Cardiovascular system Flashcards
(187 cards)
1
Q
hematocrit definition
A
percentage of RBCs in the cellular component of blood
45%
2
Q
features of erythrocytes
A
anucleate, discoid, biconcave
3
Q
formation of erythrocytes
A
in adults - axial skeleton
children - bones in fetus, liver, yolk sac and bone marrow
4
Q
regulatory hormone of erythrocytes
A
erythropoietin
5
Q
eosinophil appearance and function
A
bilobed nucleus
pink
parasitic infection
6
Q
neutrophil appearance and function
A
multilobed nucleus
pus, acute inflammation, phagocytic function
7
Q
basophil appearance and function
A
bilobed nucleus
blue
histamine, allergic response
8
Q
monocyte appearance and function
A
kidney shaped nucleus
differentiate into dendritic cells/macrophages
adaptive immunity role
9
Q
lymphocyte appearance and function
A
fried egg appearance
B/T
B lymphocyte -> plasma cell, produces antibodies
T cells mediate inflammation
10
Q
platelet features
A
anucleate and discoid
spiculated once activated
11
Q
platelet formation
A
from megakaryocytes in the bone marrow
12
Q
life span of platelets
A
5-10 days
13
Q
regulatory hormone of platelets
A
thrombopoietin
14
Q
components of plasma
A
albumin, carrier proteins, coagulation factors, immunoglobulins
15
Q
albumin formation and function
A
liver
maintaining oncotic pressure
16
Q
carrier proteins formation and function
A
liver
carry stuff
17
Q
coagulation factors formation and function
A
liver
clotting factors that can form clots
18
Q
immunoglobulins formation and function
A
plasma cells (B lymphocytes)
adaptive immunity
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
20
Q
what allows blood to stay liquid?
A
coagulation factors and platelets are inactive
21
Q
what activates platelets?
A
tissue factor - found on all cells except endothelial cells
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
23
Q
formation of the platelet plug
A
endothelium disrupted, exposing collagen fibres
platelets adhere to VWF (8) which is bound to collagen
24
Q
what does binding of platelets to VWF lead to?
A
exocytosis of secretory vesicles -> platelet amplification
25
what happens in platelet amplification?
dense granules
thrombin
spiculated
26
what binds to platelets and allows them to aggregate?
fibrinogen binds to platelets allowing more platelets to aggregate -> platelet plug
27
how does the platelet plug stay where it's wanted?
prostaglandin produced by undamaged endothelium -> inhibits aggregation
nitrogen oxide from undamaged endothelium -> vasodilation and inhibits aggregation
28
vitamin K dependent clotting factors
2, 7, 9, 10 (1972)
29
fibrinolytic pathway
plasminogen -> plasmin -> fibrin breakdown
30
22 days heart embryology
tuncus arteriosus
bulbus cordis
primitive ventricle
primitive atrium
31
apex beat
5th intercostal space on left midclavicular line
32
arch of aorta level
T4
33
borders of anterior mediastinum
anterior: sternum
posterior: middle mediastinum
34
contents of anterior mediastinum
thymus, lymph nodes, internal thoracic vessels, thyroid tissue
35
contents of middle mediastinum
pericardium and heart, ascending aorta, SVC/IVC, brachiocephalic vessels, pulmonary vessels, trachea and main bronchi, phrenic, vagus, left recurrent laryngeal nerve
36
borders of the superior mediastinum
manubriosternal joint
| inferior edge of T4 body
37
borders of posterior mediastinum
anterior: middle mediastinum
posterior: anterior thoracic vertebral column
38
contents of posterior mediastinum
oesophagus, azygous and hemizygous and descending aorta
39
structure of a cardiac myocyte
intercalated discs
centrally nucleated
striated
branching
40
ultrastructure of a myocardial cell
myosin, actin, titin, H zone, M line, A band, I band, Z line
41
myosin
2 heavy chains
| 4 light chains
42
actin
polymerised globular protein with troponin and tropomyosin incorporated
43
titin
elastic filaments that maintain alignment of sarcomere
44
M line
in middle of myosin
45
A band
overlapping myosin and actin
46
I band
just actin, containing Z line
47
H zone
just myosin, containing M line
48
