Quiz 3 Flashcards
What makes up the inferior mediastinum?
Anterior mediastinum(thymus), middle mediastinum (heart) and posterior mediastinum (lots! arteries, veins, nerves, lymphatics) ; starts at sternal angle- T4 line down to diaphragm
What makes up the superior mediastinum?
Just the superior mediastinum; starts at first rib down to sternal angle- T4 line; Infection from oral region can travel down here; the DANGER SPACE
What makes up posterior mediastinum?
From base of diaphragm and crura; has sympathetic trunk (originates T1-L2)(preganglionic axons, post- ganglionic neurons destined for sweat glands, head, neck, heart, and lungs) superior surface of diaphragm, inferior surface of thorax
Greater splanchnic nerve
(T5-T9) In posterior mediastinum; These sympathetics originate in the lateral horns; course through but don’t synapse in T5-9 ganglia; they gather and course down to abdomen; synapse with a pre-aortic ganglion (ex. celiac or superior mesenteric ganglia)
Lesser Splanchnic nerve
(T10-T11); these sympathetics originate in the lateral horn; course through but don’t synapse in the T10-11 ganglia; they gather and course down to abdomen; synapse with a pre-aortic ganglion (ex. celiac or superior mesenteric ganglia)
Least Splanchnic nerve
(T12); these sympathetics originate in the lateral horn; course through but don’t synapse in the T12 ganglia; they gather and course down to abdomen; synapse with a pre-aortic ganglion (ex. aorticorenal ganglia)
Azygous system of veins
right side of thorax has azygous vein; left side of thorax has accessory hemiazygous vein (above T8) and hemiazygous vein (below T8)
Veins of the mediastinum
SVC, right brachiocephalic vein (arm), azygos vein (T4), posterior intercostal veins, anterior intercostal veins, internal thoracic vein, anastomoses of intercostal veins (connection- in case of blockage- bp builds up and goes through system in a dif. way)
Thoracic lymphatic duct
in mediastinum; cisterna chyli; drains lymph from all tissues of the body except right side of head, neck, chest and arm which are drained by right lymphatic duct
Arteries of the mediastinum
Descending aorta (T4), posterior intercostal arteries, internal thoracic artery (internal mammillary artery), anterior intercostal arteries, anastomosis of intercostal arteries
Organs in the mediastinum
Esophagus (to T10) , trachea and primary bronchi (T4), pulmonary arteries, aortic arch
Aortic arch and it’s branches
(T2, T4) (ascending, descending aorta), brachiocephalic trunk (R. common carotid, R subclavian; exists because arterial system has to go further to go to right side due to heart location on left), left common carotid artery, left subclavian artery
Major veins of mediastinum
SVC, IVC, pulmonary veins , brachiocephalic on BOTH sides, veins bring blood to heart (color just tells you if oxygenated or deoxygenated)
Heart
pericardial sac holds heart; SVC, IVC, or coronary sinus –>R. atrium–> tricuspid (R. AV) valve–>R. ventricle–> pulmonary valve–> pulmonary trunk–> pulmonary arteries–> lungs–> pulmonary capillaries(CO2/O2 exchange in alveolus) –> pulmonary veins–> L. atrium–> bicuspid (mitral, L. AV) valve–> L. ventricle (thicker to pump blood to body)–> aortic valve –> aorta (has 2 coronary arteries coming off of it just above valve)–> systemic arteries–>systemic capillaries (CO2/O2 exchange in systemic tissue)–> systemic veins
Serous membranes
Fibrous pericardium (outermost layer), serous pericardium (more inner, 2 layers, in between there is the pericardial space- has serous fluid for lubrication), parietal pericardium (fibrous parietal pericardium, serous parietal pericardium), visceral pericardium (serous visceral pericardium)
Heart orientation
right atrium forms right border, right ventricle forms the anterior border, left atrium forms posterior border, left ventricle forms inferior border; most left chamber (apex)
Right Ventricle distinguishing factors
In right ventricle there are chordae tendinae and papillary muscles with TRICUSPID VALVE
Atrioventricular valves
