ganglia of the sympathetic trunk -parasympathetic nerves come from the vagus nerve (before it forms the oesophageal plexus)

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185
Q

Basically describe how an X-ray produces an image

A

-x-rays hit the film and converts silver halide crystals to silver (chemical rxn–>colour change to black)more x-rays reach film–> blacker imagefewer x-rays reach film–> whiter image-detector–> elect

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186
Q

Describe the appearance of air, fat, soft tissue, calcium, contrast agents and metal on an X-ray.

A

air= low electron density, (little retarding of x-rays) therefore its black fat, soft tissue, calcium and contrast agents= shades of gray metal= high electron density therefore its white

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187
Q

Describe the term silhouette sign

A

To see anatomical structures on an x-ray there must be tissues with different electron densities next to each other

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188
Q

Describe the proper technique of performing an erect PA CXR

A

-full inspiration -PA= posterior to anterior (x-rays are coming from behind the patient) -heart is closer to the film/detector because we don’t want magnification or blurriness -scapulae moved away form the chest wall (hugging x-ray cassette) -erect

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189
Q

How do you check how big the heart is on an x-ray image?

A

The max transverse diam of the heart needs to be less than 50% of the max transverse diam of the thoracic cavity (from the insides of the ribs)

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190
Q

How do you tell if the patient took a full inspiratory effort on an x-ray?

A

-you check the number of ribs visible (there needs to be 7 anterior ribs above the hemidiaphragm)

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191
Q

What is the angle of Louis?

A

-aka manubriosternal junction -the anatomical line at the manubriosternal junction and T4/5 -its used for dividing the mediastinum in an x-ray image into superior and inferior sections

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192
Q

Describe the structures in the superior mediastinum.

A

-aortic arch -SVC -branches of the great vessels -upper oesophagus -trachea -vagus nerves -LNs

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193
Q

Describe the structures in the antieror mediastinum

A

-thymus -fat -LNs

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194
Q

Describe the structures in the middle mediastinum (aka pericardium)

A

-heart -great vessels -phrenic nerves -LNs

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195
Q

Describe the structures in the posterior mediastinum

A

-oesophagus -descending aorta -azygous vein -thoracic duct -LNs

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196
Q

What happens to fluid and air respectively when they get into the pleural spaces?

A

Fluid sinks to the bases (NB: you get a meniscus) Air rises to the apices

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197
Q

How do you approach analysing an x-ray image?

A

-check patient age, sex, ethnicity -check the x-ray has been done in the correct position -check for medical devices and foreign bodies -start in the middle and move outwards

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198
Q

Describe the similarities and differences between an x-ray and CT scan

A

-cathode ray rube (same as x-ray) -electron density of tissues (same as x-ray) -has a radiation detector (not film) -has a computer monitor/film

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199
Q

Briefly describe Hounsfield units

A

They are an absolute measure of x-ray attenutation Most biological tissues sit between -100 and +100 Air= -1000 cortical bone= +1000

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200
Q

List some structures that can be seen on an CT and not on an x-ray

A

-heart chambers -right and left pulmonary artery -pulmonary trunk bifurcation -IVC

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201
Q

How is a CT image viewed and orientated

A

you are viewing the image from the persons feet up

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202
Q

What are the advantages and disadvantages of a CT chest image over CXR?

A

pros -good spatial resolution -better contrast discrimination (helped by contrast media) cons -ionising radiation exposure is greater -expensive

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203
Q

How did Garrod contribute to genetics?

A

-he formulated the one gene, one enzyme hypothesis from studying alkaptonuria -described the recessive inhiertance of enzymatic defects

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204
Q

How did Thomas Morgan contribute to genetics?

A

he discovered the white-eyed mutation in Drosophila

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205
Q

When 2 carriers of a recessive character mate what is the probability their progeny will show the recessive character?

A

1 in 4

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206
Q

What is Mendel’s First Law?

A

-parents have 2 copies of a gene for a character

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207
Q

Name some common monosomies and trisomies

A

Turners (XO) Downs syndrome (trisomy 21) Trisomy 18 Trisomy 13 Klinefelters syndrome (XXY)

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208
Q

Name an example of an incomplete dominance/50% penetrance phenotype

A

a straight haired and curly haired parents having a wazy haired child

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209
Q

List some x-linked recessive conditions

A

-red-green colour blindness -Haemophilia A -Duchenne muscular dystrophy -Lesch-Nyhan syndrome

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210
Q

What is Mendel’s second law?

A

-different characters are inherited independently (except for characters on the same chromosome=linked characters)e.g. peas can be yellow or green AND round or wrinkled

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211
Q

What is the name given to disorders that have developmental errors apparent at birth

A

congenital disorders

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212
Q

Name a congenital disorder

A

Phacomelia (shortening of limbs etc) caused by Thalidomide use for morning sickness during pregnancy

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213
Q

What is phenylketonuria?

A

-not common -recessive -lack of the enzyme phenylalanine hydroxylase -phenylalanine is not converted to tyrosine and therefore goes down another pathway -phenylalaine is converted to phenylpyruvate (a phenylketone)<

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214
Q

What is Cystic Fibrosis?

A

-most common life threatening genetic disorder in australia -3 base deletion (deletes phenylalanine 508) of the CF gene on chromosome 7 -defective or absent CFTR (chloride channel protein) -causes a build up of mucous in the lungs

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215
Q

Describe the amino acid sequence of collagen

A

-repeats of -Gly-Pro-Ala

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216
Q

What is osteogenesis imperfecta

A

-A family of diseases with defects in collagen -when glycine at position 748 mutates to cysteine it causes a kink in the triple alpha helix tertiary structure -illustrates that glycine is the only side chain that can fit into the small space

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217
Q

Name 2 condition that has defects in the structure, production or processing of collagen, or the proteins that interact with it

A

-Ehlers Danlos Syndrome (autosomal dominant) -Marfans Syndrome (fibrillin 1 gene- FBN1 is mutated)

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218
Q

Describe the cause of Albinism

A

-defect in tyrosinase -tyrosine is not converted to DOPA therefore no melanins are made -tyrosinase begins the cascade of pigment pathways

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219
Q

Describe the cause of Sickle Cell Anaemia

A

-one base change T–> A -one aa change Glutamic acid (hydrophilic) –> Valine (hydrophobic) -Val binds to the hydrophobic pocket formed when Hb is deoxygenated–> formation of an insoluble crystalline structure -however if can confer a survival advantage in Africa because it is protective against Malaria

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220
Q

Describe the cause of Porphyria

A

-failure of haem synthesis feedback inhibition (failure of negative feedback) -blistered, light damaged hands -patients plasma fluresces red in UV light

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221
Q

The majority of haemoglobinopathies are inherited in what pattern?

A

autosomal recessive

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222
Q

Describe the chains of adult haemoglobin (HbA)

A

2 alpha chains2 beta chains

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223
Q

On what chromosome are the alpha like globin chains found?

A

chromosome 16

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224
Q

On what chromosome are the beta like globin chains found?

A

chromosome 11

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225
Q

What are the 3 embryonic haemoglobin proteins?

A

Zeta 2 Epsilon 2 Zeta 2 Gamma 2 Alpha 2 Epsilon 2

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226
Q

What are the chains in fetal haemoglobin?

A

alpha 2 gamma 2

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227
Q

What are the different haemoglobin proteins found in adults and what are their proportions in adult blood?

A

HbA (alpha 2 beta 2): 97.5% HbA2 (alpha 2 delta 2): 2% HbF (alpha 2 gamma 2): 0.5%

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228
Q

What are some types of haemoglobinopathies?

A

-alpha and beta thalassaemias -structural variants -HPFH

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229
Q

What is the distrubution of alpha thalassaemia?

A

-global -south east asia

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230
Q

What is the distrubution of beta thalassaemia?

A

-global -southern european -middle eastern -north africa -south east asia -india

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231
Q

What is the distrubution of sickle cell disease?

A

-west and central africa -middle east -india

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232
Q

Briefly describe alpha thalassaemia

A

-decreased synthesis/deficiency of alpha globin chains -caused by large deletions -it affects both fetal and adult Hbs -homotetramers of gamma 4 and beta 4 separately form (less soluble) -the probability of your child inheriting the trait depends on the carriers genotype

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233
Q

Briefly describe beta thalassaemia

A

-decreased synthesis/deficiency of beta globin chains -caused by point mutations (promoter mutations, RNA splicing mutations, mutations in RNA stability and processing, nonsense mutations and frameshift mutations) -causes reduced or no beta globin chain

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234
Q

Describe the pathophysiology of untreated beta-thalassaemia

A

-ineffective erythropoiesis -increased iron absorption from gut -systemic iron overload -splenomegaly -anaemia -tissue anoxia -erythropoietin increase (extra medullary erythropoiesis–>bone marrow expansion, skeletal deformities, hepatomegaly) -frontal bossing -thinning of long bones -hair on end appearance of the skull

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235
Q

Describe what you would see on a blood film from someone with beta thalassaemia.

A

-poikilocytotic cells (abnormal shaped) -anisocytotic cells (irregularly sized) -tear drop shaped cells -hypochromic cells (pale) -microcytic cells (small) -target cells

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236
Q

What is beta thalassaemia minor

A

-the heterozygous (carrier) state for beta thalassaemia -they exhibit changes in blood parameters but are asymptomatic

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237
Q

Describe some treatments for beta thalassaemia

A

-blood transfusions -iron chelation therapy (orally) -splenectomy -hormone replacement therapy -bone marrow transplant (the only cure!)

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238
Q

Describe the pathophysiology of sickle cell anaemia

A

-caused by a point mutation A–> T -aa change Glu–> Val -anaemia -weakness -failure to thrive -splenomegaly -repeated infections -biconcave erythrocytes of HbS tetramers–> reversible sickle –> irreversible sickle–> increased adherance to endothelium–> thrombosis of small blood vessels

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239
Q

Describe the blood parameters in sickle cell disease

A

Homozygous SCD: -MCV/MCH may be normal or reduced -Hb significantly reduced -HbS seen, HbA absent Heterozygous SCD: -MCV/MCH may be normal or reduced -Hb slightly or reduced -HbS seen

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240
Q

What is the term given when an individual has two different mutations?

