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Physiology Exam Sem 1 content Flashcards

1
Q

Describe how electrical excitation leads to muscle contraction

A
  1. Electrical impulse at SAN
  2. Impulse travels to AV node
  3. Travels across bundle of His, to the purkinje fibres then to the apex where it contracts the ventricular muscle
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2
Q

What is cardiac output incl it’s equation?

A

the volume of blood ejected from the left side of the heart in one minute. CO = HR x SV

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3
Q

What is stroke volume?

A

the amount of blood ejected from the heart in one contraction

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4
Q

What are the 3 lifestyle changes that can reduce CV death rate?

A

reduce smoking, improve diet, increase exercise

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5
Q

How do drugs that reduce CVD work?

A

controlling hypertension, preventing blood clots and controlling blood cholesterol

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6
Q

What is the volume of blood in the system controlled by?

A

kidneys

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7
Q

What’s the pharmacist’s role in CVD?

A

disease prevention & supporting patients with established disease

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8
Q

What’s the refractory period and its role in conduction?

A

caused by inactivation of sodium channels, critical to conduction of action potential, prevents action potential form travelling backwards. Influx of potassium ions as vgkc slow to close.

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9
Q

What is ECG, how is it recorded and what does it tell us?

A

it’s a machine that records conduction through the heart / 10 electrodes and 12 leads, 6 on the chest, 1 on each wrist and 1 on each ankle / each lead records the potential difference between 2 electrodes to detect the direction of current flow

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10
Q

What is the isoelectric line and what does it represent?

A

a straight line (baseline) which represents the absence of electrical activity in the cardiac tissue

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11
Q

Describe what each element of the PQRST cycle represent

A

p wave: atrial repolarization, QRS complex: ventricular depolarization, T wave: ventricular repolarisation

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12
Q

What does an absent P wave represent

A

problem in atria or SAN

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13
Q

What does an absent QRS complex signify

A

problem in ventricles or conducting tissue supplying ventricles

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14
Q

What are the 6 disorders of rhythm?

A

sinus tachycardia, sinus bradycardia, atrial flutter, atrial fibrillation, ventricular fibrillation, torsade de pointes

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15
Q

How can you identify heart block on an ECG?

A

1st degree: long pq interval 2nd degree: missed QRS complex 3rd degree: p wave disconnected from QRS complex or absent

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16
Q

How can you identify a myocardial infarction on an ECG?

A
  1. the more leads on ECG the larger the infarct size
  2. abnormal Q wave and heightened T wave
  3. ST segment elevated or depressed
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17
Q

How does atrial flutter present on an ECG?

A

Absent P wave, sawtooth pattern

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18
Q

How does atrial fibrillation present on an ECG?

A

no P waves, irregularly spaced QRS waves

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19
Q

How does ventricular fibrillation present on an ECG?

A

irregular unformed QRS complexes without any clear P waves

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20
Q

How does Torsade de Pointes present on ECG?

A

QRS peaks transition back and forth across isoelectric line

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21
Q

Explain how excitable and non-excitable cells differ and give some examples of each

A

non-excitable cells do not generate action potential, they have higher resting potential

Non-excitable cell: RBCs, epithelium , endothelium, adipose

Excitable: SAN, skeletal muscle, neurone, cardiac muscle

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22
Q

What is automaticity?

A

The ability of the heart to start and maintain rhythmic activity without the use of the nervous system or without external control

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23
Q

Which two factors determine membrane potential?

A

Gradients of ions across membrane

Selectively permeable ion channels in membrane

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24
Q

What is excitation-contraction coupling?

A

The mechanism that ensures that skeletal muscle contraction does not occur without neural stimulation (excitation). At rest, cytosolic [Calcium] is low, and the troponin, tropomyosin complex covers the myosin-binding sites on actin. When the muscle is stimulated by a neuron, calcium is released from the sarcoplasmic reticulum into the cytosol of the muscle cell. Calcium binds to troponin, causing a conformation change in the troponin-tropomyosin complex that shifts it away from the myosin-binding sites. This allows myosin and actin to interact according to the sliding filament theory.

