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x 2nd Year Medicine > Renal > Flashcards

Renal Flashcards

1
Q

What is osmolarity?

A

An estimation of the osmolar conc. of plasma

Is proportional to the number of particles / litre of solution (mmol/l)

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2
Q

What is osmolality?

A

An estimation of the osmolar conc. of plasma

Is proportional to the number of particles / kg of solvent (mOsmol/kg)

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3
Q

What is tonicity?

A

Related to its affect on the volume of a cell

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4
Q

What happens to a RBC placed in a hypertonic solution?

A

Cell shrinkage

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5
Q

What happens to a RBC placed in a isotonic solution?

A

Nothing

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6
Q

What happens to a RBC placed in a hypotonic solution?

A

Cell lysis

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7
Q

Whats are RBCs very permeable to?

A

urea

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8
Q

What percentage of the weight of a male is water?

A

~60%

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9
Q

What percentage of the weight of a female is water?

A

~50%

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10
Q

How much of the total body water is Intracellular fluid?

A

67%

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11
Q

What is included in the ECF?

A

Plasma
Interstitial fluid (80%)
Lymph and transcellular fluid (negligible)

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12
Q

How can a the volume of a large body of water be calculated?

A

V(l) = D/C

Where V = unknown volume of water
D = dose of tracer added to water
C = concentration of dose present in a small volume of this water

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13
Q

What tracer can be used to obtain the total body water volume

A

3H20

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14
Q

What tracer can be used to obtain the amount of water in the ECF?

A

Inulin

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15
Q

What tracer can be used to obtain the plasma volume?

A

Labelled albumin

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16
Q

Is sodium more abundant in the ECF or ICF?

A

ECF

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17
Q

Is potassium more abundant in the ECF or ICF?

A

ICF

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18
Q

Is chloride more abundant in the ECF or ICF?

A

ECF

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19
Q

Is bicarbonate more abundant in the ECF or ICF?

A

ECF

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20
Q

What is the primary anion of the ECF?

A

Cl-

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21
Q

What are the main ions in the ICF?

A

Potassium, magnesium, negatively charged proteins

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22
Q

What organ alters the composition and volume of the ECF?

A

Kidney

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23
Q

What 2 types of nephron are found in the kidney?

A

Juxtamedullary (20%) - longer loops of Henle

Cortical (80%)

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24
Q

From deep to superficial, what are the histological layers of the glomerular capillaries?

A

Inner endothelial cells
Basement membrane
Podocytes face out into Bowman’s capsule

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25
Q

What is the juxtaglomerular apparatus?

A

The portion of the distal tubule which loops back very near to the glomerulus

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26
Q

What histologically connects the distal tubule and the glomerulus at the juxtaglomerular apparatus?

A

A thick macula densa of the distal tubule and granular cells in some of the arterioles

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27
Q

What percentage of blood that enters the glomerulus at any one time is actually filtered?

A

20%

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28
Q

How can the rate of filtration of substance X be calculated?

A

{X}plasma x GFR

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29
Q

How can the rate of excretion of substance X be calculated?

A

{X}urine x Vu (urine flow rate)

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30
Q

How can the rate of reabsorption of substance X be calculated?

A

rate of filtration - rate of excretion

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31
Q

How can the rate of secretion of substance X be calculated?

A

rate of excretion - rate of filtration

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32
Q

What barriers exist for blood filtration in the glomerulus?

A 
Glomerular capillary endothelium (RBC barrier)
Basememnt membrane (plasma protein barrier)
Slit processes of podocytes (plasma protein barrier)
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33
Q

What barriers exist for blood filtration in the glomerulus?

A 
Glomerular capillary endothelium (RBC barrier)
Basememnt membrane (plasma protein barrier)
Slit processes of podocytes (plasma protein barrier)
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34
Q

What is the normal GFR?

A

125ml/min

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35
Q

What is the extrinsic regulation of the GFR?

A

Sympathetic control via the baroceptor reflex

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36
Q

How is the GFR intrinsically controlled?

A

Myogenic mechanism and tubuloglomerular mechanism which prevent short term ABP changes affecting the GFR

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37
Q

How does myogenic regulation work to control the GFR?

A

If vascular smooth muscle is stretched (increased ABP), it contracts thus constricting the arteriole

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38
Q

How does the tubuloglomerular mechanism work to control the GFR?

