Anatomy: Muscle, Homeostasis, Blood

8/13/2019 Anatomy: Muscle, Homeostasis, Blood

1/49

ANP 1105

Muscles

There are many factors that contribute to increased contractile force, these include

a) Large number of muscle fibers activatedb) Large muscle fibers

c) Asynchronous tetanic contractions

d) Muscle and sarcomere length slightly over 100 of resting length

The velocity and !uration of "ontraction de#end on$

1) Load$ the greater the load, the longer latent #eriod %hich in turn results in slo%er

contraction and shorter contraction duration

The & sources %here muscle contraction gets its energy from is stored ATP, !irect

#hos#horylation, Aerobic res#iration and anaerobic glycolysis

a) Stored ATP

' as soon as you stimulate the muscle to contract, it is going to ma(e use of%hatever ATP there is available to be used

' ATP for cross bridge movement and detachment* "a++#um#

' These contains only &' seconds of stored ATP

b) Direct Phosphorylation of ADP by creatine phosphate

' As soon as you try to do %or(, and ATP is used, this method %ill be initiated The

"P %ill transform and transfer its #hos#hate to A!P to ma(e ATP The en-ymethat cataly-es this reaction is called creatine (inase

' This %ill last for 15'.0 seconds because the "P reserves %ill be diminished /ourmuscles %ill be at maimum #o%er during this time' Creatine Phosphate is a uniue high energy molecule that is stored in muscles

The reaction is defined as "P + A!Pcreatine + ATP

c) Aerobic respiration

' you %ill net be loo(ing to%ards glucose for energy /ou can metaboli-e it

anaerobic2aerobically The difference bet%een the t%o is utili-ing oygen' Aerobic gives you a high ATP yield* ho%ever, it is much slo%er because it

reuires many ste#s and reuires continuous su##ly of 3.and other nutrients in

order to create said ATP

' Aerobic res#iration is much more efficient #er glucose molecule but it reuiresmore time 4t generates 6 ATP #er glucose

d) Anaerobic glycolysis

' anaerobic gives you more ATP faster, but less #er glucose molecule

' 4t only generates . ATP2glucose but it is fast

' 7sually it is #yruvic acid that enters the aerobic #ath%ay 4t is converted to lacticacid


2/49


3/49

' The liver also hel#s by converting additional lactic acid to glucose2glycogen

' This is %hy after a heavy eercise, you are still breathing heavily to re#lace this

oygen debt

#eat production during muscle acti$ity

' ATP driven muscle contraction is only .0'.5 efficient The rest of the energy is

%asted and turned into heat energy %hich is dissi#ated by the body?s coolingmechanisms

uscle !iber Types

The muscle combination in every #erson is different This means that by genetics, some

#eo#le are better runners than others, etc @lo% and fast refer to their contractile ability

and their metabolism rate for generating ATP3idative im#lies that they carry out aerobic res#iration

a) Slo% oxidati$e fibers: thin cells %ith slo% acting myosin ATPases* they contract

slo%ly =red lots of myoglobin) The #rimary energy fuel is fat' contains lots of mitochondria, ca#illaries, aerobic en-ymes* 3B4!AT4CD

' fatigue resistant but they are not #o%erful =thin)' these muscles are im#ortant for endurance ty#e activities

b) !ast glycolytic fibers: large, #ale =%hite), little myoglobin and almost t%ice thediameter of slo% oidative fibers* there are fast acting myosion ATPases and

contract uic(ly

' fe% mitochondria, they are going to carry out anaerobic metabolism They %ill

need a good glycogen reserve' They %ill fatigue because there %ill be lactic acid #roduced and glycogen reserve

%ill run out, but they are very #o%erful

' These muscles are used in short term, ra#id intense movements

c) !ast oxidati$e fibers: red or #in(, cell si-e is intermediate* fast acting myosin

ATPases and contract uic(ly* high myoglobin content and oygen de#endent*fairly fatigue resistant

' the are best for intermediate activities

/our muscles reuire a different mi of these fibers in order to ada#t to certaincircumstances !ue to genetics, some #eo#le %ill have an advantage and abilities based

on their muscle com#ositions

Smooth muscle

' are very %idely distributed in the body and it is going to be in #laces %here youhave lumen

' Tend to be smaller cells %here lots of nuclei are #ushed off to the side* it is filled

%ith myofilaments


4/49

' They %ill not be arranged in an orderly %ay so you %ill not see the striation that

you see in s(eletal muscle

' They %ill still have actin and myosin* they are able to carry out contraction in onesmooth movement

' The cells are se#arated by fine "T* sheets of closely o##osed fibers* usually atleast . sheets %ith o##osite orientations

' Alternating contractions of o##osing layers #rovide miing, #eristalsis, e#elling

' There are varcosities instead of neuromuscular


5/49

a) &esponse to stretch$ more stretch =1.0 resting length) therefore

#roducing much more vigorous contraction The stretching can induce

brief contraction =gut) or can have stretch relaation res#onse =filling)' as you eat and #ut #ressure on your stomach, the smooth muscle in your stomach

%ill res#ond by relaing and e#and as you eat

b) Length and tension changes: stretches more than s(eletal* can generate

more tension than s(eletal muscles =contracts in a cor(scre%'li(e manner)

