GI Midterm Flashcards
What are the fat soluble vitamins? Describe their storage and digestion
1) ADEK
2) stored in liver and adipose tissue, can be stored for a long time and released as needed
3) Vitamins released when proteins are degraded into small peptides in the stomach (first step of digestion same for water- and fat- soluble vitamins)–> in jejunum, vitamins form micelles with bile salts –> passively transported to intestinal enterocytes (intestinal absorptive cells) –> packaged into chylomicrons and released into lymphatic system –> Travel up thoracic duct –> enter left subclavian vein –> blood circulation
* as opposed to water soluble vitamins, which are directly absorbed into the bloodstream*
Vitamin A:
1) biologically active form(s)
2) sources
3) functions
4) transport
5) excretion
1) Retinyl ester (food) –> retinol –> retinal –> retinoic acid; beta-carotene (food) –> retinal (retinol, retinal, and retinoic acid are all forms of Vit A)
2) Sources: retinyl ester from animal foods e.g. liver, beta-carotene from orange root vegetables e.g. sweet potatoes, carrots, retinol from milk and milk products
3) Functions: Retinol –> supports reproduction; Retinal –> vision esp important for night vision; Retinoic acid –> acts as transcription factor for proteins involved in cell differentiation of epithelial and goblet cells, growth, and embryonic development; Beta carotene –> antioxidant (immunity)
4) transported bound to retinol-binding proteins
5) small amount excreted in the urine
Describe the pharmacological uses of retinoids (Vitamin A)
- treatment of anemia
- acne and age spots
- Accutane - oral medication for severe acne, teratogenic so women need to be on birth control
Describe Vit A deficiency including causes, symptoms,
1) Causes: primary - inadequate intake, develops over 1-2 years; secondary - poor absorption of fats due to liver disease, cystic fibrosis, etc.
2) Symptoms: night blindness, dry eyes (due to reduction in goblet cells), Bitot gray spots (due to keratin buildup), hyperkeratosis (skin becomes dry rough and scaly), inflammation (ulcers) and softening of the cornea –> eventually blindness, impaired immunity
Describe Vit A toxicity including causes, symptoms
1) Causes: frequent consumption of liver (Abali’s example is polar bear liver), use of retinoic acid analogues e.g. Accutane during pregnancy to treat skin conditions
2) Symptoms: birth defects- craniofacial and defects of CNS, thymus, heart; reduced bone mineral density, liver + spleen enlargement, diarrhea, bone/joint pain, dermatitis
* beta-carotene excess not harmful, just turns skin yellow*
Vitamin D:
1) biologically active form(s)
2) sources
3) functions
1) Precursor derived from cholesterol in liver + UV light –> Calciferol/Vitamin D3 synthesized in skin –> hydroxylated in liver –> hydroxylated in kidneys by 1OHase –> active form = calcitriol = 1,25(OH)2D3
2) Source: need UV light (from sun) to activate, Vit D3 found in fish, fortified milk, mushrooms
3) Functions: acts as at transcription factor to increase Ca2+ absorption via CaBP from small intestine, kidney; works with PTH in bone resorption; inflammation reduction and bp regulation
Describe Vitamin D deficiency including causes, types, symptoms
1) Causes: dark skin, lack of sunlight, little dairy in diet, old people, vegans, exclusive breastfeeding (low levels of Vit D in breastmilk)
2) Types: rickets (infants) and osteomalacia (adults)
3) Rickets- bones do not calcify properly –> big head, bowed legs, growth retardation;
Ostomalacia- chronic kidney disease/anticonvulsants –> soft flexible brittle bones due to poor mineralization, + pain in legs, pelvis, lower back
Describe Vitamin D toxicity including causes, symptoms
1) Causes: occurs due to supplementation (not from excessive sunlight)
2) Symptoms: buildup of calcium which precipitates in blood vessels, kidney, heart, lungs –> can cause kidney stones, death
Vitamin E:
1) biologically active form(s)
2) sources
3) functions
1) Tocopherol (only 1 of 8 isomers is active)
2) Sources: nuts and vegetable oils, though Vit E is easily destroyed by frying
3) Function: primary defender against ROS and free radicals by donating H+ –> protects cell membrane integrity, primary lipid soluble antioxidant –> prevents platelet aggregation and monocyte adhesion; protects Vitamin A from oxidation
* after it donates its H+, vitamin E is regenerated by Vitamin C*; Vitamin E works in concert with selenium
Describe Vitamin E deficiency in terms of causes and symptoms
1) Causes: primary- inadequate intake (rare), secondary - fat malabsorption
2) Symptoms: hemolytic anemia due to oxidation of polyunsaturated fatty acids, nerve damage
Describe Vitamin E toxicity in terms of causes and symptoms
1) Causes: v high doses (nontoxic at low doses)
2) Symptoms: hemorrhage, since Vit E interferes with Vit K role in blood clotting
Vitamin K:
1) biologically active form(s)
2) sources
3) functions
1) Menaquinones, phylloquinones
2) Sources: menaquinones synthesized by bacteria in our gut, or found in fish oils and meats; phylloquinones found in green leafy vegetables, broccoli
3) Functions: Vit K is cofactor for Glu –> Gla (blood coagulation), rxn catalyzed by gamma-glutamyl carboxylase know this enzyme
Describe Vitamin K deficiency in terms of causes, symptoms
