Urinary Flashcards

0
Q

What other function does the urinary system have?

A

To excrete waste products

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1
Q

What is the main function of the urinary system?

A

Control the concentration of the ECF

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2
Q

How much water on average does a 70kg person contain?

A

40l:
25l intra cellular fluid
15l ECF: 12l interstitial, 3l plasma, lymph

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3
Q

What can a failure to control ECF result in?

A

Raised bp, tissue fluid and function

Cell shrinks or swells

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4
Q

What are the main functions of the kidney?

A

Control pH
Volume
Osmolarity
Excrete waste products

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5
Q

How many litres a day of urine do we excrete?

A

~1.5l

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6
Q

How much ECF does the kidney filter each day?

A

180l/day (refilters)

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7
Q

How much blood flow does the kidney require?

How much of the CO is this?

A

4ml/g/min

25%

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8
Q

Describe the anatomy of the kidneys

A
150g each
Retroperitoneal 
T11-T13
Right is lower due to the liver
Ribs 11th and 12th
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9
Q

Name the structures of the kidney

A
Papilla (nipple) 
Medulla - inner
Cortex - outer
Minor calyx
Major calyx 
Pelvic bladder
Renal pyramid
Renal column
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10
Q

Name the 3 outside layers of the kidney

A

Fascia
Fat
Fibrous capsule

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11
Q

Name some of the blood vessels and picture where they lay in the kidney

A
Segmental arteries and veins 
Interlobular artery and vein 
Interlobular arteries and veins 
Arcuate arteries and veins 
Renal artery and renal vein
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12
Q

What is the place where things go in and out of the kidney called and in what order?

A

Renal hilum
Vein
Artery
Ureter

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13
Q

What is the functional unit of the kidney?

A

Nephron

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14
Q

Where does most of filtration take place?

A

Glomerulus

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15
Q

What maintains the filtration pressure?

A

Afferent and efferent arterioles

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16
Q

What is the glomerular filtration rate?

A

180l/day

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17
Q

Where is the major site of reabsorption?

A

Proximal convoluted tubule

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18
Q

What specialisation does the epithelial cells have for reabsorption?

A

Polarised

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19
Q

What is the main role of the loop of henle?

A

Create a gradient of increasing osmolarity in the medulla by counter current multiplication which allows concentrated urine if water is to be preserved

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20
Q

What function does the distal convoluted tubule perform?

A

Variable reabsorption of electrolytes and water

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21
Q

Where is the collecting duct and what is its function?

A

Medulla

Produces either a high or low amount of concentration in the urine

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22
Q

What is sodium recovery controlled by?

A

Renin angiotensin system

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23
Q

What is water recovery controlled by?

A

Anti duiretic hormone

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24
Q

Where is the IVC and aorta?

A

IVC right
Aorta left
So left renal vein longer - important for transplant
Right renal artery is longer

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25
Q

Where does the IVC lie between?

A

Superior mesenteric artery and the aorta - can be compressed in an aneurysm

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26
Q

What are the 3 construction points of the ureter?

A

Junction at the renal pelvis
Where the common iliac divides into internal and external/pelvic birth
Where it pierces the bladder wall

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27
Q

What is the significance of the construction points of the ureter?

A

Stones can get trapped here as it narrows

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28
Q

What is renal colic?

A

Smooth muscle spasms at afferents to T11 and L2 presenting with flanx, loin and groin pain

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29
Q

What is the anatomical position of the bladder?

A

Rises into greater pelvis as it fills

On the pubic symphysis

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30
Q

What is the anatomical position if the prostate gland?

A

Wraps around the male urethra at the neck of the bladder

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31
Q

What are the 4 sections of the male urethra?

A

Pre prostatic - passes through neck of bladder surrounded by internal urethral spinchter
Prostatic - descends through anterior prostate
Membranous - passes through perineal pouch
Spongy - courses through corpus spongiosum in the penis

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32
Q

How long is the male urethra?

A

18-22cm

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33
Q

How long is the female urethra and what is the significance of this?

A

4cm

More prone to uti

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34
Q

For a respiratory problem, what are the changes?

A

Co2

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35
Q

For a metabollic problem, what are the changes with?

A

HCO3-

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36
Q

What if both metabollic and respiratory has changed?

A

Then you would need some form of compensation

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37
Q

If the pH is normal, what process has occurred after change?

A

Compensation

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38
Q

If the pH is abnormal, what changes have occurred?

A

Partial compensation

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39
Q

What is the normal pH in a healthy person?

A

7.38-7.42

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40
Q

Why is alkalaemia more dangerous than acidaemia?

A

Calcium concentration is affected causing tetany

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41
Q

What changes occur with acidaemia?

A

Increased potassium

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42
Q

What pHs are life threatening?

A

7.55

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43
Q

What does plasma pH depend on?

A

The 20:1 ratio of bicarbonate and carbon dioxide
Determined by respiration
Controlled by chemoreceptors
HCO3- is controlled by the kidneys

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44
Q

What occurs with respiratory acidaemia?

