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Phase 1 Notes > Cardio > Flashcards

Cardio Flashcards

1
Q

In Haemopoesis, Hemocytoblasts form?

A

Proerythroblasts - RBC
Monoblast - Monocyte
Myeloblast - Probgranulocyte -
basophil/eosinophil/neutrophil
Megakaryoblast - M.k.cyte - platelet

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2
Q

Describe RBC

A

Life span - 120 days
Young RBC = reticulocytes
Erythropeotin is secreted by kidneys to stimulate RBC production.
Has no nucleus, is biconcave and filled with haemoglobin (2a, 2beta chains and Fe)

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3
Q

Describe WBC

A

Life span - 6-10 hours
Produced in bone marrow/thymus/lymphatic organs

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4
Q

Describe platelets

A

Life span - 7-10 days
Produced in bone marrow
Contains secretory granules
-alpha
-dense
-lysosomes
-peroxisome (destroy unwanted particles)

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5
Q

What does blood contain?

A

Red blood cells
White blood cells
Platelets
Plasma:
- Water, electrolytes, proteins, albumin, hormones, coagulation factors

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6
Q

What is plasma without clotting factors called?

A

Serum

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7
Q

What is haemocrit

A

Ratio of RBC to total blood volume (0.45)

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8
Q

Describe Neutrophils

A

Inflammatory response
Multilobed with faint granules

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9
Q

Describe monocytes

A

Immature- becomes macrophages + APC
Reniform nucleus

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10
Q

Describe eosinophils

A

Antihistamine = reduces allergic response
Pink granules and IGE receptors

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11
Q

Describe basophils

A

Histamines = increases allergic response
Dark blue granules and IgE receptors

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12
Q

Describe lymphocytes

A

Cell mediated + innate response
Little cytoplasm, mostly nucleus

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13
Q

Describe production of platelets

A

Megakaryocytes undergo endomitosis (DNA doubles but cell doesn’t split)
CSM loses fragments = platelets
Inactive platelets = smooth + discoid
Activated = increased surface area + pseudopod

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14
Q

How do platelets work?

A

They release:
Energy - e- via ATP, serotonin, Ca2+
Dense granules - PDGF, VWF, Fibrinogen
To increase thromobocytosis (increases clots)
Decrease thrombocytopenia (cuts can cause bleeding)

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15
Q

Water distribution

A

Total body water = 60% = 42L
-Intracellular = 40% = 28L
-Extracellular = 20% = 14L
—Intravascular = 3L
—Interstitial = 11L

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16
Q

What is osmolality?

A

Concentration of:
2Na + 2K + urea + glucose (mmol/L)

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17
Q

Does water follow higher or lower osmolality?

A

ICF = ECF osmolality normally, but water will follow higher osmolality

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18
Q

Predominant cations in ICF vs ECF

A

ICF = K+ (110mmol/L)
ECF = Na+ (135mmol/L)

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19
Q

Why is ECF Osmolality tightly regulated?

A

Changes lead to a rapid response and could be dangerous for the brain.
Normal plasma osmolality = 275-295mmol/kg

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20
Q

Hydrostatic vs Oncotic pressure

A

Hydrostatic is pressure difference
Plasma -> Interstitial fluid

Oncotic/Osmotic is pressure difference caused by protein conc
Interstitial fluid -> plasma

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21
Q

Why don’t we give fluid intravenously?

A

Water enters blood cells causing them to expand + burst = haemolysis

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22
Q

Negative feedback loop when water deprivation increases ECF Osmolality

A
  • Water moves from ICF to ECF
  • Stimulation of thirst centre in hypothalamus
  • Release of ADH from posterior pituitary gland
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23
Q

Negative feedback loop when water deprivation decreases ECF volume (slower)

A

Angiotensinogen in the liver is converted to Angiotensin 1 then 2 by ACE in the lungs.
This causes vasoconstriction, ADH secretion, Aldosterone secretion, increased sympathetic activity and water retention.

