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Medical Physiology > Exam #3: Review Material > Flashcards

Exam #3: Review Material Flashcards

1
Q

State whether the intracellular or the extracellular concentration is higher for the following ions: K+, Na+, Cl-, & Ca++. Will the chemical driving force of their concentration gradients tend to push these ions into the cell or out of the cell?

A 
K+ = intracellular; pushed outside
Na+ = extracellular; pushed inside
Cl- = extracellular; pushed inside
Ca2+ = extracellular; pushed inside
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2
Q

Describe the conductance changes during the action potential in terms of one gate for K+ and activation and inactivation gates for Na+. Be able to describe three possible states for the rapidly inactivating Na+ channel: resting (closed), activated (open) and inactivated.

A

Resting – K+ gate is closed, Na+ activation gates closed, Na+ inactivation gates open

Depolarization – K+ gate is closed, Na+ activation gate is open, Na+ inactivation gate is closed

Repolarization – K+ gate is open, Na+ activation gate is closed, Na+ inactivation gate is open

Hyperpolarization – K+ gate is open, Na+ activation gate is closed, Na+ inactivation gate is closed

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3
Q

Describe the threshold for action potential generation.

A

The threshold is the point at which the resting potential has become positive enough, due to depolarization, to fire the action potential, and is all or nothing

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4
Q

Describe briefly how the following diseases or toxin affects synaptic transmission: Myasthenia gravis. Is the problem pre-synaptic or post-synaptic? Is it an autoimmune diseases?

A

Myasthenia gravis – autoimmune; destroys postsynaptic nicotinic Ach receptors

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5
Q

Describe briefly how the following diseases or toxin affects synaptic transmission: Eaton-Lambert Syndrome. Is the problem pre-synaptic or post-synaptic? Is it an autoimmune diseases?

A

Eaton-Lambert Syndrome – autoimmune; damages presynaptic voltage-gated Ca2+ channels

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6
Q

Describe briefly how the following diseases or toxin affects synaptic transmission: Botulinum toxin. Is the problem pre-synaptic or post-synaptic? Is it an autoimmune diseases?

A

Botulinum toxin – cleaves SNARE proteins in the presynaptic motor neuron

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7
Q

Describe briefly how the following diseases or toxin affects synaptic transmission: α-bungarotoxin . Is the problem pre-synaptic or post-synaptic? Is it an autoimmune diseases?

A

α-bungarotoxin – IRREVERSIBLY blocks postsynaptic nicotinic Ach receptors

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8
Q

Compare and contrast the contractile components (structural components) utilized in smooth muscle and skeletal muscle.

A
  • Smooth & skeletal muscle contain the same components (actin, myosin, & tropomyosin) , except smooth muscle DOES NOT contain TROPONIN
  • Myosin heads in smooth muscle face in various directions, allowing for multi-directional contraction
  • Dense bodies (smooth) = z-discs (skeletal)
  • Smooth muscle cells can shrink and bulge
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9
Q

Review the contractile events that occur in skeletal muscle, starting with the attached state.

A

1) Myosin attached to actin
2) Myosin binds ATP leading to detachment
3) ATP hydrolysis to ADP & Pi resets the myosin head
4) Cross-bridge forms & myosin binds a new position on actin
5) Pi is released leading to a change in position of myosin–>power stroke
6) ADP released

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10
Q

How does the point of regulation differ from skeletal muscle to smooth muscle?

A
  • Smooth muscle targets myosin

- Skeletal muscle uses Ca++ to regulate actin

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11
Q

Outline the events of contraction in smooth muscle.

A

1) Increased intracellular Ca++ from extracellular space
2) Ca++ binds Calmodulin
3) Calmodulin-Ca++ binds & activates myoskin light chain kinase (MLCK)
4) MLCK phosphorylates myosin regulatory chain & allows for activation of the myosin ATPase
5) Cross bridging occurs when myosin is phosphorylated at the regulatory chain

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12
Q

What is different between contraction of skeletal muscle & smooth muscle?

