exam 3 Flashcards
what is the receptor for T3?
nuclear receptor
what is the difference between growth hormone acting on the liver and growth hormone bypassing the liver?
when growth hormone acts on the liver it stimulates the release of insulin-like growth factors which stimulate the growth of cartilage, bones, and tissue, and increases blood glucose levels. when the liver is bypassed the growth of cartilage is NOT stimulated
what signals negative feedback in the growth hormone pathway?
insulin-like growth factors signal negative feedback mechanism to kick in and act on the hypothalamus and anterior pituitary gland
what is pituitary dwarfism?
insufficient growth hormone secretion in childhood which stunts vertical growth
what is giantism?
excessive growth hormone secretion in childhood which leads to excessive vertical growth
what is agromegaly?
excessive growth hormone secretion in adulthood that causes thickening of the bones
what factors stimulate the release of growth hormone?
circadian rhythm and tonic release
how does growth hormone travel in the blood stream?
half is dissolved in plasma and the other half is bound to a binding protein
what stimulates the production and secretion of parathyroid hormone?
low Calcium levels in the blood
what is the function of the parathyroid gland?
to release parathyroid hormone when low levels of calcium are detected in the blood. the release of parathyroid hormone increases the calcium concentrations in the blood
how does the parathyroid gland increase calcium levels in the blood?
- increases osteoclast activity
- increases renal calcium reabsorption
- increases intestinal calcium absorption
how do osteoclasts break down bone matter to release calcium ions into the blood?
osteoclasts release acid and enzymes to dissolve bone matter and release calcium ions into the blood. a hydrogen pump (active transport) transports the hydrogen ions out of osteoclasts into the matrix between the osteoclast and bone.
what is needed for calcium absorption in the intestines?
vitamin D3
what is calcitriol and how does the human body obtain it?
vitamin D3. we can get it through diet or exposure to sunlight
what is the function of calcitriol in the human body?
to increase calcium levels in the blood
how does calcitriol increase calcium levels in the blood?
it works in concert with parathyroid hormone to:
- increases osteoclast activity
- increases renal calcium reabsorption
- increases intestinal absorption of calcium
what is the function of calcitonin, what is its trigger, and where is it synthesized?
calcitonin decreases calcium concentration in the blood.
the trigger is excessive calcium concentration in the blood
it is synthesized and secreted from parafollicular cells in the thyroid gland
how does calcitonin decrease calcium concentrations in the blood?
- inhibits osteoclast activity
* increases renal calcium secretion in the kidneys
what is osteoporosis?
a loss of bone mass
what are these structures?
- sarcolemme
- sarcoplasm
- sarcoplasmic reticulum
- sarcomere
- muscle cell plasma membrane
- cytoplasm of muscle cell
- smooth endoplasmic reticulum of muscle cells
- functional unit of muscle cell (section of thick and thin filaments)
what are thick filaments?
myosin and myosin heads
what are thin filaments?
- troponin
- actin
- tropomyosin
what are z disks?
the ends of sarcomeres (made of thin filaments)
what is a neuromuscular junction?
the synapse between axon terminals from a motor neuron and a muscle cell
what neurotransmitter is used to excite muscle cells?
which receptors does it bind to?
acetylcholine is released from motor neuron axon terminals and binds to nicotinic cholinergic receptor channels that are located on the motor end plate of muscle cells
what is the motor end plate?
the area of sarcolemma on muscle cells at the neuromuscular junction that houses nicotinic cholinergic receptor channels. the area is ruffled to increase surface area for an increased number of receptors and acetylcholinesterase.
what stimulates the release of acetylcholine from the axon terminal of the presynaptic neuron at the neuromuscular junction?
the arrival of action potential at the axon terminal opens voltage gated calcium channels. the influx of calcium ions into the axon terminal stimulates the release of neurotransmitters
what is end plate potential(EPP)?
graded potential produced at the end plate of a muscle cell
what is the threshold for action potential in a muscle cell?
-50mV
how does action potential travel in a muscle cell?
it is reproduced just as it is in an axon along the sarcolemma into the transverse tubule. voltage gated sodium and potassium channels along the membrane are responsible for reproducing ap
describe the molecular events of muscle contraction (contraction excitation coupling)
1) acetylcholine is released into the neuromuscular junction
2) acetylcholine binds to nicotinic cholinergic receptors on the sarcolemma
3) Na+ enters cell and K+ leaves cell, cell depolarizes and produces EPP (end plate potential)
4) once threshold of -50mV is reached, localized AP is produced
5) AP is reproduced along the sarcolemma via VG ion channels (sodium and potassium) and travels to transverse tubules
6) AP arrival in the t-tubule causes DHP receptor to change conformation
7) the conformational change of the DHP receptor causes RyR (ryanodine) calcium release channels on the smooth sarcoplasmic reticulum to open
8) calcium ions are released from the smooth sarcoplasmic reticulum to the sarcoplasm and binds to troponin
9) calcium binding to troponin allows myosin heads to interact with actin protein
what is resting membrane potential for a skeletal muscle fiber?
-95mV
what does DHP stand for?
