Cardio Flashcards
(148 cards)
1
Q
In Haemopoesis, Hemocytoblasts form?
A
Proerythroblasts - RBC
Monoblast - Monocyte
Myeloblast - Probgranulocyte -
basophil/eosinophil/neutrophil
Megakaryoblast - M.k.cyte - platelet
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)
3
Q
Describe WBC
A
Life span - 6-10 hours
Produced in bone marrow/thymus/lymphatic organs
4
Q
Describe platelets
A
Life span - 7-10 days
Produced in bone marrow
Contains secretory granules
-alpha
-dense
-lysosomes
-peroxisome (destroy unwanted particles)
5
Q
What does blood contain?
A
Red blood cells
White blood cells
Platelets
Plasma:
- Water, electrolytes, proteins, albumin, hormones, coagulation factors
6
Q
What is plasma without clotting factors called?
A
Serum
7
Q
What is haemocrit
A
Ratio of RBC to total blood volume (0.45)
8
Q
Describe Neutrophils
A
Inflammatory response
Multilobed with faint granules
9
Q
Describe monocytes
A
Immature- becomes macrophages + APC
Reniform nucleus
10
Q
Describe eosinophils
A
Antihistamine = reduces allergic response
Pink granules and IGE receptors
11
Q
Describe basophils
A
Histamines = increases allergic response
Dark blue granules and IgE receptors
12
Q
Describe lymphocytes
A
Cell mediated + innate response
Little cytoplasm, mostly nucleus
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
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)
15
Q
Water distribution
A
Total body water = 60% = 42L
-Intracellular = 40% = 28L
-Extracellular = 20% = 14L
—Intravascular = 3L
—Interstitial = 11L
16
Q
What is osmolality?
A
Concentration of:
2Na + 2K + urea + glucose (mmol/L)
17
Q
Does water follow higher or lower osmolality?
A
ICF = ECF osmolality normally, but water will follow higher osmolality
18
Q
Predominant cations in ICF vs ECF
A
ICF = K+ (110mmol/L)
ECF = Na+ (135mmol/L)
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
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
21
Q
Why don’t we give fluid intravenously?
A
Water enters blood cells causing them to expand + burst = haemolysis
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
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.
24
Q
Symptoms of hyponatraemia (too much water)
A
Headache, confusion, convulsions,
Cerebral over hydration = pressure increases in skull
25
Negative feedback loop when water deprivation decreases ECF Osmolality
-Movement of water into ICF
- Inhibition of ADH secretion
- No stimulation of thirst centre
However risk of water intoxication
26
Oedema vs serous effusion
Oedema - Excess accumulation of interstitial fluid
Serous Effusion - Excess water in a body cavity
27
4 different oedema causes
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
28
2 different pleural effusions
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
29
Timeline of history of transfusion
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
30
What are the 4 major blood groups?
A, B, AB, O
31
What ABO antibodies do we have?
First true antibodies produced after 3 months
Mixture of IgM and IgG
Maximal titre at 5-10 years, decreases with age
32
What antibodies and antigens do each blood group have?
Group = Antibodies, Antigens
A = Anti-B, A
B = Anti-A, B
AB = None, A+B
O = Anti-A+B, None
33
How many Rhesus antigens are there and which one is the most important?
Over 45 different Rh antigens
RhD is the most important
34
What is haemolytic disease
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.
35
Forward typing vs Reverse typing
Forward = unknown patient blood + known antibody
Reverse = patient plasma + known antigen
36
Why do we cross match before blood donation?
Other blood groups + antigens could cause problems
37
Blood donation tests
Hep B
HIV
Hep C
…
38
Blood storage
Blood spun and plasma may be kept frozen to make FFP.
Red cells filtered for WBC then platelets removed
39
Platelet donation
Most units pooled from 4 different donations
Stored at 22 degrees with continuous agitation
7 day shelf life
40
Fresh Frozen Plasma (FFP)
From male donors only (fewer antibodies)
Born after 1996 (food chain exposure)
Pooled versions are more standardised
41
How is cryptoprecipitate formed?
Thawing FFP to 4 degrees then skimming off fibrinogen rich layer.
Used with bleeding and massive transfusion
42
What is Immunoglobulin (IVIg) used for?
