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Phase 1 > Cardioresp > Flashcards

Cardioresp Flashcards

1
Q

Haematocrit (PVC)

A

ratio of volume of red blood cells ( erythrocytes) to total volume ( 45%)

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2
Q

Haemopoiesis

A

Formation of new blood cells and platelets

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3
Q

Anaemia

A

Reduced haemoglobin or numbers of RBCs, often due to iron deficiency

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4
Q

Haemostasis

A

The arrest of bleeding, involving the physiological processes of blood coagulation and the contraction of damaged blood vessels

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5
Q

Haemophilia

A

Inability to make blood clots due to factor VIII deficiency ( haemophilia A) or factor IX deficiency ( haemophilia B - Christmas disease) A is more common.

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6
Q

Erythrocytes

A

120 day lifespan
Simple cells, no nucleus, and no mitochondria
Biconcave disc, 7.5um diameter
Contain haemoglobin and glycolysis enzymes
RBCs are removed in the spleen, liver, bone marrow (reticuloendothelial cells ) and through blood loss

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7
Q

Haemoglobin

A

Carries oxygen from lungs to tissues
Tetrameric protein with 4 globin chains, each with a haem group ( porphyrin with a central ferrous iron ion - Fe2+) capable of reversible binding oxygen
Several phenotypes exist :
Haemoglobin A - 2 a chains and 2 b chains ( 97% of adult population)
Foetal haemoglobin (HbF) 2 a, 2 y
HbA2 - 2 a, 2 d
Mutati9ns or absconded of a or b chains in adults referred to as thalassemia, potentially cashing anaemia

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8
Q

Precursors of mature cells is adults and children

A

In adults are derived from the bone marrow of the axial skeleton ( not limbs) but all bones in children.
In embryos, it is in the yolk sac, liver, spleen, and bone marrow.
Stem cells are pluripotent and can differentiate into any RBCs, white blood cells ( leukocytes) or platelets

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9
Q

Erythropoiesis

A

Production of RBCs
Hormonal stimulating factor - erythropoietin ( EPO) made in the kidneys. Low level constant release but also in response to hypoxia

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10
Q

Myelopoiesis

A

Production of WBCs
Hormonal factor : granulocyte - macrophages colony stimulating factor (GM-CSF)
will only stimulate production of myeloblastic WBCs and not lymphoid cells

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11
Q

Two types of leukocytes

A

Granulocytes - eosinophil, neutrophil, basophil
Agranulocytes - monocytes, lymphocytes

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12
Q

Eosinophils

A

Stains orange
Bi-lobed nucleus
IgE receptors
Antagonistic to basophils : lowers mast cell histamine secretion

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13
Q

Neutrophils

A

Don’t stain
( phagocyte - engulfs pathogens )
Granules -
1. Lysosomes - myeloperoxidase and acid hydrolyses
2. Inflammatory mediators
3. Gelatinises and adhesion molecules

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14
Q

Basophils

A

Satin blue
Mature into mast cells
Express surface ige and secrete histamine

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15
Q

Monocytes

A

Reinforce nucleus
Agranulocyte but have granules
Mature into macrophage

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16
Q

Lymphycytes

A

Only blood cells that divide
Large nucleus
T cell - 80%
B cell - 20%
Indistinguishable, could be T cell b cell or nk cell

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17
Q

T cell origin and maturation site

A

Originate in the bone marrow and mature in the thymus gland

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18
Q

B cell origin and maturation site

A

Bone marrow

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19
Q

Anaemia

A

Deficiency of Hb, male <130g/l and female <110g/l

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20
Q

Anaemia signs and symptoms

A

include pallor, tachycardia, hyperventilation on exertion, malaise and angina in older people.

