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Year 2 S&P > Water and Electrolytes > Flashcards

Water and Electrolytes Flashcards

1
Q

What are the intracellular and extracellular concentrations of Na?

A

Intra: 10 mM
Extra: 135-145 mM

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2
Q

What are the intracellular and extracellular concentrations of K?

A

Intra: 150 mM
Extra: 5 mM

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3
Q

Are the following ions mainly extracellular or intracellular?

  • Mg2+
  • HCO3-
  • Cl-
  • PO4(2-)
A

Mg and PO4 are intracellular

HCO3- and Cl- are extracellular

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4
Q

Describe water intake and loss in a day

A

Intake: 0.5L - 5L
Loss: 0.05L in faeces, 0.5-1L in sweat, 0.5L-4L in urine

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5
Q

What percentage of weight can be attributed to water?

A

60%

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6
Q

Describe the distribution of fluid in the body

A

2/3 is intracellular

1/3 is extracellular (20% intravascular, 80% tissue fluid)

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7
Q

What fluid is administered to increase extracellular compartment?

A

Normal (isotonic) saline 2L

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8
Q

What fluid is administered to increase intracellular compartment?

A

5% Dextrose 1L

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9
Q

What fluid is administered to decrease intracellular compartment?

A

3% Hypertonic saline 2L

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10
Q

Describe what occurs in the PCT

A

• Reabsorbs solutes
• Fluid resorption mostly isosmotic (Na = H20)
• 70% solutes and water reabsorbed
Not involved in water regulation (as fluid osmolality remains the same)

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11
Q

Describe what occurs in the descending loop

A

• The descending limb is water permeable but salt stays in

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12
Q

Describe what occurs in the ascending loop

A
  • The ascending limb is water impermeable, but salt moves out and into the interstitium
  • The thick ascending limb actively re-absorbs salt through NaKCl2 transporters
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13
Q

Describe what occurs in the distal collecting tubule

A

• Reabsorbs final 2-3% of sodium

Urine here is maximally dilute

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14
Q

Describe what occurs in the collecting duct

A

The collecting duct is:
• Basally impermeable to NaCl, which is essential to allow high NaCl concentration to create an osmotic gradient.
Vasopressin (ADH) makes the collecting duct permeable to water, and so is used to control the amount of water reabsorbed. I

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15
Q

What are the actions of ADH?

A

Vasopressin (ADH) makes the collecting duct permeable to water, and so is used to control the amount of water reabsorbed. It does this by placing aquaporins on the apical membrane

Also a direct vasoconstrictor

Also facilitates the production of vWF and FVIII

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16
Q

What stimulates ADH release?

A
  • Osmoreceptors detect an increase in plasma osmolarity (which means concentrated plasma). So ADH will increase water reabsorption from principal cells to counteract this, maintaining plams osmolarity.
  • Hypovolemia (while maintaining osmolarity) can causes ADH release. However this response is less powerful and a relatively larger depletion in plasma volume is needed to stimulate ADH release
  • Stress, pain and hypoxia are other stimulants
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17
Q

What are the effects of aldosterone?

A

Reabsorption of Na+ and Cl- and Secretion of K+
It achieves this by acting on the collecting tubules by:
• Increasing apical Na+ and K+ channels. Allowing for sodium to diffuse into the principal cell and potassium to diffuse out.
• Increasing activity of the Na/K-ATPase pump on the basal side. This moves the sodium from the cell into the plasma, generating the concentration gradient which drives the diffusion of Na+ into the cell. The rising concentration of K+ in the cell permits K+ excretion. In fact is the primary determinant of urinary K+ excretion.
• Cl- diffuses in through paracellular pathway to maintain electroneutrality.

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18
Q

What causes Renin release?

A

Renin converts angiotensinogen to angiotensin I. Renin release is stimulated by:
1. Decrease in Na+ concentration
2. Decrease in renal perfusion pressure (as detected 3. by baroreceptors in the afferent glomerular arteriole)
B1 adrenergic receptor activation

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19
Q

What stimulates aldosterone release?

A
  • angiotensin II

- rise in plasma K+

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20
Q

What are the effects of Atrial Naturetic Peptide?