A

compound heterozygote e.g. two diff types of beta globin mutations or a beta thalassaemia mutation and a sickle cell mutation

241
Q

What are some future therapies for haemoglobinopathies?

A

-RNAi to alter the imbalance of the chains -epigenetic modifications by small molecules to induce HbF (HPFH) -gene therapy using induced pluripotent stem cells

242
Q

What are the main types of dyslipidaemias?

A

-hypercholesterolaemia -hypertriglyceridaemia -mixed hyperlipidaemia

243
Q

What is dyslipidaemia?

A

-abnormal lipid profile -it can lead to atherosclerosis and an increased risk of MI and stroke

244
Q

What are some treatments for dyslipidaemia

A

-treat secondary causes (obesity, diabetes, hypothyroidism) -manage modifable risk factors (smoking, alcohol, weight, exercise, diet) -drugs

245
Q

List some drug treatments for hypercholesterolaemia and mixed hyperlipidaemia.

A

-statins -bile acid sequestrants/resins -ezetimibe -nicotinic acid/niacin

246
Q

List some drug treatments for hypertriglyceridaemia

A

-fibrates -fish oils

247
Q

What are the main sources of cholesterol?

A

-diet (animal fat, eggs) -de novo synthesis in the liver

248
Q

In what forms can cholesterol be transported in?

A

-chylomicrons -VLDL -IDL -LDL -HDL

249
Q

Where and in what form is cholesterol stored?

A

cholesterol is converted to bile acids to be stored in the gall bladder

250
Q

What is the function of lipoprotein lipase?

A

-hydrolyses the triglycerides to release FFA -FFA are then taken up into adjacent tissue and used as a source of E

251
Q

Lipoproteins must contain ______ to be able to transport lipids into artery walls.

A

apo B-100

252
Q

Describe the action of statins. Name some examples.

A

-HMG-CoA reductase inhibitors -decrease mevalonic acid and therefore cholesterol synthesis -causes an increase in hepatic LDL receptors -increased clearance of LDL -decreased plasma total cholesterol and LDL -increased plasma HDL e.g. lovastatin, atorvastatin, fluvastatin, pravastatin, simvastatin

253
Q

What are some precautions for statins

A

-avoid grapefruit juice -drug- drug interactions -levels are increased by some ABs, anti fungals, fibrates -levels are decreased by phenytoin, barbiturates, glitazones -elevates serum aminotransferase -minor increase in creatin kinase –> muscle pain and tenderness -contraindicated in pregnancy because of impaired fetal myelination

254
Q

What are some adverse effects of statins?

A

-mild GI symptoms -headache -insomnia -dizziness -myopathy (rare) -rhabdomyolysis (rare) -renal failure (rare) -hepatitis, liver failure (rare)

255
Q

Describe the action of bile acid sequestrants/resins and name some examples.

A

-oral route -non-absorbable marcomolecules that bind bile acid and prevent gut absorption -upregulation of hepatic LDL receptors -removal of LDL from plasma -increased cholesterol metabolism

256
Q

What are some adverse effects of bile acid sequestrants/resins?

A

-abdominal discomfort -bleeding -constipation -flatulence -increased TGs (rare) -faecal impaction (rare) -decreased absorption of fat soluble vitamins (rare) -decreases absorption of other drugs therefore you must give other drugs hours before or after resin

257
Q

Describe the action of ezetimibe

A

-specifically inhibits dietary cholesterol absorption in the intestine -binds to a sterol transporter -lowers LDL -doesn’t effect absorption of bile acids, fat soluble vitamins or the absorption of other drugs NB it can be used alone in statin intolerant patients or in combination with other agents

258
Q

What are some adverse effects of ezetimibe?

A

-diarrhea -headache -tiredness -allergic rxns -severe joint or stomach pain

259
Q

Describe the action of nicotinic acid/niacin

A

nicotinic acid= niacin= vit B3-mechanism is unclear -decreased secretion of VLDL from liver -reduces plasma LDL and triglycerides -increases HDL -lowers athrogenic lipoprotein a NB: not widely used. only used in combination

260
Q

What are some adverse effects of nicotinic acid/niacin?

A

-vasodilation -flushing (tolerance develops) -hypotension -nausea -vomiting -itching (rare) -glucose intolerance (rare) -uric acid retention (rare) -increase hepatic impairement (rare)

261
Q

Describe the action of fibrates and name some examples

A

-agonists at nuclear receptors -regulates gene expression of PPAR alpha -increased synthesis of lipoprotein lipase -increased lipolysis of triglycerides -reduction in plasma triglycerides -increase in HDL -used as an adjunct to dietary changes e.g. gemfibrozil, fenofibrate

262
Q

What are some common adverse effects of fibrates?

A

-mild elevation of serum aminotransferase -nausea -dry mouth -headache -rash -arrhythmias (rare) -gall stones (rare) -photosensitivity (rare) -impotence (rare) -depression

263
Q

Describe the action of fish oils in hypertriglyceridaemia

A

-reduce triglycerides and VLDL -increase HDL

264
Q

What are some adverse effects of fish oil use for hypertriglyceridaemia?

A

-aftertaste -diarrhea -abdominal discomfort -blood thinning effect

265
Q

Define ischaemic heart disease

A

an imblanace between myocardial oxygen supply and demand

266
Q

List the acute coronary syndromes

A

-unstable angina-myocardial infarction-sudden cardiac death

267
Q

List the chronic coronary syndromes

A

-stable angina-chronic myocardial ischaemia

268
Q

Coronary artery BF depends on what factors?

A

-perfusion pressure-coronary vascular resistance-external compression-intrinsic/metabolite regulation

269
Q

List the coronary artery branches

A

LM –>LAD and LCXRCA –> PD

270
Q

The anterior wall and 2/3 of the septum is supplied by

A

LAD

271
Q

The lateral wall is supplied by

A

LCX

272
Q

The posterior wall and 1/3 of the septum is supplied by

A

PD

273
Q

What is a heart attack?

A

a myocardial infarction

274
Q

What is the most common cause of myocardial infarction?

A

-acute plaque event with rupture or haemorrhage -occlusive thrombosis

275
Q

What are some other causes of myocardial infarction?

A

Non atherosclerosis -coronary artery dissection -thrombosis due to vasculitis -thromboembolism from the heart Reduced flow/oxygenation -hypotension -rapid tachycardia -hypoxaemia

276
Q

What are the main steps in the development of a myocardial infarction?

A

-Angina/reversible injury (within 30mins) -irreversable injury (past 30mins) (maybe ECG changes, intracellular changes, loss of contractility) -complications (arrhythmia, cardiac failure) -cell death -haemorrhage -oedema -necrosis and early acute inflammation (1 day) (tiger stripes) -acute inflammation (3 days) (yellowing of wall) -end of acute inflamm and start or early granulation (7 days) (macrophages ingest dead myocytes, fibroblasts produce collagen) -further complications (same as above plus mural thrombus, rupture, pericarditis, aneurysm) -early and late granulation tissue (8 weeks) (initial high cellularity and vasculariy then gradual reduction in cells and vessels with increasing collagen, grey white colour) -fibrosis/scar (8 weeks and beyond)

277
Q

What are the main types of angina? And what are the main differences between the 2?

A

stable angina -chest pain on exertion -due to atherosclerotic narrowing or endothelial dysfunction unstable angina -chest pain at rest or on exertion -due to acute plaque event or coronary artery thrombosis -it resolves -no irreversable damage occurs

278
Q

What is Chronic Myocardial Ischaemia?

A

-chronic atherosclerotic narrowing of vessels leading to -small areas of subendothelial ischaemia -patchy myocyte necrosis -replacement by fibrosis

279
Q

What is sudden cardiac death?

A

-unexpected death due to cardiac causes in a short time period of onset of symptoms in a person with no previous diagnosis of a fatal condition -the majority is due to ischaemic heart disease (an early arrythmic event or complications of a silent myocardial infarction) -other causes are –anomalous coronary arteries –LV hypertrophy –floppy mitral valve –cardiomyopathy –cardiac condution syndrome

280
Q

Define health

A

The state of complete physical, mental and social well being and not merely the absence of disease or infirmity

281
Q

Define Global Health

A

-An area of study that places priority on improving health and achieving equity in health for all people worldwide. -it involves determinants and solutins -it involves many disciplines -promotes interdisciplinary collaboration

282
Q

List some social determinants of health

A

-The social gradient -Stress -Early start -Social exclusion -Work -Unemployment -Social Support -Addition/substance depenenc -Food -Transport

283
Q

What are the 4 stages of the health transitions?

A
  1. pestilence and famine (malnutrition and infectious diseases predominate) 2. receding pandemics (improved nutrition, ppl live long enough to experience chronic disease) 3. degenerative and man made diseases (increased tobacco and alcohol use, death due to chronic conditions overtakes infectious diseases) 4. delayed degenerative diseases (CVD and cancer are the leading causes of death)
284
Q

What are some factors that more unequal countries have over equal countries?

A

-worse child bearing -lower levels of trust -higher prevalence of mental illness -more drug use -higher infant mortality rates -greater adult obesity -lower education -increased school drop outs -higher teenage birth rates -more homicides -more conflict between children -higher rate of imprisonment -greater social mobility -poorer innovation -lower levels of recycling

285
Q

What are some roles of the kidney?

A

-regulation of water and electrolyte balance -endocrine functions -excretion of endogenous waste -excretion of exogenous waste

286
Q

What are the 2 main ways drugs are eliminated?

A

-metabolism in the liver -excretion in the kidney

287
Q

What are the classes of diuretics?

A

-loop diuretics -thiazide diuretics -potassium sparing diuretics -osmotic diuretics

288
Q

How do diuretics generally work?

A

-decrease Na+ and Cl- reabsorption -increased NaCl excretion -secondary water excretion

289
Q

What is a name of a drug that affects urine pH?