Dihydropyridine
describe the interaction of thin and thick filaments in muscle cells with and without the presence of calcium
without calcium: tropomyosin blocks myosin heads from interacting with actin molecules
with calcium: calcium binds to troponin and causes tropomyosin to move which exposes actin molecules to the myosin heads and allows interaction between the two
describe the process of thin and thick filament interaction during muscle contraction starting at rest:
- (at rest) myosin head has ADP and Pi attached to it. myosin head is detached from actin because tropomyosin is blocking their interaction
- (calcium signal) when calcium is available it binds to troponin and moves tropomyosin, allowing myosin heads to bind to actin (crossbridge = myosin heads binding to actin)
- (power stroke) myosin releases Pi molecule and actin filament moves toward m-line. at the end of the power stroke ADP is released from the myosin head as well
- (tight binding in rigor state) after ADP is released there is a tight binding between the myosin head and actin molecule.
5 (ATP binds) once ATP binds to the myosin head, the myosin head releases actin. ATP is hydrolyzed by myosin head and converted into ADP and Pi. energy from this reaction is used to rotate the myosin head back into the cocked position.
when does the power stroke of contraction begin and end?
starts when : when tropomyosin unblocks myosin/actin binding site
ends when : ADP is released from myosin head
what is the enzyme in myosin heads that hydrolyzes ATP?
ATPase
SKELETAL MUSCLE
how do muscle cells stop contraction and relax?
1) sarcoplasmic Ca++ ATPase pumps calcium back into the sarcoplasmic reticulum
2) decrease in calcium in the sarcoplasm causes Calcium to unbind from troponin
3) tropomyosin recovers binding sites when myosin heads release actin. elastic elements pull filaments back into their relaxed positions
describe the: I band A band H zone Z disk M line
I band - the space between thick filaments
A band - the length of the thick filaments
H zone - the space along thick filaments between myosin heads
Z disk - the z line line that separates sarcomeres
M line - the line that travels down the middle of thick filaments
how does sarcomere relaxation take place in a muscle cell?
sarcoplasmic calcium ATPase pumps calcium back into the sarcoplasmic reticulum which causes calcium to unbind from troponin
when calcium separates from troponin, tropomyosin drops back down and blocks interaction between actin and myosin heads which stops muscle contraction
what is the difference between muscle twitch and sliding filament theory?
muscle twitch deals with the contraction of the entire muscle fiber and sliding filament theory deals with contraction of sarcomeres within the muscle fiber
what is muscle twitch?
a single contraction/relaxation cycle in a muscle fiber and produces tension
when does muscle twitch begin and end?
muscle twitch begins when the muscle fiber begins to contract and ends when the muscle fiber has relaxed
what is the latent period in muscle contraction?
the time from the start of muscle action potential to the start of muscle tension development.
(the time required for excitation contraction coupling to occur)
more crossbridges in a sarcomere does what to tension?
increases tension
describe the state of sarcomere that has the most tension potential
80%-120% while relaxed. the most tension can be achieved at rest when all myosin heads can interact with actin (more crossbridges)
why is less tension possible in greatly shortened or stretched sarcomeres?
because less myosin heads can interact with actin (less crossbridges)
how do sarcomeres maintain optimal resting length?
the CNS maintains resting muscle length near optimal
describe muscle twitch, wave summation, unfused tetanus, and fused tetanus
muscle twitch- a single muscle cell action potential causes a single contraction relaxation cycle
wave summation - a muscle cell action potential causes contraction but before it can relax another action potential causes the muscle to contract even more producing a higher contraction strength than the first
unfused tetanus - multiple muscle cell action potentials cause multiple wave summations which creates higher and higher strengths of contraction each time it contracts ( there are brief periods of incomplete relaxation between contractions)
fused tetanus - multiple high frequency muscle cell action potentials cause a stready increase in contraction strength until maximum tension is developed. there are no periods of relaxation in between stimuli
what is the myosin ATPase activity in slow twitch vs. fast twitch muscle?
slow twitch = slow
fast twitch = fast
what is the diameter in slow twitch vs. fast twitch muscle?
slow twitch = small
fast twitch = large
what is the contraction duration in slow switch vs. fast twitch?
slow twitch = long
fast twitch = short
what is the calcium ATPase activity in the SR in slow twitch vs. fast twitch?
slow twitch = moderate
fast twitch = high
what is the endurance of slow twitch vs. fast twitch?
slow twitch = fatigue resistant
fast twitch = easily fatigued
what is the use of slow twitch vs. fast twitch?
slow twitch = posture
fast twitch = jumping, quick, fine movements
what is the metabolism of slow twitch vs. fast twitch?
slow twitch = oxidative; aerobic
fast twitch = glycolytic mostly anaerobic
what is the capillary density in slow twitch vs. fast twitch?
slow twitch = high
fast twitch = low
what is the mitochondria in slow twitch vs. fast twitch?
slow twitch = numerous
fast twitch = few
what is the color of slow twitch vs. fast twitch?
slow twitch = dark red
fast twitch = pale
why is slow twitch muscle dark red?
due to the myoglobin in it
what is a motor unit?
