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Physiology Flashcards

1
Q

Wy are membranes important?

A

outer boundary

- controls entry and exit
- maintains ion conc
- functional differences in cells are to do with the composition of their plasma membrane
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2
Q

What are membranes mainly composed of?

A
  • phospholipids - form complex structures in aqueous solution
  • they can twirl vibrate and move about on their own
  • cholesterol aids in the stiffening of the cell membrane
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3
Q

What are membranes impermeable to?

A
  • water soluble substance - ions, proteins, sugars are insoluble in hydrophobic membrane core
  • small uncharged polar molecules can cross fairly freely (O2 etc)
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4
Q

Why is the lipid bilayer important (3 things)

A
  • forms basic structure of membrane
  • hydrophobic barrier serves as a barrier - maintain diff in solute composition and concentrations inside and outside the cell
  • responsible for fluidity of membrane - enables cell to change shape
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5
Q

What is the difference between peripheral and integral proteins?

A

p - not embedded within membrane, adhere tightly to surfaces of PM

I - transmembrane proteins (span lipid bilayer), embedded and linked to a lipid component of the membrane or a fatty acid that links into membrane

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6
Q

What are some functions of integral membrane proteins?

A
  • ligand binding receptors - hormone receptors
  • adhesion molecules - regulating cell shape and growth, pores and channels (conduits that allow ions to flow), carriers (facilitate or transport a molecule to other solutes) and pumps (energy from ATP to drive the transport)

can also be enzymes

docking marker acceptors - interact with secretory vesicles leading to exocytosis

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7
Q

What is the glycocalyx?

A
  • a layer of glycoproteins and glycolipids

- small amount of membrane carb is located on the outer surface of cells (sugar coating)

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8
Q

Why is the glycocalyx important?

A

self identity markers - important in cell to cell interactions and in tissue growth - cancer cells have abnormal surface markings

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9
Q

What are some specialised cell junctions that are linked?

tight, desmosomes and gap junctions

A
  • tight junctions - join lateral edges of epithelial cells near their lumen (tight or leaky)
  • desmosomes - adhering junctions that anchor cells together especially in stretch - skin heart
  • gap junctions - communicating junctions - allow movement of ions and small molecules between cells
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10
Q

What are the two things that influence whether a particle can permeate the plasma membrane or not

A
  • solubility of particle

- the size

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11
Q

How can molecules or ions penetrate membrane passively?

A
  • diffusion down a concentration gradient

- movement along an electrical gradient

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12
Q

What makes up fick’s law of diffusion?

A
  • magnitude of concentration gradient
  • surface area of the membrane across which the diffusion is taking place
  • lipid solubility of the substance
  • molecular weight of the substance
  • distance through which diffusion must take place
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13
Q

How are ions affected by electrical charge?

A
  • move passively along their electrochemical gradient
  • electrical gradient is created when there is a difference in charge in two areas, moves towards area of opposite charge
  • move through ion-specific channel proteins (leak or gated)
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14
Q

Define osmosis:

A
  • net diffusion of water down its own concentration gradient through a selectively permeable membrane
  • permeate more than expected through aquaporins (water channels)
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15
Q

What is osmolarity?

A

concentration of osmotically active particles in a solution

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16
Q

tonicity?
what is hypotonic
what is hypertonic

A
  • effect a solution has on cell volume - (iso, hypo, hypertonic) eg isotonic saline that have the same electrolytes as the plasma in the human body
  • hypotonic - water diffuses into the cell and causes swelling
  • hypertonic - water diffuses out of cell and the cell starts to shrink
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17
Q

What are some passive transport mechanisms?

A
  • diffusion down concentration gradients (simple diffusion)
  • movement along electrical gradients (ion channels)
  • osmosis - dependant on size and lipid solubility

poorly lipid soluble polar molecules - glucose + amino acids - iosn have to be transported against conc gradient

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18
Q
  • What are the two different mechanisms for selective transport
A

carrier-mediated transport or vesicular transport

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19
Q

What is carrier mediated transport and state 3 important characteristics of this

A
  • substance binds onto a specific carrier which undergoes a conformational change to transport the substance
  • can take 2 forms active or passive (facilitated)
  • faciliated uses a carrier to help move the substance down a conc gradient
  • active transport requires energy
  • 1 - specificity
  • 2 - saturation (transport maximum)
  • 3 - competition
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20
Q

how does facilitated diffusion work?

A
  • enters protein and binds

- flips protein 180 so binding site is facing the low conc - goes back to normal

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21
Q

How does active transport work?

