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Mammalian Physiology II > Exam 2: Digestion and Metabolism > Flashcards

Exam 2: Digestion and Metabolism Flashcards

1
Q

What are the 4 functions of the digestive system?

A

-take in food
-break down food into smaller molecules
-absorb molecules into bloodstream
-get rid of waste

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2
Q

What is the anatomy of the digestive system and how does food pass through?

A

-Alimentary canal (gastrointestinal tract)-> tube from mouth to anus
mouth -> pharynx -> esophagus -> stomach -> small intestine -> large intestine -> anal canal

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3
Q

What are the accessory organs of the digestive system?

A

-teeth and tongue
-gall bladder
-digestive glands (salivary glands, gall bladder, pancreas)

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4
Q

What are the 6 steps of the digestive process?

A
  1. ingestion -eating
    2.Propulsion - movement (swallowing, peristalsis)
    3.Mechanical breakdown - chewing, mixing, churning, segmentation
  2. Digestion - catabolism
  3. Absorption - GI -> blood or lymph
  4. Deification - elimination
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5
Q

What is occurring in each organ of the digestive system during the digestive process?

A

Mouth- mechanical breakdown and digestion
esophagus - propulsion
stomach - mechanical breakdown and digestion
small intestine - digestion and absorption
large intestine - water absorption

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6
Q

How does the mouth perform mechanical breakdown?

A

the teeth and tongue break food into smaller pieces to increase the surface area available for digestion

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7
Q

How does the mouth perform chemical digestion?

A

Saliva!
Mostly water
Dissolves food -> taste
Moistens food -> eases swallowing (bolus)
contains enzymes (amylase, lipase)
defense against microorganisms (antibodies, lysozyme, defensins)

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8
Q

What stimulates salivation?

A

-tasting food: taste buds and chemoreceptors
-smelling food: chemoreceptors in nose
-thinking about food: cerebral cortex

Parasympathetic innervation: receptors send signals to medulla oblongata (facial and glossopharyngeal nerves) = salivation

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9
Q

What inhibits salivation?

A

-Strong activation of sympathetic division -> constricts blood vessels to salivary glands, causes dry mouth (xerostomia)
-Dehydration -> low blood volume reduces filtration pressure in capillaries

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10
Q

What are the 2 phases of swallowing/ deglutition?

A
  1. Buccal phase: voluntary, contractions of tongue force bolus into oropharynx
  2. Pharyngeal-esophageal phase: involuntary, controlled by swallowing center in medulla and lower pons. Muscles of the pharynx and esophagus force food into esophagus
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11
Q

Describe the gastrointestinal wall:

A

Includes smooth muscle laters that are responsible for motility through the AC. Circular layer goes around AC and longitudinal muscle runs down AC.

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12
Q

Describe smooth muscle and what are the two types:

A

spindle shaped cells, 1 central nucleus, no striations, 2 types; multiunit and unitary

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13
Q

What is multiunit smooth muscle?

A

discrete, separate smooth muscle fibers that operate independently, each fiber can contract independently, controlled by nerve signals

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14
Q

What is unitary smooth muscle?

A

100s-1000s of smooth muscle fibers that contract as a single unit, arranged in sheets or bundles

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15
Q

What are the cellular components smooth muscle cells:

A

-No T-tubules
-less developed SR than skeletal muscle
-Caveolae; pouch like inholdings that hold calcium

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16
Q

How is smooth muscle similar to skeletal muscle?

A

-actin and myosin interacting by sliding filaments
-sliding process energized by ATP

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17
Q

How is smooth muscle different than skeletal muscle?

A

-thin and thick filaments are not organized into sarcomeres
thin filaments (actin) has tropomyosin but no troponin
thick filaments (myosin)- myosin heads present along entire length

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18
Q

what are dense bodies?

A

similar to Z-discs, anchor actin fibers, found attached to sarcolemma and scattered through sarcoplasm

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19
Q

what are intermediate filaments?

A

non-contractile fibers that resist tension (pulling)

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20
Q

What are the 4 steps of smooth muscle contraction?