A

Atrial Natriuretic Peptide is released from myocardial cells in the (predominantly right) atria and in some cases the ventricles. It has three effects:
• Increases excretion of Na and water
• Inhibits Na reabsorption by collecting duct.
• Inhibits renin production and aldosterone secretion
It is essentially the opposite of aldosterone and also is a direct vasodilator.

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21
Q

What are the effects of expanding the ICF? And why?

A

Expanding the ICF produces symptoms due to hyponatraemia.
These include:
confusions, followed by seizures and death

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22
Q

What are the effects of reducing the ICF? And why?

A

Reducing the ICF produces symtpoms due to hypernatraemia. These include:
thirst, anorexia, lethargy and confusion before death

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23
Q

What conditions cause a rise purely in ICF?

A
  • SIADH
  • Excessive drinking

ICF because only H20, which can rapidly equilibrate

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24
Q

What conditions cause a fall purely in ICF?

A
  • Inability to drink
  • Diabetes Insipidus

ICF because only H20, which can rapidly equilibrate

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25
Q

What conditions cause a rise purely in ECF (isolated hypervoluemia) ?

A
  • Renal failure
  • Mineralocortical excess

These will cause retention of sodium and water. Because plasma osmolarity is maintained, no fluid enters the ICF compartment.

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26
Q

What are the symptoms of having a low ECF compartment?

A
  • hypotension
  • cold
  • postural hypotension
  • oligouria
  • tachycardia (compensatory)
  • decreased consciousness
  • dry mucous membranes
  • poor skin turgor
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27
Q

What are the symptoms of having a high ECF?

A
  • hypertension
  • oedema
  • effusions
  • high juggular venous pressure
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28
Q

What conditions (and why) cause an increase in ICF and ECF?

A
  • Heart failure. Decreased renal perfusion pressure –> decreased renal function –> increased sodium retention –> hypervolumia. Compensatory release of ADH causes rise in ICF.
  • Liver cirrhosis. Low albumin in the blood means that a lot of fluid moves into the interstitial compartment rather than remaining in the intravascular compartment. This causes a decrease in blood volume, prompting release of ADH and aldosterone to increase salt and water retention.
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29
Q

What conditions (and why) cause a decrease in ECF but increase in ICF?

A
  • GI losses, diarrhoea, vomiting. Initially the loss is isotonic, and so only affects the extracellular compartment. Eventually, the decreased plasma volume causes ADH secretion, which absorbs water (but not Na+), leading to dilutional hyponatremia.
  • Mineralocorticoid deficiency. This causes a loss of Na+ reabsorption and thus an increase in ICF. The decreased Na+ reabsorption also results in a loss of water reabsorption and so a decrease in ECF. ADH again causes rise in ICF?
  • Diuretics. Inhibit Na+ and H20 reabsorption causing fall in ECF. ADH again causes rise in ICF?
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30
Q

What conditions (and why) cause a decrease in ECF and ICF?

A

Osmotic diuresis happens when you have a active osmolite such as glucose or mannitol. They increase the osmolarity of the renal tubular fluid, decreasing water reabsorption and thus increasing urinary volume. This decreases the ECF volume, and as sodium absorption is not affected causes hypernatremia and loss of ICF volume as well.

31
Q

Why is potassium an important intracellular ion?

A
  • intracellular synthesis processes

- determinant of resting membrane potential

32
Q

What is potassium excretion affected by?

A

plasma K+ and aldosterone

33
Q

What hormones affect the sodium potassium pump?

A
  • Thyroxine
  • Insulin
  • Adrenaline
  • Aldosterone (however leads to increase excretion)
    Increases Na+/K+ ATPase activity.
34
Q

What are the common causes of hypokalaemia?

A
  • (main cause) fluid loss (d&v)
  • Mineralocorticoid excess
  • Renal tubular disorders
  • Diuretics
  • Glucose, adrenaline and alkalosis causes an intracellular shift
35
Q

What are the symptoms of hypokalaemia?

A

Non-specific symptoms such as weakness. Because of its role in cell metabolism and protein and glycogen synthesis, a variety of cell function may be impaired.

36
Q

What are the common causes of hyperkalaemia?

