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
2
Q
Where are AngII receptors located
A
Vascular smooth muscle
3
Q
Rapid pressor response - RAS
A
AngII activates receptors and contracts the pre capillary arterioles
Weak vasoconstrictor action in brain, lung and skeletal
4
Q
Where is vasoconstriction maximum in rapid pressor response
A
Kidneys (efferent arteriole)
Lesser in splanchnic
5
Q
CNS effects of RAS
A
Increase in central sympathetic outflow
Attenuation of baroreceptors mediated reduction in sympathetic discharge from brain
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+
7
Q
Effect of AngII on adrenals
A
Stimulaltes synthesis and secretion of aldosterone
8
Q
What does aldosterone act on
A
Collecting and distal tubule to cause retention of Na and excretion of K+ and H+
9
Q
Source of aldosterone
A
Zona glomerulosa
10
Q
What increases secretion of aldosterone
A
AngII
K+
ACTH
11
Q
What acts as an aldosterone antagonist
A
Loss of Na and water
Hyperkalaemia
Risk of acidosis
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
13
Q
How does constriction of mesangial cells affect GFT
A
Increases
14
Q
Which drugs reduces renin secretion
A
Beta blockers
NSAIDs
Cicl;osporin
Tacrolimus
15
Q
Aldosterone and cardiac remodelling
A
1’ aldosteronism stimulates increased ECM production by vascular smooth muscle and fibroblasts
Resulting in cardiac myocyte hypertrophy
16
Q
Inhibitors of RAS
A
ACEi
ARBs
Na channel blockers
Impaired aldosterone metabolism
Aldosterone receptor blockers
Impaired release renin
17
Q
What may cause impaired aldosterone metabolism
A
Adrenal disease
Heparin
Ketoconazole
18
Q
Examples of Na channels blockers inhibiting RAS
A
Amiloride
Trimethoprim
19
Q
Classification of hyponatreamia
A
Mild: SNa+ 130-135 mmol/L
Mod: 125-129
Severe <125
20
Q
Clinical features of a/c hyponatraemia (48hrs)
A
Seizures
Coma
Resp distress
Severe cerebral oedema (if untreated)
MEDICAL EMERGENCY
21
Q
Clinical features of c/c hyponatraemia (>48hrs)
A
Frequently mild or no sx
Headache, restlessness, muscle cramps
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
23
Q
Causes of hypovolaemia hyponatreamia - low urinary Na (<20)
A
Burns
Sweating
Diarrhoea
Vomiting
Fistuale
24
Q
Causes of hypovolaemia hyponatreamia - high urinary Na
A
Diuretics - thiazides, loop diuretics
Addisons (mineralocorticoid deficency)
25
Causes of euvolaemic hyponatremia - low urinary Na
Severe polydipsia
Inappropriate fluid admin
26
Causes of euvolaemnic hyponatraemia - high urinary Na
SIADH
Hypothyroidism
27
Causes of hypervolaemic hyponatraemia
Nephrotic syn
Cirrhosis
Cardiac failure
Renal failure (high urinary Na)
28
Drugs commonly causing hyponatreamia
Thiazides
Amiloride
Carbamazepine
PPi
ACEi/ ARBs
Opiates
29
Causes of pseudo hyponatraemia
Hypertriglyceridaemia
Hyperproteinameia e.g MM
30
Cause of hypertonic hyponatreamia - increased serum osmolality
Hyperglycaemia
31
How can the causes of hypotonic hyponatreamia be divided
Assessing volume status
Hypervolaemic
Euvolameic
Hypovolameic
32
Initial ix for hyponatremaia
Measure serum Na
Measure serum osmolality
Perform fluid status assessment
Measure urinary Na
May measure TFTs and AM cortisol/ ACTH
33
Causes of SIADH
Malignancy - small cell lung, pancreas, GI, bladder
Chest disease - TB, pneumonia, lung abscesses
CNS - head injury, CVA
Drugs - carbamazepine, TCAs
34
Mx of hypovolaemic hyponatraemia
IV normal saline
Treat underlying cause
35
Mx of SIADH causing hyponatraemia
Fluid restriction
ADH receptor antagonists (deomeclocycline)
Oral sodium and furosemide
36
Mx of hypothyroidism causing hyponatraemia
Levothyroxine
37
Mx of hypervolaemia hyponatraemia
Fluid restriction
Salt restriction
Diuretics
38
Sx of central pontine myelinolysis
Occurs after 2/7
Dysarthria
Dysphagia
Paraparesis
Coma
'Locked-in syn'
39
Hypernatraemia values
Serum conc >145mmol/L
40
What does hypernatraemia represent
Deficit of water relative to Na
41
What can cause hypernatraemia
Free water losses
Inadequate free water intake
Rarely, sodium overload
42
What is hypernatraemia almost always associated w/
Hyperosmolality
43
Risk factors for hypernatraemia
Inability to drink water - ventilated pts
Infancy and older age
Severe watery diarrhoea or vomiting
Renal concentrating defect
Diabetes insipidus
Large salt intake
