Muscles, circulation and respiration Flashcards
1
Q
What is the locomotive system?
A
- structures in an organism responsible for locomotion
2
Q
What do parts of locomotive system do?
A
- Muscles contract.
- Ligaments connect bones.
- Tendons connect muscles and bones.
3
Q
What is a hinge joint?
A
- a joint that can only move in one way
- ex. elbow, knee
4
Q
What are the muscles in the arm?
A
- bicep = flexor
- tricep = extensor
5
Q
What is a joint capsule?
A
- membrane surrounding joint
- synovial fluid can’t escape
- no friction between bones
- cartilage also helps
- no friction between bones
6
Q
What is an exoskeleton?
A
- skeleton outside of the body
7
Q
What is the role of bones?
A
- facilitate movement
- anchor for muscles
- levers: bones + joints + muscles
- bones joined by joints form an axis, muscles surrounding it apply force -> movement
8
Q
How does muscle attachment work?
A
- attachment to part of skeleton which doesn’t move
- another end of the muscle pulls bone to act as lever
- move part of the body
9
Q
How do antagonistic muscles work?
A
- pairs of muscles
- contraction of one = relaxation of second
- ex.: triceps (extends), biceps (flexes)
10
Q
What are the types of joints and their examples?
A
- hinge joint
- knee, elbow
- flexion and extension
- pivot joint when flexed
- ball-and-socket joint
- hip joint
- between pelvis and femur
- flex, extend, rotate, abduction (sideways), adduction (back)
- hip joint
11
Q
What is the structure of grasshoppers hindlimb?
A
- joint
- tibia (below the joint)
- tarsus (below the joint at the basis of tibia)
- femur (above)
- large muscles
12
Q
How do muscles work in grasshoppers leg?
A
- about to jump
- flexor muscle contracts
- tibia and taurus in Z
- femur and tibia closer
- extensor muscle contracts
- tibia extends
13
Q
What are 3 types of muscles?
A
- cardiac
- involuntary
- autonomic nervous system
- smooth
- involuntary & autonomic nervous system
- skeletal (striped)
- voluntary
- somatic nervous system
14
Q
What are myofibrils?
A
- parallel, elongated structures
- consist of myofilaments (actin and myosin)
- form dark and light bands
15
Q
How is sarcomere structured?
A
- basic contractile unit
- between 2 Z-lines (centre of light bands)
- centre of dark bands: M-line
- thick myofibrils and thin actin filaments
- actin attached to Z-lines
- myosin centre of sarcomere
- myosin + 6 actin filaments
- cross-bridges during muscle contraction
16
Q
What is the structure of a muscle fiber?
A
- single muscle cell = syncytium
- many nuclei
- precursors fuse to create one cell
- many nuclei
- cytoplasm full of myofibrils
- sarcoplasm (muscle cytoplasm)
- many mitochondria (ATP for contraction)
- sarcoplasmic reticulum
- storage of Ca2+ ions
- converts the signal to contract
17
Q
What happens during muscle contraction?
A
- myosin pulls actin filaments
- towards centre
- shorter sarcomere (and muscle fiber)
- myosin heads bind to sites on actin
- cross-bridges
- force (ATP)
- regularly spaced = a lot of pulling
- cross-bridges
18
Q
How is Ca2+ involved in muscle contraction?
A
- acetylcholine released from axon terminal
- binds to receptors on sarcolemma (muscle fibre plasma membrane)
- action potential travels to T tubule
- Ca2+ released from sarcoplasmic reticulum
- in response to change of voltage
- Ca2+ binds to troponin
- cross-bridges formed
- acetylcholinesterase acts (in synaptic cleft)
- Ca2+ back to SR
- tropomyosin binds active sites of actin
- cross-bridge detachment
19
Q
What is the role of troponin and tropomyosin?
A
- tropomyosin blocks binding sites of actin
- Ca2+ when released binds to troponin
- troponin changes conformation and pulls tropomyosin
- sites exposed for myosin
20
Q
How does sliding of filaments occur?