A
  • primary - direct use of energy
  • carrier splits up ATP into ADP and P, P binds to carrier to increase affinity, ions binds to carrier which flips the site and releases the ion and the P
  • secondary - uses second hand energy from ion concentration gradients
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22
Q

What is the energy used to drive Na+ potassium pump also used for?

A

energy used to drive pump indirectly serves as the energy source for secondary active transport

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23
Q

What is the definition of secondary active transport?

A

The transfer of a solute across the membrane is always coupled with the transfer of the ion that supplies the driving force

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24
Q

what are the mechanisms involved?

A
  • symport - solute and NA move in the same direction

- antiport - solute and Na move in opposite directions

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25
Q

How does vesicular transport work?

endocytosis and exocytosis?

A
  • requires energy for vesicle formation and movement within the cell
  • endocytosis - pinching off of membrane to engulf substance
  • exocytosis - vesicle fuses with the membrane releasing its contents into the ECF - (secretion of enzymes, ways of adding carrier or channels into membrane)
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26
Q

What is membrane potential?

A
  • separation of opposite charges across the membrane

- plasma membranes of all cells are electrical polarised

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27
Q

What is responsible for potential across a membrane?

A

separated charges at each side of the membrane that form a layer along the plasma membrane

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28
Q

Is the membrane charged? what does Em refer to?

A
  • no
  • Em = difference in charge between thin layers of ECF and ICF located next to the outside and inside of the membrane, respectively
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29
Q
  • What cells have the ability to produce rapid transient changes in membrane potential?
A

nerve or muscle cells - when they are excited they produce something called action potentials

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30
Q

Why does Em exist?

A

differences in the concentration and permeability of key ions in the ECF and ICF

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31
Q

Describe the flow of potassium and sodium (conc gradient)

A
  • potassium is outward
  • sodium is inward
  • both cations the electrical gradient will always be towards the negatively charged side of the membrane
  • when at rest membrane is 100x more permeable to potassium
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32
Q

Describe the equilibrium potential for potassium ions

A
  • electrical gradient is moving the potassium back into the cell
  • concentration gradient is moving the potassium out of the cell
  • (equilibrium potential for K+ = Ek)
  • membrane potential at Ek = -90mV (negative inside the cell)
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33
Q

What is the nernst equation used for?

A

calculate equilibrium potentials for any given ion

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34
Q

What is the general resting potential for a membrane? why is this

A
  • -70mV
  • because K leaves the cell more than sodium leaves the cell therefore a lack of positive charge in the cell leaves the resting membrane potential to be negative
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35
Q

What is the goldman-hodgkin katz equation used for?

A

calculate resting membrane potentials

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36
Q

What is the sodium potassium pump used for?

A
  • it has a hyperoplarizing current

- potassium gradient is the most important thing in setting the membrane potential

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37
Q

What is the difference between depolarisation and hyper

A
  • when the membrane potential becomes less negative

- when the membrane potential gets more negative

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38
Q

what does the direction of change in potential depend upon?

A
  • the charge carried by the moving ion

- the direction of the moving ion

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39
Q

Why does sodium travel into the cell?

A
  • conc gradient is inward and so is electrical gradient
  • it moves due to cell membrane sodium selective channels
  • the driving force when negative causes inward movement of sodium
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40
Q

Why does potassium move out of the cell

A

conc gradient is outwards and has an energy that exceeds the electrical gradient which is pointing into the cell

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41
Q

what are some types of ion channels?

A

opened - gated

  • membrane voltage activated
  • chemical substances - ligand gated ion channels
  • physical stimuli - mechanical or thermal
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42
Q

Which are responsible for action potentials in neurones?

A

Voltage activated Na and K channels

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43
Q

Detail the process of action potentials in neurones

A
  • at resting potential all voltage gated channels are closed
  • depolarising event happens and when threshold is released Na channels open and K channels close
  • Na enters the cell - explosive depolarisation which generates the rising phase of the action potential
  • at peak, Na inactivation gate closes, ending net movement into the cell, at the same time potassium gate opens
  • potassium leaves the cell causing repolarisation to resting potential generating the falling phase of the action potential
  • sodium channel inactiavtion gate opens but activated gate closes resetting to respond to another depolarising event
  • further outward movement of K through still open channels causes after hyperpolarisation
  • Potassium gate closes and membrane returns back to resting potential
44
Q

What are action potentials?

A
  • brief electrical signals in which the polarity of the nerve cell membrane is momentarily reverse
  • move along nerve cell axons
  • they are generated when a threshold is reached - all or none
45
Q

How are the channels activated?

