Unit 3 &4 Flashcards
Mechanical Digestion
chewing, mixing (no bonds broken)
Chemical Digestion
food breakdown (bonds broken)
Absorption
proteins & carbohydrates move to blood & fats move to lymph
Palatine tonsils
posterior oral cavity
lingual tonsil
base of the tongue
pharyngeal tonsils
nasopharynx wall
tubal tonsils
surround auditory tube openings into the pharynx
Tongue
- Hold food during chewing
- Mix food w/ saliva
- Form bolus
- Starts swallowing r-esponse
- Speech
Salivary Glands
- Clean the mouth
- Moisten & dissolve food
- Contains salivary amylase (digests starch to maltose)
- Serous (watery) & mucus (thick) secretions
Parotid Salivary Gland
- anterior to the ear between the masseter muscle & skin
- Serous secretions
Submandibular Salivary Gland
- medial to mandible
- Serous & mucous secretions
Sublingual Salivary Gland
- under the tongue
- Mucous secretions
Pharynx
- Conducts food to esophagus
- Conducts air to trachea
Chemical Digestion: Carbohydrates
-Absorbed & transported to the liver via the hepatic portal vein
Enzymes used:
-Salivary amylase
-Pancreatic amylase
-Brush border enzymes (associated w/ microvilli):
Lactase, maltase, sucrase
Chemical Digestion: Proteins
-Absorbed & Transported to the liver via the hepatic portal vein
-Enzymes acting in the stomach:
Pepsin
Enzymes acting in the small intestine:
Pancreatic enzymes – trypsin, chymotrypsin & carboxypeptidase
Brush-border enzymes – aminopeptidases, carboxypeptidases & dipeptidases
Chemical Digestion: Lipids
-Absorbed as micelles into intestinal cells:
-Combine w/ proteins & released to the lacteal as -chylomicrons
-Enter lacteals & are transported to systemic circulation via lymph vessels
-Enzyme/chemical used:
Lipase
Bile
Chemical Digestion: Nucleic Acids
-Absorbed & transported to the liver via the hepatic portal vein
-Enzymes used:
Nucleases
Mesentery
Mesentery – peritoneum that provides:
- Blood & nerve supplies to the organs
- Hold digestive organs in place
- Store lipids (visceral fat)
Small Intestine: Microscopic Anatomy
Structural modifications to ↑surface area
Unique Features of Large Intestine
- Taenia coli – bands of longitudinal smooth muscle in the muscularis
- Haustra – pocket like sacs caused by the contractions of the taenia coli
- Epiploic appendages – fat-filled pouches of the visceral peritoneum
Internal Anal Sphincter
smooth muscle
external anal sphincter
skeletal muscle
hemorrhoids
Superficial veins around anal canal Inflammation
GI tract activity declines w/ age
- Absorption is less efficient
- Peristalsis is slowed
Hepatocyte functions:
- Produce bile
- Process nutrients
- Store fat-soluble vitamins
- Detoxification
Peptic Ulcer
-Lesions in the stomach OR duodenum wall
-Primarily caused by bacteria: Helicobacter pylori
-Treated w/:
Antacids
Pink bismuth (Pepto-Bismol)
Antibiotics
Appendicitis
Usually caused by:
- Fecal obstruction or Anatomical pinching of the appendix
- A ruptured appendix leads to peritonitis
Peritonitis
- Inflammation of the visceral peritoneum & parietal peritoneum
- Results from an infection caused by a penetrating wound
- Bacteria enter the sterile areas of the body surrounding the digestive system
- Lethal if not treated w/ high doses of antibiotics
Hepatitis
- Inflammation of the liver
- Caused by drugs, chemicals, viruses, alcohol
Viral “Hepatitis A”
caused by the ingestion of contaminated food (fecal/oral)
Viral “Hepatitis B” & “Hepatitis C”
body fluid transmitted pathogens
Diverticulitis
-Small herniations of the colon wall
-Areas can inflame & rupture
-Prevention is the treatment of choice
↑Fiber diet prevents diverticulitis
Emesis (vomiting)
- Microbes
- Allergies
- Excessive food consumption
- Poisons
Constipation
- Infrequent defecation of fecal material
- Diet low in fiber
- Diet low in water
Gall Stones (Biliary Calculi)
- Crystallization of cholesterol & bile salts
- Block the bile duct
- Fill the gall bladder
Jaundice
- Bile build-up in the skin & sclera causes a yellow appearance
- Cause: damage to the liver, gall bladder, or biliary ducts
Bulimia Nervosa
- Psychological disorder
- Patient has a fear of gaining weight
- Patient binges on food
- Purges w/ laxatives or vomiting
Anorexia Nervosa
- Psychological disorder
- Patient has a false perception of their own weight
