CVS Flashcards
1
Q
How much of the blood is the cellular component?
A
45%
2
Q
What is haemocrit and what is the normal haemocrit in a human?
A
The volume of read blood cells, normally 0.45
3
Q
What is haemopoiesis?
A
The process of the production of blood cells and platelets which continues throughout life
4
Q
Where does haemopoiesis?
A
In adults- Bone marrow
In embryonic life and infancy- Other sites
5
Q
What is the lifetime of an erythrocyte and how many are produces per second?
A
120 Days
2 million produced per second
6
Q
What is the lifetime of a platelet?
A
7-10 Days
7
Q
Where are the precursor cells of red blood cells located and what is a young red blood cell known as?
A
In adults- The axial skeleton
In children- All bones
In Utero- The yolk sac, the liver, the spleen
If they are found in the blood, it is a sign of leukaemia
Young red blood cells are known as reticulocytes
8
Q
Describe the hormonal growth factors that stimulate the precursor stem cells to proliferate?
A
Erythropoietin (made in the kidney)- Stimulates erythrocytes
G-CSF (granulocyte colony stimulating factor)- White Blood Cells
Tpo- Platelets
9
Q
What causes the oxygen disassociation curve to shift?
A
Shifts right when pH is decreased or temperature increases
10
Q
What does a red blood cell consist of?
A
Membrane to enclose haemoglobin, Enzymes of glycolysis, and haemoglobin
11
Q
Describe Haemoglobin
A
Carries oxygen from lungs to tissues where it transfers oxygen to myoglobin in muscles. Haemoglobin is formed of 2 alpha and 2 beta chains and 4 haem groups.
12
Q
How do the various blood types work?
A
There is a gene that results in the synthesis of A antigens on red blood cells, and a gene that results in the synthesis of the B antigen. Having neither= Type O (Most common) Having AB (Most rare) Having Just A (More common than B) Having just B
13
Q
What are the antibodies/antigens in the blood of each blood type?
A
Type A= has anti-B antibodies in plasma, A antigen is co-dominant
Type B= Has anti-A antibodies in plasma, B antigen is co-dominant
Type AB= neither antibodies, has A and B antigens on surface of RBC
Type O= has both antibodies in plasma and no antigens. O antigen is recessive
14
Q
What blood type is universal recipient and universal donor?
A
Universal recipient= Type AB
Universal donor= Type O
15
Q
What are the type of antibodies used in blood types?
A
Anti-erythrocyte antibodies known as natural antibodies
16
Q
Explain rhesus blood types
A
C,D,E antigens. Rhesus positive means the D antigen is present, rhesus negative means D antigen is not present
17
Q
What is the bounds for normal haemoglobin?
A
12.5-15.5 G/dl
18
Q
What is polycthaemia?
A
Higher than normal haemoglobin, caused by smoking, lung diseases, inefficient lungs meaning less O2 is exchanged so more haemoglobin is required
19
Q
What are the symptoms and signs of anaemia?
A
Symptoms- Tiredness, lethargy, malaise, reduced exercise tolerance, shortness of breath on exertion and angina
Signs- Palor, Pale mucus membranes and palmar creases, glossitis, angular stomatitis, kylonychia
20
Q
Describe iron deficiency anaemia
A
Iron is needed for haemoglobin production, lack of iron results in reduced production of small red cells
Low haemoglobin and MCV<80 fl
Causes- Occult gastrointestinal bleeding, menorrhagia, dietry
21
Q
Describe macrocytic anaemia
A
Large red blood cells. Macrocytosis can occur without anaemia (caused by liver disease, alcohol and hypothyroidism). In macrocytic anaemia, macrocytosis is a sign of it
22
Q
Describe B12 and Folate deficiency anaemia
A
Vitamin B23 and foalte are needed for DNA synthesis, thus with a B12 and folate deficiency red blood cells cannot be made in the bone marrow and thus less are released. This deficiency will effect all dividing cells but bone marrow is most active so it is affected first. Can be caused by damage to the stomach if intrinsic factor is not being produced by parietal cells, or by pernicious anaemia. Folate deficiency can be caused by malabsorbtion, dietary or an increased need.