A

1) In smooth muscle ECF Ca++ is the PRIMARY source of Ca++, NOT SR Ca++ as in skeletal muscle
2) MLCK
3) Myosin ATPase is constitutively active in skeletal muscle; smooth muscle, this is regulated
4) Cross bridging occurs as long as myosin is in the phosphorylated state

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13
Q

Describe the events of actin-myosin cross-bridging in smooth muscle.

A

1) MLCK phosphorylates Myosin ATPase to turn it ON
2) Myosin- ADP+Pi is attached to actin= cross-bridge formed
3) Release Pi + ADP from myosin= power stroke
4) ATP binds myosin= release
5) ATP hydrolysis to ADP+Pi= new cross-bridge formed

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14
Q

What is the result of decreased MLCK activation?

A

Relaxation

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15
Q

What causes relaxation in smooth muscle?

A

1) Intracellular Ca++ decreases, preventing MLCK activation & necessary phosphorylation/ activation of Myosin ATPase
2) Dephosphorylation of myosin by myosin phosphatase

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16
Q

How does the neural regulation of smooth muscle differ from skeletal muscle?

A
  • No structural neuromuscular junction like in skeletal muscle
  • Diffuse branches of nerves overlie smooth muscle
  • Multiple varicosities along the nerve fiber instead of end feet
  • Increased space between varicosity & muscle fibers
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17
Q

Define electromechanical stimulation.

A
  • Change in membrane permeability resulting in depolarization of smooth muscle

I.e. opening Na+ &/or Ca++ membrane channels leading to a depolarization

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18
Q

Define pharmacomechanical stimulation.

A
  • NOT CHANGING MEMBRANE POTENTIAL
  • Activation of signaling molecules that through the generation of second messengers activate the contractile process.

E.g. Hormone activates PLC, increasing IP3 & Ca++; increase of intracellular Ca++ causes contraction of smooth muscle

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19
Q

Define electromechanical inhibition.

A
  • Change in membrane permeability that results in hyperpolzarization of smooth muscle

E.g. close Na+ &/or Ca++ channels or open K+ membrane channels.

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20
Q

Define pharmacomechanical inhibition.

A
  • NOT CHANGING MEMBRANE POTENTIAL
  • Activation of signaling molecules that through the generation of second messengers inhibit the contractile process.

E.g. Hormone activates PKA that phosphorylates MLCK, preventing Ca++-Calmodulin from binding & activating MLCK

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21
Q

What are the two sources of Ca++ in smooth muscle? Which is the primary source?

A 
ECF= primary 
SR= secondary
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22
Q

What are the two roles of Ca++ in smooth muscle?

A

1) Membrane depolarization i.e. influx of Ca++ & Na+ are important for action potential
2) Contraction via the activation of MLCK

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23
Q

What are the two types of action potentials that occur in smooth muscle?

A

1) Spike potentials

2) Action potentials with plateaus

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24
Q

Draw a spike potential & List the different ions that important for the phases the action potential.

A

asdf

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25
Q

Draw an action potential with plateau & list the different ions that important for the phases of the potential.

A

asdf

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26
Q

What are slow wave potentials?

A

A continuous cycling of depolarization & repolarization without eliciting a spike potential that leads to a contraction.

  • Seen in some types of smooth muscle
  • Serve as pacemakers for some types of smooth muscle
  • An action potential could occur at the peak of the slow wave

*THIS IS NOT AN ACTION POTENTIAL

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27
Q

What causes slow-wave potentials?

A

Na+ pumping or rhythmic changes in ion conductance

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28
Q

What ion is primarily responsible for depolarization during action potentials in smooth muscle?

A

Ca++

*Note that Na+ does play a role, but Ca++ is primary, like cardiac action potentials.

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29
Q

What ion is responsible for the prolonged state of depolarization seen in action potentials with plateaus?

A

Ca++

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30
Q

What NT is released from all of the preganglionic fibers?

