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GIR Test 3 > B5.060 Nutrition Metabolism > Flashcards

B5.060 Nutrition Metabolism Flashcards

1
Q

rom 4 criteria for IBS

A

recurrent abdominal pain, on average, at least 1 day/ week in the last 3 months, associated with 2 or more of the following criteria:

  • related to defecation
  • associated with a change in stool frequency
  • associated with a change in stool form (appearance)
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2
Q

subtypes of IBS

A

25% IBS-C: constipation predominant
15-45% IBS-D: diarrhea predominant
IBS-M: mixed
IBS-U: unspecified

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3
Q

IBS-C screening and diagnosis

A

screen based on nutrition and clinical history (radiography, colonoscopy)
slow colonic transit
disordered rectal evacuation (increase fiber and osmotic laxatives)

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4
Q

IBS-D screening and diagnosis

A

rule out Celiac’s (4-5x more likely in IBS-D patients), disaccharidase deficiencies, food allergies, gluten intolerance, colitis, bile acid malabsorption, SIBO, stool culture, colonoscopy

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5
Q

other symptoms of IBS

A

reflux, dysphagia, early satiety, dyspepsia, nausea, bloating, gas, dysmenorrhea, fibromyalgia, increased urinary frequency/urgency

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6
Q

alarm/atypical symptoms

A 
weight loss
rectal bleeding
anemia
nocturnal
progressive
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7
Q

where are carbs, protein, and lipids digested and absorbed

A

in the small intestine

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8
Q

brush border

A

surface area for absorption in the small intestine is greatly increased

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9
Q

give an overview of carbohydrate digestion and absorption

A

only monosaccharides are absorbed
Na+ dependent cotransport: glucose & galactose
facilitated diffusion: fructose

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10
Q

classify lactase deficiency

A

70% of world population after weaning
inducible if you eat enough lactose
does not mean no dairy: cheese, butter, most yogurt and small amounts of milk and ice creams can be ok
most handle 12 g/meal of lactose

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11
Q

function of lactase

A

degrades lactose to glucose & galactose

lactose intolerance due to lactase deficiency

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12
Q

symptoms of lactose intolerance

A

bloating, diarrhea, gas

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13
Q

what are oligosaccharides

A

3-10 sugar units
ex: raffinose, stachyose
found in beans

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14
Q

dysregulation in oligosaccharide digestion

A

undigested oligosaccharides may be fermented by bacteria in large intestine

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15
Q

digestible polysaccharides

A

starch with a-glycosidic bonds

a-glucosidases in the brush border membrane hydrolyze polysaccharides to monosaccharides

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16
Q

indigestible polysaccharides

A

fiber with B-glycosidic bonds
B-glucosidases not present in our bodies
go into large intestine and become food for the gut microbiome

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17
Q

what is the FODMAP diet

A

restricting poorly absorbed carbohydrates
Fermentable Oligo, Di, Monosaccharides And Polyols
family of poorly absorbed, short chain carbohydrates
highly fermentable in the presence of gut bacteria, leading to gas and discomfort
osmotically active

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18
Q

example of FODMAP substances

A

lactose
fructose
fructo- and galacto-oligsaccharides (fructans and galactans)
polyols (sorbitol, mannitol, etc.)

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19
Q

how long should you do the FODMAP diet

A

short term - 8 weeks

during high stress periods when you have high frequency of IBS symptoms

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20
Q

example of FODMAP foods

A

fructans- wheat, rye, onions, garlic
galactans- legumes
lactose- milk
fructose- honey, apples, pears, watermelon, mango
sorbitol- apples, pears, peaches, sugar free items
mannitol- mushrooms, cauliflower, sugar free items

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21
Q

types of fiber

A

insoluble fiber such as wheat bran may exacerbate IBS

soluble fiber more beneficial

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22
Q

function of insoluble fiber

A

increase fecal bulk

decreased intestinal transit time

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23
Q

sources of insoluble fiber

A

whole grains

vegetables

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24
Q

function of soluble fiber

A

delays gastric emptying
slows glucose absorption
decreases blood choelsterol

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25
Q

sources of soluble fiber

A

fruits
vegetables
rice bran
psyllium seed

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26
Q

most common IgE associated food allergens

A 
milk
eggs
peanuts
tree nuts
soy
fish
shellfish
wheat
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27
Q

symptoms of food allergies

A

GI (70%)
cutaneous (24%)
respiratory (6%)

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28
Q

anaphylaxis

A

acute, severe allergic response that results in lowered BP, respiratory and GI distress
can be fatal

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29
Q

risk factors for allergies

A

family history of allergies
history of prior allergen exposure
GI permeability
atopic dermatitis

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30
Q

give an overview of protein digestion/absorption

A

occurs throughout small intestine
protein balance reflects the sum of protein synthesis and degradation
protein turnover is dynamic

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31
Q

describe amino acids

A

proteins are made from 20 different AAs, 9 are essential
each AA has an amino group, an acid group, a hydrogen atom, and a side group
side group makes each AA unique

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32
Q

disorders of AA metabolism and transport

A

1 in 1000 newborns

autosomal recessive

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33
Q

discuss the biochemical pathways of protein digestion

A

pancreatic juices contain proteolytic enzymes in their inactive, precursor forms
when juice enters duodenal lumen, trypsinogen contacts enterokinase expresses on enterocytes
trypsinogen is cleaved to trypsin which can activate additional trypsin and the remaining proteolytic enzymes

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34
Q

absorption of proteins

A

dipeptides and tripeptides are transported into intestinal cells
cytoplasmic peptidases hydrolyze them into AAs

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35
Q

where is excess protein stored?

