Review Tips For Physiology Finial

Justin Terrill
Loma Linda University

School of Dentistry
D.D.S. c/o 2015
jterrill@llu.edu
Tips for PHSL 505 Finals

GI Physiology
1. Know what causes lower esophageal sphincter (LES) to relax during swallowing.
a. LES relaxes well in advance of the moving bolus in response to VIP/NO [Vasoactive
Intestinal Peptide/Nitric Oxide]
Achalasia is a relatively uncommon condition associated with difficulty swallowing
(dysphagia) and a dilated esophagus proximal to a narrowed, tapered area at the
Gastroesophageal junction. Two defects are present: (1) failure of the LES to relax and (2)
impaired peristalsis in the distal two thirds of the body of the esophagus (i.e., the portion that
consists of smooth muscle). Peristalsis is intact in the proximal third of the esophagus, which
consists of striated muscle. In essence, the smooth muscle portions of the esophagus behave as
a denervated structure. The fundamental defect in achalasia is unknown but is probably related
to selective loss of inhibitory neurons that regulate the LES, the neurotransmitters of which are
VIP and NO. Treatment is either physical distention (or stretching) of the LES with a pneumatic
bag dilator or surgical cutting of the LES (i.e., an esophageal myotomy or Heller procedure).
2. Know actions of vitamin D.
a. Ca2+ is actively absorbed in the duodenum by vitamin D dependent mechanisms and
passively absorbed everywhere else in the small intestine. Vitamin D stimulates the
synthesis of calcium-binding proteins and transporters.

b. Active absorption is not tightly linked to Vitamin D, nor is it adjusted to the dietary load
of Mg2+. Mg2+ absorption = activeileum and passivesmall intestine.


3. Know the process of absorption of (heme) iron by enterocytes.

2+
a. Inorganic iron is only absorbed as Fe . Iron reductase converts Fe3+Fe2+. Fe2+ is

transported by an apical di-valent cation transporter (DCT1). DCT1 functions best when
lumen pH < intracellular pH.
b. Heme iron is transported into enterocyte via a heme carrier protein (HCP1). Heme
oxygenase cleaves heme to release iron, CO, biliverdin.
c. A basolateral transport protein, IREG1, transports iron (bound to transferrin) to plasma.
[transferrin-iron] plasma enterocyte [iron] IRP (iron regulatory protein) iron
transport protein synthesis iron absorption.
[transferrin-iron] plasma iron (Fe3+) binds IRP iron transport protein syn. iron
absorption.
4. Know characteristics of migrating motor complex during fasting (interdigestion).

a. Regions: Antrum, distal stomach, small intestine.
b. Three cyclic phases until feeding occurs.
i. Phase I
1. Slow waves, NO spikes
2. 45-60 mins
ii. Phase II
1. of slow waves relate to action potentials (intermittent
spikes/contractions)
2. 30-45 mins
iii. Phase III
1. Every slow waves associated w/action potential (spikes/contractions)
2. Short duration (5-15 mins), occur every 90-100 mins
3. Most intense phase (stomach growling)
4. Preceded by increase in plasma motilin; antrumcolon
5. Housekeeping phase, solids (i.e. penny) swept out
***Exception: hair cannot be swept out
5. Know the big picture role of the enteric nervous system in regulating gut function.
a. Enteric neurons are organized into the myenteric and submucosal plexuses, which
constitute the (ENS).
b. Sensory input to these plexuses activate programmed neural circuits that control
motility, secretion and absorption. Both excitatory and inhibitory motor neurons to
smooth muscles exist.
c. Extrinsic nerves of the autonomic nervous system (ANS) communicate with plexuses.
i. Parasympathetic innervation tends to be excitatory.
ii. Sympathetic innervation signals inhibitory.
d. Mediators of gut functions.
i. Hormones: gastrin, CCK, secretin, GIP, and motilin.
ii. Neurotransmitters: VIP/NO, ACh, GRP (gastrin releasing peptide), NE (nor-epi).
iii. Paracrines: somatostatin (SST), histamine.
e. Visceral smooth m. is organized into longitudinal/circular layer and muscularis mucosa.
Muscle cells are electrically coupled and function as a syncytium. Contractions are
phasic and tonic.


f.
Phasic contractions.
i. Preceded by an increase in intracellular Ca2+ phosphorylation of myosin
ii. Synchronized w/fluctuations in resting Vm of pacemakers cells (Interstitial cells
of Cajal)[slow waves]
1. Slow waves from Interstitial cells of Cajal
a. Always happening
i. Whether there IS an action potential (distension) or NO
action potential (fasting)
b. Does NOT cause contraction
i. Contraction occurs when an action potential is
generated (i.e. distension of the GIfood)
c. Only a characteristic of the small intestine!
g. Phasic relaxation.
i. Removal of Ca2+ by Ca2+-pumps and Na+-Ca2+ exchange.
h. Tonic contraction.
i. Intracellular Ca2+ is regulated to maintain tension as cross-bridges accumulate
w/minimal expenditure of energy.
6. Know medications that block acid production by parietal cells.
a. Effective inhibitors of acid secretion include H2-receptor blockers and proton pump
inhibitors (ppi). PPIs are the most potent, but also the most metabolically expensive!
7. Know substances that potentiate the action of gastrin on acid secretion.
a. During the gastric phase, distention stimulates parietal cells and G cells by vago vagal
mechanisms.
i. Protein digestion products stimulate gastrin release directly
ii. Dietary protein acts indirectly by its buffering effect.
b. Ingested calcium and protein stimulate acid secretion.
c. Gastrin (CCK-B) acts on ECL (enterochromaffin-like) and Parietal cells through CCKB
receptors.
8. Know about absorption of bile acid and vitamin C.
a. Active absorption (transcellular) of conjugated [primary] bile acids occur in the terminal
ileum by a Na+-dependent bile acid transporter and by an organic salt transporter
(OATP)
Bile
canaliculus
BSEP
2 Na+
Bile acids
MRP2
Organic
anions
MDR1
Organic
cations
MDR3
SInusoidal
blood
Hepatocyte
NCTP
Bile acids
OATP
Phospholipids
OCT1
Bile acids
Organic
anions
Organic
cations
Hepatocyte

b. Passive absorption (paracellular) of deconjugated/dehydroxylated [secondary] bile acids
occurs by ionic and non-ionic diffusion.
~95% bile acids (b.a.) secreted by liver are reabsorbed on each pass through intestine/returning
to liver via portal circulation. Hepatocytes extract b.a. w/high efficiency reprocessed,
resecreted into bile. The remaining 5% are filtered by renal glomerulireabsorbed in proximal
tubules.
c. Vitamin Calong w/B12are primarily absorbed in the ileum by co-transport with Na+.
9. Know what reflex causes mass movements in the colon after eating a meal.
a. Gastrocolic reflex release of CCK and gastrin non-propulsive segmentation and
mass peristalsis.
i. Mass peristalsis: 1-3 times daily. Colon contents are shifted over distance.
Segmenting contractions cease. Filling of the rectum causes distention and
stimulates the internal anal sphincter to relax as the urge to defecate occurs.
Conscious override can delay defecation.
ii. Non-propulsive (retropulsive) segmentation: produce haustra, which favor
mixing and absorption in the colon.