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21
Q

Causes of anaemia

A

Acute blood loss ( haemorrhage )
Production mismatches - hypoplastic ( not enough)
Dyshaemotpoeitic ( ineffective production)
Increased removal of RBCs - haemolytic anaemia
Deficiencies in iron, folate ( macrocytic anaemia) or vitamin B12 ( pernicious)

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22
Q

Haemostasis

A

Blood should remain fluid inside vessels and when outside, should clot.
Blood is a fluid inside vessels because :
Platelets and proteins of the coagulation cascade circulate in an inactive state
Endothelial cells , anticoagulant pathway and fibrinolytic pathways ensure fluidity

Bleeding - when blood fails to clot outside the vessel
Thrombosis - clotting inside the vessel

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23
Q

Platelets

A

Circulate in an inactive form
Anucleate
Originate from magakaryocytes which enter endomitosis where the chromosomes duplicate but the cells do not divide so more. Chromosomes than normal - polyploidy
Platelets break off from the megakaryocytes

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24
Q

Plasma

A

Fluid component of blood ( 55%)
Transportation media that contains water, salt glucose and proteins
Serum is blood plasma without any clotting factors

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25
Q

Proteins in blood plasma

A

Albumin - produced in the liver
-determines oncotic pressure of blood
- keeps intravascular fluid within that space
- lack of albumin leads to oedema
- seen in liver disease and nephrotic syndrome ( loss of protein into urine )
Carrier proteins
Coagulation proteins
Immunoglobulins - produced by activated b lymphocytes

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26
Q

Coagulation cascade

A

Process of blood clotting, ( not platelet plug formation which allows the bleeding to stop by closing the area )
Coagulation helps stabilise the plug
Ultimately converts soluble fibrinogen into fibrin which then forms a stable fibrin clot

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27
Q

Two initiating separate pathways the the coagulation cascade

A

Extrinsic and intrinsic

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28
Q

Coagulation cascade extrinsic pathway

A

Damage to endothelial lining of vessels releases tissue factor which activates factor VII.
TF VIIa then has a direct effect on factor X to initiate common part of the cascade

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29
Q

Coagulation cascade intrinsic pathway

A

Blood contacting endothelial collagen outside the lumen activates factor XII ( serum protease) > XI > IX
Factor X then activated by IXa along with cofactors VIII, phospholipids and ca2+

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30
Q

Coagulation cascade common pathway

A

Xa converts prothrombin ( factor II) into thrombin ( factor IIa)
Thrombin converts fibrinogen (I) into fibrin (Ia) and activates factor XIII
Fibrin and factor XIIIa leads to the cross linking of fibrin and a clot
Thrombin also gives positive feedback on factors V, VII, VIII and XI but also prevents over-coagulation by activating pas in which is fibrinolytic

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31
Q

Components of platelets

A

Plasma membrane
Cytoskeleton
Dense tubular system
Secretory granules
- alpha
- dense
- lysosome
-peroxisome

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32
Q

Heart shunts in embryonic development

A

Bypassing pulmonary circulation - not required in utero
Foremen ovals ( between atria)
Ductus arteriorsus ( pulmonary artery to aorta)

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33
Q

Arteries vs vein shunts in embryonic development

A

Umbilical vein carries oxygenated blood
Umbilical artery carries deoxygenated blood

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34
Q

The heart during birth

A

First breaths of life > lungs expand > the alveoli I. The lungs are cleared of fluid
An increase in the baby’s BP and a significant reduction in the pulmonary pressures reduces the need for the ductus arteriosus to shunt blood > closure of the shunt
These changes increase the pressure in the left atrium of the heart > decrease the pressure in the right atrium > foremen ovale closes > newborn circulation

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35
Q

Descriptive embryology

A

Repeated observation of last mortem specimens to determine stages of development

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36
Q

Mechanistic embryology

A

Experimentation (accidental or deliberate) to determine role of genes / proteins / environmental factors in cardiac development

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37
Q

Gastrulation

A

Mass movement and invagination of the blastula to form three layers - ectoderm, mesoderm ( middle layer) and endoderm

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38
Q

What comes from the ectoderm following gastrulation

A

( outside layer) - skin, nervous system, neural crest ( which contributes to cardiac outflow, coronary arteries )

