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Yr 2.0 Sem 3 > Urinary > Flashcards

Urinary Flashcards

1
Q

1 With which vertebral levels are the kidneys associated?

A

T11/12 to L2/3

R being more inferior

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2
Q

1 What type of epithelium is in the Proximal Convoluted Tubule?

A

Simple cuboidal with brush border / microvilli

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3
Q

1 What are the 2 layers of Bowman’s capsule?

A

Parietal layer - simple squamous epithelium

Visceral layer - processes of podocytes wrapping around capillaries of glomerulus to form filtration slits

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4
Q

1 Describe in overview the distribution of free ions across cell membranes

A 
ECF   ICF
Na+ high, low
Cl- high, low
Ca2+ high relative to ICF, v.v. low
K+ v. low, high
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5
Q

1 How are soluble vitamins prevented from being excreted in urine?

A

D3 and B12 are reabsorbed from filtrate by endocytosis when the proteins that they are bound with (D3 binding protein or transcoalbulmin respectively) bind to megalin receptors on the apical membrane of proximal tubule cells.

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6
Q

1 What happens to urea in the kidney?

A 
Freely filtered 
50% reabsorbed via Na+ dependant transporter in PCT
60% Secretion in Loop of Henle 
70% Reabsorbed in collecting duct
40% Excreted
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7
Q

1 When could a Vitamin D deficiency affect your Ca2+ levels ?

A

If you have a low calcium diet, Vitamin D3 is required for the active transcellular reabsorption of Ca2+ in the kidney.

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8
Q

1st yr On which transporters in which parts of the tubule do: amiloride, thiazide and loop diuretics exert their actions?

A

Amiloride - inhibits Epithelial Na+ Channels in DCT
Thiazide - inhibit Na+Cl- cotransporter in DCT
Loop diuretics - inhibit Na+K+2Cl-in the Thick Acending limb of Loop of Henle

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9
Q

1 How much filtered urea is normally reabsorbed?

A

50%

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10
Q

2 What factors can affect GFR physiologically?

A

Age, Pregnancy, sex, size of kidney, size of individual

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11
Q

2 How does renal agenesis arise?

A

If ureteric bud from mesonephric duct fails to interact with intermediate mesoderm then the metanephros and thus definitive kidney doesn’t form.

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12
Q

2 What’s a hypospadia and how does it occur?

A

Hypospadia is where urethra opens onto ventral surface of penis, it is caused by a defect in fusion of urethral folds.

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13
Q

2 What’s a patent urachus?

A

The urachus is a structure in the embryo that connects the urogenital sinus to the umbilicus. During development this normally closes to become the medial umbilical ligament, if it remains open (patent) it will become a conduit for urine through the umbilcus.

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14
Q

3 Why is ultra sound so good for imaging kidneys?

A

No ionising radiation, quick, cheap, fluid and calcifications can be easily differentiated.

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15
Q

3 Whats the gold standard for suspected ureteric calculi?

A

CT scan of kidneys, ureter and bladder - CT-KUB

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16
Q

3 What are the 3 most common points at which a kidney stone might get stuck?

A

Ureto-pelvic junction, pelvic brim, where ureter enters bladder

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17
Q

3 How is the ureter related anatomically to the iliac vessels?

A

Ureter crosses over the common iliac artery as it bifurcates into the internal and external iliac arteries.

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18
Q

3 Where are most nephrons in the kidney located?

A

Majority of nephrons are cortical and thus are mostly located in renal cortex.

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19
Q

3 How does blood reach the glomerulus from the renal artery?

A

segmental arteries -> interloBAR arteries -> arcuate arteries -> interloBULAR -> afferent arteriole

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20
Q

3 Explain how GFR is maintained despite transient rises of blood pressure

A

2 mechanisms contribute:
Myogenic regulation in afferent arteriole -
decreases blood flow to glomerulus when BP high via reactive contraction of vascular smooth muscle.
Glomerular-tubular feedback -
Raised BP increases tubular flow rate which increases NaCl concentration in filtrate. This is detected by macula densa cells of DCT, which signal vasoconstriction of afferent arteriole.

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21
Q

3 Describe the role of sympathetic innervation to the efferent and afferent arterioles

A

Normally little sympathetic innervation; but if circulating volume low, e.g. in ischaemia or haemorrhage, can stimulate vasoconstriction of these vessels, preserving GFR.

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22
Q

3 Describe the forces affecting filtration in the glomerulus

A

Hydrostatic pressure in Bowman’s capsule and oncotic pressure w/n capillary are opposed by the filtration-favouring hydrostatic pressure of capillary. Combination of these gives a net filtration pressure.

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23
Q

3 What are the filtration slits of the glomerulus formed by?

A

Gaps between the interdigitations of the pedicels / foot projections of the podocytes.

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24
Q

3 What is activated if the perfusion pressure in the kidney/s is low for a sustained amount of time?

A

The Renin-Angiotensin-Aldosterone System

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25
Q

What 3 hormones do the kidneys produce?

A

Renin, erythropoietin, and calcitonin (active vitamin D)

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26
Q

What is the driving force for transcellular absorption in the nephron?

A

Basolateral 3Na+2K+ATPase

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27
Q

How does amiloride work?

A

Reduces sodium and thus water reabsorption by blocking Na+ H+ exchanger in proximal convoluted tubule, and Epithelial Na channels in both the distal convoluted tubule and the cortical collecting duct.