A

Hyperventillation

Hypercapnia

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45
Q

What occurs with respiratory alkalaemia?

A

Hypoventillation

Hypocapnia

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46
Q

What detects the changes in pCO2?

A

Central medulla chemoreceptors

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47
Q

What is correction?

A

When you change the disturbances in pH and the cause is corrected for so pH is normal

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48
Q

What is compensation?

A

When the pH has changed due to a cause, the pH is compensated back to normal but the cause is not removed

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49
Q

How can pCO2 (resp) changes be compensated for (get pH back to normal)?

A

Altering the HCO3- in the kidneys

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50
Q

How is respiratory acidaemia compensated for?

A

Kidneys increase HCO3- reabsorption

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51
Q

How is respiratory alkalaemia compensated for?

A

Kidneys decrease HCO3- reabsorption

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52
Q

What is metabollic acidosis?

A

When too much acid is produced and there is a fall in HCO3- which decreases the pH

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53
Q

How is metabollic acidosis compensated for?

A

Increase ventilation which means more carbon dioxide is expelled and the pH is restored

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54
Q

What is metabolic alkalosis?

A

Plasma HCO3- rises too much

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55
Q

How is metabolic alkalosis compensated for?

A

An increase in ventilation

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56
Q

What is the problem when compensating for metabolic alkalosis?

A

You cannot increase ventilation too much or the decrease in oxygen will be far too low - therefore it can only be partially compensated for

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57
Q

Why do you get metabolic alkalosis?

A

Persistent vomiting which leads to a loss of too much acid

You need to treat the dehydration and then the alkalosis will correct itself

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58
Q

How much HCO3- is filtered every day?

A

4500mmol

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59
Q

Is 4500mmol enough HCO3-?

A

No, the body has to make more by reacting with co2 and water
OR
amino acid breakdown into ammonia plus a hydrogen ion to make ammonium so the ureters and urethras are not damaged.

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60
Q

Where is HCO3- recovered in the kidney?

A

80-90% in PCT

Remainder in TAL

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61
Q

Where is HCO3- made in the kidney?

A

Distal tubule

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62
Q

What is the minimum urine pH?

A

4.5 mmol of H+

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63
Q

How much H+ do we excrete every day?

A

50-100 mmol

Controlled by HCO3- concentration

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64
Q

What is the anion gap?

A

(Na+k) - (Cl - HCO3)

The gap is usually 10-15 mmol but changes can be accounted for if different acids have replaced HCO3-

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65
Q

Give examples of other metabollic acids created that displace HCO3-

A

Lactic acid

Ketone bodies

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66
Q

What K+ condition is associated with metabolic acidosis?

A

Hyperkalaemia

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67
Q

What K+ condition is associated with metabolic alkalosis?

A

Hypokalaemia

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68
Q

Where is most of the potassium in the body and how much?

A

ICF 98% ~ 120-150mmol

ECF 2% ~ 3-3.5mmol

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69
Q

Where is the resting membrane potential?

A

90 mmol - due to potassium
Increase in K+ depolarises membrane
Decrease in K+ hyper polarises the membrane

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70
Q

What 2 processes keep potassium regulated?

A

Internal balance

External balance

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71
Q

Explain external balance

A
The kidneys balance the k+
5-10% is lost in the GI tract 
It takes 6-12 hours to excrete a load of K+ 
LONG TERM 
TOTAL BODY K+ content
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72
Q

Explain internal balance

A

Regulates k+ in the ECF
Immediate
If ECF K+ increases - K+ moves into cells
If ECF K+ decreases - K+ moves out of cells

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73
Q

How much of ingested K+ moves into cells within minutes?

How long does excretion take?

A

4/5

6-12 hours

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74
Q

What factors promote K+ intake into cells?

A

Hormones - insulin, aldosterone, catecholamines
Alkalosis
Acidosis

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75
Q

How does insulin increase uptake of K+?

A

K+ in splanchnic blood stimulates insulin secretion from pancreas and this stimulates K+ uptake into liver and muscle cells via a Na-K-ATPase pump

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76
Q

How does aldosterone increase K+ uptake into cells?

A

K+ in bold stimulates aldosterone release which stimulates K+ uptake into cells via Na-K-ATPase

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77
Q

How do catecholamines increase K+ uptake?

A

Acts via beta 2 adrenoreceptors which in turn stimulate Na-K-ATPase

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78
Q

What promotes K+ out of cells?

A
Low ECF concentration 
Exercise (produces K+ but immediately put into cells and then exercise releases catecholamines, stopping exercise leads to low K+) 
Cell lysis 
Increase in ECF osmolatity
Acidosis to balance charges
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79
Q

Give some conditions that can give rise to hyperkalaemia

A

Addison’s disease
Diabetic ketoacidosis
Kidney failure
ACE inhibitors

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80
Q

Give some conditions that give rise to hypokalaemia

A

Cushings disease
Increased RAAS
Glucose and insulin

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81
Q

Define hyperkalaemia

A

Increase in K+ above 5mmol/L

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82
Q

Why do you get hyperkalaemia?