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39
Q

What comes from the mesoderm following gastrulation

A

Middle layer - all types of muscle, most system, kidneys, blood, bone

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40
Q

What comes from the endoderm following gastrulation

A

Gastrointestinal tract ( including liver, pancreas, but not smooth muscle,) endocrine organs

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41
Q

Where is the cardiovascular system derived from

A

Most is derived from cells situated in the mesoderm ( blood, heart, smooth muscle, endothelium)
Ther is some contribution from the cardia neural crest cells from the ectoderm

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42
Q

The heart fields

A

First heart field - future left ventricle
Second heart field - outflow tract, future right ventricle, atria
The first heart field generates a scaffold which is added to by the second heart field and cardia neural crest

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43
Q

Evolution / gene duplication

A

As organisations evolve, gene duplication occurs sporadically ( from single gene to entire genome ) each copy of each gene can then evolve separately into different ( but related) gene
This accounts for increasing complexity of development

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44
Q

Stages of cardiac formation

A

Formation of the primitive heart tube
Cardiac looping
Cardiac separation

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45
Q

Which way is left

A

All vertebrate hearts have a leftward ventricle
Any mutations are associated with improper left-right positioning ( e.g. kartagener’s syndrome )
During development, the node secretes nodal, which circulates to the left due to ciliary movement
A cascade of transcription factors ( e.g. lefty, pitx2, fog-1) transducer looping

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46
Q

Why do we need circulation to

A

Every cell in our body needs to be bathed in fluid and within 2mm of a source of oxygenation
This reproduces the extra cellular environment of primitive unix and multicellular organisms in the primeval ocean.

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47
Q

Arterial system

A

Conduits of blood ; physical properties ( elastic arteries) increase efficiency whilst regulatory control (muscular arteries) control distribution

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48
Q

Parts of the arterial system

A

Elastic arteries - major distribution vessels ( aorta, brachiocephalic, carotids, subclavian, pulmonary)
Muscular arteries - main distributing branches
Arterioles - terminal branches ( < 300mm diameter)

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49
Q

Capillaries

A

Functional part of the circulation
Blood flow regulated by precapillary sphincters
Between 3-40 microns in diameter

Three types of capillary; continuous ( most common) fenestrated ( kidney, small intestine, endocrine glands), discontinuous ( liver sinusoids)
Slow flow rate ( more nutrient exchange)

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50
Q

Venous system

A

Return blood to the heart
System of valves allows “muscular pumping”
Some peristaltic movement

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51
Q

General structure of an artery / vein

A

Tunica intima ( endothelium basement membrane )
Tunica media ( vascular smooth muscle cells )
Internal elastic laminate
Vasa vasoorum
Tunica adventitious ( fibroblasts)
External elastic lamina

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52
Q

Embryology of the circulation

A

Aberrant embryology accounts for many congenital abnormalities and fetal death
Many of the processes which pattern blood vessels in embryo are also used in post- natal physiological and pathological processes

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53
Q

Formation of the primitive heart tube

A

During the third week of development, the heart is formed from cells that form a horseshoe shaped region called the cardiogenic region
By day 19 ( third week). Two endocardia’s tubes form. These two tubes will fuse to form a single, primitive heart tube.
Day 21 : as the embryo undergoes lateral folding, the two endocardia’s tubes have fused to form a single heart tube

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54
Q

Bulbis cordis

A

Part of the primitive heart tube
Forms most of the right ventricle and parts of the outflow tracts for the aorta and pulmonary trunk

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55
Q

Primitive ventricle

A

Forms most of the ventricle

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56
Q

Primitive atrium

A

Forms the anterior parts of the right and left atria

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57
Q

Sinus venosus

A

Forms the superior vena cava and part of the right atrium
From left and right horns of the primitive heart tube

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58
Q

Cardiac looping

A

By day 22, the heart begins to beat , the bulbis cordis moves inferiority, anteriorly and to the embryos right , the primitive ventricle moves to the embryos left side, the primitive atrium and sinus venosus move superiorly and posteriorly, the sinus venosus is now posterior to the primitive atrium

