Physiology - Exam and 2 Flashcards

1
Q

How do cells communicate directly?

A

a) Juxtacrine – involves physical contact between cells involved. Trans membrane proteins and phospholipids. Signal cannot diffuse away. The signaling cell does so via membrane-bound signal molecules.
b) Gap Junctions - also involves physical contact. Specialized intercellular connection directly connects the two cytoplasms and allows free passage for molecules./ions.

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2
Q

How do cells communicate via ECF?

A
  • Autocrine (cell signal to itself)
  • Paracrine (cell signal over short distance)
  • Endocrine (hormone signal via blood stream)
  • Neuronal – long distance, target is nerve, muscle or gland. Noradrenaline and acetylcholine.
  • Neuroendocrine – combo. Neuron secretes hormone into blood.
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3
Q

In phys, what is haemostats?

A

maintenance of the extra cellular fuild

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4
Q

What are the fluid compartments?

A
  1. Extracellular Fluid (35%) (in-between cell and capillary)
    i. Interstitial Fluid (25%)
    ii. Blood plasma and lymph (8%)
    iii. Trans-cellular fluid (2%) (water in epithelial lined spaces)
  2. Intracellular Fluid (65%)
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5
Q

What separates the intracellular fluid from the interstitial fluid?

A

Cell membrane

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6
Q

What separates the interstitial fluid from plasma?

A

Capillary membrane

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7
Q

What are the main components of extracellular fluid?

A
  • Na+
  • Cl-
  • HCO3-
    There are only small amounts of K+, protein anions and ‘other’.
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8
Q

What are the main components of intracellular fluid?

A
  • K+
  • PO43-
  • Protein Anions
    There are only small amounts of Na+ and ‘other’.
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9
Q

What is a feed forward control?

A

An anticipatory alteration of effectors independent of feedback. There is adaptive control (I,e, system learns how to control ball throwing) and anticipatory control (or predictive homeostasis, i.e. increasing cardiac function in anticipation of exertion).

I.e. no negative/positive feedback necessary

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10
Q

What is the baroreceptor reflex?

A

If BP decreases, baroreceptors in the arch of aorta and carotid sinus are stretched less, and there is a decreased rate of nerve impulses. This info is relayed to the brain, which will increase sympathetic simulation, increased secretion of adrenaline and noradrenaline. This will increase heart stroke volume and heart rate, leading to increased cardiac output. There will also be constriction of blood vessels, which increases systemic vascular resistance. These factors lead to increased blood pressure and homeostasis is maintained.

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11
Q

How is plasma glucose controlled?

A

If high - insulin
If low - glucagon

If it is too high, pancreas will release insulin into blood and cells can use glucose as energy or convert it into glycogen, and liver will convert glucose to glycogen as well. Blood glucose levels drop and homeostasis in maintained.
If it is too low, pancreas will release glucagon into blood and so liver will convert glycogen into glucose, which raises blood glucose levels and homeostasis is maintained.

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12
Q

What is an example of positive feedback?

A

Oxytocin in childbirth

  • Head of fetus pushes against cervix
  • Nerve impulses from cervix transmitted to brain
  • Brain stimulates pituitary gland to secrete oxytocin
  • Oxytocin carried in blood stream to uterus
  • Oxytocin stimulates uterine contractions and pushes fetus toward cervix, when restarts the cycle
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13
Q

What causes cystic fibrosis?

A

A defective gated Cl- membrane transport protein (cystic fibrosis trans membrane conductance regulator (CFTR)) results in cells not being able to get rid of Cl- fast enough, so too much water is let in. The cells can’t regulate Cl- secretion and so mucus becomes excessively thick.

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14
Q

What are the transport processes across membranes?

A
  1. Simple Passive.
    i. through lipid bilayer
    ii. Through protein channels
  2. Carrier Mediated
    i. facilitated diffusion
    ii. Active transport
  3. Exo/Endocytosis
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15
Q

What determines diffusion of ions across a membrane in simple passive diffusion?

A

[Rate of solute movement =PΔC]. P is permeability coef. and ΔC is concentration gradient.

Diffusion of ions is determined by:

  • membrane permeability
  • concentration gradient
  • voltage gradient
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16
Q

What is Osmolarity?

A

Per L

The concentration of a solution expressed as the total number of solute particles per litre. Water moves from low to high.