10. Know enzymes present in apical membranes of enterocytes.

a. Carbohydrate Digestion
i. Maltase, -dextrinase (isomaltase), sucrase hydrolyze oligosaccharides
glucose
ii. Lactase, trehalase, sucrase disaccharides monosaccharides
1. Lactase lactose glucose & galactose
2. Trehalase trehalose glucose
3. Sucrase sucrose glucose & fructose
b. Protein Digestion
i. Enterokinase a brush border enzyme that activates trypsinogen trypsin
ii. Ecto/Endo-Peptidases {protease}(were activated by trypsin) oligopeptides
free amino acids
c. Iron Reductase converts Fe3+ Fe2+
i. ^picture on page 2, #3
11. Know what motor activity shears food mass into fine homogenate.
a. Retropulsion of contents results in shearing (grinding action). Food particle size is thus
greatly reduced.
Gastric contractions are synchronized with the gastric slow waves. The contractions mix and
propel the gastric contents. More than one contraction may be present at one time
because of the slow speed of conduction. Strong ring-like contractions propel the contents
distally toward a closed pyloric sphincter.


12. Know the secretagogue, target receptor and target cell involved in acid production by gastrin.
Secretagogues stimulate basolateral membrane receptors.

a. Vagal stimulation (in the antrum) through GRP (gastrin releasing peptide) stimulates G
cells to produce Gastrin (CCKB).
i. Products of protein digestion (amino acids/peptides) can also stimulate G cells
in the antrum.
ii. Gastrin (CCKB) binds to CCKB receptors on target cells below.
b. Gastrin {paracrine} D cell D cell releases Somatostatin (SST)
i. SST {paracrine} G cell inhibiting Gastrin release
ii. SST {endocrine} Parietal cell inhibit HCl secretion
c. Gastrin {endocrine} ECL (Enterochromaffin-like) cell ECL cell releases Histamine
(H2)
i. H2 {paracrine} Parietal cell cAMP HCl secretion
d. Gastrin {endocrine} Parietal cell Ca2+ HCl secretion **direct stimulation**

HCl
Amino
acids
2+
Ca
2+
Ca
D
CCK-B
SST
GRP
cAMP
SST
H2
M
CCK-B
Gastrin
ECL
SST
Excitatory pathway
Inhibitory pathway
CCK-B
D
13. Know muscle responses during peristalsis.

a. Peristalsis results in propulsion.
i. Circular muscle relaxes in the receiving segment (inhibitory neurons on)
ii. Circular m. contracts in propulsive segment (inhibitory neurons off)
14. Know processes that occur in each part of the stomach.
a. Proximal stomach {Reservoir function} (fundus and 1/3 of body)
i. Receptive Relaxation
1. Simultaneous relaxation (w/LES) when distension of lower esophagus by
food.
2. Vagovagal reflex: both afferent/efferent reflex are carried by Vagus n.
ii. Accommodation
1. Prevents increased intragastric pressure w/filling.
2. Compliance of gastric m. is dependent upon intact vagal fibers.
iii. Temporary storage
1. 20-25 mins contractions send food distal stomach.


iv. Contractions
1. Fundus is independent of gastric slow waves
b. Distal stomach {Preparatory function} (2/3 of body and pylorus)
i. Contractions
1. Synchronized w/gastric slow waves (interstitial cells of Cajal)
2. Mix/propel contents
3. More than one contraction may be present
4. Strong ring-like contractions propel contents distal towards closed
pyloric sphincter
ii. Emptying
1. Gastric emptying is highly regulated involving receptors in the proximal
duodenum. These receptors respond to osmolarity, [H+], caloric content
and particle size.
iii. Neural and hormonal control
1. Emptying is inhibited by gastrin, secretin, GIP and CCK. Enterogastric
and vago vagal reflexes are also involved.
15. Know the constituents of chylomicrons.

a. Enterocytes resynthesize triglycerides from absorbed products and package them into
chylomicrons.
b. Fat-soluble vitamins and other fat-soluble products are present in both mixed micelles
and chylomicrons. Chylomicrons first enter lacteal vessels (lymph system) before
entering plasma.
c. No Bile salts/acids in chylomicrons. Bile salts/acids ONLY in micelles.


16. Know the reasons for lactose intolerance.
a. Lactase deficiency causes lactose intolerance.
17. Know about recycling of bile acids.
Bile
canaliculus
BSEP
Bile acids
MRP2
Organic
anions
MDR1
Organic
cations
MDR3
SInusoidal
blood
Hepatocyte
2 Na+
NCTP
Bile acids
OATP
Phospholipids
OCT1
Bile acids
Organic
anions
Organic
cations
Hepatocyte

a. Active absorption (transcellular) of conjugated [primary] bile acids occur in the terminal
ileum by a Na+-dependent bile acid transporter and by an organic salt transporter (OATP)
b. Passive absorption (paracellular) of deconjugated/dehydroxylated [secondary] bile acids
occurs by ionic and non-ionic diffusion.
c. ~95% of bile acids secreted by liver are reabsorbed on each pass through
intestine/returning to liver via portal circulation.
d. Hepatocytes extract bile acids w/high efficiency reprocessed, resecreted into bile.
e. Bile acid that escaped the first-pass clearance by the liver (~5%) are filtered by renal
glomerulireabsorbed in proximal tubules.
18. Know about the cyclic resting membrane potential in intestinal smooth muscle cells.
a. Slow waves are due to cyclic (spontaneous) fluctuations of the RMP (Resting Membrane
Potential) from pacemaker cells. {Interstitial cells of Cajal}
i. Always happening
1. Whether there IS an action potential (distension) or NO action potential
(fasting)
ii. Does NOT cause contraction
1. Contraction occurs when an action potential is generated (i.e. distension
of the GIfood)
2. Only a characteristic of the small intestine!
b. Synchronize contractions of peristalsis and segmentation.

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19. Know how fat is handled by the body.
a. Size is important!
i. Short-chain fatty acids (SCFAs) and medium-chain fatty acids (MCFAs)
are absent from micelles and diffuse across brush-border membranes
w/glycerol into villus blood capillaries.
ii. Long-chain fatty acids (LCFAs) need micelles.
b. Emulsification of dietary lipid is accomplished by food preparation, chewing and
gastric mixing. Lingual and gastric lipase digest about 15% of the dietary fat to a
single fatty acid and diglyceride.
c. Pancreatic lipase, co-lipase, and esterases aided by bile salts complete lipid
digestion in the upper intestine.
i. Pancreatic lipase and co-lipase
1. Hydrolyze triglycerides 2-monoglyceride (2-mg) + LCFAs
d. LCFA + 2-mg are solubilized in mixed micelles.
i. Micelles diffuse across the unstirred layer before reaching the brushborder membranes.
e. The pH of the unstirred layer facilitates the shift of lipid-soluble products from
mixed micelles free state for absorption across the brush-border membrane of
enterocytes.
i. Mixed micelles are NOT absorbed, only the contents.

