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- stimulus -> receptor -> electrical potential
- receptor potential (if above threshold) = graded potential ->
- in neuron (somatic senses) -> action potential -> CNS
- in non-neural sensory receptors (special senses ex olfaction) -> neurotransmitter release
- energy transduced: open/ close channels
- depolarize(+) cell = excitatory signal in neuron Na+ channel opens
- hyperpolarzie(-) cell = inhibitory signal in neuron K+ or Cl- channels open
- spinal cord -> thalamus -> cerebral cortex *olfaction does not pass through the thalamus
- Free nerve endings
- Encapsulated nerve endings
- Specialized receptor cells: chemoreceptors -> ligand, mechanoreceptors -> touch, pressure, vibration, sound, photoreceptor -> photon, thermoreceptor -> heat and cold, Nociceptor -> pain
- has adequate stimulus: particular form of energy to which it is most responsive
multiple sensory neurons converged on one secondary neuron
level of stimulus intensity necessary for us to be aware of a particular sensation
- the sensory neuron fires action potentials as long as the receptor potential is above threshold
- slow or no adaptation
- continuous signal transmission for duration of stimulus
- monitoring of parameters that must be continually evaluated
- Ex. Baroreceptors, nocioceptors
- respond to a change in stimulus intensity but adapt if the strength of the stimulus remains constant
- fast adaptation
- cease firing if strength of a continuous stimulus remains constant
- allows body to ignore constant unimportant information
- Ex. smell
- primary: from receptor to spinal cord or medulla
- secondary: always cross over (spinal cord or medulla) -> thalamus
- tertiary: -> somatosensory cortex
- in skin and deep organs
- detects vibration (pressure)
pain in organs poorly localized -> may be displaced if -> multiple primary sensory neurons converge on single ascending neuron
- smell and taste
- olfactory receptors: bipolar neurons -> directly to the olfactory cortex
- odorant receptors: G protein coupled membrane proteins
- Taste sensations: sweet, sour, salty, bitter, umami
- taste cells: non neural cells with membrane channels or receptors that interact with taste ligands; creates Ca2+ signal -> activates primary sensory neuron
- ligands activate the taste cell
- various intracelluar pathways are activated
- Ca2+ signal in the cytoplasm triggers exocytosis or ATP formation
- Neurotransmitter or ATP is released
- primary sensory neuron fires and action potentials are sent to brain
Sweet/ Umami/ Bitter ligand
ligand -> gustducin (GPCR) -> signal transduction -> release Ca2+ -> ATP -> primary gustatory neuron
Na+ -> Na+-> cell depolarizes -> Ca2+ -> seratonin -> primary gustatory neuron
H+ -> H+ -> Ca2+ -> seratonin -> primary gustatory neuron
- cochlear nerve -> medulla -> pons -> midbrain -> thalamus -> auditory cortex
- when sound bends hair cell cilia, the hair cell membrane potential changes and alters the release of neurotransmitter onto sensory neurons
sound waves -> tympanic membrane vibrations -> ossicles transmit vibrations -> oval window -> movement of basilar membrane stimulates receptor cells -> NT release stimulates sensory neuron -> impulse to auditory cortex
- light enters eye, focused by lens onto retina -> photoreceptors (rods (b&w) cones (color)) transduce light energy into electrical signal -> electrical signals sent along neuronal pathways are processed in visual cortex
- fovea centralis: sharp vision
- photon: bundle of E
pupillary reflex is consensual:
both eyes react
path of light through eye:
- aqueous humor
- vitreous humor
lens attached to ciliary muscle via suspensory ligament (zonulas) -> ciliary muscle contracts -> releases tension on the ligaments -> lens bulges
when ciliary muscle is relaxed the ligaments pull on and flatten lens
sequence of reaction when a person looks at a distant object:
- pupils dilate
- zonulas become taut
- lenses are less convex
Phototransduction for Rhodopsin:
- retinal absorbs 1 photon
- rhodopsin splits: retinal is released from opsin due to conformational change
in darkness rhodopsin is inactive cGMP is high, and CNG and K+ channels are open
light bleaches rhodopsin; opsin decreases cGMP closes CNG channels and hyperpolarizes cell
What accessory role does the outer ear (the pinna) play in the auditory system?
the pinna funnels sound into the ear canal
How do sensory receptors communicate the intensity of a stimulus to the CNS?
sensory neurons signal intensity of a stimulus by the rate at which they fire action potentials
What is the adaptive significance of irritant receptors that are tonic instead of phasic?
irritant receptors warn the body of danger. the body should respond in some way that stops the harmful stimulus. It is important that signals continue as long as the stimulus is present, meaning the receptors should be tonic rather than phasic.
olfactory receptor cell (primary neuron)-> cranial nerve I -> secondary neuron in olfactory bulb -> olfactory tract -> olfactory cortex in temporal lobe
What is a kilohertz?