a motor neuron and the group of muscle fibers that it innervates
how does a motor unit decide how many muscle fibers to activate?
the strength of graded potential to the neuron of the motor unit higher stimulus voltage means more muscle fibers are contracted
what is muscle fatigue?
when muscles cant generate or sustain power output despite continuing stimuli
what catagories can fatigue be separated into?
central fatigue and peripheral fatigue
what are theories of central fatigue?
psychological effects
protective reflexes
what are theories of peripheral fatigue?
decreased neurotransmitter release decreased receptor activation decreased calcium release decreased calcium troponin interaction depleated PCr ATP or glycogen change in muscle cell membrane potential SR calcium leak
describe the action potential production of the sensory fibers in proprioceptor spindles in stretched, relaxed, and contracted states
stretched - high frequency of action potentials produced
relaxed - action potential production less frequent than stretched
contracted - minimal AP production
what are the functions of muscle proprioceptor spindles?
detects stretch of muscle fibers
maintains muscle tone to maintain an optimal resting length
how do muscle spindles prevent damage to muscles via stretching?
when proprioceptors sense additional load on a muscle and stretch is being detected, sensory signals will be fired off from the sensory neuron, synapse with a motor neuron in the spinal cord and a motor signal will be sent to the skeletal muscle to contract. this will prevent the muscle from being stretched.
what are the proprioceptors?
skeletal muscle spindles
golgi tendon organs
what does the golgi tendon organ respond to?
muscle tension during isometric contraction
what happens to tendons during isometric contraction?
the muscle shortens but is not strong enough to lift the load. this causes tendons to stretch
what does the golgi tendon reflex do?
protects the muscle from excessively heavy loads by causing the muscle to relax and drop the load
what is the difference between monosynaptic reflex and polysynaptic reflex?
monosynaptic reflexes use only one synapse to communicate between sensory and motor neurons
polysynaptic reflexes use more than one synapse to communicate between sensory and motor neurons
describe the pathway of the patellar tendon reflex
1) tap with the mallet stretches the quadriceps and causes spindle to send knee jerk reflex signals to the spinal cord
2) afferent neuron splits:
* a axon terminal communicates directly with an efferent neuron leading to the quadriceps and commands it to contract
* the other axon terminal communicates with an interneuron which communicates to the efferent neuron leading to the hamstrings and signals the hamstrings to relax(reciprocal inhibition)
3) knee jerks
describe the inhibition and contraction of the crossed extensor reflex
when you step on something that hurts you pull your leg away from the painful stimulus and the other leg supports your body.
nociceptors sense pain and send signals to these effectors via polysynaptic reflex
leg that feels painful stimulus :
quadriceps inhibited and hamstrings contract in order to lift leg
supporting leg:
quadriceps contract and hamstrings are inhibited in order to support your body weight
what is reciprocal inhibition
when an antagonist muscle is inhibited as part of a reflex
what is the SA node aka?
the pacemaker
what is the conduction system in the heart in order?
1) SA node
2) intermodal pathways
3) AV node
4) av bundle (bundle of his)
5) bundle branches
6) purkinje fibers (split off at the apex and travel both to the left and to the right)
what is the function of autorhythmic cells?
to spontaneously produce action potentials without input from cns
autorhythmic cells have unstable membrane potentials
what is the resting potential of autorhythmic cells?
there is no resting phase
where does membrane potential start in autorhythmic cells?
although there is no resting potential, membrane potential starts at -60mV
what is pacemaker potential and how does it work?
it is the graded potential created by autorhythmic cells
1) voltage gated If channels that transport sodium and potassium open at -60mV produce pacemaker potential (depolarize the cells)
2) to be sure the autorhythmic cell produce a threshold pacemaker potential, voltage gates calcium channels also open and allow calcium to come into the cell and depolarize it further
3) once the -40mV threshold is reached VG If channels close and additional voltage gated calcium channels open and cause a steep depolarization (AP)
4) once about 20mV is achieved VG calcium channels close and VG potassium channels open causing repolarization back down to -60mV
5) repeat steps 1-4
describe the sympathetic control on autorhythmic cells
1) epinephrine or norepinephrine binds to beta 1 adrenergic receptors
2) G protein dissociates and alpha travels to adenylate cyclase and activates it
3) adenylate cyclase reacts with ATP for form cAMP
4) cAMP activates protein kinase
5) protein kinase acts on I f channels and keeps them open longer which causes autorhythmic cells to reach threshold quicker
6) heart rate is increased
describe the effect the parasympathetic nervous system has on autorhythmic cells
1) acetylcholine binds to muscarinic cholinergic receptors on autorhythmic cells
2) g proteins dissociate and alpha proteins travel to calcium and potassium channels
3) calcium channels are closed and potassium channels are open which leads to hyperpolarization of the cell
4) when hyperpolarized it takes a longer period of time for autorhythmic cells to reach threshold
5) heart rate is decreased
what are cardiac contractile cells excited by?
