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124 Cards in this Set
- Front
- Back
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AV blocks
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Ventricular pacing
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AF
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"Caused by multi-site reentry; defibrillation, vagatonic measures (cAMP inhib and GIRLK channels open --> hyperpolarization --> shut down channels; ex0adenosine (GPCR activates GIRKS)"
If persistent: ctrl ventricular rate - verapamil (4) (Ca channel blocker); propanolol (2)(B blocker) - inhib B AR binding; digoxin |
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Vtach treatment
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"Cause by reentry, EADs and DADs; use lidocaine (1) (block Na channels), defib, verapamil (4) (block Ca channels)"
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V Fib
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"Caused by reentry, DADS, EADs; treat w/ defib, lidocaine (1) (Na channel blocker)"
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Class I
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Na channel blockers (local anesthetics) : decrease rate rise of upstroke in ventricle AP; ex-lidocaine; quinidine
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Class II
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B AR antagonists --> inhib ability of epi and norepi to bind BAR --> decrease Ca channel activity; ex-propranalol
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Class III
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Inhib K channels --> lengthen AP repol (not fighting Ca) use with reentry based arrhythmias; lenthens QT --> BAD
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Class IV
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"Ca channel antagonists --> used in SA and AV nodes --> block AP --> slow hr, prolong propagation time (PR interval); ex-verapamil"
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Arrhythmia
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"Disturbance of normal process of cardiac action potential; usually caused by more than one abnormality to rhythmic conducting system such as abnorm SA activity, pacemaker activity in tissues other than SA node, block of AP, spont generation of abnormal Aps"
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Arrythmia
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Hr > 90-100 bpm (p-p<.6)
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Tachycardia
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HR < 50-60bpm (p-p> 1)
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Bradycardia
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HR < 50-60bpm (p-p> 1)
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Heart block
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Long P-R (>.2s) --> slow AV conduction
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First degree block
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"Some Aps pass through AV, some skipped --> AV prob"
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Second degree block
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No SA Aps pass through AV; get slow QRS initiated by Purkinje or AV tissues
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Third degree block
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No SA Aps pass through AV; get slow QRS initiated by Purkinje or AV tissues
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Atrial fibrillation
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Spont uncoordinated AP throughout atria --> compromise normal blood movement from atria to ventricle; ventricle still fills passively so usually little impact on bp unless AF with rapid ventricular response --> ventricle doesn’t have time to fill, drop in bp
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Premature ventricular complex (PVC)
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Spont Aps not originating from SA; result of piece of ventricle spontaneously contracting; see unusual QRS
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Ventricular tachycardia (VT)
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hyper ventricle contraction; lots of qrsts over and over
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Ventricular fibrillation (VF)
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Random uncoordinated AP in ventricle, no contraction, drop in bp
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Reentry
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Mulitcellular mech where AP propagated by more than 1 pathways between 2 pts of heart and prop time along pathways differs (ischemia) --> get fast AP, followed by slow AP hitting after refractory pd
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delayed after depolarizaton (DAD)
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Assoc with intracell Ca overload causing inward current Na --> depol; and can be result of SR Ca overload or high cytoplasmic Ca; Digoxin can induce
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Early after depolarization
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Norm AP imm followed by abnorm depol; requires 'trigger'; more likely when long QT interval (Na and Ca channels no longer inactive); caused by decreased serum K, antiarrhyth drugs, congenital defects --> K channel defect: decrease amnt outward K avail for repol --> longer AP; Na channel defect: short inactive pd
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Heart failure
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Occurs when ventricular contraction is compromised and heart can't meet tissue demands; can be diastolic (blood filling) or systolic (contraction); drugs used to increase force of contraction
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Hypertension
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Valvular disease or congenital abnormality --> diastolyc disfunction
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In cardiac dysfunction
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Ca entry is less effective in eliciting Ca relsease; may involve disrution in coupling b/n DHPRs and RyRs
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Therapeutic agents
