ILA Flashcards

1
Q

what is the first stage of protein synthesis?

A

transcription

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2
Q

what is the second stage of protein synthesis?

A

translation

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3
Q

where does transcription occur?

A

nucleus

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4
Q

which enzyme carries out transcription?

A

RNA polymerase
NOT DNA polymerase

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5
Q

what is transcription?

A

DNA sequence is copied to make an RNA molecule

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6
Q

function of DNA helicase

A

unzips
breaks hydrogen bonds in the DNA double helix to unzip the DNA double helix and expose nucleotides

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7
Q

function of topoisomerase

A

unwinds
relieves the supercoils

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8
Q

function of single stranded binding proteins

A

SSBPs
stop DNA strands reannealing

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9
Q

where does RNA polymerase bind?

A

at the TATA promoter region

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10
Q

what is the promoter region?

A

TATA

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11
Q

in what direction does RNA polymerase move?

A

3’ to 5’

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12
Q

in what direction does RNA polymerase read?

A

3’ to 5’

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13
Q

in what direction does RNA polymerase code?

A

5’ to 3’

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14
Q

what are the stop codons?

A

UAA
UAG
UGA

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15
Q

for transcription, are one or both strands copied?

A

one

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16
Q

how does RNA polymerase work?

A

adds complementary mRNA nucleotides to the template strand to build an RNA chain

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17
Q

does the RNA transcript contain the same information as the template or non-template strand?

A

non template strand
this is called the coding strand

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18
Q

which nucleotides does RNA contain?

A

AUCG

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19
Q

what is the start and end of an mRNA strand?

A

poly-A tail (end) and 5’ cap (start)

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20
Q

product of transcription

A

pre mRNA

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21
Q

what part of pre-mRNA is removed?

A

introns

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22
Q

splicing

A

process of removing introns to form a fully coding strand

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23
Q

what part of mRNA remains after splicing?

A

exons

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24
Q

where does splicing occur?

A

in the nucleus

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25
Q

which enzymes carry out splicing?

A

spliceosomes

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26
Q

how does mRNA leave the nucleus?

A

nuclear pore

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27
Q

what is translation?

A

protein is synthesised from mRNA

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28
Q

where does translation occur?

A

ribosome in cytoplasm

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29
Q

3 bases on tRNA

A

anticodon

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30
Q

what does the tRNA anticodon bind to?

A

mRNA codon

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31
Q

3 DNA bases

A

triplet

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32
Q

describe translation

A

tRNA anticodons bind to mRNA codons
tRNA carries the correct amino acid
peptide bonds form between the amino acids
stop codon is reached

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33
Q

product of translation

A

polypeptide

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34
Q

where is mRNA broken down after translation?

A

cytosol

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35
Q

in which direction does mRNA move?

A

3’ to 5’ direction

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36
Q

transcriptome

A

the sum total of all the mRNA molecules

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37
Q

what is an SNP?

A

single nucleotide polymorphism
DNA sequence variation when a single nucleotide is substituted

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38
Q

consequences of an SNP

A

can result in a different codon which generates a different protein and thus disease

can affect recognition/ promoter/ termination sequences to change the length of proteins

most don’t (e.g if in an intron)

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39
Q

name two diseases caused by an SNP

A

cystic fibrosis
sickle cell anaemia

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40
Q

what is sickle cell haemoglobin?

A

HbS

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41
Q

genetic cause of HbS

A

SNP of adenine to thymine
GAG becomes GTG on 17th nucleotide
glutamic acid to valine
different primary structure

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42
Q

difference between sickle cell anaemia and sickle cell trait

A

sickle cell anaemia - both genes that code for haemoglobin are abnormal (HbSS)

sickle cell trait - only one chromosome carries the abnormal allele

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43
Q

how many of the beta subunits are replaced by HbS in sickle cell disease

A

just one

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44
Q

which subunits does haemoglobin have?

A

2 alpha
2 beta

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45
Q

what is normal adult haemoglobin?

A

HbA

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46
Q

is sickle cell anaemia autosomal dominant or recessive?

A

recessive

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47
Q

functional changes in HbS

A

red blood cells become sickle shaped
cells don’t live as long
lower affinity for oxygen
gets stuck in blood vessels
reduced oxygen delivery to muscles

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48
Q

primary structure of a protein

A

sequence of amino acids
covalently bonded

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49
Q

secondary structure of a protein

A

alpha helices and beta pleated sheets
hydrogen bonds

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50
Q

tertiary structure of a protein

A

3D structure of a single chain of amino acids
- London forces
- hydrogen bonds
- ionic bonds
- disulphide bonds

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51
Q

quaternary structure of a protein

A

the presence of more than one polypeptide chain

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52
Q

what fraction of water is in the intracellular fluid compartment?

A

2/3

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53
Q

what fraction of water is in the extracellular fluid compartment?

A

1/3

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54
Q

what volume of water is in the intracellular fluid compartment?

A

28L

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55
Q

what volume of water is in the extracellular fluid compartment?

A

14L

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56
Q

what volume of water is in the plasma fluid compartment?

A

3L

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57
Q

what volume of water is in the interstitial fluid compartment?

A

11L

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58
Q

what percentage of body sodium is exchangeable?

A

70%

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59
Q

what percentage of body sodium is bone crystal?

A

30%

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60
Q

what percentage of the total body sodium is in the ECF?

A

50%

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61
Q

what percentage of body sodium is in the ICF?

A

5%

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62
Q

what percentage of the body weight is water?

A

60%

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63
Q

define osmolality

A

concentration of a solution expressed as solute particles per kg

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64
Q

define osmolarity

A

concentration of solution expressed as solute particles per L

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65
Q

define oncotic pressure

A

pressure exerted by plasma proteins on capillary wall
force keeping water in a capillary

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66
Q

define osmosis

A

process by which molecules within a solvent pass through a semi-permeable membrane from a high to low concentration

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67
Q

what is hydrostatic pressure?

A

force pushing water out of the capillary

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68
Q

what part of the brain detects a low water potential?

A

osmoreceptors in the hypothalamus

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69
Q

what does the hypothalamus trigger?

A

release of ADH from the posterior pituitary

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70
Q

where is ADH released from?

A

posterior pituitary gland

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71
Q

what stimulates the posterior pituitary?

A

hypothalamus

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72
Q

what does ADH act on?

A

kidney

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73
Q

effect of ADH

A

increased fluid retention

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74
Q

is urine diluted or concentrated in the loop of Henle?

A

diluted

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75
Q

where is urine concentrated?

A

distal tubules and collecting ducts

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76
Q

is the descending limb of the loop of Henle permeable to sodium chloride and water?

A

impermeable to sodium chloride
permeable to water

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77
Q

is the ascending limb of the loop of Henle permeable to sodium chloride and water?

A

permeable to sodium chloride
impermeable to water

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78
Q

where is renin released from?

A

granular cells (juxtaglomerular cells) of the renal juxtaglomerular apparatus

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79
Q

what triggers renin release?

A
  1. reduced sodium delivery to DCT detected by macula densa
  2. reduced perfusion pressure in the kidney detected by baroreceptors in the afferent arteriole
  3. Sympathetic stimulation of the JGA via β1 adrenoreceptors
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80
Q

what inhibits renin release?