AP from autorhythmic cells
describe the state of ion channels at the various stages of contractile cell AP
depolarization - Na channels open
AP voltage 20mV - Na channels close, fast K channels open slow K channels begin to open
Plateau - Ca channels open, and fast K channels close
repolarization - slow K channels open, Ca channels close
what is the resting and AP voltage in cardiac muscle cells?
resting - -90mV
AP - 20mV
what does the opening of calcium channels at AP voltage do to membrane potential of cardiac muscle?
makes depolarization last longer
CARDIAC MUSCLE FIBERS
describe the steps of excitation contraction coupling (contraction)
1) action potential arrives in the T-tubule from adjacent cell
2) VG Ca channels open and Ca comes into the cell
3) incoming calcium signals ryanodine receptor channels to open and release calcium from the sarcoplasmic reticulum
4) calcium sparks (Ca from SR and ECF) sum together and create a calcium signal
5) calcium binds to troponin and causes tropomyosin to unblock crossbridge formation
6) contraction occurs
CARDIAC CONTRACTILE CELLS
describe the steps of excitation contraction coupling (relaxation)
**relaxation occurs when calcium unbinds to troponin **
Calcium is removed from the cell in two ways:
1) calcium is pumped back into the sarcoplasmic reticulum via calcium ATPase and stored
2) Calcium leaves the cell via NCX antiporter. sodium that enters the cell via NCX antiporter is removed immediately via sodium potassium pump
what is the purpose of muscle relaxion in cardio muscle fibers?
to allow blood to fill the chambers of the heart
what does NCX stand for?
sodium (Na) calcium (Ca exchanger
what is blood composed of?
plasma and cellular elements
what is contained within blood plasma?
- water
- ions
- organic molecules
- trace elements and vitamins
- gasses
what is contained within the cellular elements of blood?
- RBCs
- WBCs
- platelets
what percentage of blood plasma is water?
92&
what organic molecules are contained in the organic molecules of blood plasma?
- amino acids
- glucose
- lipids
- proteins
- nitrogenous waste
what percentages of plasma and cellular components make up blood?
plasma - 55%
cellular components - 45%
where are blood cells created?
red bone marrow. red bone marrow is found in:
- the axial skeleton (skull, vertebral colomn, and rib cage)
- pelvic girdle
- proximal ends of humerus and femur
- hands and feet
- scapuli
what is erythropoiesis?
what initiates it?
red blood cell formation/creation
erythropoietin made in the kidneys signals the production of RBC
how many RBCs are lost and created everyday?
about 1 million are lost and 1 million gained
what is thrombopoiesis?
what causes it?
the production of platelets
thrombopoietin, which is made in the liver signals megakaryocytes to shed platelets into the blood stream
where does erythropoiesis, thrombopoiesis, and leukopoiesis take place?
in red bone marrow
what is leukopoiesis
what causes it?
white blood cell production.
colony stimulating factors made by endothelium and fibroblasts of bone marrow stimulate leukopoiesis
what is differential white cell count?
% of white blood cells in circulation
what is the cell that all blood cells start out as?
pluripotent hematopoietic stem cell
what does pluripotent hematopoietic stem cells turn into next?
either
*uncommitted stem cells (last undifferentiated cell)
or
*lymphocyte stem cell
what is hematocrit?
% of RBCs in your total blood volume
what is the % of RBCs in total blood volume (hematocrit) in males and females?
females - 37%-47%
males 40%-54%
a centrifuged vile of blood develope what 3 layers?
plasma, buffy coat, and RBCs
what type of cellular respiration does RBCs rely on and why?
anaerobic respiration because there is no mitochondria do perform aerobic respiration. they also dont use very much energy
how long do RBCs live?
about 4 months
what is mean red cell volume (MCV)?
RBC size
what does MCV indicate?
osmilarity of the ECF of RBCs
what is normal MCV?
80-96 femtoliters (fL)
how many polypeptides make up hemoglobin?
4 polypeptides
what are the little disks within hemoglobin?
heme groups. they are the component that oxygen binds to
describe the steps of hemoglobin synthesis
1) iron (Fe) is ingested through diet
2) iron (Fe) is absorbed in the small intestines via active transport
3) the protein transferrin transports iron (Fe) in blood plasma
4) iron (Fe) arrives in the red bone marrow where it is used to make hemoglobin
what happens to excess iron in the blood?
the liver stores it as ferritin
describe the steps of RBCs destruction
1) the spleen destroys old RBCs and converts hemoglobin to bilirubin
2) the liver metabolizes bilirubin and excretes it in bile. its eventually removed from the body via feces
2a) the kidneys also excrete bilirubin in urine
what cell destroys RBCs in the spleen?
macrophages
what is anemia?
total circulating RBCs are below normal limits
describe anemia associated with blood loss
cells are normal in size and hemoglobin content but low in number
what are examples of hemolytic anemias?