1) Causes: rare since gut bacteria synthesize K, secondary deficiencies due to antibiotics, infection, or malabsorption; newborns do not have the gut bacteria so given bolus of Vit K after birth
2) Symptoms: Hemorrhage, bruising, mucosal bleeding
Describe Vitamin K toxicity in terms of causes, symptoms
No toxicity known
However, patients on coumadin (Anticoagulant which inhibits Vitamin K) should be careful not to eat too many Vit K rich foods bc it will lessen effectiveness of warfarin –> potentially lead to clots
Describe the interrelationships between the fat-soluble vitamins
Vitamin E: protects A from oxidation, is regenerated by C (primary water-soluble antioxidant), and impairs activity of K (blood clotting)
A, D, K play roles in bone growth and remodeling
Describe the digestion and absorption of water-soluble vitamins
1) Vitamins bound to protein are hydrolyzed and degraded into small peptides in the stomach –> frees vitamins from protein partners
2) Absorbed in upper small intestine (Except for B12, which is absorbed in the ileum)
3) Absorbed into portal vein and transported into liver
4) B12 is stored in the liver, the other water soluble vitamins are sent directly into the bloodstream
5) Excess vitamins excrete in urine –> need daily consumption of vitamins
Describe the differences between water and fat soluble vitamins in terms of:
1) Absorption
2) Transport
3) Storage
4) Excretion
5) Toxicity
6) Intake requirements
1) Absorption: water vitamins directly into the bloodstream, fat vitamins into lymphatic system and then the bloodstream
2) Transport: water vitamins move freely, fat vitamins may be bound to protein carriers
3) Storage: water vitamins circulate freely in water-filled parts, fat vitamins stored in cells
4) Excretion: excess water soluble vitamins excreted, fat soluble vitamins tend to remain in fat storage sites
5) Toxicity: water rare unless mega dose supplements, fat more likely due to long-term storage
6) Intake: water needed frequently, fat vitamins needed in periodic doses
What are the B water-soluble vitamins?
Many coenzymes are derived from water soluble vitamins
The - Thiamine, B1 Rhythm - Riboflavin, B2 Nearly - Niacin, B3 Proved - Pyridoxine, B6 Fully - Folate, B9 Contagious - Cobalamin, B12
B1, Thiamine:
1) biologically active form(s)
2) sources
3) functions
1) Active form: TPP - Thiamin pyrophosphate absorption reduced with alcohol consumption, folate B9 deficiency
2) Sources: meats, sunflower seeds, fortified cereals
3) Functions: found in tissues with high metabolic rate e.g brain, skeletal muscle heart – plays role in conversion of carbs to energy bc coenzyme for 4 enzymes: A) pyruvate dehydrogenase (PDH), B) alpha ketoglutarate dehydrogenase, C) branched chain alpha ketoacid dehydrogenase, D) transketolase
Describe B1 thiamine deficiency and toxicity in terms of causes, symptoms
1) Rare but found in homeless, people on Atkins, alcoholics (can progress to Wernicke-Korsakoff syndrome –> brain damage + psychosis)
2) Early symptoms: Poor appetite, weight loss, confusion, irritability
3) Late symptoms: beriberi- wet (edema, due to congestive heart failure) and dry (muscle wasting, neurological disorders)
4) No toxicity reported
B2, Riboflavin:
1) biologically active form(s)
2) sources
3) functions
1) Active form: Circulates bound to albumin, metabolized to active forms flavin mononucleotide (FMN) and FAD once taken up into the cells
* UV light, radiation destroy riboflavin but heat does not*
2) Sources: beef liver, milk producta
3) Functions: Prosthetic groups for enzymes participating in redox reactions by conversion between FAD FADH2
Describe B2 riboflavin deficiency and toxicity in terms of causes, symptoms
1) Causes: Inflammation of membranes
2) Symptoms: cheilosis (cracks at the corner of the mouth), glossitis (tongue inflammation), stomatitis (mouth inflammation), bloodshot eyes sensitive to light, flaky and scaly skin on the scalp and face
3) No toxicity reported
B3, Niacin:
1) biologically active form(s)
2) sources
3) functions
1) Active form: NAD and NADP, circulates in the blood as nicotinamide and can be made from tryptophan
2) Sources: protein-rich foods e.g. chicken, fish, peanut butter, also fortified cereal
3) Functions: coenzyme in redox rxns for breakdown of glucose, AA, fats, DNA
Describe B3 niacin deficiency and toxicity in terms of causes, symptoms
1) causes: corn-based diet, alcoholics
2) Early symptoms: loss of appetite, fatigue, weakness, depression
3) Late symptoms: Pellagra (“rough skin”) - 4Ds: Diarrhea, dermatitis, dementia, and unresolved death
4) Toxicity: from supplementation to dyslipidemia (lower LDL), niacin flush which can be avoided by taking low dose aspirin or ibuprofen
B6, Pyrodoxine:
1) biologically active form(s)
2) sources
3) functions
1) Active forms: pyridoxal phosphate (PLP), converted from pyridoxal, pyridoxine, and pyridoxamine; stored in muscle tissue
2) Sources: oatmeal, banana, pistachios, pinto beans
3) Functions: Coenzyme for metabolism of amino acids and urea; conversion of tryptophan to niacin; synthesis of heme; synthesis of neurotransmitters e.g. serotonin, dopamine, norepi
Describe B6 pyridoxine deficiency and toxicity in terms of causes, symptoms. What are the pharmacological uses of B6?