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25
Describe the arrangement of cardiac conductive tissue
myocytes, gap junctions: large pores spanning that allow ions to pass between them allowing APs to spread between cells. Intercalated discs: hold cells together and gap junction found here, nexus: where gap junction is found
26
Explain the concept of calcium induced calcium release
the process whereby calcium promotes its own release from intracellular calcium stores. Provides a means for amplification of microscopic initiation events into propagating calcium signals. During each heartbeat an influx of calcium through L-type voltage gated channels provides the trigger to induce CICR from receptors on the SR resulting in cardiac contraction
27
How does input form the autonomic nervous system affect cardiac function?
it alters rate and force of heartbeat but not required for heart to function
28
Describe nerve axon APs
simplest and fastest / specialised for rapid conduction over long distance / starts with depolarization to threshold for opening voltage gated Na+ channels / at peak Na+ influx falls, eqm is approached and Na+ channels closes and creates opposing outward flux of K+ and repolarisation occurs / brief hyperpolarization before membrane goes back to resting potential
29
Describe cardiac ventricular muscle APs
triggers ventricular muscle contraction / calcium entry during AP causes release of calcium from SR to stimulate contraction / much longer duration than axon AP
30
What are the 2 important consequences of the long plateau?
keeps sodium channels activated / allows time for calcium to enter, trigger contraction and replenish stores
31
Describe the SAN APs
heart’s pacemaker / APs spontaneous / no discernible resting potential / membrane potential changes continually
32
Explain using the neural mechanism how change in blood flow is initiated
MAP is sensed by pressure sensitive baroreceptors in ascending aorta, aortic arch & carotid sinus / afferent neuronal pathways signal change to CNS and efferent pathways wend instructions to arteries to correct / between afferent and efferent pathways, CV centre generates response when deviation from ideal map perceived
33
Explain using the paracrine mechanism how change in blood flow is initiated
local control uses paracrine mechanisms / tissues can directly adjust blood flow to meet metabolic demands / arterioles dilate in response to metabolites and increase blood flow within skeletal muscle during exercise / Hyperaemia
34
What are the implications of changing vascular smooth tone on vessel diameter and on compliance?
increasing tone will reduce compliance and the diameter of the vessel
35
What is the effect of sympathetic innervation on vascular tone?
so small arteries and arterioles are densely innervated by nerves / smooth muscle cells wrap around vessel / noradrenaline released at varicosities (nerve terminals on smooth muscle) / stimulation of NS also released adrenaline from adrenal medulla which works with noradrenaline to moderate vascular tone
36
What are the 3 distinct components of the CV centre and their function
cardiaccelerator centre – stimulates heart by increasing HR and SV, cardioinhibitor centre – slows HR by signaling via vagus nerve and vasomotor centre – controls vessel diameter by modulating smooth muscle contraction
37
What is hyperaemia and its different forms?
Hyperaemia is the local metabolically controlled increase in blood Functional/active hyperaemia is a physiological response occurring in, skeletal muscle during exercise brain in response to neuronal activity, heart in response to increased rate and GIT following meal. Reactive hyperaemia is a pathological response which follows a brief period of artery occlusion or tissue ischaemia an buildup of metabolites
38
Describe the main endocrine agents that alter vascular smooth muscle tone
adrenergic receptors evokes vasoconstriction when activated by agonists (adrenaline) / Vasopressin from hypothalamus - antidiuretic hormone which constricts blood vessels and raises blood pressure but also inhibits diuresis / Renin-angiotensin-aldosterone system - raises flow and BP as it causes vasoconstriction
39
Describe the anatomy of the barrier between blood and interstitial fluid
endothelial cells with tight junctions between each cell
40
What is the transcellular pathway?
Molecules travel through the cells, provides larger SA. It involves simple diffusion, facilitated diffusion and transcytosis
41
What is the paracellular pathway?
Molecules travel between the cells, provides smaller SA for transport. Involves simple diffusion through tight junctions between endothelial cells & bulk flow of solvent with solute which is driven by pressure difference
42
What are the physical factors governing the net movement of fluid between blood and IF?
plasma proteins, capillary walls
43
What is colloid osmotic pressure?
osmotic pressure exerted by proteins either in blood plasma or interstitial fluid
44
What is the role of colloid osmotic pressure in fluid balance?
colloid osmotic pressure generated by plasma proteins retains water in plasma, preventing it from continually flowing into extracellular space and is therefore important for fluid balance
45
What are the 3 types of capillaries?
continuous (tight), fenestrated (leaky) and discontinuous (very leaky)
46
What is oedema and what are the 4 main causes?
Fluid in the tissues. Caused by: high capillary pressure, low blood protein, lymphatic failure & capillary wall more porous to proteins
47
Give 4 types of oedema
swelling of skin following damage to local capillaries, ankle swelling (symptoms of heart failure), macular oedema , elephantiasis (mosquito borne disease found mainly in tropical areas )
48
How do particles and excess IF return to blood circulation?
