10/26/98
CHAPTER 18
ENDOCRINE = inside + to secrete
Glands that secrete to the inside
Have no duct
Secrete into body fluids
Secrete inside of the body
Product: hormones
EXOCRINE
glands that secrete to the outside
have a duct
secrete onto a surface
secrete outside of the body
Product: sweat, oil, digestive juices
Regulatory system:
1. picks up stimuli
2. integration
3. effects change
The nervous system is comparable to a hard-wired telephone system. There is an origin, hard wire, and a recipient.
The endocrine system can be compared to a cell phone that makes a broadcast via radio waves. The recipients have to
have a radio set tuned to the right frequency to receive the broadcast. The endocrine system broadcasts chemicals
(hormones) to specific recipients (glands) that have to have the right receptors to do something with it.
The endocrine system is a system of glands without any “hard-wired” connections between them. They originate from
all 3 primary tissue types: ectoderm, mesoderm, and endoderm. They all secrete the same way and they all secrete
hormones, that is the one thing they all have in common.
Types of glands
1. Wholly endocrine – thyroid, pituitary, pineal, adrenals.
2. Partially endocrine – pancreas, testes/ovaries, heart…
Types of hormones
1. Endocrine secretions – target cells (TC) are far away
2. Paracrine secretion – TC is nearby
3. Autocrine secretion – TC is the same cell: it is a self-stimulating cell
Regulation of glands
1. Neural regulation
2. Hormonal regulation – 1 hormone causes secretion of a 2nd
3. Humoral regulation (humor = body fluid) – something in the blood, glucose, Ca++ - not a hormone – causes the
regulation a certain hormone.
Example: when blood glucose is high, insulin is released, when glucose is low, glucagon is released.
Chemical structure of hormones
1. Lipid soluble – non-polar, made of fatty substance
a. Steroids – cholesterol based, non-polar ring structure, dissolves in lipids, but not H2O
testosterone, estrogen, cortisol
b. Eicosanoids – made of arachidonic acid (fatty acid), non-polar chains, easily dissolve in lipids, but not H2O
1. Prostaglandins – associated with inflammation and pain (childbirth), blood clotting
2. Leukotrienes – same structure, made of arachidonic acid, associated with immune system.
Cytokines, lymphokines, how blood cells communicate with each other.
2. Water soluble – polar, do not dissolve in lipids
a. Biogenic amines – modified amino acids: Epi, serotonin, dopamine. They are very small.
b. Peptides (short chains of AA’s) and proteins ( long chains or 2 small ones connected)
H2O soluble, polar: insulin, glucagon, hGH, ADH, oxytocin
EXCEPTION: Thyroid hormone T3/T4 – consists of 2 tyrosine molecules with a ring structure attached to it makes it an
amine and is thereby lipid soluble and water insoluble.
Water-soluble hormones leave their origin gland, are dissolved in blood, which is mostly H2O, and are that way sent to
their TC. Lipid soluble hormones require a carrier, typically a protein = binding globulin, that fits around the hormone to
enclose it and protect it from water. The protein is water-soluble and can move through the blood stream.
Lipids soluble hormones have intracellular receptors since they can get through the phospholipid bilayer without help.
This intracellular receptor and the hormone form a hormone-receptor-complex (HR). This complex moves to the
nucleus, there it interacts with the DNA, this increases DNA transcription of some genes and new proteins are formed =
enzymes they catalyze a reaction. This is called an intrinsic effect – building structures, opening channels, etc. This
is a slow process, the earliest you can expect a response is 30-45 minutes later. It is also a sustained process.
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Water-soluble hormones don’t need carriers to take them to their TC. They have extra-cellular receptors that are
located on the outside of their target cells. These receptors help them get through the phospholipid bilayer. The extracellular receptor passes the message to the interior. This is called a 2nd messenger system, where the hormone itself is
the 1st messenger. Sometimes there are even 3rd messengers.
Types of 2nd messenger systems
1. Cyclic AMP (cAMP )system ( AMP = adenosine monophosphate )
1. H2O soluble hormone comes in via blood stream, binds to its receptor at the TC. This activates a G-protein, which
acts to turn on adenylate cyclase converts ATP into cAMP
2. cAMP activates protein kinases  adds phosphates to enzymes ( phosphates all come from ATP) this activates or
inactivates enzymes  catalyzes reactions that produce physiological responses.
3. When no more hormones come to the receptor sites, the cAMP is inactivated by another enzyme
The cyclic AMP system is a very fast process, and it doesn’t last very long.
Imagine dominoes arranged in a pyramid. Take a small amount of hormone, apply it to the tip of the pyramid, and the
effect is big, a chain cascade.
Example: In the liver 1 molecule of epi causes the release of 100,000 molecules of glucagon.
2. PIP2 Bis-phosphoglycerate
Again, a H2O soluble hormone comes to its receptor site at the TC and splits into 2 reactions:
1. One reaction makes the second messenger inositol triphosphate goes to stored Ca++ center  Ca++ is released
and this is now the 3rd messenger Ca++ has an intrinsic effect and acts on Cofactors with an enzyme 
maximized effect.
2. The other reaction split makes DAG (diacylglycerate)  which acts the same as AMP activates a protein kinase
adds phosphate group to enzymes this activates or inactivates certain enzymes.
The importance of 2nd/3rd messenger systems is that different hormones, acting on the same cells, have to have different
pathways in order to create different results ( otherwise they’d just go down the same pathway and have the same effect)
Example:
Epi  liver  glucose
Glucagon liver  glucose
Glucagon uses cAMP system
Insulin uses the PIP system
Ways hormones interact
1. Synergistic interaction –
Hormone A = effect of 10
Hormone B = effect of 10
You’d expect the added effect of A and B to be 20, instead it is more like an effect of 1,000. The combined effect of A
and B is much bigger than expected. Example: estrogen and luteinizing hormone for production of oocytes.
2. Antagonistic interaction – hormone A opposes the effect of hormone B. Example: insulin promotes synthesis of
glycogen and glucagon stimulates the breakdown of glycogen in the liver.
3. Permissive effect – the actions of a hormone on a TC requires recent or simultaneous exposure to a second
hormone. Hormone A must arrive before hormone B for B to have an effect. Hormone A causes the receptor for B to
be built. Example: oxytocin needs long exposure to estrogen and progesterone in order for oxytocin receptor to be
present and cause the uterus to contract.
QUIZ 1 What effect does Oxytocin have if it is injected into a female that just had a baby? It will cause the uterus to
contract and help it get back to its pre-pregnancy size as abdominal organ. It also prevents hemorrhage. 8
Pituitary gland = Adenohypophysis (Ant. Pit.) + Neurohypophysis (Post. Pit.)
Located in the base of the brain, seated in the sella turcica. It is often called the master gland, controlled by the
hypothalamus in the diencephalon. The pituitary gland contains many nuclei that are responsible for thirst, hunger and
satiety, sleep and waking, body temp, aggression,… .The pituitary gland is made of
1. nervous tissue, 2. endocrine tissue and 3. Neuroendocrine tissue
a. Paraventricular nucleus PVN
b. SON
c. Arcuate nucleus
These nuclei produce hormones that work through the pituitary, they tell
it what to do and they use the pituitary as a storage organ
Another name for the pituitary gland is Hypophysis, which means “to grow under”. There are several parts to the pituitary
Parts of the Pituitary
1. Adenohypophysis ( Gland - under – to grow ) = anterior pituitary – glandular tissue
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Made of glandular epithelial tissue. It starts as part of the roof of the mouth = Rathke’s pouch, which pinches off and
migrates upward. There is no neural connection with the brain, but the hypothalamus still controls it hormonally
through releasing and inhibitory factors (hormones) from the hypothalamus. The adenohypophysis has a vascular
connection through a portal system: this portal system begins and ends with capillaries ( capillaries-veins-capillaries).
1. Primary capillary plexus
2. Hypophyseal portal veins
3. Secondary capillary plexus
The infundibulum connects the hypothalamus and the pituitary. It contains hypophyseal portal veins.
In a cross section of the adult pituitary, there are only 2 parts: the anterior and the posterior. In fetal and lower
animals there is also a third part: the pars intermedia, which secretes hormones, but in the adult this is taken over
by the adenohypophysis and the pars intermedia is non-existent.
Hormones secreted by the adenohypophysis
1. Somatotrophs
2. Lactotrophs
3. Thyrotrophs
4. Gonadotrophs
5. Corticotrophs
1. Somatotrophs (=body-to feed)– Somatotropin = human growth hormone hGH
A higher form of growth hormone will work on lower animals,
but a lower form of GH will not work on a higher animal.
a. Structure: Peptide – water soluble, needs no carrier, uses 2nd messenger system
b. Regulated hormonally by hypothalamus
GHRH – GH releasing hormone
GHIH – GH inhibiting hormone = dopamine
c. TC: not another endocrine gland
1. Skeleton/bone –speeds up growth in length (=interstitial growth)until adult height is reached;
speeds up growth in diameter (=appositional) throughout life
2. Skeletal muscle – stimulates some more myofibrils, causes them to switch fuel from glucose to fatty
acids  increases glycogen increases blood glucose,  can cause diabetes. GH is a diabetogenic.
3. Adipose tissue – burns fat gets ketones hGH is a ketogenic hormone , affects pH.
4. mammary gland – causes an increased production of milk.
d. Pathology
Hypersecretion of GH = pituitary tumor – an escape of the neg. feedback system causes this.
Childhood: gigantism
Adulthood: Acromegaly – bones that can grow, will ( supraorbital ridge, mandible widely spaced teeth,
wide nose)
Hyposecretion of GH = failure of gland, atrophy
Childhood: dwarfism
Adulthood: Simmons disease=primary pituitary insufficiency – pt looks like walking skeleton, thin bones,weak
2. Lactotrophs – Prolactin (=for-milk)
a. Structure:
b. Regulated hormonally by hypothalmus
PRH – prolactin releasing hormone
PIH – prolactin inhibiting hormone
c. TC: not another endocrine gland
mammary gland – causes production of milk – NOT the secretion or ejection of milk. Continues as long as
the nipple is stimulated. Prolactin is anti-reproductive, it stimulates gonadotropin releasing hormone 
gonadotropin which is a natural contraceptive  no menstrual cycle while breastfeeding.
d. Pathology
Hypersecretion:
Women - any prolactin present in a non-lactating woman is abnormal and is called amenorrhea
Men – Galactorrhea. PRL stimulates GnRH  inhibits testosterone impotence, infertility, loss of secondary
sex characteristics
Hyposecretion:
Women – inability to breastfeed
3. Thyrotrophs - TSH
a. Structure: peptide hormone needs no carrier, uses 2nd messenger system
b. Regulated hormonally by Hypothalamus
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TSH – thyroid stimulating hormone
TC: thyroid gland – butterfly shaped gland, inferior to the Adam’s apple, anterior to the trachea. The 2 lobes
are connected by the isthmus. The thyroid has a very well developed blood supply. Follicular cells made of
simple cuboidal tissue, line the follicle. Parafollicular cells in between the follicles secrete Calcitonin
1. Follicular produce Thyroglobulin which is a long protein made of lots of the same AA: tyrosine residues,
which has a ring structure attached to it and is secreted into the middle of the follicle – the colloid.
2. The iodide pump activity is increased by TSH – this is a very efficient pump that grabs iodide from the
blood, therefore blood entering the thyroid has high levels of iodide, but blood exiting the thyroid has very
low levels.
3. Iodide has to be oxidized  iodine is formed with the help of peroxidase.
4. Iodine is then attached at the tyrosine residues, 1 or 2 at each
5. The tyrosines are then hooked together in a process called coupling. Each couplet can have 2, 3, or 4
iodines attached to it.
6. The couplets are then excised:
T2 units are called Diiodothyramine – a non-functional unit that gets recycled.
T3 units are called Triiodothyramine – functional hormone
T4 units are called Thyroxine – functional hormone
7. release of T3 and T4
T3 and T4 are lipid soluble due to the ring structure, they use a transport protein
T3 is a much more potent enzyme than T4. T4 is converted to T3 before it has an effect.
TC: are nearly all body cells, with the exception of RBC’s, adult CNS cells, retina, spleen, …
T3 increases the metabolic rate (MR) is thermogenic, speeds up utilization of ATP increases muscles
MR  decreases fat stores.It is required for hair and feather production
d. Pathologies
Hyperthyroidism
Graves’ Disease – wt loss, sweats, nervousness, short attention span, insomnia, increased appetite, ruddy
looking, exopthalmus from fibrous tissue deposits behind the eyeball.
Causes for Graves’ disease”
1. LATS – long acting thyroid stimulation  auto-immune dz, since LATS looks like TSH, it does
everything TSH does  TSH levels go down, because of negative feedback. TX: thyroidectomy
2. Pituitary humor  secretes TSH
3. Thyroid tumor/cancer secretes T3/T4
Hypothyroidism –wt gain, dull, sleepy, hair loss/breakage, decreased BMR &appetite, thick skin,always cold
Causes for hypothyroidism – 1. Thyroid failure  no T3 or T4, no TSH, Goiter = enlarged thyroid
Simple goiter – thyroid became enlarged due to a lack of iodide and is therefore unable to produce T3/T4
Toxic goiter – thyroid makes lots of T3/T4
The infant’s CNS is very dependent on T3/T4. Hypothyroidism in infants is called Cretinism. Characteristics
are mental retardation, short neck, and a protruding tongue.
The parafollicular cells of the thyroid produce Calcitonin. It is a humorally regulated peptide hormone.
Calcitonin lowers blood calcium levels.
TC:
bones – it causes osteoblasts to increase their activity and lay down bone;
Kidney – excrete Ca++
Intestines – decrease absorption
No known pathologies involving Calcitonin.
c.
4. Gonadotrophs – FSH stimulates sperm and oocyte production
Luteinizing hormone (LH) stimulates secretion of testosterone and estrogen and
progesterone
5. Corticotrophs – ACTH stimulates adrenal cortex to secrete glucocorticoids
MSH excess increases skin pigmentation
Parathyroid glands – secrete parathormone or PTH. It is also a Ca++ regulator that raises Ca++ levels, but much
more potent than Calcitonin. If removed from the body, Ca++ levels fall almost immediately, causing
spasmsconvulsions coma death.
Regulated: humorally
Cells of the parathyroid gland:
1. principal cells =chief cells – have granules that stain darkly – they produce PTH
2. oxyphils = resting cells clear cells, w/o granules
TC: bone – decreases osteoblast activity, increases osteoclast activity, disolves bone increases blood [Ca++]
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Kidney – prevents excretion
Intestines – increases absorption activation of Vitamin D
Pathology: Hypersecretion – Hyperparathyroidism, increased PTH levels. Signs/Symptoms (S/S): thin, brittle,
misshapen bones, kidney stones, CNS depression, soft tissue calcifications, osteitis fibrosis cystica.
Hyposecretion: Hypoparathyroidism , decreased PTH levels. S/S: increased CNS excitability muscle contractions,
spasms, twitches tetany death. This can happen in highly lactating animals
2. Neurohypophysis ( neurons – under – gland ) = posterior pituitary – nervous tissue
The posterior pituitary starts as part of the brain, then grown down, and as it grows down, the nerves grow with it.
SON, PVN. The neurohypophysis itself makes no hormones, it just stores the ones made in the hypothalamus. Their
release causes AP’s down the hypophyseal tract
The hypophyseal tract terminates in the posterior pituitary, is a storage organ for neuro hormones: ADH
(=Vasopressin), Oxytocin. Both of these are produced by the PVN and the SON. They flow down by axoplasmic flow
and are stored in the endbulbs of those axons. When release time comes, the AP causes them to be released.
ADH = Vasopressin or Vasotocin – is structurally a 9 AA long peptide chain- water soluble, needs no carrier, 2nd
messenger system, negative feedback system.
ADH causes vasoconstriction, decreases the volume, primary TC are the kidney tubules, where they cause increased
reabsorption of water and decreased urine output. Secondary TC are the blood vessels, which are constricted and BP is
increased. The stimulus for secretion of ADH is dehydration: the increase in [Na+] in the body tissues causes the release
of ADH, which reduces urine volume (conserves H2O), increases thirst (re-hydrates), increases BP (maintains BP).
Oxytocin – is almost identical to ADH, but related to reproduction. It is structurally a 9 AA long peptide chain- watersoluble, needs no carrier, 2nd messenger system, but it works in a positive feedback system, though. Its primary TC is the
pregnant uterus, in which it causes contractions. Its secondary TC are the mammary glands, where oxytocin causes milk
let down. This is also a conditioned response ( baby crying ) which results in decreased urine output, increased thirst,
and increased BP. Recent research showed that oxytocin is also present in men in the fostering or cuddling mode.
3. Adrenal Gland = suprarenal gland is actually 2 glands
1. Adrenal medulla –central portion – made of nervous tissue – ANS – sympathetic NS – is actually a modified
sympathetic postganglionic neuron – releases Epi and Norepi into the blood – these are called neurohormones:
Catecholamines – amines – modified AA”s
Structure: polar, H2O soluble, no carrier, 2nd messenger
Tyrosine
a) receptors: alpha 1 found in all except gut, beta 1 found in heart – excitatory receptors
alpha 2 found in the gut, beta 2 are found everywhere except the heart – inhibitory receptors
Neurally regulated, since there is a direct neural connection
2. Adrenal cortex – everything with “cort” in it refers to the adrenal cortex
All adrenal cortex hormones are steroid hormones: non-polar, ring structure, lipid soluble, carrier, intracellular
receptor, intrinsic effect
Has 3 different zones:
a) Zona glomerulosa – cells are arranged in balls of cells
Mineralocorticoids are produced here – control Na+ and K+
Aldosterone- regulated by kidneys, excretion or conservation
TC is kidney, makes it save Na+, K+, and H2O ( since H2O follows Na+ and there is no active transport
of H2O, and it saves Na+ (Cl-, HCO3)
Regulation 1. Humoral: K+ and Na+, inrease K, decrease Na+ ,  secretion of aldosterone
2. Hormonally: to small degree,  ACTH and ADH from Pituitary
3. Renin/angiotensin system Na+/K+  BP, increased/decrease blood volume affects BP,
heart
Pathology: Hyperaldosteronism
Aldosteronism = Conn’s Disease: edema, increased BP, altered heart function, decreased
K+, increased Na+, affects CNS, heart, muscle contractions
Hypoaldosteronism – is typically part of a syndrome – Addison’s disease
b) Zona fasciculata – cells are arranged in columns in straight lines
Glucocorticoids – Cortisol (=primary one in humans ), hydrocortisone, cortisone, corticosterone…
Cortisol – regulation is hormonal, ACTH Adenocorticotropin hormone
Primary activity is to affect carbohydrate metabolism, normal body metabolism, affects fuel source, ATP
production
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Effects: decrease glucose met., increases glucose production, burns muscle and fat  ketogenic due to
byproducts, increases blood sugar diabetogenic, burns protein deaminates AA’s ammonia is
byproduct can cause ammonia toxicity, slows healing, causes breakdown of connective tissues,
decreases inflammation. Osmoactive, it pulls water with it.
The CNS can only use glucose for energy, so this hormone protects it.
Pathologies:
Hypersecretion  Cushing’s disease: skinny arms and legs, ascites, striae, DM, slow healing rate,
CT breakdown  blood disorders, easily broken bones and torn ligaments, moon face, buffalo hump,
odd hair distribution
Hyposecretion of Cortisol AND aldosterone:  Addison’s disease: dehydrated, increased K+ and
decreased Na+ levels cause CNS problems and heart arrhythmias, low BP. Hypoglycemia, thin, muscle
weakness, pigmentation: bronze all over, pressure points and m.m. even darker.
(This pigmentation problem is due to a cross reactivity between ACTH and MSH which causes ACTH to
mimic the action of MSH when there is no cortisol  decrease in ACTH causes pigmentation.)
c) Zona reticulosa - cells are arranged in no particular pattern, go every which way
Gonadocorticoids – produce sex hormones – teststerone, DHEA, “estrogen” (minute amounts)
DHEA seems to have no effect on anything. It goes to the testicles and the ovaries, where it is the
precursor for testosterone and estrogen, respectively. It helps maintain muscle mass, influences the sex
drive. DHEA does not seem to be on a negative feedback system. It can cause acne, hair growth, and
aggressiveness.