1) Causes: alcoholics, women on OCPs, drug interactions (e.g. isoniazid for TB, penicillamine for Rheumatoid Arthritis)
2) Symptoms: cheliosis, glossitis, dermatitis (like in pellagra, since B6 deficiency can cause niacin B3 deficiency), depression, confusion
3) Toxicity: irreversible nerve degeneration
4) Pharma uses: treatment of carpal tunnel, asthma, depression, diabetic neuropathy
B9, Folate:
1) biologically active form(s)
2) absorption
3) sources
4) functions
1) Active forms: many active forms, including tetrahydrofolate
2) Absorption: Polyglutamate in food –> all glutamates but one removed in small intestine –> folate methylated in epithelial cells –> released into circulation as methyltetrahydrofolate (inactive) and taken up by cells –> B12 activates folate and in the process becomes activated
3) Sources: dark leafy vegetables, liver, fortified breads and cereals, orange juice, lentils
4) Functions: synthesis of DNA, RNA, some AA esp for rapidly dividing cells e.g. RBCs, epithelial cells
Describe B9 folate deficiency and toxicity in terms of causes, symptoms.
1) Causes: inadequate absorption e.g. Celiac’s, Crohn’s, increased utilization e.g. pregnancy, cancer therapy (antifolates prescribed), alcoholics, elderly with poor diet, antacids
2) Symptoms: megaloblastic anemia - weakness, fatigue, headache, palpitations; folate deficiency can lead to neural tube defects in babies e.g. spina bifida, anencephaly- so women should take folate supplements;
* B12 deficiency also leads to megaloblastic anemia, but there are neurotoxic symptoms involved*
3) Toxicity: Folate supplementation may mask B12 deficiency–> irreversible neurologic deterioration; give both folate and B12 supplements
B12, Cobalamin:
1) biologically active form(s)
2) absorption
3) sources
4) functions
1) Active forms: methylcobalamin, deoxyadenosylcobalamin
2) Absorption: salivary glands produce R protein –> B12 + R move to stomach where B12 is released from meat protein partner (bc of the acidity) and binds to R; intrinsic factor (IF) released from parietal cells –> in duodenum, pancreatic enzymes cleave R, and B12 binds to IF –> IF receptors at distal ileum allow internalization of B12 –> enters portal vein, delivered to liver –> can be stored for years
3) Sources: animal products (product of bacterial fermentation in animals) + fortified or fermented foods e.g. soy milk
4) Functions: works with folate to synthesize DNA, RNA, AA; metabolism of fatty acids to maintain nerve cells
Describe B12 cobalamin deficiency and toxicity in terms of causes, symptoms.
1) Causes: decreased uptake in vegans (bc found in animal products), malabsorption due to decreased IF (autoimmune disease that kills parietal cells, which produce IF), decreased gastric acid (due to antacids/PPI, need HCl to remove B12 from bound protein), bypass/removal of terminal ileum (eg gastric bypass surgery)
2) Symptoms: pernicious anemia (IF deficiency), megaloblastic macrocytic anemia (B12 + folate deficiency), nerve damage/neurotoxicity + and swollen tongue (just B12 deficiency)
3) Toxicity: N/A
Describe the function and deficiency of B7 biotin
1) Function - coenzyme in carboxylation rxns (Adds C02), required for metabolism of carbs, fats, and proteins
2) Defiency is rare but can be due to enzyme deficiency or consumption of raw eggs (egg whites contain avidin which binds to biotin) –> weak muscles, seizures, alopecia, lactic aciduria
Describe the source, form, function and deficiency of B5 pantothenic acid
1) Source: meat, milk, veggies
2) Active form: part of coenzyme A
3) Function: Activation of fatty acids –> important in lipid metabolism
4) Deficiency/toxicity: none reported
Vitamin C, Ascorbic acid:
1) sources
2) functions
3) deficiency
4) Toxicity
1) Sources: citrus fruits
2) Function: cosubstrate for 2 enzymes used collagen formation (anchoring teeth, wound healing, tissue repair) - proline hydroxylase and lysine hydroxylase, water soluble antioxidant (donates electrons to ROS), synthesis of neurotransmitters (e.g. norepi), synthesis of carnitine (fatty acid degradation), absorption of non-heme iron
3) Deficiency: Scurvy due to alcohol, smoking, burns, old age; symptoms –> muscle weakness, loose teeth, bleeding gums, joint pain, bruised skin
4) Toxicity: diarrhea + GI distress; Vitamin C metabolized to oxalic acid, so people with tendency to form kidney stones should avoid high levels of Vit C
What are minerals? What are the two groups of minerals and what are the differences between them?
