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JMP Semester 2 > Week 19 > Flashcards

Week 19 Flashcards

1
Q

What is digestion?

A

Digestion is the conversion of the food we eat into a form that can move through our GIT epithelial cells. This process can be described by two forms of digestion mechanical (chomp chomp) and chemical (enzymes)

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2
Q

Where are carbohydrates digested?

A

Starts in the mouth but mainly Small intestine

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3
Q

Where are proteins digested?

A

Stomach and duodenum

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4
Q

Where are lipids digested?

A

Small intestine

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5
Q

What are the three main divisions of the small intestine?

A

Duodenum
Jejunum
Ileum

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6
Q

What are the five patterns of digestion in the small intestine?

A
  1. No digestion- the substance is freely absorbed by the small intestine eg glucose
    1. Luminal hydrolysis of polymer to monomers- polymeric substance digested by enzymes into monomers
    2. Oligomer hydrolysis to monomers by brush border enzymes- brush border enzymes convert oligometric substrate into monomers before absorption
    3. Intracellular hydrolysis- oligomers broken down inside cell.
    4. Luminal hydrolysis and intracellular resynthesis- digested, absorbed, reassembled.
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7
Q

What are some macronutrients absorbed into the small intestine and their digestive pathways associated?

A
  1. Glucose - no digestion needed.
    1. Protein - luminal hydrolysis of polymers to monomers (Amino acids)
    2. Sucrose- brush border hydrolysis of oligomer to monomers (glucose + fructose)
    3. Peptide- intracellular hydrolysis
    4. Triacylglycerol - luminal hydrolysis followed by intracellular resynthesis
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8
Q

Where is carbohydrates digested predominately?

A
  1. Mouth (salivary amylase)

2. Duodenum (pancreatic amylase)

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9
Q

Where and how is carbohydrate absorbed?

A

Proximal duodenum

  1. Glucose and galactose absorbed with co-transport of sodium ions (micronutrient)
  2. Fructose passively absorbed.
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10
Q

Where is proteins digested?

A
  1. Stomach (pepsin + HCl) (makes small peptides)

2. Small intestine (pancreatic enzymes) (makes small peptides)

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11
Q

Where and how are proteins absorbed?

A

Small intestines

1. Small peptides are freely absorbed
2. Brush border enzymes convert peptide to amino acids for absorption.
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12
Q

Where is fats digested?

A
  1. Mouth (salivary lipase) (enzymes are water soluble so can only act on the outer edge of a lipid drop)
    1. Duodenum- (pancreatic lipase and bile salts)
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13
Q

Where and how are fats absorbed?

A
  1. Small intestine- pancreatic lipase + bile salts to emulsify fats into smaller droplets to allow increased access by enzymes.
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14
Q

What are micronutrients?

A

Vitamins and minerals

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15
Q

What is a key factor for absorption of a micronutrient?

A

Solubility

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16
Q

What are the fat soluble vitamins?

A

A,D,E,K - absorbed with lipids as part of the chylomicron

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17
Q

What are the water soluble vitamins?

A

B,C - absorbed by active transport or specific transport proteins.

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18
Q

What are some macroscopic factors affecting absorption rates in the small intestine?

A
  1. Long (6m)

2. Huge Surface area (with many plicae (folds) and villi)

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19
Q

What are some microscopic factors affecting absorption rates in the small intestine?

A
  1. Brush border microvilli (in the mucosa layer)
    1. Goblet cells mucous secretion (mucosa layer)
    2. Inner circular and outer longitudinal muscles
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20
Q

What are some macroscopic factors affecting absorption rates in the large intestine?

A
  1. 1.5m long

2. Major site of water absorption, concentration and faeces storage

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21
Q

What are some microscopic factors affecting absorption rates in the large intestine?

A
  1. No villi
    1. Straight crypts
    2. Simple columnar epithelium
    3. High number of goblet cells (mucous secretion)
    4. High immune cell density
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22
Q

How is water absorbed in the large intestine?

A
  1. Sodium is actively pumped in from the lumen

2. Water passively follows

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23
Q

What are some vitamins absorbed in the large intestine?

A

Vitamins produced by colonic bacteria:

1. Vitamin K, vitamin B12, thiamine B1, riboflavin B2.
2. These are absorbed by specific transporters or via lymph (Vit K)
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24
Q

What structures increase surface area in the small intestine?

A
  1. Plicae (folds)

2. Villi

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25
Q

What substances are absorbed from the large intestine?