A

ANP
atrial natriuretic peptide

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81
Q

when is ANP released?

A

released by stretched atria in response to increases in blood pressure

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82
Q

where is angiotensinogen made?

A

liver

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83
Q

what converts angiotensinogen to angiotensin I?

A

renin

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84
Q

what converts angiotensin I to angiotensin II?

A

ACE
angiotensin converting enzyme

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85
Q

effects of angiotensin II

A

arteriolar vasoconstriction
Na+ reabsorption in the kidneys
triggers the sympathetic nervous system to release noradrenaline
aldosterone release from the adrenal cortex
hypothalamus - increases thirst sensation and stimulates anti-diuretic hormone (ADH) release

increases the volume of ECF and increases blood pressure

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86
Q

where is aldosterone released from?

A

zona glomerulosa of the adrenal cortex of adrenal gland

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87
Q

effect of aldosterone

A

acts on principal cells of the collecting ducts of the nephron
increases absorption of sodium and water into the blood
increases the excretion of potassium

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88
Q

where is albumin produced?

A

liver

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89
Q

what is the main plasma protein contributing to oncotic pressure?

A

albumin

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90
Q

what does low albumin cause?

A

oedema

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91
Q

what is low albumin levels called?

A

hypoalbuminemia

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92
Q

why does hypoalbuminemia cause oedema?

A

fluid moves from capillaries into interstitium

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93
Q

key routes of water loss from the body

A

urine
faeces
sweat
breath
vomiting

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94
Q

what are sensible water losses?

A

can be measured

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95
Q

what are insensible water losses?

A

cannot be measured

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96
Q

examples of insensible water losses

A

breath, sweat, faeces

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97
Q

give examples of sensible water loss

A

urine

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98
Q

what is vasopressin also called?

A

ADH

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99
Q

how does ADH/ vasopressin work?

A

binds to receptors on the collecting duct membrane
causes intracellular production of cAMP which activates protein kinase, which phosphorylates proteins that increase the rate of fusion of vesicles containing aquaporins with the membrane

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100
Q

what stimulates thirst?

A

an increase in plasma osmolarity
decrease in extracellular fluid volume
angiotensin II

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101
Q

what happens when renal blood flow is reduced?

A

juxtaglomerular cells convert prorenin to renin in the kidneys

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102
Q

what are the components of the juxtaglomerular apparatus?

A
  1. macula densa - part of DCT
  2. juxtaglomerular cells (granular cells) - afferent arterioles
  3. extraglomerular mesangial cells
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103
Q

where is the macula densa?

A

DCT

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104
Q

function of the macula densa?

A

sensitive to changes in NaCl

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105
Q

where are the juxtaglomerular (granular) cells?

A

afferent arteriole

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106
Q

function of the juxtaglomerular cells

A

release renin

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107
Q

where are mesangial cells?

A

central stalk of the glomerulus

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108
Q

what is the difference between the action of ADH and aldosterone?

A

ADH increases the nephron’s permeability to water whereas aldosterone increases the reabsorption of both sodium and water

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109
Q

effect of sodium on ECF volume, blood volume and blood pressure

A

an increase in Na+ in ECF =
- increased ECF volume
- increase in blood plasma volume
- increased blood pressure

a decrease in Na+ in ECF
- ECF decrease
- blood volume decreases
- blood pressure decreases

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110
Q

where is the thirst centre?

A

hypothalamus

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111
Q

normal homeostatic response to excess fluid

A

decrease in ECF osmolality detected by osmoreceptors
- water moves into ICF from ECF
- stops the stimulation of the thirst centre in the hypothalamus
- inhibits ADH in the posterior pituitary, leading to an increased urine volume

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112
Q

where are osmoreceptors found?

A

hypothalamus

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113
Q

consequence of excess water consumption

A

hyponatremia

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114
Q

normal homeostatic response to dehydration

A

increase in ECF osmolality detected by osmoreceptors
- water moves from ICF to ECF
- stimulates thirst centre of hypothalamus
- ADH released from posterior pituitary to decrease urine volume

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115
Q

state how much water a 70kg man has, and how much of this is intracellular, interstitial and intravascular

A

42L in total
28L is intracellular
11L is interstitial
3L is intravascular

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116
Q

estimated plasma osmolality

A

2[Na] + 2[K] + urea + glucose mol/L

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117
Q

normal range for plasma osmolality

A

270-310

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118
Q

where is ADH made?

A

hypothalamus

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119
Q

where is ADH stored?

A

posterior pituitary

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120
Q

where does ADH act?

A

kidney

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121
Q

where is aldosterone produced?

A

adrenal cortex of adrenal gland

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122
Q

where is aldosterone secreted from?

A

adrenal cortex

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123
Q

where is renin produced and secreted from?

A

juxtaglomerular cells of the kidney

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124
Q

equation for cardiac output

A

stroke volume x heart rate

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125
Q

what is cardiac output?

A

volume of blood pumped by the heart per minute

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126
Q

unit of cardiac output

A

L/ minute

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127
Q

what factors affect heart rate?

A

autonomic innervation, hormones, fitness levels, age

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128
Q

equation for stroke volume

A

SV = EDV - ESV
stroke volume = end diastolic volume - end systolic volume

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129
Q

what factors affect stroke volume?

A

contractility, preload, after load, heart size, fitness level, gender, duration of contraction

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130
Q

what is contractility?

A

how hard/ fast muscles flex

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131
Q

what is preload?

A

degree of myocardial distension prior to shortening

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132
Q

what is afterload?

A

force against which ventricle must act in order to eject blood

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133
Q

what does the LAD supply?

A

anterior 2/3 of interventricular septum, lateral wall of left ventricles and anterolateral papillary muscle

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134
Q

what does the right coronary artery supply?

A

SAN and AVN
right ventricle, right atrium

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135
Q

equation for blood pressure

A

blood pressure = cardiac output x total peripheral resistance
BP = CO x TPR

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136
Q

equation for pulse pressure

A

PP = SP - DP
pulse pressure = systolic pressure - diastolic pressure

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137
Q

equation for mean arterial pressure

A

MAP = DP + 1/3PP
mean arterial pressure = diastolic pressure + 1/3pulse pressure

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138
Q

what is pulse pressure?

A

difference between systolic and diastolic pressure

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139
Q

what is mean arterial pressure?

A

average arterial pressure throughout one cardiac cycle, systole, and diastole

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140
Q

what is stroke volume?

A

volume of blood pumped out of the left ventricle of the heart during each systolic cardiac contraction

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141
Q

which factors affect blood pressure?

A

vasopressin (ADH), aldosterone, ANP, haemorrhage, sweating, stressors, hydration, weight, muscular activity, posture

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142
Q

average cardiac output

A

5L/min

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143
Q

what is Frank Starling’s Law?

A

the greater the stretch of myocardium before systole, the stronger the ventricular contraction
stroke volume of the heart increases in response to increased volume of blood in ventricles before contraction
stroke volume increases with EDV

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144
Q

what is the physiology behind the Frank-Starling Law?

A

increased force because actin and myosin filaments are brought to more optimal degree of overlap for force generation

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145
Q

normal range of EDV

A

110-120ml

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146
Q

when is the cardiac cycle initiated?

