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MD3002 > Week 7 > Flashcards

Week 7 Flashcards

1
Q

What is the cause of a kidney tubercle?

A

Chronic inflammation

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2
Q

What are the 3 causes of kidney inflammation?

A
  • Infection
  • Acute Inflammation
  • Immunological
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3
Q

What are the 2 causes of kidney stones?

A
  • Genetic

- Metabolic

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4
Q

What is Potter Syndrome?

A

Bilateral renal agenesis

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5
Q

Describe glomerular disease?

A
  • Immunologically mediated

- HLA (human leukocytes antigen) association

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6
Q

Give example of primary glomerular disease?

A

Glomerulonephritis (plural= Glomerulonephritides)

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7
Q

Give 2 examples of secondary glomerular disease?

A
  • Vascular

- Autoimmune ie. amyloid, SLE, diabetes

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8
Q

Describe Type II Hypersensitivity kidney disease?

A
  • Anti-GBM antibodies
  • Complement fixation
  • Diffuse Damage
  • Fibrin leakage
  • Proliferated parietal endothelial cells
  • Focal disruption of BM
  • Focal loss of foot processes
  • Increase mesangial cells
  • Cresent formation
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9
Q

What is Type II hypersensitivity, autoimmune kidney disease called?

A

Goodpasture syndrome

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10
Q

What are the clinical effects of Goodpastures syndrome/Type II Hypersensitivity?

A
  • Fast
  • Haematuria in early stages
  • Some proteinuria
  • Fibrin in urine
  • Stop passing urine
  • Lung involvement
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11
Q

What are the causes of Goodpastures syndrome?

A
  • Vasculitis ANCA
  • SLE
  • Organic solvents
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12
Q

Describe Type III Hypersensitivity kidney disease?

A
  • Immune complexes
  • Size determines where deposition occurs
  • Gets stuck & forms granular deposits, causes proliferation of endothelial & mesangial cells
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13
Q

Describe Proliferative Glomerulonephritis?

A
  • Type III hypersensitivity
  • Immune complexes
  • Increased mesangial cells
  • Proliferated endothelial cells
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14
Q

What are the clinical effects of Type III hypersensitivity/Proliferative Glomerulonephritis?

A
  • Fast/slow
  • Haematuria
  • More/less urine
  • Little proteinuria
  • Pain due to swelling
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15
Q

What are the causes of Type III hypersensitivity/Proliferative Glomerulonephritis?

A
  • Postinfectious (strep.)
  • Vasculitis ANCA
  • SLE
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16
Q

Describe the characteristics of Membranous Glomerulonephritis?

A
  • Small immune complexes on the capillary walls
  • Males>females
  • 15% over 70yrs have cancer
  • Hepatitis B
  • Idiopathic
  • Penicillamine
  • SLE
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17
Q

Describe Mesangiocapillary GN 1&2?

A
  • Focal loss of foot processes
  • Immune complexes
  • Proliferated endothelial cells
  • Increased mesangial cells
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18
Q

What is the causes of minimal lesion GN?

A
  • Type IV hypersensitivity
  • Hodgkin lymphoma
  • Remission with measles
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19
Q

Who is typically effected with minimal lesion glomerulonephritis?

A

Children

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20
Q

How do you treat minimal lesion glomerulonephritis?

A

Steroids

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21
Q

What is a characteristic of minimal lesion glomerulonephritis?

A
  • Marked proteinuria

- Present with nephrotic syndrome.

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22
Q

Describe focal & segmental glomerulosclerosis?

A
  • Differential minimal change
  • Primary/secondary
  • No Immune complexes
  • Loads of Proteinuria
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23
Q

What are the 3 diseases associated with nephrotic syndrome?

A
  1. Minimal change glomerulonephritis
  2. Focal & Segmental Glomerulosclerosis
  3. Membranous glomerulonephritis
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24
Q

What does glomerular damage cause?

A
  1. Increase permeability of glomerular capillaries to protein
  2. Proteinuria
  3. Hypoproteinemia
  4. Oedema/ Hyperlipidemia
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25
Q

What are the 2 diseases associated with Nephritic syndrome?

A
  1. Proliferative glomerulonephritis

2. Mesangiocapillary glomerulonephritis

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26
Q

What are the clinical signs/symptoms associated with nephritic syndrome?

A
  • Haematuria
  • Inflammatory
  • Loin pain
  • Less proteinuria
  • Oliguria
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27
Q

What are 2 other causes of proteinuria?

A
  1. Diabetes

2. Amyloidosis

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28
Q

What are the 3 common vascular diseases affecting the kidney?

A
  • Hypertension
  • Vasculitis
  • Mesangial IgA disease
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29
Q

What causes tubulointerstitial disease?

A
  • Drug hypersensitivity
  • Acute tubular necrosis
  • Ascending infection
  • SLE
  • Ischaemia
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30
Q

Describe potential causes of Haematuria?

A
  • UTI, inflammation, vascular dilatation & blood cells leaking out of damaged vessels
  • Trauma
  • Macroscopic gross cancer, Bladder cancer.
  • Kidney neoplasm, stone, bladder infection, tumour
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31
Q

Describe potential causes of acute renal failure?

