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A&P 2 > Unit 3 &4 > Flashcards

Unit 3 &4 Flashcards

1
Q

Mechanical Digestion

A

chewing, mixing (no bonds broken)

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2
Q

Chemical Digestion

A

food breakdown (bonds broken)

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3
Q

Absorption

A

proteins & carbohydrates move to blood & fats move to lymph

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4
Q

Palatine tonsils

A

posterior oral cavity

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5
Q

lingual tonsil

A

base of the tongue

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6
Q

pharyngeal tonsils

A

nasopharynx wall

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7
Q

tubal tonsils

A

surround auditory tube openings into the pharynx

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8
Q

Tongue

A
  • Hold food during chewing
  • Mix food w/ saliva
  • Form bolus
  • Starts swallowing r-esponse
  • Speech
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9
Q

Salivary Glands

A
  • Clean the mouth
  • Moisten & dissolve food
  • Contains salivary amylase (digests starch to maltose)
  • Serous (watery) & mucus (thick) secretions
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10
Q

Parotid Salivary Gland

A
  • anterior to the ear between the masseter muscle & skin

- Serous secretions

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11
Q

Submandibular Salivary Gland

A
  • medial to mandible

- Serous & mucous secretions

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12
Q

Sublingual Salivary Gland

A
  • under the tongue

- Mucous secretions

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13
Q

Pharynx

A
  • Conducts food to esophagus

- Conducts air to trachea

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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

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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

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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

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17
Q

Chemical Digestion: Nucleic Acids

A

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

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18
Q

Mesentery

A

Mesentery – peritoneum that provides:

  • Blood & nerve supplies to the organs
  • Hold digestive organs in place
  • Store lipids (visceral fat)
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19
Q

Small Intestine: Microscopic Anatomy

A

Structural modifications to ↑surface area

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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
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21
Q

Internal Anal Sphincter

A

smooth muscle

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22
Q

external anal sphincter

A

skeletal muscle

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23
Q

hemorrhoids

A

Superficial veins around anal canal Inflammation

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24
Q

GI tract activity declines w/ age

A
  • Absorption is less efficient

- Peristalsis is slowed

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25
Q

Hepatocyte functions:

A
  • Produce bile
  • Process nutrients
  • Store fat-soluble vitamins
  • Detoxification
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26
Q

Peptic Ulcer

A

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

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27
Q

Appendicitis

A

Usually caused by:

  • Fecal obstruction or Anatomical pinching of the appendix
  • A ruptured appendix leads to peritonitis
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28
Q

Peritonitis

A
  • 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
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29
Q

Hepatitis

A
  • Inflammation of the liver

- Caused by drugs, chemicals, viruses, alcohol

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30
Q

Viral “Hepatitis A”

A

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

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31
Q

Viral “Hepatitis B” & “Hepatitis C”

A

body fluid transmitted pathogens

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32
Q

Diverticulitis

A

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

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33
Q

Emesis (vomiting)

A
  • Microbes
  • Allergies
  • Excessive food consumption
  • Poisons
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34
Q

Constipation

A
  • Infrequent defecation of fecal material
  • Diet low in fiber
  • Diet low in water
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35
Q

Gall Stones (Biliary Calculi)

A
  • Crystallization of cholesterol & bile salts
  • Block the bile duct
  • Fill the gall bladder
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36
Q

Jaundice

A
  • Bile build-up in the skin & sclera causes a yellow appearance
  • Cause: damage to the liver, gall bladder, or biliary ducts
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37
Q

Bulimia Nervosa

A
  • Psychological disorder
  • Patient has a fear of gaining weight
  • Patient binges on food
  • Purges w/ laxatives or vomiting
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38
Q

Anorexia Nervosa

A
  • Psychological disorder
  • Patient has a false perception of their own weight
  • Patient does not eat enough
  • Extreme cases are lethal
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39
Q

Cystic Fibrosis

A 
-Genetic disorder 
↑Mucus is produced
-Causes pancreatic duct blockage
-Enzymes can’t enter duodenum
-Treatment: digestive enzymes given orally
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40
Q