via the lymphatic system, the main purpose of which is to drain excess fluid, protein, large particles and debris from the interstitial space and put it back into the blood. Fluid collected from interstitial space known as lymph and is carried into lymphatic vessels. Lymphocytes contained in lymph nodes, identify and destroy foreign particles and bacteria in lymph before it’s emptied into major veins at lymphatic ducts
49
Heart failure leads to what types of oedema?
peripheral and pulmonary
50
How does peripheral oedema occur?
left ventricular dysfunction, MAP falls due to smaller CO, reflexes triggered to restore MAP, salt and water retained, plasma volume increases, venous pressure decreases, capillary pressure increases, filtration is increased
51
How does pulmonary oedema occur?
left ventricular dysfunction, reduced ejection so blood normally ejected is left behind, blood backs up into left atrium, pulmonary veins engorged with blood and hydrostatic pressure increases, pulmonary capillary pressure increases, filtration reduced and build-up of fluid in lungs
52
What are the factors that regulate cardiac output?
heart size, ventricular contractility, duration of ventricular contraction, preload and afterload
53
What are preload and afterload?
preload is how stretched the ventricles are prior to conducting, the pressure in the left atrium at the end of diastole / Afterload is the pressure in the aorta during systole
54
Which factors affect preload?
venous blood pressure, venous return, heart rate, ventricular compliance and atrial contraction
55
Which factors affect afterload?
arterial pressure & aortic valve function
56
What is the role of vascular smooth muscle tone?
provide resistance to blood flow & reduced blood vessel volume / vascular tone refers to the degree of constriction experienced by a blood vessel relative to its dilated state
57
How is vascular smooth muscle tone regulated?
by intracellular calcium which causes contraction
58
What is the frank sterling law and what does the frank-sterling curve illustrate?
the relationship between cardiac output and venous return / as the myocytes stretch and preload increased stroke volume will also increase / the more the heart fills with blood during diastole the greater the force of contraction during systole
59
What is isometric relaxation?
when all 4 valves are closed and ventricles relax , ventricle pressure falls without changing volume
60
What is isometric contraction?
when muscle contracts but there is no movement, stays the same length
61
What is the difference between volumes during isometric relaxation and contraction?
stroke volume: volume pumped by left ventricle during systole
62
What is compliance?
measure of how easily a vessel stretches in response to internal pressure
63
How can blood vessels be arranged and which arrangement has lower total resistance?
series or parallel / parallel as lower total resistance
64
How is local control of blood exerted?
by vasoactive mediators released in tissues (metabolites from muscle contraction)
65
What is poseuille’s law?
vessel resistance is directly proportional to the length of the vessel and the viscosity of the blood / inversely proportional to r4
66
What are the major blood proteins and their roles?
Haemoglobin / albumin (helps buffer plasma pH, important carrier for lipophilic molecules with low solubility, binds many drugs ,lowering their free conc in plasma)/ fibrinogen (a precursor of blood clots) / globulin (broad class of proteins that include transferrin, clotting factors, hormones and carrier proteins, functions include transport, regulation of haematocrit and immune function)
67
What does haematocrit mean?
the haematocrit is the proportion of blood which consists of red blood cells usually by volume and resented as a percentage
68
What is anaemia and how is it diagnosed?
Anaemia is a disorder of blood which becomes less effective at carrying oxygen. Caused by low conc of Haemoglobin in blood and usually reduced haematocrit
69
What is haematopoiesis?
the process of forming new blood cells starting with pluripotent haematopoietic stem cells
70
How would you describe the homeostatic reflex regulating erythropoiesis
chemoreceptors detect decrease in blood oxygen levels in the kidney which causes the release of the hormone erythropoietin which then stimulates the production of RBCs from bone marrow. Myeloid progenitor cells (precursor for RBCs) differentiate into proerythroblast then erythroblast then normoblasts then reticulocytes then erythrocyte.
71
What is the composition of blood?
Plasma made of serum and clotting proteins, Buffy coat: other cells and red blood cells
72
What is haemostasis and what 4 events are triggered when a blood vessel is cut?
haemostasis is the prevention of blood loss and the 4 events are vasospasm, formation of platelet plug, blood coagulation and the formation of fibrous tissue
73
What is the average lifespan of leukocytes, erythrocytes and platelets?
leukocytes hours, erythrocytes 120 days and platelets 10 days
74
After the ages of 20 where is haematopoietic marrow found?
only in the bones of the sternum, vertebrae and pelvis
75
What is the difference between platelet activation and coagulation?
when activated, platelets clump together to form a plug them temporarily blocks the hole in blood vessel however in coagulation fibrin forms a net which traps platelets, blood cells and other molecules to form a fibrin network. It’s a more effective longer lasting solution than a platelet plug
76
What are the mechanisms that prevent harmful clotting?
dilution of clotting factors, tissue macrophage system remove activated factors from circulation, antithrombin preventing thrombin activation and generation of neutralizing factors

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