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Urinary > Physiology > Flashcards

Physiology Flashcards

1
Q

What are some functions of the urinary system?

A

Removes metabolic waste from blood by filtration and excretion

Regulates plasma electrolytes and blood pressure (by renin angiotensin mechanism)

Help to stabilize the PH

Reabsorption of small molecules (amino acids. Glucose, and peptides)

Produces erythropoietin (a stimulant of RBC production by bone marrow)

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2
Q

What vertebral level do the kidneys lie?

A

T12-L3

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3
Q

Are kidneys intra/retroperitoneal?

A

Retroperitoneal

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4
Q

What surrounds the kidney?

A

Renal capsule, perirenal fat, renal fascia

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5
Q

What are the three constrictions of the ureter?

A

First constriction - where ureter passes over inferior renal pole?
Second constriction - ureter crosses over external iliac vessels
Third constriction - ureter traverses the bladder

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6
Q

What is the sympathetic supply to the kidney?

A

T10-L1 (Renal plexus)

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7
Q

What are the four parts of the male urethra?

A

Intramural (preprostatic)
Prostatic
Intermediate (membranous)
Spongy (penile)

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8
Q

What is the sympathetic supply to the bladder?

A

T10-L2

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9
Q

What is the parasympathetic supply to the bladder?

A

S2-S4

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10
Q

What is the somatic control of the external urethral sphincter?

A

The pudendal nerve

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11
Q

From what structures does the ejaculatory duct arise in the prostatic urethra?

A

The vas deferens and seminal vesicles

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12
Q

Which nerve constricts detrusor muscle during micturition?

A

Parasympathetic nerve

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13
Q

Which nerve constricts internal urethral sphincter during ejaculation?

A

Sympathetic nerve

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14
Q

Which is the narrowest part of the urethra in male?

A

Membranous

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15
Q

Transpyloric plane passes through which vertebral level?

A

L1

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16
Q

What is the functional unit of the kidney?

A

Nephron

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17
Q

What kind of epithelium is in the ureters/bladder?

A

Transitional epithelium

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18
Q

Name some important markers of kidney disease

A

Proteinuria

Glomerular filtration rate (GFR)

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19
Q

List some common developmental abnormalities

A

Aberrant renal arteries
Pelvic Kidney
Unilateral double kidney
Horseshoe Kidney

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20
Q

Where do the kidneys originate from embryologically?

A

Intermediate plate mesoderm

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21
Q

What does the cloaca divide to form in the embryo?

A

Rectum and Urogenital sinus

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22
Q

What does the urogenital sinus go on to form?

A

The urinary bladder

Urethra

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23
Q

How many sets of kidneys develop sequentially during nephrogenesis?

A

3

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24
Q

What does the intermediate mesoderm in the neck region of the embryo become?

A

Pronephros

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25
Q

What does the pronephric duct drain into?

A

Cloaca

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26
Q

What happens to the pronephros?

A

Degenerates (by week 5)

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27
Q

What does the Intermediate mesoderm in trunk region become?

A

Mesonephros

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28
Q

What function does the mesonephros have?

A

Functions as the kidney for approx. 4 weeks, then incorporated into developing gonad (specifically ovary in females).

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29
Q

What develops into the definitive kidney?

A

The metanephros

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30
Q

What gives rise to the rete testis?

A

The mesonephric tubules

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31
Q

What gives rise to the vas deferens?

A

The mesonephric duct

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32
Q

What is the vertebral level of the kidneys?

A

T12-L3

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33
Q

When does ascent of the kidneys stop?

A

When they come into contact with the suprarenal glands

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34
Q

Name some kidney development abnormalities

A 
Congenital polycystic kidney
Aberrant renal arteries
Lobulated kidney
Transposition of kidneys
Horshoe Kidney
Pancake Kidney
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35
Q

What di the allantois and cloaca go on to form?

A

Urinary bladder and urethra

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36
Q

What is normal GFR?

A

180 l/day (120ml/minute)

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37
Q

What are the basic renal processes?

A

Filtration
Reabsorption
Secretion

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38
Q

What is the blood flow received by the kidneys?

