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BPK305 > Midterm 1 > Flashcards

Midterm 1 Flashcards

1
Q

what is the average blood volume? How much of it is erythrocytes, neutrophils, and platelets?

A

5 L
- erythrocytes (hematocrit) ~ 40%
- WBCs (leukocytes) < 5% -> neutrophils make up 50-70% of WBCs
- thrombocytes (platelets) < 1%

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2
Q

what electrolytes are present in plasma and why are they important?

A
  • Na+ (APs)
  • K+ (APs)
  • Ca2+ (muscle contraction)
  • Mg2+ (bound to ATP)
  • H+ (regulate pH -> 7.35-7.45)
  • HCO3- (regulate pH)
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3
Q

what is plasma made of?

A
  • 92% water (electrolytes, nutrients)
  • 7% proteins
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4
Q

what nutrients are present in plasma?

A
  • glucose
  • lipids
  • cholesterol
  • vitamins
  • FFAs
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5
Q

what proteins are present in plasma?

A
  • albumin (transports FFAs)
  • globulin
  • fibrinogen (clotting)
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6
Q

what gases are present in plasma?

A
  • CO2
  • O2
  • N2
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7
Q

what are the approximate cellular constituent numbers and how much of the blood volume do they take up?

A
  • RBCs: 5 mil/uL
  • WBCs: 7000/uL
  • platelets: 250000/uL

40-45% blood volume

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8
Q

how much of each cell is produced daily through hematopoiesis?

A

75% cells produced:
- leukocytes (lifespan is from hours-days)
20-25% cells produced:
- erythrocytes (lifespan is from 90-120 days)

  • produced in bone marrow
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9
Q

what are the cytokines that regulate hematopoiesis?

A
  • colony stimulating factors - leukocytes
  • erythropoeitin (EPO) - erythrocytes
  • thrombopoeitin (TPO) - platelets
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10
Q

what does Hb production require?

A
  • iron
  • B12
  • folic acid
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11
Q

what is the structure of Hb and how does it work?

A

has 4 globin subunits
- each subunit has a heme group containing Fe to which oxygen binds
Hb binds 4 oxygen molecules
- binding is co-operative (binding of one oxygen molecule facilitates binding of another)

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12
Q

what does the oxygen dissociation curve represent?

A
  • good saturation/binding in lungs (loading)
  • poor saturation/binding in capillaries (unloading)

sigmoidal relationship

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13
Q

what factors influence hematocrit?

A
  • lower in females (increased by testosterone)
  • higher at altitude
  • higher in athletes
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14
Q

what pathophysiological term would you use to describe a hematocrit of 80%?

A

polycythemia

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15
Q

what factors regulate hematocrit?

A
  • oxygen (via EPO)
  • nutritional status
  • menstruation/hemorrhage
  • hormones
  • vit B12 complex
  • folic acid
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16
Q

what is anemia and what are the different types?

A

insufficient Hb
- hypochromic (low Hb in RBCs, Fe deficiency)
- megaloblastic (pernicious (low B12) and non-pernicious (low folic acid)) -> increased size of RBCs
- hemolytic (fragile RBCs ex. sickle cell anemia)
- aplastic (low RBC production ex. from chemotherapy radiation damage)

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17
Q

what is hyperbilirubinaemia?

A

when you cannot excrete bilirubin (byproduct of old RBCs) and it builds up in the blood
- causes jaundice
- can be reversed through urinary excretion

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18
Q

what is the normal state of cells without clotting?

A

endothelial cell lining intact generate prostacyclin which promotes vasodilation (and thus blood flow) and inhibits platelet activation (and thus clotting) by keeping them soluble

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19
Q

how does clotting occur after endothelial cell lining is damaged?

A
  • injury to endothelial cells reduces prostacyclin (platelets no longer soluble); collagen is exposed and binds and activates platelets
  • following this activation, platelet factors such as 5-HT, ADP and thromboxane A2 are released
  • factors attract more platelets causing them to aggregate and form a platelet plug
  • during this temporary hemostasis, coagulation cascade is triggered: factors I-XIII activate which convert prothrombin to thrombin, thrombin converts fibrinogen to fibrin, ultimately clotting and reinforcing the platelet plug
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20
Q

what are PMNs?

