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BUPA Physiology > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Sound of turbulent flow in the heart

A

Murmur

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2
Q

What is the sarcoplasmic reticulum’s role during depolarization?

A

The t-tubules lie in apposition to the terminal sacs/cisternae of the SR, which is triggered to flood the muscle with Ca+2 after a depolarization —> contraction

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3
Q

What happens to ventricular systole and diastole during exercise/high heart rates?

A

The time period of filling and ejection decreases; atrial systole becomes more important

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4
Q

What are some characteristics of smooth vs. cardiac vs. skeletal muscle?

A

Skeletal - many nuclei; striated fibers

Cardiac - one/two nuclei; striated disc; gap junctions

Smooth muscle - not striated; gap junction

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5
Q

What are the most muscular vessels in the body and why?

A

Arterioles, they dictate blood flow

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6
Q

Why are thick filaments considered bipolar?

A

Because the base myosin is attached tail to tail and subsequent myosins are built off of it

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7
Q

What has a higher distensibility, arteries or veins?

A

Veins

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8
Q

Which pacemaker has the highest rate of electrical activity in the heart?

A

SA node

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9
Q

Inactive form of fibrin that is always in circulation

A

Fibrinogen

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10
Q

What is secreted by healthy endothelial cells that causes vasodilation? How do one of these also regulate platelets?

A

Nitric Oxide

Prostacyclin - inhibits platelet aggregation

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11
Q

What do the different waves of the electrocardiogram correlate to?

A

P wave - atrial contraction/systole/depolarization

QRS complex - ventricular contraction/isovolumetric contraction/depolarization

T wave - ventricular relaxation/diastole/ repolarization

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12
Q

The displacement of blood per unit time

A

Flow velocity

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13
Q

What are the actions of angiotensin II?

A

Increases BP by:

  • arteriole vasoconstriction
  • NE release
  • aldosterone release (promotes renal retention)
  • stimulates thirst
  • stimulates ADH release (promotes H2O retention)
  • stimulates pressor area in medulla
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14
Q

What is the main function of the cardiopulmonary feedFORWARD receptors?

A

They respond to “anticipated” changes/events

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15
Q

What protease cleaves fibrinogen to fibrin?

A

Thrombin

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16
Q

Smooth muscle contraction reaction to stretch

A

Stretch-activation reflex

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17
Q

What is the release reaction of platelets?

A

Exocytosis of granule contents upon platelet adhesion

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18
Q

What effect does distending pressure have on stretch sensitive cationic channels?

A

Increasing distending pressure —> stretch receptors activated —> membrane depolarized —> tension increases

Vice versa: decreased activation moves membrane potential away from threshold

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19
Q

What is hypertrophic cardiomyopathy?

A

The heart can’t contract normally so it tries to compensate by developing more mass —> leads to smaller ventricles and decreases cardiac output

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20
Q

What would happen to MAP and flow (CO) if you increased heart rate?

A 
MAP = increased
CO = increased
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21
Q

What post-translational modification MUST be present on relevant clotting factors to allow Ca+2 to bind?

A

the conversion of one carboxylate (-COOH) to TWO ionized -COO-

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22
Q

How are blood samples manipulated to prevent clotting?

A

Blood tube contains Ca+2 chelator (EDTA, citrate) that binds up all the Ca+2

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23
Q

How do platelets change after “sticking”?

A
  • Express various receptors
  • Bind other platelets
  • Changes from disc to thin and spread out
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24
Q

If cross sectional area is inversely proportional to velocity, then why do capillaries have the lowest velocity?

A

Because despite the smallest radius, they have the largest TOTAL area

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25
Q

What are the 3 main steps of hemostasis?

A
  1. Vasoconstriction
  2. Platelet plug formation
  3. Fibrin clot
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26
Q

What factors are associated with hemophilia?

A

Factor IX and VIII

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27
Q

Describe the feedback reflex of the arterial baroreceptors during increased BP.

A

Increase BP —> increased firing of baroreceptors —> activates NTS —> activation of X and D (inhibition of P) —> increased vagal stimulation —> decreased heart rate and contractility

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28
Q

Relay station in the medulla for all cardiovascular input

A

NTS (nucleus of the solitary tract)

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29
Q

Why are veins called capacitance vessels?

A

Due to their high compliance, most of the blood at any one time is in the veins

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30
Q

What is the largest factor contributing to venous return?

A

Vis a tergo - “push from behind” due to heart pumping more blood through circulation

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31
Q

How do myosin crossbridges power filament sliding?

A

Myosin heads pivot when attached to actin filaments as they release the products of ATP hydrolysis

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32
Q

the pressure against which the heart must work to eject blood during systole

A

Afterload

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33
Q

Binds thick filament to the Z line

A

Titin

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34
Q

contains desmosomes and gap junctions; connects muscle cells and allows easy communication

A

Intercollated disk

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35
Q

Why are early activation components not as vital as the later-action components?

A

There are two pathways that converge into a common pathway —> if you lose one of the earlier pathways there is still another back up pathway

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36
Q

What is the baseline for D and P?

A

At baseline, P is firing to increase BP to maintain/prioritize blood supply to heart and brain (otherwise the body would shunt blood everywhere else).

*Stimulation of D inhibits P

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37
Q

What determines the tension developed in smooth muscle?

A

Frequency of spike activity (many Ca2+ dependent action potentials)

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38
Q

What are the main parts of the cardiovascular control center and what are their roles?

