Biochemical aspects of nutrition and metabolism Flashcards

1
Q

What happens during starvation

A

First use more glucose than Beta- hydroxybutyrate
As you starve start using Beta- hydroxybutyrate+ acetoacetate.
After a few days start using glucose les than Beta- hydroxybutyrate so it is predominately used
No glucose= no insulin
Carbohydrate based -> fat based
Metabolic rate decreases
Start digesting muscles as a source of protein

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2
Q

Nutritional support to treat food not accessing the intestines (From not serious to severe)

A

Oral feeding - Supplements and dietary adjustments
Ng Tube - enteral
Gastronomy- More invasive

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3
Q

What happens if there is a problem with absorption ?

A

Total Parenteral nutrition TPN
Delivered into a large vein ( central vein ideally - peripheral vein if not normally antecubital fossa) and the portal system

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4
Q

What is the composition of total parenteral nutrition TPN?

A
Nitrogen
Sodium
Potassium
Calcium
Magnesium
Phosphate
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5
Q

What happens if malnourished person is given food suddenly

A

Hyperglycemia (20% of TPN is dextrose)

therefore high insulin produced-> electrolytes shifted into cells

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6
Q

When would you use TPN?

A

When absorption into intestines is not working or when peristalsis isn’t working

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7
Q

How much calories is in TPN?

A

1800kcal

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8
Q

What is the normal source of glucose for the brain?

A

Gluconeogenesis

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9
Q

What is used for glucogenesis?

A

Glucose and amino acids

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10
Q

What is needed for ketone body formation?

A

Acetyl CoA

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11
Q

What is used to make Acetyl CoA to fuel the brain?

A

Metabolised fatty acids from adipose tissue

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12
Q

Which electrolyte will be driven into the cells by insulin? How?

A

Potassium by activating the sodium potassium pump
Magnesium
Phosphate

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13
Q

What which is used to treat breathlessness also drives potassium into cells

A

Salbutamol

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14
Q

Which electrolyte will be driven into the cells by salbutamol? How?

A

Potassium by activating the sodium potassium pump

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15
Q

What is the refeeding syndrome

A

Introduction of carbohydrates causes

  • Increased insulin secretion
  • Increase in thiamine utilisation
  • Increased metabolic rate

Increased insulin secretion causes
-Drives potassium, phosphate and magnesium into cell
Reduction in these metabolites intravascularly

Increased metabolic rate causes
-increased strain on cardiovascular and respiratory systems

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16
Q

What you need to do when you start feeding someone

A
  1. Check K, Ca, PO4, Mg and all other urea and electrolytes
  2. Proactively prophylactically give vitamin supplementation such as thymine and B12.
  3. Start feeding slowly (0.418MJ/kg/day)
  4. Increase over 4-7 days
  5. Rehydrate carefully
  6. Supplement K, PO4, Ca and Mg
  7. Monitor bloods carefully
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17
Q

What needs to be at a normal level to make potassium and calcium levels up

A

Magnesium

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18
Q

What is intestinal failure?

A

Reduction in the function of the gut below the minimum necessary for the absorption of macronutrients and/or water and electrolytes such that IV nutrition is required

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19
Q

What are the types of intestinal failure?

A
  • Type 1:Acute onset, usually self-limiting -most often seen after abdominal surgery
  • Type 2:Less common — acute onset, usually following catastrophic effect (e.g. intestinal ischaemia)
  • Type 3: Chronic — patients are metabolically stable but IV support is required over months — years. May or may not he reversible
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20
Q

What is intestinal ischaemia

A

Stroke of the gut

Clot or embolism cutting of blood supply in a portion of the bowel

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21
Q

What can happen if you have an abdominal surgery?

A

Post operative ileus

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22
Q

What is post operative ileus?

A

Bowel ‘doesn’t like it’ and hides

Therefore peristalsis stops and gut stops functioning so extra nutrition is needed

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23
Q

What types of intestinal failure are self-limiting?

24
Q

What are the causes of intestinal failure?