Immune conditions
Antibodies to viruses
43
How to ensure safe delivery of blood?
Patient identification
2 sample rue
Serologically cross matches
Check for bacterial contamination
44
What are the 3 main phases of the cardiac cycle?
LV contraction
LV relaxation
LV filling
45
Describe LV Contraction
Isovolumic contraction (both valves closed and volume stays the same)
Maximal ejection (Ejection fraction = 65%F, 55%M)
46
Describe LV relaxation
Start of relaxation and reduced ejection
Isovolumic relaxation
47
Describe LV filling
Rapid LV filling and suction
Slow LV filling (diastasis)
Atrial booster
48
Describe systole
Wave of depolarisation arrives and Ca2+ arrives at contractile proteins.
LVp rises above LAp and ejection starts
49
Describe diastole
LVp peaks then decreases
Aortic distensibility maintained and reduced ejection
50
Ventricular filling
LVp < LAp and rapid filling starts
Diastasis LVp = LAp (filling temporarily stops)
Booster creates pressure gradient and renews filling
51
Correlate the sounds to the cell cycle.
Systole = 1st to 2nd sound
Diastole = 2nd to 1st sound
In between indistinguishable clinically
52
Preload vs Afterload
Pre - Volume of blood present before LV contraction
After - Final volume of blood when contracting
53
What is Starling’s Law?
The larger the volume of the heart, the greater the energy and therefore stronger the contraction.
54
What is a positive inotropic effect?
Increased diastolic heart volume leads to increased velocity and force of contraction.
55
Elasticity definition
Myocardial ability to recover its normal shape after systolic stress
56
Definition of diastolic distensibility
Pressure required to fill the ventricle to the same diastolic volume.
57
Wave of excitation moves through:
SAN -> AVN -> Purkinje fibres -> Cardiac Myocytes
58
Describe excitation-contraction coupling
Action potential depolarises sarcoplasmic reticulum and Ca2+ moves into the cytosol.
59
Describe the bands of a sarcomere
A - whole Myosin
I - just actin
Z - Ends of sarcomere
H - middle
60
Describe myosin
2 heavy, 4 light chains with heads perpendicular and bending towards centre of sarcomere
61
Describe actin
Double stranded helix forms globular protein
62
Describe tropomyosin
Two helical polypeptide chains between two actin strands
63
Describe the 3 parts of troponin
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
Typical speed and voltage of an electrocardiogram (ECG)
Speed = 25mm/sec
Voltage = 10mm/mV
(5 big horizontal squares = 1s)
(2 big vertical squares = 1mV)
65
Rate calculations (at 25mm/s)
Rate (bpm) = (cycles in 10 secs) x 6
Rate (bpm) = 300/no. Of large squares between cardiac cycles
66
Which ions move during the phases of cardiac action potential?
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
Blood flow in organs
Liver = 27%
Kidneys = 22%
Muscle = 15%
Brain = 14%
Skin = 6%
Bone = 5%
Heart = 4%
68
Circulatory dynamics
Smaller diameter gives faster velocity
69
Which is the principal site of resistance?
Arterioles contracting, therefore
TPR= Total arteriolar resistance
70
Where is most blood in the body?
70% in veins and venules
71
Cardiac Output equation
Cardiac Output = Heart Rate x Stroke volume
72
Blood pressure equation
Blood pressure = Cardiac output x Total Peripheral Resistance
73
Pulse pressure equation
Pulse pressure = Systolic - Diastolic pressure
74
Mean arterial pressure equation
MAP = Diastolic pressure + 1/3 pulse pressure
75
Ohms Law
Flow = Pressure gradient/ resistance
76
Poiseuilles equation
Change in pressure = 8L/pi r^4
(Small change in radius = large change in flow)
77
Frank-Starling Mechanism
Increase in:
End Diastolic volume -> Stretch -> Force of contraction -> Stroke Volume -> CO
78
5 components of BP control
(Pressure inside arteries)
Auto regulation
Local mediators
Humoral factors
Baroreceptors
Central (neural) control
79
Name vasoconstrictors
Blood pressure
Endothelin 1
80
Name some vasodilators
Hypoxia
Prostacyclin
Adenosine
Bradykinin
NO
K+
CO2
81
Name some hormonal vasoconstrictors
Epinephrine
Angiotensin 11
Vasopressin
82
Name some hormonal vasodilators
Epinephrine
Atrial Natriuretic Peptide
Endothelium derived: Nitric Oxide
Prostacyclin
83
Describe baroreceptors
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
Describe heart muscle
Intercalated discs of cardiac muscle fibres joined by gap junctions.
