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MBBS - Year 3 > The Renal & Urological System - Water, Electrolyte and Acid-base balance > Flashcards

The Renal & Urological System - Water, Electrolyte and Acid-base balance Flashcards

1
Q

Function of RAAS

A

Rapid pressor response
CNS effects
Slow pressor reposne

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2
Q

Where are AngII receptors located

A

Vascular smooth muscle

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3
Q

Rapid pressor response - RAS

A

AngII activates receptors and contracts the pre capillary arterioles
Weak vasoconstrictor action in brain, lung and skeletal

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4
Q

Where is vasoconstriction maximum in rapid pressor response

A

Kidneys (efferent arteriole)
Lesser in splanchnic

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5
Q

CNS effects of RAS

A

Increase in central sympathetic outflow
Attenuation of baroreceptors mediated reduction in sympathetic discharge from brain

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6
Q

Slow pressor response of RAS

A

Produced by effect on kidneys
AngII reduces urinary excretion of Na+ and water and increases excretion of K+

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7
Q

Effect of AngII on adrenals

A

Stimulaltes synthesis and secretion of aldosterone

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8
Q

What does aldosterone act on

A

Collecting and distal tubule to cause retention of Na and excretion of K+ and H+

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9
Q

Source of aldosterone

A

Zona glomerulosa

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10
Q

What increases secretion of aldosterone

A

AngII
K+
ACTH

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11
Q

What acts as an aldosterone antagonist

A

Loss of Na and water
Hyperkalaemia
Risk of acidosis

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12
Q

Role of AngII

A

Vasoconstriction of vascular smooth muscle
Vasoconstriction of efferent arteriole
Stimulates thirst
Stimulates aldosterone and ADH release
Increase proximal Na+/H+ activity

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13
Q

How does constriction of mesangial cells affect GFT

A

Increases

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14
Q

Which drugs reduces renin secretion

A

Beta blockers
NSAIDs
Cicl;osporin
Tacrolimus

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15
Q

Aldosterone and cardiac remodelling

A

1’ aldosteronism stimulates increased ECM production by vascular smooth muscle and fibroblasts
Resulting in cardiac myocyte hypertrophy

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16
Q

Inhibitors of RAS

A

ACEi
ARBs
Na channel blockers
Impaired aldosterone metabolism
Aldosterone receptor blockers
Impaired release renin

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17
Q

What may cause impaired aldosterone metabolism

A

Adrenal disease
Heparin
Ketoconazole

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18
Q

Examples of Na channels blockers inhibiting RAS

A

Amiloride
Trimethoprim

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19
Q

Classification of hyponatreamia

A

Mild: SNa+ 130-135 mmol/L
Mod: 125-129
Severe <125

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20
Q

Clinical features of a/c hyponatraemia (48hrs)

A

Seizures
Coma
Resp distress
Severe cerebral oedema (if untreated)

MEDICAL EMERGENCY

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21
Q

Clinical features of c/c hyponatraemia (>48hrs)

A

Frequently mild or no sx
Headache, restlessness, muscle cramps

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22
Q

What can rapid correction of hyponatraemia lead to

A

Central pontine myelinolysis (osmotic demyelination syn)
At risk if Na is corrected faster than 12mmol/L/ day

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23
Q

Causes of hypovolaemia hyponatreamia - low urinary Na (<20)

A

Burns
Sweating
Diarrhoea
Vomiting
Fistuale

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24
Q

Causes of hypovolaemia hyponatreamia - high urinary Na

A

Diuretics - thiazides, loop diuretics
Addisons (mineralocorticoid deficency)

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25
Q

Causes of euvolaemic hyponatremia - low urinary Na

A

Severe polydipsia
Inappropriate fluid admin

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26
Q

Causes of euvolaemnic hyponatraemia - high urinary Na

A

SIADH
Hypothyroidism

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27
Q

Causes of hypervolaemic hyponatraemia

A

Nephrotic syn
Cirrhosis
Cardiac failure
Renal failure (high urinary Na)

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28
Q

Drugs commonly causing hyponatreamia

A

Thiazides
Amiloride
Carbamazepine
PPi
ACEi/ ARBs
Opiates

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29
Q

Causes of pseudo hyponatraemia

A

Hypertriglyceridaemia
Hyperproteinameia e.g MM

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30
Q

Cause of hypertonic hyponatreamia - increased serum osmolality

A

Hyperglycaemia

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31
Q

How can the causes of hypotonic hyponatreamia be divided

A

Assessing volume status

Hypervolaemic
Euvolameic
Hypovolameic

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32
Q

Initial ix for hyponatremaia

A

Measure serum Na
Measure serum osmolality
Perform fluid status assessment
Measure urinary Na
May measure TFTs and AM cortisol/ ACTH

