PHYL 302 Exam 1

visceral reflexes (long vs. short reflex)

- *visceral reflexes* - autonomic reflexes initiated in the viscera that can be modified by higher centers in the hypothalamus - *long reflex* - sensory neuron delivers information via dorsal roots to interneuron in the spinal cord, which then sends commands via preganglionic neuron that synapses with a ganglionic neuron in the collateral ganglia - allows for divergence (greater effect) - *short reflex* - doesn't involve CNS, uses interneurons within collateral ganglia instead of those in the spinal cord - less divergence (more localized effect)

2 factors that increase EF and 6 factors that decrease EF (4)

EF = SV/EDV or (EDV - ESV)/EDV Increase EF 1. Exercise 2. Epinephrine - sympathetic NS stimulation increases contractile force (ionotropy) Decrease EF 1. ↓preload (EDV) 2. ↑afterload - ↑pressure required for ventricles to push blood out would cause ↑ESV (amount of blood leftover after ventricular systole) 3. Cardiac tamponade - ↑pressure in the pericardial cavity, plug would close off superior and inferior vena cava and pulmonary trunk, leaving left ventricle with no blood to pump 4. ANS malfunction - sympathetic NS stimulation causes vasoconstriction, ↑afterload, and ↑ESV 5. Heart failure - chronically high afterload, heart enlarges at first to compensate, but can only enlarge so much 6. Cardiac ischemia - loss of blood flow and O₂ to part of the heart, heart cannot pump w/o ATP for muscle contraction

4 roles of thrombin

- *thrombin* - important blood clotting enzyme, activated from zymogen form *prothrombin* by *factor X* 1. Stimulates conversion of fibrinogen into fibrin 2. Activates factor XIII, which stabilizes the fibrin meshwork 3. Enhances activation of more prothrombin to thrombin (positive feedback) 4. Enhances platelet aggregation

mean corpuscular volume

average volume of RBCs, can be measured using a *hemocytometer* - machine that gives a differential count of all blood cells in a sample

vitamin C and Cu³⁺

cofactors in RBC production

hementin

protein produced by giant Amazonian leeches, dissolves clots by inhibiting thrombin

autologous transfusion

removing one's own blood from circulation and storing it for later use, patients often use this if they are having surgery so that they can be reinfused w/ their own blood to prevent chance blood incompatibility

arrhythmias (bradycardia, tachycardia, SVT, PVC, A-fib, V-fib, CHB)

- *arrhythmia* - any variation from normal HR and sinus rhythm - *bradycardia* - HR <50 bpm at rest - *tachycardia* - HR >100 bpm at rest - *supraventricular tachycardia (SVT)* - tachycardia that originates in the SA or AV node ('before the ventricles') - *premature ventricular contraction (PVC)* - when ventricles contract after the T wave but before the next P wave, caused by an *ectopic focus* (multiple Purkinje fibers become overly excitable and depolarize more rapidly than the SA node) - *atrial fibrillation* - rapid and uncoordinated atrial depolarizations w/ no definite P wave, creates turbulent blood flow (↑risk of clots), difficult to get the last 20% of blood into the ventricles - *ventricular fibrillation* - uncoordinated ventricular contractions w/ no pattern, very serious, person must be shocked back to normal sinus rhythm or death will result - *complete heart block (CHB)* - no impulse conduction b/t atria and ventricles due to AV node malfunctions, atria beat at sinus rhythm (65-70 bpm) but ventricles assume rate of Purkinje fibers (<30 bpm), QRS complexes occur at a regular rate, but much slower than P waves

3 causes of stenotic valve and 7 causes of insufficient valve (3/5)

- *stenotic valve* - stiff valve that doesn't open completely, results in 'whistling' sounds as blood is pushed through 1. congenital defect 2. Ca²⁺ buildup on valve 3. *rheumatic fever* - autoimmune disease that causes antibodies to mistakenly attack the heart valves and form scars on the valves - *insufficient valve* - valve that cannot close completely, results in 'swishing' sound as blood moves backwards and collides w/ blood moving in opposite direction 1. broken chordae tendineae 2. congenital defect 3. infection like endocarditis or syphilis (inflammatory chemicals damage chordae tendineae) 4. Marfan syndrome - causes abnormally stretchy CT such that the valve prolapses easily 5. ankylosing spondylitis - genetic disease linked to HLA-B27 mutation, causes stiffening of chordae tendineae 6. trauma 7. rheumatic fever

5 parts of AP in cardiac autorhythmic (pacemaker) cardiac myocytes

- *autorhythmic cells* - spontaneously depolarizing cardiac pacemaker cells, initiate APs but don't contract, 1% of cardiac cells - no resting MP, cells slowly depolarize to threshold (*pacemaker potential*, steps 1 and 2) and fire APs in a cyclical fashion 1. Opening of *funny (If) channels* - voltage-gated bidirectional channels that open at -60 mV and permit influx of Na⁺ and efflux of K⁺ (cell becomes more positive) 2. Halfway through pacemaker potential, If channels close and *T type (transient type) Ca²⁺ channels* open - Ca²⁺ flows in, membrane reaches threshold 3. At threshold, T type Ca²⁺ channels close, and *L type (long lasting) Ca²⁺ channels* open, Ca²⁺ influx causes depolarization (rising phase) 4. At +10 mV, L type Ca²⁺ channels close, and voltage-gated K⁺ channels open, K⁺ efflux causes repolarization (falling phase) 5. Slow closure of voltage gated K⁺ channels (don't fully close until -60 mV) causes slow decrease in K⁺ permeability, which contributes to next pacemaker potential (less efflux of K⁺ = more positive MP)

properties of blood (pH range, temperature, *liters in males and females, viscosity*)