The adrenals produce small amounts of testosterone and even smaller amounts of estrogen ( from
testosterone). Females have no other source of testosterone so it is very important for them for
regulation of sex drive, disposition.( Imagine you have 0 testosterone, and you get 1 from the adrenals,
the difference is enormous! ). Males have an other source of testosterone: the testicles. The effect of
adrenal testosterone is small. ( Imagine them having 1000 testosterones and the adrenals add 1 more )
The same goes for estrogen: males have no other source of estrogen besides the adrenals, so that
amount is very important to them. For women, the adrenal source only becomes an important factor after
a hysterectomy and post-menopausal.
Pathologies:
Hypersecretion of gonadocorticoids:
Testosterone
Estrogen
Boys: precocious puberty
feminization
Girls: virilization
precocious puberty
Men: nothing
feminization
Women:virilization
nothing
4. Pancreas
It is partially endocrine, but
a) Mostly exocrine ( duct, secretes onto surface, into a cavity, to the outside) – acinar glands
1. digestive enzymes
2. HCO3
b) pancreatic islet ( of Langerhans) – endocrine part
Has different cell types
1. alpha cells – secrete Glucagon – by structure a peptide hormone that raises blood glucose levels
TC: liver glycogenolysis and gluconeogenesis, it makes glucose from AA’s ( takes off the amine group
and converts the rest, causes increased fat utilization. Humorally regulated and by diet, hormonally by
somatostatin.
Pathologies: chronic hypoglycemia no energy, cold, sleepy, lack of concentration
2. ß-cells – secrete Insulin – by structure a protein hormone made of 2 peptides chained together. Decreases
blood sugar.
TC: liver  glycogenesis; adipose tissue  increases fat production; all cells except CNS activated
glucose carrier that enables glucose to enter the cells via facilitated diffusion.
Regulated humorally by glucose levels in the blood and diet, and hormonally by Somatostatin, digestive
enzymes, ACTH, hGH.
Pathologies: Hyposecretion: Diabetes Mellitus = copius urine- sweet. Decreased activities of carriers on
all cells glucose stays in the blood more glucose gets filtered out carriers that take sugar back in
get saturated  excess is spilled in urine. Saturation point = transport maximum. Effects: loose glucose,
can’t use glucose, and have to find alternate energy sources: fat ( causes increased ketone production
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acidic) and protein (causes muscle wasting  ammonia levels increase increased AA’s in the
blood acidic)
DM patients: acidosis causes altered CNS function, cellular problems, altered respiratory patterns.
S/S: 3 cardinal signs: polydypsia, polyuria, polyphagia. Also altered vascular function
a) Type 1 – juvenile onset – insulin dependent – caused by destruction of ß-cells – autoimmune
disease? , not heritable, rapid onset. Tx with diet and insulin
replacement.
b) Type 2 - not insulin dependent – is an insensitivity of receptors to insulin, heritable, r/t
obesity. Tx: diet, oral drugs
Acute hypoglycemia from Hyperinsulinism from incorrectly administered insulin ( IV rather than SQ)
CNS effects, sweating, anger, delirious, coma, death.
3. Delta cells – somatostatin= GHIH – inhibits the release of insulin and glucagon – paracrine secretion
4. F cells – pancreatic polypeptide – paracrine secretion regulates acinar glands.
5. Pineal gland
Part of the epithalamus of the CNS
Cells are called pinelocytes  produce melatonin – only secreted in the dark. Associated with circadian and
seasonal rhythms, it is antireproductive. Levels are highest in pre-puberty, then drop dramatically during puberty.
Levels are decreased in the eldery.
6. Thymus gland
It is partially endocrine. This gland is part of the immune system. Hormones made by the thymus are communication
factors that modify the maturation of WBC’s. All hormones produced by the thymus start with “thym”: thymic factor,
thymopoietin, thymoxin...
LAB
1. Pituitary = Hypohysis
Comes from ectoderm, is also known as the master gland.
Adenohypophysis
Secretes
TC
FSH - Follicle stimulating hormone
ovaries, testes
LH – Luteinizing hormone
ACTH – Adrenocorticotropic h.
cortex of adrenal gland
TSH – Thyroid stimulating hormone
thyroid
GH – growth hormone
muscles and long bones
PRL - Prolactin
mammary gland during lactation
MSH – Melanocyte stimulating h. (chameleon) not much in humans
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Neurohypophsis – receives hormones from hypothalamus
Secretes
TC
Oxytocin
uterine contractions
ADH – Antidiuretic h.
reduces urine volume
2. Thyroid – colloid filled cells
Secretes
T4 – Thyroxine
T3 – Odothyromine
Calcitonin
TC
metabolism and cellular oxidation
decreases blood Ca++ levels
3. Parathyroid – 4 little “dots” on posterior side of thyroid gland, chief cells produce its hormones
Secretes
TC
PTH
CaPO3 regulator
4. Adrenal gland
a) Adrenal medulla –
inside of cortex
Secretes
Epi and Norepinephrine
b) Adrenal cortex –
Secretes
Mineralocorticoids
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TC
fight or flight response
TC
regulate H2O and electrolyte balance – aldosterone
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increase blood glucose levels – cortisone, corticosterone
sex hormones – males: androgens
Females: estrogen
Glucocorticoids
Gonadocorticoids
Zones: Zona glomerulosa
Zona fasciculata
Zona reticularis ( innermost )
5. Pancreas – endocrine and exocrine function
Islets of Langerhans is where endocrine hormones are produced, alpha (glucagon), beta (insulin), and delta cells,
Endocrine
Secretes
TC
Insulin
decreases blood sugar
Glucagon
antagonist to insulin, raises blood sugar
Exocrine
Secretes
TC
Pancreatic amylase
6. Gonads
Ovaries
Secretes
Estrogen
Progesterone
Testes
Secretes
Testosterone (from interstitial cells)
7. Pineal body
Secretes
Melatonin
TC
TC
TC
inhibitory effect for early sexual development
8. Thymus – this gland is active until puberty, then it goes away. Active in immune system
Secretes
Lymphocytes: B-cells – are produced and mature in the bone marrow
T-cells – are produced in the bone marrow, then travel to the thymus where the mature, 2 types for development
POSSIBLE TEST QUESTIONS FOR TEST 1
1. COMPARE THE ROLES OF THE NERVOUS AND ENDOCRINE SYSTEMS IN CONTROLLING HOMEOSTASIS.
Both systems rely on the release of chemicals that bind to specific receptors on their TC. They share many of these
chemicals, ( epi, norepi). They both share the same goal of controlling homeostasis through coordination and regulation
of the activities of other cells., tissues, organs, and systems. Each system can inhibit or stimulate the other system.
Nervous system
Endocrine system
Effect
w/I milliseconds
seconds to hours or days
Duration
brief
longer than NS
Messengers
neurotransmitters
hormones
many are shared between systems
Cells affected
muscle, gland, neural cells
virtually all body cells
Action
muscular contraction or
changes in metabolic activities
glandular secretion
Mechanism
negative feedback primarily
negative feedback primarily
Means of transportation axons (hardwire)
blood vessels/CV system (radiowave)
2. COMPARE & CONTRAST THE MECHANISMS OF
Lipid soluble
Structure
non-polar
Transportation
carrier protein
Receptor
intracellular
forms hormone-receptor
complex that interacts w/
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ACTION OF LIPID VS. H20 SOLUBLE HORMONES.
Water soluble
polar
no carrier
extra-cellular
H. activates G-protein to make cAMP (=2nd messenger)
from ATP. cAMP then phosphorylates protein kinases,
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DNA to make new enzymes
Intrinsic effect
Slow process since hormone
is generated
which them to turn enzymes off or on.
Fast process since existing hormone is turned on or off
3. COMPARE AND CONTRAST PERMISSIVE, SYNERGISTIC, & ANTAGONISTIC HORMONE INTERACTIONS.
Synergistic interaction
The net result of 2 synergistic hormones is greater the effect either hormone would have acting alone.
Hormone A = effect of 10
Hormone B = effect of 10
You’d expect the added effect of A and B to be 20, instead it is more like an effect of 1,000. The combined effect of A
and B is much bigger than expected. Example: estrogen and luteinizing hormone for production of oocytes.
Antagonistic interaction
The net result depends on the balance between the 2 hormones. When an antagonistic hormone is present, the
observed effect will be smaller than those produced by either hormone acting unopposed.
Hormone A opposes the effect of hormone B. Example: insulin promotes synthesis of glycogen and glucagon
stimulates the breakdown of glycogen in the liver.
Permissive effect
The actions of a hormone on a TC requires recent or simultaneous exposure to a second hormone.
Hormone A must arrive before hormone B for B to have an effect. Hormone A causes the receptor for B to be built.
Example: oxytocin needs long exposure to estrogen and progesterone in order for oxytocin receptor to be present
and cause the uterus to contract.
H. acting alone
H. acting in combination
Synergistic
normal effect
> than normal effect
Antagonistic
normal effect
< than normal effect
Permissive
no effect
normal effect
4. COMPARE THE CAUSES, EFFECTS, & TREATMENTS OF TYPE 1 VS. TYPE 2 DIABETES MELLITUS
IDDM
NIDDM
Causes
destruction of ß-cells – auto-immune
insensitivity of TC receptors to insulin or ß-cell
disease?, not heritable, rapid onset.
hyposecretion of insulin; heritable, r/t obesity
typically youth or young adult
onset later in life
Effects
3 cardinal signs: polydypsia, polyuria, polyphagia.
acidosis causes altered CNS function,
cellular problems, altered resp. patterns.
& vascular function
Treatment
diet and SQ insulin replacement.
diet and oral hypoglycemic agents or insulin
5. EXPLAIN THE MECHANISM BY WHICH EFFECTS OF LOW LEVELS OF PROTEIN HORMONES ARE AMPLIFIED
Amplification is the process by which the binding of a small number of hormone molecules to membrane receptors may
lead to the release of second messengers within a cell. Imagine dominoes arranged in a pyramid. Apply a small amount
of energy (hormone) to the tip of the pyramid, and the effect is big, a chain cascade ( lots of enzymes are released)
Example: In the liver 1 molecule of epi causes the release of 100,000 molecules of glucagon.
Cyclic AMP (cAMP )system ( AMP = adenosine monophophate )
1 H2O soluble hormone comes in via blood stream, binds to its receptor at the TC. This activates a G-protein, which
acts to turn on adenylate cyclase converts ATP into cAMP
2 cAMP activates protein kinases  adds phosphates to enzymes ( phosphates all come from ATP) this activates or
inactivates enzymes  catalyzes reactions that produce physiological responses.
The cyclic AMP system is a very fast process, and it doesn’t last very long.
Hypothalamus
TRH TSH & hGH  Tri-iodothyramine and Thyroxine
GHIH = somatostatin  inhibits hGH and TSH
GHRH hGH  body growth, regulates metabolism
PRH  PRL  milk production
PIH = dopamine + TRH  inhibit PRL
CRH  ACTH  glucocorticoids and MSH  skin pigmentation
Adenohypophysis
TSH  Tri-iodothyramine and Thyroxine
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FSH sperm, oocytes, and estrogen
LH  testosterone, estrogens, ovulation, formation of corpus luteum  progesterone
PRL  milk production
ACTH  glucocorticoids
MSH  skin pigmentation
LAB
11-4-98
Spematogenesis - begins at puberty and never really ends
occurs in seminiferous tubules
spermatogonia are found in the periphery of the tubules
Under influence of FSH mitotic division produces 1 spermatogonium and 1 spermatocyte which will undergo meiosis.
Primary spermatocyte undergoes meiosis 1 to produce 2 secondary spermatocytes  meiosis 2
4 spermatids (have short tail ).
Spermiogenesis follows spermatogenesis - removes extra cytoplasm from spermatid and converts to motile form.
Sustentacular (Sertoli ) cells - nourishes spermatid
Interstitial cells - LH causes cells to produce testosterone which acts synergistically with FSH
Mature sperm
Head - contains DNA and acrosomal cap containing enzymes necessary for egg penetration
End piece - contains centriole for tail production, mitochondria for ATP
Tail - contractile protein for propulsion
Oogenesis
Oogonia in vasc. cortical tissue of ovary, about 700,000 from mitosis present at birth, encapsulated by single layer of
follicular cells and are called primordial follicles, increase in size until birth and are called primary oocytes and are at
prophase of meiosis 1.
Primary oocytes are quiet until puberty, on FSH stimulation. 1 or more follicles develop about every 24 days, first from
one ovary then from the other.
Primordial follicles epithelial cells change from squamous to cuboidal and it becomes primary follicle which begins to
produce estrogen finishes first maturation to produce 2 haploid cells of disproportionate size. One large one called
secondary oocyte and other smaller cells called polar bodies.
Polar bodies complete second maturation and produce 2 more polar bodies, which disintegrate.
2nd follicle containing secondary oocyte enlarges to Graffian vescicular follicular stage and on the 14 th day of cycle is
ovulated due to influence of estrogen and FSH and LH, secondary oocyte ovulated and finishes maturation
Spermatogenesis
Primitive stem cells = spermatogonium + FSH  1 spermatogonium + primary spermatocyte (2n)  meiosis 1 
secondary spermatocyte (2n)  meiosis 2  spermatids (n) (non-functional gametes )  spermiogenesis gets rid of
extra cytoplasm  motile sperm (n).
Oogenesis
Immature ovum w/i follice and surrounded by follicule cells or granulosa cells(=more than one layer of follicular cells)
Primitive stem cells= oogonium in ovarian cortices of developing fetusmitosis  primordial follicles primary oocytes
+ FSH at puberty  primary oocyte w/I primary follicle  meiosis 1  1 secondary oocyte and 1 first polar body. . First
polar body meiosis 2  2 more polar bodie  disintegrate…..secondary oocyte + estrogen Graafian follicle + LH
 ovulation…secondary oocyte + sperm  meiosis 2  ovum and 1 second polar body
After ovulation the ruptured follicle  corpus luteum degenerates into corpus albicans
LECTURE
11/4/98
QUIZ 3 and 4
Film
All DNA is chemically the same, but the arrangement differs.
Sperm only becomes fully mature after ejaculation. 20% of all sperm are deformed or rendered non-functional through
infection, environment, stress, smoking, chemical pollution, radiation, poor nutrition… Vagina’s acidity renders another
25% of sperm non-viable, and WBC’s destroy even more. Only 50 of 200,000,000 reach the egg!
Eyes and skin both aid in sexual arousal.
Mucin helps sperm find the uterus.
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LECTURE
11/9/98
Test 2 material Chapter 28 and 29
Chapter 28:The Reproductive System
An embryo is non-gendered until about age 5 weeks.
Gonad = middle kidney
Mesonephritic ducts – not fused on the most inferior aspect
Paramesonephritic ducts – do fuse together
What determines what sex an embryo develops into?
There are 22 autosomes and 1 sex chromosome ( xx = female, xy = male). The x chromosome is large with lots of genes
on it. The y chromosome on the other hand is small and only 2 genes have been found on it: hairy ears and the SRY
gene. This SRY gene codes for the HY antigen, this turns on at about 5 weeks of embryonic development, the protein
1. goes to the gonad and starts differentiation of the gonad into testes and produces testosterone.
2. The presence of testosterone causes the hypothalamus to become acyclic = male hypothalamus  releases
hormone at a fairly constant, low rate: GnRH
3. Testosterone also goes to the lower back muscles and causes them to develop in such a way that they can produce
the movements of copulation.
4. Testosterone causes the reproductive system to develop: the paramesonephritic duct (fused) degenerates (
therefore contributes nothing to the functional structures) and the mesonephritic duct (not fused) continues to
develop and turns into the ductus deferens. It also causes the epididymus, vas deferens, ejaculatory duct, and
seminal vesicles to develop.
5. The prostate and bulbourethral glands are endodermal outgrowths of the urethra
In the absence of the y chromosome there is no SRY gene to stimulate any testosterone production and in the absence
the SRY gene and absence of testosterone
1. the gonads develop into the ovaries
2. the hypothalamus becomes cyclic = female hypothalamus  GnRH is realeased in cycles.
3. the reproductive anatomy develops as follows: the mesonephritic duct (not fused) degenerates ( therefore
contributes nothing to the functional structures) and the paramesonephritic ducts (fused) develop into the vagina and
the uterus.
4. The greater and lesser vestibular glands develop from endodermal outgrowths of the vestibule.
The external genitalia remain undifferentiated until the 8th week. Until then both have an elevated region called the genital
tubercle, consisting of the urethral groove, paired urethral folds and paired labioscrotal swellings.
Femaleness = absence of maleness?
Homologues:
MALE
Penis
Corpora cavernosa
Corpora spongiosum
Proximal shaft of penis
Penile urethra
Bulbourethral gland
Scrotum
FEMALE
Clitoris
Erectile tissue
Vestibular bulbs
Labia minora
Vestibule
Greater vestibular glands
Labia majora
Male reproduction
Gonad = testes – descend 7th –8th month of pregnancy. Testes descend through the inguinal canal. When they descend,
they bring the peritoneum with them which forms the tunica vaginalis. They also bring the spermatic cord with them ( =
testicular artery and vein, vas deferens, and nerve). The spermatic cord is cut during castration.
Testes are outside the body cavity, because sperm is viable only if kept 3 degrees cooler than body temperature.
Every 1 degree rise in temperature decreases sperm count by 10-15%. The Pampiniform plexus is a vascular network
that controls the temperature of the testis.
Testes are surrounded by the tunica albuginea which divides the testes into lobules through septa. Each lobule contains
several seminiferous tubules. Where all these seminiferous tubules come together is the rete testes. This leads to the
vas deferens.
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Dartos muscle = smooth muscle in scrotum causes the puckered look.
Cremaster muscle is skeletal muscle in the scrotum. It is under somewhat voluntary control, and contracts during
sexual activity and excitement.
Spermatogenesis is the production of sperm. It consists of
1. Meiosis
2. Spermiogenesis
Spermatogenesis begins with cells from the yolk sac ( future gut ) that look like body cells (2n). They are called germ
cells or stem cells. There are 2 types of spermatogonia:
Spermatogonia A – these make more spermatogonia by mitosis
Spermatogonia B – make sperm
A cross-section of a seminiferous tubule looks like a life preserver. On the outer edge of it, spermatogonia are lined up all
around it. Some are type A, which means they stay on this outside edge and make more spermatogonia, so mitosis takes
place here. Some of the spermatogonia are type B and they move toward the center of the seminiferous tubule. They
enter meiosis and as soon as they do, they are called primary spermatocytes. They are diploid cells at this stage and
enter into Prophase 1 ( remember that this phase is short in males but up to 40 years in females). The DNA doubles,
there are 23 pairs of chromosomes x 2 copies of each. Next comes tetrad formation  chiasma  genetic recombination
and meiosis 1 continues  2 haploid cells = 2 copies of 1n cells. These are called secondary spermatocytes. If
allowed, these secondary spermatocytes will be destroyed by the body’s immune system, because they are different than
regular body cells ( haploid vs diploid ). Next, these secondary spermatocytes enter meiosis 2. They undergo equatorial
division of the cytoplasm the resulting 4 cells are 1n and and connected with each other. Next comes
spermiogenesis the cells are now spermatids. They are round cells that 1. Loose their cytoplasm, 2. Develop a tail
(9+2 structure of flagella), 3. Develop an acrosomal cap. The spermatids leave through the lumen of the seminiferous
tubule ( inner hole in the life preserver)
The sustenacular or Sertoli or Nurse cells are large cells that feed the sperm, and protect them from the body’s own
defenses. Since spermatocytes are haploid, the body sees them as foreign material and tries to destroy them. They also
transport spermatcytes to the epididymus.
Sustenacular cells:
1. feed spermatocytes
2. protect them from man’s immune system by forming tight junctions: the blood-testes-barrier. WBC’s can’t get into the
seminiferous tubules.
3. Move the spermatocytes around, to the epididymus
4. Connect to 100-150 sperm.
Interstitial cells or cells of Leydig are between seminiferous tubules. They are the endocrine portion of the testes that
produce testosterone.
Structure of sperm
1. Acrosome – cap on the end – contains enzyme (hyaluronidase) and enzyme inhibitors. Sperm is not fertile right after
ejaculation, it has to mature first in a process called capacitation. During this time the inhibitors wear off.
