Week 5 Flashcards

1
Q

What is an ECG?

A

Electrocardiogram

Test to check rhythm and electrical activity of heart

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2
Q

What is a cardiac impulse?

A

the wave of cardiac excitation passing from the sinoatrial node to the atrioventricular node and along the bundle of His and initiating the cardiac cycle broadly

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3
Q

What are the parts of the cardiac conduction system?

A

SA node, AV node, bundle of His, bundle branches, and Purkinje fibers

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4
Q

Describe cardiac conduction system

A

Signal from sinoatrial node moves slowly to Atrioventricular node as ventricles begin to fill
From there signal moves through bundle of His, bundle branches, to Purkinje fibers which stimulate ventricles for ejection

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5
Q

Outline the properties of the ECG paper (speed, square size)

A

Speed: 25 mm/s
Large squares: .2 second, .5 mV
Small squares: .04 second, 0.1mV

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6
Q

What is positive/negative deflection?

A

Positive - energy coming towards the lead

Negative - energy travelling away from the lead

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7
Q

How many electrodes do you use for the ECG?

A

10
Leads are a misnomer (often called 12 lead ECG) - leads are not the cables, but the line between where you put the electrodeand where you are looking for

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8
Q

Describe Einthoven’s triangle

A

Right arm, left arm, left leg

aVR, aaVL, aVF

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9
Q

What is a chest lead vs limb lead?

A

Chest leads look at heart on horizontal transverse plane

Limb leads look at heart on coronal plane

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10
Q

What is the P wave? How long should it last? Where should it be positive (1) / negative (1) on ECG?

A

First positive deflection
Atrial depolarisation
Should no be more than 0.12 seconds
Positive in lead II (negative in AVR)

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11
Q

What is the T wave? What can changes indicate?

A

Rapid phase of ventricular repolarisation

Peaked or flattened can reflect changes in potassium, metabolic process

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12
Q

What is your QRS complex related to?

A

Ventricular depolarisation
If larger than 0.12 suggests defect in intraventricular conduction
Direction determine ‘electrical axis’

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13
Q

What is the PR interval?

A

Represents time for transmission of signal from atria to ventricles through AV node
0.12-.20 second duration (3-5 small squares)

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14
Q

What is the electrical axis? What is normal?

A

Direction of the mean vector of the wave of ventricular depolarisation in the limb leads
Lead 1 is arbitrarily defined as 0 degrees
Normal axis between -30 and +90 degrees

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15
Q

Define abnormal electrical axis readings

A

beyond -30 = left axis deviation

beyond 90 = right axis deviation

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16
Q

What is the ST segment?

A

In isoelectric line between QRS and T wave
Plateau phase of repolarisation
Should not deviate above/below isoelectric line by more than 1mm
Deviation = likely damage
STEMI!

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17
Q

What is the QT interval?

A

Measures polarisation process
Prolonged (>440ms in men, >460ms women)
Prolonged due to inherited conditions, drugs
Prolonged can cause arrhythmia

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18
Q

What is the structure for reading ECGs? (5)

A

Name / age of patient / current condition
Check heart rate
Check rhythm is regular (are R waves coming regularly)
P wave - duration and shape
T wave - should be positive in I, II, aVL, aVF, V2-6

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19
Q

How to check heart rate on ECG?

A

1 large square = 300 bpm

count number of squares between R waves (300 divided by this number)

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20
Q

What are the criteria for sinus rhythm? (3)

A

Positive 1, 2, aVF AND
Negative aVR AND
Each QRS preceded by P

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21
Q

What is left ventricle hypertrophy? How can you see it on ECG?

A

enlargement and thickening (hypertrophy) of the walls of your heart’s main pumping chamber (left ventricle)
Large QRS complex - various systems to add up

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22
Q

What are the changes on ECG during myocardial infarction?

A

ST elevation during STEMI
Maybe no changes during non-STEMI (or slight T inversion)
Pathological Q waves are long term effect

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23
Q

What are the clinical signs of shock?