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33
Q

Causes of SIADH

A

Malignancy - small cell lung, pancreas, GI, bladder
Chest disease - TB, pneumonia, lung abscesses
CNS - head injury, CVA
Drugs - carbamazepine, TCAs

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34
Q

Mx of hypovolaemic hyponatraemia

A

IV normal saline
Treat underlying cause

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35
Q

Mx of SIADH causing hyponatraemia

A

Fluid restriction
ADH receptor antagonists (deomeclocycline)
Oral sodium and furosemide

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36
Q

Mx of hypothyroidism causing hyponatraemia

A

Levothyroxine

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37
Q

Mx of hypervolaemia hyponatraemia

A

Fluid restriction
Salt restriction
Diuretics

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38
Q

Sx of central pontine myelinolysis

A

Occurs after 2/7

Dysarthria
Dysphagia
Paraparesis
Coma
‘Locked-in syn’

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39
Q

Hypernatraemia values

A

Serum conc >145mmol/L

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40
Q

What does hypernatraemia represent

A

Deficit of water relative to Na

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41
Q

What can cause hypernatraemia

A

Free water losses
Inadequate free water intake
Rarely, sodium overload

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42
Q

What is hypernatraemia almost always associated w/

A

Hyperosmolality

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43
Q

Risk factors for hypernatraemia

A

Inability to drink water - ventilated pts
Infancy and older age
Severe watery diarrhoea or vomiting
Renal concentrating defect
Diabetes insipidus
Large salt intake

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44
Q

Renal concentrating defects that may cause hypernatreamia

A

Osmotic diuresis
Renal failure
Obstructive uropathy

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45
Q

What do sx of hypernatraemia depend on

A

Underlying cause and whether a/c or c/c

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46
Q

Sx of hypernatraemia

A

Neuro disturbances - lethargy, weakness, irritability, seizure
Impaired thirst
May see signs of hypovolaemia

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47
Q

Signs of hypovolaemia

A

Orthostatic hypotension
Decreased JVP
Tachycardia
Dry mucous membrane

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48
Q

Tx of hypernatraemia

A

Review med and closely ,monitor fluid chart
Oral or IV fluids
Can be given desmopressin of central diabetes insipidus
Can give thiazide diuretics if nephrogenic diabetes insipidus

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49
Q

5 R’s of IV fluid therapy

A

Resus
Routine maintenance
Replacement
Redistribution
Reassessment

50
Q

What are resus fluids aimed at

A

Rapid restoration of perfusion and expansion of circulating volume

51
Q

Preferred ways of meeting routine daily fluid and electrolyte requirements

A

Eating and drinking sufficiently is 1st and TPN is 5th

52
Q

How long is short term cover required for routine fluid maintenance

A

Less than 3/7

53
Q

Examples of continuing losses after any initial resus

A

High-output stomas
Post-AKI polyuria
Losses through vomiting
Surgical drains

54
Q

What does redistribution incl in IV fluid resus

A

Redistributing fluid into large-volume ascites
Pleural effusion
Trapped in non-motile gute w/ SBO or ileus
Leaking into interstitial in sepsis

55
Q

Most important R in IV fluid resus

A

Reassessment - adjusting composition and preventing complications from fluid therapy

56
Q

When might a pt need immediate fluid resus

A

Hypovolaemic shock

57
Q

What is shock

A

Inadequate perfusion to tissues

58
Q

Clinical signs of shock

A

Low SBP (<100mmHg)
Tachycardia
Tachypnoea
Delayed CRT
Cool peripheries
High or deteriorating EWS
Response to PLR
Confusion/ decreased LOC

59
Q

PLR

A

Pssive leg raise

60
Q

Bolus doses and admin

A

500ml over 15mins - short, fat tube in larger peripheral veins
If venous access is difficult, consider interosseous access

61
Q

What is the max vol of bolus that can eb given

A

2000ml
>2000ml requires ICU

62
Q

What can excessive NaCl in fluid therapy cause

A

Hyperchloraemic metabolic acidosis but since no K, risk of hyperkalemia (AKI, rhabdo)