2. Head – full of densely packed chromatin
3. Midpiece – a. rows of mitochondria for ATP production
b. fructose – primary energy source
4. Tail – only flagellum in human body.
Regulation of the male development
1. acyclic hypothalamus  Pituitary  gonadotrophs  gonadotropins: LH ( = ICSH) } to testis for
FSH
} sperm production
GnRH  release of LH and FSH ( constant low amounts of all 3)
FSH  testes  stimulates sustenacular cells  produce androgen(=male) binding protein ABP
LH  to interstitial cells to produce testosterone.
The testosterone binds to the ABP and causes the seminiferous tubules to produce sperm. No LH or FSH = no sperm.
Testosterone effects:
Secondary sex characteristics: facial hair, body hair, deep voice, muscle development, growth, development of
reproductive organs.
It is on negative feedback: testosterone is converted to estrogen by aromatase before it gets to the brain. Estrogen in
turn inhibits GnRH.
Obesity decreases reproduction. This seems to be hormonally linked. High levels of aromatase use testosterone and
convert it to estrogen ( neg. feedback ). Aromatase levels are high in obese people ( animals ) and so testosterone gets
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converted into estrogen (  low testosterone = loss of some secondary sex characteristics in obese males, high
estrogen further fat deposits )
Sustenacular cells produce Inhibin which works in a negative feedback loop to inhibit GnRH.
Quiz 4
Case study -
Female reproduction
Most parts are internal, suspended by ligaments.
The ovary is the female gonad. It develops due to a lack of testosterone. Primordial follicles (=sac) contain oogonia, and
unlike in the male there is a limited number of them: ca. 500,000. In a woman’s lifetime, only about 500 are “used”.
Oogonium (2n) becomes primary oocyte as soon as it enters meiosis/prophase 1. Everything up to this point occurs
during fetal development and is stuck here in suspended animation until puberty. At puberty, meiosis causes the division
of the primary oocyte  1 secondary oocyte + 1 polar body ( attached right to the oocyte ). This secondary oocyte is
ovulated. If fertilized, it goes on to meiosis 2 which yields 1 ovum and 2 more polar bodies. Fertilization has to occur in
the fallopian tube, because the ovum is only viable for 24 hours, and the trip through the tube takes it about 5 days.
Sperm lives for about 48 hours, just about the time it takes it to travel up the uterus and up the tube.
Ovarian cycle
Uterine cycle
LECTURE
11/11/98
Test 1 results: 3 A’s, 4 B’s, 4 C’s, 1 F. Highest grade 114, second highest 100 points out of 120 possible.
GnRh is produced in the hypothalmus. It is influenced by other hormones via negative and positive feedback.
negative feedback provided by - rising estrogen levels
estrogen PLUS progesterone ( very powerful )
positive feedback through – “ high” levels of estrogen
LH (from adenohypophysis)- causes production of estrogen by follicle. Once the follicle is ruptured LH makes it
luteinize (=turn yellow) and it becomes the corpus luteum which produces estrogen and progesterone.
FSH (from adenohypophysis) – causes follicle to grow and develop.
Estrogen is a steroid, causes:1.secondary sex characterisitics in females: hips, breasts, fat deposition, skin, deeper
voice.
2. uterus: perimetrium
myometrium
endometrium: stratum basalis – not affected by estrogen
Stratum functionalis – estrogen makes it grow: thicken and
develop spiral arteries
Progesterone is also a steroid, and is produced by the corpus luteum. It causes the stratum functionalis to become even
thicker and secretory ( mucus layers)
The ovarian/uterine cycle is an average of 28 days long, but can range from 25-35 days.
Day 0-5 – no estrogen or progesterone are produced. The uerus looses its support and the stratum functionalis sloughs
off because no estrogen and progesterone stops the negative feedback on GnRH  GnRH will be secreted
Adenohypophysis secretes LH and FSH
FSH causes 7-10 follicles to start growing and turn into primary follicles ( the rest remain primordial follicles ).
LH enables the follicles to secrete estrogen  est. makes menses stops and stratum functionalis grow  Rising levels
of estrogen cause neg. feedback on GnRH  GnRH levels drop most of the 7-10 primary follicles become atritic but
1 primary follicle survives and becomes a secondary follicle that secretes estrogen. The levels of estrogen now become
“high” and negative feedback switches to positive feedback on GnRH (day12). This surge of GnRH causes an increase
in LH and FSH which peaks at day 14 and causes  ovulation. (The uterus/stratum functionalis is still growing at this
time). At ovulation the follicle ruptures and  estrogen levels dip low enough to cause negative feedback to take over
control of GnRH so GnRH levels drop  LH and FSH levels drop. The ruptured follicle luteinizes under influence of LH
and it becomes the corpus luteum secretes estrogen and progesterone. Progesterone causes uterus to become
thicker and secretory. Estrogen plus progesterone exert strong negative feedback on GnRH and without GnRH there is
no more LH or FSH. The life span of the corpus luteum is limited and on day 27 it dies and turns into corpus albicans
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which is scar tissue estrogen and progesterone production ceases and without their influence, the uterus sloughs off
and on day 0 menses begins and the cycle starts over.
Ovarian cycle:
1. follicular phase – day 1-14
2. ovulation – day 14
3. luteal phase – day 15-27 or as long as corpus luteum is around
Uterine cycle:
1. menstruation – day 0-4
2. proliferative phase – day 4-14
3. secretory phase – day 15-28
Inhibin – produced by the corpus luteum
Primarily decreases FSH levels, but also LH
Relaxin – has no effect during the normal cycle
Increased levels in pregnancy
It causes smooth muscle of uterus to relax (quiescience )
It relaxes ligaments, the cervix, and the pubic symphysis
Birth control
1. Contraception – anything that prevents fertilization: barriers, sponges, condoms, spermicidals, hormones (gossipol
is a new hormone not on the market yet: it is for men to prevent spermiogenesis.)
2. Non-contraception methods – prevent implantation: RU486 (blocks progesterone receptors ), abortion, IUD ( device
just floats around in uterus, earliest one was palmdate nut ), morning after pill ( works for up to
72 hours after fertilization but before implantation on day 6 )
Development
Chapter 29
Ovulation causes the release of a secondary oocyte which may or may not be fertilized. If sperm are around, the corona
radiata surrounding the zona pellucida is a barrier they have to break. Sperm have an acrosomal cap containing
enzymes necessary for egg penetration. The enzyme is hyaluronidase. It takes many sperms’ combined hyaluronidase
to dissolve the connection between the cells of the corona radiata. As soon as 1 sperm makes it to the zona pellucia,
its tail breaks off, and a cortical reaction changes the membrane such that no more sperm can penetrate it. Only at this
point does the secondary oocyte begin meiosis 2 and it becomes an ovum.
Since the oocyte is only viable for 24 hours and sperm for 48-72 hours, conception has to take place in a narrow window
of about 3 –4 days around ovulation. The trip through the fallopian tubes takes the ovum about 5 days, so fertilization
most commonly occurs in the ampulla of the fallopian tube.
An ectopic pregnancy is any pregnancy outside of the uterus.
Early division of the fertilized ovum is called cleavage = mitosis without growth ( usually you have growth followed by
division )
The 16-32 cell stage is called morula.
At 5 days, when the egg has arrived at the uterus, it is a blastocyst = hollow ball. The blastocyst is made up of the
trophoblast and inner cell mass(=embryoblast), and an internal, hollow cavity called the blastocele. The trophoblast
and part of the inner cell mass form the membranes composing the fetal portion of the placenta, the rest of the inner cell
mass develops into the embryo.
The blastocyst “tastes” the uterine wall to see if it is ready for implantation, if it isn’t the blastocyst just tumbles down a
little further in the uterus and the check the walls’ readiness again. When it is ready, the blastocyst digests its way into
the wall of the uterus, which actually causes some inflammation and swelling and the blastocyst becomes buried in the
wall. Implantation is complete 7-12 days after fertilization (day26). At this time the trophoblast secretes HCG (human
chorionic gonadotropin) which is very similar to LH. It prevents the corpus luteum from dying and sustains its secretion of
estrogen and progesterone the walls of the uterus will be maintained.
After implantation, during the embryonic period (first 2 months), the inner cell mass of the blastocyst develops into the 3
primary germ layers: the ectoderm, the mesoderm, and the endoderm. The process by which the 2 layered inner cell
mass is converted into a structure made of the above 3 layers is called gastrulation.
Next, the embryonic (extraembryonic) membranes form: they lie outside the the embryo and protect and nourish it and
later also the fetus. These embryionic membranes are the
1. Yolk sac
2. Amnion
3. Chorion
4. Allantois
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The yolk sac is reduced in placental animals.It functions as an early site of blood formation, and contains cells that
migrate into the gonads and differentiate into primitive germ cells (spermatogonia and oogonia )
The amnion surrounds the fetus itself. It becomes filled with amniotic fluid.
The chorion surrounds the embryo and later the fetus. Later, it becomes the principle embryonic part of the placenta.
The amnion fuses to the inner layer of the chorion. a. placenta
b. chorionic villi
c. wall of the uterus
The allantois is also reduced in placental animals. It becomes part of the urinary bladder ( stores waste products in nonplacental animals ) and serves as an early site of blood formation. Later, its blood vessels serve as the umbilical
connection in the placenta between mother and fetus.
POSSIBLE TEST QUESTIONS FOR TEST 2
1. Compare and contrast the processes of spermatogenesis and oogenesis.
Spermatogenesis
Primitive stem cells = spermatogonium + FSH mitosis  1 spermatogonium + primary spermatocyte (2n)  meiosis 1
 secondary spermatocyte (2n)  meiosis 2  spermatids (n) (non-functional gametes )  spermiogenesis gets rid of
extra cytoplasm  motile sperm (n).
Spermatogenesis is the production of sperm. It consists of
3. Meiosis
4. Spermiogenesis
Spermatogenesis begins with cells from the yolk sac ( future gut ) that look like body cells (2n). They are called germ
cells or stem cells. There are 2 types of spermatogonia:
Spermatogonia A – these make more spermatogonia by mitosis
Spermatogonia B – make sperm
A cross-section of a seminiferous tubule looks like a life preserver. On the outer edge of it, spermatogonia (primitive stem
cells ) are lined up all around it. Some are type A, which means they stay on this outside edge and make more
spermatogoniathrough mitosis. Some of the spermatogonia are type B and they move toward the center of the
seminiferous tubule. They enter meiosis  primary spermatocytes (2n)  Prophase 1 (short in males but up to 40 years
in females). DNA doubles, there are 23 pairs of chromosomes x 2 copies of each tetrad formation  chiasma 
genetic recombination  meiosis 1  2 copies of 1n cells: secondary spermatocytes meiosis 2 equatorial division of
the cytoplasm 4 1n cells (connected with each other)spermiogenesis (differentiation) the cells are now mature
spermatids or spermatozoa. They are round cells that 1. Loose their cytoplasm, 2. Develop a tail (9+2 structure of
flagella), 3. Develop an acrosomal cap. The spermatids loose their attachment to the Sustenacular cells at spermiation
and leave through the lumen of the seminiferous tubule ( inner hole in the life preserver). The whole process from
spermatogonial division to spermiation takes 9 weeks.
Spermatogenesis
FSH + Primitive germ cellsmitosis 2 primitive germ cells  some continue mitosis,
Some primitive germ cells  meiosis primary spermatocytes (2n)  Prophase 1: tetrad formation, chiasma, genetic
recombination  secondary spermatocytes (2x1n)  meiosis 2  4x1n= spermatozoa or spermatids  spermiogenesis
(physical maturation) = loose attachment to sustenacular cells and enter lumen of seminiferous tubules = spermiation of
mature but immobile spermatozoa. Spermatozoa are stored in the epididymus where they mature functionally in a
process called capacitation =( mixing with with secretiions of seminal vescicles + exposure to conditions inside the
female reproductive tract )
Oogenesis
Immature ovum w/i follice and surrounded by follicular cells or granulosa cells. Primitive stem cells= oogonium in ovarian
cortices of developing fetusmitosis  primordial follicles primary oocytes + FSH at puberty prohase 1 primary
oocyte w/I primary follicle  meiosis 1  1 secondary oocyte + 1 polar body. secondary oocyte + estrogen Graafian
follicle + LH  ovulation…secondary oocyte + sperm  meiosis 2  ovum (+2 polar bodies disintegrate ) ovum  cell
division embryo
After ovulation the ruptured follicle  corpus luteum degenerates into corpus albicans
2. Graph and describe the hormonal changes that occur during a normal menstrual cycle.
At the beginning (day 0) of the menstrual cycle all hormone levels are low. Low levels of GnRH are released, and it
stimulates FSH and LH. FSH will stimulate follicular development over the next 14 days, and the LH stimulates estrogen
production by the follicle. Estrogen levels subsequently rise and this causes neg. feedback on GnRH.
In turn FSH and LH also rise. When levels of estrogen become “high”, it exerts positive feedback on GnRH and in turn on
LH (great effect) and FSH (some effect). The LH surge causes rupture of the fully mature secondary oocyte from the
Graffian follicle. After this happens, LH luteinizes the corpus hemorrhagicum and it becomes the corpus luteum. The C.L.
under influence of LH, secretes Progesterone ( levels now rise ) and some estrogen – not as much as the developing
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follicle (levels are falling). The life span of the corpus luteum is limited and it begins to degenerate into the corpus
albicans less than 2 weeks after ovulation. Progesterone and estrogen levels drop off and GnRH is once again
stimulated and the cycle starts again.
Progesterone
Menses 0-4
Proliferative 4-14
destruction of functionalis
repair/regeneration
Ovulation
Luteal Phase 15-28
Graffian follicle
UTERINE
seretory phase
Follicular Phase 1-14
follicle develops
Secretory phase 15-28
Ovulation
OVARIAN
corpus luteum  matures  corpus albicans
3. Describe the secondary sex characteristics of males and females.
Estrogen causes:1.secondary sex characterisitics in females: hips, breasts, fat deposition, skin, deeper voice.
2. uterus: perimetrium
myometrium
endometrium: Stratum basalis – not affected by estrogen
Stratum functionalis – estrogen makes it grow: thicken and
develop spiral arteries
Testosterone effects:
Secondary sex characteristics: facial hair, body hair, deep voice, muscle development, growth, development of
reproductive organs.
It is on negative feedback: testosterone is converted to estrogen by aromatase before it gets to the brain.
Estrogen in turn inhibits GnRH.
4. Name and describe the roles of the hormones involved in pregnancy.
Progesterone and Estrogen – low levels from Corpus luteum for first 3-4 months, after that the placenta produces
high levels to maintain pregnancy and prepare mammary glands, and prepare the mother’s body for delivery.
HCG – human chorionic gonadotropin – mimics LH: it prevents the corpus luteum from degenerating and stimulates
it into continuing the production of E. and P. which is necessary to allow for implantation into the uterus. HCH can be
detected by the 8th day after fertilization, and levels peak around the 9th week. It decreases after the 4th and 5th month
and levels off until childbirth.
Relaxin - It causes smooth muscle of uterus to relax (quiescience ), relaxes ligaments, the cervix, and the pubic
symphysis, and helps dilate the cervix.
HCS – Human chorionic somatomammotropin – helps prepare mammary glands for lactation, enhances growth by
increasing protein synthesis, decreases glucose use and increases fatty acid use by the mother for ATP production.
All these hormones come from the placenta, the chorion being the first part to produce E. and P.
5. Identify the embryonic/fetal membranes, and describe the location and functions of each.
they lie outside the the embryo and protect and nourish it and later also the fetus. The embryonic membranes are the
1. Yolk sac
2. Amnion
3. Chorion
4. Allantois
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The yolk sac is reduced in placental animals.It functions as an early site of blood formation, and contains cells that
migrate into the gonads and differentiate into primitive germ cells (spermatogonia and oogonia )
The amnion surrounds the fetus itself. It becomes the amniotic sac that is filled with amniotic fluid.
The chorion surrounds the embryo and later the fetus. Later, it becomes the principle embryonic part of the
placenta. The amnion fuses to the inner layer of the chorion. a. placenta
b. chorionic villi
c. wall of the uterus
The allantois is also reduced in placental animals. It becomes part of the urinary bladder ( stores waste products in
non-placental animals ) and serves as an early site of blood formation. Later, its blood vessels serve as the umbilical
connection in the placenta between mother and fetus.
TEST 3 MATERIAL
LECTURE
11/16/98
FILM
The Living Body: 2 hearts beating as one.
If man were to “recreate’ the human body, he would have to build 2 pumps to do what the heart accomplishes. The
human heart beats about 3 billion times during an average life.
An athletes’ heart can be up to 30% larger and eject about 30% more blood than a non-athlete. This makes it more
efficient and the heart can pump at a slower rate.
Coronary arteries supply the heart muscle itself first, then the rest of the body.
THE HEART
Covered by the pericardium, it consists of 2 layers, 1 thick parietal one, and the visceral, outermost layer.
The myocardium is the thick cardiac muscle tissue of the heart
The endocardium is squamous epithelium and is continuous with the endothelium.
Atria are the receiving chambers, ventricles are the pumping chambers.
Fish have a 4 chambered heart, but the chambers are all in a row.
Amphibians – the 2 systems mix, and the blood does not get very oxygenated.
Reptiles – 3 chambered heart with an incomplete septum, some, but not as much mixing of blood, more oxygenated.
Mammals and birds – completely separate ventricles.
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Separate circulatory systems:
1. Pulmonary circulatory system
2. Systemic circulation
3. coronary circulation
There are 2 receiving chambers: L and R atria, which are extremely thin walled, sit on top of the ventricles, which they
empty into, and have gravity’s assistance. Most of the emptying occurs before the atria ever contract – except when you
are standing on your head.
Valves in the heart prevent back flow. The atrioventricular valves or AV valves sit between the atria and the ventricles
Left: Bicuspid or Mitral valve ( it looks like a bishop’s miter hat)
Right: Tricuspid valve
They are made of collagen, fibrous connective tissue, tough but very flexible. It can loose its’ flexibility in which case it
develops stenosis (leaks).
The L and the R Ventricles are the pumping chambers of the heart. Their walls are much thicker. They have ridges
called trabeculae carnae in them that trap blood and force it forward and increase the contractile force.
The R ventricle leads into the pulmonary circulation, which is not a very far from the heart. The blood does not have to
flow against gravity, since the lungs are at about the same height as the heart. The lungs also don’t offer much
resistance since they are filled with only air. The maximum pressure in the right ventricle is about 40-45mmHg.
The L ventricle on the other hand, leads into the circulation. It has to go against gravity and quite a distance, too. The
left ventricle is therefore a high-pressure pump with very thick walls in comparison to the right ventricle. The pressure in
the left ventricle can exceed 120mmHg.
Both ventricles pump into large arteries. The R ventricle pumps blood into the pulmonary trunk through the
pulmonary semilunar valve. The L ventricle pumps blood through the aortic semilunar valve into the aorta (largest in
the body). The valves have strings attached to them called chordae tendinae (DRCT) and then papillary (=finger)
muscles . The papillary muscle contracts at the same time the ventricle does, it does not open the valve, but prevents
regurgitation.
The vessels that drain into the R atrium are the superior and inferior vena cava. There are no valves between the vena
cava and the ventricle.
Draining into the L atrium are the 4 pulmonary veins: 2 from the right and 2 from the left lung. Again, there are no
valves. Page 587
The coronary or cardiac circulatory system
2 coronary arteries branch off from the aorta. The heart feeds itself before it feeds anything else.
The L coronary artery branches into the
1. Anterior interventricular coronary artery – feeds mostly the left but also some of the right ventricle.
Corresponding vein – Great cardiac vein
2. Circumflex coronary artery – feeds the atria and sides of the ventricles
The R coronary artery branches into the
1. Marginal artery – feeds the right ventricle
Corresponding vein – Small coronary vein
2. Posterior interventricular
Corresponding vein – Middle coronary vein
The coronary veins all drain into the coronary sinus, which the drains into the R atrium. Page 588
Cardiac muscle cells
Striated, sarcomeres, less developed SR, T tubules. Cells are shorter, branched, thicker. Single nucleus, maybe 2. Gap
junctions – ions move freely from one to the other (Na+). Intercalated discs. Cells are highly communicative, with
functional sensitium (big cell)
Cardiac muscle is involuntary muscle because it does not have a resting potential (-90mV), BUT: cells are leaky to Na+
much more than skeletal muscle, so it moves towards threshhold  AP muscle contraction
Cardiac muscle has automaticity – it is involuntary, goes through AP’s  contractions without any signals from neurons.