A
  • neutrophils
  • eosinophils
  • basophils
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21
Q

what is the function of neutrophils?

A

neutralize foreign substances

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22
Q

what is the function of eosinophils?

A

destroy invading parasites and cells

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23
Q

what do basophils form and what is their function?

A
  • form mast cells (can enter tissues and trigger histamine release; where injury occurs causes vasodilation)
  • mediate allergic response and inflammation
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24
Q

what do monocytes differentiate into?

A

macrophages
- “big eaters” -> ingest invaders

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25
Q

what are the types of lymphocytes?

A
  • B cells (create antibodies)
  • T cells
  • natural cell killers
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26
Q

what is the annulus fibrosis?

A

supports valve integrity to prevent prolapse and strengthen electrical insulation
- separates electrical current of atria and ventricles

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27
Q

what are the layers of the ventricular wall from inner to outer?

A
  • endocardium
  • myocardium
  • epicardium
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28
Q

how can cardiomyocytes change in size?

A

pressure overload (ex. with hypertension or weight lifting)
- increased cell width
- more parallel sarcomeres
volume overload (ex. valve failure or aerobic exercise)
- increased cell length
- stretching sarcomeres

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29
Q

what are the properties of the Z-line?

A
  • forms sarcomere boundary
  • thin actin filaments run through
  • contains a-actinin (forms it)
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30
Q

what are the properties of the I band?

A
  • shortens with contraction
  • lengthens with relaxation
  • contains only actin filaments
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31
Q

what are the properties of the A band?

A
  • measures only myosin filaments
  • doesn’t change with contraction
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32
Q

what are the properties of the H zone/band?

A
  • centre of A band
  • no overlapping thin filaments
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33
Q

why is there more mitochondria in cardiac myocytes?

A

FFAs are the heart’s primary energy source, not glucose

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34
Q

how are cardiomyocytes coupled?

A

1) myocyte branching
- provides longitudinal and diagonal coupling
- coupled at intercalated discs
2) macula adherens/desmosomes
- cytoskeletal proteins
- physical coupling
3) gap junctions
- connexins
- electrical coupling
- create a functional syncytium

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35
Q

what is the structure of gap junctions?

A
  • 2 connexons per gap junction
  • a connexon is a hexamer of 6 connexins
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36
Q

what is titin?

A
  • from M-line to Z-line (half sarcomere)
  • acts like a spring (more tense in cardiac muscle)
  • stabilizes position of contractile elements
  • returns stretched muscle to resting length
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37
Q

what is nebulin?

A
  • from Z-line to thin filament ends
  • aligns thin filament
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38
Q

what are the states of cross-bridge cycling?

A

1) attached state
2) released state
3) cocked state
4) cross-bridge state
5) power-stroke state

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39
Q

what is the attached state?

A

resting state; myosin is attached to actin (ADP released from previous contraction)

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40
Q

what is the released state?

A

ATP binds to the myosin head, causing myosin to dissociate from actin

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41
Q

what is the cocked state?

A

ATP is hydrolyzed, causing myosin heads to enter a cocked position (ADP + Pi attached)

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42
Q

what is the cross-bridge state?

A

a cross-bridge forms and the myosin head binds to a new position on actin

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43
Q

what is the power-stroke state?

A

Pi is released; myosin head changes conformation, resulting in the power stroke, the filaments slide past eachother

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44
Q

what does the force pCa curve represent?

A

more Ca2+ increases tension

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45
Q

what is the structure of TnC?

A

TnC has 4 binding sites (dumbbell):
- site I: dysfunctional in cardiac muscle
- site II: binds Ca2+ -> initiates contraction
- sites III and IV: high affinity; always occupied

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46
Q

what makes up the troponin (Tn) complex?

A
  • TnT: binds tropomyosin
  • TnC: binds Ca2+
  • TnI: binds actin; inhibits cross-bridge cycling by covering binding site
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47
Q

how does Ca2+ bind to Tn to initiate contraction?

A
  • [Ca2+] increases
  • Ca2+ binds TnC
  • TnI and tropomyosin move
  • exposes myosin binding site
  • crossbridge cycling
  • contraction
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48
Q

what are the myosin heavy chains?