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f. The products of fat hydrolysis^travel to the smooth endoplasmic reticulum (SER)
via a fatty acid-binding protein (FABP).
g. Esterases re-esterify lipids.
i. 2-mg + LCFAs triglycerides
h. The triglycerides are packaged into chylomicrons.
i. During fasting, endogenous lipids are processed and secreted in VLDLs.
ii. VLDLs and chylomicrons permeate villus lacteal capillaries, NOT villus
blood capillaries!
20. Know about gallstones and how they are impacted by eating fatty foods.
a. Gallstones are either cholesterol (majority) or pigment stones. Cholesterol stones
form when there is an imbalance in normal ratio of contraction and emptying of bile.
21. Know substances absorbed and those not absorbed in the ileum.
Sites of nutrient absorption. A, The
entire
small
intestine
absorbs
carbohydrates, proteins, and lipids.
However, the absorption is greatest in
the duodenum, somewhat less in the
jejunum, and much less in the ileum. The
thickness of the arrows in the inset
indicates the relative magnitude of total
absorption at the indicated site in vivo.
The maximal absorptive capacity of a
specific segment under optimized
experimental conditions (e.g., substrate
concentrations) may be greater. B, Some
substances are actively absorbed only in
the duodenum. C, Bile acids are
absorbed along the entire small intestine,
but active absorption occurs only in the
ileum. D, The vitamin cobalamin (B12) is
absorbed only in the ileum.
a. Absorbed
i. Magnesium is actively absorbed.
ii. Vitamin C and B12 (Cobalamin) is primarily absorbed in the ileum by co-transport
w/Na+.
iii. Conjugated bile acids are actively absorbed in the terminal ileum by a Na+
dependent bile acid transporter and by an organic salt transporter (OATP).
iv. NET absorption of NaCl via Na+-H+ exchange and Cl--HCO3- exchange in the apical
membrane.

12

22. Know what is responsible for the intestinal phase of gastric acid secretion.
a. Basal (interdigestive) phase
i. The rate of acid secretion is low but the luminal [H+] is high b/c of the absence
of the buffering effect of food in the stomach.
b. Cephalic phase
i. Sight, smell, taste, and thought stimulate the dorsal motor nucleus of the Vagus
nerve. ACh stimulates parietal (oxyntic) cells, ECL cells, release of GRP, and
inhibits D cells.
ii. This phase accounts for ~30% of the total acid secretion.
c. Gastric phase
Gastric phase of gastric

acid secretion. Food in the
stomach stimulates gastric
acid secretion by two major
mechanisms:
mechanical
stretch and the presence of
digested protein fragments
(peptones).

i. Distention activates release of ACh locally and through the vago-vagal reflex.
Hydrolyzed proteins and amino acids stimulate G cells to secrete gastrin. Low
antral pH stimulates D cells to release Somatostatin (SST).
ii. This phase accounts for ~60% of the total effect.

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d. Intestinal phase
Intestinal
phase
of
gastric acid secretion.
Digested protein fragments
(peptones) in the proximal
small intestine stimulate
gastric acid secretion by
three major mechanisms.

i. Hydrolyzed protein in the duodenum stimulates duodenal G cells to secrete
gastrin. By an unknown mechanism the absorption of amino acids in the
duodenum stimulates gastric secretion of acid.
ii. This phase accounts for ~5-10% of the total acid secretion.
iii. Most of the effect of the duodenum is inhibitory.
iv. Fat, acid, and hyperosmolar contents inhibit acid secretion.
1. This is through the effects of GI hormones.
23. Know product of fat cells that affects how we respond to food.
a. Leptin exerts long-term inhibitory regulation.
b. Leptin is a product of fat cells, which also plays a role in neurological development of
the hypothalamus.
c. Low blood glucose stimulates the firing rate of neurons in the hunger center and inhibits
firing of neurons in the satiety center.
d. Leptin stimulation of leptin receptors (LepR) in the hypothalamus
i. Inhibits NPY/AGRP neurons.
ii. Stimulates POMC/CART neurons.
iii. Increases production of CRH (Corticotropin Releasing Hormone).
iv. Increases sympathetic activity.
v. Decreases secretion of insulin.

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24. Know the neurons involved in regulating hunger.

a. The arcuate nucleus of the hypothalamus houses the appetite and satiety centers.
b. Anorexigenic neurons (POMC/CART)
i. Satiety sensation decreases appetite.
1. Activation stimulates secretion of -MSH
2. -MSH stimulates synthesis of cocaine/amphetamine-related
transcripts.
3. -MSH acts on melanocortin receptors (MCR) 3 and 4 in the
paraventricular nuclei of the hypothalamus.
4. Activation of MCR 3/4 food intake/ energy expenditure.
c. Orexigenic neurons (NPY/AGRP)
i. Hunger sensation increases appetite.
1. Activation inhibits the effects of -MSH on MCR 3/4.
a. food intake.

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25. Know the process of bile acid secretion.

a. Bile synthesis.
i. Hepatocytes synthesize primary bile acids from cholesterol and conjugate
them with glycine or taurine.
ii. Conjugated (primary) bile acids exist primarily as salts in the gut lumen.
iii. Gut bacteria dehydroxylate/deconjugate primary bile acids secondary bile
acids.

b. Bile secretion.
i. Canalicular bile.
1. Formed as bile acids are actively secreted across the canalicular
membrane.
16

2. Bile acids are osmotically active and pull water across tight
junctions.
3. Other solutes including glucose, calcium, glutathione, and urea are
absorbed passively into bile.
ii. Ductule bile.
1. Product of the columnar epithelial cells (cholangiocytes) that line the
ductules.
2. Hepatic bile emerges from the ductules prior to entering the gall
bladder.
c.
Bile acid-dependent secretion.
Mechanisms involved in bile acid-

dependent secretion of bile.
Bile acids are extracted from portal
blood via co-transport w/Na+ (2), which
is dependent upon Na+-K+ exchange (1).
Secretion of bile acids into canalicular
bile is via a bile acid export pump (3).

i. Volume of bile secreted in response to recycling of bile acids.
ii. Total bile pool (~3gm) undergoes 4-12 cycles/day depending upon # of
meals/fat content.
iii. Bile acids synthesized = bile acid lost
1. Regulated by negative feedback control of 7--hydroxylase, the rate-
limiting step.
d. Bile acid-independent secretion.
i. Accomplished by water transport coupled to transport of Na+.
ii. The hormone secretin stimulates the secretion of H2O and HCO3-.
iii. CCK (cholecystokinin) potentiates this activity.

