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FRCA Physiology > General Physiology > Flashcards

General Physiology Flashcards

1
Q

What are transcription and translation

A

Transcription - sequence of DNA producing a specific mRNA
Translation - mRNA determining the final amino acid sequence via tRNA in a ribosome

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2
Q

Which enzyme unzips dna during transcription, where?
What are the strands called, which is used to create the mRNA?

A

DNA polymerase
Nucleus
Sense and anti-sense
Antisense

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3
Q

Nucleotide types and category

A

Guanine - purine
Cytosine - pyramidine
Adenine - purine
Thymine - pyramidine
Uracil - pyramidine

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4
Q

What are transcription factors?
Function

A

Proteins that bind to specific DNA sequences
Either promote or repress RNA polymerase

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5
Q

Where does translation occur
What does tRNA bind to specifically
Which way does the sequence get read

A

Ribosome
Codons
5’ to 3’

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6
Q

What are the special codons that mark key points in translation

A

Start AUG
Stop UAA, UAG, UGA

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7
Q

Where and how is the amino acid carried on tRNA
What loads it on

A

At the 3’ end covalently bonded
Aminoacyl tRNA synthetases

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8
Q

How many codon combinations are there?
How many amino acids are there

A

4^3 = 64
20

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9
Q

Where does the amino acid chain go after translation
What for

A

To the Golgi
Further processing and refinement then packaging into granules

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10
Q

What are the levels of structures of proteins with link types

A

Primary - polypeptides chain - peptide bonds
Secondary - specific geometric shape eg beta sheet or alpha helix - hydrogen bonds
Tertiary - unique folded 3d structure - van de valls, hydrogen bonds, etc.
quaternary - combination of more than one polypeptide chain creating fibrous or globular proteins

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11
Q

Structure of haemoglobin
How is it effected in SSD

A

2 alpha and 2 beta polypeptide chains with an inorganic haem group.
SSD - abnormal beta chain, lock together and thus precipitate forming sickle shaped RBCs

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12
Q

Types of genetic mutation

A

Substitution - one base for another
Insertion
Deletion

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13
Q

How can cells influence gene expression in other cells

A

Release of molecules that trigger intracellular signalling in the target cell via extracellular or intracellular receptors

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14
Q

How does oestrogen effect target cells

A

Crosses cell membrane
Bonds to receptor
Enters nucleus
Binds to DNA
Alters transcription

OR
Binds to g-protein coupled receptor

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15
Q

How does thyroid hormone effect target cells

A

Enters via transporter proteins
Enters nucleus
Binds to thyroid hormone receptor - unbound this causes transcription repression but bound causes activation

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16
Q

Thickness of cell memebrane
Main functions

A

7.5 nm
Separation of internal from external
Maintenance of concentration gradients
Control of movement in and out
Maintenance of cell shape
Cell adhesion
Cell signalling

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17
Q

What is the correlation of the structure of phospolipids in cell membranes
What holds the bilayer together

A

Hydrophilic head
Hydrophobic tail
Thus forms bilayer
Hydrophilic head out thus low permeability to ions and polarised molecules.
Van der waals, hydrogen bonds, non-covalent interactions

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18
Q

Types of protein position on cell membranes

A

Integral, peripheral, surface

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19
Q

Functions of cell memebrane proteins

A

Structure
Pumps
Carriers
Ion channels
Receptors
Enzymes

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20
Q

Types of transport across cell membranes and description

A

Diffusion - net movement of particles down concentration gradient. Simple or facilitated (through carrier protein) tending to equilibrate the gradient
Osmosis - movement of solvent molecules across a semi-permeable membrane from an area of low solute concentration to high solute concentration tending to equilibrate the concentration
Active transport - movement of particles against their concentration gradient requiring energy (primary from atp, secondary from electrochemical gradient)
Endocytosis - cell absorbs molecules by engulfing them
Exocytosis - cells direction excretory vessels out of the cell membrane.

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21
Q

What is a cell receptor, what does it react too?