63
Q

Can you resuscitate a pt w/ hyperkalemic solution

A

No

64
Q

What is the routine maintenance of electrolyte daily

A

Na/K/ cl intake should be equal
Water ~25-30ml/kg/ day

65
Q

When can human albumin solution be used in fluid resus

A

In pts w/ severe sepsis
Used for large-volume paracentesis and hepato-renal syn

66
Q

Potassium rich foods

A

Tomato
Banana
Baked potato
Orange

67
Q

Where is the majority of total body K stored

A

Mainly intracellular - 95%
In muscle, liver and interstitial fluid

68
Q

What causes movement of K from ICF to ECF

A

Acidosis
Hyperosmolality
beta-adrenergic antagonists
Cell damage

69
Q

What causes movement of K from ECF to ICF

A

Alkolosis
Insulin
Aldosterone
beta-adrenergic agonists

70
Q

How does K enter body

A

Oral intake causes K in ECF to increase
Loses K through urine and stool

71
Q

What may increase free serum K

A

Hyperglycaemia
Exercise

72
Q

Where is the majority of K absorbed

A

PCT

73
Q

What increases the secretion of K+

A

Aldosterone
Increased delivery of Na and water
High K

74
Q

Who is most likely to get hypokalaemia

A

Elderly and pts w/ reduced oral intake

75
Q

Hypokalaemia definition

A

Serum K conc <3.5mmol/L

76
Q

Clinical features of hypokalaemia - neuromuscular

A

Weakness
Constipation
Confusion

77
Q

Clinical features of hypokalaemia - cardiac

A

Arrhythmias, ECG changes, dig toxicity
HTN

78
Q

Why does hypokalaemia cause HTN

A

Increased vascular reactivity and Na retention

79
Q

Clinical features of hypokalaemia - renal

A

Polydispia/ polyuria
Metabolic alkalosis
Tubulointersitial fibrosis/ cystic changes

80
Q

Why does hypokalaemia cause polydipsia

A

Impaired renal concentrating ability

81
Q

What does hypokalaemia cause metabolic alkalosis

A

Increased acid excretion

82
Q

ECG changes in hypokalaemia

A

ST-segment depression
Flattened T-wave
U wave

83
Q

Aetiology of hypokalaemia

A

Pseudohypokalaemia
Decreased K intake/ reduced absorption
Increased entry into cells (usually caused by drugs)
Increased GI losses (D + V)
Increased urinary losses

84
Q

Cause of pseudo hypokalaemia

A

Blood sample w. large no. abnormal white cells (e.g. AML) - take up intracellular K —> reduced conc

85
Q

Why does alkalosis cause hypokalaemia

A

Metabolic or resp
H+ moves out of cell to reduce pH and K+ is moved in

86
Q

Upper vs lower GI losses causing hypokalaemia

A

Upper causes metabolic alkalosis and volume depletion due to loss of HCl –> 2’ hyperaldosteronism - renal K wasting
Lower causes metabolic acidosis due to loss of bicarb

87
Q

How do beta2-agonist cause increased K entry into cells

A

Stimulates Na-K ATPase, NaClK cotransporter

88
Q

Increased urinary losses causing hypokalaemia

A

Increased mineralocorticoid activity - hyperaldosteronim
Diuretics
Renal tubular acidosis
Barrier and Gittelman’s syn

89
Q

1’ vs 2’ hyperaldosteronismm

A

1’ - adrenal adenoma, hyperplasia or carcinoma
2’ - heart failure, nephrotic syn

90
Q

Why do diuretics cause hypokalaemia

A

Volume depletion activates hyperaldosteronism, increased distal delivery of Na and water

91
Q

Renal causes of hypokalaemia

A

Urine K+ > 20

Diuretics
Hypomagnesia
Endocrine - hyperaldosteronism, Cushing’s
Renal tubular acidosis (type 1 or 2)
Batter’s and Gitelman’s syn

92
Q

Extra renal causes of hypokalaemia

A

Inadequate oral intake
Gut losses
Redistribution into cells (e.g. beta-agonist, insulin, theophylline, alkalosis)

93
Q

Assessment of hypokalaemia

A

ECG
Bloods - U&E’s, chloride, bicarb, glucose
Urinary potassium and chloride

94
Q

Mx of mild to moderate hypokalaemia (3.0 - 3.5)

A

Oral slow release KCl
Treat causes e.g aldosterone antagonists for hyperaldosteronism
Check K regularly

95
Q

Mx of severe hypokalaemia (<2.5)