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e. Gallbladder storage/secretion of bile.

i. Bile is secreted continuously and accumulates in the gallbladder during
interdigestive periods.
ii. During storage, water is removed and concentration of bile acids increases.
iii. Cations increase in concentration while [Cl-] and [HCO3-] decrease.
iv. NHE and CFTR channels are present in the gallbladder epithelial cells.
1. NHE Na+-H+ Exchange
2. CFTR Cystic Fibrosis Transmembrane conductance Regulator
v. Rhythmic contractions of the gallbladder begin within an hour of eating.
1. This is in response to release of CCK as fat and protein products
enter the duodenum.
2. LCFAs are the main stimulator for CCK.
vi. CCK binds to CCK-A receptors in gallbladder smooth muscle.
1. CCK also causes relaxation of Oddis sphincter.
a. Bile passes through in spurts.
vii. Activation of the vago-vagal reflex releases Ach.
f.
***Dr. Teel said that if you get rid of/lower bile acids by way of medications, it will
lower cholesterol.
i. If Statin (cholesterol drug) cause loss of bile acids or b/c of increased
excretion, the liver will increases bile acid synthesis until it reaches its
maximum amountfrom there if continued lowering of bile acids occur
then it will lower cholesterol.
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26. Know how to help restore normal intestinal flora after destruction by medication.
a. Bacteria lost to antibiotics will in time repopulate.
b. Process can be accelerated by taking probiotics (i.e. certain yogurts).
***Extra Information***
Esophageal cancer has ~95% mortality rate.
Gastroporesis
Paralysis of GI delayed emptying of stomach
Can be caused by neuropathy associated w/Diabetes.
Regulation of Salivary Gland Function
Parasympathetic
Secretomotor salivary output
Sympathetic
Vasomotor salivary output
**Caveat**
Small amount of NE stimulate saliva flow
Large amount of Epinephrine/NE decrease saliva flow cause
xerostomia (dry mouth).
Aldosterone Na+-K+ exchange & ENAC channels
Sjogrens Syndrome
Chronic/progressive autoimmune disorder.
Symptoms: xerostomia, dry eyes (xerophthalmia)
Loss of salivary function
Difficulty swallowing, chewing, tasting, speaking.
Dental health issues.

Dry, erythematous mucosa.
Ulcerations.
Parotid glands are often enlarged.
Pathology
Lymphocyte infiltration of salivary glands w/subsequent damage to acinar cells.
Cl/HCO3 exchange in striated duct is compromised.
Syndrome may be secondary to other autoimmune diseases and certain

medications can cause xerostomia.
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Dr. Kirbys Section
1. Which cranial nerves innervate taste buds?

a. CN VII, CN IX, CN X
2. Which nucleus in the brainstem does taste sensation from cranial nerves travel to?

a. The Nucleus Solitarius.
3. Which sensory modality does not relay through the thalamus?
a. Olfaction (smell)
i. via CN I (Olfactory n.)
ii. Project directly into the telencephalon.
iii. Odorous molecules are drawn into nasal system during inhalation.
4. What are the forms of rhodopsin (cis or trans) that exist in light and darkness?
a. Dark: rhodopsin, in cis conformation, binds to opsin.
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b. Light: rhodopsin is isomerized by light causing a conformational change (photobleaching)
to all-trans.
c. Rhodopsin is responsible for monochromatic vision in the dark.
5. What are the other term(s) (synonym) used for the primary visual cortex?
a. Primary Visual Cortex = Area 17 = V1 = Striate Cortex
6. How are cells grouped functionally in the visual cortex?
a. Magnocellular neurons (laminae I and II) are functionally color blind, fast, high-
contrast sensitivity and low sensitivity.
b. Parvicellular neurons (laminae III through VI) are functionally color selective, slow,
low-contrast sensitivity and high resolution.
7. Where is primary visual cortex located?
a. In and around the Calcarine fissure in the Occipital lobe.
8. Receptive fields in the retina have what type of organization?

a. All with Center-Surround (C-S) receptive field.

21

9. What is the shape of receptive fields in visual cortex?
a. Receptive fields of cells in the visual cortex are larger and have more-complex stimulus
requirements than retinal ganglion cells or lateral geniculate nucleus cells (e.g., Hubel,
1963).
b. Simple cells
Gabor filter-type
receptive field typical
for a simple cell.
Blue regions indicate
inhibition, red
facilitation.

i. Responds primarily to oriented edges and gratings (bars of particular
orientation).
c.
Complex cells
i. Responds primarily to oriented edges and gratings (bars of particular
orientation).
ii. However it has a degree of spatial invariance.
1. Its receptive field cannot be mapped into fixed excitatory and inhibitory
zones.
2. It will respond to patterns of light in a certain orientation within a large
receptive field, regardless of the exact location.
3. Some complex cells respond optimally only to movement in a certain
direction.
d. Hypercomplex cells
i. Detect length in V1.
ii. Exhibit end-stopping properties.
1. When a cell's response increases as a stimulus, for example a bar,
expands to fill the receptive field, and then responds less when the
stimulus exceeds the size of the receptive field.
iii. However, later research has found them to be subclasses of the simple and
complex cells.

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10. What are the names of the two types of interneurons found in the retina?
a. Bipolar cells
i. Found in high [conc.] in the middle of the retina.
b. Amacrine cells
i. Serve to produce lateral inhibition of light [improve acuity].
c. Horizontal cells
i. Serve to produce lateral inhibition of light [improve acuity].
Dr. McLeans Section
1. Innate vs. Adaptive Immunity
Comparison of innate and adaptive immunity

Innate
Adaptive
Response time
Rapid (mins!hrs)
Slow (days)
Specificity
Antigen nonspecific
Secondary response
Same as primary
response
Faster than primary

response
Major components
Physical barriers and

phagocytes
B and T cells
Antigen specific
improves during course of
immune response
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a. Innate Immunity
i. Natural resistance that a person inherits from their parents and is born with.
ii. First line of defense against infection and is non-specific for a particular antigen.
Defense
Anatomic!
Physical barrier and acidic environment retards entry and growth of

microbes!
Mucus entraps microbes!
Cilia propel microbes out of body!
Mucous membrane!
Normal flora compete w/pathogenic microbes for nutrients and
attachment sites!
Physiologic!
Normal body temperature & fever inhibits growth of some microbes!
Temperature!
Acidic stomach kills most ingested microbes!
Low pH!
Lysozyme cleaves bacterial cell wall!
Chemical mediators! Interferon (IFN) induces antiviral state in uninfected cells!
Complement lyses microbes or facilitates phagocytosis!
Skin!
Phagocytic!
Inflammatory !
Cells internalize (endocytose) & break down foreign macromolecules!

Specialized cells (monocytes, neutrophils, macrophages) internalize
(phagocytose), kill, & digest whole microbes!
Caused by damaged tissues & infections
Leakage of vascular fluid containing serum proteins w/antibacterial
activity
Influx of phagocytic cells into the affected area!

iii. Phagocytic cells are mainly involved which engulf and destroy invading microbes.
1. Most phagocytosis is conducted by blood monocytes, neutrophils, and
tissue macrophages.
iv. Response to infection.
1. Recognition.
a. Pathogen associated molecular patterns (PAMPs) on pathogens.
b. Pattern recognition receptors (PRRs) on WBCs as well as soluble
PRRs.
2. Recruitment of.
a. Effector cells that engulf bacteria, kill virus-infected cells, or attack
protozoan parasites; secrete cytokines.

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b. Complement: serum proteins that help the effector cells by marking
pathogens with molecular flags, but also attack pathogens in their
own right.
v. Overall effect of Innate Immune System.