A

SAN fires

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147
Q

what does firing of the SAN cause?

A

atrial depolarisation

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148
Q

how is atrial depolarisation represented on an ECG?

A

p wave

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149
Q

when does atrial contraction start?

A

shortly after the p wave

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150
Q

consequence of atrial contraction

A

blood enters ventricles

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151
Q

why doesn’t ventricular volume start at zero?

A

there is a passive movement of blood from the atria to the ventricles as the AV valves are open due to the pressure gradient

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152
Q

why do the AV valves shut?

A

ventricular pressure rises above atrial pressure

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153
Q

what causes the first heart sound?

A

closing of AV valve

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154
Q

how is ventricular depolarisation represented on an ECG?

A

QRS complex

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155
Q

why does the ventricular volume initially not change?

A

semilunar valves are shut

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156
Q

what is isovolumetric contraction?

A

ventricles contract when the semilunar valves are shut, so the volume does not change

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157
Q

what is the rapid ejection phase?

A

ventricular pressure exceeds pressure in the aorta and pulmonary artery
semilunar valves open and blood is ejected out of the ventricles

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158
Q

how is ventricular repolarisation represented on an ECG?

A

T wave

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159
Q

what is the second heart sound?

A

ventricular pressure falls below aortic pressure
semilunar valves shut

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160
Q

what is isovolumic relaxation?

A

ventricles start to relax with all valves closed

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161
Q

what increases ventricular pressure on the graph?

A

contraction
filling with blood

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162
Q

when is most myocardium perfused and why?

A

diastole
subendocardial coronary vessels are compressed during ventricular systole which results in momentary retrograde blood flow
however, the epicardial coronary vessels remain open

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163
Q

blood supply to the heart muscles

A

coronary arteries

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164
Q

where does venous blood from the heart muscle go?

A

cardiac veins drain into coronary sinus, which drains into right atrium

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165
Q

what does the right coronary artery supply?

A

right ventricle, right atrium, SAN, AVN
septum

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166
Q

which is the largest coronary artery?

A

LAD

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167
Q

where does the LAD run?

A

anterior ventricular groove

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168
Q

what is the most common coronary artery occlusion?

A

LAD

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169
Q

how is the LAD occluded?

A

plaque from cholesterol
atherosclerosis

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170
Q

territory supplied by the LAD

A

anterior 2/3 interventricular septum
lateral wall of left ventricle
anterolateral papillary muscle

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171
Q

consequence of occlusion of LAD

A

block impulse conduction between atria and ventricles
left/ right heart block

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172
Q

symptoms of occlusion of LAD

A

infarction of conducting system, atheroma production, ST elevation, heart block and arrhythmia, (impulses cannot travel down left and right ventricle branches simultaneously), or heart failure, prolonged PR (type 1 heart block), nausea, shortness of breath, pain in head, jaws, arms

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173
Q

which type of coronary occlusion is called a widowmaker, and why?

A

LAD
high mortality rate

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174
Q

consequence of occlusion of right coronary artery

A

conduction of nodes affected, contractions become out of rhythm or slower, inefficient blood flow (ischaemia) and potential backflow

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175
Q

symptoms of occlusion of right coronary artery

A

chest pain, if complete block then heart muscle dies and MI results, pain radiating in arms, shoulders, jaw, neck or back, shortness of breath, weakness and fatigue

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176
Q

ways to reduce risk of heart problems

A

cut down alcohol intake
stop smoking
be more physically active
vaccination

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177
Q

how many units of alcohol per week?

A

14 units

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178
Q

effect of sympathetic stimulation on peripheral blood vessels

A

vasoconstriction to increase blood pressure

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179
Q

are peripheral blood vessels innervated by parasympathetic fibres?

A

no

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180
Q

the occlusion of which coronary artery is most likely to result in a fatal heart attack?

A

left main coronary artery

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181
Q

the occlusion of which coronary artery is most likely to result in a fatal heart attack and why?

A

left main coronary artery
supplies the largest area of heart muscle

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182
Q

which nerve supplies the pericardium?

A

phrenic
phrenic supplies the 3 p’s
pericardium, pleura, peritoneum

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183
Q

what is end diastolic volume?

A

total amount of blood in the ventricle just before systole

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184
Q

average stroke volume?

A

70ml

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185
Q

mitral valve stenosis

A

narrowing of the mitral valve
left atrium has to contract with more force to generate more pressure to overcome the valve stenosis
increase in left atrium pressure

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186
Q

what is the embryological ductus arteriosus?

A

connects the pulmonary artery to the aorta

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187
Q

what does the embryological ductus arteriosus become?

A

ligamentum arteriosum

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188
Q

what is the foramen ovale?

A

hole between the right and left atrium

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189
Q

what type of heart failure causes pulmonary oedema and why?

A

left heart failure
blood backs up in the pulmonary system

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190
Q

what type of heart failure causes peripheral oedema?

A

right heart failure

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191
Q

failure of both sides of the heart

A

biventricular failure

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192
Q

movement of oxygen and carbon dioxide in and out of the respiratory system

A

oxygen rich air from environment - nasal cavities - pharynx - trachea - bronchi - bronchioles - alveoli - oxygen and carbon dioxide exchange at alveoli - bronchioles - bronchi - trachea - pharynx - nasal cavities - carbon dioxide rich air to the environment

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193
Q

how is physiological dead space calculated?

A

anatomical (conducting) dead space + alveolar dead space

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194
Q

what is conducting/ anatomical dead space?

A

volume of the conducting airways
from the nose, mouth and trachea to the terminal bronchioles

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195
Q

what is the alveolar dead space?

A

comprises alveoli which are ventilated, but not supplied by the pulmonary arterial circulation

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196
Q

where is greatest resistance to air flow?

A

segmental bronchi

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197
Q

if diameter is doubled, how does resistance change?

A

decreases by 1/16

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198
Q

if diameter is halved, how does resistance change?

A

increases 16-fold

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199
Q

what is Poiseuille’s Law?

A

R = 8ul/pi x r^4

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200
Q

two types of pulmonary stretch receptors

A

slow and rapidly adapting

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201
Q

what is the Hering-Breuer reflex?

A

inhibits inspiration
smooth muscle response to stretch

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202
Q

what are juxtacapillary receptors?

A

in the alveolar walls, close to capillaries
also called J receptors
respond to
- irritants
- noxious agents
- interstitial fluid volume
leads to bronchoconstriction

203
Q

space between pleural membranes

A

intrapleural cavity

204
Q

what is type 1 respiratory failure?

A

hypoxemia
inadequate oxygen

205
Q

definition of type 1 respiratory failure

A

low level of oxygen with a normal or low level of carbon dioxide

206
Q

definition of type 2 respiratory failure

A

high carbon dioxide and low oxygen levels

207
Q

causes of type 1 respiratory failure

A

caused by conditions that affect oxygenation such as
- hypoventilation
- ventilation/ perfusion mismatch e.g pulmonary embolism
- low ambient oxygen at altitude
pneumonia
- shunt - oxygen blood mixes with non-oxygenated blood

208
Q

what is type 2 respiratory failure?