1000 Hz which means 1000 waves per second
Normally when cation channels on a cell open, either Na+ or Ca2+ enters the cell. Why is it K+ rather than Na+ that enters hair cells when cation channels open?
endolymph has high K+ and low Na+ so the electrochemical gradient favors K+ movement into the cell
The stereocilia of hair cells are bathed in endolymph, which has a very high concentration of K+ and a low concentration of Na+. When ion channels in the stereocilia open, which ions move in which direction to cause depolarization?
K+ entry into hair cells causes depolarization
What functions does the aqueous humor serve?
he aqueous humor supports the cornea and lens. it also brings nutrients to and removes wastes from the epithelial layer of the cornea, which has no blood supply
Brain Area Senses:
- medulla: sound, taste
- cerebrum: odors, visual, taste
- midbrain: visual
- cerebellum: equilibrium
In which two senses does the brain rely on the timing of receptors activation to determine the location of the initial stimulus?
olfaction and hearing
range of hearing for the average human ear
20 to 20,000 Hz
most acute hearing in the range
1,000 to 3,000 Hz
Which structure of the inner ear codes sound for pitch?
association of wave frequencies with different areas of the membrane
Loud noises cause action potentials to:
fire more frequently
parts of the vestibular apparatus that tell our brain about our movements through space
- SEMICIRCULAR CANALS, which sense rotation
- OTOLITH ORGANS, which responds to linear forces
List four types of cells found in the retina, and briefly describe their functions.
- rods and cones are photoreceptors that transduce light energy
- bipolar and ganglion cells carry out signal processing
sound cannot be transmitted through the external or middle ear
inner ear is damaged
auditory pathways are damaged
central hearing loss
loss of accommodation due to stiffening of the lens with age
longer than normal distance between lens and retina (near-sightedness)
shorter than normal distance (far-sightedness)
- a sympathomimetic: to dilate
- a muscarinic antagonist: blocks muscarinic receptors
- a cholinergic agonist: constrict
- an anticholinesterase: prevents breakdown of ACh
- a nicotinic agonist: constrict
contraction and dilation iris muscles
circular muscles form a ring on the inner part of the iris; when these muscles contract the pupil gets smaller. The radial muscles extend from the outer edge of the iris to the circular muscles; when they contract they pull on the relaxed circular muscles and expand the diameter of the pupil (dilate)
- regulate BP, HR, Resp, H2O balance, temp.
- sympathetic: fight or flight
- parasympathetic: rest and digest
- preganglionic neuron: from CNS synapses with
- postganglionic neuron: in autonomic ganglion
- sympathetic: long post - secret NE onto adrenergic receptors; short pre -spinal cord
- parasympathetic: long pre - from brain; short post - secrete ACh onto cholinergic muscarinic receptors
- ACh -> cholinergic (nicotinic, muscarinic) neurons and receptors; from preganglions of both divisions and post ganglions of parasympathetic
- NE -> adrenergic (alpha and beta) neurons and receptors; from postganglionic neurons of sympathetic division
- in autonomic ganglia
- curare = antagonist
- found in neuroeffector junctions of parasympathetic branch
- G-protein coupled mechanisms
- atropine = antagonist
- 1: muscle contraction
- 2: muscle relaxation
- most common NE -> much stronger response
- 1: excitation of heart
- 2: inhibitory; smooth muscle relaxation blood vessles/ bronchioles
- 3: adipose tissue
- Beta blockers: antagonists - propranolol
NE release and removal at a sympathetic varicosity
- action potential arrives at varicosity
- depolarization opens voltage gated Ca2+ channels
- Ca2+ entry triggers exocytosis of synaptic vesicles
- NE binds to adrenergic receptor on targer
- receptor activation ceases when NE diffuses away from synapse
- NE is removed from synapse
- NE can be taken back into synaptic vesicles for re-release
- NE is metabolized by (MAO)
- Somatic motor: CNS -> ACh nicotinic receptor (skeletal muscle)
- Parasympathetic: CNS -> ACh ganglion; nicotinic receptor -> ACh muscarinic (smooth muscle/glands/adipose)
- Sympathetic: CNS -> nicotinic receptors; ACh ganglion -> Alpha receptor/ Beta 1 receptors; NE
- Adrenal sympathetic: CNS -> adrenal cortex -> adrenal medulla -> E -> blood vessel -> E; Beta 2 receptor
Which type of ACh receptors do you suppose chromaffin cells have, nicotinic or muscarinic?
chromaffin cells are modified postganglionic neurons, so they have nicotinic receptors
List four things that can happen to autonomic neurotransmitters after they are released into a synapse.