23
Q
Describe haemolytic anaemia
A
Normal cell production but decreased lifespan
24
Q
What can cause congenital anaemia?
A
Membrane issues e.g. spherocytosis
Enzyme issues e.g. pyruvate kinase deficiency
Haemoglobin issues e.g. Sickle cell anaemia/ thalassaemia
25
What can cause acquired anaemia?
Autoimmune: immune system attacks own red blood cells
Mechanical: Fragmentation of red blood cells by mechanical heart valve or intravascular thrombosis in DIC
26
Explain Haemolytic disease of the foetus
Mother has rhesus negative blood and baby has rhesus positive blood. When mothers blood is exposed to babies blood, and mothers immune system recognises foreign rhesus positive blood and begins making antibodies against babies blood. First baby is unaffected since it takes time for antibodies to be produced, the mother is said to be sensitised. However if the second baby is RhD positive blood, then antibodies are produced immediately and begin destroying babies red cells.
27
Describe Neutrophils
Most numerous white cell- Lifespan is 10 hrs
Phagocytose and kill bacteria
Release chemotaxins and cytokines- important inflammatory response
Multi-lobed Nucleus and granular cytoplasm
28
Describe Eosinophils
Found in blood and in mucosal surfaces lining GI, Resp and urinary tract
Phagocytic response in parasitic infection. Neutralise histamine thereby restricting inflamatory response.
Bi or Tri lobed nucleus
Large red cytoplasmic granules and IgE receptors
29
Describe Basophils
Secrete heparin anticlotting factor and histamine in response to allergens.
Bi-Lobed nucleus and prominant dark-blue staining cytoplasmic granules. IgE receptors
30
Describe Monocytes
Monocytes are phagocytes that circulate in the blood and then migrate into tissues and organs to develop into macrophages. In the blood, monocytes play a major phagocytic role.
Reniform nucleus. Large so capable of engulfing bacteria and viruses
31
Describe lymphocytes
Lymphocytes are hard to distinguish as they all look the same.
B cells form plasma cells and secrete antibodies. Made in bone marrow and stored in secondary lymphoid organs.
T helper cells help B cells and activate macrophages. (CD4) Made in bone marrow and mature in thymus.
T cytotoxic cells kill previously marked target cells (CD8)
T suppressor cells suppress T-H cells
Natural killer cells kill virus infected cells.
32
Describe acute leukaemia
Proliferation of primative precursor cells usually found in bone marrow, proliferation without differentiation. These replace normal bone marrow cells resulting in anaemia, neutropenia infections and thrombocytopenia. The presence of primitive white precursor cells in the blood is a sign of acute leukemia.
33
Describe acute myeoblastic leukemia
Malignant proliferation of precursor myeloblasts in the bone marrow. Primarily affects adults
34
Describe acute lymphocytic leukemia
Malignant proliferation of the lymphoblast precursor cells in the bone marrow. Primarily affects children
35
Describe high grade lymphoma (hodgkins disease)
Disease of the lymph nodes that spreads to the liver, spleen, bone marrow and blood
36
Describe a platelet
Small cytoplasmic anucleate cell that blocks up holes in blood vessels
Made in bone marrow from cells called megakaryocytes. Lifespan of 5-10 days. . Circulate in an inactive state.
37
What is a reduced number of platelets?
Thrombocytopenia. Increased bleeding and spontaneous bleeding
38
What is an increased number of platelets?
Thrombocytosis. Can lead to arterial and venous thrombosis leading to increased risk of heart attack and stroke.
39
What coagulation factors is vitamin K essential for correct synthesis of?
II, VII, IX, X
40
What do the coagulation factors do?
Their function is to make a vlood clot. They convert soluble fibrinogen into insoluble fibrin polymer.
41
Where are the coagulation proteins produced and what is the key enzyme?
