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411 > W12 nutrient absorption and malnutrition > Flashcards

W12 nutrient absorption and malnutrition Flashcards

1
Q

What are secretory vesicles that leave the golgi called ?

A

Condensing granules

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2
Q

Describe enzyme synthesis and secretion in acinar cells

A

Synthesized and folded in RER on basal side —> golgi where they are glycosylated —> condensing granules leave the golgi —> mature zymogen granules (contain both zymogens and active enzymes) —> accumulate at apical end until stimulatory signal for exocytosis

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3
Q

What fats are produced by acinar cells ?

A

Lipases
Colipase
Cholesterol ester hydrolase
Phospholipase A2

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4
Q

What proteins are produced but acinar cells ?

A

Trypsin
Chymotrypsin
Elastase
Carboxypeptidase

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5
Q

What inactive enzyme fats are produced by acinar cells ?

A

Procolipase

Prophospholipase A2

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6
Q

What inactive protein enzymes are produced by acinar cells ?

A

Trypsinogen
Chymotrypsinogen
Proelastase
Pro-carboxypeptidase A and B

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7
Q

Where in the duodenum is enterokinase present ?

A

Brush border of the duodenal mucosal epithelial cells

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8
Q

What is the function of enterokinase in the duodenum ?

A

Acts on trypsinogen —> trypsin activation peptide (TAP) —> trypsin

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9
Q

What is the function of trypsin in the duodenum ?

A

Act on pancreatic pro-enzymes —> enzymes

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10
Q

Why are active enzymes important in the duodenum?

A

Cleave large peptides —> small peptides —> amino acids —> intestinal cells take up AAs

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11
Q

Describe pancreatic exocrine secretions during the cephalic phase

A

Thoughts, taste, smell of food —> pancreatic secretory stimuli
Vagal cholinergic nerves —> enteric intrinsic nerves —>
1. Release ACh to stimulate enzyme secretion by pancreatic acini
2. Release ACh and vasoactive intestinal peptide (VIP) to potentiate alkaline fluid secretion by ductal cells

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12
Q

Describe exocrine secretions of pancreas during the gastric phase ?

A

Stretch induced vasovagal reflex —> cholinergic nerves induce enteric intrinsic nerves to further:
- release ACh —> enzyme secretion by acini
- release ACh and VIP to activate alkaline fluid production by ductal cells
Peptides produced by digestion by pepsin —> enteroendocrine G cells in gastric epithelium —> Gastrin —> weak CCK receptor agonist to induce pancreatic secretions

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13
Q

Describe exocrine secretions of the pancreas during the intestinal phase

A

Neuroendocrine cells in intestine —> secrete hormones —> coordinate actions of food digestion
Chyme in SI —> secretin and CCK —> secretion of digestive enzymes from acini and alkaline fluid from ducts
CCK reinforces vago-vagal reflex arc —> maintain max pancreatic secretion
Vagovagal enteropancreatic reflex responds to presence of proteins and lipids —> acinar cells by inducing ACh release from nerves —> Ach binds to M3 receptor on acinar cells

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14
Q

_______ and ________ stimulate more secretion than _______ and _______ induce more secretion than ________

A 
Monoglycerides
Free fatty acids
Proteins
Proteins 
Carbohydrates
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15
Q

Describe ductal cell structure

A

Simple cuboidal or columnar
Form hollow tubes
Basally located nuclei
High # of mitochondria

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16
Q

How does bicarbonate secretion into the lumen occur ?

A

Via a Cl and HCO3 exchange mechanism

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17
Q

what detects low pH in the intestine ?

A

S-cells

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18
Q

What does detection of low pH of the chyme in the intestine stimulate ?

A

Secretion of secretin

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19
Q

What stimulates bicarbonate secretion in the small intestine ?

A

Ach (minor)

Secretin

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20
Q

Describe secretin —> bicarbonate secretion mechanism

A

Secretin —> bind secretin receptor on ductal cells and activates cAMP production —> activation of PKA —> CFTR (chloride ion channel) —> Cl- ions pumped into lumen —> unequal ion gradient —> H2O and Na+ pulled through intercellular junction —> contransport of Na+ and HCO3 across cell membrane brings bicarbonate into cytoplasm from submucosa
HCO3 is secreted into ductal lumen bu Cl- anti porter which recycles Cl-

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21
Q

What is critical for bicarbonate secretion ?