A

1200 mls/min (20-25% of Cardiac Output)

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39
Q

How many red blood cells are filtered into bowman’s capsule?

A

None

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40
Q

What forces is glomerular filtration dependent on?

A

Hydrostatic forces favouring filtration

And oncotic pressure favouring reabsorption

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41
Q

What factors affect filterability of solutes across the glomerular filtration barrier?

A

Molecular Size
Electrical Charge
Shape

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42
Q

In the glomerular capillaries - which pressure is favoured? Hydrostatic forces favouring filtration/Oncotic pressure favouring reabsorption

A

Hydrostatic forces favouring filtration (ONLY FILTRATION OCCURS at Glomerular capillaries)

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43
Q

What is the primary factor affecting GFR?

A

Pressure in the glomerular capillaries (Pgc).

This is dependent on afferent/efferent arteriolar diameter, and balance of their resistances

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44
Q

What 3 things extrinsically control GFR?

A
  • Sympathetic Vasoconstrictive nerves (both eff + aff constrict, more sensitive at aff)
  • Circulating catecholamines (primarily constrict aff)
  • Angiotensin II->(Constriction of efferent at low, both afferent and efferent at high)
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45
Q

What intrinsically controls GFR?

A

Autoregulation (Adjusting resistance in response to BP)

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46
Q

What is the autoregulation mean blood pressure range?

A

60-130mmHg

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47
Q

What percentage of plasma volume entering the afferent arteriole is filtered?

A

20%

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48
Q

What percentage of plasma volume entering the afferent arteriole is reabsorbed?

A

19%

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49
Q

What percentage of plasma volume entering the afferent arteriole is excreted?

A

1%

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50
Q

What types of molecules are reabsorbed via carrier proteins?

A 
Glucose
Amino acids
Organic acids
Sulphate
Phosphate
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51
Q

What happens if the maximum transport capacity is exceeded of carrier proteins in the kidney?

A

The excess substrate enters the urine.

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52
Q

What is the renal plasma threshold for glucose?

A

10mmoles/L (Beyond this, it will be excreted into urine)

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53
Q

What substances are regulated via a system of maximum transport capacity?

A

Sulphate Ions

Phosphate Ions

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54
Q

Where does the majority of Na reabsorption take place?

A

The proximal tubule

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55
Q

How is Na reabsorbed?

A

Through active transport

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56
Q

Where are the active Na+ pumps located?

A

On the basolateral surfaces - decreases Na in the epithelium, so drives passive transport from the lumen to the cell.

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57
Q

How are negative ions like chlorine transported?

A

Down the electrical gradient established by sodium active transport

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58
Q

How is water transported across the proximal tubule?

A

Drawn by the osmotic force of sodium active transport/chlorine passive transport.

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59
Q

What does the rate of reabsorption of non-actively reabsorbed solute depend on?

A
  • Amount of H20 Removed (determines extent of concentration gradient)
  • The permeability of the membrane t any particular solute
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60
Q

List a substance to which tubule membrane is moderately permeable to?

A

Urea

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61
Q

How permeable is the tubular membrane to inulin and mannitol?

A

Impermeable (can not be reabsorbed)

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62
Q

The active transport of what ion extablished the gradients down which other ions, H20 and solutes passively pass?

A

Na+

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63
Q

List some substances that share the same are transported through Na+ symporters

A

Glucose

Amino Acids

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64
Q

What does High Na+ in the tubule do to glucose transport?

A

Favours it (Na+/Glucose Symporter - SGLT)

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65
Q

Are carrier mechanisms for tubular secretion specific?

A

No. Not very.

Eg Organic acid mechanism (for lactic/uric acid) is also used for penicillin, aspirin and PAK

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66
Q

What is the normal ECF [K+]?

A

4mmoles/L

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67
Q

What happens in hyperkalaemia?

A

5.5mmoles/l = hyperkalaemia > resting membrane potential of excitable cells and eventually ventricular fibrillation and death

Killer banana!!

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68
Q

What happens in hypokalaemia?

A

< 3.5 mmoles/l = hypokalaemia > resting membrane potential ie hyperpolarizes muscle, cardiac cells > cardiac arrhythmias and eventually death.