A
  • 2 chains form coiled helix
  • tail and 2 heads
  • heads = S1
  • head has 2 binding sites: ATP and actin
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49
Q

what are the myosin light chains?

A
  • 2 pairs
  • regulatory (phosphorylatble)
  • essential (alkali)
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50
Q

what are the isoforms of myosin heavy chains?

A

different rates of ATP breakdown and contraction
- V1 (a-a) - fastest
- V2 (a-B)
- V3 (B-B) - slowest (human isoform)

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51
Q

what does thyroxine do?

A

hormonal treatment that changes gene expression of myosin chains -> creates more a-B and a-a isoforms, increasing heart rate

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52
Q

what does the active portion of the cardiac length-tension curve represent?

A

there is an optimal sarcomere length (~2.3 um) -> optimal cross-bridges are formed
- any more or less will decrease tension

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53
Q

what contributes to the L-T rising phase?

A

1) overlap of actin and myosin
2) increased myofilament Ca2+ sensitivity
3) geometric changes: stretch decreases spacing between filaments
4) stretch-activated Ca2+ channel activation
5) increased SR Ca2+ release

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54
Q

what does the passive portion of the cardiac length-tension curve represent?

A

prevents from overstretching and decreased force: titin increases sarcomere stiffness
- increased resistance
- maintain force generation

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55
Q

how does cardiac L-T relationship differ from skeletal?

A
  • skeletal has a greater range of active force
  • skeletal has more distensible non-contractile components than cardiac (different isoform of titin) making its passive force minimal
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56
Q

how does the Frank-Starling law apply to L-T relationship?

A
  • reflects combination of active and passive tension
  • no descending phase due to titin and connective tissue (protects heart muscle from overstretching)
  • EDV represents length
  • SV represents tension
  • maintenance of high level of force and stroke volume as we increase EDV
  • heart muscle adapts to venous return
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57
Q

what factors increase EDV?

A
  • exercise
  • venous constriction
  • decreased heart rate (more filling time)
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58
Q

what is preload?

A

EDV (pre-contraction)
- the force that stretches the relaxed muscle cells (ex. blood filling and stretching the myocardium in the ventricular wall during diastole)
- can be increased by greater filling of the left ventricle during diastole (increasing EDV)
- maximum systolic pressure is reached at optimal preload (further increases will decrease peak pressure)

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59
Q

what is afterload?

A

blood pressure
- the force against which the contracting muscle must act (ex. the aortic pressure that must be overcome to open the aortic valve and eject blood)
- increasing afterload can lead to higher systolic pressure (ex. by increasing peripheral resistance)
- continued increases in afterload lead to increased isovolumetric systole

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60
Q

what determines Vmax?

A

by the rate of cross-bridge cycling

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61
Q

what is the structure of Na+ channels?

A
  • 24 transmembrane segments per a subunit (1 a subunit per Na+ channel)
  • one gene product
  • 1 domain = 6 transmembrane segments; 4 domains per voltage-gated channel
  • membrane-spanning B1 and B2 subunits
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62
Q

what is the structure of K+ channels?

A
  • 1 domain = 6 transmembrane segments; 4 domains per voltage-gated channel
  • 6 transmembrane segments per a subunit (4 a subunits per K+ channel)
  • 4 gene products
  • 4 cytoplasmic B subunits
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63
Q

what is the structure of Ca2+ channels?

A
  • cytoplasmic B subunit
  • transmembrane y subunit
  • transmembrane a1 subunit, a2-delta subunit (joined by S-S bond)
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64
Q

what is Ohm’s Law?

A

V=IR
R=1/G, so V=I/G
I=deltaVG

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65
Q

what are V1 and V2?

A
  • V1= membrane potential (Vm)
  • V2 = equilibrium potential for that ion (ex. Ek)
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66
Q

what is the Nernst equation?

A

Ek = 60log10([K+]out/[K+]in)
- used for calculating the equilibrium potential of an ion

67
Q

what are the values of Ek, ENa, and ECa?

A
  • Ek = -90 mV
  • ENa = +65 mV
  • ECa = changes
    • +120 mV at rest
    • +90 mV during contraction
68
Q

what is the GHK equation and RMP? What occurs during depolarization?