1) Minerals - essential, inorganic elements required for maintaining normal body functions e.g. blood clotting, nerve impulses, bone health and growth, and as antioxidants and electrolytes; come from both plant and animal sources
2) Macrominerals - required in large amounts (greater than 100 mg/day), include Ca, P, K, S, Na, Cl, Mg;
Microminerals/trace minerals - need less than 100 mg/day
What is bioavailability? What factors affect positively or negatively
1) Bioavailability - extent to which amount of ingested nutrient is absorbed and available in the body
2) Factors that increase bioavailability: deficiency in a mineral increases absorption, cooking for legumes (breaks bond bw mineral and binders), Vitamin C for iron, zinc
3) Factors that decrease: binders including oxalates (found in veggies), phytates (Grains), polyphenols (Tea + coffee), goitrogens (iodine); too much of one mineral can affect absorption of competing minerals e.g. Zinc supplementation can reduce copper toxicity
Overall, absorption efficiency of minerals is low and tightly controlled
Iron (trace mineral):
1) Source
2) Forms
3) Functions
4) Transport
1) Source: clams, fish + meat + poultry, whole grains, legumes; Heme iron only from animal foods (e.g. meat, eggs, milk) - smaller % of daily iron intake but well absorbed; non-heme iron in both animal and plant foods - majority of iron intake but less well absorbed
2) Forms: In RBCs as part of hemoglobin, in heart/skeletal muscle as part of myoglobin, stored in intestinal mucosa cells and liver/spleen/bone marrow as ferritin or in liver/macrophages as hemosiderin (if iron levels are v high)
3) Functions: oxygen delivery, cofactor in redox rxns, part of electron carriers, prosthetic group in enzymes that destroy microorganisms
4) Free iron is toxic; transported in circulation bound to transferrin
Describe the absorption of iron and what factors affect non-heme absorption in particular
1) Absorption (duodenum): Fe3+ must be reduced to ferrous form Fe2+ to be transported into the intestinal cell –> either stored as ferritin in the cell or transported out of cell by ferroportin –> oxidized by ceruloplasmin into Fe3+ and bound to serum transferrin in the blood –> distributed to liver, muscle, bone marrow, other tissues
* if there is excess iron, it is not transported out of the cell but rather stays in the cell as ferritin and is excreted when the intestinal cells are shed*
2) Enhancing factor: increased demand, Vitamin C, Meat Protein Factor (MPF) in animal proteins, acids
3) Inhibiting factors: infections, low gastric acid or GI disease, binding agents e.g. phytates, oxalates, polyphenols, Ca Zn or Mn (bind to Fe), antacids + H+ pump inhibitors
Describe iron deficiency in terms of causes, symptoms, and diagnosis
1) Causes: most common nutrition deficiency worldwide- pregnancy/menstruation, infants/young children, inadequate intake through diet e.g. raw vegans, malabsorption e.g. Celiac’s
2) Symptoms: fatigue, feeling cold or faint, shortness of breath (–> all due to iron deficiency anemia), low IQ (infants, due to altered neurotransmitter synthesis), pica (consumption of nonfood e.g. dirt), glossitis, koilonychia (spoon nails)
3) Diagnosis: decrease in serum iron and ferritin and increase in transferrin –> decrease in transferrin saturation; iron deficiency anemia i.e. hypochromic microcytic anemia
Describe iron toxicity in terms of causes, symptoms
1) Causes: excess ingestion, transfusion, hemochromatosis (genetic disease where iron is absorbed at high rate, also called “bronze diabetes”),
2) Symptoms: diabetes, skin darkening, arthritis
Zinc (trace mineral):
1) Source
2) Absorption and transport
3) Functions
1) Source: seafood e.g. oysters and crabs, meat, eggs, also veggies but they need to be cooked well to release zinc from phytates
2) Absorption: zinc absorbed into intestinal mucosal cells and binds to metallothionein (just as ferritin binds to iron) –> metallothionein releases Zn to albumin –> bound to serum albumin and transported in blood to the rest of the body –> pancreas use zinc to make digestive enzymes –> Secrete into the intestine
* if there is excess Zinc, it is not taken up but remains in the intestinal mucosal cell and is excreted when the cells are shed*
3) Functions: cofactor for hundreds of enzymes–> used for heme, DNA, RNA synthesis; gene expression (part of Zinc finger proteins); sexual maturation; sense of taste and smell and immune function
Describe zinc deficiency in terms of causes, symptoms
1) Causes: malabsorption disorders, alcoholics (promotes Zn excretion), lactating women, vegetarians, heavy smokers, patients with ulcers, genetic condition called acrodermatitis enteropathica (inflammation of skin + diarrhea)
2) Symptoms: changes in taste, anosmia (loss of sense of smell), poor appetite, poor wound healing, impaired immunity, hair loss, growth retardation/delayed sexual maturation in children
Describe zinc toxicity in terms of causes, symptoms
1) Causes: rare, can occur with supplementation
2) Symptoms: diarrhea, naseau, vomiting, depresses immune function, impairs copper absorption –> give zinc supplementation to treat genetic condition Wilson’s disease which results from increased copper storage
Copper (trace mineral):
1) Source
2) Absorption and transport
3) Functions
1) Source: beef liver, shellfish e.g. oysters and lobster, nuts + seeds, lentils, soy, dark chocolate
2) Absorption: small intestine –> transported bound to albumin –> transported from liver as part of ceruloplasmin, increased in more acidic environment
3) Functions: component of lysyl oxidase –> production of skin + hair + connective tissue (e.g. elastin, collagen), cofactor for superoxidase dismutase –> removing ROS, maintenance of myelin sheath + nervous system, part of ceruloplasmin –> oxidation of iron so it can be bound to transferrin for transport
