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Peer teaching > Cardiovascular system > Flashcards

Cardiovascular system Flashcards

1
Q

hematocrit definition

A

percentage of RBCs in the cellular component of blood

45%

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2
Q

features of erythrocytes

A

anucleate, discoid, biconcave

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3
Q

formation of erythrocytes

A

in adults - axial skeleton

children - bones in fetus, liver, yolk sac and bone marrow

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4
Q

regulatory hormone of erythrocytes

A

erythropoietin

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5
Q

eosinophil appearance and function

A

bilobed nucleus
pink

parasitic infection

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6
Q

neutrophil appearance and function

A

multilobed nucleus

pus, acute inflammation, phagocytic function

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7
Q

basophil appearance and function

A

bilobed nucleus
blue

histamine, allergic response

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8
Q

monocyte appearance and function

A

kidney shaped nucleus

differentiate into dendritic cells/macrophages
adaptive immunity role

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9
Q

lymphocyte appearance and function

A

fried egg appearance
B/T

B lymphocyte -> plasma cell, produces antibodies

T cells mediate inflammation

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10
Q

platelet features

A

anucleate and discoid

spiculated once activated

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11
Q

platelet formation

A

from megakaryocytes in the bone marrow

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12
Q

life span of platelets

A

5-10 days

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13
Q

regulatory hormone of platelets

A

thrombopoietin

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14
Q

components of plasma

A

albumin, carrier proteins, coagulation factors, immunoglobulins

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15
Q

albumin formation and function

A

liver

maintaining oncotic pressure

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16
Q

carrier proteins formation and function

A

liver

carry stuff

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17
Q

coagulation factors formation and function

A

liver

clotting factors that can form clots

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18
Q

immunoglobulins formation and function

A

plasma cells (B lymphocytes)

adaptive immunity

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19
Q

hemostasis definition

A

maintaining balance of blood flow (so it is liquid in vessels but will clot outside)

the stopping of the flow of blood

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20
Q

what allows blood to stay liquid?

A

coagulation factors and platelets are inactive

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21
Q

what activates platelets?

A

tissue factor - found on all cells except endothelial cells

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22
Q

bleeding and clotting

A

vessel damage -> constriction

slow of blood flow to area and endothelial surfaces pressed together

bleeding stopped by platelet plug and coagulation cascade

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23
Q

formation of the platelet plug

A

endothelium disrupted, exposing collagen fibres

platelets adhere to VWF (8) which is bound to collagen

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24
Q

what does binding of platelets to VWF lead to?

A

exocytosis of secretory vesicles -> platelet amplification

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25
Q

what happens in platelet amplification?

A

dense granules
thrombin

spiculated

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26
Q

what binds to platelets and allows them to aggregate?

A

fibrinogen binds to platelets allowing more platelets to aggregate -> platelet plug

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27
Q

how does the platelet plug stay where it’s wanted?

A

prostaglandin produced by undamaged endothelium -> inhibits aggregation

nitrogen oxide from undamaged endothelium -> vasodilation and inhibits aggregation

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28
Q

vitamin K dependent clotting factors

A

2, 7, 9, 10 (1972)

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29
Q

fibrinolytic pathway

A

plasminogen -> plasmin -> fibrin breakdown

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30
Q

22 days heart embryology

A

tuncus arteriosus

bulbus cordis

primitive ventricle

primitive atrium

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31
Q

apex beat

A

5th intercostal space on left midclavicular line

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32
Q

arch of aorta level

A

T4

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33
Q

borders of anterior mediastinum

A

anterior: sternum
posterior: middle mediastinum

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34
Q

contents of anterior mediastinum

A

thymus, lymph nodes, internal thoracic vessels, thyroid tissue

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35
Q

contents of middle mediastinum

A

pericardium and heart, ascending aorta, SVC/IVC, brachiocephalic vessels, pulmonary vessels, trachea and main bronchi, phrenic, vagus, left recurrent laryngeal nerve