- Patient does not eat enough
- Extreme cases are lethal
Cystic Fibrosis
-Genetic disorder ↑Mucus is produced -Causes pancreatic duct blockage -Enzymes can’t enter duodenum -Treatment: digestive enzymes given orally
Metabolism
Metabolism = anabolism + catabolism
Catabolism
Breakdown of large molecules into smaller subunits
Catabolism or Anabolism: Digestion
Catabolism
Catabolism or Anabolism: Removal of hydrogen (H) during dehydrogenation
Catabolism
Catabolism or Anabolism: Removal of carboxyl groups (COO–) during decarboxylation
Catabolism
Catabolism or Anabolism: Removal of amine groups (NH2) during deamination
Catabolism
Diarrhea
- Movement of fecal material through the G.I. tract too rapidly (over-hydration)
- Caused by microbes, spicy foods, stress
Cirrhosis of the Liver
- Liver cells are destroyed & replaced by fibrous connective tissue
- Causes: alcohol, drugs, toxins
Flatulence
Intestinal gas results from:
Bacteria
Diet
Swallowing air
Anabolism
Synthesis of large molecules from smaller subunits
Catabolism or Anabolism: Glycogen (polysaccharide) from glucose (monosaccharide)
Anabolism
Catabolism or Anabolism: Proteins from amino acids
Anabolism
Catabolism or Anabolism: Lipids from glycerol & fatty acids
Anabolism
Reduction reaction:
if a molecule gains electrons or gains H +→ it is reduced
Oxidation reaction:
if a molecule loses electrons or loses H+ → it is oxidized
Reducing agents
donate electrons or H
Oxidizing agents
accept electrons or H
Reduction-Oxidation Reactions
- Coenzymes transport or carry
- Niacin makes NAD
- Riboflavin makes FAD
- Pantothenic Acid makes CoA
Dehydration/Synthesis Reactions
using synthesis enzymes
Hydrolysis/Breakdown Reactions
using digestive enzymes
Cellular Respiration Equation
C6H12O6 + 6O2 + 38 ADP + 38 P →
6CO2 + 6H2O + 38 ATP + Heat
Which is oxidized and reduced: NAD + 2H -> NADH + H
oxidized: NAD
reduced: NADH + H
Which is oxidized and reduced: FAD + 2H -> FADH2
oxidized: FAD
reduced: FADH 2
Glycolysis
- Anaerobic
- Cell cytoplasm
- Breaks down glucose (6C) into two pyruvic acid (3C) molecules
- ATP is made
- Reduced NAD (NADH+H+) created
How many C: Glucose
6C
How many C: Pyruvate
3C
How many C: Coenzyme A
3C
How many C: Acetyl CoA
2C
How many C: Regenerates Oxaloacetic Acid (OAA)
4C
How many C: Citric Acid
6A
Krebs Cycle
-Indirect Aerobic
-Mitochondrial matrix
4C+2C=6A
Electron Transport System (ETS)
- Mitochondrial inner membrane
- Aerobic:direct
- Makes ↑ATP + metabolic H2O + CO2
Substrate phosphorylation:
- 2 ATP (net) per glucose in Glycolysis made this way
- 2 ATP per glucose in Krebs Cycle made this way
- ATP is generated when bonds break
Oxidative phosphorylation:
- 26 ATP generated by ETS (w/ O2) made this way
- ATP is generated by H+ & e– movements
Glycogenesis
- Glycogen creation
- Anabolic
- Location: liver & muscle absorb glucose from blood
- Many glucose molecules bonded together become -glycogen
- Glucose is stored as glycogen (animal starch)
Glycogenolysis
- Glycogen breakdown
- Catabolic
- Location: liver & muscle release stored glycogen as glucose
- Liver glycogen is broken down to release glucose to blood
- Muscle glycogen is broken down to release glucose to muscle cells only
Gluconeogenesis
- Creation of glucose from non-carbohydrate sources
- Anabolic
- Location: metabolic pathways convert Krebs cycle acids, lactic acid, amino acids & lipids into glucose, LIVER
- Proteins & lipids (in the body & in food) are “sacrificed” to make new glucose
- May cause tissue deterioration
- Maintains a normal blood glucose level
Catabolism of Lipids
- Fatty acids: broken down 2 carbons at a time to acetic acid (beta oxidation)
- Acetic Acid: converted into an acetyl group
- Acetyl group: carried by coenzyme A (CoA)
- Acetyl-CoA → Krebs cycle & converted into CO2 & NADH+H+ & FADH2 & ATP
- Glycerol: converted into Phosphoglyceraldehyde (PGA)
- PGA sent to Glycolysis & converted into NADH+H+ & ATP & pyruvic acid
Beta Oxidation
- Process that breaks down fatty acids two carbon units (2C) @ a time
- Each two carbon acetyl group (2C) converts into acetyl CoA, which is then used in the Krebs Cycle to make 1ATP, 3 NADH+H+, & 1 FADH2
PROBLEM: If a fatty acid has 20 carbons, then how many acetyl units would be made?
