BRS Physio Flashcards
Characteristics of simple diffusion
Not carrier mediated
down an electrochemical gradient
Passive
Facilitated diffusion
down electrochemical gradient
passive no metabolic energy
Carrier mediated
Example: Glucose transport
Primary Active Transport
agasint electrochemical gradient
needs ATP and is active
carrier mediated
Example: Na-K-ATPas
Voltate gated channels
Opened or close by changes in membrane potential
Example: Na/K
Ligand gated channels
Open or close by hormones, second messengers or neurotransmitters
Example: Nicotinic receptor
At rest the membrane potential is far more permeable to
K over Na
Depolarization
Makes the membrane potential less negative
Hyperpolarization
Makes the membrane potential more negative
Inward current
Flow of positive current into the cell and depolarizes the membrane
Outward current
Flow of positive current outside of the cell, hyperpolarizes the membrane
What happens during the upstroke of the action potential? And what drug can block this?
Depolarization casues rapid openeing of the activation gates of the Na channels. Lidocaine
What two steps happen during depolarization
inactivation gates close of NA
K+ gates slowly open
During what condition does acommodation happen? And what is the result in the body?
hyperkalemia and muscle weakness
What two things increase conductance?
Increased fiber size
Myelination
In chemical synapses which ion enters the presynaptic terminal causing neurotransmitter release
Ca
At the neuromuscular junction what neurotransmiter is released from the presynaptic terminal? What about the post?
Pre: AcH
Post: Nicotinic
What catalyzes the formation of ACH from CoA and choline?
Choline acetyltransferase
What does Botulinum toxin do?
Blocks release of ACh from presynaptic terminals causing a total blockade
What does Neostigmine do?
Inhibits acetylcholinesterase which prolonges and enhances action of AcH at muscle end plate.
Examples of excitatory postsynaptic potentials and waht do they do?
Depolzarie cell by opening Na and K, include AcH, norepinephrine, epinephrine, dopamine, glutamate and serotonin.
Examples of inhibatory postsynaptic potentials and what they do?
hyperpolarize , open Cl- channels, GABA, glycine
Noreepinephrine
Primary transmiter from postganglionic sympathetic neurons, binds with alpha or beta receptors, removed by MAO
Epinephrine
Synthesized from NE by the action of phenylethanolamine in the adrenal medulla
Dopamine
Midbrain neurons, inhibits prolatin sectrtion
Serotonin
High concetrations in brain stem from tryptophan and is converted to melatonin in the pineal gland
Histamine
From hypothalamus
Glutamate
most prevalant excitatory neurotransmisiter
GABA/ Glycine
Inhibatory neurotransmiter
Nitric Oxide
short acting inhibatory neurotransmitter in GI. blood vessels and central nervous system.
Thick filaments in skeletal muscle
present in A band in center of sarcomere and contain myosin.
thin filaments in skeletal muscle
anchored in the Z lines are present in I bands and contain actin, tropomyosin and troponin
Troponin
Complex of T-I, T, C
4 steps in excitation/contraction of skeletal muscle
- Action potential
- Depolarization of T tubules
- Intracellular Ca increase
- Ca binds to troponin C which starts cross bridge cycling
What is the mechanism of Tetanus
Single action potential causes Ca release from CA from the SR and produced a single twitch. The muscle is then stimulated repeadly causing an increase in CA, which extends the time for cross bridge cycling resulting in no relaxation.
Primary difference in smooth and skeletal muscle structure?
Smooth has thick and thin filaments that are not arranged in sarcomeres, therefore they appear homogenous rather than striated.
Multiunit smooth muscle
densly innervated, contraction controlled by neural inneration and behaves as a separate motor unit
Unitary smooth muscle
spontaneously active, exhibits slow waves and exhibits pacemaker activity which is modulated by hormones and neurotransmitters
2 major differences in skeletal muscle vs smooth muscle contraction?