Metabolism

A

Metabolism = anabolism + catabolism

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41
Q

Catabolism

A

Breakdown of large molecules into smaller subunits

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42
Q

Catabolism or Anabolism: Digestion

A

Catabolism

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43
Q

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

A

Catabolism

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44
Q

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

A

Catabolism

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45
Q

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

A

Catabolism

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46
Q

Diarrhea

A
  • Movement of fecal material through the G.I. tract too rapidly (over-hydration)
  • Caused by microbes, spicy foods, stress
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47
Q

Cirrhosis of the Liver

A
  • Liver cells are destroyed & replaced by fibrous connective tissue
  • Causes: alcohol, drugs, toxins
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48
Q

Flatulence

A

Intestinal gas results from:
Bacteria
Diet
Swallowing air

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49
Q

Anabolism

A

Synthesis of large molecules from smaller subunits

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50
Q

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

A

Anabolism

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51
Q

Catabolism or Anabolism: Proteins from amino acids

A

Anabolism

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52
Q

Catabolism or Anabolism: Lipids from glycerol & fatty acids

A

Anabolism

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53
Q

Reduction reaction:

A

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

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54
Q

Oxidation reaction:

A

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

55
Q

Reducing agents

A

donate electrons or H

56
Q

Oxidizing agents

A

accept electrons or H

57
Q

Reduction-Oxidation Reactions

A
  • Coenzymes transport or carry
  • Niacin makes NAD
  • Riboflavin makes FAD
  • Pantothenic Acid makes CoA
58
Q

Dehydration/Synthesis Reactions

A

using synthesis enzymes

59
Q

Hydrolysis/Breakdown Reactions

A

using digestive enzymes

60
Q

Cellular Respiration Equation

A

C6H12O6 + 6O2 + 38 ADP + 38 P →

6CO2 + 6H2O + 38 ATP + Heat

61
Q

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

A

oxidized: NAD
reduced: NADH + H

62
Q

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

A

oxidized: FAD
reduced: FADH 2

63
Q

Glycolysis

A
  • Anaerobic
  • Cell cytoplasm
  • Breaks down glucose (6C) into two pyruvic acid (3C) molecules
  • ATP is made
  • Reduced NAD (NADH+H+) created
64
Q

How many C: Glucose

A

6C

65
Q

How many C: Pyruvate

A

3C

66
Q

How many C: Coenzyme A

A

3C

67
Q

How many C: Acetyl CoA

A

2C

68
Q

How many C: Regenerates Oxaloacetic Acid (OAA)

A

4C

69
Q

How many C: Citric Acid

A

6A

70
Q

Krebs Cycle

A

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

71
Q

Electron Transport System (ETS)

A
  • Mitochondrial inner membrane
  • Aerobic:direct
  • Makes ↑ATP + metabolic H2O + CO2
72
Q

Substrate phosphorylation:

A
  • 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
Q

Oxidative phosphorylation:

A
  • 26 ATP generated by ETS (w/ O2) made this way

- ATP is generated by H+ & e– movements

74
Q

Glycogenesis

A
  • 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
Q

Glycogenolysis

A
  • 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
Q

Gluconeogenesis

A
  • 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
Q

Catabolism of Lipids

A
  • 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
Q

Beta Oxidation

A
  • 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
Q

PROBLEM: If a fatty acid has 20 carbons, then how many acetyl units would be made?

A

(10 acetyl units which will turn the Krebs Cycle 10x)

80
Q

Ketone Formation

A 
-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
Q

Catabolism of Proteins

A

-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
Q

Amino Acid Catabolism

A
  • 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
Q

Deamination

A
  • 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
Q

Lipid Anabolism

A

-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
Q

Protein Anabolism

A

-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
Q

LDL Function in Cholesterol Metabolism

A

-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
Q

HDL Function in Cholesterol Metabolism

A
  • 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
Q

Saturated Fats

A
  • 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
Q

Two mechanism of hormonal

A

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

90
Q

Insulin

A

-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
Q

Glucagon

A

-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
Q

Hypoglycemia

A
  • ↑Insulin causes glucose to move from blood → cells
  • Blood glucose decreases because glucose moves into cells
  • Results: ↓blood glucose level (hypoglycemia)
93
Q