A

sodium bicarbonate(can be used to treat asprin overdose)

290
Q

What is a name of a drug that alters secretion of organic molecules in the kidney?

A

-probenecid (inhibits the secretion of banned substances in sport)

291
Q

How do loop diuretics work?

A

-most powerful of the diuretics -act on the thick acsending limb of the loop of henle -inhibits Na+/K+/2Cl- cotransporter -reduces hypertonicity of the interstitium (reduced osmotic P in the interstitium, reduced water reabsorption) -increases Na in the distal tubule (increased osmotic P in tubule, reduced water reabsorption) -well absorbed from the gut -plasma protein bound -duration of action= 3-6hrs

292
Q

What are some adverse effects of loop diuretics?

A

-K loss from distal tubule–> hypokalaemia -H excretion–> metabolic alkalosis -reduced ECF–> hypovolaemia and hypotension

293
Q

What are some clinical uses of loop diuretics?

A

-salt and water overload in(acute pulmonary oedema, chronic HF, ascites, renal failure) -hypertension

294
Q

How do Thiazide diuretics work?

A

2 types: -true thiazides -thiazide-like drugs -act on the distal conveluted tubule (they act more distally than loop diuretics) -inhibit Na+/Cl co-transporter -orally active -excreted in the urine -max effect= 4-6 hrs -duration 8-12 hours

295
Q

What are some adverse effects of thiazide diuretics?

A

-K loss from collecting ducts -increased plasma uric acid

296
Q

What are some clinical uses of thiazide diuretics?

A

-hypertension -severe resistant oedema

297
Q

How do potassium sparing diuretics work?

A

-limited diuretic effect -used in combination with K loosing diuretics to prevent K loss -there are 2 subclasses: (spironolactone) and (triamterene and amiloride) -act on the collecting tubule and ducts -Spironolactone: aldosterone receor antagonist therefore reduced activation of Na channels -Triamterene and amiloride: blocks luminal sodium channels therefore inhibits Na reabsorption

298
Q

How do osmotic diuretics work?

A

-they are pharmacologically inert -they are filtered but not reabsorbed -affects water permeable parts of the nephron (proximal tubule, descending limb of loop, collecting tubules) -reduces passive water reabsorption -minor effect on Na reabsorption

299
Q

What are some clinical uses for osmotic diuretics?

A

-for raised intracrainal P and raised intraocular P -prevention of acute renal failure

300
Q

Why is the kidney susceptible to toxicity?

A

-because it receives 25% of the blood supply (it sees a lot of drugs) -the kideny concentrates things and is therefore exposed to concentrated amounts of drugs -the kideny is able to carry out metabolism which generally produces reactive metabolites Mechanisms of damage is via direct or formation of metabolites -ROS -interference ith Ca metabolism -protein/enzyme binding

301
Q

T/F There is a positive correlation between blood LDL cholesterol levels and the risk of heart disease

A

TRUE

302
Q

T/F there is an inverse correlation between HDL cholesterol level and risk of heart disease

A

TRUE

303
Q

What are the different fates of cholesterol made in the liver?

A

-transport (assembled into VLDL for transport to tissues) -bile acids (stored in gall bladder to emulsify fats) -steroid hormones and vit D -membranes (makes them less fluid)

304
Q

Briefly outline cholesterol synthesis

A

-Aceytl-CoA is generated in the mitochondria–> HMG CoA –> mevalonic acid by HMG-CoA reductase–> cholesterol -cholesterol negatively feedsback to inhibit HMG CoA reductase

305
Q

How is cholesterol carried from one site in the body to another?

A

cholesterol is not soluble in aqueous medium and is therefore esterified (makes it more hydrophobic) and incorporated into protein/lipid composites called lipoproteins

306
Q

Describe the composition of chylomicrons

A

-triacyglycerol and cholesterol-ester from the gut -B-48 -ApoE -ApoCI,II and III -ApoA I, II, III, IV, V

307
Q

Describe the composition of VLDLs

A

-triacyglycerol and cholesterol-ester from the liver -ApoB-100 -ApoE -ApoC I, II, III -ApoA-V

308
Q

Describe the function and composition of HDL

A

-scavenges free cholesterol from membranes and cells -stops macrophages from becoming foam cells -ApoA-I (2 molecules of this make a hydrophobic ring to round up cholesterol-ester and phospholipids to mature into HDL)

309
Q

What enzyme is present in the liver to help form VLDL from cholesterol?

A

ACAT (acyl-CoA-cholesterol acyl transferase)

310
Q

What enzyme is present in the plasma to help HDL scavenge cholesterol from membranes?

A

LCAT (lecithin-cholesterol acyl transferase)

311
Q

Describe the basic steps in the pathogenesis of atherosclerosis

A

-oxidised LDL accumulates in an artery wall -endothelial cells upreg adhesion molecules -monocytes and T cells invade the tissue and secrete cytokines -macrophages take up the oxLDL using scavenger receptors–> foam cells -fibrous tissue develops to trap the foam cells -foam cells produce TF which can –> blood clot and then rupture of the plaque

312
Q

What is a main adverse effect of statin use?

A

-depletion of Q10=ubiquinone=Coenzyme Q -its involved in mitochondrial bioenergy transfer -depletion can cause skeletal and cardiac muscle complications -NB supplements of Q10 do not appear to be effective in alleviating myotoxicity

313
Q

What are the key outcomes from clinical trials?

A

-relative measures of intervention effect (relative risks, hazard ratio) -absolute measures of intervention effect (absolute risk/rate reduction, NNTT) -survival analysis

314
Q

What does randomisation mean in experiments?

A

-random allocation of subjects into each arm of a clinical trial/intervention -aim= the treatment groups are identical in all aspects other than the intervention and reduces confounding -i.e. they have the same confounders.

315
Q

What is information/measurement bias?

A

-the systematic differences in the way info is collected between/among groups being compared -arises when there is variability in methods for collecting info -subtype= recall bias

316
Q

How do you deal/minimise information bias?

A

ensure the methods for collecting info are uniform -use a standardised tool Blinding= non awareness of intervention allocation -single blind= subjects or investigators unaware -double blind= subjects and investigators unaware

317
Q

What is selection bias?

A

-systematic differences in characteristics of subjects selected for study and those not selected PLUS differences in characteristics of subjects within groups being compared

318
Q

How do you deal/minimise selection bias?

A

Careful recruitment -representative sample -obtain cases and controls from the same source Maximise response Minimise loss to follow up use ITT analysis -assume subjects remained in the randomised group they were allocated in, regardless of if they crossed over or if they drop out -it always under-estimates any treatment effect (b/c cross over introduces overlap in treatment between groups)

319
Q

What is NNT?

A

Number needed to treat= number of ppl needed to undergo the intervention in order to prevent the outcome in one person -its a marker of efficiency of the intervention NNT= 1/ (absolute risk or rate reduction)

320
Q

What does a Kaplan-Meier curve show?

A

-plot of hazard or survival vs time -its a survival analysis -captures outcomes at their time of occurrence -NB survival= avoidance of event not avoidance of death

321
Q

Define hypertrophy

A

-increase in the size of cells resulting in an increase in size of an organ -increased production of intracellular structures -nucleus increases in size and can change shape -permanent cells take this pathway -stimuli= mechanical stress, GFs, hormones

322
Q

Define hyperplasia

A

-an increase in the number of cells -stem cells are stimulated to divide by hormone or GFs -can be physiological or pathological -labile or stable cells take this pathway -often occurs at the same time as hypertrophy

323
Q

Name an example of physiological hyperplasia

A

Endometrium during menstruation changes

324
Q

Name an example of pathological hyperplasia

A

parathyroid hyperplasia -loss of fat cells replaced by cells

325
Q

Name an example of mixed hypertrophy and hyperplasia

A

Graves Disease -increase in cell size -cuboidal cells change to columnar cells -loss of colloid

326
Q

Define metaplasia

A

-a reversible change in which one adult cell type is replaced by another adult cell type (change in apperance) -occurs frequently at junctions between diff epithelial types e.g. cervix, glandular meeting squamous -stimulus= altered enviro -new phenotype can be protective against injury or it can have no added benefit -can be physiological or pathological

327
Q

Name an example of physiological metaplasia

A

At the onset of menarche, swelling of the tissues exposes the endocervical mucosa to the acidic vaginal environ. Simple columnar epithelium–> stratified squamous epithelium

328
Q

Name an example of pathological metaplasia

A

-Barrett Oesophagus (Gastro-oesophageal reflex disease) Bile acids induce metaplasia of the oesophageal stratified squamous epithelium –> intestinal type columnar with mucus secreting goblet cells (flat hat–> large hat)

329
Q

Define neoplasia

A

-dysregulated/ unregulated cell division -that can occur in the absence of a stimulus -due to genetic mutations (genome is changed) -can be benign or malignant

330
Q

Define atrophy

A

-a decrease in cell or organ size -occurs when a normal growth stimulus is decrease or lost -reversible if not accompanied by cell death or fibrosis -stimulus= decreased workload, diminsed blood supply, loss of innervation, loss of hormonal stimulation, aging

331
Q

Name an example of atrophy

A

Loss of calf muscle due to disuse Atherosclerosis in the aging brain

332
Q

What are the 2 main broad categories of myocardial hypertrophy?

A

Physiological/developmental -growth of ventricle wall in proportion to the chamber -increased cap density -no loss of systolic or diastolic function -reversible Pathological -growth of ventricle wall with reduced or enlarged cavity -switching on fetal/embryonic genes -reduced function and –> cardiac failure -depoisition of matrix -doesn’t regress

333
Q

What are the 2 main patterns of myocardial hypertrophy?

A

Concentric -increased work without stretch -increased pressure -increase diam of the wall with a reduction of the lumen Eccentric -increased work with stretch -increased volume -increase in the diam of the lumen but the walls can be thin and long

334
Q

What is the normal thickness in mm of the LV and RV? And what is the normal weight of the heart?

