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Phase 1 revision > SUGER - RENAL > Flashcards

SUGER - RENAL Flashcards

1
Q

What are the normal values for:

  • Renal blood flow
  • Glomerular filtration rate
  • Urine flow rate
A

Renal blood flow:
1l/min

Renal plasma flow:
700ml/min

Glomerular filtration rate:
125ml/min

Urine flow rate:
1ml/min

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2
Q

What percentage of your cardiac output does the kidney receive?

A

20%

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3
Q

Why is the PCT a common site of poisoning and vulnerable to toxins?

A

A lot of toxins that you want to get rid off are secreted here.

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4
Q

Name some proximal tubular disorders and the solute they affect

A

1) Glucose: renal glycosuria
2) Amino-acids: Aminoacidurias (e.g. cystinuria)
3) Phosphate: Hypophosphataemic rickets (eg XLH)
4) Bicarbonate: Proximal renal tubular acidosis
5) Multiple solutes: Fanconi syndrome

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5
Q

Renal glycosuria

  • What is it a defect in?
  • Mechanism?
  • Clinical features?
A

Defect: Sodium glucose transporter 2 (SGLT2)
Mechanism: Failure of glucose reabsorption
Clinical features: Incidental finding on testing, benign, sugar in urine but blood sugar levels normal

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6
Q

How are SGLT2 inhibitors (e.g. empaglifloxin) used to treat type 2 diabetes?
What are the positives/negatives of this?

A

The failure to absorb glucose means that these medicines make you pee out more glucose in urine. This means that people don’t put on weight, unlike other diabetes medication.
However more sugar in the urine means that they are more susceptible to infections and thrush.

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7
Q

Aminoaciduria: Cystinuria

  • What is it a defect in?
  • Mechanism?
  • Clinical features?
A

Defect: Renal basic amino acid transporter (rBAT)
Mechanism: Failure of cystine reabsorption, increased urinary cystine concentration – stone formation
Clinical features: Renal colic, recurrent stone formation

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8
Q

What is the treatment for aminoaciduria?

A

1) High fluid intake:
High urine flow rate as faster things are flowing, the harder it is for things to crystallise,lower concentration
2) Alkalinise urine:
Increases solubility of cystine
3) Chelation:
Using something to bind to the cystine to stop it getting into the urine. Penicillamine, captopril
4) Management of individual stones
(percutaneous treatment, breaking the stone up, surgery etc)

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9
Q

Hypophosphataemic rickets

  • Defect
  • Mechanism
  • Clinical features
A

Commonest form is X-linked hypophosphataemic rickets.
Defect:
PHEX – zinc dependent metalloprotease
Mechanism:
- PHEX mutation results in increased FGF-23 levels, leading to decreased expression and activity of NaPi-II in proximal tubule.
- There is less NaPi TRANSPORTERS so LESS phosphate reabsorbed in the proximal tubule so LESS mineralisation.
Clinical features:
- Bow legged deformity, impaired growth

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10
Q

What is the treatment for Hypophosphataemic rickets?

A

Phosphate replacement

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11
Q

Proximal (type 2) renal tubular acidosis

  • Defect
  • Mechanism
  • Clinical features
  • Treatment
A

Defect: Na/H antiporter
Mechanism: Failure of bicarbonate reabsorption
Clinical features: Acidosis, impaired growth
Treatment: Bicarbonate supplementation

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12
Q

What can genetic defects in carbonic anhydrase do?

A

Genetic defects in carbonic anhydrase produce a mixed proximal/distal renal tubular acidosis.

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13
Q

Which drug inhibits carbonic anhydrase?

A

Acetazolamide

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14
Q

Why can acetazolamide be used to treat altitude sickness?

A

When you go up altitude, there is less pp(O2 ), so you breathe in more.
This REDUCES the amount of C02, so the blood pH will INCREASE, leading to chronic alkalosis, this can treated by inducing acidosis. Acetazolamide inhibits carbonic anhydrase so less bicarbonate reabsorbed so pH will reduce.

