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HOM > Renal > Flashcards

Renal Flashcards

1
Q

Which hormone does the kidney use to control RBC production?

A

Erythropoietin

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2
Q

Why is plasma only 91% water?

A

Because proteins eg) albumin are very large

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3
Q

What is Van’t Hoff’s equation?

A

Osmotic pressure = osmolarity x gas constant x absolute temp

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4
Q

What is osmolality?

A

Osmoles per kg water (not osmoles per litres because 1 litre plasma isn’t 1 litre water)

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5
Q

What does it mean that osmolality is “colligative”?

A

Proportional to number not type of particle

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6
Q

Why do cells not contribute to colloid osmotic pressure?

A

They’re not dissolved

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7
Q

What provides ECF osmolality?

A

NaCl

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8
Q

What provides ICF osmolality?

A

K+, Cl- and impermeable ions

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9
Q

What is crenation?

A

Shrinking around cytoskeleton

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10
Q

How does cerebral swelling kill?

A

Compresses medulla so stops breathing, or compresses veins causing even more swelling

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11
Q

How do you measure intracellular volume?

A

Total water - ECF volume

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12
Q

Does cortex or medulla have rich blood supply and lots of mitochondria?

A

Cortex

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13
Q

Does the afferent or efferent arteriole have baroreceptors?

A

Afferent

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14
Q

What do the podocytes provide?

A

Fenestrated capillary, basement membrane, diaphragm between foot processes

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15
Q

Why are podocytes negatively charged?

A

To repeal albumin

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16
Q

Why do some cations remain in the plasma?

A

Becayse there are -ve proteins there so cations remain due to charge

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17
Q

Filtration fraction = ?

A

glomerular filtration rate / renal plasma flow

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18
Q

Why does the remaining plasma cause decreased net filtration pressure?

A

High proteins and % haematocrit

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19
Q

Kidney flow = ?

A

Change in pressure / Ra + Re

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20
Q

What does dilating afferent or constricting efferent cause?

A

Increased pressure but decreased flow

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21
Q

Glomerular capillary pressure = ?

A

Venous pressure + AV pressure gradient x efferent resistance/total resistance

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22
Q

What is the autoregulatory range?

A

Large blood pressure range across which the glomerular filtration rate doesn’t change

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23
Q

What are the two ways to reduce flow?

A

Myogenic or tubulo-glomerular

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24
Q

What is the myogenic mechanism to reduce flow?

A

High blood pressure stretches afferent so it constricts

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25
Q

What is the tubulo-glomerular feedback mechanism to reduce flow?

A

Macula densa senses NaCl uptake, releases ATP, stimulates afferent arteriole constriction

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26
Q

What do mesangial cells do?

A

Contract to reduce capillary membrane area

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27
Q

Why can severe muscle damage cause renal failure?

A

Myoglobin can block filtration pores

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28
Q

What is “clearance”?

A

Expresses rate of excretion as a function of plasma concentration

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29
Q

Clearance = ?

A

Rate of excretion / plasma concentration

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30
Q

What is excretion measured in?

A

moles/min

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31
Q

What is clearance measured in?

A

ml/min

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32
Q

Why do positive molecules have highest filterability?

A

Attracted to and pulled through membrane

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33
Q

Why do -ve molecules have higher filterability if they are very small?

A

Can slip through when small

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34
Q

What happens to clearance if renal handling is constant?

A

Stays the same because if plasma concentration is doubled then excretion rate is doubled

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35
Q

What does it mean if clearance is less than or greater than GFR?

A

If less then not freely filtered, if greater then must also be secreted

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36
Q

Rate of excretion = ?

A

GFR x plasma conc

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37
Q

Clearance = ?

A

GFR

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38
Q

Excretion = ?

A

urine production x urine concentration

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39
Q

Clearance = ?

A

urine production x urine concentration / plasma concentration

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40
Q

What is the filtration coefficient?

A

Product of surface area and hydraulic conductivity

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41
Q

What is the protein reflection coefficient?

A

Goes 0 (permeable) to 1 (impermeable)

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42
Q

What may reduce the filtration coefficient?