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28
Q

How do thiazides diuretics work?

A

Block Na+ Cl- co-transporter in distal convoluted tubule -> reduces sodium reabsorption which reduces water reabsorption leading to diuresis.

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29
Q

Why is spironolactone “potassium sparing”?

A

As well as reducing the reabsorption of sodium and hence water, it also blocks the action of renal outer medullary K+ channels reducing K excretion in the cortical collecting duct.

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30
Q

4 What is pressure naturesis?

A

Mechaism by which an increase in renal artery blood pressure reduces number of apical NaH transporters and downregulates basolateral NaKATPase. Ultimately this reduces the amount of Na+ reabsorbed so that it remains fairly constant despite increased glomerular filtration rate.

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31
Q

4 What cells are responsible for the myogenic response of auto-regulation?

A

Smooth muscle cells of afferent arterioles

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32
Q

4 Which part of the kidney tubule is most vulnerable to hypoxia and why?

A

Thick ascending limb of Loop Of Henle, because it has the highest energy requirement.

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33
Q

4 Which is the “diluting segment” of the kidney and why is it referred to as such?

A

Ascending limb of Loop Of Henle because there is absorption of ions from the filtrate but no water absorption. Thus the filtrate becomes less concentrated i.e. more diluted as it flows through this segment.

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34
Q

4 How do the macula densa cells sense renal blood flow?

A

By sensing NaCl concentration in the filtrate via concentration dependent Na+K+Cl- transporters.

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35
Q

4 How does renal artery stenosis affect systemic blood pressure?

A

Reduces the rate of blood flow to the kidneys, this activates the Renin-Angiotensin-Aldosterone-System raising systemic blood pressure.

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36
Q

4 State 2 causes of renal artery stenosis (narrowing)

A

Atheroma and fibromuscular dysplasia

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37
Q

4 What is the most osmotically effective solute in the extra cellular fluid?

A

Na+ (sodium)

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38
Q

4 Why do we need to be able to vary how much sodium we excrete?

A

To match ingestion, thus retaining sodium balance.

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39
Q

4 Where is most sodium reabsorbed?

A

Proximal convoluted tubule

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40
Q

4 Where is the majority of water reabsorbed?

A

Proximal convoluted tubule

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41
Q

4 How is water reabsorbed in the Loop of Henle what makes this possible?

A

By osmosis in descending limb (none in ascending limb) along concentration gradient set up by sodium uptake in proximal convoluted tubule

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42
Q

4 Why is some of the epithelium of the ascending limb of the Loop of Henle thin?

A

Allows passive paracellular reabsorption of Na+

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43
Q

4 Why are there K+ channels allowing K+ to flow into filtrate from the cells of the Thick Ascending Limb of the Loop of Henle?

A

To maintain activity of NKCC2 in apical membrane despite the relative lack of K+ in the filtrate at this point.

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44
Q

4 How is Calcium reabsorbed in the kidney?

A

Apical transport of ions via channels, after which calcium binds to calbindin.
This protein allows the Ca2+ to diffuse to the basolateral aspect of the cell where it is transported out via the sodium calcium exchanger (NCX).

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45
Q

4 Which hormones regulate calcium reabsorption in the kidney?

A 
Parathyroid hormone (PTH)
1,25-dihydroxy (active) vitamin D
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46
Q

4 What do the intercalated cells in the collecting duct do?

A

Actively reabsorb Cl- and secrete either H+ of HCO3- depending on which type they are.

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47
Q

4 Explain how Atrial Natriuretic Peptide supports systemic blood pressure

A

ANP is released by atrial myocytes in response to stretching of atrial wall.

It’s 2 main actions are inhibition of Na+ reabsorption in the collecting duct of the kidney (natureis) and vasodilation. Vasodilation in afferent arteriole of kidney increases GFR preventing activation of RAAS.

If effective circulating volume drops, ANP release is inhibited and so salt and thus water is retained.

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48
Q

4 Why do we need the baroreceptor reflex?

A

Regulates peripheral vascular resistance, heart rate and contractility of the heart in response to acute changes in blood pressure.

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49
Q

4 What 3 factors can stimulate renin release from the juxtaglomerular apparatus?

A

Reduced NaCl delivery to distal tubule / macula densa cells
Sympathetic stimulation of Beta 1 receptors of juxtaglomerular cells
Reduced perfusion pressure sensed by renal baroreceptors

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50
Q

4 Which cells release renin?

A

Granular cells of juxtaglomerular apparatus / near macula densa / DCT

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51
Q

4 How does aldosterone increase blood pressure?

A

Increases circulating volume by acting of principal cells of collecting ducts to stimulate Na+ reabsorption via activation of EnaC and increasing expression of basolateral NaKATPase.

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52
Q

4 What 3 effects does the sympathetic nervous system have in the kidney?

A

Stimulates renin release (from granular cells)
Vasoconstriction of arterioles
Stimulates Na+ absorption in proximal convoluted tubule. (Activates apical NaH exchanger and basolateral NaKATPase.)