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15
Q

Fanconi Syndrome

  • Mechanism
  • Clinical features
  • Causes
A

Mechanism: Generalised proximal tubular dysfunction, possibly due to failure to generate sodium gradient by Na/K ATPase
Clinical features: Glycosuria, aminoaciduria, phosphaturic rickets, renal tubular acidosis
Causes: Genetic (eg cystinosis, Wilson’s disease), myeloma, lead poisoning, cisplatin

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16
Q

Barrter’s syndrome

  • Defect
  • Mechanism
  • Clinical features (antenatal and classical)
A

Defect: NKCC2, ROMK, ClCKa/b, Barrtin
Mechanism: Failure of sodium, potassium and chloride cotransport in thick ascending limb. Salt wasting, hypokalaemic alkalosis due to volume contraction, failure of voltage dependent calcium & magnesium absorption.
Clinical features:
Antenatal: Polyhydramnios, prematurity, delayed growth, nephrocalcinosis
Classical: Delayed growth, polyuria, polydipsia

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17
Q

Polyhydramnios

A

excess of amniotic fluid in the amniotic sac.

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18
Q

Polydipsia

A

Excessive thirst

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19
Q

Name common distal tubular and collecting duct disorders

A
  • Gitelman’s syndrome
  • Distal (type 1) renal tubular acidosis
  • Disorders resembling hyperaldosteronism
  • Type 4 renal tubular acidosis
  • Nephrogenic diabetes insipidus
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20
Q

Gitelman’s syndrome

  • Defect
  • Mechanism
  • Clinical features
A

Defect: NCCT (thiazide sensitive chloride channel) in the DCT
Mechanism:
Failure of sodium/chloride cotransport in distal tubule, hypokalaemic alkalosis due to volume contraction, impaired magnesium absorption.
Clinical features: Polyuria, polydipsia, tetany

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21
Q

What is tetany?

A

Muscle spasms caused by low magnesium

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22
Q

What differentiates Gitelman’s syndrome from Barter’s syndrome?

A

In Gitelman’s there is increased calcium reabsorption but lowered magnesium re absorption. In Barters there low magnesium and calcium.

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23
Q

How will the kidney sense that the BP has reduced?

A

JGA of the kidney will sense that there is fall in sodium delivery to the distal nephron because of fall in GFR.

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24
Q

What is the action of aldosterone?

A

1) Steroid hormone – predominantly acts on transcription
2) Increase expression of ENaC, Na/K ATP-ase
3) This means that more sodium retained, and more H+ and K+ excreted.
4) Water follows the Na so BP goes up

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25
Q

What other hormone can bind to the Mineralocorticoid receptor that aldosterone binds to? What stops this happening in the renal tubules?

A

Mineralocorticoid receptor also activated by cortisol.

Cortisol entry to renal tubular cells prevented by 11-beta hydroxysteroid dehydrogenase.

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26
Q

Distal (type 1) renal tubular acidosis:

  • Defect
  • Mechanism
A

Defect: Luminal H+ ATPase or H+/K+ ATPase. Can be gentic or acquired. But specific cause not known.
Mechanism: Failure of H+ excretion and urinary acidification

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27
Q

What does excessive aldosterone activity lead to?

A

Excessive aldosterone activity produces sodium retention, hypertension and hypokalaemic alkalosis.

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28
Q

What is primary hyperaldosteronism?

A

Excessive aldosterone production when the adrenal gland is producing too much.

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29
Q

What is secondary hyperaldosteronism?

A

Secondary hyperaldosteronism is when you have problems with the renin/angiotensin system or renal artery stenosis.

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30
Q

How can renal artery stenosis cause hyperaldosteronism?

