1. Chronic stress gives rise to genuine physical pathological symptoms – relax!

2. if we just used passive diffusion, cells would certainly dry out! Instead we have a respiratory epithelium that is a flat sheet of cells devoted to gas exchange; it’s living, so it must be moist, and it minimizes the diffusion distance while maximizing surface area available

The movie Saw 3 is pack jammed with gore and horror and evil.

Many nights I just can’t sleep because of a horrific insomnia that keeps me up.

3. pathway = nose, mouth, pharynx, larynx, trachea, bronchi, lungs
it humidifies the air, warms the air for inhalation; cells are constantly secreting muscus that can trap particulates, and are ciliated- they are constant beating or waving to move the muscus upwards to the throat and mouth where it is swallowed…mucus elevator

4. see above; a production of pathogens or dust or debris produces a lot of mucus, and a stuffy nose develops

5. it controls the resistance to airflow and the distribution of air in the lungs; it is controlled by the ANS

6. there is increased mucus and generally inflammation that tightens airways, so there’s an increased chance of chronic infection in the lungs

1. abonormally low GH levels à pituitary dwarfism
normal GH, but lack of GH-R or IGFs à dwarfism as well
abnormally high GH prior to pubery à gigantism
abnormally high GH after puberty à acromegaly (thickening, sharp feat.)

2. medulla in the middle, cortex on the outside; medulla secretes catecholomines (epinephrine) and cortex secretes glucocorticoids (cortisol)

3. sympathetic nervous system extends through the cortex and into the medulla controlling it; glucocorticoid release from the cortex is stimulated by ACTH

4. epinephrine, aka adrenaline, accelerates cellular energy utilization and mobilize energy reserves; cortisol accelerates the rates of glucose synthesis and glycogen formation, increasing glucose in the blood

alarm phase: sympathetic neurons innervating the adrenal medulla, stimulating the release of epinephrine or norepinephrine, or both. This response is extremely rapid, with equally rapid effects including increased heart rate, increased vasodilation in muscle, and energy mobilization.
This response is geared to coping with short term stresses, like fighting, or the initial phase of an unexpected stimulus.
resistance phase:: usually occurs 1-5 minutes later, if the stress persists. This phase is mediated by the release of CRF from the hypothalamus, ACTH from the anterior pituitary, and glucocorticoid release from the adrenal cortex.
The glucocorticoids include cortisol, which stimulates the liver to increase blood glucose, protein breakdown to increase amino acids in the blood, and fat breakdown to increase fatty acids in the blood. It also inhibits inflammation and the immune response.
exhaustion occurs if the source of stress persists in the long term. If plasma glucocorticoids are maintained too high for too long, a number of debilitating physiological effects result, including suppression of appetite, sleep, immunity, sex drive, and GH release, and an increase in irritability and possibly neural degeneration.

1. your body temp decreases, so this stimulates the hypothalamus to release TRH, TRH heads to the anterior pituitary and stimulates the release of TSH, TSH tells the thyroid to release thyroxin (which affects the liver, heart, and muscles); thyroxin tells organs/tissues to increase the number of cellular mitochondria and metabolic enzymes, metabolic rate therefore increases, energy production increases, and body temp is raised!!! Thyroxin will feed back to the hypothalamus and anterior pituitary to inhibit them; if there’s no IODINE, thyroxin is decreased, so feedback is decreased, but TRH and TSH release still continues, so the thyroid is stimulated to mitosis so more cells might make more thyroxinà goiter

2. indirect effects: GH stimulates the liver to synthesize and release insulin-like growth factors (IGFs); IGFs are mitogens: they stimulate mitosis and protein synthesis in cells; all of this concerns the growth and maintenance of tissues
direct effects: GH will go to adipose cells, break down fats, and increase the number of fatty acids in the blood OR it will go to other cells like the liver, break down glycogen, and increase glucose in the blood; all of this concerns energy mobilization

3. see above

4. indirect effects: when blood glucose is high, direct: when it’s low

5. NO IDEA

I try to experience new things and accomplish all of my goals as best as I can.

Chemical Dependency is nothing to laugh at and has wrecked more lifes than you can imagine.

1. see above; look up phosphorylation

Managing people for the maximization of dentistry is important.

Wind power is going to be the next “big thing” soon I hope.