A
  1. Ca2+ bonds to calmodulin -> activates it
  2. Activated calmodulin activates myosin kinase
    3.Activated myosin kinase catalyzes transfer of phosphate from ATP to myosin
    4.Phosphorylated myosin forms cross-bridge with actin
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21
Q

What are unique aspects of smooth muscle contraction?

A

-takes 30x longer than skeletal but uses less than 1% of energy
-can contract for days without fatiguing
-exhibits relatively constant tension “smooth muscle tone”
-relaxes once intracellular Ca2+ levels deplete, slower reuptake of Ca2+ into SR than skeletal

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22
Q

How is skeletal vs smooth muscle regulated?

A

skeletal muscle is stimulated only by nervous system
smooth muscle is stimulated by nervous system, hormones, and local factors

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23
Q

What are smooth muscle fibers?

A

arranged in bundles of parallel fibers that are connected through gap juctions. The muscle layers function as a syncytium -> when AP occurs, it travels in all directions in the muscle, similar to cardiac

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24
Q

What are the two types of electrical activity in the AC?

A

-slow waves
-spikes
hyperpolarization and depolarization can occur

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25
Q

What is a slow wave?

A

NOT AP
slow, undulating changes in RMP stimulated by electrical pacemaker cells (interstitial cells of cajal), DONT cause contraction (no entry of Ca2+, excite appearance of spike potentials)

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26
Q

What is a spike potential?

A

APs
Ca2+ enters smooth muscle cells, occurs when RMP > -40mV, last 10-40x longer than APs in nerve fibers, Ca-Na channels are slower to open and close

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27
Q

What do depolarization and hyper polarization do to smooth muscle?

A

Depolarization makes smooth muscle more excitable, occurs by stretch, acetylcholine from parasympathetic NS, stimulatory GI hormones

Hyperpolarization makes smooth muscle less excitable, occurs by norepinherhine or epinephrine, stimulation by sympathetic NS

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28
Q

What is tonic contraction?

A

continuous contraction of smooth muscle, can occur from
continuous spike potentials
hormones (continuous depolarization of smooth muscle membrane)
continuous Ca2+ influx

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29
Q

What is the enteric nervous system?

A

NS of AC
lies within walls of AC beginning in esophagus and ending in anus
5x more neurons than in spinal cord
can function independently
also stimulated, inhibited by parasympathetic and sympathetic systems
sensory neurons can elicit reflexes

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30
Q

What are the 2 plexuses of the enteric nervous system?

A
  1. myenteric plexus: between longitudinal and circular muscle layers
  2. Submucosal plexus: Mesissner’s nerve plexus, in submucosa
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31
Q

What is the myenteric plexus?

A

chain of neurons, when stimulated, increases:
tonic contractions of AC
rate of contractions
intensity of rhythmical contractions
velocity of conduction waves along the gut wall

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32
Q

What does the myenteric plexus control?

A

gastrointestinal movements -> peristalsis, segmentation
May be inhibitory, spinchters -> control passage of food through AC

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33
Q

What is the submucosal plexus and what does it control ?

A

integrates sensory signals from AC epithelium
controls local:
secretion
absorption
blood flow
contraction of submucosal muscle (in-folding of AC)

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34
Q

What affects do the autonomic nervous system have on the AC?

A

Parasympathetic stimulation: rest and digest, increase activity of AC
Sympathetic stimulation: fight or flight, inhibit activity of AC
-> sting stimulation can block movement of food

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35
Q

What are afferent nerves?

A

stimulated by: irritation of gut mucosa, excessive stretch, presence of specific chemicals in gut
can excite or inhibit intestinal movements and secretions
signals can also go to spinal cord and brain stem (may initiate reflexes)

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36
Q

What are the reflexes in the AC?

A

May be integrated in
-enteric NS (reflexes for peristalsis and mixing contractions)
-prevertebral sympathatic ganglia (evacuation of colon, inhibition of stomach motility and secretion)
-spinal cord/brain stem - vomiting reflex, pain reflex inhibiting AC, defecation reflexes

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37
Q

What is the vomiting reflex/emesis?

