4. cardiovascular system Flashcards

Question

what are the three layers of the heart wall?

Answer 1

1. epicardium (outer); 2. myocardium (middle) 3. endocardium (inner)

Answer 2

the outer layer of the heart wall and part of pericardium (visceral serous pericardium)

Answer 3

epicardium (outer) *visceral serous pericardium

Answer 4

myocardium (cardiac muscle)

Answer 5

endocardium (continuous with endothelium of large vessels of heart)

Answer 6

the outer layer of fibrous connective tissue surrounding an organ.

Answer 7

1. right atrium (RA) receives deoxygenated blood from vena cava and coronary sinus 2. right ventricle (RV) pumps deoxygenated blood to lungs (pulmonary circulation) 3. left atrium (LA) receives oxygenated blood from lungs via pulmonary veins 4. left ventricle (LV) pumps oxygenated blood into aorta (systemic circulation)

Answer 8

right ventricle (RV) pumps deoxygenated blood to lungs = pulmonary circulation

Answer 9

left ventricle (LV) pumps oxygenated blood into aorta = systemic circulation

Answer 10

The coronary sinus is the major venous tributary of the greater cardiac venous system; it is responsible for draining most of the deoxygenated blood leaving the myocardium.

Answer 11

The coronary sulcus, also known as the atrioventricular groove, is a groove that separates the atria and ventricles of the heart. It extends from the upper medial end of the third left costal cartilage to the middle of the right sixth chondrosternal joint.

Answer 12

The right coronary artery supplies blood to the right ventricle, the right atrium, and the SA (sinoatrial) and AV (atrioventricular) nodes, which regulate the heart rhythm.

Answer 13

The left anterior descending artery branches off the left coronary artery and supplies blood to the front of the left side of the heart.

Answer 14

atrioventricular (AV) valves 1. right AV = tricuspid 2. left AV = bicuspid (mitral) semilunar (SL) valves 3. pulmonary valve 4. aortic valve

Answer 15

at origin of emerging arteries = pulmonary + aortic *leaving the heart; between ventricle and pulmonary artery/aorta

Answer 16

mitral valve

Answer 17

bicuspid/ mitral (left AV valve)

Answer 18

1. tricuspid valve (AV valve) 2. pulmonary valve (SL valve)

Answer 19

1. bicuspid/mitral (AV valve) 2. aortic valve (SL valve)

Answer 20

As the ventricles contract, ventricular pressure exceeds arterial pressure, the semilunar valves open and blood is pumped into the major arteries. However, when the ventricles relax, arterial pressure exceeds ventricular pressure and the semilunar valves snap shut.

Answer 21

In the AV valves, leaflets are connected to the ventricular myocardium by chordae tendineae, while in the SL valves, cusps are anchored directly to the arterial roots

Answer 22

The chordae tendineae connect the atrioventricular valves (tricuspid and mitral), to the papillary muscles within the ventricles. Multiple chordae tendineae attach to each leaflet or cusp of the valves.

Answer 23

To ensure that the AV valves do not turn inside-out, they are attached to small papillary muscles by tough tendons called the chordae tendineae. Papillary muscles contract in synchrony with the ventricles, thus maintaining constant tension on the valve. Papillary muscles are finger-like projections from the wall of the ventricle that anchor the chordae tendineae. This connection provides tension to hold the valves in place and prevent them from prolapsing into the atria when they close, preventing the risk of regurgitation.

Answer 24

Pectinate muscles are located in the atria (mostly in right), while papillary muscles are found in the ventricles. Pectinate muscles assist in atrial contractions, while papillary muscles help to prevent the atrioventricular valves from inverting during ventricular contraction.

Answer 25

The pectinate muscles (musculi pectinati) are parallel muscular ridges in the walls of the atria of the heart. - most prominant in right allow expansion of the heart

Answer 26

The fossa ovalis is a depressed structure, of varying shapes, located in the inferior aspect of the right interatrial septum. [1] A remnant of an interatrial opening, the foramen ovale, which has a significant role in fetal circulation, the fossa ovalis forms by the fusion of the septum primum and septum secundum. The fossa ovalis is a depression in the right atrium of the heart, at the level of the interatrial septum, the wall between right and left atrium.

Answer 27

The trabeculae carneae also serve a function similar to that of papillary muscles in that their contraction pulls on the chordae tendineae, preventing inversion of the mitral (bicuspid) and tricuspid valves towards the atrial chambers, which would lead to subsequent leakage of the blood back into the atria.

Answer 28

Patent foramen ovale (PFO) is a hole between the left and right atria (upper chambers) of the heart. This hole exists in everyone before birth, but most often closes shortly after being born. PFO is what the hole is called when it fails to close naturally after a baby is born. Every baby is born with a ductus arteriosus. After birth, the opening is no longer needed and it usually narrows and closes within the first few days of life. The fetal circulatory system bypasses the lungs and liver with three shunts. The foramen ovale allows the transfer of the blood from the right to the left atrium, and the ductus arteriosus permits the transfer of the blood from the pulmonary artery to the aorta The shunts that bypass the lungs are called the foramen ovale, which moves blood from the right atrium of the heart to the left atrium, and the ductus arteriosus, which moves blood from the pulmonary artery to the aorta.

Answer 29

1. superior vena cava 2. pulmonary arteries 3. pulmonary trunk 4. inferior vena cava

Answer 30

1. aortic arch 2. pulmonary veins 3. ascending aorta

Answer 31

1. brachiocephalic (branching to right subclavian and right common carotid) 2. left common carotid 3. left subclavian

Answer 32

The aortic arch is the portion of the aorta that is in the shape of an arch and connects the ascending aorta with the descending aorta.

Answer 33

Brachiocephalic trunk; right subclavian artery (supplies the right arm) right carotid artery (supplies the brain and right side of the head and neck). Left carotid artery; supplies your brain and the left side of the head and neck Left subclavian artery; supplies your left arm and the back of your brain.

Answer 34

The pulmonary circulation is a short loop from the heart to the lungs and back again. The systemic circulation carries blood from the heart to all the other parts of the body and back again.

Answer 35

The pulmonary circulation is a division of the circulatory system in all vertebrates. The circuit begins with deoxygenated blood returned from the body to the right atrium of the heart where it is pumped out from the right ventricle to the lungs.

Answer 36

Systemic circulation carries oxygenated blood from the left ventricle, through the arteries, to the capillaries in the tissues of the body.

Answer 37

The coronary sinus is the major venous tributary of the greater cardiac venous system; it is responsible for draining most of the deoxygenated blood leaving the myocardium

Answer 38

Coronary arteries supply blood to the heart muscle. Like all other tissues in the body, the heart muscle needs oxygen-rich blood to function. Also, oxygen-depleted blood must be carried away. The coronary arteries wrap around the outside of the heart. Small branches dive into the heart muscle to bring it blood.

Answer 39

There are two primary coronary arteries, the right coronary artery (RCA) and the left main coronary artery (LMCA). Both of these originate from the root of the aorta. The RCA emerges from the anterior ascending aorta and supplies blood primarily to the right atrium, right ventricle The circumflex artery branches off the left coronary artery and encircles the heart muscle. This artery supplies blood to the outer side and back of the heart. The left marginal artery (or obtuse marginal artery) is a branch of the circumflex artery, originating at the left atrioventricular sulcus, traveling along the left margin of heart towards the apex of the heart. aorta [right] right coronary posterior interventricular right marginal [left] left coronary circumflex left marginal diagonal anterior interventricular

Answer 40

This cardiac vein returns deoxygenated blood (metabolic waste products) from the anterior surfaces of the left ventricle.

Answer 41

to drain the venous blood of the external layer of the myocardium.

Answer 42

The middle cardiac vein collects blood from the areas supplied by the posterior interventricular artery. The small cardiac vein drains the blood from the posterior surfaces of the right atrium and ventricle. The anterior cardiac veins drain the anterior surface of the right ventricle. *The cardiac veins are veins in the heart that drain deoxygenated blood from the myocardium (the heart muscle) into the right atrium of the heart.

Answer 43

The small cardiac vein, also known as the right coronary vein, is a coronary vein that drains parts of the right atrium and right ventricle of the heart

Answer 44

blood (plasma and cells)

Answer 45

1. transportation; nutrients & waste 2. protection; immune system 3. regulation; hormones, proteins etc.

Answer 46

blood production

Answer 47

blood loss

Answer 48

1. red blood cells (erythrocytes) 2. white blood cells (leukocytes) 3. platelets (thrombocytes) 4. plasma (ECM of the blood)

Answer 49

specialised fluid connective tissue

Answer 50

red blood cells

Answer 51

white blood cells

Answer 52

thrombocytes

Answer 53

(erythrocytes) - produced in bone marrow - erythropoietin- kidney - no nucleus - haemoglobin protein - haematocrit (40-45%)

Answer 54

the percentage by volume of red cells in your blood (40-45%)

Answer 55

low number of erythrocytes; low iron

Answer 56

high number of erythrocytes; viscosity *This makes the blood thicker and less able to travel through blood vessels and organs

Answer 57

a hormone that your kidneys naturally make to stimulate the production of red blood cells

Answer 58

(leukocytes) - protection - phagocytosis - 2 major classes granulocytes; neutrophils, eosinophils, basophils agranulocytes; lymphocytes, monocytes

Answer 59

The process where these white blood cells surround, engulf, and destroy foreign substances

Answer 60

(leukocytes) granulocytes; neutrophils, eosinophils, basophils agranulocytes; lymphocytes, monocytes

Answer 61

granulocytes

Answer 62

agranulocytes

Answer 63

low WBC count; infection

Answer 64

high WBC count; inflammation

Answer 65

high= inflammation (leukocytosis) low= infection (leukopenia)

Answer 66

(thrombocytes) - cell fragments - control blood loss - fibrin clot - normal platelet count (150,000-450,000 platelets per µL

Answer 67

150,000-450,000 platelets/µL

Answer 68

platelet count >450,000 *may cause blood clots which can block blood flow to your organs

Answer 69

platelet count <150,000 *may bleed easily and have difficulty stopping the bleeding

Answer 70

- straw-coloured liquid in which the blood cells are suspended - ECM of blood - approximately half your blood is made of plasma - plasma composed of; water (92%), proteins (albumin- major protein), glucose, electrolytes)

Answer 71

Electrolytes like sodium, potassium, bicarbonate, chloride, and calcium help maintain blood pH.