A

LV = 15mm RV= 5mm Men >500g Women >400g

335
Q

What is the histological apperance of myocardial hypertrophy?

A

-enlarged rectangular nuclei -bi-nucleated myocytes -increased CT

336
Q

What are some causes of myocardial hypertrophy?

A

-HT -ischaemic heart disease -valvular disease -hypertrophic obstructive cardiomyopathy -amyloid

337
Q

What are some complications of myocardial hypertrophy?

A

-ischaemia -fibrosis -cardiac failure -arrhythmias -death

338
Q

Describe dystrophic calcification in the tricuspid aortic valve

A

-congenital bicuspid aortic valve predisposes to degenerative calcific changes -calcium and fibrosis balls -valves are still relatively normal -can cause aortic stenosis

339
Q

Describe myxomatous mitral valve

A

-aka floppy mitral valve -chordae tendinea not affected -big, bulgy leaflets -can be inherited or caused by CT disease -causes mitral valve prolapse -causes mitral regurgitation

340
Q

Describe acute rheumatic fever

A

-typically occurs in children -caused by streptococcus pyogenes -small number develop into carditis

341
Q

Describe rheumatic heart disease

A

-aberrant imm response to heart valves because of molecular mimicry of streptococcus Ag -fibrosed/thickening of whole valve -can affect all valves -causes stenosis or regurgitation -most common cause of mitral stenosis

342
Q

What are some valvular disease complications?

A

-altered cardiac BF (angina, syncope, myocardial hypertrophy, HF, arrhythmia) -thrombosis -infective endocarditis

343
Q

Describe infective endocarditis

A

-vegetations are present -looks like calcification but its not! -its softer because its thrombus not calcification -rest of the valve is not affected -valve is eaten away by the bacteria -present with fever, onset or worsening of a murmer, symptoms of embolism -bac get into blood stream via dental work, invasive procedures, IV drug use

344
Q

The heart sounds are due to what?

A

The valves closing

345
Q

What is the formula for the ejection fraction?

A

EF= SV/EDV it should be ~50% in normal ppl

346
Q

Describe valve stenosis

A

-narrowing -valve doesn’t open fully -there is restriction of glow -a P gradient across the valve exists -higher P in the chamber behind the valve e.g. LV in aortic stenosis, LA in mitral stenosis -P overload

347
Q

Describe valve incompetence

A

-aka regurgitation or leaking -valve doesn’t close fully -blood leaks back into previous chamber -heart required to pump SV to maintain CO -greater vol in ventricle–> increase EDV -increased EF -volume overload

348
Q

Desribe what turbulence is.

A

-high flow of blood over stenosed or impotenet valves -it causes murmurs

349
Q

Describe what valvular heart disease is

A

-mostly due to degnerative conditions -it used to be caused by previous rhematic fever but now this is uncommon except in NT, asia, and africa -occassionally its congenital -cardiac compensation is effective but it will eventually fail -symptoms (SOB) are a late feature and indicate poor prognosis -in regurgitation: irreversible LV changes occur at the time symtoms dev -in aortic stenosis: symptoms indicate the time to intervene

350
Q

How do you assess for valvular heart disease?

A

-Hx -examination (pulse, murmur) -ECG -Echocardiography (shows LV changes)

351
Q

What are some interventions for valvular heart disease?

A

-valve replacements (metal, plastic, bioprostheses) -valve repair -balloon valvotomy -stent valves

352
Q

Describe aortic stenosis and the compensatory mechanisms involved

A

-progressive narrowing of the aortic vavle by fibrosis and calcification -reduction in valve area -introduces a P gradient across the valve -P gradient rises during systole and then decreases towards to end of systole -P overload of the LV compensation (LV concentric hypertrophy) -wall thicken and stiffen -diastolic dysfunction -increased LV EDP required to fill the LV -atrial contraction becomes important to fill the LV -murmur= crescendo decrescendo (diamond shape) between S1 and S2 -changes often reverse with surgery

353
Q

Describe aortic regurgitation and the compensatory mechanisms involved

A

2 main mechanisms -aortic leaflets are damaged due to endocarditis or rheumatic fever -aortic root is dilated –> leaflets don’t close due to Marfans syndrome, Aortic dissection, collagen vascular disorders or syphilis -part of each SV leaks back into LV during diastole -to maintain CO, LV has to pump an increased SV -volume overload Compensation (LV dilation) -increased EDV -increased SV -increased EF -increased PP -reduced aortic diastolic P = collapsing pulse -normal ESV -early diastolic murmer (blowing sound) immediately after S2 -no symptoms if mild or moderate

354
Q

Describe what happens during decompensation in aortic regurgitation

A

-LV diastolic vol increases -LV function deceases -LV systolic vol increases -these are all irreversable changes

355
Q

What are some causes of mitral regurgitation

A

Causes include: -myxomatous degeneration (mitral valve prolapse) -ruptured chordae tendinae -infective endocarditis -MI -rheumatic fever -collagen vascular disease -cardiomyopathy= secondary mitral regurgitation

356
Q

Describe mitral regurgitation and the compensatory mechanisms involved

A

-portion of SV leaks back into the low pressure LA -to maintain CO LV has to pump greater SV -volume overload compensation (LV dilation) -increased EDV -increased SV -increased EF -normal ESV -increased LA P and vol–> atrial fibrillation, thrombus in LA, increased pulmonary venous P and artery P -systolic murmur (same intensity all the say through systole) between S1 and S2 decompensation -marked increase in LV diastolic vol -reduced EF -increased LV systolic vol -changes are irreversible

357
Q

Describe mitral stenosis and the compensatory mechanisms involved

A

-due to previous rheumatic fever -fibrotic, narrowed mitral valve -P gradient across mitral valve -reduced filling of LV -LA contraction is important -LV systolic function is NOT affected compensation (LA dilation and increased P) -increased LA P and volume can –> atrial fibrillation and thrombus -increased pulmonary venous and artery P -murmur= low pitch long sound in diastole interventions= valvotomy or valve replacement

358
Q

What is the difference between a clot and a thrombus?

A

A thrombus forms in vivo (inside someone) and a clot forms in static blood in vitro (in the lab)

359
Q

Define thrombosis

A

The pathological formation of a haemostatic plug in a blood vessel in the absence of blood loss

360
Q

Define arterial thrombus

A

-white thrombus -platelets and WBCs in a fibrin mesh -associated with atherosclerosis -breaks off–> blood vessel obstruction

361
Q

Define venous thrombus

A

-red thrombus -fibrin, platelets and RBCs -usually associated with blood stasis eg DVT with travel -breaks off–> embolus lodging in lungs or brain

362
Q

Define thromboemolus

A

A blockaged in a blood vessel caused by a dislodged thrombus

363
Q

Describe the mechanism of vasoconstriction in response to damage to a blood vessel

A

-collagen is exposed -platelets stick to collagen and activate -ADP and 5-HT (powerful vasoconstrictor) are released from platelets

364
Q

Describe the mechanism of platelet activation and adhesion in response to damage to a blood vessel

A

-ADP from activated platelets causes others to activate and change shape -granule contents are secreted (ADP and 5-HT) -mediators are synthesised (TXA2) -platelets aggregate via fibrinogen bridging between GPIIb/IIIa receptors -a soft plug is formed

365
Q

What are some stimuli for platelet activation?

A

-collagen -ADP -thrombin -thromboxane

366
Q

Describe the mechanism of fibrin deposition in response to damage to a blood vessel

A

-the extrinsic or intrinsic pathway activates prothrombin–> thrombin extrinsic= in vivo, damaged tissues release thromboplastin intrinsic= in vitro, exposed collagen or other, negative charges -thrombin convertes fibrinogen–> fibrin

367
Q

What are 2 ways to control blood coagulation?

A

-enzyme inhibitors e.g. antithrombin III -fibrinolysis by plasmi

368
Q

What are some drugs affecting fibrin formation?

A

-procoagulant drugs (vit K) -injectable anticoagulants (heparin, LMW heparin) -oral anticoagulants (warfarin, direct thrombin inhibitors, direct factor Xa inhibitors, indirect factor Xa inhibitors)

369
Q

Describe the mechanism of heparin

A

-enhances activity of antithrombin III -AT III normally inactivates Xa and thrombin -heparin binds to AT III to expose the active site

370
Q

Describe the mechanism of action of LMW heparin

A

-same effect on factor Xa but less effect on thrombin

371
Q

Describe the mechanism of action of warfarin

A

-coumarin derivative -inhibits the reduction of vit K –> inhibiting gamma carboxylation of glutamate in factors II, VII, IX, X -used for prolonged therapy -only active in vivo -doesn’t affect already active factors!! adverse effects -haemorrhage

372
Q

Describe the prothrombin time (PT)

A
  • time for clot formation of plasma after addition of Ca2+ and TF -measures the extrinsic pathway
373
Q

Describe the international normalised ratio (INR)

A

-ratio of patient PT to normal PT

374
Q

Describe some new anticoagulant agents

A

-Indirect Factor Xa inhibitors -Direct Factor Xa inhibitiors (apibaxan, edoxaban, Rivaroxaban) -direct thrombin inhibitors (dabigatran) -LMW -oral -fixed doses therefore better compliance -still in clinical trials

375
Q

What are 3 main classes of drugs that affect platelet activation and adhesion?

A

-ADP receptor antagonists e.g. clopidogrel -Thromboxane synthesis inhibitors e.g. COX inhibs ie asprin -GP IIb/IIIa receptor antagonists e.g. abciximab, tirofiban NB: you use these platelet inhibitors in conjunction with asprin

376
Q

Name 2 drugs that are fibrinolytic

A

-Streptokinase -Alteplase

377
Q

What are some symptoms of a failing heart?