- *blood* - fluid connective tissue that distributes nutrients to cells, carries metabolic wastes, and transports immune cells to sites of infection and disease - pH range: 7.35 - 7.45 - temperature: 100.4 °F - males have 4-6 L, females have 4-5 L blood - viscosity: 1.5 (plasma), 5.0 (whole blood) Poiseuilles

CO, SV, and EF equations

- *cardiac output (CO)* - amount of blood pumped by the heart in a given period of time - *stroke volume (SV) - amount of blood pumped out of each ventricle per contraction - *ejection fraction (EF)* - proportion of blood in the ventricle that is pumped out - CO = heart rate (HR) x SV - SV = end diastolic volume (EDV) - end systolic volume (ESV) - EF = SV/EDV or (EDV - ESV)/EDV

4 steps of erythropoiesis

- *erythropoiesis* - creation of new erythrocytes in red bone marrow (proximal end of a bone) - yellow bone marrow in the distal end of the bone can convert back into red bone marrow temporarily to restore RBC levels in rare cases like hemorrhage 1. Stimulus of ↓RBCs or ↓O₂ carrying capacity of blood is sensed by kidneys 2. Kidney cells release EPO 3. EPO causes ↑production and release of RBCs from red bone marrow 4. Once normal RBC level is reestablished, EPO secretion↓

Fe²⁺ vs. Fe³⁺

- *ferric iron (Fe³⁺)* - iron that is typically consumed or gained from the environment - ferrous iron (Fe²⁺) - iron that the body uses in RBCs, stomach and intestines use HCl to convert Fe³⁺ to Fe²⁺ for absorption

4 functions of the fibrous skeleton

- *fibrous skeleton* - extensive connective tissue network surrounding the heart, connects to the elastic sheath around each myocyte and the fibrous sheet around each muscle layer 1. Distributes forces of contraction - when myocytes contract, forces are transferred to the fibrous skeleton, which stretches less 2. Prevents overexpansion of heart during contractions 3. Elastic recoil after contraction - helps to fill the heart after each contraction 4. Physically isolates atrial and ventricular cells via the interatrial and interventricular septa

hemoglobin and cooperative binding

- *hemoglobin (Hb)* - protein that allows RBCs to transport O₂ and CO₂ (and sometimes CO) - composed of four 3° proteins (2 α chain, 2 β chains) in a single 4° structure - each subunit contains a molecule of *heme* - porphyrin ring that binds to *iron*, which binds to O₂) - *cooperative binding* - if one O₂ binds, the porphyrin ring changes shape so that O₂ is more likely to bind than CO₂ (and vice versa for CO₂) - in the tissues, RBCs deliver O₂ to cells - once 1 O₂ leaves and is replaced by CO₂, RBC has ↑CO₂ affinity and ↓O₂ affinity, so all O₂ is delivered to tissues and replaced by CO₂ - opposite process occurs in the lungs

histamine vs. heparin

- *histamine* - cytokine, causes general vasoconstriction, bronchoconstriction, and itchiness, but also vasodilation to allow blood to flow to the irritated area - *heparin* - anticoagulant, helps to clear allergen out of system and keeps blood from clotting (↓BP caused by vasodilation from histamine increases risk for clots) - both help with wound healing and clearing pathogens from body

hypovolemic vs. hypervolemic

- *hypovolemic* - low blood volume, caused by sweating and not rehydrating or hemorrhaging due to injury, or cholera causes confusion and disorientation - *hypervolemic* - high blood volume, usually due to excess Na⁺ in diet (draws water back into blood), could also be due to malfunction of RAAS that causes too much Na⁺ to be reabsorbed

intrinsic control vs. extrinsic control

- *intrinsic control* - also known as the *Frank-Starling law*, heart's inherent ability to vary SV through the intrinsic relationship b/t EDV and SV (↑venous return = ↑EDV = ↑SV) - ↑EDV causes cardiac myocytes to stretch more, which opens Ca²⁺ membrane channels and causes Ca²⁺ induced Ca²⁺ release from the SR, which increases strength of cardiac contractions and ↑SV - *extrinsic control* - factors that affect SV that originate outside the heart - ↑sympathetic activity = ↓ESV = ↑SV - sympathetic stimulation increases the heart's contractile force so that it squeezes out more blood (↓ESV) and ↑SV - results in leftward shift of the Frank-Starling curve - if ESV gets below minimum ventricular volume, syncope occurs

abnormal heart sounds 1. Lub-whistle-dup 2. Lub-dup-whistle 3. Lub-swish-dup 4. Lub-dup-swish

- *lub* - AV valves close, onset of ventricular systole - *dup* - semilunar valves close, onset of ventricular diastole 1. Lub-whistle-dup - stenotic semilunar valve, 'lub' means AV valves closed, 'whistle' means blood is trying to get through semilunar valves 2. Lub-dup-whistle - stenotic AV valve, whistling occurs before 'lub', which means blood is trying to get through stenotic AV valve 3. Lub-swish-dup - insufficient AV valve, 'swish' as blood rushes back through the partially closed AV valves (unable to close completely) 4. Lub-dup-swish - insufficient semilunar valve, swishing occurs after 'dup', which means blood comes back through the partially closed semilunar valves

How does the heart prevent itself from going into tetany?