A

Continuous cardiac monitoring
Check and correct Mg
IV infusion of 1L 0.9% saline w/ 40mmol KCl - 10mmol/hr via peripheral line
Treat causes

96
Q

Causes of hypokalaemia w/ HTN

A

Cushings
Conn’s synd (1’ hyperalodsteronism)
Liddle’s syn

97
Q

Causes of hypokalaemia w/ alkalosis

A

Vomiting
Thiazides
Cushing’s
Conn’s

98
Q

Causes of hypokalaemia w/ acidosis

A

Diarrhoea
Renal tubular acidosis
Acetazolamide
Partially treated DKA

99
Q

What is hyperkalaemia defined as

A

K > 5.5

100
Q

Clinical features of hyperkalaemia

A

Non-spp

Arrhythmias
N & V
Muscle weakness
SOB

101
Q

ECG changes in hyperkalaemia

A

Tall tented T waves
Widened QRS
Small/ flattened P waves

102
Q

Causes of pseudohyperkalaemia

A

Thrombosis (K leaks out of platelets during clotting)
Severe leucocytosis (CLL)
Haemolysis (tourniquet use, fist clenching)

103
Q

How can we divide causes of hyperkalameia

A

Impaired excretion - AKI/ CKD, drugs, RTA type 4, Addisons
Increased release from cells - Insulin deficiency, rhabdo, tumour lysis, BB

104
Q

Common causes of hyperkalaemia

A

3 A’s RMD

AKI
Acidosis (metabolic)
Addisons
Rhabdo
Massive blood transfusion
Drugs

105
Q

Drug that may induce hyperkalemia

A

K-sparing diuretics e.g. amiloride
ACEi
ARBs
Spiro
Ciclosporin
Heparin

106
Q

Treating hyperkalaemia w/ ECG changes

A

IV calcium gluconate (10% over 10mins) - stabilse cardiac membrane
Insulin/ dextrose infusion - shifts from ECF to ICF
Nebulised salbutamol - shifter

107
Q

Classification of hyperkalemia

A

Mild: 5.5. - 5.9
Mod: 6.0 - 6.4
Sev: >6.5

108
Q

When can sodium bicarb be given for hyperkalaemia

A

Controversial
High K w/ metabolic acidosis (HC03 <16) and volume depletion

109
Q

Removing K from body in hyperkalaemia

A

Diuretics - urinary K wasting
Dialysis - if refractory
Calcium resins - gut wasting

110
Q

Hormones affects Ca homeostasis

A

PTH
Vit D (calcitriol)

111
Q

Organs involved in Ca homeostasis

A

Intestines
Bone
Kidney

112
Q

What happens to PTH when Ca is low

A

Increased
Bone release Ca2+ and PO4-
Kidney increase PO4- production, Ca reabsorption, increased calcitriol formation (increased intestinal absorption)

113
Q

Foramtion of active vit D

A

UVB –> vit D3
25-hydroxylase in liver —-> 25 OHD (circulating form)
1alpha-hydroxylase in kidney –> 1, 25 (OH)2D (active hormonal form)

114
Q

Defence against hyperCa

A

Increased plasma Ca
Decreased PTH and increased calcitonin
Increased renal Ca excretion
Decreased conversion from 25 OHD to calcitriol
Decreased intestinal absorption

115
Q

Calcitonin vs calcitriol

A

Calcitriol is active form of vit D
Calcitonin is a hormone released from thyroid when Ca is low - inhibits osteoclasts (bone resorption)

116
Q

Sources of vit D

A

Sunlight
Fish
Cheese
Milk
Fortified cereal

117
Q

What form can vit D be stored in

A

24,25 D

118
Q

What is the metabolically active form of Ca

A

Ionised

119
Q

Causes of hyperCa w/ increased PTH

A

Hyperparathyroidism (1’. 3’)
Familial hypocalciuric hyperCa - do 24-hr urinary Ca
Malignancy (MM, PTHrP from solid tumours, bone mets)
Excess Vit A
Thyrotoxicosis

120
Q

Causes of hyperCa due to increased Ca absorption

A

Milk-Alkali syn
Excess vit D
Increased intake

121
Q

Non-spp causes of increased Ca

A

Lithium - increases pTH
Thiazide diuretics - reduce urinary Ca excretion
Rhabdo - Ca released from muscle

122
Q

Ix for hyperCa

A

ECG
LFTs
U&Es
PTH
Boine profile

MBBS - Year 3 (9 decks)

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