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17
Q

What is Osmolality,

A

Per Kg

Whereas osmolality (with an “ℓ”) is a measure of the osmoles (Osm) of solute per kilogram of solvent

1 Osmole/L = 22.4 atmospheres of pressure

Total osmolality includes all dissolved solutes and must take dissociation into account.

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18
Q

What is Tonicity?

A
  • Hypotonic solution – cell lysis (explodes)
  • Isotonic – normal (same osmotic pressure against membrane)
  • Hypertonic – shriveled
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19
Q

What is the difference between leak and gated channels?

A

i. always open – leak channels

ii. open or closed – gated channels

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20
Q

What do all carrier-mediated transport forms show?

A
  • specificity of solute binding

- saturation of transport rate at high concentrations of solute.

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21
Q

What are the two types of carrier-mediated transport?

A

a) Uniport – 1 solute transported

b) Cotransport – transport of one solute is coupled to that of another
i. Symport – same direction
ii. Antiport – opposite directions

NOTE: can still be passive

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22
Q

What is the difference between chive and passive transport?

A

The difference between active and passive is whether energy input is required or whether particle is simply moving down chemical/electro gradient. Active transport channels are ‘pumps’

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23
Q

Is Na/K an active or passive pump?

A

Active.

Against their electrochemical gradients.

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24
Q

How does active transport get its energy?

A

Active transport derives its energy from hydrolysis of ATP, therefore it needs metabolism.

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25
Q

What are the types of endocytosis?

A
  • fluid phase (literally just taking a bit out of the ocean around it – more random)
  • receptor-mediated (more specific)
  • phagocytosis (i.e. getting rid of bacteria – unique to specialized phagocytic cells)
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26
Q

What are the types of exocytosis?

A
  • constitutive secretory pathway (unregulated)

- Regulated secretory pathway

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27
Q

How is the rate of passive diffusion calculated?

A

ΔS/Δt = -D(ΔC/Δx) (Fick’s Law)

Means: rate of passive diffusion (net flow of solute) = proportionality constant (D) x concentration gradient at a point.

D and Δx are combined to form the permeability coefficient P.
Therefore, Net flow of Solute = -PΔC

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28
Q

What is the permeability coefficient governed by?

A
  • size and shape of molecule
  • lipid solubility
  • electrical charge
  • ability to form H-bonds (hydrophilic)
  • chemical structure of molecule and cell membrane
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29
Q

What factors need to be taken into account when determining the effective osmotic pressure difference?

A
  1. The total concentration of dissolved solutes = osmolarity (total number of moles of particles/L =Osmoles/L) or osmolality (Osmoles/kg).
    NOTE: Total osmolarity of typical ICF/ECF is about 300mOsmoles/L in mammals.
  2. Degree of dissociation of each dissolved solute – a solution of 100mmole/L with complete dissociation will have osmolarity of 200mOsmoles/L.
  3. Permeability of the membrane to each substance.
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30
Q

What is the equivalent hydrostatic pressure?

A

the equivalent hydrostatic pressure for a given osmolality difference across a membrane:

RULE OF THUMB: 1 Osmole/L difference = about 22.4 atmospheres (or 22.4 x 760 mmHg) of hydrostatic pressure.

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31
Q

How is the effective effective osmotic pressure difference calculated?

A

Effective Osmotic Pressure Diff (mm of Hg) = (reflection coefficient) x RTΔϕ (Vant Hoff Equation)

Δϕ is the osmolality difference calculated as per factors above.

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32
Q

What is the difference between tonicity and osmolarity?

A

Solutions can have same osmolarity (iso-osmolar) but different tonicity, leading to water flow. This is because of membrane impermeability.

Osmolarity is the total concentrations of solutes, penetrating and non-penetrating. Tonicity is only the concentration of non-penetrating solutes.

Say two solutions are 300mOsmoles/L (normal), but one solution (ECF) contains a solute that is not in the ICF but membrane is impermeable to it. Although there is a large concentration gradient, impermeability means it won’t move into the cell. The concentration of solutes will remain the same and water won’t move – ISOTONIC.

BUT if another solution contains a solute that is not in the cell but can get into the cell, it will diffuse into the cell due to the concentration gradient. All other concentrations staying the same, the ICF will now have more total solute particles than the ECF (although that PARTICULAR solute will have equal concentrations across both). Therefore water will flow into the cell. HYPOTONIC. This process will continue until membrane ruptures, expelling contents into surroundings = LYSIS.

