W10 Practise lecs on Nutrition (SG) Flashcards

IV Fluid Management, Electrolytes, Oral Enteral Parenteral Nutrition, Anaemias

1
Q

Normal physiology:
Fluid intake and output

A

*Intake is controlled by thirst; excretion is controlled by ADH/vasopressor → water reabsorption
*Total fluid intake for adults: 25-30mL/Kg/day
*Urine output: approximately: 0.5-1mL/ kg/hour

Insensible losses
*Perspiration ~900mL/day
*Exhaled moisture from lungs ~400mL/day
*Water lost through faeces ~200mL/day

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2
Q

Assess the patient-algorithm 1
What do you assess?

A

Fluid balance
blood pressure, heart rate
Capillary refill time
NEWS
Passive leg raising
Serum electrolytes

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3
Q

Hypovolaemia Symptoms:

A

HR- Tachycardia
BP- HYPOtensive
Jugular venous pressure- Decreased
Mucous membrane- Dry
Peripheries- Cool to touch
Skin tugor (elasticity)- Decreased, sunken eyes
CRT- Prolonged
Daily weight- Weight loss

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4
Q

Hypervolaemic (Fluid overload) Symptoms:

A

HR: Tachychardia
BP: HYPERtensive
Jugular venous pressure- Increased
Peripheries- Warm to touch, oedematous
Skin turgor (elasticity)- Increased, peripheral or pulmonary oedema
Daily Weight- Weight gain

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5
Q

Physiology in dehydration:

A

Sepsis- Vasodilation
Trauma- Major blood loss
Severe burns- Loss of plasma
Vomiting & Diarrhoea- Loss of electrolytes

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6
Q

Physiology in fluid overload
Terminology for where fluid overload occurs:

A

*The third extravascular space= non-
functional collection in interstitial space
developing in edema
*Peritoneal cavity→ ascites
*Pleural cavity → pleural effusion
*Pericardial cavity → pericardial effusion
*Joints → joint effusion

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7
Q

Types of fluids: CRYSTALLOID- SMALLER MOLECULES

A

Water with added salts and glucose
* 1L of 0.9% NaCl (Iso)
* 1L of 5% glucose (hyper)
* 0.18% sodium chloride in 4%
glucose (hypo+hyper)
* Hartmann’s solution (isotonic)

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8
Q

Types of fluids: Plasma-lyte 148 (Iso) 140mm

A

Larger molecules which remain in intravascular space for longer thus theoretically aids fluid retention

Human albumin- For patients with decompensated liver disease. Albumin increases plasma volume through oncotic pressure drawing in and retaining fluid (anaphylaxis risk)

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9
Q

Tonicity and Osmolality: Definitions

What is a solvent?
What is osmolality?
What is osmolarity?

A
  • Solvent: substance that can dissolve a solute → dissolving sugar in coffee
  • Isotonic fluids have the same concentration of solutes as in plasma
  • Osmolality is measure of solute concentration per unit mass of solvent. It is critical this matches blood plasma (mOsm/kg) →grams of sugar dissolved in kilograms of coffee
  • Osmolarity is the measure of solute concentration per unit volume of solvent (mOsm/L) → grams of sugar dissolved per Litre of coffee
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10
Q

What should be used for fluid resuscitation?

A
  1. Isotonic fluids should be used for fluid resuscitation
    * Prescribed as boluses to rapidly correct fluid status (fluid challenge):
    * 500mL over 15mins stat, reassess and prescribe and Rx 250-500ml again as needed (three- four times)
    * Use crystalloids that contain sodium in the range 130–154 mmol/L
    * Consider human albumin solution 4–5% for fluid resuscitation only in patients with severe sepsis.
  2. Passive leg raise
    * Concerns about ability of the heart to respond to fluid challenge
    * Patient lying flat, raise legs >45 degrees →haemodynamic improvement
    →volume replacement
    * If patient deteriorates → fluid overload
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11
Q

Algorithm 3- Routine Maintenance

A
  • 25-30mL/kg/day of water (limit to 2.5L if possible)
  • 1mmol/kg/day of Na+, K+, Cl-
  • 50-100g/day glucose (glucose 5% contains 5g/100mL)
  • Give less fluids in the older patients, cardiac failure or renal impairment
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12
Q

Algorithm 4- REPLACEMENT and REDISTRIBUTION

A
  • Replace electrolytes and address fluid losses
  • Seek expert help if patients have a complex fluid and/or electrolyte redistribution issue or imbalance, or significant comorbidity
  • Reassess the patient
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13
Q

What are the 5Rs of Fluid Maintenance?