- abnormally arranged hemoglobin such as in sickle cell
* parasitic infections such as malaria
describe aplastic anemia
red bone marrow is not producing blood cells. can be caused by certain drugs or radiation
what does iron deficiency do to blood?
causes anemia
why do these cause anemia?
iron deficiency
folic acid deficiency
vitamin b12 deficiency
iron deficiency - iron is required for heme production
folic acid deficiency - folic acid is required for DNA synthesis
vitamin B12 deficiency - b12 is required for DNA synthesis
what can vitamin b12 deficiency be caused by?
lack of intrinsic factor that the small intestine needs to absorb b12
lack of b12 in diet
what happens when erythropoietin production or release is inadequate?
this will cause a low production of RBCs and thus a low RBC count (anemia)
what is polycythemia vera?
abnormally high blood cell count (all blood cells)
what is hemostasis and what are the steps?
when a blood vessel is damaged and bleeding is occuring hemostasis is the process in which blood loss is stopped
steps:
1) vasoconstriction - blood vessels constrict to restrict blood flow thus reducing blood loss
2) platelet activation - collegen fibers in the endothelium of the damaged blood vessel activates platelets and cause them to build up and clot around the damaged area
2a) clotting factors are released from platelets
3) factors attract more platelets
4) platelets aggregate into platelet plug
what are the clotting factors that platelets release and what are their functions?
serotonin - vasoconstrictor
ADP platelet aggregation
platelet activating factors (PAF) - activates more platelets and produces thromboxane A2
how is thromboxane A2 produced?
1) membrane phospholipids from the endothelial cells in blood vessels are converted into arachidonic acid
2) arachidonic acid reacts with an enzyme called cyclooxygenase (COX1) to produce prostaglandin H2
3) prostaglandin H2 reacts with an enzyme called thromboxane synthase to produce thromboxane A2
what is the function of thromboxane A2?
- induces further vasodilation
* increases platelet aggregation (brings more platelets to the area
**factors involved with platelet function** collagen - source: activated/release stimulated by: role:
source : subendothelium extracellular matrix
activation : injury exposes platelets to collegen
role : binds platelets to begin platelet plug
**factors involved with platelet function** seratonin - source: activated/release stimulated by: role:
source : secretory vesicles of platelets
activated by : platelet activation
role : platelet aggregation
**factors involved with platelet function** adenosine diphosphate - source: activated/release stimulated by: role:
source : platelet mitochondria
release stimulated by : platelet activation or thrombin
role : platelet aggregation
**factors involved with platelet function** platelet activating factors- source: activated by/ release stimulated by: role:
source : platelets, neutrophils, and monocytes
release stimulated by : platelet activation
role : plays a role in inflammation; increases capillary permeability
**factors involved with platelet function** thromboxane A2 - source: activated/release stimulated by: role:
source: phospholipids in platelet and endothelial cell membranes
release stimulated by : platelet activating factor
role: vasoconstrictor and platelet aggregation
**factors involved with platelet function** platelet derived growth factor(PDGF) - source: activated/ release stimulated by: role:
source : platelets
release stimulated by: platelet activation
role: promotes wound healing by attracting fibroblasts and smooth muscle cells
what is thyroglobulin and where is it synthesized?
thyroglobulin is a protein that T3 and T4 molecules are synthesized on and attached to. they are synthesized in the follicular cells cytoplasm
describe T3 and T4 synthesis
1) sodium iodine symporter (NIS) transports iodine into follicular cells and a transporter called pendrin transports it out of the cell into the colloid
2) follicular cells synthesize enzymes and thyroglobulin and they move into the colloid via exocytosis
3) thyroid peroxidase attaches iodine to tyrosine to make T3 and T4
4) thyroglobulin with T3 and T4 attached moves back into the follicular cell via endocytosis
5) T3 and T4 molecules are separated from thyroglobulin by enzymes
6) T3 and T4 travel across follicular cell membrane into the ECF where they diffuse into capillaries and circulate the blood stream
what is the difference between T3 and T4?
T3 is tyrosine with 3 molecules of iodine attached
T4 is tyrosine with 4 molecules of iodine attached
where is T3 and T4 synthesized?
thyroid colloid
what are these? MIT DIT MIT + DIT DIT + DIT
MIT = monoiodotyrosine is tyrosine with one iodine attached
DIT = diiodotyrosine is tyrosine with 2 iodines attached to it
MIT + DIT = T3
DIT + DIT = T4
which thyroxine is active?
T3. T4 that moves into cells need to have an iodine removed to render it active for use by the cell
what signals the release of thyroid releasing hormone?
nothing, known as tonic release, it keeps secreting thyroid releasing hormone unless negative feedback halts it. if negative feedback kicks in secretion of TRH from the hypothalamus and TSH from the anterior pituitary gland are halted
what are the causes of hyperthyroidism?
1) thyroid cancer
2) graves disease
what is graves disease?
is an autoimmune disease where the immune system is producing thyroid stimulating immunoglobulins which stimulate the production and release of T3 and T4 from the thyroid gland. negative feedback acting on the hypothalamus and anterior pituitary gland are ineffective because they are not the source of stimulation
what are the symptoms of hyperthyroidism?
1) increased O2 consumption
2) increased metabolic heat production (heat intolerance)
3) increased protein catabolism which leads to weight loss
4) insomnia which leads to irritability
5) tachycardia
6) goiter (enlarged thyroid gland)
7) exopthalamus (pressure behind eye makes eyeballs pop out)
what is the most common cause of hypothyroidism?
iodine deficiency
what are symptoms of hypothyroidism?