Answer 72

1. water (92%) 2. proteins; major protein=albumin 3. glucose 4. electrolytes

Answer 73

plasma= 55% white blood cells and platelets= <1% red blood cells= 45%

Answer 74

network of blood vessels on the body or within an organ

Answer 75

1. arteries 2. veins 3. capillaries

Answer 76

1. tunica interna (intima) = layer of epithelium (endothelium) 2. tunica media = smooth muscle and elastic tissue 3. tunica externa (tunica adventitia) = connective tissue

Answer 77

layer of epithelial cells (endothelium)

Answer 78

smooth muscle and elastic tissue

Answer 79

connective tissue

Answer 80

1. large elastic arteries 2. medium muscular arteries 3. arterioles 4. anastomoses

Answer 81

- tunica media; mostly smooth muscle, less elastic fibres - wall thickness; 50% of total vessel diameter - resistance vessels

Answer 82

- point where 2 blood vessels join/merge - communication between atrial branches - collateral circulation (an alternative route for blood supply)

Answer 83

The circle of Willis is a loop of arteries at the base of your brain. It functions as the roundabout for the two major arteries that supply blood to your brain. It can play a role in minimizing the effects of certain brain issues, like stroke.

Answer 84

The collateral circulation is a network of specialized “endogenous bypass vessels” that is present in most tissues and provides protection against ischemic injury caused by ischemic stroke, coronary atherosclerosis, peripheral artery disease and other conditions and diseases. a network of backup blood vessels that can take over if main blood vessels are blocked or narrowed, providing alternative pathways to ensure blood flow to tissues and organs

Answer 85

- largest diameter among arteries - tunica media; lots of elastic fibres, less smooth muscle - wall thickness; <10% of total vessel diameter - conducting arteries

Answer 86

- tunica media; mostly smooth muscle, less elastic fibres - wall thickness; 25% of total vessel diameter - distribution arteries

Answer 87

conducting= large elastic arteries distribution= medium muscular arteries

Answer 88

large elastic arteries (conducting) = <10% of total vessel diameter medium muscular arteries (distribution) = 25% of total vessel diameter arterioles (resistance) = 50% of total vessel diameter

Answer 89

arterioles

Answer 90

- an inflammatory disease where cholesterol enters the vessel wall - narrows lumen and renders wall less elastic - increased resistance to blood flow and decreased circulation - arteries affected; coronary, aortic arch, abdominal aorta - causes; poor diet, high cholesterol, lack of exercise, smoking etc.

Answer 91

coronary aortic arch abdominal aorta

Answer 92

Your arteries are built to handle a lot of pressure going through them at once. This high pressure contributes to plaques.

Answer 93

- smallest blood vessels - walls; single layer of endothelial cells and basement membrane - highly permeable - exchange vessels - 3 structural types; continuous, fenestrated, sinusoid

Answer 94

single layer of endothelial cells (tunica intima) and basement membrane

Answer 95

1. continuous (intercellular cleft) 2. fenestrated (fenestrations/pored) 3. sinusoid (incomplete basement membrane and intercellular gap)

Answer 96

An intercellular cleft is a channel between two cells through which molecules may travel and gap junctions and tight junctions may be present

Answer 97

Fenestrated capillaries are capillaries that have tiny openings, or pores

Answer 98

Venules are the smallest veins and receive blood from capillaries.

Answer 99

1. post capillary 2. muscular

Answer 100

smallest - no tunica media - sparce tunica externa - very porous

Answer 101

microscopic - tunica media - 1-2 layers of smooth muscle - sparce tunica externa - no exchange with interstitial fluid

Answer 102

- structurally similar to arteries - 60-70% of blood in venous system - large lumen - poorly developed tunica media - low pressure in veins - skeletal system pumps and valves - vascular venous sinuses - anastomotic veins - superficial veins

Answer 103

Unlike deep veins, they're not surrounded by muscle. Instead, your superficial veins can be found just underneath your skin. So, you can easily see them. Your superficial veins carry blood from your outer tissues near the surface of your skin to your deep veins (via the perforating veins).

Answer 104

A circulatory anastomosis is a connection (an anastomosis) between two blood vessels, such as between arteries (arterio-arterial anastomosis), between veins (veno-venous anastomosis) or between an artery and a vein (arterio-venous anastomosis).

Answer 105

Dural venous sinuses are a group of sinuses or blood channels that drains venous blood circulating from the cranial cavity. It collectively returns deoxygenated blood from the head to the heart to maintain systemic circulation. receive blood from the veins associated with the cerebrum, cerebellum and brainstem

Answer 106

- vein walls lose elasticity - weaken and dilate - swollen (varicose) veins - incompetent valves - backflow can't be prevented - blood collects in veins; dilate even more Weakened valves, also called incompetent valves, within the veins might cause varicose veins. The weakened valves let blood pool in the veins instead of traveling to the heart. When blood pools in the veins, the veins become larger, making them show under the skin. Varicose veins are bulging, enlarged veins

Answer 107

The cardiac cycle is the sequence of events during a single heartbeat. It includes: Atrial systole: Atria contract, filling ventricles with blood. Ventricular systole: Ventricles contract, ejecting blood into the arteries. Diastole: Heart relaxes, and chambers refill with blood. This cycle ensures blood is pumped throughout the body and lungs.

Answer 108

Pressure gradients in the cardiovascular system are maintained by the heart's pumping action. Blood flows from areas of higher pressure to lower pressure. When the heart contracts, it generates high pressure in the ventricles, driving blood into the arteries. As the heart relaxes, pressure in the arteries drops, and blood flows back toward the heart. This pressure difference ensures continuous blood circulation throughout the body.

Answer 109

The autonomic nervous system (ANS) controls heart rate and contractility through the sympathetic and parasympathetic branches. The sympathetic nervous system increases heart rate and contractility by releasing norepinephrine, while the parasympathetic system slows the heart rate via acetylcholine. Starling's Law states that the heart will pump more blood if it is stretched more (i.e., the greater the ventricular filling, the greater the force of contraction). Therapeutic targets include drugs that influence heart rate, contractility, and blood vessel tone, such as beta-blockers (to reduce heart rate) or inotropes (to increase contractility) in heart failure treatments.

Answer 110

total volume of blood in body = 5L or 8.8 pints

Answer 111

volume of blood ejected by 1 ventricle in 1 minute

Answer 112

CO= stroke volume x heart rate

Answer 113

how much blood (ml) ventricle ejects ~70ml

Answer 114

SV=~70ml HR= 70bpm CO= 70 x 70 = 4900ml/min

Answer 115

dynamics of blood flow

Answer 116

circulation= 2 hydraulic circuits (systemic + pulmonary circulation) each a series of interconnected pipes that transport fluid system is pressurised and has a central pump (heart) *coronary circuit deals with a small amount of blood, therefore the other two are really driving this.

Answer 117

pressure in aorta is higher; this drops as it goes through the different types of blood vessels. Left ventricle has a thick wall so it builds up in pressure and pumps it out at a high pressure (about 110) capillary bed is around 10- essentially lost all the pressure which drove the blood out of the heart. in the veinous system the pressure goes down but not to 0; there's always some pressure (around 5). the right ventricle is around the pressure of the capillaries. it quickly reaches lungs and capillaries so you don't want the pressure in pulmonary circulation to be high.

Answer 118

A large vein that carries blood to the heart from other areas of the body. The vena cava has two parts: the superior vena cava and the inferior vena cava. The superior vena cava carries blood from the head, neck, arms, and chest.

Answer 119

**O2 rich, CO2 poor blood 110/70 mmHg [aorta and branches, left atrium, left ventricle, systemic arteries] 10-25 mmHg [capillary bed of all body tissues where gas exchange occurs] **O2 poor, CO2 rich blood 5-10 mmHg [right atrium, right ventricle, systemic veins, vena cava]] 10-25 mmHg [pulmonary arteries]

Answer 120

atria *followed by ventricles (0.1s delay)

Answer 121

0.1s delay

Answer 122

both left and right ventricle eject the SAME volume of blood

Answer 123

blood pooling and back up would occur very quickly

Answer 124

An electrical stimulus is generated by the sinus node (also called the sinoatrial node, or SA node). This is a small mass of specialized tissue located in the right upper chamber (atria) of the heart The SA (sinoatrial) node generates an electrical signal that causes the upper heart chambers (atria) to contract. The signal then passes through the AV (atrioventricular) node to the lower heart chambers (ventricles), causing them to contract,

Answer 125

The fibrous rings surround the atrioventricular and arterial orifices, and are stronger upon the left than on the right side of the heart. The atrioventricular rings serve for the attachment of the muscular fibers of the atria and ventricles, and for the attachment of the bicuspid and tricuspid valves.