- *tetanus* - when skeletal muscle fibers stay contracted for a long period of time due to summation of contractions - cardiac muscle cannot go into tetany b/c heart constantly needs to be pumping blood - skeletal muscle AP has a short refractory period compared to contraction period - in contrast, cardiac myocytes have a long refractory period of 250 msec due to the *plateau phase* of the AP, which is almost as long as contraction period (300 msec) - during this time, the heart is ejecting blood - ensures that cardiac muscle is not restimulated until contraction is almost over, allows time to refill the heart with blood

autonomic control of heart rate (sympathetic vs. parasympathetic) *Vagus*

- 2 cardiac centers in the medulla: *cardioacceleratory center* (sympathetic, ↑HR) and *cardioinhibitory center* (parasympathetic, ↓HR) - left vagus nerve (CN X) innervates the SA and AV nodes, while the right vagus nerve innervates only the SA node - sympathetic NS: ↑HR (*chronotropy*), ↑contractile force (*ionotropy*), and ↑conduction velocity (*dromotropy*) by releasing NE or E at adrenergic receptors on nodal and contractile cells - parasympathetic NS: ↓HR (chronotropy) ONLY - parasympathetic is usually dominant, so if it is turned down, then sympathetic NS has more influence and can ↑contractile force - indirect effect on ionotropy

NMJ and ANS toxins (black widow spider venom, botulinum toxin, curare, organophosphates, MG)

- ACh is released at sympathetic AND parasympathetic preganglionic synpases (nicotinic receptors), and ONLY parasympathetic postganglionic synapses (muscarinic receptors) - *black widow spider venom* - causes excess release of ACh (spastic paralysis) - *botulinum toxin* - blocks ACh release (flaccid paralysis) - *curare* - blocks ACh receptor function (flaccid paralysis) - *organophosphates* - inhibit AChE (spastic paralysis) - *myasthenia gravis* - autoimmune disease that destroys ACh receptors (flaccid paralysis)

When evaluating an EKG... - PR segment should be ___-___ small boxes. - QRS complex should be ______ small boxes. - QT interval should be _____ small boxes or _______. - Height of QRS complex should be ________.

- PR segment should be *3-5* small boxes (0.12-0.2 sec) - QRS complex should be *≤3* small boxes - QT interval should be *<11 small boxes* or *less than half the time from R wave to R wave* - Height of QRS complex should be *no more than 10 small boxes*

RBC antigens

- RBCs have many surface antigens that determine a person's blood type - *Type O* - 'HH', contains the H antigen on RBCs (oligosaccharide w/ no side chains), have anti-A and anti-B antibodies - *Type A* - have A antigens on RBCs (H antigen + A side chain), have anti-B antibodies - *Type B* - have B antigens on RBCs (H antigen + B side chain), have anti-A antibodies - *Type AB* - have A and B antigens on RBCs, don't have any antibodies - A and B surface antigens are similar to environmental antigens, so anti-A and anti-B antibodies will develop in people that do not possess A and/or B surface antigens - *Rh factor (D antigen)* - blood types can be either Rh⁺ or Rh⁻ - there are no naturally occurring antibodies against Rh factor, so Rh⁻ people do NOT make anti-Rh antibodies unless they were transfused with Rh⁺ blood or were pregnant with a Rh⁺ baby

Erythrocytes/RBCs (organelles, shape, diameter, life span, osmoregulation)

- RBCs lose most their organelles during development, rely on environment for glucose, so they contain a lot of *glycolytic enzymes* for anaerobic respiration - *biconcave* shape - thicker edges and a thinner inside, allows for large SA (high surface to volume ratio) for rapid gas exchange - critical when exercising b/c O₂ is 30x less soluble than CO₂, so need large surface area for O₂ delivery to tissues - shape also allows them to fold to squeeze through small capillaries - diameter: 7.2 to 8.4 μm - average life span of 120 days - in a hypertonic solution, RBC will take in more solute so that less water flows out - in a hypotonic solution, RBC will pump out solute so that less water flows in

cardiac tamponade

- acute compression of the heart caused by increased pressure in the pericardial cavity due to bleeding, excess fluid, or a tumor - pressure 'plugs' venous vessels and blood cannot leave the heart (like a tampon)

gradients of CO₂, O₂, and plasma protein from blood to ISF to ICF

- blood has high [O₂] and low [CO₂] b/c it exchanges CO₂ for O₂ (becomes oxygenated) in the lungs - always a gradient for O₂ from blood to interstitial fluid (ISF), and for CO₂ from ISF to blood - intracellular fluid (ICF) [O₂] is lowest b/c cells are constantly using it for metabolism, and [CO₂] is highest b/c CO₂ is a byproduct of metabolism - always a gradient for O₂ from ISF to ICF, and for CO₂ from ICF to ISF - [plasma protein] is high in the bloodstream and ICF, but they don't usually leave b/c they are too large - therefore, ISF [plasma protein] is nearly 0 (about 2 μg)

mast cells vs. basophils

- both are granulocytes and release the same inflammatory granules - same blue appearance with eosin and hematoxylin stains - but when stained with toluidine blue, mast cells are metachromatic (blue and red), while basophils are only blue - come from different cell lines and have different precursors - mast cells mature at their tissue site, basophils mature in the bone marrow

effects of sympathetic vs. parasympathetic stimulation (heart, *blood vessels*, lungs, digestive tract, bladder, eye, liver, adipose tissue, exocrine pancreas, sweat glands, salivary glands, adrenal medulla, endocrine pancreas, genitals, brain activity)