A
  • Tumour
  • Shock: dehydrated, hypovalaemic
  • Kidneys dont get enough circulation, metabolic shut down.
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32
Q

Describe potential causes of proteinuria?

A
  • Hypertension
  • Diabetes
  • Leaky porous membrane to protein
  • Amyloid or other primary glomerular disease
  • Bladder/kidney infection
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33
Q

What is Vesicoureteric reflux?

A
  • Reflux from bladder to ureter

- Increased risk of infection

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34
Q

What is Renal Artery Stenosis?

A
  • Congenital where artery doesn’t develop
  • Effected kidney is ischaemic so produces more renin which raises BP.
  • Normal kidney exposed to much higher BP than normal, so suffering affects of hypertension
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35
Q

What are the 2 genetic causes of kidney disease?

A
  1. Familial Mediterranean fever

2. Alport’s syndrome

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36
Q

What is the Mesangial cell?

A

Central part of renal glomerulus between capillaries, mesangial cells are phagocytic & separated from capillary lumina by endothelial cells

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37
Q

What are the clinical effects of Membranous glomerulonephritis?

A
  • Fast
  • More urine initially & as renal failure occurs less
  • Lots of proteinuria
  • Oedema
  • No pain due to no active inflammation
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38
Q

What are the clinical signs/symptoms of Nephrotic syndrome?

A
  • Proteinuria
  • Oedema
  • Hyperlipidaemia
  • Fall in plasma proteins
  • Unlike nephritic, is slower, non-inflammatory.
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39
Q

What is the main difference between Nephrotic and Nephritic syndromes?

A
  • NEPHROTIC syndrome involves the loss of a lot of PROTEIN

- NEPHRITIC syndrome involves the loss of a lot of BLOOD

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40
Q

What buffers the pH in the body?

A
  • Proteins
  • Haemoglobin
  • Carbonic acid/bicarbonate
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41
Q

Where is the acid/base excreted?

A
  • Lungs

- Kidneys

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42
Q

Which 3 scenarios result in acid-base balance disturbances?

A
  1. Problem with ventilation
  2. Problem with renal function
  3. Overwhelming acid/base load the body can’t handle
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43
Q

What are the normal pH levels?

A

7.35-7.45

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44
Q

What are the normal pO2 levels?

A

12-13 kPa

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45
Q

What are the normal pCO2 levels?

A

4.5-5.6 kPa

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46
Q

What are the normal bicarbonate levels?

A

22-26 mmol/l

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47
Q

How is standard bicarbonate calculated?

A

From actual bicarbonate but assuming 37oC & paCO2 of 5.3kPa

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48
Q

What does standard bicarbonate reflect?

A

Metabolic component of acid-base balance

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49
Q

What are the 4 steps to approach assessment of Arterial Blood Gases (ABG’s)?

A
  • Step 1: assess pO & oxygenation
  • Step 2: assess pH
  • Step 3: determine the primary problem
  • Step 4: is compensation occuring?
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50
Q

What is the PaO2/FiO2 ratio or P/F ratio of a healthy individual?

A

> 50

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51
Q

What is the PaO2/FiO2 ratio or P/F ratio of someone with acute lung injury?

A

<40

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52
Q

What is the PaO2/FiO2 ratio or P/F ratio of someone with ARDs?

A

<26.7

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53
Q

What does ARDS stand for?

A

Acute respiratory distress syndrome

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54
Q
  1. If pH and pCO are changing in
    the SAME direction the primary problem is _______?
  2. If pH & pCO2 are changing in DIFFERENT directions the primary problem is _______?
A
  1. Metabolic

2. Respiratory

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55
Q

What is compensation?

A

Altering in function of respiratory or renal system to change the secondary variable in an attempt to minimise an acid-base imbalance

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56
Q
  1. If pCO2 & bicarbonate are moving in the SAME direction _______ is likely to be occuring?
  2. If they are moving in DIFFERENT directions suspect __________?
A
  1. Compensation

2. Mixed Disorder

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57
Q

How is anion gap calculated?

A

Sum of routinely measured cations in venous blood minus routinely measured anions
([Na+] + [K+]) - ([Cl-] + [HCO3-])

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58
Q

What does an increase anion gap signal?

A

Presence of metabolic acidosis

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59
Q

What is a normal anion gap?

A

16

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60
Q

How can an overwhelming acid load occur?

A
  • Bodies own production
  • Ingestion (exogenous source of aspirin or ethanol)
  • Failure of excretion by kidneys
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61
Q

When does the body produce acid increasing anion gap?

A
  • Whole body hypoperfusion: shock (cariogenic, septic, hypovolaemic)
  • Part of body hypoperfusion: femoral artery embolism
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62
Q

What will hypoperfusion cause?

A

Increased anaerobic metabolism with subsequent increased production of lactic acid = LACTIC ACIDOSIS

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63
Q

In health what metabolises lactate?

A

Liver, process needs oxygen

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64
Q

What are 3 other causes of lactic acidosis?

A
  1. Severe acute hypoxia
  2. Severe convulsions (respiratory arrest)
  3. Strenuous exercise (dehydration)
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65
Q

What does the addition of lactic acid do to ionogram?

A
  • Increases the anion gap due to lactic acid being one of the unmeasured anions
  • Bicarbonate falls
  • Cl- & Na+ remain
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66
Q

Body produces acid when insulin _____ & glucagon _____?