Ca2+ in the sarcomere contraction process
calcium binds to troponin, causing conformational change and movement of tropomyosin
exposes myosin head binding site to the actin
49
binding of actin and myosin
energy from ATP for head movement
Z lines move close together
50
excitation-contraction coupling
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
51
events of the pacemaker action potential
pacemaker potential
depolarisation
repolarisation
52
pacemaker potential
slow depolarisation opening of slow Na+ channels and closing of K+ channels
53
depolarisation of pacemaker action potential
pacemaker potential reaches threshold (-40mV)
Ca2+ influx
54
repolarisation of pacemaker action potential
Ca2+ channels inactivating and K+ channels opening
55
control of pacemaker action potential
sympathetic and parasympathetic stimulation
56
sympathetic control of pacemaker action potential
adrenaline/noradrenaline binding to beta-1 receptor causing increased Na+ permeability so the threshold potential is reached faster
57
parasympathetic control of pacemaker action potential
acetylcholine binds to a muscarinic receptor causing decreased Na+ permeability
longer time taken to reach threshold potential
58
differences between cardiac myocyte action potential and regular action potential
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
59
what does the longer refractory potential in cardiac action potential do?
prevents muscle fatigue
60
stage 4 of action potential of cardiac muscles
Na+ and Ca2+ channels closed
open K+ rectifier channels keep TMP stable at -90mV
K+ from ICF -> ECF
61
stage 0 of action potential of cardiac muscles
rapid Na+ influx through open fast Na+ channels
Na+ from ECF -> ICF
depolarisation
62
stage 1 of action potential of cardiac muscles
partial repolarisation
transient K+ channels open and K+ efflux returns TMP to 0mV
K+ from ICF -> ECF
63
stage 2 of action potential of cardiac muscles
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
64
stage 3 of action potential of cardiac muscles
repolarisation
Ca2+ channels close but delayed rectifier K+ channels remain open and return TMP to -90mV
K+ from ICF to ECF
65
what does conduction spread through in nodes?
gap junctions
66
AVN conduction
less gap junctions -> delays conduction
allows for atrial emptying before contraction of ventricle
67
HP systems structure
v large fibres
highly permeable gap junction
68
artery structure
thick muscular wall to sustain force of LV contractions
elastic - cushions systole
as elastic in walls recoils, the pressure supplied is the diastolic pressure
69
arterioles structure
smooth muscle in walls
determining arterial pressure and distributing flow
70
where is the principle site of resistance to vascular flow?
arterioles
71
capillary structure
endothelial cells and pericytes
precapillary sphincters control blood flow to tissue
fenestrated (holes)
thin - movement of fluid across membranes
72
what becomes the lymph?
substances and fluid that move across into tissue become lymph
73
veins structure
main blood reservoir
low resistance
wide lumen
74
functions allowing venous return against gravity
valves - prevent backflow
muscle action peristalsis
respiratory pump
75
lymph vessels structure
low pressure
valves
76
lymph vessels function
drains excess fluid from tissues
drains into subclavian veins
77
lymph fluid contents and appearance
no erythrocytes/large proteins, can contain all other blood components
eosinophilic
78
where are precursor cells of erythrocytes found in adults and children?
bone marrow
adults: axial skeleton (skull, ribs, spine, pelvis, long bones)
children: all bones
in utero: yolk sac, liver, spleen
79
what is an important fact about precursor cells?
not found in blood - if they are, this is a sign of leukaemia
80
what do hormonal growth factors do? what are their different types?
stimulate precursor stem cells to proliferate and differentiate
EPO/erythropoietin (hormone from kidney): erythrocytes
G-CSF (granulocyte colony stimulating factor): leukocytes
Tpo: platelets
81
what is haemoglobin made of?