- both sympathetic and parasympathetic are usually partially active at all times, but one predominates - sympathetic dominance prepares body for strenuous physical activity or stressful situations (fight-or-flight) - parasympathetic dominance allows body to relax and focus on 'housekeeping' activities (rest-and-digest) 1. Heart - S: ↑HR and force of contraction (β₁) - P: ↓HR 2. Blood vessels - S: constricts (α₁), except skeletal muscle and brain vessels - P: dilates vessels in brain (cluster headaches), penis, and clitoris 3. Lungs - S: dilates airways (β₂), ↓mucus secretion (α) - P: constricts airways, ↑mucus secretion 4. Digestive tract - S: ↓movement (α₂, β₂), contracts sphincters to prevent movement (α₁), ↓digestive secretions (α₂) - P: ↑movement, relaxes sphincters to allow movement, ↑digestive secretions 5. Bladder - S: relaxes to reduce urge to urinate (β₂) - P: contracts to empty 6. Eye - S: dilates pupil (α₁), atropine - P: constricts pupil 7. Liver - S: glycogenolysis (β₂) - P: none 8. Adipose tissue - S: lipolysis (β₂) - P: retroperitoneal adipose 9. Exocrine pancreas - S: ↓digestive secretions (α₂) - P: ↑digestive secretions 10. Sweat glands - S: ↑secretion from hairy skin (α₁) - P: ↑secretion from specialized sweat glands in the armpits, genitals, and non-hairy skin (palms) 11. Salivary glands - S: ↑secretion of lipid and mucus-filled saliva - P: ↑secretion of watery saliva 12. Adrenal medulla - S: ↑NE and E secretion - P: none 13. Endocrine pancreas - S: ↓insulin, ↑glucagon (α₂) - P: ↑insulin, ↑glucagon 14. Genitals - S: ejaculation (males), organismic contractions (both) - P: erections (both) 15. Brain activity - S: inc. alertness through RAS (suprarenal medullae) - P: none

clot formation and clotting cascade pathway (what enzyme catalyzes fibrinogen → fibrin?)

- clot formation can be triggered by the intrinsic (clotting in the vascular system) or extrinsic pathway (clotting of blood that has escaped vessels and has entered tissues, shorter pathway) - *factor VIII* - joins the intrinsic and extrinsic pathways - ultimate step is the conversion of *fibrinogen* (soluble plasma protein) into *fibrin* (insoluble, threadlike molecule), catalyzed by the enzyme *thrombin* - fibrin molecules form a loose mesh that traps blood cells and aggregates platelets to form a blood clot - Ca²⁺ is an important cofactor in clotting cascade reactions

clot retraction

- dissolution of a clot, platelets contract and pull the edges of the damaged vessel closer together - occurs simultaneously with clot formation (but at a slower rate) - *factor XII* - first factor activated in clot formation, converts *plasminogen* to *plasmin*, enzyme that causes clot dissolution (deposits plasmin into the clot as it is being formed so that clot dissolves at a slow rate)

streptokinase

- enzyme derived from streptococci bacteria that prevents blood from clotting - used in the past to dissolve clots in coronary arteries, but was stopped b/c it was found to dissolve many other proteins too - better treatment is tissue plasminogen activator (tPA) b/c it is specific to dissolving clots

carbonic anhydrase

- enzyme in RBCs that is critical for CO₂ transport b/c it converts CO₂ into bicarbonate ion (HCO₃⁻) via the equation H⁺ + HCO₃⁻ → H₂CO₃ → H₂O + CO₂ - RBCs can get rid of CO₂ by either converting it to HCO₃⁻ and sticking H⁺ onto Hb (buffer), or by attaching CO₂ to Hb directly - if you don't exhale CO₂, concentrations of H⁺ and HCO₃⁻ increase (law of mass action) - since ratio of H⁺ to HCO₃⁻ is 1:600,000, body doesn't notice ↑HCO₃⁻, but ↑H⁺ causes acidosis

α₁, α₂, β₁, β₂, and β₃ receptors

- five types of adrenergic receptors - all respond to either NE from ONLY sympathetic postganglionic fibers, or E from adrenal medulla 1. *α₁ receptors* - located on most sympathetic effectors - respond to NE > E - when NE or E binds, they activate the IP₃-Ca²⁺ 2° messenger pathway, usually excitatory (preparation for stress) 2. *α₂ receptors* - located on digestive organs - respond to NE > E - when NE or E binds, they inhibit cAMP 2° messenger pathway, inhibitory (↓digestive activity) 3. *β₁ receptors* - located on the heart - respond to NE and E equally - when NE or E binds, they activate cAMP 2° messenger pathway, excitatory (↑HR and force of contraction) 4. *β₂ receptors* - located on smooth muscle of arterioles and bronchioles - only respond to E (aren't innervated so don't really get NE, but easy access to E through bloodstream) - when E binds, they activate cAMP 2° messenger pathway, generally inhibitory (dilate blood vessels and bronchioles) 5. *β₃ receptors* - located in adipose tissue, heart, and bladder - respond to NE and E equally - when Ne or E bind, they activate PLC via DAG-IP₃ 2° messenger pathway (lipolysis, ↓HR and force of contraction, relax bladder (↓ urge to urinate) - β₃ receptor is anti-diabetic b/c it mobilizes adipose tissue - abnormal receptor can cause obesity and DM in places where it is usually rare

sickle cell disease treatment

- genetic disorder caused by a point mutation that results in abnormally-shaped Hb (HbS), causes RBCs to have a crescent shape - sickled RBCs clump together and block blood flow in small vessels - treatment: *hydroxyurea* - prevents HbS formation by inhibiting DNA synthesis, which forces RBCs to go back to producing fetal Hb (HbF) - HbF isn't deformed like HbS, so it can carry O₂ better (just holds on to it tighter) - hydroxyurea also creates nitric oxide (NO), which causes vasodilation and increases the efficiency of O₂ delivery to tissues

colony-stimulating factors (CSFs) Once cells reach the _______ stage, they are 'committed' and will produce a certain type of cell.