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53
Q

4 How does Anti Diuretic Hormone cause an increase in concentration of urine?

A

Increases water absorption in DCT via Aquaporin 2

Stimulates Na+ absorption in thick ascending limb of Loop of Henle via NaKCl cotransporter

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54
Q

4 Which 3 hormones does Angiotensin II stimulate the release of?

A

ADH
Aldosterone
Noradrenaline

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55
Q

4 What are the direct effects of Angiotensin II in the kidney?

A

Vasoconstriction of afferent and efferent arterioles

Increases Na+ reabsorption in PCT (by stimulating NaH exchanger)

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56
Q

4 List 6 endocrine causes of hypertension

A

Primary hyperaldosteroneism / Conn’s syndrome
Cushing’s syndrome (excess cortisol)
Liquorice (apparent mineralcorticoid excess)
Phaeochromocytoma
Acromegaly
Hyper- or hypo-thyroidism

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57
Q

4 What are the 3 main signs of nephrotic syndrome?

A

Proteinuria >350mg/mmol
Hypoalbuminaemia
Oedema

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58
Q

5 Where is ADH produced?

A

Hypothalmus (by neurosecretory cells, then stored in posterior pituitary )

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59
Q

5 Why is osmolarity of blood reduced if there is a decrease in effective circulating volume?

A

Kidneys continue to conserve water at the expense of osmolarity in attempt to maintain circulating volume.

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60
Q

5 What does ADH do to alter the water handling in the nephron?

A

Stimulates expression of aquaporin 2 in apical membrane of collecting duct, increasing absorption of water

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61
Q

5 What is the medullary counter current mechanism?

A

Generation of vertical osmotic gradient within kidney interstitum by transport in Loop of Henle that is maintained by flow of blood in vasa recta in the opposite direction to that of filtrate flow in tubules.

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62
Q

5 Where in the kidney would you find glomeruli of the nephrons?

A

Cortex

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63
Q

5 Why does the thick Ascending Limb of the Loop of Henle need so much oxygen?

A

To produce ATP necessary for active transport of Na+ into interstitum, increasing osmolarity of interstitum which allows the variable reabsorption of water in collecting duct.

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64
Q

5 What makes urea an effective osmole in the kidney?

A

Hydrophillic so cannot cross membranes easily without transporters

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65
Q

5 What is nephrogenic diabetes insipidus?

A

Acquired insensivity of kidney nephrons to ADH resulting in production of large amounts of dilute urine

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66
Q

5 Give 2 common causes of cranial / central diabetes insipidus

A

Brain tumour

Head injury esp basillar skull fractures

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67
Q

5 Damage to which parts of the part of the brain could result in inability to produce concentrated urine?

A

Pituitary gland or hypothalamus

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68
Q

5 Give 3 pulmonary causes of SIADH

A

Pneumonia, TB, small cell lung cancer

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69
Q

5 What is the specific importance of an accurate drug history in a case of suspected SIADH?

A

Many drugs can cause SIADH including carbimazole, amitriptyline and SSRIs

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70
Q

5 How would you generally treat hyponatraemia?

A

Fluid restriction and treat underlying cause

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71
Q

5 List 3 cerebellar signs of hyponatreamia

A

Ataxic gait
Past pointing
Intention tremor

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72
Q

5 Give 4 causes of hypervolameic / oedmatous hyponatreamia

A

Renal failure
Nephrotic syndrome
Congestive heart failure
Liver failure

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73
Q

5 How do you treat cerebral/renal salt wasting syndrome?

A

IV hypertonic saline

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74
Q

5 How is cerebral/renal salt wasting syndrome differentiated from SIADH?

A

Estimation of effective circulating volume: cerebral slat wasting will be hypovolaemic

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75
Q

5 List 5 conditions that could lead to cerebral/renal salt wasting syndrome

A 
Head injury
Stroke
Brain tumour
Intracranial surgery
Tuberculous meningitis
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76
Q

6 Why does the tubule pH decrease distally?

A

Bicarbonate reabsorption in PCT

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77
Q

6 How is bicarbonate recovered from the filtrate in the kidney?

A

Reacts with H+ -> CO2 and water. CO2 diffuses across membrane into tubular cells where it reacts w/ water to reform H+ and bicarb. Then bicarb transported into capillary.

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78
Q

6 Why does it take 2-3 days for kidney to change serum [HCO3-]?

A

Creation of HCO3- in kidney involves breakdown of protein the concentration of which is a limiting factor.

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79
Q

6 What does the breakdown of glutamine produce and what happens to these products?

A

NH4+ / ammonium -> enters lumen and is excreted.

HCO3- / bicarbonate -> enters capillary via Na+HCO3- exchanger

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80
Q

6 Name 2 substances that buffer H+ in urine

A

NH3 ammonia

PO4 phosphate

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81
Q

6 How could profuse vomiting result in hypokalaemia?

A

Loss of H+ in vomit may cause metabolic acidosis causing renal K+ wasting as the kidney attempts to correct blood pH. Also some K+ lost with gastric contents

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82
Q

6 Which acid-base disturbance could diarrhoea cause?

A

Metabolic acidosis if very severe as bicarbonate ions lost

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83
Q

6 Why is there a risk of arrhythmia in hypokalaemia?

A

Increased gradient between ICF & ECF causes depolarisation of cardiac myocyte sarcolemma increasing excitability.

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84
Q

6 Give 3 symptoms of hypokalaemia

A

Weakness, polyuria and constipation

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85
Q

6 What are 3 common causes of low serum K+?

A

Hyperaldosteronism
Increased urinary flow / polyuria
Vomiting or NG drainage

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86
Q

6 Why does an increased plasma osmolarity increase extracellular [K+]?

A

Increased osmolarity of plasma induces osmosis of water into plasma, K+ follows due to solvent drag.