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69
Q

What happens to K+ filtered at the glomerulus?

A

Its reabsorbed

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70
Q

How does aldosterone regulate potassium secretion?

A

Aldosterone promotes potassium secretion

(^[K+] in ECF bathing the aldosterone secreting cells stimulates aldosterone release which circulates to the kidneys to stimulate ^in renal tubule cell K+ secretion.)

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71
Q

What is the osmolarity of the fluid leaving the proximal tubule?

A

Isosmostic with the plasma (300 mOsmoles/l)

The solute movements are accompanied by equivalent H20 movements

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72
Q

Where in the kidney are the the proximal and distal tubules located?

A

The cortex

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73
Q

What is the maximum concentration of urine produced by the kidney?

A

1200-1400 mOsmoles/l

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74
Q

What is the amount of urea, sulphate, phosphate, other waste products and non-waste ions (Na+ and K+ ) which must be excreted each day?

A

600 mOsmoles

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75
Q

What is the minimum required obligatory H20 loss?

A

500 mls

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76
Q

If no water intake happens, will the kidneys still excrete H20?

A

Yes. It is possible to urinate to death.

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77
Q

What is the mimimum [urine] in excess H20 intake?

A

30-50 mOsmoles/l

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78
Q

What are the counter-current characteristics of the ascending limb in the loop of Henle?

A
  • Actively transports Na+ and Cl- ions out of the tubule lumen into the interstitium
  • Is impermeable to H20
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79
Q

What are the counter-current characteristics of the descending limb in the loop of Henle?

A
  • Freely permeable to H20

- Relatively impermeable to NaCl

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80
Q

What is the limiting gradient of sodium being pumped out of the ascending limb?

A

200mOsm

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81
Q

What happens to the concentration of the fluid as it moves down the descending limb?

A

Progressively more concentrated

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82
Q

What happens to the concentration of the fluid as it moves up the ascending limb?

A

Progressively gets more diluted

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83
Q

What happens if the active transport of NaCl from the ascending limb is abolished (ie by furesemide?)

A

The kidney can only produce isotonic urine

84
Q

How much of the initial filtrate is removed at the loop of Henle?

A

15-20%

85
Q

Is fluid entering the distal tubule more or less than the plasma?

A

More dilute (delivers a hypotonic solution)

86
Q

What role does the vasa recta play in the countercurrent mechanism?

A

Act as a countercurrent exchanger

87
Q

What are the functions of the vasa recta?

A
  • Provide O2 for the medulla
  • In providing O2 it must not disturb gradient
  • Removes volume from the interstitium, up to 36l/day.
88
Q

What controls the permeability of the collecting duct?

A

ADH (concentrates the urine)

89
Q

Where is ADH synthesised?

A

Hypothalamus (SO and PVN nuclei)

90
Q

Where is ADH released?

A

Posterior Pituitary

91
Q

What is the half-life of ADH?

A

~10 minutes, so can be rapidly adjusted

92
Q

What is the primary control of ADH secretion?

A

Plasma osmolarity

When increases, ADH increases (must also affect tonicity!)

93
Q

What receptors mediate neuronal discharge of ADH?

A

Osmoreceptors in the anterior hypothalamus.

(Triggered by changes in volume through stretch-sensitive ion channels).

94
Q

What is normal plasma osmolality?

A

280-290 mOsm/kg H2O.

95
Q

What would increasing urea do to ADH release?

A

Nothing.

UREA IS AN INEFFECTIVE OSMOLE

96
Q

What would increasing NaCl do to ADH release?

A

Increase it!

Extra osmolarity (that increases tonicity) -> ADH release.

97
Q

What would happen with ingestion of hypertonic solutions such as saltwater?

A

Increase the solute load to be excreted and > urine flow > dehydration, because more H2O is required to excrete the solute load than was ingested with it.

98
Q

How does ADH increase the permeability of the collecting ducts?

A

Incorporation of aquaporin channels (AQP2) into the luminal membrane

99
Q

What happens to the collecting duct when ADH is present?

A

H2O is able to leave - the cortical CD becomes equilibrated with the interstitium.

If maximal ADH - becomes highly concentrated.