2 alpha and 2 beta chains and 4 haem groups
overall quaternary structure combination of 2+ tertiary structures
82
what is rhesus?
C, D, E antigens
D antigen is most important -rhesus positive means D antigen is present, rhesus negative means it's not
83
what is anaemia?
reduction of haemoglobin in blood
84
what are normal haemoglobin levels?
12.5 - 15.5 g/dl
85
what is polycthaemia caused by?
smoking, lung diseases, inefficient lungs
86
what are symptoms of anaemia?
tiredness, lethargy, malaise, reduced exercise tolerance, SOB, angina
87
what are the signs of anaemia?
palor, pale mucus membrane, palmar creases, glossitis, angular stomatitis, kylonychia (spoon shaped nails)
88
what are the classifications of anaemia?
iron deficiency, B12/folate deficiency, anaemia of chronic disorder, haemolysis, bone marrow failure/inflitration
89
what is iron-deficiency anaemia?
lack of iron -> reduced production of small red cells
needed for haemoglobin production
90
how is red cell size measured?
MCV (mean cell volume)
91
what is the normal MCV? what is the abnormal one?
82-96 fl
<80 fl
92
what are the causes of iron-deficiency anaemia?
bleeding:
occult GI: most common
menorrhagia: heavy periods. only premenopausal women or repeated child birth
dietary: not getting enough iron in diet
93
what is macrocytic anaemia?
MCV > 100fl
can occur w/out anaemia - caused by liver disease, alcohol, hypothyroidism
94
why does macrocytosis occur?
vitamin B12/folate deficieny
95
how do vitamin B12/folate affect erythrocyte production?
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
causes of B12 deficiency
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
what is pernicious anaemia?
autoimmune disease
causes antibodies to be made against gastric parietal cells -> less intrinsic factor produced -> B12 malabsorption
98
why does pernicious anaemia have a slow onset?
liver has a vast store of B12 which can last 4 years
99
where is folate found?
vegetables and fruit
100
what are the causes of folate deficiency?
malabsorption (celiac disease)
dietary (not enough fruit or vegetables)
increased need (haemolysis/increased cell division)
101
what is haemolysis?
normal or increased erythrocyte production but decreased life span < 30 days
destroyed before 120 days
102
what are types of haemolysis?
congenital or acquired
103
what is congenital haemolysis caused by?
membrane issues e.g. spherocytosis
enzyme issues e.g. pyruvate kinase deficiency
haemoglobin issues e.g. sickle cell anaemia
104
what is spherocytosis?
blood cells are spherical
get stuck in vessels easily
dominant condition, variable penetrance
105
what is pyruvate kinase deficiency?
enzyme needed to convert phosphoenolpyruvate to pyruvate is deficient -> less ATP and build up of phosphoenolpyruvate
G6PD deficiency
106
what is sickle cell anaemia?
defect in beta globin chain
sickle shaped, get trapped in vessels
107
what is thalassaemia?
mutation in haemoglobin genes (beta more common in india and Pakistan) and alpha more common in east e.g. Thailand
108
what causes acquired haemolysis?
autoimmune, mechanical, pregnancy
109
what is autoimmune haemolysis?
immune system attacks own erythrocytes, can be triggered by blood transfusion (foreign antibodies)
110
what is mechanical haemolysis?
fragmentation of erythrocytes by mechanical heart valve or intravascular thrombosis in DIC
111
what is DIC?
disseminate intravascular coagulation
112
what is HDFN?
haemolytic disease of the foetus and newborn
113
what happens in HDFN?
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
what if the mother's second baby also has RhD positive blood?
antibodies produced immediately, begin destroying babies erythrocytes -> haemolysis, anaemia and jaundice
115
what is rhesus disease?
antibodies can cross to baby via placenta and begin attacking
116
what are leukocytes?
mature cells that circulate in the blood
produced from immature precursor cells in the bone marrow which are derived from stem cells
117
what controls the rate of production of leukocytes?