A

ACh

*Regardless of system, all preganglionic fibers release ACh

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31
Q

What do the postganglionic fibers of the PNS release?

A

ACh

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32
Q

What do the postganglionic fibers of the SNS release?

A

NE/Epi or DA

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33
Q

What is the exception to postganglionic fibers of the SNS releasing NE/Epi or DA?

A

Thermoregulatory sweat glands, which posses muscarinic receptors & respond to ACh

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34
Q

What neurotransmitter do postganglionic fibers to the renal vascular smooth muscle release?

A

DA

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35
Q

What NTs are released by the adrenal medulla?

A

Epi & NE

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36
Q

What receptors are present in the target organs of the PNS?

A

Muscarinic ACh

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37
Q

What receptors are present in the thermoregulatory sweat glands?

A

Muscarinic ACh

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38
Q

What receptors are present in the target organs of the SNS? What are the two exceptions to this?

A
  • Alpha & Beta Adrenergic

- Exceptions: 1) thermoregulatory sweat, 2) renal vasculature

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39
Q

What receptors are present in the renal vasculature?

A

DA-1

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40
Q

What receptors are present in skeletal muscle?

A

Nicotinic ACh

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41
Q

How is ACh synthesized?

A

1) Uptake of choline from the ECF via the Na+ dependent choline transporter (CHT)
2) Conjugation by ChAT (AcetylCoA + Choline)
3) Final product: ACh

Note that acetylcholine is synthesized in BOTH the cytoplasm & in the mitochondria. ChAT= choline acteyltransferase

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42
Q

What drug can block the choline transporter (CHT)?

A

Hemicholiniums

*Note that these are not used clinically.

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43
Q

How is ACh stored?

A

Once ACh is synthesized, it is transported into the storage vesicle via the “vesicle assocaited transporter” (VAT)

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44
Q

What drug blocks VAT?

A

Vescamicol

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45
Q

How is ACh released?

A

1) Depolarization of nerve
2) Voltage-dependent Ca++ entry
3) Ca++ binds Calmodulin, activating “vesicle associated membrane proteins,” VAMPs & “synaptosome-assocaited proteins,” (SNAPs)
4) Exocytosis

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46
Q

What is the function of the VAMPs & SNAPs?

A

Docking storage vesicles on the inner surface of the nerve terminal facing the synapse
- Fusion of the synaptic vesicle with the neural membrane

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47
Q

What does botulinum toxin block?

A

VAMPs & SNAPs

*Botulinum toxin enzymatically removes two amino acids from one or more of these fusion peptides

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48
Q

How is ACh action terminated?

A

1) Rapid hydrolysis of ACh via acetylcholine esterase (AChE)
2) Choline re-uptake into terminals
3) ACh interaction with ACh autoreceptors

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49
Q

What does acetylcholine esterase break ACh into?

A

Choline & Acetate

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50
Q

What drug blocks Acetylcholine esterase? What happens at the synapse in response to these drugs? Give an example of an AChE inhibitor.

A
  • AChE inhibitors
  • Increase ACh concentrations & over-stimulation of receptors

*Neostigmine is an AChE inhibitor

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51
Q

What are the two major types of ACh receptors?

A
  • Muscuarinic

- Nicotinic

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52
Q

What are muscarinic receptors?

A

Transmembrane G-protein coupled receptors

*The type of G-protein associated with the particular receptor will result in a differential effect

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53
Q

What are nicotinic receptors?

A

Transmembrane Na+ ion channel

*ACh acts as a ligand that causes the channel to undergo a conformational change & opening when bound; both Na+ & K some K+ flow down their electrochemical gradients

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54
Q

What type of alpha subunit is associated with M1 & M3? What does their activation ultimately lead to?

A
  • Gq
  • Increased Ca++
  • Increased PKC
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55
Q

What type of alpha subunit is associated with M2? What does the activation of M2 ultimately lead to?

A
  • Gi/o
  • Decreased cAMP
  • Decreased PKA
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56
Q

What muscarinic receptors are present in the heart? What nervous system are they associated with?