A
  1. Decreases
  2. Increases
    (leading to ketoacidosis)
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67
Q

What are the 3 different types of ketoacidosis?

A
  1. Uncontrolled diabetes mellitus (severe, life-threatening)
  2. Alcoholic ketoacidosis
  3. Starvation ketoacidosis
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68
Q

What are the different accidental/deliberate exogenous acid load ingestions causing an increase anion gap?

A
  • Methanol (industrial solvent, windscreen wash)

- Ethylene glycol (anti freeze)

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69
Q

What are the 2 renal causes of metabolic acidosis?

A
  1. Renal failure both acute & chronic (increase anion gap)
  2. Renal tubular acidosis (normal gap)
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70
Q

What are the 2 possible causes of normal anion gap metabolic acidosis?

A
  1. Diarrhoea

2. Renal tubular acidosis

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71
Q

What 3 processes increase due to diarrhoea?

A
  1. Gut below pylorus secretes bicarbonate into gut lumen
  2. For every bicarb ion into gut, H+ ion enters ECF
  3. Volume depletion, so renin/angiotensin/aldosterone axis stimulated retaining Cl-
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72
Q

What does metabolic acidosis with normal anion gap look like on ionogram?

A
  • Bicarb decreases
  • Cl- increases
  • Unmeasured anions & Na+ remain
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73
Q

What 3 other cases can show normal anion gap with metabolic acidosis?

A
  1. Laxative abuse
  2. Ileostomy
  3. Colostomy
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74
Q

What is the compensation for metabolic problems?

A
  1. RESPIRATORY
  2. Slow metabolic (renal) correction- secrete more acid (& make new bicarb), plasma H+ decreases (pH rises) & plasma bicarb rises to normal
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75
Q

Compensation for metabolic problems can only occur if what 2 things are true?

A
  1. Metabolic acidaemia is of non-renal origin

2. Kidneys are functioning effectively

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76
Q

What happens to the pCO2 to compensate for a metabolic acidosis?

A
  • pCO2 must fall

- Minute volume must increase upto ~30l/min but difficult to maintain

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77
Q

What is Kussmaul respiration?

A

Laboured deep, rapid pattern of breathing which is limited by tiredness

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78
Q

Why is Metabolic alkalosis (alkalaemia) the least common of acid-base disturbances?

A

Because kidneys are very good at excreting excess bicarbonate

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79
Q

What are the processes which have to happen during metabolic alkalosis (alkalaemia)?

A
  1. Initiating process

2. Maintaining process

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80
Q

Describe the most common initiating process?

A
  • Loss of H+ from gut (above pylorus), from kidney (furosemide & thiazide)
  • Gain of exogenous alkali less common (massive blood transfusion)
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81
Q

Describe the 2 types of maintenance of the alkalosis?

A
  • Chloride depletion group

- Potassium depletion group

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82
Q

What happens to bicarbonate when chloride is low in renal tubular fluid?

A

Bicarbonate must be reabsorbed to maintain electrical neutrality

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83
Q

What are the 2 only anions present in appreciable quantities in ECF?

A
  1. Chloride

2. Bicarbonate

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84
Q

What happens to pCO2 to compensate for metabolic alkalosis?

A
  • pCO2 must increase

- Minute volume must fall

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85
Q

What causes abnormal electrolytes?

A
  • Primary disease state
  • Secondary consequence of multitude of diseases
  • Iatrogenic problems are very common
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86
Q

What is Iatrogenic?

A

Disease produced secondary to the treatment of the patient

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87
Q

How much [Na] & [K] are in ECF?

A 
[Na]= 140mmol/L
[K]= 5mmol/L
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88
Q

How much [Na] & [K] are in ICF?

A 
[Na]= 10mmol/L
[K]= 150mmol/L
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89
Q

What are the 2 major compartments in extracellular fluid?

A
  • Plasma

- Interstitial

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90
Q

What will happen when you decrease the volume of ECF by 4L?

A

Raise the concentration of any solute

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91
Q

What happens when you increase the excretion of a solute?

A

Decrease the solute concentration

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92
Q

What causes loss of isotonic solutions?

A
  • Haemorrhage

- Fistula fluid

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93
Q

What happens when you loose 2L of isotonic fluid?

A
  • Loss is from ECF
  • No change in [Na]
  • No fluid redistribution
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94
Q

What causes loss of hypotonic solutions?

A

Dehydration

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95
Q

What happens when you loose 3L of hypotonic fluid?

A
  • Greater loss from ICF than ECF
  • Small increase in [Na]
  • Fluid redistribution between ECF & ICF
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96
Q

What causes gain of isotonic fluid?

A

Saline drip

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97
Q

What happens when you gain 2L of isotonic fluid?

A
  • Gain is to ECF
  • No change in [Na]
  • No fluid redistribution
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98
Q

What causes gain of hypotonic solution?

A
  • Water

- Dextrose

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99
Q

What happens when you gain 3L of hypotonic fluid?

A
  • Greater gain to ICF than ECF
  • Small decrease in [Na]
  • Fluid redistribution between ECF & ICF
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100
Q

What are the 3 physiological compensatory mechanisms?

A
  1. Thirst
  2. ADH
  3. Renin/Angiotensin system
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101
Q

What are the 3 therapeutic compensatory mechanisms?