A

pump failure
ventilation failure due to hypercapnia/ hypoxaemia

209
Q

causes of type 2 respiratory failure

A

increased airway resistance
- COPD, asthma, suffocation
reduced breathing effort
- drugs
- brain stem lesion
reduction in the area of the lung available for gas exchange e.g chronic bronchitis

210
Q

what is the main driver for respiration?

A

carbon dioxide

211
Q

upper airways

A

nose, nasal cavity, pharynx, larynx

212
Q

lower airways

A

trachea, bronchi, bronchioles, alveoli

213
Q

compare the right and left main bronchus

A

right is shorter and more vertically aligned

214
Q

how many lobar bronchi does the left lung have?

A

two

215
Q

how many lobar bronchi does the right lung have?

A

three

216
Q

what do segmental bronchi supply?

A

each supplies a bronchopulmonary segment of the lung

217
Q

what are the two pontine respiratory centres?

A

pneumotaxic and apneuistic

218
Q

what are the two medullary respiratory groups?

A

dorsal respiratory group
ventral respiratory group
DRG and VRG

219
Q

which respiratory group is predominantly active during inspiration?

A

DRG

220
Q

which respiratory group is active during inspiration and expiration?

A

VRG

221
Q

are the DRG and VRG bilateral or unilateral?

A

bilateral

222
Q

function of the apneustic centre

A

positive firing
stimulates inspiration

223
Q

function of the pneumotaxic centre?

A

negative firing
antagonist to the apneustic centre
signals to the dorsal respiratory group
stimulates the external intercostals and diaphragm

224
Q

function of the dorsal respiratory group

A

signals to the ventral respiratory group
stimulates internal intercostals and accessory respiratory muscles

225
Q

where are central chemoreceptors?

A

ventral lateral surface of medulla

226
Q

function of central chemoreceptors

A

detect changes in pH of spinal fluid
so carbon dioxide levels

227
Q

where are peripheral chemoreceptors?
be specific

A

aortic body - aortic arch
carotid body - bifurcation of the common carotid

228
Q

what do peripheral chemoreceptors in the aortic body detect? and what do they not detect?

A

changes in blood oxygen and carbon dioxide but not pH

229
Q

what do peripheral chemoreceptors in the carotid body detect?

A

changes in blood oxygen, carbon dioxide and pH

230
Q

do central chemoreceptors desensitise?

A

yes

231
Q

do peripheral chemoreceptors desensitise?

A

no

232
Q

which chemoreceptors have the greater impact on ventilation?

A

peripheral

233
Q

why is carbon dioxide the main driver to breathe?

A

chemoreceptors respond to small changes in carbon dioxide but only large oxygen changes

234
Q

what happens when there is an increase in carbon dioxide levels?

A

decrease in blood pH due to production of H+ ions from carbonic acid when carbon dioxide combines with water
respiratory centre in medulla sends nervous impulses to the external intercostal muscles and diaphragm to increase breathing rate and lung volume during inhalation

235
Q

what happens when a decrease in oxygen is detected?

A

by peripheral chemoreceptors
low arterial oxygen stimulates chemoreceptors, increasing number of action potentials sent to ceentre in medulla
leads to an increase in ventilation, meaning more oxygen reaches the alveoli

236
Q

how are changes in carbon dioxide detected?

A

increased H+ concentration in extracellular fluid and arterial blood
increased stimulation of centre in the medulla and an increase in ventilation

237
Q

what does the ventral respiratory group stimulate?

A

both inspiratory and expiratory movements

238
Q

what does the dorsal respiratory group stimulate?

A

primarily inspiration

239
Q

equation for flow of air in/ out of lungs

A

flow = (p(alv) -p(atm))/R
p(alv) is alveolar pressure
p(atm) is atmospheric pressure
R is a constant

240
Q

when flow is negative, in which direction does air flow?

A

into lungs

241
Q

is alveolar pressure is less than atmospheric pressure, where does air flow?

A

into lungs

242
Q

what is Boyle’s Law, and what does it mean?

A

P1V1 = P2V2
at a constant temperature, an increase in the volume of a gas will cause a decrease in pressure

243
Q

equation for transpulmonary pressure

A

P(tp) = P(alv) - P(ip)
the difference between the alveolar pressure and intrapleural pressure
with intrapleural pressure being the pressure in the pleural space

244
Q

what is transpulmonary pressure?

A

difference in pressure between the inside and outside of the lungs

245
Q

is transpulmonary pressure always negative or positive relative to atmospheric pressure and why?

A

positive
because the lungs must always have some air in them

246
Q

what is P(ip)?

A

pressure of the intrapleural fluid surrounding the lungs

247
Q

is P(ip) negative or positive and why?

A

negative
the elasticity of the lungs and the chest wall mean they tend towards collapsing and enlarging respectively, so they move apart from each other
this reduces the pressure of the intrapleural fluid

248
Q

what is respiratory failure?

A

a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygen and carbon dioxide elimination

249
Q

what is a drop in arterial oxygen?

A

hypoxemia

250
Q

what is a rise in arterial carbon dioxide levels?

A

hypercapnia

251
Q

define hypercapnia

A

PaCO2 > 6kPa

252
Q

define hypoxemia

A

PaO2 < 8kPa

253
Q

definition of type 2 respiratory failure

A

high carbon dioxide and low oxygen levels

254
Q

role of saliva

A

enzymes, antibacterial, pH control, taste, lubrication

255
Q

muscular composition of the oesophagus

A

upper 1/3 skeletal muscle
lower 2/3 smooth muscle

256
Q

innervation of the different parts of the oesophagus?

A

upper 1/3 skeletal muscle supplied by superior laryngeal and recurrent laryngeal nerve
lower 2/3 smooth muscle supplied by enteric nervous system

257
Q

two names for the sphincter at the entrance of the stomach

A

lower oesophageal sphincter
cardiac sphincter

258
Q

what is GORD?

A

stomach acid refluxes into oesophagus
oesophageal mucosa is exposed to stomach acid, bile and pepsin which damages the lining

259
Q

what can cause GORD?

A

cardiac sphincter weakened (also called the LES)
takes less pressure for fluid to move back up
poor oesophageal motility

260
Q

passage of food from the mouth to the duodenum

A

mouth, pharynx, oesophagus, stomach, duodenum

261
Q

at which spinal level is the oesophagus continuous with the pharynx?

A

C6

262
Q

at which spinal level does the oesophagus emerge through the diaphragm?

A

T10

263
Q

arterial supply of the oesophagus

A

left gastric artery
oesophageal branches from the left inferior phrenic artery

264
Q

which regions of the abdomen does the stomach lie in?

A

umbilical, epigastric and left hypochondriac

265
Q

regions of the stomach

A

cardia, fundus, body, pylorus

266
Q

function of the stomach

A

temporary food storage
mixing and breakdown of food
digestion (gastric juices and digestive enzymes from mucosa)

267
Q

function of the duodenum

A

receives partially digested food (chyme) from stomach and secretions from the pancreas, liver and gallbladder mix with chyme in duodenum to facilitate chemical digestion

268
Q

in the oesophagus, what is the orientation of the circular and longitudinal muscle layers?

A

inner circular
outer longitudinal

269
Q

what is a primary peristaltic wave?