It also has rhythmicity because Na+ leaks at a constant rate producing a regular rate of AP’s, but every cell of the heart
has its own rhythm. However, since all cells are linked together the fastest cells takes the slower ones with it.
Contraction of the heart is called systole, relaxation or no contraction is called diastole.
Conduction system
Specialized cells that spread AP’s much more rapidly are called pacemaker cells ( P cells ). The sinoatrial node or SA
node is located at the base of the superior vena cava, at the base of the right atrium. It is the fastest with a depolarization
rate of 100 beats/min, if left to its own devices. The other fibers pick up its rhythm.
The next fastest node is the AV node – it is much slower at only 40-50 beats/min. This rate wouldn’t allow for much more
than sitting or lying around. The AV node receives an AP from the sinoatrial node and passes it along.
Next comes the AV bundle (formerly “bundle of His”) attached to the AV node, it crosses between the atrium and the
ventricle with junctional fibers. Its depolarization rate of 20-40beats/min is not enough to sustain life.
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Then there are the R and L bundle branches that go to the apex of the heart. They have a depolarization rate of
6-10 beats/min.
Lastly there are the Purkinje fibers, which are conduction fibers that conduct the AP’s to the individual cells of the
ventricles and the papillary muscle.
Muscle cells have their own intrinsic depolarization rate of 2 beats/min (BPM).
Heart block represents a problem with the junctional fibers.
Skeletal muscle releases Ca++ when an AP comes in and that causes a contraction. There is an absolute and relative
refractory period during which no AP is possible, no matter how hard the stimulus.
With cardiac muscle, the refractory period is longer ( up to 250msec instead of 2 or 3 ) than the contractory period.
It is impossible to tetanize the heart because of that difference and that is good because if it became tetanized, the heart
would not be able to fill since there would not be any relaxation.
A normal cardiac cycle takes about 0.8seconds (at a HR of 70 BPM). Each cycle consists of a contraction and relaxation.
An ECG measures AP’s as a graph on paper that is running at a certain speed.
The P wave shows atrial depolarization – ca. .1sec long. If longer, it can mean atrial enlargement or stenosis.
The QRS complex shows ventricular depolarization and atrial repolarization (hidden).
The T wave represents ventricular repolarization.
The height of the peaks, the intervals between the peaks, and the amount of area under the peaks all can be interpreted
into how the heart is performing.
The PR or PQ interval = .1sec – represents the conduction time from the beginning of atrial excitation to the beginning of
ventricular excitation. If this interval is longer, it indicates scarring or damage to the AV nodes, because the impulse has
to travel around the scar tissues.
The QT interval extends from the start of the QRS complex to the end of the T wave. It is the time form beginning of
ventricular depolarization to the end of repolarization. A prolonged QT interval can mean myocardial damage, coronary
ischemia, or conduction abnormalities.
If the Q wave is deeper or wider, it can indicate an MI.
If there is an additional U wave, electrolyte or medication problems are present or PVC’s ( =separate depolarization by
the Perkinje fibers)
Uncoupling is a rare condition caused by Ca++ problems – Ca++ is not released by the SR. The patient will have a
perfectly normal ECG, but his hear is not contracting!
Page 595
During the quiescient period (0.4sec) nothing is happening, atria and ventricles are relaxed. The atria are filling through
passive filling due to the pressure difference.
P wave (0.1sec) shows atrial contraction/systole, which is active filling. The QRS complex (0.3sec) represents ventricular
depolarization and atrial repolarization.  ventricular contraction/systole and also atrial diastole. The AV valves slam
shut when the ventricles relax and blood flows back from the pulmonary trunk and the aorta against them and that slam
is the 1st heart sound, S1 (lub) (dicrotic notch after T wave on ECG).
Ventricular filling starts when ventricular pressure drops below atrial pressure, the AV valves open and blood from the
atria rushes in. Atrial systole occurs after the P wave and accounts for only the last 20-25ml that fill the ventricle. At the
end of ventricular diastole there are about 130ml in each ventricle = EDV
Ventricular systole has to raise the pressure in the R ventricle above that of the pulmonary trunk (15-20mmHg) and in
the L ventricle higher than aortic pressure(> 80mmHg) before the semilunar valves open and ventricular ejection
begins. After that the ventricles relax , the semilunar valves close and another quiescient period begins. The closing of
the semilunar valves is what creates the 2nd heart sound, S2 (dub). The blood volume left in the ventricles after systole is
called the ESV, about 60ml. The volume of blood ejected from the ventricles per beat is called stroke volume, ca. 70ml
The T wave represents ventricular diastole.
When the ventricles contract, not all the blood gets ejected. The body has to keep a reserve for times of increased need
like exercise. Exercise shortens the quiescience period.
There are 2 more heart sounds that are not loud enough to be heard normally. S3 is associated with rapid ventricular
filling and S4 with atrial contraction.
Cardiac output is the amount of blood ejected from a ventricle in 1 minute.
Stroke volume is the amount of blood ejected from a ventricle with 1 beat.
Cardiac Output (CO in ml/min) =HR (BPM) x SV (ml/beat)
For the average person this comes to about 5 liters per minute, that means that every drop of blood in your body is
circulated through the entire pulmonary and systemic circulation every minute.
In a well trained athlete, cardiac output can be as high as 35l/min!
CO=HRxSV
HR can vary from 70 –200 BPM.
Factors that influence HR
1. Venous return – the muscle contraction forces the blood back to the heart it stretches the heart walls SA node
 increases the amount of Na++ leaking  causes faster depolarization.
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2. Autonomic ( Parasympathetic and Sympathetic ) Nervous System
a) parasympathetic NS controls the SA node only by means of the Vagus nerve ACH is released and the HR
slows down (brake system)
b) sympathetic NS controls the SA and the AV node and the heart fibers this increases the depolarization rate
 HR goes up by shortening the quiescient period, makes the heart more sensitive. (accelerator)
If you cut the vagus nerve, the HR goes up, if you cut the sympathetic components, the HR slows down.
HR is also dependent on the body’s temperature and hormones.
QUIZ 5 – (8)
What happens to the HR when you cut both the vagus nerve and the sympathetic components?
HR will be controlled by only venous return = SA node, the rate would go to 100BPM.
Preload is the stretch of the heart before it contracts.
Contractility is the forcefulness of contraction of individual ventricular muscle fibers.
Afterload is the pressure that must be exceeded before ejection of blood from the ventricles can begin.
Preload : Effect of stretching: Frank-Starling law: the more the heart is filled during diastole, the greater the force of
contraction during diastole. Preload = EDV
Ca++  uncovers binding sites in muscle more Ca++ increases contractility = iontropic effect.
The sympathetic component at the individual fibers increases the amount of Ca++ released and thereby increases
contractility.
CO=HRxSV
Stroke volume = end diastolic volume – end systolic volume  SV = EDV-ESV
Therefore CO = HR x (EDV-ESV)
CO= speed x (preload –contractility)
Fetal Heart
There is no sense in sending all the blood of a fetus to the lungs if the O2 comes from the placenta. The foramen ovale
allows for blood in the R ventricle to go to the left ventricle and from there out to the body. There is also another shunt
between the aorta and the pulmonary veins: the ductus arteriosus.
At birth, when fluid is expelled from the infant’s lungs and they are filled with air, more blood automatically goes to the
lungs because the resisitance is all of a sudden lower. Also, there a 2 muscle spasms occurring at/around birth. The
musculature of the foramen ovale goes into spasm and seals it off, it becomes the fossa ovalis. The ductus arteriosus
also goes through a spasm and it closes, becoming the ligamentum arteriosus. Page 601.
LECTURE
11/18/98
The circulatory system consists of arteries, arterioles, veins, venules, and capillaries. It forms a circle that starts and
ends at the heart. Most blood stays contained within the blood vessels, and only a small amount leaves blood through
sinusoids: in the liver, penis, clitoris, and in the brain. Blood vessels grow. No cell in the body is more than 2 or 3 cells
away from blood supply.
On cross section an artery and a vain compare as follows
Artery
Vein
3 walled vessel
3 walled vessel
smaller lumer
larger lumen
Tunica externa or Tunica adventicia surrounds it: DICT with lots of elastin: it is stretchy, strong, has recoil.
Tunica media – smooth muscle, allows for vasoconstriction/dilatation:
Thick layer
thin layer
Subendothelial: aereolar
} base
Loose connection }
Tunica interna or Tunica intima or Endothelium – SiSqEpi, solid internal coating throughout endocardium in heart,
slick surface prevents blood from clotting. It is the only layer in capillaries.
Arteries
Large: Elastic or conducting arteries – have lots of elastin in their walls, have lots of recoil to expand/contract. Their
walls bulge and come back in like a balloon with every heartbeat. It dampens the highs and lows of BP ( keeps the MAP
=, ??)This also helps to provide a continues flow of blood to the organs instead of a burst and then no blood, burst, …
Example: Aorta, subclavians, common iliacs.
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Medium : Muscular arteries – are distributing arteries, intermediate in size, these have much less elastin, but a lot of
smooth muscle to allow for vasoconstriction/dilatation. These vessels allow adjustment of blood flow to where it is
needed. Example: Brachial, tibial
Arterioles are on one end connected to an artery, on the other to a capillary bed. They change during their length and
will look like what they are closest to: when close to an artery they look like an artery, on the other side when they are
close to a capillary, they look like a capillary. They are almost microscopic in size, have lots of smooth muscle: compared
to their size, they have more smooth muscle than any other artery. The tunica externa is absent here. Arterioles are
primarily for vasoconstriction/dilatation but not for the purpose of changing distribution, but to affect BP.
Capillaries tend to occur in beds. At their opening they have a metarteriole that branches into the bed of the capillary.
They have one vessel that goes straight through the entire bed, the thoroughfare vessel. The precapillary sphincter is a
circulatory muscle that allows/prevents blood passing through the capillary bed. Capillaries consist of a single layer of
endothelium without muscle. They are very thin walled vessels that are the most important physiologically: gas exchange,
nutrient and waste product exchange by means of diffusion takes place here ( no active transport).
There are different types of capillaries, depending on location in the body. The types are dependent on how the cells
are connected to each other:
1. Continuous capillaries are connected end to end without breaks in their walls. Example: all tissues except
eptihelia and cartilage
2. Fenestrated capillaries have holes in them. Example: kidney, brain, some endocrine organs
3. Sinusoids allow blood to leak through large holes. Example: liver, BM, adrenal glands
4. True capillaries- sometimes another category referred to in textbooks.
Veins are also 3 walled, but their walls are different in thickness compared to the arteries. Veins are the largest, then
come venules.
Tunica externa is a great deal thicker in veins to allow for expansion. The tunica externa is absent in venules.
The tunica media is thinner, it doesn’t have a whole lot of muscle which decreases their ability to vasoconstrict/dilate.
The tunica interna folds in flaps that form pocket valves to prevent backflow of blood. When these valves get “blown out”
(after leaky valves have weakened them ) the result are varicose veins. Hemorrhoids are an example of varicose veins,
they prevail in women. One treatment involves injections with botulism bacteria that kills off the affected vein and allows
for regrowth.
Arteries are pressure reservoirs since they store the pressure from the ventricle’s systole, and they go back in when the
ventricle is in diastole. Veins, on the other hand, are called the volume reservoir. 60% of the blood are stored in veins
and venules. (8% in the heart, 15% in the arteries and arterioles, 5% in the capillaries, and 12% in the pulmonary
vessels). Page 617. Veins generally flow against gravity. The pressure inside them is negligible (+/- 0). Veins are
embedded in skeletal muscle. There are 2 pumps that help circulate the blood in veins:
1. Skeletal muscle pump forces the blood along inside veins
2. Respiratory pump pulls blood into the heart: when the diaphragm contracts it brings blood into the chest cavity by
means of negative pressure. This allows for an increased blood return to the heart, esp. during exercise.
If someone is not contracting their skeletal muscles for a long time, like a soldier standing at attention/guard, the blood
will pool and the person may faint.
When a limb falls asleep it is caused by ischemia in that extremity: when the blood supply is cut off to tissues and nerves
and then resumed all the blood coming in causes “weird” AP’s ( overload on the nerves?) to cause tingling.
Be able to recognize the major arteries: picture 21.18 and 21.23.
Film:
The heart beats about 100,000 times and pumps about 1835 gallons of blood a day.
When capillaries on the arterial side are blocked, it causes ischemia. When capillaries on the venous side are blocked, it
causes swelling.
In arterial obstructions atherosclerosis is most common. It begins with damage to the lining of the vessel caused by
smoking, high BP, cholesterol. In venous obstructions thrombophlebitis is most common. It begins just like
atherosclerosis, but is caused by mechanical, chemical, thermal or other agents.
Cholesterol is synthesized from unsaturated fats in the liver.
Bloodflow is like a river: in a wide, unobstructed river, flow is laminar, which means water flows in sheets, and it is
fastest in the middle because closest to the edge there is friction against the walls and that causes resistance. Velocity
is fastest in the largest vessels ( increased vessel diameter  increased velocity ). In the aorta, blood flow is the fasted
in the body, ca. 40cm/sec. In capillaries, is much slower, almost imperceptible.
As TOTAL ( all diameters of one kind of vessel) cross-sectional diameter decreases, the speed increases.
Therefore, in capillaries the velocity is slower than in the aorta: the crossectional diameter in the 1 aorta in the body is
smaller than all the diameters of all the capillaries added together, and flow is faster in the aorta.
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Flow = Q, length of vessel= L, radius= r, viscocity = N, initial pressure = P 1, final pressure = P2
Q= (P1-P2) r4 / 8 LN
Increasing P1  increases Q
Increasing P2  decreases Q
Increasing L  decreases Q
Increasing N  decreases Q
Increasing r  increases Q
Since the radius in the equation is to the 4th power, it will have the biggest effect on the final result if it is changed.
Vasoconstriction/dilatation represent a change in diameter of a blood vessel and has the greatest effect on flow.
The opposite of flow is resistance =PR
PR = 8LN/ r4
Increasing L  increases PR
Increasing N  increases PR
Increasing r  decreases PR
Peripheral resistance to blood flow is most easily controlled by vasoconstriction/dilatation
BP= COxPR
BP = [HR ( EDV- ESV ) 8LN] / r4
BP is easiest controlled by controlling the radius of the blood vessels.
There is virtually no BP at the back of the right atrium (???)
Systolic BP – Diastolic BP = Pulse pressure
120
80
= 40
(normal)
If 130
70
= 60
this larger pulse pressure indicates that there is hardening of the arteries, they
aren’t expanding and contracting as much and there is a larger difference between the systolic and diastolic BP.
BP regulation
BP = [HR ( EDV- ESV ) 8LN] / r4
The radius of blood vessels is controlled by the sympathetic component of the vasomotor center ( part of ANS ).
How does this work? AP’s are sent out at regular intervals. If they are sent out at a faster rate, the contractions will occur
faster and vasoconstriction occurs. If AP’s slow down, dilation occurs.
In blood vessels you have alpha 1 (excitatory ) receptors as well as beta 2 (inhibitory ) receptors. The beta 2 receptors
have little effect since there are more alpha receptors. If you give a pt Epi it will cause vasoconstriction. However, give an
alpha blocker first, and the response is dilatation: all the excitatory receptors will have been taken up and only inhibitory
beta receptors are available.
Changing BP
Heart rate is controlled by cardiovascular center in medulla ( sympathetic stimulation speeds it up, parasympathetic slows
it down )
Viscocity of the blood and the length of the vessel change it little.
Increasing the stroke volume increases the heart rate increases the BP
EDV=venous return
ESV =contractility
Hormones, ADH(vasopressin) change the volume of blood and thereby BP
Angiotensin 2 and aldosterone increase BP, ANP aids in Na+ excretion and thereby leads to volume decrease and BP
decrease.
Autoregulation of BP is a local event. APD levels, chemicals, histamine, bradykinase, CO2 and O2 control it.
Anaphylactic shock in response to histamine release causes systemic vasodilatation at the same time.
A BP cuff really measures the pressure in the cuff. Korotkoff sounds are the sounds that are heard while taking blood
pressure. Turbulence is created as the pressure in the cuff goes down and as the arterial blood gets through, this
turbulence causes the audible sound. The first audible sound is the systolic pressure. As pressure is lowered in the
cuff, turbulence subsides and the “first” silence is the diastolic pressure.
Systolic pressure reflects the force of left ventricular contraction, diastolic pressure provides information about vascular
resistance. The difference between systolic and diastolic pressure is called pulse pressure (PP) and it gives information
about the condition of the CV system. The normal ratio of systolic:diastolic:PP = 3:2:1. Increased PP can be indicative of
PDA or Atherosclerosis.
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Capillaries are made of single layers of simple squamous epithelium. Arteriolar and venous pressure make them leaky to
fluids between the cells, but not to RBC’s, some WBC’s, and few platelets. How much of the fluid will leak back into the
capillaries depends on the net filtration rate (NFP).
NFP = pressure favoring filtration – pressure opposing filtration
The NFP is usually right about 1mmHg, that means that there is always more pressure pushing fluid into the tissues than
there is pushing it back into the capillaries tissues would always swelling if the lymphatic system wasn’t counteracting
this swelling: it returns fluids back into the circulatory system.
LAB material for test 2
Blood composition
Plasma is a non-living matrix that has over 100 substances dissolved or suspended in it, like gases , hormones, salts,
metabolic wastes etc. It consists of 90 % water and is strawcolored.
Formed elements are the cells of the blood, ca. 45%: erythrocytes, leukocytes and platelets.
Leukocytes:
Granulocytes
1.Neutrophils – 3-7 lobed nucleus, active phagocyte, indicative of acute infection.
2.Eosinophils – bi-lobed nucleus, cytoplasm stains, phagocytize antigen-antibody complexes; ind. of
allergic and parasitic infection.
3. Basophils – large U or S shaped nucleus, few granules, contains histamine, mediates inflammatory
response.
Agranulocytes
1. Lymphocytes – smallest leukocyte, large nucleus, sparse cytoplasm, looks like blue rim, B cells:
antibody prod., T-cells: destroys cells such as grafts, tumors, virus infected cells.
2. Monocytes – largest leukocyte, kidney shaped nucleus, phagocyte, ind. of chronic infections.
Never Let Monkeys Eat Bananas – initial of leukocytes in order of highest to lowest concentration.
Platelets release thromboplastin and PF3 which together with other clotting factors and Ca help convert prothrombin
to thrombin which polymerizes fibrinogen into fibrin which forms a meshwork of fibers to trap RBC’s and form clot.
The names of a blood vessel changes every time it branches or passes through another structure.
Hematocrit is the packed cell volume (PVC) = RBC volume
Sedimentation rate: rouleaux formation, rapid settling , final packing
Anemia, normal menses, pregnancy, infectious process – increased sed rate
Polycythemia – decreased sed rate
Coagulation time: tissue factor released + PF3 + other tissue clotting factors + Ca+ ions converts prothrombin to
thrombin polymerizes fibrinogen into fibrin.
LECTURE
11/23/98
Film r.e. stroke
There are 5 billion RBC’s in 1ml of blood. 55% of blood are H20, 45% are formed substances. RBC’s can stack up like
coins when…???
RBC’s have a life span of about 120 days and 200 billion RBC’s die each day and are gobbled up by WBC’s. Dying cells
or injuries attract WBC’s to help clean up.
1,000 RBC :1 WBC
Cholesterol – crystalline form , is larger than RBC’s, embeds into the walls of arteries. Damage to the cell walls causes
the injured cells to grow and RBC’s adhere forming a plaque that later calcifies.
Chapter 19
Blood is a connective tissue made of
1. Cells
a. RBC’s - Erythrocytes
b. WBC’s - Leukocytes
c. Platelets – Thrombocytes
2. Matrix – mostly H20 – plasma, the liquid portion of blood.
a. H20
b. Electrolytes
c. Gases
d. Proteins:
1. Albumin (major component)
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2. Globulins
3. Fibrinogen – a fibrous protein made of soluble fiber. Fibrinogen is important in clotting, when it turns into
fibrin, an insoluble fiber that makes a blot clot.
The blood volume for males is about 5-6liters, for females 4-5 liters. The reason that males have more blood is
testosterone: it increases blood production. Blood makes up approximately 8% of a person’s body weight. It has a salty,
metallic taste. Fe++ gives blood not only its metallic taste but also the red color.
Buffers keep the pH of blood very tightly regulated, between 7.35-7.45. Anything lower than 7.35 is acidotic, anything
higher than 7.45 is alkalotic. A pH below 7 or above 8 usually means death.