A

Stimulants: extreme stretching of stomach, irritants like bacteria, alcohol, spicy food, drugs

Emetic/ vomiting center: in medulla oblongata
makes diaphragm and abdominal wall contract = chyme expelled

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38
Q

What does the esophagus do in the AC?

A

carries food from mouth -> stomach
propelled by peristalsis
solid food ~8s
liquid 1-2s

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39
Q

What is peristalsis?

A

wave-like contractions of smooth muscles
propels food through esophagus and intestines
churns chyme in stomach
also moves waste
can also occur in ducts, ureters, and smooth muscle tubes

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40
Q

How is peristalsis stimulated?

A

stretching of the AC, polarized (1 direction) from mouth -> anus

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41
Q

What are the 3 steps of peristalsis?

A

1.propulsion
2.grinding
3.retropulsion

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42
Q

What does segmentation do in the small intestine?

A

alternating contraction/ relaxation
mixes chyme
allows time for absorption
enteric pacemaker cells set rhythm
slowly pushes food forward
takes ~2hrs to pass through intestine

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43
Q

What is an AC secretion and their 2 functions?

A

-secretions by glands
1. chemical digestion ( digestive enzymes)
2. Lubrication and protection (mucus)

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44
Q

What are the 3 types of glands?

A

-mucus glands (goblet cells) -> single celled
-pits -> contain secretory cells
-tubular glands -> have tube for secretion

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45
Q

What are the 3 mechanisms for stimulation of the AC glands?

A

epithelial contact
autonomic stimulation
hormones

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46
Q

How dos epithelial contact stimulate the AC glands?

A

-presence of food stimulates glands in that region
-enteric NS may be stimulated
-types of stimuli: touch, chemical irritation, stretching
-Stimulates mucus cells and deeper glands to increase secretion

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47
Q

How does autonomic stimulation stimulate the AC glands?

A

Parasympathetic: increase rate of secretion. Upper AC and 1/3 of large intestine. mouth, esophagus, stomach, pancreas, and duodenum. Remaining portions of small and large intestine respond to local neural and hormonal stimuli

Sympathetic: dual effect
Alone-> slightly increase secretion
If parasympathetic stimulation is occurring, sympathetic stimulation will decrease secretions through vasoconstriction

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48
Q

How do hormones stimulate the AC glands?

A

regulate the volume and type of secretions in stomach and intestine
produced in response to presence of food
may have stimulatory or inhibitory effect

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49
Q

What is the stomach and what does it do?

A

storage tank, chemical digestion, converts bolus -> chyme, ~4L capacity

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50
Q

What are the functions of the stomach?

A

mechanical breakdown (churns)
chemical digestion (gastric juice, protein and fat digestion occurs)
little to no absorption (alcohol and aspirin are exceptions)

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51
Q

What are the stomach layers?

A

-Mucosa
–simple column of epithelial cells, secrete bicarbonate rich mucus
–gastric pits
lead into gastric glands which make gastric juices, 5 cells that secrete substance for acid production, mucous cells help protect stomach from HCl

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52
Q

Chief cells
Produce?
Product do?
how stimulated/ inhibited?

A

pepsinogen
digests proteins after becoming pepsin when reacting with HCl
stimulated by parasympathetic NS (acetylcholine) and enteric NS

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53
Q

Parietal cells
Produce?
Product do?
how stimulated/ inhibited?

A

HCl
lowers pH
stimulated by parasympathetic NS, histamine, gastrin
inhibited by somatostatin

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54
Q

ECL cells
Produce?
Product do?
how stimulated/ inhibited?

A

histamine
stimulates parietal cells
stimulated by proteins in stomach, hormones secreted by enteric NS

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55
Q

G cells
Produce?
Product do?
how stimulated/ inhibited?

A

Gastrin
stimulates ECL cells to produce histamine, stimulates chief cells
stimulated by proteins in stomach

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56
Q

D cells
Produce?
Product do?