A

Kidney failure
Metabolic acidosis
Reduced aldosterone
Cell lysis

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83
Q

What effects do hyperkalaemia cause?

A
Bradycardia
Heart block
Arrhythmia 
Smooth gut in GI paralysed 
Acidosis
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84
Q

What changes would you see in an ECG of someone with hyperkalaemia?

A

Widened QRS
Absent p wave
Prolonged PR interval
VF

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85
Q

What emergency treatment would you give for hyperkalaemia?

A

Calcium gluconate to reduce K+ effect on heart
Glucose, insulin
Salbutamol
Dialysis

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86
Q

What long term treatment would you use for hyperkalaemia?

A

Treat cause
Reduce intake
Dialysis
Oral K+ binding resins

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87
Q

Define hypokalaemia

A

K+ concentration of <3.5 mmol/L

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88
Q

Give some common causes of hypokalaemia

A
Vomiting 
Diarrhoea 
Kidney diuretic drugs
High aldosterone 
Metabollic alkalosis
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89
Q

Give some effects of hypokalaemia

A
Increased excitability of the heart 
Arrhythmia 
Smooth muscle paralysis 
Muscle weakness 
Diabetes insipidus
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90
Q

What would you expect to see on an ECG for hypokalaemia?

A

U wave
T wave flatter
Further from QRS complex

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91
Q

How would you treat hypokalaemia?

A

Cause

IV K+(BE CAREFUL)

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92
Q

When does plasma osmolarity increase?

A

If water intake is less than excretion

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93
Q

When does plasma osmolarity decrease?

A

If water intake is more than water excretion

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94
Q

On average, how much urine does someone excrete every day?

A

1-1.5l/day

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95
Q

What do disorders of water balance manifest as?

A

Changes in body fluid osmolarity

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96
Q

What do disorders of sodium balance manifest as?

A

Changes in body volume

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97
Q

What are changes in plasma osmolarity detected by?

A

OVLT in the hypothalamus
Anterior and ventral to the third ventricle
Fenestrated epithelium

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98
Q

What two pathways maintain osmolarity?

A

Thirst and ADH

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99
Q

Describe the role of ADH

A

If plasma osmolarity increases by 1% then OVLT cause release of ADH from posterior pituitary
This causes low volumes of concentrated urine to be produced
Affects water and urea reabsorption

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100
Q

What changes does ADH make in the collecting duct?

A

Addition of aquaporin 2 channels which increase water absorption
When body is normal, aquaporin 2 is removed via endocytosis

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101
Q

How does the ADH effect on urea cause body osmolarity to decrease?

A

I’m dehydration, urea is reabsorped as it acts as an osmole so water will follow it

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102
Q

Explain/draw the counter current multiplication system

A

At the bottom of the loop of Henle the concentration is high. Above this descends in concentration the higher you get on both sides. Na Cl is pumped out of the ascending loop and is impermeable to water. Water is pumped out of the descending loop causing an increase in conc the further you of down the loop of Henle. This is maintained by vasa recta which move in the opposite direction.

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103
Q

Name some functions of calcium

A

Nerve conduction
Muscle contraction
Hormone and enzyme release
Exocytosis

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104
Q

How much free calcium do we have in our body?

A

1-1.3 mmol/L

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105
Q

What is the total calcium range in plasma?

A

2.1-2.6mmol/L

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106
Q

What 3 forms does calcium exist as in the plasma and in what proportions?

A

Free ionised - 45%
Bound to albumin - 45%
Caught up in phosphates etc - 10%

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107
Q

How much calcium is in our whole body? How does it exist?

A

25-30mol but 99% is in skeleton

0.1% in ECF

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108
Q

Discuss the handling of calcium in the intestines

A

Calcium is absorbed in the intestines by the help of calcitriol binding

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109
Q

Discuss renal handling of calcium

A

Filter 250mmol per day
98-99% is reabsorbed
Calcium excretion <10mmol per day

65% reabsorped in PCT
20-25% in loop of Henle
10% in the DCT by control of PTH

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110
Q

What do you give patients if they need to lose calcium?

A

NaCl

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111
Q

Where do patients with calcium deficiency get their calcium from and what problems can this cause?

A

Bone

Brittle bones

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4
5
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112
Q

How much vitamin D does a healthy adult need a day?

A

800-1000units

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113
Q

Why do you get vitamin D deficiency?

A
Lack of sunlight 
Pigmentation 
Breast feeding 
Multiple pregnancies 
Vegetarians
Anorexia
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114
Q

What are the actions of 1,25(OH)2D?

A

Increases calcium and phosphate availability in intestines
Promotes osteoblasts
Promotes active form
Synthesis of renal-1-alpha-hydroxylase

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115
Q

What are the actions of PTH?

A

Calciferol to calcitriol
Aids bone remodelling
Increases plasma calcium and phosphate plasma conc
Increases calcium reabsorption
Decreases phosphate and HCO3- reabsorption
Increase ca release from bone

116
Q

How is PTH controlled?