(10 acetyl units which will turn the Krebs Cycle 10x)
Ketone Formation
-OAA is converted into glucose during: Starvation, ↑fat diet, diabetes mellitus -Without OAA: Acetyl CoA can’t enter the Krebs cycle Acetyl CoA accumulates -Liver converts excess Acetyl CoA into ketones (acetone) -Ketones are acidic & aromatic ↑Ketones → ketosis ↑↑Ketone levels → ketoacidosis
Catabolism of Proteins
-Proteins are broken down to amino acids
-Amino acids are deaminated & converted into energy
Ex: glycine (amino acid) is deaminated & converted into an acetyl group that becomes acetyl CoA & enters Krebs cycle
Amino Acid Catabolism
- Amino acids are catabolized by deamination
- Deamination removes amine groups (NH2) from the amino acid
- Remainder of the amino acid is used to generate ATP
Deamination
- Removal of an amine group (NH2) from an amino acid
- Prepares amino acid for entry into Glycolysis as Pyruvic -Acid or entry into the Krebs Cycle as Acetic Acid, Citric Acid, α-Ketoglutaric Acid, OAA
- Results: ↑urea formation at the liver
- Liver requires extra ATP to form urea
Lipid Anabolism
-Produces new lipids from glycerol, fatty acids
-Lipid anabolism products:
Triglycerides (adipose cell storage)
Oils (sebum)
Waxes (cerumen)
Steroids (lipid hormones)
Phospholipids (cell membrane)
Protein Anabolism
-Produces new proteins from amino acids
-Protein anabolism products:
Enzymes (anabolic & catabolic)
Antibodies (immunity)
Muscle proteins (actin & myosin)
Collagen (connective tissue)
Keratin (hair & fingernails)
LDL Function in Cholesterol Metabolism
-Low density lipoproteins (LDL): made in the liver
-Transports cholesterol to body cells (including blood vessel walls)
Contributes to plaque (atheroma) deposits w/in the wall
HDL Function in Cholesterol Metabolism
- High density lipoproteins (HDL) are made in tissues during exercise
- Transports triglycerides & cholesterol from body cells (including blood vessels) to the liver to be excreted
- HDL eliminates cholesterol from the body
Saturated Fats
- Triglycerides that contain fatty acids w/ many hydrogen atoms
- Single bonds link carbon atoms
- Stimulate the liver to make ↑cholesterol
- Stimulate the liver to ↓cholesterol release from the body
- Recommendation: unsaturated fats substitute for saturated fats in the diet
Two mechanism of hormonal
Direct Gene Activation (steoroids) and Second Messanger (protein)
Insulin
-Produced by the beta(β) cells of the islets of Langerhans in the endocrine pancreas
-Transfers glucose from blood into all body cells to promote hypoglycemia
↑Glycogenesis
↑Lipogenesis
↑Protein synthesis
↓Gluconeogenesis
Glucagon
-Produced by the alpha(α) cells of the islets of Langerhans in the endocrine pancreas
-Transfers glucose from the liver into the blood to promote hyperglycemia
↑Glycogenolysis
↑Lipolysis
↓Protein synthesis
↑Gluconeogenesis
Hypoglycemia
- ↑Insulin causes glucose to move from blood → cells
- Blood glucose decreases because glucose moves into cells
- Results: ↓blood glucose level (hypoglycemia)
Hyperglycemia
- ↑Glucagon causes glucose to move from liver cells → blood
- Blood glucose increases because glucose does not move into cells
- Results: ↑blood glucose level (hyperglycemia)
Diabetes Mellitus Type I
- Type 1 (juvenile-onset) diabetes:
- Autoimmune
- Beta cells of the pancreas are destroyed & suddenly stop producing insulin
- Results in chronic hyperglycemia
- Must be controlled by hormone replacement therapy (HRT)
Diabetes Mellitus Type II
- Type II (adult-onset) diabetes:
- Non-Autoimmune
- Poor response by cell receptors to insulin
- Poor diet
- ↓Exercise
Latent Autoimmune Diabetes in Adults (LADA)
- Type 1.5 diabetes:
- Autoimmune
- A form of Type I diabetes
- Occurs during adulthood
- Delayed onset of symptoms
Thyroid Stimulating Hormone (TSH)
-Produced by: anterior pituitary
-Stimulates: thyroid to produce & release thyroxine (thyroid hormone) as T4 (tetra-iodothyronine) or T3 (tri-iodothyronine)