Produced in the liver, key enzyme is thrombin
42
Describe albumin
Most numerous protein in the plasma. Produced in the liver. Maintains oncotic pressure. Carries fatty acids, steroids and thyroid hormones.
43
What are the classes of immunoglobulins?
IgG ( Most important)
IgM (all start off as this)
IgA
IgE
44
How do platelets become activated?
When there is damage to a blood vessel, the sub-endothelium is exposed so platelets will bind directly to collagen or via large molecules such as Von Willebrand factor, which activates the platelets.
45
When does a platelet change shape and what does this mean?
Changes shape once activated from a smooth discoid to spiculated with extending pseudopodia. This increases surface area. This makes the platelets bind together.
46
What changes does activation cause to a platelet?
Platelet shape change
Activation of further receptors on the surface of platelets
Intracellular signalling causing platelets to release their stored granular contents.
47
What are the stored granular contents of a platelet?
Dense granules contain ATP, Calcium etc. That help the platelet plug form by activating more platelets.
Alpha granules contain von Willebrand factor, fibrinogen etc. which enhance binding.
48
Briefly describe the coagulation cascade
A series of proteolytic enzymes that circulate in an inactive state are activated in a cascade in order to generate Thrombin which cleaves fibrinogen, creating fibrin (a blood clot). It is NOT an all or nothing response.
49
Describe haemophilia
Recessive X-Linked severe bleeding disorder. Bleeding into muscles and joints as not enough clotting factors in the blood= slow clotting time or long PTT.
50
What is haemophilia A?
Rare bleeding disorder. Deficiency in clotting factor VIII, treat with factor VIII
51
What is haemophilia B?
Very rare bleeding disorder. Deficiency in clotting factor IX. Treat with factor IX
52
What is Von Willebrands disease?
Autosomal dominant disease with a lack of Von Willebrands factor. Lack of VWF causes platelet dysfunction hence muco-cutaneous bleeding.
53
What happens in Vitamin K deficiency?
Vitamin K is a fat soluble vitamin, and deficiency is caused by malabsorption. Manifests as a prolonged PTT. Incorrect synthesis of coagulation factors II, VII, IX, X. Treat with IV vitamin K. Coagulation factors are still produced but they do not work
54
What drugs affect bleeding?
Asprin affects platelet function
Heparin and warfarin inhibit vitamin K, affecting the coagulation cascade.
Steroid makes tissues thin and causes bruising and bleeding
55
Describe disseminated intravascular coagulation
A rare life threatening condition caused by sepsis, obstetric issues, or malignancy. Causes a breakdown of haemostatic balance resulting in simultaneous bleeding and microvascular thrombosis. Treat underlying cause
56
What is the first response of a damaged blood vessel?
It will constrict due to neural control and release of endothelin-1. This temporarily slows the flow of blood in the affected area and presses opposed surfaces of the vessel together and this keeps them 'glued' together.
57
What breaks down a blood clot?
Plasminogen is converted by plasminogen activators into plasmin which then goes on to break fibrin down and thus the entire blood clot.
58
What is the appearance of cardiac muscle?
Striated due to regularly repeating sarcomeres composed of myosin-containing thick filaments interdigitating with thing filaments that contain actin (Troponin and tropomyosin are present in the actin thin filament)
Individual cells are relatively small with a single nucleus
Arranged in layers
Adjacent cells joined end to end with intercalating discs within which desmosomes that hold the cells and gap junctions are present
59
What are the polypeptide chains found in myosin?
2 Large heavy chains and 4 smaller light chains
| Combine to find a molecule with two globular heads and a long tail formed from the intertwined heavy chains
60
What is the structure of actin?
A globular protein composed of a single polypeptide that polymerises with other actin monomers to form a polymer made up of two intertwined helical chains
61
Where is tropomyosin found?
It occupies the grooves between two actin strands and overlies the myosin binding sites
62
What happens when calcium ions bind to troponin?
The troponin changes shape which pushes the tropomyosin exposing the myosin binding sites on actin
63
What is the A-Band?