A

-fatigue -oedema -SOB -palpitations

378
Q

Describe the action of digoxin on myocytes

A

-it inhibits the Na+/K+ ATPase pump -thereby increasing intracellular Na and decreases Ca -increases Ca in SR -so there is an increased amount of Ca released with each AP –> increased contractility

379
Q

Describe the use of glycosides in heart faliure

A

-marrow therapeutic index -affects all excitable tissues (gut, CNS, cardiac) -used for short term -used for symptomatic relief -long half life -high Vd due to high affinity for binding to muscle -increases contractility e.g. digoxin

380
Q

Describe the use of beta adrenoceptor agonists for heart failure

A

-they increase contractility -IV -short term for acute HF or cardiogenic shock -increases the risk of arrhythmias, increases cardiac work and O2 demand -can lead to loss of beta 1 sensitivity and therefore decreased symapthetic drive e.g. NA and Adr (alpha and beta non selective) dobutamine (beta 1 selective)

381
Q

Name a phosphodiesterase inhibitors for heart failure

A

-Amrinone

382
Q

Describe the use of inotropes in heart failure

A

-they increase contractile force -symptomatic relief -with long term use HF symptoms progress and you can get cardiac remodelling

383
Q

What are some classes of drugs used in heart failure that cause preload reduction

A

-venodilators -diuretics -aldosterone receptor antagonists -aquaretics

384
Q

What are the aims of treatment for HF?

A

-decrease cardiac work -improve cardiac function -reduce signs and symptoms -increase survival

385
Q

Why is the use of beta adrenoceptor antagonists for HF considered counter-intuitive therapy?

A

-because you want to increase contractility in HF which you can achieve by giving beta agonists -antagonists blocks beta 1 receptors but SV increases and cardiac work decreases -SV increases because afterload decreases (beta 1 and alpha 1 antagonists do this by causing vasodilation) -cardiac work decreases because HR decreases, renin release is inhibited, vasodilation occurs -also protects against receptor downreg

386
Q

What classes of drugs cause symptomatic relief for HF?

A

-inotropes -diuretics -venodilators

387
Q

What classes of drugs cause reduced mortality for HF?

A

-angiotensin inhibitors -beta adrenoceptor antagonists -aldosterone antagonists

388
Q

Name some alternatives to drugs for treating HF

A

Surgical -pacemakers -defibs -valve replacement -heart transplant Lifestyle changes -reduce salt, fluid, alcohol intake -stop smoking -exercise

389
Q

What is the role of tissue plasminogen activator?

A

-binds to fibrin and activates plasmin -plasmin then breaksdown the fibrin clot

390
Q

What drug is used to prevent arterial thrombosis?

A

Asprin because its a white thrombus (has high concs of platelets)

391
Q

What drug is used to prevent venous thrombosis?

A

warfarin because its a red thrombus (high conc of blood cells)

392
Q

Name a genetic cause of abnormal blood coagulability

A

-factor V leiden mutation

393
Q

Name some non genetic causes of abnormal blood coagulability

A

-oestrogen (OCP, pregnancy) -cancer -smoking -obesity -age

394
Q

Distinguish ischaemia from infarction

A

ischaemia= not enough blood supply infarction= tissue death due to inadequate blood supply

395
Q

Describe what a red infarction is.

A

-there is haemorrhage into a infarcted tissue due to -dual blood supply -collateral blood supply -venous infarction -reperfusion after necrosis(tissue dies then bleeds)

396
Q

Describe what a pale infarction is

A

-there is no haemorrhage into the infarcted tissue -this is due to a blocked end artery

397
Q

Why do we make semi-synthetic drugs as animicrobial agents?

A

-to alter the pharmacological properties of already naturally occuring compounts e.g. change kinetics, reduce toxicity, modify antimicrobial spectrum

398
Q

How can you classify antimicrobial agents?

A

-by source (natural or synthetic) -by mechanism of action (bacteriostatic, bactericidal) -by their pharmacological class

399
Q

Describe some antimicrobial agents that target bacterial cell walls

A

beta-lactams e.g. penicillins -binds to PBP which normally catalyse the fincal crosslinking step in the synthesis of peptidoglycan -therefore cell wall precursors accumulate in the cytosol–> autolysis glycopeptides e.g. vancomycin -bind to D-ala-D-ala -prevents the incorporation of the subunit into the growing peptidoglycan chain

400
Q

Name some antimicrobial agents that target bacterial cytoplasmic membrane

A

Polymyxins Polyenes

401
Q

Name some antimicrobial agents that target bacterial ribosomes

A

Aminoglycosides Chloramphenicol

402
Q

Name some antimicrobial agents that target bacterial nucleic acid

A

Rifamycins Quinolones

403
Q

Name some antimicrobial agents that target folic acid

A

Sulphonamides Trimethoprim They are selective for bacteria because we cannot make folic acid

404
Q

Describe the structure of penicillin

A

Beta lactam ring plus..

405
Q

What are some characteristics of some penicillins (pen G,V, ampicillin, methicillin, flucloxacillin, carbenicillin)? (talk about the spectrum, oral efficacy and toxicity)

A

….

406
Q

Describe the basis of vancomycin resistance and name a microbe that does this.

A

-they replace the terminal D-ala with a D-lac(sugar residue) -Enterococci bacteria -VISA (vancomycin intermediate staph aureus- they are resistant) They overproduce peptidoglycan and therefore effectively mops up vancomycin -VSSA (vancomycin susceptible staph aureus)

407
Q

Describe the basis of resistance to beta-lactams

A

-expression of chromosomally encoded or plasmid encoded beta-lactamase (breaks a bond in the beta lactam ring) -altered penicillin-binding proteins (make a new PBP that doesnt bind penicillin) e.g. MRSA= methicillin resistant staphylococcus aureus, MRSE= methicillin resistant staph epidermis

408
Q

Name some drugs that act on protein synthesis by targetting recognition

A

Aminoglycosides Tetracyclines

409
Q

Name a drug that act on protein synthesis by targetting peptidyl transfer

A

chloramphenicol

410
Q

Name a drug that acts on protein synthesis by targetting translocation

A

macrolides

411
Q

Name a drug that acts on protein synthesis by targetting isoleucyl-tRNA synthesis

A

mupirocin

412
Q

Name some drugs that act on protein synthesis by targetting formation of the initiation complex

A

oxazolidones

413
Q

Name some examples of aminoglycosides

A

gentamicin tobramycin amikacin streptomycin

414
Q

Describe the basis of resistance to aminoglycosides

A

enzymatic modification of the aminoglycosides e.g. acetylation, phosphorylation, adenylation increased efflux (not specific to aminoglycosides therefore considered low level resistance and can be overcomed by increasing dose of AB) modified outer membrane to reduce entry (not specific to aminoglycosides) ribosomal mutation leading to reduced binding

415
Q

What are the main mechanisms of resistance to antimicrobial agents?

A

Drug inactivation -by hydrolysis -by covalent modification Altering the target of drug action -modify the target to a less sensitive form e.g. MRSA, D-ala –> D-lac -overproduce the target e.g. VISA Reduce access of drug to the target -reduced entry -increased efflux Failure to activate the inactive precursor of the drug e.g TB (some ABs are prodrugs)

416
Q

What are the 2 main ways bacteria are resistant to ABs?

A

-intrinsic resistance -acquired resistane (mutation or horizontal gene transfer)

417
Q

What are the 3 main ways horizontal gene transfer can occur?

A

-transformation (only between related bac) -phage mediated transduction -plasmid mediated conjugation (direct contact, can be between entirely unrelated bac)

418
Q

Briefly describe the term temperate phage

A

a phage that undergoes the lysogenic cycle -no lysis of the bac cell -phage DNA enters the host cells genome -has the potential to go to the lytic cycle

419
Q

Briefly describe the term virulent phage

A

a phage that undergoes the lytic cycle -makes lots of copies of the phage DNA and proteins -lysis of the bacterial cell

420
Q

The right and left brachiocephalic veins unit to form what?

A

the SVC

421
Q

Describe the anatomy of left brachiocephalic vein

A

-longer than the right -more horizontal course -in front of the trachea

422
Q

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Describe the anatomy of right brachiocephalic vein

A

-shorter than the left -vertical course

423
Q

Describe the course of the aortic arch

A

-upwards, backwards and to the left

424
Q

Where does the ascending aorta change its name to the arch of the aorta?

A

-at the level of the manubrio-sternal junction

425
Q

Where does the birfurcation of the pulmonary trunk lie in relation to the arch of the aorta?

A

below the arch

426
Q

What is the ligamentum arteriosum?

A

-a fibrous ligament that connects the pulmonary trunk and the aorta -its a remnant of an embryonic duct (ductus arteriosus)

427
Q

What is the ductus arteriosus?

A

-the remnant of an embryonic duct that connects the pulmonary trunk and the aortic arch

428
Q

What are the braches of the aortic arch?

A

-brachiocephalic trunk –> right common carotid artery, right subclavian artery -left common carotid -left subclavian artery

429
Q

What 2 vessels clasp the trachea in a V?

A

-left common carotid and the brachiocephalic trunk

430
Q

What is the path of the phrenic nerve?

A

-from the cervical nexus -descend onto the scalenus anterior -passes between the subclavian artery and subclavian vein -passes anterior to the lung route structures -its the most lateral structure in the mediastinum -pierces the diaphragm on each side through the cable orifice (hole in the central tendon) at the level of T8

431
Q

What is the path of the vagus nerve?

A

-intimately associated with the arch of the aorta -its a large cranial nerve -runs posterolateral to the common carotid artery -goes up to supply the neck -also goes down with the CCA and IJV -sits lateral to the aortic arch -travels with the trachea, passes behind the lung route structures onto the anterior oesophagus -the right and left vagus nerves will ramify to form an oesophageal plexus then goes through the diaphragm through the muscular hiatus at the level of T10

432
Q

At what level does the oesophagus pass through the diaphragm?

A

at the level of T10

433
Q

What is the cisterna chyli?

A

-a collection sac adjacent to the aortic hiatus in the diaphragm (at the level of T12) collects all of the lymph from below the diaphragm

434
Q

What are the branches of the descending thoracic aorta?

A

-intercostal arteries -bronchial arteries -pericardial arteries -oesophageal arteries

435
Q

How can you measure right ventricular EDP?