(tricuspid/ bicuspid) prevent blood from flowing back into atrium; open when ventricle is filling; ventricle contraction sends blood out through any hole and AV valve snaps shut, preventing back flow into atrium, chordae tendinae and papillary muscles hold valve shut; cause the S1 sound
Semilunar valves
(aortic- middle and pulmonary- most anterior) prevent back flow from great vessels into ventricles; when ventricle relaxes and fills, something needs to prevent aortic flow from reversing (blood pushes down to go down void and catches valves which snap them shut) ; cause the S2 sound
Ventricular Diastole
Chamber fills with blood
Ventricular Systole
Chamber is contracting
Auscultation
Listening to the sounds of the heart; S1 (AV) bottom of heart [mitral on left, tricuspid on right] /S2 (semilunar) top of heart [pulmonary on left, aortic on right]; are sounds made by valves closing; sternal angle (rib 2- under it is 2nd space)-T4 line down to diaphragm
S1 (LUB)
the contracting ventricles caused the AV valves to snap shut
S2 (DUB)
the relaxing ventricles caused the semilunar valves to snap shut
Coronary circulation
coronary arteries, cardiac veins-drain to right atrium
Coronary arteries
right coronary artery–> right marginal artery (anterior), posterior descending (interventricular) artery (PDA) [if RCA supplies PDA heart is right dominant (67%)]; left coronary artery–> left anterior descending (interventricular) artery (LAD)–> left circumflex artery (LCX) (anterior to posterior) [If LCA supplies the PDA the heart is classifed as left dominant (33%)]
coronary artery innervation
sympathetic- vasodilation
parasympathetic- vasoconstriction
cardiac veins
coronary sinus (posterior)–> middle cardiac vein (posterior)–> great cardiac vein (anterior)
Heart innervation (sympathetic)
increases heart rate, increases force of contraction; T1-T4 (thoracic sympathetic cardiac nerve OR cardiopulmonary splanchnic nerve) ; T1–> sympathetic chain–>cervical sympathetic cardiac nerve; T2–> sympathetic chain–>cervical sympathetic cardiac nerve; sympathetic trunk, cardiac splanchnic nerves, cardiac plexus)
Heart innervation (parasympathetic)
decrease heart rate, decrease force of contraction; medulla–> vagus nerve; intramural ganglion; vagus nerve (CN 10), cardiac plexus
Conduction system of the heart
SA (sinuatrial) node–> AV (atrioventricular) node –>bundle of His–> anterior ventricular septum–> apex of heart–> anterior side of ventricles ; ANS to conduction system of heart (medulla–> vagus nerve, thoracic sympathetic cardiac nerve, cervical sympathetic cardiac nerve)
visceral sensory
Visceral motor (efferent) (medulla–> vagus nerve, thoracic sympathetic cardiac nerve, cervical sympathetic cardiac nerve) ; visceral sensory (afferent) (medulla T1-T4) when heart suffers damage body doesn’t know how to react; guesses what is going on; dermatomes T1-T4 (left arm, pectorals)- stabbing feeling, upper chest pain radiating to arm; DULL, DIFFUSE, non-localized pain
Visceral afferent neurons that parallel vagus nerve (heart suffers damage)
Vagus nerve pain referred to the craniofacial region (neck, tooth, jaw pain); pain in the mouth might not always be caused by a problem in the mouth
Skeletal Muscle
Attached to bones (or some facial muscles) to skin; single, very long, cylindrical, multi-nucleated cells with obvious striation; voluntary
Cardiac Muscle
Walls of the heart; branching chains of cells; uni- or binucleated cells; striation; involuntary (though can be modulated by ANS), rhythmic
Smooth musle
single- unit muscle in walls of hollow visceral organs (other than the heart); multiunit muscle in intrinsic eye muscles, airways, large arteries; single, fusiform, uninucleated; no striations; involuntary
Striated muscle cells**
Voluntary, attached to bones or skin, very long cylindrical, multinucleated cells, striated (packed with orderly arrangement of myofibrils), not self stimulating (each fiber innervated by branch of somatic motor neuron as part of motor unit), under control of nervous system; high energy requirement (lots of mitochondria, creatine phosphate, myoglobin), fast contracting, no rhythmic contractions; strength increases with stretching; fatigues easily