A

If the GFR rises, more NaCl flows through the tubule, leading to constriction of afferent arterioles

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39
Q

What is plasma clearance?

A

A measure of hoe effectively the kidneys can clean the blood.

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40
Q

How can plasma clearance be calculated?

A

Rate of excertion/ Plasma conc.

{X}urine x Vu/ {X}plasma

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41
Q

How can plasma clearance be calculated?

A

Rate of excertion/ Plasma conc.

{X}urine x Vu/ {X}plasma

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42
Q

What is the rate of inulin clearance compared to the GFR?

A

Inulin clearance = GFR

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43
Q

What is the rate of clearance of glucose?

A

0 - it is not secreted from the body

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44
Q

How does the rate of urea clearance compare to the GFR?

A

Urea clearance less than GFR

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45
Q

How doe sthe rate of H+ clearance compare to the GFR?

A

H+ clearance > GFR

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46
Q

How can renal plasma flow (RPF) be calculated?

A

Using para-amino hippuric acid (PAH)

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47
Q

Why is PAH good for measuring RPF?

A

It is freely filtered at the glomerulus
Secreted into the tubule
Completely cleared from the plasma

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48
Q

What should RPF be?

A

~650ml/min

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49
Q

What is the filtration fraction?

A

The fraction of plasma flowing through the glomeruli that is filtered into the tubules

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50
Q

How can the filtration fraction be calculated?

A

GFR/RPF

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51
Q

How can the filtration fraction be calculated?

A

GFR/RPF

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52
Q

Roughly how may times per day is the plasma filtered?

A

65

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53
Q

What do the kidneys reabsorb 99-100% of in healthy individuals?

A

Fluid - 99
Salt - 99
Glucose
Amino acids

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54
Q

How much of the urea in the blood is reabsorbed by the kidneys?

A

50%

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55
Q

What percentage of creatinine is reabsorbed by the kidneys?

A

0%

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56
Q

How much filtered fluid is reabsorbed in the proximal tubule?

A

80ml/min

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57
Q

What substances are reabsorbed in the PT?

A 
Sugars
Amino acids
Phosphate
Sulphate
Lactate
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58
Q

What substances are secreted in the PT?

A 
H+
Drugs and toxins
Hippurates
Neurotransmitters
Uric acid
Bile pigments
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59
Q

What are the 2 types of tubular reabsorption?

A

Transcellular

Paracellular

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60
Q

What are the 2 types of tubular reabsorption?

A

Transcellular

Paracellular

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61
Q

How is sodium transported into the epithelial cells of the proximal tubule?

A

Secondary active transport with glucose/amino acids

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62
Q

What is the function of the loop of Henle?

A

Generates a cortico-medullary solute conc. gradient

Enabling formation of hypertonic urine

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63
Q

What happens the the ascending limb of the loop of Henle?

A

Na+ and Cl- are reabsorbed

Water cannot easily permeate

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64
Q

What happens in the descending limb of the loop of Henle?

A

does NOT reabsorb NaCl

Is highly permeable to water

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65
Q

What ions are involved in the triple transporter?

A

K+
Cl-
Na+

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66
Q

Is fluid leaving the proximal tubule hypo, iso, or hyper tonic?

A

Isotonic

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67
Q

Is fluid entering the distal tubule hypo, iso, or hyper tonic?

A

Hypotonic

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68
Q

How does urea contribute to ~1/2 of the medullary osmolality?

A

Urea cycle adds solute to the interstitium
Distal tubule not permeable to urea
Urea diffuses passively into loop

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69
Q

How does urea contribute to ~1/2 of the medullary osmolality?

A

Urea cycle adds solute to the interstitium
Distal tubule not permeable to urea
Urea diffuses passively into loop

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70
Q

What is the purpose of countercurrent multiplication?

A

To concentrate the medullary ISF, enabling the kidney to produce different urine volumes and concs. according to the amounts of circulating ADH

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71
Q

How does ADH affect the distal tubules and the collecting ducts?

A

Increases water reabsorption

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72
Q

How does aldosterone affect the distal tubules and the collecting ducts?

A

Increases sodium reabsorption

Increases H+/K+ secretion

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73
Q

How does atrial natriuertic hormone affect the distal tubules and the collecting ducts?

A

Decreases Sodium reabsorption

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74
Q

How does PTH affect the distal tubules and the collecting ducts?

