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Kofi: Pure clinical conditions 2 > Urinary > Flashcards

Urinary Flashcards

1
Q

Which vertebral level can the kidneys be found?

A

T11/T12

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2
Q

What is the purpose of the bladder?

A

Storage of urine that empties periodically via the urethra

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3
Q

What are body fluid compartments?

A

42L of water split into:

  • 28L of intracellular fluid
  • 14L of extracellular fluid.

14L of extracellular fluid split into:

  • 11L of interstitial fluid
  • 3L of intravascular fluid
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4
Q

What is the purpose of the kidney?

A
  • Maintenance of a stable environment to enable function in all parts of the body
  • Regulation by controlling the concentrations of key substance in extracellular fluid
  • Excretion of waste products
  • Endocrine via synthesis of renin, erythropoietin, prostaglandins
  • Metabolism though the formation of the active form of vitamin D, catabolism of insulin, PTH and calcitonin
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5
Q

How is kidney function measured?

A

Glomerular filtration rate

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6
Q

What is the GFR?

A

Amount of filtrate that is produced from blood flow per unit time

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7
Q

How does advancing age affect the glomerular filtration rate?

A
  • Declines after 30 years of age
  • Rate of decline is 6-7mls/min per decade
  • Loss of functioning nephrons
  • Some compensatory hypertrophy
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8
Q

What is compensatory hypertrophy?

A
  • If the nephron number decreases
  • Exisiting nephrons get bigger
  • Healthy kidney can also get bigger
  • Occurs to much greater extent in childhood
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9
Q

What are the risks associated with compensatory hypertrophy?

A
  • Nephrons have to work harder
  • Greater risk of wearing out
  • Cortical scarring
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10
Q

What happens to the kidneys and their function in pregnancy?

A
  • GFR increases
  • Kidney size increases due to increased fluid volume
  • Nephrons number stays the same
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11
Q

What does a decline in GFR show?

A
  • Decline in the number of nephrons
  • Decline of GFR within individual nephrons

Overall the kidney function has worsened

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12
Q

A patient arrives with significant kidney damage. Their GFR has been stable but recently has decreased. Upon examination, you notice there is kidney hypertrophy. What does this tell you about the kidney function?

A

The kidney function has declined slowly so GFR didn’t fall until there was significant kidney damage

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13
Q

Why do we need a surrogate marker?

A

The actual GFR cannot be measured

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14
Q

What is the formula for clearance?

from the body

A

C=A/P

C= clearance
A= amount of substance eliminated from plasma
P= plasma concentration of substrate
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15
Q

What is the formula for Renal clearance?

A

C=(UxV)/Pa

C= clearance
U= amount in urine
V= urine flow rate
Pa= arterial plasma concentration
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16
Q

What is clearance?

A

The volume of plasma cleared of a substance per unit time where the substance is denoted as ‘x’.

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17
Q

What are the properties of substances used to measure GFR?

A
  • Produced at a constant rate
  • Be freely filtered across the glomerulus
  • Not be reabsorbed in the nephron
  • Not be secreted into the nephron
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18
Q

Why isn’t inulin used to measure GFR?

A
  • Requires a continuous IV to maintain a steady state

- Requires catheter and timed urine collections

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19
Q

When is 51 Cr-EDTA used clinically?

A
  • In children
  • Where indication renal function is required

Approximately 10% lower clearance than inulin. Radioactively labelled and cleared by renal filtration

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20
Q

What is creatinine?

A
  • Endogenous substance

- End product of muscle breakdown

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21
Q

What are the properties of creatine in regards to being an indicator of clearance?

A
  • Produced at a constant rate
  • Freely filtered across the membrane
  • Not reabsorbed along the nephron
  • However it is secreted into the nephron
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22
Q

How is creatinine clearance measured?

A
  • Urine is collected over 24 hours

- The serum creatinine is measured

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23
Q

What are the issues associated with using creatinine as a measurement of clearance?

A
  • Cumbersome and frequently inaccurate

- Overestimates GFR by 10-20% due to creatinine secretion

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24
Q

Which population is creatinine best for in terms of indicators of clearance?

A

-Pregnant women

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25
Q

What factors lead to increased creatinine measurement?

A
  • Muscle cell break down
  • Large muscle bulk
  • Black
  • Male
  • Creatinine supplements
  • Certain drugs
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26
Q

What factors lead to reduced serum creatinine?

A
  • Reduced muscle mass
  • Old
  • Hispanic/Indo-asian
  • Female
  • Vegetarian
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27
Q

What is the eGFR?

A

A ‘best guess’ of the GFR which uses models to try and better estimate the GFR from serum creatinine levels. It is not the same as GFR.

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28
Q

What are the variable for the equation for the MDRD eGFR based on?

A
  • Serum creatinine
  • Age
  • Sex
  • Caucasian or Black
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29
Q

When is MDRD eGFR inaccurate?

A
  • People without kidney disease
  • Children
  • Pregnancy
  • Old age
  • Other ethnicities
  • Amputees
  • People with significantly reduced muscle mass
  • Patient with higher levels of kidney function
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30
Q

Why is there a risk of patient being labelled as CKD due to the MDRD eGFR?

A

There is an underestimation of the true GFR when the serum creatinine is close or within normal range

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31
Q

Why is eGFR less accurate with mild kidney disease?

A
  • Reduction in GFR causes increase in blood flow
  • Reduced nephron number lead to nephron hypertrophy so no change in GFR
  • Reduced filtration of creatinine results in increased serum creatinine and increased secretion into the tubule
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32
Q

What is the sequence of arteries from the renal artery?

A

Renal artery > Segmental artery > Interlobar artery > Arcuate artery > Interlobular Artery

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33
Q

What are the 2 types of nephrons found in the kidney?

A
  • Cortical nephrons

- Juxtamedullary nephrons

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34
Q

What are the features of the cortical nephrons?

A
  • Short loop of henle which just enters the medulla
  • Peritubular capillaries covering most of the nephron
  • Rich sympathetic innervation
  • High concentration of renin
  • In the outer part of the cortex
  • Small glomerulus
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35
Q

What are the features of the juxtamedullary nephrons?

A
  • Glomerulus sits juxtaposed to the medullary boundary
  • Loop of henle is very long and penetrates deep into medullary tissue
  • Vasa recta runs in parallel to the loop of henle.
  • Poor sympathetic innervation
  • Almost no renin
  • Glomerulus is large
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36
Q

What is renal plasma flow and blood flow?

A

Renal blood flow = About 1.1 L/min

Plasma flow = (1-haemotocrit) X renal blood flow

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37
Q

What is the renal corpuscle and function of the renal corpuscle?

A

The glomerulus + bowman’s capsule

To produce ultra filtrate of plasma

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38
Q

What produces the filtration barrier in the renal corpuscle?

A
  1. Capillary endothelium - permeable. Water, salts, glucose. Filtrate moves between cells
  2. Visceral layer of Bowman’s capsule - Acellllar gelatinous later of collagen/glycoproteins which is permeable to small proteins. Glyocproteins repel protein movement
  3. Podocyte layer - Pseudopodia interdigitate froms filtration slits
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39
Q

Which molecules cannot cross the filtration barrier?

A

Cells and large proteins

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40
Q

What is the effect as a result of the negative charge on the filtration barrier being lost?

A

-Proteins are more readily filtered and result in a condition called proteinuria

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41
Q

What is the myogenic mechanism?

A
  • Arterial smooth muscle response to decrease and increase in vascular tension
  • Contribute to total auto-regulatory mechanism
  • Occurs rapidly
  • Property predominantly of the preglomerular resistance vessels
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42
Q

Why do we need Autoregulation of GFR?

A

Feedback mechanism intrinsic to the kidney to keep RBF and GFR constant. Without this a slight change in the blood pressure would cause a significant change in the GFR

Two mechanism

  • Myogenic reflex
  • Tubuloglomerular feedback
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43
Q

What is the myogenic response to an increase in blood pressure?

A

-Constriction of the afferent arteriole predomantly or dilation of the efferent arteriole to decrease the blood volume arriving to be filtered. This keep the GFR unchanged

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44
Q

What is the myogenic response to a decrease in blood pressure?

A

-Dilation of the afferent arteriole predominantly or constriction of the efferent arteriole in order to increase the blood volume arriving to be filtered. This keep the GFR unchanged.

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45
Q

How does the Tubular glomerular feedback mechanism work?

A
  • Links the sodium and chloride concentration at the macula densa with control of renal arteriole resistance (efferent and afferent)
  • Acts in response to acute deviation in the delivery of fluid and solutes to the JGA.
  • Control the distal solute delivery and hence tubular reabsorption
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46
Q

What is the action of the Tubular goloemrular feedback when the arterial pressure increases?

A
  • Increase in renal plasma flow and increase in GFR leads to increase in NACl
  • Macula densa cells detects NaCl via a concentration-dependant salt uptake through the NaKCC co-transporter and responds to changes in NaCL arriving in the distal convoluted tubule
  • Juxtaglomerular apparatus is stimulated to release adenosine which constricts the afferent arteriole by stimulating the Alpha 1 receptors. The efferent arteriole is dilated by stimulation of the Alpha 2 receptors
  • This reduces the GFR
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47
Q

When is the sympathetic innerveation of the renal vessels most active?

A

During haemorrhage, ischamia or the fight or flight response.

Vasoconstriction occurs in order to conserve blood volume and can cause a fall in GFR

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48
Q

How does the parasympathetic nervous system act on the blood vessels?

A

Release of nitrous oxide for endothelial cells and vasodilation

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49
Q

What is the glomerulotubular balance?

A

It blunts the sodium excretion in response to any GFR changes which occur do occur despite the Myogenic
and TG feedback response.

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50
Q

What is the short term regulation of blood pressure?