A
  • In renal artery stenosis, you have narrowing of the renal artery
  • The blood supply and flow rate to kidneys reduced,
  • The body thinks that the BP has dropped as you get lowered sodium delivery to the distal nephrons
  • Then the system tries to raise BP started without it actually being needed.
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31
Q

Glucocorticoid remediable aldosteronism

  • Defect
  • Mechanism
  • Treatment
A

Defect: Chimeric gene – 11beta hydroxylase and aldosterone synthetase
Mechanism: Aldoosterone produced in response to the ACTH hormone instead of renin in the adrenal, ACTH level is always higher in the body, so too much aldosterone is produced.
Treatment: Suppress ACTH using synthetic glucocorticoids

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32
Q

Liddle’s syndrome

  • Defect
  • Mechanism
  • Treatment
A

Defect: Activating mutation of ENaC
Mechanism: Sodium channel always open so constant aldosterone like effect
Treatment: Amiloride (blocks ENaC)

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33
Q

Syndrome of Apparent Mineralocorticoid Excess (AME)

  • Defect
  • Mechanism
  • Treatment
A

Defect: 11-beta hydroxysteroid dehydrogenase

Mechanism: Cortisol not broken down in the renal tubules, therefore activates mineralocorticoid receptor. This increases aldosterone activity.

Treatment: Spironolactone (mineralocorticoid receptor antagonist)

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34
Q

Hyperkalaemic distal (type 4 ) renal tubular acidosis

  • Defect
  • Mechanism
  • Treatment
A

Defect: Low aldosterone levels

Mechanism: Reduced generation of electrochemical gradient, resulting in failure of H+ and K+ excretion
Common in elderly patients with diabetes

Treatment: Diuretics or fludrocortisone

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35
Q

Nephrogenic diabetes insipidus

  • Defect
  • Mechanism
A

Defect: Vasopressin V2 receptor or aquaporin 2 water channel
Mechanism: Failure of water reabsorption in the collecting duct, resulting in inability to concentrate urine
Clinical features: Polyuria, polydipsia, hypernatraemia

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36
Q

What kind of substance needs to be used to get a X-ray of kidneys?

A

A substance that is fully filtered and excreted by the kidney therefore it is concentrated in the urine. It has a large nucleus that absorbs x-rays hence you can see the urinary tract and the bladder.

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37
Q

What level is the umbilicus at?

A

L4/5

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38
Q

What does the kidney sit against?

A

Half of the kidney is sitting against the anterior diaphragm and half sitting against Quadratus Lumborum.

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39
Q

What are sonic headhshots? What do they do?

A

Messenger released by notochord that act on the ectoderm, endoderm and mesoderm.

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40
Q

What does the intermediate mesoderm develop into?

A

Urogenital system. THREE overlapping kidney systems are formed in a cranial to caudal sequence, all developing from intermediate mesoderm.

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41
Q

What are the three overlapping kidney systems in embryology?

A

1) Pronephros
2) Mesonephros
3) Metanephros

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42
Q

Where is the PRONEPHROS found, when does it disappear and stop functioning?

A
  • Found in the cervical region
  • Non functioning, rudimentary
  • Develops in week 4 and disappears by week 5
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43
Q

Where is the MESONEPHROS found, what does it consist of, when does it disappear and stop functioning?

A
  • Found in the thoracic and lumbar region
  • Comprises a ridge and duct
  • May function for short period
  • Develops in week 4 and has a duct connecting it to the cloaca in males it persists into adulthood
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44
Q

Where is the METANEPHROS found, when does it disappear and stop functioning?

A
  • develops in the pelvis

- becomes the permanent kidney

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45
Q

What will the mesonephric duct form into?

A

Mesonephric duct will form the Vas deferens in the male.

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46
Q

Where does the mesonephric duct end?

A

In the cloaca

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47
Q

What does the bladder form from?

A

The cloaca

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48
Q

Describe what happens to the cranial tubules and the caudal tubules by the eighth week.