A
  • M2

- PNS

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57
Q

What type of G-protein is associated with the M2 receptor in the heart?

A

Gi/o= inhibitory G-protein

Decrease cAMP & PKA

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58
Q

What do M2 receptors inhibit in the heart?

A
  • SA node= negative chronotrope
  • AV node= decreased conduction velocity
  • Atrial muscle= decreased atrial contracion
  • Ventricular muscle= decreased ventricular contracion
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59
Q

What type of muscarinic receptor is present in the lungs?

A

M3

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60
Q

What is the effect of M3 activation in the lungs?

A
  • Contraction of the bonchi & bronchioles
  • Secretion from submucosal glands

*DO NOT use drugs in asthma patients that have PNS activity

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61
Q

What type of muscarinic receptor is present in the stomach? What is the effect of stimulation of these receptors?

A

M3, motility & cramps

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62
Q

What type of muscarinic receptor is present in the glands? What is the effect of stimulation of these receptors?

A

M1, secretion

63
Q

What type of muscarinic receptor is present in the intestine? What is the effect of stimulation of these receptors?

A

M3, contraction–diarrhea & involuntary defecation

64
Q

Describe the mechanism of M1 & M3 receptor activation.

A

1) Receptor activation
2) Gq (activation)
3) PLC
4) PIP2–>IP3 & DAG
5) Increase Ca++ & PKC

65
Q

Describe the mechanism of M2 receptor activation.

A

1) Receptor activation
2) Gi
3) Adenylul Cyclase inhibited
4) Decrease cAMP
5) Decrease PKA

66
Q

Name the three locations of nicotinic ACh receptors.

A

1) PNS ganglia
2) Targets of the somatic nervous system, skeletal muscle
3) Adrenal medulla

67
Q

What type of nicotinic receptor is present in the adrenal medulla? What is the response to ACh binding?

A
  • Nn

- Secretion of Epi & NE

68
Q

What type of nicotinic receptor is present in the autonomic ganglia? What is the response to ACh binding?

A
  • Nn
  • Stimulation

*Note that all autonomic ganglia have nicotinic AChR

69
Q

What type of nicotinic receptor is present in the neuromuscular junction? What is the response to ACh binding?

A
  • Nm
  • Stimulation i.e. twitch & hyperactivity of skeletal muscle

Remember skeletal MUSCLE, N-M

70
Q

How are catecholamines synthesized?

A

1) Tyrosine is converted to DOPA via Tyrosine Hydroxylase*
2) DOPA is converted to Dopamine
3) Dopamine is converted to Norepinephrine

Note that this is the rate-limiting step

71
Q

What drug blocks tyrosine hydroxylase? What step of the catecholamine synthesis process does this drug block?

A
  • Metyrosine

- Conversion of Tyrosine to DOPA

72
Q

What part of catecholamine synthesis only occurs in the adrenal medulla?

A

Norepinephrine is converted to Epinephrine

73
Q

How are catecholamines stored?

A

Synthesized catecholamines are transported into vesicles for storage via the “Vesicular Monoamine Transporter (VMAT)”

*Note that the conversion of norephinephrine to epinephrine occurs in the vesicle, if the converting enzyme is available.

74
Q

What blocks VMAT? What is the mechanism of action?

A

Reserprine, blocks VMAT & causes a depletion of catecholamine stores

Still used today for “resistant hypertension

75
Q

How are the catecholamines released?

A

Similar exocytosis mechanism as ACh

76
Q

What drug blocks VAMP?

A

Bretylium

77
Q

How is catecholamine transmission terminated?

A

1) Diffusion into the circulation & metabolized by liver COMT (catechol-O-methyl transferase)
2) Binding to an autoreceptor on the pre-synaptic nerve terminal
3) Neuronal Re-uptake via NET1 (NE transporter on the presynaptic nerve terminal), where:
- Repackaged in vesicles
- Metabolized by mitochondiral monoamine oxidase (MAO)
4) Extraneuronal uptake via extraneuronal transporters (ENT or NET2)

78
Q

Where are alpha-1 receptors located?