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36
Q

borders of the superior mediastinum

A

manubriosternal joint

inferior edge of T4 body

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37
Q

borders of posterior mediastinum

A

anterior: middle mediastinum
posterior: anterior thoracic vertebral column

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38
Q

contents of posterior mediastinum

A

oesophagus, azygous and hemizygous and descending aorta

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39
Q

structure of a cardiac myocyte

A

intercalated discs

centrally nucleated

striated

branching

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40
Q

ultrastructure of a myocardial cell

A

myosin, actin, titin, H zone, M line, A band, I band, Z line

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41
Q

myosin

A

2 heavy chains

4 light chains

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42
Q

actin

A

polymerised globular protein with troponin and tropomyosin incorporated

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43
Q

titin

A

elastic filaments that maintain alignment of sarcomere

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44
Q

M line

A

in middle of myosin

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45
Q

A band

A

overlapping myosin and actin

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46
Q

I band

A

just actin, containing Z line

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47
Q

H zone

A

just myosin, containing M line

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48
Q

Ca2+ in the sarcomere contraction process

A

calcium binds to troponin, causing conformational change and movement of tropomyosin

exposes myosin head binding site to the actin

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49
Q

binding of actin and myosin

A

energy from ATP for head movement

Z lines move close together

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50
Q

excitation-contraction coupling

A

action potential arrives, travels down T tubules

depolarisation -> L-type Ca2+ channels to open

Ca2+ binds to ryanodine receptors (RyRs) in sarcoplasmic reticulum -> more Ca2+ release

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51
Q

events of the pacemaker action potential

A

pacemaker potential

depolarisation

repolarisation

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52
Q

pacemaker potential

A

slow depolarisation opening of slow Na+ channels and closing of K+ channels

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53
Q

depolarisation of pacemaker action potential

A

pacemaker potential reaches threshold (-40mV)

Ca2+ influx

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54
Q

repolarisation of pacemaker action potential

A

Ca2+ channels inactivating and K+ channels opening

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55
Q

control of pacemaker action potential

A

sympathetic and parasympathetic stimulation

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56
Q

sympathetic control of pacemaker action potential

A

adrenaline/noradrenaline binding to beta-1 receptor causing increased Na+ permeability so the threshold potential is reached faster

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57
Q

parasympathetic control of pacemaker action potential

A

acetylcholine binds to a muscarinic receptor causing decreased Na+ permeability

longer time taken to reach threshold potential

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58
Q

differences between cardiac myocyte action potential and regular action potential

A

cardiac action potential has Ca2+ leaving the cell to cause a plateau

cardiac action potential is 200-300 ms, regular is ms

cardiac action potential has a longer refractory period

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59
Q

what does the longer refractory potential in cardiac action potential do?

A

prevents muscle fatigue

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60
Q

stage 4 of action potential of cardiac muscles

A

Na+ and Ca2+ channels closed

open K+ rectifier channels keep TMP stable at -90mV

K+ from ICF -> ECF

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61
Q

stage 0 of action potential of cardiac muscles

A

rapid Na+ influx through open fast Na+ channels

Na+ from ECF -> ICF

depolarisation

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62
Q

stage 1 of action potential of cardiac muscles

A

partial repolarisation

transient K+ channels open and K+ efflux returns TMP to 0mV

K+ from ICF -> ECF

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63
Q

stage 2 of action potential of cardiac muscles

A

plateau

influx of Ca2+ through L-type Ca2+ channels is electrically balanced by K+ efflux through delayed rectifier K+ channels

Ca2+ from ECF to ICF
K+ from ICF to ECF

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64
Q

stage 3 of action potential of cardiac muscles

A

repolarisation

Ca2+ channels close but delayed rectifier K+ channels remain open and return TMP to -90mV

K+ from ICF to ECF

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65
Q

what does conduction spread through in nodes?

A

gap junctions

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66
Q

AVN conduction

A

less gap junctions -> delays conduction

allows for atrial emptying before contraction of ventricle

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67
Q

HP systems structure

A

v large fibres

highly permeable gap junction

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68
Q

artery structure

A

thick muscular wall to sustain force of LV contractions

elastic - cushions systole

as elastic in walls recoils, the pressure supplied is the diastolic pressure

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69
Q

arterioles structure

A

smooth muscle in walls

determining arterial pressure and distributing flow

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70
Q

where is the principle site of resistance to vascular flow?

