bio 328 full semester package

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Class: BIO 328

Lecture/Exam: Full Semester Package

School: SBU

Semester: N/A

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Lecture 1 Spinal Cord Reflexes

Motor Functions are split into 2 ways

o Descending systems systems from above brain stem called

Upper Motor neuron systems

Basal Ganglia, cerebellum, motor cortex and brainstem centers

o The Lower motor neuron systems the motor neurons in the

ventral horn of the spinal cord

Form synapses at the neuromuscular junction and release AcH, thereby causing muscle contraction

These are the Piano Keys in order to get the Tune e.g. movement.. you must play the Piano keys activate

these motor neurons

Also called the Final common pathway

A Skeleton muscle cannot be inhibited- only the level of contraction

can change based on the concentration of acetylcholine

o To relax a muscle, you must inhibit the motor neuron.

Many different things can cause motor neuron excitation. All of these

things go to the spinal cord, which will then play the keys on the

piano

o Nociceptor Sensory Receptors in skin

o Skeletal muscle sensory receptors

o Receptors in tendons

Spinal cord is arranged by levels

o Cerivcal spinal cord =

hands/arms and chest, etc.

Spinal Cord has 2 colors

o Gray matter these are

neurons in the center

bowtie of the spinal cord

Dorsal Horn sensory input

Intermediate Regions Interneurons

Fingers on the keys of the piano

Ventral Horn The Motor Neurons reside here o White Matter These are the axons traveling up and down the

spinal cord. White due to some myelination

Antero - Lateral pain input

Ventral lateral motor function/ standing

Dorsal - touch/sensory input


Dorso-lateral descending motor control

2 Major enlargements of the bowtie

o Cervical spinal cord

o Lumbar Spinal cord

o This is because this is where the most motor and sensory

information is needed hands and legs

Spinal cord is suspended in CSF Cerebral spinal cord

2 roots to the spinal cord

o Ventral Root

o Dorsal root

Contains the dorsal root ganglion cell body for sensory o These Roots combine to make up the peripheral nerve which

contains both motor and sensory axons

Some are myelinated, some arent.

Types of nerve fibers in peripheral nerves

o Somatic neurons

Muscle Spindles

Axon 1A tells spinal cord about length and movement

of the muscle.

This is parallel to the muscle fibers

Golgi Tendons provide info about muscle tension

Sits in series with the muscle fibers

Free nerve endings measure potential pain.. as well as temperature and crude touch

o Motor Neurons

Alpha Motor neuron this is the main one it synapses at the neuromuscular junction (NMJ)

Gamma Motor Neuron innervates a sensory receptor this is critical to the functioning of the Alpha motor neuron

Reflexes a sterotyped motor responses elicited by a defined sensory

stimulus

o Can be overridden if you think hard enough

Reflex Classifications

o Autonomic or somatic

o Where the reflex is integrated cranial or spinal cord

o When the reflex develop - learned or born with it?

o The Number of neurons in the reflex loop

Skeletal Muscle Sensory Receptor initiated reflex Muscle Stretch

Reflex patellar stretch reflex

o Muscle Spindle the sensory apparatus. Intrafusal Muscle Fiber


This is in parallel with the muscle fibers. It detects how long the muscle is, and how its changing

o Afferent Sensory neuron inputs on the monosynaptic nerve

junction

o Motor neuron causes contraction (more Ach) for the quadriceps

muscle and relaxation (less Ach) for the hamstring muscle

Monosynaptic excitatory reflex

Polysynaptic inhibitory reflex o Ipsilateral (same side) and negative feedback. No afterdischarge

no sustained contraction

Alpha Gamma Co-activation occurs in the stretch reflex

o Alpha Motor Neuron actually causes the contraction

o Gamma motor neuron it targets the intrafusal muscle fiber and

innervates its contractile material to contract.

This is important because it keeps the muscle spinal taut so that the length of the muscle can be reported

Nociceptor Reflex ex. Ball of the foot crossed extensor/flexor

withdrawal reflex

o Lift foot when stepped on something sharp.. and kept it up..

also balanced the rest of body

o Polysynaptic pathway that is a protective reflex

o First, free endings detect pain and

transmit to the spinal cor dand

contract the quadriceps (flexors)

on the foot with pain.

o It does the opposite on the other

foot.

o Afterdischarge is active you

dont stop withdrawing your leg and

put it back down.