1) decreased O2 consumption
2) decreased metabolic heat production(cold intolerant)
3) decreased protein synthesis which leads to thin/dry skin, brittle nails, thin hair
4) slow speech and thought process
5) fatigue
6) bradycardia
7) goiter (enlarged thyroid gland)
8) myxedema (bags under eyes)
what does hypothyroidism do to infants?
cretinism (stunted nervous system development)
are thyroid hormones hydrophobic or hydrophilic?
hydrophobic
how does T3 and T4 travel in the blood?
they bind to thyroxine-binding globulin and albumin
what is coagulation cascade?
the formation of solid clots
describe coagulation cascade pathways
- intrinsic pathway:
1) in addition to activating platelets, collagen fibers also activate clotting factor 12 (factor 12 becomes active 12)
2) additional factors are activated using calcium ions until the pathway gets to the common pathway
3) active factors activate factor 10 in the common pathway - extrinsic factor:
1) damaged cells in the damaged area exposes tissue factor 3 (thromboplastin)
2) tissue factor 3 activates factor 7
3) tissue factor 3 and active 7 move along to the common pathway - common pathway (used by both intrinsic and extrinsic pathways)
4) active 7 and tissue factor 3 along with calcium activate factor 10
5) active 10 activates prothrombin changing it to thrombin
6) thrombin activates fibrinogen, converting it to fibrin
7) fibrin is arranged in a cross linked fibrin polymer which is what a solid clot is made of
describe the feedback mechanisms of the intrinsic and extrinsic pathways of coagulation cascade
POSITIVE FEEDBACK MECHANISM
in intrinsic pathway thrombin activates factor 11 which creates more thrombin and activates even more factor 11
in extrinsic pathway active 10 activates factor 12 which activates even more factor 10
**COAGULATION CASCADE** collagen 1) source: 2) activated or released in response to: 3) role:
1) subendothelial extra cellular matrix
2) injury that exposes collagen to plasma clotting factors
3) starts intrinsic pathway
**COAGULATION CASCADE** tissue factor 3 (thromblastin) 1) source: 2) activated or released in response to: 3) role:
1) most cells except platelets
2) damage to tissue
3) starts extrinsic pathway
**COAGULATION CASCADE** prothrombin and thrombin 1) source: 2) activated or released in response to: 3) role:
1) liver and plasma
2) platelet lipids, calcium ions, and factor 5
3) fibrin production
**COAGULATION CASCADE** fibrinogen and fibrin 1) source: 2) activated or released in response to: 3) role:
1) liver and plasma
2) thrombin
3) form insoluble fibers that stabilize platelet plug
**COAGULATION CASCADE** calcium ions (factor 4) 1) source: 2) activated or released in response to: 3) role:
1) plasma ions
2) N/A
3) required for several steps of the coagulation cascade
**COAGULATION CASCADE** Vitamin K 1) source: 2) activated or released in response to: 3) role:
1) diet
2) N/A
3) needed for synthesis of factors 2, 7, 9, and 10
what does low vitamin K do to coagulation cascade?
since it is needed for synthesis of several clotting factors, vitamin K will make it difficult for your body to form a clot and you will bleed longer
what is fibrinolysis?
dissolution of clot by plasmin
describe how fibrinolysis works
1) plasminogen is always circulating in the blood stream.
2) once it comes in contact with tissue plasminogen activator (tPA) plasminogen is activated and becomes plasmin
3) plasmin breaks down fibrin clots
describe the basic steps of hemostasis
1) vasoconstriction
2) platelets aggregate into loose platelet plug
3) clot :reinforced platelet plug
4) fibrinolysis
5) intact blood vessel wall
how to healthy blood vessels prevent clot formation and activation of platelets?
1) endothelium - secretes prostacyclin and nitric oxide
2) anticoagulants - our body produces heparin, antithrombin 3, protein C, these anticoagulants block clotting factors
3) vitamin K antagonist
4) asprin
how is prostacyclin produced?
prostacyclin begins as membrane phospholipids of endothelial cells
1) membrane phospholipids
2) membrane phospholipids is converted into arachidonic acid
3) an enzyme called cyclooxygenase (COX2) converts arachidonic acid into prostaglandin H2
4) an enzyme called prostacyclin synthase converts prostaglandin H2 into prostacyclin
what is the function of prostacyclin?