A

occurs when food enters the oesophagus during swallowing and forces food down to stomach

270
Q

what is a secondary peristaltic wave?

A

if a bolus gets stuck, stretch receptors in oesophageal lining are stimulated and a second wave happens

271
Q

what does GORD stand for?

A

gastro-oesophageal reflux disease

272
Q

which cells make HCl?

A

parietal cells

273
Q

physiology of acid production in the stomach

A

water and carbon dioxide combine in the parietal cell to form carbonic acid (H2CO3)
this is catalysed by carbonic anhydrase
carbonic acid dissociates into a proton (H+) and a bicarbonate (HCO3-)
H+ enters the stomach lumen via an H+ - K+ ATPase on the apical membrane
this channel uses ATP to exchange k+ ions in the stomach with H+ ions in the parietal cells
bicarbonate ion is transported out of the cell into the blood in exchange for a chloride ion (Cl-) using an ion exchanger located on the basolateral membrane
chloride ion is transported into the stomach lumen through a chloride channel
the H+ and Cl- associate in the stomach lumen to form HCl

274
Q

3 ways of increasing acid production

A

ACh from vagus nerve
- released firstly during the cephalic phase of digestion
- activated upon seeing food
- directly stimulates parietal cells
- also produced during the gastric phase of digestion when intrinsic nerves detect distension of the stomach, stimulating ACh production

gastrin
- hormone secreted from stomach G cells
- G cells activated by vagus nerve
- gastrin released into blood until it reaches the parietal cells
- gastrin binds to CCK receptors on the parietal cells

enterochromaffin like cells in the stomach secrete histamine which binds to H2 receptors on the parietal cells
these cells secrete histamine in response to the presence of gastrin and ACh

275
Q

decreasing stomach acid production

A

low pH
- accumulation of acid in the stomach between meals leads to a lower pH
- inhibits gastrin secretion via the production of somatostatin from D cells

when food passes into duodenum, enterogastric reflex
- inhibitory signals sent to stomach via enteric nervous system
- signals to medulla to reduce vagal stimulation of the stomach

presence of chyme in the duodenum stimulates entero-endocrine cells to release cholecystokinin and secretin
- both complete digestion and inhibit gastric acid secretion

276
Q

defences of gastric and duodenal mucosa against acid damage

A

produce HCO3-
- alkaline neutralises stomach acid on top of epithelial surface
mucous production

277
Q

which glands in the duodenal mucosa secrete alkaline mucus?

A

Brunner’s glands

278
Q

what is dyspepsia?

A

group of symptoms altering doctors to consider disease of the upper GI tract
- nausea
- vomiting
- heartburn

279
Q

risk factors for GORD

A

family history
older age
obesity
hiatus hernia

280
Q

risk factors for reflux

A

overweight
- extra pressure on stomach/ diaphragm

smoking
- loosen sphincter

alcohol
- damage stomach lining/ glands

large meals
- stomach stretches increasing pressure on lower oesophageal sphincter

pregnancy
- more pressure on sphincter
- generalised smooth muscle relaxation due to progesterone

281
Q

why can acid reflux cause a sore throat?

A

acid enters pharynx

282
Q

what divides the liver into anatomical left and right lobes?

A

falciform ligament

283
Q

how is the liver divided into a functional left and right?

A

line vertically halfway through the IVC and gallbladder

284
Q

which lobes are present on the visceral surface of the liver?

A

caudate and quadrate

285
Q

which accessory lobe of the liver is superior?

A

caudate

286
Q

what separates the caudate and quadrate?

A

porta hepatis

287
Q

what is the porta hepatis?

A

bundle of blood vessels, nerves and ducts entering or leaving the liver

excludes the hepatic vein which drains into the IVC

288
Q

arrangement of hepatocytes

A

hexagonal lobules
portal triad at each corder
surround a central vein

289
Q

what is the portal triad?

A

venule of a portal vein
arteriole of hepatic artery
bile duct

along with lymphatics and vagus nerve fibres

290
Q

function of sinusoids

A

deliver blood to central vein

291
Q

what is the space of Disse?

A

between the sinusoid endothelium and hepatocytes

292
Q

what does the space of Disse contain?

A

blood plasma

293
Q

where are Ito cells found?

A

space of Disse

294
Q

another name for Ito cells

A

hepatic stellate cells

295
Q

function of Ito cells

A

store fat
produce proteins such as collagen when liver is damaged

296
Q

action of Kupffer cells in the walls of the sinusoids

A

phagocytose blood borne pathogens

297
Q

what happens to old erythrocytes in the liver, bone marrow and spleen?

A

phagocytosed by macrophages
globin portion of Hb is metabolised into amino acids and reused for protein synthesis
organelles are recycled
haem portion is broken down into biliverdin for transport in the blood
the iron ions bind to the blood protein transferrin for transport
unused haem groups can be used for haematopoesis or converted into bilirubin and used to make bile in the liver
iron ions can be transferred into ferritin for storage in the liver

298
Q

where are old red blood cells broken down?

A

spleen, liver, bone marrow

299
Q

how are old red blood cells broken down?

A

macrophages

300
Q

when red blood cells are broken down, what happens to the globin portion?

A

it is protein
metabolised into amino acids and reused for protein synthesis

301
Q

when red blood cells are broken down, what happens to the cell organelles?

A

recycled

302
Q

when red blood cells are broken down, what happens to the haem groups?

A

separated into iron ions and haem group
haem group broken down into biliverdin for transport in the blood
biliverdin is used in haemopoesis or converted into bilirubin for bile
iron ions bind to the blood protein transferrin for transport
iron ions stored as ferritin in liver or used for haemopoiesis

303
Q

describe the formation and recycling of bile

A

formed from haem group
haem portion is converted to biliverdin by haem oxygenase (Fe2+ is liberated)
biliverdin is converted into unconjugated bilirubin by biliverdin reductase 6
unconjugated bilirubin undergoes biotransformation to form bilirubin in the liver
bilirubin dissolves in bile, and through digestive processes end up in the small intestine
bacteria remove glucuronic acid to form urobilinogen
urobilinogen is recycled by enterohepatic circulation or oxidised by different bacteria to form stercobilin
stercobilin is excreted in faeces to give it a brown colour

304
Q

subcostal plane

A

10th costal cartilage
lower most bony point of the rib cage
body of L3 vertebra

305
Q

which spinal level does the inferior mesenteric artery arise from?

A

L3

306
Q

which part of the duodenum is at L3?

A

third

307
Q

transtubecular plane

A

unites the tubercles of the iliac crests
upper border of L5
confluence of the common iliac veins (i.e IVC origin) lie on this plane

308
Q

where and how does the IVC originate?

A

confluence of the common iliac veins
L5

309
Q

what is haemolytic/ pre-hepatic jaundice?

A

increased unconjugated bilirubin due to excess erythrocyte breakdown, exceeding the capacity of the liver to transport it

310
Q

which jaundice is present in newborns and why?

A

haemolytic/ pre-hepatic
foetal haemoglobin is broken down

311
Q

causes of pre-hepatic jaundice

A

infection, trauma to erythrocytes, sickle cell anaemia, drugs and toxins and antibodies

312
Q

signs of haemolytic/ pre-hepatic jaundice

A

absence of bile pigments in urine and normal stool colour
this is because unconjugated bilirubin is insoluble so not filtered by kidney and bile can circulate to enter the intestine as normal

313
Q

what is hepatocellular/ hepatic jaundice?