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59
Q

Cardiac septation

A

At this stage in heart development, there is one common atrium and one common ventricle they are connected by an internal opening called the atrioventricular canal
Blood first enters the atrium
Passes through the atrioventricular canal and into the ventricle then exits through the turn us arteriosus
Masses of tissue called endocardia’s cushions grow from the sides of the atrioventricular canal to partition it into two separate openings.
As the endocardia’s cushions grow together, the atrioventricular canal also is being repositioned to the right of the heart.
The superior and inferior endocardia’s cushions fuse, forming two separate openings that are now called the right and left atrioventricular canals and become the right and left atrioventricular openings of the heart ( now as blood flows through the heart, it will pass from the atrium, through both atrioventricular openings, into the ventricle and up through the truncus arteriosus

60
Q

Days 17-21

A

Formation of blood islands
Vascularisation of the yolk sac, chorionic villus and stalk,
Vasculogenesis commences
This is added to by angiogenesis
( driven by angiogenic growth factors and takes place via proliferation and sprouting )

61
Q

1st and 2nd aortic arches

A

Become minor head vessels
1st - small part of maxillary
2nd - artery to stapedius

62
Q

3rd aortic arches

A

Portion between 3rd and Ruth arch disappears
Become common carotid arteries, and proximal internal carotid arteries
Distal internal carotids come from extension of dorsal aortae

63
Q

Right dorsal aorta and right 4th aortic arch

A

R dorsal aorta looses connections with midline aorta and 6th arch, remaining connected to r 4th arch
Acquires branch 7th cervical intersegmental artery which grows into r upper limb
Right subclavian artery is derived from right 4th arch, right dorsal aorta and right 7th intersegmental artery

64
Q

Left dorsal aorta and left 4th aortic arch

A

Left dorsal aorta continues into trunk
Left 7th cervical intersegmental artery, which grows into left subclavian artery
Right subclavian artery is derived from right 4th arch, right dorsal aorta, and right 7th intersegmental artery

65
Q

6th aortic arches

A

Right arch may form part of pulmonary trunk
Left arch forms ductus arteriosus - communication between pulmonary artery and aorta

66
Q

4 major types of blood

A

A B AB O

67
Q

ABO antigens inheritance

A

Mendelian pattern
Gene on chr 9 codes for an enzyme rather than the sugar itself
Another gene codes for the sugar base of the ABO antigen

68
Q

ABO antibodies

A

Infants <3 months produce a few ( first true abo antibodies >3 months )
Mix of igM and IgG
IgM mainly fro group Aand B.
IgM antibodies don’t cross placenta but rhesus antibody (IgG) can cross the placenta

69
Q

Rhesus antigens

A

> 45 different Rh antigens
2 genes, hromosome 1 ( RHD - codes for Rh D and RHCE - codes for Rh C and Rh E )
Highly immunogenic
Can cause haemolytic transfusion reactions and haemolytic disease of the foetus and newborn ( HDFN)

70
Q

Haemolytic disease of the foetus/newborn (HDFN)

A

RhD sensitisation most common cause
Develop anti-Rh antibodies
Severe fetal anaemia
Hydrous fetalis
Prevention - detect mothers at risk, maternal fetal free DNA, anti D prophylaxis
( mothers antibodies attacks baby’s erythrocytes

Mother (dd) has kids with DD/Dd
1st child - no immune response- treated like foreign material by the mother because it has no anti-d antibodies
( mother will make rhesus D auntibodies )
2nd child - rapid immune response - Rhd antibodies from birth and attack foetus can ¡dad to anaemia and death.

71
Q

Indirect anti globulin test

A

( indirect Coombs test)
Blood grouping for ABO and rhesus d
Detects antibodies in patients serum

72
Q

Blood donation exclusion criteria

A

Temporary- travel, tattoos/body piercings, lifestyle
Permeant - certain diseases, received blood products or organ/tissue transplant since 1980, notified risk of vCJD

73
Q

Indications for transfusions

A

Hypovolaemia due to blood loss
Severe anaemia with inadequate oxygenation of tissues
Anaemia - check b12 deficiency before considering blood transfusion, not included for iron deficiency of b12 deficiency

74
Q

Early hazards of transfusions

A

ABO incompatibility reaction - can be fatal
Fluid overload - pulmonary oedema
Febrile reaction - antigens target donor antigens. Can cause life- threatened respiratory failure
Bacterial and malarial infection.