Answer 126

Your heart's tissue sends electrical impulses that travel through pathways called bundle branches. These impulses normally travel through the bottom chambers of your heart (ventricles). Your heart's two ventricles usually contract at the same time. The bundle branches, or Tawara branches, transmit cardiac action potentials (electrical signals) from the bundle of His to Purkinje fibers in heart ventricles. They are offshoots of the bundle of His and are important to the electrical conduction system of the heart

Answer 127

The fibrous skeleton of the heart acts as an insulator for the flow of electrical current across the heart. It stops the flow of electricity between the different chambers of the heart so that electrical impulses do not flow directly between the atria and ventricles. (creates delay)

Answer 128

atrial depolarisation, initiated by the SA node causes (first bump in electrogram) with atrial depolarisation complete, the impulse is delayed at the AV node. (flat in electrogram) ventricular depolarisation begins at apex, atrial repolarisation occurs. (big peak in electrogram)

Answer 129

1. ventricular filling (0.5s) 2. isovolumetric contraction (0.05s) 3. ejection (0.3s) 4. isovolumetric relaxation (0.08s)

Answer 130

- ventricular filling - AV valves open/SL valves closed - driven by venous pressure - ventricle walls expand as they fill - atria contract and add 10-20% extra at rest (more with age/exercise) - end diastolic volume =~120ml - as soon as ventricular pressure exceeds atrial AV valves shut

Answer 131

as soon as ventricular pressure exceeds atrial - AV valves shut papillary muscles pool on the chordae tendinae

Answer 132

venous pressure

Answer 133

AV = open SL= closed

Answer 134

AV= closed SL= closed *pressure in ventricles begins to climb rapidly

Answer 135

during isovolumetric contraction

Answer 136

AV = closed SL= open

Answer 137

when ventricular pressure > atrial pressure

Answer 138

3/4 blood ejected in the first 0.15s of ejection - causes bulging of elasctic arteries

Answer 139

End-systolic volume (ESV) is the volume of blood in a ventricle at the end of contraction, or systole, and the beginning of filling, or diastole

Answer 140

Diastole represents ventricular filling, and systole represents ventricular contraction/ejection. Systole occurs when the heart contracts to pump blood out, and diastole occurs when the heart relaxes and refills after contraction.

Answer 141

rate at which blood is transported to the peripheral arteries exceeds the blood leaving the ventricles so pressure in ventricles fall SL vales closed/AV valves closed (until ventricular pressure falls below atrial pressure) then AV valves are pushed open and blood begins to fill ventricles again. atria have already been filling

Answer 142

AV= closed SL= closed

Answer 143

collection of myocytes that spontaneously depolarise at regular intervals (sinoatrial node) *The SA (sinoatrial) node generates an electrical signal that causes the upper heart chambers (atria) to contract. The signal then passes through the AV (atrioventricular) node to the lower heart chambers (ventricles), causing them to contract, or pump. The SA node is considered the pacemaker of the heart.

Answer 144

the smallest subunit of all muscular tissues and organs throughout the body also known as muscle cells, are the fundamental contractile cells of muscle tissue, including skeletal, smooth, and cardiac muscle, and are responsible for muscle contraction

Answer 145

SA node the activity of the pacemaker is NOT governed by extrinsic nerves

Answer 146

the rate at which the myocytes depolarise is determined by extrinsic nerves- ANS nerves *parasympathetic vs sympathetic

Answer 147

Tachycardia (tak-ih-KAHR-dee-uh) is a fast heartbeat. The heart rate is greater than 100 beats a minute. Bradycardia (brad-e-KAHR-dee-uh) is a slow heartbeat. The heart rate is less than 60 beats a minute tachycardia=sympathetic bradycardia= parasympathetic

Answer 148

tachycardia= sympathetic bradycardia= parasympathetic

Answer 149

parasympathetic

Answer 150

via the vagus nerve. the vagal motor nuclei in brainstem (medulla)

Answer 151

in the medulla of the brainstem

Answer 152

right side= SA node left side= AV node *The SA node (sinoatrial node) is the heart's natural pacemaker, initiating the electrical signal that causes the heart to beat. The AV node (atrioventricular node) acts as a "gatekeeper" between the atria and ventricles, delaying the electrical impulse to allow the atria to contract and empty blood into the ventricles before the ventricles contract.

Answer 153

Muscarinic acetylcholine receptors (mAChRs) are acetylcholine receptors that form G protein-coupled receptor complexes in the cell membranes of certain neurons[1] and other cells. They play several roles, including acting as the main end-receptor stimulated by acetylcholine released from postganglionic fibers. They are mainly found in the parasympathetic nervous system, but also have a role in the sympathetic nervous system in the control of sweat glands.[

Answer 154

acetylcholine

Answer 155

decreases rate of SA node depolarisation by making membranes hyperpolarised (more negative) *parasympathetic

Answer 156

Hyperpolarization is when the membrane potential becomes more negative at a particular spot on the neuron's membrane, while depolarization is when the membrane potential becomes less negative (more positive).

Answer 157

Hypopolarization is the initial increase of the membrane potential to the value of the threshold potential. The threshold potential opens voltage-gated sodium channels and causes a large influx of sodium ions. This phase is called the depolarization. During depolarization, the inside of the cell becomes more and more electropositive, until the potential gets closer the electrochemical equilibrium for sodium of +61 mV. This phase of extreme positivity is the overshoot phase. After the overshoot, the sodium permeability suddenly decreases due to the closing of its channels. The overshoot value of the cell potential opens voltage-gated potassium channels, which causes a large potassium efflux, decreasing the cell’s electropositivity. This phase is the repolarization phase, whose purpose is to restore the resting membrane potential. Repolarization always leads first to hyperpolarization, a state in which the membrane potential is more negative than the default membrane potential. But soon after that, the membrane establishes again the values of membrane potential.

Answer 158

T1-T5 *long nerve fibres that run along the great vessels

Answer 159

right supply atria left supply ventricles

Answer 160

NT= noradrenaline receptor= B1 adrenoreceptors

Answer 161

- Increase AV conduction velocity (<0.1s) Faster transmission of electrical impulses to maintain coordination between atrial and ventricular contraction. - Decrease myocyte AP length Shorter AP duration for quicker repolarization and preparation for the next beat. - Increase rate of relaxation Faster relaxation of the heart muscle to facilitate efficient filling of the chambers. - Increase contractile force (increase SV) Stronger heart contractions, leading to increased stroke volume. *SV= stroke volume AP= action potential Norepinephrine is released from sympathetic nerve endings and binds to beta-1 adrenergic receptors on heart cells. This increases the rate of depolarization in the SA node, increasing heart rate. It also increases conduction velocity through the heart's electrical pathways and increases the force of contraction of the heart muscle.

Answer 162

stroke volume = the volume of blood in millilitres ejected from the each ventricle due to the contraction of the heart muscle which compresses these ventricles. SV is the difference between end diastolic volume (EDV) and end systolic volume (ESV).

Answer 163

HDL cholesterol can be thought of as the “good” cholesterol because a healthy level may help protect against heart attack and stroke. HDL carries LDL (bad) cholesterol away from the arteries and back to the liver, where the LDL is broken down and passed from the body.

Answer 164

1. central venous pressure (CVP) 2. mean arterial pressure (MAP) 3. systolic and diastolic blood pressure

Answer 165

stroke volume (SV) = ~70ml end diastolic volume (EDV) = ~120ml end systolic volume (ESV) = ~50ml

Answer 166

~70ml (stroke volume)

Answer 167

~120ml (end diastolic volume)

Answer 168

~50ml (end systolic volume)

Answer 169

Increase in contractile energy with stretch (diastolic distension) Greater stretch of muscle fibres= greater contractile energy *increase: CVP, pressure in RV, SV, pulmonary circulation pressure, pressure in LV, SV

Answer 170

increase in contractile energy with stretch

Answer 171

starling law (greater stretch of muscle fibres= greater contractile energy)

Answer 172

CVP- central venous pressure

Answer 173

fainting - blood pools at feet - cvp drops - shortens fibres in diastole - contractions weaken - sv drops - arterial pressure drops

Answer 174

- blood pools in feet - cvp drops - shortens fibres in diastole - contractions weaken - sv drops - arterial pressure drops

Answer 175

changes in blood vessel diameter (tone) can influence pressure and flow characteristics.

Answer 176

1. autonomic 2. metabolic (targets for therapeutics)

Answer 177

baroreceptor reflex

Answer 178

1. baroreceptors; initiated by stretch receptors in walls of major arteries 2. brainstem; communicates with nerves which control the heart and blood vessels 3. heart rate, stroke volume, blood vessel diameter; changes occur in cardiac output, peripheral resistance and venous capacitance 4. blood pressure; restores arterial BP to normal levels (85-100mmHg)

Answer 179

Baroreceptors are a type of mechanoreceptors allowing for relaying information derived from blood pressure within the autonomic nervous system. Information is then passed in rapid sequence to alter the total peripheral resistance and cardiac output, maintaining blood pressure within a preset, normalized range.

Answer 180

The arterial baroreceptors can be found on the wall of the aortic arch as well as on the wall of the carotid sinus, which is basically a bulge of the internal carotid artery just above its split from the common carotid artery in the neck.

Answer 181

The afferent impulses which follow baroreceptor stimulation by a blood pressure rise relay within the nucleus of the solitary tract in the brainstem (vagus nerve which originates in brainstem). This is followed by inhibition of brainstem sympathetic centers and stimulation of brainstem parasympathetic centers.

Answer 182

1. hypotentsion (<90mmHg) 2. hypertention (>140mmHg)

Answer 183

through vascular remodelling; thicker arterial walls (destructive +ve feedback cycle) = the thicker they get to accommodate increases in blood pressure, increases the pressure even more *happens naturally with ageing- blood vessels stiffen

Answer 184

Normal blood pressure is usually considered to be between 90/60 mmHg and 120/80 mmHg. For over-80s, because it's normal for arteries to get stiffer as we get older, the ideal blood pressure is under 150/90 mmHg

Answer 185

~120/80 Systolic blood pressure is the first number. It measures the pressure your blood is pushing against your artery walls when the heart beats. Diastolic blood pressure is the second number. It measures the pressure your blood is pushing against your artery walls while the heart muscle rests between beats.

Answer 186

high systolic pressure and MAP Hypertension also impairs SV; pressure opposing outflow increases afterload in ventricles

Answer 187

The Mean Arterial Pressure (MAP) calculates mean arterial pressure from measured systolic and diastolic blood pressure values.

Answer 188

decrease blood pressure diuretics reduce overall blood volume, therefore weak heart doesn't have to pump such a large volume of blood around.

Answer 189

blood vessel diameter

Answer 190

Q=(P1-P2)/R Q (blood flow) P1 (pressure at start) P2 (pressure at end) R (resistance)

Answer 191

Q=(P1-P2)/R Arterial blood pressure is regulated by the nervous system (85-100mmHg) so P1 is not easily altered. Resistance (R) is easier.