A
  1. Intravenous therapy
  2. Diuretics
  3. Dialysis
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102
Q

Describe ADH?

A
  • Produced by median eminence & release increases when osmolality rises
  • Decreases renal water loss
  • Increases thirst
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103
Q

What are the simple tests to ascertain ADH status?

A
  • Measure plasma & urine osmolality. Urine > plasma suggests ADH active
    or
  • Measure plasma & urine urea. Urine&raquo_space; plasma suggests water retention
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104
Q

What activates the Renin-angiotensin system?

A

Reduced intra-vascular volume (IVV)

  • Na depletion
  • Haemorrhage
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105
Q

What does the Renin-angiotensin system cause?

A

Renal Na retention

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106
Q

What is the simple test to ascertain Renin-angiotensin status?

A
  • Measure plasma & urine Na

- If urine <10mmol/L suggests renin-angiotensin active

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107
Q

What happens when you replace the loss of 2L of isotonic fluid with isotonic fluid?

A
  • No change in [Na]

- No fluid redistribution

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108
Q

What happens when you replace the loss of 2L of isotonic fluid with hypotonic fluid?

A
  • Fall in [Na]

- Fluid redistribution

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109
Q

What happens when you replace the loss of 3L of hypotonic fluid with isotonic fluid?

A
  • [Na] slightly increased

- No fluid redistribution

110
Q

What happens when you replace the loss of 3L of hypotonic fluid with hypotonic fluid?

A
  • [Na] restored

- Fluid redistribution

111
Q

What is urea?

Where is it filtered?

A
  • Breakdown product of protein metabolism

- Filtered at glomerulus

112
Q

In dehydration what is 1st to show change?

A

Urea

113
Q

What are often parallel to each other during fluid correction?

A

Sodium & Urea concentrations

114
Q

When is urea elevated?

A
  • CCF
  • Shock
  • MI
  • Severe burns
115
Q

What is Creatinine?

Where is it filtered?

A
  • Breakdown product of protein & muscle

- Freely filtered at glomerulus

116
Q

What happens to urea & creatinine in loss of renal function?

A
  • Decrease in filtered volume
  • Increase in plasma concentration
  • Markers of renal dysfunction
117
Q

What is the best overall measure of kidney function?

A

Glomerular filtration rate

118
Q

What is Glomerular Filtration rate (GFR)?

A

Volume of fluid passing through glomerulus, in a given time period

119
Q

What is glomerular filtration rate influenced by?

A
  • Renal perfusion pressure
  • Renal vascular resistance
  • Glomerular damage
  • Post-glomerular resistance
120
Q

What is eGFR?

A
  • “e” = estimated
  • Aid “staging” of kidney disease
  • Based on creatinine
121
Q

Describe Hyponatraemia?

A
  • Too little Na in ECF
  • Excess water in ECF
  • (pseudo hyponatraemia due to increase protein/lipid)
122
Q

Describe Hypernatraemia?

A
  • Too little water in ECF

- Too much Na in ECF

123
Q

Describe dehydration?

A
  • Water deficiency

- Fluid (Na & water) depletion

124
Q

What 2 things can cause Hyponatraemia?

A
  • Diuretics

- Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

125
Q

What 3 things can cause Hypernatraemia?

A
  • Decreased water intake
  • Osmotic diuresis
  • Aldosterone
126
Q

What 4 things are necessary to take into account when understanding electrolyte problems?

A
  • Steady state conditions
  • Patient’s clinical state
  • Effects of the compensatory mechanisms
  • Drugs & infusions
127
Q

What is the normal range of potassium?

A

3.6-5.0mmol/L

128
Q

What can cause potassium values of <3.0 or >6.0?

A
  • Cardiac conduction defects

- Abnormal neuromuscular excitability

129
Q

What is total body potassium determined by?

A

Total cell mass

small proportion of total K+ in plasma

130
Q

What is the potassium intake?

A

60-200mmol/day

131
Q

What is the relationship of potassium to hydrogen ions?

A
  • K+ & H+ exchange across cell membrane

- Both bind to negatively charged proteins (Hb)

132
Q

What happens to potassium during acidosis?

A

Moves OUT of cells –> hyperkalaemia

133
Q

What happens to potassium during alkalosis?

A

Moves INTO cells –> hypokalaemia

134
Q

What are the 2 Renal causes of hyperkalaemia?

A
  • Acute renal failure

- Chronic renal failure

135
Q

What are the 2 Mineralocorticoid dysfunction causes of hyperkalaemia?

A
  • Adrenocortical failure

- Mineralocorticoid resistance ie. sprinonlactone

136
Q

What is the cell death cause of hyperkalaemia?

A

Cytotoxic therapy

137
Q

What is the treatment for hyperkalaemia?

A
  • Correct acidosis
  • Stop unnecessary supplements/intake
  • Glucose & insulin drives potassium into cells
  • Ion exchange resins: GIT potassium binding
  • Dialysis: short & long-term
138
Q

What are the 3 increased urine losses causing potassium depletion?

A
  • Diuretics/osmotic diuresis
  • Tubular dysfunction
  • Mineralocorticoid excess
139
Q

What are the 3 GIT losses causing potassium depletion?

