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APSM  2442  FINAL  STUDY  GUIDE  
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Nervous system vs
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Ex
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Davis)
§ Freely floating through blood, then binds to a receptor which activates g
protein à activates adenylate cyclase
§ Activated adenylate cyclase converts ATP to cAMP
§ cAMP is second messenger to activate protein kinase
§ Activated protein kinase phosphorylates cellular proteins
§ Millions of phosphorylated proteins cause reactions = physiological responses
§ Basically, hormone reacts outside of cell
Factors that determine how effective a hormone is at acting on a receptor cell:
o Amount of hormone released by endocrine gland
o Amount of receptors present on target organ
o Rate of removal of hormone from blood stream by liver or kidneys
Hormone interactions:
o Permissive – when a hormones requires simultaneous or recent exposure to another
hormone to act on target cells
o Synergistic – when effect of 2 hormones working together is greater than the effect of
a single hormone acting alone; could work alone but less effective
o Antagonistic – when a hormone opposes the action of another hormone (insulin and
glucagon)
o Agonist –
§ Ex
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Insulin à pancreas releases insulin when blood glucose levels are high,
insulin stimulate glucose uptake, blood glucose level drops
o Positive – body enforces result of stimulus
§ Ex
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Hormone
is made in hypothalamus and packaged in cell body of neuron then vesicles are transported

APSM  2442  FINAL  STUDY  GUIDE  

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down the cell
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Hormone is then
released from vesicle through hypophyseal portal vein into blood
o Oxytocin – enhances uterine contractions and stimulates milk ejection; transported
along hypothalamohypophyseal tract to posterior pituitary from hypothalamus and
released into blood via portal vein
o Antidiuretic Hormone (ADH) – decreases urine production
Thyroid Gland
o Thyroxine (T4), Tetraiodothyronine (T3) and calcitonin
o T3 and T4 are synthesized via interaction of iodine and Thyroglobulin (TGB)
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F and then
blood, but have to be carried by transport protein Thyroxine-binding globule (TGB)
§ Actions of TH: increases basal metabolic rate, stimulates synthesis of
NA+/K+ pumps, normal for body temp maintenance, stimulates protein
synthesis and increased use of glucose and FA for ATP production, increases
lipolysis and cholesterol excretion, enhances catacholamines by upregulating
beta receptors, accelerates body growth
§ Disorders: Grave’s disease (hyperthyroidism), Goiter (insufficient iodine)
o Calcitonin – decreases level of plasma calcium by inhibiting osteoclasts; produced by
parafollicular cells
§ Hypothalamus releases TRH à anterior pituitary secreted TSH à thyroid
secretes calcitonin
o Parathyroid Gland – increases plasma calcium by increasing osteoclast activity,
increases bone resorption, promotes calcitrol formation to increase calcium
absorption
§ Secretes PTH in response to low CA2+ plasma concentration
o Adrenal Glands
§ Capsule
§ Cortex
• Glomerulosa = aldosterone à mineralcorticoid
• Fasciulata = cortisol à glucocorticoid
• Reticularis = DHEA à weak androgens (more important for men)
§ Medulla = catecholamines (epinephrine and norepinephrine)

CARDIOVASCULAR SYSTEM
• Functions of blood:
o Transportation – gases, nutrients, hormones, waste
o Regulation – pH, body temp, osmotic pressure
o Protection – WBC, clotting
• Characteristics:
o Dense and sticky
o 38 degrees Celsius
o pH 7
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o TOTAL BLOOD VOLUME = 5-6 L males, 4-5 L females
• Blood = 55% plasma, 45% formed elements
o PERCENTAGES ON CHART
• Hematocrit = % of total blood volume occupied by RBC; 38-46% in females, 40-54% males