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"Diuretics, vasodilators, angiotensin II receptor antagonists, agents to increase cardiac contraction strength (inotrip): sympathomimetics, phosphodiesterase inhibitors, DIGITALIS; beta blockers"
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Digitalis
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Binds and partially inhibits sarcolemmal Na/K pumps --> increases intracellular Na --> decreases Ca export in Na/Ca exchanger -> increases myoplasmic Ca available to be sequester in SR --> more Ca released in AP; used in atrial fib with rapid ventricular response and HF
"Can cause cardiac arrhythmias --> delayed after depolarization (DADs): too much Ca in SR --> spontaneous Ca release into myoplasm --> exchanger moves Ca OUT, Na IN --> Na causes depolarization --> AP" |
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Ca Induced Ca Release
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Ca induced Ca Release:
1) Voltage gated L type Ca channels activated in plateau phase of AP 2) Extracellular Ca enters myoplasm near RyR receptor 3) Ca binds RyR --> SR Ca release channels open --> lots Ca into myoplasm 4) Ca binding TnC initiates crossbridge cycling 5) Contraction occurs until myoplasmic Ca reduced to resting levels through sarcolemma Na/Ca exchange pump (3 Na IN, 1 Ca OUT), SRCa ATPase pump, and mitochondrial Ca uptake |
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Andrenergic regulation of contraction magnitude
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Andrenergic Regulation of contraction magnitude:
1) Symp systim activates B AR (epi binds) --> --> PKA activated 2) Ca pump phosphorylated --> larger SR release trigger 3) RyRs phosphorylated --> increased Ca sensitivity and release 4) SRCa ATPase pump phosphorylated --> more Ca to release 5) Troponin phosphorylated --> decreased sensitivity to Ca |
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skel muscle vs cardiac muscle ec coupling
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Involves T tubules and SR networks
"" AP provides stim for Ca channel (DHPR) activation "" DHPR activation leads to SR Ca release channel opening "" Increase in myoplasmic Ca results in crossbridge cycling "" Voluntary contraction Involuntary contraction Activate by neuron stimulation Continuously active Cells not interconnected Gap junctions all communication between cells Triad Diad Extracellular calcium not required --> plunger mech Extracellular ca required to initiate SR Ca release Magnitude of contraction influenced by temp sum, recruitment, length tension, hypertrophy Magnitude of contraction influenced by length tension, hypertrophy and adrenergic regulation Moderate length AP Long ventricular AP Moderate number mitochondria Mitochondria larger and more plentiful contractile Contractive tissues (atria, ventricle), specialized automatic (SA AV nodes) and conductive (purkinje) fibers |
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parasympathetic pathway
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1) Vagal nerve activity results in releasing of Ach --> Ach binds muscarinic receptor on nodal cell memb
2) Activates G protein --> inhibits adenylate cyclase (no cAMP) --> decreases pacemaker channel activiation --> decrease rate of pacemaker depolarization and AP initiation --> decrease heart rate 3) PKA activity decreased --> Ca channels not phosphorylated --> decrease AP duration 4) G protein activates G protein coupled inward rectifier K channels (GIRKs): open --> increase hyperpolarization of memb potential by increasing background K conductance --> more negative after potential --> harder for pacemaker to depol SA node to threshold --> slower heart rate |
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Autonomic nervous system
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"Ctrls heart rate, cardiac contractility, blood pressure; 2 divisions: sympathetic and parasympathetic"
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Parasymphathetic stimulation
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"Vagus nerve (CNX) acts on SA and AV nodes resulting in Ach release (binds muscarinic receptor on nodal cell memb); results in: decrease pacemaker channel activity: decreased heart rate (longer pp interval); decrease Ca channel activity: decreased AP duration (shorter p-r, q-t); more negative after-potential: slows heart rate"
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Sympathetic stimulation
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Controls electrical activity of heart through symphatheic nerves that directly innervate heart: use norepinephrine; chemical transmitter: epinephrine; effects entire heart
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sympathetic stimulation
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Norepinephrine and epinephrine bind B-adrenergic receptors in cardiac cells --> biochemical signaling cascade --> ampliphication
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sympathetic stimulation
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Controls electrical activity of heart through symphatheic nerves that directly innervate heart: use norepinephrine
Chemical transmitter: epinephrine released by adrenal medula; all parts of heart affected Norepinephrine and epinephrine bind B-adrenergic receptors in cardiac cells --> biochemical signaling cascade --> ampliphication Results in: faster pacemaker depol --> faster heart rate, shorter p-p interval; increase Ca channel activity --> larger AP amplitude and faster AV node conduction; see decreased p-r interval ; reduced ventricular AP duration --> decreased QT interval" |
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sympathetic pathway
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1) Epineph binds B-AR --> G protein --> increase activity of adenylate cyclase -> catelyzes transfer of intracell ATP --> cAMP
2) cAMP: increases rate of activation of pacemaker channels (start AP, in AV and some in SA nodes) -> increases heart rate 3) cAMP increases PKA activity; PKA: catalyzes Phosphorylation of voltage gated Ca channels in AV/SA nodal cells; Purkinje fibers and atrial and ventricular cells --> increases activity of Ca channels --> stronger muscle contractions --> increase amount blood pumped /beat =larger AP amplitude 4) PKA phophorylates Iks channels --> increases Iks activity --> reduce ventricular AP duration --> leaves time for ventricular filling |