A

Baroreceptor reflex

  • Adjust sympathetic and parasympathetic inputs to the heart to alter the cardiac output
  • Adjust sympathetic input to peripheral resistance vessels to alter TPR
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51
Q

What are the hormonal responses to low renal perfusion?

A
  • Renin-angiotensin aldosterone system
  • Sympathetic nervous system
  • Prostaglandins
  • ADH
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52
Q

What is the long term regulation of blood pressure?

A

Neurohormonal resposes to affect salt and water balance

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53
Q

What factors stimulate the renin release?

A
  • Reduced NaCl delivery to the macula densa of distal tube
  • Reduced perfusion pressure in the kidney causes the release of renin
  • Sympathetic stimulation (B1) of the juxtaglomerular increases release of renin
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54
Q

Where is renin released from?

A

Juxtagomerular cells of the afferent arteriole in response to reduced perfusion pressure and stimulation by the sympathetic nervous system

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55
Q

What are the direct actions of angiotensin 2 on the kidney?

A
  • Vasoconstriciton of the efferent and to a lesser extent the afferent arteriole
  • Enhanced sodium reabsorption at the proximal collecting tubule by stimulation of Na-H(NHE3) exchanger in the apical membrane
  • Increase in mesangial matrix
  • Increase in mesangial cell proliferation
  • Glomerular permeability to proteins
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56
Q

What are some indirect effects of angiotensin 2 on the kidney to control blood pressure?

A
  • Release of aldosterone

- Release of ADH

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57
Q

What are the actions of aldosterone on the kidney?

A

Acts on principal cells of distal convoluted tubule and collecting ducts to:

  • Stimulate Na+ and therefore water reabsorption
  • Activates apical Na+ channel and apical K+ channel
  • Increases basolateral Na+ extrusion via Na/K/ATPase
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58
Q

What are the actions of the sympathetic nervous system in response to low blood pressure?

A
  • Reduction of the renal blood flow by vasocontrcitin of arterioles and decrease in the GFR
  • Activates apical Na/H exchanger and basolateral Na/K ATPase in proximal collecting tubule
  • Stimulates renin release from JG cells
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59
Q

What are effects of prostaglandins in the kidney?

A
  • Causes vasodilation of the afferent arteriole

- Enhances renin release

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60
Q

What triggers the release of prostaglandins in the kidney?

A
  • Angiotensin 2
  • Noradrenaline
  • Anti diuretic hormone
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61
Q

What is the net effect of the interaction of prostaglandins and the RAAS system?

A
  • Systematic vasoconstrinon
  • Vasoconstriction of the efferent artriole
  • Vasodilation of the afferent arteriole
  • The GFR is preserved as a result
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62
Q

What is action of ADH?

A
  • Formation of concentrates urine by retaining water to control the plasma osmolarity. Reabsorption of water is increased at the distal nephron
  • Vasoconstriction
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63
Q

What stimulate release of ADH?

A
  • Increase in plasma osmolarity stimulates release of ADH

- Severe hypovolaemia stimulates release of ADH

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64
Q

What are the 2 major actions for atrial natriuretic peptide?

A
  1. Causes vasodialtion

2. Inhibits Na+ reabsorption especially in the collecting duct causing natriuresis

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65
Q

What triggers the release of ANP?

A

Low circulating volume. It acts to support the blood pressure

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66
Q

What is hypertension?

A

-Persistent increase in blood pressure

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67
Q

What is pressure natriuresis?

A

Increasing blood pressure gradually resets the kidneys for salt concentrations and water volume and this means the regulatory mechanisms aren’t working as well. It is thought to be one of the causes of hypertension

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68
Q

What is hypertension?

A

-Persistent increase in blood pressure

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69
Q

What are some causes of secondary hypertension?

A
  • Reno-vascular hypertension
  • Coarctation of the aorta
  • Primary hyperaldosteronism (Conn’s syndrome)
  • Cushing’s syndrome
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70
Q

What are the 2 main types of renovascualr disease?

A
  • Atheroma

- Fibromuscular dysplasia

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71
Q

What causes renovascular disease?

A

-Renal artery stenosis which is narrowing of the renal artery

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72
Q

Why does renovascular disease lead to hypertension?

A
  • Lack of blood supply to the kidney causes the kidney to sense hypovolaemia in the body
  • This means that it triggers changes in order to increase the blood pressure
  • This causes hypertension because the mechanism are constantly trying to increase blood pressure even though the blood is normotensive
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73
Q

What happens with unilateral renal artery stenosis?

A
  • One kidney triggers mechanism to increase blood pressure by activating the RAAS system because it senses hypovolaemia
  • One kidney works normally and sense the increase in sodium so acts to excrete the sodium. It suppresses the RAAS system.
  • Net effect is hypertension with no fluid overload and salt as the kidney that works normally excrete the extra salt and water
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74
Q

What happens with bilateral renal artery stenosis?

A
  • RAAS system is activated
  • Kidney does not get rid of the extra salt and water and hypertension persists
  • Risk of acute pulmonary oedema
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75
Q

What is coarctation of aorta

A

Stenosis in the aorta vessels

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76
Q

What is the mechanism that causes hypertension due coarctation of the aorta?

A
  • Less renal blood flow

- Kidney triggers the RAAS system as it senses hypovolaemia wrongly

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77
Q

What is primary hyperaldosteronism and the causes?

A

Excess secretion of aldosterone

  • Adrenal adenoma
  • Adrenal hyperplasia
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78
Q

What are the clinical features of primary hyperaldosteronism?

A
  • Hypertension

- Can cause hypokalemia

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79
Q

What is used in the diagnosis of the the primary hyperaldosteronism?

A
  • Aldosterone:renin ratio is high
  • Look for adenoma with a CT scan and remove if present
  • If no adenoma treat by blockage of aldosterone
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80
Q

What is the effect of excess liquorice on the blood pressure?

A
  • Blocks an enzyme
  • Cortisol can’t be converted to cortisone
  • Cortisol interacts with mineralocorticoid receptor triggering the same effect as aldosterone
  • Blood pressure increase
  • Similar mechanism as Cushing’s
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81
Q

What is chronic kidney disease?

A

Irreversible and sometime progressive loss of renal function over a period of months to years. Renal injury can cause renal tissue to be replaces by extracellular matrix in response to tissue damage
Leads to hypertension and fluid overload (oedema)

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82
Q

What are the indications of nephrotic syndrome?

A
  • Proteinuria
  • Hyperalbuminaemia
  • Oedema
  • High cholesterol
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83
Q

Which ion primarily affects the effective circulating volume?

A
  • Sodium ions

- Water in the extracellular fluid compartment depends on the sodium ion content.

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84
Q

What would be the effect of changing the amount of sodium that is ingested (without kidney action)?

A
  • Amount of water in the extra cellular fluid would change
  • Effective circulating volume would also change
  • Blood pressure also changes as a result
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85
Q

Why does the kidney Na+ excretory rates have to vary over a wide range?

A
  • The kidney needs to match excretion of sodium to ingestion to remain sodium balance.
  • Urinary water excretion can be varied physiologically
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86
Q

What can you do to increase the plasma volume?

A

-Add an isosmotic solution

Adding water alone affect plasma osmolarity

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87
Q

How can we add or remove an isosmotic solution?

A
  • Movement of osmoles

- Water will follow

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88
Q

What can affect the proximal tubule Na+ reabsorption?

A
  • Changes in osmotic pressure and hydrostatic pressure

- RAAS system can stimulate proximal tubule Na+ reabsorption

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89
Q

What causes pressure natriuresis and pressure diuresis when renal blood pressure increases?

A
  • Increased renal artery blood pressure
  • Reduced number of Na-H and reduced Na-K ATPase activity in proximal tubule
  • Causes reduction in sodium and water reabsorption in proximal tubule
  • Leads to pressure natriuresis and pressure diruresis together in order for the ECF volume to be decrease and diminish the BP rise.
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90
Q

What are the sodium channels in the proximal tubule?

A

Na-H antiporter
Na-Glucose symporter
Na-AA co-transporter
Na-Pi

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91
Q

What are the sodium channels in the loop of henle?

A

NaKCC symporter

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92
Q

What are the sodium channels found in the early distal tubule?

A

NaCl symporter

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93
Q

What are the sodium channels found in the late distal tubule and collecting tubule?

A

ENaC (epithelial Na channels)

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94
Q

What are the histological features of the proximal tubule?

A
  • Brush border
  • Large outside diameter
  • Lots of mitochondria (incredibly active)
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95
Q

What are the solutes transported in the 1st segment of the proximal tubule?

A 
-Apical
Na-H exchange 
Co-transport with glucose
Co-transport with amino acid or carboxylic acids
Co-transprt with phosphate

-Basolateral
3 Na-2K ATPase
NaHCO3- co transporter for acids and bases

  • Aquaporin channels
  • Chloride concentration increases
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96
Q

What are the solutes transported in the 2nd segment of the proximal tubule?

A

Basolateral
3Na-2K ATPase

Apical
Na+ is reabsorbed via Na-H exchanger

Paracellular and transcellular transport of Cl-

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97
Q

What is the overview of the function of the proximal collecting tube?

A
  • Highly water permeable so bulk transport of water reabsorption
  • Reabsorption is isosmotic with plasma
  • Reabsorbs 65% water, 100% glucose and amino acids, 67% of sodium
  • Driving force for reabsorption is osmotic gradient established by solute absorption, hydrostatic force in the interstitum, oncotic force in peritubular capillary due to loss of 20% filtrate at glomerulus but cells and proteins left in blood
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98
Q

What are the features of the thin descending limb?

A
  • Lots of aqua porin channels
  • No mitochondria
  • Loose junctions
  • No brush border
  • Thin
  • Flattened
  • Passive in nature
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99
Q

What are the features of the thick segment of the ascending limb?

A
  • Impermeable to water
  • Many mitochondria
  • No aqua porin
  • Lots of active transport for sodium reabsorption
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100
Q

What is the function of the thick and thin descending limb?