A
  • Vomiting
  • Diarrhoea/laxatives
  • Fistulae
140
Q

What are the 2 hypokalaemia without depletion causes for potassium depletion?

A
  • Alkalosis

- Insulin/glucose therapy

141
Q

What are the effects of chronic potassium depletion in ICF?

A
  • Lethargy, muscle weakness, heart arrhythmias
  • Polyuria, alkalosis (increase renal HCO3 production)
  • Vascular
  • Gut
142
Q

What is the treatment of potassium depletion?

A
  • Prevention: adequate supplementation

- Replacement of deficit: oral (48mmol/day + diet), IV (<20mmol/L)

143
Q

How do diuretics work?

A

Direct action on cells of the nephron to alter ionic pumps or indirectly to modify content of filtrate

144
Q

What do diuretics cause an increase in?

A

Excretion of Na+ & water from body

145
Q

What do diuretics cause a decrease in?

A

Net absorption of Na+ & Cl- ions from filtrate to cause natriuresis

146
Q

Where are the 3 main sites of action of diuretics therapeutically?

A
  1. Thick ascending loop of Henle
  2. Early distal convoluted tubule
  3. Collecting tubules & ducts
147
Q

What are the most powerful diuretics?

A

Loop diuretics (furosemide)

148
Q

Where do the loop diuretics work?

A

Act on thick ascending limb of loop of Henle

149
Q

What does loop diuretics inhibit?

A
  • Na+/K+/2Cl- carrier in luminal membrane

- Thereby inhibit transport of NaCl out of tubule into interstitial tissue

150
Q

What does loop diuretics increase?

A

Delivery of Na+ to distal tubule causing loss of H+ and K+

151
Q

What may loop diuretics produce?

A

Metabolic alkalosis

152
Q

What are the 4 indications that you would use loop diuretics in?

A
  1. Pulmonary oedema due to LVF
  2. Chronic heart failure
  3. Resistant hypertension
  4. Oedema
153
Q

How are loop diuretics helpful in cardiac failure?

A

Reduce pre-load & contribute to venodilation, which helps after load

154
Q

What are the 4 potential side effects of loop diuretics?

A
  • Hypokalaemia
  • Hypotension
  • Urinary retention (if enlarged prostate)
  • Gout
155
Q

Where do thiazide diuretics act?

A

Distal tubule

156
Q

What are the 2 main examples of thiazide diuretics?

A
  • Bendroflumethiazide

- Indapamide

157
Q

How do thiazide diuretics work?

A
  • Decrease reabsorption of Na+ & Cl- by binding to the Na+/Cl- co-transport system
  • Inhibit co-transporter’s action
158
Q

What is the additional extra renal actions thiazide diuretics possess?

A

Produce vasodilatation

159
Q

What are the 4 indications that you would use thiazide diuretics in?

A
  • Hypertension
  • Mild heart failure
  • Severe resistant oedema
  • Nephrogenic diabetes insipidus
160
Q

What are the potential side-effects of thiazide diuretics?

A
  • Increase cholesterol, glucose, uric acid, calcium
  • Decrease potassium, sodium, magnesium, BP
  • Metabolic acidosis
161
Q

Where do potassium sparing diuretics act?

A

Collecting tubules

162
Q

What are weak diuretics?

A

Potassium sparing diuretics

163
Q

What are the 2 main examples of potassium sparing diuretics?

A
  • Amiloride

- Spironolactone

164
Q

How do Amiloride & Trimterene potassium sparing diuretics work?

A

Blocking sodium channels controlled by aldosterone’s protein mediator

165
Q

How do Spironolactone & Eplerenone potassium sparing diuretics work?

A

Antagonists at aldosterone receptor

166
Q

When would you use Potassium sparing diuretics?

A

Alongside K+ losing diuretics (loop or thiazide) to prevent K+ loss, esp if this loss could be hazardous

167
Q

What are the 3 indications that you would use Spironolactone?

A
  • Heart failure
  • Conn’s (primary hyperaldosteronism)
  • Secondary hyperaldosteronism
168
Q

What are the 3 potential side-effects of K+ sparing diuretics?

A
  • Hyperkalaemia
  • GI upset
  • Metabolic acidosis
169
Q

Give 1 example of an osmotic diuretic?

A

Mannitol

170
Q

What are the indications for when you would use Mannitol?

A

Cerebral oedema + raised intra-ocular pressure

171
Q

Give 1 example of diuretic combination?

A

Co-amilofruse

amiloride + furosemide

172
Q

What are the 2 indications for when you would use co-amilofruse?

A
  • Oedema

- Issues with medication compliance (1 pill rather than 2)

173
Q

Give 1 example of carbonic anhydrase inhibitor?

A

Acetazolamide

174
Q

What are the 2 indications for when you would use Acetazolamide?

A
  • Mountain sickness

- Glaucoma (v weak diuretic)

175
Q

What does ABC stand for when talking about diuretics?

A

A- Furosemide
B- Bendroflumethiazide
C- Spironolactone

176
Q

What does SIADH stand for?

A

Syndrome of inappropriate ADH secretion

177
Q

Describe SIADH?

A

Inappropraite ADH secretion from posterior pituitary or from ectopic source despite low serum osmolality

178
Q

What is SIADH associated with?