- group of hormones secreted by bone marrow that promote growth and differentiation of hematopoietic stem cells - once cells reach the *blast* stage, they are 'committed' and will produce a certain type of cell

mediastinum

- heart is located in the *mediastinum*, directly posterior to the sternum - mediastinum also contains major blood vessels (aorta, superior and inferior vena cava, trachea, thymus, and esophagus) - heart is twisted within the mediastinum so that the left ventricle is posterior and the right ventricle is anterior

orientation of a normal heart

- heart lies slightly left of the midline, with the apex of the heart pointing toward the left foot - anterior side is mostly right atrium and ventricle - posterior side is mostly left atrium and ventricle - *base* - superior part of the heart - *apex* - inferior part of the heart, mainly formed by the left ventricle

erythroblastosis fetalis

- hemolytic disease of newborn, caused by a Rh⁻ mother's anti-Rh antibodies attacking fetal Rh+ RBCs during 2nd pregnancy with a Rh⁺ baby - during second pregnancy, anti-Rh antibodies are IgG that can cross the placental wall and attack fetal RBCs - treatment is to infuse mother with *Rhogam* - Rh immunoglobulin, prevents mother's immune system from producing anti-Rh antibodies against baby's Rh⁺ blood

intercalated discs

- interconnections b/t cardiac muscle cells - at each intercalated disc, there are two membrane junctions 1. *desmosomes* - cell adherence junctions that mechanically hold cells together and prevent them from being ripped apart during contractions 2. *gap junctions* - allow electrical potential from cardiac pacemaker cells to spread from one cardiac cell to adjacent cells to generate APs and contract as a single *functional syncytium* - the atria and ventricles each form a function syncytium and contract as separate units

suprarenal medullae (effects)

- modified paired sympathetic ganglionic neurons (one in each adrenal gland) - preganglionic neuron cell bodies in lateral gray horns of spinal cord at T₁ to L₂ or L₃ → axons enter ventral roots → combine w/ dorsal roots to form spinal nerve → *white ramus* branches from each spinal nerve carrying LONG preganglionic fibers, pass through sympathetic chain and celiac ganglia without synapsing, then synapse ganglia in the suprarenal medullae that contain *anaxonic neurons* (no axons) - release neurohormones (20% NE, 80% E, sometimes dopamine) - major effects: ↑alertness (RAS), ↑cardiovascular and respiratory activity, ↑smooth muscle tone (sphincters), mobilization of glucose and lipids

sympathetic chain (__________) ganglia (also known as sympathetic _________)

- paired ganglionic neurons located on each side of the vertebral column, also called the paravertebral ganglia or sympathetic trunk - 3 cervical, 11-12 thoracic, 2-5 lumbar, 4-5 sacral, 1 coccygeal - preganglionic neuron cell bodies in lateral gray horns of spinal cord at T₁ to L₂ or L₃ → axons enter ventral roots → combine w/ dorsal roots to form spinal nerve → *white ramus* branches from each spinal nerve carrying preganglionic fibers to synapse w/ ganglionic neurons (release ACh) in the sympathetic chain ganglion - postganglionic fibers leave via *gray ramus* → spinal nerve → innervates visceral effectors (release mostly NE and E) in the thoracic cavity, head, body wall, and limbs (THB L) - major effects: ↑HR, dilates pupils, ↑blood flow to skeletal muscles, constriction of cutaneous blood vessels, ↑sweat gland secretion, arrector pili muscle stimulation

hematocrit (other names, average male and female)

- percentage of whole blood that contains formed elements (essentially only RBCs since they are 99.9% of formed elements) - also called *volume of packed red cells (VPRC)* or *packed cell volume (PVC)* - average male hematocrit: 45% (5.4 million RBCs per μL) - average female hematocrit: 42% (4.8 million RBCs per μL)

hemopoiesis

- process of blood cell formation - hematopoietic stem cells from the embryonic yolk sac migrate into the embryo and colonize fetal bone marrow, liver, spleen, and thymus - red bone marrow forms all blood cells - liver stops producing blood cells at birth, but spleen and thymus continue WBC formation

varicosities, MAO, and COMT

- sympathetic preganglionic neurons release ACh → ganglionic neurons → postganglionic fibers release NE or E (sometimes ACh) onto viscera at neuroeffector junctions - neuroeffector junctions form an extensive branching network, with each branch containing several *varicosities* - bulges in the nerve packed with mitochondria and NTs - neuroeffector juntion ≠ synaptic cleft - *monoamine oxidase (MAO)* - enzyme that breaks down NE, found in outer mitochondrial membrane (NOT in bloodstream) - NE diffuses away from the varicosity (high → low concentration) and sometimes enters the bloodstream - once in blood, NE isn't broken down until it reaches the liver or kidneys, which contain *catechol O-methyl transferase (COMT)*

nicotinic vs muscarinic receptors

- two types of cholinergic receptors 1. *Nicotinic receptors* - located on sympathetic AND parasympethatic postganglionic cell bodies and on anaxonic neurons in the adrenal medulla, and on motor end plates of skeletal muscle - respond to ACh (cholinergic) from sympathetic AND parasympathetic preganglionic fibers (and from somatic motor neurons) - when ACh binds, they open cation channels that allow flow of Na⁺ and K⁺ (ionotropic), excitatory 2. *Muscarinic receptors* - located on effector cell membranes (cardiac and smooth muscle, most exocrine and some endocrine glands) - respond to ACh (cholinergic) from ONLY parasympathetic postganglionic fibers - when ACh binds, they activate GPCRs and signal transduction (metabotropic), can be excitatory or inhibitory

universal donors and recipients

- universal donor of RBCs only: Type O⁻ (no surface antigens for people with other blood types to react with) - universal donor of plasma only: Type AB (no anti-A or anti-B antibodies to attack other blood types) - universal recipient of RBCs only: Type AB (no anti-A or anti-B antibodies that would react to other transfused RBCs) - universal recipient of plasma only: Type O (no surface antigens for anti-A or anti-B antibodies in other blood types to react with)

