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Flashcards in Unit 3 &4 Deck (134):
1

Mechanical Digestion

chewing, mixing (no bonds broken)

2

Chemical Digestion

food breakdown (bonds broken)

3

Absorption

proteins & carbohydrates move to blood & fats move to lymph

4

Palatine tonsils

posterior oral cavity

5

lingual tonsil

base of the tongue

6

pharyngeal tonsils

nasopharynx wall

7

tubal tonsils

surround auditory tube openings into the pharynx

8

Tongue

-Hold food during chewing
-Mix food w/ saliva
-Form bolus
-Starts swallowing r-esponse
-Speech

9

Salivary Glands

-Clean the mouth
-Moisten & dissolve food
-Contains salivary amylase (digests starch to maltose)
-Serous (watery) & mucus (thick) secretions

10

Parotid Salivary Gland

-anterior to the ear between the masseter muscle & skin
-Serous secretions

11

Submandibular Salivary Gland

-medial to mandible
-Serous & mucous secretions

12

Sublingual Salivary Gland

-under the tongue
-Mucous secretions

13

Pharynx

-Conducts food to esophagus
-Conducts air to trachea

14

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

15

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

16

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

17

Chemical Digestion: Nucleic Acids

-Absorbed & transported to the liver via the hepatic portal vein
-Enzymes used:
Nucleases

18

Mesentery

Mesentery – peritoneum that provides:
-Blood & nerve supplies to the organs
-Hold digestive organs in place
-Store lipids (visceral fat)

19

Small Intestine: Microscopic Anatomy

Structural modifications to ↑surface area

20

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

21

Internal Anal Sphincter

smooth muscle

22

external anal sphincter

skeletal muscle

23

hemorrhoids

Superficial veins around anal canal Inflammation

24

GI tract activity declines w/ age

-Absorption is less efficient
-Peristalsis is slowed

25

Hepatocyte functions:

-Produce bile
-Process nutrients
-Store fat-soluble vitamins
-Detoxification

26

Peptic Ulcer

-Lesions in the stomach OR duodenum wall
-Primarily caused by bacteria: Helicobacter pylori
-Treated w/:
Antacids
Pink bismuth (Pepto-Bismol)
Antibiotics

27

Appendicitis

Usually caused by:
-Fecal obstruction or Anatomical pinching of the appendix
-A ruptured appendix leads to peritonitis

28

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

29

Hepatitis

-Inflammation of the liver
-Caused by drugs, chemicals, viruses, alcohol

30

Viral “Hepatitis A”

caused by the ingestion of contaminated food (fecal/oral)

31

Viral “Hepatitis B” & “Hepatitis C”

body fluid transmitted pathogens

32

Diverticulitis

-Small herniations of the colon wall
-Areas can inflame & rupture
-Prevention is the treatment of choice
↑Fiber diet prevents diverticulitis

33

Emesis (vomiting)

-Microbes
-Allergies
-Excessive food consumption
-Poisons

34

Constipation

-Infrequent defecation of fecal material
-Diet low in fiber
-Diet low in water

35

Gall Stones (Biliary Calculi)

-Crystallization of cholesterol & bile salts
-Block the bile duct
-Fill the gall bladder

36

Jaundice

-Bile build-up in the skin & sclera causes a yellow appearance
-Cause: damage to the liver, gall bladder, or biliary ducts

37

Bulimia Nervosa

-Psychological disorder
-Patient has a fear of gaining weight
-Patient binges on food
-Purges w/ laxatives or vomiting

38

Anorexia Nervosa

-Psychological disorder
-Patient has a false perception of their own weight
-Patient does not eat enough
-Extreme cases are lethal

39

Cystic Fibrosis

-Genetic disorder
↑Mucus is produced
-Causes pancreatic duct blockage
-Enzymes can’t enter duodenum
-Treatment: digestive enzymes given orally

40

Metabolism

Metabolism = anabolism + catabolism

41

Catabolism

Breakdown of large molecules into smaller subunits

42

Catabolism or Anabolism: Digestion

Catabolism

43

Catabolism or Anabolism: Removal of hydrogen (H) during dehydrogenation

Catabolism

44

Catabolism or Anabolism: Removal of carboxyl groups (COO–) during decarboxylation

Catabolism

45

Catabolism or Anabolism: Removal of amine groups (NH2) during deamination

Catabolism

46

Diarrhea

-Movement of fecal material through the G.I. tract too rapidly (over-hydration)
-Caused by microbes, spicy foods, stress

47

Cirrhosis of the Liver

-Liver cells are destroyed & replaced by fibrous connective tissue
-Causes: alcohol, drugs, toxins

48

Flatulence

Intestinal gas results from:
Bacteria
Diet
Swallowing air

49

Anabolism

Synthesis of large molecules from smaller subunits

50

Catabolism or Anabolism: Glycogen (polysaccharide) from glucose (monosaccharide)

Anabolism

51

Catabolism or Anabolism: Proteins from amino acids

Anabolism

52

Catabolism or Anabolism: Lipids from glycerol & fatty acids

Anabolism

53

Reduction reaction:

if a molecule gains electrons or gains H +→ it is reduced

54

Oxidation reaction:

if a molecule loses electrons or loses H+ → it is oxidized

55

Reducing agents

donate electrons or H

56

Oxidizing agents

accept electrons or H

57

Reduction-Oxidation Reactions

-Coenzymes transport or carry
-Niacin makes NAD
-Riboflavin makes FAD
-Pantothenic Acid makes CoA