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33
Q

How can haemolysis be detected?

A

When RBC’s are intact, they scatter light so that cell suspension look cloudy. When they are lysed, they release their contents and are ghosts – no longer scatter light and suspension looks clear but often reddish (as they have lost their contents into the solution).

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34
Q

What did NaCl solution of low osmolarity cause?

A

When NaCl solution (ECF) had osmolarity much less than ICF (20m and 100m), the suspension looked clear because lysis had taken place. Cell is only partially permeably to Na+ and Cl-, so concentrations stayed higher in cell. Water flowed into cell until membrane ruptured– it was a hypotonic solution.

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35
Q

What is Osmotic Fragility ?

A

an index of the susceptibility of lysis of RBC’s. Can be used in diagnostic measurements of conditions in which RBC membrane structure, or its fragility, is altered.

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36
Q

From the prac, what was the time taken to achieve lysis?

A

At point where edges of light are clearly visible, 75% of RBC’s have lysed.

Solute a: Urea – mean hemolysis time = 11.4s
Solute b: Ethylene Glycol – 17.8s

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37
Q

Why do urea and ethylene glycol have different times to achieve lysis?

A

Urea has lower molecular weight which means RBS membrane is more permeable to it, but EG has much greater Kether value which is an index of lipid solubility, indicating it may be more permeable. But there are many more factors affecting permeability not taken into account.

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38
Q

What are the main cations in Plasma and interstitial fluid, and intracellular fluid?

A

Plasma and interstitial:
Na+
Tiny amounts of K+

Intracellular:
K+
Tiny amounts of Na+

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39
Q

What are the main anions in Plasma and interstitial fluid, and intracellular fluid?

A

Plasma and interstitial:

  • Cl-
  • HCO3-
  • Protein anions (plasma only)

Intracellular:

  • PO43-
  • protein anions (> than plasma)
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40
Q

What does a Na/K-ATPase pump move?

A

3Na+ out
2K+ in

Therefore makes cell more negative

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41
Q

Compare the diffusional vs electrical forces of K, Cl, Na and Ca across a cell membrane.

A

K has diffusional forces going outside cell, but electrical forces going inside sell. Cl is the opposite. Na and Ca have both diffusional and electrical pressure towards inside of cell.

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42
Q

Why does some K leak back out?

A

Asymmetric ion distribution is established/maintained by active transport – 3Na out, 2K in. But K+ has leak channels – membrane is 50-75x more permeable to K than Na, so K also leaks back out.

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43
Q

What are the types of ion channels?

A
  1. Leak channels (always open)
  2. Ligand-gated channels (open or shut when bound by specific chemical messenger)
  3. Voltage-gated channels (open/close as a specific membrane potential)
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44
Q

What are the passive membrane properties of Na and K?

A
  • influx of Na causes depolarization

- efflux of K causes hyperpolarization

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45
Q

What is an action potential?

A

an active electrical excitability, with positive feedback after the threshold value is exceeded. It does not diminish over distance.

When the membrane potential reaches threshold value, a positive feedback response is triggered and the membrane potential shoots up and becomes positive.

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46
Q

What is the step by step mechanism of an action potential?

A
  1. When we receive a stimulus (i.e. loud bang), SOME voltage-gated Na channels open up and we get some further depolarization (i.e. MP becomes less negative and moves towards threshold).
  2. If threshold is exceeded (-55mV), ALL voltage-gated Na channels open and Na flows in very quickly due to both concentration and electrical forces. This is the positive feedback step, and results in a spike in MP (now is highly +ve compared to ECF).
  3. At the peak of the curve, Na channels shut once cell reaches a certain MP and voltage gated K channels open.
  4. K floods out of cell down electrochemical gradient causing repolarization.
  5. As K channels are slow to close, the ICF becomes more negative than at rest.
  6. After repolarization, there is low K in cell and Na is being pumped out. Concentrations have switched.
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47
Q

What is the refractory period?