A

it can’t be

need to eat protein every day or the body breaks down tissues

36
Q

what is Kwashiorkor protein malnutrition

A 
fat & lean mass is lost
edema from low plasma oncotic pressure
hair pluckability & color change, skin breakdown, poor wound healing, dermatitis, edema
trauma/sepsis patients susceptible
requires aggressive nutrition support
37
Q

marasmus

A

body fat stores have been exhausted due to starvation and muscle wasting follows

38
Q

cachexia

A

state that involves substantial loss of fat and lean body mass in the presence of chronic inflammation and disease

39
Q

nutritional consequences of kidney failure

A

accumulation of nitrogenous waste
decreased production of active vit D
decreased production of EPO
decreased glucose production
decreased degradation of bioactive peptides
accumulation of water, Na, K, inability to handle phosphorus, magnesium, or other vitamins and minerals

40
Q

diet for persons with CKD (stage 4)

A 
energy intake: 25-35 kcal.kg
low protein
low sodium
no fluid restriction
low potassium
low phosphorus
moderate calcium
individualize vit D, iron, and zinc
41
Q

why control energy intake in CKD?

A 
minimize protein energy malnutrition
tissue catabolism increases the kidney load of nitrogenous waste
indirectly limits phosphorus
less protein-induced hyperfiltration
lowers intraglomerular pressure
42
Q

effects of protein restriction of diabetic nephropathy

A

slows progression

43
Q

what is celiac disease

A

adverse response to gluten storage proteins (gliadin) that triggers an immune response resulting in damage to the mucosa of the small intestine

44
Q

3 components necessary for development of Celiac’s

A
  1. you must inherit the gene (HLA, DQ2 and/or DQ8)
  2. consume gluten
  3. have the gene triggered (stress, trauma, viral infection)
45
Q

health risks associated with celiac

A 
classic steatorrhea
increased stool mass
weight loss, weakness
iron def anemia
metabolic bone loss
inflamed mucosa
46
Q

symptoms of inflamed mucosa

A

edema, protein malabsorption
non-absorption of healing agents
leaky gut

47
Q

long term effects of celiacs

A

undiagnosed or poor diet adherence have increased mortality
metabolic bone disease
increased risk of DM1 and thyroiditis
increased risk of non Hodgkin lymphoma

48
Q

effect of gliadin

A

triggers immune response

more permeable intestine increases gliadin peptide access to immune cells

49
Q

consequences of gliadin ingestion

A

villous atrophy
decreased surface area for absorption
chronic inflammation downregulates transport proteins in epithelium
decreased CCK and secretin resultin in pancreatic insufficiency
bacterial overgrowth

50
Q

diarrhea in celiac

A

steatorrhea due to changes in jejunal mucosal function
secondary lactase deficiency
bile acid malabsorption
endogenous fluid secretion from crypt hyperplasia

51
Q

long chain triglyceride digestion and absorption

A
  1. digestive phase that includes lipolysis and micelle formation requiring pancreatic lipase and conjugated bile acids respectively
  2. absorptive phase for mucosal uptake and re-esterification
  3. postabsorptive phase that includes chylomicron formation and exit into lymphatics
52
Q

medium chain triglyceride digestion and absorption

A
  1. do not require pancreatic lipolysis, absorbed intact by intestinal epithelim
  2. after absorption, MCTs are hydrolyzed by MCFAs
  3. MCT exit is via portal vein and not lymphatics
53
Q

malabsorption of lipid

A 
usually do to lipase deficiency
-pancreatic disease > inadequate lipase
-hypersecretion of gastric > low duodenal pH > inactive lipase
depleted bile acids pool
-ileal resection
-bacterial overgrowth
54
Q

symptoms of malabsorbed sugars

A

bloating
gas
explosive diarrhea

55
Q

symptoms of protein malabsorption

A

dry hair
hair loss
fluid retention (edema, swelling)

56
Q

symptoms of fat malabsorption

A

light colored, foul smelling stools that are soft and bulky

57
Q

diet for person on stage 5 dialysis

A 
increased energy intake from stage 4
increased protein from stage 4
low sodium
fluid restriction
low phosphorus
moderate calcium
moderate potassium
58
Q

multivitamin for person on dialysis

A

renal vitamin to supplement B and C vitamins
sometimes have zinc and iron too
take after dialysis so nutrients aren’t lost

59
Q

fat soluble vitamins and dialysis

A

A,D,E,K

too large to pass through dialyzer membrane, can accumulate in blood at dangerous levels