A
  • Decreased sodium
  • Increased urine osmolality
  • Euvolaemia
179
Q

What is SIADH caused by (4)?

A
  1. Neurological- tumour, trauma, infection, GBS, MS, SLE
  2. Pulmonary- lung small cell cancer, mesothelioma, pneumonia
  3. Malignancy- stomach, pancreas
  4. Drugs- thiazide & loop diuretics, SSRIs & PPIs
180
Q

Describe the presentation of SIADH?

A
  • Nausea
  • Vomiting
  • Cramps/tremors
  • Depressed mood, irritability, personality change, memory issues, hallucinations
  • Seizures
  • Coma
181
Q

What is Erythropoietin (EPO)?

A

Hormone produced by kidney (peritubular interstitial cells) that promotes RBC formation in bone marrow, process driven by anoxia

182
Q

What happens when someones kidneys do not work?

A

Kidneys produce less EPO & person becomes anaemic

183
Q

Describe the uses of Erythropoietin drug?

A
  • Artificial version of hormone which can boost body to make RBC’s
  • 1/2 people on dialysis
  • Some of the drugs are also called ESA (erythropoeisis stimulating agent)
184
Q

What are the 3 naturally occurring Cortical hormones (adrenal hormones)

A
  1. Glucocorticoids ie. cortisol
  2. Mineralocorticoids ie. aldosterone
  3. Androgens
185
Q

What are the 2 naturally occurring Medullary hormones (catecholamines)?

A
  1. Adrenaline

2. Noradrenaline

186
Q

What are the 3 different synthetic glucocorticoids?

A
  1. Topical steroids ie. beclomethasone
  2. Inhaled steroids ie. budesonide
  3. Oral or parenteral steroids ie. hydrocortisone, prednisolone, dexamethasone
187
Q

What is the 1 example of synthetic mineralocorticoids?

A

Fludrocortisone

188
Q

When would you use topical steroids?

A

Inflammatory skin conditions ie. eczema, psoriasis

189
Q

When would you use inhaled steroids?

A

Asthma

190
Q

When would you use oral steroids?

A
  • IBD
  • Asthma
  • Acute transplant rejection
  • Congenital adrenal hyperplasia
  • Cerebral oedema
  • Acute hypersensitivity
  • Anaphylaxis
191
Q

What are the potential side effects of synthetic glucocorticoids?

A
  • Topical treatment can thin the skin
  • Adrenal suppression/atrophy
  • Psychiatric effects
  • Diabetes
  • Osteoporosis
  • Cushing’s syndrome
  • Growth restriction
  • Peptic ulceration
  • Increased susceptibility to infections
192
Q

What can synthetic glucocorticoids lead to?

A

Suppressive action on hypothalamic-pituitary-adrenal axis

193
Q

What are the 2 indications for when you would use Fludrocortisone (mineralocorticoid)?

A
  • Replacement in adrenocortical insufficiency

- Addison’s

194
Q

What are the 3 potential side effects of Fludrocortisone (mineralocorticoid)?

A
  • Hypertension
  • Sodium & water retention
  • Potassium & Calcium loss
195
Q

How much of the Scottish population have at least 1 LTC (long-term chronic condition)?

A

~2million, 40%

196
Q

What are the 6 quality dimensions?

A
  1. Patient centred
  2. Safe
  3. Effective
  4. Efficient
  5. Equitable
  6. Timely
197
Q

What does HEAT stand for?

A

Health, efficiency, access & treatment targets

198
Q

What are the 5 HEAT targets for LTC (2009-2010)?

A
  1. T6- reduce long term conditions admissions/bed days
  2. T7- improve quality of health care experience
  3. T8- increase complex care at home
  4. T10- reduce rate of attendance at A&E
  5. T12- reduce 65+ emergency bed days
199
Q

What are the 4 different levels to individualised stepped care, an organisational perspective?

A

Level 0- Inequalities targeted high risk primary prevention
Level 1- self management
Level 2- Poorly controlled single condition
Level 3- Complex co-morbidity

200
Q

Describe Level 1: Self management?

A

Collaboratively helping individuals & their carers to develop the knowledge, skills & confidence to care for themselves & their condition effectively

201
Q

Describe Level 2: Disease-specific care management?

A

Providing people with complex single need/multiple conditions with responsive, specialist services using multi-disciplinary teams & disease-specific protocols & pathways such as National Service Frameworks & Quality & Outcomes Framework

202
Q

Describe Level 3: Intensive care/case management?

A
  • Requires identification of very high intensity users of unplanned secondary care.
  • Care patients is managed using case management approach, to anticipate, coordinate & join up health & social care
203
Q

What is self-management?

A
  • Concept where the person takes ownership & is central
  • Process of becoming empowered to manage life with LTC
  • Required individuals & health professionals working in partnership
204
Q

What 3 things is self management concerned with?

A
  • Problem solving
  • Decisions making
  • Confidence
205
Q

What are the 5 principles of self-management?

A
  1. Be accountable to me & value my experience
  2. I am the leading partner in management of my health
  3. I am a whole person & this is for my whole life
  4. Self management does not mean managing my LTC alone
  5. Clear information helps me make decisions that are right for me
206
Q

What are the 3 roles of self-management programmes?

