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Y1 Medicine > CV&R Non-Anatomy > Flashcards

CV&R Non-Anatomy Flashcards

1
Q

What are 5 risk factors for atherosclerosis?

A

Age
Male
Family history
Smoking
Obesity
Hypertension

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2
Q

What are the 4 causes of chest pain ?

A

Cardiac
Respiratory
GI
Musculoskeletal
(+others)

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3
Q

What can cause cardiac chest pain ?

A

Ischaemia
Aortic dissection
Pulmonary embolism
Aortic stenosis
Pericarditis
Myocarditis

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4
Q

What are the two classifications of cardiac chest pain ?

A

Troponin positive
Troponin negative

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5
Q

What bare Troponin Positive cardiac conditions ?

A

Type 1 and 2 MI, SCAD, coronary spasm

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6
Q

What’s are Troponin Negative cardiac conditions ?

A

Angina (stable or unstable)
Cor spasm
Micro vascular/endothelial

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7
Q

What is the investigation pathways for cardiac conditions ?

A

Exercise tolerance test ( ETT) ——— stress echo, perfusion scan, CT coronary angiogram or stress perfusion cMR ———invasive coronary angiogram

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8
Q

What shows an ischaemia on an ECG ?

A

ST wave depression (during ETT)

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9
Q

What drug treatments can be used for angina ?

A

Beta blockers (-olol)
Calcium agonists (-dipine for smooth muscle + verapamil on the heart)
Nitrates (GTN spray)

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10
Q

What are the 3 acute coronary syndromes ?

A

Unstable angina - unstable plaque without myocardial necrosis
NSTEMI - thrombus without total vessel occlusion (ST depression)
STEMI - total vessel occlusion (ST elevation)

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11
Q

What are lipids ?

A

Water insoluble
3 classes = cholesterol, triglycerides, phospholipid

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12
Q

What is cholesterol a precursor to ?

A

Steroid hormones (oestrogen, testosterone, cortisol, aldosterone )
Endogenous vitamin D production

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13
Q

What is the structure of a lipoprotein ?

A

Central hydrophobic lipid core (triglycerides and cholesterol esters)
Surface layer of polar components (phospholipids + free cholesterol + apolipoproteins)

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14
Q

What is the LDL calculation ?

A

LDL = TOTAL CHOLESTEROL — HDL — TRIGLYCERIDES/5

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15
Q

Describe anticoagulant HEPARIN mechanism of action

A

Binds to and enhances antithrombin III, this bind to and inhibits clotting factors II,IX,XI and XII

Given intravenously or sub-cutaneously

Side effects = allergic reactions, haemorrhage, HIT, hyperkalaemia

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16
Q

Describe anticoagulant Warfarin mechanism of action

A

Structural Analogue of Vit K

Blocks vit. k reductase and therefore carboxylation
Blocks coagulation factor synthesis in the liver

Oral administration

Side effects = haemorrhage, crosses placenta and BBB (foetal haemorrhage)

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17
Q

Deceive aspirins use as an anti-thrombolytic agent

A

Used in low doses

It inhibits platelet synthesis, and COX irreversibly

Prevents re infarction (lowers risk by 20%)

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18
Q

Describe tissue plasminogen activator (t-PA) as a fibrinolytic ?

A

Enzyme produced by vascular endothelium

Only activate s plasminogen bound to fibrin (clot selective)

Side effects = haemorrhage

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19
Q

What are platelets derived from ?

A

Megokaryocytes in bone marrow

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20
Q

What normally suppresses platelet activation ?

A

Prostacyclin
Nitric oxide
Antithrombin III

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21
Q

What do fibrin strands enmesh ?

A

Erythrocytes and platelets

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22
Q

What is Von Willebrand disease ?

A

A deficiency in Von Willebrand factor (binds platelets to collagen)

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23
Q

What is Haemophilia A ?

A

Deficiency of factor VIII (8)

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24
Q

What is Haemophilia B ?

A

Deficiency of factor IX (9)

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25
Q

What is Haemophilia C ?

A

Deficiency of factor XI (11)

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26
Q

What digests fibrin I to soluble degradation products ?

A

Plasmin (activated by t-PA)

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27
Q

What is the treatment for venous thrombosis ?

A

Anticoagulants

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28
Q

What is the treatment for arterial thrombosis ?

A

Fibrinolytics (immediate)
Antithrombotics (long-term)

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29
Q

What is coronary steal ?