A

Filtration pores becoming blocked or mesangial cells contracting to reduce capillary membrane area

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43
Q

What may increase Pc - Pb?

A

Increased in UTI obstruction

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44
Q

How do you measure clearance?

A

Find something produced at a constant rate and freely excreted then use clearance = rate of excretion / plasma conc eg) creatinine

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45
Q

What does the clearance ratio compare?

A

The clearance of something to the clearance of inulin

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46
Q

What is the clearance ratio of PAH like? Why is this useful?

A

Greater than 1 because it’s very efficiently secreted, so clearance of PAH is effective renal plasma flow (use Fick principle for this but need arterial and venous concentrations)

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47
Q

For protein channels, what is flux proportional to?

A

Electrochemical gradient ( x permeability)

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48
Q

What is the maximum rate of transport for carrier proteins called?

A

Transport maxima

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49
Q

Why doesn’t NaCl concentration in tubule not change?

A

Water follows it

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50
Q

What are some possible anions in the Cl- anion exchanger?

A

OH-, HCO2-, HCO3-, oxalate or sulphate

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51
Q

Where is Cl- reabsorption greatest?

A

Late PCT

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52
Q

Which anions are secreted in the PCT?

A

Prostaglandins, cAMP, bile salts, drugs eg penicillin

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53
Q

Which cations are secreted in the PCT?

A

Creatinine, adrenaline, noradrenaline, dopamine and drugs eg morphine

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54
Q

How are -ve ions transported into a -ve cell?

A

Enters in exchange for an anion, anions are recycled because there’s more Cl- to reabsorb than anions to secrete

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55
Q

What is the evidence for isotonic reabsorption?

A

Either inject inulin and use micropuncture to compare early and late PCT (PCT has higher conc) or use split oil drop to test how things are absorbed

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56
Q

What happens to anions in the tubule?

A

Protonated and are then uncharged so can diffuse back

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57
Q

Why is the tubule acidic?

A

Because of Na+/H+ exchanger

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58
Q

When is K+ released?

A

Exercise, acidosis (displaced by H+), dehydration (cellular shrinkage) and cell lysis

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59
Q

When is K+ taken in/ when does K+ conc decrease?

A

Hyperhydration, insulin, adrenaline

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60
Q

What happens to the ECG during hyperkalaemia?

A

QRS gets smaller because cardiac muscle gets inexcitable and T wave gets faster because of inwardly rectifying K+ channels

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61
Q

What happens to K+ during hypokalaemia?

A

T wave gets smaller and you get a U wave

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62
Q

Why do you get arrhythmias outside normal K+ range?

A

More excitable atria and slower repolarisations because of changes in channel conductance and inwardly rectifying channels

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63
Q

Which is the main regulatory hormone of K+?

A

Aldosterone

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64
Q

In what area is aldosterone important for Na+ reabsorption?

A

DCT

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65
Q

What stimulates aldosterone?

A

Angiotensin II

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66
Q

How does ADH affect K+ control?

A

Keeps excretion constant but alters concs, increases SK activity and reduces tubular flow rate

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67
Q

Why is renal K+ control slow?

A

Only 2% of body K+ is in the ECF

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68
Q

What detects high extracellular K+? WHat does it release?

A

Zona glomerulosa - aldosterone

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69
Q

Which pump does aldosterone stimulate

A

Na+/K+

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70
Q

Which hormones stimulate Na+/K+ pump?

A

Aldosterone, adrenaline, insulin

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71
Q

How does insulin stimulate Na+/K+ pump?

A

Stimulates Na+/glucose which stimulates Na+/K+

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72
Q

What causes hypokalaemia?

A

Diuretics, diarrhoea, vomiting, reduced food intake

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73
Q

What causes hyperkalaemia?

A

Renal failure, doctor error, cell lysis, acidosis

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74
Q

How do you treat hyperkalaemia?

A

Ca2+ will stabilise membrane potentials and adding glucose and insulin makes Na+/K+ pump work faster

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75
Q

How does plasma pH affect plasma conc Ca2+?

A

Influences charge on albumin - albumin binds to Ca2+ so if H+ changes then plasma conc of Ca2+ will change

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76
Q

What happens to bone during chronic acidosis?