A

Negative feedback of calcium levels

117
Q

What are the causes of hypercalcaemia?

A

Primary Hyperparathyroidism
Haematological malignancy- due to action of PTHrp
Non haematological malignancy - “

118
Q

What are the symptoms of hypercalcaemia?

A

Nausea and vomitting/depression/lethargy/decreased cognitive abilities/constipation/anorexia/pancreatitis/polyurea and polydypsia/hypertension

119
Q

What is classed as a high calcium and what kind of importance is it?

A

> 3.5 mmol/L

Medical emergency

120
Q

How do you manage hypercalcaemia?

A
Bisphosphonates
Calcitonin
Hydration 
Loop duiretics 
Treat underlying condition
121
Q

Name the 3 types of Hyperparathyroidism

A

Primary - renal plasma calcium
Secondary - low or normal plasma calcium
Tertiary - raised plasma calcium

122
Q

Discuss calcium stone formation

A

Due to increased levels of calcium in the urine
Low urine volume
Low urine pH (<5.47)

123
Q

How do you diagnose renal stone formation?

A

History
Urine
Blood screen
Radiograph

124
Q

How do you manage renal stone formation?

A

Increasing fluid intake, reducing dietary calcium, dietary restriction of calcium and animal protein

125
Q

What controls the short term measure of blood pressure?

A

Baroreceptors in the carotid sinus and arch of aorta - they detect the stretching of the vessels and send a signal to the medulla

126
Q

What controls the medium and long term blood pressure?

A

RAAS
ANP
ADH
Sympathetic nervous system

127
Q

Explain the RAAS

A
Renin converts angiotensinogen to angiotensin I
Ace converts angiotensin I to angiotensin II 
causes: release of aldosterone 
Sympathetic stimulation 
Vasoconstriction 
ADH release
Na reabsorption 
Noradrenaline release
128
Q

What is the function of aldosterone?

A

Acts on principle cells of the collecting duct to activate ENaC and apical K+ channels
Increases Na extrusion via Na-K-ATPaae

129
Q

What is the adverse effect of ace inhibitors?

A

Breaks down bradykinin into peptides

130
Q

What does the sympathetic nervous system do in enters of blood pressure?

A

Vasoconstriction
Decreases renal blood flow and therefore decreases GFR and Na excretion
Stimulates renin
Activates Na-K-ATPase

131
Q

What does ADH do in terms of blood pressure?

A

Forms concentrated urine

Acts on thick ascending limb to stimulate NaKCC2 transporter and increase urea absorption

132
Q

What does ANP do?

A
Promotes sodium excretion 
Released by atrial myocytes in response to stretching 
Vasodilation 
Increase blood flow
Decrease sodium reabsorption
133
Q

What is the function of prostaglandins?

A

Decrease sodium reabsorption
Enhance GFR
Vasodilators

134
Q

What is the adverse effect of NSAID’s?

A

Inhibit prostaglandins

135
Q

What is hypertension?

A

Blood pressure over 140/90 mmHg

136
Q

What are the 2 forms of hypertension?

A

Essential hypertension which has an unknown cause and is 95% of cases
Secondary hypertension where there is a known cause

137
Q

Name some causes of secondary hypertension

A
Conns syndrome 
Cushings disease
Pheochromocytoma 
Renal vascular disease 
Aldosteronism
138
Q

What are some outcomes of hypertension?

A
MI
Stroke
Aneurysm 
Renal failure 
Retinopathy 
Heart failure
139
Q

How do you treat hypertension?

A
ACE inhibitors 
Diuretics
Vasodilators 
Beta blockers
Diet
Exercise 
Stop smoking and drinking 
Decrease salt intake
140
Q

Define isosmotic

A

Same concentration as plasma

141
Q

Define hyposmotic

A

Lower concentration than plasma

142
Q

Define hyper osmotic

A

Higher concentration than the plasma

143
Q

What happens with auto regulation when you increase BP?

A

Afferent arteriole constriction - adenosine released

144
Q

What happens with auto regulation when you decrease blood pressure?

A

Afferent arteriole dilation - prostaglandins released

145
Q

Describe the common organisms that cause UTI

A
Enterococci faecalis
E. coli
Coliforms
Proteus spp
Coag negative staphs
146
Q

Which of the bacteria is common in hospital UTI?

A

Coagulase negative staphylococcus

147
Q

What would you do for an uncomplicated UTI?

A

Urine dipstick test

See for nitrates, leukocyte esterase, blood, proteins

148
Q

Who is likely to get an uncomplicated UTI?

A

Young, healthy women with no abnormalities

149
Q

Who is likely to get a complicated UTI?

A

Pregnant, males, young children, elderly patients, catheterised, urinary tract abnormalities, poly nephritis,

150
Q

Do you need to culture the urine with an uncomplicated UTI?

A

No

151
Q

What sample collection method would you use for a complicated UTI? (Adults, children, catheterised, supra pubic)

A

Mid stream specimen for adults
Adhesive bag over genitals for children
Catheter samples taken with a needle in the catheter tube for catheterised patients
Supra pubic aspiration

152
Q

How are urine samples stored/transported?

