Nutrition And Fluids Flashcards

1
Q

What is MOVU?

A

Minimum obligatory volume of urine to dissolve waste products
0.5-1ml/kg/h. About 30 ml/h in average human. Or 1l per day.

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2
Q

Effects of crystalloids v colloids on fluid volume/compartments.

A

Crystalloids: electrolytes in water. No oncotic pressure. Easily distributed in ECF spaces. Eg. Normal saline 0.9% isotonic; 5% dextrose hypotonic. Hartman’s solution (lactate, K, Ca with NaCl) aka physiological.
Initially: only in ECF (plasma is only 3l of 14l in ECF) so only 214ml stay in plasma (distribution time in minutes). 1l IV dextrose 5% (hypotonic) dilutes ECF relate to ICF. SO 70ml would stay in plasma.
Colloids: contain large molecules so increase IV oncotic pressure = draw fluid back into circ. Stay in circ for longer. Maintain BP. No O2 carrying capacity. E.g. Haemaccel/volplex containing gelatine.
500ml colloid IV would all stay IV. No change in osmotic pressure, no distribution into cells (ICF).

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3
Q

Insensible fluid losses?

A

In faeces, from lungs (500ml) from sweat/skin (500ml) per day.
In total unavoidable losses= 1.5-2l per day. In healthy adult at rest. Up to 3l if & activity.
Salt losses: K 60mM, Na 100mM per day.

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4
Q

First post-op day est fluid prescription.

A

~2l on day 1. As water tends to be retained more due to stresses of surgery. 2l 5% dextrose. NB. Don’t just prescribe dextrose alone for several days. Pt will be hyponatraemic. Normal saline every 3rd bag.

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5
Q

Third space losses?

A
8l of secretion reabsorbed into bowel per day. If post-op ileus= fluid secreted is not reabsorbed (completely). = reduced ECF = fluid depleted. 
But you don't know the size so- rely on urine output.
Sudden diuresis (d2/3) ?recovery from ileus.
Pancreatitis: several litres of fluid lost into peritoneal cavity. But very difficult to tell how much! -> Vigorous replacement to maintain urine output + correct electrolytes according to daily U&Es.
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6
Q

What percentage of body is water? In an average 70kg man how much of each fluid does he have?

A
2/3 water (increase with age and Female)
70kg man= 42l water
ICF -28l
ECF-14l
Plasma- 3l
Interstitial- 10l
Transcellular 1l
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7
Q

A 70yo male presents to A&E with syncope, dyspnoea, and peripheral oedema. His CXR shows Kerley B lines, batwing shadowing, and a heart >50% of the thorax diameter. What do you expect his blood results to show? How would this guide your management?

A

DD: Congestive cardiac failure causing pulmonary oedema
Expected blood results: Hypovolaemic hyponatraemia
Management: normal physiological response to CCF, so treat the underlying cause,I.e. Heart failure. Otherwise: Fluid restriction, consider diuretics, use hypertonic solutions if needed.

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8
Q

80yo F is referred by her GP with increasing dyspnoea, low sodium, and an abnormal CXR. Explain the pathological process underlying this presentation. What else would you expect to elucidate from her history?

A

Euvolaemic hyponatraemia. Suspected SIADH, from a bronchial carcinoma, likely to be a small cell lung cancer secreting ADH inappropriately. Expect increased exposure to carcinogens e.g. Large pack history.

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9
Q

A 15yo known type 1 diabetic presents to A&E after found to be vomiting and sluggish at school. What do you expect to find on his blood results and his clinical examination? What is the underlying pathology.

A

Expect clinical examination: confusion, fruity breath (ketones), kussmaul respiration- deep and rapid with occasional apnoeas (air hunger to compensate for acidosis)
Bloods: high glucose, high ketones (large osmolar gap), acidotic with very low pCO2, high K
DD: Diabetic ketoacidosis due to not taking insulin (makes you gain wt). Metabolic acidosis due to ketones, attempted respiratory compensation by hyperventilation. Hyperkalaemia due to movement of H into ICF in exchange for K, hopefully will resolve on fixing the DKA e.g. Insulin.

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10
Q

Management of Hyperkalaemia?

A

If <6 or >6and no symptoms or ECG signs- treat it promptly. Treat the underlying cause and review drugs, monitor carefully until downwards trend established.
If >6 and symptoms or ECG changes
Anyone with
- hyperkalaemia (any) and ECG changes
- K>6 with symptoms/signs
- K>7
should be treated as a medical emergency.

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11
Q

Emergency management of Hyperkalaemia

A

Get help from Med Reg. And do ABCDE…
Repeat test URGENTLY but do not delay treating
Give IV Ca gluconate
Give IV insulin. And dextrose IV
If still uncontrollable consider dialysis/haemofiltration.
Monitor BM for at least 6h after last admin of insulin.

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12
Q

Which hormones control sodium and water excretion respectively?