A

Pale, sweaty, dizzy, cold/clammy skin

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24
Q

What is blood pressure? What maintains it? (4)

A
Pressure exerted by the circulating blood against the walls of the arteries
Maintained by:
1. contraction of left ventricle
2. resistance of small blood vessels
3. elasticity of arterial walls
4. volume / viscosity of blood
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25
Q

What are the UK parameters for optimal, normal and high-normal blood pressure?

A

less than 120/80
less than 130/85
130-139/85-89

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26
Q

What are the parameters for grade 1-3 hypertension?

A

Grade 1 - 140-159 / 90-99
Grade 2 - 160-179 / 100-109
Grade 3 - More than 180 / 110

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27
Q

What is blood pressure homeostasis?

A

Maintenance of steady state of blood pressure

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28
Q

What are the three factors that control blood pressure?

A

Contraction of left ventricle
Resistance of small blood vessels
Volume of the blood

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29
Q

Why do we need blood pressure?

A

To move blood through vascular system

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30
Q

What are the characteristics that contribute to blood pressure stability? (3)

A

The mechanism that contribute to BP stability are:
powerful (it has rapid and slow components)
highly redundant (if something happens, there is back-up)
Able to cope/adjust (e.g physical activity, threats, trauma)

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31
Q

What is cardiac output? How do you calculate it?

A

amount of blood pumped out by the heart per minute (=Stroke volume x Heart rate)

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32
Q

What are the markers of low BP? (3)

A

low stroke volume, slow or very fast heart rate, or reduced peripheral vascular resistance

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33
Q

What are the markers of high BP? (2)

A

High stroke volume

High peripheral vascular resistance

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34
Q

How do you calculate vascular resistance?

A

Poiseuille’s law

Resistance = 8 x length of blood vessel x viscosity divided by pi x the radius of blood vessel ^4

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35
Q

What is the distribution of blood volume?

A

Arteries 13%
Capillaries 6%
Veins 81%

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36
Q

Blood pressure regulation - which four systems work together?

A

CVS, Renal, nervous, endocrine

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37
Q

What is the most important factor in regulation of blood pressure?

A

Salt

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38
Q

Describe role of renal system in BP regulation

A

RAAS system responds to low blood pressure and stimulates increase
Kidney filters more than 170 L of plasma every day, filtering 23,000mmol of sodium

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39
Q

Types / percentages of Na absorption on nephron - what is being absorbed? (4 sections with approximate percents of absorption of sodium)

A

Proximal tubule: Na+/H+ exchanger = 60% absorption
Thick ascending limb of Henle: Na-K-2Cl co-transporter= 30%
Distal convoluted tubule: Na-Cl co-transporter = 7%
Cortical collecting tubule: ENaC = 2%

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40
Q

Describe (simply) the RAAS system? location, purpose, main elements

A

xxx

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41
Q

Drugs that act on different stages of the RAAS system?

A
ACE inhibitors (between Angiotensin I and II)
Beta blockers and renin inhibitors (between angiotensinogen and angiotensin I)
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42
Q

What is malignant hypertension?

A

extremely high blood pressure that develops rapidly and causes some type of organ damage.

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43
Q

What is the role of the sympathetic nervous system on BP?

A

Short-term variations (stress, exercise, changes in posture)

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44
Q

What is pressure naturesis?

A

central component of the feedback system for long-term control of BP
When pressure is very high, kidney will lose salt

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45
Q

What was the result of renal sympathetic dennervation?

A

Blocking sympathetic nerve pathways helped to lower blood pressure if those resistant to treatment. Research ongoing

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46
Q

What are baroreceptors? What happens if you put pressure on the neck?

A

Pressure receptors
The carotid sinus and aortic arch sense high pressure and the hear and pulmonary artery sense low pressure
Cause bradycardia and low blood pressure

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47
Q

Describe (simply) the activity of endocrine control of BP

A

hormonal mechanism for the regulation of blood pressure by managing blood volume

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48
Q

Why don’t you give epinephrine during shock?