A

4 degrees

Boric acid

153
Q

What is the purpose of boric acid?

A

It stops the division of bacteria to keep the sample representative of collection time

154
Q

What investigations are you to do with a urine sample?

A
Look for turbidity (cloudiness)
Look for leukocyte esterase
Look for nitrates
Look for proteins
Look for blood
155
Q

What does screening of urine in labs detect?

A

Blood
Bacteria
WBC
Casts

156
Q

Why do we culture urine?

A

To investigate children, males and complicated infections

157
Q

How predictive is a single urine specimen?

A

80% predictive

158
Q

How can you interpret the culture of urine collected?

A
Qualify 
Delays in culture
Organisms
Microscopy
Symptoms
Previous antibiotics
159
Q

What is sterile pyuria?

A

When a UTI is present however unable to identify and culture an organism

160
Q

What are the causes of sterile pyuria?

A
Previous antibiotics
Chlaymdia, gonorrhoea, tb 
Appendicitis 
Chemical inflammation
Vaginal inflammation
161
Q

What percentage of women actually have a UTI?

A

50% significant bacteria

50% urethral syndrome

162
Q

What are the non antibiotic treatments of a UTI?

A

Increase fluid intake

Address underlying disorders

163
Q

For an uncomplicated UTI, what antibiotics would you recommend and for how long?

A

3 day course

Nitrofurantoin or trimethoprim

164
Q

What antibiotics are not effective with UTI?

A

Amoxicillin

165
Q

What antibiotics would you use for a complicated UTI and for how long?

A
5-7 days
Cephalexin
Nitrofuratoin
Trimethoprim 
Ciprofloxacin
166
Q

What antibiotics would you use for poly nephritis?

A

14 days

Co amoxilav, ciprofloxacin, gentamicin IV

167
Q

When is prophylaxis appropriate?

A

3 or more episodes of UTI in one year
No treatable or underlying condition
Single, low, nightly dose of antibiotics
Trimethoprim or nitrofurantoin used

168
Q

What is the problem with diagnosing UTI with catheters?

A

No indication of pain passing urine or frequency

169
Q

What percentage of GP consultations do urine infection take up?

A

1-3%

170
Q

What are the host factors that make them susceptible to infection?

A

Short urethra
Valve incomplete
Incomplete bladder emptying, residual urine
Obstruction from stones, tumour, pregnancy, prostate

171
Q

What bacterial factors can lead to an increased susceptibility to infection?

A

K antigens - polysaccharide capsule produced all
Adhesion - fimbriae and adhesins allow attachment to epithelia
Haemolysin - damage membranes
Urease - breaks down urea
Faecal flora - gets into the urinary tract

172
Q

Define diuresis

A

Diuresis is the increased urine production

173
Q

What is a diuretic?

A

A drug that increases urine production

174
Q

Name some diseases causing diuresis

A

Diabetes mellitus because glucose acts as an osmole
Cranial diabetes insipidus as it inhibits ADH release
Nephrogenic diabetes insipidus inhibits ADH effect on collecting ducts
Psychogenic polydypsia increase thrist secondary effect

175
Q

Name some substances that can cause diuresis other than diuretic drugs

A

Alcohol as it inhibits ADH release
Coffee as it increases GFR and decreases Na absorption
Demeclyocycline and lithium inhibit ADH release on collecting ducts

176
Q

What are diuretics used to treat?

A
Congestive heart failure
Nephrotic syndrome
Cirrhosis and liver disease
Hypercalcaemia
Glaucoma
Kidney failure 
Hypertension
Pulmonary oedema
Cerebral oedema
177
Q

Explain oedema formation in congestive heart failure

A

Decrease in venous systemic pressure leads to oedema
OR
deceased CO, RAAS, sodium and water retention, ECF expansion and oedema

178
Q

Explain oedema formation in nephrotic syndrome

A

Low plasma albumin, decreased oncotic pressure, oedema, reduced circulatory volume, RAS activated, water and sodium retention

179
Q

Explain oedema formation in cirrhosis of the liver

A

Low plasma albumin, decreased oncotic pressure, oedema, reduced circulatory volume, RAS activated, water and sodium retention

180
Q

Where do loop duiretics act?

A

Loop of Henle

181
Q

What is the mechanism of loop duiretics?

A

Inhibits Na-K-2Cl
More sodium retained and potassium is lost in urine
Causes hypokalaemia

182
Q

What are loop diuretics used for?

A

Heart failure
Hypercalcaemia as it inhibits ca reabsorption
Acute pulmonary oedema
Nephrotic syndrome

183
Q

Name 2 examples of loop diuretics

A

Furosemide

Bumetanide

184
Q

Where do thiazide diuretics act?

A

DCT

185
Q

What do thiazide diuretics do?

A

They inhibit Na Cl symporter
Increase calcium absorption
Decrease k absorption

186
Q

When are thiazide diuretics ineffective?