A

Resuscitation
Routine Maintenance
Replacement and redistribution
Reassessment

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14
Q

Potassium 3.5 – 5.3 mmol/L

A
  • Potassium is the primary intracellular cation
  • Has a vital role in cell metabolism
  • A small amount is in extracellular fluids and is maintained within a narrow range
  • Sodium-potassium adenosine triphosphate (ATPase) pump stands guard and maintains the balance.
  • Maintenance for an adult is 1mmol/kg/day
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15
Q

Hypokalaemia
What are the signs and symptoms?
What drugs can cause Hypokalaemia?
What is given?

A
  • ECG changes, arrhythmias
  • Metabolic changes
  • Postural hypotension
  • Constipation
  • Ileus
  • Diuretics
  • Laxatives
  • Amphotericin, aminoglycosides,
  • Insulin e.g. in treatment of diabetic ketoacidosis
  • Caffeine, theophylline, adrenaline, salbutamol
  • Magnesium depletion
  • Oral/ enteral: Sando K, Kay-Cee-L
  • IV Peripherally
  • IV via central line
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16
Q

Hyperkalaemia:
What are the Signs and symptoms?
What drugs can cause hyperkalaemia?
What is the treatment?

A

Signs and symptoms:
* ECG changes, bradycardia
* Muscle pain, weakness, numbness
* Oliguria/ anuria

Causes
* ACEi, ARBs
* Potassium-sparing diuretics
* Renal and diabetic complications
* Lithium
* Digoxin

Treatments
* Calcium gluconate → reduce arrhythmias by antagonising cardiac membrane excitability without affecting K+ levels (protect cardiac myocytes)
* Rapid-acting insulin to shift potassium back into cells
* Remove k+ by giving diuretic (cation exchange resin if chronic); kindey filtration, correction of metabolic disease
* Prevent recurrence

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17
Q

What is the reference range for calcium?
function?

A
  • 2.2-2.6mmol/L
  • Most of calcium is incorporated in bones
    and remaining 1% is used in neural
    conduction, muscle activity and blood
    coagulation.
  • 10% of calcium is complexed with phosphate and citrate and the remainder is
    bound to proteins (mainly albumin
  • Maintenance for an adult is 0.1-0.2
    mmol/kg/day
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18
Q

Hypocalcemia
Signs and Symptoms?
Causes?
Treatment?

A
  • Hypotension
  • QT prolongation
  • Arrhythmia
  • seizures

Causes
* Total thyroidectomy
* Partial/total parathyroidectomy
* Severe vit D deficiency
* Cytotoxic drug-induced

  • Adcal, Calcichew
  • Load vitamin D if depleted
  • Correct magnesium first
  • IV calcium gluconate with ECG monitoring, repeating until asymptomatic
  • Give in glucose as sodium chloride has a calciuric effect
  • Ca gluconate can precipitate arrhythmias and digitalis toxicity

Mild >1.9 mmol/L, asymptomatic
Severe <1.9 or symptomatic

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19
Q

Hypercalcemia:
Signs and symptoms?
Causes?
Treatment?

A
  • Polyuria and thirst
  • Nausea and vomiting
  • Abdominal pain
  • Constipation
  • Renal stones
  • Fatigue, muscle weakness
  • 90% due to hyperparathyroidism or
    malignancy
  • Drug causes: thiazides, lithium, theophylline toxicity, excessive vit A or D
  • thyrotoxicosis
  • Rehydration with sodium chloride (4-6 L in 24hrs)
  • Haemodyalysis
  • Bisphosphonates
  • Off-label: steroids, denosumab, calcitonin
  • Avoid thiazides and phosphate salts

mild: >3mmol/L
severe: >3.5mmol/L or symptomatic

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20
Q

What is the reference range for magnesium?
function?

A
  • Magnesium (0.7 to 1.0 mmol/litre)
  • Usually the first electrolyte that you need to replace.
  • Magnesium is involved in energy transfer and storage, skeletal development, nerve conduction, muscle contraction
  • > 50% in bone, >40% in muscle and soft tissue, 1% in extracellular fluids
  • Maintenance for adults is 1mmol/kg
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21
Q

Hyomagnesaemia:
Causes?
Treatment?