A

hepatocytes are damaged so unable to transport bilirubin into the biliary system, so it enters the bloodstream instead
the bilirubin may be conjugated

314
Q

which type of bilirubin is elevated in haemolytic/ pre-hepatic jaundice?

A

unconjugated

315
Q

which type of bilirubin is elevated in hepatocellular/ hepatic jaundice?

A

conjugated and unconjugated

316
Q

what causes heptocellular/ hepatic jaundice?

A

hepatitis, cirrhosis and congestive liver disease

317
Q

signs of hepatocellular/ hepatic jaundice

A

dark amber urine due to water soluble conjugated bilirubin that has been filtered by the kidneys
normal stools because some bile pigment manages to be excreted into the biliary tract and intestine

318
Q

what is cholestatic/ obstructive/ post-hepatic jaundice?

A

obstruction in the biliary system due to anatomical obstructions e.g gallstones, cancers of the pancreas of ampulla of Vater

319
Q

what causes post hepatic jaundice?

A

hepatitis
intrahepatic cholestasis
extra hepatic cholestasis

320
Q

signs of post-hepatic jaundice

A

amber urine - bilirubin is conjugated so can be filtered by kidneys
pale stools as the bile cannot enter the intestine
itching of the skin as bile salts build up below skin, triggering an inflammatory response

321
Q

function of the frontal lobe

A

motor cortices and association areas
regions controlling behaviour, decision making and personality (prefrontal association area)
Broca’s area in the left frontal lobe - responsible for fluent speech

322
Q

role of Broca’s area

A

motor control of speech

323
Q

consequence of damage to Broca’s area

A

expressive aphasia
no motor control of speech
when you know what you want to say, but you have trouble saying or writing your thoughts

324
Q

blood supply to Broca’s area

A

middle cerebral artery

325
Q

blood supply to Wernicke’s area

A

middle cerebral artery

326
Q

role of temporal lobe

A

auditory cortices
medial temporal lobe for long term memory and emotion
- hippocampus
- entorhinal and perirhinal cortex
limbic system
Wernicke’s area for understanding speech and written language

327
Q

role of Wernicke’s area

A

understanding speech and written language

328
Q

consequence of damage to Wernicke’s area

A

receptive/ fluent aphasia
when someone is able to speak well and use long sentences, but what they say may not make sense

329
Q

function of the parietal lobe

A

somatosensory cortices

330
Q

where is the primary somatosensory cortex?

A

postcentral gyrus
parietal lobe

331
Q

function of the occipital lobe

A

vision

332
Q

where exactly is the primary visual cortex?

A

calcarine fissure of occipital lobe

333
Q

function of the cerebellum

A

balance, posture, receiving information from vestibulocochlear organs

334
Q

symptoms of cerebellar damage

A

DANISH
dysdiadokokinesia, ataxia, nystagmus of eyes, intention tremor, slurring of speech, heel-shin test positive

335
Q

parts of midbrain

A

tectum and tegmentum

336
Q

parts of the brainstem

A

midbrain, pons, medulla

337
Q

grey matter surrounding the cerebral acqueduct

A

periaqueductal grey

338
Q

function of the pons

A

breathing, sleeping, swallowing, bladder control

339
Q

function of the medulla

A

autonomic regulation, corticospinal pyramids

340
Q

what does the anterior cerebral artery supply?

A

corpus callosum and medial region of the brain

341
Q

what does the middle cerebral artery supply?

A

lateral parts of the hemisphere and anterior deep structures

342
Q

what does the posterior cerebral artery supply?

A

posterior region and the posterior inferior structures
e.g caudate nucleus, occipital lobe

343
Q

draw and label the circle of willis

A

.

344
Q

what is myasthenia gravis?

A

autoimmune destruction of nicotinic ACh receptors

345
Q

role of upper motor neurons

A

cell body originates in the cerebral cortex or brainstem and terminates within the brainstem or spinal cord

346
Q

role of lower motor neurons

A

alpha motor neurons exiting the spinal cord to innervate muscles

347
Q

cause of upper motor neuron weakness

A

brain injury and trauma
capsular stroke
spinal cord lesion
cerebral palsy

348
Q

symptoms of upper motor neuron lesion

A

effects will be mainly contralateral if damaged above the medulla, or ipsilateral if below
develop spasticity and stiffness over time
abnormal increased reflexes, such as babinski’s sign
clonus

349
Q

cause of lower motor neuron weakness

A

peripheral trauma
Guillain-Barre syndrome
botulism
nonclassical polio
cauda equina syndrome
amyotrophic lateral sclerosis

350
Q

symptoms of lower motor neuron lesion

A

weakness and atrophy of muscle
spontaneous neuronal discharge causing fasciculations
loss of reflexes - areflexia

351
Q

does the frontal lobe control movement in the ipsilateral or contralateral part of the body?

A

contralateral

352
Q

which hemisphere is dominant in a right handed person?

A

left

353
Q

which sulcus separates the frontal and parietal lobes?

A

central sulcus

354
Q

function of the primary somatosensory cortex

A

receive and interpret sensations e.g pain, touch, pressure

355
Q

which cranial nerves originate from the cerebrum?

A

olfactory and optic

356
Q

two major groups of descending tracts

A

pyramidal and extrapyramidal

357
Q

why do the pyramidal tracts have that name?

A

they pass through the medullary pyramids of the medulla oblongata

358
Q

where do pyramidal tracts originate?

A

cerebral cortex

359
Q

what are descending tracts?

A

pathways by which motor signals are sent from the brain to lower motor neurons in efferent neurons
the lower motor neurons then directly innervate muscles to produce movement

360
Q

function of the pyramidal tracts

A

voluntary control of body and face musculature

361
Q

which pyramidal tract supplies the musculature of the body?

A

corticospinal

362
Q

which pyramidal tract supplies the facial and neck muscles?

A

corticobulbar

363
Q

where do the corticobulbar tracts begin?

A

lateral aspect of primary motor cortex

364
Q

path of corticobulbar tracts

A

cortex, descends through internal capsule, crus cerebri, brainstem (pons and medulla), terminate on motor nuclei of cranial nerve

365
Q

where do extrapyramidal tracts originate?

A

brainstem

366
Q

what aspect of the primary motor cortex supplies the facial and neck muscles?

A

corticobulbar tract - lateral

367
Q

function of extrapyramidal tracts

A

involuntary and autonomic control of musculature
carry motor fibres to spinal cord from brain stem

368
Q

name the extrapyramidal tracts

A

vestibulospinal, reticulospinal, rubrospinal, tectospinal

369
Q

function of the vestibulospinal tract

A

balance and posture
has medial and lateral pathways

370
Q

function of the medial reticulospinal tract

A

facilitates voluntary movement by increasing muscle tone

371
Q

function of the lateral reticulospinal tract

A

inhibits voluntary movements by decreasing muscle tone

372
Q

function of the rubrospinal tract

A

fine control of hand movement

373
Q

function of the tectospinal tract

A

coordinates movement of head in relation to visual stimuli

374
Q

where do upper motor neurons travel between?