58

Dehydration/Synthesis Reactions

using synthesis enzymes

59

Hydrolysis/Breakdown Reactions

using digestive enzymes

60

Cellular Respiration Equation

C6H12O6 + 6O2 + 38 ADP + 38 P →
6CO2 + 6H2O + 38 ATP + Heat

61

Which is oxidized and reduced: NAD + 2H -> NADH + H

oxidized: NAD
reduced: NADH + H

62

Which is oxidized and reduced: FAD + 2H -> FADH2

oxidized: FAD
reduced: FADH 2

63

Glycolysis

-Anaerobic
-Cell cytoplasm
-Breaks down glucose (6C) into two pyruvic acid (3C) molecules
-ATP is made
-Reduced NAD (NADH+H+) created

64

How many C: Glucose

6C

65

How many C: Pyruvate

3C

66

How many C: Coenzyme A

3C

67

How many C: Acetyl CoA

2C

68

How many C: Regenerates Oxaloacetic Acid (OAA)

4C

69

How many C: Citric Acid

6A

70

Krebs Cycle

-Indirect Aerobic
-Mitochondrial matrix
4C+2C=6A

71

Electron Transport System (ETS)

-Mitochondrial inner membrane
-Aerobic:direct
-Makes ↑ATP + metabolic H2O + CO2

72

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

73

Oxidative phosphorylation:

-26 ATP generated by ETS (w/ O2) made this way
-ATP is generated by H+ & e– movements

74

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)

75

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

76

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

77

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

78

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

79

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)

80

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

81

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

82

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

83

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

84

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)

85

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)

86

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

87

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

88

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

89

Two mechanism of hormonal

Direct Gene Activation (steoroids) and Second Messanger (protein)

90

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

91

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

92

Hypoglycemia

-↑Insulin causes glucose to move from blood → cells
-Blood glucose decreases because glucose moves into cells
-Results: ↓blood glucose level (hypoglycemia)

93

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)

94

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)

95

Diabetes Mellitus Type II

-Type II (adult-onset) diabetes:
-Non-Autoimmune
-Poor response by cell receptors to insulin
-Poor diet
-↓Exercise

96

Latent Autoimmune Diabetes in Adults (LADA)

-Type 1.5 diabetes:
-Autoimmune
-A form of Type I diabetes
-Occurs during adulthood
-Delayed onset of symptoms

97

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

98

Thyroxine (Thyroid Hormone)

-Produced by follicles of the thyroid gland
-↑Cell metabolism (↑BMR)
-Stimulates:
Growth
Repair
Temperature regulation

99

↑Thyroxine leads to:

Hyperthyroidism
↑Metabolism (↑BMR)
Exophthalmia
↓Body weight

100

↓Thyroxine leads to:

Hypothyroidism
↓Metabolism (↓BMR)
Endophthalmia
Goiter
Obesity
Cretinism

101

Cretinism

-Disease of very young children
-Occurs when ↓thyroxine produced
-Results in:
↓Metabolism
↓Growth
↓Development
Mental retardation

102

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

103

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

104

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

105

Dwarfism

-Below normal secretion of human Growth Hormone (hGH)
-Occurs in young children
-Slow growth
-Very reduced stature

106

Esophagus

-Muscular tube
-Between laryngopharynx & stomach
-Moves through mediastinum & diaphragm
-Connects to the cardia of the stomach

107

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)

108

Deglutition (Swallowing)

-Coordinated activity of:
Tongue
Soft palate
Pharynx
Esophagus
-22 different muscle groups
-Bolus is moved by peristalsis to the stomach

109

Primary Teeth

20 teeth erupt at ½ – 2 yrs

110

Permanent

32 teeth erupt at 6 – 12 yrs

111

Incisors

chisel-shaped (cutting)

112

Canines

fang-like (tearing)

113

Premolars & molars

broad crowns w/ rounded tips (grinding)

114

Substrate + Enzyme → Product of Salivary Amylase
Source:
Optimum pH

Starch + Amylase → Maltose (disaccharide)
Salivary gland
7.0

115

peristalsis

moving

116

segmentation

mixing

117

Name the layers of the G.I. from most inner to outer

mucosa, submucosa, muscularis, serosa

118

Mucous cells

alkaline mucus

119

Parietal cells

-HCl & Intrinsic Factor
I.F. ↑vit. B12 absorption

120

Chief cells

pepsinogen
-HCl activates pepsinogen to pepsin

121

G cells

secrete the hormone gastrin

122

Cephalic Phase begins

Sight, taste, smell, or thought of food
-begins before food entry

123

Gastric Phase begins:

-Stomach distension (stretch receptors)
-Protein, caffeine, & ↑pH (basic)
-Gastrin (hormone)
-begins if food enters stomach

124

Intestinal: begins

if chyme enters duodenum

125

HCl secretion stimulated by

1) ACh, 2) histamine & 3) gastrin through second-messenger systems

126

cells of Cajal

-Basic electrical rhythm is initiated by pacemaker cells
-Peristaltic waves move at rate of 3/minute

127

Bile leaves liver by:

Right & left hepatic ducts → common hepatic duct → cystic duct → common bile duct → sphincter of Oddi

128

Secretin

-stimulates the liver to ↑bile
-stimulates the pancreas to ↑bicarbonate-rich secretions

129

cholecystokinin (CCK)

-stimulates gallbladder to contract
-stimulates Sphincter of Oddi to relax (bile & pancreatic secretions enter duodenum)

130

Pancreas Exocrine Function

Enzymes to break down all organic compounds

131

Pancreas Endocrine Function

Insulin & Glucagon production

132

Pancreatic Secretions

-Watery, alkaline (HCO3–) solution of enzymes
-Neutralizes acidic chyme
-Provides optimal (basic) pH for pancreatic enzymes

133

Pancreatic Secretions Enzymes

-Trypsinogen is activated to trypsin
-Procarboxypeptidase is activated to carboxypeptidase
-Amylase
-Lipase
-Nucleases

134

Small Intestines

All nutrient absorption takes place in the small intestine