Golgi Tendon Reflex (Deep tendon reflex)

o The Golgi tendon organ is in series

with the muscle

It encodes info about tension o 1B Afferent axon

o It detects information about muscle contraction

o It prevents overstretching of the muscles tendon by causing

some inhibition of the muscle that was being contracted, and

contracts the antagonist muscles.

o Opposite of the myotatic reflex (stretch reflex)

Lecture 2: Sensory & Motor Pathways

Principles of sensory system organization


o Specific sensory receptor types are sensitive to certain

modalities (like pain, light, etc.)

o Labeled lines a pathway codes for a particular modality

o Sensory info is processed by the opposite side of the brain

o Sensory pathways synapse in the thalamus on

their way to the cortex

Dermatome map (topographic organization)

Sensory input at different levels of spinal cord is

mapped out across the body

o Not precise for touch, pressure, vibration

o Accurate for pain and temperature

The body is mapped to the somatosensory cortex

o The cortical area is proportional to

sensory sensitivity

o Homunculus a representative body that is

made proportionate to the brains cortex.

Sensory Pathway

o 1st Order Neurons

Sensory, cell bodies in the PNS in the dorsal root ganglia and synapse in the dorsal horn

o 2nd order neurons

CNS neurons in the spinal cord or medulla o 3rd Order Neurons

Located in the contralateral (opposite side) of the brain in the thalamus

o All Ascending systems cross before the thalamus. The thalamic

projections to the cortex are the same side.

Mechanosensory system Dorsal Column medial lemniscal System

o Receptors in the skin touch pressure vibration, proprioception

(limb location)

o 1st Order neurons branch and

synapse in the dorsal horn, but

also send information to the brain

via the ipsilateral dorsal column

white matter.

Axons are organized such that the lower body is medially

organized, and upper body is

lateral in the white matter

somatotopical organization

o 1st order neuron terminates on the 2nd order neuron in the dorsal

column nuclei in the medulla

One nucleus for upper limb, one for lower o 2nd order medullary neurons project to the contralateral side of

the thalamus through a fiber called Medial Lemniscus


o 3rd order neurons are in the thalamus. These project to the

cortex. This is also somatotopically organized.

Pain Pathway Spinothalamic/anterolateral pathway

o 1st Order sensory receptors free nerve endings detect pain

Different receptors from mechanosensory system

Bodies are located in the dorsal root ganglia

o 2nd order neurons are located in the

dorsal horn.

The axons from 2nd order neuron crosses the midline and travels in the anterolateral white

matter

These axons form the spinothalamic tract

2nd order axons synapse on the neurons at many different levels, ipsilaterally and contralatterally (for example,

the foot withdraw

reflex acts on both

sides)

Some axons go

direct to the

thalamus

contralaterally

3rd order neuron is in the thalamus and

goes to the cortex

o Mechanosensory (right) vs

pain (left) pathways:

Mechanosensory & Pain pathways

from the face via Cranial

nerve V Trigeminal nerve

Referred pain

o The somatosensory cortex is missing representations for things

such as the heart, lungs, etc. all visceral organs

o Visceral organs refer pain to specific sections of skin

o This probably because the organ also synapses on the same neuron

in the spinal cord

Phantom Limb Pain

o When someone loses a limb, central pathways can still be active

in the absence of stimuli

o People can still feel the missing limb and feel lots of pain


o Difficult to treat destroying parts of pathway dont relieve

pain

Sensory Deficits after Spinal cord

injury Spinal Hemisection-

destruction half of the spinal

cord

o Spinal reflexes below the

lesion still work

Topic 3 CNS Motor

Interneurons are fingers on the

piano that cause the keys (motor

neurons) to play

The descending systems access these keys to cause tunes to be played

o Upper Motor Neurons

There are 2 types of pathways : Direct & Indirect

Direct Pathways Called Lateral Pathways

o Cortispinal tract/pathway

Originates from the cerebellar motor cortex

These go through the pyramidal system to the medulla

Crosses via pyramidal dissection while going through

the pyramidal tract

Synapses in the spinal cord and interneurons there. o Rubiospinal pathway

Originates from the red nucleus (Midbrain)

Synapse in the spinal cord and interneurons

o Both Pathways are still crossed

o They travel in the lateral white

matter on dorsal side


The Spinal cord is somatotropically organized

o distal muscles are lateral and vice versa

o Lateral muscles synapse on lateral nuclei

Lesions of the motor cortex cause issues with

fine motor control but not all movements.