A

During vasodilation, When blood is diverted to already well perfumed areas

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30
Q

What do beta1-adrenoceptor blockers do ?

A

Competitive antagonists if adrenaline and noradrenaline at cardiac beta1-adrenoceptors

Decrease HR and SV, decrease myocardial O2 demand

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31
Q

What does Ivabradine do ?

A

Blocks Na current causing delay in SA node depolarisation

Decreases HR (not force), decreases myocardial O2 demand

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32
Q

What is after-load ?

A

Force against which LV contracts

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33
Q

What is pre-load?

A

Diastolic pressure that distends LV

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34
Q

What causes reduces after-load ?

A

Dilation of arteries

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35
Q

What causes reduced pre-load ?

A

Dilation of veins

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36
Q

What is the Bainbridge Reflex ?

A

Initiated by increased blood in atria

Causes stimulation of SA node

Stimulates barorecptors in the atria, causing increased SNS stimulation

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37
Q

What does P in the ECG wave show ?

A

Atrial depolarisation

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38
Q

What does P-Q show in ECG waves ?

A

Delay at AV node

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39
Q

What happens at Q of ECG wave ?

A

Conduction through bundle branches

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40
Q

What also happens at Q of ECG wave ?

A

Conduction through purkinje fibres

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41
Q

What happens at the QRS complex of ECG waves ?

A

Ventricular depolarisation

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42
Q

What happens at S-T of ECG waves ?

A

Plateau phase of re polarisation

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43
Q

What happens at T wave of ECG ?

A

Rapid Repolarisation

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44
Q

What causes a U wave to sometimes be present on an ECG ?

A

Repolarisation of Purkinje fibres

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45
Q

Which leads are unipolar ?

A

aVR
aVL
aVL
Chest leads 1-6

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46
Q

Which leads are bipolar ?

A

I = RA-LA

II= RA-LL

III= LA-LL

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47
Q

Which ECG leads are anterior ?

A

V1-V4

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48
Q

Which ECG leads are inferior ?

A

II , III, aVF

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49
Q

Which ECG leads are lateral ?

A

I, aVL, V5 + V6

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50
Q

What does a wave look like that is horizontal -ve to +ve from L to R ?

A

All positive wave

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51
Q

What does a wave look like that is horizontal -ve to +ve from R to L ?

A

All negative wave

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52
Q

What does an ECG wave look like that is -ve to +ve superiority to inferiorly ?

A

Positive and negative parts STANDARD PQRST ECG WAVE

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53
Q

How do you calculate HR from ECG ?

A

300/no. of big squares between each QRS

OR

No. of QRS complexes across ECG (10 seconds) x 6

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54
Q

What is normal angle for the QRS axis ?

A

-30 to +90 degrees (from limb lead I)

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55
Q

How do you find the QRS axis ?

A

By finding lead with most positive QRS complex

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56
Q

What shows left axis deviation ?

A

-30 to -90 degrees
Positive QRS in I
Negative in II and aVF

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57
Q

What shows normal axis ?

A

-30 to +90
Positive QRS in I and II

58
Q

What shows right axis deviation ?

A

+90 to +180 degrees

Negative QRS in I
Positive QRS in aVF

59
Q

What shows extreme axis deviation ?

A

+180 to -90 degrees

Negative QRS in I and II
Positive QRS in aVR

60
Q

What do normal T waves show in relation to QRS ?

A

Same polarity

61
Q

What is absolute risk ?

A

Incidence of disease in a given population

62
Q

How do you calculate absolute risk ?

A

Number of new cases per population over a specified time
E.g. 1000 obese, 100 develop CAD in 1 year = 10/1000 pa = 0.1

63
Q

How do you calculate relative risk ?

A

Compare the absolute risk of those who have the risk factor and those who don’t

Express as how many times greater or smaller among exposed

64
Q

Case-control study calculation ?

A

(exposed have disease x not exposed don’t have disease) / (not exposed have disease x exposed that don’t have disease)

65
Q

Attributable risk (AR)

A

AR = incidence of disease in exposed - incidence of disease in unexposed

66
Q

AR% calculation ?

A

(AR/ incidence of disease in exposed ) x100

67
Q

Population attributable risk (PAR) calculation

A

PAR = AR x prevalence of exposure

68
Q

PAR% calculation

A

(PAR / incidence of disease in the population)x100

69
Q

What are normal cholesterol ranges ?