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24
Q

Symptoms of hyponatraemia (too much water)

A

Headache, confusion, convulsions,
Cerebral over hydration = pressure increases in skull

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25
Q

Negative feedback loop when water deprivation decreases ECF Osmolality

A

-Movement of water into ICF
- Inhibition of ADH secretion
- No stimulation of thirst centre
However risk of water intoxication

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26
Q

Oedema vs serous effusion

A

Oedema - Excess accumulation of interstitial fluid
Serous Effusion - Excess water in a body cavity

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27
Q

4 different oedema causes

A
  1. Inflammatory - Increased micro vascular permeability allows Albumin and so more water out
  2. Venous - Water leaving at venous end instead of entering
  3. Lymphatic - Lymph vessels blocked
  4. Hypoalbuminaemic - Low protein content so nothing draws water back at the venous end
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28
Q

2 different pleural effusions

A

Normal pleural space contains 10ml of fluid
Transudate - High pressure, low protein forces water out of capillaries
Exudate - Inflammation increases permeability of capillaries to protein and water follows

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29
Q

Timeline of history of transfusion

A

Transfusion from one animal to another
1666- From animal to human
1667- From human to human
1930- Discovers ABO
1912- Develops surgical technique for transfusion
1915- Develops anticoagulant for storage
1921- First blood donor service established
1940- Identify rhesus antigen
1940- Develops fractionation of plasma proteins

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30
Q

What are the 4 major blood groups?

A

A, B, AB, O

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31
Q

What ABO antibodies do we have?

A

First true antibodies produced after 3 months
Mixture of IgM and IgG
Maximal titre at 5-10 years, decreases with age

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32
Q

What antibodies and antigens do each blood group have?

A

Group = Antibodies, Antigens
A = Anti-B, A
B = Anti-A, B
AB = None, A+B
O = Anti-A+B, None

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33
Q

How many Rhesus antigens are there and which one is the most important?

A

Over 45 different Rh antigens
RhD is the most important

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34
Q

What is haemolytic disease

A

Rh+ baby blood enters Rh- mother and causes production of Rh antibodies.
Rh antibodies remain in mothers bloodstream and attach Rh+ second baby causing Rh disease.

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35
Q

Forward typing vs Reverse typing

A

Forward = unknown patient blood + known antibody
Reverse = patient plasma + known antigen

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36
Q

Why do we cross match before blood donation?

A

Other blood groups + antigens could cause problems

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37
Q

Blood donation tests

A

Hep B
HIV
Hep C
…

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38
Q

Blood storage

A

Blood spun and plasma may be kept frozen to make FFP.
Red cells filtered for WBC then platelets removed

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39
Q

Platelet donation

A

Most units pooled from 4 different donations
Stored at 22 degrees with continuous agitation
7 day shelf life

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40
Q

Fresh Frozen Plasma (FFP)

A

From male donors only (fewer antibodies)
Born after 1996 (food chain exposure)
Pooled versions are more standardised

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41
Q

How is cryptoprecipitate formed?

A

Thawing FFP to 4 degrees then skimming off fibrinogen rich layer.
Used with bleeding and massive transfusion

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42
Q

What is Immunoglobulin (IVIg) used for?

A

Immune conditions
Antibodies to viruses

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43
Q

How to ensure safe delivery of blood?

A

Patient identification
2 sample rue
Serologically cross matches
Check for bacterial contamination

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44
Q

What are the 3 main phases of the cardiac cycle?