A
  • Paracellular reuptake of water due to increased intercellular concentrations of sodium
  • Concentrates sodium and chloride ions in the lumen of the descending limb ready for active transport in the ascending
  • Highly permeable to water due to AQP (1 channels always open)
  • Impermebale to Na
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101
Q

What is the function of the thin ascending limb?

A

Passive sodium reabsorption due the actions of the descending limb.
Epethelium permits passive reabsorption by paracellular route

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102
Q

What is the function of the thick ascending limb?

A
  • NKCC2 transrptoer that transports sodium, (2)chloride and potassium from lumen to cells
  • Na+ ions move into the interstitum due to the action of 3Na-2K-ATPase
  • ROMK channels move potassium from the cell into the lumen to allow the NKCC2 channels to work
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103
Q

What is the clinical significance of the thick ascending limb?

A

Sensitive to hypoxia due to the amount of energy use

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104
Q

Give an overview of the loop of henle reabsorption.

A
  • Descending limb reabsorbs water and not NaCl
  • Ascending limb reabsorbs NaCl but not water
  • The tubule fluid leaving the loop is hypo-osmotic compared to plasma
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105
Q

Outline features of reabsorption in the distal convoluted tubule

A
  • Hypo-osmotic fluid enters (100 mOsm/Kg)
  • Active transport of 5-8% of Na+
  • Water permeability is low
  • Has 2 regions DCT1 and DCT1
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106
Q

What are the channels present in DCT1?

A

Apical

-NaCl enters via electro-neutral NCC transporter which is sensitive to thiazides diuretics

Basolateral

-3Na-2K-ATPase

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107
Q

What are the channels present in the distal convoluted tubule 2?

A

Apical

  • Na+ enter via ENaC
  • NaCL enters by the NCC

Basolateral

  • 3Na-2K-ATPase
  • KCC4
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108
Q

Which channels are affected by amiloride diuretics?

A

ENaC channels

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109
Q

What detects changes in plasma osmolarity?

A

Hypothalmic osmoreceptors

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110
Q

What are the 2 efferent pathways to regulate plasma osmolarity and their effect?

A
  • ADH: Acts on the kidney to control renal water excretion

- Thirst: Trigger brain for drinking behaviour to cause an effect on the water intake

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111
Q

Where are osmoeceptors found?

A
  • Located in the OVLT of the hypothalamus.

- Leaky endothelium is exposed directly to the systemic circulation to sense the changes in plasma osmolarity

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112
Q

What physiologically inhibits ADH?

A

-Decreased osmolarity inhibits ADH

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113
Q

What happens to the osmotic and haemodynamic relationship in circulatory collapse?

A
  • Kidney continues to conserve H2O even though this will reduce osmolarity of body fluids
  • Volume is more important than osmolarity if volume crashes
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114
Q

Describe the efferent pathway of thirst?

A
  • Stimulated by an increase in fluid osmolarity
  • Salt ingestion is the analogue of thirst
  • Large deficits in water only partially compensated for in the kidney and ingestion is the ultimate compensation.
  • Stop when sufficient fluid has been consumed
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115
Q

What is central diabetes insipidus?

A
  • Plasma ADH levels are too low
  • Damage done to the hypothalamus or pituitary gland
  • Brain injury
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116
Q

What is nephrogenic diabetes insipidus?

A

-Acquired insensitivity of the kidney to ADH

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117
Q

How are problems with ADH secretion managed?

A
  • In both water is inadequately reabsorbed so a large quantity of urine is produced
  • Managed clinically by ADH injections or by ADH nasal spray
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118
Q

What is SIADH?

A

Syndrome of inappropriate ADH secretion

  • Characterised by excessive release of ADH from posterior pituitary gland or another source
  • Dilutional hyponatraemia in which the plasma sodium levels are lowered and total body fluid is increased
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119
Q

What happens to the aqua porin channels when plasma osmolarity decreases?

A
  • No ADH stimulation
  • No stimulation of Aqua porin 2 in apical membrane
  • AQP3 and 4 on basolateral membrane only of the latter DCT and collecting ducts and act as an exit for water entering AQP2
  • Limited water reuptake in latter DCT and collecting duct
  • Loss of large amount of hypo osmotic urine
  • Diuresis
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120
Q

What happens to the aqua porin channels when plasma osmolarity increases?

A
  • Release of ADH causes the insertion of AQP2 channels into the apical membrane
  • Water moves out of the collection duct into hyper osmotic environment if there are AQP in both the apical and the basolateral epithelium of the tubule cells
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121
Q

Which part of the kidney loop is crucial to generate the medullary gradient?

A

-Thick ascending limb of the loop of henle

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122
Q

What is the maximum osmolaitly at the tip of the Loop of Henle?

A

1200 mOsm/Kg in medulla

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123
Q

What is counter current multiplication?

A
  • Na+ is actively transported out of the ascending limb of LH
  • Concentration increases in the interstitial fluid surrounding the loop of Henle
  • Increased concentration in the interstitial fluid achieved by loop of Henle
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124
Q

What is the range for the vertical osmotic gradient in the kidney?

A
  • 300 mOsm/kg at corticomedullary border

- 1200 mOsm/kg in medullary interstitum at papilla

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125
Q

What are the essential mechanisms to maintain the vertical osmotic gradient?

A
  • Active NaCl transport in thick ascending limb
  • Recycling of urea (effective osmole)
  • Unusual arrangement o blood vessels in medulla descending components in close opposition to ascending components
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126
Q

Why is urea an effective osmole?

A
  • Doesnt cross the membrane easily
  • Urea reabsorption from medullary collecting duct
  • Cortical collecting duct cells are impermeable to urea
  • Movement into interstitum and diffusion back in Loop
  • Under the influence of ADH fraction excretion of urea decreasing and urea re-cylcing increases
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127
Q

How does the vasa recta maintain the concentration gradient?

A

Flow in vasa recta is in the opposite redirection to fluid flow in the tube, the osmotic gradient is maintained. Vasa recta acts as a counter current exchanger.

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128
Q

Vasa recta can actively transport. True/False

A

False

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129
Q

What happens in the descending limb of the vasa recta?

A
  • Isoosmotic blood in vasa recta enter hyper osmotic medullary region
  • Na+,Cl- and urea diffuse into the lumen of vasa recta
  • Osmolarity of the blood in vasa recta increases as it reaches tip of hairpin loop
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130
Q

Why is blood flow in the vasa recta slow?

A

Blood flow is compromised to :

  • Deliver nutrients
  • Maintain medulaary hyper tonicity
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131
Q

How does the shape of the vasa recta and loop of henle allow for the courter current exchange?

A

-Both hairpin configurations

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132
Q

What happens in the ascending limb of vasa recta?

A
  • Blood ascending towards cortex will have higher solute content than surround interstitum
  • Water moves in from the descending limb of the loop of henle
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133
Q

What is a diuretic?

A

A substance that promotes a diuresis by increase in renal excretion of water and sodium to reduce ECF volume

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134
Q

When are diuretic used clinically?

A

Conditions where sodium and water retention cause expansion of ECF volume

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135
Q

What is the effect of diuretics reducing ENaC activity on K+ secretion?

A

Reduction of K+ secretion

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136
Q

How do Diuretic work? (4 ways)

A
  • Direction action on cell to block Na+ transporters in luminal membrane (Loop diuretic, Thiazide Diuretics, K+ sparing diuretics)
  • By antagonising the action of aldosterone
  • By modification of filtrate content
  • By inhibiting activity of enzyme carbonic anhydrase
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137
Q

How do loop diuretics work?

A
  • Block apical NKCC transporter
  • Na and Cl not absorbed so medullary tonicity is less
  • This reduces water reabsorption further down the tubule
  • Leads to Na+ and water loss

Very potent diuretics

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138
Q

What are the effect of loop diuretics in heart failure?

A

Used in heart failure for treatment of symptoms

  • Diuretic effect
  • Vaso and veno dilation to decreased after load/preload
  • Reduces symptoms but no effect on reducing mortality
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139
Q

What is given in acute pulmonary oedema?

A

-IV Furosemide

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140
Q

When are loop diuretics used?

A
  • Heart failure
  • Nephrotic syndrome
  • Renal failure
  • Cirrhosis of liver
  • Hyper calcaemia
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141
Q

What are the effect of loop diuretics on calcium absorption?

A

Blockage of the NKCC channels:

  • Impairs calcium reabsorption as lumen positive potential isn’t created by K+ drifting into the lumen
  • More calcium is exerted in urine
  • Furosemide given together with IV fluids
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142
Q

What are the effects of Thiazide diuretics?

A
  • Secreted into lumen in PCT
  • Block Na-Cl transporter in DCT
  • Travel downstream to act at DCT
  • Increase Na+ loss in urine
  • Reduces Ca2+ loss in urine
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143
Q

When are thiazide diuretics used?

A

-Widely used in hypertension

ineffective in renal failure as less potent compared to loop diuretics

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144
Q

What are the side effects of thiazide diuretics?

A

-Higher incidence of hypokalaemia

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145
Q

What are the type of K+ sparing diuretics?

A

Act on late distal tubule and collecting duct

  • Inhibitors of ENaC (amiloride)
  • Aldosterone antagonists (spironolactone)
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146
Q

What are the mechanism of action for potassium sparing diuretics?

A
  • Reduces ENaC activity directly or indirectly
  • Reduce loss of K+
  • Both can produce life threatening hyperkalaemia especially if used with ACE inhibitors, K+ supplement or in patients with renal impairment
  • Both are mild diuretics affecting only 2% of Na+ reabsorption
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147
Q

What are the non diuretic situations that feature the use of aldosterone antagonists?

