CV Anatomy/ Physiology

Question 1

• Right and left heart arranged in? Meaning? Systemic circulation? Meaning? Exception?
• Vessel with high compliance? Arteries walls? Arterioles? Veins?
• Microcirculation: Blood movement controlled by?
• Layers of the heart?
• 3 layers of the vasculature? Made of?

Answer 1

• Series; output on left must equal right; in parrallel; oxygenated blood only visits one organ; hepatic circulation (hepatic blood is via intestinal circulation)
• Aorta; thick to decrease expansion; highly innervated with lots of smooth muscle for vascular resistance; storage/capacitance vessels
• concentration and smooth muscle sphincters
• pericardium, epi, myo, endo cardium
• Tunica adventitia (mostly CT); Tunica Media (Inervated smooth muscle); Tunica Intima (CT and endothelium)

Question 2

• Cardiac muscle: Cells imbedded in? Lots of? (2)
• Myosin: Chains?
• Actin: Bound to?
• TN-C? TN-I? TN-T? TM?
• High afterload with velocity of shortening?
• Length-tension relationship: Small length (preload)? Greater length? (2) Peak tension length?
• Titin?
• Frank- Starling Law?

Answer 2

• Collagen; myofibrils and mito
• 2 heavy and 4 light
• TN and TM
• Has 1 Ca binding domain (SM = 2); Unique 32 AA N terminal with highly regulated phos; binds TM; only alpha isoform
• Slow velocity
• Less tension; more tension and force; 2.2-2.3Um
• Very stiff isoform (low compliance)
• More sacromere stretch equals more force and tension

Question 3

• Phosphorylation of LTCR?
• Phos. of RYR? Effect?
• Phos of PLB? Efects? (2)
• Phos of TN-I? Effect?
• ANS control of HR (chronotropy):
  1. ) HCN (funny current) gate: Sympathetic? Para?
  2. ) LTCR: Sympathetic? Para?
  3. ) GIRK channels: Para?

Answer 3

• Slower inactivation; increased inotropy
• Less ca needed to stimulate them; incr. inotropy
• Inhibitor of SERCA removed; more Ca re-uptake; increase inotropy and lusitropy
• Decrease Ca sensitivity; lowers inotropy; increases lusitropy
  1. ) Stimulate SA nodal cells to increase cAMP which binds HCN which makes channel more likely to open and increase diastolic depolar; Ach activates M2 receptor coupled with Gi (Ga subunit inhibits AC to decr. cAMP)
  2. ) Icreased Ca load in nodal cells leading to increased spontaneous release and NCX activity which increase diastolic depol.; ACh activates M2, decrease PKA
  3. ) Primary mechanism of para; GBy subunit binds GIRK which allows K to enter cell and slow firing rate

Question 4

• Differences b/n vascular smooth muscle and cardiac muscle: Sarcomere? Ca? Contraction? Troponin? Regulation?
• VSMC contraction? (5 steps)
• A1 adrenergic receptors? Vasoconstriction independent of?
• Arterial baroreceptor reflex: Neurons where? Respond to stretch by? Steps? (4) Effect? (4)

Answer 4

• SM has none; SM doesn’t need Ca from SR to contract; SM is long and sustained; SM has none; SM = thick
  1. ) Ca enters cyto and bind calmodulin 2.) Ca-Cal complex bind myosin light chain kinase 3.) MLCK phosph. myosin 4.) MLCP dephos. it 5.) cAMP inhibits MLCK causing relax
• NE –> Gq –> PLC –> DAG and IP3; IP3 activates receptors increasing Ca release and vasocontriction; depolarization
• Pressure sensitive Na+ neurons in aortic arch and carotid sinus; depolarizing baroreceptors act on brain stem (medulla); Incr. BP –> Incr. BR firing –> Decr. sym output/ incr. para input = Lower HR, inotropy, vasodilation, BP

Question 5

• Metbolites controlling flow through cap beds? (4)
• What is the myogenic response?
• NO regulates? Steps? (5)
• Endothelin: Stimulated by? (3) Effect? counterpart? Acts on? To do what?
• Humural control of vasculature: RAAS: Regulates? Mediated by? Renin released by? Stimulated via? (3) AT2 direct effect? Indirect? (4) Aldosterone does what? ADH?
• Atrial Neutritic peptide: Released by? When? Effects on cardiocytes? Kidney? Vasculature? Adrenals?

Answer 5

• PO2, CO2/Ph, K+, Adenosine (from hydrolising ATP = causes vaso dilation)
• Intrinsic to VSMC; stretch causes more Ca release and vasoconstriction to maintain flow
• VSM tone; NO diffuses to VSM –> activates Gc –> Increase cGMP –> PKG –> activates SERCA and inhibits LTCC = vasodilation
• AT2, ADH, Thrombin; NO acts on Gq to vasoconstrict
• BV; Kidney; juxtoglomerular cells; sympathetic, low BP in renal artery, Low Na reabsorption; vasoconstrictor; Incr. sym, aldo, endothelin, ADH; Promote Na+ and water retention; increase water retention
• Atrium; stretched; increase SERCA uptake; Na excretion; vasodilation; inhibit renin/aldo

Question 6

• Relaxation channels used by myoplasm? (3)
• ECC in SM? ECC in CM?
• NCX works how? Vr? Possible problem? But?
• Glycosides (digitalis) work how?
• Beta adrenergic receptors: Activation leads to? Effect on LTCC? RYR2? PLB? Troponin?
• Timothy syndrome?
• Brugada syndrome?
• CPVT syndrome?

Answer 6

• SERCA 2 (most important); NCX (no ATP); PMCA
• Does not require external Ca; does require ex CA
• 3 Na/ 1 Ca either way; -74; too much calcium can lead to increased Na and more depolar.
• Inhibit Na/K ATPase to increase Ca2+ with HF
• Increased contraction strength and relaxation via cAMP and PKA; Inc. inotropy; incr inotropy; incr. Ino and lusi; incr. lusi
• Denovo CaV1.2 leading to AV block and Incr. Q-T
• Na and Ca mutations with reduced LType Ca entry; shortened Q-T
• RYR2 more sensitive to Ca; more NCX activity and tachy follows