44
Renal concentrating defects that may cause hypernatreamia
Osmotic diuresis
Renal failure
Obstructive uropathy
45
What do sx of hypernatraemia depend on
Underlying cause and whether a/c or c/c
46
Sx of hypernatraemia
Neuro disturbances - lethargy, weakness, irritability, seizure
Impaired thirst
May see signs of hypovolaemia
47
Signs of hypovolaemia
Orthostatic hypotension
Decreased JVP
Tachycardia
Dry mucous membrane
48
Tx of hypernatraemia
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
49
5 R's of IV fluid therapy
Resus
Routine maintenance
Replacement
Redistribution
Reassessment
50
What are resus fluids aimed at
Rapid restoration of perfusion and expansion of circulating volume
51
Preferred ways of meeting routine daily fluid and electrolyte requirements
Eating and drinking sufficiently is 1st and TPN is 5th
52
How long is short term cover required for routine fluid maintenance
Less than 3/7
53
Examples of continuing losses after any initial resus
High-output stomas
Post-AKI polyuria
Losses through vomiting
Surgical drains
54
What does redistribution incl in IV fluid resus
Redistributing fluid into large-volume ascites
Pleural effusion
Trapped in non-motile gute w/ SBO or ileus
Leaking into interstitial in sepsis
55
Most important R in IV fluid resus
Reassessment - adjusting composition and preventing complications from fluid therapy
56
When might a pt need immediate fluid resus
Hypovolaemic shock
57
What is shock
Inadequate perfusion to tissues
58
Clinical signs of shock
Low SBP (<100mmHg)
Tachycardia
Tachypnoea
Delayed CRT
Cool peripheries
High or deteriorating EWS
Response to PLR
Confusion/ decreased LOC
59
PLR
Pssive leg raise
60
Bolus doses and admin
500ml over 15mins - short, fat tube in larger peripheral veins
If venous access is difficult, consider interosseous access
61
What is the max vol of bolus that can eb given
2000ml
>2000ml requires ICU
62
What can excessive NaCl in fluid therapy cause
Hyperchloraemic metabolic acidosis but since no K, risk of hyperkalemia (AKI, rhabdo)
63
Can you resuscitate a pt w/ hyperkalemic solution
No
64
What is the routine maintenance of electrolyte daily
Na/K/ cl intake should be equal
Water ~25-30ml/kg/ day
65
When can human albumin solution be used in fluid resus
In pts w/ severe sepsis
Used for large-volume paracentesis and hepato-renal syn
66
Potassium rich foods
Tomato
Banana
Baked potato
Orange
67
Where is the majority of total body K stored
Mainly intracellular - 95%
In muscle, liver and interstitial fluid
68
What causes movement of K from ICF to ECF
Acidosis
Hyperosmolality
beta-adrenergic antagonists
Cell damage
69
What causes movement of K from ECF to ICF
Alkolosis
Insulin
Aldosterone
beta-adrenergic agonists
70
How does K enter body
Oral intake causes K in ECF to increase
Loses K through urine and stool
71
What may increase free serum K
Hyperglycaemia
Exercise
72
Where is the majority of K absorbed
PCT
73
What increases the secretion of K+
Aldosterone
Increased delivery of Na and water
High K
74
Who is most likely to get hypokalaemia
Elderly and pts w/ reduced oral intake
75
Hypokalaemia definition
Serum K conc <3.5mmol/L
76
Clinical features of hypokalaemia - neuromuscular
Weakness
Constipation
Confusion
77
Clinical features of hypokalaemia - cardiac
Arrhythmias, ECG changes, dig toxicity
HTN
78
Why does hypokalaemia cause HTN
Increased vascular reactivity and Na retention
79
Clinical features of hypokalaemia - renal
Polydispia/ polyuria
Metabolic alkalosis
Tubulointersitial fibrosis/ cystic changes
80
Why does hypokalaemia cause polydipsia
Impaired renal concentrating ability
81
What does hypokalaemia cause metabolic alkalosis
Increased acid excretion
82
ECG changes in hypokalaemia
ST-segment depression
Flattened T-wave
U wave
83
Aetiology of hypokalaemia
Pseudohypokalaemia
Decreased K intake/ reduced absorption
Increased entry into cells (usually caused by drugs)
Increased GI losses (D + V)
Increased urinary losses
84
Cause of pseudo hypokalaemia
Blood sample w. large no. abnormal white cells (e.g. AML) - take up intracellular K ---> reduced conc
85
Why does alkalosis cause hypokalaemia
Metabolic or resp
H+ moves out of cell to reduce pH and K+ is moved in
86
Upper vs lower GI losses causing hypokalaemia
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