Lesions of the spinal cord causes inability to do

individual movements of limbs.. limb moves in

only one direction.

o Pitcher on a mound, but cant pitch the ball

Indirect (Extrapyramidal) pathways Brainstem/ventromedial Pathways

o Reticular Nuclei Posture & Walking

o Superior Colliculus vision & Vestibular nuclei balance

Tectospinal tract visual system

Vestibulospinal tract vestibular system o These innervate more of the proximal muscles

o Arise from Circuits originating in cortex, brainstem, cerebellum

o Synapse on neurons in the brainstem

o Brainstem neurons project into the spinal cord

o Really important in the maintenance of posture and coordinated

head/eye movements

Motor deficits after spinal

cord injury- spinal hemisection

o Flaccid paralysis on the

ipsilateral side

o Spastic Paralysis

reflexes are still

present, but no input from

the brain

o Clonus tap on the

patellar tendon, and itll

keep going up and down

instead of just doing it

once.

Descending input is needed to stop the oscillation.

Brown sequard Syndrome- Sensory & motor deficits following a

hemisection

Topic 4 Cerebral cortex and function


3 types of cells in the CNS

o Neurons

o Glia (10x the amount of neurons)

Astrocytes

Oligodendrocytes myelin in the CNS

Microglia phagocytes. Immune system of brain o Ependymal cells line the Ventricles

Choroid plexus modified ependymal cells that produce CSF

CSF fills ventricles & subarachnoid space

o Produced 500 ml/ day. 150 ml in total. Turns over 3-4x / day.

o 2 foramens that let the CSF into the subarachnoid space

o Hydrocephalus the inability to absorb/drain CSF

A shunt is used to drain csf to the abdomen o CSF is chemically regulated

Important in chemosensory function

More acidic than blood

Due to the blood brain barrier

Meninges

o Dura Mater

2 Sinuss are created by folds of the dura mater and these drain the CSF from the brain.

Subdural space contains venous system o Arachnoid Mater

Subarachanoid space is between the arachnoid & Pia mater

The CSF resides here.

Contains arterial system

Arachnoid granulations arachnoid mater poking through the dura mater and drains csf into the venous sinus

o Pia mater

Subdural bleeding

o pushes the brain from the outside

Subarachnoid bleeding

o Bleeds into the brain and balloons inside the brain

Blood Brain Barrier

o Capillaries are one cell thick

o Astrocyte feet combine together to form the blood brain barrier

o Tight junctions restrict diffusional passage of large molecules

Prevents transport of everything not small, lipid soluble or gas

o Other molecules cross the barrier through many specific membrane

transporters

Cerebral Cortex

o Frontal cortex motor and function


Personality and emotion

Orbital frontal cortex addictive behaviors o Parietal Cortex sensory functions & integration

Contralateral neglect syndrome if right side is damaged, you cant process some things from the left visual field

Occipital lobe primary visual cortex

o The brain processes the image upside down versus the visual

field and location of the brain

o The outer part of the cortex does more with macular (main part

of field) while inner parts do binocular parts

Temporal Lobe Audition learning, memory, facial recognition,

language

o If temporal lobe is damaged AGNOSIAS

Difficult recognizing, identifying and naming categories of objects

Right cortex unable to recognize faces

Separation of complex functions between cerebral hemispheres

o There is a lateralization (left/right)

o Wada Procedure disproved that left/right handedness indicated

which hemisphere of the brain was dominant

Injection of a fast acting barbiturate into the left/right carotid artery so that the hemisphere goes to sleep

Language repeating a spoken word

o Wernickes area processes the sound

from the auditory cortex, and passes

it through the angular gyrus

(yellow) to brocas area.

o Brocas area has to do with the

motor function for speech and

projects to the motor cortex

Repeating a written word

o Visual Cortex Angular Gyrus

wernickes area brocas area motor cortex

Corpus Callosum connects the two hemispheres - ~200 million axons

o Cutting the corpus callosum helps severe epileptic

o Its very difficult to figure out what the deficit of cutting

the corpus callosum was

o Sterognosis Experiment

Objects is held in the left hand (right hemisphere)

Object held in left hand cant be named

Object held in right hand can be named

The effects of stroke

o Aphasia change in expression or comprehension


o Brocas Area unable to speak but can understand language

Motor or expressive aphasia o Wernickes Area unable to comprehend spoken or visual info

Sensory or receptive aphasia

Brain Death

o Patient came in a coma and its not medically induced

o Greatly reduced cerebral circulation

o No response to painful stimuli other than spinal reflexes

o Brainstem must be dead as well

Midbrain eyes, relays auditory and visual info, descending control of skeletal muscles

No pupillary light reflexes

Pons coordinates respiration, maintenance of upright posture, vestibular system induced eye movement

No eye movements with vestibular stimulation

Medulla blood pressure, heart rate, respiration, standing

Apnea w/ co2 level over 60 mmhg (very high)

Topic 5: Endocrine Thyroid & Glucose stuff

Hormone chemical messenger secreted by a cell that is transported

to a distant target where the hormone exerts its effects in low conc.