A

used for calculating the resting membrane potential using the equilibrium potential and conductance for each ion
- the membrane potential is closest to the eqm potential of the ion that permeates the membrane most freely
- RMP ~-80 mV
- membrane potential moves toward ENa (~30mV)

69
Q

what is conductance of an ion determined by?

A
  • whether ion channels are open
  • number of channels present
70
Q

how is tension regulation different in cardiac myocytes vs skeletal muscle?

A
  • 100% recruitment occurs with every beat
  • no tetany (no summation) due to long AP duration
71
Q

what occurs in phase 4 of a ventricular AP?

A

resting membrane potential
- Kir2.1 channel is open; Ik1 (inward rectifier) current is flowing

72
Q

what occurs in phase 0 of a ventricular AP?

A

depolarization
- Nav1.5 channel is open; INa current is flowing
- opening threshold ~-55mV
- sensitive to tetrodotoxin (TTX)

73
Q

what occurs in phase 1 of a ventricular AP?

A

rapid repolarization
- Kv4.3 channel is open; Ik,to (transient outward) is flowing

74
Q

what occurs in phase 2 of a ventricular AP?

A

plateau (point of regulation of contraction)
- Cav2.1 channel opens; ICa is flowing, depolarizing
- INCX is flowing (3Na+ in, 1Ca2+ out - net depolarizing)
- Kir2.1 (Ik1) is blocked by polyamines
- Ik,dr is the repolarizing drive (Kv1.5 (Ikur) and Kv11.1(Ikr) open respectively)

75
Q

what occurs in phase 3 of a ventricular AP?

A

repolarization; Ik,dr (delayed rectifier) opens 3 channels in this order:
- Kv1.5 channel opens, Ikur (ultra-rapid delayed rectifier) current is flowing
- Kv11.1 channel opens, Ikr (rapid delayed rectifier) current is flowing
- Kv7.1 channel opens, Iks (slow rectifier) current is flowing

76
Q

what happens when ICa is inhibited with diltiazem?

A
  • shorter AP duration
  • less Ca2+ entry
  • less forceful contraction
77
Q

what is rectification?

A

conductance of ions through a channel is greater in one direction that the other

78
Q

what is a delayed rectifier?

A

only passes outward current; “delayed” because slower than INa

79
Q

what are the stages of the refractory period?

A
  • absolute refractory period: most Nav+ channels are inactivated making it impossible to produce another AP (long in cardiac muscle, preventing tetanus)
  • relative refractory period: another AP can be elicited but only with a greater stimulus
80
Q

what are the determinants of AP propagation?

A
  • difference in voltage between cells (large gradient = more depol)
  • resistance between cells (different gap junctions have different resistances)
  • threshold for AP firing
  • size of cells
  • expression of Nav+ channels
81
Q

what are pacemaker channels?

A

hyperpolarization-activated cyclic nucleotide gated channels (HCN channels)
- structure like a K+ channel
- non-selective cation channel (Na+ and K+)
- gated by cAMP

82
Q

what is the pathway of electrical activity in the heart?

A

sinoatrial (SA) node -> atrioventricular (AV) node -> bundle of His -> bundle branches -> Purkinje fibres

83
Q

what are the phases of an SAN AP?

A

1) slower upstroke velocity (lack Na+ channels, depolarized by ICa
2) reduced plateau duration (ICa inactivated after upstroke)
3) diastolic depolarization (due to pacemaking HCN channel)
4) higher “resting” potential (lack Ik1 - important for RMP)

84
Q

what is the SAN AP missing?

A
  • strong inward rectifier (Kir2.1)
  • Na+ channel
85
Q

how does ANS stimulation affect the diastolic depolarization slope?

A
  • S = increased slope = increased AP frequency
  • PS = decreased slope = decreased AP frequency
86
Q

how does sympathetic stimulation affect HCN channels?

A
  • NE binds B1-adrenergic receptors, activating the associated Gs protein
  • Gs protein activates adenylyl cyclase (AC)
  • AC converts ATP to cAMP
  • more cAMP becomes available and binds to more HCN channels, increasing HR (faster diastolic depol)
  • right shift of I-V
87
Q

how does parasympathetic stimulation affect HCN channels?