A
  • Cranial tubules start to degenerate whilst caudal tubules are still forming
  • By week eight all but the most caudal tubules have disappeared
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49
Q

What happens to the caudal tubules in males and females?

A

In the male these few caudal tubules form the efferent ducts of the testis

In the female all tubules disappear, maybe have one or two remnants.

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50
Q

How does the adult kidney form?

A

1) A ureteric tube buds off the distal end of the mesonephric duct
2) The tube grows into an area of mesoderm called the metanephric blastema
3) Once the ureteric bud enters the blastema it divides and dilates, forming the primitive renal pelvis. It repeatedly divides forming the major and minor calyces
4) The metanephric blastema forms the glomeruli and tubules of the kidney
4) The ureteric tube forms the collecting ducts and ureter

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51
Q

How many collecting ducts grow from the minor calyces to form the renal pyramids?

A

Approximately 1 to 3 million collecting tubules grow from the minor calyces to form the renal pyramids. Reduces as you age.

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52
Q

How does the position of the kidney come into play?

A

The kidney develops in the pelvis but shifts to a more cranial position in the abdomen, this is achieved by a diminution of body curvature and growth of the lumbar and sacral regions.

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53
Q

How does the Bowman’s capsule and loop of henle form ?

A

1) Ureters grows and starts to divide, this produces a chemical that stimulates the renal vesicle.
2) That elongates and one end attaches to the ureter and the other end becomes the Bowman’s capsule.
3) Once the Bowman’s capsule develops, you get a tuft of blood vessels grow into it that develop into the glomeruli
4) The middle part elongates to form the loop of henle.

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54
Q

Medullary sponge kidney. How can you tell in-utero?

A

MSK occurs when small cysts (sacs) form either on tiny tubes within the kidney (known as tubules) or the collecting ducts (a channel where urine is collected for removal). These cysts can reduce the outward flow of urine from the kidneys. One or both kidneys can be affected.

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55
Q

Function of the kidney in utero?

A

Metanephros starts functioning at the 12th week. Urine is passed into the Amniotic cavity and mixes with the amniotic fluid. The fluid is swallowed by the fetus and recycles through the kidneys.

During embryonic and fetal life the kidneys are not responsible for excretion of waste products since the placenta is doing that function.

56
Q

Cloaca

A

A common passage for the bowel, urinary and genital tracts

57
Q

Allantois

A

Allantois is formed as an anterior outgrowth of the Cloaca, it forms the bladder.

58
Q

During week 4 and 7 what is the cloaca divided into by the mesodermal septum?

A

= The Urorectal septum forming an anterior Urogenital Sinus and a posterior Anorectal Canal

59
Q

What do the ureters develop from? What do they drain into?

A

The ureters, develop as an outgrowths from the Mesonephric ducts and drain into the urogenital sinus.

60
Q

Why do the ureters and the mesonephric ducts enter the bladder seperately?

A

During differentiation of the cloaca and formation of the bladder, the caudal portions of the Mesonephric ducts are absorbed into the wall of the urinary bladder.

The openings of mesonephric ducts move close together to enter the Prostatic Urethra and in the male become the ejaculatory ducts.

61
Q

Development of the prostrate

A
  • At the end of the 3rd month, epithelium of the prostatic urethra (endodermal in origin) begins to proliferate
  • Forms a number of outgrowths that penetrate the surrounding mesenchyme and form the glands of Prostate.
  • Prostatic connective tissue and smooth muscles are derived from the Mesoderm.
  • In female, the Urethral epithelium gives rise to the Urethral and Paraurethral glands
62
Q

What is the equation for pH?

A

pH = -log10[H+]

63
Q

What is the normal range for blood pH?

A

7.35 to 7.45

64
Q

What is the minimum urine pH?

A

4.5

65
Q

Base

A

accepts H+ ions

66
Q

Acid

A

donates H+ ions

67
Q

What are the two arms of pH control?

A

The respiratory arm and the renal arm.