A

CFTR function

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22
Q

What are the consequences of reduced exocrine function ?

A 
Exocrine insufficiency 
Acute pancreatitis 
Chronic pancreatitis 
Diabetes 
Pancreatic ductal adenocarcinoma
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23
Q

What are the 4 basic GI processes ?

A

Motility, secretion, digestion, absorption

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24
Q

What is digestion ?

A

Biochemical breakdown of nutrients into their molecular components

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25
Q

What are carbohydrates composed of ?

A

Monosaccharides
Disaccharides
Polysaccharides

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26
Q

What enzymes are involved in the breakdown of carbohydrates ?

A

Amylase, sucrase, lactase, maltase

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27
Q

What enzymes are involved in the breakdown of proteins ?

A

Pepsin, trypsin, chymotrypsin, carboxypeptidase, aminopeptidases

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28
Q

What enzyme is involved in the breakdown of fats ?

A

Lipase

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29
Q

Where does absorption of digested nutrients, water and electrolytes primarily occur ?

A

Across the membrane of epithelial cellls in the small intestine

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30
Q

What happens to carbohydrate and protein breakdown products when they travel through the epithelial cells ?

A

Enter the blood

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31
Q

What happens to fat breakdown products when they travel through the epithelial cells ?

A

They enter the lymphatic system

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32
Q

What is the purpose of the alkaline fluid secreted by the pancreas ?

A

Neutralize acidic gastric chyme

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33
Q

What do duct cells in the pancreas secrete ?

A

Secrete aqueous NaHCO3 solution

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34
Q

What do acinar cells in the pancreas secrete ?

A

Digestive enzymes

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35
Q

What 3 enzymes secreted by the pancreas hydrolyse peptide bonds?

A

Trypsinogen
Chymotrypsinogen
Pro carboxypeptidase

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36
Q

Why does the pancreas secrete trypsin inhibitor ?

A

To inhibit any activated trypsin in the pancreas

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37
Q

What activates trypsinogen (—> trypsin) ?

A

Enterokinase

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38
Q

What is the only enzyme that can digest fats ?

A

Lipase

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39
Q

What causes steatorrhea ?

A

Lack of lipase —> ingested fats remain too large to absorb

~60-70% of ingested fats are excreted in the feces

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40
Q

How much pancreatic aqueous alkaline solution is secreted each day ?

A

1-2 litres

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41
Q

How is bile delivered to the duodenum ?

A

The sphincter of Oddi

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42
Q

Where are the majority of bile salts reabsorbed ?

A

Terminal ileum

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43
Q

Composition of bile salts

A

Deprotonated molecules, negatively charged

Derived from cholesterol but with negatively charged hydrophobic tail

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44
Q

What is lecithin

A

A component of cell membranes

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45
Q

What regulates the release of bile ?

A

CCK triggers the contraction of the gall bladder and the relaxation of the sphincter of Oddi
Vagal efferents augment this response

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46
Q

What regulates the production and secretion of bile ?

A

Neuronal- vagal input increases bile production

Hormonal- secretin stimulates the production and secretion of the NaHCO3 component of bile

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47
Q

What causes the inhibition of bile ?

A

Fats have left duodenum:
- CCK levels drop
- the sphincter of Oddi closes
—> bile cannot enter the duodenum

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48
Q

when do hepatocytes stop manufacturing bile ?

A

When the circulating bile salt concentration in the enterohepatic circulation declines

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49
Q

How are fats digested in the small intestine and what components are absorbed ?

A

Completely hydrolysed by pancreatic lipase

Monoglycerides and free fatty acids are absorbed

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50
Q

How are proteins digested and absorbed in the small intestine ?

A

Reduced to small peptide chains and some unitary amino acids by pancreatic proteolytic enzymes
Peptide fragments require further hydrolysis by aminopeptidases in the epithelial brush border prior to their absorption

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51
Q

How are carbohydrates digested and absorbed by the small intestine

A

Broken into disaccharides and some monosaccharides

Further hydrolysed by disaccharidases in the epithelial brush border.

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52
Q

What secretes amylase ?

A

Salivary glands in mouth

Exocrine pancreas

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53
Q

What is the site of action for pepsin ?