A

Increases Calcium reabsorption

Decreases phosphate

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75
Q

How does PTH affect the distal tubules and the collecting ducts?

A

Increases Calcium reabsorption

Decreases phosphate

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76
Q

What happens in the early distal tubule with ions?

A

Na+K+2Cl- transport

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77
Q

What happens the the late distal tubule with ions?

A

Calcium reabsorption
H+ secretion
Na+ and K+ reabsorption

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78
Q

What does aldosterone do in the late distal tubule?

A

Causes K+ secretion when the K+ secretory cells are activated

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79
Q

What happens in the early collecting duct?

A

Calcium reabsorption
H+ secretion
Na+ and K+ reabsorption

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80
Q

What happens in the late collecting duct?

A

There is low ion permeability and permeability to water is determined by ADH secretion

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81
Q

What happens in the late collecting duct?

A

There is low ion permeability and permeability to water is determined by ADH secretion

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82
Q

From what and where is ADH synthesised?

A

Octapeptide by the hypothalamus is transported down nerves where it is stored in granule form in the posterior pituitary gland

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83
Q

Where is ADH released into and what does it cause to happen?

A

Released from the posterior pituitary into the blood where APs down nerves lead to Ca2+-dependant exocytosis

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84
Q

What is the plasma half-life of ADH?

A

10-15mins

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85
Q

What effect does ADH have on the collecting duct membranes?

A

Increases their permeability to H20 by inserting aquaporins

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86
Q

What happens when there is maximal ADH concentration in the plasma?

A

Water moves from the collecting duct lumen along the osmotic gradient into the ISF thus enabling creation of hypertonic urine

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87
Q

How does urine travel from the kidneys to the bladder?

A

Propelled down the ureters by peristalic contractions

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88
Q

What is the micturition reflex?

A

Once the bladder has 250-400mls urine in it, stretch receptors in the wall of the bladder cause involuntary emptying of the bladder by bladder contraction and opening both the internal and external urethral sphincters

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89
Q

How can the micturition reflex be overridden?

A

Through voluntary control of the external sphincter

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90
Q

How can homeostasis of body fluid be obtained?

A

Monitoring and regulation of ECF osmolarity and volume

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91
Q

How is filtration in the kidneys regulated?

A

Changes in BP and the size of the filtration slits (podocytes)

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92
Q

What regulates the secretion/absorption in the kidneys?

A

Changes in solute conc.

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93
Q

What regulates the excretion function of the renal system?

A

Bladder function under neural control

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94
Q

How does activation of stretch receptors in the upper GI tract affect ADH?

A

Exerts a feed-forward inhibition of ADH

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95
Q

What effect does nicotine have on ADH?

A

Stimulates release

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96
Q

What effect does alcohol have on ADH?

A

Inhibits release

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97
Q

What effect does alcohol have on ADH?

A

Inhibits release

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98
Q

How does salt imbalance manifest itself?

A

Changes in ECFV

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99
Q

What regulates the amount of Na+ reabsorbed?

A

RAAS

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100
Q

In relation to ion concentrations when is aldosterone secreted?

A

When K+ conc rises or Na+ conc falls (or activation through RAAS)

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101
Q

What does aldosterone stimulate to occur in the kidney?

A

Na+ reabsorption

K+ secretion

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102
Q

How does the JGA control rennin release?

A

Reduced BP in the afferent arteriole stimulates rennin release
Low NaCl detected by the macula densa cells stimulates rennin release
Sympathetic activity on the granular cells, causes them to release rennin

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103
Q

How does the JGA control rennin release?

A

Reduced BP in the afferent arteriole stimulates rennin release
Low NaCl detected by the macula densa cells stimulates rennin release
Sympathetic activity on the granular cells, causes them to release rennin

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104
Q

What can an abnormal increase in the RAAS system cause?

A

Hypertension

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105
Q

How is hypertension caused by RAAS stimulation treated?

A

Low salt diet
Loop diuretics
ACEIs

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106
Q

What does ANP stand for?

A

Atrial Natriuretic Peptide

107
Q

What produces ANP and where is it stored until use?

A

The heart stores it in atrial muscle use until it is needed

108
Q

What causes ANP release?

A

Mechanical stretching of the atrial muscle cells due to increased PV

109
Q

What are the effects of ANP on the body?

A

Excretion of Na+ and diuresis

Lowers BP

110
Q

What is the role of erythropoietin released from the kidney?