A
  1. Do not conflict with existing programmes or treatment
  2. Designed to enhance regular treatment & condition-specific education
  3. Teach patients skills to co-ordinate all the things needed to manage health & keep active
207
Q

What are the treatment of choice for people with persistent pain?

A

Pain management programmes based on cognitive behaviour principles

208
Q

What is self-efficacy (Bandura)?

A

The belief in ones capabilities to organise & execute the course of action required to manage prospective situations

209
Q

What 4 things does self-efficacy influence?

A
  1. Choices we make
  2. Effort we put in
  3. How long we persist when we have obstacles in our way
  4. How we feel
210
Q

What do people with low/high self-efficacy tend to do?

A
  • LOW self-efficacy toward task are more likely to AVOID it

- HIGH self-efficacy toward task are more likely to ATTEMPT it

211
Q

What 5 things is self-efficacy based on?

A
  1. Past performance
  2. Vicarious experiences
  3. Verbal experiences
  4. Physiological cues
  5. NOT a stable trait
212
Q

What does EPP stand for?

A

Expert Patient Programme

213
Q

What is EPP?

A

6 weekly Self-management programme for people living with a long-term (chronic) condition

214
Q

The aim of EPP is to support people by what 3 things?

A
  1. Increase their confidence
  2. Improve their quality of life
  3. Helping them manage their condition more effectively
215
Q

What 6 topics does the initial EPP course cover?

A
  1. Dealing with pain & extreme tiredness
  2. Coping with feelings of depression
  3. Relaxation techniques & exercises
  4. Healthy eating
  5. Communicating with family, friends and healthcare professionals
  6. Planning for the future
216
Q

What does KPMP stand for?

A

Kingdom Chronic Pain Self-Management Programme

217
Q

What is the KPMP?

A
  • 10 weekly sessions
  • 2-2.30hrs
  • Delivered by multidisciplinary team in primary/secondary care
  • Education & guided practice on pain, healthy function, problem-solving, relaxation
  • Cognitive behavioural principles
218
Q

What does the KPMP aim to improve?

A

Physical, psychological, emotional & social dimensions of quality of life of people with chronic pain

219
Q

What are the 10 contents of KPMP?

A
  1. Introduction to Pain Management
  2. Understanding Chronic Pain
  3. Setting Goals & Pacing Your Activities
  4. Positive responses to Pain
  5. Getting Fitter & Being More Active
  6. Managing Your Medicines & Managing Sleep Problems
  7. Everyday Activities
  8. Relationships & Assertiveness
  9. Managing Stress & Problem Solving
  10. Flare-ups & Maintenance
220
Q

What are 2 good examples of programmes with help to achieve effective management of chronic conditions in the UK?

A
  1. The Expert Patients Programme (NHS England)

2. ALLIANCE (Scotland)

221
Q

What is the meaning of equality?

A

Sameness

222
Q

What is the meaning of inequality?

A

Unequal

223
Q

What is the meaning of equity?

A

Fairness

224
Q

What is the meaning of inequity?

A

Unfair or Unjust

225
Q

What does the inverse care law state?

A

Availability of good medical care tends to vary inversely with the need for it in the population served

226
Q

What 3 things can measure health inequalities?

A
  • Measuring Health need
  • Measuring access to healthcare
  • Measuring quality of healthcare
227
Q

What does Aristotle’s theory of distributive justice definite horizontal equity as?

A

Equity between people with the same health care needs

228
Q

What does Aristotle’s theory of distributive justice definite vertical equity as?

A

Those with unequal needs should receive different or unequal healthcare

229
Q

Describe “felt” need?

A

Individual perceptions of variations from normal health

230
Q

Describe “expressed” need?

A

Individual seeks help to overcome variation from normal health (demand)

231
Q

Describe “normative” need?

A

Professional defines interventions appropriate for the expressed need

232
Q

Describe “comparative” need?

A

Comparisons between needs for severity, size, range of interventions, cost

233
Q

What are examples of causes of Calculi?

A
  • Hypercalcaemia ie. sarcoid, renal tubular acidosis, hyperPTHism
  • Gout
  • Obstruction ie. vesico-ureteric reflux
  • Genetic
  • Dehydration
234
Q

What makes up a calculi?

A
  • Calcium 25%
  • Uric acid 20+% (can’t see on plain x-ray)
  • Infection
  • Cystine 1%
235
Q

Describe the characteristics of bladder disease?

A
  • Inflammation
  • Infection
  • Calculi
  • Neoplasia
236
Q

What are the 2 common urinary tract neoplasms/tumours?

A
  1. Bladder- urothelial (transitional cell) carcinoma

2. Renal- 4/5 are clear cell carcinoma (ccRCC)

237
Q

What are the 4 uncommon urinary tract neoplasms/tumours?

A
  1. Renal carcinomas other than clear cell including transitional cell
  2. Renal nephroblastoma (Wilm’s Tumour)
  3. Ureter transitional cell carcinoma
  4. Renal/bladder sarcoma
238
Q

Describe Wilm’s tumour?

A
  • Children
  • WT1 tumour suppressor gene
  • Histology resembles immature or embryonal blastema
  • Younger patients have better prognosis
  • Surgery, radio, chemo leads to 90% survival
239
Q

Describe Renal Cell Carcinoma?