A
  • GI losses (diarrhoea, malabsorption)
  • Malnutrition
  • Chronic alcoholism
  • Loop and thiazide diuretics
  • PPI
  • Aminoglycosides, amphotericin B
  • Magnesium tablets or sachets
  • Contraindicated in eGFR <30ml/min
  • IV replacement using magnesium sulphate 50%
  • (5 gram = 20mmol = 10mL) injection
  • Administer slower if giving peripherally

Severity & Range
Mild: 0.4-0.7 mmol/L, asymptomatic
Severe: <0.4 mmol/L or symptomatic

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22
Q

Hypermagnesemia
Causes?
Treatment?

A
  • Most common cause is renal failure
  • Reduced GI transit time (gastroparesis),
  • Lithium treatment, antacids, bowel preparations/ laxatives
  • Hypothyroidism
  • Concomitant hypocalcaemia
  • Remove source of magnesium
  • Maintain good urine output (can enhance with diuretic-not thiazide)
  • Calcium gluconate 10% injection directly antagonises the neuromuscular and cardiovascular effects of magnesium.
  • Calcium enhances the effect of glycosides (digoxin)

Severity & Range
Mild: 2-4 and asymptomatic
Severe: >4 mmol/L or symptomatic

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23
Q

What is the reference range for phosphate?
function?

A
  • 80% of phosphorus is incorporated in skeleton as a calcium salt.
    The remainder is in soft tissue, metabolic and enzymatic processes
  • Phosphate is regulated by renal excretion; parathyroid hormones reduce renal tubular reabsorption of phosphate
  • Intestinal absorption is enhanced by vit D
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24
Q

Hypophosphatemia
Causes?
Treatment?

A
  • Redistribution of phosphate into cells due to insulin therapy
  • Increased urinary excretion
  • Decreased intestinal absorption e.g. diarrhoea, laxative abuse, vit D deficiency, antacid abuse
  • Phosphate Sandoz
  • Phosphate polyfusor; dose is weight dependent
  • Speed of administration of IV depends on urgency for repletion
  • Correct calcium before correcting phosphate

Severity & Range
Mild >0.6 mmol/L
Moderate 0.3-0.6 mmol/L
Severe <0.3 mmol/L or symptomatic

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25
Q

Hyperphosphatemia
Causes? (2)
Treatment?

A
  • Usually caused by renal failure
  • Can be due to cell breakdown causing phosphate release. This would be due to rhabdomyolysis, during chemotherapy
  • Treat underlying cause
  • Low phosphate diet
  • Phosphate binders e.g. calcium acetate or
    sevelamer
  • Haemodialysis in renal failure

Classed as >1.5 mmol/L

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26
Q

What is the reference range for sodium?
function?

A

134-150 mmol/L
Sodium’s role in the body is to propagate nerve conduction, muscle contraction and maintain osmotic pressures through
balancing water and electrolytes.

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27
Q

Hyponatremia
Causes? (2)
Treatment?

A
  • Acute: drop by >10mmol/L in <48hrs
  • Chronic: over more than 48hrs
  • Pseudo: due to hyperglycaemia, raised
    triglycerides
  • Na <130mmol/L is associated with a cognitive decline even when not reported by the patient.
  • lethargy, anorexia, nausea,
    agitation, dizziness,
    disorientation
  • Seizures
  • Coma.

mild: 125-133mmol/L
moderate: 115-125mmol/L
severe: <115mmol/L or symptomatic

28
Q

Hypernatremia
Causes? (2)
Treatment?

A
  • Results from pure water loss, blood loss, salt gain
  • Should be corrected slowly over 48-72 hrs
  • Symptoms of fluid depletion
  • CNS symptoms related to the degree and rate of sodium rise
  • Coma
  • Seizures

mild: 145-150mmol/L
moderate: 150-159mmol/L
severe: >160mmol/L or symptomatic

29
Q

Assessment of fluid status:

A

Hyponatraemia:

Hypovolaemic:
* diuretics, D+V, AKI
* Assess urinary sodium
* Hypervoleamic:
* CCF, chronic liver disease
* Treat underlying condition
* Euvolaemic:
* thiazides, ACEi, antidepressants,
PPIs, SIADH
* Check TFTs, cortisol- endocrine
disorder?
* Check plasma and urine
osmolality

Hypernatraemia
* Results from pure water loss, blood loss, salt gain
* If mild-moderate, push water orally/ enterally
* If severe, give 1L of glucose over 6hrs

30
Q

Case study:
59yrs diabetic patient with pyelonephritis, treated with gentamicin. Blood test reveals serum potassium of 2.2 mmo/L.