@mooth can contract 150 versus s(eletal muscle that contracts only 0@mooth muscle can also be stretched by hormonal messages

c) #yperplasia: eam#le$ estrogen and uterine smooth muscle cells

d) Secretory functions:collagen, elastin' ma(e their o%n connective tissue

Single'unit smooth muscle

( contracts as a unit and rhythmically

* electrically cou#led by ga#


6/49


7/49

#"E"STAS-S

Control mechanisms

As ;alter "annon describes it$

:omeostasis is the ability of the body Gto maintain relatively stable internal conditionseven though there is continuous change in the outside %orldH

' not changing$ rather a dynamic state of euilibrium involving many systems$

i) adeuate blood levels of vital nutrients

ii) heart activity2blood #ressure monitored and ad


8/49

Aging is associated %ith #rogressive decrease in our ability to maintain homeostasis

greater ris(s for illness as you age

Example: temperature regulation

' ;hen you have a fever, your body drives to increase the tem#erature* %hich in

turn %ill increase your body?s metabolism rate' 4t involves #ositive feedbac( because it %ill allo% the body to (ee# doing this in

order to increase body tem#erature until a desired tem#erature is achieved

' There is also negative feedbac( involved because once you hit an o#timaltem#erature* it %ill sto# the #ositive to (ee# increasing to maintain stability of

tem#erature

Autonomic /er$ous System 0A/S)

' auto self* nom govern' AN@ regulates bodily functions that you do not need to %orry about or do not

reuire to consciously thin( about doing these things =breathing, heart beating etc)thus given the descri#tion GautomaticH

' Performs a##ro#riate res#onse %ithout you mentally controlling these actions' The motor division is divided into . divisions

1 the somatic system is directed to the s(eletal muscles

Parasym#athetc$ digestion, rest@ym#athetic$ 9et through stress

AN@ the system of motor neurons to smooth and cardiac muscle and glands to allo%res#onses usually %ithout our a%areness

a) shunt blood to more needy areasb) s#eed2slo% heart and res#iratory ratesc) ad


9/49

4n the sympathetic ner$ous di$ision of the A/S1 it consists of neurons that are not as

long as the somatic N@* it %ill target ganglia first Then the ganglia %ill release

nore#ine#hrine for the #ost ganglionic neuron %hich %ill target the designated area

Also, it can stimulate the adrenal medulla$ the inside of the medulla is made u# of neural

tissue /ou %ill have neuron stimulating neural tissue %hich is the adrenal medulla* theadrenal medulla %ill then release e#ine#hrine and nore#ine#hrine =nore#ine#hrine no%

acting as a hormone) 4t is sent into the blood stream to travel to the heart and other #arts

of the body %hich is reuired to be stimulated

Ior the #arasym#athetic division of the AN@, instead of directly arriving at a target, it

lands on ganglion and it %ill release Ac:

@7MMAF/

Somatic ner$ous system: effects s(eletal muscle

A/S: smooth muscle, cardiac muscle and glands

Path%ays and ganglia

Somatic: thic(, heavily myelinated aon from s#inal cord to s(eletal muscle* ra#id

conduction of im#ulses =no ganglia)

A/S: t%o'neuron chain$ #reganglionic neuron$ originates in the brain or s#inal cord*

#reganglionic aon syna#ses %ith .ndmotor neuron =#ostganglionic) in ganglion outside

"N@#ostganglionic aon to the effector organ

"onduction is slo%* #reganglionic aons are thin and lightly myelinated* #ostganglionic

aons are thinner and unmyleninated

Parasympathetic Di$ision

' active in non'stressful situations =resting and digestive system)

' (ee#s body?s energy use lo% %hile regulationhouse(ee#ing activities

=digestion, elimination of feces and urine)

' G!H system$ digestion, defecation, diuresis' Dam#le$ after you eat dinner, you read the ne%s#a#er /our #arasym#athetic

nervous division does the follo%ing$ digestion by stimulating events in your

stomach* slo% do%n heart rate, #u#ils constrict in order to read, slo% res#iration

rate

Sympathetic Di$ision

' Gfight or flightH system* also im#ortant during eercise$ increased heart rate,

ra#id, dee# breathing, cold s%eaty s(in, dilated eye #u#ils

' GDH system$ eercise, ecitement, emergency, embarrassment' 4t could be immediate short term stress or long term stress


10/49

' 4t %ill gear you u# for things to come* all the things that %ill come into #lay %hen

you are in a stressful situation

Somatic ner$ous system and $ascular tone al#ha bloc(ing drugs to treat

hy#ertension* blood shunting #ossible via vasoconstriction2vasodilation

' This is the only #lace in your body that is res#onsible for regulating blood vesseldiameter

' ;ith the heart, a tonic effect of slo%ing do%n heart rate /ou %ill then override it

%ith the @N@ %hen you are eercising or reuire an increase of heart rate

Peripheral ner$ous system and tone: heart, smooth muscle of 94 and urinary tracts

can be overridden by the @N@

-nteractions of the Autonomic di$isions: the most visceral organs receive dual

innervation

Antagonistic -nteractions: eam#le$ activity of the heart, 94 system, res#iratory system

S/S: 4f the @N@ is dominant, you %ould see$ increased heart rate, decreased 94, increaseres#iratory system function

P/S: if PN@ is dominant, you %ill see decreased heart rate, increased 94, decreasedres#iratory system

Cooperati$e effects: regulation of eternal genitalia during intercourse

a) PN@$ dilation of blood vessels in the #enis in males and clit in femalesb) @N@$ e