A
  • Na channels now closed
  • Absolute refractory period – neuron cannot be made to reach AP and all Na channels are inactivated
  • Relative refractory period – neuron can generate AP, but requires greater stimulus. Some Na channels are re-activated.
  • After Action potential, neurons need to recover – need to re-establish polarization and Na/K-ATPase pumps Na out and K in.
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48
Q

How do electrical events pass from cell to cell?

A
  1. Synaptic transmission (travelling AP)
  2. Direct Electrical Transmission (rare – cardiac and some smooth muscle)
  3. Chemical Mediator – common. Nerve and muscle, nerve and nerve - neurotransmitters
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49
Q

What is the difference between electrical and chemical synapses?

A

Electrical Synapses - AP travels through gap junctions between presynaptic and postsynaptic neurons.

Chemical Synapses – neurotransmitter molecules cross the synapse and signal the postsynaptic neuron by binding receptors and inducing change. (Need to know about noradrenaline and acetylcholine)

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50
Q

What is the difference between an excitatory and inhibitory post synaptic potential?

A

Excitatory post synaptic potential (EPSP):

  • depolarize membrane (more +ve, as above)
  • open some Na channels
  • Increase probability of AP (depends on whether MP depolarizes enough to reach threshold MP)

Inhibitory post synaptic potential (IPSP)

  • hyperpolarize membrane (more –ve)
  • open some Cl channels
  • Decreased probability of AP
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51
Q

What are the results of the sympathetic nervous system?

A
  • Increased HR and cardio output (CO)
  • Constriction of arteriolar and venous smooth muscle (increased BP)
  • Respiratory airways open (relaxation of airway smooth muscle)
  • Break down of glycogen in liver and muscle and adipose tissue to increase concentration of plasma glucose and FFA.
  • Skeletal muscle blood vessels dilate to increase blood flow
  • Pupils dilate and adjust for far vision
  • Digestive and urinary activities are shit down
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52
Q

What are the results of the parasympathetic nervous system?

A
  • Increased gut activity
  • Emptying of urinary bladder
  • Rapidly slow down activities enhanced by sympathetic stimulation
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53
Q

What are the exceptions to this?

A

S and PS are not always antagonistic to each other. Examples:
- Salivary glands – stimulated by both

Some organs don’t receive dual intervention. Examples:

  • Sweat Glands (S)
  • Blood vessels (S) – except penis and clitoris
  • Sympathetic tone
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54
Q

What parts of the CNS regulate the ANS?

A
  • Cerebral cortex (has influence)
  • Hypothalamus – (hunger, thirst, major visceral motor control centre)
  • Midbrain, pons and medulla (cardiac and vasomotor control, salivation, swallowing, sweating, bladder control and pupillary changes)
  • Spinal cord reflexes (defecation and micturition reflexes, but brain can consciously inhibit these responses)
55
Q

Describe the neural pathways of the somatic NS and ANS.

A
  1. Somatic nerve goes from CNS to effector organ, uses Ach
  2. ANS – Parasympathetic nerve has 2 neurons. The second is post ganglion neurotransmitter and always uses Ach. Both pre and post ganglionic neuron are cholinergic (use ACh).
  3. ANS – Sympathetic NS has two options:
    - 1 – 2 nerves. The first uses Ach and the second NE
    - 2 – 1 nerve (Ach) and then bloodstream (neuroendocrine). The nerve uses Ach and then neurotransmitter (i.e. epi) is sent to effector organ via bloodstream.
    The first nerve is always cholinergic, but the second is adrenergic (noradrenaline) or cholinergic (acetylcholine).
    - ANS ganglions closer to CNS
56
Q

Where to the PSNS and SNS connect to the CNS?

A

PSNS connects to cranio-sacral division of spine/chord and its ganglions are fairly far.

SNS connects to the thoraco-lumbar division and has ganglion close to start.

57
Q

What are NANC neurotransmitters?

A

non-adrenergic non-cholinergic. I.e. ATP, nitric oxide, VIP, GRP, other peptides.

58
Q

What does noradrenaline do?

A

Causes constriction in most vascular smooth muscle, but causes relaxation of vascular smooth muscle in skeletal muscles and relaxation of bronchial smooth muscle (because somatic = flight or fight). The reason for this is noradrenaline has 5 different receptors, and the effect will depend on the receptor.

59
Q

What are the two types of Acetylecholin receptors?

A

a) muscarinic (excitatory or inhibitory)

b) nicotinic (excitatory).