A

arterioles

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71
Q

capillary structure

A

endothelial cells and pericytes

precapillary sphincters control blood flow to tissue

fenestrated (holes)

thin - movement of fluid across membranes

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72
Q

what becomes the lymph?

A

substances and fluid that move across into tissue become lymph

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73
Q

veins structure

A

main blood reservoir

low resistance

wide lumen

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74
Q

functions allowing venous return against gravity

A

valves - prevent backflow

muscle action peristalsis

respiratory pump

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75
Q

lymph vessels structure

A

low pressure

valves

76
Q

lymph vessels function

A

drains excess fluid from tissues

drains into subclavian veins

77
Q

lymph fluid contents and appearance

A

no erythrocytes/large proteins, can contain all other blood components

eosinophilic

78
Q

where are precursor cells of erythrocytes found in adults and children?

A

bone marrow

adults: axial skeleton (skull, ribs, spine, pelvis, long bones)
children: all bones
in utero: yolk sac, liver, spleen

79
Q

what is an important fact about precursor cells?

A

not found in blood - if they are, this is a sign of leukaemia

80
Q

what do hormonal growth factors do? what are their different types?

A

stimulate precursor stem cells to proliferate and differentiate

EPO/erythropoietin (hormone from kidney): erythrocytes

G-CSF (granulocyte colony stimulating factor): leukocytes

Tpo: platelets

81
Q

what is haemoglobin made of?

A

2 alpha and 2 beta chains and 4 haem groups

overall quaternary structure combination of 2+ tertiary structures

82
Q

what is rhesus?

A

C, D, E antigens

D antigen is most important -rhesus positive means D antigen is present, rhesus negative means it’s not

83
Q

what is anaemia?

A

reduction of haemoglobin in blood

84
Q

what are normal haemoglobin levels?

A

12.5 - 15.5 g/dl

85
Q

what is polycthaemia caused by?

A

smoking, lung diseases, inefficient lungs

86
Q

what are symptoms of anaemia?

A

tiredness, lethargy, malaise, reduced exercise tolerance, SOB, angina

87
Q

what are the signs of anaemia?

A

palor, pale mucus membrane, palmar creases, glossitis, angular stomatitis, kylonychia (spoon shaped nails)

88
Q

what are the classifications of anaemia?

A

iron deficiency, B12/folate deficiency, anaemia of chronic disorder, haemolysis, bone marrow failure/inflitration

89
Q

what is iron-deficiency anaemia?

A

lack of iron -> reduced production of small red cells

needed for haemoglobin production

90
Q

how is red cell size measured?

A

MCV (mean cell volume)

91
Q

what is the normal MCV? what is the abnormal one?

A

82-96 fl

<80 fl

92
Q

what are the causes of iron-deficiency anaemia?

A

bleeding:

occult GI: most common
menorrhagia: heavy periods. only premenopausal women or repeated child birth

dietary: not getting enough iron in diet

93
Q

what is macrocytic anaemia?

A

MCV > 100fl

can occur w/out anaemia - caused by liver disease, alcohol, hypothyroidism

94
Q

why does macrocytosis occur?

A

vitamin B12/folate deficieny

95
Q

how do vitamin B12/folate affect erythrocyte production?

A

needed for DNA synthesis

erythrocytes can’t be made in the bone marrow, so less are released

affects all dividing cells, bone marrow is most active so it’s affected first

96
Q

causes of B12 deficiency

A

intrinsic factor produced by gastric parietal cells is needed for B12 absorption in the terminal ileum - less intrinsic factor -> less B12 absorbed

pernicious anaemia

97
Q

what is pernicious anaemia?

A

autoimmune disease

causes antibodies to be made against gastric parietal cells -> less intrinsic factor produced -> B12 malabsorption

98
Q

why does pernicious anaemia have a slow onset?

A

liver has a vast store of B12 which can last 4 years

99
Q

where is folate found?

A

vegetables and fruit

100
Q

what are the causes of folate deficiency?

A

malabsorption (celiac disease)

dietary (not enough fruit or vegetables)

increased need (haemolysis/increased cell division)

101
Q

what is haemolysis?