How do beta2-agonist cause increased K entry into cells
Stimulates Na-K ATPase, NaClK cotransporter
88
Increased urinary losses causing hypokalaemia
Increased mineralocorticoid activity - hyperaldosteronim
Diuretics
Renal tubular acidosis
Barrier and Gittelman's syn
89
1' vs 2' hyperaldosteronismm
1' - adrenal adenoma, hyperplasia or carcinoma
2' - heart failure, nephrotic syn
90
Why do diuretics cause hypokalaemia
Volume depletion activates hyperaldosteronism, increased distal delivery of Na and water
91
Renal causes of hypokalaemia
Urine K+ > 20
Diuretics
Hypomagnesia
Endocrine - hyperaldosteronism, Cushing's
Renal tubular acidosis (type 1 or 2)
Batter's and Gitelman's syn
92
Extra renal causes of hypokalaemia
Inadequate oral intake
Gut losses
Redistribution into cells (e.g. beta-agonist, insulin, theophylline, alkalosis)
93
Assessment of hypokalaemia
ECG
Bloods - U&E's, chloride, bicarb, glucose
Urinary potassium and chloride
94
Mx of mild to moderate hypokalaemia (3.0 - 3.5)
Oral slow release KCl
Treat causes e.g aldosterone antagonists for hyperaldosteronism
Check K regularly
95
Mx of severe hypokalaemia (<2.5)
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
Causes of hypokalaemia w/ HTN
Cushings
Conn's synd (1' hyperalodsteronism)
Liddle's syn
97
Causes of hypokalaemia w/ alkalosis
Vomiting
Thiazides
Cushing's
Conn's
98
Causes of hypokalaemia w/ acidosis
Diarrhoea
Renal tubular acidosis
Acetazolamide
Partially treated DKA
99
What is hyperkalaemia defined as
K > 5.5
100
Clinical features of hyperkalaemia
Non-spp
Arrhythmias
N & V
Muscle weakness
SOB
101
ECG changes in hyperkalaemia
Tall tented T waves
Widened QRS
Small/ flattened P waves
102
Causes of pseudohyperkalaemia
Thrombosis (K leaks out of platelets during clotting)
Severe leucocytosis (CLL)
Haemolysis (tourniquet use, fist clenching)
103
How can we divide causes of hyperkalameia
Impaired excretion - AKI/ CKD, drugs, RTA type 4, Addisons
Increased release from cells - Insulin deficiency, rhabdo, tumour lysis, BB
104
Common causes of hyperkalaemia
3 A's RMD
AKI
Acidosis (metabolic)
Addisons
Rhabdo
Massive blood transfusion
Drugs
105
Drug that may induce hyperkalemia
K-sparing diuretics e.g. amiloride
ACEi
ARBs
Spiro
Ciclosporin
Heparin
106
Treating hyperkalaemia w/ ECG changes
IV calcium gluconate (10% over 10mins) - stabilse cardiac membrane
Insulin/ dextrose infusion - shifts from ECF to ICF
Nebulised salbutamol - shifter
107
Classification of hyperkalemia
Mild: 5.5. - 5.9
Mod: 6.0 - 6.4
Sev: >6.5
108
When can sodium bicarb be given for hyperkalaemia
Controversial
High K w/ metabolic acidosis (HC03 <16) and volume depletion
109
Removing K from body in hyperkalaemia
Diuretics - urinary K wasting
Dialysis - if refractory
Calcium resins - gut wasting
110
Hormones affects Ca homeostasis
PTH
Vit D (calcitriol)
111
Organs involved in Ca homeostasis
Intestines
Bone
Kidney
112
What happens to PTH when Ca is low
Increased
Bone release Ca2+ and PO4-
Kidney increase PO4- production, Ca reabsorption, increased calcitriol formation (increased intestinal absorption)
113
Foramtion of active vit D
UVB --> vit D3
25-hydroxylase in liver ----> 25 OHD (circulating form)
1alpha-hydroxylase in kidney --> 1, 25 (OH)2D (active hormonal form)
114
Defence against hyperCa
Increased plasma Ca
Decreased PTH and increased calcitonin
Increased renal Ca excretion
Decreased conversion from 25 OHD to calcitriol
Decreased intestinal absorption
115
Calcitonin vs calcitriol
Calcitriol is active form of vit D
Calcitonin is a hormone released from thyroid when Ca is low - inhibits osteoclasts (bone resorption)
116
Sources of vit D
Sunlight
Fish
Cheese
Milk
Fortified cereal
117
What form can vit D be stored in
24,25 D
118
What is the metabolically active form of Ca
Ionised
119
Causes of hyperCa w/ increased PTH
Hyperparathyroidism (1'. 3')
Familial hypocalciuric hyperCa - do 24-hr urinary Ca
Malignancy (MM, PTHrP from solid tumours, bone mets)
Excess Vit A
Thyrotoxicosis
120
Causes of hyperCa due to increased Ca absorption
Milk-Alkali syn
Excess vit D
Increased intake
121
Non-spp causes of increased Ca
Lithium - increases pTH
Thiazide diuretics - reduce urinary Ca excretion
Rhabdo - Ca released from muscle
122
Ix for hyperCa
ECG
LFTs
U&Es
PTH
Boine profile