85
Nernst Equation
E(Na) = (61.5/z)log10(Ions out/ Ions in)
=-90mv at 37 degrees (resting potential)
86
Describe the 4 stages of an action potential of cardiac myocytes
0. Depolarisation Na+ floods in
1. Na+ close and transient outflow of K+
2. Plateau Ca2+ enters and maintains depolarised state
3. Repolarisation K+ floods out
87
What principles allow wave of excitation to spread?
All or nothing principle - Na+ channels are either open or closed (Gap junctions allow cell to cell propagation)
Refractory period
88
Describe excitation-contraction coupling in detail
.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
Which has longer contraction times- skeletal or cardiac?
Cardiac are up to 15x longer in duration due to slower calcium channels and decreased permeability to potassium after an action potential.
90
Describe how SAN depolarisation is different
Has special ion channels so is gradually depolarising until -35mv (threshold) then rapid depolarisation via Ca2+ influx. No resting membrane and no plateau
91
Phase 4 ‘resting’ SAN slope is affected by what 5 things?
Autonomic tone
Drugs
Hypoxia
Electrolytes
Drugs
92
Chronotropic vs Ionotropic
Sympathetic
Positively chronotropic increases heart rate
Positively ionotropic increases force of attraction
Parasympathetic is the opposite
93
Sympathetic stimulation of SAN controlled by
Adrenaline
Noradrenaline
cAMP
94
Parasympathetic stimulation of SAN controlled by
Acetylcholine
M2 receptors
95
How is the AVN different to the SAN?
AV fibres are smaller and have fewer gap junctions.
Delays impulses so limits dangerous tachycardias
96
Describe His-Purkinje fibres
Very large fibres and high permeability at gap junctions to allow rapid and coordinated ventricular contraction.
97
Which is the fastest - SAN / AVN / Purkinje fibres
SAN
If SAN fails, AVN will pick up.
Myocardium is the slowest and is thought to improve dynamics of contraction
98
Absolute vs Relative Refractory period
After absolute, some Na+ channels still activated and only strong stimuli can cause action potentials
99
Describe the PQRST phases in an ECG
P = Atrial depolarisation
QRS complex = Ventricular depolarisation
T = Ventricular Repolarisation
100
Atrial fibrillation vs Atrial flutter
Fibrillation- Random atrial activity and ventricular capture. Irregular irregular rhythm
Flutter - Short circuit so organised atrial activity of 300/min. Usually regular
101
PR Interval time
120-200ms
(3 to 5 small squares)
102
QRS complex timing
Less than 120ms
(3 small squares)
If QRS > 120, most likely bundle branch block
103
QT timings
Men 350-440ms
Women 350-460ms
104
Electrode vs Lead
Electrode - physical connections (10 to measure a 12 lead ECG)
Lead - Graphical representation of electrical activity in a particular vector
105
Where are the 4 limb electrodes placed?
RA
RL
LL
LA
(Positive voltage means current flows to electrodes)
106
Bipolar vs Unipolar leads
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
Which electrode is the neutral electrode?
RL
- Reduces artefact and is not directly involved in ECG measurement
108
What is Reading 1
RA to LA
109
What is reading 2?
RA to LL
110
What is reading 3?
LA to LL
111
What does a larger voltage represent?
Bigger current flow to specific electrode
(Directions of voltage show directions of current)
112
What direction is aVR?
Heart to RA
113
What direction is aVL?
Heart to LA
114
What direction is aVF?
Heart to LL
115
Rules of thumb for normal axis
Positive 1+2 = normal
Positive 1 + negative 2 (Leaving) = Left axis deviation
Negative 1 + positive 2 (Reaching) = Right axis deviation
116
Which walls correspond to which arteries?