A

normal or increased erythrocyte production but decreased life span < 30 days

destroyed before 120 days

102
Q

what are types of haemolysis?

A

congenital or acquired

103
Q

what is congenital haemolysis caused by?

A

membrane issues e.g. spherocytosis

enzyme issues e.g. pyruvate kinase deficiency

haemoglobin issues e.g. sickle cell anaemia

104
Q

what is spherocytosis?

A

blood cells are spherical

get stuck in vessels easily

dominant condition, variable penetrance

105
Q

what is pyruvate kinase deficiency?

A

enzyme needed to convert phosphoenolpyruvate to pyruvate is deficient -> less ATP and build up of phosphoenolpyruvate

G6PD deficiency

106
Q

what is sickle cell anaemia?

A

defect in beta globin chain

sickle shaped, get trapped in vessels

107
Q

what is thalassaemia?

A

mutation in haemoglobin genes (beta more common in india and Pakistan) and alpha more common in east e.g. Thailand

108
Q

what causes acquired haemolysis?

A

autoimmune, mechanical, pregnancy

109
Q

what is autoimmune haemolysis?

A

immune system attacks own erythrocytes, can be triggered by blood transfusion (foreign antibodies)

110
Q

what is mechanical haemolysis?

A

fragmentation of erythrocytes by mechanical heart valve or intravascular thrombosis in DIC

111
Q

what is DIC?

A

disseminate intravascular coagulation

112
Q

what is HDFN?

A

haemolytic disease of the foetus and newborn

113
Q

what happens in HDFN?

A

mother has Rhesus negative blood, and baby has RhD positive

when mothers blood is exposed to babies, her immune system recognises foreign RhD positive blood and starts making antibodies - first it’s unaffected as this takes time
mother sensitised to RhD positive

114
Q

what if the mother’s second baby also has RhD positive blood?

A

antibodies produced immediately, begin destroying babies erythrocytes -> haemolysis, anaemia and jaundice

115
Q

what is rhesus disease?

A

antibodies can cross to baby via placenta and begin attacking

116
Q

what are leukocytes?

A

mature cells that circulate in the blood

produced from immature precursor cells in the bone marrow which are derived from stem cells

117
Q

what controls the rate of production of leukocytes?

A

G-CSF (hormonal control)

118
Q

what are neutrophils? what do they do?

A

most numerous leukocyte

10 hours lifespan

phagocytose and kill bacteria, release chemotaxins and cytokines

119
Q

what does lack of number or function of neutrophils lead to?

A

recurrent bacterial infections

120
Q

what is a chemotaxin?

A

substance released by bacteria, injured tissue and leukocytes that induces movement of neutrophils and leukocytes to the injured area

121
Q

what is a cytokine?

A

broad category of small proteins used in cell signalling

can’t cross lipid bilayer

122
Q

what types of lymphocytes are there?

A

B and T cells

123
Q

what are the functions of lymphocytes?

A

vital to immunity

generate antibodies against specific foreign antigens e.g. bacteria and viruses

immunological memory - generates immunity and allows vaccination

124
Q

what are B lymphocytes? what do they do?

A

made in bone marrow, stored in secondary lymphoid organs

differentiate into plasma cells and produce immunoglobulins when stimulated by exposure to foreign antigen

125
Q

what are T lymphocytes? what do they do?

A

made in bone marrow, mature in thymus

some are helper cells (CD4, help B cells in antibody generation, responsible for cellular/cell mediated immunity), some are cytotoxic cells (CD8), some are suppressive

126
Q

what is acute leukaemia?

A

proliferation of primitive precursor cells usually found in bone marrow without differentiation - replaces normal bone marrow cells

127
Q

what does acute leukaemia lead to?

A

anaemia (palor and lethargy)

neutropenia (infections, as white cells aren’t differentiating)

thrombocytopenia (excessive bleeding)

128
Q

what is a sign of acute leukemia?

A

presence of primitive white precursor cells in the blood

129
Q

what is acute myeloblastic leukaemia? who does it affect?

A

malignant proliferation of the precursor myeloblasts (unipotent stem cells) in bone marrow

adults

50% survive 5 years

130
Q

what is acute lymphocytic leukemia? who does it affect?