11/49

, increases mental alertness

5 increases s#eed2strength of muscle contraction

They all lin( together and they are all res#onsible by the @N@

+ Le$els of &egulation of Autonomic function

( 6rain Stem and Spinal Cord Controls

These are motor reflees* there %ill be incoming information %ith regards to %hat isgoing on in those systems and %ill res#ond accordingly

Motor centres in ventro'lateral medulla =eam#le$ cardiovascular centreheart rate,blood vessels* also 94, res#iratory centres)

Cagus nerve afferents convey sensory information

* #ypothalamic Controls:

' also is the site of hormone #roduction' it is the integration centre of the #arasym#athetic and sym#athetic nervous

system 4t %ill it to collaborate and determine %hat is the best action to do during

the s#ecific body state' :y#othalamus$ integration centre of AN@

' Medial and anterior regions#arasym#athetic

' Lateral and #osterior areassym#athetic' :y#othalamus contains centres to coordinate heart activity, blood #ressure, body

tem#erature, %ater balance, endocrine activity* also, centres that hel# mediate

emotions and biological drives

+ Cortical Controls:

' eam#le$ meditation and biofeedbac( allo% some conscious control over visceralactivities

' eam#le$ during meditation, you can consciously lo%er heart and breathing rates,

oygen use, metabolic rate' bio feedbac( to im#rove management of migraine headaches, stress and cardiac

function

#omeostatic -mbalance of A/S

' eam#le$ hy#ertension

T#E E/D"C&-/E S7STE

A chemical substance released into the Dtra "ellular Iluid that regulates the metabolicfunction of other cells in the body


12/49

' :ormones must bind to s#ecific rece#tors to influence target cell function

' hormones are specific* level of target cell activation de#ends on$

i) hormone concentrationii) target cell rece#tor content

iii) affinity of hormone for rece#tor

echanisms of #ormone Action

' hormones alter levels of cell activity$a) membrane #ermeability2#otential =channels)

b) synthesis of en-ymes %ithin cells

c) en-yme activation2deactivation

d) induction of secretory activitye) stimulation of mitosis

+ structural groups of hormones:

i) amino acids, #e#tides, #roteins

ii) steroid hormones =derivatives of cholesterol)* they are li#ids, ma(ing them tobe #ermeable to cell membranes

iii) eicosanoids =from arachadonic acid)

* main mechanisms of action:

a) Peptide8protein hormones:bind to cell surface rece#toractivation of

membrane'bound 9 #rotein#roduction of .ndmessenger =eg$ cAMP, calcium)

activation of #rotein (inases to regulate activity of (ey en-ymes

b) Steroid hormones1 etc: entry into nucleus and activation of gene transcri#tion


13/49

#alf'life1 "nset and Duration of #ormone Acti$ity

' hormones are potent* they do not reuire high concentrations They are very

strong =#otent)

' blood level of hormone de#ends on$ rate of synthesis, and rate ofdegradation2clearance from blood

' #alf life:#ersistence of a hormone in the blood* usually J 1 min to 60 min

' time to onset of hormone action variable$ en9yme acti$ationra#id =minutes)*

en9yme synthesishours to days

' some hormone ssecreted as prohormones* activated once reach target cell

' duration of hormone action also variable =hours to days)

Control of #ormone &elease

' usually negati$efeedbac( =set#oint)* sometimes #ositive feedbac( =goal)' 6 ty#es of stimuli$ humoral, neural and hormonal

a) #umoral stimuli: hormone secretion in direct res#onst to change in blood levelof a nutrient, ion Keg$ #arathyroid hormone =PT:) and blood calcium* insulin and

blood glucose

b) /eural stimuli:not as common, eg$ sym#athetic ns and e#ine#hrine release by

adrenal medulla, hy#othalamic neurons and oytocin releasec) #ormonal stimuli:6'tiered system involving hy#othalamus, #ituitary and target

endocrine glandconce#t of hy#othalamic'#ituitary ais


14/49

Thyroid'releasing hormone =TF:), hy#othalamus

Thyroid'stimulating hormone =T@:), anterior #ituitary

Thyroid hormones =T6and T&), thyroid gland

:y#othalamus is neural* #roduces a number of releasing factors =hormones) %hich travel

to anterior #ituitary via hy#o#hyseal #ortal system

Pituitary land:

' si-e and sha#e of #ea' infundibulum connects #ituitary to hy#othalamus

Posterior lobe:

' aon terminals

' hormone storage area' antidiuretic hormone oytocin

They are structurally similar =nona#e#tides) but very different functions

&eleasing #ormone Anterior Pituitary #ormone Target

land

Thyroid releasing hormone =TF:) Thyroid stimulating hormone

=T@:)

Thyroid

gland

"orticotro#in releasing hormone

="F:)

Adrenocorticotro#ic hormone

=A"T:)

Adrenal

glands

9:4: =@omatostatin) 9F: or

9:F:

9ro%th hormone Liver

9onadotro#in releasing hormone

=9nF:)

Iollicle stimulating hormone

=I@:)Luteini-ing hormone =L:)

3varies

Testes

P4: do#amine

PF: TF:, oytocin

Prolactin Ereast


15/49


16/49


17/49

"$er$ie% of 6lood Circulation

' blood leaves the heart via arteries that branch re#eatedly until they becomeca#illaries

' 3ygen =3.) and nutrients diffuse across ca#illary %alls and enter tissues

' "arbon dioide ="3.) and %astes move from tissues into the blood' 3ygen'deficient blood leaves the ca#illaries and flo%s in veins to the heart