A

Stimulates stem cells to produce more RBCs to increase the O2 supply in tissues if this is too low

111
Q

How can pH be calculated?

A

log*1/{H+}

112
Q

What is the pH of arterial blood?

113
Q

What is the pH of venous blood?

114
Q

What can acidosis do to the CNS?

A

Leads to depression of CNS

115
Q

What can alkalosis do to the CNS?

A

Leads to overexcitability of the NS and then CNS

116
Q

What do changes in {H+} affect in the body?

A

Enzyme activity

K+ levels

117
Q

What 3 sources constantly supply the body with H+?

A

Carbonic acid formations
Inorganic acids produced during the breakdown of nutrients
Organic acids from metabolism

118
Q

What makes up a buffer system?

A

A pair of substances, one of which can yield free H+ as {H+} decreases; and one which can bind free H+ as {H+} increases

119
Q

What makes up a buffer system?

A

A pair of substances, one of which can yield free H+ as {H+} decreases; and one which can bind free H+ as {H+} increases

120
Q

What is the most important physiological buffer system?

A

The CO2-HCO3 buffer

121
Q

How does the kidney affect the plasma conc. of HCO3-

A

Varies the amount reabsorbed depending on need

Can also add new HCO3- to the blood (by excreting acid there is a net gain of HCO3-)

122
Q

What does H+ secretion from the tubule do?

A

Drives absorption of HCO3-
Forms acid phosphate
Forms ammonium ions

123
Q

What is the vast majority of H+ secretion used for?

A

HCO3- reabsorption to prevent acidosis occuring

124
Q

What does excretion of acid phosphate (Titratable acid) and NH4+ do?

A

Rids the body of excess acid and regenerates the NCO3- buffer stores

125
Q

What is compensation of an acid-base disturbance?

A

Restoration of pH to normal regardless of what happens to pCO2 and {HCO3-}p

126
Q

What is correction of an acid base distrbance?

A

Restoration of pH AND pCO2 and {HCO3-}p to normal levels

127
Q

What is correction of an acid base distrbance?

A

Restoration of pH AND pCO2 and {HCO3-}p to normal levels

128
Q

What happens immediately following a blood pH change?

A

There is immediate dilution of the acid or base in ECF

129
Q

What conditions can cause a retention of CO2 by the body (resp acidosis)?

A 
Chronic bronchitis
Chronic emphysema
Airway restriction
Chest injuries
Respiratory depression
130
Q

What happens to {H+}p in acidosis?

131
Q

What indicates uncompensated respiratory acidosis?

A

pH less than 7.35 and PCO2 > 45mmHg

132
Q

What drives the compensation is respiratory acidosis?

A

Renal system

133
Q

How does the renal system manage to compensate for a respiratory acidosis?

A

H+ secretion is stimulated and all filtered HCO3- is reabsorped
H+ continues to be secreted and generates TA and NH4+
Acid is excreted and “new” HCO3- is added to the blood

134
Q

How is respiratory acidosis CORRECTED?

A

Restoring normal ventilation and lowering PCO2

135
Q

What is respiratory alkalosis?

A

Excessive removal of CO2 by the body

136
Q

In what conditions does respiratory alkalosis occur in?

A

Low inspired PO2 at altitude
Hyperventilation
Hysterical overbreathing

137
Q

What happens to {H+}p in respiratory alkalosis?

138
Q

How is uncompensated resp alkalosis defined?

A

If pH >7.45 AND PCO2 is less than 35mmHg

139
Q

How is uncompensated resp alkalosis defined?

A

If pH >7.45 AND PCO2 is less than 35mmHg

140
Q

How does the renal system compensate for resp. alkalosis?

A

HCO3- is excreted and the urine is alkaline

No “new” HCO3- is added to the blood

141
Q

How is resp. alkalosis CORRECTED?

A

Restoration of normal ventilation

142
Q

What is metabolic acidosis?

A

Excess H+ from any source other than CO2

143
Q

What can cause a metabolic acidosis?

A

Ingestion of acids/acid-producing foodstuffs
Excessive metabolic production of H+ (lactic acid build up)
Excessive loss of base from the body (diarrhoea)

144
Q

What happens to {HCO3-}p in metabolic acidosis?

145
Q

How is uncompensated metabolic acidosis defined?

A

pH less than 7.35 and {HCO3-}p is low

146
Q

How does the body compensate for metabolic acidosis?