A

malignant proliferation of the lymphoblast precursor cells in the bone marrow

children

80% cured

131
Q

what is high grade lymphoma?

A

lymphocytes in lymph nodes becoming malignant

Hodgkins disease and non-hodgkins lymphoma, disease usually of the lymph nodes that spreads to the liver, spleen, bone marrow and blood

132
Q

what determines PT?

A

platelets determine prothrombin time

133
Q

what are platelets?

A

small cytoplasmic anucleate cells that block up holes in blood vessels

spherical, anucleate - can’t repair themselves

134
Q

where are platelets made from?

A

bone marrow from cells called megakaryocytes

135
Q

what is the life span of platelets?

A

5-10 days

136
Q

what is the normal number of platelets?

A

140-400 x 10^9/L

137
Q

what is reduced numbers of platelets?

A

thrombocytopenia (main risk is cerebral bleeding)

< 80 - increased bleeding

<20 - spontaneous bleeding

138
Q

what is high numbers of platelets? what can it lead to?

A

thrombocytosis

can lead to arterial and venous thrombosis -> increased risk of heart and stoke

139
Q

where are coagulation proteins made?

A

liver

140
Q

what is the key enzyme in coagulation?

A

thrombin - makes platelet plug

141
Q

what is essential for correct synthesis of coagulation factors?

A

vitamin K

2,7,9,10
1972

142
Q

what is the function of coagulation proteins?

A

circulate in inactive form

make blood clot

convert soluble fibrinogen into insoluble fibrin polymer

143
Q

what proteins are in the plasma?

A

albumin, carrier proteins, immunoglobulins

144
Q

what is albumin? what is its function? where is it produced? what does it carry?

A

most numerous protein in plasma

maintain oncotic pressure

lack of it -> oedema

liver

fatty acids, steroids and thyroid hormones

145
Q

what are immunoglobulins?

A

antibodies produced by plasma cells (differentiated B lymphocytes)

IgG (most important), IgM (all start off as this), IgA, IgE

produced in response to non self protein antigens

146
Q

what is haemostasis?

A

arrest of bleeding

involves physiological processes of blood coagulation and the contraction of damaged blood vessels

147
Q

why is blood usually fluid inside blood vessels?

A

proteins of coagulation cascade and platelets circulate in an inactive state

proteins and platelets are only activated by tissue factor, which is present on every cell apart from endothelial cells -> when endothelium is punctured, blood contacts tissue factor and starts clottig

148
Q

what is thrombosis?

A

blood clots inside vessels

149
Q

what is a bleeding disorder?

A

blood fails to clot outside vessels

150
Q

what is the key enzyme involved in the coagulation cascade?

A

thrombin - cleaves fibrinogen to create fibrin polymerisation

151
Q

graduation of coagulation

A

v complex, multiple steps allow for biological amplification and allow for regulation - not all or nothing response, graduated in response to severity of challenge

152
Q

what is haemophilia?

A

recessive X-linked severe bleeding disorder

bleeding into muscles and joints

not enough clotting factors in blood -> slow clotting time or long prothrombin time

only affects males due to C linked inheritance

females are carriers

153
Q

what is haemophilia A?

A

bleeding into muscles and joints

1/10000 males

deficiency in clotting factor VIII - treat with factor VIII

154
Q

what is haemophilia B?

A

bleeding into muscles and joints

1/50000 males

deficiency in clotting factor IX - treat with factor IX

155
Q

why is haemophilia B less common than A?

A

gene is smaller

156
Q

what is von Willebrands disease?

A

autosomal dominant inheritance

lack of vWF

usually a mild bleeding disorder

up to 1% - unrecognised and undiagnosed

157
Q

what is the type of bleeding seen in von Willebrands disease? what are its symptoms?

A

muco-cutaneous bleeding: bleeding in skin and mucous membranes

easy bruising, prolonged bleeding from cuts, nose bleeds, spontaneous gum bleeding/GI loss

158
Q

what are acquired bleeding disorders?

A

recent onset, no lifelong/family history

may be generalised or local bleeding

159
Q

what is the most common cause of acquired bleeding disorders?