Cardiac muscle cells **
Involuntary, found only in heart, branching chains of cells connected by porous intercalated discs, with single nucleus and striation, striated (many myofibrils in orderly arrangement), self stimulating (impulse spreads from cell to cell), under control of nervous and endocrine systems and various chemicals, intermediate energy requirement, intermediate speed of contraction yet contraction spreads quickly through tissue due to intercalated discs, rhythmic contractions, strength increases with stretching, doesn’t fatigue
Smooth muscle cells**
involuntary, line walls of most internal organs, single, tapering, cells with a single nucleus, not striated (fewer myofibrils of varying lengths), self stimulating (not individually innervated, impulse spreads from cell to cell), under control of nervous and endocrine systems and various chemicals an stretching, lower energy requirement (fewer mitochondria, etc), slower contracting and rhythmic in some organs producing peristaltic waves along organ, rhythmic contractions, stress- relaxation response, doesn’t fatigue
The motor unit of skeletal muscle
The functional unit of a muscle is the motor unit which is composed of the alpha motor neuron and all of the muscle cells it innervates; the site if innervation is the neuromuscular junction (NMJ); each alpha motor neuron’s axon branch to synapse with up to thousands of different muscle fibers, but each individual muscle fiber is only connected to one alpha motor neuron (allows control over muscle fibers that are recruited); contrasts with cardiac and smooth muscles, whom both undergo rhythmic contractions, and are self stimulating (not innervated, impulse spreads cell to cell)
Sarcoplasmic Reticulum (SR)
intracellular organelle that stores and releases Ca2+ ions (reservoir); terminal cisternae are the enlarged portion of SR nearest the t-tubules; Ca2+ is released from the SR via channels called ryanodine receptors (RyRs); since Ca2+ concentrations in the SR are higher than in cytoplasm, energy (ATP) is required to pump it back into SR via the Ca2+ pump, SERCA (ATP dependent process)
Transverse (T) tubules
smaller tube like structures perpendicular to the sarcolemma (muscle membrane); invaginate into the muscle near the SR in regular intervals; APs propagate down the T-tubules during excitation-contraction coupling
Sarcomere**
extends from one Z disc to the next; an anchor point for actin filaments (myosin/actin)
A-band
the darker band, myosin- containing band; length (~1.5mm) in relaxed muscle does NOT change during contraction
I-band
the lighter band, includes actin filament and Z-disc; shortens during contraction
H-zone
center of the A band, where actin and myosin do not overlap; shortens during contraction
M-line
located in the center of the H zone; accessory proteins anchor myosin to M-line
Titins
anchor thick filaments to Z disc and runs within the thick filaments to the M line; holds thick filaments in place; helps muscle spring back into shape after contraction or stretching
Sliding Filament theory
During contractions, myosin (thick filament) heads form cross bridge connections with actin (thin filaments) which slide the actin filament towards the M-line to shorten the sarcomere in an ATP dependent process (relaxation is also ATP dependent) ; no change in the length of the actin or myosin filaments themselves; both the I band the H zone shorten during contraction; this process is the same in both skeletal and cardiac muscle, but different in smooth muscle
Tropomyosin and Troponin regulating the thin filament
When the muscle is relaxed (when cytoplasmic Ca2+ is low; myosin head at 90 degrees) the actin binding sites are shielded by tropomyosin such that the myosin head can’t bind; when muscle is initially stimulated (when cytosolic Ca2+ increases) Ca2+ binds to troponin and shifts it, pulling tropomyosin protein and exposing the binding sites on actin to allow myosin to form cross-bridges; the higher the Ca2+ concentration, the greater the number of tropomyosin molecules that move to expose myosin binding sites