G-CSF (hormonal control)
118
what are neutrophils? what do they do?
most numerous leukocyte
10 hours lifespan
phagocytose and kill bacteria, release chemotaxins and cytokines
119
what does lack of number or function of neutrophils lead to?
recurrent bacterial infections
120
what is a chemotaxin?
substance released by bacteria, injured tissue and leukocytes that induces movement of neutrophils and leukocytes to the injured area
121
what is a cytokine?
broad category of small proteins used in cell signalling
can't cross lipid bilayer
122
what types of lymphocytes are there?
B and T cells
123
what are the functions of lymphocytes?
vital to immunity
generate antibodies against specific foreign antigens e.g. bacteria and viruses
immunological memory - generates immunity and allows vaccination
124
what are B lymphocytes? what do they do?
made in bone marrow, stored in secondary lymphoid organs
differentiate into plasma cells and produce immunoglobulins when stimulated by exposure to foreign antigen
125
what are T lymphocytes? what do they do?
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
what is acute leukaemia?
proliferation of primitive precursor cells usually found in bone marrow without differentiation - replaces normal bone marrow cells
127
what does acute leukaemia lead to?
anaemia (palor and lethargy)
neutropenia (infections, as white cells aren't differentiating)
thrombocytopenia (excessive bleeding)
128
what is a sign of acute leukemia?
presence of primitive white precursor cells in the blood
129
what is acute myeloblastic leukaemia? who does it affect?
malignant proliferation of the precursor myeloblasts (unipotent stem cells) in bone marrow
adults
50% survive 5 years
130
what is acute lymphocytic leukemia? who does it affect?
malignant proliferation of the lymphoblast precursor cells in the bone marrow
children
80% cured
131
what is high grade lymphoma?
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
what determines PT?
platelets determine prothrombin time
133
what are platelets?
small cytoplasmic anucleate cells that block up holes in blood vessels
spherical, anucleate - can't repair themselves
134
where are platelets made from?
bone marrow from cells called megakaryocytes
135
what is the life span of platelets?
5-10 days
136
what is the normal number of platelets?
140-400 x 10^9/L
137
what is reduced numbers of platelets?
thrombocytopenia (main risk is cerebral bleeding)
< 80 - increased bleeding
<20 - spontaneous bleeding
138
what is high numbers of platelets? what can it lead to?
thrombocytosis
can lead to arterial and venous thrombosis -> increased risk of heart and stoke
139
where are coagulation proteins made?
liver
140
what is the key enzyme in coagulation?
thrombin - makes platelet plug
141
what is essential for correct synthesis of coagulation factors?
vitamin K
| 2,7,9,10
1972
142
what is the function of coagulation proteins?
circulate in inactive form
make blood clot
convert soluble fibrinogen into insoluble fibrin polymer
143
what proteins are in the plasma?
albumin, carrier proteins, immunoglobulins
144
what is albumin? what is its function? where is it produced? what does it carry?
most numerous protein in plasma
maintain oncotic pressure
lack of it -> oedema
liver
fatty acids, steroids and thyroid hormones
145
what are immunoglobulins?
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
what is haemostasis?
arrest of bleeding
involves physiological processes of blood coagulation and the contraction of damaged blood vessels
147
why is blood usually fluid inside blood vessels?
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
what is thrombosis?
blood clots inside vessels
149
what is a bleeding disorder?
blood fails to clot outside vessels
150
what is the key enzyme involved in the coagulation cascade?
thrombin - cleaves fibrinogen to create fibrin polymerisation
151
graduation of coagulation
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
what is haemophilia?