A

somatostatin
inhibits parietal cells

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57
Q

What are the 3 phases of gastric secretion regulation?

A

1.cephallic phase
2. gastric phase
3. intestinal phase

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58
Q

What happens during the 1st phase of gastric secretion regulation?

A

Cephalic (reflex) phase
Triggered by: sight, smell, thought
sensory receptors -> medulla oblongata -> vagus nerve (parasympathetic NS) -> secretory cells -> gastric juices

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59
Q

What happens during the 2nd phase of gastric secretion regulation?

A

Gastric phase
Triggered when: food reaches stomach, 2/3 gastric juices made over these 3-4 hours
Stimulation:
1. stomach distension -> stretch receptors-> secretory cells -> gastric juices
2.proteins and other chemicals -> secretory cells -> gastric juices

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60
Q

What happens during the 3rd phase of gastric secretion regulation

A

Intestinal phase
triggered when: food reached duodenum, provides feedback to stomach
2 phases:
1. stimulatory phase (weaker):
intestinal cells -> gastrin -> stomach -> secretory cells -> gastric juices
2. Inhibitory phase (dominant):
intestinal cells -> enterogastrones (secretin, CCK) -> stomach-> no gastric juices

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61
Q

What is the gastric mucosal barrier?

A

protects surface of stomach from acidic conditions and enzymes
bicarbonate rich mucus neutralized pH, tight junctions, highly regenerative cells

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62
Q

What are the 3 parts of the small intestine?

A

duodenum
jejunum
ileum
Chemical digestion!!

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63
Q

What are the functions of the small intestine?

A

absorb nutrients and finish digestion

64
Q

What are the accessory organs to the small intestine?

A

Liver
pancreas
gall bladder

65
Q

What are the functions of the liver?

A

processes and stores nutrients (glycogen, fat soluble vitamins, makes proteins)
detoxifies (ammonia -> urea)
makes bile

66
Q

What is bile?

A

yellow-green alkaline fluid
bilirubin (pigment formed from heme)
bile salts: derived from cholesterol, emulsify/breakdown fats

67
Q

What is pancreatic juice?

A

alkaline fluid containing digestive enzymes

68
Q

Trypsin and chymotrypsin

A

digest proteins

69
Q

pancreatic amylase

A

digest sugar and carbs

70
Q

lipases

A

digest fats

71
Q

nucleases

A

digest DNA/RNA

72
Q

How is bile and pancreatic secretion regulated?

A

chyme eneters small intestine-> its acidic!

low pH stimulates secretin release from enteroendocrine cells -> tells liver to secrete bile, tells pancreas to secrete bicarbonate ions

Protein and fat stimulate CCK release from enteroendocrine cells -> tells pancreas to secrete digestive enzymes and tells gall bladder to release bile

73
Q

Carbohydrate digestion :

A

starch/polysacc. -> smaller polysac. -> disaccharide -> monosacride to be absorbed

74
Q

Protein digestion:

A

protein -> polypeptide -> smaller polypeptide -> amino acids to be absorbed

75
Q

Nucleic acid digestion:

A

RNA/DNA -> -> ribose sugar, N-containing bases, phosphate ions

76
Q

Lipid digestion:

A

fat globule -> triglyceride + triglyceride -> fatty acids and glycerol to be absorbed

77
Q

How does absorption occur in the small intestine?

A

circular folds force chyme to slowly spiral through intestines and increase surface area, villa aid in absorption by increasing surface area

78
Q

What is villa?

A

many capillaries
central lacteal, lymphatic vessel
aid in absorption by increasing surface area

79
Q

How does absorption occur?

A

most nutrients are taken up through capillaries -> hepatic portal vein -> liver but fats are taken up through lacteals

80
Q

How does monosaccharide, amino acid, and nucleic acid absorption occur?

A

co-transported with Na+ into intestinal cell, enter capillaries through facilitated diffusion

81
Q

How are fats absorbed?

A

fatty acids and glycerols are taken up via passive diffusion. inside of the small intestine: fatty acids and glycerol reform triglycerides -> packaged with proteins to form chylomicrons -> exocytsed -> enter lacteals

82
Q

What is the bacterial flora?