A

It buffers H+ so get demineralisation

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77
Q

What are the symptoms of acidosis?

A

Central sympotoms - nausea, fatigue, confusion, coma, death

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78
Q

What are the symptoms of alkalosis?

A

Muscle symptoms - hypokalaemia, hypocalcaemia because more -ve plasma buffers, hyperexcitability, cramps, tetany

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79
Q

Metabolism of which amino acids produces H2SO4?

A

Cysteine and methionine

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80
Q

Metabolism of which amino acids produces HCO3-?

A

Aspartate and glutamate

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81
Q

Why is it more common to be pushed toward acid production?

A

Can’t be breathed out like CO2 can?

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82
Q

What are some fast extracellular buffers?

A

HCO3-, HPO42-, bone and plasma proteins

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83
Q

What are some slow intracellular buffers?

A

HCO3-, HPO42-, proteins esp. histidine

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84
Q

Why must kidney produce new HCO3-?

A

Needs to be added to reduce losses to metabloic acids but there isn’t enough so kidney has to produce it

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85
Q

What is a problem with HCO3- production?

A

Would produce H+ so must be secreted and buffered

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86
Q

What is the main filtrate buffer?

A

HPO42-

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87
Q

How is the kidney a net bicarb producer but almost none is excreted?

A

H+ secreted, HCO3- reabsorbed as CO2, so more bicarb produced because if CO2 is increasing then too much bicarb is being used to buffer H+

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88
Q

Which cells secrete bicarb?

A

Type B intercalated in the collecting duct

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89
Q

Which amino acid is bicarb produced from?

A

Glutamine

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90
Q

What is ammoniagenesis?

A

Making ammonia from glutamine in PCT

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91
Q

What happens to the glutamine in ammonia genesis?

A

Glutamine > glutamic acid > alphaKG > Krebs cycle > glucose. SO get 2HCO3-, excrete 2NH4+ and make half a glucose

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92
Q

What happens to the ammonium produced from glutamine?

A

Splits to ammonia in cell and recombined in tubule - now trapped so excreted

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93
Q

Where is NH4+ reabsorbed?

A

Ascending limb

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94
Q

What does NH4+ substitute for on which transporter?

A

K+ on the Na+-K+-2Cl- co-transporter

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95
Q

What do osmoreceptors in the hypothalamus detect?

A

Osmotic pressure, not [Na+]

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96
Q

What is AVP?

A

Arginine vasopressin (ADH)

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97
Q

Where is ADH broken down?

A

PCT

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98
Q

What are the two ADH receptors?

A

V1 = vascular smooth muscle, low affinity V2 = collecting duct, high affinity

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99
Q

Which circulatory factors affect ADH production?

A

Arterial baroreceptors can stimulate or inhibit release, so can cardiopulmonary receptors via vagus and glossopharyngeal

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100
Q

Which osmoregulatory factors affect ADH release?

A

Nervous inputs from GI tract via vagus, liver osmoreceptors detecting water absorption from food

101
Q

What kind of neurone terminals do act pots from osmoreceptors arrive at?

A

Magnocellular

102
Q

What kind of neurones does ADH travel down?

A

Magnocellular

103
Q

WHich organ contains the osmoreceptors?

A

OVLT (organum vasculosum laminae terminalis)

104
Q

How does osmodetection link cell size to ion channel activity?

A

When cells shrink they depolarise to increase action potential frequency because stretch-inactivated non-selective cation channels show increased activity

105
Q

How do you show osmotic pressure regulated ADH release?

A

Make diuresis easy to detect by stomach-tubing water. Exteriorise carotid arteries to form carotid loops so solutions can be introduced here not into veins. Hypertonic NaCl caused reduction in urine flow rate in carotid artery but not vein. Urea had no effect.

106
Q

What is the integrated response of osmoreceptors and circulatory stretch receptors?

A

Largest changes in plasma ADH if osmotic pressure and blood pressure are reduced

107
Q

Which aquaporins does the adluminal membrane always have?

A

AQP3 and AQP4

108
Q

If ADH decreases, which aquaporins is removed by endocytosis?

A

AQP2

109
Q

What’s the maximum urine osmotic pressure?