60
Q

water soluble vitamins and dialysis

A

B,C

pass through membrane and removed from body with fluid and wastes

61
Q

normal fat soluble vitamin absorption

A

A,D,E,K
ingested as esters
digested by cholesterol esterase
highly insoluble in gut, absorption dependent on incorporation into micells

62
Q

normal water soluble vitamins absorption

A

thiamin, riboflavin, niacin, pyridoxine, pantothenate, biotin and ascorbic acid are Na+ dependent co-transport
folate is Zn dependent
B12 more complicated

63
Q

causes of B12 def

A

decreased absorption ability

achlorhydria, esp in elderly

64
Q

consequences of B12 def

A

pernicious anemia
nerve degeneration, weakness
tingling/numbness in extremities
paralysis and death

65
Q

calcium digestion and absorption

A

30-80% of ingested is absorbed
intestinal transport process regulated by calcitriol
calcitriol level falls with increased plasma Ca2+
absorption increased with Ca2+ def

66
Q

iron digestion and absorption

A

3-6% of ingested iron is absorbed
most of iron in diet is ferric, but ferrous (Fe2+) is absorbed
Fe3+ reduced to Fe2+ by ascorbic acid in lumen
absorption regulated by dietary intake, current state of iron stores, and state of EPO

67
Q

anabolic pathways

A

reactions that form cellular molecules
energy requiring
molecules are building blocks for macromolecules (proteins, nucleic acids, lipids, etc)

68
Q

catabolic pathways

A

CHO, protein, and fat oxidized to CO2 and H2O and liberated electrons passes to O2 to make ATP
principle pathways: glycolysis, TCA, ETC, oxidative phosphorylation, hexose monophosphate shunt

69
Q

hormones secreted in fed state

A

glucose dependent insulinotropic peptide (+ insulin)
CCK (+ gallbladder contraction)
gastrin (+gastric motility and gastric acid release)
secretin (+pancreatic juice and enzyme secretion)

70
Q

chemical messengers stimulating hormone secretion in fed state

A

glucose
AAs
FAs

71
Q

importance of insulin

A

primary hormone responsible for direction of energy metabolism during fed state

72
Q

very fast insulin effects

A

insulin stimulated membrane changes

GLUT4 translocation

73
Q

fast insulin effects

A

activation of inhibition of enzymes

insulin stimulated synthesis of glycogen, TG, and protein while inhibiting opposing catabolic actions

74
Q

slower insulin effects

A

further regulation of enzyme action by selective induction or repression of enzyme synthesis
increased glucokinase synthesis by promoting gene activity

75
Q

slowest insulin effects

A

promotion of growth through mitogenesis and cell replication

76
Q

effects on insulin on muscle and adipose

A

uptake of glucose via translocation of GLUT4

77
Q

effects of insulin on adipose

A

increases fatty acid uptake and TAG storage via increase in activity of lipoprotein lipase
concomitantly, insulin decrease lipolysis via decrease in activity of hormone sensitive lipase

78
Q

endocrine function in fasting state

A

liver glycogenolysis is used to maintain blood glucose levels and fatty acids are used to make ketone bodies for organ systems and tissues to use for gluconeogenesis decreasing overall demand and depletion of glucose use and stores

79
Q

substrates for gluconeogenesis in liver

A

lactate
glycerol
alanine

80
Q

stimulants of hepatic gluconeogenesis

A

glucagon
epi & NE
low levels of insulin

81
Q

glucagon overview

A

synthesized in a cells of pancreas
secreted when circulating glucose is low (some AAs like alanine stimulate secretion)
primary site of action is liver
increased cAMP levels in cell to phosphorylate proteins

82
Q

glucose metabolism in fed state

A

liver takes up blood glucose and stores as glycogen or converts to adipose

83
Q

fat metabolism in fed state

A

packed into CM or packaged at liver in VLDL and transported in circulation to adipose for storage

84
Q

AA metabolism in fed state

A

processed at liver to be stored as glycogen, used to make fat, or sent to muscle
used by various tissues to synthesize proteins and nitrogen-containing compounds

85
Q

glucose metabolism in postabsorptive early fasting state

A

liver glycogen major provider of glucose for whole body
when glycogenolysis is occurring, synthesis of glycogen and TG in the liver is diminished and gluconeogenesis begins to increase to help maintain blood glucose levels
-lactate from muscle and RBCs important source of carbons for GNG
-glucose-alanine cycle provides pyruvate for GNG
-glycogen lasts 24 hours

86
Q

overall changes during fasting state (18-48 hours)

A

glycogen depleted and GNG picks up
AA from muscle breakdown provide man of the substrates for GNG
glycerol from lipolysis also and lactate from anaerobic metabolism of glucose also contributes the some extent

87
Q

metabolism during the starvation state >2-3 days

A

metabolic shift to spare body protein
GNG to lipolysis as fat becomes major supplies of GNG to spare protein
glycerol liberated from TG breakdown still used by liver to make glucose
blood levels of FA increase sharply
amount of excess stores determine survival time

GIR Test 3 (19 decks)

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