1) vasodilation
2) inhibits platelet aggregation
what is the function of nitric oxide?
vasodilation
what does asprin do to hemostasis?
inhibits cyclooxygenase (COX1) which is neccessary for thromboxane A2 production
what is hemophilia?
defective or lacking clotting factors 8 and 9 makes it difficult for patients to form a clot
how do people get hemophilia?
it is passed on genetically via X chromosome
CARDIAC CONTRACTILE CELLS
what is the purpose of the long refractory period?
what is the long refractory period due to?
the long refractory period in cardiac contractile cells ensure that muscle twitches are not summed
the opening of calcium ion channels after depolarization has occured creates the plateau period and makes the refractory period much longer
when does the refractory period of cardiac contractile cells begin and end?
it begins when the cell starts to contract and ends when the cell is almost fully relaxed
what is the resting membrane potential of skeletal muscle cells, cardiac muscle cells, and autorhythmic cells?
skeletal muscle fibers : -95mV
cardiac muscle fibers : -90mV
autorhythmic cells : no resting membrane potential but it starts at around -60mV
what events lead to membrane potential threshold in skeletal muscle fibers, cardiac muscle fibers, and autorhythmic cells?
skeletal muscle cells: net sodium ion entry via nicotinic cholinergic receptors
cardiac muscle cells : depolarization enters cell via gap junctions
autorhythmic cells : net sodium entry via If channels and depolarization is reinforced by the opening of calcium ion channels
what causes action potential depolarization in skeletal muscle fibers, cardiac muscle fibers, and autorhythmic cells?
skeletal muscle cells : entry of sodium via VG sodium ion channels
cardiac muscle cells : entry of sodium via VG sodium ion channels
autorhythmic cells : entry of calcium via VG calcium ion channels
what is the cause and speed of the repolarization phase of skeletal muscle cells, cadiac muscle cells, and autorhythmic cells?
skeletal muscle cells : caused by : potassium efflux// speed: fast
cardiac muscle cells : caused by: potassium efflux// speed: fast
autorhythmic cells : caused by: potassium efflux// speed fast
what is the cause of hyperpolarization in skeletal muscle cells, cardiac muscle cells, and autorhythmic cells?
skeletal muscle cells : due to excessive potassium efflux at period of high potassium permeability. resting is restored by leak of potassium and sodium
cardiac muscle cells : none
autorhythmic cells : normally none but muscarinic cholinergic receptors can cause hyperpolarization by closing calcium channels and opening potassium channels
how long is AP in skeletal muscle fibers, cardiac muscle fibers, and autorhythmic cells?
skeletal muscle cells: short/1-2msec
cardiac muscle: extended/200+msec
autorhythmic cells: variable/generally 150+msec
describe the electrical conduction pathway through the heart (autorhythmic cells and chambers)
1) SA node (pacemaker) depolarizes
2) electrical activity travels rapidly to the AV node via intermodal pathways
3) depolarization spreads more slowly across the atria and conduction slows through AV node
4) depolarization travels rapidly through the AV bundle (bundle of his), AV branches, and perkinje fibers to the apex of the heart
5) depolarization wave spreads upward from the apex contracting the ventricles
how is electrical activity in the heart monitored or measured?
electrocardiogram (ECG/EKG)
what is the function of an electrocardiogram?
records electrical activity of the heart;shows summed AP by all cells (cardiac contractile cells and autorhythmic cells)
what is einthovens triangle?
an EKG where 1 lead is attached to right arm, one lead attached to the left arm and 1 lead attached to the left foot
1 lead = 2 electrodes
describe the PQRST waves
P wave : atrial depolarization
PR segment : conduction through AV node and AV bundle//atria contract
QRS complex : ventricle depolarization (atrial repolarization also occurs here)
ST segment : ventricals contract
T wave : ventricle repolarization
(EKG)
what is a wave?
Deflection
(EKG)
what is a segment?
the baseline between waves
(EKG)
what is an interval?
a wave + segment
(EKG)
how many heart beats occur in waves P, Q, R, S, and T
these waves make up one heart beat
when does atrial repolarization occur in an EKG?
during the R wave
what is diastole and systole?
diastole = time while cardiac muscle relaxes systole = time while cardiac muscle is contracted
between which waves are atrial diastole and systole?
between which waves are ventricular diastole and systole?
atrial diastole = between the last half of R wave and the first half of P wave
atrial systole = between the last half of P wave and the first half of R wave
ventricular diastole = between the end of T wave and the first half of R wave
ventricular systole = between the last half of R wave and the end of T wave
ORGAN CONTRACTION - HEART
describe the mechanical steps of contraction
1) late diastole - both sets of chambers are relaxed and ventricles fill passively
2) atrial systole - atrial contraction forces a small amount of additional blood into the ventricles
3) isovolumic ventricular contraction - the first phase of contraction pushes AV valves closed but does not create enough pressure to open semilunar valves
4) ventricular ejection - as ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected
5) isovolumic ventricular relaxation - as ventricles relax, pressure in the ventricles drops. once BP in the arteries surpasses the BP in the ventricles, semilunar valves snap shut
what makes the “Lub” “Dub” sounds of the heart beat?
Lub is made by the closing of the AV valves during ventricular contraction, Dub is made by the closing of the semilunar valves during ventricular relaxation
when do the AV valves of the heart open?
during late diastole when the heart muscles are relaxed. the valves open due to increased weight of blood entering the atria via gravity
what does EDV stand for and what is it?
end diastolic volume. this is the volume of the ventricles when they are completely full.
EDV of each ventricle is approximately 135mL
what is EDV and ESV?
EDV (end diastolic volume) is the volume of blood in one ventricle when it is completely full (right before contraction)
ESV (end systolic volume) is the volume of blood left in one ventricle after it has contracted and pumped blood out
what is stroke volume?
the amount of blood ejected by a ventricle after contraction
what is the formula for stroke volume?
end diastolic volume - end systolic volume = stroke volume
what is the typical EDV and ESV?
what is the stroke volume?