2. the effect of the target cell depends on the nature of the proteins affected, by the phosphrylation of membrane proteins can open ion channels; other enzymes inside the cell can only be activated through phosphorylation

3. we can degrade the second messenger (cAMP) using phosphodiesterase, we can endocytose the H/R complex, or we can dephosphorylate the target proteins

4. thyroid hormone (thyroxin) has a nuclear receptor that stimulates the transcription of GH receptor…this increases the abundance of the GH receptor and the cell’s sensitivity to GH therefore increases

5. draw the axis and explain

6. posterior lobe of the pituitary is neural tissue- axons from the hypothalamus extend into the posterior pituitary; hypothamalic neurons synthesize hormones and release it in/from the posterior pituitary; these hormones are oxytocin and ADH

7. anterior lobe of the pituitary is glandular tissue- it therefore synthesizes and secretes its own hormones; the hypothalamus affects the anterior lobe by releasing regulating hormones that either stimulate (TSH, FSH, LH, GH, ACTH) or inhibit (PRL, MSH) the anterior lobe; if we cut out the anterior pituitary, we’d have less GH and more PRL, for example

8. ADH: anti-diuretic, decreases urine production and helps conserve h20
oxytocin: affects smooth muscle contraction esp. in the uterine and mammary muscles; in men, it helps the prostate release sperm

1. - effects on smooth muscle: gastrin
- growth effects: GH
- reproductive effects: androgens, estrogens
- osmoregulation effects: ADH
- stress effects: NE/E, glucocorticoids

2. amino acid derivatives: amines *not lipid soluble
peptides: small proteins – insulin, glucagons *not lipid soluble
lipid derivatives: cholesterol, steroid hormones and…
…fatty acids: prostaglandins (role in immune system, fever) *lipid soluble

3. PASS THROUGH: if the H can pass through, that means the receptor is in the cytosol or the nucleus; H binds to the receptor and becomes the H/R complex; H/R complex migrates to the nucleus and binds to the DNA on regulatory regions (transcription factor) which affects transcription of certain genes; genes get turned on or off and some proteins in the cell will increase or decrease à effect!

CAN’T PASS THROUGH: receptors are in the membrane; H/R complex in the membrane activates G-protein; G-protein activates adenylate cyclase inside the cell; this plus ATP leads to cAMP which acts as a second messenger to activate the kinase…there are then alterations in enzyme activity and opening of ion channels à effect!

1. pressure is low and blood may pool

2. muscular compression and respiration are impaired, leading to a decline in cardiac output- blood supply to brain is reduced and fainting can occur

3. Venous return is achieved by a system of one-way valves in veins – when skeletal muscles contract, they squeeze veins, producing pressure and moving blood back toward the heart. Also, during normal breathing, pressure changes within the chest cavity affects similar pressure changes in the vena cava, the major vein entering the heart from the systemic circulation. (muscular compression and respiratory pump)

4. i.e. brachial artery: external pressure applied to cut off artery and then is slowly deflated; when turbulent flow resumes, that is systolic pressure; when the sound stops and flow is smooth, that is diastolic pressure

5. see and study picture in notes; The pancreas has beta-cells which secrete insulin in response to increased blood sugar – insulin stimulates several tissues to take up sugar for storage. Meanwhile, a decrease in blood sugar stimulates pancreatic alpha-cells to secrete glucagon – this hormone primarily stimulates the liver to release glucose into the blood for immediate use. These two peptide hormones help maintain blood glucose within tolerable limits.

6. a chemical messenger that carries a signal from one location to another, often through the blood

– affect the synthesis of other hormones: ?
- metabolic effects: ?

1. TURBULENCE – flow is not uni-directional; we have Laminar Flows which are parallel flow lines =>, or turbulence caused by obstructions; if blood gets too watery, it increases the chance of turbulent flow
2. ?; blood pressure declines away from the heart as a result of friction between the blood and the vessel walls; arteries are typically way thicker than veins and help to dampen the oscillation for even flow through the capillaries
3. systolic pressure is our blood pressure while pumping; diastolic is our blood pressure at rest; we maintain 80 mm/Hg during diastole because arteries have lots of elastic tissue that will snap back (elastic recoil or elastic rebound)- this propels blood forward during diastole when the semilunar valves are closed
4. see above; elastic rebound is greatest near the heart and drops in succeeding arterial sections- by the time blood reaches a precapillary sphincter, there are no pressure oscillations and the blood pressure remains steady
5. hydrostatic pressure from the arterial end is low, but still pushes enough to move fluid through the capillary; colloid osmotic pressure moves water across the capillary walls; because capillary pressure higher at the arterial end and COP is constant, water tends to move out at the arterial end and in at the venous end; capillary and COP are equal right in the middle (see 396)