A

Molecules that receive specific chemical signals from environment via ligands (peptides, neurotransmitters, hormones, drugs, toxins).

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22
Q

Types of cell receptors

A

Peripheral membrane proteins - eg elastin
Transmembrane proteins - eg G protein or ligand gated ion channel
Intracellular receptors - eg hormone receptors

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23
Q

How many transmembrane domains do G protein coupled receptors have?
How do they exert their action
How are they deactivated

A

7
Conformational change on ligand binding allows GDP to be exchanged for GTP of the Galpha subunit
Subunit disassociate to Galpha-GTP and beta-gamma.
Subunits act on effector organs or on ion channels to effect response
GTPase exchanges the GTP back to GDP and all subunits re-associate on the receptor

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24
Q

Examples of ligands for tyrosine kinase receptors

A

Insulin
Erythropoietin

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25
Q

How do tyrosine kinase receptors work

A

Ligand binds to extracellular N terminal, beta unit spans membrane, effect exerted by intracellular c-terminal
At the c-terminal kinase enzymes cause phosphorylation. Phosphorylation of tyrosine leads to activations of signal transduction pathways in the cell

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26
Q

How does insulin work via its receptor (very simply)

A

Binds to tyrosine kinase receptor
Cascade triggers release of vesicle with GLUT transporters to membrane allowing glucose into cell

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27
Q

What are ionotropic receptors
How do they work

A

Ligand gated ion channels open and close in response to ligand binding

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28
Q

Examples of ligand gated ion channels

A

Nicotinic ACh receptor
NMDA receptor
GABA receptor

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29
Q

What is the term when a ligand binding site is away from the active site

A

Allosteric

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30
Q

What does NMDA and GABA stand for

A

N-Methyl-D-Aspartic acid
Gamma-AminoButyric Acid

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31
Q

Structure of a nicotinic AcH receptor
Function

A

5 membrane spanning sub units (each made of 4 helical domains) with ion channel centrally, ACH binding sites on the 2 alpha subunits, other units beta gamma and epsilon
Conformational change on both domains bound ACH - Na + Ca flow in and K out down concentration gradients

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32
Q

Structure of an NMDA receptor

A

4 membrane spanning sub units (each made of 3 full and 1 partial helical domaine) with central ion channel
Glycine binding sites on N2 subunits
Glutamate binding sites on N1 subunits
Transmits sodium and calcium ions.

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33
Q

Structure of a GABA receptor

A

5 membrane spanning subunits (each with 4 helical domains) around a central channel binding site for benzodiazepines between alpha and beta subunits
Transmits chloride ions

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34
Q

Another name for G protein coupled receptor (broader type)

A

Metabotropic - a receptor that uses signal transduction through the membrane

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35
Q

Definition of full agonist

A

Induces a receptors maximal response

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36
Q

Definition of partial agonist

A

Induces a receptors submaximal response

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37
Q

Definition of inverse agonist

A

A drug that induces the opposite effect to the intrinsic agonist

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38
Q

Definition of Competitive antagonist

A

A drug that competes with the intrinsic agonist for the receptor and thus blocks its activity

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39
Q

Definition of non-competitive antagonist

A

A drug that binds at a different site to the intrinsic agonist and prevents receptor activation

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40
Q

Definition strong and weak acid

A

Acid - proton donor
Strong - fully dissociates in solution
Weak - partially dissociates in solution

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41
Q

Definition strong and weak base

A

Base - proton acceptor
Strong - fully dissociates
Weak - does not fully dissociate

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42
Q

What is an acid base buffer
Action

A

A weak acid and it’s conjugate base (the anionic product of an acid)
Limits the effect of a proton load in any physiological solution

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43
Q

Definition of pH including constituent units

A

Negative log base 10 of hydrogen ion concentration in nmol/l

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44
Q

What is physiological ph and h+ concentration

A

7.4
40nmol/l

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45
Q

What is a neutral pH?
Effect of temperature?

