Exam 1 Flashcards
What cell types are effector cells of the Autonomic Nervous system?
smooth muscle, cardiac muscle, gland cells
What neurotransmitter does both neurons of the parasympathetic system release?
acetylcholine
What receptor does acetylcholine bind to?
cholinergic receptor
Pharmacology of the ANS
- Acetylcholinesterase inhibitors
- Nicotine
- Muscarine
In the sympathetic system, what does the postganglionic neuron release, and onto what?
norepinephrine onto a norepinephrine receptor
Neurochemistry of Parasympathetic Pathway
- CNS stimulates action potential
- preganglionic neuron always releases acetylcholine at parasympathetic ganglion
- ACh binds to a receptor on postganglionic neuron (nicotinic)
- postganglionic neuron release ACh on target cell
- ACh binds to receptor (muscarinic)
Neurochemistry for Sympathetic system
- CNS stimulates action potential in preganglionic
- pregang neuron release ACh at sympathetic ganglion
- ACh binds to receptor on post ganglionic neuron (nicotinic)
- postganglionic neuron release norepinephrine onto target cell
- Norepinephrine binds to adrenergic receptor
What are the subtypes of Adrenergic receptors?
Alpha 1: causes contraction of smooth muscle
Alpha 2: usually found on the varicosities of sympathetic postganglionic neurons; negative feedback to inhibit further norepinephrine release
Beta 1: found on cardiac muscle cells
Beta 2: usually cause relaxation of smooth muscle
What are the two ways to activate targets in the sympathetic system?
- Activate individual preganglionic neurons through connections in the CNS
- Activate release of epinephrine from adrenal gland; this activates receptors
What is “fight or flight”
activation of all sympathetic neurons as well as release of epinephrine into the blood stream
How does the parasympathetic system operate?
By activation of individual preganglionic neurons by the CNS, does not activate all at once
Agonist drug
Binds to a receptor and stimulates the same response in the cell as binding the transmitter
Antagonist drug
Binds to a receptor but does not create a response in the cell; it blocks the action of the transmitter by occupying the binding site
Can the body activate all parasympathetic pathways at once?
No, this can only be caused by drugs
1. Acetylcholinesterase inhibitors
2. nictoine
3. muscarine
Acetylcholinesterase inhibitors
any drug that blocks the breakdown of acetylcholine prolongs activation of ANS stimulation
Nicotine
a drug that turns on BOTH sympathetic and parasympathetic systems by activating the nicotinic acetylcholine receptor at all ganglionic synapses
Muscarine
a drug found in certain mushrooms; activates all muscarinic receptors at target organs (tearing, drooling, sweating, slow heart rate, difficulty breathing)
Norepinephrine
a neurotransmitter of the sympathetic nervous system; it activates all adrenergic receptors
Epinephrine
a hormone released from the adrenal gland; it also activates all adrenergic receptors (epinephrine=adrenaline)
Homeostasis
the maintenance of a relatively stable internal environment
Hypothalamus as the Master regulator
receives info from
-frontal lobe
-limbic system
-circulating hormones and signals
-neural signals from sensory
pathways
sends instructions to
-pituitary gland (endocrine output)
-brainstem centers (neural:automic)
-brainstem centers (neural: somatic)
-spinal cord centers (neural: autonomic)
Somatic nervous system
-cell bodies in CNS
-single neuron from CNS to effector organs (skeletal muscle)
Autonomic nervous system
-autonomic pathways are part of the motor system
-anatomically and functionally different from the somatic nervous system
-the 2 divisions of the ANS each have their own anatomy
-sympathetic and parasympathetic divisions work together
What systems control homeostasis
nervous and endocrine
Anatomy of the parasympathetic nervous system
-craniosacral system
-rest and digest
-preganglionic neurons in cranial nerves III, IX, X
Anatomy of the Sympathetic nervous system
-thoracolumbar system
-preganglionic neurons form all thoracic spinal cord levels and lumbar levels L1 and 2
-fight or flight
Dual innervation
most organs receive both sympathetic and parasympathetic control
What regulates organ function?
transmitters and receptors of the ANS
Effector cells of the ANS
-smooth muscle: ANS can increase or decrease the amount of contraction in a bed of smooth muscle
-Cardiac muscle: ANS can increase or decrease the amount of contraction in the wall of the heart, and regulate the rate of contraction
-gland cells: ANS can increase or decrease the amount of secretion produced and released from a gland
Neurochemistry of the ANS
-CNS stimulates action potential
-neurotransmitter binds to a receptor on postganglionic
-binding of transmitter stimulates action potential
-postganglionic releases neurotransmitter onto the target the cell
-binding of transmitter stimulates the target cell (smooth, cardiac, or gland cell)
What are the two exceptions in the sympathetic system?