- diffuse away from the synapse
- digested by enzymes in the synapse
- taken back into the presynaptic neuron
- bind to a membrane receptor
main enzyme responsible for catecholamines degradation
MONOAMINE OXIDASE (MAO)
enzyme that breaks down ACh
What kind of receptor is found on the postsynaptic cell in a neuromuscular junction?
nicotinic cholinergic receptors
What is the advantage of divergence of neural pathways in the autonomic nervous system?
divergence allows one signal to affect multiple targets
Ganglia contain the cell bodies of:
- postganglionic autonomic neurons
- sensory neurons
If nicotinic receptor channels allow both Na+ and K+ to flow through, why does Na+ influx exceed K+ efflux?
the electrochemical gradient for Na+ is greater than that for K+
What happens to a monkey hit by a dart with curare; a plant toxin that binds to and inactivates nicotinic ACh receptors?
skeletal muscles would become paralyzed
Contractile organelles of myofiber:
- 6 types of proteins:
- actin & myosin -> contractile
- tropomyosin & troponin -> regulatory
- titin & nebulin -> accessory
Sliding filament theory:
- contraction occurs when thin and thick filaments slide past each other as myosin binds to actin, swivels, and pulls actin toward the center of the sarcomere
- sarcomere = unit of contraction
- myosin = motor protein: chemical energy -> mechanical energy of motion
- joint stiffness
- begins 2-4hr post mortum
- caused by leakage of Ca2+ ions into cell and ATP depletion
initiation of muscle action potential:
- somatic motor neuron releases at neuromuscular junction
- Net entry of Na+ through ACh receptor-channel initiates a muscle action potential
Excitation Contraction Coupling:
- Net Na+ creates EPSP
- AP to T-tubules
- DHP receptors in t tubules sense depolarization
- DHP receptors open Ca2+ channels in cytoplasm
- intracellular Ca2+ increase
- Ca2+ reuptake into SR
ATP for muscle contraction from?
- COH: aerobic and anaerobic respiration
- fatty acid breakdown always require O2 (too slow for heavy exercise
Muscle Fiber Classification:
- Slow twitch- type 1 oxidative only; aerobic, steady power, endurance
- Fast twitch- type 2 oxidative (can convert to type 1 when exercising) or glycolytic; anaerobic, explosive power, fatigues easily
- endurance: more mitochondria, more enzymes for aerobic respiration, more myoglobin (store more O2), no hypertrophy
- resistance: more actin and myosin (sarcomeres), more myofibrils (stores more glycogen), muscle hypertrophy
Electrical and mechanical events in muscle contraction:
too much or too little overlap of thick and think filaments in resting muscle result in decreased tension
Why are the ends of the A band the darkest region of the sarcomere when viewed under the light microscope?
because they are where the thick and thin filaments overlap
What is the function of t-tubules?
allow action potentials to travel from the surface of the muscle fiber to its interior
What are the three anatomical elements of a neuromuscular junction?
a neuromuscular junction consists of axon terminals from one somatic motor neuron, the synaptic cleft, and the motor end plate on the muscle fiber
Each myosin molecule has binding sites for what molecules?
ATP and actin
What is the different between F-actin and G-actin?
F-actin is a polymer filament of actin made from globular G-actin molecules
Name an elastic fiber in the sarcomere that aids relaxation.
In the sliding filaments theory of contraction, what prevents the filaments from sliding back to their original position each time a myosin head releases to bind to the next actin binding site?
the crossbridges do not all unlink at one time, so while some myosin heads are free and swiveling, others are still tightly bound
Which part of contraction requires ATP? Does relaxation require ATP?
the release of myosin heads from actin requires ATP binding. Energy from ATP is required for the power stroke. Relaxation does not directly require ATP, but relaxation cannot occur unless Ca2+ is pumped back into the sarcoplasmic reticulum using a Ca2+-ATPase.
What events are taking place during the latent period before contraction begins?