A

suppress pathogenic bacteria
some synthesize vitamins K and B
digest any undigested carbs via fermentation (cellulose, beans, lactose if intolerant)
fermentation creates gas (CO2, methane, dimethyl sulfoxide)

83
Q

What is the ileocecal valve?

A

located between ileum and cecum
regulated by ileocecal sphincter
when relaxed, chyme enters large intestine
referred to as feces after passing this point
prevents back flow

84
Q

What is the function of the large intestine?

A

absorb water and electrolytes from feces
Imbalance as:

diarrhea: too little water absorbed
causes: excessive intestinal motility
excessive osmotically active particles (lactose)

constiptaion: too much water absorbed
causes: reduced intestinal motility
lack of dietary fiber

85
Q

What is the thick mucosa of the large intestine?

A

simple columnar epithelium AND
stratified squamous epithelium
lots of goblet cells and mucous to ease passage of feces

86
Q

How is motility in the large intestine?

A

usually quiet -> not much movement
4 mass movements a day
-> powerful contractions that push contents towards rectum

87
Q

what is the defecation reflex?

A

initiated by feces in rectum (stretch receptors)
stimulates involuntary contraction of sigmoid colon and rectum -> involuntary relaxation of internal anal sphincter
then external anal sphincter is voluntary

88
Q

what is the composition of feces?

A

3/4 water, 1/4 solid matter
brown color from bilibriubin from the breakdown of RBC

89
Q

What is the liver lobule?

A

functional unit of the liver, 50,000-10,000 lobules in liver, lots of components

90
Q

What is the central vein in the lobule?

A

empties into hepatic vein and then the vena cava

91
Q

What is the cellular plates in the lobule?

A

2 cells thick with bile candlicuili between them, produces bile which empties into the bile ducts

92
Q

What is the portal veins in the lobule?

A

bring blood from AC, flows into hepatic sinusoids then to central vein

93
Q

What is the hepatic arteries in the lobule?

A

supply blood to liver tissues, also empty into sinusoids

94
Q

What is the endothelial cells in the lobule?

A

line sinusoids, highly permeable

95
Q

What is the space of disse in the lobule?

A

collect excess fluid and drain into lympathic vessels

96
Q

What is the Kupner cells in the lobule?

A

line sinusoids, macrophages that phagocytize bacteria and forge in cells, cleanses blood

97
Q

How much blood flows and is stored in liver?

A

1350mL
1050 from portal vein
300 from hepatic artery
27% of resting cardiac output

98
Q

What happens to the liver if right arterial pressure increase?

A

liver can store 500-1000 mL more
cardiac failure
liver can supply extra blood if blood volume decreases

99
Q

What happens to resistance in the liver?

A

small drop in pressure as blood travels through the liver, resistance decreases

100
Q

what is cirrhosis of the liver?

A

liver cells destroyed and replaced with fibrous tissue -> contracts around blood vessels and increases resistance
causes: chronic alcoholism, excess fat accumulation in liver, infections

101
Q

Describe lymph flow

A

hepatic sinusoids are very permeable, so fluid and proteins are drained as lymph
1/2 lymph formed in body comes from liver

102
Q

What is ascites?

A

large amount of free fluid in the abdominal cavity
If pressure in hepatic veins rises 3-7mmHg above normal -> excess fluid forms lymph and leaks into abdominal cavity

blockage of portal vein will increase capillary pressure in the AC-> which will cause edema or ascites

103
Q

What are the metabolic functions of the liver?

A

liver has many cells with high metabolic rate
process and synthesize molecules
metabolizes carbs, fats, and protein

104
Q

Explain carbohydrate metabolism in the liver

A

liver: stores glycogen, converts galactose and fructose to glucose, generates glucose from amino acids and glycerol

helps maintain normal blood glucose:
stores glucose when BG is high
releases glucose when BG is low

105
Q

Explain lipid metabolism in the liver:

A

liver: oxidizes fatty acids-> creates ATP, synthesizes lipids (cholesterol)
80% of cholesterol produced by liver is converted to bile salts

106
Q

Explain protein metabolism in the liver:

A

liver: deaminates amino acids and synthesizes molecules from them, forms urea from ammonia as ammonia is toxic in body fluids, forms plasma proteins (90%, liver disease -> decrease in albumin (responsible for OP) -> generalized edema)

107
Q

What are the 4 other metabolic functions of the liver?