A

Ventilation quickly increases to blow off more CO2

147
Q

What is {H+}p in metabolic acidosis?

148
Q

How is metabolic acidosis corrected?

A

New HCO3- is generated due to H+ secretion continuing
An acid load is excreted and {HCO3-}p is restored
Ventilation can then be normalised

149
Q

How is metabolic acidosis corrected?

A

New HCO3- is generated due to H+ secretion continuing
An acid load is excreted and {HCO3-}p is restored
Ventilation can then be normalised

150
Q

What is metabolic alkalosis?

A

Excessive loss of H+ from the body

151
Q

What can cause a metabolic alkalosis?

A

Loss of HCl from the stomach (vomitting)
Ingestion of alkali or alkali-producing foods
Aldosterone hypersecretion (causes increased acid secretion and excretion)

152
Q

What happens to {HCO3-}p in metabolic alkalosis?

153
Q

How can uncompensated metabolic alkalosis be defined?

A

pH >7.45 or increased {HCO3-}

154
Q

How does the body compensate in metabolic alkalosis?

A

Slowing ventilation, thus more CO2 is retained

155
Q

How is metabolic alkalosis corrected?

A

HCO3- is secreted in urine and the plasma conc falls back to normal

156
Q

How does GN show?

A

Glomerular tufts with secondary tubulointestinal changes
Non-infective
Usually diffuse but can be focal
Immunological mechanisms are often implicated but there is no single cause

157
Q

What is pyelonephritis?

A

A bacterial infection of the renal pelvis, calyces, tubules and interstitium
May be acute or chronic with patchy distribution
E.coli most common organism
Other causes include psuedomonas and strep. faecalis
Much commoner in females

158
Q

What is the pathogenesis of nephritis

A

Blood-borne (rare) in septicaemia, post surgery

Ascending infection - cystitis is often present

159
Q

What are the risk factors for developing nephritis?

A 
Young and female
obstruction
pregnancy
diabetes
instrumentation
Vesico-ureteric reflux (VUR)
160
Q

How does acute polynephritis appear macroscopically?

A

Ulcers on kidney tissue

161
Q

How does acute polynephritis appear microscopically?

A

Renal tubules have neutrophil polymorphs

162
Q

How does chronic pyelonephritis present?

A

Often no UTI history
Vague symptoms
Hypertension and/or uraemia
Large urine volumes
Renal imaging shows coarse cortical scarring and distortion of calyces
Kidneys may shrink
Lymphocytes and plasma cells on histology

163
Q

How does tuberculous polynephritis present?

A

Haematogenous spread from lungs
Weight loss, fever, loin pain and dysuria
Sterile pyuria
Caseous foci

164
Q

What organisms can cause cystitis?

A

E.coli
Klebsiella
Proteus
Pseudomonas

165
Q

How does cystitis present?

A

Acute inflammation

166
Q

What can cause a urinary tract obstruction?

A

Stricture, posterior urethral valves, prostatic disease

Hypertrophy of detrusor muscle

167
Q

What is hydronephrosis?

A

Dilation of the pelicalcyceal system with parenchymal atrophy

168
Q

What are the unilateral causes of hydronephrosis?

A

Calculi
Neoplasm
Pelvi-ureteric obstruction
Strictures

169
Q

What are the bilateral causes of hydronephrosis?

A

Urethral obstruction
VUR
Neurogenic disturbance
Bilateral obstruction

170
Q

What are the bilateral causes of hydronephrosis?

A

Urethral obstruction
VUR
Neurogenic disturbance
Bilateral obstruction

171
Q

What is agenesis of the kidneys?

A

absence of 1 or both kidneys

172
Q

What is hypoplasia of the kidneys?

A

Small kidneys but normal development

173
Q

What is a “horseshoe” kidney?

A

Fusion at either kidney pole - usually lower

174
Q

What is a duplex system?

A

More than 1 ureter of part of kidney on 1 side

175
Q

How do simple kidney cysts present?

A

v.common with usually no functional disturbance
may be multiple and large
May occur secondary to long standing kidney disease

176
Q

How does infantile PCKD present?

A

Rare with various subtypes
AR inheritance
Uniform bilateral renal enlargement
Elongated cysts - dilatation of medullary collecting ducts
Reniform shape maintained
Associated with congenital hepatic fibrosis

177
Q

How does adult PCKD present?