A

Worsens the vasoconstriction, tissues aren’t getting enough blood

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49
Q

What is atrial natriuretic peptide? What does it do (3)? and why?

A

It increases excretion via kidneys - 3 methods:

  1. Reducing water reabsorption in collecting ducts
  2. Relaxes renal arterioles
  3. Inhibits sodium reabsorption in DCT

Starts these processes in response to stimulation of atrial receptors

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50
Q

In what order will you organs shut down with high BP? (2 early)

A

Skin, kidney, etc.

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51
Q

What is convection?

A

Mass movement of fluid caused by pressure difference

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52
Q

Describe Darcy’s Law of flow states

A

Flow is equal to the pressure drop divided by resistance to flow

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53
Q

Relationship between blood flow and cardiac output

A

They are equal

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54
Q

How does heart beat? (source, 4 steps)

A

Generates its own electrical activity (does not need external nerves)
Starts at SA node, spread out via gap junctions
Spreads to AV node, delays conduction to allow ventricles to fill
Depolarisation rapidly through bundle of His into ventricles

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55
Q

How does the heart beat? (from what part of the heart)

A

From apex (bottom) to base (line between atria and ventricles)

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56
Q

What are the general principles of the cardiac cycle?

A
  1. Electrical activity conducted from SA node to atria and then ventricles causing CONTRACTIONS, CHAMBER PRESSURE CHANGES, MOVEMENT OF BLOOD
  2. Blood flows from high pressure to low pressure (unless blocked)
  3. Valves open / close depending on pressure change
  4. Left and right side are doing the same thing but pressure on the right is lower
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57
Q

Movement of blood through right side of the heart (describe path, valves) - 6

A
Blood returns from superior and inferior vena cava
Enters right atrium
Flows throw tricuspid valve
Gathers in right ventricle
pushed through pulmonary semilunar valve
into pulmonary arteries to lungs
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58
Q

Movement of blood through left side of the heart (describe path, valves) - 6

A
Blood from lungs is sent to heart by pulmonary veins
Enters left atrium
Flows through mitral (bicuspid) valve
Gathers in left ventricle
pushed through aortic semilunar valve
into aorta to systemic circulation
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59
Q

Describe process of cardiac cycle (where is blood going, what is happening?) - 4 phases

A
  1. ventricular filling
  2. isovolumetric contraction
  3. ejection
  4. isovolumetric relaxation
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60
Q

What is ejection fraction? What are normal values and what does a lower value indicate?

A

Ensures blood that is coming into ventricles is being ejected
SV / EDV
Normal value is 2/3rd or more; lower indicates heart failure

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61
Q

Describe the pressure changes as blood moves into/through right atrium

A

Pressure is going up in the right atrium during diastole, until so high the tricuspid valve opens
Blood moves from the atrium to ventricle, tricuspid closes
Blood leaves ventricle as atrium starts filling again
Repeats

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62
Q

Why do you look at the jugular? What does normal look like?

A

Low at SCM, pulse may be visible put should not be elevated

Jugular pressure can indicate if pressure in right atrium is too high, possible right sided heart failure

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63
Q

Describe the 4 basic heart sounds and what you are hearing

A

S1 - lubb - tricuspid / mitral valves close - beginning of systole
S2 - dupp - aortic / pulmonary valves close - beginning of diastole
S3 - occasional - turbulent blood flow into ventricles (common in young people)
S4 - pathological in adults - forceful atrial contraction against stiff ventricle

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64
Q

Outline the role of the parasympathetic nervous system on the circulatory system (route, receptors, where)

A

Vagus nerve sends messages from CNS (brainstem cranial nerves) to muscarinic M2 receptors on SA and AV node through acetyl choline

65
Q

Outline the role of the vagus nerve in heart control - which nervous system, origin, where does it connect with heart, what sort of receptors