- Sweat gland: ACh binds to muscarinic receptor
- Adrenal medulla: epinephrine and some norepinephrine get release into the blood, then it leaves the bloodstream and bind to any cell with adrenergic receptor
Acetylcholinesterase inhibitors
any drug that blocks the breakdown of ACh prolongs activation of ANS stimulation
2 main components of blood
- plasma
- formed elements
Hemopoises
aka Hematopoiesis
- the process of blood cell formation
-occurs in the hollow center of bone (red marrow)
-with aging, marrow cavity becomes filled with fat (yellow marrow)
Hemocytoblasts
stem cells that divide to form all types of blood cells; aka pluripotent stem cells
Erythrocytes
-red blood cells
-carry oxygen to cells in the body
account for slightly less than half the blood volume, and 99.9% of the formed elements
Hematocrit
measures the percentage of whole blood occupied by formed elements
Erythropoiesis
formation of new red cells
-RBCs pass through erythroblast and reticulocyte stages, during which time the cell actively produces hemoglobin
-process speeds up within the presence of erythropoietin
EPO
erythropoiesis stimulating hormone
Bioconcave disc
-provides a large surface-to-volume ratio to maximize rate of gas diffusion through membrane
-RBCs lack organelles: no nucleus
-shape allows RBCs to stack, bend, and flex
Hemoglobin
-accounts for 95% of the proteins in RBCs
-globular protein, formed from 2 pairs of protein subunits
-2 alpha and 2 beta
-each subunit contains 1 molecule of heme
-each heme has an iron ion at its center
-the iron binds and releases an oxygen molecule
-one hemoglobin can bind up to 4 oxygen molecules
Recycling hemoglobin
-aged and damaged RBCs are engulfed by macrophages of spleen, liver, and bone marrow; the hemoglobin is broken down
-raw materials are made available in blood for erythrocyte synthesis
Disorders of the blood
-jaundice
-anemia
-sickle cell anemia
Jaundince
-of the bilirubin formed in RBC breakdown, approximately 85% is removed from the blood and processed by the liver
-failure of the liver to “keep up” with RBC breakdown or blockage of the bile ducts leads to a buildup of bilirubin in the blood
-bilirubin then diffuses out into tissues all over the body, giving yellow color
Anemia
-a decrease in the oxygen-carrying capacity of blood
-symptoms: lethargy, weakness, muscle fatigue, low energy
-can include iron deficiency, hemorrhagic, and anaplastic
Sickle Cell anemia
-caused by a mutation of the amino acid sequence of the beta chain hemoglobin
-without sufficient oxygen bound to it, hemoglobin molecules cluster into rods and force the cell into a stiffened, curved shape which can get stuck in capillaries
Leukocytes
-WBCs
-can leave the blood stream in response to chemical signals by squeezing through gaps in vessel wall=diapedesis
Granulocytes (WBC)
-Neutrophil: 50-70% total WBC
-Eosinophil: phagocytes
-Basophil: migrate to damaged tissue and release histamine and heparin
Agranulocytes (WBC)
-lymphocyte: immune system cells
-monocyte: leave circulation to become macrophage
Complete Blood Count (CBC)
-one of the most common clinical tests performed
-simple blood test measuring most parameters of blood
-hematocrit and hemoglobin concentrations
-platelet count
-white blood cell count
What granular leukocytes come from a Myeloid stem cell?
-eosinophils
-basophils
-neutrophils
What agranular leukocytes form from a lymphoid stem cell?