A

Vascular smooth muscle

79
Q

Describe the mechanism of alpha-1 receptor activation.

A

1) Catecholamine binding to alpha-1 receptors leads to simulation
2) Gq subunit activated
3) Gq activates PLC
4) PLC leds the the release of IP3 & DAG
5) IP3 stimulates the release of sequestered Ca++
6) Ca++ then activates Ca++ dependent protein kinases

80
Q

Describe the mechanism of B1 & B2 activation.

A

1) Catecholamine binding to B1 or B2 receptor leads to stimulation
2) Gs subunit activated
3) Activation of adenlyl cyclase
4) Increased cAMP
5) Increase PKA

81
Q

Describe the mechanism of alpha-2 activation.

A

1) Catecholamine binding to alpha-2 receptor
2) Gi subunit activated
3) Inactivation of adenlyl cyclase
4) Decrease cAMP
5) Decrease PKA

82
Q

Where are alpha 1 receptors located in the eye?

A

Radial (dilator muscle)

83
Q

Where are B1 receptors located in the eye?

A

Ciliary body epithelium

84
Q

Where are B2 receptors located in the eye?

A

Ciliary muscle

Ciliary body epithelium

85
Q

What is the effect of stimulating alpha 1 receptors in the eye?

A
  • Alpha-1 receptors are associated with the radial (dilator) muscle
  • Contraction of the muscle results in dilation/ mydriasis
86
Q

What is the effect of stimulating B1 receptors in the eye?

A
  • B1Rs are associated with the ciliary body epithelium

- Increased production of aqueous humor?

87
Q

What is the effect of stimulating B2 receptors in the eye?

A
  • B2Rs are associated with the ciliary body epithelium &ciliary muscle
  • Constriction & increased production of aqueus humor?
88
Q

What is the effect of stimulating alpha 1 receptors in the arterioles?

A

Contraction of the smooth muscle leading to an increase in total peripheral resistance, diastolic pressure, & afterload

89
Q

What is the effect of stimulating alpha 1 receptors in the veins?

A

Contraction of the smooth muscle leading to an increase in venous return & an increase in preload

90
Q

What is the effect of stimulating alpha 1 receptors in the liver?

A

An increase in glycogenolysis

91
Q

What is the effect of stimulating alpha 1 receptors in the male sex organs?

A

Ejaculation

92
Q

What is the effect of stimulating alpha 1 receptors in the bladder & internal sphincter?

A

Contraction & urinary retention

93
Q

What is the effect of stimulating alpha-2 receptors in the platelets?

A

Aggregation

94
Q

What is the effect of stimulating alpha-2 receptors in the pancreas?

A

Decreased insulin secretion

95
Q

Where are B1 receptors located?

A 
Heart 
- SA Node
- AV Node 
- Atrial & Ventricular Muscle
- His Purkinje 
Kidney
96
Q

What is the effect of B1 receptor activation in the heart?

A

SA Node= positive chronotrope
AV Node= positive dromotrope
Atrial & Ventricular M.= positive ionotrope

97
Q

What is the effect of B1 receptor activation in the kidney?

A

Increased renin release

98
Q

Where are B2 receptors located?

A 
Blood vessels
Uterus 
Bronchioles 
Skeletal Muscle 
Liver 
Pancreas
99
Q

What is the effect of B2 receptor activation in the blood vessels?

A

Vasodilation leading to a decrease in total peripheral resistance, diastolic blood pressure, & afterload

100
Q

What is the effect of B2 receptor activation in the uterus?

A

Relaxation

101
Q

What is the effect of B2 receptor activation in the bronchioles?

A

Dilation

102
Q

What is the effect of B2 receptor activation in the skeletal muscle?

A
  • Glycogenoylsis

- Contractility/ tremor

103
Q

What is the effect of B2 receptor activation in the liver?