The events of the latent period include creation of the muscle action potential, release of Ca2+ from the sarcoplasmic reticulum, and diffusion of Ca2+ to the contractile filaments.
What is the response of a muscle fiber to an increase in the firing rate of the somatic motor neuron?
increased motor neuron firing rate causes summation in a muscle fiber, which increases the force of contraction
What is the difference in how contraction force is varied in multi-unit and single-unit smooth muscle?
multi unit smooth muscle increases force by recruiting additional muscle fibers; single-unit smooth muscle increases force by increasing Ca2+ entry
What happens to contraction if a smooth muscle is placed in a saline bath from which all calcium has been removed?
without ECF Ca2+, contraction either decreases or stops altogether because little or no Ca2+ is available to initiate the process
How do pacemaker potentials differ from slow wave potentials?
Slow wave potentials are variable in magnitude and may not reach threshold each time
Explain how hyperpolarization decreases the likelihood of contraction in smooth muscle.
many Ca2+ channels open with depolarization; therefore, hyperpolarization decreases the likelihood that these channels open. The presence of Ca2+ is necessary for contraction
Z disk - ends of a sarcomere, I band- Z disk in the middle, A band (thick filaments) darkest, H zone- lighter region of A band, M line divides A band in half; thick filaments link to each other
Briefly explain the functions of titin and nebulin.
they keep actin and myosin in alignment. Titin helps stretched muscles return to resting length
Explain he roles of troponin, tropomyosin, and Ca2+ in skeletal muscle contraction.
Ca2+ binds to troponin, which repositions tropomyosin, uncovering actin’s myosin-binding sites
fast-twitch glycolytic fibers
- has largest diameter
- uses anaerobic metabolism; fatigues quickly
- used for quick, fine movements
- has some myoglobin
- also called red muscle
slow-twitch oxidative fibers
- has most blood vessles
- has myoglobin
- red muscle
- most mitochondira
single contraction-relaxation cycle in a skeletal muscle fiber
action potentials in motor neurons:
result from inward Na+ current and outward K+ current through voltage gated channels, triggers ACh release
action potentials in skeletal muscles:
result from inward Na+ current and outward K+ current through voltage gated channels, triggers Ca2+ release from the sarcoplasmic reticulum
Pressure gradient in blood vessels:
pressure of fluid in motion decreases over distance because of energy loss due to friction
Contractile Cardiac Muscle Cells:
- intercalated discs -> gap junctions and anchoring junctions
- sSR smaller than in skeletal muscle
- abundant mitochondria
EC coupling and relaxation in cardiac muscle
- action potential enters from adjacent cell
- voltage gated Ca2+ channel opens; Ca2+ enters cell
- Ca2+ induces Ca2+ release through RyR channels
- local release causes Ca2+ spark
- summed Ca2+ sparks create Ca2+ signal
- Ca2+ ions bind to troponin to initiate contraction
- relaxation occurs when Ca2+ unbinds from troponin
- Ca2+ is pumped back into SR for storage
- Ca2+ is exchanged with Na+ by NCX antiporter
- Na+ gradient is maintained by the Na+-K+ATPase
Action Potential of a contractile cardiac cell
- Na+ channel opens
- Na+ channel close
- Ca2+ channel open; fast K+ channel close
- Ca2+ channel close; slow K+ channel open
- resting potential
- also called pacemaker cells
- spontaneous AP generation
- dont have normal resting potential
- If channels (funny) -> Na+ influx > K+ efflux -> slow depolarization -> Ca2+ channels start reopening
- at threshold lots of Ca2+ channels open
- repolarization due to K+ as always
Phases in myocardial cells:
- steep repolarization phase of AP is due to K+
- importance of plateau phase of AP is preventing tetanus
Refractory Periods in skeletal and cardiac muscle:
caridac refractory periods = LONGER
AP in cardaic autorhythmic cells:
- pacemaker potential gradually becomes less negative until it reaches threshold -> triggers action potential
- ion movements during an action and pacemaker potential Ca2+ in K+ out
- If channel open -> Ca2+ open; If close -> lots of Ca2+ open -> Ca2+ close; K+ open -> K+ close -> If open
- increased Na+ intracellular
- Na+ concentration gradient decreased
- lower E pot. for Na+
- Na+ Ca2+ pump works less
- Ca2+ intracellular increased
- stronger myocardial contraction
A drug that blocks all Ca2+ channels in the myocardial cell membrane is placed in the solution around the cell. What happens to the force of contraction in that cell?