' This blood flo%s to the lungs %here it releases "3.and #ic(s u# 3.' The oygen rich blood returns to the heart

Composition of 6lood

' blood is the body?s only fluid tissue' it is com#osed of liuid #lasma and formed elements

' formed elements include$

1 erythrocytes, or red blood cells =FE"s)

. leu(ocytes, or %hite blood cells =;E"s)6 #latelets

' hematocritthe #ercentage of FE"s out of the total blood volume

Physical Characteristics and ;olume

' blood is a stic(y, o#aue fluid %ith a metallic taste

' color varies from scarlet to dar( red' the #: of blood is 865'8&5

' tem#erature is 6 degress "

' Average volume$ 5'L for males, and &'5L for females

' Elood accounts for a##roimately of body %eight

!unctions of 6lood

' blood #erforms a number of functions dealing %ith$

1 substance distribution

. regulation of blood levels of #articular substances6 body #rotection


18/49

Distribution:blood trans#orts$

' oygen from the lungs and nutrients from the digestive tract

' metabolic %astes from cells to the lungs and (idneys for elimination' hormones from endocrine glands to target organs

&egulation:blood maintains$' a##ro#riate body tem#erature by absorbing and distributing heat

' normal #: in body tissues using buffer systems =bicarbonate ions)

' adeuate fluid volume in the circulatory system =osmotic #ressure)

Protection

Elood #revents blood loss by$

' activating #lasma #roteins and #latelets' initiation clot formation %hen a vessel is bro(en

Elood #revents infection by$

' synthesi-ing and utili-ing antibodies' activating com#lement #roteins

' activating ;E"s to defend the body against foreign invaders

6lood plasma

Elood #lasma contains over 100 solutes, including$

' proteins: albumin =ma


19/49

"3MP3NDNT@ 3I ;:3LD EL33!

Erythrocytes 0&6C)

' biconcave discs, anucleate, essentially no organelles' ma


20/49

' Dach heme grou# bears an atom of iron, %hich can bind to one oygen molecule

' Dach :b molecule can trans#ort four molecules of oygen

#emoglobin 0#b)

' 3yhemoglobin:b bound to oygen* oygen loading ta(es #lace in the lungs

' !eoyhemoglobin:b after oygen diffuses into tissues =reduced :b)' "arbaminohemoglobin:b bound to carbon dioide* .0 on heme, rest on

#e#tide

' "arbon dioide binds to the #e#tide bac(bone, Not heme' The ma


21/49

' too fe% FE" lead to tissue hy#oia* cannot deliver enough oygen to tissues

' too many FE" causes undesirable blood viscosity* blood gets too viscous and it

#um#s uncontrollably

Drythro#oiesis is hormonally controlled and de#ends on adeuate su##lies of iron, amino

acids, and E vitamins

#ormonal Control of Erythropoiesis

Drythro#oietin =DP3) is released by the (idneys %hich is triggered by =sensing oygen

levels in the blood)$

' hy#oia due to decreased FE"s

' decreased oygen availability' increased tissue demand for oygen

' oygen availability is the signal

Dnhanced erythro#oeisis increases the' FE" count in circulating blood

' 3ygen carrying ability of the blood

!ialysis #atients become anemic because they are unable to trigger DP3 to synthesi-e

ne% FE"1 Stimulus: :y#oia due to decreased FE" count, decreased amount of

haemoglobin, decreased availability of 3.. (idney =and liver to smaller etent) releases erythro#oietin

6 erythro#oietin stimulates red bone marro%& enhanced erythro#oiesis increases FE" count

5 3ygen carrying ability of blood increases

Dietary &e3uirements of Eryhtropoiesis

Drythro#oiesis reuires$' #roteins, li#ids and carbohydrates

' iron, vitamin E1., and folic acid

' The body stores iron in :b =5), the liver, s#leen, and bone marro%' 4ntracellular iron is stored in #rotein'iron com#lees such as ferritin and

hemosiderin

' "irculating iron is loosely bound to the trans#ort #rotein transferring

!ate and Destruction of Erythrocytes

' the life s#an of an erythrocyte is 100'1.0 days

' 3ld FE"s become rigid and fragile, and their :b begin to degenerate because you

start to get oygen damage done to the #roteins

' !ying FE"s are engulfed by macro#hages


22/49

' :eme and globin are se#arated and the iron is salvaged for reuse

' :eme is degraded to a yello% #igment called bilirubin

' The liver secretes bilirubin into the intestines as bile' The intestines metaboli-e it into urobilinogen

' This degraded #igment leaves the body in feces, in a bro%n #igment called

stercobilin' 9lobin is metaboli-ed into amino acids and is released into circulation

' :b released into the blood is ca#tured by ha#toglobin and #hagocytised

Erythrocyte Disorders

Anemia:blood has abnormally lo% oygen carrying ca#acity

' it is a sym#tom rather than a disease itself' blood oygen levels cannot su##ort normal metabolism

' signs2sym#toms include fatigue, #aleness, shortness of breath, and chills

Anemia

-nsufficient erythrocytes' #emorrhagic anemia: result of acute or chronic loss of blood

' #emolytic anemia:#rematurely ru#tured FE"s' Aplastic anemia:destruction or inhibition of red bone marro%

Anemia decreased haemoglobin content

4ron deficiency anemia results from

' a secondary result of hemorrhagic anemia

' inadeuate inta(e of iron'containing foods

' im#aired iron absor#tion

Pernicious anemia results from' deficiency of vitamin E1.' lac( of intrinsic factor needed for absor#tion of E1.