A

-catheter inserted via a vein across the tricuspid valve -measure JVP

436
Q

How can we measure left ventricular EDP?

A

-catheter inserted via an artery across the aortic valve -catheter inserted into the pulmonary artery will measure the pulmonary venous pressure (measure the pulmonary artery wedge pressure)

437
Q

What are the starling forces across a capillary wall?

A

-hydrostatic P forces fluid out -osmotic P (due to plasma proteins) forces fluid in

438
Q

What are some causes of oedema?

A

-increased venous pressure -decreased osmotic pressure -blocked lymphatics -increased capillary permeability

439
Q

What are the main mechanisms of cardiac failure?

A

-loss of myocardial muscle -pressure overload -volume overload

440
Q

What are the symptoms of left heart failure?

A

-SOB -fatigue -tachycardia -lung creps

441
Q

What are the symptoms of right heart failure?

A

-peripheral oedema

442
Q

What are the main mechanisms of right heart failure?

A

-global heart disease -specific right heart disease -left heart failure

443
Q

Describe concentric hypertrophy?

A

-increase in LV mass -increase in relative wall thickness–> reduces wall stress so maintains systolic funciton, CO and LV EDP -due to pressure overload -sarcomeres are in parallel

444
Q

Describe eccentric hypertrophy

A

-increase in LV mass -normal relative wall thickness therefore its dilation–> maintains SV by increasing LV EDV and EF -due to volume overload -sarcomeres are in series

445
Q

What are the 4 patterns of hypertophy?

A

-thick -dilated -thick and dilated -neither

446
Q

What are the mechanisms behind hypertrophy decompensation?

A

-LV dilation–> increase in LV EDV and LV ESV -decreased EF -reduced systolic function and CO -increase in LV EDP (increased ventricular filling) -increased LA and pulmonary vein pressure -pulmonary congestion -eventual cardiac failure

447
Q

What are the characteristics of left ventricular hypertrophy on an ECG?

A

-tall voltages of QRS -T wave inversion

448
Q

Describe what hypertrophic cardiomyopathy is?

A

-autsomal dominant disorder -mutation in sarcomere proteins -mutation in 12 genes -increased LV wall thickness espc septum -cellular hypertophy -LV outflow tract obstruction (the muscle gets in the way of the ejecting blood) -diastolic dysfunction -ventricular arrhythmias

449
Q

Describe what the athlete’s heart is

A

-wall thickness <14mm -eccentric hypertrophy -has normal cardiac function -will regress with deconditioning -heart especially the RV will enlarge -can cause ventricular arrhythmias

450
Q

List the layers of a blood vessels wall

A

-intima -media -adventitia

451
Q

Describe the tunica intima layer

A

-interacts with blood -lined by endothelium -thin layer of CT (collagen, elastin, fibroblasts) -lined by simple squamous epithelium

452
Q

Describe the tunica media layer

A

-middle layer -smooth muscle arranged concentrically/helically -constricts the lumen -smooth muscle secretes CT in which it’s embedded in (collagen type III, elastin, ground substance) -this layer is thicker in arteries than in veins (extra elastin allows pulsation BF and maintenance of BP)

453
Q

Describe the layers evident in elastic arteries.

A

elastic arteries= those closest to the heart that have to deal with the highest BP fluctuations e.g, Aorta, carotid arteries Many layers -layers of elastin in the media -they store E and compress the blood in the lumen which allows passive contraction–> BF is pulsatile but continuous

454
Q

Describe the layers in muscular arteries

A

-function= distribute blood to the tissues, contractions of its media layer regulate BP Have the normal 3 layers plus the internal and external elastic lamina -little elastin in the media -the elastin is concentrated in the internal and (external) elastic laminae

455
Q

Describe the tunica adventitia layer

A

-anchors to surrounding tissue -CT (collagen type I, elastin, ground substance, embedded fibroblasts) -has it’s own blood supply in larger vessels called vasa vasorum -thicker in veins than in arteries to contain large volumes of blood

456
Q

Define arteriosclerosis

A

-intimal damage and thickening in ARTERIES -it includes atherosclerosis -it’s common in age or with HT -arteries loose elasticity and can become narrowed -complications= impairs arteries role in controlling BP, can impair BF to downstream tissues

457
Q

Define arteriolosclerosis

A

-intimal damage and thickening in ARTERIOLES -smooth muscle cells produce too much matrix -proteins from blood leak -aka hyaline arteriolosclerosis -complications= poor BF to tissues (ischaemia), micro aneurysms and haemorrhage

458
Q

Define atherosclerosis

A

-build up of inflammatory fibrotic, necrotic and fatty material in arteries= fibroinflammatory lipid plaque=atheroma -can slowly narrow arteries or rupture

459
Q

What makes up an atheroma?

A

Fibrous cap Necrotic lipid core

460
Q

Describe the stages in the formation of atherosclerosis

A

1 fatty streaks 2 damage, inflammation, cholesterol and fibrosis 3 stable atherosclerotic plaque 4 unstable atherosclerotic plaque

461
Q

Describe the microscopic features of atherosclerosis

A

-fibrous cap -necrotic core -foam cells -cholesterol clefts -inflammatory cells -calcification -neovascularisation -narrowed lumen -thickened intima -thinned media

462
Q

What are the 2 main types of calcification

A

Dystrophic calcification -in areas of cell degeneration Metastatic calcification -serum calcium and phosphate levels are too high they reach their precipitation threshold and fall out of solution

463
Q

List some acute plaque events

A

-plaque rupture -haemorrhage into plaque -erosion of endothelium Leads to -thrombosis -thromboembolism -atheroembolism -chronic ischaemia -aneurysm

464
Q

What are the risk factors for atherosclerosis?

A

Non modifiable -age -gender -family Hx -genes -already having atherosclerosis Modifiable -HT -smoking -diabetes -cholesterol -sedentary lifestyle

465
Q

Describe the inflammatory environment in atherosclerosis

A

-oxidised LDL is taken up by macrophages which then form foam cells -these secrete ROS, MMP, cytokines to recruit more inflamm cells

466
Q

What is the role of smooth muscle in the development of atherosclerosis?

A

-smooth muscle migrate into the intima and change phenotype -proliferate -produce collagen–> thickens fibrous cap

467
Q

Define aneurysm

A

-abnormal dilation of vv -due to weakness of the media from inflammation, infection or congenital -complications= rupture, haemorrhage -morphology= saccular or fusiform -types= true aneurysm or false aneurysm (wall is broken and blood seeps out and forms the dilation)

468
Q

Describe abdominal aortic aneurysm (AAA)

A

-associated with atherosclerosis -inflamm environ weakens ECM -intimal thickening interferes with wall perfusion -rupture can occur when the dilation is above 5cm -often contains thrombus

469
Q

Describe berry aneurysm

A

-occurs in the cerebral circulation espc circle of Willis -weakening of a congenital defect -it’s the major cause of subarachnoid haemorrhage

470
Q

Describe dissection

A

-blood in the media -associated with HT -generally affects the aorta espc the ascending aorta -can compress arteries -can rupture into the pericardium–> cardiac tamponade -can rupture into the thorax–> exsanguination

471
Q

Name the 3 layers of the heart wall

A

-Epicardium -Myocardium -Endocardium

472
Q

Describe the epicardium layer of the heart wall

A

-outer layer -simple sqamous epithelium -subepicardial CT -vv -fat -nervous tissue

473
Q

Describe the myocardium layer of the heart wall

A

-cardiac muscle cells -capillaries

474
Q

Describe the endocardium layer of the heart wall

A

-inner layer -endothelial layer -subendocardial CT -conducting tissue

475
Q

Describe the histological apperance of perkinje fibres

A

-modified cardiac muscle cells (larger) -limited contractile machinery -full of glycogen -form bundles in the subendocardium

476
Q

Endothelium secretes what 2 vasoactive substances, which can on the tunica media?

A

-endothelin (vasoconstrictor) -NO (vasodilator)

477
Q

Describe the layers found in arterioles

A

Arterioles= very small arteries less than 0.1mm in diam -normal layers -have 1-3 layers of smooth muscle in the media -function= contribute most to BP changes

478
Q

Describe the transition of arterioles into capillaries

A

-arterioles–> meta-arteriole–>capillaries -meta-arterioles have an imcomplete s muscle coat -single s muscle cells act as sphincters aka precapillary sphincters to control capillary flow

479
Q

Describe the structure of capillaries

A

-less than the diam of a RBC -thin walled (1 endothelial cell)–> facilitates exchange -endothelial cell sealed with a tight junction -has a basal lamina -no smooth muscle in the media -sometimes associated with a pericyte (media) -surrounded by only a few collagen fibres (adventitia)

480
Q

Describe the structure of fenestrated capillaries

A

-walls are thinner than normal capillaries -contain pores that are often covered by diaphragms (thin membrane)

481
Q

Describe the structure of veins

A

-have the same layers as arteries -BUT the media is thinner and the adventitia is thicker–> helps withstand hydrostatic P -contains valves types of veins= larger veins, medium veins, venules,

482
Q

Describe the structure of venules

A

-little veins -function=collects blood from capillaries, exchnage across its wall and its the site of diapedesis -media is initially pericytes but is soon replaced by smooth muscle as they get bigger and closer to the heart -are affected by histamiine and cytokines

483
Q

Describe the structure of medium to large veins

A

-larger diam than arteries -subendothelial CT -adventitia enlarged often at the expense of media -sometimes you have longitudinal s muscle bundles in the adventitia= stiffening

484
Q

Describe the structure of lymphatic vessels

A

-made up of a single epithelial cell initially but by the time they get back to veins they have the normal structure of a vein -LACK RBCs -valves -the large ones look like veins

485
Q

Describe cross sectional studies

A

-sample of pop selected and information obtained AT ONE POINT/PERIOD IN TIME -NO follow up -data is collected via questionnaires, examinations, investigations -yields mostly descriptive outputs e.g. prevalence -explores associations -cheap and easy -BUT, you need a representative sample, and it doesn’t give info on temporal relationships and gives weak evidence of causality