collateral (___________) ganglia

- unpaired sympathetic ganglionic neurons, located anterior to the vertebral column - 3 collateral ganglia: celiac, superior mesenteric, and inferior mesenteric - preganglionic neuron cell bodies in lateral gray horns of spinal cord at T₁ to L₂ or L₃ → axons enter ventral roots → combine w/ dorsal roots to form spinal nerve → *white ramus* branches from each spinal nerve carrying preganglionic fibers, pass through sympathetic chain ganglia without synapsing and form paired *splanchnic nerves* (greater, lesser, lumbar, sacral) that release ACh and synapse on the 3 collateral ganglia (celiac, superior mesenteric, and inferior mesenteric, respectively), postganglionic fibers innervate visceral organs (release mostly NE and E) in the abdominopelvic cavity - sacral splanchnic nerve ends in the hypogastric plexus - major effects: constriction of blood vessels to abdominopelvic viscera, ↓activity of digestive and urinary systems, mobilization of glucose and lipids, some aspects of sexual function

quick count used for EKGs

- used to calculate approximate heart rates from EKGs - if distance from R wave to R wave is 1 big box (0.2 sec), HR = 300 bpm (60/0.2) - if distance is 2 big boxes (0.4 sec), HR = 150 bpm (60/0.4) - if distance is 3 big boxes (0.6 sec), HR = 100 bpm - if distance is 4 big boxes (0.8 sec), HR = 75 bpm - if distance is 5 big boxes (1 sec), HR = 60 bpm - if distance is 6 big boxes (1.2 sec), HR = 50 bpm

blood doping

- using RBC transfusions or RBC-enhancing drugs like erythropoietin (stimulates RBC production) to cause polycythemia improve athletic performance - ome athletes remove whole blood weeks before an event and then reinfuse it right before an event - allows them to carry more oxygen and perform better - however, there is a risk of heart attack or stroke with this method - same effect can be achieved by training at higher altitude - lower barometric pressure causes O₂ molecules to be farther apart, so body thinks it has an O₂ deficiency, so it makes more RBCs (naturally-induced polycythemia)

components of whole blood

- whole blood consists of plasma (liquid component w/ dissolved proteins and other solutes, 55%) and formed elements (blood cells, 45%) Components of plasma 1. water (92%) 2. plasma proteins (7%) - *albumin* (60%) - transport protein, keeps water and small molecules in vascular system - *globulins* (35%) - transport proteins (α and β globulins), immune function (γ globulins, C-reactive proteins) - *fibrinogen* (5%) - blood clotting 3. other solutes (1%) - *electrolytes* - ions like Na⁺, Ca²⁺, K⁺ - *organic nutrients* - lipids, carbohydrates, and amino acids - *organic wastes* - urea, uric acid, creatinine (breakdown product of creatine phosphate, byproduct of muscle metabolism), bilirubin (byproduct of RBC catabolism), ammonium - wastes are excreted through lungs (exhalation), kidneys (excretion), GI (defecation), and skin (blood to sweat glands, evaporation) Components of formed elements 1. Erythrocytes/RBCs (99.9%) 2. Leukocytes/WBCs (<0.1%) 3. Platelets (<0.1%)

3 types of anemia

1. *Aplastic anemia* - caused by failure of stem cells in the bone marrow to generate mature blood cells, can be caused by destruction of bone marrow by toxic chemicals, exposure to radiation, cancer, or chemotherapy 2. *Renal anemia* - caused by lack of erythropoietin (EPO), can be caused by kidney disease since kidneys release EPO 3. *Hemorrhagic anemia* - caused by blood loss from an acute wound or chronic illness like menorrhagia

4 exceptions to dual innervation (arterioles and veins, sweat glands, adipose tissue, submandibular salivary gland)

1. *Arterioles and veins* - most only get sympathetic input, but some exceptions - parasympathetic fibers from CN IX and CN X innervate carotid and aortic bodies/sinuses, respectively - parasympathetic nerves carry pain messages to the head through vasoactive intestinal peptide (VIP) and substance P and cause cluster headaches 2. *Sweat glands* - most only get sympathetic input, but some exceptions - parasympathetic nerves control sweating on non-hairy skin (palmar sweat response) 3. *Adipose tissue* - most only get sympathetic input (mobilization of adipose tissue), but new research has found that retroperitoneal adipose has parasympathetic input 4. *Submandibular salivary gland* - innervated by both divisions, but they are NOT antagonistic - parasympathetic releases watery saliva, sympathetic releases lipid and mucus-filled saliva (Ex. - if you exercise hard (↑sympathetic), you get dry mouth)

branches of the peripheral nervous system

1. *Autonomic nervous system (ANS)* - innervates visceral effectors (involuntary) - afferent pathways originate in visceral receptors - efferent pathways innervate visceral organs - two divisions: (1) sympathetic or thoracolumbar, and (2) parasympathetic or craniosacral 2. *Somatic nervous system* - innervates skeletal muscles (voluntary)

3 reasons for blood transfusions

1. *Hypovolemia* - most commonly caused by dehydration or hemorrhaging, or could also be *cholera* - bacterial disease characterized by hypovolemia and dehydration due to diarrhea, interferes with Na⁺ transporters so that Na⁺ cannot be reabsorbed, so water leaves body with Na⁺ - treatment is infusion with IV saline + carbohydrates - causes cells to switch to using a different glucose-Na⁺ transporter to bring Na⁺ into cells 2. *Erythroblastosis fetalis* - hemolytic disease of newborn, caused by a Rh⁻ mother's anti-Rh antibodies (created during 1st pregnancy) attacking fetal Rh⁺ RBCs during 2nd pregnancy with a Rh⁺ baby 3. *Detoxification* - drug poisoning or autoantibodies (Ex. - Grave's disease) can be diluted by adding more volume to blood