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Upward deflections
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AP (depolarization) propagating toward positive lead or Repolarization propagating away from positive lead
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Downward deflections
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Depolarization propagating away from positive lead
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P wave
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Depolarizing phase in atrial muscle
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QRS complex
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Depolarizing phase in ventricular muscles; large because lots of tissue and large upstroke from Na channels; positive because flowing towards extremities
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T wave
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"Repolarization phase in ventricular muscle; positive because AP on outer wall of heart = shorter duration than inner side (last to depol, 1st to repol) --> moving AWAY from positive electrode"
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PR interval
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Est of time for AP to pass through AV node
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EKG Normal values
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Heart rate: 60-100
<60 -bradycardia >100 - tachycardia PR interval: .12-.2 QRS:<.1 QT: <.44 |
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SA Node
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"Fast; Pacing; sends AP to atrial muscles --> contract; pacemaker channels, Ca based AP; ion channels have no 'resting potential' b/c no stable dominnat channce conductance"
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Atrial Muscle
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"Na based AP, Ca/K channels prolong plateau of AP; somewhat fewer voltage gated K channels compared to delayed rectivier --> less prominent plateau --> less Ca influx --> smaller contractile strength; P wave of EKG shows depol"
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AV Node
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"Slow = institutes delay so ventricles have time to fill b/n contractions; Ca based AP (same channels as SA, just less HCN4 channels to slow conduction by increasing time to return to resting potential), has some latent pacemaker activity; PR interval of EKG tells time it takes AP to pass through AV node"
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Purkinje fibers
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"Fast, uniform spread; Controls ventricular muscle contraction; NA based AP, Ca/K channels create plateau --> prevents AP from propagating in wrong direction; has some latent pacemaker activity"
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Ventricular Muscle
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"IKR (K OUT) sets resting potential; Na based AP w/ fast, synchronous propogation; competition between Ca and K channels creates plateua --> assures strong ventricular muscle contraction (lots Ca IN --> Ca-induced-Ca release from SR --> muscle contraction); QRS complex of EKG shows depol (tells about ventrical conductance); T wave in EKG shows repol; QT shows time needed for AP repolarization"
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Gap junctions
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Electrically link cells in heart
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Pacemaker Channels
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"=If or HCN4; activated by negative potentials, normal reversal potential ~-20mV; not particularly selective (Na and K through); main action = Na IN to cell --> depol; slow opening and slow closing --> sets heart rate ~60 hz; in SA and AV nodes, fewer found in AV node --> slows conduction in AV"
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Voltage Gated L Type Ca Channels
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"=CACNL1A1; Ltype =DHP sensitive; structure sim to Na channels, sim function --> depol opens Ca channels (Ca IN to cell); SLOW to open, very slow/incomplete inactivation, generates much less current than Na channels; in SA and AV nodes and presynaptic nerve termina at NMJ"
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Voltage Gated delayed rectifier K channels
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Repolarization; K OUT of cell; results in undershoot --> activates HCN4 channels; in SA and AV nodes
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Inward Rectifier K Channels
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"=IRK1; in cardiac and skeletal muscle --> set resting potential (~-90mV) which keeps voltage gated Na and K channels closed; no voltage sensor - consitutively active;net K mov't OUT of cell --> as gets less -, Mg tries to move OUT of cell --> blocks channel during AP; when memb pot = negative again --> Mg gets out of way"
*at high extracellular K --> Mg kept away from channel (charge-charge repulsion) --> makes depol harder --> less/weaker contractions of heart muscle |
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Cardiac Na Channels
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"Almost identical to nerve Na channels; open FAST, have inactive state; difference from nerve: NOT TTX sensitive; expressed only in non-nodal cardiac tissue; initiate and propogate AP"
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Cardiac Voltage-gated K channels
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In cardiac muscle tissue; K IN to cell; create plateau by antagonizing Ca flux depolarization; structurally similar to nerve Ltype channels: inactivate slowly and incompletely
*at high extracellular K --> Mg kept away from channel (charge-charge repulsion) --> makes depol harder --> less/weaker contractions of heart muscle I kur: ultrarapid - fights Ca to repol --> plateua Ikr and Iks: rapid, slow; structurally and functionally complex; cause repolarization" *Ikr increases with high exteracellular K conc --> gives faster repolarization --> shorter AP --> less Ca IN --> weaker ventricular contraction *w/o I kr and I ks (such as due to defect in beta subunit of Ikr channel) --> Ca would keep depol longer --> open more Ca channels --> new AP --> cardiac arrhythmias |