486
Q

Describe case control studies

A

-compares previous exposure status between subjects with the outcome of interest with those subjects without the outcome -control are matched with cases by confounders -NO longitudinal follow up -but it does give info on temporal relationship bw exposure and outcome -useful for studying rare outcomes -key output= OR (approximation of RR of outcome conferred by exposure)

487
Q

What is OR and its formulae

A

OR= approximation of RR of outcome conferred by exposure OR= (odds of exposure to non exposure among cases) / (odds of exposure to non exposure among controls) OR= ad/bc

488
Q

Describe cohort studies

A

-compares outcomes between subgroups -longitudinal -follow up -collects incidence data -derives RR -gives knowledge about the temporal relationship bw exposure and outcome -types= prospective (outcome hasn’t occurred yet) vs retrospective (outcome has already occurred by the time the researcher comes in) -can include multiple exposures and outcomes -research hypothesis can be addressed post hoc -BUT its difficult to study rare outcomes, its not cheap or easy -yet cohorts can be established as part of routine clinical care

489
Q

Define bias

A

-an unintentional error that –> systematic differences between and among groups -it leads to under or over estimation of true results -types= selection bias and information/measurement bias

490
Q

Define confounding variable

A

-a variable that affects the relation between the independent and dependent varaible -it independently predicts the outcome -it can show a false correlation between the exposure and outcome when it may nor really be there or it may not be as strong as we thought

491
Q

What are some common confounders?

A

-Age -Sex

492
Q

How do you minimise confounders

A

In the design stage of a study -matching by confounders -restriction In the analysis stage of a study -restriction -stratification (analysis by subgroups) -multivariate analysis

493
Q

What study type is most susceptible to confounders?

A

observational studies

494
Q

HT is defined as

A

BP >140/90 mmHg

495
Q

What are some RFs for HT

A

-smoking -diet -weight -stress

496
Q

What are the main anti-hypertensive drugs?

A

ABCD and others A= angiotensin system inhibitors B= Beta adrenoceptor antagonists C= Calcium channel blockers D=Diuretics Others= alpha (1+2) adrenoceptor antagonists, vasodilators, renin inhibitors

497
Q

What are the main types of angiotensin system inhibitors used as anti-hypertensives?

A

ACE inhibotors Angiotensin receptor antagonists

498
Q

Describe the use of ACE inhibitors in the treatment for HT.

A

-‘prils’ -inhibit the conversion of ang I–> ang II -decreases vasulcar tone, decreased aldosterone production, decreases cardiac hypertrophy, decreased Na and water reabsorption -prevents bradykinin breakdown

499
Q

List some ACE inhibitors

A

captopril enalapril perindopril ramipril

500
Q

What are some adverse effects of ACEinhibs?

A

-first does hypotension -dry coug -loss of taste -hyperkalaemia -acute renal failure -itching, rash, angiooedema -foetal malformations

501
Q

Describe the use of Ang receptor antagonists in the treatment for HT.

A

-‘sartans’ -blockage of AT1 receptors -decrease vasoconstriction, decrease aldosterone, decrease cardiac hypertrophy, decreased SNA

502
Q

Name 2 angiotensin receptor antagonists used for treating HT

A

losartan candesartan

503
Q

Describe the use of beta adrenoceptor antagonists in the treatment for HT

A

-‘olols’ -decrease CO by decreasing rate and contractility -decrease renin release –>decreases blood vol and TPR

504
Q

Name some beta adrenoceptor antagonists used in the treatment of HT

A

non selective -propranolol -timolol selective -atenolol -metoprolol partial agonist -pindolol

505
Q

What are some adverse effects of using Ang receptor antagonists for the treatment of HT?

A

-hyperkalaemia -headache -dizziness

506
Q

What are some adverse effects of using beta adrenoceptor antagonists in HT?

A

-cold extremities (reflex alpha 1 constriction, blockade of dilatory beta 2) -fatigue (beta 1 blockade–> decreased cardiac response, beta 2 blockade–> constriction of skeletal muscle vv) -dreams and insomnia -bronchoconstriction (beta 2 blockade in airways s muscle)

507
Q

What are some contraindications of beta adrenoceptor antagonists?

A

-asthma -diabetes -AV block -HF -metabolic syndrome

508
Q

Describe the use of calcium channel blockers in HT

A

-inhibit voltage gated L type Ca channels -decrease cardiac and vascular contractility -decrease vascular resistance

509
Q

Name some calcium channel blockers used in HT

A

non selective -verapamil -diltiazem vascular selective -felodipine -nifedipine Reduces vascular resistance -dihydropyridines

510
Q

What are some adverse effects of using calcium channel blockers in HT

A

Verapamil, Diltiazem -oedema, flushing -headache -bradycardia Dihydropyridines -same as above except there is reflex tachycardia

511
Q

Describe the use of diuretics in HT

A

-aka thiazide diuretics -inhibits Na/Cl co-transporter in the distal tubule -decreases Na and Cl reabsoprtion, increases their excretion -increased K loss -decreases blood vol -decreases BP

512
Q

Name a thiazide diuretic used in HT

A

Hydrochlorothiazide

513
Q

What are some adverse effects of using thiazide diuretics in HT?

A

-K loss -gout -hyperglycaemia -allergic rxn

514
Q

Briefly describe the parasympathetic control of HR

A

-targets the SA node and AV node -uses Ach -targets M2 receptors -affect= decreases HR -M antagonist= atropine and causes tachycardia

515
Q

Briefly describe the sympathetic control of HR

A

-targets the SA node, conducting tissues (bundle of His, perkinji fibres) and myocardial cells -uses NA and circulating Adr -targets Beta 1 receptors -affect= increases HR, increases contractility/force (positive inotropic effect) -Beta antagonist= propranolol

516
Q

Which has greater control on HR: sympathetic NS or parasympathetic NS?

A

Parasympathetic NS

517
Q

Describe the phases in the SA node AP

A

phase 4 -unstable MEMPOT -spontaneous depolarisation -Na and Ca in Phase 0 -depolarisation -Ca in Phase 3 -repolarisation -K out Phase 4

518
Q

Describe the affect of PNA and SNA on the SA node AP

A

PNA -opens K channels -slows Na and Ca fluxes -slow pre-potential (phase 4) -longer to reach threshold -slows AV conduction SNA -opens Ca channels -increases slope of phase 4 -increased SA node firing -increases AV conduction

519
Q

Describe the phases in the ventricular AP

A

Phase 4 -stable MEMPOT Phase 0 -depolarisation -Na in Phase 1 -rapid repolarisation -K out Phase 2 -plateau -Ca in, K out Phase 3 -repolarisation -K out Phase 4

520
Q

Define dysrhythmia

A

-aka arrhythmia -any variation from the normal rhythmn of the heart beat -a more forceful contraction after a missed beat -sensed as a palpitation or fluttering -diagnosis is by an ECG (assess Rhythmn and Rate)

521
Q

What are the symptoms of a dysrhythmia?

A

-SOB -chest pain -fainting -fatigue

522
Q

What are the different mechanisms underlying dysrhythmias?

A

-altered impulse FORMATION -altered impulse CONDUCTION -triggered activity

523
Q

Name the 4 classes of anti-arrhythmia drugs

A

-Na channel blockers (1a, 1b, 1c) -Beta adrenoceptor antagonists -K channel blockers -Ca channel blockers

524
Q

Name some Na channel blockers used in arrhythmias

A

-quinidine (class 1a) -lignocaine (class 1b) -flecainide (class 1c)

525
Q

Name a K channel inhibitor used in arrhythmias

A

amiodarone

526
Q

Name a Ca channel blocker used in arrhythmias

A

verapamil

527
Q

What are some other treatment approaches for arrhythmias other than the main 4 drug classes?

A

-M antagonists -Adenosine -Cardiac glycosides -Electrolyte supplements -DC shock Pacemakers -Defibrillators

528
Q

What are the basic ethical principles?

A

-Beneficence -non-maleficience -Respect for autonomy -respect for privacy -justice

529
Q

How is the inferior mediastinum defined?

A

-central compartment in the thorax -from vertebrae 5–> 8

530
Q

What is the inferior mediastinum further divided into?

A

-anterior -middle -posterior

531
Q

Describe the layers of the pericardium

A

-2 layers -outer fibrous pericardium layer -inner serous pericardium layer (further divided into outer parietal layer of serous pericardium and inner visceral layer of serous pericardium)

532
Q

Where is the apex beat normally found?

A

-in the 5th intercostal space at the mid clavicular line

533
Q

The internal aspect of the anterior part of the RA is lined by what?

A

-musculi pectinati

534
Q

Musculi pectinati terminate at a verticle ridged called?

A

crista terminalis

535
Q

The posterior surface of the RA is smooth and called?

A

sinus venarum

536
Q

The oval imprint on the wall of the RA is called?

A

Fossa ovalis -used to bypass RV in the foetus

537
Q

The venous return from the heart itself returns to the RA via

A

the coronary sinus

538
Q

The RVs walls are lined with what?

A

-trabeculae carnae

539
Q

The smooth outflow tract of the RV is called?

A

-conus arteriosus or infundibulum

540
Q

How many cusps and papillary muscles does the mitral valve have?

A

-2 cusps -2 papillary muscles

541
Q

Describe the fibrous skeleton of the heart

A

-4 rings (2 rings and 2 coronets) and 2 trigones -surround orifices of the 4 valves -pair of coronets surrounds aorta and pulmonary valves -pair of rings surrounds AV valves -2 trigones binds the 4 rings of the fibrous skeleton tog -functions= anchors atrial and ventricular masses separately, electrically isolates them, provides attachment for base of each valve cusp

542
Q

Name the cusps in the tricupsid valve

A

-anterior cusp -septal cusp -posterior cusp

543
Q

What are the cups made of?

A

-endocardium (the lining tissue of the heart)

544
Q

How many chordae tendineae attah to each cusp?