Functions of blood
1. Transportation of O2, CO2, nutrients, wastes, hormones, heat.
2. Maintain pH
3. Maintain fluid volume
4. Protection
Buffy coat is the portion that settles in between the RBC’s and the plasma when you spin a tube of blood for HCT. It
contains WBC’s and platelets.
Plasma is everything in the blood minus the blood cells ( the clear liquid that is in a preserved tube of blood spun down )
Serum is the plasma minus the fibrinogen ( or: the clear liquid in a preservative free tube of blood that has clotted )
Hemopoietic stem cells undifferentiated cells that are made in the red bone marrow.
Hormones initiate hemopoiesis: the differentiation of stem cells
1. EPO – erythropoietin  Erythropoiesis  RBC’s = erythrocytes
Hemoglobin  anuclear, no mitochondria anaerobic glycoloysis – RBC’s don’t use the product they carry and
therefore can carry more of it/ be more efficient. Nucleus is extracted during this process.
2. CSF – colony stimulating factors Leukopoiesis  WBC’s = leukocytes
3. Thrombopoietin  Thrombopoiesis  platelets – they are not really cells since they aren’t alive, platelets are
pieces of cells ( megakaryocytes )
RBC’s or Erythrocytes are 8nm ( nm???) large biconcave discs, that are sunken in where the nucleus used to be. Very
red due to hemoglobin, flexible due to spectrin, which gives it tensile strength and allows it to go through small arterioles
of 3-5nm size. Erythrocytes have a life span of about 120 days, during which they make it through the entire body about
1,000 times a day. With age, RBC’s become less and less flexible and since they are anuclear, they can’t fix themselves.
So when they travel through the spleen “later in their life”, they are likely to rupture there because the vessels in the
spleen are very small, too small for the less flexible RBC’s to make it through unharmed. That is why the spleen is also
called the RBC graveyard.
There are about 5x106 RBC/mm3 (=ca 1ml), therefore in 5 liters of blood there are 25x109(trillion)RBC’s in a human body.
Hemoglobin surrounds the Fe++ molecule
There are 4 polypeptide chains: 2 alpha, 2 ß. Each chain is assoicated with 1 heme. 4 Fe++/Hb
Each heme can loosely and reversibly bind with O2, so each Fe++ binds 1 O2.
Hemoglobin values of the blood range from 12-20Hb /dl
The spleen degrades Hb
Since Hb is a protein, it is easily chopped up into individual AA’s which are recycled.
From the Heme the Fe++ is separated, carried to the liver by transferrin, there it is stored and sent back prn to the red
BM where it is recycled.
The porphyrin ring is very stable and hard to get rid of, it has lots of nitrogen, which is actually toxic to the body and
needs to be eliminated. The non-iron portion of the heme is converted to biliverdin (= green pigment ) and then into
bilirubin (=orange pigment) which is excreted into the intestine, where, under influence of bacteria it turns into urobilin,
some of which is sent to the kidney to be excreted ( gives urine its color), the rest or the urobilin is converted to
stercobilin and excreted in the feces (gives feces its normal color ).
Therefore, RBC’s give feces and urine their characteristic colors.
Fetal Hb is a different form of Hb. At birth, it needs to be excreted.
The male body is very conservative with its Hb, unlike the pre-menopausal female that excretes some every month.
Therefore, men and postmenopausal women should not take Fe supplements.
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Blood cell production is controlled by negative feedback: when levels are down, production is increased. EPO is released
by the kidneys when the kidney becomes hypoxic ( not enough RBC’s carrying O2 to the kidneys). Luckily, synthetic
EPO is now available for all the dialysis patients whose kidneys do not function normally.
Anemia = too few RBC’s
1. Hemolytic anemia –RBC’s rupture due to bacteria, viruses,…
2. Aplastic anemia – caused by destruction of red BM
3. Hemorrhagic anemia – due to hemorrhage
4. Pernicious anemia – insufficient hemopoiesis due to lack of intrinsic factors ( needed for B12 absorption from gut)
Polycythemia – too many RBC’s ( >55%Hct) increases the work load of the heart by increasing the viscosity of the blood.
WBC’s or Leukocytes are nucleated, have no hemoglobin, and can be very long lived, 20 years. There are 5,00010,000/mm3 .
Chemotaxis is a WBC’s ability to move toward or away from certain chemicals.
Diapedesis is the WBC’s ability to squeeze through capillaries
Integrins
Selectins
Amoeboid action – cytoplasmic streaming
Granular WBC’s
1. Neutrophils – 2-5 lobes – polymorphonuclear (PMN) 60-70% of WBC’s, respiratory burst makes them into Kamikaze
cells ( they mix H2O2 and chlorox ). A large number of neutrophils goes to an injured site and make pus – yellow
color.
2. Eosinophils have granules that stain red. They are about 2-4% of all WBC’s. Eos are involved in parasitic infections,
they are weakly phagocytic, and release enzymes to kill parasites.
3. Basophils (=”love basic stain”) have granules that stain blue, they are the least common at 0.5-1%. They can leave
the blood and once they do, they are called mast cells that release histamines, kinenes, and heparin when they come
in contact with receptors for antibodies associated with allergic reactions.
Agranular WBC’s
1. Monocytes are the largest of the WBCs. They have a kidney bean or horse-shoe shaped nucleus, make up about 38% of WBCs. These as well can leave the circulation, and once they do they are called macrophages which are very
phagocytic.
2. Lymphocytes are fairly small in comparison to RBCs. They have a large nucleus for their size, and are the second
most common type of WBC.
T lymphocytes
B lymphocytes
NK – natural killer cells
Leukemia – too many leukocytes, 1 single WBC goes crazy and becomes immortal, and then it divides and divides and
the resulting cells are all immortal.
Leukopenia – WBC count of <5,000.
Thrombocytes – platelets
2 nm big and anuclear, these are not really cells at all, but fragments of macrophages. They have granules, and
“live”/exist for 2-5 days.
Thrombocytopenia – not enough platelets hemorrhaging
Thrombosis – high platelet count, platelets are too active, cause wild blood clots.
Hemostasis is a process to prevent blood loss. It has several steps to it:
1. Vascular spasm – vasoconstriction - can last minutes to hours.
2. Platelet plug formation – when platelets come in contact with a rough surface or collagen, they swell up and become
sticky chemicals are released: Prostaglandin Thromboxane A2 which affects more platelets to stick to the sticky
ones and eventually this will plug up the hole ( injury).
3. Coagulation – procoagulants = clotting factors made by the liver. These are proteins in the blood that have a
domino/cascade effect by 2 pathways:
a. Extrinsic pathway: injury to a vessel or tissue  TF(tissue factor) is released and with Ca++ and Factor 7 a
domino effect is activated.
b. Intrinsic pathway: injury to blood itself: concussion, bruise, bacterial injury causes release of Factor 12
After this, both extrinsic and intrinsic follow the
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Common pathway: prothrombinase converts prothrombin to thrombin  converts fibrinogen to fibrin  once
this happens fibrin falls out of solution and forms a net-like web which catches RBCs and WBCs and forms a
plug. Then Factor 13 interacts with this plug and pulls it tight into a clot.
Most clotting factors require Vitamin K to work.
Moldy clover is a cow dz that causes the release of dicumerol, from which Coumadin is derived, a drug given to reduce
clotting. ASA, a prostaglandin inhibitor, is also given to reduce clotting.
Any clot that is not “useful” is called a thrombus, a clot in an uninjured vessel or where it is not supposed to be.
An embolus is a free floating clot.
Hemophelia a condition characterized by the inability to make clotting factors bleeders.
1. Classsical or type A hemophelia – no factor 8 is made intrinsic pathway is not possible.
2. Alternate or type B hemophelia – no factor 9 is made, and again, the intrinsic pathway is not possible.
c.
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1. NAME THE WAVES AND THE INTERVALS PRESENT ON AN ELECTROCARDIOGRAM, AND STATE WHAT
ELECTRICAL ACTIVITY IS REPRESENTED BY EACH. WHAT GENERAL CARDIAC PROBLEMS CAN BE
IDENTIFIED FROM AN ECG?
An ECG measures AP’s as a graph on paper that is running at a certain speed.
During the quiescient period (0.4sec) nothing is happening, atria and ventricles are relaxed. Atriafilling through
passive filling due to the pressure difference.
The P wave shows atrial depolarization or active filling. Atrial systole occurs after the P wave and accounts for only
the last 20-25ml that fill the ventricle. – ca. .1sec long. If longer, it can mean atrial enlargement or stenosis.
The PR or PQ interval = .1sec = conduction time from the beginning of atrial excitation to the beginning of
ventricular excitation. Longer = scarring or damage to the AV nodes ( impulse has to travel around the scar
tissues).
The QRS complex shows ventricular depolarization and atrial repolarization (hidden)  ventricular
contraction/systole and also atrial diastole. The AV valves slam shut when the ventricles relax and blood flows back
from the pulmonary trunk and the aorta against them and that slam is the 1st heart sound, S1 (lub) (dicrotic notch
after T wave on ECG). 0.3sec. Deeper or wider Q wave  possible MI
The T wave represents ventricular repolarization (diastole) The QT interval extends from the start of the QRS
complex to the end of the T wave. It is the time form beginning of ventricular depolarization to the end of
repolarization. The closing of the semilunar valves after ventricular ejection is what creates the 2 nd heart sound, S2
(dub).
A prolonged QT interval can mean myocardial damage, coronary ischemia, or conduction abnormalities.
2. STATE THE FRANK-STARLING LAW OF THE HEART AND EXPLAIN ITS RELATIONSHIP TO CARDIAC OUTPUT
USING THE APPROPRIATE FORMULA FOR DETERMINING CARDIAC OUTPUT.
Preload : Effect of stretching: Frank-Starling law: the more the heart is filled during diastole, the greater the force of
contraction during diastole. Preload = EDV ( end diastolic volume )
Contractility is the forcefulness of contraction of individual ventricular muscle fibers.
CO=HRxSV
Stroke volume SV = EDV – ESV
Therefore CO = HR x (EDV-ESV)
CO= speed x (preload –contractility)
This explains the Frank-Starling law: The greater the EDV/preload, the higher the resulting SV that is multiplied with
the HR to get the CO.
3. DESCRIBE THE STRUCTURAL DIFFERENCES BETWEEN FETAL AND POSTNATAL CIRCULATION. EXPLAIN
THE FUNCTIONS OF THE SPECIAL STRUCTURES DESCRIBED. Page 662
There are differences because the lungs, kidneys, and liver begin to work at birth. After birth, the infant’s body is
responsible for its own O2, CO2, waste and nutrient balance. The placenta is no longer managing these things for
the infant.
Since the liver is not needed in utero the umbilical vein that returns oxygenated blood from the placenta sends
only a small portion of this blood through the liver and the most part goes into the vena cava by way of the
ductus venosus. The blood from the liver joins this a little more superiorily. After the umbilical cord is cut at birth and
blood flow ceases through the umbilical arteries and veins, the arteries fill with connective tissue and become the
medial umbilical ligaments.The umbilical vein becomes the ligamentum teres ( round ligament ) that attaches the
umbilicus to the liver. The ductus venosus becomes the ligamentum venosum, a fibrous cord on the inferior surface
of the liver.
There is no sense in sending all the blood of a fetus to the lungs when the O2 comes from the placenta. The
foramen ovale allows for blood in the R ventricle to go to the left ventricle and from there out to the baby’s body.
There is also another shunt between the aorta and the pulmonary veins that allows for more mixing of blood: the
ductus arteriosus. At birth, when fluid is expelled from the infant’s lungs and they are filled with air, more blood
automatically goes to the lungs because the resistance is all of a sudden lower. Also, there are 2 muscle spasms
occurring at/around birth. The musculature of the foramen ovale goes into spasm and seals it off, it becomes the
fossa ovalis. The ductus arteriosus also goes through a spasm and it closes, becoming the ligamentum
arteriosus.
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4. A WOMAN WHO IS BLOOD TYPE A HAS A BABY WHOSE BLOOD IS O. HER HUSBAND INSISTS THAT THE
CHILD CANNOT BE HIS BECAUSE HE IS BLOOD TYPE B. IS HIS CLAIM JUSTIFIED OR NOT? WHAT ARE THE
POSSIBLE BLOOD TYPES OF THE BABY'S MATERNAL GRANDPARENTS? EXPLAIN YOUR ANSWER.
IAIA or IAi  A
IBIB or Ibi  B
IAIB  AB
ii  O
so the baby received one i from its mom, and one i from its dad.
The mom is IAi and the dad is IBi. His claim that the baby CANNOT be his is not justified.
The possible maternal grandparents are IAIA and IAi, or IAIA and ii, or IAIA and IBi.
5. DESCRIBE THE PROCESS OF COAGULATION OF BLOOD.
Hemostasis is a process to prevent blood loss. It has several steps to it:
1. Vascular spasm – vasoconstriction - can last minutes to hours.
2. Platelet plug formation – when platelets come in contact with a rough surface or collagen, they swell up and
become sticky chemicals are released: Prostaglandin Thromboxane A2 which affects more platelets to stick to
the sticky ones and eventually this will plug up the hole ( injury).
3. Coagulation – procoagulants = clotting factors made by the liver. These are proteins in the blood that have a
domino/cascade effect by 2 pathways:
a. Extrinsic pathway: injury to a vessel or tissue  TF (tissue factor) is released and with Ca++ and
Factor 7 a domino effect is activated.
b. Intrinsic pathway: injury to blood itself: concussion, bruise, bacterial injury causes release of Factor 12
After this, both extrinsic and intrinsic follow the
c. Common pathway: prothrombinase converts prothrombin to thrombin  converts fibrinogen to fibrin  once
this happens fibrin falls out of solution and forms a net-like web which catches RBCs and WBCs and forms a
plug. Then Factor 13 interacts with this plug and pulls it tight into a clot.
LECTURE TEST 3 MATERIAL
11/28/98
Film: The coming Plague
Quiz: 8
Ebola virus first broke out 20 years ago in Zayr. It kills 8 out of 10 people infected. It could jump from one continent to
another in a few weeks. Ebola has been found in fruitbats, and outbreaks seem to be every 2 years, which could tie them
to the blossoming of the fig tree. With good hospital technique, Ebola withers, otherwise it spreads through the hospitals
like wildfire.
In 1950 polio was a major threat to the people and Jonas Salk is the man that came up with a vaccine for it in April 1955.
The CDC was first set up to fight malaria.
Small pox are uniquely human: man is the causative virus’ natural host. In 1806 Jefferson wrote to E. Genner (worked on
a cure ) that people in the future would only know small pox by history. Soon thereafter a vaccine was found and
Jefferson had his whole household immunized. Small pox became “eradicated” in the 1970s.
Emerging epidemics: Lassa fever is another hemorrhagic disease caused by a virus that dissolves the walls of organs. A
small rat is its natural host. Lassa fever is transmitted by poor technique in mission hospitals.
May 1981: AIDS’ first PCP cases diagnosed. In Kenya, 25% of women are infected, and 10% of infants.
War and VD have always gone hand in hand.
Syphilis – Treatment was found by Paul Ehrlich: Arsenic. Untreated, it can cause blindness, heart disease, sterility, and
madness. 25% of young men supposed to enter the army in 1918 were infected. That’s when the government stepped in.
The cure was found with PCN at the end of WW2.
Gonorrhea is the most prevalent bacterial infection in the world.
Test 2 results: raw score of 89 was highest = 100
LAB TEST 3 MATERIAL
11/22/98
Immune System Chapter 36
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FILM
Humoral immunity attacks directly
Lymphocytes come from stem cells, they are produced in the bone marrow (BM) or the fetal liver.
T lymphcytes or T cells render cell mediated immunity, they help the B cells
T and B cells look identical but are found in different places. They have surface receptors, 10 million different ones in
each of us.
Epitopes or antigenic determinants = small immunogenic part of a large foreign antigen (fig22.13 Tortora)
Hapten = small molecule that becomes immunogenic when it attaches to a body protein.
Secondary antibody response is slow, but if you survive the initial attack, you are likely to have lifelong protection.
Antigen = Non-self protein ( not ALWAYS a protein). Antigens are large, but only a small portion needs to be recognized
Antibodies are 4 proteins bound together by disulfide bonds. 2 heavy and 2 light chains with a variable and a constant
region on both of them. The variable regions allow for individualization, and respond to different antigenic peptides
(pieces of foreign proteins ) There are 60 –70 AA’s on the light chains. There are membrane bound and soluble forms of
antibodies in plasma or in lymph.
are immunoglobulins:
1. IgG – most common, provides passive immunity: you are not the one who made the antibodies, crosses placenta
2. IgA – crosses breast milk, can also be secreted in mucus secretions, also provides passive immunity
3. IgM – initial response, 1st to appear after infection
4. IgE – goes to work after IgM, responsible for most allergies
5. IgD – is usually membrane bound, not found floating around unless it has just been shed by B cells after clonal
expansion after selection of B cell
Variable to the antigen class, antibodies can switch from M to G, A, or E.
Primary cell mediated response and antibody response have 3 characteristics in common:
1. Specificity
2. Memory
3. Differentiation of self and non-self cells (auto-immune problems start here )
Lymphatic system is a one-way system: it carries lymph to the heart. It consists of:
1. Lymph vessels – are very thin walled, made of 3 tunics, and have many valves ( more than veins)
2. Lymph nodes
3. Lymphoid organs: tonsils, thymus, spleen (= single largest mass of lymphatic tissue in the body )
1. Lymphatic vessels are blind end capillaries that are present in nearly all tissues. They pick up the interstitial fluid with
H20 and proteins into lymphatic collecting vessels. Fluid in the lymphatic vessels is moved along by the skeletal and
respiratory pumps. Lymphatic trunks receive the lymph from the lymphatic collecting vessels until it returns to the
vascular system through one of the two large ducts:
The smaller R lymphatic duct drains into the R subclavian vein. It collects lymph from the R side of the body superior to
the diaphragm.
The larger Thoracic duct receives lymph from the body inferior to the diaphragm and from the L side of the body
superior to the diaphragm and then drains into the L subclavian vein.
Cisterna chyli is an enlarged terminus at the base of the thoracic duct that receives lymph from the lower abdomen,
pelvis, and lower limbs.
In humans, both ducts empty the lymph into the venous circulation at the junction of the internal jugular and the
subclavian vein.
2. Lymph nodes are bean shaped and there are 1000’s of them. They cluster around vessels
Macrophages, phagocytes that destroy bacteria, CA cells and other foreign materials.
There are large collections of nodes in the following areas:
1. Inguinal
2. Axillary
3. Cervical
4. Peyer’s patches in the intestine
Swollen glands are a sign that fluid is trapped in the nodes during an infection.
The lymph node is enclosed within a fibrous capsule. Trabeculae made of very fine connective tissue form septa in these
capsules ( just like in the testes).
There is an outer region, the cortex with germinal centers (= cells arranged in globular masses). The germinal centers
contain B-cells which are dividing, the rest of cells are T cells that circulate continuously, moving from the blood into the
node and then leaving the node in the lymphatic stream. The medulla is the internal portion of the gland. Most of these
cells are macrophages, that play an important role in “presenting” the antigens to the T cells. Each node has many
afferent vessels though which lymph enters the nodes, and it leaves through fewer efferent vessels at the hilus. Since
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there are fewer efferent then afferent vessels, lymph stagnates in the node and allows for the immune response, and for
the macrophages to do their jobs.
3. Primary Lymphoid organs: thymus and bone marrow
Bone marrow makes stem cells for B and T cells
B cells mature in the bone marrow, recognize self. They are the memory cells for secondary responses. Plasma cells
produce antibodies  immune response
T cells travel to the thymus to mature. They provide cellular immunity. Types of cells:
1. Memory cells
2. Killer cells ( Tc ) – have CD8 surface markers, punch holes into the cells they attack
3. Helper cells (Th ) – have CD4 markers, activate B cells and T cells
For test: there will be more questions on the lymphatic system than identification. Know the picture of the lymph node in
the book, page 371. Joe will cover respiratory system Wednesday, 11/25.
LAB
11/25/98
Pulmonary system anatomy
Exercise 37, page 374…
Nasal cavity – warms filters moistens
External nares = nostrils
Vestibule – right inside ext. nare
Septum separates nares, front part cartilaginous, back is bone, infection can be in one side only
Nasal conchae and meatus = or turbinates, swirl air around, are covered by highly vascular mm to trap particulate
matter and moisten air and warms it, and filters it.