A
  • Reduction of mortality in heart failure (used in the long term treatment of heart failure)
  • Preferred duct for ascites and oedema in cirrhosis
  • Used as additional therapy in hypertension if other treatment aren’t effective
  • Treatment of hypertension in Conn’s syndrome
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148
Q

What are ENaC blockers like amiloride used in combination with?

A

K+ losing diuretics

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149
Q

How can diuretics contribute to hypokalaemia?

A
  • Diuretics may lead to reduced circulatory volume
  • Activtion of RAAS
  • Increase in Aldosterone secretion
  • Increase in Na+ absorption and K+ secretion
  • Hypokalaemia
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150
Q

How can K+ sparing diuretic cause hyperkalemia?

A
  • Reduction in Na+ reabsorption
  • Reduces potassium loss in urine as negative potential for movement of potassium isn’t created
  • Hyperkalaemia
151
Q

What is the reason for use of loop/thiazide diuretics and a K+ sparing diuretic in combination?

A

-Used to minimise changes in potassium

Thiazide/Loop diuretics can be used with only potassium supplements if necessary

152
Q

What should be avoided with use of K+ sparing diuretics?

A
  • Potassium supplement
  • Impaired renal function
  • Increase in risk of hyperkalaemia

Concomitant use with ACEI/ARB - regular K+ monitoring required

153
Q

What is activated in nephrotic syndrome?

A
  • Reduced circulatory volume
  • RAAS activated
  • Na+ and water retention
  • Expansion of ECF
  • More oedema
154
Q

What are the adverse effects of diuretics?

A
  • Potassium abnormalities
  • Hypovolaemia especially in loop diuretic
  • Hyponatraemia
  • Increase in uric acid levels in blood (with Thiazides, Loop Diuretics) can precipitate attack of gout
  • Metabolic effects (glucose intolerance, LDL levels)
  • Thiazides (erectile dysfunction)
  • Spironolactone causes gynaecomastia
155
Q

How do carbonic anhydrase inhibitors work?

A
  • Inhibits action of carbonic anhydrase in brush border and PCT cells
  • Loss of HCO3- so osmolarity of lumen increases
  • Can cause metabolic acidosis due to loss of HCO3- in urine
156
Q

Which condition in the eye are carbonic anhydrase inhibitors useful to treat?

A
  • Useful in the treatment of Glaucoma

- Reduces formation of aqueous humour in the eye by about 50%

157
Q

What is the mechanism for osmotic diuretics?

A
  • Acts by altering the osmolarity to affect renal water absorption
  • Small inert molecule increase the plasma osmolarity thus drawing out fluid from tissues and cells
  • Osmolarity of the filtrate in increased in the kidney
  • Loss of water, Na+ and K+ in the urine
  • Doesn’t inhibit enzymes or transport proteins
158
Q

What are other substances with diuretic action?

A
  • Alcohol (inhibits ADH release)
  • Coffee (increase GFr and decreases Na+ reabsorption)
  • Drugs that inhibit action of ADH on collecting ducts
159
Q

What are some diseases causing diuresis?

A
  • Diabetes Mellitus
  • Cranial Diabetes Insipidus
  • Nephrogenic Diabetes insipidus
  • Psychogenic polydipsia
160
Q

How is the detrusor muscle controlled?

A

Parasympathetic (Pelvic nerve S2, S3, S4).

161
Q

How is the sphincter muscle controlled?

A

Somatic innervation via the Pudendal nerve

S2, S3, S4

162
Q

What is the features of the bladder phases?

A

Storage phase

  • Compliance
  • Sensation of bladder filling
  • No detrusor contraction

Voiding phase

  • Voluntary initiation
  • Complete emptying
163
Q

What is the effect of a lower motor neurone lesion?

A
  • Low detrusor pressure
  • Large residual urine
  • Reduced perianal seasntion
  • Lax anal tone

+/- overflow incontinence

164
Q

What is the effect of an upper motor neurone lesion?

A
  • High pressure detrusor contractions
  • Poor coordination with sphincters

Stops the inhibitor of the parasympathetic nerves

165
Q

What are the types of incontinence?

A
  • Stress Urinary incontinence
  • Urge Urinary Incontinence
  • Mixed Urinary Incontinence
  • Overflow Incontinence
166
Q

What are risk factors for incontincnece?

A
  • Pregnancy and childbirth
  • Pelvic surgery
  • Pelvic prolapse
  • Race
  • Family predisposition
  • Anatomical abnormalities
  • Neurological abnormalities
  • Menopause
  • Drugs
  • UTI
  • Co-morbidities
  • Obesity
  • Age
  • Increase in intra-abdominal pressure
167
Q

How is uriniary incontinence examined?

A

History to categorise type of UI

Examination

  • BMI
  • Abdominal exam
  • Digital Rectal examination (prostate, limited neurological examination)
  • Females (external genitalia stress test, vaginal exam)
168
Q

What are investigations undertaken for urinary incontinence?

A
  • Urine dipstick mandatory
  • Basic non-ivasic urodynamics (frequency-volume chart, bladder diary, post micturition residual volume)

Optional
Invasive urodynamic
Pad tests
Cystoscopy

169
Q

What are the conservative management options for Urinary Incontinence?

A
  • Modify fluid intake
  • Weight loss
  • Stop smoking
  • Decrease caffeine intake
  • Avoid constipation
  • Timed voiding - fixed schedule
170
Q

What is contained incontinence?

A
  • Indwelling catheter
  • Sheath device
  • Incontinence pads

For patient suitable for surgery who have failed conservative or medical management

171
Q

What are the management options for stress urinary incontinence?

A

Initial management
-Pelvic floor muscle training

Pharmacological Management
-Duloxetine for combined noradrenaline and serotonin uptake inhibitor and increased activity in striated sphincter during filling phase

Surgery. Permanent (P) and Temporary (T)

Females

  • Low tension vaginal tapes (P)
  • Open retropubic suspension procedures (P)
  • Classic sling procedures (P)
  • Intramural bulking agents (T)

Males

  • Artificial urinary sphincter
  • Male sling procedure
172
Q

What are the specific management of Urge Urinary Incontinence?

A

Initial management
-Bladder training (schedule of voiding for at least 6 weeks)

Pharmacological management

  • Anticholinergics (oxybutynin) which acts on muscurrinic receptors (M2,M3). Has side effects on other sites.
  • B3 adrenoreceptor agonist (Mirabegron) to increase bladder’s capacity to store urine
  • Intravesical injection of Botulinum toxin to inhibit release fo Act at pre-synaptic neuromuscular junction causing flaccid paralysis

Surgery

  • Sacral nerve neuromodulation
  • Autoaugmentaion
  • Augmentation cystoplasty
  • Urinary diversion
173
Q

Which areas can pathology in kidney affect?

A

Glomerulus
Tubular compartment
Interstitium
Vascular

174
Q

What can the glomerular filter leaking cause?

A
  • Proteinuria
  • Haematuria

One or both

175
Q

What is area of the glomerulus is affected in nephrotic syndrome?

A

Podocyte/Sub-epithelial damage

176
Q

How is nephrotic syndrome managed?

A

Oedema - Salt and fluid restriction, diuretics
Proteinuria - ACE inhibitors
Hypercholesteraemia - Statins

Treat the underlying cause

177
Q

What are the common primary causes of nephrotic syndrome?

A
  • Minimal change glomerulonephritis
  • Focal segmental glomerulosclerosis
  • Membranous glomerulonephritis
178
Q

What are the features of minimal change glomerulonephritis?

A
  • Usually arises in childhood and adolescence.
  • Responds to steroid but may recur if the steroid are stopped
  • Doesn’t usually progress to renal failure
179
Q

What is minimal change glomerulonpehristes?

A
  • Damage to podocyte layer so patient can’t selectively filter so proteins pour out of the glomerulus.
  • Thought to be immune associated
180
Q

What is focal segmental glomerulosclerosis?

A
  • Damage to podocyte layer so patient can’t selectively filter so proteins pour out of the glomerulus.
  • Heals by scarring after being damaged by circulating factors in the blood (haven’t found out which it is)
181
Q

What are the features of focal segmental glomerulosclerosis?

A
  • Scarring of the glomerulus occurs
  • Less effectively treated by steroids
  • Progression rapidly to renal failure
  • Patients can get FSGS even after they have a kidney transplant
182
Q

What is membranous glomerulonephritis?

A
  • Autoimmune

- Immune complex deposits on sub-epithelial layer causing damage to the podocyte layer

183
Q

What are the features of membranous glomerulonephritis?

A
  • Rule of thirds
  • Commonest in adults
  • May be secondary for example lymphoma
184
Q

What are secondary causes of nephrotic syndrome?

A
  • Amyloidosis

- Diabetes Mellitus

185
Q

What are the pathological changes that occur in diabetes mellitus?

A
  • Hyperfiltation/Capillary hypertension
  • Glomerular basement membrane thickening Mesangial expansion
  • Podocyte injury
  • Glomerular sclerosis
186
Q

Why does hyperfiltation/capillary hypertension occur in diabetes mellitus?

A

Occurs in early course of disease.Related to hyperglycaemia

  • Increase in glucose levels
  • Upregulates SGLT2 transporter
  • Less glucose passed out in urine
  • Increase in reabsorption of sodium
  • Less sodium gets to the macula densa
  • Less effect on JGA
  • Afferent vasodilation
  • Efferent vasoconstriction
  • Glomerular hypertension occurs as a result
  • GFR increases
187
Q

What are the risk factors for diabetes mellitus?

A
  • Genetic susceptibility
  • Race
  • Hypertension
  • Hyperglycaemia
  • High level of hyper-filtration
  • Increasing age
  • Duration of diabetes
  • Smoking
188
Q

What are the stages of of diabetic nephropathy?

A
  1. Hyperfiltration and hypertrophy
  2. Latent stage
  3. Microalbuminuria
  4. Overt proteinuria
  5. ESRD
189
Q

What happens in the latent stage of diabetic nephropathy?