Answer 192

arterioles= resistance vessels change happens locally to redistribute flow to where it is needed. Arterioles, small blood vessels that carry blood away from your heart, are connectors between your arteries and capillaries. They control your blood pressure and blood flow throughout your body, using their muscles to change their diameter.

Answer 193

long narrow tubes; higher resistance than short wide tubes = arterioles

Answer 194

large arteries (2%) arterioles (60%) capillaries (20%) venous system (15%)

Answer 195

R=8η/πr^4 the velocity of the steady flow of a fluid through a narrow tube (as a blood vessel or a catheter) varies directly as the pressure and the fourth power of the radius of the tube and inversely as the length of the tube and the coefficient of viscosity. shows the enormous influence that vessel diameter has on the blood flow rate that circulates through the vessel

Answer 196

1. large arteries (2%) 2. venous system (15%) 3. capillaries (20%) 4. arterioles (60%)

Answer 197

The capillaries are small and offer high resistance, but because they are arranged in parallel, the total capillary resistance decreases with increasing numbers of capillaries; more surface area.

Answer 198

determined by local metabolic rate in tissues e.g. skeletal muscle 20% oxygen consumption - therefore receives 20% cardiac output - exceptions= kidneys, cardiac muscle, brain continual adjustment - standing - stress - exercise done by changes in 'vascular tone'; both intrinsic and extrinsic mechanisms

Answer 199

Vascular tone, the contractile activity of vascular smooth muscle cells in the walls of small arteries and arterioles, is the major determinant of the resistance to blood flow through the circulation. Vascular tone refers to the degree of constriction experienced by a blood vessel relative to its maximally dilated state.

Answer 200

determined by local metabolic rate in tissues e.g. skeletal muscle 20% oxygen consumption - therefore receives 20% cardiac output - exceptions= kidneys, cardiac muscle, brain

Answer 201

1. standing 2. stress 3. exercise

Answer 202

Blood pressure is the force your circulating blood exerts against the walls of your arteries. Blood flow is the movement of blood through your body, and resistance is the pushback that's against the blood flow in the circulatory system. Blood pressure, flow, and resistance are all closely related.

Answer 203

(basal level of vascular tone) - myogenic response - endothelial secretions - vasoactive metabolites - temperature increase in arterial pressure= increase vascular tone = constriction decrease in arterial pressure= decrease in vascular tone = dilation

Answer 204

bayliss myogenic response = myocytes depolarise when stretched

Answer 205

vasoconstrictors= endothelin-1 vasodilators= nitric oxide (NO) amounts governed by shear stress: frictional force of blood on the vessel wall

Answer 206

endothelin-1 * frictional force of blood on the vessel wall

Answer 207

nitric oxide (NO) * frictional force of blood vessel wall

Answer 208

metabolic activity of myocardium, skeletal muscle etc. blood flow is diverted there within seconds. several candidates (H+, K+, ATP, CO2, adenosine) Actively metabolizing cells surrounding arterioles release vasoactive substances that cause vasodilation. This is termed the metabolic theory of blood flow regulation. Increases or decreases in metabolism lead to increases or decreases in the release of these vasodilator substances.

Answer 209

1. H+ 2. K+ 3. ATP 4. CO2 5. adenosine

Answer 210

skin= origin of temperature regulation blood flow here can change > 100 fold sympathetic vasoconstrictor fibres; actively influences by hypothalamic temp-regulating centre dilate with heat= physically contain more blood (skin reddens) constrict with cold= physically less blood (pale/bluish colour) to protect and conserve core temperature

Answer 211

dilate with heat= physically contain more blood (skin reddens) constrict with cold = physically less blood (pale/bluish colour) *protects and conserves core temperature

Answer 212

sympathetic vasoconstrictor fibres influenced by hypothalamic temp-regulating centre

Answer 213

raynaud's syndrome

Answer 214

spasm of small arteries supplying extremities in response to: - cold - stress - most cases cause is unknown *in severe cases cells and tissue death can occur- gangrene theres an overeaction to what hypothalamus is telling arteries women more prone

Answer 215

1. cold 2. stress 3. most cases cause is unknown

Answer 216

gangrene - cell and tissue death can occur

Answer 217

mechanism that overrides intrinic mechanism necessary to have effect on entire body

Answer 218

1. vasomotor nerves 2. vasoactive hormones (higher level of control- overrides intrinsic controls to meet needs of the whole body)

Answer 219

- sympathetic vasoconstrictors - NT= noradrenaline; a-receptors on vascular myocytes - sympathetic vasodilators (NT= NA or ACh) - parasympathetic vasodilators (NT= ACh) (a decrease in the firing rate of a sympathetic vasoconstrictor can cause vasodilation too)

Answer 220

The preganglionic neuron travels from its origin in the brain or spinal cord to a ganglion (collection of cytons outside the CNS). The postganglionic neuron begins in and travels from the ganglion to the smooth muscle or gland being innervated.

Answer 221

vasodilation a decrease in the firing rate of a sympathetic vasoconstrictor can cause vasodilation too

Answer 222

noradrenaline (NA) acetylcholine (ACh)

Answer 223

acetylcholine (ACh)

Answer 224

alpha receptors on vascular myocytes

Answer 225

Vascular smooth muscle cells (VSMCs) constitute the major cells in the wall of blood vessels. The main role of vascular smooth muscle is to redistribute blood within the body by contracting and dilating in response to stimuli, thus changing the volume of blood vessels and the local blood pressure.

Answer 226

adrenaline- constriction/dilation (same action as NA in the sympathetic NS) vasopressin (ADH)- constriction angiotensin - constriction atrial natriuretic peptide (ANP) - dilation insulin - dilation

Answer 227

1. adrenaline 2. vasopressin (ADH) 3. angiotensin

Answer 228

1. adrenaline 2. atrial natriuretic peptide (ANP) 3. insulin

Answer 229

adrenalin binds to same a-receptors on SMC's in arterioles it also binds to b-receptors on SMCs =dilation where b-receptors outnumber a-receptors (active skeletal muscles; myocardium; liver) blood is redistributed from the stomach to other parts of the body more vital to survival digestion in supressed also causes the body's muscles to tighten, including the stomach muscles *Adrenaline (epinephrine) interacts with both alpha and beta adrenergic receptors, but its effects on alpha receptors can be more prominent at higher concentrations, leading to vasoconstriction and increased vascular tone. While beta receptors primarily mediate vasodilation, alpha receptors can override this effect at higher doses due to their greater abundance

Answer 230

Norepinephrine is continuously released into circulation at low levels while epinephrine is only released during times of stress. Norepinephrine is also known as noradrenaline. It is both a hormone and the most common neurotransmitter of the sympathetic nervous system. Epinephrine is also known as adrenaline

Answer 231

Hormones are produced in endocrine glands and are secreted into the blood stream. Neurotransmitters: Neurotransmitters are released by presynaptic nerve terminal into the synapse. Hormones: Hormones are transmitted through blood. Neurotransmitters: Neurotransmitters are transmitted across the synaptic cleft.

Answer 232

Electrical impulses carried by the sympathetic nervous system are converted to a chemical response in the adrenal gland. Chromaffin cells contained in the adrenal medulla act as postganglionic nerve fibres that release this chemical response into the blood as a circulating messenger.

Answer 233

total peripheral resistance x cardiac output

Answer 234

heart rate x stroke volume

Answer 235

optimal: systolic= <120 diastolic= <80 normal: systolic= <130 diastolic= <85 high-normal: systolic= 130-139 diastolic= 85-89

Answer 236

1 (mild) systolic= 140-159 diastolic= 90-99 2 (moderate) systolic= 160-179 diastolic= 100-109 3 (severe) systolic= >_180 diastolic >_110

Answer 237

1: 140-159 (systolic) <90 (diastolic) 2: >_160 (systolic) <90 (diastolic)

Answer 238

1. smoking 2. obesity 3. diet (e.g. salt) 4. exercise (lack of) 5. genetic (occurs in ~90% of people)

Answer 239

e.g. renal hypertension/pheochromocytoma -known underlying cause (occurs in <10% of people)

Answer 240

Primary hypertension (which occurs in about 90% of people) has no identifiable cause. Secondary hypertension (about 10% of people) has a known underlying cause, such as renal, endocrine, or vascular disorder, or the use of certain drugs

Answer 241

Page's Mosaic Theory provided a framework for us to study the various hypertension “forces” at a molecular and cellular levels. A paradigm has arisen based on this work in which that common molecular events occur in diverse sites, including the brain, the kidney and the vasculature. original: chemical; reactivity; volume; vascular caliber; viscosity; cardiac output; elasticity; neural revised: genetic; environmental; anatomical; adaptive; neural; endocrine; humoral; hemodynamics

Answer 242

1. atherosclerosis 2. stroke 3. myocardial infarction 4. heart failure 5. renal failure 6. retinopathy

Answer 243

antihypertensive therapy -> 40% reduction of stroke 25% reduction in myocardial infarction >50% reduction in heart failure

Answer 244

1. block of sympathetic nervous system: reduce effects on heart (b1-blockers). reduce effect on on blood vessels (a1-blockers. reduce renin release from kidney (b1-blocker) 2. kidney: reduce blood volume (diuretics) 3. hormones: inhibit renin-angiotensin-aldosterone (angiotensin converting enzyme 'ACE' inhibitors and angiotensin receptor blockers) 4. vasodilation of peripheral resistance arterioles: Ca2+ channel blockers

Answer 245

Renin is released into your bloodstream when your blood pressure drops too low or when there's not enough sodium in your body. Specifically, renin secretion happens when: Baroreceptors (pressure-sensitive receptors) in your arterial vessels detect low blood pressure. Your kidneys detect low salt (sodium) levels.

Answer 246

reduce effects on heart (B1-blockers) reduce effects on blood vessels (a1-blockers) reduce renin release from kidney (b1-blockers)

Answer 247

The primary function of the kidneys is to regulate the fluid environment in the body. This is done through the formation of urine. By making urine, the kidneys are able to: Regulate blood volume by removing excess fluid from the body.