A

anti-platelet or anti-coagulation medication

160
Q

what are other causes of acquired bleeding disorders?

A

liver disease, vit K deficiency, drugs, DIC

161
Q

how does liver disease cause acquired bleeding disorders?

A

synthesises coagulation factors and fibrinogen

disease often associated with bleeding and prolonged prothrombin time

most common cause of liver disease is alcohol

162
Q

how does vitamin K deficiency cause acquired bleeding disorders?

A

vit K needed for correct synthesis of coagulation factors II, VII, XI, X

vit K is a fat soluble vitamin

163
Q

what is vitamin K caused by?

A

malabsorption, esp. in obstructive jaundice

164
Q

what does vitamin K deficiency manifest as?

A

prolonged PTT

165
Q

what is vitamin K deficiency causing bleeding disorders treated with? in babies?

A

intravenous vitamin K

newborns are born vitamin K deficient, given it at birth

166
Q

how do different drugs affect bleeding?

A

aspirin affects platelet function

heparin and warfarin (most widely used oral anticoagulant - inhibits vit K) affect coagulation cascade

steroid makes tissues thin and cause bruising and bleeding

167
Q

what is DIC?

A

disseminated intravascular coagulation

breakdown of haemostatic balance

simultaneous bleeding and microvascular thrombosis

life threatening

168
Q

what are the causes of DIC?

A

sepsis, obstetric (anything that goes wrong with pregnancies), malignancy

169
Q

what is the mechanism of DIC?

A

activation of coagulation cascade inside blood vessels, thrombin produced, causing fibrinogen -> fibrin. forms microvascular thrombosis (platelet plugs) everywhere

170
Q

what does DIC cause?

A

deficiency of clotting factors and platelets as they’ve been used up in formation of microvascular thromboses

171
Q

what is the treatment of DIC?

A

treat underlying cause

stop generation of intravascular thrombin

transfuse new platelets

172
Q

what is the response of the blood vessel to damage?

A

constriction

173
Q

what causes a blood vessel to constrict?

A

neural control and release of endothelin-1 (released by endothelial cells)

174
Q

what temporarily closes a blood vessel when it’s damaged?

A

constriction of vessel by endothelin-1 and neural control, which presses opposed endothelial surfaces of the vessel together

this contact induces a stickiness that keeps vessels glued together

175
Q

where does permanent closure of vessels occur?

A

permanent closure by constriction and contact stickiness occur in v small vessels of the microcirculation

176
Q

what does the stopping of bleeding depend on?

A

independent processes that occur in rapid succession: formation of a platelet plug and blood coagulation

177
Q

what happens when a vessel is injured/ruptured?

A

disrupts the endothelium - exposure of collagen fibres

178
Q

how to platelets adhere to collagen fibres?

A

via an intermediary VWF. also attached to the collagen via a receptor on the platelet membrane - glycogen 1b receptor

179
Q

what does binding of the platelets to the collagen fibre wall trigger?

A

platelet releases contents of their secretory vesicles via exocytosis

180
Q

what do platelet dense granules release?

A

ADP - acts on P2Y1 and P2Y12, causing platelet amplification

181
Q

what causes platelet amplification?

A

ADP from platelet dense granules acting on P2Y1 and P2Y12

ATP binding to P2X1

182
Q

what causes platelet activation?

A

thrombin binding to PAR1 and PAR4 receptors - induces platelet activation and further thrombin release (positive feedback)

183
Q

what are changes in platelet activation?

A

platelet changes shape from a smooth discoid shape to a more spiculated (spiky) shaped with pseudopodia

increases SA

184
Q

what does platelet activation cause?

A

increase in expression of glycoprotein IIb/IIIa receptors on platelets which bind to fibrinogen, enabling new ones to adhere to old ones (positive feedback)

185
Q

what do GP IIb/IIIa bind to?

A

fibrinogen

186
Q

what is fibrinogen from?

A

alpha granules

187
Q

what is platelet aggregation?

A

new platelets adhering to old ones (positive feedback mechanisms)

GP IIb/IIIa receptors on platelets bind to fibrinogen from alpha granules

Peer teaching (10 decks)

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