A
- myosin heads attach to actin sites
- ATP binds to myosin head
- cross-bridge broken (detachment)
- ATP –> ADP + P
- myosin heads change angle (they are cocked)
- storing potential energy from ATP
- myosin heads change angle (they are cocked)
- myosin heads attach to actin site further from the centre than previous one
- ADP and P released
- heads push actin inwards = power stroke
- cycle repeats
21
Q
What did William Harvey discover regarding blood system?
A
- blood in vessels
- too high pressure to be all around in body
- veins have valves preventing backflow
- unidirectional flow
- veins and arteries connected by capillaries
22
Q
What are the characteristics of systemic and pulmonary circulation?
A
- pulmonary (to lungs)
- oxygenates blood
- CO2 blood –> lungs –> O2 blood
- lower pressure (capillaries too delicate)
- systemic
- nutrients and oxygen to cells
- takes metabolic waste
23
Q
What are the steps of cardiac cycle?
A
- atrial systole
- atria contract (blood into ventricles)
- atrioventricular valves open
- ventricles relax
- pressure in arteries drops
- ventricular systole
- AV valves close
- ventricular pressure rises
- semilunar valves open (arteries low pressure)
- maximises arterial blood pressure
- atrial pressure drops
- semilunar valves open (arteries low pressure)
- ventricles relax
- pressure drops
- semilunar valves close
- diastole
- pressure in ventricles low
- AV valves open
- blood from veins into atria
- pressure in ventricles low
24
Q
What causes cardiac muscle contractions?
A
- heart does not use motor neuron to contract
- myogenic
- sinoatrial node
- small region of cells located in right atrium
- proteins that trigger contraction
- membrane depolarises and activates adjacent cells
- heart pacemaker (if deficient, an artificial is needed)
25
Q
How is atrial and ventricular contraction controlled?
A
- sinoatrial node sends signal
- gap junctions allow electric charges to flow freely between cells
- interconnections on atrial fibres allows for propagation
- fibres branched → signal branched
- rapid spreading
- time delay → signal gets to ventricles
26
Q
What characterises cardiac muscle?
A
- shorter and wider than skeletal
- one nucleus
- Y-shaped cells
- joined muscle fibres (interconnected cells)
- junction = intercalated disc
- gap junctions → connected cytoplasm
- movement of ions and low electrical resistance
- joined muscle fibres (interconnected cells)
27
Q
How is the delay in contraction of atria and ventricles caused?
A
- SA node —> atrioventricular (AV) node
- Purkinje fibres spread the signal
- fibres carrying signal from SA to AV nodes slowly
- 0.12 sec delay
- AV slower
- smaller in diameter
- reduced Na+ channels, more negative potential, longer refractory period
- fewer gap junctions
- more non-conductive tissue
- delay allows for atrial systole before AV valves close
28
Q
What happens after AV node received the signal?
A
- AV bundle receives the impulse (now has to be fast)
- left and right branch
- impulses through wall between ventricles
- connect at the apex to Purkinje fibres (contraction begins)
- Purkinje fibres spread to ventricles
- fewer myofibrils
- bigger diameter
- more Na+ channels + mitochondria + storage of glucose
29
Q
How is heart rate regulated?
A
- 2 nerves in medulla
- cardiovascular centre
- one nerve causes increase, the other decrease
- signal to sinoatrial node
- pH and oxygen levels control
- receptors in brain
- low blood pressure, pH and oxygen
- needs speeding up
- more carbon dioxide needs to be removed
- high pressure, oxygen and pH
- needs slowing down
30
Q
How do hormones control heart rate?
A
- epinephrine = adrenaline
- adrenal glands
- rises during vigorous activity
- fight or flight
- hunters, athletes (warm-up)
31
Q
What are the characteristics of arteries?
A
- thick walls
- small lumen
- high pressure
- collagen layers
- elastin fibres store energy during systole, release at diastole
- muscular
- go out of heart
- transport blood outside of heart
32
Q
What are characteristics of veins?
A
- thin walls
- large lumen
- blood to heart (atria)
- exception: portal vein (from stomach and intestine to liver)
- low pressure
- valves (prevent back flow)
33
Q
What is the structure of arterial wall?