A
  • ACh binds m2-muscarinic receptors, activating the associated Gi protein
  • Gi protein inhibits AC
  • less ATP is converted to cAMP
  • less HCN channels open, decreasing HR (slower diastolic depol)
  • left shift of I-V
88
Q

what happens when the cardiac vagus nerve is stimulated?

A

causes ACh release, slowing down diastolic depolarization (slowing heart rate)

89
Q

what are the specialized features of the AVN?

A
  • smaller cells
  • fewer gap junctions
  • slower intrinsic diastolic depol rate
  • more negative Em
90
Q

what is Wolff-Parkinson-White syndrome?

A

accessory AVN pathway: electrical activity leaks from atria to ventricle due to breakdown in annulus fibrosis
- causes delta waves (pre-excitation)

91
Q

what are the times for the conduction pathway?

A

a) AVN -> bundle of His (130 ms)
- slow conduction creates delay between atrial and ventricular depol
b) bundle of His -> apex (30 ms)
c) endocardium -> epicardium (30 ms)

92
Q

how do Purkinje fibres conduct APs so quickly?

A
  • wide diameter (low resistance)
  • large number of gap junctions (low resistance)
93
Q

why is ventricular repolarization a positive deflection?

A

the subepicardium has a shorter AP duration than the subendocardium (starts after, finishes before)
- creates a voltage gradient that presents as a net positive charge moving towards the electrode (upwards deflection)

94
Q

what are the advantages of ECGs?

A

simple and cheap; provides info about:
- axis of heart
- chamber sizes (hypertrophy)
- arrhythmias and conduction blocks
- myocardial ischemia
- myocardial infarction (heart attack)
- congenital defects

95
Q

what are the components of a 12 lead ECG?

A
  • 3 bipolar limb leads
  • 9 unipolar leads
    • 3 augmented voltage limb leads
    • 6 precordial (chest) leads
  • reference electrode
    10 electrodes total
96
Q

what lead views the conduction system? what is Einthoven’s Law?

A

lead II
I + III = II

97
Q

what are the augmented voltage limb leads?

A
  • aVR = right arm
  • aVL = left arm
  • aVF = left foot (leg)
98
Q

what are the precordial (chest) leads?

A
  • V1 and V2 = septal
  • V3 and V4 = anterior
  • V5 and V6 = lateral
99
Q

what is a normal PR interval? what can cause a long PR interval?

A
  • normal = 120-200 ms
  • AVN block: takes longer to conduct from atria to ventricles
100
Q

what causes a short PQ interval?

A

WPW syndrome (pre-excitation, delta waves)
- faster conduction from atria to ventricles

101
Q

what is a normal QRS complex? what causes a long QRS complex?

A
  • <120 ms
  • bundle branch block (BBB): ischemia in bundle branches; longer conduction through bundle of His
102
Q

what is a normal QT interval? what causes a long and short QT interval?

A
  • 360-440 ms
  • short and long can be inherited and can cause arrhythmias
103
Q

what is the quadrant method when calculating mean electrical axis?

A
  • look at lead I; if positive QRS complex, fill in right half
  • look at lead aVF; if positive QRS complex, fill in bottom half
  • overlapping quadrant is axis
104
Q

what is a right axis deviation? what causes it?

A
  • lead I has a negative QRS complex; lead aVF has a positive QRS complex (+90 to +180)
    causes:
  • RV hypertrophy
  • infants (have large hearts relative to body, gets weighed down)
  • tall and thin (abdominal organs not supporting heart; hangs down)
105
Q

what is a normal axis?

A

0 to +90

106
Q

what is a left axis deviation? what causes it?

A
  • lead I has a positive QRS complex; lead aVF has a negative QRS complex (0 to -90)
    causes:
  • obesity
  • pregnancy
    (heart pushed up physically by other structures)
  • LV hypertrophy
107
Q

what is extreme axis? what causes it?

A
  • lead I and lead aVF have negative QRS complex (-90 to 180)
    causes:
  • dextrocardia: heart on right side of chest
  • cardiac pacemaker: pacemaker wires in bottom of left ventricle, so signal is going in the other direction
108
Q

what is the isoelectric method for calculating mean electrical axis?