A

pH 7 and hydrogen and hydroxyl concentrations equal. True at 25oC, at 37oC neutral pH is 6.8

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46
Q

pH of:
Gastric juices
Urine
Arterial blood
Venous blood
CSF
pancreatic fluid

A

Gastric juices 1-3
Urine 5-6
Arterial blood 7.38-7.42
Venous blood 7.37
CSF 7.32
pancreatic fluid 7.8-8

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47
Q

Definitions of acidosis and acidaemia

A

Acidosis - excess of acid moieties within physiological system
Acidaemia - pH <7.4

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48
Q

What processes are most impacted by deranged pH in the body

A

Oxidative phosphorylation
Enzyme function
Carrying power of Hb (Bohr effect)
Chemical reactions
Ionic flux

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49
Q

What is the H+ ion concentration at pH
7.4
7.7
7.1
6.8

A

7.4 - 40nmol/l
7.7 - 20nmol/l
7.1 - 80nmol/l
6.8 - 160nmol/l

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50
Q

What is the main source of body acid production

A

CO2 from glucose metabolism

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51
Q

What process produces non-volatile acids in the body

A

Amino acid metabolism

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52
Q

What systems are involved in hydrogen ion control, over what timeframes

A

Buffer - seconds
Resp - minutes
Renal - hours
Hepatic - hours

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53
Q

Definition of pK

A

Neg log base10 of the dissociation constant for a chemical reaction

Also happens to be pH at which a buffer is most efficient and at which the system is at 50% ionisation

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54
Q

Blood based buffers and their pK

A

Bicarbonate 6.1
Histidine on haemoglobin 7.8
Amino/carboxyl in plasma proteins 7.4

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55
Q

Interstitial buffers and their pK

A

Bicarbonate 6.1

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56
Q

Intercellular buffers and their pK

A

Proteins - 7.4
Phosphates 6.8

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57
Q

What is the Henderson-hasselbach equation?

A

pH = pK + log10[A-]/[HA]

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58
Q

How is the Henderson-hasselbach equation derived

A

H+A <=> HA
k1 [H][A] = k2 [HA] With k being rate constant
[H] = K [HA]/[A] with K being k2/k1
Log10 then -log10 both sides

Log10[H] = log10K + log10[HA]/[A]

-Log10[H] = -log10K - log10[HA]/[A]

Substitute pH and pK

PH = pK + log10[A]/[HA]

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59
Q

Why is the bicarbonate buffer system so effective

A

Easily regulated components
CO2 by lungs and HCO3 by kidneys

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60
Q

What is the Henderson hasselbach equation for the bicarbonate buffer system

A

PH = 6.1 + Log [HCO3-] / pCO2 x 0.225

0.225 is the solubility coefficient for CO2

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61
Q

How much CO2 is dissolved in typical arterial blood

A

5.3 kPa x 0.23 = 1.2 mmol/L

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62
Q

What is the most powerful buffer and provides 75% of all intracellular buffering

A

Histidine residues on haemoglobin

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63
Q

What is the relationship between buffer systems termed
What is it

A

Isohydric principle

When in a compartment all buffer pairs are in equilibrium with the same H+ concentration. Only those buffers with a pK within 1 pH unit of that in the solution participate effectively in the buffering of the pH

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64
Q

What is the respiratory response to excess hydrogen ions

A

Increased CO2
Detected by chemoreceptors in the medulla and carotid bodies
Increased alveolar ventilation

Increased H+ directly on the respiratory centre in the medulla

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65
Q

What is control effectiveness

A

The ability of a physiological homeostatic mechanism to deal with change in the parameter it controls.

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66
Q

What is the control effectiveness of the respiratory system to hydrogen ion concentration
Example numbers

A

50-75%
Will deal with 5-7.5nmol of a 10nmol change in H+

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67
Q

How do kidneys affect acid base balance

A

H+ secretion
HCO3- filtered
HCO3- generated

68
Q

How is H+ secreted in the kidneys

A

Secreted by epithelial cells in the collecting system by primary and secondary active transport
Also by interaction between hydrogen ions and bicarbonate within the collecting system.