A

LV contraction
LV relaxation
LV filling

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45
Q

Describe LV Contraction

A

Isovolumic contraction (both valves closed and volume stays the same)
Maximal ejection (Ejection fraction = 65%F, 55%M)

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46
Q

Describe LV relaxation

A

Start of relaxation and reduced ejection
Isovolumic relaxation

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47
Q

Describe LV filling

A

Rapid LV filling and suction
Slow LV filling (diastasis)
Atrial booster

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48
Q

Describe systole

A

Wave of depolarisation arrives and Ca2+ arrives at contractile proteins.
LVp rises above LAp and ejection starts

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49
Q

Describe diastole

A

LVp peaks then decreases
Aortic distensibility maintained and reduced ejection

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50
Q

Ventricular filling

A

LVp < LAp and rapid filling starts
Diastasis LVp = LAp (filling temporarily stops)
Booster creates pressure gradient and renews filling

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51
Q

Correlate the sounds to the cell cycle.

A

Systole = 1st to 2nd sound
Diastole = 2nd to 1st sound
In between indistinguishable clinically

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52
Q

Preload vs Afterload

A

Pre - Volume of blood present before LV contraction
After - Final volume of blood when contracting

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53
Q

What is Starling’s Law?

A

The larger the volume of the heart, the greater the energy and therefore stronger the contraction.

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54
Q

What is a positive inotropic effect?

A

Increased diastolic heart volume leads to increased velocity and force of contraction.

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55
Q

Elasticity definition

A

Myocardial ability to recover its normal shape after systolic stress

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56
Q

Definition of diastolic distensibility

A

Pressure required to fill the ventricle to the same diastolic volume.

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57
Q

Wave of excitation moves through:

A

SAN -> AVN -> Purkinje fibres -> Cardiac Myocytes

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58
Q

Describe excitation-contraction coupling

A

Action potential depolarises sarcoplasmic reticulum and Ca2+ moves into the cytosol.

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59
Q

Describe the bands of a sarcomere

A

A - whole Myosin
I - just actin
Z - Ends of sarcomere
H - middle

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60
Q

Describe myosin

A

2 heavy, 4 light chains with heads perpendicular and bending towards centre of sarcomere

61
Q

Describe actin

A

Double stranded helix forms globular protein

62
Q

Describe tropomyosin

A

Two helical polypeptide chains between two actin strands

63
Q

Describe the 3 parts of troponin

A

TnT - binds tops in to tropomyosin
TnI - with tropomyosin inhibits actin and myosin interaction
TnC - ca2+ binding sites signal contraction and drives TnI away from myosin

64
Q

Typical speed and voltage of an electrocardiogram (ECG)

A

Speed = 25mm/sec
Voltage = 10mm/mV
(5 big horizontal squares = 1s)
(2 big vertical squares = 1mV)

65
Q

Rate calculations (at 25mm/s)

A

Rate (bpm) = (cycles in 10 secs) x 6
Rate (bpm) = 300/no. Of large squares between cardiac cycles

66
Q

Which ions move during the phases of cardiac action potential?

A

Absolute refractory period:
0. Depolarisation= Na+ and Ca2+ enters
1. Na+ channels close
2. Ca2+ enters and K+ leaves
3. Repolarisation = Ca2+ channels close and K+ leaves
4. Resting potential = Leaky K+ channels

67
Q

Blood flow in organs

A

Liver = 27%
Kidneys = 22%
Muscle = 15%
Brain = 14%
Skin = 6%
Bone = 5%
Heart = 4%

68
Q

Circulatory dynamics

A

Smaller diameter gives faster velocity

69
Q

Which is the principal site of resistance?

A

Arterioles contracting, therefore
TPR= Total arteriolar resistance

70
Q

Where is most blood in the body?

A

70% in veins and venules

71
Q

Cardiac Output equation

A

Cardiac Output = Heart Rate x Stroke volume

72
Q

Blood pressure equation

A

Blood pressure = Cardiac output x Total Peripheral Resistance

73
Q

Pulse pressure equation

A

Pulse pressure = Systolic - Diastolic pressure

74
Q

Mean arterial pressure equation

A

MAP = Diastolic pressure + 1/3 pulse pressure

75
Q

Ohms Law

A

Flow = Pressure gradient/ resistance

76
Q

Poiseuilles equation

A

Change in pressure = 8L/pi r^4
(Small change in radius = large change in flow)