Mechanisms all work via 2nd messenger systems

o Hormones work by binding to ligand gated receptors and then:

o Alter membrane potentials/regular transport/cause exocytosis

Classes of hormones

o Peptides derived from amino acids. Ex. Insulin, TRH, TSH

o Amines derives from tyrosine. Ex. E, NE, thyroid hormones

o Steroids Derived from cholesterol. Ex. Cortisol, aldosterone

Thyroid hormones they are always required

o Required for normal maturation of the nervous system

o Required for normal bodily growth

o Required for normal alertness and reflexes

o Major determinate of the rate at which the body produces heat

o Facilitates the activity of the sympathetic nervous system by

stimulating the synthesis of Beta receptors for E & NE

Thyroid Hormone release can be controlled via hormones,

neurotransmitters or ion/nutrient changes

Release of T3/T4 (thyroid hormones)

o The Hypothalamus releases TRH (thyrotropin-releasing hormone)

that goes to the anterior pituitary via portal capillaries

o The TRH binds to the a G protein phospholipase C, IP3 DAG

receptor in the anterior pituitary.

Ip3 calcium release


o The anterior pituitary releases TSH thyroid stimulating

hormone

o The TSH binds to a follicular cell in the thyroid to a G protein

coupled Adenylyl cyclase, cAMP second messenger pathway

This is a complex pathway

TSH pathway

o Enhances the transport of iodine into the follicular cell

o Iodination of tyrosine residues that is sitting in a long

peptide chains waiting.

This is why the hormones can be stored everything is stored on the thyro-globulin peptide chain in the colloid

o The protein can then be endocytosed to an endosome in the

follicular cell that chops up the thyroglobulin into T3 & T4

o TSH exerts a growth factor effect and causes hyperplasia of the

follicular cells as well.

T3 & T4 then bind to thyroxin binding protein which carries the

hormones through the blood stream.

o T4 = Thyroxin. 4 iodines

o T3 = more biologically active. 3 iodines.

o T3 is involved in negative feedback to regulate the levels of

TRH & TSH

Hypothyroidism 2 ways it can happen

o Follicular cells are making too little T3/T4. Because of this,

TSH & TRH are very high. This causes hyperplasia (TSH) Goiter

Hashimotos disease an autoimmune disorder o Secondary hypothyroidism too little T3/T4 due to too little

TRH/TSH.

No goiter because too little TSH

Hyperthyroidism

o Tumor Too much T3/T4 and low TRH/TSH no goiter

o Graves Disease due to TSI thyroid stimulating immunoglobin

is a TSH receptor antibody that stimulates TSH receptor

Causes goiter because of TSH like effects

Autoimmune disease

o Secondary hyperthyroidism too much TSH/TRH goiter o Hyperthyroidism affects B receptors and causes increased

contractility in the heart

Glucose Stuff

Increase in Plasma concentration of glucose causes the stimulation of

beta islet cells in the pancreas. >100 mg/dL is the threshold

o Glucose level rises in the B Cell

o ATP Production will increase due to the glucose increase

Closes a potassium ATP Channel


o Membrane potential will depolarize

o Causes a voltage gated calcium to open calcium influx

Calcium induced calcium release o Calcium causes release of insulin vesicles

Increase levels of insulin

o Causes glucose uptake in muscles and fat cells

o Causes glucose release to stop in the liver and causes uptake

Increase in synthesis of glucagon and triglycerides

Insulin Receptor tyrosine kinase receptor

o Causes insertion of GLUT4 transporters in the cell.

o Brain, kidney and intestines arent insulin dependent they use

GLUT1 transporters instead

Glucose tolerance test a way to test for diabetes

o Can differentiate between non diabetic and type 1 & 2

o Oral Test

Fast overnight & glucose is measured in the blood

Drink a known Conc. Of glucose

Normal person sugar spikes and drop rapidly

Diabetic sugar spikes and goes down really slowly

Type 2 the insulin will still be made so youll see

it affect the curve, but you wont see it with type 1

Type 1 Diabetes Insulin Hyposecretion insulin dependent

o 10% of diabetics

o Autoimmune disease

o Glucosuria the kidneys cant reabsorb all glucose so its

excreted it.