Treatment is intramuscular in


23/49

' secondary #olycythemia =smo(ers, burn victims)* lose fluid, therefore increase in

hematocrit

' blood do#ing' DP3 abuse

Platelets' #latelets are fragments of mega(aryocytes %ith a blue'staining outer region and a

#ur#le granular center

' #latelet formation regulated by thrombo#oietin' granules contain clotting factors and en-ymes

' #latelets function in the clotting mechanism by forming a tem#orary #lug that

hel#s seal brea(s in blood vessels

' #latelets not involved in clotting are (e#t inactive by N3 and #rostocyclinreleased from endothelium

' Lifes#an is 10 days* .50'500000 #latelets2mL

enesis of Platelets' the stem cell for #latelets is the hemocytoblast

@tem cell!evelo#mental #ath%ay

:emocytoblastMega(aryoblastPromega(aryocyteMega(aryocytePlatelets

#emostasis

@eries of reactions for sto##age of bleeding

!uring hemostasis, three #hases occur in ra#id seuence' vascular s#asms$ immediate vasoconstriction in res#onse to in


24/49

#emostasis: ;ascular Spasms

' vasoconstriction in res#onse to in


25/49

Platelets do not stic( to each other or to blood vessels

7#on damage to blood vessel endothelium #latelets$

' ;ith the hel# of von ;illebrand factor =C;I) adhere to collagen' Are stimulated by thromboane A.

' @tic( to e#osed collagen fibers and form a #latelet #lug

' Felease serotonin and A!P, %hich attract still more #lateletsThe #latelet #lug is limited to the immediate area of in


26/49

Coagulation Phase (: T%o path%ays to Prothrombin Acti$ator

' May be initiated by either the intrinsic or etrinsic #ath%ay

i) Triggered by tissue'damaging events

ii) 4nvolves a series of #rocoagulants

iii) Dach #ath%ay cascades to%ard factor B' 3nce factor B has been activated, it com#lees %ith calcium ions, PI6, and factor

Ca to form #rothombin activator

These are the #rocesses leading u# to the formation of #rothrombin activator ;hen youactivated the etrinsic #ath%ay, it activates the intrinsic #ath%ay

The more severe the %ound, the more #ath%ays %ill be o#en to do this #rocess more

ra#idly

' The formation of #rothrombin activator =PA) is the rate'limiting ste#

' After PA accumulates, clotting #roceeds in 10'15 seconds

Coagulation Phase +: Common Path%ays to the !ibrin esh

' thrombin cataly-es the #olymeri-ation of fibrinogen into fibrin' insoluble fibrin strands form the structural basis of a clot


27/49

' fibrin causes #lasma to become a gel'li(e tra#

' fibrin in the #resence of calcium ions activates factor B444 that$ cross'lin(s fibrin,

strengthens and stabili-es the clot

Clot &etraction and &epair

' clot retractionstabili-ation of the clot by suee-ing serum from the fibrin

strands

' Fe#air i) Platelet'derived gro%th factor =P!9I) stimulates rebuilding of blood vessel

%all

ii) Iibroblasts form a connective tissue #atchiii) @timulated by vascular endothelial gro%th factor =CD9I), endothelial cells

multi#ly and restore the endothelial lining

"$er$ie% of Coagulation


28/49

Clot remo$al: !ibrinolysis

' removal of clot %hen no longer needed

' Iibrin clots is digested by Plasmin =#recursor #lasminogen)' Plasminogen is activated by tissue Plasminogen Activator =tPA) released by

endothelial cells

' Eegins %ithin . days and continues until clot is dissolved

!actors Limiting Clot ro%th or !ormation

' t%o homeostatic mechanisms #revent clots from becoming largei) @%ift removal of clotting factors by normal blood flo%

ii) 4nhibition of activated clotting factors

-nhibition of Clotting !actors

' fibrin acts as an anticoagulant by binding thrombin and #reventing its #ositive

feedbac( effects of coagulation

' Thrombin not absorbed to fibrin is inactivated by antithrombin 444 in #lasma

' :e#arin on the endothelium enhances antithrombin 444 activity

!actors Pre$enting 2ndesirable Clotting

' unnecessary clotting is #revented by endothelial cells lining the blood vessels

' Platelet adhesion is #revented by$

i) The smooth endothelial lining of blood vesselsii) N3 :e#arin and P94.secreted by endothelial cells

iii) Citamin D uinine, a #otent anticoagulant

#emostasis Disorders : Thromboembolytic Conditions

' Thrombusa clot that develo#s and #ersists in an unbro(en blood vessel

i) Thrombi can bloc( circulation, resulting in tissue deathii) "oronary thrombosisthrombus in blood vessel of the heart

' Embolus a thrombus freely floating in the blood stream

' Pulmonary emboli can im#air the ability of the body to obtain oygen' "erebral emboli can cause stro(es

Pre$ention of 2ndesirable Clots

' @ubstances used to #revent undesirable clots

i) As#irin$ an anti#rostaglandin that inhibits thromboane A.ii) :e#arin$ an anticoagulant used clinically for #re and #ost o#erative cardiac

careiii) ;arfarin$ used for those #rone to atrial fibrillation

#emostasis Disorders: 6leeding Disorders

' Thrombocytopenia: condition %here the number of circulating #latelets is

deficient

i) Patients sho% #etechiae due to s#ontaneous, %ides#read hemorrhage


29/49

ii) "aused by su##ression or destruction of bone marro% =eam#le$ malignancy,

radiation)

iii) Platelet counts less than 00002mm6is diagnostic for this conditioniv) Treated %ith %hole blood transfusions

