W12 nutrient absorption and malnutrition Flashcards
(166 cards)
1
Q
What are secretory vesicles that leave the golgi called ?
A
Condensing granules
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
3
Q
What fats are produced by acinar cells ?
A
Lipases
Colipase
Cholesterol ester hydrolase
Phospholipase A2
4
Q
What proteins are produced but acinar cells ?
A
Trypsin
Chymotrypsin
Elastase
Carboxypeptidase
5
Q
What inactive enzyme fats are produced by acinar cells ?
A
Procolipase
Prophospholipase A2
6
Q
What inactive protein enzymes are produced by acinar cells ?
A
Trypsinogen
Chymotrypsinogen
Proelastase
Pro-carboxypeptidase A and B
7
Q
Where in the duodenum is enterokinase present ?
A
Brush border of the duodenal mucosal epithelial cells
8
Q
What is the function of enterokinase in the duodenum ?
A
Acts on trypsinogen —> trypsin activation peptide (TAP) —> trypsin
9
Q
What is the function of trypsin in the duodenum ?
A
Act on pancreatic pro-enzymes —> enzymes
10
Q
Why are active enzymes important in the duodenum?
A
Cleave large peptides —> small peptides —> amino acids —> intestinal cells take up AAs
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
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
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
14
Q
_______ and ________ stimulate more secretion than _______ and _______ induce more secretion than ________
A
Monoglycerides Free fatty acids Proteins Proteins Carbohydrates
15
Q
Describe ductal cell structure
A
Simple cuboidal or columnar
Form hollow tubes
Basally located nuclei
High # of mitochondria
16
Q
How does bicarbonate secretion into the lumen occur ?
A
Via a Cl and HCO3 exchange mechanism
17
Q
what detects low pH in the intestine ?
A
S-cells
18
Q
What does detection of low pH of the chyme in the intestine stimulate ?
A
Secretion of secretin
19
Q
What stimulates bicarbonate secretion in the small intestine ?
A
Ach (minor)
Secretin
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-
21
Q
What is critical for bicarbonate secretion ?
A
CFTR function
22
Q
What are the consequences of reduced exocrine function ?
A
Exocrine insufficiency Acute pancreatitis Chronic pancreatitis Diabetes Pancreatic ductal adenocarcinoma
23
Q
What are the 4 basic GI processes ?
A
Motility, secretion, digestion, absorption
24
Q
What is digestion ?
A
Biochemical breakdown of nutrients into their molecular components
25
What are carbohydrates composed of ?
Monosaccharides
Disaccharides
Polysaccharides
26
What enzymes are involved in the breakdown of carbohydrates ?
Amylase, sucrase, lactase, maltase
27
What enzymes are involved in the breakdown of proteins ?
Pepsin, trypsin, chymotrypsin, carboxypeptidase, aminopeptidases
28
What enzyme is involved in the breakdown of fats ?
Lipase
29
Where does absorption of digested nutrients, water and electrolytes primarily occur ?
Across the membrane of epithelial cellls in the small intestine
30
What happens to carbohydrate and protein breakdown products when they travel through the epithelial cells ?
Enter the blood
31
What happens to fat breakdown products when they travel through the epithelial cells ?
They enter the lymphatic system
32
What is the purpose of the alkaline fluid secreted by the pancreas ?
Neutralize acidic gastric chyme
33
What do duct cells in the pancreas secrete ?
Secrete aqueous NaHCO3 solution
34
What do acinar cells in the pancreas secrete ?
Digestive enzymes
35
What 3 enzymes secreted by the pancreas hydrolyse peptide bonds?
Trypsinogen
Chymotrypsinogen
Pro carboxypeptidase
36
Why does the pancreas secrete trypsin inhibitor ?
To inhibit any activated trypsin in the pancreas
37
What activates trypsinogen (—> trypsin) ?
Enterokinase
38
What is the only enzyme that can digest fats ?
Lipase
39
What causes steatorrhea ?