A

Stomach antrum

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54
Q

Where do trypsin, chymotrypsin and carboxypeptidase act?

A

Small intestine lumen

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55
Q

Where do aminopeptidases act ?

A

Small intestine brush border

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56
Q

What secretes aminopeptidases ?

A

Small intestine epithelial cells

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57
Q

What increases the surface area of the small intestine for absorption ?

A

Circular folds
Villi
Brush border
- microvilli

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58
Q

What holds together epithelial and mucous cells?

A

Tight junctions

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59
Q

What does the brush border contain ?

A

Enzymes that hydrolyse peptides/disaccharides
Enterokinase
Transmembrane carrier proteins

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60
Q

What is contained in the crypts of Lieberkuhn ?

A

Mucous cells: primary locus for success entericus secretion

Stem cells that constantly produce new epithelial cells

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61
Q

Why is bile neccassary for the digestion of fats ?

A

Lipase can only act on the surface of fat aggregates

Bile salts act as a detergent and emulsify large fat aggregates into smaller pieces

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62
Q

How do fat droplets repel other droplets ?

A

The negatively charged hydrophilic tails of of bile salts repel each other

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63
Q

What is the function of colipase ?

A

Anchor lipase to the bile salts at the surface of a fat droplet

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64
Q

Describe the structure and function of micelles

A

4-7 nm in diameter
Composed of bile salts, lecithin and cholesterol (core), hydrophilic tail shell
Shuttle digested fat molecules to the epithelial surface

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65
Q

What hydrolyses disaccharides into their constituent monosaccharides ?

A

Disaccharidases in the brush border

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66
Q

How are glucose and galactose absorbed

A

Secondary active transport

  • co-transported into the cell with Na+ ions
  • passively diffuses into the interstitial fluid through a membrane channel
  • enter a capillary
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67
Q

How does fructose pass through the epithelium ?

A

Passively diffuses through the epithelial cell by means of facilitated diffusion

68
Q

What are the 3 sources of endogenous proteins ?

A

Digestive enzymes that have been digested themselves
Proteins from sloughed epithelial cells
Plasma proteins that have leaked into the GI tract lumen

Up to 1/2 of each days protein absorption

69
Q

What are peptide fragments hydrolysed by and where ?

A

Aminopeptidases in the brush border

70
Q

How are peptide fragments absorbed ?

A

Secondary active transport with Na+ ions

Enter capillaries in the laminate propria of the villus

71
Q

How does fat absorption differ from that of proteins and carbohydrates ?

A

Completely digested by pancreatic lipase

72
Q

How do digested fats cross the brush border?

A

Diffusion

73
Q

What is combined to form triglycerides in the cytosol ?

A

Monoglycerides and free fatty acids

74
Q

What forms chylomicrons ?

A

Triglycerides and bipolar lipoproteins

75
Q

Where do chylomicrons go ?

A

Into the central lacteal of the lymphatic system

76
Q

What are the two categories of motility ?

A

Mixing movements

Propulsive movements

77
Q

What are the accessory organs of the GI system ?

A

Pancreas, liver, gallbladder, and salivary glands

78
Q

What 4 factors regulate the motility and secretion of the GI tract

A

Intrinsic electrical properties of smooth muscle cells
enteric nervous system
Autonomic nervous system
GI hormones

79
Q

Where do preganglionic sympathetic fibres from the CNS synapse ?

A

In prevertebral ganglia

80
Q

Where do preganglionic parasympathetic fibres from the CNS synapse when they enter into the GI wall?

A

Postganglionic fibres within the ENS

81
Q

What are the 3 different pairs of salivary glands outside the oral cavity?

A

Parotid
Submandibular
Sublingual

82
Q

What are the most important proteins and enzymes in saliva ?

A

Amylase, lysozyme and mucus

83
Q

What is the function of lysozyme ?

A

Lyses the cell wall of some bacteria —> some protection against infection

84
Q

What control is the rate of production of saliva under ?

A

Autonomic control

85
Q

How does parasympathetic activation affect production of saliva ?

A

Increased production of all secretions

86
Q

How does sympathetic stimulation affect saliva?