Describe copper deficiency in terms of causes, symptoms
1) Causes: rare, seen in premature infants, in individuals with Menke’s syndrome (poor copper absorption), nutritional disorders e.g. kwashiorkor, anemia, Celiac’s
2) Symptoms: anemia, connective tissue damage –> excessive bleeding; silver, brittle hair
Describe copper toxicity in terms of causes, symptoms, treatment
1) Causes: consumption of acidic beverages in copper containers, Wilson’s genetic condition (Copper cannot be excreted in bile –> increased copper deposits in brain, kidney, cornea, liver + decreased blood copper levels)
2) Symptoms: abdominal pain, naseau, vomiting, diarrhea; Wilson’s –> Kayser-Fleischer ring (Greenish discoloration of cornea), low blood copper levels but increased copper deposits in brain, kidney cornea, liver
3) Treatment: Zinc supplementation (to impair copper absorption), Copper chelation therapy through penacillamine
Selenium (trace mineral):
1) Source
2) Forms
3) Absorption and transport
4) Functions
1) Source: based on soil content, brazil nuts
2) Forms: selenocysteine (biologically active form), selenomethionine (Storage)
3) Absorption: regulated through urinary excretion, highest concentration in liver pancreas muscle kidneys thyroid; not much known about transport
4) Functions: component of 2 proteins, part of the antioxidant enzymes –> protect against ROS (works with Vitamin E) e.g. glutathione peroxidase (GPx) which breaks down peroxides to water, thyroid metabolism –> conversion of T4 to T3, immune function,
Describe selenium deficiency and toxicity in terms of causes, symptoms
1) Deficiency: rare, noted for Keshan disease (poor soil content) –> enlarged heart with poor cardiac function
2) Toxicity: also rare, caused by industrial accidents or supplementation; symptoms –> garlic odor breath, fatigue, joint pain, hair loss, GI upset
Fluoride (trace mineral):
1) Source
2) Function
- fluoride is NOT an essential nutrient*
1) Source: fluoridated water or toothpaste/mouthwash
2) Function: no natural metabolic function, but promotes tooth mineralization and healthy enamel and prevents development of cavities
Describe fluoride deficiency and toxicity in terms of causes, symptoms
1) Deficiency: accelerates formation of cavities
2) Toxicity: accidental swallowing; symptoms –> discolored teeth, enamel pitting, but no health risk
Iodine (trace mineral):
1) Source
2) Absorption
3) Functions
1) Source: seafood, iodized salt, plants from iodine rich soils
2) Absorbed in the small intestine, 40% of body iodine is in thyroid gland; goitrogens are vegetables (turnips, cabbage, cauliflower, broccoli) which decrease absorption of iodine in the gut cooking destroys goitrogen activity
3) Part of thyroid hormone –> regulates basal metabolic rate, growth, energy metabolism, blood cell production, growth, nerve and muscle function
Describe iodine deficiency in terms of causes, symptoms, treatment
1) Causes: deficient intake, excessive Calcium intake, tobacco/alcohol consumption, pregnancy
2) Symptoms: goiter and hypothyroidism since T3/T4 production declines and TSH secretion increases –> lethargy, dry skin, reduced muscle and skeletal growth, weight gain; cretinism (irreversible mental retardation, in infants)
3) Iodized salt, thyroid hormone
Describe iodine toxicity in terms of causes, symptoms
1) Causes: excessive dietary intake
2) Symptoms: body can adapt to higher intake, but can lead to goiter
Describe the sources and uses of chromium in the body and its relationship to diabetes.
1) Sources: egg yolks, whole grains, pork, mushrooms
2) Function: enhances insulin action
3) Chromium deficiency linked to glucose intolerance (DMII)
Describe the sources and uses of cobalt in the body and its relationship to megaloblastic anemia
1) Source: animal foods containing Vitamin B12
2) Function: part of Vitamin B12
3) Same symptoms as Vitamin B12 deficiency –> megaloblastic anemia, nerve damage, and swollen tongue
Define peritoneal and primary and secondary retroperitoneal organs + give examples + venous drainage
1) Peritoneal - contained within the peritoneal cavity and covered by visceral peritoneum e.g. stomach, liver, spleen, first part of duodenum, ileum, jejenum, cecum, transverse colon, sigmoid colon, tail of pancreas; drained via the hepatic portal system and connected to the parietal peritoneum via mesentary (conduit for vessels/nerves)
2) Primary retroperitoneal - lie between parietal peritoneum and the abdominal wall, covered by parietal peritoneum e.g. kidney, adrenals, ureter, aorta, IVC, lower rectum, anal canal; drained via the caval system
3) Secondary retroperitoneal - initially peritoneal and suspended in mesentary, but migrated behind the peritoneum during development e.g. head neck body of pancreas, rest of duodenum, ascending and descending colon; drained via the hepatic portal system
Describe the organs of the GI tract including components and function:
1) Esophagus
2) Stomach
3) Small intestine
4) Large intestine
1) Esophagus - conduit for ingested food, no digestion
2) Stomach - 3 muscle layers (others have 2) for churning and digesting food; pyloric sphincter guards entry into small intestine; mucosa has gastric pits that are continuous with gastric glands (Secrete HCl + enzymes)
3) Small intestine: duodenum (bw foregut and midgut), jejunum, ileum; responsible for digestion and nutrient absorption, have crypts + villi, epithelium contains enterocytes (intestinal absorptive cells) + goblet cells
4) Large intestine/colon: cecum, ascending colon, transverse colon, descending colon, sigmoid colon (continuous with rectum and anal canal); contain haustra outpocketing and taenia coli muscle bands; NO villi + increased # goblet cells
Describe the accessory digestive organs, including their development from the gut tube:
1) Salivary glands