Lack of lipase —> ingested fats remain too large to absorb
| ~60-70% of ingested fats are excreted in the feces
40
How much pancreatic aqueous alkaline solution is secreted each day ?
1-2 litres
41
How is bile delivered to the duodenum ?
The sphincter of Oddi
42
Where are the majority of bile salts reabsorbed ?
Terminal ileum
43
Composition of bile salts
Deprotonated molecules, negatively charged
| Derived from cholesterol but with negatively charged hydrophobic tail
44
What is lecithin
A component of cell membranes
45
What regulates the release of bile ?
CCK triggers the contraction of the gall bladder and the relaxation of the sphincter of Oddi
Vagal efferents augment this response
46
What regulates the production and secretion of bile ?
Neuronal- vagal input increases bile production
| Hormonal- secretin stimulates the production and secretion of the NaHCO3 component of bile
47
What causes the inhibition of bile ?
Fats have left duodenum:
- CCK levels drop
- the sphincter of Oddi closes
—> bile cannot enter the duodenum
48
when do hepatocytes stop manufacturing bile ?
When the circulating bile salt concentration in the enterohepatic circulation declines
49
How are fats digested in the small intestine and what components are absorbed ?
Completely hydrolysed by pancreatic lipase
| Monoglycerides and free fatty acids are absorbed
50
How are proteins digested and absorbed in the small intestine ?
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
51
How are carbohydrates digested and absorbed by the small intestine
Broken into disaccharides and some monosaccharides
| Further hydrolysed by disaccharidases in the epithelial brush border.
52
What secretes amylase ?
Salivary glands in mouth
| Exocrine pancreas
53
What is the site of action for pepsin ?
Stomach antrum
54
Where do trypsin, chymotrypsin and carboxypeptidase act?
Small intestine lumen
55
Where do aminopeptidases act ?
Small intestine brush border
56
What secretes aminopeptidases ?
Small intestine epithelial cells
57
What increases the surface area of the small intestine for absorption ?
Circular folds
Villi
Brush border
- microvilli
58
What holds together epithelial and mucous cells?
Tight junctions
59
What does the brush border contain ?
Enzymes that hydrolyse peptides/disaccharides
Enterokinase
Transmembrane carrier proteins
60
What is contained in the crypts of Lieberkuhn ?
Mucous cells: primary locus for success entericus secretion
| Stem cells that constantly produce new epithelial cells
61
Why is bile neccassary for the digestion of fats ?
Lipase can only act on the surface of fat aggregates
| Bile salts act as a detergent and emulsify large fat aggregates into smaller pieces
62
How do fat droplets repel other droplets ?
The negatively charged hydrophilic tails of of bile salts repel each other
63
What is the function of colipase ?
Anchor lipase to the bile salts at the surface of a fat droplet
64
Describe the structure and function of micelles
4-7 nm in diameter
Composed of bile salts, lecithin and cholesterol (core), hydrophilic tail shell
Shuttle digested fat molecules to the epithelial surface
65
What hydrolyses disaccharides into their constituent monosaccharides ?
Disaccharidases in the brush border
66
How are glucose and galactose absorbed
Secondary active transport
- co-transported into the cell with Na+ ions
- passively diffuses into the interstitial fluid through a membrane channel
- enter a capillary
67
How does fructose pass through the epithelium ?
Passively diffuses through the epithelial cell by means of facilitated diffusion
68
What are the 3 sources of endogenous proteins ?
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
What are peptide fragments hydrolysed by and where ?
Aminopeptidases in the brush border
70
How are peptide fragments absorbed ?
Secondary active transport with Na+ ions
| Enter capillaries in the laminate propria of the villus
71
How does fat absorption differ from that of proteins and carbohydrates ?
Completely digested by pancreatic lipase
72
How do digested fats cross the brush border?
Diffusion
73
What is combined to form triglycerides in the cytosol ?
Monoglycerides and free fatty acids
74
What forms chylomicrons ?
Triglycerides and bipolar lipoproteins
75
Where do chylomicrons go ?
Into the central lacteal of the lymphatic system
76
What are the two categories of motility ?