A

1200mosm

110
Q

What are the main waste solutes?

A

SO4 2- and HPO4 2-

111
Q

What is the mechanism of activation of AQP2?

A

ADH > V2 receptor (GPCR) > adenyl cyclase > cAMP > PKA > vesicles phosphorylated using serine 256 > fuse with collecting duct luminal membrane

112
Q

How does ADH increase urea permeability of medullary collecting duct and thin ascending limb?

A

Stimulating phosphorylation and activation of urea transporters in luminal membrane

113
Q

What is the main urea transporter?

A

UT-A1

114
Q

What is the luminal/adluminal membrane urea transporter?

A

UT-A3

115
Q

What is the urea transporter in the thin descending limb?

A

UT-A2

116
Q

What does angiotensin stimulate?

A

Na+/H+ exchange

117
Q

What does aldosterone stimulate

A

K+/H+-ATPase

118
Q

What pH is cortisol released in response to?

A

Low

119
Q

What does PTH cause in prolonged acidosis?

A

Acid secretion

120
Q

What decreases and increases metabolic acid?

A

Vomiting decreases, HCO3- loss increases

121
Q

If pH is normal what is causing the PCO2 change?

A

Non-respiratory causes

122
Q

What is the ideal glomerular filtration rate?

A

125ml/min

123
Q

What is normal tissue fluid osmolarity? Why is it the same in tubular fluid?

A

280 mosm - isotonic reabsorption

124
Q

If low Na+ conc, what happens to the fluid at the top of the loop of Henle? What if high Na+ conc?

A

Just excrete the hyposmotic solution. If high, add aquaporins

125
Q

Osmolality control is at the expense of what?

A

Volume control

126
Q

What does hyponatraemia cause?

A

Nausea

127
Q

Why is 200mosm the maximum gradient? What is used instead?

A

Fixed stoichiometry of pumps, back-leakage, instead use countercurrent multiplication

128
Q

Is fluid from the DCT hyposmotic or hyperosmotic?

A

Hyposmotic

129
Q

If conc triples, how much water is reabsorbed?

A

2/3

130
Q

Where does most H2O reabsorption occur?

A

Cortex

131
Q

What does heart failure cause?

A

Lower effective circulating volume, causing response in kidney like hypovolaemia so blood volume expands causing oedema

132
Q

What can be used to treat heart failure?

A

HKCC2 or KCC blocker

133
Q

Where does urea diffuse from and to?

A

Collecting duct > thin ascending limb

134
Q

What does high medullary urea allow?

A

Water reabsorption from descending limb so NaCl because concentrated and can be passively absorbed

135
Q

What does countercurrent exchange avoid?

A

Filling medulla with water, balanced by vasa recta

136
Q

What are the three stimuli to thirst?

A

High plasma osmotic pressure, reduced extracellular fluid volume, dry throat

137
Q

What is osmotic thirst due to?

A

High osmotic pressure detected by less sensitive hypothalamic osmoreceptors in the OVLT

138
Q

What is hypovolaemic thirst due to?

A

Reduced extracellular volume detected by arterial and cardiopulmonary stretch receptors - inputs inhibit thirst centres and angiotensin stimulates thirst in hypovolaemia

139
Q

What are the two types of diabetes insipidus?

A

Nephrogenic (failure to respond to ADH) or neurogenic (failure to produce ADH)

140
Q

How do you treat neurogenic diabetes insipidus?

A

Fake ADH called desmopressin acetate

141
Q

What determines the volume of the ECF? Why?

A

[Na+] because volume = amount/conc

142
Q

Why does increase filtration fraction mean more is reabsorbed?

A

Peritubular capillary collid osmotic pressure raised and hydrostatic pressure lowered, Na+/fluid reabsorbed because renal interstitial hydrostatic pressure falls

143
Q

How does extracellular fluid expansion increase ABP which increases Na+ excretion?

A

Higher ABP means higher net filtration rate and GFR, more filtered and less reabsorbed so more lost in urine, pressure natriuresis because water follows so decreased extracellular fluid volume, increased colloid osmotic pressure increases Na+ excretion

144
Q

What modulates activity of renal sympathetic nerves?