A
  • Normal albuminuria

- GBM thickening & mesangial expansion

190
Q

What happens in the microalbuminuria stage of diabetic nephropathy?

A
  • Variable mesangial expansion/sclerosis
  • Increase GBM thickening
  • Podocyte changes
  • GFR normal
191
Q

What happens in the overt proteinuria phase of diabetic nephropathy?

A
  • Diffuse histopathological changes
  • Systemic hypertension
  • Falling GFR
  • Mesangial expansion/sclerosis leads to reduced surface area for filtration
  • Microvascular changes (hyalinosis of arterioles) leads to tissue ischaemia
192
Q

What is the primary prevention of diabetic nephropathy?

A
  • Tight blood pressure control
  • SGLT2 inhibitors (Reduced hyper-filtration)
  • Statin therapy
  • Cardiovascular risk management (diet, exercise)
  • Moderate protein intake
193
Q

How is diabetic nephropathy managed?

A
  1. Hyper-filtration & hypertrophy – primary prevention
  2. Latent stage – primary prevention
  3. Microalbuminuria -RAAS Blockage to reduced glomerular hyper filtration. Hyperkalaemia limits use with advanced CKD
  4. Overt proteinuria
  5. ESRD
194
Q

What are the clinical features of hypertensive renal disease?

A
  • Microalbuminuria is the first sign
  • Slow and progressive
  • Disease of exclusion (no evidence of hypertensive disease elsewhere)
195
Q

What is the management of hypertension renal disease?

A
  • Slow progression
  • Good BP control
  • ACE inhibitors or angiotensin receptor blockers with albimunuria
196
Q

What are the histoligcal changes that occur in hypertensive nephrosclorosis?

A
  • Vascular changes
  • Fibro-elastic intimal thickening leading to lumen narrowing
  • Hyalinosis of the afferent arterial wall (diabetes affects efferent as well)
  • Secondary insult causing glomerular changes such as wrinkling of glomerulus and glomerulosclerosis
  • Leads to CKD
197
Q

What is renal disease associated with acute severe hypertension?

A
  • Damage to endothelium leading to haematuria
  • Activation of RAAS
  • Glomerulus is punched out so acute kidney injury.
  • Fibrinoid necrosis of arterioles so ischaemia which leads to activation of RAAS
  • Haemolytic anaemia due to shearing of blood vessels
  • Associated with Scleroderma and Haemolytic uraemic syndrome
  • Leads to AKI
198
Q

What are the differentiating factors between hypertensive renal disease and renal vascular disease?

A
  • Hypertension is often more acute in renal vascular disease and refractory to treatment
  • Decline in GFR often more rapid
  • Evidence of atherosclerosis elsewhere
  • Acute worsening with RAAS blockade leads to reduction in GFR even more as kidney thinks its hypovolaemia
199
Q

What are the primary features of nephritic syndrome?

A
  • Loss of protein
  • Blood in urine
  • Acute renal failure usually
  • Hypertensive
  • Low GFR
200
Q

How is nephritic syndrome managed?

A
  • Blood pressure control
  • Treatment of oedema
  • Cardiovascular risk management
  • Disease specific treatment such as immunosuppressant
201
Q

What are the conditions that cause nephritic syndrome?

A
  • Anti-GBM disease

- Vasculitis

202
Q

What are the site affected by glomerular injury?

A
  • Basement membrane
  • Podocyte
  • Sub-epithelial
  • Sub-endothelial
203
Q

What are the causes of haematuria?

A

Blood vessels are commonly injured

Non nephrological

  • IgA Nephropathy
  • Thin glomerular basement membrane nephropathy
  • Hereditary Nephropathy (Alport)

Cancer

  • Renal cell carcinoma (RCC)
  • Upper tract transitional cell carcinoma (TCC)
  • Bladder cancer
  • Advanced prostate carcinoma

Other causes

  • Stones
  • Infection
  • Inflammtion
  • Benign prostatic hyperplasia
204
Q

What is IgA nephropathy?

A
  • Commonest glomerular membrane
  • IgA is naturally secreted into mucosal membrane. IgA deposited in the kidney. If you get infected you produce more IgA.
  • IgA is deposited in the mesangium as there is nothing to stop it getting into the mesangium
  • Causes the capillary loop to become fragile as a result which leads to haematuria (visible/invisible)
  • Can also get protein in urine
205
Q

How is IgA nephropathy managed?

A
  • Can detect abnormal IgA

- No effective treatment. ACE inhibitors can slow it down but not that underlying cause

206
Q

What are the features of thin glomerular basement membrane nephropathy?

A
  • Doesn’t progress

- Benign

207
Q

What is Hereditary Nephropathy (Alport syndrome) ?

A
  • X-linked
  • Abnormal collagen 4
  • Associated with deafness as collagen 4 is used in the ear
  • Abnormal appearing glomerular basement membrane
  • Progress to renal failure
208
Q

What are the symptoms of chronic kidney disease?

A
  • Fatigue / malaise
  • Loss of appetite / Loss of weight
  • Acute illness / recent infection
  • Ankle swelling
  • Haematuria / nocturia
209
Q

What are the symptoms of acute kidney disease?

A
  • Dysuria
  • Change in urine –amount / colour
  • Pain (supra-pubic / loin / joints)
  • S/E of drugs with renal metabolism
  • Nausea & vomiting
  • Ankle swelling / SoB
  • Fatigue / Malaise
  • Fever
210
Q

What are risk factors of acute kidney disease?

A
  • Ishaemic heart disease
  • Hypertension
  • Cerebrovascular disease
  • Known CKD (risk factor for AKI)
  • Diabetes mellitus
  • In younger patient – enuresis in childhood, problems in pregnancy
211
Q

What examination are undertaken for acute kidney disease?

A
  • Blood pressure
  • Urine dipstick
  • Urine microscopy if dipstick positive
212
Q

Why can inacrurances occur in urine dipstick?

A
  • Extreme exercise can cause proteinuria and haematuria
  • Menstruation
  • Indwelling catheters (always have an infection
213
Q

What are general examination for acute kidney infection?

A
  • General appearance (Pallor, Uraemia, Nails, Rashes, Bruises)
  • CVS/RS (BP, Fluid balance – (JVP, RR, O2 saturation, Chest sounds), Heart sounds – (Additional sounds, murmurs), Bruits)
  • GIS/GUS (Palpable masses including bladder, Pain, Ballotable kidneys, Abdominal bruits, Urine outputs)
214
Q

What are the features of urine microscopy?

A
  • Infection – send for culture
  • Crystals (Look under microscope, Gout, Pseudogout)
  • Casts
  • Red cell casts
215
Q

What are the predisposing factors to UTI?

A
  • Shorter urethra
  • Obstruction
  • Neurological problems
  • Ureteric reflux
216
Q

Which organism is commonly associated with UTI?

A

E-Coli

217
Q

What are the virulence factors of E.coli that allow it to evade the immune defence?

A
  • Fimbriae allow attachment to host epithelium
  • Haemolysins damage host membranes and cause renal damage
  • K antigen permits production of polysaccharide capsule
  • Urease breaks down urea creating a favourable environment for bacterial growth
218
Q

What are common syndromes presented as a result of UTI?

A
  • Cystitis –frequency & dysuria (lower UTI)
  • Acute pyelonephritis (upper UTI)
  • Chronic pyelonephritis
  • Asymptomatic bacteriuria (e.g. pregnancy)
  • Septicaemia +/- shock
219
Q

What are the clinical symptoms of lower UTI?

A
  • Dysuria
  • Frequency
  • Urgency
  • Low grade fever sometimes
220
Q

What are the clinical symptoms of upper UTI?

A
  • Fever
  • Loin Pain
  • May have dysuria and frequency
221
Q

What is an uncomplicated UTI?

A

Defined as infection by a usual organism in a patient with a normal urinary tract and normal urinary function.

222
Q

What is a complicated UTI?

A

UTI when one or more factors are present that predispose the person to persistent infection, recurrent infection, or treatment failure.

223
Q

What are examples of predisposing factors to complicated UTI?

A
  • Abnormal urinary tract (e.g., vesico-ureteric reflux, indwelling catheter, etc).
  • Virulent organism (e.g.Staph. aureus).
  • Impaired host defences (e.g. poorly controlled diabetes, immunosuppression).
  • Impaired renal function
224
Q

What are most cases of UTI in children, men and pregnant women treated as?

A

Complicated UTI

225
Q

What is the investigation undertaken in UTI?

A
  • In healthy non-pregnancy women of child-bearing age, no need ot culture urine
  • Culture urine in complicated UTI
226
Q

How are patient screened for UTI?

A
  • Turbidity

- Dipstick testing (useful to exclude UTI)

227
Q

When is a dipstick testing not useful for in diagnosis of UTI?

A
  • Acute uncomplicated UTI in women
  • Men with typical/severe symptoms
  • Catheterised patients
  • Older patient without features of infection
228
Q

When is imaging considered in UTI investigation?

A
  • Considered in all children with UTI
  • Valuable in septic patients to identify renal involvement
  • Males: posterior urethral valves
  • Female – vesico-ureteric reflux
229
Q

What is the treatment for uncomplicated UTI?

A
  • Increase fluid intake
  • Address underlying disorders
  • 3 days course of Trimethoprim or nitrofurantoin
  • Check with cultures post treatment in children and pregnant women
230
Q

What is the treatment for simple cystitis?

A
  • Uncomplicated infections can be treated with trimethoprim or nitrofurantoin
  • 3 days course
231
Q

How are complicated lower UTI’s treated?

A
  • Trimethoprim
  • Nitrofurantoin – specific to bladder
  • Cephalexin
232
Q

What is the treatment for pyelonephritis/septicaemia?

A
  • Co-amoxiclav
  • Ciprofloxacin (7 days also effective)
  • Gentamicin IV
233
Q

How is UTI prophylactically prevented?