77
Q

Frank-Starling Mechanism

A

Increase in:
End Diastolic volume -> Stretch -> Force of contraction -> Stroke Volume -> CO

78
Q

5 components of BP control

A

(Pressure inside arteries)
Auto regulation
Local mediators
Humoral factors
Baroreceptors
Central (neural) control

79
Q

Name vasoconstrictors

A

Blood pressure
Endothelin 1

80
Q

Name some vasodilators

A

Hypoxia
Prostacyclin
Adenosine
Bradykinin
NO
K+
CO2

81
Q

Name some hormonal vasoconstrictors

A

Epinephrine
Angiotensin 11
Vasopressin

82
Q

Name some hormonal vasodilators

A

Epinephrine
Atrial Natriuretic Peptide
Endothelium derived: Nitric Oxide
Prostacyclin

83
Q

Describe baroreceptors

A

Primary in carotid sinus and aortic arch
Short term regulation of BP
BP -> Firing to medulla -> CO/TPR -> BP
Long term regulation of BP is blood volume (Renin-angiotensin)

84
Q

Describe heart muscle

A

Intercalated discs of cardiac muscle fibres joined by gap junctions.

85
Q

Nernst Equation

A

E(Na) = (61.5/z)log10(Ions out/ Ions in)
=-90mv at 37 degrees (resting potential)

86
Q

Describe the 4 stages of an action potential of cardiac myocytes

A
  1. Depolarisation Na+ floods in
  2. Na+ close and transient outflow of K+
  3. Plateau Ca2+ enters and maintains depolarised state
  4. Repolarisation K+ floods out
87
Q

What principles allow wave of excitation to spread?

A

All or nothing principle - Na+ channels are either open or closed (Gap junctions allow cell to cell propagation)
Refractory period

88
Q

Describe excitation-contraction coupling in detail

A

.Ca2+ influx through surface ion channels
.Amplication of Ca2+ influx with NaCa channels
.Ca2+ activates release of Ca2+ from sarcoplasmic reticulum
.Ca2+ binds to troponin and conformational change reveals myosin binding sites
Myosin head cross links with actin
Myosin heads pivot causing contraction

89
Q

Which has longer contraction times- skeletal or cardiac?

A

Cardiac are up to 15x longer in duration due to slower calcium channels and decreased permeability to potassium after an action potential.

90
Q

Describe how SAN depolarisation is different

A

Has special ion channels so is gradually depolarising until -35mv (threshold) then rapid depolarisation via Ca2+ influx. No resting membrane and no plateau

91
Q

Phase 4 ‘resting’ SAN slope is affected by what 5 things?

A

Autonomic tone
Drugs
Hypoxia
Electrolytes
Drugs

92
Q

Chronotropic vs Ionotropic

A

Sympathetic
Positively chronotropic increases heart rate
Positively ionotropic increases force of attraction
Parasympathetic is the opposite

93
Q

Sympathetic stimulation of SAN controlled by

A

Adrenaline
Noradrenaline
cAMP

94
Q

Parasympathetic stimulation of SAN controlled by

A

Acetylcholine
M2 receptors

95
Q

How is the AVN different to the SAN?

A

AV fibres are smaller and have fewer gap junctions.
Delays impulses so limits dangerous tachycardias

96
Q

Describe His-Purkinje fibres

A

Very large fibres and high permeability at gap junctions to allow rapid and coordinated ventricular contraction.