Answer 248

inhibit renin-angiotensin-aldosterone system (angiotensin converting enzyme 'ACE' inhibitors and angiotensin receptor blockers)

Answer 249

Ca2+ channel blockers

Answer 250

[sir james black] - late 1950s- black notes that dichloroisoprenaline (DCI) can block the effects of adrenaline on the heart - sees potential for a drug which protects the heart from adrenaline release during stress/emotion - substitutes chlorine atoms on DCI to get first beta blocker (pronethalol) - quickly replaced by propranolol due to side effects in patients and animals - 1988; awarded Nobel prize for development of beta blockers and anti-ulcer drugs

Answer 251

pronethalol -> propranolol dichloroisoprenaline (DCI) can blcok effect of adrenaline on the heart; chlorine atoms substituted (pronethalol); quickly replaced by propranolol due to side effects in patients and animals

Answer 252

e.g. propranolol (β1 and β2) and atenolol (β1 selective) competitive reversible antagonists - decrease blood pressure via blockage of β1 sympathetic tone on heart and reduction in renin release from kidney - decrease in heart rate and stroke volume - decrease in cardiac output

Answer 253

1. exacerbate asthma (block of β2-absolute contraindication) 2. intolerance to exercise 3. hypoglycaemia 4. vivid dreams

Answer 254

phentolamine (α1 and α2) doxazosin, prazosin (α1 selective) competitive reversible antagonists decrease blood pressure via decrease in sympathetic tone in arterioles (α1) decrease in peripheral resistance

Answer 255

In the case of a reversible competitive antagonist, the bond to the receptor site is chemically reversible, so that the blocking action depends on the concentration of the antagonist and is reduced by a higher concentration of the neurotransmitter.

Answer 256

Sympathetic tone refers to the continuous activity of sympathetic nerves that regulate blood pressure by controlling cardiac and vascular functions.

Answer 257

1. postural hypotension (loss of sympathetic venoconstriction) 2. reflex tachycardia (via baroreceptors)

Answer 258

If blood pressure decreases, the heart beats faster in an attempt to raise it.

Answer 259

e.g. captopril and enalapril - angiotensin converting enzyme on vascular endothelial surface converts angiotensin I to the active angiotensin II lower blood pressure by: 1. reduced formation of the vasoconstrictor angiotensin II (decrease in peripheral resistance) 2. reduced blood volume (loss of angiotensin II- stimulated release of aldosterone, this reduction of renal reabsorption of Na+ and water)

Answer 260

captopril enalapril

Answer 261

phentolamine (α1 and α2) doxazosin, prazosin (α1 selective)

Answer 262

propranolol (β1 and β2) atenolol (β1 selective)

Answer 263

angiotensin converting enzyme (on vascular endothelial surface)

Answer 264

generally well tolerated but: a) sudden fall in BP on 1st dose b) persistent irritant cough- due to reduced breakdown of bradykinin, a peptide that activates sensory nerves in lung tissue

Answer 265

persistent irritant cough- due to reduced breakdown of bradykinin, a peptide that activates sensory nerves in lung tissue

Answer 266

- two receptor subtypes: AT1 and AT2 - AT1 receptor mediates vasoconstrictor and aldosterone-releasing action of angiotensin II - losartan and candesartan (AT1 blockers) - useful antihypertensive agents - side effect profile appears good- no irritant cough as seen with ACE inhibitors

Answer 267

AT1 blockers

Answer 268

Angiotensin receptor blockers (ARBs), also known as angiotensin II receptor antagonists, are used to treat high blood pressure and heart failure. They are also used for chronic kidney disease and prescribed following a heart attack. They include irbesartan, valsartan, losartan and candesartan.

Answer 269

Angiotensin II is the main effector molecule of the RAS. It causes increases in blood pressure, influences renal tubuli to retain sodium and water, and stimulates aldosterone release from adrenal gland.

Answer 270

bendroflumethiazide (thiazide)

Answer 271

e.g. bendroflumethiazide lower blood pressure by reducing blood volume mechanism is though reduced renal reabsorption of Na+ and water (additional vasodilator action may also contribute: decrease in peripheral resistance)

Answer 272

decrease in plasma K+ *Diuretics, particularly loop and thiazide diuretics, decrease plasma potassium (K+) levels primarily because they increase the delivery of sodium (Na+) to the distal tubule, which stimulates the sodium-potassium pump and leads to increased potassium excretion in the urine. This process, coupled with the activation of the renin-angiotensin-aldosterone system (RAAS) due to volume depletion, further promotes potassium loss

Answer 273

verapamil diltiazem nifedipine

Answer 274

e.g. verapamil, diltiazem, nifedipine L-type voltage operated calcium channels - open upon membrane depolarisation - calcium entry into cardiac and vascular smooth muscle reduce Ca2+ entry into vascular smooth muscle and cardiac muscle by blocking L-type voltage operated calcium channels

Answer 275

verapamil diltiazem (mechanism of L-type channel block)

Answer 276

nifedipine (mechanism of L-type channel block) * act as allosteric modulators of L-type calcium channels, influencing their activity without directly binding to the channel's primary binding site.

Answer 277

smooth muscle nifedipine>diltiazem>verapamil cardiac muscle verapamil>diltiazem>nifedipine

Answer 278

nifedipine > diltiazem > verapamil

Answer 279

verapamil> diltiazem > nifedipine

Answer 280

verapamil has strongest effect on heart nifedipine has strongest effect on smooth muscle (diltiazem has moderate effects on both)

Answer 281

1. reducing peripheral resistance (block of Ca2+ entry into vascular smooth muscle->vasodilatation) 2. reducing cardiac output (block of Ca2+ entry into cardiac muscle- heart rate and stroke volume both reduced) **1>>2: reduction in peripheral resistance (1) is the primary or more significant factor in lowering blood pressure compared to the reduction in cardiac output (2)

Answer 282

1. headache 2. constipation 3. cardiac dysrhythmias (negative chronotropic effect and slowed conduction) 4. gum hyperplasia

Answer 283

an oral condition that causes your gums to overgrow

Answer 284

A cardiac dysrhythmia (arrhythmia) is an abnormal or irregular heartbeat. If you have a dysrhythmia, your heart might beat too fast or too slowly. Or your heart's rhythm might be disrupted, leading you to feel like your heart skipped a beat.

Answer 285

calcium channel blockers (negative chronotropic effect and slowed conduction)

Answer 286

- chest pain due to myocardial ischaemia - build-up of metabolites (adenosine, CO2, lactate, K+ ions) activates sensory nerves *not disease itself ischaemia due to myocardial O2 demand which is not met

Answer 287

Myocardial ischemia occurs when the blood flow through one or more of your coronary arteries is decreased. The low blood flow decreases the amount of oxygen your heart muscle receives. Myocardial ischemia can develop slowly as arteries become blocked over time.

Answer 288

1. adenosine 2. CO2 3. lactate 4. K+ ions activates sensory nerves

Answer 289

1. stable angina (most common) 2. unstable angina 3. variant angina (least common)

Answer 290

most= stable least= variant

Answer 291

(most common) - attacks predictable, e.g. exercise, stress - myocardial O2 demand not met - involvement of chronic occlusive coronary artery disease i.e. atherosclerosis; use of cholesterol-lowering drugs (statins)

Answer 292

- attacks unpredictable - coronary artery occlusion due to platelet adhesion to ruptured atherosclerotic plaque; use of anti-platelet drugs)

Answer 293

(least common) - attacks unpredictable - coronary artery occlusion by vasospasm

Answer 294

Coronary artery occlusion is a partial or complete blockage of one of your coronary arteries, which can lead to a heart attack. The underlying cause of coronary artery occlusion is usually coronary artery disease (CAD). CAD results from plaque buildup inside your coronary arteries, causing them to narrow.

Answer 295

Atherosclerosis is thickening or hardening of the arteries caused by a buildup of plaque in the inner lining of an artery. Risk factors may include high cholesterol and triglyceride levels, high blood pressure, smoking, diabetes, obesity, physical activity, and eating saturated fats

Answer 296

to reduce myocardial O2 demand

Answer 297

by vasodilator drugs: arteries; decrease after-load (force against which left ventricle contracts) decrease myocardial work decrease myocardial O2 demand veins; decrease pre-load (diastolic pressure that distends the relaxed left ventricle) decrease venous return decrease pre-load decrease stretch of ventricle and atria decrease strength of contraction decrease myocardial work decrease myocardial O2 demand

Answer 298

after-load: force against which left ventricle contracts pre-load: diastolic pressure that distends the relaxed left ventricle

Answer 299

brainbridge (atrial) reflex- a sympathetic reflex initiated by increased blood in the atria causes stimulation of the SA node stimulated baroreceptors in the atria, causes increases SNS stimulation **The Bainbridge reflex helps increase heart rate when venous return increases and can be less active when venous return is reduced.

Answer 300

1. glyceryl trinitrate 2. amyl nitrite 3. isosorbide dinitrate 4. isosorbide mononitrate

Answer 301

(most commonly used anti-anginals) - GTN (nitroglycerine, 10% in inert lactose base) -> taken as sub-lingual tablet/spray -> not orally active (destroyed by first-pass metabolism) - amyl nitrite (volatile liquid) -> vials opened and inhaled -> not now used clinically but has become drug of abuse (poppers) *both drugs rapid in onset, but action short lived uses: - prophylaxis in stable angina (i.e. taken immediately before exercise) - rapid relief of ongoing anginal attack (all forms)

Answer 302

cause both arterial and venous smooth muscle dilation by the intracellular release of nitric oxide.

Answer 303

nitric oxide (NO) - all nitrovasodilators are pro-drugs - lipophilic; readily enter smooth muscle cells and are reduced to nitric oxide (NO) - termed 'NO donors' - mimic action of endothelium-derived NO

Answer 304

NO is a free radical which not only is present in the environment but also can be produced in the body as a vital signaling molecule. In the vasculature, NO stimulates sGC to produce cGMP, decreases the intracellular concentration of calcium, causes relaxation of vascular smooth muscle and thus is a potent vasodilator.