Hyperglycemia

A
  • ↑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
Q

Diabetes Mellitus Type I

A
  • 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
Q

Diabetes Mellitus Type II

A
  • Type II (adult-onset) diabetes:
  • Non-Autoimmune
  • Poor response by cell receptors to insulin
  • Poor diet
  • ↓Exercise
96
Q

Latent Autoimmune Diabetes in Adults (LADA)

A
  • Type 1.5 diabetes:
  • Autoimmune
  • A form of Type I diabetes
  • Occurs during adulthood
  • Delayed onset of symptoms
97
Q

Thyroid Stimulating Hormone (TSH)

A

-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
Q

Thyroxine (Thyroid Hormone)

A

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

99
Q

↑Thyroxine leads to:

A

Hyperthyroidism
↑Metabolism (↑BMR)
Exophthalmia
↓Body weight

100
Q

↓Thyroxine leads to:

A 
Hypothyroidism 
↓Metabolism (↓BMR) 
Endophthalmia
Goiter 
Obesity 
Cretinism
101
Q

Cretinism

A

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

102
Q

human Growth Hormone (hGH)

A

-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
Q

Gigantism

A
  • 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
Q

Acromegaly

A
  • 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
Q

Dwarfism

A
  • Below normal secretion of human Growth Hormone (hGH)
  • Occurs in young children
  • Slow growth
  • Very reduced stature
106
Q

Esophagus

A
  • Muscular tube
  • Between laryngopharynx & stomach
  • Moves through mediastinum & diaphragm
  • Connects to the cardia of the stomach
107
Q

Esophageal Characteristics

A
  • 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
Q

Deglutition (Swallowing)

A 
-Coordinated activity of: 
Tongue
Soft palate 
Pharynx 
Esophagus 
-22 different muscle groups
-Bolus is moved by peristalsis to the stomach
109
Q

Primary Teeth

A

20 teeth erupt at ½ – 2 yrs

110
Q

Permanent

A

32 teeth erupt at 6 – 12 yrs

111
Q

Incisors

A

chisel-shaped (cutting)

112
Q

Canines

A

fang-like (tearing)

113
Q

Premolars & molars

A

broad crowns w/ rounded tips (grinding)

114
Q

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

A

Starch + Amylase → Maltose (disaccharide)
Salivary gland
7.0

115
Q

peristalsis

A

moving

116
Q

segmentation

A

mixing

117
Q

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

A

mucosa, submucosa, muscularis, serosa

118
Q

Mucous cells

A

alkaline mucus

119
Q

Parietal cells

A

-HCl & Intrinsic Factor

I.F. ↑vit. B12 absorption

120
Q

Chief cells

A

pepsinogen

-HCl activates pepsinogen to pepsin

121
Q

G cells

A

secrete the hormone gastrin

122
Q

Cephalic Phase begins

A

Sight, taste, smell, or thought of food

-begins before food entry

123
Q

Gastric Phase begins:

A
  • Stomach distension (stretch receptors)
  • Protein, caffeine, & ↑pH (basic)
  • Gastrin (hormone)
  • begins if food enters stomach
124
Q

Intestinal: begins

A

if chyme enters duodenum

125
Q

HCl secretion stimulated by

A

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

126
Q

cells of Cajal

A
  • Basic electrical rhythm is initiated by pacemaker cells

- Peristaltic waves move at rate of 3/minute

127
Q

Bile leaves liver by:

A

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

128
Q

Secretin

A
  • stimulates the liver to ↑bile

- stimulates the pancreas to ↑bicarbonate-rich secretions

129
Q

cholecystokinin (CCK)

A
  • stimulates gallbladder to contract

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

130
Q

Pancreas Exocrine Function

A

Enzymes to break down all organic compounds

131
Q

Pancreas Endocrine Function

A

Insulin & Glucagon production

132
Q

Pancreatic Secretions

A
  • Watery, alkaline (HCO3–) solution of enzymes
  • Neutralizes acidic chyme
  • Provides optimal (basic) pH for pancreatic enzymes
133
Q

Pancreatic Secretions Enzymes

A
  • Trypsinogen is activated to trypsin
  • Procarboxypeptidase is activated to carboxypeptidase
  • Amylase
  • Lipase
  • Nucleases
134
Q

Small Intestines

A

All nutrient absorption takes place in the small intestine

A&P 2 (7 decks)

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