A

TC = <5 mmol/L
HDL = >1 mmol/L
Non-HDL = <4mmol/L
TC to HDL ratio = <6

70
Q

What is the pathophysiology of asthma ?

A

Loss of airway epithelium
Thickening of BM
Hypertrophy of smooth muscle layer

71
Q

What are possible triggers of asthma ?

A

Inflammation - allergy, infection, exercise
Drugs - beta blockers, NSAIDs
Cold air + scents

72
Q

What is the presentation of asthma ?

A

Bronchospasm = wheeze, dyspnoea, exercise intolerance
Inflammation = cough

73
Q

What is the management of asthma ?

A

Bronchorelaxation = beta 2 agonists
Anti-inflammatories = corticosteroids, leukotrine receptor blockade, monoclonal antibodies (-mab)

74
Q

What is the maximum peak flow rate ?

A

900L/minute
Achieved by firm but flexible airway walls

75
Q

What are ways of airway narrowing ?

A

Dynamic = rapid muscle contraction, secretions
Fixed = smooth muscle bulk, thickening of BM

76
Q

What is different about smooth muscle in asthma ?

A

There are mast cells present

77
Q

What do the mast cells in smooth muscle in asthma cause ?

A

Variable airway calibre , leading to diurnal variation (nighttime or morning)

78
Q

How to measure asthma via enhanced nitric oxide ?

A

Increased eosinophilic inflammation
Normal value 30ppb

79
Q

Describe how spirometers can be used to measure asthma ?

A

Narrow airway relaxes in response to salbutamol (approx 15% improvement)

80
Q

What are the 3 phases of asthma ?

A

1) smooth muscle only - triggered by mediator ,rare wheezy episodes
2) chronic inflammation- irritates smooth muscle, regular wheezy episodes
3) acute inflammation- viral infection, clinical exacerbations

81
Q

Describe type 2 inflammation in asthma

A

Cells = lymphocytes, eosinophils and mast cells
Cytokines = IL-4, IL-5
Prostanoids = PGE2, Leukotrine D4
Immunoglobulins = specific IgE

82
Q

What does histamine in asthma mast cell mediation cause ?

A

Smooth muscle contraction

83
Q

What type of immune cell fights viruses ?

A

Neutrophils and lymphocytes

84
Q

What type of immune cells fight parasitic infection ?

A

Eosinophils

85
Q

What type of immune cells fight bacterial infection ?

A

Neutrophilic

86
Q

What is the mechanism of action of B2 Agonists ?

A

Bind to B-2 adrenergic receptors activating a G protein
Cyclic AMP acts as a second messenger
Smooth muscles relaxes widening the airway

87
Q

What is the main side effect associated with B-2 adrenoceptor agonists such as salbutamol) ?

A

Tremor

88
Q

What is the partial pressure of O2 in alveoli ?

A

102

89
Q

What is the partial pressure of CO2 in alveoli ?

A

40

90
Q

What is the distance between alveoli and red blood cells ?

A

1-2um : includes type 1 alveolar epithelium, capillary endothelium and BM

91
Q

How quickly do red blood cells pass through capillaries ?

A

Less than 1 second

92
Q

For each mmHg of Po2 how much oxygen is there ?

A

0.003ml/100ml of blood

93
Q

How many ml of O2 per litre of blood in the arteries ?

A

3ml O2/L blood

94
Q

How do pH and temperature effect the oxygen dissociation curve ?

A

High pH or high temperature decrease oxygen affinity for Hb

95
Q

At what O2 saturation does Hb affinity loss become steep ?

A

60mmHg

96
Q

What is the respiratory exchange ratio ?

A

Ratio of expired CO2 to O2 uptake

97
Q

What is the respiratory exchange ratio in normal conditions?

A

0.8

98
Q

Which 3 forms is CO2 carried in the blood ?

A

Dissolved (7%)
Bound to Hb (23%)
Converted to bicarbonate (70%)

99
Q

What is the bicarbonate equation ?

A

H2O + CO2 —> H2CO3 —> H+ + HCO3-

100
Q

What is the V/Q ratio for lungs ?

A

0.8-1.2

101
Q

What are possible V/Q ratios for individual alveoli?

A

V/Q > 1 = ventilation exceeds perfusion

V/Q < 1 = perfusion exceed ventilation

102
Q

Where does the brain receive neural signals from for breathing control ?

A

Chemoreceptors: feedback on blood Po2, PCo2 and pH
Mechanoreceptors : feedback on mechanical status of lungs, chest wall and airways

103
Q

Where in the brain controls breathing ?