A

Glycogenolysis

104
Q

What is the effect of B2 receptor activation in the pancreas?

A

Insulin secretion

105
Q

What is the rate-limiting step in catecholamine synthesis?

A

Conversion of Tyrosine to DOPA via Tyrosine Hydroxylase

106
Q

What ion is the cell most permeable to at rest? What is the effect of this?

A
  • The cell membrane is most permeable to K+ at rest

- Resting membrane potential is closest to the equilibrium potential for K+

107
Q

Describe the general sequence the cardiac action potential in terms of cellular permeability & ion channels.

A

1) Fast Na+ channels open, leading to Na+ entry & rapid depolarization
2) Slow Ca++ channels open leading to the plateau phase caused by Ca++ influx
3) Change in K+ permeability throughout the action potential leads to K+ efflux & causes repolarization

108
Q

What is the resting membrane potential in a cardiac myocyte?

A

-90mV

109
Q

What is phase 0 of the AP in a ventricular myocyte?

A

Depolarization due to opening of Fast Na+ channels

110
Q

What is phase 1 of the AP in a ventricular myocyte?

A

Early repolarization when Fast Na+ channels inactivate (close) & some K+ channels open

111
Q

What is phase 2 of the AP in a ventricular myocyte?

A
  • Plateau phase where the membrane potential is approximately 0
  • Due to slow Ca++ channels with Ca++ influx, BALANCED by K+ efflux
112
Q

What is phase 3 of the AP in a ventricular myocyte?

A

Rapid repolarization as Ca++ channels are closing, & K+ channels open

113
Q

What is phase 4 of the AP in a ventricular myocyte?

A

Resting membrane potential; only K+ channels are open

114
Q

How does the nodal action potential compare to the ventricular myocyte action potential?

A
  • Missing phases 1 &2 i.e. no rapid influx of Na+ b/c no fast Na+ channels
115
Q

What happens during phase 3 in nodal cell?

A

Repolarization as K+ channels open

116
Q

What happens in phase 4 in the nodal cell?

A

Slow leak of Na+, called the “funny current” slowly changes the membrane potential until threshold is reached

117
Q

What is the effect of NE on pacemaker cells?

A
  • Increases Ca++ permeability

- More positive charge enters the cell & cell reaches threshold faster

118
Q

What is the effect of ACh on pacemaker cells?

A

Increases permeability of K+

119
Q

What is the effect of Beta-adrenergic stimulation on the SA node?

A
  • Increased conduction velocity

- Increased pacemaker rate

120
Q

What is the cholinergic effect on the SA node?

A
  • Decreased pacemaker rate

- Decreased conduction velocity

121
Q

What does the PR interval correspond to? What is the normal duration of a PR interval?

A
  • Atrial myocyte plateau phase (Ca++ IN & K+ OUT)

- 0.12-0.2 sec

122
Q

What causes the QRS complex? What is the normal duration of a QRS complex?

A
  • Ventricular depolarization

- 0.03-0.12 sec

123
Q

How much time passes between 5mm?

A

0.2 sec (1 large box)

124
Q

How much time passes between 1mm?

A

0.04 sec (1 small box)

125
Q

What is the pathophysiology underlying a PR interval that is longer than normal?

A

1st degree AV block

126
Q

What is the pathophysiology underlying a PR interval that is shorter than normal?

A

Junctional rhythm or accessory pathway between the atria & ventricles

127
Q

What is the pathophysiology underlying a few very large & wide QRS complexes appearing in a lead with mostly normal QRS complexes?

A

PVCs

128
Q

What is the pathophysiology underlying all very large & wide QRS complexes?

A

Ventricular rhythm

Extreme hyperkalemia

129
Q

What is the pathophysiology underlying a p-wave that occurs without a subsequent QRS complex?

A

AV Block

130
Q

Draw the Renin- Angiotensin II- Aldosterone system.

A

p. 163 Costanzo

131
Q

Outline the cardiopulmonary baroreceptor reflex.

A

p. 165 Costanzo

132
Q

What is albumin? What are the functions of albumin?