A
  • sodium - opening of a few channels opens more - positive feedback
  • potassium - self limiting - outward movement casues repolarisation which turns off the stimulation for opening - negative feedback
46
Q

What is responsible for the refractory period?

A

inactivation of sodium channels contributes to the repolarizing phase of action potential + ref period

47
Q

What is absolute and relative refractory period?

A
  • absolute = no stimulus can elicit a second action potential due to sodium channels all being inactivation
  • relative - stronger stimulus may elicit a second action potential, membrane is hyper polarised
48
Q

What allows a greater local current spread

A
  • increase in AP conduction velocity

- the less ‘leaky’ the axon the greater the local current spread

49
Q

how is passive current spread increased?

A
  • increased axon diameter (increase current spread)
  • decrease of leak - adding insulating material (myelin) provided by schwann cells in the PNS and oligodendrocytes in the CNS - both are types of macroglia
50
Q

How is the action potential spread(saltatory conduction - from the latin saltare - to hop or to leap)

A
  • jumps from one node of ranvier to the next

- demyelinating disorder such as CNS and Guillian barre syndrome causes slowing or cessation of nerve conduction

51
Q

What are the hormones involved in controlling glucose?

A
  • In absorptive and post-absorptive states
    o Insulin and glucagon (pancreas)
  • In emergencies
    o Adrenaline (adrenal gland)
  • During starvation
    o Cortisol (adrenal) and growth hormone (pituitary)
52
Q

What are the different pancreatic islets of langerhans?

A
  • Alpha cells = glucagon
  • Beta cells = insulin
  • Delta cells = somatostatin
53
Q

What happens during the absorptive state?

A
  • Glucose rises
  • Insulin rises
  • Glucagon falls
54
Q

What is insulin and what are its effects?

A

Hormone of the fed state:

  • Favours anabolism
  • Glucose  glycogen
  • Fatty acids  triglycerides
  • Amino acids  protein

Effects:
o Lowers glucose by stimulating uptake from blood and activating liver enzymes
- Promoting secretion
o Increased glucose, amino acids, parasympathetic activity, glucagon,
- Inhibiting secretion
o Decreased glucose, increased sympathetic activity

55
Q

What is glucagon and what are its effects?

A
  • Favours catabolism
  • Glycogenglucose
  • Triglycerides  fatty acids
  • Hormone of the hungry state!!!
  • Effects
    o Raises glucose by increasing glycogenolysis, inhibiting liver glycogen synthesis, promoting liver gluconeogenesis, lipolysis (also in adipose tissue)
  • Stimulation of release
    o Decreased blood glucose
    o Amino acids
    o Sympathetic nerve activity
  • Inhibition of release
    o Raised blood glucose
    o Insulin
56
Q

Detail the difference of Type 1 and type 2 diabetes

A 
-	Type 1 
o	Early onset 
o	Little/no insulin secretion 
o	Defect in beta cells 
o	Insulin injections required 
-	
Type 2 
o	Adult onset 
o	Insulin secretion may be normal 
o	Defect in insulin sensitivity 
o	Diet/exercise/oral drugs
57
Q

What does adrenaline do?

A
  • Raises glucose
  • Stimulates glycogenolysis
  • Stimulates gluconeogenesis
  • Released during short term emergencies
58
Q

What does cortisol do?

A
  • Raises glucose
  • Stimulates protein catabolism
  • Stimulates gluconeogenesis
  • Stimulates lipolysis
  • Not important for rapid mobilisation of fuel
59
Q

Why is the growth hormone important?

A
  • Anterior lobe of pituitary
  • In response to starvation
    o Decreases glucose uptake by muscle
    o Mobilises glucose from liver
    o Promotes lipolysis in fat cells
60
Q

Where are baroreceptors found and what is their function?

A

Baroreceptors – located in Aortic Arch and Carotid Sinus.

Sensitive to stretch, firing rate increases when MAP increases and decreases when MAP decreases. They only respond to acute changes (firing decreases if high blood pressure is sustained)

61
Q

Define blood pressure

A

The outwards hydrostatic pressure exerted by the blood on the vessel walls

62
Q

What is systolic pressure?

A

– is when the heart is contracting (normally <140 mmHg

63
Q

Why is diastolic pressure?

A

– is when the heart is relaxed (normally <90 mmHg)

64
Q

What is MAP?

A

MAP – the average arterial blood pressure during a single cardiac cycle. (Normally 70 -105 mmHg)

65
Q

How do you calculate MAP?