A

1) find the limb leads
2) find the lead with the most biphasic QRS complex
3) identify the lead 90 degrees to it
4) determine if the QRS complex is upwards (towards) or downwards (away)

109
Q

what are the length independent factors of cardiac contraction?

A

changes in contractility

110
Q

what are examples of positive inotropes (increased contractility)?

A
  • norepinephrine
  • epinephrine
  • cocaine
  • amphetamines
  • digitalis (digoxin)
111
Q

what are examples of negative inotropes (decreased contractility)?

A

-propanolol (B-blocker -> sympathetic antagonist)
- nifedipine (blocks Ca2+ channels)
- ACh (parasympathetic agonist)

112
Q

what is the process of EC coupling?

A
  • AP enters ventricular myocyte and travels down the T-tubule causing L-type Ca2+ channels (Cav1.2) to open
  • causes calcium-induced calcium release (CICR) -> Ca2+ binds to SR RyR2s and triggers channel opening, releasing Ca2+ from the SR
  • Ca2+ binds to TnC and causes cross-bridge cycling -> contraction!
113
Q

how is the Na+/K+ pump significant in EC coupling?

A

3Na+ out, 2K+ in
- brings membrane to resting for another AP
- creates Na+ gradient for NCX to move Ca2+ out of the cell, facilitating relaxation

114
Q

what does phospholamban (PLB) do?

A

regulates SERCA
- slows down SERCA, slowing down Ca2+ movement into SR

115
Q

how does sympathetic regulation increase contractility?

A

increased cAMP levels due to increased AC activity activates protein kinase A (PKA); phosphorylates:
- PLB
- Cav1.2 (B subunit)
- TnI
- RyR

116
Q

how does PKA increase SERCA activity (increase contractility?)

A

PKA phosphorylates PLB
- inhibits the brake effect it has on SERCA
- SERCA is more active, moving more Ca2+ into the SR at a faster rate
1) faster relaxation
2) more SR Ca2+ release (b/c more Ca2+ is loaded into SR)

117
Q

how does PKA increase contractility through phosphorylation of Cav1.2 and RyR2?

A
  • increases probability of their opening
  • increases Ca2+ current and CICR
118
Q

how does PKA increase contractility through phosphorylation of TnI?

A
  • decreases the affinity of TnC site II for Ca2+ (increases offloading of Ca2+ from TnC)
  • promotes faster relaxation
119
Q

what are sympathomimetics?

A

stimulate SNS
- cocaine: blocks NE reuptake by neurons
- amphetamine: release NE from storage vesicles

120
Q

what are sympatholytics?

A

inhibit SNS
- propanolol (B blocker)

121
Q

how is digitalis (digoxin, foxglove) a positive inotrope?

A

inhibits Na+/K+ ATPase
- elevates intracellular Na+, reduces intracellular K+
- causes reversal of NCX (Ca2+ comes in, Na+ goes out) due to their close proximity
- causes more Ca2+ in the myocyte, increased contractility

122
Q

what is EDV, ESV, and SV? what are their normal values?

A
  • EDV = end diastolic volume; volume during isovolumetric contraction (120 mL)
  • ESV = end systolic volume; volume during isovolumetric relaxation (50 mL)
  • SV = stroke volume = EDV - ESV = 70 mL
123
Q

what is the ejection fraction?

A

SV/EDV
- how much we ejected vs how much we had available
- normal = 55%
- low = <50% (common after an MI)

124
Q

where are systolic and diastolic pressure on the P-V loop? what is pulse pressure?

A
  • systolic = E (peak)
  • diastolic = D (when aortic valve opens)
  • pulse pressure = s - d ~ 40 mm Hg
125
Q

where are the ECG waves on the P-V loop?

A
  • P wave (atrial depolarization) - before bump before C (atrial contraction)
  • QRS complex (ventricular depolarization - C (before isovolumetric contraction)
  • T wave (ventricular repolarization) - E
126
Q

what do the heart sounds indicate?

A
  • S1 (lub) = closure of mitral valve
  • S2 (dub) = closure of aortic valve
127
Q

what is the dicrotic notch and what is it caused by?

A

brief increase in aortic pressure; due to:
- closure of aortic valve
- elastic recoil of aorta

128
Q

how does increased preload (increased blood coming back to heart) affect the PV loop?