A

brain and brainstem to ventral horn of the spinal cord

375
Q

where do lower motor neurons travel between?

A

ventral horn of the spinal cord to the peripheral muscles

376
Q

what is the cortical homunculus?

A

contains the motor and sensory homunculus
region of the brain dedicated to processing motor and sensory functions for different parts of the body

377
Q

motor homunculus

A

motor processing for different bodily anatomical positions

378
Q

where does the motor homunculus handle signals coming from?

A

premotor area of frontal lobes

379
Q

sensory homunculus

A

sensory processing for different anatomical positions

380
Q

where does the sensory homunculus handle signals coming from?

A

thalamus

381
Q

what is the corona radiata?

A

white matter sheet that continues ventrally as the internal capsule and dorsally as the centrum semi ovale
group of nerves key for sending messages between regions of the brain

382
Q

internal capsule

A

white matter structure situated in the inferomedial part of the cerebral hemisphere of the brain, carrying information past the basal ganglia
connects the midbrain and cerebral cortex

383
Q

which blood vessels are part of the anterior circulation?

A

anterior and middle cerebral arteries

384
Q

which blood vessels are part of the posterior circulation?

A

posterior cerebral, vertebral, basilar and their branches

385
Q

what links the posterior and anterior circulations?

A

circle of Willis

386
Q

largest terminal branch of the internal carotid arteries

A

middle cerebral artery

387
Q

occlusion of which artery causes hemianopia?

A

posterior cerebral artery
this stroke affects the visual pathways from the optic chiasm onwards towards the occipital lobe

388
Q

can a stroke of the posterior circulation also cause muscle weakness? why?

A

corticospinal tracts have to travel through the brainstem and spinal cord

389
Q

which neurotransmitter do upper motor neurons use?

A

glutamate

390
Q

which receptors detect the neurotransmitter glutamate?

A

glutamatergic receptors

391
Q

function of lower motor neurons

A

receive impulses from the upper motor neurons and connect the spinal cord and brainstem to the muscle fibres

392
Q

do upper or lower motor neuron disorders cause spacicity?

A

upper

393
Q

do upper or lower motor neuron disorders cause flaccidity?

A

lower

394
Q

symptoms of an upper motor neuron lesion

A

muscle weakness in the extensors (in the flexors for the legs)
hypermedia and muscle spacicity
weakness on the contralateral side of the lesion due to 85% of the fibres crossing over (decussation)

395
Q

upper or lower motor neurons cause forehead sparing?

A

upper

396
Q

symptoms of lower motor neuron lesions

A

severe atrophy, hypotonia, hypoflexia, flaccid muscle weakness
affects the whole side of the body, including the forehead

397
Q

what is muscular dystrophy?

A

X-linked genetic disorders resulting in malformed dystrophin
loss of cell membrane cytoskeletal connections, unregulated influxes of calcium to sarcolemma
e.g Duchenne’s

398
Q

what is the CNS?

A

brain and spinal cord

399
Q

is the somatic nervous system always stimulatory?

A

yes

400
Q

function of the somatic nervous system

A

voluntary movement - skeletal muscles
reflex arcs involving muscles

401
Q

functions of the ANS

A

heart rate, digestion, salivation, urination, digestion

402
Q

main parasympathetic neurotransmitter

A

ACh

403
Q

main sympathetic neurotransmitter

A

noradrenaline

404
Q

what is the resting potential?

A

-70mV

405
Q

which pump maintains the resting potential and how?

A

Na+/ K+ pump
3 Na out, 2 K in

406
Q

describe the physiology of an action potential

A

action potential begins with a depolarising stimulus e.g neurotransmitter binding to ion channel
cell is depolarised (becomes less negative)
voltage gated Na+ channels open
influx of sodium ions
threshold potential reached at -55mV
action potential occurs if threshold potential reached
influx of sodium ions continues until +30mV via a positive feedback loop
the sodium channels close
potassium voltage gated channels open and potassium ions leave the cell to repolarise the membrane
membrane potential approaches resting potential
potassium channels experience a delay in closing resulting in hyperpolarisation
once voltage gated potassium channels close, resting potential is restored

407
Q

what is hyperpolarisation

A

potassium voltage gated channels experience a delay in closing
potential falls below -70mV

408
Q

what is the absolute refractory period?

A

no stimulus can produce a second action potential

409
Q

what is the relative refractory period?

A

second action potential can happen, but needs stronger stimulus

410
Q

is there a higher or lower concentration of sodium ions on the inside or outside during the resting potential of the cell?

A

outside

411
Q

what do sensory receptors respond to?

A

stimuli

412
Q

what are sub-modalities?

A

different variations within a stimulus e.g pitch and volume in audible stimuli

413
Q

how are sensory receptors triggered?

A

ion channels if the stimulus is large enough

414
Q

types of sensory receptors

A

tonic - slow adapting receptors
phasic - rapid adapting receptors

415
Q

which receptors detect pain?

A

nociceptors

416
Q

are nociceptors phasic or tonic?

A

phasic

417
Q

what are Pacinian corpuscles?

A

phasic receptors
respond to pressure changes and vibration

418
Q

which spinal segments control the knee jerk reflex?

A

L3 L4

419
Q

describe the knee jerk reflex

A

patellar ligament is struck
afferent signal travels to spinal cord
synapses with 1 interneurons and 2 alpha-motor neurons
inhibitor - via interneuron, goes to flexor (hamstrings). polysynaptic
excitatory, via alpha motor neurons, to extensor (quadriceps)
monosynaptic
extensor contracts and flexor relaxes
knee jerks

420
Q

brown sequard syndrome

A

an incomplete spinal cord lesion, typically in cervical region
lesion in one half of the spinal cord due to hemisection
usually cervical
weakness on one side (hemiparaplegia) and loss of sensation on the opposite side (hemianaesthesia)
ipsilateral loss of
- motor function
- vibration
- proprioception
- deep touch
to lesion
contralateral loss of
- pain
- temperature

421
Q

how does diameter affect conduction speed?

A

larger fibre has a faster action potential as more ions can flow in a given time

422
Q

are sodium channels found in the nodes of ranvier or myelinated regions?

A

nodes of ranvier

423
Q

what is saltatory conduction?

A

action potentials jump from node to node

424
Q

what are the four aspects of a stimulus?

A

modality, intensity, location, duration
MILD

425
Q

absence of the patellar reflex

A

Westphal’s sign

426
Q

causes of brown sequard - traumatic and non traumatic

A

traumatic
- bullet, stab wound, kick, car accident
non-traumatic
- tumour
- disc hernia
- MS

427
Q

what happens if the lesion is below the point of decussation?

A

ipsilateral side is affected

428
Q

what happens if the lesion is above the point of decussation?

A

contralateral side is affected

429
Q

what is the spnothalamic tract?

A

ascending tract which carries pain sensation

430
Q

does the spinothalamic tract decussate, and where?