Answer 305

nitric oxide activates soluble guanylate cyclase (sGC) - cytoplasmic (soluble ) enzyme - receptor on soluble guanylate cyclase contains ferrous (Fe2+) haem moiety (like O2 binding site of haemoglobin) - NO binds to haem receptor --> enzyme activation --> converts GTP to cGMP --> increases cGMP --> vasodilation

Answer 306

soluble (cytoplasmic) guanylate cyclase = sGC ->NO binds to haem receptor on enzyme -> enzyme activation -> converts GTP to cGMP -> increase in cGMP causes vasodilation *receptor on sGC contains a ferrous (Fe2+) haem moiety

Answer 307

venous dilatation > arterial dilatation nitrovasodilators primarily work by reducing venous return (preload), which lowers the heart's workload and oxygen demand, thereby helping to relieve the chest pain associated with angina.

Answer 308

- headache (dilation of cerebral arteries) - tolerance on prolonged use; need drug free 'washout' period to restore efficacy

Answer 309

- recently introduced to treat angina (all forms) - blocks If (Na+) current that contributes to SA node depolarisation towards threshold - decreases heart rate bit not force - decrease myocardial O2 demand

Answer 310

Positive inotropic medications are medications that increase the force of muscle contraction of the heart, resulting in an increased cardiac output.

Answer 311

a state in which the heart fails to maintain an adequate circulation for the needs of the body despite an adequate venous filling pressure.

Answer 312

1. heart rate 2. filling 3. outflow resistance 4. contractile state of heart

Answer 313

haemodynamic overload: - excess pressure (e.g. essential hypertension, aortic stenosis) - excess volume (e.g. valve regurgitation, obesity) neurohumoral overload (e.g. thyrotoxicosis) tissue damage (e.g. myocardial infarction) genetically determined excessive hypertrophic response to pressure (human familial hypertrophic cardiomyopathy)

Answer 314

left ventricular failure - fatigue - pulmonary oedema (orthopnoea) right ventricular failure - venous distension - oedema - cyanosis

Answer 315

left ventricular failure - fatigue - pulmonary oedema (orthopnoea) right ventricular failure - venous distension - oedema - cyanosis

Answer 316

Pulmonary oedema is a condition caused by too much fluid in the lungs. This fluid collects in the many air sacs in the lungs, making it difficult to breathe.

Answer 317

Orthopnoea (or-thaap-nee-uh) is shortness of breath (dyspnea) that happens when you're lying on your back (in a supine position).

Answer 318

Jugular vein distention is the bulging of the major veins in your neck. It's a key symptom of heart failure and other heart and circulatory problems. It's not a painful symptom, but it can happen with conditions that can be life-threatening.

Answer 319

Oedema is a build-up of fluid in the body which causes the affected tissue to become swollen. The swelling can occur in one particular part of the body or may be more general, depending on the cause.

Answer 320

Cyanosis is where your skin or lips turn blue or grey

Answer 321

Thyrotoxicosis: In an overactive thyroid state, there is increased metabolism, which increases heart rate and cardiac output. The heart has to work harder, and over time, this can lead to heart failure, especially if the condition is not treated.

Answer 322

Essential hypertension: Chronic high blood pressure forces the heart to pump against a higher resistance, increasing the workload on the heart, particularly the left ventricle. Over time, this can cause left ventricular hypertrophy (LVH), which can lead to heart failure if not controlled.

Answer 323

Aortic stenosis: A narrowing of the aortic valve increases resistance for the left ventricle to overcome, leading to a pressure overload. This can also result in left ventricular hypertrophy and eventual heart failure if left untreated.

Answer 324

Valve regurgitation (e.g., mitral or aortic regurgitation): The backflow of blood through a faulty valve increases the volume of blood the heart has to pump, leading to volume overload, which can cause dilation of the heart chambers and eventually heart failure.

Answer 325

Obesity: Increased body mass demands more from the heart, leading to volume overload and increased cardiac output. Over time, this can lead to heart failure due to the excessive strain on the heart.

Answer 326

Myocardial infarction (heart attack): When part of the heart muscle dies due to lack of blood flow, it reduces the heart's ability to contract effectively. This leads to a decrease in cardiac output, which can progress to heart failure.

Answer 327

Familial hypertrophic cardiomyopathy (FHC): This is a genetic condition where the heart muscle (especially the left ventricle) thickens excessively, often in response to pressure overload. This thickening can impair the heart's ability to pump blood effectively and lead to heart failure. The hypertrophic response in FHC is abnormal and genetically determined, contributing to heart failure.

Answer 328

increase in central venous pressure ->increase pre-load -->increase end-diastolic volume --->increase stroke volume

Answer 329

increase peripheral vascular resistance ->diastolic arterial pressure -->increase afterload --->increase cardiac work

Answer 330

The preload refers to the amount of blood already in your ventricles when you're ready to pump it out, and the afterload refers to the pressure against which your heart has to pump that blood.

Answer 331

to reduce the preload/afterload or make the heart work harder (positive inotropes)

Answer 332

objective is to reduce preload/afterload or to make the heart work harder (positive inotropes) commonly used - diuretics; reduce fluid volume by excreting Na+ - ACE inhibitors; lower BP and indirect Na+ excretion other treatments - vasodilators e.g. nitrates to reduce preload - low dose b-blockers - POSITIVE INOTROPES

Answer 333

dopamine; acts via dopamine receptors (D1 and D2) but also via release of noradrenaline dobutamine; acts mainly via B1 and B2 adrenoceptors *short term inotropic support in advanced heart failure in patients who have not responded to standard treatment

Answer 334

- intracellular calcium concentration - Ca2+ entry via ion channels - Na+/Ca2+ exchange - Ca2+ storage in sarcoplasmic reticulum

Answer 335

calcium (Ca2+) is the key trigger for cardiac muscle contraction. When calcium ions enter the cardiac muscle cell during an action potential (through L-type calcium channels), calcium is released from the sarcoplasmic reticulum (SR), which leads to actin and myosin filaments interacting. This interaction is what generates the force of contraction in muscle cells. Contraction happens when calcium binds to troponin on the actin filaments, allowing the myosin heads to bind to actin and pull, creating the muscle contraction.

Answer 336

after contraction, the muscle needs to relax so it can fill with blood again for the next cycle. For this to happen, calcium must be removed from the cytoplasm: ATP-dependent pumps are responsible for removing calcium from the cytoplasm: 1. sarcoplasmic reticulum Ca2+ ATPase (SERCA): pumps calcium back into the SR for storage 2. Na+/Ca2+ exchanger (NCX): this transporter moves calcium out of the cell in exchange for sodium. For this to work efficiently, the sodium-potassium ATPase pump (Na+/K+ pump) is crucial, as it maintains low sodium levels inside the cell. *if calcium is not properly removed, the muscle can remain in a state of contraction, which leads to problems like diastolic dysfunction or heart failure

Answer 337

Na+ is pumped out of the cell, and K+ is pumped in. This helps keep the intracellular sodium concentration low. If this pump becomes impaired (as might occur with digoxin or foxglove plant-derived drugs), there is increased intracellular sodium. This reduced the driving force for the Na+/Ca2+ exchanger meaning the exchanger can't pump out as much calcium as needed. The reduced calcium extrusion leads to calcium accumulation inside the cell. This can increase the force of contraction because intracellular calcium is higher, which is the mechanism by which digitalis-like drugs (e.g. digoxin) increase the contractility of the heart (a phenomenon called positive inotropic effect)

Answer 338

The sodium-potassium pump system moves sodium and potassium ions against large concentration gradients. It moves two potassium ions into the cell where potassium levels are high, and pumps three sodium ions out of the cell and into the extracellular fluid.

Answer 339

Digoxin (from the foxglove plant) is an example of a drug that effects the Na+/K+ ATPase pump. By inhibiting this pump, digoxin increases the intracellular calcium concentration because the sodium gradient is disrupted, which leads to increased contractility of the heart. This is beneficial in conditions like heart failure, where the heart's pumping ability is weakened.

Answer 340

Beta-receptor agonists (e.g. dobutamine/dopamine) increase the force of contraction by enhancing the activity of calcium channels and increasing intracellular calcium. -> these drugs act through the b1-adrenergic receptors on cardiac cells, leading to increased cAMP levels. Higher cAMP levels activate protein kinase A (PKA), which then phosphorylates various proteins that enhance calcium influx into the cell (via L-type calcium channels) and increase calcium release from the sarcoplasmic reticulum -> the result is an increased intracellular calcium concentration, which enhances the contractile force of the heart (this is another example of positive inotropic effect)

Answer 341

calcium-sensitising drugs (e.g. levosimendan) do not increase intracellular calcium but increase the sensitivity of troponin to calcium, making the actin-myosin interaction more efficient -> this means that less calcium is needed to generate a stronger contraction. These drugs are useful in conditions like heart failure where you want to increase the force of contraction without increasing the intracellular calcium load (which can be harmful over time)

Answer 342

levosimendan

Answer 343

dobutamine dopamine

Answer 344

low therapeutic index severe adverse effects -> cardiac arrhythmias -> early signs of toxicity -> nausea -> vomiting -> altered colour vision elimination reduced in the elderly and those with renal failure interactions with e.g. diuretics (reduce K+) or amiodarone, verapamil, quinidine (increase its plasma concentration)

Answer 345

Digoxin has a low therapeutic index, meaning the difference between the therapeutic dose (the dose that provides benefit) and the toxic dose (the dose that causes harm) is quite small. This makes monitoring its plasma concentration important when the drug is used.

Answer 346

Reduced Elimination in the Elderly: As we age, kidney function often declines, and digoxin is primarily eliminated by the kidneys. This means that elderly patients may accumulate digoxin in their system more easily, increasing the risk of toxicity. Renal Failure: Since digoxin is excreted by the kidneys, patients with renal failure (impaired kidney function) have a reduced ability to clear the drug, which can result in elevated plasma levels and increased risk of toxicity.