69
Q

How does secondary active transport result in H+ excretion in the kidneys
Where does it occur

A

Proximal collecting duct
Small but significant electrochemical gradient against diffusion.
Primary active transport transports Na from the renal tubule into the cells, with hydrogen ions transported the other way by countercurrent transport.

70
Q

How does primary active transport result in H+ excretion in the kidneys
Where does it occur

A

Distally in collecting duct
Large electrochemical gradient to work against
Hydrogen transporting ATPase on tubule membrane expel hydrogen into the tubule against its concentration gradient. The bicarbonate is moved back into the extracellular fluid in exchange for chlorine which moves right through with the hydrogen into the renal tubule

71
Q

What happens to secreted H+ in the tubules? What is the net effect

A

Combines with a buffer (bicarbonate, phosphate, ammonia)
Net effect is increased bicarbonate in the blood

72
Q

What enzyme is activated int he renal tubules in response to decreasing pH
What does it do

A

Glutaminase
Increased activity producing more ammonia for secretion acting as a urinary buffer.

73
Q

What is the livers role in acid base management?

A

Carbon dioxide produce
Metabolism of organic acid anions
Plasma proteins production
Metabolism of ammonium
Ureagenesis - regulates urea produce in the face of the need to either conserve or consume bicarbonate

74
Q

What is the distinction between type A and B hyperlactaemia

A

Type A impaired normal oxygen delivery, type B from other cause (e.g. leukaemia, renal failure, drugs)

75
Q

Causes of hyperlacataemia

A

Increased cellular production
Reduced uptake or use of oxygen (causing anaerobic metabolism)
Reduced lactate clearance
Adrenergic stimulation causing increased glycolysis

76
Q

What is the significance of the lactate:pyruvate ratio? What is it normally?

A

Normally 10:1
If >10:1 indicates tissue hypoxia

77
Q

What is the anion gap?
What is the formula?
Normal values

A

The difference between the sun of measured cations and anions
(Na+K)-(Cl+bicarb)
3-11

78
Q

Sources of error in anion gap calculations

A

Blood sample not processed immediately - contained leukocytes continue metabolism increases bicarb concentration
Haemolysis alters k concentrat

79
Q

Causes of high anion gap acidosis

A

Electroneutrality maintained by extra unmeasured anions - bicarb levels drop binding with the H+ leaving the unmeasured anion around.

M - methanol
U - uraemia
D - DKA
P - paraldehyde
I - Isonicotinc acid
L - Lactic acid
E - ethanol
S - salicylates

80
Q

Causes of Normal anion gap acidosis

A

Hyperchloraemic acidosis, fall in bicarb compensated by rise in cl-

Diarrhoea
Proximal renal tubular acidosis
Renal failure
Distal renal tubular acidosis
Ammonium chloride
Acetazolamide
TPN
Alcohol (!)

81
Q

What causes a low anion gap acidosis?

A

Low albumin (constitutes 80% of unmeasured anions)
Increase in cations eg paraproteins or lithium

82
Q

What is the distinction between standard and actual bicarbonate on an ABG

A

Standard - bicarb corrected to normal temp and CO2 level - reflects true metabolic picture
Actual - calculated by Henderson hasslbach from rest of ABG

Ie standard controls for respiratory component

83
Q

What is the base excess?

A

The amount of acid that must be added to the sample of blood in vitro to restore the sample to pH 7.4
WHILE THE CO2 IS HELD AT 5.33kPa

84
Q

What issues may effect an ABGs gas and acid base interpretation, why?

A

Air bubbles (esp froth as lrg surface area) - time dependant change in O2 as bubbles with have a PaO2 of 21kpa
Time delay - ongoing metabolism in cells (worse in leucocytosis)
Heparin in syringe - dilution
Catheter dilution - withdrawing blood from a line still contaminated with a drip
Halothane - messes with pO2 electrode
Temp - when blood is cooled CO2 becomes more soluble so PaCO2 falls and pH rises as HB accepts more hydrogen ions when cooled.
Syringe type - old plastic can interfere - modern plastic used or glass

85
Q

What are the two scientific methods of blood gas interpretation?
Brief description

A

Alpha stat - ionisation of imidazole on histidine (haemoglobin) remains constant at different temps - ie. Intracellular pH is maintained at different temps so no need to alter patient parameters to maintain pH in the face of change of temp

pH stat - correct blood gases for temp, physiological parameters should be altered to maintain pH in the face of changing temps.