A
  1. Sodium- to draw water in

2. Vitamins K,B12,B1,B2.

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26
Q

What is the general relationship between motility and absorption?

A
  1. Motility up = absorption decrease

Motility decrease = absorption increase

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27
Q

What is the source, target and action of Gastrin?

A 
Source = G cells, antrum of stomach
Target = parietal cells in body of the stomach
Action = increase H+ ion secretion (more stomach acid)
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28
Q

What is the source, target and action of Somatostatin?

A

Source = D cells in stomach and duodenum, cells of pancreatic islets
Target = Stomach, Intestine, Pancreas, Liver
Action =
Stomach- reduces gastrin release
Intestine- increases fluid absorption/ decreases secretion
Pancreas reduces endocrine/exocrine secretions
Liver- reduces bile flow

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29
Q

What is the source, target and action of VIP?

A

Source = ENS neurons
Target = small intestine, pancreas
Action = small intestines - decreases smooth muscle relaxation and increases small intestine secretions
Pancreas- increases secretions

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30
Q

What is malabsorption?

A

A defect in the digestion and absorption of food nutrients.

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31
Q

What is the different types of malabsorption issues?

A
  1. Can effect a single nutrient- lactose intolerance

2. Can effect multiple nutrients- coeliac disease

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32
Q

What is the common presentations of malabsorption issues?

A
  1. Diarrhoea (steatorrhea)

2. Weight loss

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33
Q

What can malabsorption lead to?

A

Malnutrition and anaemia.

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34
Q

What are some systemic effects of malabsorption?

A 
Malnutrition
Weight loss
Growth retardation
Oedema
Anemia
Muscle cramps (loss of calcium)
Osteoporosis
Bleeding deficiencies
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35
Q

What are some GIT localised effects of malabsorption?

A

Diarrhoea
Impaired carbohydrate/electrolyte absorption - leading to osmotic diarrhoea
Unabsorbed fats lead to mucosa irritation
Pale, bulky, frequent stool with foul odour.

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36
Q

What is the consequences for inadequate intake of carbohydrate?

A
  1. Tissue wasting

2. Metabolic acidosis resulting from accelerated fat use for energy requirements

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37
Q

What are the two types of dietary fatty acids?

A

Saturated (no double bonds)

Unsaturated (double bonds etc)

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38
Q

What is meant by an essential fatty acid?

A

They cannot be synthesized in the body and have to be supplied though diet.

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39
Q

What is a characteristic of all essential fatty acid structure?

A

They are all polyunsaturated.

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40
Q

What is the consequence of essential fatty acid deficiency

A
  1. Poor growth
    1. Skin legions
    2. depression
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41
Q

What is meant by essential amino acid?

A

Cannot be made by body must be supplied by diet

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42
Q

What are conditionally essential amino acids?

A

Needed only in certain situations, illness, pregnancy etc

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43
Q

What is the difference between complete and incomplete food proteins?

A

Complete- has all essential amino acids (usually animal origin)
Incomplete- lacks one or more essential amino acids (usually plant origin)

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44
Q

What are the consequences of inadequate protein intake?

A
  1. Weight loss
    1. Tissue wasting
    2. Growth retardation in children
    3. Anemia
    4. Oedema
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45
Q

Define vitamin

A

Organic compounds that catalyze/support a number of biochemical reactions

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46
Q

Define minerals

A

Inorganic elements/compounds that are part of metabolic reactions or provide structural support in body tissues.

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47
Q

What is a coenzyme?

A

Small organic molecules that temporarily bind to enzymes and are essential to that enzymes functioning. Coenzymes are a form of cofactors.

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48
Q

What are all B-vitamins?

A

Co-enzymes or precursors to coenzymes.

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49
Q

What are the consequences of folate deficiency?

A
  1. Anemia
    1. Gastrointestinal problems
    2. Spina bifida risks in newborns (open spine)
    3. Neural deficits
    4. Vascular disease
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50
Q

What are the consequences of Vitamin B12 deficiency?

A
  1. Macrocytosis (large red blood cell size)
    1. Peripheral neuropathy
    2. Ataxia (uncoordinated muscle movements
    3. Depression
    4. Weakness
    5. Smooth tongue
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51
Q

What are some consequences of Vitamin C deficiency?