A

vitamin storage (A,D,B12), prevents deficiency for months+
iron storage (blood iron buffer)
forms substances involved in coagulation
excretes drugs and hormones (detoxifies or excretes many drugs, liver damage can lead to excess hormone levels and overactivity)

108
Q

Explain paralysis of swallowing mechanism:

A

damage to CN, polio, muscular dystrophy
may cause: complete failure of swallowing, failure of epiglottis to close (food travels into lungs), failure of soft pallet and uvula to close (food refluxes into nose)
may occur during anesthesia: vomit travels into trachea because swallowing reflex is blocked

109
Q

What is achalasia and megaesophagus?

A

lower esophageal sphincter fails to relax during swallowing
from: damage to myenteric plexus in esophagus (normally inhibits sphincters)
Megaesophagus: esophagus becomes distended due to food

110
Q

What is gastritis and chronic gastritis?

A

inflammation of gastric mucosa
causes: bacterial infection, alcohol, aspirin
makes increase in permeability of gastric barrier -> acid damages mucosa
chronic gastritis: atrophy of stomach, reduction in secretions, vitamin B12 absorption is affected, decrease in RBC pridtcion, pernicious anemia

111
Q

What are ulcers?

A

damage to stomach/ intestinal mucosa
Helicobacter pylori: causes 75% of ulcers, damages mucosal barrier and increases HCl production

112
Q

What is pancreas failure and pancreatitis?

A

failure of pancreas to secrete pancreatic juice (up to 60% fat, 1/3-1/2 of carbs, and proteins may not be absorbed)
Pancreatitis: inflammation of pancreas
excess alcohol consumption and blockage by gallstone

113
Q

What are gallstones?

A

hard deposits of bile
causes: too much cholesterol, excess bilirubin (cirrhosis), failure of gall bladder emptying

114
Q

What is sprue?

A

inadequate absorption in small intestine, can be caused by gluten
only some people are sensitive
detsroys villi, reducing absorption surface area

115
Q

What is megacolon?

A

may be caused by deficiency of ganglion cells in myenteric plexus
defecation reflex and peristalsis doesn’t occur in large intestine, feces accumulate, leading to distention of colon

116
Q

What happens if a spinal cord injury occurs?

A

defecation reflex functions
voluntary control is disrupted, making defecation difficult -> can be stimulated with small enema

117
Q

What can cause an obstruction

A

cancer, ulcer, spasm, paralytic ileum, adhesions

118
Q

What is metabolism?

A

sum of all chemical reactions occurring in the body, may be catabolic or anabolic

119
Q

What is a catabolic reaction?

A

breakdown large organic molecules into smaller molecules, releases energy contained in bonds
most energy is released as heat but some is transferred to ATP

120
Q

What is an anabolic reaction?

A

building a larger molecule from smaller ones, requires energy in the form of ATP

121
Q

What is ATP?

A

energy currency of cells, produced by catabolic reactions and used in anabolic reactions, like RNA nucleotide with 2 extra phosphates
can be synthesized and recycled by re-adding phosphate groups using energy from body or food stores

122
Q

Why does ATP have a lot of potential energy?

A

phosphate groups are negatively charged, the bond linking them carriers potential energy due to repulsive forces
energy is released when phosphates are removed by hydrolysis

123
Q

Give an overview of cellular respiration

A

produces ATP from a molecule with high potential energy, usually glucose but can be other things, 4 stages with multiple steps

124
Q

Quick summary of the 4 stages of cellular respiration:

A
  1. glycolysis
    glucose breakdown to pyruvate
  2. pyruvate processing
    pyruvate is oxidized to acetyl-CoA
  3. Krebs cycle: actely-CoA is oxidized to CO2
  4. ETC + chemisomosis: compounds that were reduced in steps 1-3 are oxidized in reactions leading to ATP production
125
Q

What is a redox reaction?