A

Renal failure

187
Q

How much sodium is inhibited with thiazide diuretics?

A

5%

188
Q

How much sodium is inhibited with loop diuretics?

A

25%

189
Q

What are thiazide diuretics used for?

A

Hypertension

Hypercalcaemia

190
Q

What is a side effect of thiazide diuretics?

A

Erectile dysfunction
Gout
Glucose intolerance
Hyperlipidaemias

191
Q

Name 2 examples of diuretics

A

Metalazone

Bendroflumethiazone

192
Q

Give 2 examples of K+ sparing diuretics

A

Amiloride

Triamtrene

193
Q

Where does amiloride act?

A

Collecting ducts

194
Q

How does amiloride function?

A

Inhibits ENaC
Decreases the Na channel
Causes hyperkalaemia as there is a decrease in K+ in the urine because more positive charge from sodium is lost

195
Q

How do aldosterone antagonists act?

A

They block aldosterone by competitively inhibiting it

Which blocks am reabsorption

196
Q

What are aldosterone antagonists used to treat?

A

Best treatment for hypertension
Ascites and cirrhosis because it doesn’t cause hypokalaemia
Used in heart failure with loop diuretics

197
Q

How is hyperkalaemia caused with diuretics?

A

Block aldosterone -decreases Na absorption- K+ is kept in the cell

198
Q

How can you minimise changes in K+ with diuretics?

A

Give a loop and thiazide with a k+ sparing or aldosterone antagonist

199
Q

What 2 diuretics are not used?

A

Carbonic anhydrase inhibitors

Osmotic diuretics

200
Q

How do osmotic diuretics work?

A

Act as an osmole

201
Q

What are osmotic diuretics used to treat?

A

Cerebral oedema

202
Q

What are carbonic anhydrase inhibitors used to treat?

A

Glaucoma

203
Q

Where do carbonic anhydrase inhibitors act?

A

PCT

Interferes with Na and HCO3- reabsorption.

204
Q

What can carbonic anhydrase inhibitors cause?

A

Metabolic acidosis

205
Q

Name a carbonic anhydrase inhibitor

A

Acetazolamide

206
Q

Name an osmotic diuresis

A

Mannitol

207
Q

Give an example of an aldosterone antagonist

A

Spironolactone

208
Q

Describe the anatomy of the detrusor muscle

A

Inner longitudinal, middle circular, outer longitudinal
Gives bladder strength to stretch
Rugae on inner folds to stretch

209
Q

Describe the anatomy of the internal ureteral spinchter

A

Continuation of the detrusor
Smooth muscle
Physiological spinchter

210
Q

Describe the anatomy of the external urethral spinchter

A

Anatomical spinchter
Derived from pelvic floor muscles
Skeletal muscle
Somatic

211
Q

What is the innervation of the detrusor muscle?

A

S2-S4 parasympathetic pelvic nerve
Stimulated by Ach acting on M3

T10-L2 hypogastric nerve
Sympathetic
B3 receptors

212
Q

What is the innervation of the internal urethral spinchter?

A

T10-L2 hypo gastric nerve
Sympathetic
Alpha 1 receptors
Sympathetic - relaxation

213
Q

What is the innervation of ge external urethral spinchter?

A

Pudendal nerve
S2-S4
Acts on nicotinic receptors to cause contraction

214
Q

What is the parasympathetic system responsible for in terms of micturation?

A

Peeing
Contraction of detrusor
Relaxing of internal spinchter

215
Q

What is the sympathetic system responsible for in terms of micturation?

A

Storage of urine
Relaxing detrusor
Contracting internal spinchter

216
Q

Describe voiding of urine

A

Relaxation of bladder allows for storage of urine
At about 500ml, temp and pain signals tell the brain voiding is necessary and also stretch receptors
Contraction of detrusor, relaxation of both spinchters, passage of urine
In males the bulbospongiosus muscle expels the last few drops of urine

217
Q

Does the pressure increase when bladder is full?

A

No, bladder is relaxed and contraction of spinchters also help to reduce the pressure

218
Q

What occurs when you need to store urine?

A

Bladder relaxes
Spinchter contracts
Bladder expands
Prevention of urine passing

219
Q

Define stress urinary incontinence

A

This is when you leak urine when you cough or sneeze for example

220
Q

Define urge urinary incontinence

A

This is leakage associated with urgency to urinate

221
Q

Define mixed urinary incontinence

A

This is when a combination of involuntary leakage on urge and exertion such as sneezing or coughing causes leakage

222
Q

Define overflow urinary incontinence

A

When the bladder is full there is leakage

223
Q

Describe the prevalence of urinary incontinence with age

A

Increases

224
Q

Describe the risk factors associated with urinary incontinence

A
Pregnancy
Obesity
Drugs
UTI
Familial
Pelvic prolapse
225
Q

Describe the investigation of urinary in continence

A
Record amount of fluid they pass for 2 or 3 days
Number of pads patient wears 
Pad test
Urine dipstick 
Cystoscopy
226
Q