86
Q

What method is used to correct ABGs for temperature

A

Rosenthal correction

87
Q

What can commonly cause metabolic alkalosis

A

Diuretics
Ingestion of alkali
Loss of chloride
Excess aldosterone

88
Q

How might pyloric stenosis cause a metabolic alkalosis

A

Loss of chloride and hydrogen ions from vomiting
Dehydrated kidneys respond by conserving sodium at expense of hydrogen thus also paradoxical renal hydrogen loss.

89
Q

What diuretic produces a metabolic acidosis rather than alkalosis? Why?

A

Acetazolamide
Inhibits carbonic anhydride preventing the regeneration of bicarb in the kidney

90
Q

What effect do salicylates have on acid base

A

Stimulate resp centre producing resp alkalosis
Uncouple oxadative phosphorylation producing metabolic acidosis

91
Q

What is the strong ion difference in acid base theory?
Normal value

A

Sum of +ve ions minus major -ve charge ions. (Strong ions which dissociate fully in solution)
40-42mEq/L

92
Q

Why does the Stewart hypothesis suggest alkalosis occurs in vomiting

A

Loss of chloride increasing the SID
NOT H+ loss as water provides an inexhaustible supply of H+

93
Q

What is the effect on acid base of administrating large volumes of normal saline

A

Hyperchloraemic acidosis
Reduction in SID and increased water dissociation

94
Q

What are the three principles of Stewart’s theory of acid base

A

Dissociation - strong ions separate fully, others only partially dissociate (eg weak acids
Electroneutrality - aqueous solutions will always have equal +ve to -ve ions
Mass conservation

95
Q

What acid base disturbance results from albumin loss according to Stuart? How does the body react

A

Alkalosis - albumin is a weak acid
Decreasing the strong ion gap

96
Q

How would the Stewart approach to acid base suggest sodium bicarb raises ph

A

Increases plasma sodium thus increasing SID and reducing plasma water dissociation and a fall in fee H+

97
Q

What changes ph in Stewart equation of acid base?

A

Not H+, there is an inexhaustible supply from breakdown of water
Independent variables
CO2
Strong ions
Weak acids

98
Q

How does SID differ from anion gap?

A

Bicarb is not a strong ion

Sid = (na k ca mg) - (cl lactate)

99
Q

According to Stewart how does sid influence ph
What is normal range of sid

A

Sid has a strong effect on electrochemical gradient of water hence on h concentration.
Low sid causes dissociation of H and low pH
40-44 mol/L

100
Q

What are the main weak acids in Stewart’s theory of acid base
What term represents them?

A

Albumin
Phosphate

Atot = (AH+A-)

101
Q

How would the Stewart approach consider renal input into acid base balance

A

Loss of chlorine ions increases SID thus causes acidosis,
No effect of H or bicarb loss as will be replenished from water

102
Q

How does the liver impact on acid base balance via the kidneys

A

Production of ammonium which is excreted with Cl increasing anion gap
Production of glutamine in response to acidaemia used by the kidneys to produce ammonium

103
Q

How would varied GI losses impact on SID

A

Stomach losses - high Cl loss - increased SI D
Pancreatic or large intestine losses - loss of high SID fluid with low Cl thus decreased SID

104
Q

How is hartmans neutral according to Stewart acid base

A

Sid slightly smaller than Plasma thus slightly acidotic
However, contains no ATOT (albumin) thus tends back to neutral

105
Q

How does hypovolaemia cause alkalosis by Stewart acid base

A

Proportionally greater na retention than Cl thus increased SID

106
Q

What is the strong ion gap of Stewart’s acid base?