Answer 347

Diuretics (especially potassium-wasting diuretics, like furosemide or hydrochlorothiazide): These diuretics can lower potassium levels in the blood (hypokalemia), and low potassium can increase the effects of digoxin, making it more likely to cause arrhythmias or toxicity. Amiodarone, Verapamil, and Quinidine: These drugs can increase digoxin plasma concentration by slowing its elimination. Amiodarone and verapamil can reduce digoxin clearance, and quinidine can displace digoxin from tissue binding sites, increasing the free plasma concentration. Drug interactions (e.g., with diuretics, amiodarone, verapamil, and quinidine) can increase digoxin's plasma concentration, heightening the risk of toxicity.

Answer 348

levosimendan; binds to troponin C at high intracellular calcium. - may only sensitise to calcium during systole (on-off effect) - PDE inhibitor at higher concentrations - vasodilator K+ ATP channels - once daily administration - in phase III trials in UK - meta-analysis of data from 326 patients (6RCTs) using intermittent levosimendan. Associated with a significant reduction in mortality at the longest follow-up available Calcium sensitization: Binds to troponin C in high calcium conditions to improve contraction without increasing intracellular calcium. Phosphodiesterase (PDE) inhibition: At higher concentrations, it increases cAMP, promoting vasodilation and reducing afterload. Vasodilation: Opens K_ATP channels, leading to smooth muscle relaxation and lowering systemic vascular resistance. Once-daily dosing: Convenient regimen that improves patient compliance. Promising results: Meta-analysis suggests significant reduction in mortality in heart failure patients using intermittent levosimendan.

Answer 349

This on-off effect is thought to be advantageous because levosimendan sensitizes the heart muscle to calcium only during systole (the contraction phase of the cardiac cycle). This selective effect allows for improved contractility during contraction, without overwhelming the heart with excessive calcium during relaxation (diastole). This helps reduce the risk of arrhythmias that can occur with other inotropic agents, which increase calcium in the cell indiscriminately.

Answer 350

At higher concentrations, levosimendan acts as a phosphodiesterase (PDE) inhibitor. PDE inhibitors increase levels of cAMP in cells, which leads to smooth muscle relaxation and vasodilation. This helps lower afterload (the resistance the heart must pump against), which makes it easier for the heart to pump blood. By inhibiting PDE3, levosimendan promotes vasodilation in vascular smooth muscle, reducing the workload of the heart.

Answer 351

inflammatory disease (previously thought of as only a disease of lipid/cholesterol storage)

Answer 352

develops slowly over many years- can be asymptomatic

Answer 353

Damage to the endothelium upsets the balance between vasoconstriction and vasodilation and initiates a number of events/processes that promote or exacerbate atherosclerosis; these include increased endothelial permeability, platelet aggregation, leukocyte adhesion, and generation of cyto- kines.

Answer 354

- platelet adhesion - migration of smooth muscle cells; PDGF to form fibrous cap - uptake of modified LDLs- LOX-1 - formation of lipid-laden foam cells (monocytes-macrophages) - release of MMPs by macrophages - compensatory vessel remodelling

Answer 355

- formation of fibrous cap (healing) - foam cells burst/die - necrotic core (lipid debris) - further monocyte recruitment - oxidation of LDLs within plaque

Answer 356

- fibrous cap thins/ulcers (oxidant and shear stress) - thrombus formation - intraplaque haemorrhage - vessel occlusion - myocardial infarction

Answer 357

Modified LDL (low-density lipoprotein), especially oxidized LDL, is taken up by macrophages through the LOX-1 receptor. This leads to the formation of foam cells, which contribute to plaque buildup.

Answer 358

Damage to the endothelium disrupts the balance between vasoconstriction and vasodilation, triggering a cascade of events such as increased endothelial permeability, platelet aggregation, leukocyte adhesion, and cytokine generation. This sets the stage for atherosclerosis development.

Answer 359

Fatty streaks represent the early stages of atherosclerosis. They are formed by the accumulation of lipids and foam cells (lipid-laden macrophages) under the endothelium.

Answer 360

Modified LDL (low-density lipoprotein), especially oxidized LDL, is taken up by macrophages through the LOX-1 receptor. This leads to the formation of foam cells, which contribute to plaque buildup.

Answer 361

As the plaque develops, smooth muscle cells migrate from the vessel media to the intima in response to growth factors like PDGF (platelet-derived growth factor). These cells proliferate and help form a fibrous cap over the lipid core. This cap is important in stabilizing the plaque.

Answer 362

As the lesion advances, foam cells may burst, contributing to the formation of a necrotic core filled with lipid debris. This core is a hallmark of more complicated plaques, which are more likely to rupture.

Answer 363

The thinning and potential ulceration of the fibrous cap (due to oxidative stress and shear stress) can expose the underlying lipid core. This leads to platelet adhesion and the formation of a thrombus (blood clot), which can further obstruct the vessel.

Answer 364

Blood vessels within the plaque can rupture, leading to intraplaque hemorrhage. This can worsen the plaque and increase the risk of rupture.

Answer 365

As the thrombus grows, it can cause partial or complete vessel occlusion. If it occurs in coronary arteries, it can lead to myocardial infarction (heart attack), which often happens when a vulnerable plaque ruptures.

Answer 366

The plaque undergoes compensatory remodeling, with the vessel enlarging in some cases to accommodate growing plaque. However, further recruitment of monocytes and macrophages to the site can aggravate inflammation and further destabilize the plaque.

Answer 367

Macrophages in the plaque release MMPs, which are enzymes that degrade the extracellular matrix. This can weaken the fibrous cap and increase the likelihood of plaque rupture.

Answer 368

LDL is harmful when elevated because it contributes to plaque buildup in arteries, increasing the risk of cardiovascular disease. - Carries cholesterol to cells, but can deposit it in the arteries; carries from liver to cells throughout body HDL is protective, helping remove excess cholesterol and reduce the risk of plaque formation and cardiovascular events. - Removes excess cholesterol from the blood, preventing plaque formation; carries back to liver

Answer 369

1. Atherosclerotic plaque formation in the coronary arteries. 2. Plaque rupture exposes the lipid core to the bloodstream. 3. Thrombus (blood clot) formation that blocks the artery. 4. Ischemia (lack of oxygen) causes heart muscle damage. 5. If untreated, this damage leads to myocardial infarction (heart attack), which can result in permanent heart damage, heart failure, or arrhythmias

Answer 370

1. incorporating into cell membranes 2. maintaining membrane fluidity and permeability 3. production of steroids and fat soluble vitamins 4. the liver

Answer 371

- monitors cholesterol levels - regulates this through synthesis, absorption and bile secretion - drugs to treat hyperlipidaemia target this process in the liver/gut

Answer 372

1. Synthesis: The liver produces cholesterol, which is essential for cell membranes, hormones, and bile production. 2. Transport: Cholesterol is carried through the bloodstream by lipoproteins (LDL and HDL). LDL delivers cholesterol to cells, while HDL transports excess cholesterol back to the liver. 3. Excretion: The liver excretes cholesterol in bile, which aids digestion and is partially eliminated from the body. 4. Regulation: The liver adjusts its cholesterol production based on the body’s needs, maintaining balance in cholesterol levels. 5. Impact of Diet: Saturated fats and trans fats can raise LDL cholesterol, while unsaturated fats can help raise HDL cholesterol.

Answer 373

The liver is the primary organ responsible for producing cholesterol. It synthesizes cholesterol from acetyl-CoA, a molecule derived from the breakdown of fats, carbohydrates, and proteins.

Answer 374

Cholesterol is converted into bile acids in the liver, which are essential for the digestion and absorption of dietary fats

Answer 375

Lipoproteins are particles made of protein and fats (lipids). - They carry cholesterol through your bloodstream to your cells.

Answer 376

1. chylomicrons; carry TGs from intestines to liver, muscle and adipose tissue 2. VLDL; carry newly synthesised TGs from liver to adipose tissue 3. IDL; an intermediate between VDL and LDL 4. LDL; major reservoir of cholesterol, taken up via LDL receptors by endocytosis 5. HDL; absorb cholesterol released by dying cells, also act as 'reverse transport' to take cholesterol to liver

Answer 377

triglycerides a type of fat (lipid) found in the body. Triglycerides are composed of glycerol (a sugar alcohol) and three fatty acids. They are the main form of fat stored in the body and are used by cells for energy.

Answer 378

carry TGs from intestines to liver, muscle and adipose tissue (lipoprotein)

Answer 379

carry newly synthesised TGs from liver to adipose tissue (lipoprotein)

Answer 380

intermediate between VLDL and LDL (lipoprotein)

Answer 381

major reservoir of cholesterol carries cholesterol from liver to various tissues such as the adrenal gland, gonads, muscle, and adipose tissue. (lipoprotein)

Answer 382

taken up via LDL receptors by endocytosis

Answer 383

Endocytosis is a cellular process in which substances are brought into the cell. The material to be internalized is surrounded by an area of cell membrane, which then buds off inside the cell to form a vesicle containing the ingested materials.

Answer 384

1. VLDL (very low-density lipoproteins) are secreted by the liver, carrying triglycerides to tissues. 2. As cells extract triglycerides, VLDL particles shrink and become IDL (intermediate-density lipoproteins). 3. Further triglyceride removal from IDL results in LDL (low-density lipoprotein), which is cholesterol-rich and carries cholesterol to tissues. 4. LDL cholesterol can contribute to atherosclerosis if elevated in the bloodstream.

Answer 385

1. LDL (very bad) 2. IDL (bad) 3. VLDL (bad) 4. chylomicron 5. HDL (good)

Answer 386

The exogenous lipoprotein pathway describes how lipids, particularly dietary triglycerides (TGs) and cholesterol, are absorbed from the intestines, transported through the bloodstream, and delivered to tissues in the body. This pathway primarily involves chylomicrons, which are special lipoprotein particles responsible for the transport of dietary fats.

Answer 387

1. Dietary fats are digested and absorbed in the small intestine. 2. Chylomicrons are formed in the intestinal cells, carrying triglycerides, cholesterol, and apolipoproteins. 3. Chylomicrons enter the lymphatic system, then the bloodstream, and are transported to peripheral tissues. 4. Lipoprotein lipase (LPL) in capillary walls breaks down triglycerides into free fatty acids, which are taken up by muscle and adipose tissue. 5. The chylomicron remnants, now depleted of most triglycerides but rich in cholesterol, are cleared by the liver.