A

Parasympathetic nervous system
Sends messages from CNS to SA and AV nodes
Originates in brain stem
Muscarinic M2 receptors

66
Q

Outline the role of the sympathetic nervous system on the circulatory system

A

Act on heart and blood vessels
Adreniline and noradrenialine
a1 and b1 receptors SA and AV nodes and at ventricles
Origin - thoracic and lumbar regions

67
Q

Role of adrenaline and noradrenaline

A

Both catecholamines, regulation
no
Noradrenaline (synonymous with norepinephrine), the main neurotransmitter of the sympathetic nervous system, maintain blood pressure

Adrenaline is a key determinant of responses to metabolic or global challenges to homeostasis, such as glucoprivation, and of manifestations of emotional distress

68
Q

Effect of sympathetic on CVS - what does it do? Where?

A

Major effect of sympathetic system is to mediate increases in CO and TRP to increase in BP
Does this by increasing heart rate and contractility and by stimulating vasoconstriction

69
Q

How does stimulation of B1 adrenoceptor induce an increase in HR?

A

Targeted activation of the beta-1 receptor in the heart increases sinoatrial (SA) nodal, atrioventricular (AV) nodal, and ventricular muscular firing, thus increasing heart rate and contractility. With these two increased values, the stroke volume and cardiac output will also increase

If channel allows sodium through, causes polarisation, transfer of calcium and potassium drives ongoing polarisation/depolarisation

70
Q

How does stimulation of B1 adrenorecptors induce an increase in contractility?

A

Inotrophic effect??
More calcium, more contraction
Calcium stores within cells released when stimulated, Tropinin

71
Q

Define chrono, dromo, ino, lusitrophic

A

chrono - heart rate
dromo - conduction
ino - contractility
lusi - relaxation

72
Q

Drugs that stimulate or inhibit B1 receptors - what are they, examples, used for what conditions?

A

B agonists increase cardiac activity - used for cardiac arrest anaphylaxis, cardiogenic shock (during sepsis)
Non-selective - Adrenaline, dobutamine

B antagonists reduce cardiac activity - used for angina, hypertension, arrhythmia, HF
B1 - atenolol
B1 & 2 (non selective) - propranolol

73
Q

Describe sympathetic nerve activity on blood vessels - what does it control?

A

Radius of blood vessels (so important for TPR)
Affected by release of NA from sympathetic nerves and adrenaline / NA from adrenal medulla
Acts at Ai adrenoreceptors on smooth muscle cells in arterioles

74
Q

Describe activity of alpha adrenoceptor agonists (and 2 examples)

A

A agonists increase vasoconstriction
Adrenaline (in high doses)
NORAD / noradrenaline (non-selective a agonist)
Phenylephrine (selective a1 agonist)

75
Q

Describe activity of alpha adrenoceptor antagonists (and 2 examples, for what treatment)

A

A antagonists reduce vasoconstriction

Prazosin, phenoxybenamine (a1 selective antagonists) - hypertension and Phaeochromocytoma (adrenal gland tumour)

76
Q

What happens if you give beta and alpha blockers together? And example combo

A

Very strong treatment for hypertension, cardiac protective

Carvedilol and metoprolol

77
Q

What is the effect of the parasympathetic nerve activity on the heart?

A

Stimulation of vagus nerve decreases cardiac output
Vagus nerve releases acetyl choline which acts on M2 receptors on the heart
Reduces frequency at SA node, reduction in heart rate

78
Q

How does stimulation of M2 muscarinic induce a decrease in HR?

A

Vagus nerve releases acetyl choline which acts on M2 receptors on the heart. Reduces frequency at SA node, reduction in heart rate

79
Q

Outline Mus receptor agonist and antagonist and examples of each

A

Mus agonists decrease cardiac activity
Pilocarpine (relieves intraocular pressure in glaucoma), bethanechol
Mus antagonists increase cardiac activity
Atropine, hyocine - used to address sinus bradycardia post myocardial infarction

80
Q

What is the exception to the rule (that parasympathetic activity generally doesn’t effect blood vessels)?