A
  • Albumin is a plasma protein (anion, most abundant–58%–plasma protein)
  • Responsible for 70-80% of colloid osmotic pressure, or oncotic pressure, that drive water into the vasculature
  • Transporter in the blood (important for drugs)
133
Q

Clinically, what does hypoalbuminemia lead to?

A

Edema

  • Note that the causes of hypoalbuminemia are generally three-fold:
    1) Decreased synthesis
    2) Increased volume distribution
    3) Increased excretion & degradation
134
Q

What is the function of Transferrin?

A

Transferrin binds iron to allow for iron transport to the bone marrow for erythropoesis

Note that free iron in the circulation is TOXIC.

135
Q

What is the function of Haptoglobin?

A
  • Haptoglobin binds free Hemoglobin that enters the plasma following intravascular hemolysis (lysis of RBCs)
  • Haptoglobin then transports Hemoglobin to the liver & spleen, where the complex undergoes endocytosis by macrophages
  • Within macrophages, heme is degraded, and iron & amino acids are recycled
136
Q

What is the diagnostic utility of Haptoglobin concentrations?

A

Diminished Haptoglobin concentrations are indicative of Intravascular hemolysis as more Haptoglobin binds Hemoglobin (& has a short half-life), leaving less free Haptoglobin in the plasma

137
Q

What is hematopoesis? Where does hematopoesis occur?

A

Hematopoesis is the process by which all blood cells are formed. It occurs in different locations throughout life.

  • Prenatally= yolk sac, then spleen & liver
  • Postnatally= bone marrow ONLY

Splenic hematopoesis as an adult is ABNORMAL

138
Q

What are the important characteristics of RBCs? Include both shape & important enzymes.

A
  • Biconcave
  • No nucleus
  • No organelles (mitochondria)

Contain significant lactate dehydrogenase & carbonic anhydrase

139
Q

What is important about the shape of the RBC?

A

The biconcave shape of the RBC:

  • Increases the SA/V ratio
  • Makes RBCs easily deformable, which is necessary for passage through the narrow vessels of the spleen

*Note that aging of RBC makes them less deformable & therefore, more likely to get stuck in the spleen–>recycling

140
Q

What is the function of erythropoietin (EPO)?

A

Erythroid progenitors, produced from myeloid progenitors, express an EPO receptor; EPO binding to its receptor is REQUIRED for continued RBC differentiation

141
Q

How is EPO produced?

A

The kidney senses oxygen levels & produces EPO when O2 levels decrease

Note that chronic renal failure can REDUCE the amount of EPO produced; thus, decreasing erythrocyte production, leading to anemia

142
Q

What factors cause an increase in EPO production?

A

EPO is produced in response to low oxygen levels (sensed at the kidney). Factors that may lead to low oxygen include:

1) Low blood volume
2) Anemia
3) Impaired Hb function
4) Poor blood flow
5) Pulmonary disease

143
Q

How are levels of oxygen detected? What is the effect on EPO when oxygen levels are low?

A

Hypoxia inducible factor 1alpha (HIF-1a) facilitates EPO transcription

  • HIF-1a is continuously transcribed & translated under normal oxygen saturations, & then DEGRADED
  • In hypoxic conditions, HIF-1a is NOT degraded & leads to an increase in EPO production

Specifically, HIF-1a is degraded via an intermediate, VHL (von Hippel Lindau protein). In normal circumstances, a protein hydroxylates a proline residue in HIF-1a, VHL then ubiquinates HIF-1a, & it is degraded. In hypoxic conditions, the protein that hydoxylayes, no longer functions.

144
Q

What is hematocrit? What is a normal hematocrit?

A

A percentage: volume RBCs/ Total Blood Volume

  • Male normal= 40-54%
  • Female normal= 36-48%
145
Q

What is a reticulocyte? What do increased & decreased numbers of reticulocytes indicate?