Describe the examination of a patient with suspected incontinence

A

Height weight
Abdo exam
Digital rectal exam for males
Vaginal exam or external gentitalial exam for women

227
Q

Explain how you would manage a patient with incontinence

A
Modify lifestyle - weight loss, fixed schedule, decrease caffeine
Catheter
Sheath device
Pads 
Bladder training
Pelvic floor training
228
Q

Describe the pharmaceutical management of incontinence

A

Duloxetine - only last resort - increases contraction of external urethral spinchter
Anticholinergics - act on m3 receptors to stop contraction of detrusor
Botulinum toxin - inhibits Ach, prevents detrusor contraction

229
Q

Describe the surgical management of incontinence in women

A

Low tension vaginal tapes (not suitable for goes who want babies)
Correcting anatomical position of urethra
Sling
Intramural bulking agents such as collagen - for those who want babies

231
Q

Describe the surgical management of incontinence in men

A

Artificial spinchter

Male sling

232
Q

How much of the cardiac output does the kidney recieve?

A

25%

233
Q

What is the definition of AKI?

A

A decline in GFR that occurs during a period of less than 2 weeks

234
Q

How is AKI measured?

A

By an increase in serum creatinine

235
Q

Define oligouria

A

A decrease in urine production <500ml a day

236
Q

Define anuria

A

No urine production, <100ml a day

237
Q

Define uraemia

A

The clinical signs and symptoms of kidney failure leading to a lack of secretory and excretory function

238
Q

Define azotaemia

A

An increase in urea in the blood

239
Q

What are the 3 causes of AKI?

A

Pre-renal
Post-renal
Intrinsic

240
Q

What is pre-renal AKI?

A

This is due to reduction in perfusion
60% of all AKI
Kidney unable to maintain bloodflow
REVERSIBLE as injury has not yet occurred

241
Q

What is post-renal AKI?

A

This is due to an obstruction such as an enlarged prostate, stones, or at the bladder

242
Q

What is intrinsic kidney disease?

A

This is damage to the interstitial kidney/glomerulus/tubules

243
Q

What treatment is there available for AKI?

A

Volume correction for pre-renal
Urological intervention for post-renal
Supportive treatment
Dialysis

244
Q

Define haematuria

A

Bleeding into the urinary tract from anywhere between the glomerulus to the urethra

245
Q

Define nephrological haematuria

A

Glomerular inflammation and bleeding

glomerulonephritis

246
Q

Define urological haematuria

A

Renal stones, RCC, TCC

247
Q

Define glomerulonephritis

A

Renal disease characterised by inflammation of the glomeruli or small blood vessels in the kidney
Can present with haematuria/proteinurea

248
Q

Define nephrotic syndrome

A

Protein over 3.5g/day in the urine

249
Q

Define nephritic syndrome

A
Haematuria
Proteinurea
Renal impairment
Salt and water retention
Hypertension
250
Q

What are some glomerulonephritis giving haematuria?

A

IgA neuropathy
Mesangiocapillary glomerulonephritis
Post streptococcal glomerulonephritis

251
Q

What are some systemic diseases causing glomerulonephritis?

A

SLE
Bacterial endocarditis
Vasculitis
Anti GBM disease

252
Q

What are some investigations of haematuria?

A
Urine microscopy
Assessment of renal function
Qualification of 24 hour protein excretion
Immunological tests
Renal imaging
<45 then a renal biopsy
253
Q

What are the investigations of proteinurea?

A
Assessment of renal function
Blood sugar/serum albumin/serum cholesterol 
Immunological tests
Renal Imaging
Urine:Creatinine ratio
254
Q

What is minimal change glomerulonephritis?

A

Need an electron microscope to see damage, will show epithelial cell foot process effacement
Light microscopy normal

255
Q

What is membranous glomerulonephritis?

A

Increase in thickness of BM with sub epithelial depositation of electron dense deposits on electron microscopy
Gives silver spikes stain on microscopy
Little proliferation but mesangial sclerosis may occur in advanced cases
All glomeruli involved

256
Q

What is focal segmental glomerularsclerosis?

A

Sclerosis of some glomeruli

In early cases mostly juxtamedullary glomeruli involved

257
Q

How does oedema occur in glomerular disease?

A

Hydrostatic pressure causes fluid to move into the interstitium
At the distal end fluid moves back in due to oncotic pressure
Proteinurea lowers oncotic pressure by lowering serum albumin so fluid does not reenter. Also activates RAAS

258
Q

What is nephritic syndrome?

A

A collection of signs associated with disorders affecting the kidneys, characterised by having pores in the basement membrane large enough to permit proteins and red blood cells

259
Q

What is rapidly progressive glomerular nephritis?

A

A clinical situation whereby glomerular injury is so severe that renal function deteriorates over days. Patient presents as a uraemic emergency

260
Q

Define chronic kidney disease

A

Irreversible and sometimes progressive loss of renal function over months to years.

261
Q

What happens in CKD?