Initiation of contraction
- Ca2+ levels increase in cytosol 2. Ca2+ binds to troponin 3. Troponin Ca2+ complex pulls tropomyosin away from G-actin binding site 4. Myosin binds to actin and completes power stroke 5. actin filament moves
Cross bridge cycle **
This cycle can continue as long as the muscle is activated, ATP is available, and the limit of shortening has not been reached. Cross bridges cycle independently of one another 1. binding of myosin to actin (Ca2+ activation allows cross bridge formation by binding to troponin) [inorganic phosphate is released] 2. Power stroke (~10nm movement per stroke; actin gets pulled toward middle of sarcomere) [ADP is released] 3. Rigor (myosin in low energy form) [new ATP binds to myosin head; Ca2+ back to storage; for detachment to occur, a new ATP must bind to myosin head and undergo partial hydrolysis] 4. Unbinding of myosin and actin [ATP is hydrolyzed] 5. Cocking of the myosin head (myosin in high energy form) “energized” or “cocked” myosin head: MADPPi [Ca2+ activation allows cross bridge]
Rigor
If cellular energy stores are depleted (as happens after death) the cross bridges can’t detach due to lack of ATP and cycle stops in the attached state. This produces stiffness of the muscle known as rigor. Thus, rigor mortis that sets in shortly after death. Need energy to relax OR contract. Contraction is thus an energy demanding process- lots of ATP is needed
Excitation- Contraction Coupling
The physiological process of converting an electrical stimulus (AP) to a mechanical response (contraction) at the NMJ. 1. Motor neuron AP 2. Ca2+ enters voltage gated channels 3. ACh is released and diffuses across the synaptic cleft and attaches to ACh receptors on the sarcolemma 4. Na+ entry into motor end plate 5. local current between depolarized end plate and adjacent muscle plasma membrane 6. Muscle fiber AP initiated 7. Propagated AP in muscle plasma membrane 8. Ach degradation
Excitation Contraction coupling in motor endplate
ACh is released and diffuses across the synaptic cleft and attaches to ACh receptors on the sarcolemma 1. AP generated is propagated along the sarcolemma and down the T tubules 2. AP triggers Ca2+ release from the terminal cisternae of SR 3. Ca2+ ions to troponin which changes shape, removing the blocking action of tropomyosin; actin active sites are exposed 4. Contraction: myosin cross bridges alternately attach to actin and detach, pulling the actin filaments toward to center of the sarcomere; release of energy by ATP hydrolysis powers the cycling process 5. Removal of Ca2+ by active transport into the SR after the action potential ends (SERCA) [can shut down 3-4] 6. Troppmyosin blockage restored blocking actin active sites; contraction ends and muscle fiber relaxes
Cardiac Muscle part 2
Cross- striated, elongated, branched cells link to one another at intercalated disks; desmosomes (specialized cell junctions at the intercalated disks - proteins that spot weld the junction and allow force to be transferred and the heart to hold together as it beats despite mechanical stress); Gap junctions (provide electrical conduction to allow beating as single conductive unit [syncyntium]); auto rhythmicity due to intrinsic pacemaker cells( no external innervation required, generate own beat), almost exclusively uses aerobic respiration (large mitochondria thus resistant to fatigue, high myoglobin content since myoglobin can function as an O2 storage mechanism; cardiac tissue is very vulnerable to hypoxia (plasma troponin and myoglobin levels are measured to assess damage over time after heart attacks)
Smooth muscle part 2