A

Decrease in fluid volume but increase in mucous production —> dry sticky mouth

87
Q

Describe fluid volumes as it moves through the small and large intestine

A

~8200 mL enters small intestine daily
~6700 mL reabsorbed from small intestine
~1400 mL reabsorbed in large intestine
100 mL excreted in feces

88
Q

What is the succus entericus ?

A

Aqueous salt and mucous solution secreted from the small intestine
~1.5 litres / day

89
Q

What is the function of the succus entericus

A

Lubricate passage through lumen
protects mucosa from acid injury
Hydrolysis

90
Q

How is water reabsorbed in small intestine

A

Na+ actively pumped into interstitium via Na+/K+ ATPase
Na+ ions in interstitial fluid —> hypertonic —> attract water from the lumen
Hydrostatic pressure moves water into capillary network

91
Q

How is Na+ absorbed in the small intestine ?

A

Into epithelial cells: via Na+ channels
Absorbed passively
Through tight junctions (when luminal Na+ concentration is high)

92
Q

How is Cl- absorbed in small intestine ?

A

Cl- ions passively follow the electrical gradient established by Na+ active movement into the interstitium

93
Q

What can produce an acid base imbalance

A

Large loss of electrolytes via vomiting or diarrhea

94
Q

What acid base imbalances do diarrhea and vomiting result in?

A

Vomiting: metabolic alkalosis
Diarrhea: metabolic acidosis

95
Q

What are the consequences of prolonged diarrhea ?

A

Malnutrition
Dehydration
Acid-base disturbance

96
Q

What are the possible causes of diarrhea ?

A

Excessive intestinal motility
Hyper-osmotic chyme
Toxins

97
Q

How can excessive intestinal motility cause diarrhea?

A

Irritation of the GI tract wall
Bacterial/viral infection
Emotional stress

98
Q

How can hyper-osmotic chyme result in diarrhea?

A

—> luminal fluid accumulation

99
Q

Mechanism of diarrhea caused by toxins

A

Inhibit Na+ absorption or stimulate Cl- excretion into intestinal lumen —> osmotic fluid movement into the lumen

100
Q

Differentiate between maldigestion and malabsorption

A

Maldigestion: defective hydrolysis of nutrient s
Malabsorption: defective mucosal absorption

101
Q

Examples of luminal defects that can cause maldigestion/malabsorption

A

Bile acid deficiency
Lactase deficiency
Pancreatic enzyme deficiency
Atrophic gastritis

102
Q

Examples of mucosal defects that can cause maldigestion/malabsorption

A

Celiac disease
Crohn disease
Congenital defects of transporters
Intestinal resection

103
Q

Examples of transport defects that can cause maldigestion/malabsorption

A 
Vasculitis
Portal hypertension 
Cardiac disease
Intestinal lymphangiectasis 
Retroperitoneal fibrosis
104
Q

What is anthropometry?

A

Measures of body composition

  • BMI
  • height, weight
  • hip to waist ratio
  • skinfold
  • muscle bulk
105
Q

Screening tests for nutritional status

A

Subjective global assessment (SGA)
- physical exam: sc fat, edema, muscle bulk
Mini nutritional assessment
- includes BMI or sc fat

106
Q

What are the criteria for classifying a patient as well nourished ?

A
  • weight loss and muscle wasting

- currently eating well and gaining weight

107
Q

What are the criteria for a classification as mild/moderate malnutrition?

A 
Moderate weight loss (5-10%) 
Compromise in food intake 
Continued weight loss 
Progressive functional impairment 
Moderate stress
108
Q

What are the criteria for classifying a patient as having severe malnutrition?

A

Severe weight loss (>10%)
Poor nutrition intake
Progressive functional impairment
Muscle wasting

109
Q

What blood tests can be useful in accessing nutritional status?

A 
CBC 
Electrolytes 
Lipid panel 
Liver panel 
Ca, PO4, Mg 
Coag 
B12, folate
TSH 
Anti-tTG IgA
110
Q

What stool tests can be useful in disease of malabsorption/maldigestion ?

A

Fat
Elastase , chymotrypsin
PH
C&S, O&P, Cdiff

111
Q

What is a hydrogen breath test and what does it test for ?

A
  • measures lactose levels
  • increase >20 ppm after ingesting 20-50g lactose —> lactose absorption issues
    If baseline is high —> too much bacteria in GI
112
Q

What does the Schilling test look for ?