Osmotic diuresis loss of lots of water due to glucose

Polyuria excessive urination

Polydipsia excessive thirst o Body will break down glycogen and fats for energy polyphagia

o Diabetic ketoacidosis build up of ketones from fat break down

will cause acidity in the blood and can lead to coma

Insulin Shock hypoglycemia

o Insulin excess

o Causes the body to take up too much glucose and reduces the

glucose available in the blood for the brain to use

Type 2 Diabetes

o Caused by genetics and being overweight

o Insulin resistance defect in the B cells ab ility to secrete

insulin

Gestational diabetes 4% of pregnancies

o Women can become diabetics due to insulin resistance

o Insulin resistance is connected to levels of progesterone and

cortisol


o May be due to peptide hormone hPL (human placental lactogen)

o Problems go away after delivery

Topic 6: Cardiac Output and excitation coupling in vascular smooth muscle

Mean arterial pressure we cannot change this directly; it is

changed by cardiac output and stroke volume and peripheral resistance

Main features of the CV system

o Heart is a double pump and each side is equal volumes

o Arterial system is high pressure, venous is low pressure

o Right atrium Right ventricle lungs left atrium Left

Ventricle aorta (body)

Coordination of the heart beat

o SA Node (pacemaker) AV Node (delays contractions of ventricles

from atria) bundle of his purkinje fibers o ECG analysis

P wave = atrial depolarization

Q wave = depolarization through bundle of his

RS Wave = ventricular r depolarization

T Wave = ventricular repolarization o ECG Pathology

PR interval lengthening indicates 1st degree AV conduction block

QRS loss after P waves indicate 2nd degree AV block

Lengthening of QT interval indicates congenital defects in voltage gated Na+ or K+ channels.

A Singularly most important function of the CV system is to ensure

continuous system is to ensure adequate blood flow through

capillaries

Poiselles law

o P = F * R

Delta P = pressure gradient along the tube

F = flow of fluid

R = resistance to fluid flow

Mean Arterial Pressure (MAP) cardiac version of poiselles law

o MAP = CO * R

MAP = Mean pressure in aorta mean pressure at right atrium

CO = cardiac output - liters/min

CO = Heart Rate * Stroke Volume


R = peripheral resistance (TPR or SVR)

SA Node Cell

o Able to be autorhythmic

o As the membrane repolarizes, an HCN non-specific cation channel

opens

This helps to depolarize the action potential o Nodal cells lack voltage gated Na+ channels. They use calcium

channels instead.

Heart Rate Control

o SA Node cells are pacemaker cells 100 bpm

o Av node cells are at lower rate 40-60 bpm

o Unregulated heart rate 100 bpm

o Decreasing heart rate

Increase parasympathetic activity. Muscarinic receptor causes K+ channel to open and hyperpolarize the potential.

Because of this, it takes longer for the pacemaker

potential to fire. (chronotropic effect)

Dromotropic (conduction) effect does the same o Increasing the heart rate

E & NE increase sympathetic activity via B receptors

Mechanical

events in the

cardiac cycle

o Systole

Period of

Contraction

o Diastole

period of

relaxation

The heart has

isovolumetric

contraction and

relaxation of

the ventricles

Stroke volume =

end diastolic

volume end

systolic


Pressure Volume Loop for the left ventricle

Should be able to determine if stroke volume changed and whether it

was due to frank-starling

or due to change in

contractility

Regulating stroke volume

o Frank Starling law

o Increasing

Contracility

Frank-starling law

o Increasing sarcomere

length of muscle

fibers can increase

stroke volume

Increase EDV Increase SV

o Tension can be

increased rapidly as

the sarcomere length.

Skeletal muscle cant increase as

much

Cardiac Function curve is

the same as the frank

starling curve, just

different axes

o Increase in blood volume or venous

pressure, you will increase EDV

thereby stroke volume/ cardiac

output

Role of the veins

o Holds 60% of the blood of the body

o Increasing sympathetic nerve activity causes venoconstriction.