-Thyroid requires:
Iodine + TSH → Thyroxine
Thyroxine (Thyroid Hormone)
-Produced by follicles of the thyroid gland
-↑Cell metabolism (↑BMR)
-Stimulates:
Growth
Repair
Temperature regulation
↑Thyroxine leads to:
Hyperthyroidism
↑Metabolism (↑BMR)
Exophthalmia
↓Body weight
↓Thyroxine leads to:
Hypothyroidism ↓Metabolism (↓BMR) Endophthalmia Goiter Obesity Cretinism
Cretinism
-Disease of very young children
-Occurs when ↓thyroxine produced
-Results in:
↓Metabolism
↓Growth
↓Development
Mental retardation
human Growth Hormone (hGH)
-Produced by: anterior pituitary gland
-Increases:
Fat utilization (lipolysis)
Protein synthesis
Tissue development
-Most hGH is released during sleep
-Decreasing amounts are released as age increases
-Youth hormone
Gigantism
- Caused by ↑human Growth Hormone (hGH) before bone growth-plate fusion
- Occurs in children
- Results in excessive height/weight for the person’s age
Acromegaly
- Caused by ↑human Growth Hormone (hGH) after bone growth-plate fusion
- Occurs in adults
- Excessive growth to the body such as: hands, feet, head, jaw & internal organs
- Longevity is limited
Dwarfism
- Below normal secretion of human Growth Hormone (hGH)
- Occurs in young children
- Slow growth
- Very reduced stature
Esophagus
- Muscular tube
- Between laryngopharynx & stomach
- Moves through mediastinum & diaphragm
- Connects to the cardia of the stomach
Esophageal Characteristics
- Epithelium – stratified squamous
- Empty esophagus is folded & flattened
- Expands if food is present
- Glands secrete lubricating mucus
- Bolus moves through the esophagus
- Muscle changes from skeletal muscle (superiorly) to smooth muscle (inferiorly)
Deglutition (Swallowing)
-Coordinated activity of: Tongue Soft palate Pharynx Esophagus -22 different muscle groups -Bolus is moved by peristalsis to the stomach
Primary Teeth
20 teeth erupt at ½ – 2 yrs
Permanent
32 teeth erupt at 6 – 12 yrs
Incisors
chisel-shaped (cutting)
Canines
fang-like (tearing)
Premolars & molars
broad crowns w/ rounded tips (grinding)
Substrate + Enzyme → Product of Salivary Amylase
Source:
Optimum pH
Starch + Amylase → Maltose (disaccharide)
Salivary gland
7.0
peristalsis
moving
segmentation
mixing
Name the layers of the G.I. from most inner to outer
mucosa, submucosa, muscularis, serosa
Mucous cells
alkaline mucus
Parietal cells
-HCl & Intrinsic Factor
I.F. ↑vit. B12 absorption
Chief cells
pepsinogen
-HCl activates pepsinogen to pepsin
G cells
secrete the hormone gastrin
Cephalic Phase begins
Sight, taste, smell, or thought of food
-begins before food entry
Gastric Phase begins:
- Stomach distension (stretch receptors)
- Protein, caffeine, & ↑pH (basic)
- Gastrin (hormone)
- begins if food enters stomach
Intestinal: begins
if chyme enters duodenum
HCl secretion stimulated by
1) ACh, 2) histamine & 3) gastrin through second-messenger systems
cells of Cajal
- Basic electrical rhythm is initiated by pacemaker cells
- Peristaltic waves move at rate of 3/minute
Bile leaves liver by:
Right & left hepatic ducts → common hepatic duct → cystic duct → common bile duct → sphincter of Oddi
Secretin
- stimulates the liver to ↑bile
- stimulates the pancreas to ↑bicarbonate-rich secretions
cholecystokinin (CCK)
- stimulates gallbladder to contract
- stimulates Sphincter of Oddi to relax (bile & pancreatic secretions enter duodenum)
Pancreas Exocrine Function
Enzymes to break down all organic compounds
Pancreas Endocrine Function
Insulin & Glucagon production
Pancreatic Secretions
- Watery, alkaline (HCO3–) solution of enzymes
- Neutralizes acidic chyme
- Provides optimal (basic) pH for pancreatic enzymes
Pancreatic Secretions Enzymes
- Trypsinogen is activated to trypsin
- Procarboxypeptidase is activated to carboxypeptidase
- Amylase
- Lipase
- Nucleases
Small Intestines
All nutrient absorption takes place in the small intestine