A

Sodium excretion = aldosterone

Water excretion = ADH

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13
Q

Where is aldosterone secreted? What causes it’s secretion

A

Secreted from adrenal cortex (glomerulosa).
Stimulated by renin-angiotensin system (RAAS) which is stimulated by a decrease in renal perfusion (Renin release).
It causes sodium reabsorption in DCT and water retention.

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14
Q

How does the autonomic nervous system respond to a decrease in effective arterial blood volume?

A

Increased sympathetic activity -> systemic arteriolar VASOCONSTRICTION AND constriction of renal AFFERENT arterioles

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15
Q

Where is sodium? Normal intake and excretion in 24h?

A

Sodium is primarily an extracellular cation (total approx 4000mmol or 4 moles) some is complexed in bone (30%)
Normal intake: 100-200mmol
Normal losses (Kidney, gut, skin) <20mmol
So the excess is excreted in urine.

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16
Q

46yo M, received recent Vincristine therapy with packed red cells for progression of Acute Lymphoblastic Leukaemia. 4/7 later he had mild abdominal pain and distention, bowel sounds present, continuing mild constipation. 6/7 more abdominal distention and vomiting, reduced bowel sounds. What do you do?

A

Order abdominal x-ray: check for perforation and ileus (multiple fluid levels).
ABG
Prescribe IV fluids- with extra sodium.
Stop diuretics/opiates.
Nasogastric tube to aspirate contents.
Vincristine can cause neurotoxicity -> colonic demyelination/axonal degeneration -> constipation -> paralytic ileus (3rd space loss of sodium and water) -> hyponatraemia.
1000mmol of sodium is secreted into gut in 24h. Normally it’s reabsorbed- and can be fatal if not (i.e. Paralytic ileus)

17
Q

Sources of sodium losses in disease states

A
  • Renal: 25 000 mmol filtered in 24h. It MUST be reabsorbed.
  • GI: 1000mmol secreted in 24h. It must be reabsorbed.
    (Total body sodium = 4000mmol)
18
Q

What is Conn’s syndrome?

A

Excess mineralocorticoids:

Primary adrenal disease

19
Q

Commonest causes of Conn’s syndrome?

A

Adrenal adenoma
Bilateral hypertrophy of zona glomerulosa
GC remediable aldosteronism (Auto Dom, where ACTH controls Aldo)
Adrenal carcinoma

20
Q

Signs of Conn’s Syndrome?

A

Hypokalaemic, Alkalosis

Hypertension, High-normal Na

21
Q

Differentials for Conn’s Syndrome?

A

Liquorice, 11B hydroxysteroid dehydrogenase deficiency.

22
Q

Causes of hyperaldosteronism?

A

Primary: conn’s syndrome
Secondary: increased plasma renin activity (CCF, liver cirrhosis, nephrotic syndrome, Na losing nephritis, renal artery stenosis)

23
Q

How to distinguish 1o or 2o hyperaldosteronism?

A

Na: (1o normal-high) (2o <138)
HTN: in primary, occasional in secondary
CCF, ascites, nephrotic syndrome: rare in primary;
Plasma renin: low in 1o; high in 2a.

24
Q

How to screen for hyperaldosteronism? What is important pre-test?

A

[aldo]/[renin] in plasma.

Need to have stopped spironolactone at least 6w before

25
Q

How to confirm hyperaldosteronism?

A

Saline suppression test (4h): 2l saline in 4h (aldo should decrease)
Sodium loading and fludrocortisone (4d) risk of severe hypokalaemia

26
Q

How to differentiate Na v water depletion?

A

Isotonic depletion: Na (-), HCT+++, urine volume(-), urine conc(+). More effect on peripheral circulation UNLESS severe then plasma volume preservation > osmolality.
water depletion: Na+, HCT(+), urine volume—, urine conc+++

27
Q

What is the anion gap?

A

[Na + K] - [Cl + HCO3]

Normal: 10-18

28
Q

Causes of a raised anion gap?

A

MUDPILES: methanol/metformin, Ureamia, DKA, Paraldehyde, Iron, Lactate, Ethanol, Salicylates

29
Q

What is the cause of the normal anion gap?

A

Phosphate and lactate

30
Q

Initial management of DKA

A

NG tube: prevents inhalation
Rehydration
Insulin replacement
K replacement (total K is low)

31
Q

What must be done in the first hour of DKA management

A

PANICS
Potassium: check hourly; omit if ?anuria or serum level >5.5
Acidosis: check pH and ketones
Normal saline: 500ml over 15mins if syst<90; otherwise 1l in 1st hr
Insulin infusion: by wt, fixed rate, 0.1units/kg/hr
Catheter and cultures (urine, blood)
Stomach aspiration if drowsy; ET tube if no gag reflex.

32
Q

Venous fasting blood glucose diagnostic of diabetes

A

7.0

33
Q

Venous blood glucose diagnostic of diabetes 2h after oral glucose load (OGTT)

A

11.1

34
Q

HbA1c diagnostic of diabetes?

A

48mmol/mol