60
Q

What are the adrenergic receptors?

A

a1 - vascular smooth muscle - contract

a2

b1 - heart - increased heart rate and force

b2 - smooth muscle - relax

b3

61
Q

What do the nicotinic receptors do?

A

activate post g nerve

62
Q

What do the muscarinic receptors do?

A

m1

m2 - heart - decrease heart rate

m3 - smooth muscle and glands - contract and secrete

63
Q

How do drugs work on the ANS?

A

They work by mimicking or blocking the effects of the two primary neurotransmitters – Ach and A/NA:

  • Receptor Agonists – stimulated, active receptors
  • Receptor Antagonists – block receptors
64
Q

How does myosin crawl along actin?

A
  1. ATP binds to myosin head (on ATPase), which is attached to surface of actin. Myosin ‘head’ then ‘releases’ actin.
  2. ATP goes to ADP + P + energy with help of ATPase. ‘Cocks’ myosin protein to high-energy conformation (like a spring loaded position), which means head aligns itself next notch along actin.
  3. P released from Myosin, releasing energy myosin has in ‘cocked’ position (like releasing a spring), and causes myosin to push on actin filament. Therefore it effectively can crawl along actin.
  4. ADP released which brings us to back to start.
65
Q

How to Tropomyosin and Troponin help regulate muscle contraction?

A
  • Tropomyosin protein is coiled around actin, and it is attached to actin by Troponin. When muscle isn’t contracting, tropomyosin blocks myosin from being attached to actin where it usually attaches, or keeps it from moving – i.e. doing its walking procedure.
  • Only way to unblock this process is for the Troponins nailing down tropomyosin to change their conformation. The only way troponins do this is if we have a HIGH concentration of Ca2+ ions. The Ca2+ ions bind to troponin and change it’s conformation, and tropomyosin is therefore moved out of the way.
  • If concentration of Ca2+ ions becomes really low, troponin releases them and goes back to standard conformation, and so tropomyosin can block myosin again and muscle will relax.

a) High concentration of Ca2+ ions = contraction
b) Low concentration of Ca2+ ions = relaxation

66
Q

What is a sarcolemma?

A

cell membrane of a striated muscle fiber

67
Q

What are the key components to a sarcomere?

A
  • Myosin
  • Actin + tropomyosin (strand) + troponin
  • Titin holds myosin in place
  • a-Actin holds actin in place
  • Z line
  • M line
  • I zone
  • H zone
  • A zone

I and H zone move during contraction

A sarcomere is a structural unit of a myofibril in striated muscle, consisting of a dark band and the nearer half of each adjacent pale band.

68
Q

What is a T-tubule?

A

Tubule in surface of muscle membrane

69
Q

What is the sarcoplasmic reticulum and how does it work?

A

Organelle inside muscle. Main function is storage.

  1. It has Ca ion pumps on membrane (which are ATPases). Ca ion will attach to pump, and when ATP hydrolizes, the Ca ion is pumped in.
  2. As a result, resting muscle will have a very high concentration of Ca ions on the inside of Sarcoplasmic reticulum.
  3. When muscle need to contract, Ca ions get dumped back out into cytoplasm of muscle cells, which can then bond to the troponin, moving the tropomyosin out of the way and allowing myosin to move.
70
Q

What are the main features of cardiac muscle?

A

Nucleus: Single
Striated: Y
Voluntary: N
Other features: Fibers branch and are interconnected by intercalated discs

71
Q

What are the main features of smooth muscle?

A

Nucleus: Single
Striated: N
Voluntary: N
Other features: Lines internal structures. Small, elongated spindle shaped cells.

72
Q

What are the main features of skeletal muscle?

A

Nucleus: Many
Striated: Y
Voluntary: Y

73
Q

What is a monocyte?

A

Muscle cell = ‘muscle fiber’ (NOT fibril)

Myocytes are made up of myofibrils, which are tubular protein chords found in muscle fibers that appear striated under microscope, and are the contractile fibers in muscle tissue.

74
Q

What is the cytoplasm in a muscle cell called?

A

Sarcoplasm

75
Q

What are the anatomical features of a muscle?

A

Connected to periosteum of bone via tendon.

Coverings:

a) Endomysium - covers each myocyte
b) Perimysium - binds myocytes together into a fascicle
c) Epimysium - bings fascicles together into a muscle

76
Q

What is muscle tension?