' 4nability to synbthesi-e #rocoagulants by the liver results in severe bleedingdisorders

' "auses can range from vitamin > deficiency to he#atitis and cirrhosis

' 4nability to absorb fat can lead to vitamin > deficiencies as it is a fat'solublesubstance and is absorbed along %ith fat

' Liver disease can also #revent the liver from #roducing bile, %hich is reuired for

fat and vitamin > absor#tion

' #emophilias hereditary bleeding disorders caused by lac( of clotting factors

i) :emo#hilia A$ most common ty#er =6 of all cases) due to a deficiency offactor C444

ii) :emo#hilia E$ due to a deficiency of factor 4Biii) :emo#helia "$ mild ty#e, due to a deficiency of factor B4

' :emo#hilia A and E are B'lin(ed

' :emo#hilia " is autosomal recessive

' @ym#toms include #rolonged bleeding and #ainful and disabled


30/49

' AE3 blood grou#s may have various ty#es of antigens and #reformed antibodies

=agglutinins)' Agglutinins absent in ne%borns, a##ear by . months, #ea( at '10 years

' Agglutinogens and their corres#onding agglutinins cannot be mied %ithout

serious haemolytic reactions

&h 6lood roups

' There are eight different Fh agglutinogens, three of %hich =", !, and D) are

common' Presence of the Fh agglutinogens on FE"s is indicated as F:+

' Anti'Fh antibodies are not s#ontaneously formed in Fh'individuals' :o%ever, if an Fh'individual receives Fh+blood, anti'Fh antibodies form

' A second e#osure to Fh+blood %ill result in a ty#ical transfusion reaction

#emolytic Disease of the /e%born

' :emolytic disease of the ne%born$ Fh+antibodies of a sensiti-ed Fh'mother

cross the #lacenta and attac( and destroy the FE"s of an Fh+baby

' Fh'mother becomes sensiti-ed %hen e#osure to Fh+blood causes her body tosynthesi-e Fh+antibodies

' The druge Fho9AM can #revent the Fh'

mother from becoming sensiti-ed' Fho9AM is an anti'F: agglutinin antisera' Treatment of haemolytic disease of the ne%born involves #re'birth transfusions

and echange transfusions after birth

Transfusion &eactions

' transfusion reactions occur %hen mismatched blood is infused

' !onor?s cells are attac(ed by the reci#ients #lasma agglutinins causing$


31/49

i) !iminished oygen'carrying ca#acity

ii) "lum#ed cells that im#ede blood flo%

iii) Fu#tured FE"s that release free haemoglobin into the bloodstream' "irculating haemoglobin #reci#itates in the (idneys and causes renal failure

6lood Typing' %hen serum containing anti'A or anti'E agglutinins is added to blood,

agglutination %ill occur bet%een the agglutinin and the corres#onding

agglutinogens' #ositive reactions indicate agglutination

A6" 6lood Typing

Elood Ty#e Eeing Tested FE" Agglutinogens @erum Feaction @erum Feaction

Anti'A Anti'E

AE A and E + +

E E ' +

A A + '3 None ' '


32/49

#eart Anatomy

' a##roimately the si-e of your fist

' T%o side'by'side #um#s' Location

i) @u#erior surface of dia#hragm

ii) Left of the midline, from .nd

rib to 5th

intercostal s#aceiii) Anterior to the vertebral column, #osterior to the sternum

iv) GmediastinumH

+ layers of the heart

' Pericardium$ outer sac

' Myocardium$ muscle, bul( of mass

' Dndocardium$ inner lining

Co$ering of the #eart: Anatomy

Pericardium a double %alled sac around the heart com#osed of$' A su#erficial fibrous #ericardium

' A dee# t%o'layer serous #ericardiumi) The #arietal layer lines the internal surface of the fibrous #ericardium

ii) The visceral layer or e#icardium lines the surface of the heartiii) They are se#arated by the fluid filled #ericardial cavity

Co$ering of the #eart: Physiology

The #ericardium$

' #rotects and anchors the heart

' #revents overfilling of the heart %ith blood' allo%s for the heart to %or( in relatively friction'free environment

D#icardiumvisceral layer of the serous #ericardium

#eart


33/49

' fibrous s(eleton of the heartcrisscrossing, interlacing layer of connective

tissue, insulation, su##orts great vessels

Endocardium endothelial layer of the inner myocardial surface* continuous %ithvessels leaving and entering the heart

External #eart: a=or ;essels of the #eart 0Anterior $ie%)Cessels returning blood to the heart include$

' su#eriour and inferior vena cava, one goes to organs above heart, the other goes

belo%' right and left #ulmonary veins

Cessels conveying blood a%ay from the heart$' #ulmonary trun(, %hich s#lits into right and left #ulmonary arteries

' Ascending aorta =three branches)brachioce#halic, left common carotid, and

subclavian arteries

External #eart: ;essels that supply8drain the #eart' Arteriesright and left coronary =in atrioventricular groove), marginal,

circumfle, and anterior interventricular arteries

' Ceinssmall cardiac, anterior cardiac, and great cardiac veins

External #eart: a=or ;essels of the #eart 0posterior $ie%)