A

Functioning renal tissue is replaced by ecf and scar tissue so sclerosis and fibrosis occurs. Excretory and hormone functions are both lost. Characterised by proteinurea and hypertension

262
Q

What do most patients die of in CKD?

A

CVS causes

263
Q

What is the classification used for CKregD?

A
5 stages
1 - GFR >90 - early
2 - GFR 60-89
3 - GFR 30-59
4 - GFR 15-29
5 - GFR <15 established renal failure
264
Q

At what stage do most patients present with CKD?

A

Stage 3 present to GP
Generally asymptomatic
85% of CKD patients are found from regisries of IHD, diabetes and hypertension

265
Q

What makes CKD develop quicker?

A

Badly controlled BP

266
Q

What are the chances of death with stages 2 3 and 4 of CKD after 5 years?

A

2 - 20%
3 - 25%
4 - 45%

267
Q

How would you investigate CKD?

A

24 hour creatinine clearance
Inulin
51CR EDTA or Iohexol

268
Q

What is the problem with measuring creatinine for CKD?

A

It can be normal when GFR is <60%

Depends upon age, sex and ethncitiy - black patients, young, males tend to have higher muscle bulk

269
Q

How can you assess CKD?

A
Cause
Diagnosis and Prognosis 
Degree of renal impairment
Imaging
Compliment/immunoglobulins/antibodies/ANCA
CRP 
SPEP/UPEP
270
Q

What are the cardiovascular complications of CKD?

A

Cardiomyopathy
Atheroscerosis
Pericarditis

271
Q

What are the causes of CKD?

A
Immunological - glomerulonephritis
Idiopathic
Genetic - alports or PKD
Infection - pyelonephritis 
Obstruction 
Systemic - myeloma/diabetes 
Vascular 
Hypertension
272
Q

What are the haematological complications of CKD? And how does it occur?

A
Anaemia 
Decreased RBC survival
Resistance to erythropoeitin 
Decreased erythropoeitin 
Blood loss
(Eryhropoeitin stimulates bone marrow for rbc production)
273
Q

What are the bone complications of CKD?

A

Renal bone disease
Decreased Vitamin D - lowers calcium - secondary hyperparathyroidism - osteomalacia
Increase in phosphate which lowers free calcium levels which causes secondary hyperparathyroidism, osteitis fibrosis cystica
Non bone calcification

274
Q

What are the CNS complications of CKD?

A

Coma
Seizures
Neuropathy

275
Q

What are the general symptoms of CKD?

A
Tired
Breathless
Nausea and vomitting 
Restess legs 
Aches and Pains 
Itching 
Chest pain
276
Q

How can you conservatively manage CKD?

A
Diet
Exercise
Stop smoking
ACE inhibitors/Angiotensin receptor blockers 
Treat diabetes
Statins
Treat blood pressure
277
Q

What does RRT (renal replacement therapy) consist of?

A

Either renal transplant or dialysis

Peritoneal dialysis or haemodialysis

278
Q

What are the indications for dialysis?

A
Uraemic symptoms
Acidosis 
Pericarditis
Fluid overload
GR <10ml/min
279
Q

What is required for haemodialysis?

A
Artificial kidney
Logistics
Purified water supply
Anti-coagulation
Vascular access 
HD machine
280
Q

What procedure do you need to perform to allow haemodialysis as often as 3 times a week?

A

Create an arterio-venous fistula between radial artery and cephalic vein so blood flows from artery to vein and the vein builds up smooth muscle, allows cannulation 3x a week as a normal vessel would not be strong enough for this.

281
Q

What are the advantages of haemodialysis?

A

High survival rate
4/7 days free of treatment
Dialysis dose is easily prescribed

282
Q

What are the disadvantages of haemodialysis?

A
Expensive
Can't travel 
CVS instability
Fluid and diet restrictions 
Can't pass urine
Access problems
283
Q

What is peritoneal dialysis?

A

This is where dialysis occurs across the peritoneal membrane and the waste products are also excreted across the peritoneal membrane. Requires peritoneal blood flow, membrane and peritoneal dialysis fluid.

284
Q

What are the advantages of peritoneal dialysis?

A
Can be done at home
Low technology
Easily learned
CVS stability
Better for elderly and diabetics possibly 
Allows mobility
285
Q

What are the disadvantages of peritoneal dialysis?

A
No long term survivors as of yet
High revenue costs 
Frequent exchanges - 4 a day roughly
Peritonitis
Treatment failures
Limited dialysis dose range
286
Q

What are the sources for kidney transplant?

A
Emotional relation
Relative
Alturistic donor 
Non-heart beating donor
Deceased donor
287
Q

Where is the kidney put in the patient?

A

Into the iliac fossa and connected via the iliac vessels and into the bladder

288
Q

What are the advantages for renal transplant?

A
Near normal renal function
High survival rate
Allows mobility 
Cheaper
Long term good results
289
Q

What are the disadvantages about renal transplantation?

A
Hard to find donors or a match
CKD still in patient 
Operation - morbidity and mortality
Life long immunosuppression 
Not all are suitable - eg malignancy