This causes more venous return to the heart

venous pressure venous return atrial pressure

EDV Stroke Volume Cardiac Output


o This changes the pressure

volume loop preload increase

Contraction of ventricular muscle

o Gap junction depolarizes from

the action potential.

o A voltage gated L type Ca2+

channel in t tubule opens

Calcium induced calcium release

o Calcium released from SR binds

to troponin and allows the

actin/myosin to interact and

contract the sarcomere

o Changes in contractility is all about how the muscle is handling

calcium

Increasing contractility Increased Contracility Graph

o Increasing in developed

tension without changing

muscle length

o B adrenergic receptor

activates cAMP and

phosphorylates the L type

Ca2+ channel so it opens

longer

Ryanodine receptor (Ca channel in SR) also

phosphorylated

Ca transporter back into the SR is also

phosphorylated

o Ejection Fraction (EF) = SV/EDV

Normally 50% -75%

Contracility = Ejection Fraction

Frank-starling property represents changes due to increase in

EDV/venous return. Increasing contractility represents intrinsic

changes in the muscle performance

Another way to alter mean arterial pressure, you can change

peripheral resistance

o CV variables for resistance to blood flow

L = length of CV system (constant)

n = viscosity of the blood

r = radius of the blood vessel

Main thing that alters resistance

Smooth Muscles


o Not striated

o Innervated by the autonomic nervous system sympathetic system

o Contains actin & myosin, tropomyosin, but NOT troponin

Troponin = calcium binding that causes tropomyosin shift o Can develop comparable max tension as striated muscle, but the

timing is different. Such as time taken to generate smooth

muscle

o Smooth muscle can be relaxed by neurotransmitter, unlike

skeletal muscle

o Smooth muscle lacks a specialized end plate/junction for

neurotransmitter release

o Contraction of smooth muscle can be initiated by hormones and

paracrines, unlike skeletal muscle

Ex. E, cortisol, angiotension II, nitric oxide, histamine o Unlike skeletal muscle, smooth muscle can be initiated by

mechanical stretch

o Actin and myosin are arranged in diagonal bundles and dont have

sarcomeres. Cross bridges are much slower

o Smooth muscle membrane is more complex.

Has voltage gated Ca2+ channel

Alpha receptors bind E or NE

G protein/phospholipase C / Ip3. IP3 opens Ca channel

in SR

Smooth Muscle Contraction

o Cytosol level of Calcium increases (IP3 of Ca induced Ca)

o No Troponin. Ca binds to calmodulin (CaM)

o CaM associates with MLCK. MLCK phosphorylates a protein in the

light chain in head of myosin

o Once myosin is phosphorylated, it binds actin and shortens.

o Relaxation is done via lowering calcium conc.

o Myosin phosphatase takes off the phosphate from the myosin

Topic 7: Vascular System

Most drop in blood pressure covers over the arterioles

o They are the primary determinant of blood flow resistance

o Determine the relative distribution of blood to body parts

This is done by changing radius. Radius flow

Control of the arteriolar radius

o Local control

Myogenic activity. Pressure Stretch


Causes vasoconstriction

Paracrines from metabolism O2 Co2 H+, K+ Osmolarity

Causes vasodilation

Paracrine signal molecules

NO, histamine, adenosine - Vasodilation

Endothelin-1 Vasoconstriction

o Extrinsic control

Nervous - sympathetic input (NE alpha receptor)

Causes vasoconstriction

Neurons can release NO and cause vasodilation

Hormonal

Epinephrine

o Alpha 1 receptor vasoconstrict

o Beta 2 receptor vasodilation

o Different vessels have different receptors

Angiotensin II vasoconstriction

Arginine vasopressin (AVP) vasoconstriction

Cortisol vasoconstrict

Atrial natriuretic peptide (ANF) vasodilator

Local Control autoregulation

o Active hyperemia when organs increase activity

PO2 Arterioler radius Blood Flow o Flow Autoregulation due to drop in pressure (like bleeding)

Arterial pressure blood flow to organ PO2

metabolites Vessel wall stretch Arterioler radius Blood Flow

Doesnt have to be only drop in Pressure, also works

for increase in pressure

Autoregulation of Glomerular filtration rate(GFR) in kidney is an example of flow regulation

Capillary exchange and bulk flow

o Diffusion, facilitated diffusion and transcytosis

Bulk Flow

o Mass movement of water and dissolved solutes between and blood

and interstitial fluid

o Main function is to distribute the extracellular fluid

o Result of the balance between hydrostatic (blood pressure) and

osmatic pressures (due to conc. Gradients)

o Interstitial fluid can be thought of as a reservoir

Capillary wall is highly permeable to everything but large proteins

o This creates a osmotic pressure

o As you pass through a capillary, hydrostatic pressure decreases.