Cessels returning blood to the heart include$

' right and left #ulmonary veins

' su#erior and inferior vena cavaCessels conveying blood a%ay from the heart include$

' aorta

' right and left #ulmonary arteries

;essels that Supply8Drain the #eart 0posterior $ie%)

' arteriesright coronary artery =in atrioventricular groove) and the #osterior

interventricular artery =in interventricular groove)

' veinsgreat cardiac vein, #osterior vein to left ventricale, coronary sinus, and

middle cardiac vein

Atria of the #eart

' atria are the receiving chambers of the heart

' each atrium has a #rotruding auricle

' #ectinate muscles mar( atrial %alls' blood enters right atria from su#erior and inferior vena cava and coronary sinus

' blood enters left atria from #ulmonary veins

;entricles of the #eart

' ventricles are the discharging chambers of the heart' Pa#illary muscles and trabeculae carneae muscles mar( ventricular %alls

' Fight ventricle #um#s blood into the #ulmonary trun(


34/49

' Left ventricle #um#s blood into the aorta

Path%ay of 6lood Through the #eart and Lungs

' right atriumtricus#id valveright ventricle

' right ventricle#ulmonary semililunar valve#ulmonary arterieslungs' lungs#ulmonary veinsleft atrium

' left atriumbicus#id valveleft ventricle

' left ventricleaortic semilunar valveaorta

' aortasystemic circulation


35/49

Pulmonary circuit$ short, lo% #ressure

@ystemic circuit$ Long #ath%ay, 5 #ressure =more resistance)

Coronary Circulation

' coronary circulation is the functional blood su##ly to the heart muscle itself' collateral routes ensure blood delivery to heart even if ma


36/49

Coronary Circulation

' many anastomoses, %hich #rovide alternate routes for nourishment if a given

artery begins to be occluded* total occlusion results in com#lete bloc(age1 actively deliver blood %hen heart is relaed

. largerly ineffective %hen ventricles are contracting

' heart 12.00 of body but reuires 12.0 of blood su##ly =es#ecially left ventricle)

Coronary $enous supply

Irom ca#illariescardiac veins =great, middle and small)coronary sinusright

atrium

Also some anterior cardiac veins

directly into right atrium anteriorly


37/49

#eart ;al$es

' heart valves ensure unidirectional blood flo% through the heart

' atrioventricular =AC) valves lie bet%een the atria and the ventricles' AC valves #revent bac(flo% into the atria %hen ventricles contract

' "hordae tendineae anchor AC valves to #a#illary muscles

' Aortic semilunar valve lies bet%een the left ventricle and the aorta' Pulmonary semilunar valve lies bet%een the right ventricle and #ulmonary trun(

' @emilunar valves #revent bac(flo% of blood into the ventricles

' No valves for vena cava and #ulmonary veins

Atrio$entricular ;al$e !unction


38/49

@emilunar Calve Iunction

icroscopic Anatomy of #eart uscle

' cardiac muscle is striated, short, fat, branched, and interconnected

' the connective tissue endomysium acts as both tendon and insertion' intercalated discs anchor cardiac cells together and allo% free #assage of ions' heart muscle behaves as a functional syncytium

' 1 or . nuclei2cell

' Iull of mitochondria =.5 vs . s(eletal)' Fesist fatigue

Physiological properties of cardiac muscle fibers %ith those of s.eletal muscle cells

"ardiac Muscle @(eletal Muscle

' shorter, fatter

' single or double nuclei

' intercalated dis(s =desmosomes, ga#


39/49

-ntercalated discs and * aspects of their structure to the support of Cardiac

!unction

' an area %here there is a high concentration of ga#


40/49

Phase 1 de#olari-ation due to Na+influ =#ositive feedbac()

Phase . #lateau maintained by "a.+influ =Gslo%H "a.+channels)

Phase 6 re#olari-ation %ith >+ efflu

Cardiac Action Potential and Contraction of Cardiac uscle

' absolute refractory #eriod muscle t%itchallo%s heart to fill again

' heart needs to be stimulated in


41/49

-ntrinsic conduction system of the heart allo%s it to function as a pump

AP generated by @A node #asses to$. AC node =short delay)$ Eottlenec(* it is easy for signal to #ass do%n to the ventricles

3nly one #ath%ay Therefore, it %ill be direct and it gives time for atria to contract and

fill u# ventricles before the ventricles contract6 AC bundle

& rt and lt bundle branches

5 Pur(in+* ma(es diastolic #otentials more negative

. Sympathetic /S:increases de#olari-ation and re#olari-ation rates' tonic #arasym#athetic dam#ening effect on heart rate* constantly slo%ing do%n

the @A nodeSinus rhythm: normal regular heartbeat set by the sinoatrial node

6radycardia: heart is slo%er than normal heart rate

Tachycardia: heart is faster than normal heart rate

Delineate the extrinsic inner$ation of the heart and contrast the influences of P/S

and S/S on heart rate

' cardiac centres located in medulla oblongata


42/49

' fibers to #rimarily @A node, AC node, coronary arteries

' Cardioaccelatory centre 0sympathetic)motor neurons in T1'T5=referring to

thoracic region) level of s#inal cord#ostganglionic neurons eventually to heart

increase both rate and force of heartbeat

' Cardioinhibitory centre 0parasympathetic)to dorsal vagal nucleus in

medullainhibitory im#ulses to heart via branches of vagus nerve

EC tracing and the nature of the information it is encoding

Electrocardiogram: records electrical changes during heart activity relies on conductile

activity of body fluids

i) P'%a$e > atrial de#olari-ation

ii) ?&S complex > ventricular de#olari-ationiii) T'%a$e > ventricular re#olari-ation