A
Acute :
-Fistula/obstruction
-Small bowel dysfunction:
   ->Ileus
   ->Enteritis caused by:
      --Chemotherapy 
      --Infection
Chronic
-Gut bypass
-Short bowel caused by:
   ->Jejunum-colon
   ->Jejunostomy
-Small bowel dysfunction
   ->Dysmotility
   ->Enteritis caused by:
      --Irradiation
      --Crohn's disease
25
What is enteritis?
Inflammation of the small intestine
26
Where in the small intestine is Folate absorbed?
Proximal small intestine
27
Where in the small intestine is vitamin B12 absorbed?
Distal small intestine
28
What is absorbed in the proximal small intestine?
``` Fat Sugars Peptides and amino acids Iron Folate Calcium Water Electrolytes ```
29
What is absorbed in the distal small intestine?
Bile acids Vitamin B12 Water Electrolytes
30
What is absorbed in the middle small intestine?
``` Sugars Peptides and amino acids Calcium Water Electrolytes ```
31
Where in the small intestine is fat absorbed?
proximal small intestine
32
Where in the small intestine are sugars absorbed?
proximal and middle small intestine
33
Where in the small intestine are peptides and amino acids absorbed?
proximal and middle small intestine
34
Where in the small intestine is iron absorbed?
proximal small intestine
35
Where in the small intestine is calcium absorbed?
proximal and middle small intestine
36
Where in the small intestine is water absorbed?
the whole small intestine
37
Where in the small intestine are electrolytes absorbed?
the whole small intestine
38
Where in the small intestine are bile acids absorbed?
distal small intestine
39
What is short bowel syndrome?
a syndrome where you've got a section of the bowel that's not working. referring to having a base of the small intestine not being there
40
What causes short bowel syndrome?
``` Post operative Mesenteric ischaemia Crohn's disease Trauma Neoplasia Radiation enteritis ```
41
What part of the gut can you live without? What cant you live without?
Sections of the colon | Any part of the small intestine
42
What water/electroyte management is there? Mild to severe
Oral gluose/saline and Sodium chloride Enteral- Ng tube Parental going into vein
43
What are the inputs and outputs of the urea cycle?
Glutamine/ amino acid NH3 through protein metabolism and carbamoyl phosphate Urea -product
44
What is the urea cycle for?
Detoxify anomia into urea
45
If a patient has a defect in the Urea Cycle, what might happen if they are unable to eat?
Hyperammonaemia
46
What is MCADD short for?
Medium chain acyl-CoA dehydrogenase deficiency
47
What is MCADD?
Defect in fatty acid oxidation
48
What is the most common fatty acid oxidiation disorder
MCADD
49
What happens to people with MCADD in the fed state?
Nothing- because they are utilising glucose from carbohydrated and it is a fatty acid disorder
50
What happens to people with MCADD in the fasted state?
Hypoglycemia as fatty acids are utilised when starving
51
How does MCADD impact a baby?
Hypoglycemia therefore fatal for baby
52
When should we test for MCADD?
At birth
53
How is MCADD tested
Heel prick test
54
What criteria are there for an effective screening test/programme?
The condition should be an important health problem. There should be an accepted treatment for patients with recognized disease. Facilities for diagnosis and treatment should be available. There should be a recognizable latent or early symptomatic phase. There should be a suitable test or examination. The test should be acceptable to the population. The natural history of the condition, including development from latent to declared disease, should be adequately understood. There should be an agreed policy on whom to treat as patients. The cost of case-finding (including a diagnosis and treatment of patients diagnosed) should be economically balanced in relation to possible expenditure on medical care as a whole. Case-finding should be a continuous process and not a "once and for all proiect.
55
What is screened in the newborn screening programme
``` Sickle cell disease Cystic fibrosis Congenital hypothyroidism Phenylketonuria MCADD (Medium chain acyl-CoA dehydrogenase deficiency) Isovaleric acidaemia Glutaric aciduria type I Homocystinuria ```