68
Q

What is the normal range for [H+] ?

A

45-35nmol/l

69
Q

What are the dietary acid loads in terms of carbohydrate, protein and fats?

A

Carbohydrate + Fats → Carbonic acid → CO2 - lung

Protein → Non-carbonic acids → sulphur AA – kidney

70
Q

Bicarbonate buffer equation

A

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-

71
Q

Henderson- hasselbach equation

A

pH = pKa + log([A-]/[HA])

pH = pKaH2CO3 + log([HCO3-]/[H2CO3])

pH = 6.1 + log([HCO3-]/0.03 x pCO2)

72
Q

Base excess

A

Quantity of acid required to return plasma pH to normal.

73
Q

Standard base excess

A

Quantity of acid required to return extracellular fluid (ECF)
back to normal

74
Q

Acidosis

A

Disorder tending to make blood more acid than normal

75
Q

Alkalosis

A

Disorder tending to make blood more alkaline than normal

76
Q

Acidemia

A

Low blood pH

77
Q

Alkalemia

A

High blood pH

78
Q

What is the anion gap?

STEWARTS THEORY

A

The difference between measured anions (negative) and cations (positive)
Anion gap = [Na+] + [K+] - [Cl-] - [HCO3-]

79
Q

What is the normal range for the anion gap?

A

Normal: 10-16

80
Q

What does a wide anion gap mean?

A

= lactic acidosis, ketoacidosis, ingestion of acid, renal failure

81
Q

What does a narrow anion gap mean?

A

= GI HCO3- loss, renal tubular acidosis

82
Q

Titrable acidity

A

Quantity base to bring pH to 7.4

83
Q

What is the most common urinary buffer?

A

Alkaline phosphate (HPO4 2-) is the most commonest urinary buffer.

84
Q

Describe how alkaline phosphate acts as a urinary buffer in the proximal tubule

A

1) When all of the filtered HCO3- has been combined with secreted H+, the additional H+ secreted (from the sodium/hydrogen antiport) then starts combining with the HPO4 2-
2) H+, generated from the dissociation of H2CO3
from within the tubular epithelial cells, combines
with HPO4 2- to form H2PO4- dihydrogen phosphate which is then excreted in urine

85
Q

How does the action of the alkaline phosphate alkalinze the blood?

A
  • In bicarbonate reabsoprtion there is NO NET GAIN on HCO3- (reabsorption replaces filtered).
  • In PHOSPHATE BUFFER there is no absorption of HCO3- from teh tubular lumen BUT HCO3- diffues into the interstial fluid still so there is a NET GAIN of HCO3-
  • The conc of HCO3- increases so the pH blood plasma
86
Q

When does the H+ combine in the urinary phosphate buffer?

A

Significant amounts of H+ combine with filtered non

bicarbonate buffers such as HPO4 2- ONLY AFTER the filtered HCO3- has virtually ALL BEEN REABSORBED

87
Q

What triggers urinary ammonium buffer?

A

It is an apadative response to acid load. It increases when acid load increases.

88
Q

Describe how ammonium acts as a urinary buffer in the proximal tubule

A

1) Tubular cells, mainly those of the PROXIMAL
TUBULE, take up glutamine from both the glomerular filtrate & peritubular plasma and METABOLISE it to form
NH3 (ammonia) & HCO3- (bicarbonate)

2)The NH3 then reacts with the H+ in the cell (either
derived from the dissociation of H2CO3 or from that absorbed as a result of Na+ reabsorption) to form NH4+ (ammonium ion)

3) The NH4+ is then actively secreted via Na+/NH4+ countertransport into the lumen and excreted
4) The HCO3- moves into the peritubular capillaries and thereby increases HCO3- levels (net gain of HCO3-) thereby ALKANISING the blood plasma

89
Q

Net acid excretion equation

A

= titratable acidity + ammonium EXCRETED – HCO3- REABSORBED

90
Q 
Respiratory Acidosis 
LEVELS OF: 
- pH
- HCO3-
- pCO2
A

Fail to get rid of CO2 resulting in a decrease in pH as CO2 builds

up.
- pH decreased
- HCO3- increased
- pCO2 increased

91
Q

Causes of respiratory acidosis

A
  • Hyperventilation»»hypercapnia (too much CO2)
  • COPD
  • Any cause of respiratory failure (pulmonary embolism : Type 1, hypoventilation: Type 2)
92
Q

What is the typical actions for respiratory disorders and metabolic disorders of acidosis and alkalosis?