Note$ D"9 records only voltage =current flo%) and time* sho%s only electrical events, but

from these can deduce contractile events 4t is not sho%ing you atrial contraction, it issho%ing you de#olar and re#olari-ation of atria and ventricles


43/49

@tandard limb leads for recording D"9 tracingsThere are 1. leads altogether

Measure com#osite of all APs from nodal and contractile cells

Three bi#olar leads measure voltage difference bet%een arms or bet%een arms and legs

Diagnostic EC inter$als

' RF@ com#le ventricular de#olarisation and contraction =GbigH F:y#ertro#hy) Dither bigger heart from %or(ing out and ecercising or muscle

failure of a #art of the heart so that the other functional #arts are com#ensating for

the damaged #art* hence more #ressure


44/49

' P'F =or P'R) interval time from atrial ecitation to ventricular

ecitation2contraction

' @'T segment entire ventricle de#olari-ed =cardiac ischemia)' R'T interval time from ventricle de#olari-ation to re#olari-ation =ventricular

arrhythmias

@A node$ sinus rhythm =85b#m)@A im#aired Sunctional Fhythm by AC node =&0'0 b#m)* heart rate is slo%er* not

getting de#olari-ation throughout the atria* blood is not to##ing u# in the ventricles

:eart bloc( defective AC node =uncou#ling of P'%ave)

Sinus &hythm 0a) and non'functional SA node

*nd

degree heart bloc. and $entricular fibrillation


45/49

Explain the e$ents of each phase of the cardiac cycle

Systole: contraction of heart* #um#ing 37T

Diastole: relaation of heart* filling

Cardiac cycle: atrial systole + diastoleventricular systole + diastole

@tart mid'to'late diastole$

1 Period of $entricular filling: mid to late diastole#ressure lo% =butPatria O Pventricles) AC valves 3PDN* @L valves "L3@D!

After 80 ventricular filling, AC valves begin to closeP %ave and atrial systole*

atrial #ressure increases and final 60 of blood enters ventricles =end diastolic volume or

D!C)atrial diastole for rest of cycle

. ;entricular systole 0comprises ?&S complex and T %a$es): ventricles

begin to contractincreased #ressure closes AC valves #eriod of

isovolumetric contraction =volume constant* a closed system)increased#ressure o#ens @L valvesventricular e


46/49

b) blood flo%s from higher to lo%er #ressure through any available o#ening* this is %hy

it is so im#ortant for the AC valves to shut %hile e


47/49

Cardiac "utput 0C") in terms of heart rate and stro.e $olume

"3 amount of blood #um#ed from left ventricle into aorta2min

' average "3 for resting, healthy male 5L2min' @C D!C D@C =D!C end diastolic volume, D@C end systolic volume)

"3 :F @C = :F is heart rate, and @C is stro(e volume)

-nfluence of exercise on #& and S;

' "3 increases &'5 times in a fit #erson

' "3 increases 8 times in a %ell trained marathon runner' "ombined effects on :F and @C =cardiac reserve)

Detailed mechanisms for the regulation of #& and S;

' :eart rate is determined by rate of s#ontaneous de#olari-ation of @A nodei) autonomic fibers innervating @A node

ii) circulating hormones =eg$ e#ine#hrine)

iii) #lasma electrolyte concentration ="a++, Na+, >+, :+)

iv) body tem#erature =useful ins surgery)

' Nore#ine#hrine =sym#athetic N@)$ increasesthe rate of s#ontaneous

de#olari-ationheart rate is increased

' Ach =#arasym#athetic N@)$ decreasesrate of s#ontaneous de#olari-ation =>+

influ hy#er#olari-es #acema(er cells)heart rate is decreased' &esting conditions: PN@ is dominant =vagal tone)

' Tachycardia 0O150'180 b#m) leads to reduced cardiac out#ut

' This is because that the heart is #um#ing too fast* %hich in turn, ventricles %ill

not have enough time to fill u# to o#timal volume Therefore the "3 %illdecrease

!ran. Starling La% of the #eart and intrinsic regulation of S;

Preload: Iran( @tarling La% of the :eart$ %ithin defined limits, the heart %ill #um#

%hatever volume of blood it receives* over a fairly %ide range, there is a #ro#ortionalrelationshi# bet%een D!C and stro(e volume


48/49

"ardiac muscle has o#timal length for contraction = length'tension relationshi#)* resting

shorter than o#timal length' each ventricle is regulated inde#endently and beat'to'beat$ I@ mechanism hel#s

ensure that each ventricle #um#s same volume of blood over a #eriod of time

' Dam#le$ if right heart O left heart O 1ml2beatin 0 minutes, the %hole bloodvolume in lungs if the right heart gets ahead of the left heart* increased return to

left heart let it catch u#

4f you have high EP, you do not allo% the heart to rest adeuetly The ventricles have to

%or( harder to overcome semilunar bac( #ressure 4n eercise, you are only doing this for

a short #eriod of time, allo%ing the heart to recover

Afterload and its influence in stro.e $olume

Afterload >#ressure that ventricles must overcome to force o#en valves and e


49/49

Documents

Anatomy: Muscle, Homeostasis, Blood