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87
Q

6 How might salbutamol affect plasma [K+]?

A

Increases it, as it agonises beta 2 adrenoreceptors in the kidney tubules, stimulating basolateral 3Na+2K+ATPase, increasing rate of K+ reabsorption.

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88
Q

6 Liddle’s syndrome stimulates epithelial Na+ channels in the collecting duct. How does this result in high blood pressure with low [K+]?

A

Stimulating ENaC increases renal Na+ reabsorption.
This leads to
1. water retention increasing circulating volume and hence blood pressure
2. increased K+ secretion in collecting ducts

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89
Q

6 Explain why a high urinary flow rate would increase K+ secretion

A

Reduces electrochemical and concentration gradients opposing secretion. This is because

  1. luminal K+ is passes through tubule more quickly due to the high flow
  2. Na+ re-absorption is increased as there is a greater filtered load, thus increasing electronegativity of lumen
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90
Q

6 How does magnesium affect the bones?

A

Increases osteoblast proliferation and hence bone strength

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91
Q

6 Where is most filtered Mg2+ reabsorbed?

A

Thick Ascending Limb of Loop of Henle (50-70%)

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92
Q

6 How might mild hypomagnesaemia present?

A

Fatigue, muscle spasms, anxiety, depression, headache

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93
Q

6 What serum concentration would confer a severe hypomagnesaemia?

A

<0.4mmol/l

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94
Q

6 If a patient had low serum [Mg2+] what changes may you see in their other electrolytes?

A

Lower K+ and calcium

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95
Q

6 Give 4 signs of severe hypomagnesaemia

A

Hyperreflexia, tetany, seizures, cardiac dysrrythmias

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96
Q

6 Which 4 commonly used therapeutics can cause hypomagnesaemia?

A

PPIs
Aminoglycosides (gentamycin etc)
Loop diuretics
Thiazide diuretics

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97
Q

1st year Which hormones control serum calcium levels?

A

Parathyroid hormone / PTH

Calcitriol / active vitamin D

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98
Q

6 Where in the kidney tubules is calcium reabsorbed?

A

PCT, TAL of LoH and DCT

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99
Q

6 How does the collecting duct of the nephron help prevent the formation kidney stones?

A

Calcium sensors in apical membrane inhibit local aquaporin and proton pumps when concentration of calcium in filtrate is high.

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100
Q

6 Which symptom of hypocalaceamia would you be most concerned about?

A

Laryngospam (tetany of associated muscles associated with vocal cords)

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101
Q

6 Give 2 cardaic consequences of hypocalaceamia

A

Reduced myocardial contractilty, long QT interval

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102
Q

6 What changes in mental state could hypocalaceamia cause?

A

irritability, confusion, memory loss, hallucination and paranoia

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103
Q

6 In what regions of their body is a hypocalcemic patient likely to be experienced parathesia?

A

Lips and finger tips

104
Q

6 What are the 2 main causes of hypocalceamia?

A

Vitamin D deficiency and lack of parathyroid hormone

105
Q

6 Why are loop diuretics used in heart failure?

A

Rapidly cause veno and vasodilation to reduce symptoms such as breathlessness and oedema (no effect on mortality!)

106
Q

6 Which is the most potent type of diuretics?

A

Loop diuretics

107
Q

6 Why is furosemide useful in hypercalaemia?

A

Impairs absorption of and increases secretion of calcium and so can be given with IV fluids to reduce serum calcium concentration.

108
Q

6 What is the most common use for thiazide diuretics?

A

Hypertension (due to is vasodilatory effects)

109
Q

6 Which diuretic would you use for a patient in renal failure?

A

Loop diuretic

not thiazide as is ineffective

110
Q

6 Use of which diuretic reduces mortality in heart failure patients?

A

Spironolactone

111
Q

6 When would you use spironolactone for hypertension?

A

If ACE inhibitors, Ca2+ channel blockers and thiazides are all either not tolerated, ineffective or are not having enough of an effect.

112
Q

6 Where in the nephron do potassium sparing diuretics act?

A

DCT and collecting duct

113
Q

6 Which ion channel does amiloride act on?

A

Epithelial Na+ channel / ENaC (inhibits)

114
Q

6 What % of sodium reabsorption do thiazides inhibit?

A

5%

115
Q

6 Give one use for osmotic diuretics

A

Cerebral oedema eg due to a local tumour

116
Q

6 What type of diuretic is used in glaucoma ?

A

Carbonic anhydrase inhibitor (eg acetazolamide)

117
Q

6 How does liver cirrhosis cause ascites?

A

Fibrosis in liver impedes flow -> portal hypertension -> increases venous pressure in splanchnic circulation. -> Increases hydrostatic pressure in peritoneal capillaries, overwhelming force of oncotic pressure retaining water inside capillaries -> fluid leaks into peritoneal cavity.

