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Foundation block > C: Physiology > Flashcards

C: Physiology Flashcards

1
Q

Main functions of blood (4)

A

delivery, waste collection, communication routes (endocrine), defense

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2
Q

Composition of blood

A

plasma (cell free)- 55%, buffy coat, white bloat cells, platelets (1%), erythrocytes (45%)

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3
Q

Serum definition

A

Liquid component of blood, no clotting factors (plasma with no clotting factors)

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4
Q

Serum functions (3)

A

transport, inflammatory response/immunity, oncotic pressure

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5
Q

Albumin and its function (2)

A

Most abundant plasma protein.
- Regulates oncotic pressure (solubilised and retained in blood stream) + transport (charged, polar, non-specific binding)

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6
Q

Serum protein electrophoresis (SPE) process/ goal

A

Uses agarose/ polyacrylamide gel electrophoresis and is able to separate proteins based on charge and size. (Used for diagnosis, monitoring disease progression and assessing organ function)
- Limitations: changes missed, some proteins too low to detect

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7
Q

Albumin levels (serum protein)- increases/decreases as disease signals

A
  • decrease: prolonged malnutrition, chronic liver/ renal disease
  • Increase: dehydration
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8
Q

Alpha-globulins levels (serum protein)

A
  • increase: acute inflammatory disease
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9
Q

Beta-globulin levels (serum protein)

A
  • Increase: liver disease
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10
Q

Gamma-globulins levels (serum protein)

A
  • Decrease: immune suppression/ deficiency
  • Increase: broad band= chronic infection, sharp band= multiple myeloma
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11
Q

Acute phase proteins levels (serum protein)

A
  • increase: response to inflammation
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12
Q

How are serum enzymes used in diagnosis?

A
  • Cellular enzymes are normally LOW
  • Enzyme activity in serum may be increased by cell proliferation of damage.
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13
Q

Haemotosis

A

formation and dissolution of blood clots

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14
Q

Clotting (and what things are involved)

A

Forming solid mass of blood to plug vessels. Uses platelets (secretory specialists) and clotting factors.

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15
Q

Thrombosis

A

Clot attached to blood vessel walls

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16
Q

Embolus

A

Detached thrombosis that blocks blood flow in diff part of bodyh

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17
Q

Blood clot stages

A
  1. Formation of unstable clot (primary haemostasis)
  2. Formation of fibrin clot (secondary haem..)
  3. Clot degradation (fibrinolysis)
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18
Q
  1. Unstable clot (primary haemostasis)
A
  • Injury and collagen is exposed, Von Willebrand’s factor secreted, platelets activated
  • Platelets change shape (spidery/sticky), form clump and adhere
  • positive feedback
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19
Q
  1. Fibrin clot (secondary haemostasis)
A
  • Initial plug stabilised by mesh fibrin derived from soluble fibrinogen
  • Fibrinogen/ fibrin regulated by thrombin (proteases that cuts proteins) that activates clotting factors
  • Thrombin activation: prothrombin cleaved creating thrombin.
20
Q

Thrombin activation (clotting cascade)

A

Intrinsic, extrinsic and common.
- Can be used for positive feedback
- Proteases have multiple points of regulation
- Coagulation complexes dependent on Vitamin K

21
Q

Intrinsic clotting cascade

A

Blood can clot without any other biological agents.
- Initiated with surface contact with collagen
- Cascade of protease cleaving + activating other factors

22
Q

Extrinsic clotting cascade

A

Requires factors not found in blood
- tissue damage, protein tissue factor (TF) exposed to blood

23
Q

Common clotting cascade

A

X -> Xa -> cleaves prothrombin -> thrombin

24
Q
  1. Clot degradation (Fibrinolysis)
A

Limiting clot formation + degradation/breakdown of clot
- Limiting clot: proteases inhibitors
- Clot breakdown: Plasmin breaks down fibrin mesh

25
Q

Excitable cells

A

Generate and conduct electrical impulses (nerve + muscle)

26
Q

What drives membrane excitability and flow of ions

A

Electrochemical gradients when ions are able to move through the membrane via ion channels and ionic gradients
- Ions flow until it reaches equilibrium potential (calculated using Nernst Equation

