Unit 3 &4 Flashcards
(134 cards)
1
Q
Mechanical Digestion
A
chewing, mixing (no bonds broken)
2
Q
Chemical Digestion
A
food breakdown (bonds broken)
3
Q
Absorption
A
proteins & carbohydrates move to blood & fats move to lymph
4
Q
Palatine tonsils
A
posterior oral cavity
5
Q
lingual tonsil
A
base of the tongue
6
Q
pharyngeal tonsils
A
nasopharynx wall
7
Q
tubal tonsils
A
surround auditory tube openings into the pharynx
8
Q
Tongue
A
- Hold food during chewing
- Mix food w/ saliva
- Form bolus
- Starts swallowing r-esponse
- Speech
9
Q
Salivary Glands
A
- Clean the mouth
- Moisten & dissolve food
- Contains salivary amylase (digests starch to maltose)
- Serous (watery) & mucus (thick) secretions
10
Q
Parotid Salivary Gland
A
- anterior to the ear between the masseter muscle & skin
- Serous secretions
11
Q
Submandibular Salivary Gland
A
- medial to mandible
- Serous & mucous secretions
12
Q
Sublingual Salivary Gland
A
- under the tongue
- Mucous secretions
13
Q
Pharynx
A
- Conducts food to esophagus
- Conducts air to trachea
14
Q
Chemical Digestion: Carbohydrates
A
-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
Q
Chemical Digestion: Proteins
A
-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
Q
Chemical Digestion: Lipids
A
-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
Q
Chemical Digestion: Nucleic Acids
A
-Absorbed & transported to the liver via the hepatic portal vein
-Enzymes used:
Nucleases
18
Q
Mesentery
A
Mesentery – peritoneum that provides:
- Blood & nerve supplies to the organs
- Hold digestive organs in place
- Store lipids (visceral fat)
19
Q
Small Intestine: Microscopic Anatomy
A
Structural modifications to ↑surface area
20
Q
Unique Features of Large Intestine
A
- 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
Q
Internal Anal Sphincter
A
smooth muscle
22
Q
external anal sphincter
A
skeletal muscle
23
Q
hemorrhoids
A
Superficial veins around anal canal Inflammation
24
Q
GI tract activity declines w/ age
A
- 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