A

Trimethoprim or nitrofurantoin

  • Single nightly dose
  • Ensure all breakthrough infections documented
  • Three or more episodes a year but not treatable underlying conditons
234
Q

What substances give false positives of haematuria on dipstick?

A

Myoglobin, Bacterial Peroxidases, Bleach

235
Q

What is the management of a patient with Haematuria?

A
  • Stabilise the patients
  • Blood
  • 3 way catheter and irrigation
  • CT angiogram if significant bleed
  • If it doesn’t settle then intervention such as cystoscopy/interventional radiology
236
Q

Which substances presents with false negatives?

A

-Vitamin C

237
Q

What is the mechanism for acute urinary retention?

A
  • Bladder outlet obstruction
  • Low bladder contractile power
  • Interrupted sensory or motor innervation of bladder and/or sphincter
238
Q

What are investigations done for acute urinary retention?

A
  • History and examination
  • Bloods
  • Bladder scan
  • Neurological documentation important
239
Q

What are the causes of acute urinary retention in men?

A
  • BPH
  • Prostate cancer
  • Urethral stricture
  • Prostatic infection
240
Q

What are the causes of acute urinary retention in women?

A
  • Prolapses
  • Masses
  • Post botox
  • Fowler’s syndrome
241
Q

What are the causes of acute urinary retention in both males and females?

A
  • Clots
  • Drugs
  • Pain
  • Major abdominopelvic surgery
  • Spinal cord compression
  • Spinal cord injury
  • Spina bifida
  • Urinary tract infections
  • Constipation
  • Urethral damage/rupture
  • Diabetic nephropathy
  • Neurological degeneration
242
Q

What are management options for acute urinary retention?

A
  • Urethral Catheterisation
  • Suprapubic (if difficult)
  • Preferable as long-term condition
  • Risk of bowel perforation with insertion
  • Should have ultrasound if laparotomy
243
Q

What differentiates acute urinary retention from chronic?

A

It is very painful

244
Q

Where can stones from in the urinary tract?

A
  • Renal
  • Ureteric (constrictions)
  • Bladder (due to incomplete emptying)
  • Prostatic calculi (no clinical significance )
  • Urethral calculi in men (rare)
245
Q

What are the effects of a ureteric obstruction?

A
  • Therefore, a unilateral obstructive stone globally impairs renal function.
  • Can also get bilateral calculi of kidney or ureters
246
Q

What are features of renal and ureteric colic?

A
  • Causes a lot of pain
  • Present with renal colic
  • Loin to groin pain
  • Testicular pain sometimes
247
Q

What are the investigations dow for renal and ureteric colics?

A
  • History
  • Examination
  • Urinalysis
  • CT KUB non-contrast
  • Abdominal X-ray
248
Q

What are the management options for renal and ureteric colics?

A
  • Conservative management
  • Non- Invasive management (Shockwave lithotripsy)
  • Invasive management (Cystoscopy + lasertripsy, Percutaneous nephrolithotomy, Uteroscopy)
249
Q

What are signs and symptoms of ureteric stones?

A
  • Very painful
  • Impairment in renal function
  • May get stuck
250
Q

What are the management options for ureteric stones?

A

Symptoms and stone size guide treatment

  • Most stone will pass if small enough (less than 4mm)
  • Pain mandates a stent and sometimes primary URS + lasertipsy
251
Q

What is the pathophysiology of urosepsis?

A
  • Blocked upper renal tract to ureteric orifice
  • Standing column of septic urine in the upper urinary tract including the kidney is called pyelonephroisis
  • Infection can spread to blood
252
Q

What is the management for urosepsis?

A
  • Stenting
  • Nephrostomy

To drain urine

253
Q

What are causes of AKI?

A
  • Pre-renal
  • Renal vein
  • Renal artery
  • Small vessel disease – intrinsic
  • Glomerular disease - intrinsic
  • Acute tubular necrosis – intrinsic
  • Acute interstitial nephritis - intrinsic
  • Intratubular obstruction
  • Post renal obstruction
254
Q

What is imaging undertaken in AKI?

A
  • Ultrasound – perform if obstruction suspected. Not need for pre-renal/ATN
  • Chest X-ray – to look for fluid overload
255
Q

Why is bipsy taken if AKI suspected?

A
  • Pre-renal and post-renal AKI ruled out
  • A confident diagnosis of ATN cannot be made
  • Systemic inflammatory symptoms/sign are present
256
Q

What is the pathophysiology of pre-renal failure in AKI?

A
  • Actual GFR is reduced due to decreased renal blood flow.
  • No cell damage so kidney works hard to restore blood flow
  • Avidly reabsorbs salt and water (ADH + Aldosterone)
  • Responds to fluid resuscitation
257
Q

What are causes of pre-renal failure in AKI?

A
  • Hypovolaemia – blood loss, fluid loss
  • Systemic vasodilation – sepsis, cirrhosis, anaphylaxis
  • Pre-glomerular vasoconstriction – sepsis, NSAIDs
  • Post glomerular vasodilation – Ang2 antagonist, ACE inhibitors
258
Q

How does the kidney attempt to correct pre-renal failure and what happens if it fails?

A
  • In mild hypo-perfusion, autoregulation ensures renal blood flow preserved
  • Dilation of afferent arteriole - prostaglandin
  • Constriction of efferent arteriole - RAAS
  • If compensatory responses overwhelmed, AKI occurs
  • Occurs below 80mmHg or higher if hypertensive
259
Q

How do ACE inhibitor and NSAIDs affect renal perfusion to cause pre-renal failure?

A
  • NSAIDs acts against vasodilators (prostaglandins)
  • ACE inhibitors act against formation of Ang 2
  • The intrinsic auto-regulatory mechanism are overridden
260
Q

What is the pathophysiology in acute tubular necrosis?

A
  • Cells are damaged which cannot be reversed immediately but can be eventually if treated
  • Damaged cells cannot reabsorb salt and water efficiently or expel excess water
  • Proximal tubule is particularly at risk of ischaemia if pre-renal AKI persists
261
Q

What are the causes of acute tubular necrosis?

A
  • Ischaemia
  • Nephrotoxins
  • Sepsis
  • Thombotic-microangiopathy
  • Acute tubule-interstitial nephritis
262
Q

What examples of endogenous nephrotoxins?

A
  • Myoglobin
  • Urate
  • Bilirubin
263
Q

What are examples of exogenous nephrotoxins?

A
  • Endotoxin
  • X-ray
  • Drugs
  • Poisons
264
Q

How can myoglobin cause damage to the kidney?

A

Due to muscle necrosis leading to rhabdomyolysis. Myoglobin filtered at glomerulus and is toxic to tubule cells. Can also cause obstruction

  • Crush injury
  • AKI in wars and natural disasters
  • Drug users (unconscious so don’t move)
  • Elderly - fall
265
Q

What is the pathophysiology of thrombotic microangiopathy?

A
  • Caused by endothelial damage
  • Platelet thrombi
  • Partial obstruction of small arteries
  • Destruction of Red Blood cells
  • Leads to micro-angiopathic anaemia
266
Q

What can cause acute tubule-insterstitial nephritis?

A
  • Toxin induced (Many drugs)

- Infections (Caused by an inflammatory response)

267
Q

What is the pathophysiology of post renal failure?

A
  • Obstruction with continuous production
  • Rise in intraluminal pressure
  • Dilatation of renal pelvis (hydronephrosis)
  • Decrease in renal function
268
Q

What are the causes of post renal failure?

A
  • Within the lumen (stones, blod clot, tumours)
  • Within the wall (congenital megareter, stricture post TB)
  • Pressure from outside (enlarge prostate, tumour, aortic aneurysm, ligation of ureter)
269
Q

How is AKI managed?

A
  • Treat volume overload (restriction of sodium and water, diuretic)
  • Treat hyperkalemia (restrict dietary K, Calcium gluconate)
  • Treat acidosis
  • Dialysis
270
Q

When is dialysis used in the AKI?

A
  • High K+ refractory to treatment
  • Metabolic acidosis where the sodium bicarbonate is not appropriate
  • Fluid overlaod refractory to diuretic
  • Signs of uraemia
  • Presence of dialysable nephrotoxin
271
Q

How does renal cell carcinoma present?

A
  • Localised or advanced
  • Haematuria
  • Incidental finding on imaging
  • Palpable mass is rare

If advanced

  • Large varicoele may be present
  • Pulmonary/tumour embolus
  • Loss of weight/loss of appetite
  • Hypercalcaemia
272
Q

How does a transitional cell carcinoma present?

A
  • Localised
  • Haematuria
  • Incidentl finding on imaging

If advanced

  • Loss of weight/loss of apetite/symptom of metastasis
  • DVT
  • Lymphoedema
273
Q

What is the percentage of patient with visible haematuria and over 45 that present with cancer?

A

20%

274
Q

What is the history undertaken if cancer in urinary tract is suspected?

A

History
• Smoking
• Occupation
• Painful or painless – painless is more worrying from a cancer point of view. Painful is likely external
• Other LUTS – beginning of steream. Prostate cancer
• Family history

275
Q

What is the examination undertaken if cancer in urinary tract is suspected?

A
  • BP
  • Abdominal mass – ulickly to be cancer
  • Varicocele
  • Leg swelling – lympadema (blockage of lymph node by cancer)
  • Asses prostate by DRE (Size, Texture)
276
Q

What are the types of test undertaken for haematuria?

A
  • Radiology
  • Endoscopy
  • Urine
  • Blood tests
277
Q

What are the radiological test performed in haematuria?

A
  • Ultrasound (can pick up bladder cancer but not the smallest of cancer)
  • CT (need good kidney function to be able to inject contrast)
278
Q

What is an example of an endoscopic test?

A

-Flexible cystoscopy to look inside the bladder

279
Q

What are the Urine tests done?