APSM  2442  FINAL  STUDY  GUIDE  

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o Anemia = below normal hematocrit, more common in females and chemo patients
o Polycythemia = hematocrit above normal, usually caused by EPO and blood doping
Hemopoiesis – process by which all of the formed elements of blood develop à blood cells
are formed in and mature in the red bone marrow
Erythrocytes – Red blood cells
o We make 2 million new RBCs / second
o Glycolipids on membrane yield blood type
o Hemoglobin – oxygen carrying protein
Heart is located in mediastinum
Pericardium – membrane that surrounds and protects the heart
o Fibrous pericardium – tough, elastic, dense irregular conn
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Problems with autorrhythmic fibers result in
arrhythmias
Sinoatrial (SA) node – in right atrial wall, no stable resting potential
o Repeatedly depolarize to threshold spontaneously à acts as pacemaker potential,
when it reaches threshold it triggers and action potential
o Each AP form SA node propagates through both atria by gap junctions à the 2 atria
contract at the same time
AP reaches Atrioventricular (AV) node via conduction along atrial muscle
o At AV node, action potential slows because of structural differences, the delay allows
time for atria to empty blood into ventricles
From AV node, AP travels to Atrioventricular (AV) Bundle aka Bundle of His à bundle
is only place where AP can conduct from atria to ventricles
After AV bundle, AP goes to Left and Right Bundle branches and extends through
interventricular septum towards apex
Purkinje Fibers conduct AP from apex upwards to rest of ventricular myocardium à
ventricles contract and push blood towards SL valves
Autorrhythmic fibers on their own:
o SA node = 100bpm
§ Controlled by hormones and ANS
o AV node = 50bpm
§ Sped up by sympathetic NS and release of vagus nerve; should get pacemaker
if AV node is damaged
o AV bundle, bundle branches, purkinje fibers
§ Need pacemaker if SA and AV are both damaged
AP goes through conduction system to excite contractile fibers (atrial and ventricular
muscle fibers)
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Plateau – maintained depolarization due to slow voltage gated calcium channels
opening in sarcolemma
• Calcium ions flow into cell
• Increased calcium triggers contraction
• K+ channels open and K+ leaves contractile fiber
• Calcium inflow and K+ outflow balances

APSM  2442  FINAL  STUDY  GUIDE  
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Repolarization
• More K+ channels open and K+ flows out
• Calcium channels close
• Outflow K+ restores membrane potential of -90mV
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HEART WAVES
o P-wave – first wave, represents atrial depolarization (SA node through contractile
fibers in atria)
o QRS Complex – starts going down then spikes way up then drops
• Rapid ventricular depolarization because AP is spreading through ventricular
contractile fibers
o T wave – long, slight upward dome shape
• Ventricular repolarization, occurs as ventricles are starting to relax
• Smaller and wider than QRS because repolarization is slower than
depolarization
• *During plateau, EKG is flat
• Problems:
o Enlarged P wave = enlarged atria
o Enlarged Q wave = myocardial infarction
o Enlarged R wave = enlarged ventricles
o T wave is flatter than normal when heart muscle is not receiving enough
oxygen à coronary artery disease, hyperkalemia (?)
• ECG intervals
o P-Q interval – time required for AP to travel through atria, AV node, and
fibers
§ Long PQ = AP detouring around scar tissue
o S-T segment – time that ventricular contractile fibers are depolarized during
plateau phase
o Q-T interval – start of QRS complex to end of T wave, time from beginning of
ventricular depolarization to end of ventricular repolarization
§ Long if there is myocardial damage or conduction abnormalities
EXTRINSIC INNERVATION OF HEART
o Heartbeat is modified by ANS
o Cardiac centers are located in medulla
§ Cardioacceleratory center innervates SA and AV nodes, heart muscle
and coronary arteries through sympathetic neurons
§ Cardioinhibitory center inhibits SA and AV nodes through
parasympathetic fibers in vagus nerves
Cardiac Cycle = all events associated with blood flow through the heart in one heartbeat
o Systole – contractile phases
o Diastole – relaxation (filling) phases
o Systole and Diastole in atria and ventricles alternate!!
o Forces blood from higher to lower pressure

APSM  2442  FINAL  STUDY  GUIDE  

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o During the relaxation period, both atria and ventricles are relaxed – the faster the heart
beats, the shorter the relaxation period
Auscultation – sound of heartbeat caused by blood turbulence from valves closing, 4 sounds
but only 2 are loud enough to be heard
o Lub – AV valves close
o Dub – SL valves close
Cardiac Output – volume of blood ejected from left or right ventricle into aorta or
pulmonary trunk each minute
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resting male – 5
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3 important
factors!!
§ Blood viscosity
§ Total blood vessel length – longer the vessel, the greater the resistence
§ Blood vessel diameter
§ Resistance = Length x viscosity / Radius^4
o Sources of vascular resistance:
§ MAP decreases throughout systemic circulation
§ Largest drop occurs across the arterioles
o Venous Return (VR) = volume of blood returning to heart from veins, equal to CO;
aided by:
§ Pressure gradients
§ Venous valves
§ Vasoconstriction
§ Skeletal muscle pump
§ Respiratory muscle pump – negative pressures in the thoracic and abdominal
cavities generated during inspiration to pull venous blood towards the heart
o Venous Reserve: at rest, systemic veins and venules contain a large percentage of the
blood volume that can be diverted quickly if needed; if BP drops stimulation of
sympathetic NS will cause venoconstriction, allowing a greater volume of blood to
flow to skeletal muscles
*Hormonal regulation of BP and BF à renin – angiotensin – aldosterone system, ADH

APSM  2442  FINAL  STUDY  GUIDE  
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Autoregulation of BP – ability of a tissue to automatically adjust its blood flow to match the
metabolic demands of the tissue
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They do not
participate in gas exchange!!
Respiratory muscles: diaphragm, intercostals, etc

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