A
  • Mineralocorticoid deficiency
  • ACE inhibitors
  • Renal failure
  • Intracellular shift (out of cell) by insulin insufficiency, acidosis, and cell lysis.
37
Q

What is the potassium ‘feed-forward loop’?

A

Insulin promotes entry of K+ into skeletal muscle and liver by increasing Na+/K+ ATPase activity. Serves to minimise plasma K+ rise by concurrent K+ intake with glucose intake.

38
Q

What are the symptoms of hyperkalaemia?

A
  • weakness
  • bradycardia
  • ECG abnormalities
39
Q

List the ECG abnormalities seen in hyperkalaemia

A
  • Tented T waves (more specific)
  • Loss of P waves
  • Broad QRS
  • Bradycardia (dangerous and can be fatal)
40
Q

How is hyperkalaemia treated?

A
  1. Calcium chloride. It has no effect on plasma potassium, but has an effect on cardiac excitability and treats bradycardia. Works quickly
  2. 50% glucose (sometimes with insulin) allows potassium to be taken into cell. Takes half an hour to work and works for 4 hours before potassium starts leaking out
  3. 1/2 L of sodium bicarbonate.
41
Q

What are the consequences of lowered pH?

A
  • Impaired ventricular function
  • Arrythrmias, lowering fibrillation threshold
  • Vasodilation, catecholamine resistance
  • Impaired oxygen delivery
  • Bronchoconstriction
  • Reduced hepatic and renal blood flow
  • Impaired consciousness
  • Respiratory muscle fatigue
  • Protein catabolism
  • Insulin resistance
42
Q

What are the two main component of the carbonic acid buffer?

A

bicarbonate ions and pCO2

43
Q

What does BE measure?

A

The non-CO2 element of the acid-base change

44
Q

For what pCO2 values are respiratory alkalosis/acidosis indicated?

A

pCO2 less than 4.5 is resp alkalosis

pCO2 more than 6 is resp acidosis

45
Q

What are the causes of respiratory alkalosis?

A
  • hyperventilation
  • Type 1 respiratory failure:
    • High altitude
    • Focal lung disorders that affect ventilation-perfusion mismatch.
    • Diffusion problem
    • pnuemonia
    • pulmonary embolism
    (last two are most common)
46
Q

How would you differentiate between pneumonia and a pulmonary embolism when investigating the cause of respiratory alkalosis?

A

Do an X-ray:
Pneumonia will show an abnormal x-ray
PR will show a normal x-ray

47
Q

Differentiate between Type 1 and Type 2 Respiratory failure

A

Type 1 respiratory failure is a drop in O2 without an increased level of CO2 in the blood.
Type 2 is caused by inadequate ventilation, where CO2 and O2 are low.

48
Q

What are the causes of respiratory acidosis?

A

Type 2 respiratory failure:

- increased airway resistance such as from COPD, asthma, pulmonary fibrosis, chronic bronchitis

49
Q

What are the causes of metabolic acidosis?

A
  1. (those that present with high chloride) Renal failure, mineralocorticoid deficiency, diarrhoea
  2. (anion gap) lactic or ketoacidosis
50
Q

What is the normal range for the anion gap?

A

12+/-4

51
Q

What are the most common causes of metabolic alkalosis?

A

Diuretics
Mineralo-corticoid excess
Vomiting

52
Q

What is the general link between conditions that affect K+ and those that affect H+?

A

Conditions usually increase or decrease both together. For example diuretics and mineralocorticoid excess causes low K+ and low pH. Renal failure and aldosterone deficiency causes high K+ and high pH.

53
Q

Where does compensation usually occur in acid-base inbalances?

A

For the acidosis’

  • metabolic acidosis is immediately compensated by increased resp. rate
  • respiratory acidosis is slowly compensated by kidney.
54
Q

What are the functions of the kidney, and so the consequences of renal failure?

A

• Maintains fluid compartments
- When goes wrong can be oedema
• Electrolyte (acid-base) balance
- When they stops doing this you develop metabolic acidosis
- Hyperkalaemia
• Excretion of metabolic wastes
- When goes wrong leads to vomiting and drowsiness
• Hormone, produces erythropoietin and 1-a-hydroxylase
- When goes wrong causes anaemia and bone weakness

55
Q

Why can creatinine be used to measure kidney function?