A
  • Culture and sensitivity

- Cytology

280
Q

Describe the epidemiology of Renal Cell Carcinoma.

A
  • 7th most common cancer in Uk
  • 95% of all upper urinary tract tumours
  • Rising incidence and mortality
  • Common in men and whites
  • 30% metastases on presentation
281
Q

What is the aetiology of RCC?

A
  • Smoking
  • Obesity
  • Dialysis
282
Q

Where does renal cell carcinoma spread?

A
  • Spread to the right atrium via IVC (can embolise to the lung to cause a pulmonary embolism)
  • Perinephric spread
  • Lymph node metastases
283
Q

What is the treatment for localised renal cell carcinoma?

A
  • Surveillance
  • Excison via radical nephrectomy or partial nephrectomy
  • Ablation (cyroablation, radiofrequency ablation)
284
Q

What is the treatment for metastatic Renal Cell Carcinoma?

A

Palliative (Chemo- and radio- resistant)

  • Biological therapies – act on the cell cycle, vaccine, monoclonal antibodies.
  • Those targeting angiogenesis are now 1st choice. Tyrosine kinase inhibitors given
285
Q

Describe epidemiology of Bladder

A
  • In UK, 8th most common cancer in men and 14th in women.
  • Incidence is decreasing
  • Presentation is often more advanced in women
  • 3X more in men
  • More in White than non-white
286
Q

What are risk factors of Bladder TCC?

A
  • White
  • Male
  • Smoking
  • Occupational exposure
287
Q

What are some occupational exposure for bladder TCC?

A
  • Dye more carcinogenic
  • Handling of poly aromatic hydrocarbons
  • Painters, mechanics, printers, hairdressers
288
Q

What is the initial treatment for bladder TCC?

A

-TUR bladder tumour

289
Q

What is the staging of bladder TCC?

A 
Ta – rare chance of death
T1
T2 -– low survival as muscle invasive from here
T3
T4
290
Q

What is the histological grading of TCC?

A
  • Normal
  • Grade 1
  • Grade 2
  • Grade 3
  • Carcinoma in Situ (grade 3 tumour that has yet to invade)
291
Q

What are further treatments for high risk and low risk non muscle-invasive TCC?

A

High-Risk

  • Check cystoscopies
  • Intravesical immunotherapy

Low-risk

  • Check cystoscopies
  • Intravesical immunotherapy or not
292
Q

What is further treatment for muscle invasive TCC?

A
  • Neoadjuvant chemotherapy
  • Radical (Cystectomy or Radiotherapy)

If not curative, Palliative chemotherapy/radiotherapy

293
Q

What is the aetiology for Upper Urinary Tract TCC?

A
  • Smoking
  • Phenacetin abuse
  • Balkan’s Nephropathy
294
Q

Describe the epidemiology of Upper urinary tract TCC

A

5% of all malignancies of upper urinary tract.

295
Q

What are initial investigation for suspected Upper urinary tract TCC?

A
  • Ultrasound
  • CT Urogram (Filling defect, Ureteric stricture)
  • Retrograde pyelogram
  • Ureteroscopy (Biopsy, Washings for cytology)
296
Q

What is the standard treatment for upper urinary tract TCC?

A

-Nephro-ureterectomy

297
Q

What is the treatment for metastatic TCC?

A

-Systemic chemotherapy (Traditionally cisplatin-based but needs reasonable kidney function for this to ha[pen

-Biological therapies
Immunotherapy (New)

298
Q

Describe the biological therapy used in metastatic TCC.

A

Cancer cells employ a protective mechanism to avoid destruction by the immune system

  • One anti-TCC strategy is to introduce antibodies to block this protective mechanism
  • Targeting the Programmed Cell Death Receptor 1 (can be given in the presence of poor renal function
299
Q

Describe the epidemiology of Prostate Cancer.

A
  • Commonest cancer in men
  • 2nd most common cause of death from cancer in men
  • Rare in men lower than 50 years of age
300
Q

What are risk factors for prostate cancer?

A
  • Age
  • Family history (BRCA2 gene mutation)
  • Ethnicity (Black>white>Asian)
301
Q

Describe screening for prostate cancer.

A

PSA screening

  • Enzyme
  • If it is higher doesn’t means prostate cancer
  • If it is low/normal doesn’t mean you do not have prostate cancer
  • Cant rely on PSA within 6 weeks of a urinary retention
  • You need glands to make PSA. If they are replaced by the cancer then you can’t make it
302
Q

What the issue with PSA screening

A
  • Over diagnosis -
  • Over treatment
  • QOL (co-morbidities of established treatment. Our screening isn’t good enough)
  • Cost- effectiveness
  • Other causes of raised PSA (Infection, Inflammation, Large prostate, Urinary retention)
303
Q

What is the presentation of prostate cancer?

A
  • Urinary symptoms
  • Bone pain – spread to bone
  • Had their PSA check then biopsied
  • DRE for another reason – change in bowel habit
  • Incidental finding at transurethral resection of prostate (TURP) for retention/urinary symptoms
304
Q

Why do patient with prostate cancer experience bone pain?

A
  • Bone metastases
  • Sclerotic as it is osteoblastic
  • Hot spots on bone scan
  • Highly unlikely if PSA <10 ng/ml)
305
Q

What is the diagnostic pathway for prostatic cancer?

A
  • DRE
  • Serum PSA (If abnormal for the previous : Transrectal ultrasound guided bipsy of prostate)
  • LUTS tract symptoms (Transurethreal resection of prostate)
306
Q

What is the treatment for local prostate cancer?

A
  • Established Rxs (Surveillance, Robotic radical prostatectomy)
  • Radiotherapy (External beam, Brachytherapy)
307
Q

What is the treatment for locally advanced prostate cancer?

A
  • Surveillance (Rapid rise in PSA)
  • Hormones
  • Hormones and radiotherapy
308
Q

What are the treatment types for hormones and palliation?

A
  • Hormone (+-chemotherapy)

- Palliation

309
Q

What are the types of hormonal treatments for metastatic prostate cancer?

A
  • Surgical castration

- Medical castration using LHRH agonists to decrease testosterone

310
Q

Describe the palliative treatment for metastatic prostate cancer?

A
  • Single dose radiotherapy
  • Bisphosphonates
  • Zoledronic acid (Chemotherapy )
  • New treatments (eg abiraterone, enzalutamide)
311
Q

What are factors affecting treatment decisions for prostate cancer?

A
  • Age
  • DRE (Localised, Locally-advanced, Advanced)
  • PSA level
  • Biopsies (Gleason grade, Extent)
  • MRI scan and bone scan (Nodal and visceral metastases)
312
Q

What is acute polycystic kidney disease?

A
  • Autosomal dominant (+new mutations)
  • Mutation in PKD 1 gene and PKD 2 gene
  • Cysts grow with age generally presents in adulthood
  • Big kidneys
  • Diagnosed with ultrasound and Genetic testing
313
Q

What are secondary complications from cyst in APCKD?

A
  • Pain
  • Bleeding into cyst
  • Infection
  • Renal stones)
314
Q

What is the clinical disease in APCKD?

A
  • Cyst fluid filled
  • Hypertension very common
  • Increase incidence of intra-cranial aneurysms
  • Increased incidence of heart valve abnormalities
315
Q

What is done to investigate al renal diseases?

A
  • Blood pressure

- Urine dipstick

316
Q

What is the aetiology of CKD?

A
  • Diabetes
  • Hypertension
  • Immunologic
  • Infection
  • Genetic – APKD, Alport
  • Obstruction and reflux nephropathy
  • Vascular
  • Systemic disease
317
Q

What are the risk factors of CKD?

A
  • Elderly
  • Multi-morbid
  • Ethnic minorities
  • Socially disadvantaged
318
Q

Describe the staging of CKD

A 
G1 – normal or >90
G2 – 60-90
G3a – 45 - 59
G3b – 30-44
G4 – 15-29
G5 - <15

A1 - normal
A2 - microalbuminuria
A3 – proteinuria

319
Q

What are the principles of CKD?

A
  • Define degree of renal impairment
  • Define cause of renal impairment
  • Provide patient with diagnosis and prognos
  • Identify complication
  • Plan long term treatment (delay progression and plan for dialysis or transplantation)
320
Q

What are the general blood tests used for investigation of CKD?

A
  • Urea & Electrolytes
  • Bone chemistry
  • Liver function tests (albumin for proteinuria)
  • Full blood count
  • CRP

+/- iron levels (check iron stores first before EPO treatment)
+/- parathyroid hormone

321
Q

What are blood tests used to determine the cause of the CKD?

A
  • Autoantibody screen
  • Complement levels
  • Anti neutrophil cytoplasmic antibody
  • Serum immunoglobulin
322
Q

What are other investigations done in CKD?

A
  • Ultrasound scan (Kidney size, evidence of obstruction)
  • Kidney biopsy (cause unknown, Haematuria, Proteinuria)
  • Other for specific causes (CT scan, MRI scan, MR angiogram)
323
Q

What are methods used to manage CKD?

A
  • Modifiable risk factors of CKD (Lifestyle, Smoking, Diet , Lack of Exercise)
  • Stopping proton pump inhibitors/NSAIDS
  • Uncontrolled diabetes
  • Hypertension (antihypertensive, diuretics, fluid restriction)
  • Proteinuria
  • Lipids
324
Q

What are the effects of CKD on water/salt handling by the kidney?

A
  • Reduced GFR
  • Lose ability to maximally dilute and concentrate urine
  • Small glomerular filtrate but same solute load cause osmotic diuresis and nocturia
  • Low volume of filtrate reduced maximum ability to excrete urine therefore maximum urine volume is much smaller
325
Q

What are the effects of acidosis in CKD?

A

Msucle
Bone
Renal function progression to worsen

326
Q

What is acidosis in CKD treated with?

A

Treat with NaHCO3 tablets

327
Q

What are the predisposing factors to hyperkalemia in CKD?