A

Respiratory disorder – renal compensation

Metabolic disorder – respiratory compensation

93
Q

Why is Hyperkalemia a consequence of acidosis?

A

Hyperkalemia in acidosis is becuase the cells try to get rid of excess H+ in the blood by bringing it into cells, as they do this they have to force potassium out of the cells. This means that the concentration of potassium increases in the blood.

94
Q

Compensation

pH, HCO3-, pCO2 levels

A

pH normalised, disturbed levels of HCO3- or pCO2

95
Q

Correction

pH, HCO3-, pCO2 levels

A

pH, HCO3- , pCO2 all normalised

96
Q

What is the renal compensation for respiratory acidosis?

A

1) The kidneys will increase H+ secretion (in the form of ammonium (NH4+)
2) Kidneys will also release more HCO3- into the plasma which will increase pH, as a result of the use of the ammonium buffer
3) The increase in pH will take DAYS

97
Q 
Respiratory Alkalosis
LEVELS OF: 
- pH
- HCO3-
- pCO2
A 
Too much CO2 lost resulting in an increased pH as CO2 is lost.
LEVELS OF: 
- pH increases 
- HCO3- decreases
- pCO2 decreases
98
Q

What are the causes of Respiratory Alkalosis?

A
  • CO2 depletion due to hyperventilation»hypocapnia
  • Hypoxia
  • Type 1 respiratory failure e.g. pulmonary embolism - decrease in
    O2 and a decrease/no change in CO2
99
Q

What is the renal compensation for Respiratory Alkalosis?

A

1) The kidneys will decrease H+ secretion thereby retaining H+ and helping return pH to normal
2) The decrease H+ secretion will also result in a decrease in HCO3- reabsorption resulting in more HCO3- excretion and thus a fall in plasma HCO3- further helping to increase pH and return it back to
normal

100
Q 
Metabolic acidosis
LEVELS OF: 
- pH
- HCO3-
- pCO2
A 
Excess acid production (intercalated cells release acid) resulting in
a decrease in pH. 
LEVELS OF: 
- pH decreases
- HCO3- decreases
- pCO2 decreases
101
Q

What are the causes of metabolic acidosis?

A

1) Renal failure
2) GI HCO3- loss
3) Dilution of blood - more H2O in blood the more acidic it gets
4) Failure of H+ excretion i.e. hypoaldosternonism whereby insufficient aldosterone is released so less Na+ reabsorbed meaning less H+ secreted using Na+/H+ countertransporter
5) Excess H+ e.g. ketoacidosis

102
Q

What is the respiratory compensation for metabolic acidosis?

A

The decrease in pH will stimulate chemoreceptors of the lung resulting in enhance respiration resulting in a fall in CO2 resulting in an increase in pH.

103
Q 
Metabolic Alkalosis
LEVELS OF: 
- pH
- HCO3-
- pCO2
A 
Lack of acid production (intercalated cells release less acid) resulting in a increase in pH.
LEVELS OF: 
- pH increases
- HCO3- increases 
- pCO2 increases
104
Q

Causes of Metabolic Alkalosis

A

1) Vomiting (due to the loss of gastric secretions which are rich in HCL)
2) Volume depletion
3) Alkali ingestion
4) Hyperaldosteronism
5) Hyperkalaemia - resulting in increased aldosterone release

105
Q

What are the respiratory compensation of Respiratory Alkalosis?