-monocytes
-B lymphocytes
-T lymphocytes
Where do myeloid and lymphoid stem cells come from?
hematopoietic stem cell (hemocytoblast)
Disorders of the blood
-Leukemia (lymphoid and myeloid)
-immature and abnormal cells enter circulation, invade tissues
Platelets
fragments of a megakaryocyte
Steps in platelet formation
- hemocytoblast
2.megakaryoblast - megakaryocyte (II/III)
- megakaryocyte (IV)
- platelets
Steps in blood clotting
- smooth muscle contracts (vasoconstriction)
- injury to lining of blood vessel exposes collagen fibers; platelets adhere
- platelets release chemicals that make nearby platelets sticky; platelet plug forms
- fibrin forms a mesh that traps RBCs and platelets, forming the clot
Coagulation
-many blood proteins involved
-liver problems give coagulation problems
-drugs can interfere with clotting process
-final step: thrombin catalyses conversion of fibrinogen to fibrin threads
Fibrinolysis
breakdown of clot
-an inactive plasma enzyme called plasminogen is converted to plasmin
-plasmin digests fibrin threads of clot and clot eventually breaks down
Systemic circuit
-blood passes to and from most organs of the body
-arteries carry oxygenated blood
-veins carry deoxygenated blood
Pulmonary circuit
-blood passing to and from the lungs
-pulmonary arteries carry deoxygenated blood to lungs (need to be oxygenated)
-pulmonary veins carry oxygenated blood to left side of the heart
Where do arteries carry blood?
away from the heart
Where do veins carry blood?
toward the heart
Where does the RS of the heart receive blood from?
RS of heart receives deoxygenated blood through the superior and inferior vena cavae
Where does the RS pump blood to?
the pulmonary arteries
Where does the LS of heart receive blood from?
The LS of heart receives oxygenated blood from lungs via the pulmonary veins
Where does the LS of heart pump blood through?
aorta, to the rest of the body
How many layers make ip a blood vessel?
3
Tunica intima
-innermost layer of a blood vessel
-lined by epithelium
-supported by connective tissue
Tunica media
-middle layer of a blood vessel
-smooth muscle with various amounts of elastic fibers
Tunica externa
-outermost layer of a blood vessel
-connective tissue
Composition of arteries
-stronger, thicker walls than veins of the same size
-arteries generally contain more smooth muscle and often more elastic fibers
Blood vessels where have the largest diameter?
closest to the heart
Elastic arteries
largest arteries closest to heart contain lots of elastic fibers, and swell with each heart pump
Muscular arteries
smaller diameter arteries distributing to organs
Resistance vessels
arterioles are small diameter with a few layers of smooth muscle; constriction or relaxation
Exchange vessels
capillaries are the only vessels where materials move through the vessel wall
Capacitance vessels
veins have little muscle or elastic fibers; little ability to stretch, hold most of blood
How do veins move blood up from the lower body?
valves and muscular pump
function of valves
prevent blood from flowing backward
muscular pump
skeletal muscle activity around deep veins compresses veins and pushes blood toward heart
Capillaries
-how substances pass through a capillary wall
-through the epithelial cell membrane
-through fenestrations in the epithelial cell membranes
-through spaces between epithelial cells
3 types of capillaries
-continuous
-fenestrated
-sinusoidal
Continuous capillaries
-continuous endothelial lining
-permit diffusion of water, small solutes and lipid-soluble solvents
-least leaky
Fenestrated capillaries`
-have small fenestrations
-permit rapid exchange of water and larger solutes between plasma and interstitial fluid
-medium leakiness
Sinusoidal capillaries
-have large gaps between adjacent endothelial cells
-permit free exchange of water and large plasma proteins
-most leaky
Precapillary sphincter
-regulate blood flow through a capillary bed
-smooth muscles in vessels as they branch into a capillary network
-sphincters contract, acting as a valve to decrease blood flow
Where does the heart lie in the body?