75
Q

Late hazards of transfusions

A

Rhesus d and other antibody sensitisation
Delayed transfusion reaction
Viral infection, hepatitis b, c and hiv
Prior infection
Iron overload resulting in cardiac, hepatic and endocrine damage

76
Q

Operative erythropoietin alternative to transfusion

A

Stimulates RBC production

77
Q

Plasma alternative to transfusion

A

Can be used as it is of fractioned to produce concentrates of specific components such as factor 8 or 9.

78
Q

Fresh frozen plasma alternative to transfusion

A

Contains coagulation proteins and clotting factors. Used in massive transfusion , dilutions and coagulopathy ( impaired coagulation), liver disease, and disseminated intravascular coagulation ( DIC).

79
Q

Cryoprecipitate alternative to transfusion

A

Frozen blood rich in fibrinogen. Used in DIC and massive transfusion is there is a lack of fibrinogen in coagulation cascade

80
Q

Platelet use in alternative to transfusion

A

Used in thrombocytopenia ( low platelet count ) however not useful if deficiency is due to immune anti-platelet antibody

81
Q

Albumin alternative to transfusion

A

Can be used in cases of oedema to correct the oncotic pressure of blood and keep fluid in. Used in liver disease or nephrotic syndrome

82
Q

Anti-D globulin alternative to transfusion

A

Collected from people sensitised to D and used to prevent Rh D disease

83
Q

Intravenous immunoglobulin alternative to transfusion

A

Pooled immunoglobulin, use din immunodeficiency, congenital or acquired and some auto-immune diseases.

84
Q

Cardiac output

A

Volume of blood ejected by each ventricle per minute
Co = hr x sv

85
Q

Extra-embryonic blood vessel formation day 17-21

A

Lateral plate mesoderm - blood islands - vasculogenesis

86
Q

Extra-embryonic blood vessel formation day 28

A

Angiogenesis - proliferation and sprouting - mesodermal cell recruited for tunica media and adventitia

87
Q

Arteries

A

Low resistance, high pressure - maintain perfusion during diastole
Elastic - largest and closest to the heat x elastin in tunica media / external - expand / recoil to absorb pressure
Muscular - includes coronary arteries, thick muscular walls

88
Q

Arteriole

A

High resistance
Myogenic auto regulation - increase stretch - vasoconstriction : smooth muscle contraction ( thermogenesis) - more pressure and more perfusion.

89
Q

Capillary

A

Slow flow - enables time for nutrient/ waste exchange
Continuous, discontinuous or fenestrated
Pericytes regulate flow
Flow determined by : arteriolar resistance, pre capillary sphincters and plasma/ifs flow

90
Q

Vein

A

Low resistance capacitance vessels : contain 70% of blood volume
Venous return is aided by :
Valves - unidirectional blood flow
Skeletal muscle contraction
Sns mediated vasoconstrictions
Respiratory pump - diaphragm contraction creates pressure difference

91
Q

Sphygmomanometer

A

Compress brachial artery with cuff above sbp- deflate
Systolic : pressure in arteries when heart beats - 100-150 mmHg x korotohoff sounds start -turbulent blood flow
Diastolic : pressure in arteries when heart is at rest beats 60-90 mmHg - korotohoff sounds stop : laminar blood flow

92
Q

Baroreceptors

A

Present in the carotid sinus ( carotid artery birfurcation) and aortic arch primarily. Secondary found in vein, myocardium and pulmonary vessels
Afferent - glossopharyngeal nerve to medulla
Efferent - sympathetic and vagus x.
Firing rate proportional to medulla

93
Q

How Baroreceptrs work

A

Increased bp sensed by baroreceptors which is then sent via the glossopharyngeal nerve ( is) to the medulla where there is increased firing which results in stimulation of parasympathetic ( x) nerves and decrease in sympathetic stimulation
. Results in decreased co and tar. By = co x tpr

94
Q

Arterial baroreceptors

A

Short term regulation of bp. New baseline formed if arterial pressure has deviated from the normal baseline for more than a few days. Can lead to hypertension if new baseline is higher.