1. Induce a state of inflammation (condition of heat, pain, redness, swelling).
2. Within mins after injury, the inflammatory process begins w/activation and
increased [conc.] of acute-phase proteins inducing both local/systemic
responses.
Acute-Phase Response!
Local responses!
Systemic responses!
Activation of kinins:
!Act on vascular endothelial
cells (e.g. bradykinin)
causing them to contract,
leading to vascular
permeability
!Responsible for pain and
itching
!Fever induction
!Increases WBC number
!Production of C-reactive peptide
(this binds the microbes membrane
and activates complement system
resulting in cell lysis or enhanced
phagocytosis)
Activation of the
coagulation pathway (clot)!
25

3. Cytokines Induce Vasodilation [refer to Figure 1-6, pg. 25^]
a. T cells and macrophages are the main cells that produce cytokines.
b. Increases blood flow (causing warmth and redness).
c. Causes gaps between cells of vessels allowing blood plasma to leak
into tissues.
d. Change blood vessels surfaces causing them to attract white blood
cells (WBCs).
e. WBCs at the site of infection become inflammatory cellscells that
release substances contributing to inflammation.
b. Adaptive Immunity
i. Acquired or protective immunity.
1. Acquired after immunizations, requires education.
2. Adds to an ongoing innate immune response.
ii. Highly specific!
iii. Little/no effect against infection by different pathogen.
iv. B & T lymphocytes are the cells responsible for adaptive immunity.
1. B lymphocytes
a. Humoral Immune Response (HIR).
b. Synthesize/secrete specific antibodies against antigens into the
bloodstream.
2. T lymphocytes
a. Cell-Mediated Immunity.
b. Recognize antigens presented by antigen presenting cells (APCs).
26
Adaptive [Acquired] Immunity!

Natural [Passive/Active]!
Artificial [Passive only]!
Artificial [Active only]!

v. Primary Immune Response
1. The first time that an adaptive immune response is made to a given
pathogen.
vi. Secondary Immune Response
1. Occurs following subsequent exposure to the same pathogen.
2. Rapid response repels the pathogen before detectable symptoms occur.
3. Responses are specific to the pathogen causing the primary immune
response.
vii. Vaccinations (active artificial)
1. Stimulates the immune system to generate memory cells by administration
of a pathogens antigens in a form that cannot cause disease.
2. Usually made from weakened or killed pathogens.
a. Injection killed (inactivated) form
b. Inhaled weakened (attenuated) form
3. Adjuvant: added to vaccines to enhance immune response.
4. Routes of Administration
a. Oral route
i. Attenuated live viruses.

27

ii. Rotavirus and oral typhoid.
b. Intranasal (inhaled) route
i. Attenuated live virus.
ii. Influenza only.
c. Injection route
i. Killed (inactivated) form.
ii. Two types Intramuscular (IM) & Subcutaneous (SC).
5. Pathogens that mutate rapidly may change to render the secondary
immune response ineffective.
a. Example: influenzaa new vaccination is needed each year.
>>Just a review picture<<

SCID (Severe Combined Immunodeficiency Disease)
Both T and B cell defects.
Patients die early in infancy w/o bone marrow transplant or gene therapy.
AIDS (Acquired Immune Deficiency)
Caused by the Human Immunodeficiency Virus (HIV).
HIV selectively infects CD4 T cells!!!! [MHC II CD4+).
28
Eventual depletion of CD4 T cells results in the loss of the adaptive immune response and
ultimately death due to opportunistic infections.
2. Hematopoiesis.
a. The developmental process where HSCs give rise to all of the cells of the blood.
b. Hematopoietic Stem Cells (HSCs) are pluripotent.
c. Site of hematopoiesis changes with age:

d. HSCs derivatives.
29

e. Hematopoietic Growth Factors (Extra/probably dont need to know).
IL-3 &
IL-3 &

f.
Hematopoiesis = Erythropoiesis + Leukopoiesis

i. Erythropoiesis
1 day!
3 days!
120 days!
1 day!
1 day!
1 day!

1. Red Blood Cell (RBC) formation.

30

ii. Leukopoiesis
1. White Blood Cell (WBC) formation.
2. Myelopoiesis
a. Granulopoiesis [B.E.N.]
i. Basophils, Eosinophils, Neutrophils.
b. Monocytopoiesis
i. Monocytes [agranular].
c. Megakaryocytopoiesis (Thrombopoiesis)
i. Megakaryocyte
1. Fragmentation forms platelets (thrombocytes).
a. Important in hemostasis (blood clotting).
3. Lymphopoiesis
a. B & T cells, Natural Killer (NK) cells.
g. Self-Renewal when HSCs divide and some of the daughter cells remain HSCs.
h. The other daughter cells will become different kinds of stem cells with more limited
developmental potential.
i. Erythroid, Myeloid, and Common Lymphoid Progenitors.
i.
Erythroid Progenitor cells.

i. Erythrocytes [RBCs].
j.
Myeloid Progenitor cells.

i. Granulocytes
a. Leukocytes w/prominent cytoplasmic granules containing
substances that kill microorganisms and enhance phagocytosis.
2. Basophils
a. Allergic reactions.
3. Eosinophils
a. Provides defense against parasites such as worms.

31

4. Neutrophils

a. Carry out phagocytosis.
i. Engulfing, and breaking down pathogens or dead cells and
debris in the body.
b. Short-lived and the primary leukocyte that destroys pathogens in
both innate and adaptive immunity.
c. Stored in the bone marrow/released to fight infection.
ii. Monocytes Macrophages
1. Monocyte circulating precursor to macrophage.
2. Long-lived leukocytes that destroy pathogens in both innate and adaptive
immunity.
3. Carry out phagocytosis
4. Large cells containing many vacuoles with engulfed material.
iii. Megakaryocytes
1. Fragmentation forms platelets (thrombocytes).
a. Important in hemostasis (blood clotting).
iv. Myeloid Dendritic cells
1. Star-shaped cells that cooperate w/lymphocytes to initiate adaptive
immune responses.
v. Mast cells.
1. Expulsion of parasites from body through release of granules containing
histamine and other active agents.

32

k. Common Lymphoid Progenitor cells.
i. Natural Killer cells
1. Granular.
2. Function in innate immunity.
3. Important in defense against viral infections, also tumor/cancer cells.
ii. B lymphocytes
1. Develop in bone marrow (acquire B cell receptor).
2. Function in adaptive immunity.
3. Express immunoglobulins (Igs) as recognition molecules on the cell surface.
4. Differentiate into plasma cells upon activation by infection.
5. Plasma cells make antibodies.
a. Soluble forms of Igs that are released into the blood and body
fluids.
iii. T lymphocytes
1. Begin development in bone marrow, migrate to thymus (acquire T cell
receptor).
2. Function in adaptive immunity.
3. Express molecules known as T cell receptors (TCRs) on their surfaces as
recognition molecules.
4. Activated to differentiate into effector T cells.
a. Helper T (TH) cell
i. Have CD4+ MHC class II receptors.
1. MHC II molecules on APCs (antigen presenting cells)
ii. Secrete substances that activate other cells of the immune
system.
b. Cytotoxic T (TC) cell
i. Have CD8+ MHC class I receptors.
1. MHC I molecules are present on almost all cells.
ii. Kill cells infected w/viruses or other intracellular pathogens.
3. Immunogenicity.
a. An antigens ability to elicit a Humoral (antibody mediated) and/or cell-mediated immune
response.