A

The increase in pH inhibits the chemoreceptors of the lung thereby reducing respiration thereby increasing CO2 resulting in a decrease in pH

106
Q

How does the kidney act as an endocrine organ?

A
  • Produces erythropoietin

- Site of Vitamin D activation

107
Q

Erythropoetin EPO

  • where is it produced?
  • what does it stimulate
  • increases in response to?
  • decreases in response to?
A

1) Produced in the peritubular cells in the interstitial space of the renal cortex
2) Stimulates bone marrow MATURATION OF RED BLOOD CELLS (erythrocytes)
3) Increases in response to; anaemia, altitude & cardiopulmonary disorders
40 Decreases in response to; polcythaemia (abnormally increased haemoglobin in
blood), renal failure

108
Q

Function of Hypoxia-inducible factor (HIF)-2

A

It regulates erythropoietin (EPO).

Maybe this can be used to treat anaemia.

109
Q

What is standard bicarbonate standardised to?

A

pCO2 5.3kPa and temp 37oc

110
Q

What can base excess be used to calculate?

EQUATION

A

Can be used to calculate bicarbonate dose to correct acidosis.
0.3xWtxBase excess

111
Q

In acidosis what value is the base excess?

A

Base excess is negative in acidosis, can be referred to as base deficit.

112
Q

What is an Arterial Blood Gas (ABG)?

A

TEST THAT MEAUSRES:

  • pH
  • pO2
  • pCO2
  • Std HCO3-
  • Std Base excess
  • May include other measures (eg lactate, Na+, K+)
113
Q

Clinical features of metabolic acidosis

A

Sighing respirations (Kussmaul’s resps), tachypnoea

114
Q

ABG interpretation steps

A
  • pH (acidosis or alkalosis)
  • pCO2 (respiratory component/not)
  • Std HCO3- (metabolic component/not)
  • Base excess (if negative = acidosis)
115
Q

What is urine flow through the ureters to the bladder propelled by?

A

Urine flow through the ureters to the bladder is propelled by contractions of the
ureter wall SMOOTH MUSCLE

116
Q

What is classes as the lower urinary tract?

A
  • The bladder
  • The bladder neck
  • The prostate gland (in the man)
  • The urethra and urethral sphincter
117
Q

What is the function of the urinary tract?

A
  • To collect urine
  • Store it under safe LOW PRESSURE conditions
  • Store it until it is socially acceptable to release urine
118
Q

Detrusor Muscle

  • what type of muscle?
  • innervation during filling
  • innervation during micturition
A
  • It is a smooth muscle
  • Parasympathetic innervation
  • inhibited during filling
  • stimulated during micturition
119
Q

Internal urethral sphincter

  • what type of muscle?
  • innervation during filling
  • innervation during micturition
A
  • smooth muscle
  • sympathetic innervation
  • stimulated during filling
  • inhibited during micturition
120
Q

External sphincter

  • what type of muscle?
  • innervation during filling
  • innervation during micturition
A
  • slow twitch skeletal muscle (voluntary)
  • somatic motor
  • stimulated during filling
  • inhibited during micturition
121
Q

Describe the muscles of the bladder and their actions on the bladder.

A
  • Bladder is a balloonlike chamber with walls of smooth muscle collectively known as the DETRUSOR MUSCLES
  • Contraction of the detrusor muscles squeezes on the urine in the bladder lumen to produce urination
  • Part of the detrusor muscles at the neck of the bladder where the urethra begins functions at the internal urethral sphincter
  • Just below the internal urethral sphincter, a ring of SKELETAL MUSCLE surrounds the urethra - this is the external striated urethral sphincter (also known as the
    RHABDOSPHINCTER)
  • Contraction of this can prevent urination even if the detrusor muscles are contracting strongly
122
Q