A
  1. Scurvy (degeneration of skin, teeth, blood vessels)
    1. Weakness
    2. Delayed wound healing
    3. Impaired immunity
    4. Gastrointestinal upset (extreme deficiency)
    5. Kidney stone (extreme deficiency)
    6. Gout (extreme deficiency)
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52
Q

What is Vitamin C for?

A

Critical co-factor in hydroxylation of collagen and proline residues
As collagen is main structural protein in connective tissues leads to things like scurvy if there is a deficiency.

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53
Q

What are some consequences of Vitamin A deficiency?

A
  1. Night blindness
    1. Dry, scaling skin
    2. Increased infection
    3. Immune dysfunction
    4. For extreme deficiency- headache, irritability, vomiting, hair loss, blurred vision, liver and bone damage.
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54
Q

What are some consequences of Vitamin D deficiency?

A
  1. Rickets (bone deformities in children)
    1. Soft bones in adults
    2. Poor muscle tone
    3. Joint pain
    4. Vulnerable to infections
    5. Increased cancer risk
    6. In extreme cases- brain, cardiovascular and kidney damage, calcification of soft tissues, fatigue, weight loss.
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55
Q

What is Anaemia?

A

Anaemia is a condition that develops when your blood lacks enough healthy red blood cells or haemoglobin.

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56
Q

What are some consequences in Iron deficiency?

A
  1. Iron deficiency anemia
    1. Weakness
    2. Impaired immunity
    3. Impaired cognition in children
    4. Fatigue
    5. In extreme cases- liver damage, hemochromatosis.
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57
Q

What are some consequences in Iodine deficiency?

A
  1. Goiter (enlarged thyroid)
    1. Cretinism (stunted physical and mental development)
    2. Myxedema (depression of thyroid hormone production)
58
Q

Where is intestinal epithelium located?

A

Luminal surfaces of small and large intestine of the GIT

59
Q

What layer is the intestinal epithelium apart of?

A

Intestinal mucosa

60
Q

What are some of the features of intestinal epithelium functional organisation?

A
  1. The cells are joined together by tight junctions- forming a contiguous and relatively impermeable membrane.
    1. They have crypts in between villi (go further into the tissue base)
    2. They have villi (protrudes out from the tissue base)
    3. Cells line the villi and the crypts
    4. The individual cells have microvilli (brush border)
61
Q

What is the general sequence of carbohydrate absorption?

A

Polysaccharide –> Disaccharide –> Monosaccharides

62
Q

What is the process of starch digestion (polysaccharides)?

A
  1. Salivary amylase - makes shorter polysaccharides
    1. Stomach acid inactivates salivary amylase
    2. Pancreatic amylase - polysaccharides into maltose, maltotriose and dextrin (short oligosaccharides (polymers of 3-6 monosaccharides))
    3. Oligosaccharides then hydrolysed by disaccharidases (enzymes) into simple sugars (monosaccharides) in the small intestine
63
Q

How are monosaccharides absorbed?

A
  1. Secondary active transport (Na+ and energy required)

2. Or for fructose - facilitated diffusion.

64
Q

What is the mechanism of glucose transport on the luminal side of the intestines?

A
  1. The Na+/K+ ATPase enables the construction of a Na+ gradient from the lumen –> cell environment (it drives Na+ from the cell into the blood)
    1. Na+ - glucose cotransporter (symport) then utilises this Na+ gradient to pump Na+ and glucose into the cell.
65
Q

What is the mechanism of glucose transport on the basolateral side of the intestines?

A
  1. Glucose leaves the cell and enters the bloodstream via facilitated diffusion using the GLUT2 glucose uniporter.
66
Q

What is required for secondary active transport?

A

Electrochemical gradient of ions. (not ATP)

67
Q

What is required for facilitated diffusion?

A

No energy, ions travel down concentration gradient

68
Q

What happens after monosaccharides enter the capillaries of the intestinal villi?

A
  1. Travel via the portal vein into the liver

2. Galactose and fructose are converted to glucose.

69
Q

How are proteins digested generally?

A

Protein–> smaller peptides–> amino acids

70
Q

Where does protein digestion begin?

A

Stomach

1. where proteins are denatured (lost 3D structure) by HCl
2. Cleaved by pepsin into smaller peptides
71
Q

How are proteins then digested after the stomach?

A

Small intestine

1. Peptidases (pancreatic and intestinal)
2. Peptidases recognise various R group patterns and cut the peptide bonds at those places.
3. Peptides eventually (some may be di or tri peptides in need of further cleaving within the epithelial cell) all cleaved into amino acids.
72
Q

What are the two forms of peptidases?