A

Inputs from cardiopulmonary receptors and arterial baroreceptors (reduced volume/ABP inhibits sympathetic outflow less)

145
Q

What does NA to alpha1 receptors on PCT do?

A

Increase NHE3 activity so more Na+ reabsorbed

146
Q

Which hormones affect Na+ excretion?

A

Angiotensin II, aldosterone, ANP

147
Q

Where is angiotensinogen always present?

A

Blood

148
Q

Where is renin released from?

A

Juxtaglomerular cells

149
Q

When is renin relased?

A

If ABP decreases - either detected by afferent arteriole or decreases cardiopulmonary and arterial stretch > sympathetic nerves > NA > beta1 > renin release

150
Q

What does macula densa sense and what does it do about it?

A

Detects low NaCl, increases renin release using prostaglandin

151
Q

What does angiotensin promote secretion of?

A

Renin as more NaCl reabsorbed (+ve feedback)

152
Q

What does selective efferent constriction ensure?

A

Some filtration remains to remove waste products

153
Q

Which exchanger does angiotensin stimulate and what does this cause?

A

Na+/H+ exchanger, increases Na+ reabsorption

154
Q

What 4 things does angiotensin II do?

A

Increases Na+ reabsorption, constricts efferent arteriole, stimulates Na+ appetite, stimulates aldosterone release

155
Q

What does aldosterone act on?

A

Cortical collecting duct

156
Q

What does aldosterone promote?

A

Na+ reabsorption, K+ secretion and excretion and H+ excretion

157
Q

What does aldosterone act as a transcription factor for?

A

Three genes (aldosterone induced proteins)

158
Q

What does aldosterone do in principal cells?

A

Increased Na+ channel to stimulate Na+/K+ channel and increased Ca2+-activated K+ channel by DNA. Upregulates SK and ENaC

159
Q

What does aldosterone do in type A intercalated cell?

A

Increases K+/H+ exchanger (non-genomic effect)

160
Q

What are the stimuli to release aldosterone?

A

AII, increased plasma [K+], decreased plasma [Na+]

161
Q

What is aldosterone deficiency?

A

Addison’s disease

162
Q

What symptoms does aldosterone deficiency cause?

A

Reduced plasma volume, circulatory collapse, deregulation of extracellular K+

163
Q

What does aldosterone excess cause?

A

Conn’s disease?

164
Q

What are symptoms of excess aldosterone?

A

High ABP, high ECF, K+ depletion, alkalosis because exchanged with H+

165
Q

How does MSP drop cause renin release?

A

Detected by low-pressure baroreceptors > brain stem > renal sympathetic nerve > granule cells > NA > renin release

166
Q

ECF expansion has opposite effect to haemorrhage EXCEPT WHAT?

A

ANP secretion increased

167
Q

What happens during low volume?

A

Lower MSP > decreased renal blood pressure > GFR > less NaCl in filtrate

168
Q

What are the seven role of angiotensin?

A

Peripheral vasoconstrictor, dipsogen, simulates Na+ hunger, increase NHE in PC, constrict efferent, causes aldosterone release

169
Q

What secretes ANP?

A

Atrial myocytes during increased atrial stretch

170
Q

What does ANP cause?

A

Opposite to aldosterone and AII. Has natriuretic effect so it increases Na+ loss and decreases ECF volume

171
Q

How does ANP work?

A

Increases cGMP > PKG > decreased ENaC and Na+/K+ATPase

172
Q

What does ANP inhibit secretion of?

A

Renin, aldosterone, ADH

173
Q

Why does ANP cause dopamine release?

A

Slows Na+/K+ATPase so less solutes reabsorbed and isotonic fluid excreted

174
Q

What does ADH do to the afferent arteriole? WHY?

A

Dilates it for pressure natriuresis

175
Q

Why does ANP dilate mesangial cells?

A

Increases filtration surface area so increases GFR

176
Q

What can hypocalaemia cause?

A

Spontaneous action potentials because threshold is decreased and -ve charge on glycoproteins isn’t bound which mimics depolarisation, motor nerves susceptible so can cause contraction of larynx muscles, prolonged QT interval, tetany of respiratory muscles

177
Q

What can hypercalaemia cause?