A
- tunica externa
- connective tissue (most outer)
- tunica media
- smooth muscle and elastic fibres (elastin)
- thick layer
- tunica intima
- smooth endothelium (lining of artery)
34
Q
How is blood pressure measured?
A
- systolic – during ventricular systole (contraction)
- diastolic – during ventricular diastole
- blood occlusion
- blocking of blood flow
- systolic pressure
- higher, yes pulse
- diastolic pressure
- lower, no pulse
35
Q
What is arterial occlusion?
A
- atherosclerosis
- fatty tissue (atheroma) in artery wall
- LDL accumulate
- phagocytes engulf it
- once they die, form a plaque
- stiff walls, low resistance = low blood pressure
- older people affected
36
Q
What is coronary occlusion and its consequences?
A
- narrowing of coronary arteries
- supply blood to the heart
- pain = angina
- no ability to contract
- faster heart beat
- fibrous cap on atheromas rupture
- blood clot block arteries
- causes: high LDL and glucose levels, high blood pressure, smoking, trans fats damage endothelium, Chlamydia pneumoniae
37
Q
What are characteristics of capillaries?
A
- connect arterioles and venules
- single endothelial cells
- easier substance exchange
- short diffusion distance
- easier substance exchange
- 10µm diameter
- branched (high surface area)
- slow blood flow
- increases time for diffusion
- control of substance transported
- tight junctions and pores (plasma leaks out)
38
Q
What is the structure of valves in veins?
A
- three cup-shaped flaps of tissue
- blood flowing backwards is stopped
- blood towards the heart pushes valves to the sides
- one-way flow
39
Q
What causes heartbeat sounds?
A
- AV closes = lub
- ventricles empty —> semilunar valves close = dub
40
Q
How do artificial pacemakers work?
A
- malfunctioning sinoatrial node
- maintains rhythm (not fast, fault in electrical system)
- not detected heartbeat = starts working
41
Q
What does ECG represent?
A
- contraction due to electrical signal (can be measured)
- heart pathology
- first wave (P) = atrial systole
- highest peak (QRS complex) = ventricular systole
- height of R wave compared: standing / lying
- third wave (T) = ventricular diastole
- measured before and after mild exercise
42
Q
How is defibrillator used?
A
- cardiac arrest = reduced blood supply to heart
- no O2
- result: ventricular fibrillation
- chaotic contractions
- diagonal line between paddles
- heart in the middle
- electric discharge given off if there’s fibrillation
43
Q
What are the causes and consequences of thrombosis?
A
- blood clot blocks blood flow
- myocardial infarction / heart attack
44
Q
What are the causes and consequences of hypertension?
A
- resistance to flow of blood —> slows down
- more pressure on arterial walls
- narrow and stiff arteries
- walls weaken = bulge forms (aneurysm)
- can burst
- stroke – weak blood vessels (leak)
- kidney failure
45
Q
What are factors contributing to thrombosis and hypertension?
A
- family history of heart attacks
- age
- post-menopause risk
- low oestrogen (males at risk)
- smoking —> increase in blood pressure
- high-salt diet
- saturated fats and cholesterol
- height
- sedentary lifestyle (no exercise)
46
Q
What is the path of air entering the body?
A
nasal passage / oral cavity —> larynx —> pharynx —> trachea (cartilage wall keeps it open no matter pressure) —> bronchi (cartilage) —> bronchioles (smooth muscle tissue) —> alveoli
47
Q
What happens during inspiration?
A
- external intercoastal muscles contract
- rib cage opens
- diaphragm contracts
- volume increases (pressure decreases)
- air goes from high to low pressure
48
Q
What happens during expiration?
A
- exhalation is passive
- internal intercoastal muscles contract (only during deep exhalation)
- rib cage closes
- diaphragm relaxes
- volume decreases (higher pressure)
- air out
49
Q
How is ventilation monitored?
A
- ventilation rate = number of times air is drawn in or expelled / minute
- tidal volume = volume of air drawn
50
Q
What are the causes of lung cancer?