A

MAP = [(2x Diastolic) + Systolic] divided by 3
OR
MAP = DBP + 1/3 difference between SBP and DBP

66
Q

What is the MAP equation?

A

Mean Arterial Pressure (MAP) = Cardiac Output (CO) x Total Peripheral Resistance (TPR)

67
Q

What is the cardiac output?

A

Stroke volume x the heart rate

68
Q

How is MAP regulated?

A

MAP can be regulated by regulating HR, Stroke volume, and total peripheral resistance.

69
Q

What are the major resistance vessels?

A

Arterioles

70
Q

What is homeostasis?

A

components of our bodies internal environment must be maintained within narrow ranges

71
Q

What do Homeostatic Control Systems do?

A
  • Sense deviations from normal
  • Integrate this information
  • Make appropriate adjustments to restore controlled variable to a desired variable
72
Q

What are intrinsic and extrinsic controls?

A
  • Local controls inherent in an organ
  • Regulatory mechanisms initiated outside an organ
  • Accomplished by nervous and endocrine systems
73
Q

What is feedforward

A

Responses made in anticipation of change

74
Q

Feedback?

A 
-	Responses made after a change has occurred 
o	Primary type
o	Opposes initial change 
o	
Components are 
	Sensor 
	Control centre 
	Effector 
o	Promotes stability by regulation of a controlled variable through flow information along a closed loop
75
Q

What is the core temperature of the body?

A
  • Temperature of the structures deep within the body

- Homeostatically maintained at about 37.8

76
Q

Sites for monitoring Body temp?

A
  • Ear drum (35.5 – 37.5)

- Rectal (36.7 – 37.5)

77
Q

What are the ways in which the body can gain heat?

A
  • Metabolic heat
    o Basal Metabolic Rate – basic level of heat production
     Can be increased by hormones – adrenaline, noradrenaline, thyroxine
    o Muscle activity can be increased enormously (shivering)
  • Radiation
    o Emission of heat energy in the form of electromagnetic waves
    o About ½ body’s heat loss

Convection
o Transfer of heat energy by air currents, combines with conduction
-
Conduction
o Transfer of heat between objects in contact
o Dependent on temperature gradient and thermal conductivity

78
Q

How can the body loose heat?

A
  • Convection
    o Air next to skin warmed by conduction, warmed air less dense and rises while cooler air moves next to the skin
  • Conduction
  • Radiation
  • Evaporation
    o Passive – water passively diffuses from surface of the skin and the linings of the respiratory airways
    o Active – sweating controlled by sympathetic nervous system
79
Q

How does the negative feedback system work that controls the body’s core temperature?

A
  • Sensor detects change in controlled variable
  • Sends signal to hypothalamus
  • Effectors (e.g. skeletal muscles, Skin arterioles, sweat glands) triggered to respond and restore variable to normal
80
Q

Provide some details on the hypothalamus?

where is the posterior hypothalamic centre?

A
  • Body’s thermostat
  • Posterior hypothalamic centre = cold
    o Vasoconstriction
    o Increased muscle tone
    o Shivering
-	Anterior hypothalamic centre = warmth
o	Vasodilatation 
o	Sweating 
o	Decreased muscle tone 
-	Sympathetic nervous system stimulates sweating
81
Q

How is a fever created?

A

Macrophages release chemicals which act as an endogenous pyrogen >
Stimulates Hypothalamus to release Prostaglandins >
This ‘resets’ the thermostat to higher temp >
Hypothalamus initiates mechanism to heat the body (cold response) >
Thermostat reset to normal if pyrogen release is reduced/stopped.

Fever = 38-40 C

82
Q

What is pulse pressure?

A

the difference between systolic and diastolic blood pressures

83
Q

What is the normal range of MAP

A

70-105 (60 needed for perfusion or organs)

84
Q

What is vasomotor tone and what is it caused by?

A
  • vascular smooth muscle partially constricted at rest; tonic discharge of sympathetic nerves resulting in continuous release of noradrenaline
  • increase in sympathetic discharge will increase vasomotor tone, increase constriction which increases SVR and MAP
  • decrease will do the opposite
85
Q

-Where does excitation of the heart come from?

A
  • pacemaker cells in the sino atrial node
  • these initiate heart contractions
  • SA node is located in the upper right atrium
86
Q

What is the definition of stroke volume?

A

the volume of blood ejected from each ventricle each heartbeat

87
Q

What is the role of the angiotensin aldosterone system?