A

Increased threshold for action potentials, phosphates may precipitate causing kidney stones, muscle weakness

178
Q

WHich two hormones are hypercalcaemic?

A

PTH and 1,25-DHCC

179
Q

Which hormone is hypocalcaemic?

A

Calcitonin

180
Q

Where is the non-free calcium in the blood found?

A

Bound to proteins or complexed with anions

181
Q

What secretes PTH?

A

Chief cells of the four parathyroid glands

182
Q

What does PTH do?

A

Raises Ca2+, lowers PO4 2-

183
Q

What does PTH act on?

A

Bone and kidney directly,, via 1,25-DHCC in gut

184
Q

What’s the process of PTH inhibition following calcium detection?

A

Low-affinity GPCR receptor > PLC > DAG and IP3 > IP3 binds to EP so calcium released > PKC activated > PTH synthesis and secretion inhibited

185
Q

What do osteoprogenitor cells differentiate into?

A

Osteoclasts and osteoblasts

186
Q

Where do osteoprogenitor cells come from?

A

Haematopoietic stem cells

187
Q

What do osteoblasts do?

A

Lay down bone, secrete collagen, secrete Ca2+ and phosphate to form matrix

188
Q

What do osteoclasts do?

A

Break down bone using acid and enzymes

189
Q

What is an osteocyte?

A

Mature bone cell surrounded by calcified matrix connected by cytoplasmic extensions

190
Q

How does PTH cause rapid output of Ca2+ from bone fluid and slower mineralisation of bone?

A

Reduces laying down of bone by osteoblasts (stimulates them to secrete RANK-L and IL-6 which are cytokines which stimulate osteoclasts), stimulates Ca2+ uptake in osteocytes where it travels down cytoplasmic extensions and is released into ECF and interstitial fluid

191
Q

Where is most filtered Pi reabsorbed?

A

PCT

192
Q

What are the three types of Na+/Pi transporter?

A

IIa = 3:1, IIb = 3:1, IIc = 2:1

193
Q

How does PTH affect phospahte reabsorption transport?

A

Decreases Tmax

194
Q

How does decreasing plasma Pi cause rise in free Ca2+?

A

Favours calcium phosphate dissolution

195
Q

Which kind of plasma Ca2+ is filtered?

A

Free

196
Q

Where is most Ca2+ reabsorbed?

A

PCT

197
Q

How is Ca2+ transported out of tubule?

A

NCX

198
Q

How does most Ca2+ enter the tubule?

A

TRPV5/6 (channels)

199
Q

What allows calcium shuttling from luminal to adluminal membrane?

A

Calbindin-D

200
Q

Why can Ca2+ movement be regulated in the DCT and CD?

A

Movement here is transcellular not paracellular

201
Q

How does PTH affect calcium reabsorption in the PCT?

A

Decreases it

202
Q

What does PTH phosphorylate to increased calcium reabsorption?

A

NCX

203
Q

How is the type IIa transporter controlled?

A

PTH produces PKA and PKC which phosphorylate NHERF-1 so it dissociates from the transporter which is then available for endocytosis

204
Q

What does a thyroparathyroidectomy cause?

A

Lowered ability to recover from hypo/hypercalcaemia

205
Q

What is the pathway of 1,25-DHCC production from cholesterol?

A

Cholesterol > vitamin D3 > 25-HCC > 1,25-DHCC or 24,25-DHCC

206
Q

Where does vitamin D3 > 25-HCC?

A

Liver

207
Q

Where does 25-HCC > 1,25-DHCC or 24,25-DHCC?

A

Kidney

208
Q

What stimulates and inhibits 25-HCC > 1,25-DHCC?

A

Ca2+ inhibits, PTH, growth hormone and prolactin stimulate

209
Q

What stimulates and inhibits 25-HCC > 24,25-DHCC?

A

Ca2+ stimulates, PTH, growth hormone and prolactin inhibits

210
Q

What does 1,25-DHCC do?

A

Increases calcium and phosphorus reabsorption in kidney and increases absorption in the small intestine enabling bone mineralisation

211
Q

What is a synergist of 1,25-DHCC?