A

Brainstem

104
Q

Where are peripheral chemoreceptors found ?

A

Aortic arch and carotid sinuses

105
Q

Which nerve do aortic chemoreceptors use ?

A

Vagus (X)

106
Q

What nerve do carotid chemoreceptors use ?

A

Glossopharyngeal (IX)

107
Q

Where do the nerves send chemoreceptor signal to in the brainstem ?

A

Nucleus Tractus Solitarius (NTS)

108
Q

What chemoreceptors are responsible for hypoxia response ?

A

Peripheral

109
Q

What chemoreceptors are responsible for hypercapnia or pH decrease responses ?

A

Central

110
Q

What are central chemoreceptors?

A

Clusters of neurones in the brainstem

111
Q

Which type of chemoreceptor plays a major role in moment to moment breathing ?

A

Central

112
Q

What do mechanoreceptors do ?

A

Detect movement of the lung and chest wall

113
Q

What nerve do mechanoreceptors signal through ?

A

Vagus (X)

114
Q

What are the locations and functions of mechanoreceptors?

A

Airway smooth muscles = terminate inspiration
Airway epithelium = sigh or shortened expiration

115
Q

What makes up the ventral respiratory group in the brainstem ?

A

Pattern and rhythm generating neurones

116
Q

What do respiratory pattern generating neurones do ?

A

2 types : inspiratory and expiratory active during their respective phases of breathing

117
Q

What do respiratory rhythm neurones do ?

A

Produce rhythmic output through the spinal nerves to respiratory muscles (diaphragm + intercostals) to produce rhythmic breathing

118
Q

What are the 3 major components of acid-base regulation ?

A

Buffering
Ventilation
Renal regulation

119
Q

What are buffers ?

A

Weak acids partially dissolved in solution

120
Q

What is the Henderson hasselbach equation ?

A

CO2 + H2O —> H2CO3 —> HCO3 + H+

121
Q

What is metabolic acidosis ?

A

Low HCO3 therefore low pH

122
Q

What is metabolic alkalosis ?

A

high pH

123
Q

What is respiratory acidosis ?

A

High CO2 therefore low pH

124
Q

What is respiratory alkalosis ?

A

Low CO2 therefore high pH

125
Q

What is the ADME pneumonic ?

A

Absorption
Distribution
Metabolism
Excretion

126
Q

Which method of drug administration is preferred ?

A

Oral

127
Q

Volume of distribution calculation ?

A

Dose (mg) / concentration ( mg/L-1)

128
Q

How to calculate dose for individual ?

A

Typical weight adjusted volume x weight

129
Q

Dose calculation?

A

Dose = concentration x volume

130
Q

What is loading dose ?

A

A single dose which brings a drug to its target range

131
Q

What is the clinical significance of first pass metabolism ?

A

Differences (due to age + gender)
Some drugs undergo more first pass metabolism than others
Impact peak drug concentrations

132
Q

What is bioavailability?

A

The fraction of the drug that reaches systemic circulation after oral administration

F= effective dose after oral / effective does after IV
(F=%effective dose)

133
Q

What are the routes of clearance of drugs ?

A

Total = renal + hepatic + other

134
Q

What is clearance ?

A

The rate at which drug is removed from the body

135
Q

What is clearance proportional to ?

A

Drug concentration

136
Q

What is a drug-drug interaction ?

A

When a second drug alters the effects of the first drug

137
Q

What are inhibitors ? (CYP450 enzyme)

A

They reduce clearance by inhibiting drug metabolism, increasing half life, meaning drug can accumulate with repeated dosing

138
Q

What do inducers do ? (CYP450)

A

Accelerated clearance of drugs metabolised, shorter half life

139
Q

What are the features of type 1 respiratory failure ?

A

Low O2 = <8kPa
Pneumonia
Cardiac failure
Pulmonary embolism

140
Q

What are the features of type 2 respiratory failure ?

A

Low O2 = < 8kPa
High CO2 = >6kPa
Opiate overdose
Neuromuscular weakness
Advanced COPD
Severe respiratory fatigue

141
Q

What are the symptoms of heart failure ?

A

Breathlessness
Ankle swelling (oedema)
Fatigue

142
Q

What are the 3 goals of HF treatment ?

A

Relief of symptoms
Avoid admission or readmission
Prevent premature death

Y1 Medicine (5 decks)

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