95
Q

Cardiopulmonary baroreceptors

A

Atria, ventricles and pulmonary artery. When these baroreceptors are stimulated, you have a decreased vasoconstrictor and decreased bo. Decreased release of angiotensin, aldosterone and vasopressin leads to fluid loss - key in blood volume regulation.

96
Q

Blood vessel auto regulation

A

Is both intrinsic (responds to blood flow ; should be constant)
And extrinsic ( myogenic vasocontriction / dilation)
Myogenic tone of blood vessels - smooth muscle never relaxes

97
Q

Hyperaemia

A

Increased blood flow
Active - metabolic response ( increases intensity e.g. excersize )
Reactive - occluded tissue - once removed more blood flow to it

98
Q

Peripheral chemoreceptors

A

Aortic arch and carotid sinus
Sensitive to
High co2
Hypoxia ( low oxygen)
And low ph

Will always act ina sympathetic way to increase blood pressure
Does this by sending impulses to the pressor region of the medulla

99
Q

Arterial baroreceptors

A

Aortic arch and carotid sinus
Responds to high bp

More distortion of baroreceptors means higher firing rate
Sends impulses to depressor centre of medulla

Lowers bp in a parasympathetic way

100
Q

Cardiopulmonary baroreceptors

A

In atria ventricle and pulmonary artery
Responds to high blood volume

Increased by - increased bp = more distorted baroreceptors
Impulses to depressor region of medulla

Lowers bp in a parasympathetic way

101
Q

Central control of circulation

A

Medulla
Two centres
Pressor - sympathetic
Depressor - parasympathetic

102
Q

Cardiac output equation

A

Stroke volume x heart rate

103
Q

Blood pressure equation

A

Cardiac output x total peripheral resistance

104
Q

Pulse pressure equation

A

Systolic - diastolic

105
Q

Mean arterial pressure equation

A

Diastolic pressure + 1/3 of pulse pressure

106
Q

Pouisseile’s law

A

Blood flow = (pi) r ‘4/ 8 x length x viscosity

107
Q

Frank starling law

A

Higher end diastolic volume ( more vent filling) = harder contraction

( higher edv means more myocytes stretching - contraction strength - higher stroke volume so higher cardiac output

108
Q

Starling forces acting of blood vessels

A

Force keeping blood in = oncotic pressure ( by albumin pressing on by walls )

Force squeezing fluid out = hydrostatic pressure ( by more pressures of fluid inside - pressure gradient high to low )

109
Q

Controlling blood pressure long term

A

Fluid intake
RAAS
ADH

Failing hearts go have a lower cardiac output
We can treat by increasing sv ( increase volume of extra cellular fluid by giving blood ) or increase hr

110
Q

regulating circulation

A

Vasodilators
Hypoxia
Low ph / high h+ / high co2
Bradykinin
NO
prostacyclin ( ( released by healthy endothelium)
High K+
Acetylcholine (Ach) - acting on muscularinic type 2 receptors
ANP ( released by dialated atria when bp high j

Vasoconstrictors
Endothelin 1 ( released by injured endothelium)
Angiotensin II
ADH
NAd ( noradrenaline)

111
Q

Stroke volume

A

Ventricular ejection at systole

112
Q

Co

A

Ventricular ejection / unit time

113
Q

TPR

A

total peripheral systemic resistance ( highest in the arterioles)

114
Q

Preload

A

Amount of myocyte stretch in ventricular filling ; ( a volume )

115
Q

After load

A

Resistance myocytes contract against in ventricular systole ( a resistance)

116
Q

Contractility

A

How hard heart beats

117
Q

Compliance

A

How easily heart fills in diastole

118
Q

Diastolic distensibility

A

Pressure to fill ventricles at diastole to edv

119
Q

Parasympathetic and sympathetic effects of cv system

A

Parasympathetic
ach - muscularinic type 2 (M2) receptors
Decrease in hr (chrinotropic )
Decrease in force if contraction ( ionotrophic )