100
Q

In the absence of ADH, what happens in the collecting duct?

A

Impermeable to H2O - so the medullary interstitial gradient isnt effective in inducing H2O movement > a large volume of dilute urine is excreted.

101
Q

What happens to urea in the presence of high ADH?

A

The urea is also permeable, so tends to move into the interstitium (reabsorbed), and reinforces the gradient in the loop of Henle.

Uraemia can occur.

102
Q

Why is it important for urea to also be absorbed?

A

If it wasn’t, it would exert an osmotic effect to hold H2O in the tubule.

The conservation of H2O is more important than the consequence of urea retention.

103
Q

What does increasing ECF do to ADH secretion?

A

Decreases it. (Encourage diuresis)

104
Q

What does decreasing ECF do to ADH secretion?

A

Increases it. (Inhibits diuresis)

105
Q

Where are the low pressure stretch receptors located?

A

L + R atria and great veins

Also called ‘volume receptors’

106
Q

Where are the high pressure stretch receptors located?

A

Carotid and Aortic arch baroreceptors

107
Q

What do moderate decreases in ECF volume primarily affect?

A

The atrial receptors

(Normally tonically inhibit ADH release, but in reduced ECF, increase ADH release).

108
Q

What receptors are affected if volume changes enough to affect MBP?

A

Carotid and aortic receptors

Important to think about in haemorrhage. There is an increase in ADH even going from lying down to standing up.

109
Q

What other stimuli increase ADH secretion?

A

Pain, emotion, stress, exercise, nicotine, morphine.

Following traumatic surgery, inappropriate ADH secretion occurs, need to be careful about monitoring H2O intake.

110
Q

What other stimuli decrease ADH secretion?

A

Alcohol, suppresses ADH release.

111
Q

What are the major ECF osmoles?

A

Na+ and Cl-

112
Q

What are the major ICF osmoles?

A

K+ salts

113
Q

Approximately how much water makes up TBW?

A

42L

114
Q

What fraction of TBW is ICF?

A

2/3rds (28L)

115
Q

What is the renal response to decreased ECF volume (eg salt and H2O loss from vomiting, diarrhoea, excess sweatng etc) ?

A

^Sympathetic discharge -> ^VC -> ^TPR -> ^BP towards normal

->^Renal Arterial constirction
+ ^Renin -> ^Angiotensin II > ^proximal tubule Nacl and H20 reabsorption/^ Aldosterone -> ^ distal tubule Nacl and H20 reabsorption

116
Q

What action does angiotensin II have on the proximal tubule?

A

^ Na+ reabsorption from the proximal tubule and less Na+ excreted.

117
Q

What action does aldosterone have on the distal tubule?

A

^ Na+ reabsorption from the distal tubule and less Na+ excreted.

118
Q

Why is there an increase in Na+ reabsorption with angiotensin release?

A

Greater reabsorptive forces in the peritubular capillaries.

119
Q

How is GFR maintained in relation to constriction of the afferent/efferent arterioles?

A

Constriction of afferent - due to sympathetic VC

Constriction of efferent - due to angiotensin II

120
Q

What comprises the juxtaglomerular apparatus?

A

Juxtaglomerular cells + The Macula Densa

121
Q

What do juxtaglomerular cells produce?

A

Renin

122
Q

What does Renin act on?

A

Angiotensinogen -> Angiotensin I

123
Q

What converts Angiotensin I to Angiotensin II?

A

ACE

124
Q

What actions does angiotensin II have?

A
  • Vasoconstict arterioles
  • ^Cardiovascular response in cv centre in medulla oblongata
  • ^ADH and Thirst via Hypothalamus
  • ^Na reabsorption via adlosterone release from adrenal cortex
125
Q

Where is aldosterone released from?

A

The zona glomerulosa of the adrenal cortex.

126
Q

What increases renin release?

A
  • When pressure falls in afferent arteriole at level of JG cells (act as baroreceptors - less distension, more renin!)
  • ^Sympathetic nerve activity (via B1 effect)
  • Decreased NaCl delivery at macula densa
127
Q

What decreases renin release?

