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Biology HL > Muscles, circulation and respiration > Flashcards

Muscles, circulation and respiration Flashcards

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1
Q

What is the locomotive system?

A
  • structures in an organism responsible for locomotion
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2
Q

What do parts of locomotive system do?

A
  • Muscles contract.
  • Ligaments connect bones.
  • Tendons connect muscles and bones.
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3
Q

What is a hinge joint?

A
  • a joint that can only move in one way
    • ex. elbow, knee
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4
Q

What are the muscles in the arm?

A
  • bicep = flexor
  • tricep = extensor
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5
Q

What is a joint capsule?

A
  • membrane surrounding joint
  • synovial fluid can’t escape
    • no friction between bones
      • cartilage also helps
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6
Q

What is an exoskeleton?

A
  • skeleton outside of the body
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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
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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
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9
Q

How do antagonistic muscles work?

A
  • pairs of muscles
    • contraction of one = relaxation of second
    • ex.: triceps (extends), biceps (flexes)
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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)
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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
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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
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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
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14
Q

What are myofibrils?

A
  • parallel, elongated structures
  • consist of myofilaments (actin and myosin)
    • form dark and light bands
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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
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16
Q

What is the structure of a muscle fiber?

A
  • single muscle cell = syncytium
    • many nuclei
      • precursors fuse to create one cell
  • cytoplasm full of myofibrils
  • sarcoplasm (muscle cytoplasm)
    • many mitochondria (ATP for contraction)
  • sarcoplasmic reticulum
    • storage of Ca2+ ions
    • converts the signal to contract
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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
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18
Q

How is Ca2+ involved in muscle contraction?

A
  1. acetylcholine released from axon terminal
    • binds to receptors on sarcolemma (muscle fibre plasma membrane)
  2. action potential travels to T tubule
  3. Ca2+ released from sarcoplasmic reticulum
    • in response to change of voltage
  4. Ca2+ binds to troponin
    • cross-bridges formed
  5. acetylcholinesterase acts (in synaptic cleft)
  6. Ca2+ back to SR
  7. tropomyosin binds active sites of actin
    • cross-bridge detachment
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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
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20
Q

How does sliding of filaments occur?

A
  1. myosin heads attach to actin sites
  2. ATP binds to myosin head
    • cross-bridge broken (detachment)
  3. ATP –> ADP + P
    • myosin heads change angle (they are cocked)
      • storing potential energy from ATP
  4. myosin heads attach to actin site further from the centre than previous one
  5. ADP and P released
    • heads push actin inwards = power stroke
  • cycle repeats
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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
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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
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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
  • ventricles relax
    • pressure drops
    • semilunar valves close
  • diastole
    • pressure in ventricles low
      • AV valves open
    • blood from veins into atria
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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)
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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
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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
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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
  1. blood occlusion
    • blocking of blood flow
  2. systolic pressure
    • higher, yes pulse
  3. 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
  • 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
  • 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)

Biology HL (14 decks)

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