33

b. Immunogen
i. Any agent capable of inducing an immune response.
4. Antigenicity.
a. Ability of an antigen to combine w/the final products that arise from an immune response
such as antibodies and cell surface receptors (but not elicit a response).
**All immunogens are antigens but NOT all antigens are immunogens (e.g. haptens)**
5. Structure of an antibody.
a. Variable (V) region (varies greatly from one antibody to the next) and is responsible for
binding pathogens.
b. Constant (C) region contains binding sites for receptors on phagocytes and complement
proteins and is responsible for recruiting cells and molecules for pathogen destruction.
c. Hinge regionflexible region of the antibody where all of the arms of the Y come together,
allows the Ig to be flexible for binding to antigen and proteins that mediate immune
responses.
d. 2 identical H chains and 2 identical L chains [Lambda () or kappa () L chains].
i. Heavy = VDJ; Light = VJ
e. Fab - contains the antigen-binding site. Obtained by papain (from papaya fruit) digestion.
f.
F(ab)2 - obtained by pepsin digestion.
g. FC regionthe portion of the constant region that forms the "stem" of the Y shaped Ig
molecule.
h. Hypervariable regions (paratope) 3 regions of high variability within the V domain,
designated HV1, HV2, HV3.

34

i.
Framework regions the regions of the V domain between the hypervariable domains,
which are relatively invariant.

6. Antigens.
Epitope
Paratope

a. Epitope (antigenic determinant)
i. Part of an antigen to which an antibody binds or gives rise to the MHC-binding
peptide that is recognized by a TCR.
ii. 4 types of B cell epitopes.
35

iii. T cell dependent antigens [most common]
1. Requires the presence of helper T cells to stimulate antibody production by
B cells.
iv. T cell independent antigens
1. Trigger B cells to produce antibodies without the presence of T cells.
b. Paratope
i. Small regions of antibodies, which bind to epitopes.
c. Mitogens Nonspecifically activate T and/or B cells.
i. Pokeweed mitogen [B & T cell].
d. Super antigens Antigens that bind to TCR of T helper cells and MHC class II of APC eliciting
a massive T cell activation by binding to 1-10% of lymphocytes inducing large cytokine
release.
i. Toxic Shock Syndrome.
7. Major Histocompatibility Complex I/II.

a. Activation of Nave T cell (CD4/8) requires co-stimulatory (B7 ligand) on APC, binds to CD28.
b. MHC class I molecules
i. Present on almost all cells.
ii. Bind to CD8+ Cytotoxic T cells.
c. MHC class II
i. Present on APCs.
ii. Bind to CD4+ Helper T cells.

36

8. B cell development.
a. Involves the rearrangement of immunoglobulin genes.
b. Immature B cellsonly IgM on surface.
i. Negative selectionSelf-reactive immature B cells are inactivated by deletion
(apoptosis) or anergy (mature but do not respond to subsequent antigen exposure).
ii. Receptor editingchange in the Ig specificity of an autoreactive B cell.
c. Mature (Nave) B cellsB cells that have not encountered specific antigen express IgM and
IgD.
i. When activated by exposure to antigen they differentiate into plasma cells and
memory B cells.
ii. Plasma cells
1. Become highly specialized toward antibody secretion.
2. No longer express surface Ig or MHC class II and therefore are unresponsive
to antigen or T cells.
3. Have a life span of about 4 weeks.
iii. Memory B cells.
1. Persist for long periods of time.
2. Are generated after proven successful antigen specificities have been
produced.
3. Are much more easily activated on encounter with antigen.
4. Allow a much quicker and stronger response to antigen than in the primary
response.
d. Somatic hypermutation mutations that occur in the V (variable region) genes of heavy
and/or light chains of a B cell.
e. Isotype switching an individual B cell switches to make an antibody of a different class
such as IgG, IgA or IgE.
9. Functions of Immunoglobulins.
a. 5 Isotypes of heavy chains.
i. Mu ()- IgM, Delta ()- IgD, Gamma ()- IgG, Alpha ()- IgA, Epsilon ()- IgE
37

b. Soluble proteins that recognize antigens (secreted or membrane bound).
c. Neutralization: Neutralizing antibodies directly inactivate a pathogen or toxin by binding
tightly to it and preventing it from interacting with human cells to cause harm.
d. Opsonization: coating of a pathogen with an immune system protein (phagocytosis or
complement).
e. IgG
i. 80% of total Igs; longest lasting at 23 days.
ii. Pass through the placenta, the only one!!!
iii. Possesses both anti-viral and antibacterial activity.
f.
IgM
i. Can form a pentamer.
ii. A soluble form is produced in a primary immune response.
iii. When it is bound to B cells it forms the B cell receptor.
iv. It functions in complement activation with high activity.
v. It has high agglutination ability.
g. IgA
i. Dimeric form is most common.
ii. Predominant antibody in saliva and tears.
iii. Possess anti-viral and antibacterial activity when in the presence of lysozymes.
iv. Mother can pass IgA to infant during breastfeeding-it is passive natural.
h. IgD
i. They are present on B lymphocyte surfaces with little known activity.
i.
IgE
i. Shortest half-life of 2 days.
ii. Present on surfaces of basophils and mast cells.
iii. 3. It is involved in allergic reactions.
38

10. Cytokines.
a. Soluble protein molecules that regulate the immune system.
b. IL-2
i. Controls differentiation of T cells.
ii. An important cytokine in immunosuppressant drugs, b/c if you block activation of IL-
2 than there will not be an immune response.
39
Macrophages ! Secrete: IL-1, IL-6, TNF-!

Cytokine!
Function!
IL-1!
Induces inflammation
Induces fever
Induction of acute phase protein synthesis
!
IL-6!

Stimulates T cell activation
Stimulates B cell immunoglobulin production
Stimulates IL-2 production
!
TNF-!
Induces inflammation
Induces fever
Neutrophil activation!

TH1 cells ! Secrete: IL-2, INF, TNF (lymphotoxin), IL-3, GM-CSF

Cytokine
IL-2
INF-
TNF-
Function
**T cell proliferation
NK activation and proliferation
Activates macrophages
Increases expression of MHC-I and MHC-II
molecules
Increases antigen presentation
Inhibits TH2 cells
Inflammation
Plays a role in killing target cells by cytotoxic CD8
T cells

40
TH2 cells ! Secrete: IL-4, IL-5, IL-10, IL-13, IL-3, GM-CSF

Cytokine
Function
IL-4
B cell proliferation
TH2 proliferation
IgE synthesis
IL-5
B cell proliferation and secretion of antibodies

Eosinophil activation
IL-10
Inhibits TH1 production and macrophage function
IL-13
B cell proliferation
IgE synthesis

11. TH1 and TH2.

a. Can down-regulate each other.
i. TH2 secrete IL-10 inhibit TH1 response.
ii. TH1 secrete IFN- inhibit TH2 response.
b. TH1
i. Secrete cytokines at site of infection.

41

ii. Biased towards cell-mediated immune response.
1. Macrophage activationleads to inflammation.
a. Needs cytokine IFN- and CD40 ligand CD40 receptor on
macrophage for activation.
b. Granuloma forms if not effective.
2. Cytotoxic (CD8) T cell activity.
iii. Viruses and bacteria favor the production of TH1 cells.
c. TH2
i. Secrete cytokines in secondary lymphoid organs.
ii. Biased towards Humoral immune response.
1. Dominated by B cell differentiation and the production of antibodies (Igs).
iii. Allergens and parasites favor TH2 induction.
d. TC cells
i. Induce apoptosis by two mechanisms.
ii. Fas-ligand binds to Fas-ligand receptor on target cell induces apoptosis.
iii. Lytic granules perforin forms holes in target cell granzyme enters cell and
initiates apoptosis.
e. Suppressor (Regulator) CD4 T cells
i. Antigen specific T cells that inhibit immune responses.
ii. Identified by the expression of CD25.
iii. Must have physical contact with their target T cells.
12. Complement Cascade.
a. System of blood proteins that permanently marks a pathogen or antigen as foreign and
targets it for removal by the immune system.
42
C1
Esterase
Inhibitor
acts here!
(Mannose associated serine protease)!