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Denervation atrophy
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Initial increase in Ach release --> spasms; hypersensitivity occurs because AChR looking for stimulus --> nonvisible contractions; with time muscle fiber degenerates and is replaced by fat and fibrous tissue
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Myotonia
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Hyperexcitability in skel muscle fibers where activation is caused by runs of repetitve Aps --> results in delay of muscle relaxation;
result of Na channels conduction giving small depols at rest --> Na depol low enough for recovery but with 2nd stimulus (ex - K) high enough to cause repeat APs |
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Paralysis
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Temporary loss of motor fuction; result of Na channels w/ high enough Na depol that 2nd hit (hyperkalemia - K) makes Na level so high channels are inactivated and AP is blocked
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impact magnitude contraction for skel muscle
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"Force of muscle contraction generated by number crossbridges acting in parallel. Number crossbridges acting in parallel depends on:
1) Number myofibrils per muscle fiber (hypertophy increases diameter and number) 2) Isometric length tension relationship 3) Recruitment of motor units (increase motor units, increase cell body size, requires more excitatory stimulus for impact) 4) Temporal summation: contractions add till reach tetanus as long as new contraction occurs before end of last one |
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Excitation contraction coupling (EC)
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Aps excite muscle fibers so they contract as a result of a dramatic increase in intracellular Ca
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Sarcomeres
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Fundamental contractive unit delimited by Z lines
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Myofibrils
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Sarcomeres linked end to end
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I band
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"Thin only: actin, troponin, tropomyosin (shorten in contraction)"
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H zone
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Thick only: shortens in contraction
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Types of troponin
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TpT: binds tropomyosin; TpC: binds Ca; TpI: inhibits actin-myosin interaction
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Types of actin
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"G Actin: single, globular actin molec; F Actin: actin filaments (= multi globular molecs)"
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Z line
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"Actin only, adjacent bands linked together, ends of sarcomere"
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A band
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Thick filaments = myosin molec length (doesn't change in contraction)
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Sarcoplasmic reticulum
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Baglike structures encircling myofibrils; = Ca reservoirs; contains Ca ATPase transport protein to pump Ca back into SR following muscle contraction
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Transverse tubule system (T Tubules)
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Sarcolemma invaginations that run deep inside muscle fiber to form elaborate plasma memb network; terminal pt of T Tubule syst adjacent to SR; contain inward rectifier K channels and chloride channels to establish and maintain resting memb potential; contain Na and K channels that propogate Aps deep in muscle fibers; contain DHPR voltage sensor channels that detect and trigger RyR receptor opening in SR
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Triad
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2 Terminal T tubules to 1 SR; 1 triad/sarcomere
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Brody disease
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Painless muscle cramping and exercise induced impairment of muscle relaxation exacerbated by cold; result of Ca-ATPase mutation: collects Ca from myoplasm after contraction; w/o CaATPase -->extended contraction bc Ca lingering
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Malignant Hyperthermia
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"During/after general anesthesia --> hypermetabolism, skel muscle rigidity, hyperthermia, death; result of mut in RyR and voltage sensor --> makes hypersens to voltage; more easily excitable therefore even small depol elicits Ca vomit --> more ca hanging around waiting to be used; treat w/ dantrolene"
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Dantrolene
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Inhibits Ca release from RyR selectively in skel muscle (not heart)
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Contraction
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I band and H zone shorten; A band remains same; sarcomere length =same
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Myosin structure
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Dimer with 2 globular heads (4 light chains) and supercoiled tail (2 heavy chains); head has ATPase activity and actin binding site; cleavages sites allow flexibility
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skel muscle EC coupling steps
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1) AP at NMJ travels down T tubules (containing Na channels) --> effects DHPR (dihydropyradine receptor) = Voltage Sensor (=L type Ca channels)