- No troponin in smooth muscle
2. In smooth, hormones and neurotransmitters can also directly release Ca from the SR through IP3 gated channels.
In the ANS where are parasympathetic ganglia located?
Near effector organs
In the ANS where are sympathetic ganglia located?
Paravertebral chain
Where are the preganglionic neurons of the sympathetic nervous system?
T1-L3 aka Thoracolumbar region
Where are the preganglionic neurons of the parasympathetic nervous system?
Nuclei of cranial nerves and S2-S4
Adrenergic neurons release what as the neurotransmitter?
Norepinephrine
Cholinergic neurons release what as the neurotransmitter?
ACh
Nonadrenergic/NonCholinergic release what?
Substance P, VIP or NO
Structure of parasympathetic nerves
Long preganglionic releases ACH onto Nicotonic receptor on short postganglionic which releases ACH onto muscarinic receptor
Structure of sympathetic nerves
Short preganglionic rleases ACh on nicotonic receptor on long postganglionic which releases NE onto adrenergic receptor
Alpha 1 : location, G protein, receptor
Smooth muscle, Gq, Increases IP3/Ca, excitation via NE
Alpha 2: location, G protein, Receptor
GI, Gi, decreases CAMP, inhibtion,
Beta 1: location, G protein, Mechanism
Heart(SA,AV,Ventr), Gs, increases CAMP, excitation
Beta 2
Smooth muscle,Gs, increaes CAMP, relaxation, most sensitive to epi
Nicotinic receptors
Autonomic ganglia, activated by ACH or nictoine, excitation,
Muscarinic receptors
inhibatory on the heart, activated by ACh and muscarine
Systolic pressure
highest arterial pressure during cardiac cycle, measured after contraction
Diastolic pressure
lowest arterial pressure, measured during relaxation
P wave of ECG
atrial depolarization
PR interval of ECG
Initial depolarization of the ventricle, length depends on conduction velocity through AV node. Decreased by stimulation of sympathetic, increased by stimulation of parasympthathetic
QRS ECG
Depolarization of ventricles
QT of ECG
Entire period of depolarizatiopn and repolarization of the ventricles
ST of ECG
isoelectric, period when ventricles are depolarized
T of ECG
ventricular repolarization
Phase 0 of cardiac action potential
upstroke, transient increase in Na conductance which depolarizes the membrane
Phase 1 of cardiac action potential
Brief period of initial repolarization caused by an outward current in part because of the movement of K ions out of the cell
Phase 2 of cardiac action potential
The plateau of the action potential, caused by a transient increase in Ca conductance.
Phase 3 of cardiac action potential
The repolarization, CA conductance decreaes and K conductance increases and predominates
Phase 4 of cardiac action potential
Resting membrane potential, period during which inward and outward currents are equal.
When is the absolute refractory period in the heart?
begins with upstroke of action potential and ends after plateau
Cardiac Cycle (A) Atrial systole
Atrial vs Vent pressure: > Arterial vs Vent pressure: > AV: Open SLV: Closed EKG: P wave Heart Sounds: 4th heart sound
Cardiac Cycle (B) Isovolumetric Ventricular Contraction
Atrial vs Vent pressure: < Arterial vs Vent pressure > AV: Closed SLV: Closed EKG: QRS Heart Sounds: First heart sound
Cardiac Cylce (C) Rapid Ventricular Ejection
Atrial vs Vent pressure: < Arterial vs Vent pressure: < AV: Closed SLV: Open EKG: QRS onset of T wave Heart Sounds: Most of stroke volume is ejected
Cardiac Cycle (E) Isovolumetric Relaxation
Atrial vs Vent pressure: < Arterial vs Vent pressure: > AV: Closed SLV: Closed EKG: T wave Heart Sounds: Second heart sound
Cardiac Cycle (F) Rapid Ventricular Filling
Atrial vs Vent pressure: > Arterial vs Vent pressure AV: Open SLV: EKG: Heart Sounds: third
Cardiac Cycle (G) Reduced Ventricular Filling
Longest phase