A

yes
spinal cord

431
Q

which spinal segments are responsible for
a. achilles
b. patellar
c. biceps
d. triceps
reflexes

A

S1, S2 - achilles
L3, L4 - patellar
C5, C6 - biceps
C7, C8 - triceps

1,2 buckle my shoes
3,4 kick down the door
5,6 pick up the sticks
7,8 lay them straight

432
Q

layers of the kidney

A

outer cortex
inner medulla

433
Q

kidney anatomy

A

pyramids taper to form the papilla
from the papilla, the urine drips into a minor calyx
several minor caylx form a major calyx
major calyx empty into the renal pelvis
pelvis empties into ureter

434
Q

where does the ureter narrow?

A

where the pelvis of the kidney becomes ureter (ureteropelvic junction)
pelvic brim
where the ureter passes through the bladder (uretovesical junction)

435
Q

what stops urine passing back up from the bladder into the ureter?

A

ureter enters bladder at oblique angle
as pressure in bladder rises, it presses on part of ureter which is in the bladder wall so stops urine from passing back up to the kidney

436
Q

what is the tube through which urine passes from the bladder to the exterior?

A

urethra

437
Q

length of female urethra

A

2 inches

438
Q

length of male urethra

A

8-10 inches long

439
Q

where does the female urethra end?

A

inferior to clitoris and superior to vaginal opening

440
Q

where does the male urethra end?

A

tip of the penis

441
Q

functional unit of the kidney

A

nephron

442
Q

cortical nephron

A

tubules extend only a short distance into medulla then back into cortex

443
Q

juxtamedullary nephrons

A

tubules extend deep within the medulla - have a vasa recta around them

444
Q

what is the part of the nephron in which blood plasma is filtered?

A

renal corpuscle

445
Q

glomerulus

A

capillary tuft formed by the afferent and efferent arterioles and encased in Bowman’s capsule

446
Q

where does bulk of reabsorption happen?

A

PCT

447
Q

what type of epithelium is the PCT?

A

cuboidal epithelium

448
Q

what type of epithelium is the loop of henle?

A

squamous epithelium

449
Q

is the descending limb permeable or impermable to water?

A

permeable

450
Q

where does solute reabsorption take place in the LOH?

A

ascending limb

451
Q

is the ascending limb permeable or impermeable to water?

A

impermeable

452
Q

function of the DCT

A

fine regulation of Ca2+, Na+, K+ and HCO3

453
Q

what size molecule can get through tthe filtration barrier?

A

10kDa

454
Q

what prevents albumin getting through the filtration barrier?

A

podocytes with negatively charged foot processes

455
Q

what does the Bowman’s capsule contain?

A

glomerular filtrate

456
Q

whaich factors affect the filtration of the glomerulus?

A

size of molecule
pressure
charge of molecule
rate of blood flow

457
Q

what percentage of cardiac output is renal blood flow?

A

20%

458
Q

normal cardiac output

A

5L min

459
Q

normal renal blood flow (RBF)?

A

1L/ min

460
Q

volume of liquid filtered by the kidneys per day/ GFR per day

A

180L

461
Q

GFR per minute

A

125ml/ min

462
Q

how many times is the blood plasma filtered per day?

A

60

463
Q

how many capillary beds does the nephron have?

A

two

464
Q

when does glomerular filtration occur?

A

blood hydrostatic pressure exceeds hydrostatic pressure of glomerular capsule and blood colloid pressure

465
Q

blood filtration barrier layers

A

fenestrated capillary endothelium
glomerular basement membrane
podocytes

466
Q

GFR means

A

glomerular filtration rate
volume of fluid filtered by the renal glomeruli per unit time

467
Q

renal clearance

A

virtual plasma volume per minute, from which a substance is completely eliminated

468
Q

which types of substances have serum concentrations in direct dependence with GFR?

A

substances with exclusive glomerular filtration (without tubular secretion or reabsorption)

469
Q

what percentage of glomerular filtrate is reabsorbed?

A

99%

470
Q

what does the PCT have to increase surface area?

A

villi

471
Q

function of the PCT

A

reabsorption of Na, Cl, glucose, amino acids, bicarbonate

472
Q

what is diabetes insipidus?

A

deficiency of ADH
massive diuresis and excessive thirst

473
Q

which protein is produced in the nephron?

A

Tamm Horsfall/ uromoduliin

474
Q

urine flow rate

A

1ml/kg/hr

475
Q

what is the rate determining step of RAAS?

A

renin

476
Q

which cells release renin?

A

granular cells of juxtaglomerular apparatus

477
Q

what 3 things trigger renin release?

A

reduced NaCl delivery to distal tubule detected by macula densa
reduced perfusion pressure in kidney detected by baroreceptors in afferent arteriole
sympathetic stimulation of JGA cells

478
Q

which nerve fibres innervate JGA cells?

A

beta 1 adrenergic sympathetic nerve fibres

479
Q

where is angiogensinogen produced?

A

liver

480
Q

action of renin

A

cleaves angiotensinogen to angiotensin 1

481
Q

action of ACE (angiotensin converting enzyme)

A

converts angiotensin I to angiotensin II

482
Q

where is ACE found?

A

renal endothelium , lungs, capillary endothelium

483
Q

action of angiotensin II

A

ADH release
aldosterone release
sympathetic stimulation

484
Q

another name for ADH

A

vasopressin

485
Q

what are mineralocorticoids?

A

class of steroid hormones that regulate salt and water balances

486
Q

which is the principal mineralocorticoid?

A

aldosterone

487
Q

which cells does aldosterone act on?

A

principal cells of the collecting duct

488
Q

action of aldosterone

A

regulates blood pressure by altering the amount of Na that is reabsorbed
increases the retention of sodium and excretion of potassium

489
Q

action of ADH

A

affects blood pressure by causing release of aquaporin channels into the membrane of principal cells of the collecting duct
causes increased water retention

490
Q

causes of chronic renal failure

A

high blood pressure
diabetes
high cholesterol

491
Q

complications of chronic renal failure

A

fluid retention - oedema
hyperkalaemia - usually excess potassium is removed from the blood by the kidneys
cardiovascular disease - chronic renal failure causes high blood pressure
weak bones

492
Q

how is GFR regulated?

A

myogenic reflex
tubuloglomerular feedback
RAAS system

493
Q

describe the kidney myogenic reflex

A

not dependent on nerve supply or blood-bornee substances
intrinsic property of the smooth muscle in the capillaries of glomerulus

494
Q

what happens to the GFR when the macula densa detect a fall in sodium chloride levels?

A

increases

495
Q

which mechanism regulates GFR?

A

tubuloglomerular feedback

496
Q

if a substance is not secreted or reabsorbed in the renal tubules, how do we measure renal clearance?

A

GFR

497
Q

what is the most common drive for reabsorbtion?

A

sodium potassium pump

498
Q

what is prerenal kidney failure?

A

sudden reduction of blood flow to the kidneys

499
Q

causes of pre-renal kidney failure?

A

hypotension
volume depletion e.g vomiting
oedema

500
Q

what is renal kidney failure?

A

direct damage to kidney

501
Q

causes of renal kidney failure

A

glomerular disease
acute interstitial nephritis
eclampsia
allergic reactions to medications

502
Q

what is post-renal kidney failure?

A

obstruction in the urinary tract

503
Q

causes of post renal kidney failure

A

kidney stones
urethral stricture
bladder tumour