2) Pancreas
3) Liver
- all accessory glands are outgrowths of the forming digestive tract*
1) Salivary gland: ducts emerge from gut tube –> terminate by generating acini; acini secrete digestive enzymes into the ducts to access the lumen of the gut
2) Pancreas: ducts emerge from gut tube –> terminate by generating acini; some acini which lose their connection to the ducts become the islets of langerhans (endocrine function) –> produce insulin, glucagon, somatostatin and secrete into the bloodstream
3) Liver: bud from duodenum –> branches to form gall bladder and liver –> hepatic branch encounters venous pool and develops into cords/lines of hepatocytes; sinusoids lying between hepatocytes are continuous with the portal system (Receive blood from portal vein and hepatic artery)
What is portal hypertension? Describe cause and symptoms
1) Hepatic portal system- blood from peritoneal and secondary retroperitoneal organs passes through liver en route to the heart; liver damage –> fibrosis (Scar tissue) –> blood cannot flow and backs up –> blood seeks alternate routes via anastomotic connections to the caval system
2) Increased blood flow in anastomotic veins –> veins enlarge and walls weaken
A) esophageal varices patients can die from blood loss
B) anorectal varices
C) caput medusae in abdominal body wall
Describe the arterial blood supply to the GI organs
- 3 major arteries that arise from the aorta*
1) Foregut - celiac artery e.g. spleen, liver, stomach, pancreas
2) Midgut - superior mesenteric artery e.g. pancreas, small intestine (cecum, asending), large intestine
3) Hindgut - inferior mesenteric artery e.g. large intestine, (Transverse, descending, sigmoid), rectum
Define and describe:
1) Dietary Reference Intake (DRI)
2) Recommended Dietary Allowance (RDA)
3) Adequate Intake (AI)
4) Upper Limit (UL)
5) Estimated Average Requirement (EAR)
6) Estimated Energy Requirement (EER)
- established for HEALTHY individuals*
1) DRI - set of reference values to assess nutrient intake, include RDA, AI, and UL
2) RDA - goal to ensure that intake is adequate in an individual (sufficient intake for 97% of pop)
3) AI - likelihood that intake is adequate when no RDA is set for the nutrient
4) UL - likelihood of toxicity or excess
5) EAR - likelihood that intake is adequate in a population (sufficient intake for 50% of pop)
6) EER - average dietary energy intake to maintain energy balance - no upper level e.g. active 20 year old man requires 3000 kcal, sedentary requires 2500 kcal
What are the major nutrient categories? What are micronutrients vs macronutrients?
1) Water, Minerals, Vitamins, Carbs, Proteins, Lipids (can also argue Oxygen and Alcohol)
2) Macronutrients: need >1g/day, include water, carbs, proteins, lipids
3) Micronutrients: need less than 1g/day, includes minerals and vitamins
Define:
1) Essential nutrient
2) Conditionally essential nutrient
1) Essential nutrient - one the body cannot make, and we need to survive
2) Conditionally essential - depends on the condition e.g. choline for prenatal
* Whether something is nutritious depends on the dose*
What is the energy that can be yielded from the following nutrients:
1) Carbs
2) Protein
3) Fat
4) Alcohol
1) Carbs = 4kcal/g
2) Protein = 4 kcal/g
3) Fat = 9 kcal/g
4) Alcohol = 7 kcal/g (estimate)
What are the ABCD methods of nutritional assessment?
A) Anthropometry e.g. height, weight, circumferences
B) Biochemical measurements e.g. blood, urine
C) Clinical assessments e.g. medical history, visible signs or symptoms of illness
D) Dietary assessment e.g. food diary
Describe the three groups of polysaccharides (complex carbs) including sources and functions:
1) Starch
2) Glycogen
3) Fiber *elaborate on soluble vs insoluble and harmful effects of excessive fiber intake
1) Starch - found in corn, rice, wheat, legumes; glucose storage in plants –> amylose (unbranched chain of glucose molecules) and amylopectin (branched chain)
2) Glycogen - highly branched chain of glucose –> can be easily broken down for fast energy (fasting, exercise), storage in liver and muscle
3) Fiber - cannot be digested; promotes growth of beneficial intestinal bacteria –> protects against disease, binds dietary fat and cholesterol –> decreases blood cholesterol, promotes satiety
A) soluble = fermentable in water, found in apples, gums,; softens feces and relieves constipation
B) insoluble = non-fermentable, found in whole grains, green leafy veggies; increases bulk of feces and also releases constipation (though too much causes constipation)
C) Overintake: GI obstruction –> gas, diarrhea, too many phytates prevent absorption of minerals
Define:
1) Glycemic index
2) Glycemic load
1) Glycemic index - rise in blood glucose after eating 50g of carbs; 1=glycemic index of glucose
2) Glycemic load - rise in blood glucose based on how many carbs you actually eat; GL = (GI/100) x #carbs
* eating low GI and GL foods is associated with better health*
What are the simple vs complex carbs? How are carbs metabolized
1) Simple carbs: monosaccharides (glucose, fructose, galactose) + Disaccharides (lactose, sucrose, maltose)
2) Complex carbs: oligosaccharides (3-10 sugar units) + polysaccharides (>10 sugar units, glycogen, starch, dietary fiber)
3) Metabolized into glucose, stored as glycogen in liver + muscle –> fuels body’s cells
* carbs are NOT essential nutrients*
Explain the protein-sparing action of complex carbohydrates
Need adequate dietary carbohydrate to prevent the breakdown of protein into amino acids –> glucose for energy
What are the functions of protein in the body?
1) Structural materials
2) Enzymes
3) Hormones
4) Fluid balance –> can cause edema
5) Acid-base balance
6) Transportation
7) Antibodies
8) Provide fuel, and glucose if needed
9) Other - fibrin for clotting, collagen for scars, opsin for vision
How is excess nitrogen excreted?