Mixing movements
| Propulsive movements
77
What are the accessory organs of the GI system ?
Pancreas, liver, gallbladder, and salivary glands
78
What 4 factors regulate the motility and secretion of the GI tract
Intrinsic electrical properties of smooth muscle cells
enteric nervous system
Autonomic nervous system
GI hormones
79
Where do preganglionic sympathetic fibres from the CNS synapse ?
In prevertebral ganglia
80
Where do preganglionic parasympathetic fibres from the CNS synapse when they enter into the GI wall?
Postganglionic fibres within the ENS
81
What are the 3 different pairs of salivary glands outside the oral cavity?
Parotid
Submandibular
Sublingual
82
What are the most important proteins and enzymes in saliva ?
Amylase, lysozyme and mucus
83
What is the function of lysozyme ?
Lyses the cell wall of some bacteria —> some protection against infection
84
What control is the rate of production of saliva under ?
Autonomic control
85
How does parasympathetic activation affect production of saliva ?
Increased production of all secretions
86
How does sympathetic stimulation affect saliva?
Decrease in fluid volume but increase in mucous production —> dry sticky mouth
87
Describe fluid volumes as it moves through the small and large intestine
~8200 mL enters small intestine daily
~6700 mL reabsorbed from small intestine
~1400 mL reabsorbed in large intestine
100 mL excreted in feces
88
What is the succus entericus ?
Aqueous salt and mucous solution secreted from the small intestine
~1.5 litres / day
89
What is the function of the succus entericus
Lubricate passage through lumen
protects mucosa from acid injury
Hydrolysis
90
How is water reabsorbed in small intestine
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
How is Na+ absorbed in the small intestine ?
Into epithelial cells: via Na+ channels
Absorbed passively
Through tight junctions (when luminal Na+ concentration is high)
92
How is Cl- absorbed in small intestine ?
Cl- ions passively follow the electrical gradient established by Na+ active movement into the interstitium
93
What can produce an acid base imbalance
Large loss of electrolytes via vomiting or diarrhea
94
What acid base imbalances do diarrhea and vomiting result in?
Vomiting: metabolic alkalosis
Diarrhea: metabolic acidosis
95
What are the consequences of prolonged diarrhea ?
Malnutrition
Dehydration
Acid-base disturbance
96
What are the possible causes of diarrhea ?
Excessive intestinal motility
Hyper-osmotic chyme
Toxins
97
How can excessive intestinal motility cause diarrhea?
Irritation of the GI tract wall
Bacterial/viral infection
Emotional stress
98
How can hyper-osmotic chyme result in diarrhea?
—> luminal fluid accumulation
99
Mechanism of diarrhea caused by toxins
Inhibit Na+ absorption or stimulate Cl- excretion into intestinal lumen —> osmotic fluid movement into the lumen
100
Differentiate between maldigestion and malabsorption
Maldigestion: defective hydrolysis of nutrient s
Malabsorption: defective mucosal absorption
101
Examples of luminal defects that can cause maldigestion/malabsorption
Bile acid deficiency
Lactase deficiency
Pancreatic enzyme deficiency
Atrophic gastritis
102
Examples of mucosal defects that can cause maldigestion/malabsorption
Celiac disease
Crohn disease
Congenital defects of transporters
Intestinal resection
103
Examples of transport defects that can cause maldigestion/malabsorption
```
Vasculitis
Portal hypertension
Cardiac disease
Intestinal lymphangiectasis
Retroperitoneal fibrosis
```
104
What is anthropometry?
Measures of body composition
- BMI
- height, weight
- hip to waist ratio
- skinfold
- muscle bulk
105
Screening tests for nutritional status
Subjective global assessment (SGA)
- physical exam: sc fat, edema, muscle bulk
Mini nutritional assessment
- includes BMI or sc fat
106
What are the criteria for classifying a patient as well nourished ?
- weight loss and muscle wasting
| - currently eating well and gaining weight
107
What are the criteria for a classification as mild/moderate malnutrition?