A

increased volume -> increased stretch -> increased length -> increased tension
- increased SV (wider and taller loop)

129
Q

how does increased afterload (increased pressure in aorta) affect the PV loop?

A

increased pressure to open aortic valve -> increased isovolumetric contraction time -> early closing of aortic valve -> increased ESV
- decreased SV (narrower and taller loop)
- causes hypertrophy

130
Q

how does increased contractility affect the PV loop?

A

increased contractility -> increased force of contraction -> increased max systolic P -> decreased ESV
- increased SV and force of contraction (wider and taller loop)

131
Q

what is cardiac muscle’s primary energy source? how does it differ from skeletal muscle? what else can cardiac muscle use?

A
  • 70-90% FFAs (skeletal muscle uses 5% FFAs, glucose is dominant)
  • cardiac muscle cannot work anaerobically (skeletal can through glycolysis)
  • cardiac muscle can also use glucose, glycogen, and lactate
132
Q

how is the heart designed for fat use?

A

heart has a high expression of:
- FABP (allows diffusion from capillary to myocyte)
- CAT (allows diffusion from cytosol to mitochondria)
- mitochondria

133
Q

how are FFAs released into blood and how do they enter the muscle cell and the mitochondria?

A
  • FFAs released from adipose tissue by lipolysis circulate blood bound to albumin
  • to enter the cell: fatty acid binding protein (FABP)
  • to enter mitochondria: Carnitine AcylTransferase (CATs)
134
Q

how are FFAs used to generate ATP?

A

aerobic:
- bypass glycolysis and undergo B-oxidation to produce acetyl-CoA for Kreb’s cycle (2 Cs removed each cycle to produce 1 acetyl-CoA; costs 2 ATP)

135
Q

how does glucose make ATP anaerobically?

A

GLUT4 (transporter) brings glucose into the myocyte
glycolysis:
glucose -> glucose-6-P -> 2 triose-P -> 2 pyruvate -> 2 ATP and lactate

136
Q

how does glucose make ATP aerobically?

A

2 pyruvate (pyruvate dehydrogenase moves it into the mitochondria) -> acetyl-CoA -> Kreb’s cycle -> 36 ATP

137
Q

how is glucose metabolism regulated?

A

i) glucose uptake:
- concentration gradient
- insulin increases GLUT4
ii) enzymatically - PDH vs LDH choice is determined by presence of O2
iii) high B-oxidation of FFAs suppresses glucose metabolism

138
Q

how does lactate make ATP?

A
  • lactate cotransporter (with H+) brings lactate into the myocyte
  • lactate is converted to pyruvate with lactate dehydrogenase (unique to cardiac cells)
  • 1 molecule of pyruvate produces 18 ATP
139
Q

what are the arterial layers, from lumen to outside?

A

1) tunica intima
2) tunica media
3) tunica adventitia

140
Q

what are characteristics of the tunica intima?

A
  • endothelium
  • one cell layer thick
  • paracrine functions
  • present through vasculature
141
Q

what are characteristics of the tunica media?

A
  • variable number of cell layers thick
  • contains EC matrix, elastic, collagen (more elastic + contractile)
  • contains smooth muscle cells
142
Q

what are the characteristics of the tunica adventitia?

A
  • site of sympathetic nerves (regulates vasoconstriction/dilation)
  • vaso vasorum - some blood vessels are so big, they have their own blood supply
  • extensive ECM
143
Q

how does branching affect cross-sectional area (CSA)? how is velocity related to CSA?

A
  • branching increases CSA (when a vessel branches, total CSA of daughter vessels > parent vessels)
  • velocity is inversely proportional to CSA
144
Q

what is the equation for linear velocity of an RBC through a tube?

A

velocity = Q/A (slower in wider vessels, faster in narrower vessels)
- Q = flow (volume of blood through vessel per unit time) -> constant
- A = CSA

145
Q

what is the hemodynamic equivalent for Ohm’s Law (V=IR)?

A

P=QR
- deltaP (driving force between 2 points -> large pressure gradient increases flow (Q))
- Q = flow in L/min
- R = resistance
- determines the flow for a given P
- most important variable that controls flow

146
Q

what 2 things determine resistance?