Right coronary artery - Inferior LV Wall
Left circumflex - Lateral LV Wall
LAD - Anterior LV Wall
117
Which readings correspond to which walls?
Lateral - 1, aVL
Inferior - 2, 3, aVF
118
Describe the positions of the unipolar chest leads
(Septal) V1, V2 either side of septum 4th intercostal space
(Anterior) V3, V4,
(Latera) V5, V6 diagonally down until 6th rib midaxillary
119
Describe antherogenesis
Build up of fatty fibrous plaque.
If it ruptures/ thrombosis occurs myocardial infarction, ischaemic stroke etc could occur
120
Describe platelet activation
Shape change from smooth discoid to pseudopodia (finger like extensions increase SA and cell interaction)
121
Describe platelet adhesion (+aggregation)
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
Describe platelet amplification pathway - Thromboxane A2
Activated platelets release Thromboxane A2 which activates next platelet (aspirin inhibits)
Rapid response = cross linking of GP2b/3a for platelet aggregation
123
Name the different agonists that cause platelet activation (rapid response to bleeding)
Thrombin
Thromboxane A2
Collagen
ADP
124
Describe the cyclooxygenase pathway of endothelial cells
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
Describe the cyclooxygenase pathway of platelets
Arachidonic Acid
(COX1 - Mediates platelet aggregation)
- Low dose aspirin inhibits
Prostaglandin H2
Thromboxane A2
Platelet aggregation
126
Describe the ADP signalling pathway
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
Describe amplification loops via dense granules
Activated platelets release dense granules which release ADP. This activated P2Y12 and sustains platelet aggregation.
128
Describe amplification loops via Thrombin Par1
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
What is the fibrinolytic system?
Checks in system to regulate activation pathways
130
Describe the fibrinolytic system
Endothelium -> tPA catalyses
Plasminogen -> Plasmin catalyses
Fibrin -> Fibrin degradation products
131
Name the inhibitors which regulate the fibrinolytic system
PAI-1 inhibits
tPA catalyst
Antiplasmin inhibits
Plasmin catalysts
132
Describe haemoglobin structure
2 alpha and 2 beta chains, each containing a heme group and Fe2+ for O2 association
133
Innate vs adaptive immunity
Innate - Non-specific phagocytosis (All other wbc)
Adaptive - Antigen specific antibodies (T/B cells)
Both release cytokines
134
Humoral vs Cell mediated Immunity
Humoral - B cells secrete antibodies
Cell mediated - T cells defend
135
What do cardiac myocytes do?
Heart pumping depends on interaction between contractile proteins and its muscular wall transforming chemical energy into mechanical energy.
136
Main neural influences on medulla
Baroreceptors
Chemoreceptors
Hypothalamus
Cerebral Cortex
Skin
Change in blood O2, CO2
137
Describe chemoreceptors control of respiration
Central in medulla: Increased PaCO2 -> vasoconstriction-> peripheral resistance -> Increased BP
Peripheral: Effects of PaO2
138
Function of alpha granules
Mediates release of surface P-selection (monocyte bind to) and release of inflammatory mediators, adhesion molecules and coagulation factors
139
Embryology: Day 17-21
Formation of blood islands on yolk sac turns into vascularisation of yolk sac, chorionic villus and stalk
140
Embryology: Day 18
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
What happens to each aortic arch?
1 - Maxillary (head)
2 - Ear
3 - common carotid
4 - Subclavian
5 - Disappears
6 - Pulmonary trunk and ductus arteriosus
142
Where is the cardiovascular system derived from embryology?
Mesoderm
143
Embryology: What develops better cardiac function?
More transcription factors and duplicated genes
= more complex
= better survival
144
Embryology: 3 stages of cardiac formation
Formation of primitive heart tube
Cardiac looping
Cardiac septation
145
Describe formation of the primitive heart tube
Cells from the carcinogenic region form two endocardial tubes which fuse and form a single primitive heart tube. (Day 19)
146
Describe cardiac looping
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
Embryology: How is left determined?
Node secretes nodal which circulates to the left due to ciliary movement. A cascade of transcription factors transduce looping.
148
Describe cardiac septation
Endocardial cushions grow from the sides of the atrioventricular canal to partition it into 2 separate openings