1) AA –> ammonia (NH3) toxic
2) 2 NH3 –> 1 Urea (NH2)2CO
3) Urea released into blood
4) Kidneys filter urea out of blood, excreted in urine
Define nitrogen balance and give examples of different states
Nitrogen balance = Nitrogen intake - nitrogen output
1) Positive nitrogen status - body synthesizes more N than it degrades –> protein added e.g. growing children, pregnancy, people recovering from illness, increased insulin/GH secretion
2) Negative nitrogen status - body degrades more N than it synthesizes e.g. starvation, stress, cancer, surgery, increased T4/cortisol secretion, deficiency of essential amino acids (e.g. PVT TIM HLL)
What is the PDCAAS method of ranking dietary proteins? Contrast protein quality bw animal vs plant sources. Explain the concept of protein complementation
1) PDCAAS - evaluating protein quality based on AA requirements (does it have essential AA? N-containing AA?) and digestibility
2) Animal proteins e.g. egg, milk protein, poultry have high PDCAAS ~1; plant proteins e.g. kidney beans, whole wheat bread, generally have lower PDCAAS scores although soy=1
3) Protein complementation = combining low-quality proteins to provide adequate levels of essential AA e.g. combining beans (Ile, Lys) with rice (Met, Trp)
Discuss the forms of protein-energy malnutrition including causes and symptoms:
1) Kwashiorkor
2) Marasmus
1) Kwashiorkor - wasting due to sudden and recent deprivation of food, or due to lack of protein but not calories (e.g. rice diet); symptoms: distended belly/edema, 60-80% body weight for age, poor appetite
2) Marasmus - wasting and stunting due to severe deprivation of food for long time, both calorie and protein deficit; symptoms: muscle wasting, less than 60% body weight for age, good appetite
What is the importance of dietary protein? What is the recommended intake
1) Need dietary protein bc its the only source of essential AA (mnemonic: PVT TIM HLL) and practical source of Nitrogen
2) RDA for adults: 0.8 g/kg body weight/day
Describe the structural features of fatty acids.
What are common foods rich in different types of fatty acids?
1) Carboxylic acid with long aliphatic chain that can be saturated (solid) or unsaturated (liquid) fats spoil when exposed to 02
2) 18-C fatty acids abundant in food: saturated from animal fats, coconut oil, butter; monounsaturated (1 double bond) in olive, canola oils; polyunsaturated (1+ double bonds): omega-6 in corn, soybean, sunflower oils; omega-3 in flaxseed and fish (salmon) oils
* double bonds are numbered based on distance from methyl end of carbon chain*
What is hydrogenation? What is the difference between saturated fatty acids and trans fats?
1) Hydrogenation - conversion of unsaturated fats –> saturated fats (trans-fats)
2) Trans fats are not found in nature, are worse for us than saturated fats, although both increase incidence of coronary heart disease
A) Sat fats: increase LDL, promote blood clotting
B) Trans fats: increase LDL, lower HDL, interfere with enzyme function, raise blood levels of atherogenic lipoprotein (which causes plaque formation)
Describe the structure, functions, and sources of the following lipids:
1) Phospholipid
2) Sterols
3) Triglycerides
1) Phospholipid - hydrophilic head, hydrophobic tails; lipid bilayer of cell membrane + emulsifiers; found in chocolate
2) Sterols - made in body, another component of cell membranes; found in cholesterol, plant sterols
3) Triglyceride=triacylglyceride=TAG - glycerol + 3 fatty acids; provide cells with energy, secrete hormones, skin insulation + shock absorption; found in foods high in cholesterol, saturated fats that lower HDL e.g. red meat, butter
What are the essential fatty acids, in what foods are they found, and what are their health benefits?
What are eicosanoids? What is their function?
Two essential FAs (can be used to make other FAs):
linoleic acid and linolenic acid
1) Linoleic acid (omega-6) found in vegetable oils (corn, soybean, sunflower) and meats –> lower LDL, increase HDL, reduces risk of coronary heart disease
2) Linolenic acid, EPA, DHA (omega-3) found in flaxseed oil, fish (salmon) –> little effect on LDL, HDL, reduces risk of coronary heart disease + cancer
3) Eicosanoids are prostaglandins, leukotrienes etc. derived from omega-6 and omega-3 FAs (ideally in 2:1 ratio, though realistically its much higher); one major pathway is omega 6 linoleic acid–> arachidonic acid
4) “local hormones” with health benefits: regulate inflammation, immunity
What is the main driver of high cholesterol? What are ways to lower cholesterol
1) It is NOT dietary cholesterol (e.g. eggs, cheese), but rather saturated fats that are the top determinant of LDL cholesterol; sources include meats, whole milk products, tropical oils
2) Replace saturated fats with unsaturated fats, consume omega-3 fatty acid foods or supplements
What are the guidelines for fat intake?
~1/3 daily energy from fat, including essential FAs
limit intake of harmful fats: saturated fats, trans fat, cholesterol
Describe the four types of lingual papillae including histology, function, and whether or not there are taste buds:
1) Filiform
2) Fungiform
3) Foliate
4) Circumvallate
Papillae - mucosal projections on the tongue, formed by highly vascular CT core and covered by strat squamous epithelium
1) Filiform: narrow conical shape, smallest, most numerous, NO taste buds, keratinized stratified epithelium –> breaks up food into smaller particles
2) Fungiform: mushroom shape, taste buds on dorsal surface
3) Foliate: three fingers of dermal papillae sticking into epithelial layer, taste buds along a furrow/trench, von Ebner glands which flush material from the trench so taste buds can respond rapidly
4) Circumvallate: rectangle shaped, largest, taste buds along a furrow/trench, von Ebner glands
Describe the histology and function of the major salivary exocrine glands:
1) Parotid
2) Sublingual
3) Submandibular
* Which gland has the most common benign tumor?