A
- smoking (87%)
- mutagenic chemicals
- passive smoking (3%)
- air pollution (5%)
- diesel fumes, nitrogen oxides, burning coal
- radon gas (radioactive from granite)
- asbestos, silica and other solids (dust)
51
Q
What are the consequences of lung cancer?
A
- difficulties breathing, coughing (even blood)
- chest pain
- loss of appetite, weight loss, fatigue
- high mortality if metastatic
- chemo and radiotherapy
52
Q
What are the causes of emphysema?
A
- smaller number of air sacs with thicker walls
- surface area down
- distance of diffusion greater
- less elasticity
- phagocytes produce elastase to kill bacteria in vesicles
- enzyme inhibitor A1AT prevents elastase from digesting alveoli
- genetic factor
- smokers have more phagocytes
- enzyme inhibitor A1AT prevents elastase from digesting alveoli
- chronic disease
- lack of energy
53
Q
How does gas exchange work?
A
- diffusion between air in alveoli and blood in capillaries
- air in alveolus: higher oxygen, lower CO2
- maintaining gradient
- stale air out, new in = ventilation
54
Q
What are the characteristics of type I pneumocytes?
A
- a lot of alveoli with large surface area
- alveoli built of epithelium
- most, type I pneumocytes
- capillary also from epithelium
- small distance of diffusion
55
Q
What are characteristics of type II pneumocytes?
A
- 5% of alveolar surface area
- secrete fluid (with surfactant)
- oxygen in alveolus dissolves and diffuses
- CO2 can evaporate and be exhaled
- similar to phospholipids
- hydrophilic heads facing water hydrophobic tails air
- reduction of surface tension
- prevents water from causing walls to adhere and collapse
56
Q
What do oxygen dissociation curves represent?
A
- haemoglobin – protein transporting oxygen
- degree of binding is determined by partial pressure of oxygen (pO2)
- difference in pO2 = concentration gradient
- oxygen curve shows saturation of haemoglobin
- at low pO2 → few heme bound to oxygen
- at high pO2 → more heme groups bind, making it easier
- small change in structure
- in low oxygen, oxygen is released
57
Q
What is the difference between haemoglobin and myoglobin?
A
- myoglobin has higher oxygen affinity at low pO2
- oxygen released from heme attaches to myoglobin
- more sensitivity for workouts
- binds one oxygen only
58
Q
What is the difference between foetal and adult haemoglobin?
A
- higher affinity for O2
- O2 is transferred to foetus from maternal blood across placenta
59
Q
What are the consequences of altitude on gas exchange?
A
- low pO2 in air
- haemoglobin not fully saturated, less oxygen in tissues
- red blood cells production increases
- ventilation rate increases
60
Q
What is the treatment for emphysema?
A
- cannot be cured —> prevention
- oxygen administering equipment
- breathing techniques
61
Q
How is carbon dioxide transported?
A
- dissolved as CO2
- converted to bicarbonate ions (HCO3-) dissolved
- less toxic
- in red blood cells (catalysed by carbonic anhydrase)
- reversible
- in tissues more HCO3- = lower pH
- in lungs back to CO2
- bound to plasma proteins
62
Q
What is the Bohr shift?
A
- increased metabolism = more CO2 released in blood
- lower pH
- acidic environment, shifts curve to right
- greater release of oxygen by haemoglobin
- O2 released when needed
- in lungs pCO2 lower (more oxygen binds)
63
Q
How is pH of blood controlled?
A
- usually between 7.35 - 7.45
- if lower
- chemoreceptors signal to respiratory centre
- hyperventilation (more CO2 out)
- if higher
- bicarbonate secreted in kidney
- buffers work
64
Q
How is ventilation rate controlled?
A
- respiratory centre
- medulla oblongata
- 2 sets of nerves: intercoastal, phrenic (diaphragm)
- lungs stretch —> signal sent by stretch receptors
- inspiration + new signal
65
Q
What is the role of chemoreceptors?
A
- in carotid artery and aorta
- sending signal to breathing centre (medulla oblongata)
66
Q
How does CO2 changes ventilation rate?
A
- more metabolism = more CO2
- pH low
- increase in ventilation rate
- expelling CO2 in alveoli (hyperventilation)