in the thoracic cavity aka the mediastinum, between the two lungs
Pericardial sac
the fibrous sac in which the heart is enclosed
-pericardial cavity within sac surrounds the heart
Visceral pericardium
adhered to the hearts surface
Parietal pericardium
outer layer of pericardium
Right side of the heart
-right atrium
-right ventricle
Left side of the heart
-left atrium
-left ventricle
Apex
most inferior part of the heart
Base
superior end of the heart where great vessels attach
Arteries on the left side of the heart
-left coronary immediately splits into circumflex artery and left anterior descending (LAD)
Coronary veins
collect deoxygenated blood from heart wall and return it to the right atrium
Endocardium
innermost layer of the heart, supported by connective tissue
Myocardium
middle layer of the heart, cardiac muscle
Epicardium
outer layer of the heart, connective tissue with fat, coronary vessels, and visceral pericardium
Atrioventricular valves
-between atria and ventricles
-right AV valves has 3 flaps (tricuspid)
-left AV valve has 2 flaps (bicuspid or mitral)
Semilunar valves
-between ventricles and their exit vessel
-leaving right ventricle: pulmonary valve
-leaving left ventricle: aortic valve
Anatomy of AV valves
-cusps are anchored by string like chordae tendinae to muscular pegs called papillary muscles
When the AV valves are open then atrial pressure is ___ than ventricular pressure
greater
When the AV valves are closed then the atrial pressure is ___ than ventricular pressure
less
Blood flow through the heart
- blood –> inferior and superior vena cavae –> right atrium
- right atrium –> tricuspid valve–> right ventricle
- right ventricle–> pulmonary valve–> pulmonary trunk
- pulmonary trunk–> right and left pulmonary arteries –> lungs
- lungs–> 2 left and 2 right pulmonary veins–> left atrium
- left atrium–> bicuspid valve–> left ventricle
- left ventricle–> aortic valve–> aorta–> body
Conducting system of the heart
- SA node (pacemaker)
- AV node
- AV bundle
- bundle branches
- purkinje fibers
P wave
atrial depolarization, initiated by the SA node
before QRS
when depolarization is complete, impulse is delayed at the AV node
QRS
ventricular depolarization begins at apex, atrial repolarization occurs
after QRS
ventricular depolarization is complete
T
ventricular repolarization begins at apex
after T
ventricular repolarization is complete
bradycardia
slow HR
tachycardia
fast HR
pumping blood
a mechanical event initiated by electrical events
electrical event
distribution of electrical excitation, normally initiated by pacemaker cells of the SA node, passed to the contractile cells of the heart wall
mechanical event
contraction of myocardial cells, which exert pressure on the blood within the chambers to create a driving force for moving blood
Action potential of a single contractile cardiac muscle cell
- Na+ channels open
- Na+ channels close
- Ca2+ channels open; fast K+ channels close
- Ca2+ channels close; slow K+ channels open
- resting potential
the role of calcium ions in cardiac contractions
-contraction is produced by an increase in calcium ion concentration around myofibrils (very sensitive to extracellular Ca+ concentrations)
Calcium channel blockers
a group of powerful medications for heart patients, reduce calcium in myocytes so they contract less forcefully
How long does an action potential last in a contractile cardiac muscle cell?
as long as the contraction
one cardiac cycle
the start of one heartbeat to the start of the second heart beat
2 stages of activity in the heart chamber?
systole and diastole
systole
contraction of myocardium
diastole
relaxation of myocardium
what do purkinje fibers produce?
action potentials in contractile myocardial cells of both right and left ventricles
ventricular systole
when both ventricles begin contracting from apex to base
ventricular diastole
ventricles relax
atrial diastole
atria relax
Stages of heart contraction
- ventricular filling and atrial contraction (mid-to-late diastole)
2a. isovolumetric contraction phase
2b. ventricular ejection phase
(ventricular systole) - isovolumetric relaxation (early diastole)
- ventricular filling (repeats)
1st heart sound
closure of AV valves
2nd heart sound
closure of semilunar valves
end diastolic volume
the amount of blood in the left ventricle just before contraction
end systolic volume
the amount of blood left in the left ventricle after contraction
cardiodynamic
control of cardio output
cardiac output
the volume of blood pumped by the left ventricle in 1 minutes
CO= HR x SV
Stroke volume (SV)
the amount pumped out of the left ventricle during systole
SV= EDV-ESV
Heart rate is directly proportional to___
cardiac output
cardiovascular center
medulla oblongata in the brainstem drives the autonomic nervous system the cardiac center regulates heart activity
Cardioacceleratory center
increases heart rate
-controls sympathetic neurons, causes them to release norepinephrine at SA node
Cardioinhibitory center