A

-more than 1 for each cusp -and a group of chordae tendineae attach to adjacent sides of 2 cusps therefore when the papillary muscles contract the chordae tendinea pull 2 cups tog to create a seal

545
Q

What type of valves are the aortic and pulmonary valves and how many cusps do they have?

A

-they are semilunar valves -they have 3 cusps

546
Q

Are there papillary and chordae tendinae associated with the semilunar valves?

A

NO

547
Q

Where do the coronary arteries begin?

A

-at the beginning of the aorta

548
Q

Where are the SA node and the AV node in the RA?

A

SA node -at the top of the cristae terminalis, infront of the SVC AV node -between the opening of the coronary sinus and the AV valve

549
Q

The breast is made up of what?

A

-glandular tissue -fibrous tissue -adipose tissue -blood vessels -nerves -lymphatics

550
Q

What is the retromammary space?

A

-aka submammary space -space filled with CT -separates breast from pectoralis major muscle -allows breast movement

551
Q

Describe the blood supply and lymphatic supply of the breast

A

Artery supply= lateral side from axillary artery, medial side from internal thoracic artery Venous supply= lateral side from axillary vein, medial side from internal thoracic veins Lymphatic supply= axillary LNs, intercostal LNs, parasternal LNs

552
Q

Describe the articulation pattern of the 12 thoracic ribs

A

-upper 7 have costal cartilage that articular with the sternum directly -ribs 8,9,10 have costal cartilage that articulates with the rib above each -ribs 11,12 are floating ribs

553
Q

Describe the divisions of the sternal complex

A

-manubrium -sternum -xyphoid process

554
Q

Describe the structure of a typical rib

A

-head with 2 smooth articular facets -neck -tubercle with 2 facets, 1 smooth, 1 rough -body/shaft -sternal end (anterior)

555
Q

What ribs are atypical?

A

-ribs 11,12 -ribs 1,2

556
Q

what 3 things distinguish a thoracic vertebra from others?

A

-costal facets for ribs on the body -facets on transverse process -long spinous process

557
Q

Describe the joints and ligaments involve in joining ribs to vertebrae

A

Costovertebral joints -head of rib articulates with demi facets on 2 consecutive vertebrae -reinforced via radiate ligament Costotransverse joints -facet between the facet of the transverse process and the medial tubercle of the rib (neck) -has 3 parts to the strong costotransverse ligament

558
Q

Describe the attachments of the diaphragm

A

-attaches to the xyphoid process anteriorly -attaches to the costal margin to the tips of ribs 11 and 12 and the vertebral column laterally -2 arcuate ligaments attach it to quadratus lumborum and psoas major muslces -left and right crus attach it to the lumbar vertebrae posteriorly

559
Q

Describe the span of the left and right crus

A

left crus from L1,2 only right crus from L1,2,3 Right dome of the diaphragm goes higher because of the liver

560
Q

At what level does the oesophagus pass through the diaphragm?

A

at the level of T10 through the muscular part, to the left of midline

561
Q

At what level does the IVC pass through the diaphragm?

A

at the level of T8 through the central tendon, to the righ of midline

562
Q

At what level does the aorta pass through the diaphragm?

A

at the level of T12 in the midline

563
Q

Each dome of the diaphragm is supplied by what nerves?

A

the left and right phrenic nerves

564
Q

Describe the intercostal muscles

A

External ICM -front pocket -replaced anteriorly by a membrane -muslce of inspiration Internal ICM -back pocket -replaced posteriorly by a membrane -accessory muscle of expiration Innermost ICM -back pocket -discontinous -subnames= transversus thoracis (anterior space) and subcostalis (posterior space)

565
Q

The intercostal nerve is from which rami and what does it run between?

A

-from the ventral rami -it runs between the innermost and internal ICMs

566
Q

Describe the artery and venous supply of the ribcage

A

arteries -anterior artery from the internal thoracic artery -posterior artery from the descending thoracic aorta veins -anterior vein drains into the internal thoracic vein -posterior vein drains into the azygous system

567
Q

Where are baroreceptors found?

A

-carotid sinus -aortic arch

568
Q

Where in the brainstem is the cardiovascular control centre?

A

-in the medulla -it has pressor and depressor centres

569
Q

Sympathetic nerves innervate what?

A

-SA node -ventricles -Arterioles -veins

570
Q

Parasympathetic nerves innervate what?

A

-SA node

571
Q

Describe the phrase baroreceptor resetting

A

When baroreceptors are exposed to a diff P than normal for a prolonged period of time their threshold for baroreflex firing is changed. This occurs within 1-2 days

572
Q

Baroreceptors stop firing below what P?

A

60mmHg

573
Q

Where are chemoreceptors found and what do they respond to?

A

-found in the carotid body and aortic body outside arteries -they respond to very low O2 because they are stimulated by very low MAP (which indicates low BF, low O2, high CO2 and low pH)

574
Q

Describe the relationship between sex and BP

A

-men have higher BP than women

575
Q

Describe the relationship between age and BP

A

-SBP rises with age -DBP rises until 60 y/o after which it doesnt rise (bc of hardening of arteries)

576
Q

Describe the relationship between body size and BP

A

the bigger the body the bigger the BP

577
Q

Describe the diurnal variation in BP

A

-BP decreases at night by 20mmHg -less variability at night -less SNA at night

578
Q

Describe the seasonal variation in BP

A

-BP in summer are 3 mmHg lower than winter bc -there is increased vasodilation -increased sweating, decreased blood vol, decrease CO -decreased body weight (bikini body phase)

579
Q

Describe the population paradox in relation to cardiovascular deaths and BP

A

-in a pop, more deaths occur in a larger no. of ppl at moderate risk than in the small no. of ppl at highest risk -i.e. most ppl who die from CVD have average BP and not HT -bc those with high BP are given meds to decrease their BP -and those wih moderate BP dont get meds

580
Q

‘What are the 2 diff sources of arachidonic acid?

A

Dietary PUFA -usually omega-6 PUFA e.g. linoleic acid C18:2 which is converted by desaturation, elongation and desaturation into arachidonic acid -Omega-3 PUFA e.g. eicosapentaenoic (EPA) C20:5, linolenic acid C18:3, docosahexaenoic (DHA) C22: 6 Esterified in the membrane phospholipids (attached to 2nd C) (plasma and nuclear)

581
Q

What is another name for arachidonic acid? And describe the structure of it.

A

Eicosatetraenoic acid -20 C -4 double bonds -omega 6 FA

582
Q

How is arachidonic acid released from membranes?

A

-via phospholipase A2 -PLA2 is activated by increase in intracellular Ca (hence its a Ca dependent enzyme) -snake venoms can contain the enzyme

583
Q

What substance can inhibits PLA2?

A

-glucocorticoids -annexin 1

584
Q

Arachidonic Acid is metabolised to cyclic endoperoxides by what enzyme?

A

COX1= constitutive COX2= inducible by inflammatory stimuli

585
Q

Arachidonic acid can be metabolised to another substance 5-HPETE, that isn’t a cyclic endoperoxide, by what enzyme? And where is this enzyme expressed?

A

-5-LOX -in inflammatory cells e.g. eosinophils, neutrophils, mast cells

586
Q

What are the cyclic endoperoxides rapidly converted into? And why?

A

-they are highly unstable and are therefore rapidly converted into the stable prostaglandins (PGE2, PGD2, PGF2)

587
Q

Describe the action of PGE2

A

-relaxes vascular s muscle therefore its a vasodilator and natriuretic -hyperalgesic (sensitises nerves) when in conjunction with bradykinin -pyrogenic -angiogenic

588
Q

Describe the action of PGF2alpha

A

-bronchoconstrictor

589
Q

Describe the action of PGD2

A

-bronchoconstrictor

590
Q

How are the stable prostaglandins removed from the body?

A

-they only act locally at the site of production (last 3-5mins) -they don’t circulate in the blood -they are degraded by endothelial cells of pulmonary capillaries (in the lung)

591
Q

Describe how IL-1beta increases pain sensitivity

A

it induces -increase in BK1 receptors -increase in COX2 and PLA2

592
Q

Describe how prostaglandins are invovled in the development of fever

A

-inflammation –>macrophages to become activated–> produce cytokines–> stimulate PGE2–> cAMP increase–> raises temp in hypothalamus

593
Q

Where do NSAIDs work in the arachidonic acid pathway? What are their benefits? What are their adverse effects?

A

-act on COX -benefits= anti-inflammatory, analgesic, antipyretic -adverse effects= loss of gastro-protective role of PGE2, gastric irritation/ulceration

594
Q

Describe prostacyclin

A

-chemically unstable -t 1/2= 3 mins -produced by endothelial cells -vasodilation -anti-aggregation of patelets -protects against CAD -NB its not a prostaglandin bc it doesnt have the cyclopentane ring

595
Q

Describe thromboxane A2

A

-chemically unstable -t 1/2= 30 secs -produced by platelets -vasoconstrictor -pro-aggregation -also not a prostaglandin -promotes CAD

596
Q

Describe the action of asprin

A

Acetylation of COX and vascular protection at low doses -platelets in GI circulation are exposed to high concs of asprin -platelets have no nucleus and therefore cannot resynthesise COX (platelets lifespan= 8 days) -conc of asprin is lower in the systemic circulation and endothelium re-synthesis of COX occurs within hours -TxA2 levels are reduced more and for longer than PGI2 bc platelets cant resynthesise COX and therefore TxA2 -PGI2/TxA2 ratio is increased Asprin-triggered lipoxins -produces analogues of endogenous lipoxins which are inflammation resolving lipids

597
Q

5-HPETE produces what substances in the arachidonic acid pathway?

A

-LTA4 which produces LTB4 or LTC4, LTD4, LTE4 (the leukotrienes)

598
Q

Describe the actions of leukotrienes

A

-bronchoconstrictors -vasoactive -leaky vessels

599
Q

Name a drug that acts on the cysteinyl-leukotriene 1 receptor

A

montelukast

Danielle's MD1 (6 decks)

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