A
  • Angiotensin II feedback

- ADH inhibits renin release

128
Q

If there is sufficient volume change does this take precedence over disturbances in osmolarity?

A

Yes

129
Q

What does ANP do to Na+?

A

Promotes excretion

130
Q

What happens if aldosterone is given to normal subjects?

A

Na+ Retention, and therefore weight gain due to H20 retention.

K+ loss

131
Q

Does ANP act the same or counter the action of Aldosterone?

A

It counters it.

Volume expansion - ‘aldosterone escape’

132
Q

In Conn’s syndrome (primary hyperaldosteronism) - what happens to Na+ and K+ levels?

A

K+ depleted due to the aldosterone, but Na+ loss is countered by ANP production

(so hyperkalaemia, but not hypernatraemic,)

133
Q

What condition uncontrolled can lead to osmotic diuresis?

A

Diabetes Mellitus

134
Q

In osmotic diuresis what happens to the [Na+] in the lumen of the proximal tubule?

A

It’s decreased - because a larger volume is present due to the osmotic drive for glucose.

The ability to absorb glucose is therefore also impaired. (as the gradient is depeleted for the Na+-Glucose symporter)

135
Q

What happens to the interstitial gradient of the ascending limb in osmotic diuresis?

A

It is eventually abolished

136
Q

In uncontrolled diabetes what can cause a hyperglycaemic coma?

A

Hypotension - due to severe salt and water depletion in osmotic diuresis.

137
Q

What type of drugs can cause potassium wasting?

A

Loop diuretics

138
Q

What is the normal pH of arterialized blood?

A

7.4

139
Q

What are sources of H+?

A
  • Respiratory Acid (Carbonic acid)

- Metabolic Acid (Inorganic acids - sulphuric/phosphoric Organic - Fatty/Lactic)

140
Q

With a normal diet is there a net gain or loss of hydrogen?

A

Gain (50-100 mmoles per day)

141
Q

What is the major source of alkali in the body?

A

Oxidation of organic anions such as citrate

142
Q

What is a buffer?

A

Minimises changes in PH when H+ ions are added or removed (bicarbonate acts as an Extracellular buffer)

143
Q

What is the normal value of pCO2?

A

5.3kPa (40mmHg)

144
Q

What is the normal value of HCO3-

A

24 mmoles

145
Q

What is the equation of the buffer system?

A

^H+ + HCO3- H2CO3 H2O + CO2^ -> ^ventilation and \/CO2

in increasing ^H+

146
Q

How is [HCO3-] regulated?

A

Renal regulation

147
Q

How is PCO2 regulated?

A

Respiratory regulation

148
Q

What other buffers are there in the ECF?

A

Plasma proteins

Dibasic phosphate

149
Q

List some intracellular buffers?

A

Proteins, Organic/inorganic phosphates and haemoglobn

Also bone carbonate - chronic renal failure -> bone wasting

150
Q

What can acidosis do to plasma K+ levels?

A

Increase it - leading to hyperkalaemia -> VF and death

Need to maintain electrochemical neutrality

151
Q

How does the kidney regulate [HCO3-]?

A
  • Reabsorbing filtered HCO3-

- Generating new HCO3-

152
Q

How is HCO3- reabsorbed?

A

Through conversion into CO2 via active H+ secretion from proximal tubule cells

153
Q

What is the minimum/maximum pH of urine in humans?

A

Minimum 4.5-5.0,

Maximum 8.0

154
Q

What are some weak acids and bases used in titratable acidity?

A

Dibasic phosphate (HPO42-)
Uric Acid
Creatinine

155
Q

What is generated in titratable acidity?

A

New HCO3-, and H+ is excreted

156
Q

What is the source of new HCO3- produced?

A

Indirectly from CO2 in the blood

157
Q

What is the principle site of titratable acidity?

A

Distal tubule

This is where unreabsorbed dibasic phosphate becomes highly concentrated

158
Q

What is generated in ammonium excretion?

A

New HCO3-, and H+ is excreted

159
Q

What does renal glutaminase do?

A

Produces NH3 via deanimation of amino acids

160
Q

What is the main adaptive response of the kidney to acid loads?