(Mannose binding lectin)!
C3a!
! The most important and

abundant complement
molecule is C3.
! All 3 complement pathways

generate enzymes that act
as C3 convertasean
enzyme that cleaves C3.
Final result
outcome is
MAC!!!
Which is
mainly
composed of
C9s!

b. Deficiency of C1 esterase inhibitor can cause hereditary angioedema.

43

13. Initiations for Complement.
~~Classical pathway.
a. Triggered by antibodies bound to the surface of the pathogen. (Helps in adaptive).
~~Lectin-mediated pathway.
b. Triggered by mannose binding proteins that are bound to molecules on the surface of
pathogens. (No antibodies, so helps in innate).
~~Alternative pathway.
c. Triggered directly by components of bacterial cell surfaces. (No antibodies, so helps in
innate).
14. Anaphylatoxins.
a. Smaller complement components 3a, C4a and C5a.
b. Induce anaphylaxis, an acute systemic inflammatory response.
c. Order of potency: C5a > C3a > C4a.
d. Also aids in phagocytosis.

15. Type I&IV allergic reactions (know all though).
a. Type I hypersensitivity [immediate-type].
i. Caused by binding of antigen to specific IgE bound irreversibly to its Fc receptor,
principally on mast cells.
1. Histamine (preformed granule) is released.
2. Leukotriene (formed after activation) released/more potent.
ii. Site of activation.
1. Inhaled allergens activate mast cells in respiratory tract rhinitis/asthma.
2. Insect stings deliver antigens into skin where mast cells mediators cause
urticaria (hives), angioedema, atopic dermatitis (eczema).
44

3. Allergens in food trigger mast cells in GI tract vomiting/diarrhea.
4. Allergens in blood cause systemic mast cell activation anaphylaxis.
b. Type II hypersensitivity.
i. Related to IgM and IgG.
ii. Caused by antibodies specific for altered components of human cells.
c. Type III hypersensitivity.
i. Caused by immune complexes formed from IgG and soluble antigens.
ii. Complement can remove if they are large complexes, but if small
1. Initiate tissue-damaging inflammatory reactions.
d. Type IV hypersensitivity [Delayed-type].
i. Caused by effector T cells specific for the sensitizing antigen.
ii. Occurs 1-3 days after contact with antigen
iii. Best-studied example is the tuberculin test.
1. Small amount of protein antigen from M. Tuberculosis is injected in the skin.
Inflammatory rxn 24-72 hours later.
iv. Another example: Dermatitis from contact with Poison Ivy and Poison oak.
**Type I, II, III involves antibodies**
**Type IV involves T cells**

16. Leptin.
a. Coded for by obesity gene [ob].
b. Acts as a hormone.
c. From adipose tissue promotes negative energy balance.
i. Suppressing appetite.
ii. Increasing energy expenditure.
d. From stomach is released in response to food presence.
e. Levels rise w/increasing BMI to try and diminish appetite, but to no availLeptin resistance.
17. Adiponectin.
a. Lean people have higher amounts.

45

b. Inhibits inflammation and protects against insulin resistance & cardiovascular disease.
18. Know how to calculate x gram of fat = y kcal.
a. Ex. 10 grams of body fat =? kcal
i. 9 kcal (10 grams) = 90 kcal
ii. 90 kcal (0.87) = 78.3 kcal [from fat].
b. Fat 9 kcal/gram.
i. 1 lb. fat = 3500 kcal.
ii. Body fat 87% fat.
c. Protein/Carbohydrate 4 kcal/gram.
19. Vitamin overview & deficiencies.

a. Vitamin K is the ONLY fat soluble vitamin with a coenzyme function.
b. Vitamin A, D, K are important in bone and tooth development!!!
c. Vitamin names&deficiencies.
i. B1: Thiamine
1. Beriberi
a. Severe thiamine deficiency found where polished rice is the major
component of the diet.
b. Affects nervous system (dry beriberi) or cardiovascular system (wet
beriberi).
c. Muscle wasting and edema.
2. Wernicke-Korsakoff syndrome
46

a. Seen primarily in association with chronic alcoholism and due to
dietary insufficiency or impaired absorption of the vitamin.
b. Apathy, loss of memory, ataxia, and a rhythmic to and fro motion of
the eyeballs (nystagmus).
ii. B2: Riboflavin
1. No major disease.
2. Dermatitis.
3. Cheilosis (fissuring at the corners of the mouth).
4. Glossitis (tongue appearing smooth and purplish or red).
iii. B3: Niacin
1. Pellagra: disease of the skin, GI tract and CNS.
a. Symptoms: Dermatitis, diarrhea, dementia (3Ds)
b. If untreated death (4D).
iv. B5: Pantothenic Acid
v. B6: Pyridoxine (more common of the 3), pyridoxal, and pyridoxamine
1. ONLY water-soluble vitamin with significant toxicity.
a. Neurological damage; > 200 mg/day
2. Scaly dermatitis, anemia, depression, confusion, convulsions.
vi. B7: Biotin
vii. B9: Folic Acid
1. Most common vitamin deficiency in the US.
a. Particularly among pregnant women and alcoholics.
2. Anemia.
3. Neural tube defects: Spina bifida and anencephaly.
viii. B12: Cobalamin
1. Pernicious (deadly) anemia.
a. Deficiency in red blood cells.
d. Vitamin C: Ascorbic acid
i. Scurvy:
1. Sore and spongy gums, loose teeth, fragile blood vessels, swollen joints, and
anemia.

47

e. Vitamin A
i. Night Blindness, xerophthalmia [dry eyes, lack of tear production], keratomalacia
[softening of the cornea].
f.
Vitamin D (calciferol)
i. Rickets [children]
1. Inadequate calcification resulting in misshapen bones (bowing of leg).
ii. Osteomalacia [adults]
1. Poor bone mineralization.
2. Soft, flexible, brittle and deformed bones.
iii. Osteoporosis [adults]
1. Loss of calcium.
2. Results in fractures.
g. Vitamin E (tocopherols)
i. Red blood cell breakage.
ii. Nerve damage.
h. Vitamin K (Quinone derivatives)
i. Hemorrhaging.
20. Minerals & deficiencies.
a. Major minerals: > 100mg/day
i. Ca, P, K, Na, Cl, Mg, and S
b. Trace minerals: < 100mg/ day
i. Fe, I, Zn, Cr, Se, F, Mo, Cu, and Mn
c. Sodium
i. Muscle cramps, mental apathy and loss of appetite.
d. Calcium
i. Stunted growth in children.
ii. Bone loss (osteoporosis) in adults.
e. Phosphorus
i. Important in genetic material.
ii. Muscular weakness, bone pain.
f.
Fluoride
i. Reduces dental caries 50-70%.
48

g. Iron
i. Deficiency disease is anemia.
h. Iodine
i. Goiter may arise from lack of Iodine.
21. BMI [Body Mass Index] ranges.