A

Immature RBC with no nucleus

*However, the reticulocyte does contain some organelles that are NOT found in the mature RBC

When there is an increased production of red blood cells to overcome chronic or severe loss of mature red blood cells, such as in a haemolytic anemia, people often have a markedly high number and percentage of reticulocytes. A very high number of reticulocytes in the blood can be described as reticulocytosis.

Abnormally low numbers of reticulocytes can be attributed to chemotherapy, aplastic anemia, pernicious anemia, bone marrow malignancies, problems of erythropoietin production, various vitamin or mineral deficiencies (B9, B12, iron), disease states (anemia of chronic disease) and other causes of anemia due to poor RBC production.

146
Q

Outline the process of thrombopoesis.

A

1) Megakaryocyte-progenitor cells differentiate into megakaryocyte precursors, via thrombopoietin (TPO), which is secreted constitutively via the liver & bone marrow
2) Megakaryocyte precursors undergo endomitosis, causing them to become large multi-nucleated cells
3) Platelets are produced via cytoplasmic budding
4) Platelets contain TPO receptors, which lessens the stimulus for the production of further platelets

147
Q

Outline that mechanism by which activated thrombin is destroyed.

A

Tissue Factor Pathway Inhibitor (TFPI) is secreted by the vasculature
- TFPI reduces thrombin formation by inhibiting the Factor VIIa/Tissue factor complex

Antithrombin is a circulating plasma protease produced by the liver; it inhibits thrombin production & destroys thrombin already produced

148
Q

What is the role of Heparin sulfate in anticoagulation?

A

Heparin sulfate binds to antithrombin & speeds thrombin proteolysis (x1000)

*Note that Heparin has NO DIRECT ANTICOAGULATION effect

149
Q

Outline the pathway of the reduction in thrombin production.

A
  • Thrombin can decrease further production of itself by interacting with Thrombomodulin
  • Thrombomodulin is an integral membrane protein of endothelial cells
  • Thrombomodulin can bind thrombin & protein C (blood plasma protein) to form APC (activated protein C)
  • APC interaction with a cofactor, protein S, to form a serine protease that degrades Factors VIIIa & Factor Va
150
Q

What is Factor V Leiden thrombophilia?

A

A mutation in Factor V prevents it from being inactivated & leads to a hypercoagulable state

151
Q

What is the function of the fibrinolytic system?

A

Degradation of fibrin clots after an injury has healed

Degradation of fibrin clots that form at inappropriate sites

152
Q

Outline the Fibrinolyitc system.

A
  • Plasmin is created by the cleavage of plasminogen by tPA (Tissue Activating Factor)
  • Plasmin is a serine proteases the cleaves fibrin; thus, degrading clots
153
Q

What are the functions of Plasminogen, plasmin, tissue plasminogen activator (tPA), plasminogen activator inhibitor
(PAI), α2-plasmin inhibitor?

A

The fibrinolytic system functions to dissolve fibrin clots that occur in undamaged tissues and to remove
the clot after an injury has healed. The fibrinolysis process begins when the circulating plasma protein
called plasminogen is converted into an active serine protease called plasmin. Plasmin can then cleave
fibrin; thereby, dissolving clots. Plasminogen is activated by the serine protease tissue plasminogen
activator (t-PA), which is expressed by endothelial cells. t-PA is kept under tight control to prevent the
removal of necessary fibrin clots at wounds. This is accomplished by rapid removal of circulating t-PA
and the inhibition of circulating t-PA by plasminogen activator inhibitor (PAI). PAI is released from
platelets, macrophages, and endothelial cells. Thrombin also directly inhibits the fibrinolytic system by
activating the thrombin-activatable fibrinolysis inhibitor (TAFI). The plasmin inhibitor α2-antiplasmin
also negatively regulates the fibrinolytic system by inhibiting plasmin that is not already bound to fibrin.
Thus, free plasmin circulating in blood is quickly inactivated. α2-antiplasmin, which is produced and
secreted by the liver, is present in blood plasma at relatively high concentrations.

Medical Physiology (74 decks)

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