Answer 388

lipoprotein lipase (LPL)

Answer 389

Nascent HDL (or empty HDL) refers to newly synthesized HDL particles that are initially cholesterol-poor and contain high amounts of phospholipids and apolipoproteins, particularly apoA-I. These nascent particles are essential for initiating reverse cholesterol transport. Once nascent HDL collects cholesterol from tissues, it matures into a larger, cholesterol-rich HDL particle, which can then transport the cholesterol back to the liver. Mature HDL has the capacity to carry cholesterol and deliver it to the liver for: -> Bile acid synthesis (excretion in bile), -> Hepatic recycling for use in cell membranes or hormones.

Answer 390

The remnant receptor (LRP1) on liver cells facilitates the uptake and clearance of chylomicron remnants, which are cholesterol-rich particles that result after triglycerides are removed from chylomicrons.

Answer 391

The liver synthesizes triglycerides from excess dietary carbohydrates and fatty acids and packages them into VLDL particles. VLDL is secreted into the bloodstream, where it circulates to tissues like muscle and adipose tissue.

Answer 392

1. As VLDL circulates through the bloodstream, it comes into contact with lipoprotein lipase (LPL), an enzyme located on the endothelial cells of capillaries (especially in muscle and adipose tissue). 2. LPL breaks down the triglycerides in VLDL into free fatty acids and glycerol, which are taken up by muscle cells (for energy) and adipose tissue (for storage). 3. This loss of triglycerides causes the VLDL particle to shrink and become smaller and denser. This transformed particle is now referred to as IDL (Intermediate-Density Lipoprotein).

Answer 393

lipoprotein lipase (LPL) LPL breaks down the triglycerides in VLDL into free fatty acids and glycerol, which are taken up by muscle cells (for energy) and adipose tissue (for storage). This loss of triglycerides causes the VLDL particle to shrink and become smaller and denser. This transformed particle is now referred to as IDL (Intermediate-Density Lipoprotein).

Answer 394

1. Be taken up by the liver via specific receptors (LDL receptors or remnant receptors) 2. Continue to lose more triglycerides, becoming LDL (Low-Density Lipoprotein).

Answer 395

VLDL has the highest amount of triglycerides relative to cholesterol, as its main role is to transport triglycerides to peripheral tissues. IDL higher cholesterol content than VLDL and lower triglyceride content LDL is primarily cholesterol-rich, making it the major carrier of cholesterol in the blood. HDL, while having significant cholesterol content, also has some triglycerides but plays a critical role in reverse cholesterol transport, removing excess cholesterol from tissues and returning it to the liver.

Answer 396

As IDL loses more of its triglycerides (via LPL activity), it becomes LDL, a lipoprotein that is cholesterol-rich and contains more cholesterol than triglycerides. LDL carries cholesterol to peripheral tissues, where it is used for various functions, such as: -> Incorporation into cell membranes, -> Synthesis of steroid hormones, -> Production of bile acids in the liver. LDL particles have the apolipoprotein apoB-100, which is recognized by LDL receptors on peripheral cells and liver cells, facilitating cholesterol uptake. Excess LDL in the bloodstream can lead to cholesterol buildup in blood vessel walls, contributing to atherosclerosis.

Answer 397

- high circulating levels of free and bound cholesterol and TGs - It results from an inability to break down lipids or fats in your body, specifically cholesterol and triglycerides. - secondary causes; diabetes mellitus, alcoholism, hypothyroidism, liver disease, drugs, diet

Answer 398

1. diabetes mellitus 2. alcoholism 3. hypothyroidism 4. liver disease 5. drugs 6. diet

Answer 399

Primary hyperlipoproteinemia is often genetic. It's a result of a defect or mutation in lipoproteins. These changes result in problems with accumulation of lipids in your body. Secondary hyperlipoproteinemia is the result of other health conditions that lead to high levels of lipids in your body.

Answer 400

[STATINS] simvastatin pravastatin rosuvastatin

Answer 401

statins e.g. simvastatin, pravastatin, rosuvastatin - competitive inhibitors of rate-limiting step in cholesterol biosynthesis - marked decrease in cholesterol levels may stimulate LDL receptor up-regulation

Answer 402

most effective at night since this is when most cholesterol biosynthesis occurs

Answer 403

group of disorders of heart and circulatory system 1. coronary heart disease 2. cerebrovascular disease 3. peripheral arterial disease 4. rheumatic heart disease 5. congenital heart disease 6. DVT/pulmonary embolism

Answer 404

of blood vessels suppling the heart

Answer 405

of blood vessels suppling the brain

Answer 406

of blood vessels suppling arms and legs

Answer 407

heart muscle and valve damage due to rheumatic fever

Answer 408

malfunction of heart structure from birth

Answer 409

blood clots in veins which can move to heart and lungs

Answer 410

Rheumatic fever is an inflammatory condition that can affect the heart, joints, brain, and skin. Rheumatic fever can develop if strep throat, scarlet fever, or impetigo aren't treated properly.

Answer 411

Rheumatic heart disease is a condition where the heart valves have been permanently damaged by rheumatic fever. Rheumatic fever is an inflammatory disease that can affect many connective tissues, especially in the heart. Untreated or undertreated strep infections put a person at increased risk.

Answer 412

As it progresses, some plaques evolve to take on a more unstable phenotype with greater degrees of inflammation. Eventually, plaque rupture can occur, and contact of blood with the exposed subendothelial matrix and plaque content causes the formation of occlusive thrombi.

Answer 413

partial= angina pectoris (ischemic heart disease) total= myocardial infarction (MI)

Answer 414

partial= transient ischemic attack total= cerebrovascular accident (CVA)

Answer 415

A stroke happens when there is a loss of blood flow to part of the brain. Your brain cells cannot get the oxygen and nutrients they need from blood, and they start to die within a few minutes. This can cause lasting brain damage, long-term disability, or even death

Answer 416

a brief episode of neurological dysfunction resulting from an interruption in the blood supply to the brain or the eye, sometimes as a precursor of a stroke.

Answer 417

aneurysm -occlusion - rupture and haemorrhage

Answer 418

peripheral vascular disease - gangrene and amputation

Answer 419

1. dyslipidemia 2. stress 3. lack of PA 4. T2D 5. diet (sat fat) 6. hypertension 7. metabolic syndrome 8. inflammation 9. obesity 10. age, race, gender 11. smoking 12. sleep 13. prior event (genetics/family history)

Answer 420

physical activity can have an indirect role in reducing other risk factors such as sleep, stress, T2D, hypertension, metabolic syndrome and obesity

Answer 421

Dyslipidemia refers to abnormal levels of lipids in the bloodstream, which poses a significant risk factor for cardiovascular (CV) diseases. Dysregulation in these lipid levels, whether due to genetic predispositions or lifestyle factors, can lead to atherosclerosis and other CV complications.

Answer 422

Metabolic syndrome is a cluster of conditions that occur together, increasing your risk of heart disease, stroke and type 2 diabetes. These conditions include increased blood pressure, high blood sugar, excess body fat around the waist, and abnormal cholesterol or triglyceride levels.

Answer 423

physical activity: any bodily movement produced by the skeletal muscles that requires an increase in energy expenditure

Answer 424

vary positively correlated with physical fitness; planned/structured and repetitive bodily movement; objective to improve or maintain physical fitness

Answer 425

those performing insufficient amount of MVPA for health (not meeting the WHO recommended minimum required MVPA)

Answer 426

Moderate to Vigorous Physical Activity (MVPA) an intensity level of physical activity required to meet health and fitness outcomes.

Answer 427

sedentary behaviour is defined as any waking behaviour characterised by an energy expenditure <_1.5 METs while in a sitting, reclining or lying posture

Answer 428

physical activity improves endothelial function, which enhanced vasodilation and vasomotor function in blood vessels

Answer 429

physical activity contributes to weight loss, glycaemic control, improved blood pressure, lipid profile and insulin sensitivity

Answer 430

1. cardiac growth (hypertrophy, hyperplasia) 2. vascular (flow, vasoreactivity, anglogenesis) 3. metabolism (ox. phosphorylation) 4. function (stroke volume, cardiac output, improved Ca+ handling, T-tubule organisation) 5. cardioprotection (ischemic injury)

Answer 431

Ischemic injury is a pathological condition that occurs when the blood supply to organs and tissues is temporarily restricted or cut off, depriving them of nutrients, oxygen, and sugar.

Answer 432

Hyperplasia and hypertrophy are two ways that the size of cells can increase. Hyperplasia is an increase in the number of cells, while hypertrophy is an increase in the size of cells. During hypertrophy, the cells enlarge as they fill with more cytoplasm. This can lead to an increase in the strength or function of the tissue.

Answer 433

Angiogenesis is the formation of new blood vessels. This process involves the migration, growth, and differentiation of endothelial cells, which line the inside wall of blood vessels

Answer 434

skeletal muscle (hypertophy, hyperplasia, fibre type switching) vascular (flow, vasoreactivity, angiogenesis) metabolism (insulin sensitivity, Ox.phosphorylation, adipose 'browning')

Answer 435

cAMP and PKA facilitate the increased influx of sodium and calcium ions into the heart cells, which accelerates the depolarization process.

Answer 436

It increases the conduction velocity, ensuring rapid transmission of electrical signals to coordinate efficient heart contractions.

Answer 437

Sympathetic activation shortens the duration of the myocyte action potential, allowing for faster repolarization and quicker preparation for the next beat.

Answer 438

Lusitropy refers to the rate of relaxation of the heart muscle. Sympathetic activation increases the rate of relaxation to facilitate efficient filling of the heart during diastole.

Answer 439

By releasing norepinephrine, sympathetic activation increases calcium availability in the heart muscle cells, enhancing contraction strength (positive inotropy).

4. cardiovascular system Flashcards

(474 cards)