A

Endopeptidases - cleaves peptide bonds inside the polypeptide (trypsin etc)
Exopeptidases- cleaves bonds at the ends of a polypeptide (aminopeptidase etc)

73
Q

How are amino acids absorbed into the epithelial cells and then the bloodstream?

A
  1. Similarly to glucose rely on a Na+ gradient maintained by Na+/K+ ATPase
    1. Na+ gradient allows functioning of sodium-dependent amino acid symporter (there is a different symporters for acidic, basic and neutral amino acids)
    2. Facilitated diffusion allows amino acids access to the bloodstream from the epithelial tissue.
74
Q

How are peptides absorbed into the epithelium and then the bloodstream?

A
  1. Peptide carriers with cotransport of H+ into the cell. (secondary active trans)
    1. Peptides then digested into amino acids via intracellular peptidases
    2. Amino acids go into the blood stream via facilitated diffusion.
75
Q

What are the mechanisms of lipid digestion in the mouth?

A

Salivary glands release lingual lipase- has pretty limited action

76
Q

What are the mechanism of lipid digestion in the stomach?

A

Stomach mixes fats with water - limited lipase action

77
Q

What is emulsification mean?

A

Large fat globules are converted into small droplets for increase surface area of action for lipases.

78
Q

What are the mechanisms of lipid digestion in the small intestine?

A
  1. Lipid arrival into the duodenum stimulates bile secretion
    1. Bile salts emulsify fats in the small intestine - allows for GIT enzyme access
    2. Pancreatic and small intestinal lipases hydrolyze triglycerides to free fatty acids and monoglycerides.
79
Q

What is bile made from and where is it secreted?

A

Made in liver from cholesterol and is secreted by the gallbladder.

80
Q

Why is some fat excreted?

A

Trapped in fiber, exit in faeces

81
Q

What are the membrane transport mechanisms for sugar uptake?

A
  1. Facilitated diffusion (fructose)

2. Secondary active transport (Na+/glucose symporter) (glucose and galactose Needs Na+ gradient. From Na+/K+ ATPase

82
Q

What are the membrane transport mechanisms for amino acid?

A
  1. Secondary active transport
    1. Sodium dependent amino acid symporter (similar to Na+/ glucose symporter)
    2. Required a Na+ gradient
    3. Different symporter for acidic, neutral and basic amino acids.
83
Q

What is the membrane transport mechanism for dipeptides?

A
  1. Secondary active transport
    1. Requires a peptide carrier (symporter) with H+ ions
      Needs a H+ ion gradient.
84
Q

What happens to free fatty acids and monoglycerides which have been digested by lipase?

A

They enter the intestinal epithelial cells were they are then used to resynthesize triglycerides.

85
Q

How do free fatty acids and monoglycerides enter the epithelial cells?

A

Through micelle contact.

86
Q

What happens to free fatty acids and monoglycerides in the epithelial cell?

A

They are resynthesized into triglycerides.

87
Q

What are chylomicrons?

A
  1. They are packages of triglycerides, apolipoproteins, cholesterol and phospholipids.
    1. They are released into central lacteals by exocytosis.
    2. Largest lipoprotein produced by the intestine.
88
Q

What are central lacteals?

A

Lymphatic capillaries

89
Q

Where do lipid soluble molecules go after absorbed by the epithelium?

A
  1. Packaged with other lipids into chylomicrons
    1. Chylomicrons sent to the lymph (via lacteals)
    2. Lymph then feeds chylomicrons into the blood where they disassociate and the lipids within are utilised.
90
Q

Where do water soluble molecules go after being absorbed by the epithelium?

A

They are passed directly into the blood stream except vitamin B12.

91
Q

What is the difference between fat soluble and water soluble vitamin absorption?

A
  1. Water soluble - diffusion into the epithelium in the upper parts of the small intestine
    1. Fat soluble - absorption required bile salts, they are carried by micelles and then diffuse into absorptive cells.
92
Q

What is the difference between fat soluble and water soluble vitamin excretion from epithelium?

A
  1. Water soluble - direct to blood

2. Fat soluble- chylomicrons –> lymph –> blood

93
Q

What are the absorption strategies for vitamin B12?

A
  1. Vitamin B12 binds to intrinsic factor to resist digestion by GIT enzymes
    1. B12- Intrinsic factor complex recognised by surface receptors on mucosal cells at terminal ileum
    2. Absorbed via endocytosis
94
Q

What is intrinsic factor released by?