A

energy can be transferred by moving electrons between molecules
when something loses and electron, it is oxidized, when something gains an electron, it is reduced OIL RIG
each electron transferred from one molecule to another during redox is usual accompanied by a proton
the reduced molecule gains a proton and has higher potential energy
the oxidized molecule loses a proton and has lower potential energy

126
Q

Explain glycolysis

A

in cytoplasm
Starts w: glucose
Products: costs 2 ATP, gain 4 ATP, net gain of 2 ATP,2 NADH(electron carriers), 2 molecules of pyruvate

127
Q

Explain pyruvate processing

A

in mitochondria
Starts w: pyruvate 2x
Products: CO2, NADH, acetyl-CoA

128
Q

Explain Krebs cycle

A

in mitochondria
Starts w: acetyl-CoA 2x
Products:2 ATP, 6 NADH, 2 FADH2
can be turned on or off at multiple points, if ATP or NADH levels are high, then cycle will be inhibited

129
Q

Explain electron transport chain

A

in mitochondria
Starts w: electron carriers NADH and FADH2
Products: LOTS of ATP

electrons are carried to ETC by electron carriers NADH and FADH2, electrons are passed between proteins which pump protons into intermmebrane space (building high proton concentration)

130
Q

What is an electron carrier?

A

molecules that help move electrons in redox reactions

131
Q

What is the chemiosmotic hypothesis?

A

ETC does not make ATP directly. instead, it pumps protons from the mitocondiral matrix -> inner membrane space which creates an electrochemical gradient that can be used to make ATP

132
Q

What is ATP synthase?

A

the proton gradient set up by ETC allows proteins to flow down their concentration gradient
protons flow through F0 unit of ATP synthase, which spins the F1 unit
This produces energy to convert ADP
+ Pi to ATO

133
Q

How is energy harvested by extracting electrons?

A

series of oxidation/reduction reactions slowly harvests energy from glucose in gradual steps. electron carriers remove electrons and carry them to ETC

134
Q

What is glucose?

A

80% of carbs absorbed are digested into glucose, most remaining monosaccharides are converted to glucose, 95% of all monosaccharides circulating in blood are glucose

135
Q

How can glucose be transported?

A

-down concentration gradient -> glucose carrier proteins
-against concentration gradient -> sodium-glucose co transport, only certain epithelial cells

136
Q

What does insulin do?

A

released by pancreas in response to increase in blood glucose, increase rate of abspotipn into cells except RBC, Brian, liver, kidney and lining of small intestine, skeletal muscle and adipose cells are targets

137
Q

How is glucose stored?

A

in cells, glucose is utilized or stored as glycogen
liver cells store 5-8% of their weight
muscle cells store 1-3% of their weight

138
Q

What is glycogenolysis?

A

breakdown of stored glycogen
stimulated by hormones:
epinephrine; released by adrenal medulla when sympathetic NS sis simulated
glucagon-> released by pancreas when blood glucose levels decrease

139
Q

What is the difference between type 1 and type 2 diabetes?

A

1: autoimmune diseased affecting beta cells in pancreas, cells no longer produce insulin
2: cells become resistant to effects of insulin, insulin secretion is increased, but cells become exhausted, often reversible with diet and exercise

140
Q

What are the early and later effects of diabetes?

A

early: excessive urination and thirst
later: injury to tissues, especially blood vessels and nerves, without glucose cells rely on fats for fuel -> ketones

141
Q

What is basal metabolic rate?

A

energy per unit time that a person needs to keep body functioning at rest

breathing, blood circulation, control of body temperature, brain and nerve function, contraction of muscles

60-75% of daily calorie expenditure
declines 1-2% per decade after 20 years because decrease in muscle mass

142
Q

What are calories?