27
Q

Membrane potential and calculations

A

Diff in electrical charge. Changes depending on permeability
- Calculated using Goldman (GHK) equation

28
Q

Closed ion channels types (2)

A
  • Ligand-gated (acetocholine binds)
  • Voltage-gated (depends on cell membrane potential
29
Q

Action potential stages (nerve)

A

1) Resting potential
2) Depolarisation: Pushed over threshold, Nat channels open and move out. Process terminates, Na channels enter refractory period.
3) Repolarisation: K channels open and enter. K overshoots
4) Na/K pump bring back to resting

30
Q

Action potential stages (myocyte)

A

4) resting
0) activation of voltage-gated Na channels, out
1) early repolarisation due to largely inactivation of Na channels
2) plateau phase, inward current slowly activating and inactivation of voltage-gated Ca channels
3) repolarisation phase, K enter

31
Q

Action potential in nerves (characteristics)

A
  • All or nothing, very rapid
  • Starts with initiating event (stimulation or receptor), triggers events down the line
  • Speed depends on size of axon (wide = faster) and myelination (ability to skip)
32
Q

Nervous system reflex

A
  • Fast, involuntary, stereotypical motor response to stimulus
  • Mediated by synapses in CNS + some higher control (voluntary control)
33
Q

Autonomic Nervous System

A

Sympathetic (action) and parasympathetic (rest + digest)
- Controlled by hypothalamus + parts of limbic system
- Sympathetic - more diffusion/ widespread (neurocrine + adrenaline)

34
Q

Similarities between sympathetic and parasympathetic ANS

A
  • Many structures receive input from both (outflow may activate separately)
  • Always working together
  • CNS coordinates both
35
Q

Differences between sympathetic and parasympathetic ANS

A
  • System receives both signals, balance of both = outcome
  • Same transmitter may interact with diff types of receptors in diff cells
36
Q

Blood pressure regulation

A

W/ negative feedback system in ANS (using baroreceptor)

37
Q

Partial pressure

A

Pressure exerted by particular gas in a mixture. (Bound gas exerts no partial pressure)

38
Q

PA, Pa and Pv (what does it stand for)

A

O2 content in alveolae (PA), arterial (Pa) and venous (Pv)

39
Q

PO2 gradient cascade

A

Po2 in lungs must remain high to drive diffusion into tissues. Highest in lungs, decreases as it moves through body

40
Q

How is oxygen transported in blood?

A
  1. Bound to haemoglobin
  2. Dissolved in solution
41
Q

Oxygen dissociation curve

A
  • At lungs: high pH and high affinity for O2 (more O2 taken up, Hb has higher affinity for O2)
  • At tissues: Low pH and lower affinity for O2 (Bohr shift: more oxygen given up at tissues, lower Hb O2 affinity)
42
Q

CO2 transport in blood

A
  1. Chemical form of HCO3- (formed by CO2 + H2O-> H2CO3 -> H+ +HCO3-)
  2. Combined with Hb
  3. Dissolved in solution
43
Q

Chloride shift

A

HCO2- exchanges for Cl0 to prevent HCO3- build-up and slow uptake of new CO2

44
Q

How can oxygen be independent of O2 content of inspired air?

A

Gas transport with Hb due to flat part of saturation curve. (only max amount that Hb can carry)

45
Q

Why is the close regulation of CO2 in blood necessary?

A

Regulates blood pH

46
Q

How is breathing regulated?

A
  1. Respiratory centre in brainstem: Pre-Botzinger complex regulating regular breathing pattern. Can be altered by higher centres (modulatory inputs- eating) or sensory inputs - metabolism
  2. Chemical regulation:
    - Peripheral chemoreceptors sensing low PaO2 and high PaCO2 and fires action potential to respiratory network.
    - Central chemoreceptors: indirectly sensitive to PaCO2 (sense H+)
47
Q

List some adaptations to life at altitude

A
  • Low PaCO2 and high pH= inhibition of peripheral/ central chemoreceptors = no increased ventilation
  • Increased HCO3- excretion from kidneys that will eventually stabilize
  • Increased arterial ventilation, low PaO2, and high pH in blood

Foundation block (10 decks)

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