Causes of hypokalaemia?
Characterise as mild, moderate, severe?
treatment?

A

=severe hypokalaemia (<2.5mmol/L)
due to aminoglycoside abx (gentamicin)

31
Q

Case study:
73yrs osteoporotic patient with vit D deficiency. She is on long-term steroid treatment due to lymphoma. Albumin-adjusted calcium is 2.2 mmol/L

Causes of hypocalcaemia?
Characterise as mild, moderate, severe?
treatment?

A

=Mild
due to severe vitamin D deficiency

32
Q

Case study:
58yo alcoholic patient admitted due gastroenteritis. Serum magnesium is 0.54 mmol/L
Causes?
Characterise as mild, moderate, severe?
treatment?

A

GI fluid loss due to gastroenteritis and chronic alcoholism
mild hypomagnesaemia (0-4-0.7mmol/L,asymptomatic)

33
Q

Hypophosphataemic patient (0.23 mmol/L)
and weighs 72kg
Treatment?

A

Severe hypophosphataemia (<0.3mmol/L)
Phosphate polyfusor (dose is weight dependent) - 35mmol phosphate, 350ml polyfusor (from chart on slide)

34
Q

What is oral nutrition?
Who uses it?

A
  • Sterile liquids, semi-solids or powders which provide micro and macro nutrients- BAPEN definition
  • Used in individuals who cannot meet their nutritional requirements through oral diet alone e.g. due to short bowel syndrome, IBDs, chronic or acute malnutrition…
  • Can be gluten or lactose free, halal or kosher.
  • Can be for specific group e.g. pre-operative or for 65+ years old at risk of vit D deficiency
35
Q

Examples of oral nutrition

A
  • Juice
  • Milkshake
  • High-energy powders
  • Soup
  • Semi-solid: thickened liquids, smooth pudding
  • High protein
  • Low volume high concentration (shots)
  • Specialist
36
Q

Monitoring for oral nutrition?

A
  • Meeting nutritional requirements
  • Weight has increased to target (and BMI within healthy range)
  • The individual’s medical condition has changed, e.g. an individual with a swallowing difficulty recovers some/ all of their functionality
  • The individual can no longer tolerate them due to taste fatigue
37
Q

What is the definition of oral nutritional supplements and give three examples of patients who might benefit from
them

A

Sterile liquids, semi-solids or powders which provide micro and macro nutrients.
* 65+ and Risk of vit D deficiency
* Pre Op
* IBD

38
Q

Who is enteral nutrition indicated for?
4 types of tubes?

A

Enteral nutrition is indicated for patients who are unable to take oral nutrition but in whom the GIT is functioning

Naso-gastric Short-term <30 days e.g. early on post-stroke, reduced oral intake, acute onset dysphagia
Naso-jejunal Short-term <90 days e.g. due to gastroparesis, oesophagus or stomach pathology
Gastrostomy (PEG) Long-term >30 days e.g. long term in neurological disease, oesophageal pathology, head and neck
cancer, brain injury
Jejunostomy Long-term >30 days e.g. gastroparesis, as NJ but longer term

(refer to NEWT guidelines)

39
Q

Enteral feeding considerations

A
  • Use enteral syringe
  • Liquids are usually the preferred preparation. Caution in sorbitol-containing liquids due to diarrhoea risk
  • Syrups require additional dilution
  • Some suspensions may block the tube
  • Injections are usually more expensive. Ampoules may have glass particles so would need additional filtration

(this is off-license on SPC refer to NEWT guidelines)

40
Q

Additional guidance for enteral nutrition:

A
  • Crush tablets well and flush to prevent clogging
    -Dispersible/ effervescent tabs- look out for sodium intake
    -Film-coated- coating particles may block tube
    -Enteric-coated- designed to bypass stomach for absorption in intestines so may not be effective and cause ADRs. Chunks can then bind together and block the tube
  • Consider buccal and sublingual tablets
  • MR formulations- DO NOT CRUSH due to dose dumping and unlikeliness to dissolve fully
  • Cytotoxic medicines- hazardous to staff
  • Chewable tablets- advice varies- check individual monographs
  • Capsules- check individual advice. May be unpalatable or cause irritation.
41
Q

Using your BNFs, can ciprofloxacin be given enterally?
Can sucralfate be administered enterally?
What about warfarin?
Consider a patient on Pentasa®; can it be administered via the PEG tube
Can finasteride tablets be crushed?