A
  • Originates in ducts esp PCT
  • Commonest type is “clear cell” due to glycogen
  • Papillary, chromophobe
  • Mostly sporadic
  • Smoking & obesity
  • Genetics
  • Grows along renal vein to IVC
240
Q

What are the 3 types of genetic susceptibilities for Renal Cell Carcinoma?

A
  1. von Hippel-Lindae Syndrome
  2. autosomal dominant RCC
  3. Hereditary papillary
241
Q

Who is more prone to Renal Cell Carcinoma (RCC) men or women?

A

Men > Women

242
Q

Describe the clinical presentation of Renal Cell Carcinoma (RCC)?

A
  • Haematuria most common
  • Pain
  • Metastases
  • Paraneoplastic syndromes ie. pyrexia, hormones (EPO)
243
Q

When do “cannonball lesions” occur?

A

When Renal Cell Carcinoma metastasises to lung

244
Q

What is the % of 5 year survival rate for Renal Cell Carcinoma?

A

50% but very stage dependant

245
Q

What are the 3 different types of localisation for bladder (urothelial) cancer?

A
  1. Posterior & lateral wall 70%
  2. Trigone & bladder neck 20%
  3. Dome 10%
246
Q

What is the typical pattern of bladder (urothelial) cancer?

A

Papillary 80%

247
Q

What is the aetiology of bladder (urothelial) cancer?

A
  • Smoking

- Industrial ie. aniline dyes

248
Q

What is the presentation of bladder (urothelial) cancer?

A
  • Haematuria
  • Dysuria
  • Obstruction
  • Tend to recur
249
Q

What are the 3 different types of acute/chronic renal failure?

A
  1. Pre-renal
  2. Renal
  3. Post-renal
250
Q

What are the different “pre-renal” causes of acute renal failure?

A
  • Shock

- Major trauma

251
Q

What are the different “renal” causes of acute renal failure?

A
  • Some glomerulo-nephritides
  • Toxic ie. drugs, Analgesics
  • Malignant
  • Hypertension
  • Vasculitis
252
Q

What is the “post-renal” cause of acute renal failure?

A

Obstruction

253
Q

What are the features of acute renal failure?

A
  • Potassium high
  • Creatinine high
  • May be oliguria
  • Hypertension
  • Lipids in nephrotic syndrome
254
Q

What is the “pre-renal” cause of chronic renal failure?

A

Atherosclerosis

255
Q

What are the “renal” causes of chronic renal failure?

A
  • Glomerulonephritis
  • Diabetes
  • Hypertension
  • Polycystic
256
Q

What is the “post-renal” cause of chronic renal failure?

A

Obstruction

257
Q

What are the effects of chronic renal failure?

A
  • Potassium high
  • Creatinine high
  • May be oliguria
  • Hypertension
  • Anaemia
  • Small kidneys due to scarring
258
Q

Give some examples of intrinsic and extrinsic obstructive uropathy?

A
  • Ureteropelvic stricture
  • Transitional cell carcinoma of renal pelvis
  • Ureteral stone
  • Blood clot
  • Pregnancy
  • Urothelial carcinoma
  • Urethral stricture
259
Q

What is hydronephrosis?

A
  • Distension & dilation of renal pelvis & calyces, usually caused by obstruction of free flow of urine from kidney
  • Must be bilateral for Post-renal failure/ unilateral if patient has 1 kidney
260
Q

List some potential causes of bladder outflow obstruction leading to post-renal renal failure?

A
  • Prostate enlargement in men
  • Uterine prolapse in women
  • Calculi
  • Tumours
  • Urethral strictures
  • Neurological damage
261
Q

What are the different intrinsic causes of obstruction leading to post-renal renal failure?

A
  • Within the wall: intrinsic tumour ie. transitional cell carcinoma
  • In the lumen: calculi, blood clot etc
262
Q

What are the clinical features of renal failure?

A
  • Anaemia
  • Immunosuppression
  • Bone disease
  • Neuropathy
  • Neoplasia
263
Q

What is Renal Osteodystrophy?

A
  • Bone disease when your kidneys fail to maintain proper levels of calcium and phosphorus in the blood
  • It’s common in people with kidney disease & affects dialysis patients
264
Q

What is the purpose of renal replacement therapy?

A
  • Electrolytes
  • Fluid
  • Excretion
  • Erythropoietin
265
Q

Describe haemodialysis?

A
  • Blood inflow then goes through semipermeable membrane
  • Dialysate return
  • Negative pressure
  • Dialysate inflow
  • Blood return
266
Q

Describe Peritoneal Dialysis?

A

Dialysate absorbs waste & fluid from blood, using your peritoneum as a filter to clean blood

267
Q

What does continues ambulatory peritoneal dialysis need?

A

Permanent catheter

268
Q

What are the different potential donors for transplantation?

A
  • Cadaveric
  • Live related
  • Liver unrelated
269
Q

What 3 risks does immunosuppression during transplantation cause?

A
  • Risk of infection ie. BK virus
  • Risk of skin cancer ie. HPV
  • Risk of lymphoma
270
Q

What are the 4 different types of transplantation rejection?

A
  • Acute cellular rejection
  • Acute antibody mediated rejection
  • Acute vascular rejection
  • Chronic allograft nephropathy (chronic rejection)

MD3002 (15 decks)

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