The region of the sarcomere occupied by thick and a few overlapping thin filaments
64
What is the I-Band?
The area occupied only by thin filaments that extend to the centre of the sarcomere from the Z lines
65
What are the Z lines?
Two successive Z lines define the limits of one sarcomere
66
What is the H zone?
The area occupied by only thick myosin filaments
67
What is the M line?
The centre of the H zone
68
Describe titin
Elastic protein filaments in sarcomeres that extend from the Z-Line to the M line, linked to both proteins.
69
What is the sarcoplasmic reticulum and what importance does it have during contraction?
It is a membrane network that surrounds the contractile proteins. It releases calcium ions when calcium ions binds it to ryanodine receptor
70
Why is the resting membrane potential -90mV?
The membrane is much more permeable to K+ which is leaving the cell as k+ channels are open. Pumps then move 3Na+ ions out for every 2 K+ ions pumped in, which means the inside is relatively more negative.
71
How does a cardiac cell get a positive action potential?
An action potential arrives, and Na+ voltage gated ion channels are opened. Na+ entry depolarises the cell, triggering more Na+ channels to open in a positive feedback effect.
72
What happens when a cardiac cell gets an action potential of +52mV?
The voltage gated Na+ channels close, and voltage gated K+ channels open, partially repolarising the cell.
73
What triggers the opening of the slow Ca2+ voltage gated ion channels, and where are these found?
An action potential
| Found at T-tubules
74
What causes the plateau value of 0mv?
K+ flowing out of the cell and Ca2+ fllowing into the cell
75
What does the binding of Ca2+ to ryanodine receptors on the sarcoplasmic reticulum cause?
Release of many Ca2+ into the sarcoplasm, initiating cardiac muscle contraction
76
What happens when myosin can bind to the actin filament?
The inorganic phosphate is dropped, and the ADP still remains attached to the head. The ADP is then dropped to allow the myosin to contract and pull the actin filament.
77
How does the myosin detatch from the actin?
ATP binds to the myosin head detaching the head from the actin filament. ATPase in the myosin head hydrolyses the ATP into ADP and Pi ready for the next contraction
78
How is cardiac contraction different to skeletal contraction?
Cardiac contraction last longer than in skeletal muscle due to the slow calcium channels
79
Why is there a refractory period?
To prevent excessive frequent contraction and to allow adequate filling time
80
Where do coronary arteries exit from main circulation?
Behind the aortic valve cusps in the very first part of the aorta
81
Where do the coronary arteries drain back into the heart?
Via the coronary sinus which empties into the right atrium
82
What are the gap junctions importance during propagation?
They allow action potentials to spread from one cell to another
83
Where is the sinoatrial node located?
The right atrium, near the entrance to the superior vena cava
84
What is the resting membrane potential of the sinoatrial node and how is this maintained?
-55 to -60 mV
| Maintained do to slow Na+ inflow
85
What are F-type channels and where are they found?
Channels that open when the membrane potential is at negative values. Found in the pacemaker cells
86
What are T-type Ca2+ channels and where are they found?
Calcium ion channels that open very briefly but contribute to an inward current of Ca2+
Found in the pacemaker cells
87
Why does the SA node normally initiate action potentials over the AV node?
The pacemaker cells in the SA node bring them to threshold more rapidly than the AV node
88
Where is the atrioventricular node located?
Located at the base of the right atrium
89
What does the slow propagation through the AV node mean?
It allows time for the atria to empty blood into the ventricles before ventricular excitation occurs
90
What nerve supplies parasymptathetic stimulation to the heart?
Vagus nerve (CN10)
91
What compound is used to supply parasympathetic stimulation to the heart?
Acetylcholine
92
What does an increased parasympathetic stimulation do to the heart?
Decrease rate (negatively chronotropic)
Decrease force of contraction (negatively inotropic)
Decrease cardiac output
93
What nerve fibres innervate the heart sympathetically?
Postganglionic fibres
94
What compounds control sympathetic stimulation to the heart?