Internal nares – where air leaves nares and enters pharynx
Pharynx – throat, connects the nasal and oral cavities to the larynx and esophagus inferiorily. 3 areas (back of throat)
1. Nasopharynx – where nares empties into throat, serves only as air passage. Pharyngotympanic tubes drain
into lateral aspect
2. Oropharynx - Where oral cavity empties into back of throat, serves as common conduit for food and air
3. Laryngopharynx – accommodates air and food.
Hyoid bone is right in front of larynx, holds tongue
Larynx consists of 9 cartilages: 1. Thyroid cartilage = Adam’s apple
2. Crichoid cartilage
Glottis – opening to trachea (or Rima glottidis)
Epiglottis – falls over glottis w/ swallowing, only cartilage of the larynx made of elastic cartilage, all
others:hyaline
vestibular folds –above vocal cords
Vocal folds – right before you get into the trachea, males’ are looser for lower voice. Females have higher
pitched voice due to tighter vocal folds
Trachea – ringed-shaped hyaline cartilage or C-shaped or D-shaped if you take the trachealis muscle into consideration.
divides at the carina into L and R primary bronchus and then it branches again into the secondary bronchi.
Ciliated columnar pseudostratified epithelium inside of trachea.
Hyaline cartilage next
Dense connective tissue outside
Trachea  Primary bronchus  Secondary bronchus  Tertiary bronchus  bronchioles 
Terminal branches: respiratory bronchioles alveolar ducts  alveolar sacs made of alveoli
With branching the amount of cartilage in the bronchi decreases and smooth muscle increases.
Lobes – compartments in the lungs: 3 on the right, 2 on the left. The lobes are divided by oblique and horizontal fissures.
Cardiac notch is an area on the left lobes where the lung tissue is notched out to make room for the heart.
Alveoli – air sacs in the lung, simple squamous epithelium, ( thin – allows rapid diffusion )
Alveolar capillary walls + basal laminas = respiratory membrane or air-blood barrier
Pulmonary capillaries – arterioles and venules, cover the alveoli, also made of simple squamous epithelium again
allows for easy diffusion
Type 2 or septal cells – make surfactant – changes surface tension of the alveoli to prevent them from collapsing
Macrophages – make sure that any foreign substances are taken care of and phagocytosed, keep the area clean. Coal,
smoke, asbestos are things they can’t get rid of, so they show up as black spots on x-ray
External intercostal muscles pull rib cage up and out, diaphragm contracts down and increases the volume of the
lungs. Internal intercostals work on active expiration to expel air.
Exhaling is passive, inhalation is active
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Trachealis muscle in back of trachea
The terminal branches of the bronchioles are called respiratory bronchioles These in turn subdivide into several alveolar
ducts which terminate in alveolar sacs made of alveoli. They are made of simple sqamous epthelium a thin basal lamina.
The alveoli are densely spider-webbed with pulmonary capillaries and this is called the respiratory membrane or airblood barrier.
Gas exchange occurs by simple diffusion across the respiratory zone structures, and the area from the nasal cavity to
the bronchioles is known as the conducting zone structures or anatomical dead space.
Respiratory physiology
Gas exchange occurs by simple diffusion.
The pleura are made up of 2 layers: the parietal pleura that adheres to the thoracic wall and the diaphragm. The visceral
pleura covers the lung tissue. The pleural space produces a lubricating serous fluid.
Vital capacity VC (3600-4800ml) is the maximum amount of air that can be exhaled after a maximum inspiration
VC = TV+ IRV+ ERV
Tidal volume TV (500ml) is the amount of air inhaled or exhaled with each breath under resting conditions.
Inspiratory reserve volume IRV ( 3100ml) is the amount of air that can be forcefully inhaled after normal tidal volume
inhalation.
Expiratory reserve volume ERV (1200ml) is the amount of air that can be forcefully exhaled after normal tidal volume
exhalation. This amount is reduced in COPD.
Residual volume RV (1000-1200ml) is the amount of air that remains in the lungs that can’t be exhaled.
Total lung capacity TLC = VC + RV
Inspiration: external intercostals and diaphragm ( together = inspiratory muscles) contract, size of thoracic cavity
increases, diphragm flattens. External intercostals lift rib cage, increasing thoracic size and since the pleura adhere to
the thoracic wall it also increases pulmonary volume and air pressure in the lungs decreases. Vacuum created this way
pulls air into the lungs = inspiration.
Expiration: inspiratory muscles relax, elastic lung tissue recoils and intrathoracic and intrapulmonary volumes decrease.
Intrapulmonary pressure increases higher than atmospheric pressure, air flows out of the lungs. Pressure inside and
outside the lungs is equalized with expiration.
Lecture material for test 4
11/30/98
Immune System
Lymphoid tissues are the tonsils, thymus, spleen, Peyer’s patches, BM…
Its primary purpose is protection. It is a system of WBCs.
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2 Branches: the non-specific immune system and the specific branch
 1. Non-specific immune system – this is shared with every live creature, it has no specificity, is the same every
time and with nothing tailored to a specific pathogen. It has no memory. The non-specific immune system consists of
phagocytes that engulf and destroy organisms.
a. Barriers – 1) Skin through keratin is waterproof – it is hard for bacteria to move without water.
2) Mucus membranes – line the cavities of the body, they are not nearly as good as skin in their
protective abilities, but they secrete mucus to trap organisms.
b. Chemicals – 1) Lysozyme – an enzyme in saliva, tears, and nasal secretions that lyses certain bacterial walls.
2) Complement – 20 proteins in the blood (C1…..C1b) that have the ability to latch on an create a
hole in the membrane of bacteria – they form membrane attack complexes (MAC) by
a. Classical pathway
b. Alternate pathway
These pathways converge after completion
Complement attachment causes 1. dilatation of arterioles
2. release of histamine from mast cells
3. chemotaxis
4. opsonization –(to make tasty)–makes it easier for phagocytes
5. MAC
c. Phagocytes – primarily macrophages and neutrophils
B lymphocytes
Pseudopods  1. adherence
2. ingestion
3. digestion
4. exocytosis
Antigen presenting cells are phagocytes that eat something, chop it up, and then display it on their surface as
antigenic determinants ( epitopes )
Inflammation is the non-specific activity that goes on once you have been infected/ the barrier has been crossed:
1. Vasodilation
2. Increased capillary permeability ( bigger things like complement can get out )
3. Chemotaxis
4. Diapedesis
5. Heat
6. Redness
7. Swelling/edema  compression of neurons  pain
8. Pain from chemicals being released
9. Loss of mobility if inflammation is near a joint
10. Fibrinogen  clot formation  walls of the area to prevent infection from spreading systemically
Cardinal signs of inflammation: heat, redness, swelling, pain ( and immobility )
Neutrophils – respiratory burst makes them into Kamikaze cells ( they mix H2O2 and chlorox to take care of a pathogen,
and it kills them as well). A large number of neutrophils goes to an injured site and make pus – a collection of cell debris
and dead neutrophils – yellow color.
Interferons – appear during viral invasion only. They are specific in one way. A virus is an intracellular parasite that
cannot reproduce outside of a cell. After invasion by a virus, a cell become a virus factory. The cell’s last ditch effort
before becoming a virus factory is to produce interferons to send to the other cells to prevent their viral infection.
Several kinds of interferons: a. alpha interferon – can be made by any cell in the body. It slows cell growth, prevents
viral infection and tumor formation
b. beta interferon – has essentially the same activities and characteristics as alpha
c. gamma interferon – is only made by certain WBCs, so only certain cells can make it. It
increases phagocytosis and natural killer cell.
 2. Specific or Immune response consists primarily of lymphocytes.
Characteristics
a. Specific - it tailors its attack to the individual pathogen
b. memory – a 2nd infection causes a response that doesn’t allow the infection to take hold immunity
2 types of specific immune responses
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 1) Cell mediated immunity – more complicated – cells are workers that produce the response right there at the site.
(T cells are our defense against abnormal cells and pathogens living inside living cells )
 2) Humoral or Antibody mediated immunity – the cells don’t do the actual killing  antibodies are like seeking
missiles that attack while floating around in the body. (B cells – provide our defense against antigen (pathogens) in
body fluids.
Lymphocytes are
a. T lymphocytes or T cells move to the thymus to mature ( Thymus dependent cells) – about 80% of circulating
lymphocytes are T cells.
b. B lymphocytes or B cells mature in the Bursa equivalens ( Bone marrow dependent cells ) – account for 1015% of circulating lymphocytes. B cells can differentiate into plasma cells when stimulated, and then secrete
antibodies (immunoglobulins) that react with specific antigens (pathogens, mostly proteins)
c. NK cells or Natural killer cells – account for the remaining 5-10% of circulating lymphcytes. These are also
known as large granular lymphocytes that will attack foreign cells, normal virus infected cells, and cancer cells.
They perform immunological surveillance.
1. Cell mediated immunity is lymphocyte controlled – a small nucleated cell produced in the BM that starts out
immature, it has to leave the BM to mature.
The thymus atrophies after age 12 or 13. It is
1. site for lymphocyte maturation
2. endocrine – when the lymphocytes are here, the thymus makes hormones that are involved in and control
lymphocyte maturation.
3. As the lymphocytes mature they develop a receptor, whose shape is very important. There are 4 genes on the V
strand, 12 on the D, and about a 100 on the J strand. As lymphocytes mature they fold the DNA ( into something
shaped like an ohm sign). This leaves over 1 billion (1-109) combinations and every combination gives rise to a
slightly different shaped receptor – before you ever encountered any pathogen to fit any of those receptors!
The receptors are made for proteins. If one of those receptors fits your own cell, it chews your own cells up. So
before the matured lymphocytes leave the thymus, they must pass 2 tests:
a. positive and
b. negative selection
T cells must recognize non-self protein and must not be activated by self proteins (= must recognize self ) ( which
is which of a and b???)
If a T cell fails to recognize self proteins it gives rise to auto-immune diseases. The T and B cells??? are
activated by self proteins and cause diseases like Lupus, or Graves disease.
Receptors are designated by clusters of differentiation (CD)
T cells exhibit CD4
1. T helper cells or TH – stimulate the activation and function of T and B cells
2. T delayed type hypersensitivity or TDTH B cells exhibit CD8
1. T cytotoxic or TC – attack foreign/body cells infected by viruses by direct contact. Primary cells involved in
production of cell mediated immunity.
2. T suppressor or TS – inhibit the activation and function of both T and B cells.
Before an immune response can begin, T cells must be activated. This does not happen by direct contact with a
pathogen. T cells recognize antigens that are bound to glycoproteins in cell membranes.
Cells check surface proteins. One big one is Major Histocompatibility Complex (MHC or HLAs – Human Leukocyte
Antigens). All cells exhibit it. There are 2 major classes.
Class 1 – MCH1 – are found on all nucleated cells. They pick up small peptides from the surrounding cytoplasm: if they
are self protein
they will be ignored by the T cells. If not, the will soon appear in the cell membrane and activate T cells. This will lead to
the destruction of the abnormal cell.
Class 2 – MCH2 are found on Antigen presenting cells (phagocytes) have MCH2 on them
1. Macrophages
2. B cells
3. dendritic cells ( in MM, vagina )
Antigen is anything your immune system responds to.
1. Complete antigen – is big enough to be noticed. It will initiate a response and then react with the products of that
immune response.
2. Hapten – a little antigen that is actually to little to initiate a response. A hapten by itself will not initiate a response but
if a response has already been initiated it will react with the product. A hapten becomes conjugated ( attached to ) a
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blood protein – this is not a voluntary process – this blood protein being big enough to produce a response. The
hapten then interacts with the products. Page 689.
Antibodies consist of 2 parallel pairs of polypeptide chains, 1 heavy and 1 light. Each chain consists of a constant and a
variable segment. Constant segments are what classify an antibody as IgE… The tips of the light chains contain the
antigen binding sites.
APC complex – Antigen with MHC2 puts it on its surface to present it to another cell.
APCs have MHC1 and MHC2 depending on the MHC
MHC1  CD8 presents it to T cytotoxic cells and T suppressor cells  MHC1 has to interact with CD8
MHC2  CD4 presents it to T helper cells and T delayed type hypersensitivity cells  MHC2 has to interact with CD4
T cells ignore pathogens that are free since they don’t have the MHC, so they only interact with intracellular pathogens
(Virus or fungus – but always intracellular pathogens) after they have learned about the pathogens from the APC.
T cytotoxic cells work by using perforin (they are also called the “kiss of death”): it touches the cell and it explodes. But the
T cytotoxic cells can’t do this alone, they need help from the interleukins, lymphokines, etc. and the T helper cells are the
necessary to get this process going.
T cytotoxic cells are all different in their receptors. When the antigen matches the APC receptor ( antigen selects it), the cell
goes through mitosis  clonal expansion results in the production of a bunch of identical cells and all of them circulate
around looking for that antigen being presented, and when they find it, they destroy it.
An allergy is an inappropriate immune response.
T DTH cells are cells that are associated with “allergies”, poison ivy, graft rejection…
T cytotoxic cells kill infected body cells
T helper cells help by producing interleukins
T supressor cells also help by stopping/suppressing the clonal expansion by producing interleukins ( different ones )
2. Humoral or Antibody mediated response
B cells are also produced in the BM and undergo positive and negative selection
But the variable chain where the AG binds is different on every B cell. B cells react with free AGs in the blood, T cells or
lymphocytes, they will react with them. Again there is selection of a cell, the B cell in this case, and clonal expansion
takes place. Then other things happen to the B cells:
1. they loose their receptor
2. they develop rough ER for protein synthesis and it starts making tons of protein ( 100,000 in 6 seconds) called
antibodies or immunoglobulins (Ig). At this point they become plasma cells.
The antibodies look just like the receptors, with 2 heavy and 2 light chains, 1 constant region and 1 variable region – the
part that actually matches the antigen.
Immune globulins
1. IgG – most common – single unit = monomer (looks like a Y made of double lines) is found In body fluids and
crosses placenta, so an infant is born with it, provides passive immunity: you are not the one who made the
antibodies.
2. IgA – is a dimer in structure ( like 2 Y’s put together ) crosses breast milk, can also be secreted in mucus secretions,
provides passive immunity.
3. IgM – initial response, 1st antibody to appear after infection, is a pentimer (5 Y’s put together) and therefore can
combine with 10 antibodies  causes clumping.
4. IgE – goes to work after IgM, responsible for most allergies, mast cells have receptors for IgE degranulation 
histamine release. Allergy shots cause the production of IgG and that then takes care of the allergen.
5. IgD – is a surface receptor of the B cell, usually membrane bound, not found floating around unless it has just been
shed by B cells after clonal expansion after selection of B cell, it is another monomer.
Variable to the antigen class, antibodies can switch from M to G, A, or E.
B cells also need help, they depend on the T
helper
cells as well.
The 1st response to an antigen is usually slow, maximum response after about 7 days. However, a 2nd response to the
same antigen causes a 100-fold reaction usually within 24 hours. This can only happen if the B and T cells remember 
they make memory cells that have been exposed to the antigen and that are extremely long lived, up to 20 years.
How do antibodies kill things? There are lots of different ways:
1. The antibodies fix the antigen and help complement to come along and make it easier for it to atack.
2. They optionize (=”to make tasty”) – make it easier for the phagocyte
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3. They agglutinate
4. Neutralizatin – anitbodies bind to toxins’ binding sites, making it unable to attach itself to a cell.
5. They precipitate ( fall out of solution )
Autoimmune diseases
Rheumatic fever – repeated exposure to strep causes antibodies to be made that are similar to a protein on the heart.
Then the body doesn’t recognize the difference and attackes its own heart tissues.
Lupus, Hashimoto’s thyroiditis, Juvenile onset DM.
************************
Respiratory Anatomy
Pharynx – throat, connects the nasal and oral cavities to the larynx and esophagus inferiorly. 3 areas (back of throat)
1. Nasopharynx - is made of hyaline cartilage, where nares empties into throat, serves only as air passage.
Pharyngotympanic tubes drain into lateral aspect
Thin epithelium, passage for air only
Lots of mucus secreting cells
Nasal conchae and meatus - turbinates clean the air passing through them, warm and hydrate it.
Mouthbreathers don’t get these benefitsair that reaches their lungs is not as clean are more prone
to respiratory infections.
Pharyngeal tonsils = adenoids – lots of WBCs and IgA here.
2. Oropharynx – is subjected to more abrasions, so it is made of stratified squamous epithelium.
Where oral cavity empties into back of throat, serves as common conduit for food and air.
Uvula – can block off breathing, is removed prn for sleep apnea
Palatine and lingual tonsils are located here.
3. Laryngopharynx – accommodates air and food, where respiratory and digestive system separate.
Larynx – the voice box, is the beginning of the bronchial tree, no food is supposed to go through here.
consists of 9 cartilages, 3 unpaired cartilages:
1. Thyroid cartilage = Adam’s apple
2. Crichoid cartilage
3. Epiglottis – prevents food from going down the bronchial tree, falls over glottis w/
swallowing, only cartilage of the larynx made of elastic cartilage, others: hyaline
and 3 paired cartilages: 1. Cuneiform
2. Corniculate
3. Artynoid
Glottis – opening to trachea (or Rima glottidis)
Crichothyroid ligament is where a tracheostomy is performed.
Trachea is made of hyaline cartilage that is in the shape of a C. The open area is “closed up” by muscle tissue. The
esophagus is right behind it, and when food is swallowed, the esophagus bulges into the opening of the C into the
trachea to accommodate the food bolus. The tracheal lining is pseudostratified ciliated columnar epithelium, which has
lots of goblet cells. It has a very well developed basement membrane (stains bright blue on a slide). Cilia are constantly
beating to move this mucus, and all the particles trapped in it, up so they can be excreted.
L and R primary bronchi – the R is wider and more vertical, the L is narrower and more horizontal. They divide further
into the secondary bronchi. The further down you get, the less cartilage you find, and the more smooth muscle. Then
you get to the tertiary bronchi, to the bronchioles and then the terminal bronchioles
From the nose to the terminal bronchioles the area is called anatomical dead space, because there is no gaseous
exchange. Anything smaller than the terminal bronchioles, like the respiratory bronchioles and there is gas exchange
taking place. Alveoli are made of simple squamous epithelium. There are 2 types of cells here:
1. Mostly type 1 cells – SSE that makes up the wall
2. Some type 2 or septal cells that are cuboidal or even columnar. They produce surfactant – a phospholipid
substance that forms a thin layer on the inside of the alveoli, it reduces the surface tension of water and prevents the
collapse of the alveoli.
Alveolar macrophages clean up inhaled dust.
IRDS – Infant Respiratory Distress Syndrome is caused by absence of surfactant. If it is unavoidable that an infant is
delivered prematurely, the mother can be given cortisol which stimulates surfactant production. The infant can also be
given surfactant after birth.
Respiratory Physiology
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O2 and CO2 exchange takes place by diffusion of only, from high to low concentrations. Blood is high in CO2 and low in
O2, air is low in CO2, and high in O2. The higher the distance, the lower the diffusion rate, so you only want a short
distance/ thin membrane for the molecules to diffuse across. Diffusion in the lungs takes place across a membrane that is
only 0.5 micron thick and consists of the following layers: 1. SSE of capillaries ( Endothelium )
2. Basement membrane of capillaries
3. Basement membrane of alveolus
4. SSE of alveolus
5. Surfactant
This layer becomes thicker when inflammation or swelling (pulmonary edema) is present
There are 500 million alveoli, their surface area added together would equal ca. 70m2 – a tremendous amount.
Considering the average person has ca. 5 liters of blood, that is an extremely thin layer covering this surface.
Musculature involved with respirations
Muscles involved in inspiration: a. external intercostals pull the ribs up and out.
b. diaphragm flattens when contracted
Both serve to increase the volume of the thoracic cavity. That is all they do.
Muscles involved in expiration: a. internal intercostals pull the ribs down and in and decrease the volume of the thoracic
cavity.
b. abdominal muscles ( transverse abdominus, rectus abdominus, internal and external
obliques) compress the abdomen.