If all calcium channels in the muscle cell membrane are blocked, there will be no contraction. If only some are blocked, the force of contraction will be smaller than the force created with all channels open.
At the molecular level, what is happening during the refractory period in neurons and muscle fibers?
the refractory period represents the time required for the Na+ channel gates to reset
Lidocaine is a molecule that blocks the action of voltage-gated cardiac Na+ channels. What happens to the action potential of a myocardial contractile cell if lidocaine is applied to the cell?
If cardiac Na+ channels are blocked with lidocaine the cell will not depolarize and therefore will not contract
Do you think that the Ca2+ channel is autorhythmic cells are the same as the Ca2+ channels in contractile cells?
the Ca2+ channels in autorhythmic cells are not the same as those in contractile cells. autorhythmic Ca2+ channels open rapidly when the membrane potential reaches about -50mV and close when it reaches about 20 mV. the Ca2+ channels in contractile cells are slower and do not open until the membrane has depolarized fully.
Name two functions of the AV node. What is the purpose of AV node delay?
the AV node conducts action potentials from atria to ventricles. it also slows down the speed at which those action potentials are conducted, allowing atrial contraction to end before ventricular contraction begins
Where is the SA node located?
upper right atrium
If vasodilation occurs in a blood vessel:
Trace an action potential from the SA node through the conducting system of the heart.
SA node to internodal pathways to AV node to bundle of His to purkinje fibers to ventricular myocardium
volume of blood in ventricle at end of contraction
volume of blood in the ventricle at the beginning of contraction
What events cause the two principal heart sounds?
vibrations from AV closure cause the “lub” sound and from semilunar valve closure causes the “dup” sound
volume of blood in the ventricle before the heart contracts
volume of blood that enters the aorta with each contraction
volume of blood that leaves the heart in one minute
volume of blood in the entire body
Compare and contrast the structure of a cardiac muscle cell with that of a skeletal muscle cell. What unique properties of the cardiac muscle are essential to its function?
cardiac muscle has strong cell to cell junctions, gap junctions for electrical conduction, and the modification of some muscle cells into autorhythmic cells
Define inotropic effect. Name two drugs that have a positive inotropic effect on the heart.
an effect on force of contraction. norepinephrine and cardiac glycosides
Two drugs used to reduce cardiac output are calcium channel blockers and beta receptor blockers. What effect do these drugs have on the heart that explains how they decrease cardiac output?
calcium channel blockers slow heart rate by blocking Ca2+ entry and decrease force of contraction by decreasing Ca2+- induced Ca2+ release. Beta blockers decrease effect of NE and E preventing increased heart rate and force of contraction
Calculate cardiac output if stroke volume is 65 mL/beat and heart rate is 80 bpm.
5200 mL/min or 5.2 L/min
Calculate end-systolic volume if end-diastolic volume is 150 mL and stroke volume is 65 mL/beat.
The formula given for calculating MAP applies to a typical resting heart rate of 60-80 bpm. If heart rate increases, would the contribution of systolic pressure to mean arterial pressure decrease or increase, and would MAP decrease or increase?
if heart rate increases, the relative time spent in diastole decreases. In that case, the contribution of systolic pressure to mean arterial pressure increases, and MAP increases.
Peter’s systolic pressure is 112 mm Hg, and his diastolic pressure is 68 mm Hg. What is his pulse pressure? His mean arterial pressure?
pulse pressure is 112-68 = 44mm Hg. MAP is 68 + 1/3 (44) = 82.7 mm Hg
Resistance to blood flow is determined primarily by which?
blood vessel diameter
The extracellular fluid concentration of K+ increases in exercising skeletal muscles. What effect does this increase in K+ have on blood flow in the muscles?
extracellular K+ dilates arterioles, which increases blood flow
What happens when E combines with beta1 receptors in the heart? With beta2 receptors in the heart? Which heart tissue possess the different types of beta receptors?
E binding to myocardial beta1 receptors increases heart rate and force of contraction. E binding to beta2 receptors on heart arterioles causes vasodilation
Skeletal muscle arterioles have both alpha and beta receptors on their smooth muscle. E can bind to both. Will the arterioles constrict or dilate in response to E?
alpha receptors have lower affinity for E than beta2 receptors so the beta2 receptors dominate and arterioles dilate
A person with liver disease loses the ability to synthesize plasma proteins. What happens to the colloid osmotic pressure of his blood? What happens to the balance between filtration and absorption in his capillaries?
loss of plasma proteins will decease colloid osmotic pressure. Hydrostatic pressure will have a greater effect in the filtration-absorption balance, and filtration will increase
Why did this discussion refer to the colloid osmotic pressure of the plasma rather than the osmolarity of the plasma?
using osmotic pressure rather than osmolarity allows a direct comparison between absorption pressure and filtration pressure, both of which are expressed in mm Hg.