118
Q

6 Why would you not use a thiazide diuretic if the patient has high serum calcium levels?

A

It reduces urinary loss of calcium

119
Q

6 What do you need to be careful of if using ACE inhibitors and spironolactone or amiloride?

A

Serum K+ as these diuretics are potassium sparing so risk hyperkaleamia (which can be life threatening)

120
Q

6 State a common side effect of thiazide diuretics

A

Erectile dysfunction (reversible when drug stopped)

121
Q

6 Which type of diuretic is most likely to cause HYPOkaleamia?

A

Thiazides (loop diuretics also cause it but less frequently)

122
Q

6 How do loop & thiazide diuretics affect gout?

A

They increase the concentration of uric acid in blood so can precipitate attacks of gout

123
Q

6 Why might you choose to use a newer aldosterone agonist drug eg eplererone rather than spironolactone in a young man?

A

Spironolactone can cause gynaecomastia (due to its oestogen like effect) however eplerenone has less of this effect

124
Q

6 Why can thiazide and loop diuretics increase the risk of diabetes mellitus?

A

They increase glucose tolerance (and also LDL levels )

125
Q

6 What 3 things should you monitor to ensure a patient on loop diuretics doesn’t become hypOvoleamic?

A

Weight for loss
Blood pressure for postural drop
Skin turgor / mucous membranes for dehydration

126
Q

6 How do you minimise serum K+ changes in patients on diuretics?

A

Use K+ losing diuretics (Loop and thiazides) in combination with K+ sparing diuretics or with K+ supplements

127
Q

7 Which part of the brain controls the storage phase of micturation?

A

L / pontine storage centre in pons

128
Q

7 What does the M centre of the pons synapse with?

A 
Ganglia in wall of bladder (excitory)
L centre (inhibitory)
129
Q

7 What are the spinal roots of the bladder’s innervation?

A

S2, 3 and 4

130
Q

7 Which types of receptors does the sympathetic innervation of the bladder affect?

A

Beta 3 receptors of detrusor muscle
Alpha 1 receptors of internal sphincter
Nicotinic ACh receptors of external sphincter

131
Q

7 How is bladder voiding initiated?

A

Voluntary control via cerebellum which has excitory synpases with M centre of pons.. otherwise (eg in infants) M centre excited by high levels of stretch in bladder wall.

132
Q

7 What is the effect of parasympathetic innervation of the bladder?

A

Synapses w/ M3 receptors stimulating rhythmic contractions of detrusor muscle

133
Q

7 Describe the composition of the detrusor muscle

A

Smooth muscle arranged in 3 layers: inner and outer longitudinal and middle circular

134
Q

7 In males, how is retrograde ejaculation prevented?

A

Contraction of internal urethral sphincter

135
Q

7 What is the most common cause of urinary incontinence in women?

A

Damage to pelvic floor during childbirth

136
Q

7 What is the 1st line treatment for stress urinary incontinence?

A

Thrice daily pelvic floor muscle training for at least 3 months

137
Q

7 In principle how do you manage mixed urinary incontinence?

A

Manage the urge incontinence first (bladder training)

138
Q

7 What initial investigations are do you need to do in urinary incontinence?

A

Dipstick for blood, protein, glucose, leukocyte esterase
Non-invasive urodynamics such as a bladder diary, frequency-volume chart, and evaluation of post micturation residual volume

139
Q

7 What is the gold standard for surgically treating urinary incontinence in males?

A

Artificial urinary sphincter

140
Q

7 Give 6 lifestyle interventions recommended for urinary incontinence

A 
Modify fluid intake
Decrease caffeine intake
Stop smoking
Timed voiding on fixed schedule
Weight loss
Avoid constipation
141
Q

7 What is the most commonly used surgical treatment for female urinary incontinence?

A

Low tension vaginal tapes (to support mid urethra)

142
Q

7 What drugs are used for first line treatment of urinary urge incontinence?

A

Anti-cholinergics
(eg oxybutynin)

Beta 3-adrenoreceptor agonist (Mirabegron)

143
Q

1st year Describe the distribution of muscarinic receptors

A

Smooth muscle, CNS, the eyes and salivary glands

(M1 - CNS and salivary glands
M2 - heart smooth muscle
M3 - ocular and intestinal smooth muscle and salivary glands
M4 - CNS
M5 CNS, eye)
144
Q

7 Which muscarinic receptors are targeted by drugs used to treat urinary incontinence?

A

M2 and M3

145
Q

10 Why is serum creatinine not a great measure of GFR in acute kidney injury?

A

Creatinine change lags behind GFR by a few days (doesn’t peak until ~7 days after, % change used instead)

146
Q

8 Quantify the range of proteinuria that may be present in nephritic syndrome

A

up to 3.5g / 24 hours

147
Q

8 What are the defining features of nephrotic syndrome?

A

Proteinuria (>3.5g/24hrs)
Hypoalbumineamia
Oedma
And often hyperlipideamia

148
Q

8 Where is the likely site of injury in nephrotic syndrome?

A

Podocyte layer / subendothelial

149
Q

8 What is the most common cause of nephrotic syndrome?

A

Membranous glomerulonephritis

150
Q

8 What is the most common cause of nephrotic syndrome in black people?

A

Focal segmental glomerulosclerosis

151
Q

8 Why does membranous glomerulonephritis look “spikey” on microscopy?

A

Immune complex deposition (IgG) on the glomerular membrane (binds to antigen on podocytes)

152
Q

8 What’s the prognosis in focal segmental glomerulosclerosis?

A

Progresses to renal failure, often rapid decline to end stage

153
Q

8 Why is a kidney transplant often unsuccessful for focal segmental glomerulosclerosis?

A

Damage to podocytes due to a circulating factor which donor kidney will then be exposed to