A

AD inheritance with a defect on chromosome 16 or 4
Mid-life as an abdo mass, haematuria, hypertension and CKD
Massive bilateral kidney enlargement
Multiple cysts of varying sizes
Reniform structure distorted

178
Q

Other than in the kidneys, where other can cysts from adult PCKD present?

A

In 1/3 cases:
Liver
Pancreas
Lung

179
Q

What vascular disorder is PCKD associated with?

A

Berry aneurysms in the circle of Willis –> subarachnoid haemorrhage

180
Q

What are the benign types of renal tumours?

A

Fibroma
Adenoma
Angiomyolipoma
JCGT

181
Q

How does a renal fibroma appear?

A

Medullary in origin

White nodules

182
Q

How does a renal adenoma appear?

A

yellowish nodules less than 2cm in size

Cotrical origin

183
Q

How does a renal angiomyolipoma appear?

A

Mixture of fat, muscle and blood vessels
May be multiple and bilateral
Associated with tuberoussclerosis

184
Q

How does a renal JGCT appear?

A

Juxtaglomerular cell tumour

Increased Rennin production leading to secondary hypertension

185
Q

How does a renal JGCT appear?

A

Juxtaglomerular cell tumour

Increased Rennin production leading to secondary hypertension

186
Q

What are the malignant renal tumours?

A

Nephroblastoma (Wilm’s tumour)
Urothelial carcinomas
Renal cell carcinoma
Transitional cell carcinoma

187
Q

What is a nephroblastoma?

A

Commonest intra-abdo tumour in children

Arises from residual primitive renal tissue

188
Q

Where do urothelial carcinomas affect?

A

Renal pelvis and calyces

189
Q

What is a Renal Cell Carcinoma?

A

Arises from renal tubule epithelium
Commonest primary renal tumour in adults
Commonest in males 55-60

190
Q

How does a renal cell carcinoma present?

A 
Abdo mass
Haematuria
Flank pain
Ploycythemia
Hypercalcaemia
191
Q

What does a renal cell carcinoma look like?

A

A large well-circumscribed mass centered on the cortex

Yellow with solid, cystic, necrotic and haemorrhagic areas

192
Q

Where can renal cell carcinomas spread to?

A

Renal vein extension is common

Lung and bone via blood

193
Q

What is a transitional cell carcinoma?

A

Tumour from the transitional epithelium which accounts for 90% of all bladder tumours

194
Q

What are the risk factors for developing transitional cell carcinoma?

A 
Analine dyes
Rubber industry
Benzidine
Cyclophosphamide
Anagesics
SMOKING
195
Q

How does a transitional cell carcinoma present?

A

Haematuria

some occur ureteric obstruction and so those symptoms may also be present

196
Q

What does a transitional cell carcinoma look like?

A

Papillary or solid

Papillae have a thicker lining than normal urothelium

197
Q

Where can a transitional cell carcinoma spread to?

A

local lymph nodes (obturator)
Lungs
liver

198
Q

What is the commonest malignant bladder tumour in children?

A

Embryonal rhabdomyosarcoma

199
Q

What tumours can affect the penis?

A

Squamous cell carcinoma in situ

Bowen’s disease - erythroplasia of Queyrat

200
Q

What are the features of penile tumours?

A

Full thickness dysplasia of the epidermis

Only 5% lead to invasive carcinoma

201
Q

What is benigh nodular hyperplasia of the prostate (BPH)?

A

Irregular proliferation of both glandular and stromal prostatic tissue

202
Q

How common in BPH?

A

At least 75% of men >70 are affected but only 5% are symptomatic

203
Q

What can cause BPH?

A

Hormonal imbalance
Alteration of the androgen/oestrogen ratio
Central (peri-urethral) gland is involved (oestrogen responsive)

204
Q

What can cause BPH?

A

Hormonal imbalance
Alteration of the androgen/oestrogen ratio
Central (peri-urethral) gland is involved (oestrogen responsive)

205
Q

How can BPH affect the bladder sphincter mechanism

A

Physical obstruction

Physiological interference - peri-urethral glands at the internal urethral meatus

206
Q

What does prostatism cause?

A

Difficulty in starting micturition
Poor stream
Overflow incontinence

207
Q

What are the complications of acute or chronic urinary retention?

A

Bladder hypertrophy
Diverticulum formation
If untrated may lead to hydroureter, hydronephrosis or infection

208
Q

How is BPH managed?