```
Moderate weight loss (5-10%)
Compromise in food intake
Continued weight loss
Progressive functional impairment
Moderate stress
```
108
What are the criteria for classifying a patient as having severe malnutrition?
Severe weight loss (>10%)
Poor nutrition intake
Progressive functional impairment
Muscle wasting
109
What blood tests can be useful in accessing nutritional status?
```
CBC
Electrolytes
Lipid panel
Liver panel
Ca, PO4, Mg
Coag
B12, folate
TSH
Anti-tTG IgA
```
110
What stool tests can be useful in disease of malabsorption/maldigestion ?
Fat
Elastase , chymotrypsin
PH
C&S, O&P, Cdiff
111
What is a hydrogen breath test and what does it test for ?
- measures lactose levels
- increase >20 ppm after ingesting 20-50g lactose —> lactose absorption issues
If baseline is high —> too much bacteria in GI
112
What does the Schilling test look for ?
B12 deficiency
113
What is fecal elastase/chymotrypsin a good measure of ?
Low —> pancreatic insufficiency
114
What is pernicious anemia ?
Vitamin B12 anemia caused by a lack of intrinsic factor being secreted from the stomach —> intestine cannot properly absorb B12
115
What is step 2 of the Schilling test ?
Confirm cause
| - stomach (intrinsic factor), pancreas (pancreatic insufficiency), bacterial (SIBO)
116
What might you see on a CT scan in a patient with Crohn disease
Terminal ileum inflammation
117
What makes up the celiac iceberg ?
```
Classic
Atypical
Silent
Latent
Potential
Refractory
```
118
What is atypical celiac disease ?
Gluten sensitive enteropathy, extra intestinal symptoms and signs (short, anemic, osteoporosis, infertile)
119
What is latent celiac disease ?
Normal villus architecture on gluten containing diet but have had/ will have gluten sensitive villus atrophy
120
What is potential celiac disease ?
Never had a biopsy consistent with celiac disease but show immunological abnormalities characteristic for the disease
121
What damage is seen in the mucosa of the small intestine in someone with celiac disease?
Villus atrophy
Crypt hyperplasia
Enterocyte disarray
Inflammatory infiltrates
122
What happens to the release of bile salt and pancreatic enzyme in response to meals in patients with celiac ?
Decreases
123
What serologies can be done to diagnose celiac disease?
anti-tTg IgA
Anti-endomysial antibody
Anti-gliadin antibodies (IgA, IgG)
124
What should be done to diagnose celiac disease?
Small bowel biopsy
125
What might you see on endoscopy of a patient with celiac disease?
Scalloping of duodenum
| Marbelization of duodenum
126
Anorexia definition
Loss of appetite or reduced caloric intake
127
What is cachexia ?
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
Definition of anorexia-cachexia syndrome
Involuntary loss of weight and appetite with advanced illness
- distinct from FTT, sarcopenia (age related muscle loss) and starvation (reversible)
129
What is the pathogenesis of anorexia cachexia ?
Cytokine driven causing dysregulation in 3 main groups:
- altered intake
- inflammation/catabolism
- anabolic dysbalance
130
What causes altered intake in anorexia cachexia
Abnormal satiety signals, neuro-hormones, autonomic dysfunction
—> lack of hunger, taste abnormalities, early satiety
131
What causes inflammation/catabolism in anorexia cachexia
Increased resting energy expenditure/hyper metabolism
| —> increase in acute phase proteins, fever, fatigue, decreased haemopoiesis
132
What causes anabolic dis balance in anorexia cachexia ?
Alteration of hypothalamic regulated anabolic hormones —> muscle wasting
133
Treatment for anorexia cachexia
Medical optimization of secondary nutrition impact symptoms and acute/chronic conditions
134
Non-pharmacological treatment of anorexia cachexia
Counseling/education
| Consultation with nutritionist
135
Pharmacological treatment of anorexia cachexia
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
What is important to note in artificial hydration and nutrition in patients with anorexia cachexia ?