This is due to decreasing resistance.


o Plasma osmotic (oncotic) inwards water movement

o NFP = net filtration pressure = filtration absorption

o NFP is usually positive more filtration than absorption

o Excess filtrate is taken up by the lymph system

o Pc= Hydrostatic pressure (out)

o Pif= interstitial fluid pressure

o if osmotic force due to if

fluid protein conc. (out of cap)

o c osmotic force due to protein conc in blood (into cap.)

Pulmonary capillaries capillary exchange processes are identical

except there is a small net filtration

o Pc is very low and large if

Vascular function curve

o Measures change in the

atrial pressure as cardiac

output changes

o No cardiac output central venous pressure (7mmhg) only

o As cardiac pressure

increases, atrial pressure

will decrease.

o Hypovolemia causes a

downward shift while

hypervolemia causes an

upward shift

Flipping the axes of the vascular

function curve and plotting cardiac

function leads to 2 intersecting

curves called the steady state point

o Transfusion vascular curve

moves to the right, steady state

point moves up

o Increase in contractility will

shift the cardiac curve up and

left

Lecture 8: Regulation of arterial blood pressure

Short Term regulation

o Baroreceptors blood pressure receptors in the aorta and in the

carotid arteries

One is located at the arch of the aorta and the other is in the carotid arteries

o Only variables heart rate, stroke volume and resistance


Fixing high blood pressure

o Sympathetic outflow decreases. Less NE & excitation.

o Increase parasympathetic signals decrease heart rate

o Stroke volume cant change EDV, but you can change

contractility by reducing sympathetic outflow

Fixing Low Blood Drive

o More sympathetics More NE & E, increasing resistance and heart

rate and contractility.

o Withdraw parasympathetic brake and all activity

Long Term Regulation of high blood pressure decrease blood volume

o Kidneys will increase urinary loss of water and sodium

Lower activity of RAAS renin angiotensin-aldosterone system. Causes more Na+ excretion

Renin causes angiotensin II (by ACE enzyme) to go and produce aldosterone

Decrease Kidney tubular reabsorption of NA+ o If high Blood Volume is detected first

Activity of low pressure baroceptors detect blood volume and tells the medulla

AVP (anti diuretic hormone) secretion decreases causes more diuresis

Atrial natriuretic peptide (ANP) pathway

As plasma volume increases, atrial fibers release ANP

It decreases aldosterone

Afferent dilation and efferent constriction in kidney

arterioles Increase in GFR.

Decreases Na+ reabsorption

Regulation of aterial blood pressure

in shock

o Shock = sustained drop in mean

arterial blood pressure

Septic shock infection

Hypovolemic shock

o Hemorrhage 10%-20% rapid loss

of blood volume

o Short term regulation

Drop in blood volume

drop in EDV Drop in SV

Increase heart rate and contractility

Increase peripheral resistance baroreceptor reflex

Increase Sympathetic system, EDV rise in cardiac output

Reflex compensations work towards normalcy

Use the RAAS system


o RAAS system

MAP GFR Renin Release

Renin converts angiotensinogen into angiotensin I

ACE converts Angiotensin I to angiotensin II

Angiotensin II goes to adrenal cortex and releases aldosterone

Aldosterone causes na+ and H20 to be retained

AVP cases vasoconstriction and aldosterone to be released

GFR wont be the same anymore because no auto regulation o Long term response

Drop in capillary hydrostatic pressure Increased fluid

absorption from interstitial compartment increase in

plasma volume restore MAP

Increase absorption because of starling forces in the

capillary more water leaves from interstitial fluid

(reservoir) and enters blood plasma

Called autotransfusion redistribution not replacement o Sometime after hemorrhage plasma rises back and beyond

original value, but erythrocyte cant regenerate.

o Red blood cell replacement can be done via erythropoietin

release by the kidney to stimulate more production, but takes

days to weeks for replacement.