A

Proportional to the number of actin-myosin cross bridges (i.e. amount of overlap).

77
Q

What is the length-tension curve?

A

Sarcomere length vs tension

As sarcomere shortens, tension increases to the point where all myosin heads are touching actin.

Peak tension maintained from where all myosin heads touching to where actin meets up with itself.

As actin filaments overlap, tension decreases even though sarcomere length is still shortening.

78
Q

What is the passive force of a muscle?

A

due to passive recoil of muscle filaments where actin and titan act as rubber bands.

79
Q

What is the active force of a muscle?

A

due to sarcomere shortening

80
Q

What is the relationship between active and passive muscle force?

A

length-tension

At first peak (as length increases), active tension is predominant and maximal overlap of sarcomeres is reached. Active tension then starts to drop, but passive tension increases causing total tension to increase again.

Total force = active + passive

81
Q

What is excitation-contraction coupling?

A

Excitation–contraction coupling is the process by which a muscular action potential in the muscle fiber causes the myofibrils to contract.

Note: latent period

82
Q

What is a motor unit?

A

Each muscle fiber has only one neuromuscular junction, but each motor neuron may have many muscle fibers. A motor unit is a single motor neuron and the multiple muscle fibers that it innervates. Motor end plate is also called synapses. If you want something to have fine muscle control (I.e. eye muscles – rectus lateralis), then you want as little myofibres per motor unit, as opposed to ones where you don’t need fine control, i.e. gastrocnemius.

83
Q

What is motor-unit recruitment?

A

More/different motor units can be recruited for different tasks. Motor unit recruitment is a measure of how many motor neurons are activated in a particular muscle, and therefore is a measure of how many muscle fibers of that muscle are activated. The higher the recruitment the stronger the muscle contraction will be.

84
Q

What are the 3 main skeletal muscle fibre types?

A
  • Type I – SO – Slow contracting, fatigue resistant, low strength
  • Type IIa – FO – Fast contracting, fatigue resistant, high strength
  • Type IIb – FG – Fast contracting, fast fatigue, highest strength, and also the largest. Myosin ATPase activity is the fastest here.

O = oxidative, meaning cell can supply their own fuel. G is glycolytic, which means cell can’t supply it’s own fuel for very long but it is very fast.

85
Q

How does a motor neurone cause a contraction?

A

An action potential in a motor neuron triggers the release of acetylcholine from its terminal. Acetylcholine then diffuses onto the muscle fiber’s plasma membrane (or sarcolemma) and binds to receptors in the motor end plate, initiating a change in ion permeability that results in a graded depolarization of the muscle plasma membrane (the end- plate potential). Events eventually land up in contraction, and the entire process is called excitation-contraction coupling.

86
Q

What is a twitch?

A

Mechanical response to a single action potential. It has three phases:

  1. Latent Period
  2. Contraction Phase (ends when muscle tension peaks)
  3. Relaxation phase (peak tension until end)
87
Q

What happens as we increase the voltage that triggers a twitch?

A

The active force increases (motor unit recruitment) but the latent period stays the same.

88
Q

What is muscle tension?

A

Tension = muscle force. The force generated by a whole muscle reflects the number of active motor units at a given moment, with each unit developing maximal tension.

89
Q

How does motor unit recruitment increase muscle force?

A

It increases the number of active motor units.

90
Q

What is the threshold voltage?

A

the smallest stimulus required to induce an action potential in a muscle fibre’s plasma membrane, or sarcolemma. As more voltage is delivered, more fibers are activated.

91
Q

What is maximal tension?

A

Maximal tension in the whole muscle occurs when all the muscle fibers have been activated by a sufficiently strong stimulus (referred to as the maximal voltage).

92
Q

What happens as we increase the voltage (not in terms of a twitch - constant)?

A

At first, as we increase voltage the active force remains at 0 until threshold voltage is reached. Then, as we increase voltage, the active force increases at a decreasing rate, and then plateaus (maximal tension).

93
Q

What is treppe?

A

Treppe is the progressive increase in force generated when a muscle is stimulated in succession, such that muscle twitches follow one another closely, with each successive twitch peaking slightly higher than the one before. Step-like increase. For the first few twitches, each successive twitch produces slightly more force than the previous twitch as long as the muscle is allowed to fully relax between stimuli and the stimuli are delivered relatively close together.