A

Ciprofloxacin
Enteral feeds decrease the exposure to Ciprofloxacin. Manufacturer makes no recommendation.

Sucralfate
Sucralfate increases the risk of blocked enteral or nasogastric tubes when given with Enteral feeds. Manufacturer advises separate administration by 1 hour.

Warfarin
Enteral feeds (vitamin-K containing) potentially decrease the anticoagulant effect of Warfarin. Manufacturer makes no recommendation.

Percutaneous Endoscopic Gastrostomy (PEG)

Finasteride crushing: not to be handled by women of childbearing potential

42
Q

What is Parenteral nutrition?
What is TPN?

A
  • Parenteral nutrition (PN) refers to the provision of nutrients by the intravenous route.
  • Total Parenteral Nutrition (TPN) implies that all macronutrient and micronutrient and fluid requirements are met by an intravenous nutrient solution and no significant nutrition is obtained from other sources.
    -Macronutrients=fats, protein, carbohydrates
    -Micronutrients= vitamins, minerals, electrolytes
  • Parenteral nutrition is typically indicated in patients who are malnourished or at risk for malnutritionwhen a contraindicated to EN exists or the patient does not tolerate adequate EN or lacks suffcient bowel function to maintain or restore nutrition status
43
Q

Short-term indications for PN?

A
  • Prolonged NBM status following major surgery
  • Multi-organ failure where nutritional requirements cannot
    be met by enteral route
  • Severe pancreatitis
  • Mucositis following chemotherapy
  • High output stoma
  • Intractable vomiting
  • Pre-operatively in the
    malnourished patient
44
Q

Long-term indications for PN?

A
  • Extreme short bowel syndrome
  • Inflammatory bowel disease
  • Radiation enteritis
  • Motility disorders
  • Chronic mal-absorption
45
Q

Consequences of malnutrition?

A
  • Reduced ability to fight infection
  • Reduced muscle function
  • Impaired wound healing
  • Impaired kidney function
  • Changes in mood and mental health
  • Increased length of hospital stay
  • Increased numbers of patients who are readmitted to hospital
  • Increased numbers of deaths
46
Q

Consequence of PN?

A

*Line sepsis
*Risk of fluid and electrolyte imbalance (re-feeding syndrome)
*Metabolic disturbances
*Hypertriglyceridemia
*Abnormal LFT’s
*Hyperglycaemia
*Bacterial translocation
*Thrombophlebitis

47
Q

Should a patient receive PN?

A
  1. Reason for referral/ indication?
    * Functioning gut?, Diagnosis, medical history, NG output, ?BO, flatus? Why nbm? Length time since surgery, number of surgical procedures
  2. Nutritional status: MUST screening tool identifies patients at risk of malnutrition
    * Malnutrition Universal Screening Tool
    * MUST must be assessed for all patients within 24 hours of admission
  3. Dedicated line? Central or peripheral?
  4. Expected time scale for use of PN
  5. Fluid balance. Added IV fluids being administered. Fluid losses. Electrolyte losses
  6. Biochemistry results (trends) / Re-feeding risk?
  7. Relevant blood tests? triglycerides? ALP rise? Hypoalbuminaemia? BGL?
    Sliding scale?
48
Q

Calculate MUST score in a patient;
34yo patient BMI OF 16. Lost 5% body
weight in last 4 months due to cancer.
Admitted due to gastroenteritis and
had no intake for 6 days.

A

Step 1: BMI Score:
BMI = 16kg/m2 - (+2)
Step 2: Weight loss score:
Unplanned weight loss 5% (+1)
Step 3: Acute disease effect score:
Acutely ill and no nutritional input for >5 days (+2)
Step 4: Overall risk of malnutrition = 5 (High risk of malnutrition)

(used guidelines from slide)

49
Q

Peripheral access
Benefits?
Risks?

A
  • Catheter tip lies within the peripheral vein
  • 1.5µm filter within giving set should be used

Benefits: Quick, easy access, non-invasive

Risks:
* Peripheral vein thrombosis
* ↑ risk Thrombophlebitis (local inflammation) vein collapses due to increased pressure (GTN patch)
* Limited use of PN bags available as maximum osmolarity = 800-900 mOsmoL/kg
* Pain especially if PN is cold
* Should only be used short-term (max 5-7 days)

50
Q

Central access: not assessed
Benefits?
Risks?