A

SIG = SID - HCO3- - albumin
Should be 0 ie net negative of bicarb and albumin counter positive sid

The gap is unknown elements eg ketones

107
Q

Bonds in forming protein tertiary structure

A

Hydrogen
Ionic
Hydrophobic
Disulphide bridges

108
Q

What is the general function of enzymes

A

Protein catalysts - increase rate of chemical reaction without being changed themselves. Lower activations energies associated with the uncatalysed reation

109
Q

What model replaced lock and key for enzyme substrate binding

A

Induced fit - enzyme active site changes shape.

110
Q

What is the term for other molecules needed to assist an enzyme in its function? Broad categories and examples?

A

Cofactors
Metal ions eg - mg for hexokinase, zn for carbonic anhydrase

Coenzymes
Organic molecules eg - coenzyme A in acyl group reactions or coenzyme B12 in alkyl group reaction.

111
Q

What can effect rate of an enzyme reaction?

A

Concentration of substrate
Intrinsic ability of enzyme
Temperature
pH

112
Q

What is the relationship between enzyme reaction speed and temp

A

Generally increases until reaches a certain point where enzyme denatures and rapidly falls.

113
Q

What is the michaelis mention equation in relation to enzyme kinetics?

A

E+S reversible ES unidirectional E+P
With rate constants k1 and k1- over the reversible stage and k2 over the unidirectional

V0 (initial max velocity) = Vmax[S] (max velocityxsubstrate ) / Km+[S] (rate constant + substrate)

The rate constant being k-1+k2 /k1

114
Q

What plot type is used to evaluate enzyme kinetics
What are the axis
What are the values of x intercept, y intercept

A

Lineweaver burke
X is 1/[s], intercept gives -1/km
Y is 1/v0, intercept is 1/vmax

115
Q

What is the effect on the enzyme substrate relationship of an increasing Km, how can it be read on a graph of substrate vs V0

A

Increasing Km means lower affinity of substrate to enzyme (higher concentration of substrate required for same reaction velocity)
It is the substrate concentration when velocity is half v max

116
Q

What are the characteristics of a competitive enzyme inhibitor?
Effect on enzyme graphs

A

Reversible binds the enzyme usually at active site stopping substrate from binding
If binds away from active site causes shape change that stops substrate from binding
Both methods are overcome by increasing substrate concentration
Causes a right shift on a substrate velocity graph - Km increases but vmax is unaffected (just takes longer to get there
On a lineweaver burke steepens the line (crosses x axis closer to 0 larger Km) but crosses y axis in same place vmax same

117
Q

Characteristics of non competitive inhibitor
Graph effects

A

Binds away from active site often permanent (covalently)
Substrate binding ineffective but still occurs
Net effect is decrease in the amount of functional enzyme
Thus lowers vmax but Km the same
On a substrate vs velocity reaches a lower v max (shifted down) but same Km
On a lineweaver Burke same end point on x axis but steeper line crossing the y axis higher (lower vmax)

118
Q

What enzymes do not exhibit michalas menton kinetics? How do they appear to act?
Example?

A

Allosteric enzymes - their kinetics influenced by other molecules
Sigmoid curve indicating binding of Allosteric molecule.
Can also exhibit changes to vmax much like non competitive inhibition and Km like competitive
Haemoglobin (binding of oxygen)

119
Q

What characteristic makes Allosteric enzymes important?

A

Allows an end product in a series of reactions to effect earlier enzymes providing a negative feedback system.

120
Q

What are pro enzymes?
Common use

A

Inactive enzymes or zymogens
Proteolytic enzymes left inactive until in the desired location

121
Q

Percentage of body water by compartments

A

Whole body 60% weight is water
66% in ICF
34% in ECF
APPROX:
Intravascular - 9% of water
Interstitial - 21% of water
Transcellular - 2% of water
Bone and connective tissue - 2% of water

122
Q

What are the constituents of intravascular fluid? Percentages

A

Plasma (55%) blood cells

123
Q

What does plasma consist of? Percentages?