A

Renal function can be measured by calculating GFR by measuring creatinine. Creatinine is filtered very easily and not absorbed anywhere. It is a cheap widely available test that can be done at all hours.

56
Q

What is the relationship between GFR and creatinine?

A

However, the relationship between GFR and Serum Creatinine is NON-LINEAR. You can lose a lot of function, without creatinine levels increase. The test is not very sensitive, not good at detecting mild degree of dysfunction.

57
Q

What are creatinine levels dependent on apart from GFR?

A
  • age
  • diet
  • body build
58
Q

What are the signs of renal failure, in order of appearance?

A
  1. fluid retention
  2. anaemia
  3. bone disease
  4. high potassium
  5. anorexia/wasting
  6. confusion/coma
59
Q

How can renal failure be categorised?

A
  • pre-renal
  • post-renal
  • intrisnic
60
Q

What are the types/causes of pre-renal failure?

A
  • hypovolumia (e.g haemorrhage, dehydration)

- heart failure

61
Q

What are the types/causes of post-renal failure?

A
  • ureteric (e.g bilateral calculi)
  • bladder outflow
  • enlarged bladder
  • hydronephrosis
62
Q

What are the types/causes of intrinsic renal failure?

A
  • Acute Tubular Necrosis (ATN) can either be ischaemic or toxic
  • Diabetes
  • Nephritis
  • Reflux
  • Hereditary
63
Q

Describe the initial management in renal failure (first few hrs)

A
  1. Make patient safe - by treating hyperkalaemia (IV Ca, IV Glucose or IV bicarbonate)
  2. Optimise ECF - may be dehydrated (if so treat with IV saline) or overloaded (bicarb>)
  3. Check drug chart for drugs that are contraindicated)
  4. Check if dialysis is needed - if so move to specialist unit.
64
Q

What drugs are contraindicated in renal failure?

A
  • Gentamicin
  • NSAIDs
  • Acyclovir
  • Heparin
65
Q

Describe the ‘secondary’ (after first hours) management of renal failure

A

Get imaging checking for hydronephrosis and kidney size
Screening checking for metabolic toxins (CK) or autoantibodies (ANA/ANCA)
Specialist advice due to nephritis or chronicity

66
Q

What are the types of Renal Replacement Therapy?

A
  • Haemodialysis
  • Peritoneal dialysis
  • Kidney transplantation
67
Q

Summarise Haemodialysis for a patient

A
  • Uses a man-made membrane to filter waste and remove extra fluid from blood
  • Need to be in hospital, and nurses will monitor weight
  • 3x per week
  • universal and can be performed indefintely
68
Q

Summarise Peritoneal Dialysis for a patient

A
  • Uses the peritoneal membrane and dyalysis fluid to filter waste and extra fluid from body
  • Can be done at home
  • 3-4x per day
  • suitable for people who are capable of doing their own treatment.
  • Gets more difficult after 5 years (dialysis becomes less efficient)
69
Q

List the access complications in haemodialysis

A
  • Enlarged fistulas
  • Distal ischaemia (fingers then need to be chopped off)
  • Line infection
  • Blockages to major veins
70
Q

What other treatments are necessary when on dialysis?

A
  • vitamin D tablets

- blood transfusions/erythropoietin for anaemia

71
Q

What are the causes of mortality of someone on dialysis?

A

In order:

  1. Cardiac disease
  2. Uncertain causes
  3. Infection
  4. Treatment withdrawal
  5. Other
  6. Malignancy
  7. Cerebrovascular disease
72
Q

Summarise Renal Transplantation for a patient

A
  • placed in lower abdomen
  • must be fit for surgery
  • best survival (despite increased risk of dying 3 months in)
  • allows independence
  • graft survival is around 10 years
73
Q

What are the complications of a renal transplant?

A
  • Renal vein thrombosis
  • Rejection
  • Immunosuppression allowing for opportunist infections, such as fungal brain abscess. Also more prone to malignancies such as skin and lymphoid tumours.
74
Q

What behavioural changes are recommended if someone develops CKD?

A

The most important things you should do if you develop CKD is stop smoking and take tablets to control blood pressure. Buying a flat in Ealing may help as that’s where most of the dialysis units are located :P.

Year 2 S&P (4 decks)

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