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
what is haemophilia A?
bleeding into muscles and joints
1/10000 males
deficiency in clotting factor VIII - treat with factor VIII
154
what is haemophilia B?
bleeding into muscles and joints
1/50000 males
deficiency in clotting factor IX - treat with factor IX
155
why is haemophilia B less common than A?
gene is smaller
156
what is von Willebrands disease?
autosomal dominant inheritance
lack of vWF
usually a mild bleeding disorder
up to 1% - unrecognised and undiagnosed
157
what is the type of bleeding seen in von Willebrands disease? what are its symptoms?
muco-cutaneous bleeding: bleeding in skin and mucous membranes
easy bruising, prolonged bleeding from cuts, nose bleeds, spontaneous gum bleeding/GI loss
158
what are acquired bleeding disorders?
recent onset, no lifelong/family history
may be generalised or local bleeding
159
what is the most common cause of acquired bleeding disorders?
anti-platelet or anti-coagulation medication
160
what are other causes of acquired bleeding disorders?
liver disease, vit K deficiency, drugs, DIC
161
how does liver disease cause acquired bleeding disorders?
synthesises coagulation factors and fibrinogen
disease often associated with bleeding and prolonged prothrombin time
most common cause of liver disease is alcohol
162
how does vitamin K deficiency cause acquired bleeding disorders?
vit K needed for correct synthesis of coagulation factors II, VII, XI, X
vit K is a fat soluble vitamin
163
what is vitamin K caused by?
malabsorption, esp. in obstructive jaundice
164
what does vitamin K deficiency manifest as?
prolonged PTT
165
what is vitamin K deficiency causing bleeding disorders treated with? in babies?
intravenous vitamin K
newborns are born vitamin K deficient, given it at birth
166
how do different drugs affect bleeding?
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
what is DIC?
disseminated intravascular coagulation
breakdown of haemostatic balance
simultaneous bleeding and microvascular thrombosis
life threatening
168
what are the causes of DIC?
sepsis, obstetric (anything that goes wrong with pregnancies), malignancy
169
what is the mechanism of DIC?
activation of coagulation cascade inside blood vessels, thrombin produced, causing fibrinogen -> fibrin. forms microvascular thrombosis (platelet plugs) everywhere
170
what does DIC cause?
deficiency of clotting factors and platelets as they've been used up in formation of microvascular thromboses
171
what is the treatment of DIC?
treat underlying cause
stop generation of intravascular thrombin
transfuse new platelets
172
what is the response of the blood vessel to damage?
constriction
173
what causes a blood vessel to constrict?
neural control and release of endothelin-1 (released by endothelial cells)
174
what temporarily closes a blood vessel when it's damaged?
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
where does permanent closure of vessels occur?
permanent closure by constriction and contact stickiness occur in v small vessels of the microcirculation
176
what does the stopping of bleeding depend on?
independent processes that occur in rapid succession: formation of a platelet plug and blood coagulation
177
what happens when a vessel is injured/ruptured?
disrupts the endothelium - exposure of collagen fibres
178
how to platelets adhere to collagen fibres?
via an intermediary VWF. also attached to the collagen via a receptor on the platelet membrane - glycogen 1b receptor
179
what does binding of the platelets to the collagen fibre wall trigger?
platelet releases contents of their secretory vesicles via exocytosis
180
what do platelet dense granules release?
ADP - acts on P2Y1 and P2Y12, causing platelet amplification
181
what causes platelet amplification?
ADP from platelet dense granules acting on P2Y1 and P2Y12
ATP binding to P2X1
182
what causes platelet activation?
thrombin binding to PAR1 and PAR4 receptors - induces platelet activation and further thrombin release (positive feedback)
183
what are changes in platelet activation?
platelet changes shape from a smooth discoid shape to a more spiculated (spiky) shaped with pseudopodia
increases SA
184
what does platelet activation cause?
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
what do GP IIb/IIIa bind to?
fibrinogen
186
what is fibrinogen from?
alpha granules
187
what is platelet aggregation?
new platelets adhering to old ones (positive feedback mechanisms)
GP IIb/IIIa receptors on platelets bind to fibrinogen from alpha granules