3 steps of leukocyte (WBC) movement to site of infection

1. *Margination* - WBCs roll along the capillary wall and slow down via *selectin*, then become attached via *integrin* 2. *Diapedesis* - WBCs squeeze through the endothelial lining of capillaries 3. *Chemotaxis* - WBCs follow the chemical gradient to the site of infection

6 phases of the cardiac cycle on EKG

1. *P wave* - atrial depolarization (systole) due to SA node firing 2. *PR segment* - AV nodal delay, no current detected b/c too small 3. *QRS complex* - ventricular depolarization (systole) and atrial repolarization (diastole) simultaneously, no separate wave for atrial diastole b/c occurs at the same time as ventricular systole 4. *ST segment* - complete depolarization of ventricles, cardiac myocytes in plateau phase of AP 5. *T wave* - ventricular repolarization (early diastole) 6. *TP interval* - ventricles are relaxed and passively filling (80%) until next P wave

4 autonomic activities controlled by the CNS

1. *Prefrontal association areas* - tie ANS activity is tied to emotional states (Ex. - blushing when embarrassed) 2. *Hypothalamus* - integrates autonomic, somatic, and endocrine responses that accompany some emotional and behavioral states (Ex. - ↑HR w/ anger and fear) 3. *Medulla* - regulatory centers for cardiovascular, respiratory, digestive, and urinary systems 4. *Autonomic reflexes* - integrated at the spinal cord, but also controlled by higher levels (Ex. - urination, defecation, and erections)

parasympathetic division pathway

1. *Preganglionic neurons* - cell bodies located in (1) brainstem (cranial division, 75%), CN III, VII, IX, and X, and (2) sacral spinal nerves S₂ to S₄ (sacral division, 25%), LONG axons, release ACh onto ganglionic neurons 2. *Ganglionic neurons* - located either inside target organs (intramural ganglia) or near them (terminal ganglia, includes ciliary, pterygopalatine, submandibular, and otic ganglia) 3. *Postganglionic fibers* - SHORT axons from ganglionic neurons, release ACh to innervate target organs

sympathetic division pathway

1. *Preganglionic neurons* - cell bodies located in lateral horns, SHORT and myelinated axons enter ventral roots, exit through the lateral gray horns of T₁ to L₂ or L₃, release ACh onto ganglionic neurons 2. *Ganglionic neurons* - located near the spinal cord, consists of (1) sympathetic chain ganglia, (2) collateral ganglia, and (3) suprarenal medullae, or adrenal glands 3. *Postganglionic fibers* - LONG and UNmyelinated axons from ganglionic neurons, release mostly NE and E (few ACh) to innervate target organs

3 steps of hemostasis

1. *Vascular spasm* - immediate constriction of a cut or torn blood vessel to stop bleeding temporarily, causes a sharp pain 2. Formation of a *platelet plug* at the site of the tear 3. *Blood coagulation* - transformation of blood from liquid to solid gel (clotting)

causes of abnormal RBC shape

1. Abnormal *spectrin* - cytoskeletal protein that maintains cell structure, bound to plasma membrane by *ankyrins* 2. Vitamin B12 or folic acid deficiency - compounds that increase speed of RBC production

6 phases of the cardiac cycle

1. Atrial systole - atria contract and push last 20% of blood into ventricles 2. Atrial systole ends, and atrial diastole continues until the start of the next cardiac cycle 3. Ventricular systole, phase 1 - ventricles contract (↓volume, ↑pressure), AV valves close to prevent regurgitation 4. Ventricular systole, phase 2 - ventricles contract (↑ pressure) until ventricular pressure > pressure in pulmonary artery and aorta, then semilunar valves open 5. Ventricular diastole, early - ventricles relax (↑volume, ↓pressure) and blood flows into the atria, retrograde blood flow pushes semilunar valves closed 6. Ventricular diastole, late - ventricles relax (↓pressure) until ventricular pressure < atrial pressure, then AV valves open and ventricles passively fill to 80% full

4 functions of plasma proteins

1. Establish plasma colloid osmotic pressure - plasma proteins are dispersed as a colloid to help keep fluid in vascular system b/c they prevent excessive fluid loss (albumin) 2. Help buffer changes in pH - plasma proteins carry H⁺ and OH⁻ on their surfaces and release them when needed to prevent acidosis or alkalosis 3. Immune response (Ig) 4. Clot formation (fibrinogen)

sympathetic vs. parasympathetic NS (origin of preganglionic fiber, origin of postganglionic fiber, length/myelination of preganglionic fiber, length/myelination of postganglionic fiber, preganglionic NT released, postganglionic NT released, preganglionic receptor, postganglionic receptor, divergence)

1. Origin of preganglionic fiber - S: lateral gray horns of T₁ to L₂ or L₃ - P: CN III, VII, IX, X (and V), and sacral nerves S₂ to S₄ 2. Origin of postganglionic fiber - S: sympathetic chain (paravertebral) ganglia or collateral (prevertebral) ganglia - P: terminal ganglia or intramural ganglia 3. Length/myelination of preganglionic fiber - S: short, myelinated - P: long, myelinated 4. Length/myelination of postganglionic fiber - S: long, unmyelinated - P: short, unmyelinated 5. Preganglionic NT released - S: ACh - P: ACh 6. Postganglionic NT released - S: NE (usually) - P: ACh 7. Preganglionic receptor - S: nicotinic - P: nicotinic 8. Postganglionic receptor - S: α or β - P: muscarinic 9. Divergence - S: high (widespread), one preganglionic neuron may innervate as many as 32 ganglionic neurons in different ganglia - P: low (localized), one preganglionic neuron may innervate 6 ganglionic neurons in the same ganglia