A

Regulation of ammonium excretion. (Increases in acidosis)

161
Q

What is respiratory acidosis?

A

PH has fallen - due to a respiratory change. (PCO2 must have increased)

162
Q

What can cause acute respiratory acidosis?

A

Drugs which depress the medullary respiratory centres - barbituates/opiates

Obstruction of major airways

163
Q

What can cause chronic respiratory acidosis?

A

Lung disease (Bronchitis, emphysema, asthma)

Increases HCO3 as well as co2 - does not correct the initial disturbance

164
Q

What can cause acute respiratory alkalosis?

A

Voluntary hyperventilation, aspirin, first ascent to altitude

(Increased blow-off of CO2)

165
Q

What can cause chronic respiratory alkalosis?

A

Long term residence at altitude, \/ Po2 to < 60mmHg (8kPa) stimulates peripheral chemoreceptors to increase ventilation

166
Q

What can cause metabolic acidosis?

A
  • Increased H+ production of a diabetic/lactic acidosis
  • Failure to excrete the normal dietary load of H+ as in renal failure
  • Loss of HCO3- as in diarrhoea
167
Q

What kind of ventilation can take place in renal failure/diabteic ketoacidosis?

A

Kussmaul breathing (Increased in depth of breathing - maximum of 30L/min)

168
Q

What can cause metabolic alkalosis?

A
  • Increase H+ ion loss - vomiting loss of gastric secretions
  • ^Renal H+ loss - aldosterone excess, excess liquorice ingestion
  • Excess administration of HCO3- in patient with renal impairment
  • Massive blood transfusions
169
Q

What would you do in a patient with combined metabolic and respiratory acidosis?

A

Think potassium!

  • Insulin - stimulates uptake of potassium
  • Calcium resonium (also for hyperkalaemia)
  • Ca gluconate (iv) - \/ excitability of heart
170
Q

What takes precedence - restoration of volume of correcting metabolic acidosis?

A

Restoration of volume

171
Q

What us the anion gap?

A

Difference between the sum of the principal cations and the principal anions in the plasma

172
Q

In what acidotic situations might the anion gap increase?

A

Lactic/Diabetic Acidosis

173
Q

The following blood gas values were seen in a patient. Which simple Acid/Base Disturbance has he got?

pH = 7.32, [HCO-3]= 15 mM, PCO2 = 30mmHg (4kPa)

A

Metabolic Acidosis

PH fallen, PCO2 fallen, HCO3- fallen

174
Q

The following blood gas values were seen in a patient. Which simple Acid/Base Disturbance has he got?

pH = 7.32, [HCO-3]= 33 mM, PCO2 = 60mmHg (8kPa)

A

Respiratory Acidosis (Chronic)

(PH fallen, HCO3 risen (compensation!), PCO3 risen)

(In chronic resp acidosis, HCO3- rises to try to compensate)

175
Q

The following blood gas values were seen in a patient. Which simple Acid/Base Disturbance has he got?

pH = 7.45, [HCO-3] = 42 mM, PCO2 = 50mmHg (6.7kPa)

A

Metabolic Alkalosis

PH Risen, HCO3- risen, PCO2 risen

176
Q

The following blood gas values were seen in a patient. Which simple Acid/Base Disturbance has he got?

pH = 7.45, [HCO-3]= 21 mM, PCO2 = 30mmHg (4kPa)

A

Respiratory Alkalosis

PH Risen, HCO3- fallen, PCO2 fallen

177
Q

A 75 year old man has the following blood gas values:
pH = 7.31, PCO2 = 7.7.kPa, (58mmHg), [HCO3-] =36mmoles/l.
1. It is likely that he has renal disease.
2. He may have an acute respiratory infection.
3. It is possible that he may have chronic bronchitis.
4. There will be a decrease in his excretion of ammonium ions.
5. His plasma potassium will be reduced.