1. Heart sounds are the lub-dup we are all familiar with; the lub occurs when the AV valves shut, and the dup occurs when the semilunar valves shut, but the sound itself is the turbulent flow of blood against the closed valves
2. Stroke volume is the amount that a full ventricle can hold, which is normally 70 mL in humans; cardiac output is the stroke volume times the heart rate = 70 mL x 70 beats/min = 4900 mL/min
3. this occurs when the incoming blood (or cardiac return) causes the cardiac muscle to stretch, increasing the force of the next contraction; increasing cardiac return causes an increase in the whole system! It is based on need…
4. PARASYMPATHETIC – vagus nerve uses Ach to hyperpolarize the nodal cells it innervates, decrease rate of APs, decrease heart rate (if you cut the vagus nerve, heart rate will increase)
   SYMPATHETIC – cardiac nerve uses nor/epinephrine to depolarize the nodal cells and ventricular muscles it innervates, increase conductance of APs, increase heart rate
5. right we totally already answered this in #3
6. hmmm…

VASCULAR RESISTANCE – friction with the blood vessel wall that will increase or decrease with blood vessel diameter (how?)
VISCOSITY – a fluid resistance; friction against itself (i.e. water is 1, blood is 5, honey is a lot more)

1. see above; depriving tissues of O2 can lead to cell damage and/or cell death; cardiac cells are non-regenerative and are replaced with a patch of fibrous connective tissue – this diminishes pumping efficiency and the normal functioning capabilities of the heart drop
2. diastole – rest, systole – pump
3. see pg 380; diastole: the atria fill with blood, the A.V. valves open and the ventricles fill to about 80% while semilunar valves are still closed…

atrial systole: atria pump blood to ventricles, they fill to 100%…
atrial diastole: atria start filling with blood again, and
ventrical systole: AV valves shut, SL valves open, blood goes to either the lungs or the body

4. Cardiac muscle contractions are different than skeletal muscle contractions because they involve V-Ca++ gates! An AP is fired in the following steps: V-Na+ gates open first, sodium rushes in, V-Ca++ gates open and stay open, causing a plateau of depolarization inside the cell, V-K+ gates open and the rest of the AP steps follow; the plateau phase guarantees that another AP won’t fire before the contraction is done, therefore preventing tetanus
5. nodal tissue is made up of specialized cardiac muscle cells with an unstable resting membrane potential – a constant leakage of ions lets the sinoatrial (SA) nodes fire APs on its own~ setting a pace at about 70 APs/minute (or 70 beats/min)
6. AP spreads through the atria first, they contract, then the AP reaches the second node (AV node) that follows the lead of the sinoatrial node, delays signal to the ventricles, allows completion of the atrial contractions, and it relays the signal down specialized conduction fibers called Perkinje fibers- they spread the AP into the ventricles

1. right – pulmonary – to serve the lungs

left – systemic – to serve the rest of the body

2. atria are think, weak, “floppy dog ears” that receive blood; ventricles are thicker and are what pumps the blood out of the heart (left ventricle is thicker than the right because it’s harder to pump blood to the rest of the body than to the lungs)
3. right atrium, right ventricle, pulmonary artery, arterioles, capillaries in the lungs (O2 in, CO2 out), venules, pulmonary vein, left atrium, left ventricle, aorta, arteries, arterioles, capillaries (02 out, CO2 in), venules, veins, vena cava
4. they are striated and involuntary; they are also connected to each other end to end by intercolated disks and by gap junctions (in gap junctions, the cytoplasm is continuous with a number of other cells (see pg 371); cardiac cells are very aerobic and need a lot of O2… there’s lots of mitochondria and lots of hemoglobin
5. Coronary vessels are so named because they look like a “crown;” they surround the heart; blockage of coronary vessels can starve the heart of O2 which can lead to a heart attack (myocardial infarction); angina is the pain caused by reduced blood flow from coronary vessels