A

Parietal cells

95
Q

How is B12 transported around the body and what is different about its storage?

A
  1. Transported by transcobalamin II
    1. Stored mainly in the liver. Different because other water soluble vitamins are not stored. (Liver has up to a 3 year supply!)
96
Q

What are the absorption strategies for calcium?

A
  1. Active transport across intestinal epithelium - limited passive diffusion via paracellular route.
    1. Active Vitamin D promotes expression of Calcium transporters (carrier, channels and pumps)
97
Q

What are the absorption strategies for Iron?

A
  1. Haeme iron (Fe2+) easily transported via haeme transporter (20-40% absorbed)
    1. Non haeme iron (Fe3+) must first be reduced by duodenal cytochrome B to be absorbed. Can be absorbed by DMT1 transporter but only (2-4%)
    2. Iron absorption increased by ascorbic acid when body stores are low.
98
Q

What is Ferritin?

A

Intracellular iron storage protein

1. Acts as buffer against iron deficiency/overload
2. Serum levels directly related to amount of iron stored in the body
99
Q

What is the blood iron carrier protein?

A

Transferrin

100
Q

What is an intolerance?

A
  1. It is a hypersensitivity reaction when immune activation occurs to an innocuous (not harmful) stimuli
101
Q

What is required for a hypersensitivity to form?

A

A pre-sensitized immune state of the host - from prior exposure to an antigen or allergen.

102
Q

What is a food allergy?

A

Occurs when an immune response is activated by an otherwise harmless food antigen

103
Q

What is a food intolerance?

A
  1. Occurs when the body has a non-immune reaction to eating a particular food or drink.
  2. Cannot cause severe allergic reactions (anaphylaxis)
  3. Cannot be detected by allergy testing
104
Q

How is an immune intolerance established?

A
  1. Intact mucosal barrier
  2. Active Treg differentiation
  3. Protective IgA antibody production
  4. Dampened innate/adaptive immunity
105
Q

How is a food allergy established?

A
  1. Leaky, damaged mucosal barrier
  2. Th2 immune activation
  3. IgE antibody production
  4. Mast cell, eosinophil, basophil accumulation
106
Q

What is the main difference between lactose intolerance and a milk allergy?

A
  1. Lactose intolerance is a sensitivity (to lactose, a milk carbohydrate)
    1. Milk allergy is an actual immune system reaction to milk protein.
107
Q

How common is lactose intolerance after infancy?

A

4% of the population (rising), up to 90% of adults in some east Asian countries.

108
Q

What is the mechanism of lactose intolerance?

A
  1. Deficiency of Lactase enzyme in brush border cells
  2. Lactase converts D-galactose and D-glucose
  3. Results in unabsorbed lactose
  4. From this there is an increased osmotic load (increased water in lumen to cause diarrhoea)
  5. Along with diarrhoea the lactose is then fermented by colonic microbes leading to short chain fatty acids and GAS which can cause bloating, abdominal pain and flatulence.
109
Q

What is the mechanisms for establishment of food allergy?

A
  1. Food bypasses the tissue through weakened tight junctions between epithelial cells
  2. Leads to loss of tolerance, immune activation and ongoing tissue damage
110
Q

What are some of the reasons tight junctions may be weakened to allow food allergy?

A
  1. Immaturity (infants)
  2. Alcohol ingestion
  3. Inflammation in the gut epithelium and other tissue
111
Q

Why are infants particularly at risk of cows milk protein allergy?

A
  1. Digestive enzymes not fully active
  2. Immature/ low secretory IgA fail to inhibit allergen entry
  3. Increased mucosa permeability
  4. Undigested proteins exposed to immune system
112
Q

How are food allergies diagnosed?

A
  1. Clinical history
  2. Food specific IgE testing
  3. Food avoidance trials
  4. Oral challenges (under controlled conditions)
113
Q

What are some clinical symptom differences between lactose intollerance and milk protein allergy?

A
  1. Lactose - persistent diarrhoea, stomach bloating, Abdo pain, nausea/vomiting
  2. Allergy- bloody/mucous diarrhoea, blood vomiting, iron deficiency, eosinophilia
114
Q

What type of disease in Coeliac?

A

Autoimmune

115
Q

What is Coeliac disease?

A
  1. Gluten sensitivity, causes malabsorption due to impaired function of mucosal tissue.
  2. Predominantly affects Caucasians
116
Q

What is the events that lead to tissue damage in Coeliac?