A

B12 deficiency

113
Q

What is fecal elastase/chymotrypsin a good measure of ?

A

Low —> pancreatic insufficiency

114
Q

What is pernicious anemia ?

A

Vitamin B12 anemia caused by a lack of intrinsic factor being secreted from the stomach —> intestine cannot properly absorb B12

115
Q

What is step 2 of the Schilling test ?

A

Confirm cause

- stomach (intrinsic factor), pancreas (pancreatic insufficiency), bacterial (SIBO)

116
Q

What might you see on a CT scan in a patient with Crohn disease

A

Terminal ileum inflammation

117
Q

What makes up the celiac iceberg ?

A 
Classic
Atypical 
Silent 
Latent 
Potential 
Refractory
118
Q

What is atypical celiac disease ?

A

Gluten sensitive enteropathy, extra intestinal symptoms and signs (short, anemic, osteoporosis, infertile)

119
Q

What is latent celiac disease ?

A

Normal villus architecture on gluten containing diet but have had/ will have gluten sensitive villus atrophy

120
Q

What is potential celiac disease ?

A

Never had a biopsy consistent with celiac disease but show immunological abnormalities characteristic for the disease

121
Q

What damage is seen in the mucosa of the small intestine in someone with celiac disease?

A

Villus atrophy
Crypt hyperplasia
Enterocyte disarray
Inflammatory infiltrates

122
Q

What happens to the release of bile salt and pancreatic enzyme in response to meals in patients with celiac ?

A

Decreases

123
Q

What serologies can be done to diagnose celiac disease?

A

anti-tTg IgA
Anti-endomysial antibody
Anti-gliadin antibodies (IgA, IgG)

124
Q

What should be done to diagnose celiac disease?

A

Small bowel biopsy

125
Q

What might you see on endoscopy of a patient with celiac disease?

A

Scalloping of duodenum

Marbelization of duodenum

126
Q

Anorexia definition

A

Loss of appetite or reduced caloric intake

127
Q

What is cachexia ?

A

Multifactorial syndrome of continuous involuntary loss of skeletal muscle mass, which cannot fully be reversed by conventional nutritional support and includes 3/5 of:

  • decreased muscle strength
  • reduced muscle mass
  • fatigue
  • anorexia
  • biochemical alterations (anemia, inflammation)
128
Q

Definition of anorexia-cachexia syndrome

A

Involuntary loss of weight and appetite with advanced illness
- distinct from FTT, sarcopenia (age related muscle loss) and starvation (reversible)

129
Q

What is the pathogenesis of anorexia cachexia ?

A

Cytokine driven causing dysregulation in 3 main groups:

  • altered intake
  • inflammation/catabolism
  • anabolic dysbalance
130
Q

What causes altered intake in anorexia cachexia

A

Abnormal satiety signals, neuro-hormones, autonomic dysfunction
—> lack of hunger, taste abnormalities, early satiety

131
Q

What causes inflammation/catabolism in anorexia cachexia

A

Increased resting energy expenditure/hyper metabolism

—> increase in acute phase proteins, fever, fatigue, decreased haemopoiesis

132
Q

What causes anabolic dis balance in anorexia cachexia ?

A

Alteration of hypothalamic regulated anabolic hormones —> muscle wasting

133
Q

Treatment for anorexia cachexia

A

Medical optimization of secondary nutrition impact symptoms and acute/chronic conditions

134
Q

Non-pharmacological treatment of anorexia cachexia

A

Counseling/education

Consultation with nutritionist

135
Q

Pharmacological treatment of anorexia cachexia

A

May improve quality of life.

  • progesterone analogs: weeks to take effect
  • corticosteroids: days for effect, improve appetite, pain, energy nausea, but have side effects: delirium, insomnia, gastritis
  • cannabinoids
136
Q

What is important to note in artificial hydration and nutrition in patients with anorexia cachexia ?

A

No evidence that it prolongs life or improves quality of life
—> generally not indicated

137
Q

What is required for transmission of a parasite ?

A

Reservoir host

A route of infection

138
Q

How can parasites cause disease in humans?

A

Mechanical effects
Invasion and destruction of host cells
Allergic or inflammatory immune reaction
Competition for specific nutrients

139
Q

What are the two forms of Protozoa ?