154
Q

8 What is the main cause of membranous glomerulonephritis?

A

Autoimmmune

155
Q

8 How can diabetes mellitus lead to nephrotic syndrome?

A

Microvascular damage to glomerular capillaries

Mesangium sclerosis causing thickening of glomerular basement membrane

156
Q

8 What are the 4 main principles of nephrotic syndrome managment?

A

Treat underlying cause
Treat oedema with diuretics
Limit protein loss in urine w/ ACE inhibitors
Treat hyperlipideamia to prevent atheroma

157
Q

8 What are the 3 key features of nephritic syndrome?

A

Haematuria
Acute renal failure
Hypertension

158
Q

8 How is the kidney damaged in nephritic syndrome?

A

Endothelium disrupted causing inflammatory response and damage to glomerulus

159
Q

8 What protein is dysfunctional in Alport syndrome?

A

Collagen IV

160
Q

8 Which chromosome is different in Alport syndrome?

A

Most commonly X chromosome

161
Q

8 What happens to the glomerular basement membrane in Alport syndrome?

A

Splits and laminates

162
Q

8 Where in the kidney are immune complexes deposited in IgA nephropathy?

A

Mesangium

163
Q

8 What is the most common type of glomerulonephritis?

A

IgA nephropathy

164
Q

8 Why is important to catch cases of Goodpasture’s syndrome / anti-GM disease early?

A

It is rapidly progressive but treatable by immuno suppression and plasmaphoresis if caught early

165
Q

8 What is ANCA?

A 
Anti Neutrophil
Cytoplasmic Antibody (associated with vasculitis)
166
Q

8 What does vasculitis in the kidney look like on histology?

A

Segmental necrosis with crescents of cellular reaction

167
Q

8 What are the 5 stages of diabetic nephropathy?

A 
Hyperfiltration and hypertrophy
Latent 
Microalbumineamia
Overt proteinuria
End stage renal disease
168
Q

8 What are the 2 main microscopic changes in glomeruli affected by diabetic nephropathy?

A

Thickened glomerular basement membrane

Expansion of mesganium

169
Q

8 What is the most common cause of end stage renal disease?

A

Diabetic nephropathy

170
Q

8 How does hyperglyceamia cause activation of the renin-angiotensin-aldosterone system?

A

Apical SGLT2 in proximal tubule upregulated, increasing reabsorption of glucose and Na+. Thus there is less Na+ to be delivered to distal parts of tubule. In DCT macula densa senses low NaCl conc and activates RAAS

171
Q

8 Why is a thicker glomerular basement membrane a problem?

A

Increases pore size so bigger molecules such a proteins can pass through - it gets leaky bascially

172
Q

8 What is the pathognemonic histological sign of diabetic nephropathy?

A

Kimmelsteil-Wilson nodules

173
Q

8 Describe the changes in GFR that occur in diabetic nephropathy

A

Increased during hypertrophic stage

Then decreases, passes through normal at microalbuminuria stage

174
Q

8 What is the first clinical sign of diabetic nephropathy?

A

Microalbuminuria

175
Q

8 How does mesangial expansion / sclerosis affect kidney function?

A

Reduced surface area for filtration (and so GFR reduced)

176
Q

8 In a patient with normal GFR and proteinuria <100mg/mmol why would you want to know if they’re diabetic?

A

If non diabetic confers mild kidney disease, if diabetic prognosis much worse

177
Q

8 What interventions are important in preventing diabetics developing nephropathy?

A

Tight BP control
Tight blood glucose control
~Smoking cessation advice
~Statins

178
Q

8 Which ethnicities are more at risk of diabetic nephropathy?

A

Black and Asian

179
Q

8 Why would you consider starting a patient with diabetic nephropathy on statins?

A

Prevent CV disease, DN confers increasing cardiovascular risk

180
Q

1st year What (quantitively) is a normal blood glucose level ?

A

<48 mmol/mol or <6.5%

181
Q

8 Why is early intervention for diabetic nephropathy important?

A

Can reverse initial hyperfiltration and delay microalbuminuria with tight glycaemic control

182
Q

8 What is the 2nd commonest cause of end stage renal disease?

A

Hypertension

183
Q

8 Presence of any of which 3 factors in a patient’s history would suggest that kidney damage is due to hypertension and not vice versa?

A

Hypertension preceding proteinuria / ↓GFR by long time-frame
Left ventricular hypertrophy
Hypertensive eye disease

184
Q

8 How are the renal arteries and arterioles affected by hypertensive nephrosclerosis?

A

Fibroelastic intimal thickening → narrowing of lumen

Hyalinosis of afferent arteriolar walls

185
Q

8 How do vascular changes in the kidney affect the glomeruli?

A

Leads to ischaemia which causes:
Wrinkling of glomerular tuft
Glomerulosclerosis (patchy)

186
Q

8 What drugs would you give for hypertension?

A

ACE inhibitors

or Ang II blockers if albuminuria

187
Q

8 How does a hypertensive emergency cause haematuria?

A

High BP damages endothelium of glomeruli

188
Q

8 How can an acute INcrease in blood pressure activate the RAAS?

A

Causes fibrinoid necrosis of arterioles in kidney leaing to ischaemia

189
Q

8 Where does ANCA-associated vasculitis affect?

A

Small arterioles, often kidneys and lungs

190
Q

8 Where can depositis form in lupus nephritis?

A

Bascially anywhere..