97
Q

Which is the fastest - SAN / AVN / Purkinje fibres

A

SAN
If SAN fails, AVN will pick up.
Myocardium is the slowest and is thought to improve dynamics of contraction

98
Q

Absolute vs Relative Refractory period

A

After absolute, some Na+ channels still activated and only strong stimuli can cause action potentials

99
Q

Describe the PQRST phases in an ECG

A

P = Atrial depolarisation
QRS complex = Ventricular depolarisation
T = Ventricular Repolarisation

100
Q

Atrial fibrillation vs Atrial flutter

A

Fibrillation- Random atrial activity and ventricular capture. Irregular irregular rhythm
Flutter - Short circuit so organised atrial activity of 300/min. Usually regular

101
Q

PR Interval time

A

120-200ms
(3 to 5 small squares)

102
Q

QRS complex timing

A

Less than 120ms
(3 small squares)
If QRS > 120, most likely bundle branch block

103
Q

QT timings

A

Men 350-440ms
Women 350-460ms

104
Q

Electrode vs Lead

A

Electrode - physical connections (10 to measure a 12 lead ECG)
Lead - Graphical representation of electrical activity in a particular vector

105
Q

Where are the 4 limb electrodes placed?

A

RA
RL
LL
LA
(Positive voltage means current flows to electrodes)

106
Q

Bipolar vs Unipolar leads

A

Bi - Measures potential difference between two electrodes (one designated positive)
Uni - Measures the potential difference between an electrode (positive) and a combined reference electrode

107
Q

Which electrode is the neutral electrode?

A

RL
- Reduces artefact and is not directly involved in ECG measurement

108
Q

What is Reading 1

A

RA to LA

109
Q

What is reading 2?

A

RA to LL

110
Q

What is reading 3?

A

LA to LL

111
Q

What does a larger voltage represent?

A

Bigger current flow to specific electrode
(Directions of voltage show directions of current)

112
Q

What direction is aVR?

A

Heart to RA

113
Q

What direction is aVL?

A

Heart to LA

114
Q

What direction is aVF?

A

Heart to LL

115
Q

Rules of thumb for normal axis

A

Positive 1+2 = normal
Positive 1 + negative 2 (Leaving) = Left axis deviation
Negative 1 + positive 2 (Reaching) = Right axis deviation

116
Q

Which walls correspond to which arteries?

A

Right coronary artery - Inferior LV Wall
Left circumflex - Lateral LV Wall
LAD - Anterior LV Wall

117
Q

Which readings correspond to which walls?

A

Lateral - 1, aVL
Inferior - 2, 3, aVF

118
Q

Describe the positions of the unipolar chest leads

A

(Septal) V1, V2 either side of septum 4th intercostal space
(Anterior) V3, V4,
(Latera) V5, V6 diagonally down until 6th rib midaxillary

119
Q

Describe antherogenesis

A

Build up of fatty fibrous plaque.
If it ruptures/ thrombosis occurs myocardial infarction, ischaemic stroke etc could occur

120
Q

Describe platelet activation

A

Shape change from smooth discoid to pseudopodia (finger like extensions increase SA and cell interaction)

121
Q

Describe platelet adhesion (+aggregation)

A

On surface of platelet is glycoprotein 2b/3a receptors which increase upon activation. Fibrinogen links the receptors and binds the platelets together.
GP2b/3a also bind to Von Willebrand factors (VWF) attached to exposed sub endothelial collagen on damaged vessel walls.

122
Q

Describe platelet amplification pathway - Thromboxane A2

A

Activated platelets release Thromboxane A2 which activates next platelet (aspirin inhibits)

Rapid response = cross linking of GP2b/3a for platelet aggregation

123
Q

Name the different agonists that cause platelet activation (rapid response to bleeding)

A

Thrombin
Thromboxane A2
Collagen
ADP

124
Q

Describe the cyclooxygenase pathway of endothelial cells

A

Arachidonic Acid
(COX1 - Mediates platelet aggregation)
(COX2 - Mediates inflammation and inhibits aggregation)
- High dose aspirin inhibits both
Prostaglandin H2
Prostacyclin
Platelet aggregation (limits blood flow to prevent bleeding)

125
Q

Describe the cyclooxygenase pathway of platelets

A

Arachidonic Acid
(COX1 - Mediates platelet aggregation)
- Low dose aspirin inhibits
Prostaglandin H2
Thromboxane A2
Platelet aggregation

126
Q

Describe the ADP signalling pathway

A

P2Y1 and P2Y12 on the membrane are activated by ADP and attached.
G proteins attached to P2Y1 starts aggregation
G proteins attached to P2Y12 amplify aggregation

127
Q

Describe amplification loops via dense granules

A

Activated platelets release dense granules which release ADP. This activated P2Y12 and sustains platelet aggregation.