5 parts of AP in contractile cardiac myocytes

1. Resting MP at -90 mV due to *leaky K⁺ channels* 2. When AP arrives via gap junctions and cells reach threshold (-70 mV), membrane rapidly depolarizes due opening of voltage gated Na⁺ channels 3. At +30 mV, Na⁺ channels close, and *transient K⁺ channels* open very briefly - fast and transient repolarization due to K⁺ efflux 4. *Plateau phase* - flattening of AP (maintain + charge) for 250 msec due to (1) opening of *L type Ca²⁺ channels*, slow influx of Ca²⁺ keeps MP +, and (2) slow ↓K⁺ permeability due to closing of transient K⁺ channels and leaky K⁺ channels (no K⁺ efflux, MP stays +) 5. After 250 msec (about 0 mV), L type Ca²⁺ channels close, and then *ordinary voltage gated K⁺ channels* open - fast repolarization due to fast K⁺ efflux 6. Once cell reaches resting MP again, ordinary voltage gated K⁺ channels close and leaky K⁺ channels open

5 steps in movement of electrical impulses through heart

1. SA node spontaneously depolarizes 2. Depolarization spreads to the AV node 3. AV node delays spread of electrical activity to the AV bundle (bundle of His) while atrial contraction occurs 4. After atrial contraction, electrical impulses travel along the AV bundle within the interventricular septum to the apex of the heart, and to the papillary muscles by the moderator band (closes the AV valves) 5. The impulse is distributed throughout the ventricular myocardium to cause ventricular contraction

5 steps of platelet plug formation

1. When the endothelial lining of a blood vessel rips, *von Willebrand factor (vWF)* (plasma protein) adheres to the exposed collagen - platelets bind to vWF as they flow past - vWF is later deactivated by *ADAMST13* - bound platelets become spiky and become more adherent to collagen - contractile filaments within the platelet plug contract and pull broken edges closer together 2. Activated platelets release *ADP* 3. ADP causes nearby platelets to adhere to the platelet plug, which release more ADP - positive feedback loop 4. ADP causes formation of *thromboxane A₂*, a vasoconstrictor that promotes platelet aggregation 5. ADP stimulates release of *prostacyclin* and *nitric oxide (NO)* from undamaged endothelium to inhibit platelet aggregation (confines platelet plug to site of injury)

excitation-contraction coupling and relaxation in contractile cardiac myocytes

Contraction 1. AP from adjacent myocyte travels down T tubules 2. L type Ca²⁺ channels open, large influx of Ca²⁺ from the ECF 3. *Ca²⁺ induced Ca²⁺ release* - Ca²⁺ binds to SR and causes small amount of Ca²⁺ 4/5/6. Ca²⁺ binds to troponin, which causes tropomyosin to expose binding sites on actin, cross bridges form and cardiac muscle contracts Relaxation 7. Ca²⁺ unbinds from troponin 8. Ca²⁺ pumped back into the SR 9. *Na⁺/Ca²⁺ exchanger (NCX)* - pumps 1 Na⁺ in and 1 Ca²⁺ out to get Ca²⁺ back into the ECF 10. Na⁺/K⁺ ATPase restores resting MP

4 heart valves

Two AV valves 1. Right AV (tricuspid) valve - 3 cusps, deoxygenated blood flows through from the right atrium to the right ventricle 2. Left AV (bicuspid or mitral) valve - 2 cusps, oxygenated blood flows through from the left atrium to the left ventricle - 2 cusps forms a stronger seal, good b/c greater pressure on the left side of the heart (systemic circulation) - both AV valves close when papillary muscles contract and pull on the chordae tendineae - the AV valves open when atrial pressure > ventricular pressure (atrial systole), and close when ventricular pressure > atrial pressure (early ventricular systole) Two semilunar valves 3. Pulmonary semilunar valve - 3 half moon-shaped cusps, deoxygenated blood flows through from the right ventricle to the pulmonary trunk 4. Aortic semilunar valve - 3 half-moon shaped cusps, oxygenated blood flows through from the left ventricle to the aorta - semilunar valves don't have chordae tendineae or papillary muscles - close due to backward pressure gradient created by retrograde blood flow toward ventricles - fills the indentations in the valves and shuts them (like water running into a cul-de-sac) - semilunar valves open when ventricular pressure > pulmonary trunk/aortic pressure (late ventricular systole), and close when pulmonary trunk/aortic pressure > ventricular pressure (late ventricular diastole)

cranial division vs. sacral division terminal ganglia vs. intramural ganglia

Two types of parasympathetic preganglionic neurons 1. *Cranial division* (75%) - preganglionic cell bodies are located in nuclei of CN III, VII, IX, and X → long axons release ACh → ganglionic neurons (terminal and intramural) → postganglionic fibers release ACh → target organs - CN III → *ciliary ganglion* (*terminal*, next to target organ) → innervates intrinsic eye muscles (constrict pupils) - CN VII → *pterygopalatine* and *submandibular ganglia* (terminal) → innervate nasal, tear, and salivary glands (↑secretions) - CN IX → *otic ganglion* (terminal) → innervates parotid salivary gland (↑secretions) - CN X → *intramural ganglion* (inside target organs → innervates viscera of the neck, thoracic cavity, and most of the abdominal cavity (peristalsis, constriction of respiratory passageways,↓HR and contraction force) 2. *Sacral division* (25%) - preganglionic cell bodies are located in sacral spinal nerves S₂ to S₄ → long axons release ACh → intramural ganglia → postganglionic fibers release ACh → innervates viscera in the inferior abdominopelvic cavity (defection, micturition, sexual arousal)

tissue plasminogen activator (tPA)

activates plasmin within the tissues to dissolve random clots that form in the blood vessels due to random conversion of fibrinogen to fibrin

trigeminal-parasympathetic reflex

parasympathetic reflex that causes lacrimal gland secretion, linked to CN V (trigeminal nerve)