Sympathetic
Noradrenaline- beta 1 (B1) receptors in heart
( increase hr - positive chronotropic )
Increase in force of contraction- positive ionotropic )

120
Q

Pulmonary vs systemic vessels

A

Pulmonary
Thin walled
Hypoxia - vasoconstrict
Sys/ dia pressure - 25/8 ( trying to oxygenate deoxygenated blood from right side of the heart - only passing through the lungs so can’t have too high pressure )

Too high pressure can cause oedema- as hydrostatic pressure in vessels would be too big to withstand keeping fluid inside )

Systemic
Thick walled
Hypoxia - vasodilate
120/80

121
Q

Precursor to all blood cells

A

Haematocytoblast - pluripotent

Proerythroblast - rbc
Monoblast - monocyte
Lymphoblast - t + b lymphocyte
Myeloblast - progranulocyte - basophil, eosinohil, neutrophil
Megakaryoblast - megakaryocytes - platelet

122
Q

Granulocyte

A

Have visible granules
Neutrophils, (inflam response, multilobed, faint granules
eosinophil, ( antihistamines, pink granules, IgE receptors
basophil ( histamines, dark blue granules, IgE receptors

123
Q

Agranulocytes

A

Monocytes - ( immature, become macrophages and arcs, reinforce nucleus
Lymphocytes ( cell mediated innate response, very little cytoplasm, mostly nucleus

124
Q

Platelets

A

Megakaryocyte undergoes endomitosis ( dna doubles but cell doesn’t divide
C.s.m “ blebs “ ( ejects fragments = platelets )
Inactive platelets - smooth and discoid
Activated - increase sa and pseudopoid

Release e- granules ( energy)
Adp, ca2+, atp, serotonin

And dense granules ( scaffold )
Fibrinogen, pdgf ( platelet dense growth factor ) , heparin antagonist

125
Q

Too high or low platelets

A

High - thrombocytosis ( more clots )
Thrombocytopenia ( cutes can cause bleeding)

126
Q

Vascular contraction

A

Step before platelet plug formation
Endothelin 1 from damaged endothelium = vasoconstriction
( healthy endothelium = prostacyclin and NO release vasodilates and keeps vessels open

127
Q

Platelet plug formation

A

Con willebrand factor ( vwf) ( factor 8) binds to exposed collagen at injured endothelium ( using the platelet receptor factor GP1b).
Platelet adhesion - bind to VWF on collagen via GP IIa / IIIb
Platelet activation - exocytosis of dense and e- granul3s - result = amplified +ve feedback to activate more platelets

This forms initial platelet plug

128
Q

Coagulation cascade following platelet plug formation

A

Forms a mesh of fibrin 1 over primary platelet plug to form a stable secondary platelets plug
Intrinsic pathway - uncommon, trauma inside the blood vessels ( internal endothelial damage)
Factor 12 - 11 - 9 - 8 -10
Extrinsic pathway - common, extra vascular trauma
Tissue factor 3 from damaged tissue activates 7 then 10

Common pathway - 10 in centre - activates 2 ( with the help of 5) ( prothrombin- thrombin)
2 activates 1
Fibrinogen - fibrin

129
Q

Hydrolysis the secondary platelet plug

A

tPa ( tissue plasminogen activator ) converts plasminogen to plasminogen
Plasmin eats fibrin; fibrin - fibrinogen (. It’s inactive form )

All clotting factors bar VIII ( VWF) produced by the liver
Vitamin k dependant factors are 10 9 7 2

130
Q

Conduction of a heartbeat

A

SAN ( in wall of the right atrium, in one of the grooves in the right oricle) ( 60-80 bpm autorythmic sinus pattern - Myogenic and doesn’t need any neural signals to beat it does it on its own )

Electrical impulses to atria via bacchman bundles

AVN - delayed about 0.1s for ventricles to;fill
Lower condiction speed As less gap junctions and smaller fibre diameter