A

Trophozites: motile
Cysts: resting stage

140
Q

Common type of amoeba

A

Entameoba

141
Q

Common type of flagellate

A

Simple trophozoites and cysts:
Giardia
Trichomonas

142
Q

Describe and give an example of a sporozoa

A

Intracellular, complex, more than one host

Cryptosporidium

143
Q

What is the clinical presentation of giardia lamblia?

A

A symptomatic carriage
Watery diarrhea, cramping, bloating
Chronic malabsorption, weight loss

144
Q

Risk factor for infection of giardia lamblia

A

Contaminated well or stream water
Day care centres
Sexual transmission (MSM)

145
Q

How is giardia lamblia diagnosed and treated?

A

Stool sample — > wet mount
Antigen detection

Metronidazole

146
Q

Clinical presentation of entameoba histolytica

A

Asymptomatic carriage
Diarrhea, abdominal pain, dysentery
Liver, lung, brain abscess

147
Q

Risk factors for infection with entameoba histolytica

A

Contaminated water or food
Travellers/immigrants
Sexual transmission (MSM)

148
Q

Diagnosis and treatment of entameoba histolytica infection?

A

Stool sample—. Wet mount
Antigen detection
Antibody detection

Metronidazole
Iodoquinol/paramomycin

149
Q

Describe helminths (worms)

A

Complex, multicellular
Adults reproduce sexually within the vertebrate host
Eggs and larvae exist within or external to the host

150
Q

What are the 3 groups of helminths ?

A 
Trematodes 
- schistosomes vs. Non shistosomes 
Nematodes (round worms) 
-filaria vs soil transmitted 
Cestodes (tapeworms)
151
Q

What are the big 3 soil transmitted helminths?

A

Roundworm, hookworm, whipworm

152
Q

How do worms cause malnutrition?

A

Feeding on host tissues and blood —> iron and protein loss
Competing for nutrients and causing malabsorption
Causing appetite loss, diarrhea and dysentery

153
Q

What impact can worms have on children from 3-8 ?

A

Growth stunting
Malnutrition
Cognitive impairment

154
Q

What is the most common helminth infection?

A

Ascaris lumbricoides (roundworm)

155
Q

How do hookworms infect humans?

A

Filariform larva penetrates skin of foot

156
Q

What are the 2 broad groups of malnutrition?

A

Under nutrition and micronutrient deficiencies

Overweight, obesity, diet related non communicable diseases

157
Q

What are the 3 underlying principle of food security?

A

Availability: sufficient, consistent
Access: resources to obtain food
Utilization: knowledge of basic nutrition, water ad sanitation, safe storage

158
Q

What are some of the causes of hunger?

A 
Poverty
World population 
Climate change 
Conflict 
Disasters
Pandemics
Harmful economic systems 
Food and agriculture policy
159
Q

Who are most at risk of malnutrition?

A 
Children under 5 
Adolescents and elderly 
Pregnant and lactating women 
Persons living with chronic disease 
People with infectious diseases
People in areas of poor food security, post-disaster, chronic civil conflict
160
Q

What groups of people in canada are vulnerable for becoming malnourished ?

A

Poverty, low employment
Refuges, new immigrants
Adopted children from resource poor countries
Aboriginal population
Patients with chronic disease causing anorexia
Elderly

161
Q

Define protein energy malnutrition

A 
Decreased macronutrients (protein, carbs, fats) 
Growth failure
Two types: wasting (acute), stunting (chronic)
162
Q

Define micronutrient deficiency

A

Deficient in vitamins, minerals and trace elements

163
Q

Describe the characteristics of Kwashiorkor

A

Usually 6m-3y
Rapid: often due to acute illness, infections, trauma
Protein deficiency

164
Q

Describe marasmus characteristics

A

Usually under 1 y
Slow, chronic (prolonged starvation), famine, conflict
Protein and calorie deficiency
Withering

165
Q

Define stunting

A

Low height for age
Look younger than age
Poor cognitive development (sometimes)

166
Q

What are the factors in the malnutrition cycle?

A

Malnutrition —> less schooling —> less employment and poverty —> lower birth weight offspring —> higher infant morbidity and mortality —> malnutrition —> etc

411 (16 decks)

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