A

Can occur once eGFR is less that 20 mls/min

Less likely when good durine output maintined

328
Q

How is hyperkalaemia managed in CKD?

A

May require

  • Stopping ACE-ihibitor/ Angiotensin receptor blocker
  • Avoidance of potassium
  • Altering diet to avoid food with high potassium
329
Q

What are the effects of accumulation of waste products in CKD?

A
  • Contribute to uraemic syndrome
  • Reduce apetite
  • Nausea and vomiting
  • Pruritis
330
Q

What is the effect of CKD on drug management?

A
  • Lots of drugs require dose alteration in CKD/ERSD due to reduced metabolism and elimination
  • Drug sensitivity can be increased even if elimination unimpaired meaning side effects more likely
331
Q

What are the causes of anaemia in CKD?

A
  • Decreased EPO
  • Absolute iron deficiency. High hepcidin so less iron absorbed from gut
  • Blood loss
  • Short red blood cell life span
  • Bone marrow suppression
  • Mineral and bone disorders
  • ACE inhibitor can cause anaemia
  • Deficiency in B12 and folate
332
Q

Why is treating anemia in CKD important for the patient?

A
  • Improve exercise capacity
  • Improve cognitive function
  • Helps regulate left ventricular hypertrophy
  • Helps slow progression of renal disease
  • Reduces mortality
333
Q

How does mineral bone disease occur in CKD?

A
  • Phosphate retention
  • Leads to bone resistance to PTH and low Vitamin D levels
  • Leads to Hypocalcaemia
  • Parathyroid hormone is triggered
  • Phosphate retention leads to less calcium sensors and less vitamin D sensors
  • This leads to secondary parathyroidism
334
Q

What are the effects of mineral bone disease in CKD?

A
  • Leads to bone loss
  • Can cause bone cysts
  • Non bone calcification (deposits in the skin which causes ulceration, deposits in joints)
335
Q

What are the treatment for mineral bone disease in CKD?

A
  • Phosphate intake
  • Phosphate binders
  • 1 alpha calcidol
  • Vitamin D
336
Q

What are the symptoms of CKD?

A
  • Tiredness (Overwhelming fatigue, Guilt, physically and mentally incable)
  • Difficulty sleeping
  • Difficulty concentrating
  • Volume overload
  • Nausea vomiting
  • Itching
  • Restless legs
  • Sexual dysfunction/ reduce fertility
  • Increased risk of infections
337
Q

What are advantages and disadvantages of haemodyalysis?

A

Advantages

  • Less responsibility
  • Days off

Disadvantages

  • Travel time/waiting
  • Tied to dialysis times
  • Big restriction on fluid/food intake
338
Q

What are the contraindications of haemodyalysis?

A
  • Failed vascular access
  • Heart failure a relative contraindication
  • Coagulopathy a relative contraindication
339
Q

What are advantages and disadvantage of peritoneal dialysis?

A

Advantages

  • Self sufficient/independence
  • Generally less fluid/food restrictions
  • Fairly easy to travel with CAPD
  • Renal function may be better preserved initially

Disadvantages

  • Frequent daily exchanges and overnight
  • Responsibility
340
Q

What are the contradictions of peritoneal dialysis?

A
  • Failure of peritoneal membrane (surface area)
  • Adhesion, previous abdo surgery, hernia, stoma
  • Patient unable to connect
  • Obese or large muscle mass
341
Q

What are the complications of peritoneal dialysis?

A
  • Peritonitis
  • Ultrafiltration failure
  • Leaks
  • Development of a hernia
342
Q

Describe the pH of the filtrate as it flows through the tubules?

A
  • 7.4 when filtered
  • 6.7 at the end of the PCT
  • 4.5 - 8 at the collecting duct
343
Q

What is the minimum urine pH?

A

4.5

344
Q

What are the buffers of the urine that helps to control the H+ (pH) ?

A

(HPO4)2-
NH4+

Excess H+ removed by ammonia system as phosphate is only secreted at 25-30 mmol/d

345
Q

What is the difference in acid-base status between vomitig and diarrhoea?

A

Vomiting

  • Loss of H+
  • Loss of K+
  • Result in metabolic alkalosis

Diarhoea

  • Loss of K+
  • Loss of bicarbonate
  • Results in metabolic acidosis
346
Q

What are the side effects of furosemide?

A
  • Contirbutes to chloride loss

- Also contribute to potassium, salt and water loss

347
Q

What is the distribution of potassium in the body?

A

-Mostly intracellular

348
Q

How does the body prevent excess potassium in the ECf?

A
  • Quick K+ uptake into cells

- K+ excretion in urine

349
Q

What increases 3Na+/2K+ ATPase activity?

A
  • K+ concentration in plasma
  • Insulin
  • Noradrenaline effect on B2 arenoreceptors
350
Q

What increases potassium movement out of the cell?

A
  • High osmolality
  • Acidosis
  • Cell damage
  • Exercise
351
Q

What reduces potassium moving out of the cell?

A

Alkalosis

352
Q

What increase potassium movement into the cell? 3Na+/2K+

A
  • ECF (K+)
  • Insulin
  • B2 receptor agonists
  • NA/Salbutamol
  • Aldosterone
353
Q

What inhibits potassium movement into cells?

A
  • Digitalis

- Chronic disease

354
Q

How is potassium excreted?

A

Under normal circumstance

  • Small amounts of potassium are lost in faeces and sweat
  • Kidney predominantly responsible for excretion in urine. 15 mmol/day
  • Potassium is regulated by excretion not absorption
355
Q

How is variable potassium excretion controlled?

A
  • If plasma potassium concentration is low, less excretion in DCT and CD
  • If plasma potassium concentration is high, more excretion occurs in DCT and CD
356
Q

What causes increases potassium secretion?

A
  • Increased intracellular K+
  • Electronegative lumen
  • Permeability of luminal membrane
  • Decreased luminal K+
357
Q

Explain the aldosterone paradox in volume depletion

A
  • Aldosterone stimulates the ENaC channels
  • Ang 2 inhibits ROMK
  • Ang 2 stimulate NaCL channel
358
Q

Explain the aldosterone paradox after consuming a big K+ load in a meal.

A
  • Aldosterone stimulate ROMK and ENaC

- Decreased Ang2 so inhibits of NaCL

359
Q

What is the effect of hypokalaemia on membrane potential?

A
  • Low serum K+ leads to bigger K+ gradient between intracellular and extracellular compartment
  • Depolarisation lead to increased excitability
  • Risk of arrhythmia
360
Q

What is the effect of hyperkalaemia on membrane potential?

A
  • High serum K+ leads to smaller K+ gradient
  • Decreased membrane excitability
  • Risk of cardiac arrhythmias
361
Q

What are the symptoms of hypokalaemia?

A
  • Weakness
  • Polyuria (low potassium causes ADH resistance)
  • Constipation
  • Arrhythmias
362
Q

What are the causes of hypokalaemia?

A
  • Reduced dietary intake
  • Increased entry into cells
  • Increased GI loss
  • Increased urine loss
363
Q

How is a patient with hypokalaemia assessed?

A
  • History
  • Fluid balance
  • Acid base status
  • If K+ loss unclear from the above then urine K+ excretion
364
Q

How is hypokalaemia treated?

A
  • Oral K+ supplement

- Slow IV potassium

365
Q

What are the issues with calcium?

A
  • Difficult to keep in solution
  • Cysrtalization would occur without inhibitors at usual concentrations
  • High calcium in urine can lead to kidney stones
366
Q

What is the distribution of calcium in the body?

A

Mostly intracellular

Extracellular calcium is

  • Protein bound (50%)
  • Free ionised
  • Complexed
367
Q

What are the symptoms of hypocalcaemia?

A

Muscular

  • Fatigue
  • Muscle weakness
  • Paraesthesia
  • Tetany
  • Laryngospasm

Neurological

  • Irritabiliy
  • Memory loss
  • Confusion
  • Hallucination
  • Paranoia
  • Long QT
368
Q

What are causes of hypocealcaemia?

A
  • Vit D deficiency
  • Lack of PTH
  • Reduced intake
  • Malabsorption
  • Pancreatitis
  • Chronic diarrhoea
  • Hypercalciuria
  • Hyperphosphateamia
  • Hypomagnesaemia
  • ECF expansion
  • Acidosis
  • Loop diuretics
369
Q

What is the function of magnesium in the body?

A
  • Intracellular signalling
  • Co factor for protein and DNA synthesis
  • Control of neuronal activity in the brain
  • Cardiac excitability
  • Neuromuscular transmission
  • Osteoblast proliferation and bone strength
370
Q

How is the intake of magnesium controlled?

A
  • Magnesium in diet absorbed by gut (30-50% absorbed)
  • Some magenisu in gut secretions
  • Some magnesia is lost in faeces
  • If dietary intake or serum magnesium is low, Gut can increase absoroption to 80% of the daily intake
371
Q

What are symptoms of hypomagnesaemia?

A
  • Fatigue
  • Muscle spasm
  • Anxiety or Headache
  • Headache
less than 0.4
Cardiac dysrhtmias 
Hyperreflexia
Tetany
Seizures
Hypokalemia
Hypocalcaemia
372
Q

What are causes of hypomagnesaemia?

A
  • Decreased intake
  • Drugs (loop diuretic, thiazide diuretics)
  • GI loss
  • Renal loss (diuretics, polyuria)
  • Misceaneous (alcoholism)
373
Q

What is the treatment for hypomagnesaemia?

A
  • Oral magnesium salts

- Intravenous magnesium sulfate

374
Q

When does hypermagnesaemia occur?

A
  • Renal impairment
  • Adrenal insufficiency
  • Usually iatrogenic (IV magnesium, purgatives, babies born to mother given IV magnesium)

Kofi: Pure clinical conditions 2 (5 decks)

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