A

energy needed or ingested is measured in calories, need 1500-2000 calories/day
dependent on body weight, age, height, gender, activity level, and amount of exercise

143
Q

what is our caloric content?

A

15% protein
40% fat
45% carbs
nonwestern countries carbs>protein

144
Q

what is a caloric imbalance?

A

if energy intake equals energy expenditure no change in body weight
excess energy is stored as fat
if energy intake is insufficient, loss of body mass and starvation occurs

145
Q

What is starvation?

A

stored carbs are only a few hundred grams, mainly glycogen in liver and muscle cells, only has energy for ~1/2 day
next, proteins and fats are depleted due to energy content

146
Q

what are the 3 phases of starvation?

A

o 1. Rapid depletion: mobilized proteins converted to glucose and mostly used by brain
o 2. Slowed depletion: remaining protein not easily removed, fats are converted to ketones which can cross blood brain barrier and be used by brain cells, helps preserve protein stores
o 3. Rapid depletion again: stores depleted, proteins used again, proteins are essential for cell function, so death occurs when protein depleted to ½ normal level

147
Q

What are the protein requirements?

A

body breaks down 20-30g of protein per day to produce compounds, must be replaced. intake 30-50g of protein to maintain stores

148
Q

What is the difference between hunger and satiety?

A

hunger is the feeling associated with a craving for food
satiety is a feeling of fullness and satisfaction after eating a meal

149
Q

How does the hypothalamus regulate hunger?

A

o Feeding center: lateral nuclei, stimulation causes voracious feeding, destruction leads to loss of desire for food
o Satiety center: ventromedial nuclei, provides sense of satisfaction that inhibits feeding center, stimulation causes a lack of appetite, destruction leads to continuous eating
o Influenced by:
 Signals from stretch receptors in stomach
 Signals from AC and adipose hormones
 Signals from cerebral cortex (sight, smell, taste)
o Also regulates secretion of hormones that regulated energy balance and metabolism
 Ex: hormones from thyroid, adrenal glands, and pancreas

150
Q

What are examples of regulation by the hypothalamus?

A

o Peptide YY, CCK, and insulin
 Suppresses further feeding
o Ghrelin
 Released by stomach during fasting, stimulates appetite
o Leptin
 Produced in increased amounts by fat calls as they increase in size, inhibits food intake

151
Q

What does ozempic do?

A

semaglutide imitates glucagon like peptide GLP-1
o Originally used to treat diabetes (stimulates insulin secretion), off label use for weight loss as it inhibits food intake, increases feeling of satiety, weight may be regained when stopped

152
Q

What is short-term feedback?

A

What turns of feeding when we have eaten enough?
o Not enough time for energy stores to change, food absorption takes hours
o Stretch receptors in AC, AC hormones (CCK released when fat and proteins enter duodenum, peptide YY released from ileum and colon), food passing through mouth meters intake (once a certain amount passes through the feeding center becomes inhibited)

153
Q

What is long term feedback?

A

feeding control is geared toward nutritional balance
o When blood concentration of glucose, amino acids, or lipids decreases, feeding is stimulated
o Interaction between temperature regulating and feeding regulating centers in hypothalamus
 Cold -> feeding because an increase in food -> increase in metabolic rate -> increase in heat also increase in fat for insulation, heat -> decrease in feeding
o Leptin produced by adipose cells decreases appetite through a few mechanisms (in notes)

154
Q

How is temperature regulated?

A
  • Temperature regulation: tightly regulated (97.7-99.5 degrees F)
    o 60% of energy produced is in form of heat
    o Regulated by hypothalamus through negative feedback
155
Q

What happens when temperature is too high?

A

o Superficial arteries are dilated
 Increase heat loss to air
o Sweating initiated in skin
o Thyroid stimulates cells to decrease metabolic heat production

156
Q

What happens when temperature is too low?

A

o Superficial arteries are constricted
 Decrease heat loss to air
o Shivering increases aerobic respiration in muscles -> releases heat
o Thyroid stimulates cells to increase metabolic heat production

Mammalian Physiology II (3 decks)

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