A
  • Poisuille’s Law
  • arrangement of the blood vessels
147
Q

what is Poisuille’s Law?

A

R=8nL/pir^4
- n = blood viscosity (constant; controlled by hematocrit)
- L = length of vessel (constant)
- r = radius (most important, not constant)

  • explains the importance of resistance determined by radius
148
Q

how does radius affect flow? how is radius regulated?

A
  • if P=QR then doubling the radius will increase Q by 16
  • radius affected by nerves, hormones, paracrines, metabolites
149
Q

how is the arrangement of blood vessels related to resistance?

A
  • blood vessels in series have higher resistance (R=R1+R2+R3)
    • one path for blood to travel
  • blood vessels in parallel have lower resistance (1/R=1/R1+1/R2+1/R3)
    • alternate paths for blood to travel
150
Q

what is compliance? what does high compliance mean?

A

compliance=change in volume/change in pressure
- high compliance implies high distensibility (stretchy)
- large volume change for a given pressure change
- high compliance decreases pulsatility of flow
- the vessel wall absorbs the cardiac pulse wave (Q =/ during diastole, makes output smoother rather than stopping and starting over -> reduces pulse pressure)

151
Q

what happens to compliance as we age? what does this entail?

A

compliance decreases with age; reduced compliance leads to:
- increases pulsatility
- impairs baroreflex function (senses BP)- contributes to hypertension with aging
- increases systolic pressure and afterload

152
Q

what are characteristics of arterioles?

A

1) resistance is high (small radius=high R - causes large P drop)
2) site of regulation of R - major determinant of flow (allows us to have lower pressure downstream which is important for gas exchange)

153
Q

why aren’t capillaries considered the major determinant of flow?

A

have the highest R but:
- they are in parallel
- R is not variable (r cannot be changed)

154
Q

how is thick filament unique in vascular smooth muscle?

A
  • low ability to break down ATP
  • site of contractile regulation (SMC contraction is thick filament regulated - in skeletal it is actin)
155
Q

how is thin filament unique in vascular smooth muscle?

A
  • no nebulin, TnI, TnC, TnT
  • calponin and caldesmon inhibit myosin-actin interactions
  • thin filaments anchor into dense bodies (irregular pattern, no striations)
156
Q

how do gap junctions present in SMCs?

A
  • multi unit (not coupled): do not required coordinated contraction or regulated flow, allow for distensibility
    (eg. aorta)
  • single unit (coupled): work together to change radius, etc. (eg. arterioles)
157
Q

what allows mechanical coupling between SMCs?

A

adherens junctions (dense plaques)

158
Q

how is VSM different than skeletal and cardiac muscle?

A
  • myofilaments occupy most of cytosol
  • few myofilaments near PM
  • actin:myosin > 6
  • smooth muscle cells can proliferate
159
Q

how are VSM organelles arranged differently from the heart?

A
  • SR is less regular (some associates with PM, some extends towards myofilaments)
  • caveoli instead of t-tubules (specialized lipid rafts)
    • contain Ca2+ channels and other ion channels
    • can localize signaling molecules
  • fewer mitochondria (glycolysis can support non-contractile ATP needs)
160
Q

how is Ca2+ use different in smooth muscle vs striated muscle?

A
  • striated: Ca2+ acts as a disinhibitor
  • smooth: Ca2+ directly activates contraction via MLCK
161
Q

how is MLC phosphorylation significant?

A
  • enables cross-bridge cycling (thick filament regulated)
  • relaxation requires MLC phosphatase (MLCP)
  • the system remains active even after Ca2+ elevations subside, if MLC remains phosphorylated -> sustained force
162
Q

what inhibits MLCP?

A

RhoA
- favours contraction
- Ca2+ sensitization

163
Q

what is the process of VSM contraction?

A
  • Ca2+ binds calmodulin
  • calmodulin changes configuration (becomes Ca-CaM)
  • Ca-CaM activates MLCK
  • MLCK phosphorylates regulatory MLC
  • actin-myosin cross-bridges
  • cross-bridge cycling and contraction
164
Q

what is the process of VSM relaxation?

A
  • MLCP and decreased Ca2+
  • dephosphorylates regulatory MLC
  • prevents new cross-bridges from forming
  • relaxation

BPK305 (3 decks)

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