94
Q

What is wave summation?

A

When a skeletal muscle is stimulated repeatedly, such that the stimuli arrive one after another within a short period of time, muscle twitches can overlap with each other and result in a stronger muscle contraction than a stand-alone twitch. Wave summation occurs when muscle fibers that are developing tension are stimulated again before the fibers have relaxed. Thus, wave summation is achieved by increasing the stimulus frequency. Wave summation occurs because the muscle fibres are already in a partially contracted state when subsequent stimuli are delivered.

95
Q

What will happen as you increase frequency of stimulus?

A

As frequency of stimulus increased, the force generated increased until it plateaued (maximal tetanic tension).

96
Q

What is unfused tetanus?

A

if stimuli continue to be applied frequently to a muscle over a prolonged period of time, the maximum possible muscle force from each stimulus will eventually reach a plateau state known as unfused tetanus

97
Q

What is fused tetanus?

A

If stimuli are then applied with even greater frequency, the twitches will begin to fuse so that the peaks and valleys of each twitch become indistinguishable, known as fused tetanus.

98
Q

What is Maximal Tetanic Tension

A

When the stimulus frequency reaches a value beyond which no further increases in force are generated by the muscle, the muscle has reached its maximal tetanic tension.

99
Q

What is an isometric contraction vs isotonic?

A

When a muscle attempts to move a load that is equal to the force generated by the muscle, the muscle contracts isometrically. During an isometric contraction, the muscle stays at a fixed length (isometric means “same length”).

The other is isotonic contraction. In isotonic contraction, the tension in the muscle remains constant despite a change in muscle length. It will shorten if muscle tension is greater than the force opposing it, and elongate if muscle tension is less than the force opposing it.

100
Q

What are the equations for CO and BP?

A
  1. CO = HR x SV
    (Cardiac output = Heart Rate x Stroke Volume)
  2. BP = CO x SVR
    (Blood Pressure = Cardiac Output x Systemic Vascular Resistance)
101
Q

How are these parameters controlled?

A

All parameters in the above relationships are controlled by the sympathetic and parasympathetic fibres of the ANS. The heart receives both types of innervation, while the smooth muscle of small muscular arteries, arterioles and veins receives innervation mainly from the sympathetic division

102
Q

What are the effects of increased parasympathetic tone?

A

Decreases:

  • HR
  • CO
  • BP
  • SVR (systemic vascular resistance)

Increases:

  • LV EDP
  • SV
  • Pulse pressure

No effect on:

  • RA pressure
  • mean systemic pressure
103
Q

What are the effects of increased sympathetic tone?

A

Increases:

  • HR
  • CO
  • BP
  • SVR (systemic vascular resistance)
  • mean systemic pressure

Decreases:

  • LV EDP
  • SV

No effect on:
- RA pressure

104
Q

If the ANS is working, what will happen during a haemorrhage?

A

Increased:

  • HR
  • SVR
  • SNS tone

Decreased:

  • CO
  • BP
  • LV EDP
  • RA pressure
  • SV
  • mean systemic pressure
  • pulse pressure
  • PSNS tone
105
Q

If the ANS is not working, what will happen during a haemorrhage?

A

Increased:

  • SV
  • BP >
  • LV EDP ~
  • RA pressure ~
  • SV
  • Pulse Pressure~
  • SNS Tone

No Change:
- SVR

106
Q

How to a-adrenergic antagonists work?

A

They block a-adrenergic receptors.

These receptors cause vascular smooth muscle to contract.

Less sensitive to epi than b, but when activated they override vasodilation mediated by b, therefore high levels of epi cause vasoconstriction.

At low levels, b dominates and we get vasodilation, therefore decreased peripheral vascular resistance.

107
Q

What are the effects of taking an a-adrenergic antagonist?

A

Decreased:

  • CO
  • SVR
  • BP
  • LV EDP
  • RA Pressure
  • SV
  • mean systemic pressure

Increased:
- pulse pressure?

No effect:

  • HR
  • PSNS tone
  • SNS tone
108
Q

What are the different components of blood?

A
  • 55% fluid (plasma)
  • ## 45% RBCs
109
Q

What is plasma made of?