A

Blood vessels to penis, arousal stimulates CNS to drive release of NO, which produces cycle that increases blood flow which causes an erection

81
Q

What is a risk factor?

A

Aspect of personal behaviour or lifestyle, environmental exposure, inborn or inherited characteristic ASSOCIATED with particular disease or condition.

82
Q

What is the healthy entrant effect?

A

People who are unhealthy may be excluded from study which makes the pool of entrants healthier than the general population

83
Q

How can we quantify risk?

A

Probability event will occur

Compare risk of those who are exposed, to those who aren’t

84
Q

How do you calculate a relative risk (RR)?

A

Ratio of absolute risks

Exposed : unexposed group

85
Q

What are confounding factors? Provide examples

A

A confounding factor is one that is associated with the risk factor, without being a consequence of it. Furthermore, it is associated with the disease (independently of the risk factor).

86
Q

What are the limitations of cohort studies? (6)

A
there are unknown (and therefore not measured) risk factors.
Confounding factors
Time / expense
Bias due to loss of follow up
Behaviour change
Doesn't work if diseases are rare
87
Q

Why / how do you calculate incidence rate?

A

In cohort studies, people have been studied for different numbers of years (varying length of exposure)
Incidence rate: Total number occurrences of outcome divided by total number of years at risk.

88
Q

What are the advantages to cohort studies? (2)

A

Prospective designs help establish when people are exposed to risk and when they develop the disease
Population based samples can make findings very helpful

89
Q

What is a prospective vs retrospective study?

A

xxx

Retrospective - using past data from electronic databases - introduces different bias such as missing data

90
Q

What are the challenges explaining findings from a cohort study to a patient?

A

Study looks at risks in a mixed group with varying demographics - not at their specific situation

91
Q

What are the four phases of drug movement in the body?

A

Administration/Absorption
Distribution
Metabolism
Excretion

92
Q

What factors effect whether a drug can exert its actions? (3)

A
  1. must reach target
  2. correct concentration
  3. correct duration
93
Q

What does pharmacokinetics mean?

A

Drug movement

How body handles drug

94
Q

What are the routes of administration? (3) How is each route absorbed?

A

Enteral - absorbed via GI tract
Parenteral - bypasses GI tract
Topical - for local action (can also be systemic)

95
Q

What are the types of enteral administration?

A

Absorbed vial GI tract
Oral
Buccal, sublingual
Rectal

96
Q

What are the types of parenteral administration?

A
Bypasses GI tract
Injection:
Intradermal 
Subcutaneous
Intramuscular
Intravenous
Injected into other body cavity
97
Q

What are the types of topical administration?

A

For local action (or systemic effect)

Eye drops, inhalers, cream/ointments/patches, nose/ear/eye drops

98
Q

How do drugs move between fluid compartments, across physiological barriers?

A

Across cell membrane (lipid soluble by passive diffusion, water soluble by protein transporters)
Between cells - some can pass between cells depending on nature of epithelia

99
Q

What is bioavailability?

How else can you measure/define this?

A

The proportion of the drug administered that is available for therapeutic effect
Look at proportion that reaches systemic circulation
Biggest risk for oral treatments

100
Q

What are the factors affecting bioavailability? (4)

A

Pharmaceutical formulation
Absorption
Metabolism / elimination
Local factors - disease / interactions

101
Q

Why is sublingual better than oral for bioavailability?