Adrenaline and noradrenaline
95
What does an increased sympathetic stimulation do to the heart?
Increases heart rate (positively chronotropic)
Increases force of contraction (positively inotropic)
Increases cardiac output
96
What does an ECG measure?
The currents generated in the extracellular fluid
97
What is phase 0 of myocyte action potential?
Rapid depolarisation, inflow of Na+
98
What is phase 1 of myocyte action potential?
Partial depolarisation, inward Na+ current deactivated and outflow of K+
99
What is phase 2 of myocyte action potential?
Plateau, slow inward Ca2+ current
100
What is phase 3 of myocyte action potential?
Repolarisation, K+ outflow Ca2+ current deactivated
101
What is phase 4 of myocyte action potential?
Pacemaker potential, slow Na+ inflow
102
What is the P wave showing?
Atrial depolarisation
103
What is the PR interval showing?
The time taken for atria to depolarise and electrical activation to get through AV node
104
What is the QRS complex showing?
Ventricular depolarisation
105
What is the ST segment showing?
The interval between depolarisation and repolarisation
106
What is the T wave showing?
Ventricular repolarisation
107
What is tachycardia?
Increased heart rate
108
What is bradycardia?
Decreased heart rate
109
What is dextrocardia?
Heart on right side of chest instead of left
110
How can anterolateral myocardial infarction be seen on an ECG?
ST segments are raised in anterior (V3-V4) and lateral (V5-V6) leads
111
How can acute inferior myocardial infarction be seen on an ECG?
ST segments are raised in inferior (II, III aVF) leads
112
What are the standard limb leads and where are they?
I, II, III
| form a triangle between electrodes on the wrists and left leg
113
What are the augmented leads and where are they?
aVR, aVL, aVF
| Bisect the angles of the triangle of the standard limb leads
114
What are the precordial leads and where are they?
V1-V6
| Recording electrodes placed on the chest
115
How much time does a small square on an ECG show?
40ms
116
In a normal ECG, are p waves positive or negative in every lead except aVR?
Positive
117
In a normal ECG, are T waves positive or negative in every lead except aVR and sometimes V1/V2?
Positive
118
How long does systole last?
0.3 seconds
119
What is isovolumetric contraction?
Contraction of the ventricles with valves closed so volume of blood does not change but pressure increases
120
When does maximal ejection from the ventricles occur?
When pressure in the ventricles exceeds that in the aorta and pulmonary trunk so the aortic and pulmonary valves opens
121
What percentage of blood is left in the ventricles after maximal ejection?
33%
122
How long does diastole last?
0.5 seconds
123
What are the stages of systole?
Isovolumetric contraction of ventricles
| Maximal ejection of ventricles
124
What are the stages of diastole?
```
Reduced ejection
Isovolumetric ventricular relaxation
Rapid left ventricle filling and ventricle suction
Slow ventricular filling
Atrial booster
```
125
What is diastasis?
Pressure equalisation in the atrium and ventricles
126
Define stroke volume?
The volume of blood ejected from each ventricle during systole
127
Define cardiac output
The volume of blood each ventricle pumps as a function of time (L/min)
128
Define total peripheral resistance
The total resistance to flow in systemic blood vessels from beginning of aorta to vena cava- arterioles provide the most resistance
129
Define preload
The volume of blood in the left ventricle which stretches the cardiac myocytes before left ventricular contraction
130
Define afterload
The pressure the left ventricle must overcome to eject blood during contraction
131
Define contractility
The force of contraction and the change in fibre legnth
132
Define elasticity
Myocardial ability to recover normal shape after systolic stress
133
Define diastolic dispensibility
The pressure required to fill the ventricle to the same diastolic volume
134
Define compliance
How easily the heart chamber expands when filled with blood volume
135
What is starlings law?
The force of contraction is proportional to the end diastolic length of cardiac muscle fibre
136
How is blood pressure increased on standing?