A
  1. Chronic Bronchitis

Chronic respiratory acidosis

(PH has fallen, PCO2 has risen HCO3- has risen)

178
Q

The following acid/base values were obtained:
pH = 7.25, [HCO3-] = 12mmoles/l, PCO2 = 3.3kPa (25mmHg)

They are indicative of a respiratory acidosis
The reduction in Pco2 is a result of under-breathing
The subject has probably been taking bicarbonate of soda
It could be related to impaired renal function
The subject may have been vomiting very badly

A

Impaired renal function
(Failure to excrete normal dietary load of H+)

Metabolic Acidosis

(PH has fallen, PCO2 has fallen, HCO3 has fallen)

179
Q

What two clinical situations is measuring GFR particularly useful in?

A
  • In patients with renal disease - a measure of disease progression
  • Adjusting doses of certain drugs that are removed through excretion (digitalis, many antibiotics etc)
180
Q

How is plasma clearance measured?

A

Plasma clearance of X, CX= [UX] V/[PX]

units are mls/min
UX = Urine concentration of X,
V = urine flow rate,
PX = plasma concentration of X

181
Q

What are the gold standards for substances used in plasma clearance

A

Inulin Clearance, Polyfructose,

loading IV dose of Inulin,

182
Q

What is used in clinical practice for plasma clearance?

A

51Cr-EDTA (a suitable radioactive substance)

183
Q

What is used routinely as an estimate of GFR?

A

Creatinine clearance

(GFR is approximately proportional to 1/[Plasma CR], but not a linear relationship!

184
Q

What factors can affect serum creatinine?

A

Muscle mass, dietary intake, drugs, ketoacidosis.

185
Q

What is normal GFR?

A

Approximately 100mls/min/1.73m2

186
Q

Is the clearance of urea less or greater than inulin?

A

Less. Some urea is absorbed.

187
Q

What is the clearance of glucose in normal physiology?

A

0

188
Q

What organic anion is used to measure real plasma flow (RPF)?

A

Para-amino-hippuric acid

189
Q

Is the clearance of penicillin less or greater than inulin?

A

Penicillin has a greater clearance than inulin because some penicillin is secreted from the capillary into the tubule (+the filtered)

190
Q

How does urine flow from the kidney to the ureters?

A

Smooth muscle peristaltic contraction

191
Q

What is the smooth muscle of the bladder called?

A

Detrusor muscle

192
Q

Which of the sphincters of the bladder (internal/external) is the true sphincter?

A

External sphincter (voluntary somatic control)

193
Q

What other structures does the bladder lie in front of?

A

Reproductive system and rectum

194
Q

What makes up the trigone of the bladder?

A

-2 vesicoureteric openings and the urethreal opening

195
Q

What is normal daily urine production?

A

750-2500 mls in temperate climates

196
Q

What is the parasympathetic supply of the detrusor muscle?

A

Pelvic nerves from s2-s4 (Increases bladder contraction)

197
Q

What is the sympathetic supply of the detrusor muscle?

A

Hypogastric nerves L1-L3 (Inhibits bladder contraction, also prevent semen reflux into bladder)

198
Q

What innervates the skeletal muscle that forms the external urethral sphincter?

A

Somatic motorneurones (pudendal nerves) S2-S4

Keeps the sphincter closed against string contractions

199
Q

What provides the sensory innervation?

A

Stretch receptor afferents from the bladder wall discharge to the spinal cord via interneurones.

(Excites parasympathetic, inhibits sympathetic, inhibits somatic motoneurones, pathways to sensory cortex -> sensation of fullness)

200
Q

Why is the micturition reflex essentially a spinal process in babies?

A

Higher brain connections have yet to be established

201
Q

What is the volume of urine in bladder required to initiate the spinal reflex in an adult?

A

300-350mls

202
Q

How is delay of the micturition reflex accomplished?

A

Descending pathways from many brain centres - inhibit parasympathetic and stimulate somatic nerves to external sphincter

203
Q

How does remaining urine get expelled from the male urethra?

A

Contractions of the bulbocavernous muscle?

204
Q

What are the 3 major types of micturition abnormalities?

A
  • Interruption of afferent nerves
  • Interruption of afferent and efferent nerves
  • Interruption of facilitatory and inhibitory descending pathways from the brain
205
Q

How may some paraplegic patients train themselves to initiate voiding?

A

Through afferent stimuli of one reflex (mild mass reflex) irradiating to evoke the bladder reflex.

Urinary (3 decks)

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