A

PTH

212
Q

What happens if there’s inadequate 1,25-DHCC?

A

Abnormal bone mineralisation

213
Q

How does 1,25-DHCC work?

A

Increases TRPV5/6 and calbindin-D in DCT, CD and small intestine, increases type II Na+/Pi absorbers and type III in the small intestine

214
Q

What secretes calcitonin?

A

C cells of the thyroid gland

215
Q

What does calcitonin do?

A

Inhibits absorption of bone by osteoclasts so bone deposition favoured

216
Q

How does calcitonin work?

A

Ca2+ acts on receptor, forms IP3, Ca2+ increases stimulating calcitonin (feed-forward)

217
Q

What GI hormone stimulates calcium release?

A

Gastrin

218
Q

What are the renal effects of calcitonin?

A

None

219
Q

How does calcitonin protect maternal bone against excessive demineralisation?

A

Ensures demand met by gut absorption, sex steroids stimulate production so after menopause there’s increased osteoclast activity so bone demineralisation

220
Q

What problem with the thyroid causes hypercalcaemia? Hypocalcaemia?

A

Hyperparathyroidism, hypoparathyroidism

221
Q

What causes milk fever?

A

Insensitivity to PTH

222
Q

What happens in PTH excess?

A

Ca2+ excretion increases due to increased filtered load

223
Q

What is the reversal potential?

A

Eqm potential

224
Q

What is nAChR permeable to?

A

Sodium in and potassium out

225
Q

Where are positive charges on channel which cause rotation and opening?

A

S4 section

226
Q

What is K channel blocker?

A

Tetraethylammonium

227
Q

What is Na channel blocker?

A

TTX

228
Q

What is NaKATPase blocker?

A

Digitalis and ouabain

229
Q

What is the descending limb permeable to?

A

Water

230
Q

What is the thin ascending limb permeable to?

A

Solute passively

231
Q

What is the thick ascending limb permeable to?

A

Solute actively

232
Q

What do osmorecetors detect is isotonic fluid or haemorrhage?

A

No change

233
Q

What does the pneumotaxic centre do?

A

Inspiratory cutoff

234
Q

What does the apneustic centre do?

A

Drive inspiration, phrenic nerve

235
Q

Another name for the CPG?

A

Pre-Botzinger complex

236
Q

Where is NHE found and what does it do?

A

Proximal tubule, for ion and water reabsorption (makes tubule acidic and cell alkaline)

237
Q

Where is bicarb transporter found and what does it do?

A

Early proximal tubule for ion and water reabsorption

238
Q

What is the difference between SGLT-1 and SGLT-2?

A

SGLT-1 is for late proximal tubule and and is for 2Na+, SGLT-2 is for early proximal tubule and is for one Na

239
Q

Where is the anion-Cl- transporter and what is it for?

A

Late proximal tubule for ion reabsorption

240
Q

Where is KCC transporter and what is it for?

A

Late proximal tubule, for ion reabsorption, unregulated K+ absorption, active NaCl transport, water reabsorption

241
Q

Where is the NKCC2 transporter and what does it do?

A

Think ascending limb, for unregulated K+ reabsorption, active NaCl transport, water reabsorption

242
Q

Why is NKCC2 energetically favourable?

A

Low intracellular NaCl conc

243
Q

Where is SK found and what is it for?

A

Distal tubule and collecting duct, regulating K+ secretion

244
Q

Where is NHE3 found and what does it do?

A

Proximal tubule and ascending limb, for bicarb reabsorption and ammoniagenesis

245
Q

What stimulates NHE3?

A

Sympathetic nerves and angiotensin

246
Q

Where is NBC1 and what does it do?

A

Proximal tubule and ascending limb, for bicarb reabsorption and ammoniagenesis

247
Q

Where is Cl-/bicarb exchanger and what is it for?

A

Type A intercalated cell of collecting duct for bicarb reabsorption, ammonia trapping and ammoniagenesis

248
Q

Where is K+-H+ATPase found and what is it for?

A

Collecting duct for ammonia trapping

249
Q

Where is H+-ATPase and what is it for?

A

Collecting duct, for ammonia trapping (makes lumen acidic)

HOM (7 decks)

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