191
Q

9 What are the 2 most common symptoms of renal disease?

A

Tired all the time

Malaise

192
Q

9 What can give a false positive for white cells on a urine dipstick?

A

Vaginal secretions

193
Q

9 What does it mean if a patient has nitrites on dipstick urinanalysis?

A

Presence of urinary tract infection or indwelling urinary catheter

194
Q

9 History of which medical conditions would you want to ask a patient with renal signs / symptoms about specifically?

A 
DM
Hypertension
IHD
Cerebrovascular disease
Known CKD (major risk for AKI)
195
Q

9 What are the 2 most vital elements of an examination of a patient with renal symptoms?

A 
Blood pressure
Urine dipstick (if they are passing urine)
196
Q

9 Do you get more uraemic symptoms in acute or chronic kidney injury?

A

Acute

197
Q

9 What colour is a “uraemic skin tone”?

A

Grey / brown / sallow

198
Q

9 Why is an early morning urine needed to confirm proteinuria?

A

Negates orthostatic effect and reduces effect of exercise which can give false postives

199
Q

9 What are some non-renal causes of proteinuria?

A 
Lower UTI / cystitis
Fever
Exercise
Amyloidosis
Myeloma (Bence Jones Protein)
Haematuria
Eclampsia &amp; pre-eclampsia in pregnancy
200
Q

9 What other than UTI might cause positive leukocytes on urine dipstick (sterile pyuria)?

A 
Chlamydia trachomatis 
Neoplasms
Stones
Glomerular nephritis
False pos due to vaginal secretions
Chemical inflammation
201
Q

9 What are the symptoms of a upper UTI / pyelonephritis?

A

Fever
Loin pain
+/- dysuria / urgency / frequency

202
Q

9 When would you want to treat asymptomatic bacteruria?

A

Pregnancy as can cause pre-term labour

203
Q

9 Suggest 4 reasons why UTIs are more common in patients with CKD

A

Damaged kidneys more vulnerable to infection
Often malnourished
Ureamia interferes with immune system
Often on immuno-suppressants to treat cause of CKD

204
Q

9 How often are symptoms of urethritis in females associated with significant bacturia?

A

50% (others are “urethral syndrome” for which causes incl STIs or vaginal infection/inflammation)

205
Q

9 Why is a neuropathic bladder prone to infection?

A

Often leads to incomplete emptying and thus residual urine as can’t sense when bladder is empty or not

206
Q

9 Give 3 obstructive causes of incomplete emptying of the bladder

A

Calculi
Bladder neck hypertrophy
Urethral strictures

207
Q

9 What type/s of bacteria are most commonly associated with UTIs?

A

Gut flora eg E coli and other coli forms

often Gram negative

208
Q

9 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 (eg catheter, virulent organism, diabetes, immunosuppression
Also kids, men and pregnant ladies often managed as complicated)

209
Q

9 When is urine culture needed in suspected UTI?

A

Complicated UTI, pregnant, male, kids, treatment failure, recurrent infections

210
Q

9 What 5 things would you look for in a suspected UTI urine sample (near patient testing)?

A 
Turbidity
Dipstick for:
leucocyte esterase
nitrite
haematuria
proteinuria
211
Q

9 Why is it important to look at nitrite and leukocyte esterase together on dipstick?

A

Nitrite alone has v. poor sensitivity and leuc est alone has fairly poor specificity

212
Q

9 Why is is not very useful to do a urine dipstick in older patients without features of infection?

A

Asymptomatic bacteriuria

common in >65s and not associated with inc risk of morbidity/mortality

213
Q

9 What causes presence of nitrite in urine in UTI?

A

Bacterial ureases

214
Q

9 What are the 3 main principles of UTI treatment?

A

Increase fluid intake
Appropriate antibiotics
Address underlying disorders

215
Q

9 What would you prescribe for simple cystitis (assuming they have tried conservative management)?

A

3 day course of trimethoprim or nitrofurantoin

216
Q

9 Give 2 examples of pathogens that are common causes of complicated UTIs

A

Klebsiella spp

Staphlococcus aureus

217
Q

9 How would you treat pyelonephritis / UTI associated

septicaemia? UHL 2017

A

14 day co-amoxiclav
OR 7 day ciprofloxacin
OR 14 day IV gentamicin (with close monitoring of kidney function as nephrotoxic)

218
Q

9 Why would nitrofurantoin not be useful for treating pyelonepritis?

A

It only penetrates as far as bladder, and can’t use if GFR reduced

219
Q

10 When would you not use eGFR?

A

In AKI, amputees, extremes of muscle mass

220
Q

10 What is AKI?

A

Acute Kidney Injury of an abrupt (days to weeks) decline in actual GFR (glomerular filtration rate)

221
Q

10 What are the 2 most common causes of AKI?

A

Dehydration and hypotension

222
Q

10 How do ACE-Inhibitors and NSAIDs affect renal perfusion?

A

NSAIDs cause pre-glomerular constriction
ACEi cause post-glomerular vasodilatation
Both of these effects impair renal autoregulation

223
Q

10 Why is it important to recognise poor renal perfusion early?

A

If poor renal perfusion is not recognised and treated promptly then acute tubular
necrosis will develop

224
Q

10 How in principle treat would you treat AKI that has a pre-renal cause?

A

Fluid resuscitation

225
Q

10 How can liver failure cause kidney failure?

A

Impaired metabolism and excretion of bilirubin which then accumulates and damages kidney tubule cells

