C: Physiology Flashcards
Main functions of blood (4)
delivery, waste collection, communication routes (endocrine), defense
Composition of blood
plasma (cell free)- 55%, buffy coat, white bloat cells, platelets (1%), erythrocytes (45%)
Serum definition
Liquid component of blood, no clotting factors (plasma with no clotting factors)
Serum functions (3)
transport, inflammatory response/immunity, oncotic pressure
Albumin and its function (2)
Most abundant plasma protein.
- Regulates oncotic pressure (solubilised and retained in blood stream) + transport (charged, polar, non-specific binding)
Serum protein electrophoresis (SPE) process/ goal
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
Albumin levels (serum protein)- increases/decreases as disease signals
- decrease: prolonged malnutrition, chronic liver/ renal disease
- Increase: dehydration
Alpha-globulins levels (serum protein)
- increase: acute inflammatory disease
Beta-globulin levels (serum protein)
- Increase: liver disease
Gamma-globulins levels (serum protein)
- Decrease: immune suppression/ deficiency
- Increase: broad band= chronic infection, sharp band= multiple myeloma
Acute phase proteins levels (serum protein)
- increase: response to inflammation
How are serum enzymes used in diagnosis?
- Cellular enzymes are normally LOW
- Enzyme activity in serum may be increased by cell proliferation of damage.
Haemotosis
formation and dissolution of blood clots
Clotting (and what things are involved)
Forming solid mass of blood to plug vessels. Uses platelets (secretory specialists) and clotting factors.
Thrombosis
Clot attached to blood vessel walls
Embolus
Detached thrombosis that blocks blood flow in diff part of bodyh
Blood clot stages
- Formation of unstable clot (primary haemostasis)
- Formation of fibrin clot (secondary haem..)
- Clot degradation (fibrinolysis)
- Unstable clot (primary haemostasis)
- Injury and collagen is exposed, Von Willebrand’s factor secreted, platelets activated
- Platelets change shape (spidery/sticky), form clump and adhere
- positive feedback
- Fibrin clot (secondary haemostasis)
- 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.
Thrombin activation (clotting cascade)
Intrinsic, extrinsic and common.
- Can be used for positive feedback
- Proteases have multiple points of regulation
- Coagulation complexes dependent on Vitamin K
Intrinsic clotting cascade
Blood can clot without any other biological agents.
- Initiated with surface contact with collagen
- Cascade of protease cleaving + activating other factors
Extrinsic clotting cascade
Requires factors not found in blood
- tissue damage, protein tissue factor (TF) exposed to blood
Common clotting cascade
X -> Xa -> cleaves prothrombin -> thrombin
- Clot degradation (Fibrinolysis)
Limiting clot formation + degradation/breakdown of clot
- Limiting clot: proteases inhibitors
- Clot breakdown: Plasmin breaks down fibrin mesh
Excitable cells
Generate and conduct electrical impulses (nerve + muscle)
What drives membrane excitability and flow of ions
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
Membrane potential and calculations
Diff in electrical charge. Changes depending on permeability
- Calculated using Goldman (GHK) equation
Closed ion channels types (2)
- Ligand-gated (acetocholine binds)
- Voltage-gated (depends on cell membrane potential
Action potential stages (nerve)
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
Action potential stages (myocyte)
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
Action potential in nerves (characteristics)
- 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)
Nervous system reflex
- Fast, involuntary, stereotypical motor response to stimulus
- Mediated by synapses in CNS + some higher control (voluntary control)
Autonomic Nervous System
Sympathetic (action) and parasympathetic (rest + digest)
- Controlled by hypothalamus + parts of limbic system
- Sympathetic - more diffusion/ widespread (neurocrine + adrenaline)
Similarities between sympathetic and parasympathetic ANS
- Many structures receive input from both (outflow may activate separately)
- Always working together
- CNS coordinates both
Differences between sympathetic and parasympathetic ANS
- System receives both signals, balance of both = outcome
- Same transmitter may interact with diff types of receptors in diff cells
Blood pressure regulation
W/ negative feedback system in ANS (using baroreceptor)
Partial pressure
Pressure exerted by particular gas in a mixture. (Bound gas exerts no partial pressure)
PA, Pa and Pv (what does it stand for)
O2 content in alveolae (PA), arterial (Pa) and venous (Pv)
PO2 gradient cascade
Po2 in lungs must remain high to drive diffusion into tissues. Highest in lungs, decreases as it moves through body
How is oxygen transported in blood?
- Bound to haemoglobin
- Dissolved in solution
Oxygen dissociation curve
- 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)
CO2 transport in blood
- Chemical form of HCO3- (formed by CO2 + H2O-> H2CO3 -> H+ +HCO3-)
- Combined with Hb
- Dissolved in solution
Chloride shift
HCO2- exchanges for Cl0 to prevent HCO3- build-up and slow uptake of new CO2
How can oxygen be independent of O2 content of inspired air?
Gas transport with Hb due to flat part of saturation curve. (only max amount that Hb can carry)
Why is the close regulation of CO2 in blood necessary?
Regulates blood pH
How is breathing regulated?
- Respiratory centre in brainstem: Pre-Botzinger complex regulating regular breathing pattern. Can be altered by higher centres (modulatory inputs- eating) or sensory inputs - metabolism
- 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+)
List some adaptations to life at altitude
- 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