Cardiogenic shock due to congestive heart failure

o Lower cardiac output

o Consequence of prolonged hypertension diastolic dysfunction

Serious hypertrophy and ventricular volume decreases o Systolic dysfunction consequence of damage to ventricular

tissue due to decreased coronary blood flow (heart attack)

o Coronary arteries provide the heart muscles with blood from the

base of the aorta

o Left anterior descending branch widowmaker can get blocked

left ventricle loses blood

Cardiovascular responses to cardiac failure / systolic dysfunction

o Decreased CO triggers baroreceptor reflex

Increases HR, SV, Contractility, and Resistance

Initially beneficial restoring CO & MAP

Long term leads to massive expansion of extracellular

fluid volume. RAAS Aldosterone AVP H20 retention

Causes EDV SV to increase CO

o This is bad because heart is damaged

o Frank starling curve is significantly lower

o Asking the heart to work harder


o Cardiac function graph much lower due to

hypervolemia. More atrial pressure and less

cardiac output.

Ventricle muscles will start to tear

o EDV is too big.. tension needed is too much

Peripheral Edema(Swelling of the body) occurs

Pulmonary edema fluid build in the lungs

o Gas cant really diffuse well through the water

Increase in peripheral resistance more work load

Heart Failure Treatments

o Diuretics causes excretion of water

o Increase cardiac contractility - cardiac ionotropic drugs -

Digitalis (digoxin) poisons the Na/K ATPase pumps

Causes increase Ca+ in the cell o Inhibit AVP binding to receptors in kidney and vascular muscles

Increases excretion of water o Inhibit the RAAS system ACE inhibitors

ACE inhibitors block formation of angiotension II / aldosterone

o Vasodilators organic nitrates / nitroglycerin

Anaphylaxis an extreme allergic reaction

o A type of allergic response classified as immediate

hypersensitivity

o Rapid onset. Mediated by IgE immunoglobulins, mast cells, and

basophils

o Immunity stuff

Humoral immune response Memory B cells make antibodies

Cell mediated responses T cells cytotoxic T cells and helper T cells

Helper T cells when activated, make the humoral

response much larger and better. Cytotoxic not used.

Humoral response recognizes the antigen and makes antigens and the antigens wait for the next time.

Mast cell has IgE on its surface and binds to the allergen.

Releases histamine and other inflammatory mediators

Inflammatory response will divert more fluid away from

blood increase vascular permeability o Histamine will cause hypotension by binding to smooth vascular

muscles

o Swelling of the tissue around airways (Angio-edema)

o Bronchiolar smooth muscle contraction

o Epinephrine (epi-pen) is used to reverse anaphylaxis.

Vasoconstriction of the blood via A1 receptor


Bronchodilation via B2 receptor

Hypertension

o Chronically increased MAP 140/90 +

o Major abnormality is increased peripheral resistance

o Baroreceptor reflexes reset to a different resting value

o Could also be due to kidney dysfunction in a small subset of the

population

o This will call diastolic dysfunction

o Hypertension will increases the chances of having a stroke

Treatments for hypertensive disease

o Diuretics

o B1 adrenergic blocks decrease CO, HR & SV. Decrease CO & MAP

o Calcium channel blocks decreases total peripheral resistance,

but can increase risk of heart attack (due to calcium channels

in the heart)

o ACE inhibitors

Renal hypertension is best treated with ACE inhibitors

Vasovagal syncope : emotional fainting

o Happens due to sudden drop in Blood pressure due to vasodilation

o Inhibition of smooth muscle & sympathetic innervation

o Baroreceptor reflex becomes uncoupled

Hyponatremia

o Occurred in 1% of new York marathoners in the past

o Cause by salt lost in sweat, though runners were hydrated

o Overhydration dilutes the plasmas Na+ content and blood flow to

kidneys is significantly lower

Interstitial Na content remains normal

Due to this imbalance, water flows into the interstitial space

Swelling of hands, feet, constriction of chest

People died due to brain swelling, fainting, coma, death o Treatment hypertonic saline IV

Ecstasy induced hyponatremia article key points

Due to genetic variation one can metabolize MDMA slower

MDMA forms inhibitor complexes with CYP2D6 an enzyme that is used

to breakdown MDMA. This can lead to acute toxicity

o CYP2D6 is also affected by other drugs as well

MDMA causes a lot of dehydration and fever.

Acute Kidney Injury can occur

o Dose dependent correlation of proximal tubule damage

Hyponatremia

o Excessive water intake is associated with MDMA use. People try

to hydrate to prevent fever


o HMMA is a metabolite of MDMA that is a more potent inducer of

ADH (antidiuretic hormone (AVP) )

o Serum sodium conc. Drops, causing hyponatremia

bio 328 full semester package

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