A

Water 90%
Proteins 7%
Ions

124
Q

Rough volume of intravascular space in adult

A

70-75ml/kg - appprox 5L in adult
2 litres of which are RBC

125
Q

Roughly how much interstitial fluid is there in an average sized adult 70kg
Contents
Function

A

10L
Water and ions (no proteins)
Transport medium
Lymphatics

126
Q

How does the ionic composition of icf and plasma compare? Implication?

A

Same composition and same osmolality
Fluid administered into intravascular space freely exchanges with ICF

127
Q

What is transcelluar fluid
Examples

A

Secreted fluid separate from plasma
Eg GI fluid, csf, urine, aqueous humour, bile

128
Q

What determines waters distribution across a semipermeable membrane?

A

The concentrations of the respective solutions
Water will move from a low solute concentration to a high solute concentration to equalise the concentrations

129
Q

What is osmotic pressure?

A

The hydrostatic pressure required to prevent the movement of water across a semipermeable membrane (the minimum pressure that needs to be applied to a solution to prevent the inflow of its pure solvent across a semipermeable membrane)

130
Q

What are
Osmoles
Osmolality
Osmolarity

A

Osmoles - osmotic ally active particles
Osmolality - number of Osmoles per kg of water
Osmolarity - number of Osmoles per litre of water (depends on temperature)

131
Q

What is plasma osmolality typically
How can it be calculated

A

280-305 mosmol/kg
Plasma osmolality = urea + K + (2xNa)

132
Q

What is the principle determinate of water distribution between ECF and ICF

A

ECF solute concentration - very little change in ICF concentration but ECF changes radically at times. Mainly this is dependant on ECF Na concentration

133
Q

What controls fluid distribution within the ECF

A

Relative volumes of compartments as ions can move freely between blood and ISF
The size of compartment is determined by number of solute particles rather than osmolality.
Fluid is also pushed out of vessels by hydrostatic pressure and kept in by oncotic pressure (osmotic effect of proteins)

134
Q

How is water intake regulated in the awake patient

A

Sensor - osmoreceptors in hypothalamus respond to changes in ECF toxicity (reflecting Na concentration)
Controllers - mechanisms in hypothalamus
Effectors - thirst (resulting in conscious intake of more water), ADH release from pituitary causing water reabsorption in collecting ducts

135
Q

What is Ficks Law

A

Rate of diffusion across a membrane of unit area is proportional to concentration gradient

136
Q

What is grahams law

A

Rate of diffusion is inversely proportional to square route of molecular weight

137
Q

Width of capillary wall
Width of interstitial space
Rough time frame to equilibriate in ideal conditions by diffusion.

A

10 micro meters
1.2 micro meters

0.05s

138
Q

What is ion trapping
Relevance to clinical anaesthesia

A

Unionised weak acid travels through cell membrane by diffusion then dissociates
Relevant in obstetrics where local anaesthetics pass to baby then dissociate in lower foetal blood pH

139
Q

What is osmosis

A

Diffusion of solvent across a membrane that is impermiable to its solute from a region of low to high solute concentration so to equalise the solute concentrations.

140
Q

What conditions are required for 1 mol of a substance to produced 1 atmosphere of osmotic pressure

A

Dissolved in 22.4L at 0degrees Celsius across a semipermeable membrane

141
Q

Hoffs formula for calculating osmotic pressure

A

P = RT Sum(c1-c2)
Osmotic pressure = universal gas constant x temp (K) x sum of differences in ion concentrations across membrane

142
Q

Universal gas constant with units

A

8.31 joules/kelvin/mole

143
Q

What is the osmolarity of proteins in the blood
What is the specific term
Oncotic pressure exerted?

A

1-2 mOsmol/L
Oncotic pressure
3.5kPa (26mmHg)

144
Q

What is the ideal gas equation

A

PV=nRT
Pressure x volume = number of moles x universal gas constant x absolute temp

145
Q

What is tonicity

A

The behaviour of cells when bathed in solution as a comparison of osmolarity of plasma and solution. (Ie a hypo, iso hypertonic solution)

146
Q

What is the function of sodium potassium atpase in detail
What is the normal sodium concentration gradient

A

Moves 3 na out of the cell and 2 k in for 1 atp to adp.
15mmol/l to 145mmol/l

147
Q

What ion does nakatpase need for normal function
What upregulates it?
What down regulates it?