A
  • Examples: PICC, Hickman, CVC, femoral…
    (neck, arm, directly below neck, using arteries)
  • A port must be dedicated for PN administration and labelled as such
  • 1.5µm filter within giving set should be used
  • Patients may be on continuous or cyclical regimes

Benefits: either peripheral or central PN can be administered, can be used for longer term PN

Risks:
* Catheter occlusion
* Line sepsis
* Pneumothorax
* Embolism

51
Q

Examples of macronutrients,micronutrients and electrolytes?

A

Macronutrients: carbohydrate, nitrogen and lipid (SMOF)
* SMOF: Soyabean oil + medium chain triglycerides + olive oil + fish oil
* Anti-inflammatory? Improved liver tolerability? Reduced cholesterol?
Micronutrients: Vitamins, trace elements and minerals
* Storage
* Pabrinex?
Electrolytes:
sodium, potassium, magnesium, phosphate, chloride, calcium

52
Q

Monitoring requirements?

A
  • Fluid balance
  • Blood sugars
    -6hrly first 48 hrs if stable once daily
    -If unstable – may require sliding scale
    -5% dextrose (caution!)
  • Weight
  • Signs of infection: sepsis, temperature, inflammatory markers
  • Food chart
  • Access route
  • Medication
  • LFTs
  • Renal function
53
Q

Calculate the minimum micronutrients requirements for a 60kg patient. If the patient vomited 250mL four times, how
would this change their potassium intake?

Electrolyte: Average req per day (mmol/kg)
Sodium - 1-1.5
Potassium- 1-1.5
Magnesium- 0.1-1.5
Calcium- 0.1-0.2
Phosphate 0.5-0.7

A

Na= 60
Potassium= 60
Magnesium= 6
Calcium= 6
Phosphate= 30

You may need approx. 14 mmol of potassium to counteract the loss

54
Q

What is the definition of Refeeding syndrome?
What does it depend on?

A

Defined by BAPEN as potentially fatal shifts in fluids and electrolytes that may occur in malnourished patients on re-feeding following a period of starvation.

  • BMI, % of unintentional weight loss,
  • Nutritional intake in the past 5-10days or more
  • Previous low levels of electrolytes prior to feeding
  • History of alcohol or drug misuse, using insulin, chemo, antacids or diuretics
  • To mitigate the risks of referring:
  • Replace electrolytes and thiamine beforehand.
54
Q

What are some definitions of Anaemia?
What are the symptoms?

A
  • Reduction in one or more of RBC measurements obtained as part of a full blood count (Hb concentration, haematocrit, RBC count)
  • Hb lower than 100g/dL
  • Result in reduced oxygen delivery to tissues
  • Symptoms: SOB, increased HR, headaches, dizziness, fainting, atrophic glossitis (inflamed/ swollen tongue), changes in nails (brittle, ridged, spoon shaped), angular cheilitis (corners of mouth inflamed)
  • Ranges differ in age (?co-morbidities), sex, ethnicity, in athletes, in pregnancy
  • Higher values which may mask underlying anaemias: smokers (due to CO), hypovolaemia/dehydration (anaemia will be more apparent after fluid replacement), hypoxia due to high altitudes
55
Q

Diagnosis of anaemia?

A
  • Underlying medical condition which can cause anaemia
  • Family history of anaemia
  • Causes of acquired anaemia:
  • Dietary practices e.g. vegan diet lacks B12
  • Parasitic infections after travel
  • Infections
  • Heavy bleeding (menses, melena)
  • Gastric surgery
  • Starvation or anorexia nervosa
  • Chronicity of anaemia
  • Symptoms suggestive of haemolysis:
  • Dark ursine, jaundice
  • Hx of gallstones
  • Anaemia with certain food or drug disease e.g. fava beans or oxidant drugs
  • Symptoms suggestive of kidney, liver or hypersplenism
  • Response to treatment
56
Q

Blood tests- Red Cells (for reference)

A
  • Haematocrit: % of total blood volume occupied by red
  • cell
  • RBC
  • Mean Cell Volume: mean volume of red cells
    -Microcytic = < 80 (iron deficiency anaemia)
    -Normocytic = 80 – 100
    -Macrocytic = > 100 (e.g. Vit B12, Folate)
    -Red cell Distribution Width: variation in RBC size or volume (may be early diagnosis of B12/folate or iron deficiency.
  • Mean Cell Volume: average quantity of Hb present in a single RBC. This would be low in iron deficiency anaemia
  • Mean Cell Haemoglobin Concentration: amount of Hb per unit volume. This may be normal/ slightly reduced in MACROcytic anaemia
  • Platelets: low=thrombocytopaenia
  • Pancytopenia: low red cells, white cells and platelets
57
Q

What is Sickle cell anaemia?