No evidence that it prolongs life or improves quality of life
—> generally not indicated
137
What is required for transmission of a parasite ?
Reservoir host
| A route of infection
138
How can parasites cause disease in humans?
Mechanical effects
Invasion and destruction of host cells
Allergic or inflammatory immune reaction
Competition for specific nutrients
139
What are the two forms of Protozoa ?
Trophozites: motile
Cysts: resting stage
140
Common type of amoeba
Entameoba
141
Common type of flagellate
Simple trophozoites and cysts:
Giardia
Trichomonas
142
Describe and give an example of a sporozoa
Intracellular, complex, more than one host
| Cryptosporidium
143
What is the clinical presentation of giardia lamblia?
A symptomatic carriage
Watery diarrhea, cramping, bloating
Chronic malabsorption, weight loss
144
Risk factor for infection of giardia lamblia
Contaminated well or stream water
Day care centres
Sexual transmission (MSM)
145
How is giardia lamblia diagnosed and treated?
Stool sample — > wet mount
Antigen detection
Metronidazole
146
Clinical presentation of entameoba histolytica
Asymptomatic carriage
Diarrhea, abdominal pain, dysentery
Liver, lung, brain abscess
147
Risk factors for infection with entameoba histolytica
Contaminated water or food
Travellers/immigrants
Sexual transmission (MSM)
148
Diagnosis and treatment of entameoba histolytica infection?
Stool sample—. Wet mount
Antigen detection
Antibody detection
Metronidazole
Iodoquinol/paramomycin
149
Describe helminths (worms)
Complex, multicellular
Adults reproduce sexually within the vertebrate host
Eggs and larvae exist within or external to the host
150
What are the 3 groups of helminths ?
```
Trematodes
- schistosomes vs. Non shistosomes
Nematodes (round worms)
-filaria vs soil transmitted
Cestodes (tapeworms)
```
151
What are the big 3 soil transmitted helminths?
Roundworm, hookworm, whipworm
152
How do worms cause malnutrition?
Feeding on host tissues and blood —> iron and protein loss
Competing for nutrients and causing malabsorption
Causing appetite loss, diarrhea and dysentery
153
What impact can worms have on children from 3-8 ?
Growth stunting
Malnutrition
Cognitive impairment
154
What is the most common helminth infection?
Ascaris lumbricoides (roundworm)
155
How do hookworms infect humans?
Filariform larva penetrates skin of foot
156
What are the 2 broad groups of malnutrition?
Under nutrition and micronutrient deficiencies
Overweight, obesity, diet related non communicable diseases
157
What are the 3 underlying principle of food security?
Availability: sufficient, consistent
Access: resources to obtain food
Utilization: knowledge of basic nutrition, water ad sanitation, safe storage
158
What are some of the causes of hunger?
```
Poverty
World population
Climate change
Conflict
Disasters
Pandemics
Harmful economic systems
Food and agriculture policy
```
159
Who are most at risk of malnutrition?
```
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
What groups of people in canada are vulnerable for becoming malnourished ?
Poverty, low employment
Refuges, new immigrants
Adopted children from resource poor countries
Aboriginal population
Patients with chronic disease causing anorexia
Elderly
161
Define protein energy malnutrition
```
Decreased macronutrients (protein, carbs, fats)
Growth failure
Two types: wasting (acute), stunting (chronic)
```
162
Define micronutrient deficiency
Deficient in vitamins, minerals and trace elements
163
Describe the characteristics of Kwashiorkor
Usually 6m-3y
Rapid: often due to acute illness, infections, trauma
Protein deficiency
164
Describe marasmus characteristics
Usually under 1 y
Slow, chronic (prolonged starvation), famine, conflict
Protein and calorie deficiency
Withering
165
Define stunting
Low height for age
Look younger than age
Poor cognitive development (sometimes)
166
What are the factors in the malnutrition cycle?
Malnutrition —> less schooling —> less employment and poverty —> lower birth weight offspring —> higher infant morbidity and mortality —> malnutrition —> etc