A

Treatment goes into capillaries under tongue

102
Q

Considerations when choosing rate of administration (5)

A

Administration - Convenience, acceptability
Absorption -Bioavailability and Speed
Site of action
Local effects/ side effects
Effect of disease on route of administration

103
Q

Advantages (3) / disadvantages (4) of IV administration

A

Excellent bioavailability
Ensure patient gets medicine
Can be used when enteral route not available (e.g. vomiting)

Usually needs input from healthcare professional
Risk of cannula infections
High concentrations from bolus may cause side effects
Expensive

104
Q

Advantage (4) / disadvantages (5) of transdermal

A

Acceptable to patients
Easy to administer
May aid adherence to treatment
Can be stopped easily

Local side effects
Many drugs not absorbed
Patches may come off
Affected by skin disease
Slow to initiate effect
105
Q

What happens during drug distribution? (3 steps)

A
  1. dissolved in body water
  2. bound to plasma proteins
  3. distributed to tissues
106
Q

Calculating volume of distribution

A

total amount of drug in the body / plasma concentration of the drug

107
Q

What is the significance of a high volume of distribution?

A

Need loading dose before maintenance dose

108
Q

In body, which drug molecules are active vs inactive?

A

Free state drugs are active, protein bound are inactive

109
Q

Why are albumin levels in patients important before starting treatment?

A

If high levels, will inactivate more of the drug

If low, more of the drug will be active

110
Q

What is the significance of a drug being protein bound?

A

Protein-bound drugs act as a reservoir when free-state drugs are removed by metabolism or excretion
Protein-bound drugs therefore have a longer half-life

111
Q

What are the characteristics of drugs that bind to tissues? (2) Examples (3)

A

Extensive binding to tissue delays elimination and increases the drug half life.

These include many lipid-soluble drugs, which may enter fat stores
E.g. benzodiazepines, verapamil, lidocaine.

112
Q

What happens during systole?

A

ventricles contract and atria relax

113
Q

What happens during diastole?

A

ventricles relax and atria contract

114
Q

What are the three components that drive the cardiac cycle?

A

Pacemaker
Conduction system
Contractile element

115
Q

Describe cardiac muscle tissue

A

Striated cells containing numerous mitochondria joined at intercalated discs

116
Q

Describe intercalated discs

A

Come together through physical connection (desmosomes) and xxx gap junctions

117
Q

What are the characteristics of a cardiac myocyte? (4)

A

Automaticity: ability to spontaneously initiate an impulse.
Excitability: indicates how well a cell responds to electrical stimuli.
Conductivity: ability of cell to transmit an impulse to another cell.
Contractility: ability to contract after receiving an impulse

118
Q

What is resting potential?

A

Net balance of ions inside/out of cell
Na moving in, K moving out
Ca Na exchanger

119
Q

Describe what happens during depolarisation and repolarisation

A

Depolarisation
Voltage-gated activation
Triggers release of sarcoplasmic reticular Ca++
Sarcomeric contraction

Repolarisation
Restoration of resting membrane potential
Sarcomeric relaxation

120
Q

What are the two main cell types in the heart?

A

Contractile cells - atrial and ventricular tissue in layers, low automaticity, highly contractile/excitable

Automatic / auto-rhythmic cells - pacemaker and conduction tissue
High automaticity and conductivity

121
Q

Describe contractile cell action potential (0-4 phase)

A
Phase 0: rapid depoliarisation
- Na rapidly into cell, Ca slowly into cell
Phase 1: early repolarisation
- Na channels close
Phase 2: plateau phase
- Ca continues in, K flows out
Phase 3: rapid repolarisation
- Ca channels close, K flows out rapidly
Phase 4: resting potential
- Active transport through Na-K pump, cell impermeable to Na, K may leave cell
122
Q

Describe the autorhythmic cell action potential

A

Phase 4: Pacemaker potentials – the ‘ funny current – If ’Inward diffusion of sodium ions
Phase 0: Depolarisation due to inward diffusion of calcium. Concludes when fast calcium channels open.
Phase 3: Repolarisation due to outward diffusion of potassium

123
Q

Where is there non-conductive tissue in the tissue?

A

Between atria and ventricles

124
Q

What is ‘re-entry’? What is the circus movement?