A

Surgery (transurethral resection)

Drugs (alpha-blockers, 5-alpha-reductase inhibitors)

209
Q

How prevalent is prostate carcinoma?

A

Common
Responsible for 11% of cancer deaths in males
Peak incidence = 60-80

210
Q

Where does prostate cancer originate from?

A

Periphera; ducts and glands esp. in the posteior lobe

Peri-urethral zone may become involved at a later stage

211
Q

How does prostate carcinoma spread?

A

Local - urethral obstruction, capsular penetration, seminal vesicles, bladder, rectum
Lymphatic - sacral, iliac, para-aortic nodes
Blood - bone, osteosclerotic mets lungs, liver

212
Q

How does prostate carcinoma spread?

A

Local - urethral obstruction, capsular penetration, seminal vesicles, bladder, rectum
Lymphatic - sacral, iliac, para-aortic nodes
Blood - bone, osteosclerotic mets lungs, liver

213
Q

How is prostate carcinoma diagnosed?

A

RP exam
Imaging - US, x-rays, DEXA
Biochem - PSA
Biopsy - 8-12 needle biopsies from US-guided trans-urethral resection

214
Q

How is prostate carcinoma managed?

A

Hormonal therapy - anti-androgens. Oestrogens, cyproterone
Radiotherapy - for bone mets
Surgery - radical prostatectomy

215
Q

How common are testicular tumours?

A

Relatively uncommon although incidence is rising

1% of all cancer deaths - commonest solid organ malignancy in young adult males

216
Q

What is the usual clinical picture for testicular carcinoma?

A

Painless testicular enlargement

May be associated with hydrocele, gynaecomastia or other common malignancy symptoms

217
Q

What is a major risk of developing testicular tumours?

A

Undescended testes

218
Q

What are the different types of testicular tumours?

A

Germ Cell Tumours (90%) - Seminoma, teratoma, mixed
Others - Lymphoma, leukaemia, stromal tumours, mets
Paratesticular tumours - adenomatoid tumour, sarcomas

219
Q

What are the different types of testicular tumours?

A

Germ Cell Tumours (90%) - Seminoma, teratoma, mixed
Others - Lymphoma, leukaemia, stromal tumours, mets
Paratesticular tumours - adenomatoid tumour, sarcomas

220
Q

What is a seminoma?

A

Commonest GCT (40%)
Occurs in 30-50y/o
Solid, homogenous, pale, macroscopic appearance (potato tumour)
Consists of large, clear tumour cells with variable stromal lymphocytic infiltrate

221
Q

What are the variants of seminoma?

A

Spermatocytic and anaplastic

222
Q

How can seminomas spread?

A

Lymphatic - para-aortic nodes

Blood - lungs and liver

223
Q

How are seminoma treated?

A

Radio/chemo
V. radiosensitive
>95% cure rate

224
Q

What is the peak incidence for teratoma occurrence?

225
Q

How can teratomas appear macroscopically?

A 
v variable
Solid areas
Cysts
Haemorrhage
Necrosis
226
Q

What tumour markers exist to monitor treatments of seminomas and teratomas?

A

bHCG - trophoblastic componenets
AFP - yolk-sac componenets
PLAP - seminoma

227
Q

What is the gross structure of the kidney?

A

Bean shaped organ
Encapsulated by dense collagen fibres
Has a cortex and a medulla
Medulla is divided into pyramids

228
Q

What makes up a nephron?

A

Renal corpuscle and renal tubules

229
Q

What makes up the renal corpuscle?

A

A tuft of capillaries called the glomerulus and the Bowman’s capsule

230
Q

What cell type makes up the Bowman’s capsule?

A

Simple squamous epithelium

231
Q

How does the thin limb of the loop of Henle appear histologically?

A

Simple squamous lining with nuclei protruding into the lumen

232
Q

How does the thick ascending limb of the loop of Henle appear histologically?

A

cuboidal epithelial cells with absent mitochondria

233
Q

What is the vasa recta?

A

A group of thin-walled blood vessels which dip down into the medulla from above and then climb back up to the cortex

234
Q

What cell type lines the distal convoluted tubule?

A

Simple cuboidal epithelial cells

235
Q

What cell type lines the collecting ducts?

A

Simple columnar epithelium

236
Q

What is the macula densa?

A

On the side of the DCT nearest the afferent arterioles, the DCT cells are tall, crowded together and nuclei are intensily stained. These function in sensing ion composition in the DCT

237
Q

What are juxtaglomerular cells?