22. Extras from nutrition.
a. Maltose = glucose + glucose
b. Sucrose = glucose + fructose
c. Lactose = glucose + galactose
d. Hydroxyapatite Ca10 (PO4)6(OH)2
i. Acid makes more soluble.
ii. Fluoride makes it more insoluble.
e. RDA (recommended daily allowance)
i. Carbs 130 mg/day
1. 45-60% cals should be from carbs.
2. < 25% of sugar.
ii. Fat 20-35% of calories.
iii. Protein 0.8 g/kg of body weight.
1. 10-35% of cals.
2. Pregnant women additional 30 mg.
3. Infants 2 g/kg/day.
f.
Linoleic acid is an essential fatty acid (Omega-6).

i. Lowers LDL & HDL.
49

g. -linolenic acid (essential fatty acid) [Omega-3].
i. Lowers blood pressure.
ii. Scaly dermatitis, hair loss and poor wound healing.
h. Order [badgood].
i. Trans unsaturated saturated [solid] monounsaturated [liquid]
polyunsaturated [-3 & -6].

i.
20 amino acids.
i. 9 essential A.A.
1. Cannot be synthesized (or produced in sufficient amounts) by the body.
2. Phenylalanine, Valine, Threonine, Tryptophan, Methionine, Histidine,
Leucine, Lysine, Isoleucine.
ii. Non-essential A.A.
1. Synthesized in sufficient amounts by the body.
j.
Protein structure.
50

k. Condensation reaction.

l.
Proteins have negative charges.
m. If there is low protein in the blood water will try to replace it *(disease related to this).
n. Nitrogen Balance.
i. Adequate protein intake in adults.
o. Positive Nitrogen balance.
i. Net increase in the amount of nitrogen in the body.
1. Children or individuals undergoing healing.
p. Negative Nitrogen balance.
i. Net decrease in the amount of nitrogen in the body.
ii. In wasting or degeneration.

51

23. Nutrition Diseases.
a. Type 1 diabetes {Insulin-Dependent}:
i. Pancreas fails to produce insulin.
b. Type 2 diabetes {Insulin-Independent}:
i. Cells fail to respond to insulin.
ii. Usually adult onset.
c. Hypoglycemia.
i. Blood glucose below normal level.
ii. Normal 70-105 mg/dL.
d. Elevated levels of LDL cholesterol.
i. Increased risk for CHD.
e. Elevated levels of HDL cholesterol.
i. Decreased risk for CHD.
f.
Excess protein.
i. Nephrolithiasis (kidney stones).
ii. Osteoporosis*****
iii. Heart disease
1. Homocysteine.
iv. Cancer.
v. Accelerates kidney disease.
vi. Raise the acidity (lower pH) of the blood.
g. Too little protein.

i. < 130 g/day.
ii. Provide carbon skeletons for the synthesis of glucose.
iii. Protein energy malnutrition (PEM).
1. Developed countries.
a. Most frequently seen in patients with medical conditions.
2. Developing countries.
a. Inadequate intake of protein and/or energy is the primary cause.
3. Depressed immune system with a reduced ability to resist infection.
a. Death from secondary infection is common.

52

iv. Kwashiorkor [PEM]
1. Sudden and recent deprivation of food (acute).
2. Lacking protein.
3. Frequently seen in children after weaning between 18 months and 2 years
of age, when their diet consists predominantly of carbohydrates.
4. Edema.
a. Swollen feet swollen abdomen
b. **Distinguishing feature between Kwashiorkor and Marasmus.
v. Marasmus [PEM]
1. Severe deprivation of food over a long time (chronic).
2. Lacking protein & carbohydrates [nutrients in general].
3. Children from 6 18 months of age in impoverished areas of the world.
4. Learning disability.
a. Brain normally grows to almost full adult size within first 2 years of
life.
5. Arrested growth, extreme muscle wasting, weakness, and anemia.
h. Anorexia nervosa.
i. Major psychological component.
ii. Refusal to maintain a normal body weight.
iii. Intense fear of gaining weight or becoming obese.
iv. Disturbance of body image resulting in a feeling of being fat or having fat in certain
areas even when extremely emaciated.
i.
Bulimia nervosa.
i. Major physiological component.
ii. Episodic binge eating followed by behaviors designed to prevent weight gain,
including purging, fasting and excessive exercise.
j.
Binge eating disorder.

i. Can be over-weight.
ii. Binge eating, rarely purging, exert less restraint than bulimics during times of
dieting.
53

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Justin Terrill

Loma Linda University

Tips for PHSL 505 Finals

Tips for PHSL 505 Finals

a. Inorganic iron is only absorbed as Fe . Iron reductase converts Fe3+Fe2+. Fe2+ is

Tips for PHSL 505 Finals

Tips for PHSL 505 Finals

Tips for PHSL 505 Finals

Tips for PHSL 505 Finals

Tips for PHSL 505 Finals

Tips for PHSL 505 Finals

13. Know muscle responses during peristalsis.

Tips for PHSL 505 Finals

Tips for PHSL 505 Finals

Tips for PHSL 505 Finals

Tips for PHSL 505 Finals

Tips for PHSL 505 Finals

Gastric phase of gastric

Tips for PHSL 505 Finals

Tips for PHSL 505 Finals

Tips for PHSL 505 Finals

Tips for PHSL 505 Finals

Bile acid-dependent secretion.

Mechanisms involved in bile acid-

Tips for PHSL 505 Finals

Tips for PHSL 505 Finals

Paralysis of GI delayed emptying of stomach

Can be caused by neuropathy associated w/Diabetes.

Regulation of Salivary Gland Function

Secretomotor salivary output

Vasomotor salivary output

Aldosterone Na+-K+ exchange & ENAC channels

Chronic/progressive autoimmune disorder.

Symptoms: xerostomia, dry eyes (xerophthalmia)

Loss of salivary function

Difficulty swallowing, chewing, tasting, speaking.

Dental health issues.

Parotid glands are often enlarged.

Lymphocyte infiltration of salivary glands w/subsequent damage to acinar cells.

Cl/HCO3 exchange in striated duct is compromised.

Syndrome may be secondary to other autoimmune diseases and certain

Tips for PHSL 505 Finals

Tips for PHSL 505 Finals

Tips for PHSL 505 Finals

Tips for PHSL 505 Finals

Comparison of innate and adaptive immunity

Faster than primary

Physical barriers and

Tips for PHSL 505 Finals

Physical barrier and acidic environment retards entry and growth of

Cells internalize (endocytose) & break down foreign macromolecules!

Tips for PHSL 505 Finals

Tips for PHSL 505 Finals

Tips for PHSL 505 Finals

Adaptive [Acquired] Immunity!

Artificial [Active only]!

Tips for PHSL 505 Finals

Both T and B cell defects.

AIDS (Acquired Immune Deficiency)

Caused by the Human Immunodeficiency Virus (HIV).

HIV selectively infects CD4 T cells!!!! [MHC II CD4+).

Tips for PHSL 505 Finals

Tips for PHSL 505 Finals