128
Q

Describe amplification loops via Thrombin Par1

A

Thrombin from the coagulation cascade activated Par1 which releases Ca2. This inhibits translocase and activates scramblase which leads to expression of aminophospholipids on the outer membrane. More thrombin is released to amplify the pathway. This causes shape change and cross links between GP2b/3a receptors (aggregation)

129
Q

What is the fibrinolytic system?

A

Checks in system to regulate activation pathways

130
Q

Describe the fibrinolytic system

A

Endothelium -> tPA catalyses
Plasminogen -> Plasmin catalyses
Fibrin -> Fibrin degradation products

131
Q

Name the inhibitors which regulate the fibrinolytic system

A

PAI-1 inhibits
tPA catalyst
Antiplasmin inhibits
Plasmin catalysts

132
Q

Describe haemoglobin structure

A

2 alpha and 2 beta chains, each containing a heme group and Fe2+ for O2 association

133
Q

Innate vs adaptive immunity

A

Innate - Non-specific phagocytosis (All other wbc)
Adaptive - Antigen specific antibodies (T/B cells)

Both release cytokines

134
Q

Humoral vs Cell mediated Immunity

A

Humoral - B cells secrete antibodies
Cell mediated - T cells defend

135
Q

What do cardiac myocytes do?

A

Heart pumping depends on interaction between contractile proteins and its muscular wall transforming chemical energy into mechanical energy.

136
Q

Main neural influences on medulla

A

Baroreceptors
Chemoreceptors
Hypothalamus
Cerebral Cortex
Skin
Change in blood O2, CO2

137
Q

Describe chemoreceptors control of respiration

A

Central in medulla: Increased PaCO2 -> vasoconstriction-> peripheral resistance -> Increased BP
Peripheral: Effects of PaO2

138
Q

Function of alpha granules

A

Mediates release of surface P-selection (monocyte bind to) and release of inflammatory mediators, adhesion molecules and coagulation factors

139
Q

Embryology: Day 17-21

A

Formation of blood islands on yolk sac turns into vascularisation of yolk sac, chorionic villus and stalk

140
Q

Embryology: Day 18

A

Angioblastic cords form throughout embryonic disc
Vasculogenesis of axial blood vessels from mesoderm commences and angiogenesis adds to. Driven by growth factors, proliferation and sprouting occurs

141
Q

What happens to each aortic arch?

A

1 - Maxillary (head)
2 - Ear
3 - common carotid
4 - Subclavian
5 - Disappears
6 - Pulmonary trunk and ductus arteriosus

142
Q

Where is the cardiovascular system derived from embryology?

A

Mesoderm

143
Q

Embryology: What develops better cardiac function?

A

More transcription factors and duplicated genes
= more complex
= better survival

144
Q

Embryology: 3 stages of cardiac formation

A

Formation of primitive heart tube
Cardiac looping
Cardiac septation

145
Q

Describe formation of the primitive heart tube

A

Cells from the carcinogenic region form two endocardial tubes which fuse and form a single primitive heart tube. (Day 19)

146
Q

Describe cardiac looping

A

Day 22: The heart begins to beat
Primitive atrium and sinus venous moves superioris and posteriorly
Primitive ventricle moves to left
Bulbis cordis moves inferiorly, anteriorly.

147
Q

Embryology: How is left determined?

A

Node secretes nodal which circulates to the left due to ciliary movement. A cascade of transcription factors transduce looping.

148
Q

Describe cardiac septation

A

Endocardial cushions grow from the sides of the atrioventricular canal to partition it into 2 separate openings

Phase 1 Notes (9 decks)

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