A

Modified smooth muscle cells in the wall of the afferent arteriole which contain and secrete Rennin

238
Q

What is the pathway of urine flow?

A 
Produced at the renal papilla
Collected into the minor calyx
Flows into the major calyx
Renal Pelvis
Ureter
Bladder
Urethra
Exits the body
239
Q

What cells line the conducting part of the urinary tract?

A

Transitional epithelium or Urothelium

240
Q

What are the cells on the luminal surface of the urinary tract known as?

A

Umbrella cells - they are domed like umbrellas

Have a thickened and inflexible membrane

241
Q

What are the cells on the luminal surface of the urinary tract known as?

A

Umbrella cells - they are domed like umbrellas

Have a thickened and inflexible membrane

242
Q

What lies below the transitional epithelium of the urinary tract?

A

Lamina propria

2-3 layers of smooth muscle

243
Q

What is the histological structure of the proximal ureter?

A 
Internally = transitional epithelium
Middle = Thick layer of lamina propria
Externally = Thin layer of muscularis externa
244
Q

What is the histological structure of the distal ureter?

A

Like proximal ureter but lamina propria is thinner and muscularis externa is thicker

245
Q

What is the histological structure of the urinary bladder?

A

From internal to external:
Urothelium
Lamina propria
Thick layers of smooth muscle

246
Q

What is the histological structure of the female urethra?

A

3-5cm length

Transitional epithelium to a stratified squamous epithelium at its termination

247
Q

What is the histological structure of the male urethra?

A

20cm length
Prostatic urethra = 3-4cm lined by a transitional epithelium
Membranous urethra = 1cm lined by a stratified columnar epithelium
Penile urethra = 15cm lined by stratified columnar and changing to stratified squamous at its termination

248
Q

What is the histological structure of the prostate gland?

A

Tubulo-alveolar glands lined by a simple secretory columnar epithelium with a fibromuscular stroma

249
Q

How does oedema occur?

A

An imbalance between the rate of formation and rate of absorption of ISF

250
Q

What is the nephrotic syndrome?

A

A disorder of glomerular filtration which allows protein to appear in the filtrate

251
Q

How does congestive HF cause oedema?

A

Expansion of blood volume due to low CO, leading to increased venous and capillary pressures

252
Q

How does hepatic cirrhosis cause oedema?

A

Increased pressure in the hepatic portal vein, combined with decreased albumin production causes a loss of fluid into the abdo cavity

253
Q

How does hepatic cirrhosis cause oedema?

A

Increased pressure in the hepatic portal vein, combined with decreased albumin production causes a loss of fluid into the abdo cavity

254
Q

What drug blocks the Na+/H+ exchange which occurs in the PCT?

A

Carbonic Anhyrase inhibitors

255
Q

What drug blocks the Na+/K+/2cl- co-transport in the ascending loop of Henle?

A

Loop diuretics

256
Q

What drug blocks Na+/Cl- co-transport in the DCT?

A

Thiazide diuretics

257
Q

What drug blocks the Na+/K+ exchange in the collecting tubule?

A

Potassium sparing diuretics

258
Q

What is the site of action for many diuretics?

A

Apical membrane of tubular cells

259
Q

What 2 transport systems exist for allowing drugs enter the filtrate to access the apical membrane of tubular cells?

A

Organic Anion Transporters (OATS)

Organic Cation transporters (OCTs)

260
Q

What type of drugs to OATs transport?

A

Acidic drugs e.g. thiazide and loop agents

261
Q

What type of drugs do OCTs transport?

A

Basic drugs e.g. triamterene and amiloride

262
Q

How do OATS work to allow acidic drugs to access the apical membrane of tubular cells?

263
Q

How do OATS work to allow acidic drugs to access the apical membrane of tubular cells?

A

At the basolateral membrane, organic anions enter a cell by either diffusion or in exchange for alpha-ketogluarate via the OATS.
At the apical membrane organic anions enter the lumen via either MRP2 or OAT4.

264
Q

How do OCTS work to allow acidic drugs to access the apical membrane of tubular cells?

A

At the basolateral membrane, organic cations enter the cell either by diffusion, or OCT
At the apical membrane, organic cations enter the lumen via either MDRP1 or OC+/H+ antiporters

x 2nd Year Medicine (10 decks)

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