A

Reentry can be subdivided into three subcategories: (1) circus movement, (2) reflection, and (3) Phase 2 reentry. Reentry occurs when a propagating impulse fails to die out after normal activation of the heart and persists to re-excite the heart after expiration of the refractory period
Scar and fibrosis can form slow component of re-entry circuit

125
Q

Factors that can affect blood pressure measurements

A

anxiety, technique, personality of taker, instrument characteristics, cuff size, environment, number of readings

126
Q

What tends to happen to someone’s blood pressure after repeated readings?

A

Regression to the mean - they will tend to return towards normal after multiple readings

127
Q

Why is high blood pressure an important problem? (2)

A
  • Strongly associated with higher risks of CVD, especially CHD and stroke
  • Common in general population
128
Q

If these complications (3) are present it’s particular important to control BP to reduce risk of CVD

A
  • left ventricular hypertrophy
  • proteinuria or renal impairment
  • hypertensive retinopathy
129
Q

What makes blood pressure quantitative rather than qualitative?

A

It is the value that matters, not just the existence of high blood pressure

130
Q

How do we define hypertension / high blood pressure?

A

The level at which treatment becomes beneficial - where it is better to treat than leave it

131
Q

What are the causes of high blood pressure?

A

Small number have specific medical cause (secondary hypertension)
Most have no specific medical cause (primary hypertension)

132
Q

Common causes of secondary hypertension (5)

A

-Coarctation of aorta
-Renal and renal vascular disease
-Adrenal disease
cortical 1 hyperaldosteronism,
Cushing’s syndrome
medulla phaeochromocytoma
-Pregnancy
-Drugs esp OCP, HRT

133
Q

Other factors that may cause ‘essential’ hypertension

A

high BMI, high alcohol intake, high salt intake, low potassium intake, low fibre / high fat diet, physical inactivity, stress

134
Q

What do migration studies show in studies about high blood pressure?

A

People who move to a higher blood pressure population will generally have their BP increase to match host population within 6 months

135
Q

What is attributable risk?

A

Excess risk

Risk in the ‘exposed’ group (those with high blood pressure) - risk in ‘unexposed’ (those w/o high blood pressure)

136
Q

How do you lower blood pressure (non pharma)? (6)

A

Weight loss, reduce alcohol, reduce salt, increase fruit/vegetable, increase exercise, reduce saturated fat intake

137
Q

What are main pharmacological tools used to lower blood pressure? (6)

A

(A) ACE inhibitors
(B) beta blockers
(C) calcium-channel blockers
(D) diuretics

138
Q

How has the view on who needs their blood pressure lowered changed?

A

People who are at high CVD risk should be treated, others maybe not (old view was that everyone with high BP should be treated)

139
Q

What is relative risk vs attributable risk?

A

Attributable risk is the excess risk (difference in risk between exposes and unexposed groups) whereas the relative risk is a ratio

140
Q

Advantages (3) / disadvantages (3) of oral

A

Acceptable to patients
Easy to administer
Cheapest route

Interrupted by vomiting, GI problems 
Bioavailability may be limited by: 
Poor absorption 
First pass metabolism 
Interactions in GI lumen 
GI upset common side effect
141
Q

Advantages (1) / disadvantages (3) of rectal

A

Can be used for people who can’t swallow

Socially undesirable
Local factors influence absorption
Local irritation

142
Q

Advantages (4) / disadvantages (4) of IM

A

Easier than IV
Bioavaliability better than oral
Depot of drug absorbed slowly may be useful e.g. in contraception/antipsychotic, for administration at monthly or longer intervals.
Can be used when enteral route not available (e.g. vomiting)

Painful
Risk of infection
Drug may not be absorbed if blood pressure low
Usually needs to be done by healthcare professional

143
Q

Advantages (1) / disadvantages (2) of subcutaneous

A

Useful to self-administer drugs

Absorption may be slow and unreliable
Local side effects e.g. repeat insulin injections can cause lipoatrophy

144
Q

Advantages (3) / disadvantages (3) of topical

A

Straight to site of action
Limits systemic exposure and side effects
Acceptable to patients

Local side effects
May be messy/inconvenient
Rapid clearance may need regular administration

145
Q

What are you hearing during ‘lub’ and ‘dub’?