There is a decreased venous return due to gravity, thus cardiac output decreases which causes a drop in blood pressure, stimulating baroreceptors to increase blood pressure
137
What is intrinsic autoregulation?
When the arterioles either vasoconstrict or vasodilate in response to changes in resistance with the aim to maintain constant blood flow
138
What is myogenic autoregulation?
When blood flow is increased and stretches vascular smooth muscle, the muscle automatically constricts until the diameter is normalised or slightly reduced
139
What is hyperemia?
An increase in blood flow
140
What is active hyperemia?
Increase in blood flow when metabolic activity is increased
141
What is reactive hyperemia?
When an organ or tissue has had its blood supply completely occluded a profound transient increase in its blood flow occurs if blood flow is reastablished
142
How many heart sounds are there normally?
3
143
What is the first heart sound?
A soft, low pitched lub, associated with the closure of the AV valves
144
What is the second heart sound?
A louder dub, associated with the closure of the aortic and pulmonary valves
145
What is the third heart sound?
The sound of blood rushing into the left ventricle
146
What does MAP stand for?
Mean arterial pressure
147
What is the equation for MAP?
MAP=DP+1/3(SP-DP)
148
Where is the pressure region and what is it?
It is located in the medulla. It is sympathetic, and increases blood pressure by increasing vasoconstriction, cardiac output and contractility.
149
Where is the depressor region and what is it?
It is located in the medulla. It is sympathetic and decreases blood pressure by inhibiting the pressor region
150
What do the central chemoreceptors in the medulla normally respond to?
A decrease in pH
151
Where are the cardiopulmonary baroreceptors located?
The atria, ventricles and pulmonary artery
152
What can the cardiopulmonary baroreceptors inhibit?
Pressor region, vasoconstrictor centre, renin-angiotensin and aldosterone system, vasopressin
153
How do cardiopulmonary baroreceptors bring about a decrease in blood pressure?
Promoting vasodilation and fluid loss
154
What is the principal site of resistance to vascular flow?
Arterioles
155
What is endothelin-1?
A peptide released by endothelium cells resulting in vasoconstriction
156
What are the vasodilators?
```
Hypoxia
Increased CO2
Decreased pH
Bradykinin
Nitric oxide
Increased K+
H+
Tissue breakdown products
Prostacyclin
```
157
What is prostacyclin?
A lipid released by endothelial cells that triggers vasodilation
158
What are the vasoconstrictor hormones?
Angiotensin II, Vasopressin and adrenaline
159
What are the vasodilator hormones?
Atrial natriuretic peptide, adrenaline
160
Where are the peripheral chemoreceptors located?
In the aortic arch and carotid sinus
161
How are the peripheral chemoreceptors stimulated?
A fall in PaO2 and a rise in PaCO2 and a fall in pH causing blood pressure to increase
162
Where are the arterial baroreceptors located?
One found in the aortic arch, two found at the carotid sinus (division of the left and right carotid)
163
What is the equation for cardiac output?
Heart rate x stroke vol
164
What is the equation for blood pressure?
CO x Total peripheral resistance
165
What is the equation for pulse pressure?
Systolic-diastolic pressure
166
What is the equation for stroke vol?
End diastolic vol- end systolic vol
167
What is poiseuille's equation?
Flow=radius to the power 4
168
What is ohms law?
Flow=pressure gradient/resistance
169
What is the composition of the intima of an artery?
An inner surface lining of endothelial cells and a very small amount of collagen
170
What is the composition of the adventitia of an artery?
Mainly collagenous connective tissue
171
What are the layers of an artery wall?
Intima, media, adventitia
172
Where is the endothelium of capillaries fenestrated?
Liver, kidney, glomeruli and endocrine tissues
173
What do pericytes do?
Have muscle fibres and regulate blood flow
174
What is the composition of a wall of a vein?
Collagen and little muscle and elastic with the wall and a single internal elastic lamina
175
Why do veins have valves?
For one way flow to the heart
176
Why do some veins have skeletal muscle?
It can contract to increase vein pressure and ensure blood flows back to the heart