Impulses conducted down bundle of his ( spread from right and left ventricles down to the apex of the heart )

Then transmitted to lateral regions of the ventricles by purkinje fibres ( fastest conduction)

131
Q

Myocytic contraction

A
  1. AP wave of depolarisation; Na + influx
  2. Plateau phase (2) ; ca ++ in causes ca ++ release via Ryr -2 receptors from sarcoplasmic reticulum ( Ca++ induced Ca++ release)
  3. Ca++ binds to troponin c ( protein that sits on top of tropomyosin and inhibits actin forming cross bridges with the myosin)
    - changes shape ; removes tropomysin from myosin head. Actin myosin bridges form

After this - atp needed to break cross bridges ( so myosin can move along / muscle can relax) and to return ca++ to sarcoplasmic reticulum.

132
Q

Excitation contraction coupling ; contractile cell

A

Phase 4 - resting membrane potential ( -90 mV )
Increase in mV value to the threshold ( -70)
once threshold is exceeded - massive influx in Na+ ( fast sodium ion channels open) - phase 0

This cause’s potential difference of cell to increase to + 20.

Shutting of fast na + channels and transient k + open ( these allow k+ to leave ) causes minor decrease in potential diff in cell.

L type ca ++ channels open ( proportional to rate of transient k + ions leaving ) so charge will not change

Ca ++ L type channels eventually close and more k+ channels open to k+ can leave ( potassium rectifying channels) until rmp is reestablished.

No hyperpolsrisztion as heart muscle is autorythmic and continuous so needs to be consistent.

Refractory periods
Absolute - phase 1 and 2 - no further ap generated at this point
Relative - phase 3 can generate ap but stimulus needed.

133
Q

Nodal cell depolarisation

A

cells that transmit electrical impulses

Rmp of -60. Threshold -40

T type ca ++ channels open allow small ca ++ influx

L type will open at threshold value and allow a bigger calcium influx

K+ channels open allow k effluent

This sinus rhythm generation needs to be shorter than contractile mechanism

134
Q

ECG reading

A

P wave - atrial systole ( depolarisation)
QRS - ventricular systole ( depolarisation) and atrial repolarisation
T wave - ventricular repolarisation

135
Q

St elevation

A

St segment isn’t isoelectric
So ventricles repolarise ( relax ) less
Lowered edv and co
Widow maker - cardiac arrest

136
Q

Pr interval

A

Start of p to start of qrs

137
Q

12 lead ecg

A

10 sticky pads
12 leads

A. 3 unipolar - aVR, aVL , avF
B. 3 bipolar - I, II, III ( 4 sticky pads)
C. 6 chest - ( 6 sticky pads)

A & B - 4 pads on each limb ( right leg emitted ; value 0)
- aVL, aVR, aVF correspond in one direction to a sticky pad on e limbs from heart
The 3 pads correspond with each other too ( bipolar leads).

C. 6 chest leads
V1-V6

138
Q

Heart views of the 12 lead ecg

A

Septal - v1v2
Anterior - v3v4
Lateral - v5v6 II aVF
inferior - II IIaVF

139
Q

What part of heart does the RCA supply

A

SAN, AVN, post IV septum

140
Q

What part of heart does the RMA supply

A

RV & apex

141
Q

What part of heart does the PDA supply

A

RV, LV, post 1/3 IV septum

142
Q

What part of heart does the LCA supply

A

LA, LV, septum, AV, bundle of his

143
Q

What part of heart does the LAD supply

A

Ant 2/3 of IV septum, RV, LV

144
Q

What part of heart does the LMA supply

A

LV

145
Q

What part of heart does the circulflex artery supply

A

LA, LV

146
Q

Heart failure

A

Systolic failure - heart doesn’t pump hard enough
Diastolic - heart doesn’t fill to full volume

Left failure x blood backs up in lungs - pulmonary oedema

Right failure - blood back up in rest of body - peripheral oedema ( most commonly legs )

Phase 1 (8 decks)

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