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Abdominal symptoms > Biochemical aspects of nutrition and metabolism > Flashcards

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?

A

1 and 2

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
Q

What is enteritis?

A

Inflammation of the small intestine

26
Q

Where in the small intestine is Folate absorbed?

A

Proximal small intestine

27
Q

Where in the small intestine is vitamin B12 absorbed?

A

Distal small intestine

28
Q

What is absorbed in the proximal small intestine?

A 
Fat
Sugars
Peptides and amino acids
Iron
Folate
Calcium
Water
Electrolytes
29
Q

What is absorbed in the distal small intestine?

A

Bile acids
Vitamin B12
Water
Electrolytes

30
Q

What is absorbed in the middle small intestine?

A 
Sugars 
Peptides and amino acids 
Calcium 
Water 
Electrolytes
31
Q

Where in the small intestine is fat absorbed?

A

proximal small intestine

32
Q

Where in the small intestine are sugars absorbed?

A

proximal and middle small intestine

33
Q

Where in the small intestine are peptides and amino acids absorbed?

A

proximal and middle small intestine

34
Q

Where in the small intestine is iron absorbed?

A

proximal small intestine

35
Q

Where in the small intestine is calcium absorbed?

A

proximal and middle small intestine

36
Q

Where in the small intestine is water absorbed?

A

the whole small intestine

37
Q

Where in the small intestine are electrolytes absorbed?

A

the whole small intestine

38
Q

Where in the small intestine are bile acids absorbed?

A

distal small intestine

39
Q

What is short bowel syndrome?

A

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
Q

What causes short bowel syndrome?

A 
Post operative 
Mesenteric ischaemia 
Crohn's disease 
Trauma
Neoplasia
Radiation enteritis
41
Q

What part of the gut can you live without? What cant you live without?

A

Sections of the colon

Any part of the small intestine

42
Q

What water/electroyte management is there? Mild to severe

A

Oral gluose/saline and Sodium chloride
Enteral- Ng tube
Parental going into vein

43
Q

What are the inputs and outputs of the urea cycle?

A

Glutamine/ amino acid
NH3 through protein metabolism and carbamoyl phosphate
Urea -product

44
Q

What is the urea cycle for?

A

Detoxify anomia into urea

45
Q

If a patient has a defect in the Urea Cycle, what might happen if they are unable to eat?

A

Hyperammonaemia

46
Q

What is MCADD short for?

A

Medium chain acyl-CoA dehydrogenase deficiency

47
Q

What is MCADD?

A

Defect in fatty acid oxidation

48
Q

What is the most common fatty acid oxidiation disorder

A

MCADD

49
Q

What happens to people with MCADD in the fed state?

A

Nothing- because they are utilising glucose from carbohydrated and it is a fatty acid disorder

50
Q

What happens to people with MCADD in the fasted state?

A

Hypoglycemia as fatty acids are utilised when starving

51
Q

How does MCADD impact a baby?

A

Hypoglycemia therefore fatal for baby

52
Q

When should we test for MCADD?

A

At birth

53
Q

How is MCADD tested

A

Heel prick test

54
Q

What criteria are there for an effective screening test/programme?

A

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
Q

What is screened in the newborn screening programme

A 
Sickle cell disease
Cystic fibrosis
Congenital hypothyroidism
Phenylketonuria
MCADD (Medium chain acyl-CoA dehydrogenase deficiency)
Isovaleric acidaemia
Glutaric aciduria type I
Homocystinuria

Abdominal symptoms (7 decks)

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