Respiration is moving air in and out
1. (pulmonary) Ventilation – 1 inhalation(or inspiration) and 1 exhalation ( or expiration)
2. External respiration – exchange of air O2 and CO2 between air and blood
3. Internal respiration – exchange of O2 and air between blood and cells
4. Cellular or True respiration –
Pulmonary ventilation
Lungs are surrounded by pleura: parietal and visceral, with serous fluid between them. They stick together ( compliance
elasticity). The pleura are sealed off, therefore the pressure inside the thoracic cavity is dependent on the outside. The
lungs, on the other hand are patent: the pressure inside the lungs is the same as outside.
Air pressure is the weight of the air, the closer to the earth, the higher the pressure. The higher up on a mountain you
are, the lower the pressure. The average pressure is 760mmHg or torr, or 14.7lbs/in 2 at sea level. Air is a mix of gases:
21% O2, .3% CO2, 70% N2, H2O, Ag, Ne. All gases contribute an amount equal to their percentages to the weight of air.
The air and intrapulmonary pressure are equal.
The intrathoracic pressure is lower, though, and can be manipulated.
Fig 23.14
The intrathoracic pressure is 756mmHgalways lower than atmospheric pressure. This is what keeps the walls of the
lungs always slightly inflated. The only way they collapse is when there is a pneumothorax (hole in the pleura through
which air can enter).
Inspiration – the inspiratory muscles contract, the diaphragm flattens, the external intercostals pull the ribcage up, and
the volume of the cavity increases.
Dalton’s law – pressure and volume are inversely related
P1V1=P2V2  the larger the volume, the lower the pressure  as the volume increases in the lungs, the pressure
decreases and air enters the lungs until equilibrium is reached. ( Boyle’s law)
Expiration – in mammals this is a passive process. Forced exhalation or inspiration, however, is active respiration.
During expiration, everything contracted during inspiration relaxes. The volume of the thoracic cavity decreases
pressure increases, and air leaves the lungs until the pressure inside and out is equalized. Since the pressure in the
thoracic cavity is always lower than the pressure in the lungs, you cannot exhale all the air in the lungs. The remaining air
is called residual volume.
Vital capacity VC (3600-4800ml) is the maximum amount of air that can be exhaled after a maximum inspiration
VC = TV+ IRV+ ERV
Tidal volume TV (500ml) is the amount of air inhaled or exhaled with each breath under resting conditions.
Inspiratory reserve volume IRV ( 3100ml) is the amount of air that can be forcefully inhaled after normal tidal volume
inhalation.
Expiratory reserve volume ERV (1200ml) is the amount of air that can be forcefully exhaled after normal tidal volume
exhalation. This amount is reduced in COPD.
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Residual volume RV (1000-1200ml) is the amount of air that remains in the lungs that can’t be exhaled.
Total lung capacity TLC = VC + RV (5000ml)
O2 is used in the Krebs cycle. 21% of air is O2. At 760mmHg this comes out to 160mmHg partial pressure of O2. Since
the pressure is lower at higher altitudes, this is of course, comes out to less mmHg at higher altitudes.
pO2= 160mmHg= partial pressure of O2 at sea level
CO2=0.3mmHg =pCO2. This is so low, that getting rid of it is not a problem in diffusion
Fresh air begins to mix in the nose as soon as it enters. In the nose, the pO2 is already down to 104mmHg , and the
pCO2 is up to 40mmHg. At this point, the dumping of CO2 becomes more difficult.
At the alveolar capillaries pO2 is only 40mmHg, and pCO2 is up to 45mmHg.
??? Equilibrates O2 100mmHg, CO2 40mmHg
At the body cells
pO2 = 40mmHg
and 104mmHg in the blood, so the diffusion goes  into the cells
At the body cells
pCO2 = 45mmHg
and 40 mmHg in the blood, so the diffusion goes  into the blood
Expired air is O2= 120mmHg and CO2= 27mmHg, so giving mouth to mouth resuscitation actually gives someone
oxygen.
Transport of O2 (fig 23.18)
Very little of O2 dissolves in the blood/H2O: only 1.5%. The remaining 98.5% of the O2 combine with Hgb to form an
oxyhemoglobin complex, so Hgb is very valuable. It attaches to Iron molecules in the heme, and since there is 1 Fe++
per heme, each Hgb can carry 4 O2 molecules.
CO2 transport into the cell
CO2 is more soluble in H2O than O2. 7% are dissolved in plasma, 23% attach to Hgb ‘s AA residues to form
carbaminohemoglobin. 70% combine with H2O chemically and is then carried as HCO3- (bicarb) in the plasma.
CO2+H2O  H2CO3 H+ +HCO3- This is a very slow reaction, but it happens all by itself. However, if carbonic
anhydrate is present, this reaction happens very quickly. Carbonic anhydrase is present in RBCs.
For every negatively charged bicarb molecule that leaves the RBC, a negatively charged Cl- ion comes in. This chloride
shift helps to keep the inside charge of the RBC neutral with respect to the tissues.The same shift occurs at the lungs,
except the entire process is reversed, the Cl- leaves the RBC and the HCO3- comes in.
Tissues CO2 + H2O  H+ + HCO3- (leaves to go out to the tissues) Cl- comes into the RBC.
Lungs Cl- leaves the RBC, HCO3- comes in HCO3- + H+  CO2 + H2O
Henry’s law: The amount of a gas dissolved in liquid is proportional to the partial pressure of the gas and its solubility
coefficient over the liquid, when the temperature remains constant.
Diving: The bend
The air breathed in from the tank is high pressure, but the Primary gas in air is N2 (nitrogen), and when it is under high
pressure, more of it becomes dissolved in the blood. The deeper you go, the more N2 goes into the blood, and this is ok,
unless you releave the pressure quickly and the N2 forms bubbles in the blood. This is a very painful process that causes
people to bend over, therefore the name “The bend”. (Movie: The Abyss)
Hgb is a molecule with 4 hemes with 1 Fe++ in each. O2 binds loosely and reversibly with Fe++ ( this is ferrous iron, and
is the only form of Fe that O2 binds with; Fe+++ is the oxidized form that has lost 1 electron through oxidation, it is nonfunctional. If someone were to accidentally replace his Fe++ with Fe+++, IV methylene blue will reverse this process =
TV show “ER”, where a boy had been around organophosphate compounds. )
Allosterism –( per Steadman’s dictionary: the influence of an enzyme activity, or the binding of a ligand to a protein, by a
change in the conformation of the protein, brought about by the binding of a substrate or other effector at an allosteric
site other than the active site of the protein )
Not all O2s bind or come off the Fe++ with the same ease, the 1st is hard, but the 4th is easy. If they all bound/came off
with the same ease, we would have a straight line representing O2-hemoglobin saturation graphically in the Oxygenhemoglobin dissociation curve. However, the curve is sigmoidal, (fig 23.19 on page 733 ), meaning that it allows for
loading up ( in the lungs ) or unloading of O2 ( in the tissues) in a small range of pO2.
Loading – takes place in the lungs – don’t need as much to fill a Hgb
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Unloading – takes place in the tissues – the tissues don’t have to be as deprived before O2 is dumped off. All due to
Allosterism.
This Oxygen-hemoglobin dissociation curve can be shifted.
A R shift makes it easier to unload – Hgb has a reduced affinity for O2  unloads it easier.
A L shift makes it easier to load – Hgb has an increased affinity for O2 loads it easier.
Factors that can cause a curve shift:
1. Temperature: a. increased temp causes a R shift = easier to unload  fever increased resp rate
b. decreased temp causes a L shift = easier to load
2. pH: a. acidity causes a R shift = makes it easier to unload O2 in the tissues  acidosis  increased resp rate
CO2+H2O  H2CO3 H+ +HCO3Increased CO2  increased H+  decreased pH
b. alkalinity causes a L shift = it is easier to load O2 in the lungs
CO2+H2O  H2CO3 H+ +HCO3Decreased CO2  decreased H+  increased pH
3. 23DPG – Bisphosphoglycerate – a substance in the blood that acts like a wedge in “keeping the heme open”
The more you have in your blood the further the curve will be shifted to the R – O2 is easier unloaded.
4. Fetal hemoglobin causes a shift to the L, basically, the fetus is “stealing” the O2 from the mother’s blood, so its Hgb
has to have a higher attraction for the O2 for it to come off.
Regulation of respirations
1. 4 respiratory centers
a. 2 in the medulla:
1) inspiratory – controls rate and depth via reverberating circuit
2) expiratory – inhibits inspiratory center and sometimes the expiratory muscles
b. 2 in the pons: 1. Apneustic center – stops respirations, inhibits the inspiratory center in CO2 is down ( pH up)
2. Pneumotaxic center – emergency center – excites the inspiratory center in times of
suffocation ( air hunger )
Hering-Breuer reflex or Inflation reflex
Bronchial baroreceptors become stretched during overinflation stimulates vagus inspiratory center is inhibited 
expiration begins baroreceptors no longer stimulated inhibition stops new inspiration begins. Possibly this reflex is
mainly a protective mechanism rather than key component of normal respiration.
There are peripheral receptors – these are chemoreceptors for increased CO2 levels= hypercapnia ( and some decrease
O2=hypoxia). Hypercapnia is what drives human respirations.
The central chemoreceptors in the medulla and the hypothalamus detect mostly CO2 levels.
A person can have normal CO2 levels and low O2 levels in high altitude and COPD.
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POSSIBLE QUESTIONS FOR TEST 4
1. Draw and label the oxygen-hemoglobin association/dissociation curve. Explain “curve shifting” and list the
reasons for and the directions of the shift.
Not all O2s bind or come off the Fe++ with the same ease, the 1st is hard, but the 4th is easy. If they all bound/came
off with the same ease, we would have a straight line representing O2-hemoglobin saturation graphically in the
Oxygen-hemoglobin dissociation curve. However, the curve is sigmoidal, (fig 23.19 on page 733 ), meaning that it
allows for loading up ( in the lungs ) or unloading of O2 ( in the tissues) in a small range of pO2.
Loading – takes place in the lungs – don’t need as much to fill a Hgb
Unloading – takes place in the tissues – the tissues don’t have to be as deprived before O2 is dumped off. All due to
Allosterism.
This Oxygen-hemoglobin dissociation curve can be shifted.
A R shift makes it easier to unload – Hgb has a reduced affinity for O2  unloads it easier.
A L shift makes it easier to load – Hgb has an increased affinity for O2 loads it easier.
Factors that can cause a curve shift:
1. Temperature: a. increased temp causes a R shift = easier to unload  fever increased resp rate (RR)
b. decreased temp causes a L shift = easier to load
2. pH:
a. acidity causes a R shift = makes it easier to unload O2 in the tissues  acidosis  increased RR
CO2+H2O  H2CO3 H+ +HCO3Increased CO2  increased H+  decreased pH
b. alkalinity causes a L shift = it is easier to load O2 in the lungs
CO2+H2O  H2CO3 H+ +HCO3Decreased CO2  decreased H+  increased pH
3. 23DPG – Bisphosphoglycerate – a substance in the blood that acts like a wedge in “keeping the heme open”
The more you have in your blood the further the curve will be shifted to the R – O2 is easier unloaded.
4. Fetal hemoglobin causes a shift to the L, basically, the fetus is “stealing” the O2 from the mother’s blood, so its
Hgb has to have a higher attraction for the O2 for it to come off.
2. Using the knowledge you have about the immune system, list reasons for:
a. the T helper cell being the primary target of HIV
in the human body, the virus binds to CD4 – which is characteristic of T helper cells
the virus then turns the T helper cell into a virus factory, unable to do its regular job of fighting infection
b. why HIV is so devastating to the immune system
the virus slowly destroys T cells
when an infection occurs, suppressor factors released by T suppressor cells inhibit an immune response
before the few surviving T helper cells can stimulate the formation of T cytotoxic cells or plasma cells in
adequate numbers.
T helper cells are unavailable to produce cytokines
c. the ways in which HIV is spread ( why body fluids?)
the virus is found free and in macrophages of blood, semen, vaginal secretions, and breast milk
3. Write out the chemical formula that describes the conversion of carbon dioxide to bicarbonate ion, and
use the formula to explain why hyperventilation and hypoventilation affect the acid base balance.
CO2+H2O  H2CO3 H+ +HCO3Hyperventilation can be caused by a fever or acidosis. In both cases, hyperventilation tries to cause a left shift in
the O2/CO2 association/dissociation curve, combining the HCO3- and H+ to form CO2 and H2O in an attempt to
bring the pH back to homeostasis.
Acidosis results in hyperventilation in an attempt to raise the pH by L shifting the equation.
Hyperventilation results in alkalosis in an attempt to bring the pH back up from an acidotic state.
Alkalosis results in hypoventilation in an attempt to lower the pH by R shifting the equation.
Hypoventilation results in acisdosis in an attempt to bring the pH down from an alkalotic state.
4. Name the five immunoglobulin classes, and describe the functions of each.
Immune globulins are part of the body’s humoral or antibody mediated response response
6. IgG – most common – single unit = monomer (looks like a Y made of double lines) is found In body fluids
and crosses placenta, so an infant is born with it, provides passive immunity: you are not the one who made
the antibodies.
7. IgA – is a dimer in structure ( like 2 Y’s put together ) crosses breast milk, can also be secreted in mucus
secretions, provides passive immunity.
8. IgM – initial response, 1st antibody to appear after infection, is a pentimer ( looks like 5 Y’s put together) and
therefore can combine with 10 antibodies  causes clumping.
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9. IgE – goes to work after IgM, responsible for most allergies, mast cells have receptors for IgE
degranulation  histamine release. Allergy shots cause the production of IgG and that then takes care of the
allergen.
10. IgD – is a surface receptor of the B cell, usually membrane bound, not found floating around unless it has
just been shed by B cells after clonal expansion after selection of B cell, it is another monomer.
5. You have just moved from your home on the Atlantic coast to a small town high in the Rocky Mountains.
Explain the effects of this move or your respiratory system. What are the short-term and long term
compensations you might expect your body to make to this new environment?
For a few days, I would experience mild hypoxia because of the high altitude. Normal/sea level pO2 at 760mmHg
is 160mmHg, but at higher altitude this drops and lower pO2 results in less O2 being available to the cells mild
hypoxia hyperventilation respiratory alkalosismild cerebral edema headache, insomnia, tachypnea,
nausea.
My kidneys would respond to the hypoxia by producing Erythropoietin which is needed for RBC differentiation.
After a few days my body would have compensated for the lower pO2 pressure by circulating a higher number of
RBCs. The alkalinity also causes a L shift in the O2/CO2 association/dissociation curve and that makes it easier
to load O2 in the lungs: Hgb has an increased affinity for O2 loads it easier.
Lab notes for test 4
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Renal system
Kidney – renal fascia – anchors peritoneum to abdominal wall.
Adipose capsule – fatty tissue surrounding tissue.
Renal capsule – fibrous layer that adheres to the kidney.
Cortex – light reddish brown – 1 million corpuscles ( glomerular capsule and glomerulus )
Glomerulus – the filter through which the wastes pass through that make up urine – it is a minute capillary bed.
Nephron – the functional unit of the kidney. Glomerulus, proximal convoluted tubule, descending limb, ascending limb,
Outer 2/3 of cortex - Cortical nephrons The cortical nephrons are located entirely within the cortex.
Inner 1/3 of cortex – juxtamedullary nephrons have loops of Henle that extend well into the medulla.
Medullary renal pyramids ( 6-18) are separated by renal columns, terminating at renal papilla, minor calyx, major calyx,
renal pelvis.
Calyx – minor an major – are fingerlike extensions of the pelvis. The minor calyxes are subdivisions of the major one.
The minor calyces also terminate in cuplike areas that enclose the apexes of the medullary pyramids and collect urine
draining from the pyramidal tips into the pelvis.
Path of blood flow through the kidneys: (KNOW!)
Renal artery  segmental arteries interlobar arteries  arcuate arteries  interlobular arteries  afferent arterioles
 glomerular capillaries  efferent arterioles  peritubular capillaries and/or vasa recta  interlobular veins  arcuate
veins  interlobar veins  segmental veins  renal veins.
Ureters enter posteriorly in bladder. Bladder median umbilical ligament connects bladder to abdominal wall.
Two lateral ligaments connect it to the posterior body wall. Trigone is the triangular region of the bladder that
encompasses both ureteral orifices and the single urehtral orifice.
The internal urethral orifice has an internal sphincter which is involuntary.
In females, the urethra is short and straight, ca 4cm long. Due to its proximity to the anus, females are more prone to
bladder infections. In the male, the urethra is about 20cm long, and merges with the spermatic cords and continues
through the penis to the external urogenital opening. The urogenital diaphragm is the muscular floor of the pelvic cavity.
Urine is clear in turbidity, pale yellow to amber in color, urochrome due to destruction of hemoglobin. The pH will range
from pH 4.5 –6, with an average of 6. A high protein diet will yield a more acidic urine, whereas a vegetarian diet results
in a more alkaline urine.
Specific gravity - 1.001-1.030 is the relative weight compared to the same weight of de-ionized (DI) water.
Albuminuria is the presence of albumin in the urine – usually, albumin is too large to cross the capillary wall.
Presence of glucose in urine – glycoseuria
Ketoneuria – from fat metabolism
Red blood cells in the urine = hematuria
Bile pigments – bilirubinemia
WBCs, casts, cellular crystals
Unorganized sediments – uric acid, ammonium nitrates, cholesterol, calcium oxalates, calcium carbonates, and calcium
phosphates.
Organized sediments are not normally present – squamous epithelial cells, transitional epi. cells, WBCs ( neutrophils ),
RBC’s, granular casts, RBC casts, hyaline casts, fatty casts.
Lab
12/7/98
DI water – should lead to increase in urine volume, SG decrease
0.1% NaHCO3- - should lead to little increase in urine volume, then conserving H20, increase in SG.
0.9% NaCl – leads to slight increase in urine output, then same. Increases specific gravity.
2.0% NaCl – leads to conservation of urine , no output.
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Digestive system
Alimentary canal or GI tract + accessory digestive organs = digestive system
Mouth – vestibule – carbos start being digested here
Salivary glands empty their secretions into the oral cavity
1. Parotid glands – large, located near the ear – mainly serous – contains amylase
2. Submandibular glands – at mandible – mucin and amylase
3. Sublingual glands in floor of mouth – mucin and amylase
Oropharynx
Laryngopharynx
Esophagus
Lower esophageal sphincter
Stomach – 3 muscle layers: circular, longitudinal, oblique
Protein starts digestion here
Pyloric sphincter – valve into small intestine
Rugae – folded lining of stomach allows for expansion – has columnar pits
Greater and lesser curvatures
Greater and lesser omentum – suspends stomach – lesser connects stomach to the liver, greater goes around
small intestine
Small intestine –Duodenum – short – 10 cm, digestion of fat and carbos
Jejunum
Ileum – 6 feet
Large intestine – 5 feet – from iliocecal valve to anus, longitudinal muscle is called teniae coli.
cecum
appendix
colon – ascending
hepatic/ right colic flexure
transverse
splenic/ left colic flexure
descending colon
sigmoid colon – no water removal here
rectum
anal canal
anal orifice
Accessory structures
Liver – produces bile salts for lipid digestion. Sends them to gall bladder for storage via hepatic duct
4 lobes: Left and right, Caudate, and Quadrate.
Gall bladder – stores bile salts, cystic duct
Cystic duct and hepatic duct merge into the common bile duct
Pancreas – acinar cells  lipases Pancreatic ducts. We have 2 pancreatic ducts because during fetal development
we have 2 pancreas, and they fuse, but the ducts don’t, they become the large and small pancreatic ducts.
The ductus venosum is a fetal structure that later on becomes the round ligament. It suspends the liver from the body
wall.
LAB
12/9/98
Mastication starts in the mouth.
Labia – lips
Vestibule – between lips and teeth
Teeth – enamel, dentin, gingiva, pulp cavity, root canal, cementum, periodontal ligaments, apical foramen ( know picture
on page 405)
Oral cavity – hard palate, soft palate, uvula (tonsils and uvula have immune function: they trap stuff )
Stomach – food from here on down is called chyme.
The salivary glands release enzymes for carbohydrate digestion: amylase – a starch enzyme.
Protein digestion starts in the stomach with the gastric juices.
Peristalsis is movement by the longitudinal and circular muscles that propulses food down and around.
The stomach is the only structure with an oblique muscle layer.
Gastric glands
Pyloric sphincter
Plica are folds in the small intestine that increase the surface area for absorbtion
Three slides of the small intestine:
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1. Duodenum – has fewer plica than the jejunum and they are less tall. Bile salts enter here and pancreatic juices like
amylase, bicarb, lipases, proteolytic enzymes.