226
Q

10 What changes in serum biochemistry do you need to look out for in AKI?

A 
• Metabolic acidosis
• Hyperkalaemia
• Hyponatraemia
• Hypocalcaemia and hyperphosphataemia
(also urea and creatinine always high in AKI)
227
Q

10 What is the typical progression of ECG changes in untreated hyperkalaemia?

A
  • Tall T waves
  • Small or absent P waves
  • Increased P-R interval
  • Wide QRS complex
  • ‘Sine wave’ pattern
  • Asystole
228
Q

10 How would you treat hyperkalaemia?

A 
Calcium gluconate (to protect heart)
Restrict dietary K
Stop K-sparing diuretics, ACEi, ARB
Exchange resin
Dextrose &amp; insulin
229
Q

10 What are the 2 main groups of patients most at risk of AKI?

A
  • Advanced age

* CKD

230
Q

10 In what type of patients are you most liekly to see an obstructive cause of AKI?

A

Elderly

231
Q

10 What are the 3 most commonly used types of drugs that can cause AKI?

A

Antibiotics
NSAIDs
Proton pump inhibitors

232
Q

10 What does myoglobinuria look like?

A

Flat Coca cola

233
Q

10 What are the 2 most common causes of rhabdomyolysis in the UK?

A

Drug use - unconscious so don’t move

Elderly – fall over and unable to get up

234
Q

10 List 3 endogenous nephrotoxins

A

Myoglobin
Urate
Bilirubin

235
Q

10 Which parts of the kidney tubule tend to be damaged in ATN?

A

Proximal convoluted tubule

Thick ascending limb of Loop of Henle

236
Q

10 What 4 things could cause obstruction of urinary tract but not from within the lumen?

A

Enlarged prostate
Local tumour
Abdominal aortic aneurysm
Post-TB stricture

237
Q

10 How can infection lead to an AKI?

A

Inflammatory immune response causes systemic vasodilation reducing effective arterial blood volume

238
Q

10 What is a big clue as to whether a case of urinary retention is acute or chronic?

A

If patient is in pain - acute is painful, chronic not

239
Q

10 Give 5 indications for dialysis in AKI

A

(Mnemonic AEIOU)
Acidosis - metabolic cause, where NaHCO not appropriate
Electrolyte abnormality - High K+ refractory to treatment
Ingestion of a dialysable nephrotoxin e.g. aspirin, antifreeze etc
Overload of fluid that isn’t responding to diuretics
Uraemic signs: pericarditis, intractable nausea and vomiting, reduced consciousness / encephalopathy

240
Q

10 What 3 substances can give a false positive for blood on a urine dipstick?

A

Myoglobin, bleach and bacterial peroxidases

241
Q

10 Give 1 substance that can cause false negatives for haematuria on urine dipstick

A

Vitamin C

242
Q

11 When do we use PSA testing?

A

Opportunistic screening for prostate cancer in men who are already concerned about it

243
Q

11 Why is Digital Rectal Examination performed for suspected prostate maligancy?

A

Cancers tend to form in peripheral zone of prostate which is just anterior to the rectum and so can easily be palpated. They also tend to feel craggy so can be differentiated from smooth benign prostate enlargement.
PSA test results normal in some cases of prostate cancer.

244
Q

11 What grading system is used for prostate cancer?

A

Gleason grading - based on derangement of gland structure

245
Q

11 Describe the racial distribution of prostate cancer risk

A

Black > white > asian

246
Q

11 What 2 factors in family history would confer increased risk of prostate cancer?

A

Presence of BRCA2 mutation

1st degree relative diagnosed with prostate cancer when under 60 years old

247
Q

11 Describe the age distribution of prostate cancer

A

Rare <50 y.o.

V.V. common >80, but typically not cause of death

248
Q

11 Why might a non-symptomatic prostate cancer present?

A

PSA test result
Incidental finding on DRE performed for another reason eg change of bowel habit
(Rarely, incidental finding on TransUrethral Resection of Prostate)

249
Q

11 What types of symptoms does prostate cancer usually present with?

A

Urinary symptoms eg weak stream, urgency, frequency, nocturia
Bone pain, eg persistent back pain

250
Q

11 When would haematuria be a red flag symptom in primary care?

A

Visible haematuria if middle aged or older

=>2 week wait referral

251
Q

11 How can advanced Renal Cell Carcinoma present?

A 
Large varicocele may be present
Pulmonary/tumour embolus
Loss of weight/loss of appetite/symptom from metastasis
Hypercalcaemia
Palpable mass
Haematuria
252
Q

11 How does advanced Transitional Cell Carcinoma present?

A
  • Haematuria
  • Loss of weight/loss of appetite/symptom of metastasis
  • DVT
  • Lymphoedema
253
Q

11 What distant sites does renal cell carcinoma tend to spread to and how?

A

Right atrium via IVC

Lung & Liver via lymph node metastases

254
Q

11 What potentially curative treatments are available for bladder TCC?

A 
Radical cystectomy (followed by ileal conduit or reconstruction w/ bowel) or radiotherapy
\+/- chemotherapy
255
Q

11 Suggest why bladder cancer often presents at a more advanced stage in women than men?

A

Lower urinary tract symptoms very common in women esp as recurrent UTIs very common

256
Q

11 Suggest why bladder cancer often presents at a more advanced stage in women than men?

A

Lower urinary tract symptoms very common in women esp as recurrent UTIs very common too

Yr 2.0 Sem 3 (5 decks)

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