A
  • Water (approx. 90% of mass)
  • Plasma proteins
  • Salts
  • Nutrients
  • Wastes
  • Dissolved Gases
110
Q

What are the functions of plasma?

A
  • Maintenance of internal environment
  • Rapid transport system
  • Plasma protein functions
    a. Colloidal osmotic presure
    b. pH buffering
    c. Transport
    d. Immunity
    e. Blood coagulation
111
Q

Where are the sites of haematopoiesis?

A

Embryo: yolk sac

2-7 months gestation: liver, spleen, lymph nodes

7 months: bone marrow

Birth to 5years: All bones

Adult: Axial skeleton

112
Q

Characteristics of Haematopoietic Stem Cells

A
  • Produce all formed elements: RBC, WBC, Platelets
  • Self-renewing and pluripotent
  • Regulated by factors such as nutrition, PO2 and infection via hormones and growth factors
  • Marrow churns out 30mL of blood containing 100 billion cells everyday
113
Q

What are the functions of Platelet

A
  • Prevent blood loss by forming thrombi
  • Adhere to damaged blood vessel walls
  • Aggregate together to form platelet plug
  • Aid coagulation enzymes in forming insoluble strands of fibrin that holds platelet plug and trapped RBCs to form blood clot
114
Q

What are found in leukocytes

A
  • Neutrophils
  • Basophils
  • Eosinophils
  • Monocytes
115
Q

Function of Neutrophils

A
  • Phagocytic (bacteria)
  • Most abundant
  • Rapid to infection site
116
Q

Function of Eosinophils

A

Weakly phagocytic
Destroys parasites extracellularly
Roles in allergies and inflammation

117
Q

Function of Basophils

A

Inflammation and allergic reactions

118
Q

Monocytes

A

Become macrophages
Release messenger molecules (cytokines)
Enhance immune response

119
Q

Types of Lymphocytes and functions

A

B-Lymphocytes

  • 20% of all lymphocytes
  • proliferate and become plasma cells that produces antibodies (humoral immunity)

T-lymphocytes

  • 80% of all lymphocytes
  • Proliferate and become activated T-cells (cell-mediated immunity)
    a. cytotoxic T-cells (kills foreign cells)
    b. Helper T-cells (releases cytokines)
120
Q

What do RBCs consist of

A
  • water
  • electrolytes
  • haemoglobin
  • metabolic enzymes e.g. carbonic anhydrase
  • no nucleus or organelles
121
Q

Functions of RBC

A
  • Oxygen transport
    a. 1g Hb binds 1.39ml O2
  • Carbon dioxide transport
122
Q

How many subunits does RBC contain and what does the subunits consist of?

A

4 subunits

  • Globin (polypeptide chains)
  • HbA: 2 x alpha-globin and 2 x beta-globin
  • Haem unit: 1 x Fe2+ and 1 x protoporphyrin molecule
123
Q

Amount of O2 loaded depends on?

A

P02

124
Q

What percentage of O2 is unloaded in tissues?

A

20-25%

125
Q

Binding of RBC is reduced by?

A
  • High DPG
  • High Temp
  • Acidosis
126
Q

Bind of RBC is increased by?

A
  • Reduced DPG
  • Reduced Temp
  • Alkalosis
127
Q

How is erythropoiesis regulated?

A
  • Too few RBCs
  • Too many RBCs
  • Hypoxia
128
Q

What is erythropoiesis stimulated by?

A
  • Erythropoietin (EPO)

- Released from kidneys in response to hypoxia

129
Q

Why are RBCs removed?

A
  • Reduced flexibility
  • Altered membrane surface
  • Rupture
130
Q

What are the normal Red Cell Measurements (male and females)

A

Red cell count (RBC)
= 5.0 x 1012 cells/L (M)
= 4.8 x 1012 cells/L (F)

[Haemoglobin] ([Hb])
= 150 g/L (M)
= 135 g/L (F)

Haematocrit (PCV)
= 0.45 (M)
= 0.42 (F)

131
Q

Formula of Mean Cell Volume

A

Mean Cell Volume (MCV) = PCV/RBC

132
Q

Formula of Mean Cell Hb

A

Mean Cell Haemoglobin (MCH) = [Hb]/RBC

133
Q

Formula of Mean Cell Hb Conc.

A

Mean Cell Hb Concentration (MCHC) = [Hb]/PCV