The left ventricle fails to pump normally, blood backs up into what set of blood vessels? Where would you expect edema to occur?
if the left ventricle fails, blood backs up into the left atrium and pulmonary veins, and then into lung capillaries. Edema in the lungs is known as pulmonary edema.
Baroreceptors have stretch-sensitive ion channels in their cell membrane. Increased pressure stretches the receptor cell membrane, opens the channels, and initiates action potentials. What ion probably flows through these channels and in which direction?
the most likely ion is Na+ moving into the receptor cell
- their diameter can be altered by neural input
- are the main site of variable resistance
- store pressure generated by the heart
- have walls that are both stiff and elastic
- have thin walls of exchange epithelium
- blood flow slowest through these vessels
- carry low-oxygen blood
- act as a volume reservoir
- their diameter can be altered by neural input
- have lowest blood pressure
- carry low-oxygen blood
- have thin walls of exchange epithelium
List the four tissue components of blood vessel walls, in order from inner lining to outer covering. Briefly describe the importance of each.
endothelium: capillary exchange and paracrine secretion; elastic tissue: recoil; smooth muscle: contraction; fibrous connective tissue: resistance to stretch
What is the equation used to calculate the strength of this pressure wave?
pulse pressure = systolic pressure - diastolic pressure
List the factors that aid venous return to the heart.
one way waves in the veins, skeletal muscle pump, and low pressure in the thorax during breathing
What is hypertension, and why is it a threat to a person’s health?
elevated blood pressure can cause a weakened blood vessel to rupture and bleed
What is hyperemia? How does active hyperemia differ from reactive hyperemia?
a region of increased blood flow. active: increased blood flow is in response to an increase in metabolism; reactive: increase in flow follows a period of decreased blood flow
With which three physiological systems do the vessels of the lymphatic system interact?
immune, circulatory, and digestive systems
Define edema. List some ways in which is can arise.
excess fluid in the interstitial space. causes include lower capillary oncotic pressure due to decreased plasma proteins or blockage of the lymphatic vessels by a tumor or other pathology
blood flow through a tissue
colloid osmotic pressure:
the contribution of plasma proteins to the osmotic pressure of the plasma
a decrease in blood vessel diameter
growth of new blood vessels, especially capillaries, into a tissue
small vessels between arterioles and venules that can act as bypass channels
cells surrounding the capillary endothelium that regulate capillary leakiness
The two major lipoprotein carriers of cholesterol are HDL and LDL. Which type is bad when present in the body in elevated amounts?
LDL-C is bad in elevated amounts
Calcium channel blockers prevent Ca2+ movement through Ca2+ channels. Explain two ways this action lowers blood pressure. Why are neurons and other cells unaffected by these drugs?
preventing Ca2+ entry decreases ability of cardiac and smooth muscles to contract. Decreasing Ca2+ entry into autorhythmic cells decreases heart rate. Neurons and other cells are unaffected because they have types of calcium channels not affected by the drugs
Left ventricle failure may be accompanied by edema, shortness of breath, and increased venous pressure. Explain how these signs and symptoms develop.
left ventricular failure causes blood to pool in the lungs, increasing pulmonary capillary hydrostatic pressure. This may cause pulmonary edema and shortness of breath when oxygen has trouble diffusing into the body. Blood backing up into the systemic circulation increases venous pressure.
Fluid exchange at capillary
- Filtration in systemic capillaries; increased hydrostatic pressure (fluid out), decreased colloid osmotic pressure (fluid in)
- relationship between capillaries and lymph vessels; arterioles -> net filtration -> lymph vessels -> net absorption -> venule; the excess H2O and solutes filter out of capillary are picked up by the lymph vessels and returned to the circulation
The developement of atherosclerosis plaques:
- LDL accumulates and is oxidized, macrophages inject LDL become foam cells, smooth muscle cells begin to take up cholesterol
- lipid core accumulates, scar tissue forms wall of lipid core, smooth muscle cells divide thicken intima, calcifications; deposit with in plaque
- platelets exposed to collagen -> blood clots, macrophages release enzyme to dissolve collagen plaque making stable plaque -> unstable plaque