all salivary glands have myoepithelial cells
1) Parotid: 95% serous secreting acini, has adipocytes, can sometimes see facial nerve VII
* clinical correlation: pleomorphic adenoma is most common benign salivary gland tumor- nodular mass, needs to be resected*
2) Submandibular: serous acini + adipocytes, also serous demilunes (mucous cell capped with serous cells, looks like mushroom)
3) Sublingual: 95% mucous secreting acini, lighter in color bc mucous doesnt stain, flattened basal nuclei
* much fewer intercalated and striated ducts bc mucous secretion doesnt need to be modified/buffered*
Describe the duct system in the salivary glands
1) Intralobular ducts (within lobule):
A) Intercalated ducts - connect acini with striated duct, modify serous secretion (which contains amylase) by secreting bicarb and absorbing Cl
B) Striated ducts - connect intercalated duct to interlobular duct, modify secretion by secreting K and bicarb and absorbing Na+, appear striated bc of infoldings with mt
2) Interlobular ducts (bw lobules):
A) Excretory ducts - transport saliva to exterior surface, surrounded by lots of CT, will see goblet cells
Describe the histology of the mucosa and the muscle layers of the organs of the GI tract and how it relates to their function: Esophagus
1) Mucosa: Stratified squamous epithelium, Large mucosa that allows bolus of food to fit in the lumen, submucosa has mucous glands to lubricate epithelium, and counteract the acidity of stomach
* only esophagus and duodenum have submucosal glands*
2) Muscle: large muscularis externa to move food down to the stomach- striated skeletal muscle closer to mouth, smooth closer to stomach
Describe the histology of the mucosa and the muscle layers of the organs of the GI tract and how it relates to their function: Stomach
1) Mucosa: Simple columnar epithelium with gastric pits that extend into glands, NO villi or goblet cells, Mucosa has transient folds called rugae which open up to expand stomach surface area
Pit:gland length ratio–> Cardia - 1:1, fundus/body - 1:3 (most colorful bc of chief and parietal cell staining), pylorus - 3:1 (NO chief or parietal)
2) Muscle: Thick muscularis externa bc three layers of muscle (all other organs have 2)
Describe the 6 types of cells that make up the epithelium of the stomach (in the gastric pit and gland):
1) Surface mucous
2) Neck mucous
3) Stem
4) Parietal *differentiate bw active and inactive
5) Chief
6) DNES *differentiate bw open and closed
1) Surface mucous - located in the gastric pit, cells produce bicarb & granules which contain glycoproteins that combine with the bicarb to form surface protective insoluble gel
2) Neck mucous - located at juncture of gastric pit –> gland, produce soluble gel eventually differentiate into surface mucous
3) Stem - need active stem cell pop bc cells die due to abrasion, takes 4-5 days to mature
4) Parietal - produce HCl (gastric acid) and intrinsic factor (for B12 absorption –> otherwise develop pernicious anemia);
A) Inactive cell has lots of mt and membrane reserve (tubules, vesicles) in the cytoplasm
B) Active cell - membranes coalesce to increase surface area, prominent intracellular canaliculus
5) Chief - located in basal half of gastric glands, produce pepsinogen and gastric lipase, v basophilic (stains v dark), stimulated by ACh and secretin
6) DNES - communication –> interact with other DNES cells, neurons, influence motility and digestion, secrete secretin, glucagon, other hormones into ECM –> blood circulation (NOT the lumen, so fenestrated capillaries are on basal side)
A) Open - extend to lumen, Closed - stay on basal side
What are the protective and destructive factors in the stomach?
1) Protective: bicarbonate rich mucous secretion, prostaglandins (increase local circulation and bicarb secretion), tight junctions, pepsinogen (not active form), pepsinogen, stem cells
2) Destructive: HCl, pepsin, stress + aspirin + NSAIDs (inhibit prostaglandins –> decreased bicarbonate production –> “heartburn” symptoms), H. pylori
Describe the histology of the mucosa and the muscle layers of the organs of the GI tract and how it relates to their function: Small intestine
1) Mucosa: Simple columnar epithelium with goblet cells, villi (evaginations) and crypts of Lieberkuhn (invaginations) –> increase surface area; plicae circularis = folds of submucosa that encircle the small intestine, covered by villi;
A) duodenum submucosa has Brunner’s glands –> produce alkaline mucous to protect epithelium from acid that spills over from stomach
B) Jejunum has long villi
C) Ileum has short and fat villi, Peyer’s patches (lymphoid nodules)
2) Muscle: 2 muscle layers, smaller than that of the stomach - inner circular and outer longitudinal
* only esophagus and duodenum have submucosal glands*
Describe the 6 types of cells found in the epithelium of the small intestine including histology, function, and where they are found:
1) Enterocytes
2) Goblet
3) Immune
4) Paneth
5) Stem
6) DNES
1) Enterocytes - absorptive cell located in villi and crypts; absorb lipids, sugars, AA, ions, etc., digest proteins and carbs, produce enzymes associated with glycocalyx
2) Goblet - located in villi; produce layer of mucous
3) Immune - located in villi e.g. lymphocytes, macrophages, M cells
4) Paneth- located at base of crypts; produce lysozyme (controls gut flora), TNF-alpha (pro-inflammatory), defensins (antimicrobial)
5) Stem - located at the base of crypts
6) DNES - located in villi and crypts, for communication