2. Jejunum has lots of tall plica. Absorbtion of nutrients takes place here.
3. Ileum – contains Peyer’s patches and large number of local flora like E.coli. They are required for digestion.
The colon has longitudinal muscle concentrated in 3 strips called Taenia Coli. Since these bands are shorter than the
rest of the wall of the intetine, they cause the wall to pucker into small pocketlike sacs called haustra.
The layers of the colon are from inside out: mucosa, submucosal layer ( basal lamina ) muscularis, outer capsule layer.
The mesocolon is a layer of mesentery between the ascending, transverse, and descending colon, it attaches the
transverse colon to the posterior body wall.
The pancreatic-duodenal sphincter ( sphincter of Oddi) regulates the release of pancreatic amylase into the
duodenum.
FOOD  lips  mouth  in the oral cavity food is masticated, made into bolus by tongue  oropharynx 
laryngopharynx esophagus gastroesophageal sphincter stomach pyloric sphincter duodenum
jejunumileum ileocecal valve cecum ascending colon  transverse colon descending colon sigmoid colon
rectum anal canal  anal sphincter FECES
LECTURE MATERIAL FOR TEST 5
Kidney
Functions are:
1. Urine formation:
a. blood volume
b. composition
c. BP – primary long term regulation are kidneys
2. Metabolism
a. gluconeogenesis
b. EPO
c. Vitamin D
3. Electrolyte levels
4. pH
12/7/98
The renal fraction is about 20-25%, that means that the renal arteries deliver 20-25% of the resting cardiac output to the
kidneys.
Path of blood flow through the kidneys: (KNOW!)
Renal artery  segmental arteries interlobar arteries  arcuate arteries  interlobular arteries  afferent arterioles
 glomerular capillaries  efferent arterioles  peritubular capillaries and/or vasa recta  interlobular veins  arcuate
veins  interlobar veins  segmental veins  renal veins.
Microscopic anatomy
1. Nephrons – functional unit of the kidney where urine is produced
a. vascular portion – made of simple squamous epithelium - afferent arteriole
glomerular capillary bed is made of fenestrated capillaries which drain into the
efferent arteriole which drains into the
peritubular capillary network
b.
tubular portion – Bowman’s capsule surrounds glomerular capillary bed – it is a hollow structure attached to a
network of tubules, made of simple cuboidal cells
1) proximal convoluted tubule drains into
2) loop of Henle ( hairpin ) drains into the medulla
3) Distal convoluted tubule drains into
4) Collecting duct
There are 2 types of nephrons:
1. Juxtamedullary nephrons have long loops of Henle that extend well into the medulla of the kidney. This allows for
production of more concentrated urine, the volume is decreased, the waste amount is increased. These are primary
in animals that live in the desert.
2. Cortical nephrons have short loops of Henle that are basically confined to the cortex. These are prevalent in
animals that do not need to conserve water.
Humans have about equal number of both types.
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Urine formation is the primary duty of the nephron. This is done in 2 steps:
1. Filtration – the forcing of fluids and dissolved substances across a filter. BP pushes the liquid portion of blood and its
dissolved substances across a filter. Things that are filtered out include small stuff like AAs, Na+ Ca+, Glucose, K+,
Cl-, urea, NH4. This filtrate must then be manipulated. There are forces favoring filtration and those opposing
filtration. Subtract one from the other and the result is the Net Filtration Pressure ( NFP). The kidneys are good at
increasing vasoconstriction and –dilation and BP. The pressure in the arteriole into the kidneys is 55mmHg ( normal
body cell pressure is 35mmHg ). The resulting NFP in the kidneys is 10mmHg, and if you compare that to the body
cell, it means that 10 times the amount of fluid will be filtered in the kidneys. The NFP is easiest controlled by
controlling the blood hydrostatic pressure ( BHP). Page 862.
2. Reabsortion is the active transport ( pinocytosis ) from the tubule back into the blood. There is lots of control over it.
More detail below.
3. Secretion is the moving of something from the blood into the urine to enhance the amount we will get rid of. More
detail below.
The filter is in the capillary bed in the glomerulus. It filters in 3 stages:
1. Capillaries in the endothelium are fenestrated. They filter out all the blood cells and largest proteins.
2. The basement membrane of the capillaries also has pores, but smaller the endothelial ones. It excludes the large
and most medium sized proteins.
3. Bowman’s capsule has 2 layers, the visceral layer has podocyte with pedicles, which looks like a ball with a hand
on it, the pedicles are the fingers which are interlaced. They also have slit pores, which are even smaller and
exclude all medium sized proteins, but anything small gets through.
The filtrate is anything that gets through the filters: water, glucose, electrolytes, organic acids, urea, NH4, vitamins, AAs,
dissolved gases ( CO2, HCO3), O2, smallest proteins, and peptides.
The filtration fraction is the amount of fluid that comes through, about 16-20%. This amounts to about 125ml/minute
and is called the Glomerular Filtration Rate (GFR). The glomerular filtration is about 180 liters per day ( 45 gallons ).
If the GBHP goes down, so does the NFP.
GFR increases if afferent arterioles are vasodilated or efferent arterioles are vasoconstricted.
GFR decreases if the afferent arterioles are vasoconstricted, and the efferent arterioles are vasodilated.
Vasoconstriction/dilation is controlled by the sypmathetic division of the autonomic nervous system. It regulates the size
of the afferent arterioles and efferent arterioles and causes vasoconstriction. If there is less input from the sympathetic
branch, dilation occurs.
Hormonal control:
1. Angiotensin 2
2. Aldosterone – controls BP
3. ADH – controls BP
4. ANP – decreases BP
Reabsorbtion occurs mostly in the proximal convoluted tubule ( PCT).
1. Small proteins are recovered by pinocytosis – they adhere to the wall of the tubule and are then engulfed by the
tubule.
2. Glucose and AAs are reabsorbed by active transport. When the glucose transport maximum is reached ( i.e. all the
carriers are filled ) glucose is spilled in the urine. ( diabetics ). 2 nd symport or facilitated diffusion is used first with
gradients.
100% of proteins and AAs should be reabsorbed from the urine. K+, Na+ are reabsorbed by active transport. HCO3- by
simple diffusion. There is no active transport of water anywhere in the body. 65% of water filtered out is reabsorbed by
osmosis in the PCT, so 35% of 180 liters are filtered.
Distal convoluted tubule (DCT)
15% of water is reabsorbed here by osmosis. 5% of Na+ by active transport.
Collecting duct
9% more water are reabsorbed here, and the rest of the Na+.
In the end, 99% of water has been reabsorbed, and all the Na+ and HCO3-.
Secretion
H+ ion are secreted in the PCT and DCT to regulate pH. A pH of 4.5 is the most acidic for urine, so there is a limit to how
much HCO3- can be secreted.
K+ is secreted according to aldosterone levels ( saves Na+).
Antibiotics are secreted at a high rate.
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The loop of Henle mainly functions in water conservation and salts. The deeper you get into the kidney, the higher the
salt content. In the cortex Na levels are 300mos, in the medulla it is 1200mos.
The descending loop is permeable to water, so as you go down the descending loop towards the medulla, water is being
reabsorbed to dilute the ever increasing levels of Na+, so the Na+ content rises to 1200mos as the water is being saved.
The ascending loop, however, is impermeable to water, so the water cannot come back into the tubule. Here, Na+ is
actively transport out of the tubule to equalize the Na+ content so the higher you get up in the ascending loop, the closer
the Na+ levels drop back to 300mos.Since the walls of the ascending tubule are thicker, this is also called the thick limb
sometimes.
This explains why animals living in the desert have long loops of Henle so they can absorb the most water back. Animals
living in water have short loops of Henle.
The collecting duct goes right back through the medulla, so it is subjected to the same gradient of Na+. It has a variable
water permeability though, which is controlled by ADH:
The higher the ADH levels, the higher the permeability. Water and alcohol inhibit ADH, so water is not conserved.
A low ADH level decreases the permeability, so water is conserved.
GFR is what controls the volume of urine to some extent. The GFR is most controlled by BP, and BP is affected by:
1. sympathetic NS
2. ADH and Aldosterone
3. ANP
This is local control. The distal collecting tubule is right next to the afferent arteriole – and where they touch is called the
juxtaglomerular apparatus – it has specialized cells.
a) Macula densa cells – are part of the wall of the DCT and count the number of Na+ and Cl- ; they have specialized
receptors that keep a running total ( I love Lucy episode in chocolate factory at conveyor belt ). Macula densa cells
also monitor GFR: if it falls, renin is released. Renin is an enzyme released by the DCT into the blood where it
combines with angiotensin  angiotensin 1  to the lungs  + convertase  angiotensin 2 = potent
vasoconstrictor of the body. It increases blood pressure and thereby GFR, and that speed up of GFR inhibits further
renin release.
b) Juxtamedullary cells ( JG cells) are part of an amino acid , they cause dilation of the afferent arterioles and
constriction of the efferent arterioles, thereby increasing GFR.
A decreased GFR rate increases renin release  increases angiotensin 2  also causes release of aldosterone (saves
Na+ and H2O)  increases blood volume  increases BP  increases GFR. ADH release is increased when the
hypothalamus detects an increase in Na+  to the collecting duct  water is saved, thirst increases, as does BP and
GFR.
Digestive system
Functions:
1. Digestion ( to break apart )
a. Mechanical ( movement ) – mostly by chewing, churning.
b. Chemical – by actual chemicals or enzymes
Anatomy or the digestive tract ( or GI tract)
It is a long tube that is open at both ends. Things that are inside the GI tract are external, and not in the body
Accessory structures
Teeth, liver, gallbladder, tongue,…
Cross section of the GI tract
1. Serosa is the outer layer – equal to the visceral peritoneum, made of connective tissue, gives the tube strength and
shape. Also reduces friction.
2. Muscularis – mostly smooth muscle, some skeletal, in the esophagus, pharynx, and mouth. 2 layers:
a. Longitudinal layer is the outer layer – when it contracts the tube gets shorter.
b. Circular layer is the inner layer – it decreases lumen size
These 2 layers allow for mixing and peristalsis. The stomach has a 3rd layer:
c. Oblique layer – allows for even more mixing and some mechanical digestion
3. Submucosal layer – loose areolar connective tissue – lots of space in here for
a. lots of blood vessels
b. lymphatics
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myenteric plexus – forms nervous network, coordinates the movement of contents through
it. By controlling the smooth muscle of the muscularis, this plexus is the major regulator of GI
motility.
d. Glands
4. Mucosal layer – lining of the hollow space – epithelium, changes dramatically depending where you are
a. Esophagus – stratified squamous ( many layers, non-keratinized )
b. Stomach – simple cuboidal and simple columnar – single layer arranged in gastric pits. Has
villi ( fingerlike projections ) to increase surface area
c. Large intestine – smooth surface made of simple columnar epithelium
d. Anal mucosa – stratified columnar
Mouth or buccal cavity – between cheeks and teeth
Oral cavity – behind teeth
Tongue – skeletal muscle, has to do with speech but also moves food. It produces a bolus – which is an amount of food
that can be swallowed – and it pushes food back. Swallowing is voluntary at first, then it becomes involuntary.
Teeth are the hardest substance in the body. Humans have deciduous teeth which fall out, and permanent teeth, which
start coming in around age 6 or 7. Dentition is a collective term for the types of teeth found in a mouth. They tell you
what foods are/were eaten by that animal:
Incisors are for biting. Canines are for tearing flesh. Bicuspids and molars are for grinding food ( plants ). Omnivores
can eat everything.
Associated with the mouth are salivary glands:
1. Parotids release the most amylase. These are infected in mumps.
2. Submandibulars are located at the angle of the mandible.
3. Sublinguals release the least amylase. They are located underneath the tongue, above the sumandibulars.
The salivary glands release saliva:
a. mostly water
b. mucin – makes it slick
c. Lysosyme which breaks down bacterial walls
d. Ions – Na+, K+
e. Amylase – digests starch (plant storage form of glucose) into 2-glucose units called maltose
The salivary glands are under autonomic control: sympathetic stimulation decreases secretion, parasympathetic
increases it. Function of saliva: it moistens, lubricates, begins chemical digestion, and decreases bacteria. That is why
open mouth breathers often have bad breath: the lysosyme isn’t there to take care of the bacteria. This also causes the
bad taste in your mouth in the morning: you have been sleeping with your mouth open.
c.
The esophagus is made of smooth muscle and is normally collapsed until a bolus of food is in it. Once it passes through,
the esophagus goes back to its collapsed state. The esophagus passes through the
1. Diaphragm which helps keep the esophagus closed. A hiatal hernia is condition where the usually tight hole in the
diaphragm is larger than normal and allows stomach contents to back up into the esophagus.
2. Cardiac or lower esophageal sphincter – also helps keep it closed. It is mostly contracted.
The stomach has a greater and a lesser curvature to it. It has 3 layers of muscle. The epithelium inside is folded into
rugae until the stomach is all filled up and all stretched out. Gastric pits in the stomach are narrow channels that extend
deeply into the lamina propria of the stomach mucosa. They are lined with mostly 1. simple columnar but also 2.
parietal cells which make and release HCl – which lowers the pH in the stomach to 2 or less. This acidic environment
can be damaging to other cells, and therefore 3. mucus cells produce mucus to protect the tissues from the HCl. The
4. Zymogenic cells release pepsinogen which combines with the acid  pepsin  digests proteins into peptides.
All enzymes have a favorite pH where they work best. Amylase stops working in the acidic stomach. 5. Endocrine cells
release gastrin which aids in ralaxation of the ileocecal valve.
Food in the stomach is called chyme. Some absorbtion takes place in the stomach: Water, alcohol ( that’s why an empty
stomach intoxicates faster) and Vitamin B12.
The pyloric sphincter at the duodenal end of the stomach opens periodically once food has reached a certain
consistency  chyme squirts into the duodenum at a pH of 1-2. The small intestine is 13 feet long, all folded up.
1. The duodenum is the shortest section, it forms a loop.
2. The jejunum is the longest
3. Ileum
The pancreas lies in a fold of the duodenum.. It has partially endocrine, partially exocrine functions. The pH of 1-2 is too
low for the small intestine, so the pancreas will secrete bicarbonate to raise the pH to >7.
1. The exocrine accini cells produce digestive enzymes
a. Aminopeptidase for chemical digestion of proteins
b. Carboxypeptidase for chemical digestion of proteins
c. Trypsin for chemical digestion of proteins
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d. Chymotrypsin for chemical digestion of proteins
e. Amylase for chemical digestion of starch
f. Maltase for chemical digestion of maltose
g. Lipase for chemical digestion of fat
2. The F cells secrete pancreatic polypeptide – paracrine secretion that regulates acinar glands.
The liver is the 2nd largest organ – right after the skin. Made of 4 lobes, it consists of the R and L lobe, the caudate and
the quadrate lobe. It detoxifies poisons, stores fat soluble vitamins ( A, D, E, and K) and glucose (glycogen), Fe. It
produces bile which is made up of cholesterol, bile salts, water, lecithin, several ions, and bile pigments from the
breakdown of blood (biliverdin green). Bile is an emulsifier for fat ( it surrounds it )  micelle – allows the fat to disolve
in the stomach. Bile can form stones from cholesterol.
In the small intestine the submucosal layer has lots of blood vessels and lymphatics ( lacteals ) for fat absorbtion. All
cells in the small intestine have microvilli for increased absorbtion capabilities. Water , AAs, glucose, vitamins, and
electrolytes are absorbed here. From the ileum, the chyme leaves via the ileocecal valve into the large intestine,
specifically the cecum. This is a short pouch that is actually below the valve. Minimal bacterial digestion takes place
here. The vermiform appendix is a lymphoid tissue in function. It is a vestigial part of the digestive system.
The colon consists of the ascending, transverse, and the descending colon. It has pits = intestinal glands, but little
digestion occurs here by our system. This is the main place for bacterial digestion. Water absorbtion, Vitamin B and K,
takes place here as well. The colon concentrates and then eliminates waste materials via the rectum and then through
the anus. The anal sphincter is circular with columnar epithelium. The internal sphincter is smooth muscle and
therefore involuntary, the external sphincter is skeletal muscle and therefore voluntary.
Feces, the final elimination product, are still over half water. The second largest contributor are bacteria, then epitelial
cells.
When food enters the stomach, it causes mass peristalsis. This is a strong peristaltic wave that begins in the middle of
the transverse colon and quickly drives the contents of the colon into the rectum. This is known as the gastrocolic reflex.
Defecation reflex is caused by distension of the rectal wall ( it ultimately causes the contraction of the longitudinal
muscles of the colon, causing it to get shorter, increasing the pressure inside. This pressure, along with parasympathetic
stimulation opens the internal sphincter and defecation occurs.
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POSSIBLE QUESTIONS FOR TEST 5
1. Describe the digestive activities occurring in the stomach.
Continued mechanical digestion of all foods, chemical digestion of proteins and carbohydrates ( continued ).
When stretch receptors detect distension of stomach or chemorecpetors the rise of chyme pH, parasympathetic
fibers are stimulated in the submucosal plexus. These cause waves of peristalsis and gastric juice release from
parietal, chief, and mucosal cells. When the food has been mixed enough, a small amount squirts into the duodenum
past the pyloric sphincter. This causes the stomach to be less distended and the pH is lower, so the negative
feedback cycle turns off.
Gastrin is also released due to the parasympathetic fiber stimulation and subsequent acetylcholine stimulation. The
target cells are the gastric glands. Gastrin causes the growth of gastric glands, the secretion of gastric juice,
contraction of the esophageal sphincter, increases the motility of the stomach, relaxes the pyloric and ileocecal
sphincters. Gastrin is inhibited when the pH of gastric juice drops below 2.0 and is stimulated when the pH rises. This
helps maintain an optimal pH for pepsin to work, the killing of microbes, and denaturing of proteins.
2. Identify the protein-hydrolyzing enzymes in the digestive tract, and name their sources. Why are these
enzymes released in an inactive form?
The zymogenic cells of the stomach produce Pepsinogen, which turns into Pepsin under influence of HCl.
The exocrine accini cells of the pancreas produce the following protein hydrolyzing enzymes:
Trypsin, Chymotrypsin, Elastase, and Carboxypeptidase.
Aminopeptidase is produced by the brush border in the intestine.
If they were active upon release, they could digest the protein in the body cells around them when there is no
food/protein around.
3. Describe in detail the renin-angiotensin negative feedback loop that helps regulate blood pressure and
glomerular filtration rate.
Some stressor causes BP and therefore GFR to drop  macula densa cells of the JGA detect the decrease and the
decrease of Na+, Cl-, and water  DCT releases renin ( enzyme ) directly into the blood where it interacts with
angiotensin and makes angiotensin 1. This passes through the lungs, where it is converted by convertase into
angiotensin 2, which is a potent vasoconstrictor. Angiotensin 2:
1. Vasoconstricts the afferent arterioles  GFR increases.
2. Vasoconstricts arterioles in the body  raises BP
3. stimulates aldosterone secretion Na+ is saved along with water  increases blood volume  BP and GFR rise
4. stimulates thirst center in hypothalamus
5. stimulates ADH secretion from neurohypohysis
Angiotensin 2 increases blood pressure and thereby GFR, and that speed up of GFR inhibits further renin release.
4. Predict the effect on GFR and NFP of each of the following; Explain you reasoning in each case
1) Hemorrhage  initially compensated, then decreased GFR and NFP. The body tries to maintain homeostasis
and increases GFR and NFP by increasing BP. As blood loss continues, this is no longer possible and GFR and
NFP drop. If GBHP drops below 45mmHg, filtration stops  anuria.
2) increased permeability of the endothelial-capsular membrane  would increase GFR and NFP slightly – the
membrane only filters out the largest of proteins, so instead of being filtered out they would now get through,
thereby increasing colloid pressure exerted by the filtrate resulting in more fluid being filtered.
3) constriction of the lumen of the proximal convoluted tubule  decreases GFR and NFP since there is less
blood coming through to the filter.
5. List the functions of the kidneys
1. Urine formation:
d. blood volume
e. composition
f. BP – primary long term regulation are kidneys: renin-angiotensin pathway
2. Metabolism
d. gluconeogenesis
e. EPO
f. Vitamin D
3. Electrolyte levels
4. pH – secretion of variable amounts of H+ ions
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