2) Conformational change --> DHPR interacts mechanically with RYR receptor on SR --> open RYR (ryanodine receptors) 3) Ca released from SR into myoplasm (therefore extracellular Ca not necessary for skel muscle contraction --> mechanical opening of SR Ca channel) 4) Ca binds Troponin C (TnC) --> conformational change 5) Troponin + tropomyosin move away from myosin binding site on actin 6) Myosin (at rest) is bound to ADP and Pi with myosin head perpendicular to actin; when myosin binding sites on actin exposed --> myosin attaches to binding sites (form transfilament cross bridges) 7) ADP and Pi dissociate from myosin --> myosin head turns 45 degress and pulls actin = Power Stroke (=Rigor Complex --> ATP required to release myosin from actin) 8) Actin-Myosin complx binds ATP --> actin dissociates from myosin 9) Myosin's intrinsic ATPas activity hydrolyzes ATP 10) Myosin returns to perp conformation with ADP and Pi 11) Ca dissociates from TnC or Myosin binds actin again |
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Inward Rectifier K Channels
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K selecting (K Out); set muscle resting potential (-90mV); in skel muscle memb and cardiac; nongated = constitutively active; Mg can block
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Voltage Gated Ca Channel
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In presynaptic nerve terminal; mediates NT release; structurally similar to Na channels except activation occurs at more + potentials = slower inactivation
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Nicotine Ach Receptor Channel
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"In NMJ in skel muscle; mediate electrical transmission from nerve to muscle; ligand (Ach) gated channel; relatively nonselective monovalent cation channel (K, Na go through) --> main action = Na in until close to Nerst potential --> then = amnt Na in and K out"
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Electrical synapse
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Electric current flows from pre --> post synaptic cell through large proteins (=gap junctions)
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Chemical synapse
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Presyn call releases NT --> diffuses across synaptic cleft --> receptors on postyn memb --> ion channel open --< change in memb voltage or cascade of biochem events alter electrical properties of postsyn cleft
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Neuromuscular junction
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Specialized synapse between alpha-motoneuron (in spinal cord) and skelectal muscle fiber via nicotine-Ach receptor
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End plate potential
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"Large depolarization on post syn cell following Ach binding receptor channel, opening pore to Na IN (and K OUT)"
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Miniature end plate potential (MEPP)
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"Small, infrequent depolarizations of approx same size; too small to trigger AP in muscle cell; summation of many MEPPS = normal EPP --> AP"
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Motor unit
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Muscle fibers innervated by one motorneuron + neuron; Each muscle fiber innervated by 1 motoneuron through 1 EPP complex containing numerous NMJ end-plates; fine motor skills have lower nerve to muscle motor unit innervation ratios
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Neuromuscular blockade
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Temporary paralysis to skel muscle; occurs when Ach binding receptor is competitively inhib (ex - Botox); reverse using anti-cholinesterases --> increases Ach in cleft --> competitvely inhib binding of blocking drugs
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Myasthenia gravis
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Autimm --> ab to nicotinic Ach receptor; (Nicotinic Ach receptor perm to Na and K --> brings membrane pot to ~-10mV) = postsynaptic fatigue disorder;
"see progressive decrease in Ach receptors AND Ach release --> decrease in muscle AP amplitude with successive stimulations (normally decrease in number Ach vesicles released on successive stim doesn't matter because high safety factor; in MG - low safety factor, as Ach vesicles decreases, impact visible b/c only a few AChRs)" treat with anti-cholinesterase --> increase Ach concentration within cleft |
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Insecticides and nerve gas
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Disrupt neurotransmission by covalently binding cholinesterases --> Ach lingers in synaptic cleft --> at low does: spont asynch excitation and fibrillation of muscle; at high dose: chronic depolarization --> Na channels inactivate --> no AP --> prob at respirator nerve-muscle junctions
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Lambert-Eaton syndrome
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Autoimm--> ab to presynaptic Ca channels at motor nerve channel --> Ach release decreased --> decrease muscle response
-if stim repeatedly: 1st compound muscle AP = small; more stim --> bigger AP amplitude (bringing in more Ca before Ca is cleared) |
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NMJ Process
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1) AP invades terminal pt of axon
2) Depolarization of axon opens Ca channels 3) Ca induces fusion of vesicles with presyn memb 4) Ach released and diffuses across cleft 5) Ach binds nicotine - Ach receptors 6) Channel pore open to Na and K 7) Na into cell --> depol = EPP 8) Meanwhile, Ach unbinds from receptor -->channel closes 9) Ach hydrolized by Ach E --> choline and acetate 10) Choline taken up into nerve terminal 11) Choline resynth into Ach and repackaged into vessicle |
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TTX
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Photoxin with high affinity for Na channel --> clogs --> lung failure
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Local anesthetics
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"Block Na channel proteins; structure: aromatic (greasy) tail, intermediate chain, amino end (may or may not be protonated); act via tonic block or hydrophilic pathway"
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LA Tonic block
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Occurs no matter what; low efficiency; hydrophobic pathway; nonprotonated LA (hydrophob) --> diffuse into NA channel and blocks