A
  • Sickle cell disease is caused by a genetic defect producing an abnormal type of
    haemoglobin called haemoglobin-S, which alters the shape of red blood cells, especially in conditions of low oxygen concentration, causing the cells to become crescent, or sickle-shaped.
  • Acute painful sickle cell episodes (also known as painful crises) are caused by blockage of the small blood vessels.
  • The red blood cells in people with sickle cell disease behave differently under a variety of conditions, including dehydration, low oxygen levels and elevated temperature.
  • Changes in any of these conditions may cause the cells to block small blood vessels and cause tissue infarction (necrosis). Repeated episodes may result in organ damage.
  • Sickled cells deliver less oxygen to the tissues and are more likely to become stuck in smaller blood vessels, breaking into pieces and interrupting blood flow.
  • The sickle cells are broken down after only 20 days compared with 120 days for normal red blood cells, causing pressure on folic acid levels.
  • The disease causes chronic pain and fatigue
58
Q

Haematinics- Iron screen
what is screened?

A
  • Serum iron: concentration of iron circulating in blood. 70% in RBC, 20% as ferritin (iron storage protein) and stored in liver, spleen…
  • TIBC: amount of transferrin available for iron to bind to. When iron is low, liver produces more transferrin to transfer iron to where it’s needed
  • If all low except for TIBC= iron deficiency anaemia
  • % iron saturation: how many sites on transferring are occupied by
    iron. If deficiency, binding sites will by empty so this % would be low

Iron, Total Iron Binding Capacity (TIBC), % iron saturation, ferritin serum, vitamin b12 serum, folate serum

59
Q

Macrocytic anaemias
2 categories?
examples?

A
  • Megaloblastic
    -Folate deficiency
    -Vitamin B12 deficiency
    -Copper deficiency
    -Drug-induced
  • Non-megaloblastic
    -Liver disease
    -Alcohol use
60
Q

Vitamin B12:

A
  • Vit B12 is required for the action of key enzymes in synthesis of DNA during cell division.
  • Common dietary sources: Meat (liver high in B12), Fish, Dairy Products
  • Lack of B12 may occur when: Low dietary intake (vegan diet),
  • Malabsoption (Crohn’s, GI surgery) If stomach acid not produced (PUD or with PPIs) If Intrinsic Factor not produced by stomach (pernicious anaemia).
  • May lead to MACROCYTIC ANAEMIA
61
Q

Folate

A
  • Absorbed in upper small intestine, transported in blood to bone marrow in free form or bound to albumin.
  • Stored in LIVER but only capacity to store enough to last 3
    months on a folate free diet.
  • Folic Acid is in GREEN LEAFY vegetables and liver ( broccoli, Brussels sprouts, asparagus, peas, chickpeas and brown rice).
62
Q

Microcytic anaemias (TAILS)
examples?

A
  • Thalassaemia
  • Anaemia of chronic disease
  • Iron deficiency
  • Lead poisoning
  • Congenital Sideroblastic anaemia
63
Q

Iron preparations

A
  • Ferinject
  • Monofer- similar to ferinject but different doses
  • Cosmofer- Ganzoni formula
  • Test doses

Before initiating treatment for anaemia, it is essential to determine which type is present. Iron salts may be harmful if given to patients
with anaemias other than those due to iron deficiency

64
Q

Haemolytic anaemias e.g. Glucose-6-phosphate dehydrogenase -deficiency (G6PD)

A
  • Shortage of an enzyme found in RBC
  • Common among populations originating from parts of the world where malaria is or was common: that is, sub-Saharan Africa, Asia, the Mediterranean region, and the Middle East
  • Babies are often born jaundiced due to the breakdown of RBC
  • It is linked to the X chromosome
  • Patients need to avoid certain foods and drugs to avoid haemolysis - (this info is in BNF but not in an interaction checker as it is drug-disease)