Bladder filling explain the process

A

1) While the bladder is filling; the PARASYMPATHETIC INPUT to the detrusor muscles is minimal
2) As a result the muscle is relaxed - due to the
arrangement of the smooth muscle fibers, when the detrusor muscle is relaxed, the internal urethral sphincter is passively closed
3) At the same time there is strong sympathetic input to the internal urethral sphincter & strong input by the somatic motor neurones to the external urethral sphincter
4)this means that the internal & external urethral sphincters are CLOSED

123
Q

Bladder stretch reflex:

Briefly describe it

A
  • This is a primitive spinal reflex, in which micturition is stimulated in response to stretch
  • It is similar to a muscle stretch reflex e.g the patella reflex
  • During toilet training at a young age the spinal reflex is overridden by the higher centres of the brain to provide voluntary control over micturition
124
Q

Explain the bladder reflex arc

A
  1. Bladder fills with urine, and the bladder walls stretch
  2. Sensory nerves (afferent) detect the stretch and transmit to the spinal cord
  3. Interneurones within the cord relay the signal to the parasympathetic efferents (PELVIC NERVE)
  4. The pelvic nerve acts to contract the detrusor muscle and thus stimulate micturition
125
Q

What is special about the bladder reflex?

A
  • This stretch reflex is NOT FUNCTIONAL post childhood
  • But can regain function in spinal injuries or neurodegenerative disease where the
    DESCENDING SOMATIC PATHWAY can be damaged resulting in the loss of voluntary micturition - INCONTINENCE
126
Q

Explain the process of urination as the bladder fills

A

1) As the bladder fills with urine, the pressure within it increases, which then stimulates stretch receptors in the bladder wall
2) The afferent neurones from these receptors enter the spinal cord and stimulate the parasympathetic neurones which then cause the detrusor muscles to CONTRACT
3) When the detrusor muscle contract, the change in bladder shape pulls open the internal urethral sphincter
4) Simultaneously the afferent input from the stretch receptors reflexively inhibits the sympathetic neurones to the internal urethral sphincter which further contributes to opening
5) The afferent input also inhibits the somatic motor neurones to the external urethral sphincter causing it to RELAX
6) This activity results in the opening of both sphincters and the contraction of the detrusor muscles is then able to produce URINATION

127
Q

Sympathetic nervous supply to the bladder

  • nerve
  • type
  • action
A
  • Via the HYPOGASTRIC NERVE (T12-L2)
  • causes the RELAXATION of the detrusor muscle therefore promoting urine retention
  • when inhibited to the internal sphincter causes then to open
128
Q

Parasympathetic nervous supply to the bladder

  • nerve
  • type
  • action
A

The parasympathetic system communicated with the bladder via the PELVIC SPLANCHNIC NERVE (S2-S4).

Increased signals from this nerve causes
CONTRACTION of the detrusor muscles - thereby stimulating micturition

129
Q

Somatic motor nervous supply to the bladder

  • nerve
  • type
  • action
A

The somatic system supply gives voluntary control over micturition.
It innervates the external urethral sphincter, via the PUDENDAL NERVE (S2-S4)
It can cause it to constrict (storage phase) or relax (micturition).

130
Q

How do we know when we need to go to the toilet?

A

There are sensory (afferent) nerves that report to the brain, located in the bladder wall they signal the need to urinate when the bladder becomes full.

131
Q

Continence

A

The ability to control movements of the bowels and bladder

132
Q

What are the key factors in the normal bladder filling?

A
  • Continence
  • Sensation of bladder volume
  • Compliance - bladder holds urine at low pressure via receptive
    relaxation
133
Q

What is voiding?

A

When urine is released through the urethra

134
Q

What are the key factors in the normal bladder voiding?

A
  • Voluntarily initiated

* Complete emptying

135
Q

What are the consequences of bladder dysfunction?

A
  • Incontinence
  • Infection & bladder stones
  • Upper urinary tract injury - due to high pressure

Phase 1 revision (5 decks)

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