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LA Hydrophillic block
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"=Use Dependent Block; more effective at high firing rates and with chronic depolarization; nonprotonated LA --> crosses memb --> protonated --> block channel, ball holds in place = stable (hard to remove); therefore more AP fired, more it is blocked"
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Ester LA
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Metabolized by esterases (common --> therefore short acting)
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Amide LA
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Metabolized by liver enzymes (less common --> therefore long acting)
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Conduction velocity
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Depends on diameter of nerve (smaller = slower) and myelination
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Myelin
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Produced by specialized cells (oligodendrocytes - CNS; schwann cells - PNS)
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Tetrodoxin
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"Nerve toxin in puffer fish; blocks Na channels --> less Na = slower rise, smaller amplitue --> slower conduction velocity"
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Multiple sclerosis
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Inflammation in brain and/or spinal cord; autoimmune --> ab to central myelin; disrupts myelin --> low safety factor for AP propagation --> delay AP or fails entirely; genetic and environmental factors
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Rising phase
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"Depolarization phase; Na channels open, Na into cell (approach Vna); overshoot; Na channel inactivates"
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Falling phase
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"Repolarization phase; Na channels inactivate, K channels open, K out of cell (approach Vk); channels close; undershoot"
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Relative Refractory Pd
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"During undershoot, Permeability of K still high, 2nd stim within this period will result in slightly different AP"
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Absolute Refractory Pd
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"During AP, permeability of Na low (most Na channels inactive), K high; 2nd stim at this point will NOT generate an AP"
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Purpose of refractory pd
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Assure unidirectional AP propagation; limits neuron firing rates --> don't get more Na in than Na/K ATPase pump can pump out
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Action potential
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Transient change in membrane potential of nerve cells
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Voltage gated K channels
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"K out of cell; many types and roles, 4 subunits (homotetramer) p loop --> pore, 4th memb spanning protein - +++ Aas = voltage sensor, 2 conformational states, slow to open, stay open"
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Voltage gated Na channels
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"Na into cell; Few types, 1 roles - initiate and propagate AP; more complex than K, loop forming 'ball blocking mechanism'; 3 conformational states; fast to open, slow to inactivate"
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Patch clamp
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"Glass pipette on cell memb --> trap 1 ion channel --> apply voltage, measure membrane potential changes"
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Phosphlipid bilayer membrane properties
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"Permeable to water and small greasy molecs; impermeable to ions, proteins and large non-greasy substs"
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NA/K Pump
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"Large, ATPase memb protein: 3 Na out of cell, 2 K into cell (large [K] inside cell, large [Na] outside cell)"
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Ca Transport
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Low intracellular [Ca]: Ca ATPase pump - Ca out of cell; Na/Ca exchange proteins (Na IN - dwn gradient; Ca out - against gradient)
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Nernst Potential
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Membrane potential at which ion will be in equilib; Vm=61log[Xo]/[Xi]
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Resting Potential
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No net current across cell; use Golman-Hodgkins-Katz eqn:
Vo=61log(Pna[Na o] + Pk[K o]/(Pna[Na i] + Pk[K i]) Edit P=permiability (how readily ion wants to leave) |
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Na concentrations
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I: 10mM O: 140mM (136-145mM)
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K concentrations
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I: 140mM O: 4mM (3.5-5mM)
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Ca concentrations
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I: 50nM O: 2.4mM
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Cl concentrations
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I: 58mM O: 103mM (98-106mM)
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Voltage-gated Na channel diseases
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"Cardiac arrhythmias, myotonias, periodic paralyses, epilepses"
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Voltage-gated K channel diseases
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"Cardiac arrhythmias, epilepsies, ataxias"
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Voltage-gated Ca channel diseases
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"Cardiac arrhythmias, periodic paralyses, ataxias"
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