Spindle shaped, mononucleated cells under involuntary control of their slow, rhythmic (wave-like) contractions; grouped into sheets on the walls of hollow organs and some vessels; no sarcomeres (not striated), actin fibers attach to the cell wall and the dense bodies in the cytoplasm that serve as anchors. When activated, actin fibers slide over the myosin bundles causing shortening of the cell walls (No troponin present); Ca2+ plays a prominent role in the initiation of contraction, but the source of the Ca2+ differ in smooth muscle vs others (influx through voltage or ligand gated plasma membrane channels and/or efflux from intracellular stores through either RyRs or inositol triphosphate receptors (IP3R) Ca 2+ channels); lacks troponin so Ca2+ binding to troponin does not enable smooth muscle contraction (increased myosin ATPase activity and binding of myosin to actin; crossbridge cycling causes contraction of myosin and actin complexes, in turn causing increased tension along the entire chains of tensile structures, resulting in contraction of the entire smooth muscle tissue.) Relaxation of smooth muscle does not always happen when Ca2+ levels decrease (Dephoshorylation of myosin by myosin light chain phosphatase can lead to relaxation or….; Myosin cross bridges can remain attached to actin despite lowered Ca2+ allowing sustained contractions with little expenditure of energy; Muscle relaxation occurs when the Ca2+-calmodulin complex dissociates or other mechanisms intervene)
Skeletal Muscle Overview
Makes up ~40% of nonfat body weight of the human body; it can help maintain body temp in response to cold (aka shivering) since shivering increases metabolic rate; it is typically attached to bone (tongue is exception); responsible for supporting and moving the skeleton; it is striated (due to sarcomeres); it doesn’t contract without nervous stimulation, is under voluntary control ; high energy demands so fatigues easily
Main events in skeletal muscle contraction**
- AP initiated and propagates through motor neuron 2. AP triggers ACh release at presynpatic membrane of neuromuscular junction 3. ACh diffuses across synpatic cleft from axon terminal to post synaptic membrane in muscle fiber (aka motor endplate) 4. Since Na+ influx> K+ efflux, local depolarization occurs (aka end plate potential- EPP) 5. EPP triggers AP in the skeletal muscle cell that propagates into the t-tubules 6. AP triggers Ca2+ release from sarcoplasmic reticulum 7. Ca2+ binds to troponin on the thin (actin) filament, shifting tropomyosin and revealing the myosin binding sites on the actin filaments 8. energized myosin heads bind to actin and rotate causing shortening (cross bridge cycling) and contraction 9. cytoplasmic Ca2+ falls as it is pumped back into SR causing relaxation in an ATP dependent fashion 10. The cross-bridge cycle is terminated by the loss of calcium from the troponin 11. Tropomyosin translocates to cover the cross-bridge binding sites 12. The calcium returns to the sarcoplasmic reticulum, the muscle relaxes & returns to the resting state
Roles of Ca2+ in muscle contraction
- promotes presynaptic neurotransmitter release 2. Ca2+ released from the SR binds to troponin to initiate sliding filaments 3. Ca2+ promotes glycogen breakdown and ATP synthesis by activating essential enzymes; Thus the same ion that stimulates muscular contraction also activates phosphorylase kinase, which them activates glycogen phosphorylase, which releases Glucose 1 phosphate from glycogen, which can be used to make ATP to support muscular contraction
Sources of ATP production
Free cytosolic ATP provides the immediate source of energy for muscle contractions. However, it is only sufficient to fuel ~ 5-6 seconds of intense activity. Other sources are creatine phosphate, glycogenolysis (anaerobic respiration), or cellular (aerobic) respiration
Creatine phosphate
Direct phosphorylation [couple reaction of creatine phosphate (CP) and ADP to form creatine and ATP]; energy source is CP, no O2 use, 1 ATP produced per CP, creatine; duration of energy provision is 15 s
Glycogenolysis (anaerobic) respiration
Anaerobic mechanism (glycolysis in cytosol–>pyruvic acid–> lactic acid formation) energy source is glucose (from glycogen breakdown or delivered from blood); no O2 used, produces 2 ATP per glucose, lactic acid is released in blood; duration of energy provision 30-60 s