Detail how the system works

A

regulating plasma volume and SVR

renin is released from the kidneys and stimulates the production of angiotensin 1 by angiotensinogen by the liver

  • angiotensin 1 is then converted to angiotensin 2 by ACE (produced by pulmonary vascular endothelium)
  • angiotensin 2 stimulates the release of aldosterone from the adrenal cortex
  • it also causes vasoconstriction - increases SVR stimulates thirst and ADH release - contribues to increasing plasma volume mainly brought about by aldosterone
88
Q

How does aldosterone work?

A

steroid hormone than acts on kidneys to increase sodium and water retention - increases plasma volume

89
Q

What is the role of ADH?

A
  • peptide hormone derived from hypothalamus and stored in posterior pituitary
  • secretion stimulated by - reduced ECF or increased ECF osmolality
  • plasma osmolality (how many chemiclas etc have been dissolved in your blood)
  • monitored by osmoreceptors in the brain in close proximity to the hypothalamus
  • ADH release is stimulated by increased plasma osmolality
  • acts on kidneys to retain water or concentrate urine - increase extracellular volume which increases BP
90
Q

What are natriuretic peptides?

A
  • peptide hormones - syntheised by heart and brain etc
  • released in response to cardiac distention
  • casue excretion of salt and water in the kidneys - reducing blood volume and blood pressure
  • decrese renin release = decrease BP
  • vasodialtors - decrease SVR and decrease blood pressure
  • counter regulation for RAAS
91
Q

What is cardiac afterload?

A

Cardiac AFTERLOAD means the resistance into which heart is pumping

92
Q

What is Shock?

A

An abnormality of the circulatory system resulting in inadequate tissue perfusion and oxygenation

93
Q

Hypovolaemic shock?

A

caused by loss of blood volume
haemorrhagic
non-haemorrhagic

94
Q

Cardiogenic shock?

A

caused by sudden severe impairment of cardiac function – heart suddenly unable to pump sufficient blood to provide adequate tissue perfusion
e.g. severe heart attack (severe acute myocardial infraction)

95
Q

Obstructive shock?

A

caused by physical obstruction to circulation either into or out of the heart
e.g. cardiac tamponade, tension pneumothorax, pulmonary embolism, severe aortic stenosis

96
Q

Distributive shock?

A

caused by excessive vasodilation and abnormal distribution of blood flow
neurogenic e.g. spinal cord injury
Vasoactive e.g. septic shock, anaphylactic shock

97
Q

What is the EDV controlled by?

A

The venous return to the heart

98
Q

What is the origin of conduction and cardiac impulse?

A

Auto rhythmicity and excitation of the heart originates in the SA Node, this is sinus rhythm.

SAN located in RA close to SVC entry point.

Has Spontaneous Pacemaker Potential:

  • pacemaker potential due to decrease in K+ efflux and transient influx of sodium (HCN channels - funny current) and Calcium from T Cells.
  • Rising phase of action potential (depolarisation) due to activation of L-type Ca channels, causing Ca++ influx.
  • Falling phase (repolarisation) due to activation of K+ channels resulting in K+ efflux.
99
Q

What are the phases of ventricular muscle action potential?

A 
0 - fast sodium influx 
1 - closure of sodium channels and transient K efflux 
phase 2 - Ca influx 
3 - closure of Ca channels and K efflux
4 - resting membrane potential
100
Q

How is mucle tension produced?

A

Muscle tension is produced by sliding of actin filaments on myocin filaments

101
Q

Structure of Striated Muscle Fibre?

What are myofibrils?

What causes the change in colour of appearance

What are sarcomeres?

A

Each muscle fibre (cell) contains many MYOFIBRILS. These are the contractile units of muscle

The myofibrils have alternating segments of thick and thin protein filaments

The ACTIN (thin filaments) causes the lighter appearance in myofibrils and fibers

The MYOCYIN (thick filaments) causes the darker appearance

Within each myofibril: actin and myocin are arranged into SARCOMERES

102
Q

What cranial nerves carry exclusively parasympathetic nerves?

A

Cranial nerves II, VII, IX and X carry exclusively

parasympathetic nerve fibres.

103
Q

How does the frank starling mechanism battle an increased afterload (unable to eject to its full stroke volume)

A

increasing end diastolic volume, increased afterload continues to exist (ventricular mass will eventually become hypertrophic)

104
Q

What is the main way the body increases preload in response to heart failure ?

A

Increases renin secretion

105
Q

What is sodium-glucose co-transport an example of?

A

Secondary active transport - movement in a way other than through the use of ATP

106
Q

What can lead to leg oedema following right sided cardiac failure

A

Increased venue hydrostatic pressure

Principles (10 decks)

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