A

“lub” is the first heart sound, commonly termed S1, and is caused by turbulence caused by the closure of mitral and tricuspid valves at the start of systole

The second sound,” dub” or S2, is caused by the closure of aortic and pulmonic valves, marking the end of systole

146
Q

What are the branches of the aorta and what do they supply?

A

Coronary arteries - heart
Brachiocephalic trunk - head and right arm (through right common carotid and right subclavian)
Left common carotid - head
Left subclavian - head and left arm

147
Q

What are the branches of the descending thoracic aorta? Where does it start? end?

A
Descending starts at about T3, ends at aortic hiatus through diaphragm T12
Paired posterior intercostal
Bronchial
Oesophageal
Mediastinal
148
Q

Common variations of aortic branches (2) & clinical significance

A

Double - splitting of the ascending aorta into two limbs that pass to either side of the trachea and oesophagus. May result in trachael or oeosphageal obstruction
Right-sided - aorta courses to right of trachea, three different types with varying complications

149
Q

What is the azygous system? How does it relate to caval system?

A

azygos vein serves to drain most of the posterior intercostal veins on the right side of the body, and the hemiazygos vein and the accessory hemiazygos vein drain most of the posterior intercostal veins on the left side of the body.

Blood can circumvent vena cava if there is a blockage through the azygous system

150
Q

What is the thoracic duct? where?

A

The thoracic duct is the largest lymphatic vessel within the human body
A large portion of the body’s lymph is collected by this duct and then drained into the bloodstream near the brachiocephalic vein between the internal jugular and the left subclavian veins.
Starts at T12 (and extends to the root of the neck)

151
Q

What is the relationship of the ligamentum arteriosum to the left vagus nerve?

A

ligamentum arteriosum is closely related to the left recurrent laryngeal nerve, a branch of the left vagus nerve. After splitting from the left vagus nerve, the left recurrent laryngeal loops around the aortic arch behind the ligamentum arteriosum, after which it ascends to the larynx

152
Q

What are the locations of the oesophageal and pulmonary plexuses and superficial and deep cardiac plexuses?

A

Pulmonary about T3
Oesophageal about T7
Cardiac between bifurcation of trachea (carina) and arch of aorta

153
Q

How does the heart actually sit in the body? What is anterior/posterior?

A

Right ventricle to the anterior, left posterior

apex pointing to left side of chest

154
Q

What are the remnants of foetal structures present in the adult heart and great vessels? (3 terms)

A

foramen ovale - passage between left/right atrium
fossa ovalis - indentation where passage used to be
ligamentum arteriosum - small ligament that is the remnant of the ductus arteriosus formed within three weeks after birth. At the superior end, the ligamentum attaches to the aorta

155
Q

What are the valves of the heart?

A

Tricuspid valve
Pulmonary valve
Mitral (bicuspid valve)
Aortic valve

156
Q

Significance and location of coronary sinuses

A
Above aortic valve 
provide pooling spot for entrance to coronary arteries which provide blood to heart 
Left - left coronary artery
Right - right coronary artery
Posterior - non-coronary sinus
157
Q

How do the valves work?

A

Pulmonary and aortic are semilunar and close when back flowing blood starts to put pressure of them
Mitral and Tricuspid have chordae tendineae - blood moves into ventricles down pressure gradient, chrodae tendineae hold them closed as blood moves from ventricles through the semilunar valves

158
Q

What is the role of the lymphatic system? What are the key lymphatic organs?

A

Tonsils, spleen, liver, thymus
the lymphatics that drain fluid from the tissue (only move in one direction - from periphery to neck)
(2) one of the most important functions of the lymphatic system is in host defence as it houses most of the immune system.