slows heart rate
-controls parasympathetic neurons of vagus nerve, leading to acetylcholine release at SA node
SV is directly proportional to
cardiac output
filling time
duration of ventricular diastole
-longer fill time= longer fill volume
-slower heart rate= more fill time
venous return
rate of blood flow during ventricular diastole
-determined by venous pressure
-level of vasoconstriction alters venous pressure
increased sympathetic activity ___ the degree of constriction, dilating the vessel to increase blood flow=vasoconstriction
increases
decreased sympathetic activity ___ the degree of constriction, dilating the vessel to increase blood flow= vasodilation
decreases
preload
stretch on ventricle wall during diastole
-directly proportional to EDV
-more blood=more stretch on contractile cells
contractility
how hard the ventricle contracts
-directly proportional to stroke volume
beta blockers
block receptors for epinephrine and norepinephrine, so decrease contractility (decrease workload on heart)
calcium channel blockers
decrease calcium entry or release in contractile cells; less calcium= less actin (myosine interaction=less tension)
afterload
force the ventricle needs to produce to open the semilunar valve and eject blood
-inversely related to cardiac output
ejection fraction
important clinical measure of heart function
-50-75% = normal
-36-49% = below normal
-35% and below = ability is low
flow
a function of pressure and resistance
difference in BP/ peripheral resistance
mean arterial pressure (map)
diastolic pressure + 1/3 pulse pressure (usually 93)
pulse pressure
difference between systolic and diastolic pressure
vascular resistance
-due to friction between blood and the vessel wall
blood viscosity
resistance caused by molecules and suspended materials in a liquid
turbulance
swirling action within vessel that disturbs smooth flow
diffusion
movement of ions or molecules along a concentration gradient from high concentration to low concentration
filtration
water and small solutes squeezed out of the capillary tube into the interstitial fluid
reabsorption
water drawn back into the capillary from the interstitial fluid
-mainly pulled by osmotic pressure exerted by large plasma proteins trapped in blood
net filtration pressure
the difference between net hydrostatic pressure and net osmotic pressure
lymphatic vessels
return interstitial fluid to the blood stream
edema
the accumulation of interstitial fluid due to abnormal leakage from capillaries
Autoregulation
causes immediate, localized adjustments
-local regulation of blood flow within tissues
-adjusted by changing peripheral resistance by changing diameter of vessel
Neural mechanisms
respond quickly to changes
-cardiovascular center controls both heart and vessels
-CNS regulates systematic BP with the baroreceptor reflex
Endocrine mechanisms
slowest, long-term changes
-activation of hormone pathways
Cardiovascular adaptation: standing up
sympathetic activation causes HR and ventricular contraction to increase so stroke volume increase and restores cardiac output and BP
Cardiovascular adaptation: light exercise
increase in venous return, causes increase in EDV and preload, so theres an increase in stroke volume and cardiac output
Cardiovascular adaptation: strenuous exercise
sympathetic activity increase which causes HR and contractility to increase= CO increases
short term response to hemorrhaging
fixing BP
long term response to hemorrhaging
body uses hormones to increase fluid retention
circulatory shock
life threatening failure of circulatory system to get enough oxygen to tissue
Heart Attack
decrease in coronary blood flow, can lead to angina pain and eventually to a heart attack
Athersclerosis
inflammatory disease of the vessel wall
-stiffening of the walls due to the fatty deposits
-high levels of LDL (not good)
-reduces blood flow, increases resistance
Treatment for blocked coronary artery
-coronary artery bypass graft surgery (CABG)
-ballon angioplasty
-insert a stent
hypertension
high BP
Arrhythmia
-atrial fibrillation
-ventricular fibrillation
Atrial fibrillation
-atrial wall quivers
-blood clots may form near atrial walls
Ventricular fibrillation
-ventricle wall quivers and fails to pump blood out of heart
-leads to cardiac arrest
Abnormalities in the heart
-ventricular septal defect
-atrial septal defect
-causes mixing of low O2 blood and high O2 blood
heart failure
the heart cannot pump enough blood to the heart
congestive heart failure
heart pumps inadequately, blood backs up on venous side, which can go to the lungs (edema) and interfere with breathing
common drug treatments for cardiovascular disease
-alpha blockers
-beta blockers
-calcium channel blockers
alpha blockers
used to dilate blood vessels and decrease BP
beta blockers
used to decrease contractility to ease workload and decrease HR- decrease CO (lower BP)
calcium channel blockers
used to decrease contractility in ventricle to decrease SV, CO, and BP