A

Mg
Upregulated by insulin, thyroid hormone, aldosterone
Dow regulated by cardiac glycosides, dopamine

148
Q

How does insulin impact on Glut?

A

Causes vesicles containing GLUT 4 to merge with cell membrane increasing number of glucose transporters

149
Q

How is glucose taken up in the gut?

A

Secondary active transport -
NaKatpase at basal membrane creates sodium gradient out of cell
Na is taken up from gut along with glucose through sodium dependant glucose transporters

Facilitated diffusion
Glucose diffuses through GLUT 2 carrier proteins at basal membrane into blood.

150
Q

Characteristic points of a membrane channel

A

When open allow access from both sides of membrane
Contain one or more binding site in a transmembrane sequence
Provide a rapid portal through the membrane which approaches the free rate of diffusion
Can be open or gated for control

151
Q

What are aquaporins. How are they activated?
Where are the types found?

A

Water channels. Located in endosomes. Moved to luminal surface when vasopressin binds to V2 receptor
1-3 in the kidney (2 in the collecting duct)
4 - in the brain
5 - in the salivary, lacrimal and respiratory glands.

152
Q

What sorts of gated channels are there?

A

Voltage - eg in nerves, open and close due to electrical signal
Chemical - open and close due to chemical signal, either directly - ligand gated channels where ligand receptor is part of channel or indirectly - ligand gated channel where ligand binds remotely causing an release in an intracellular messenger e.g. G protein coupled receptors
Mechanical - e.g stretch activated channels on sensory nerve terminals

153
Q

What is transcytosis?

A

Endocytosis or exocytosis
Proteins that could not otherwise cross the membrane passed in or out via vesicle formation/fusion with membrane.

154
Q

Types of Endocytosis and description
Key protein involved

A

Phagocytosis - cell pushes out to engulf external object
Pinocytosis - external object into internal invagination
receptor mediated Endocytosis - pinocytosis with receptors

Key protein is clathrin - stabilise vesicle structure

155
Q

What are The flask shaped invaginations that are needed for Endocytosis called? What protein pinches them off?

A

Caveoli
Dynamin

156
Q

What triggers exocytosis

A

Usually increased calcium concentration. Needs atp .

157
Q

How many subunits does a nakatpase have

A

2

158
Q

What is the Gibbs-Donnan effect

A

When ions on one side of a membrane can’t diffuse through it the distribution of diffusible ions is also effected (e.g. non diffusible anions hinder diffusion of diffusible cations)
Results in electrochemical gradient
High protein in blood and cells trap ions

159
Q

What equation calculates equilibrium potential across membrane

A

Nernst equation

160
Q

What is the resting potential

A

A diffusion potential due to distribution of K -90mV
Some movement of Na and Cl drop it to -70mV

161
Q

What is the Nernst equation?

A

E = RT ln(c1/c2) +ZFv

162
Q

What is the most predictive measurement of morbidity in obesity

A

Waist circumference NOT BMI

163
Q

What pathways are involved in obesity

A

Hyperinsulinaemia - increased deposition of fat
Insulin resistance - t2dm
Suppressed leptin - reduced satiety
Insulin mediated reduction in dopamine clearance - increased food reward

164
Q

What is the site of release, function of leptin

A

Released from adipose tissue
Signals adipose tissue mass and thus adequacy of energy supply to CNS
Overall reduces food intake and permits energy expenditure

165
Q

What is the CNS effect of insulin

A

Similar to leptin
Reduces feeding, causes satiety
Activates SNS

166
Q

Where in the brain senses leptin and insulin levels

A

Hypothalamus

167
Q

What are the end effects of leptin and insulin centrally

A

Increased saitity to decrease meal size
Increased SNS activity causing energy expenditure - glycogen breakdown, lipolysis

FRCA Physiology (1 decks)

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