A
  1. Gluten damages mucosa through an autoimmune process
  2. Partially digested gluten form a immune reactive fragment (gliadin)
  3. Intestinal mucosa becomes permeable to gliadin
  4. Gliadin cross links with transglutaminase and the complex is detected as antigenic
  5. CD4 T cells are activated and anti transglutaminase antibodies (IgG) are formed.
  6. Immune reaction causes inflammation (mucosal villi become blunt or flat) kills cells.
117
Q

What kind of specific autoimmune disease is coeliac?

A
  1. TH1 autoimmune

2. Does not involve IgE or allergic response

118
Q

What is autoimmunity?

A
  1. A misdirected immune response against host tissue
  2. Associated with a breakdown in immune tolerance, which limits immune activation to self antigens
  3. Complex interaction between genetic susceptibility and environmental exposure (triggers)
119
Q

What generally is the hygiene hypothesis?

A

Lack of early childhood exposure to infectious agents and symbiotic microorganisms increased the susceptibility to allergic and autoimmune diseases by stunting the immune system development.

120
Q

What are some of the early life exposures that promote a healthy intestinal microbiota?

A
  1. Breast milk
    1. Vaginal delivery
    2. Infection
    3. Lots of siblings
    4. Furred pets
121
Q

What ate some of the early life exposures that trend towards dysbiotic (unhealthy) intestinal microbiota?

A
  1. Infant formula
    1. Caesarean delivery
    2. Antibiotic exposure
    3. No/low number of siblings
122
Q

What is the relationship between helminths and the rate of autoimmune disease?

A

Inverse. More helminths = less autoimmune disease e.g. in Asia there is more helminths

123
Q

What are general feeding requirements of babies-infants?

A
  1. Milk as long as you like first 12 months or longer preferred.
  2. Food starts around 6 months (milk not enough on its own past 12 months)
124
Q

What are some of the benefits of breastfeeding?

A
  1. Ideal nutrition (no risk of milk protein allergy)
    1. Antibodies in breast milk
    2. Associated with reduced disease risk
    3. Helps uterus contract post birth
    4. Reduces risk of post natal depression
    5. Cheaper
    6. Helps babies microflora environment develop
125
Q

What are normal patterns or growth?

A

Head, weight and height all track normally

126
Q

What is an abnormal pattern of growth?

A

Growth rates that drop a centile grade

127
Q

What are common causes of poor growth in young children?

A
  1. Family history
    1. Growth hormone deficiency
    2. Hypothyroidism (underactive thyroid)
    3. Poor nutrition
    4. Malabsorption
    5. Severe stress
128
Q

How often should a babies poo in the first 6 weeks?

A
  1. Breastfed- 3 per day but 4-12 can still be considered normal
    1. Formula fed- 1-4 per day, after first month may only be once a day.
129
Q

How should babies poo appear in the first 6 weeks?

A
  1. Breastfed- Runny and yellow

2. Formula fed- light brown or green

130
Q

How will stool change after solid foods?

A
  1. Breastfed- more stool

2. Formulafed- 1-2 stools a day

131
Q

How often should adults poo?

A

3 times per day - 3 times per week

132
Q

What are some dietary effects on stool patterns?

A
  1. Fibre reduces transit time
133
Q

Define diarrhoea.

A

a condition in which faeces are discharged from the bowels frequently and in a liquid form. Over 3 watery stool per day.

134
Q

What is the name for fatty faeces?

A

Steatorrhea- pale, oily

135
Q

Chronic diarrhoea causes?

A 
Coeliac
Cystic fibrosis
Crohns
Ulcerative colitis
Surgical resection
C.diff
Giardia
IBS
Laxatives
Other medications
Malabsorption syndromes
Bile salt malabsorption
136
Q

What are the dietary sources of essential amino acids?

A

Meat
Eggs
Seafood
Dairy

137
Q

What are the dietary sources of essential fatty acids?

A

Fish
Nuts
Plant oils

138
Q

What are signs of malnutrition and or malabsorption?

A 
Weight loss
Muscle wasting
Fatigue
Depression
Weakness
etc
139
Q

some indicators for a baby in pain:

A

Draws legs up

Grabs at area of pain.

140
Q

Where is B12 absorbed?

A

Terminal ileum.

141
Q

B12 deficiency symptoms

A

depression, psycosis, palor

etc

JMP Semester 2 (8 decks)

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