EDV = 135mL ESV = 65mL SV = 70mL
how much BP do the ventricles need to produce in order to eject blood into blood vessels?
the ventricles need to build enough bp in the ventricle to overcome the bp in the blood vessels to open semilunar valves and eject blood into vessels
what is normal sinus rhythm?
normal heart rate and rhythm
what is tachycardia?
fast heart rate (hr > 100bpm)
what is bradycardia?
slow heart rate (HR < 60bpm)
what is arhythmia?
when the heart beats in an irregular or abnormal rhythm
what is heart block (AV block)?
when electrical conduction is disrupted at the AV node
what is 1st degree heart block (AV block)?
when PR interval is constant but lasts excessively long
what is 2nd degree heart block?
when the QRS complex is periodically skipped.
pr intervals also progressively increase in duration at times
what is 3rd degree heart block?
aka complete heart block. this is where the SA node and av node are completely out of sync. the SA node fires more frequently than the AV node creating more p waves and less QRS complexes
what is PAC?
premature atrial contraction
what is PVC?
premature ventricular contraction
why is PVC serious?
often times this can be a precurser to myocardio infarction
what is heart flutter?
extremely fast HR (200-300bpm)
what is fibrillation?
rapid, irregular, and unsynchronized contraction
how do you fix fibrillation?
electrical shock with a defibrillator
what is asystole?
no contraction of the heart muscles. flat line, call coroner
which proprioceptor is associated with maintaining muscle tone for optimal resting length of sarcomeres?
skeletal muscle spindles
how do you calculate cardiac output (CO)?
cardiac output = heart rate x stroke volume
CO=HRxSV
what is the force of cardiac contraction influenced by?
- contractility
* EDV
EDV varies with…
venous return
what is venous return aided by?
- skeletal muscle pump
* respiratory pump
how does sympathetic innervation and epinephrine effect cardiac output?
increases contractility and venous constriction
what determines the stroke volume of a cardiac contraction?
force of contraction in the ventricular myocardium
what is a - chronotropic effect?
decreased HR
what is + chronotropic effect?
increased HR
how do you calculate stroke volume(SV)?
stoke volume = end diastolic volume - end systolic volume
SV=EDV-ESV
what happens to stroke volume with increased contractility?
increased contraction strength = increased stroke volume
what factor influences EDV?
the amount of venous return
what is the resting length of sarcomeres in cardiac muscle fibers when the ventricles are empty?
they are very short to the point where there is overlap of actin
what effects the length of sarcomere beside contraction and relaxation?
EDV, the more blood in the ventricles, the more stretched out the sarcomeres are
what does increased venous return do to EDV and ventricular wall stretch?
increased venous return means increased EDV and increased ventricular wall stretch thus increased sarcomere length
what is contractility?
cardiac muscles intrinsic ability to contract
it is dependent on ICF Calcium ion availability
why is contractility dependent on ICF calcium availability?
more calcium ions means more calcium/troponin interaction and more crossbridge formation
what is + ionotropic effect?
more forceful contraction of the heart
describe the pathway and effects of sympathetic nervous system on cardiac contractile cells
1) epinephrine/norepinephrine binds to beta1 adrenergic receptors
2) g-proteins activate second messenger system which results in the phosphorylation of VG calcium channels and SR calcium ATPase
3) open time of VG calcium channels leads to increased open time and increased entry of calcium ions from ECF
3a) increased SR calcium ATPase activity causes more calcium to be stored in the SR which leads to increased calcium release from SR during contraction which causes more forceful contraction of contractile cells
3b) increased SR calcium ATPase activity also causes faster calcium removal from the sarcoplasm and and shortens Ca/troponin binding time and a shorter duration of contraction
this process causes a + ionotropic effect*
what is a - ionotropic effect?
a decrease of contractile cell contraction force
what is digoxin (digitoxin) and what effect does it have on cardiac contractile cell?
it is a toxin that blocks sodium/potassium pumps on cardiac contractile cells
- when sodium/potassium pumps are blocked, it traps sodium coming into the contracile cell via NCX transporter and sodium concentrations in the cell climb.
- once sodium concentrations get high enough in the sarcoplasm, the NXC transporter does not function and calcium becomes trapped in the cell.
- without a way to get calcium out of the sarcoplasm, calcium/troponin interaction cannot stop and the contractile cell cant relax.
- this causes the heart to seize in a contracted state
this is concidered a + ionotropic effect
can digoxin (digitoxin) be used as a medicine?
yes, given the right dosage, digoxin can be used to increase contraction force of the heart
what is cardiac preload?
the degree of cardiac muscle stretch before contraction which is created by EDV
what is stroke volume of the heart?
ejected volume
how do you calculate ejection fraction and what is it?
stroke volume / end diastolic volume x 100
SV/EDVx100=ejection fraction
ejection fraction is the percentage of EDV that is pumped out of the heart in a single contraction
how do you calculate afterload?
afterload = EDV + arterial resistance