A

NTS - input relay station
X - cardio-inhibitory center (location of vagal a cell bodies)
D - depressors; decrease BP
P - pressors; increase BP

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39
Q

What does the phosphorylation of troponin I do?

A

Increases offloading of Ca+2 from Troponin C WITHOUT any affect on force

Decreased affinity of TnC for Ca+2 —> increases influx of Ca+2 back in SR —> decreased duration of contraction

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40
Q

What are the effects on epinephrine on the veins?

A

It binds to alpha-1 and increases venous tone

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41
Q

Provide a molecular track for the myosin crossbridge “engine” while stimulating the myosin ATPase

A

Actin “thin” filament

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42
Q

What is the equation for flow?

A

Q = deltaP/R

DeltaP = change in pressure
R = resistance
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43
Q

In a series arrangement, the greatest pressure drop is in which segment?

A

The segment with the highest resistance

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44
Q

How can threshold be reaching in GI smooth muscle to cause an action potential?

A

Stretch
Hormones
Nerve stimulation (vagal)

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45
Q

What pathway initiates the clotting cascade?

A

Extrinsic pathway

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46
Q

What is characteristic of laminar flow?

A

It have a parabolic velocity

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47
Q

What are the 3rd/4th heart sounds and what is unique about them?

A

They occur during filling and atrial systole; can be auscultated in children but not adults generally

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48
Q

What affect do cardiopulmonary receptors and arterial baroreceptors have on ADH release from the posterior pituitary?

A

Normal activation of CP and baroreceptors leads to tonic inhibition of ADH

Inactivation of these receptors leads to removal of inhibition of ADH (aka. ADH release)

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49
Q

What are the 3 proteins of troponin and what are their roles?

A

Troponin T - links troponin to tropomyosin
Troponin I - inhibits the interaction of myosin and actin
Troponin C - binds Ca+2 to relieve troponin I inhibition

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50
Q

Describe the changes in pressure as you move inferiority down the body.

A

The pressure is 1 mmH20 higher for every 1 cm below the heart

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51
Q

What would happen if you removed troponin/tropomyosin?

A

The myosin would be able to bind to the actin without calcium

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52
Q

Describe the feed forward mechanism when you lift your feet in the air?

A

Lift legs —> pressure in veins drops below ATM pressure —> veins collapse —> Increased venous return (no change in arterial pressure) —> cardiopulmonary receptors (right atrium) activated —> flow in aorta increases (decreased resistance via dilation) to keep pressure decreased

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53
Q

The amount of blood in the ventricle immediately before a contraction begins

A

End diastolic volume (EDV)

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54
Q

What is released by damaged tissue to activate the extrinsic pathway? What does it bind to/activate?

A

Tissue thromboplastin (tissue factor)

Binds to factor VII (with Ca+2, protein, and phospholipid) to activate factor X

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55
Q

Amount of blood ejected with each contraction

A

Stroke volume

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56
Q

What happens to baroreceptors with chronic hypertension?

A

They get pushed further into the wall and the threshold for firing decreases

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57
Q

What is the hemodynamic equation for CO?

A

CO = (Paorta - PRA)/TPR

Paorta = pressure of aorta
PRA = pressure of right atrium
TPR = total peripheral resistance
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58
Q

How is smooth muscle able to shorten extensively (up to 30%)?

A

Side-polar filaments prevent extreme overlap and also actin is not restricted by collisions with Z-bands

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59
Q

What are the effects of epinephrine on the heart?

A

It binds to beta-1 and increases HR and contractility

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60
Q

How does the afterload affect stroke volume?

A
  • aortic pressure
  • decreases ejection velocity
  • less shortening leads to lower SV
  • increases latent period (more pressure —> takes more time to generate)
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61
Q

What changes will leads to increased arterial pressure?

A
  • increased SV
  • increased ejection velocity
  • increased TPR
  • increased diastolic pressure
  • increased HR
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62
Q

What would happen to MAP and flow (CO) if you increased venous tone?

A 
MAP = increased
CO = increased
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63
Q

What is the role of NE on veins?

A
  • increases venous tension
  • decreases compliance
  • raises venous pressure
  • increases venous return
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64
Q

The theory that there is a basal tone in smooth muscle with an oscillating membrane

A

Myotonic hypothesis

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65
Q

What is the equation for flow velocity?

A

V = Q/A

A = cross sectional area

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66
Q

What does and doesn’t shorten during contraction in a sarcomere?

A

Shortens: I band, H zone

Remains the same: A band

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67
Q

How does calcium regulate phosphorylation of light chains on myosin?

A

Ca+2 enters cells —> binds calmodulin —> complex activates myosin light chain kinase (MLCK) —> myosin kinase phosphorylates light chains on myosin —> crossbridge binds toactin

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68
Q

What happens when there is a loss of secondary hemostasis?

A

*platelet plug is too weak

Formation of platelet plug —> vasoconstriction wanes —> pressure increases —> plug breaks —> more platelets deposit —> process repeats

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69
Q

If overlap of thick and thin filaments is directly proportional to force, than why does extreme overlap lead to decreased force?

A

The thick filament sees the myosin from opposite half of sarcomere which is in the wrong direction, thus decreasing force

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70
Q

Contraction in which the muscle stays the same length; at high load with maximized force

A

Isometric

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71
Q

Firm mechanical attached net between cardiac cells

A

Desmasomes

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72
Q

The sound of the aortic valve closing

A

2nd heart sound (DUB)

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73
Q

Contraction in which the muscle shortens; at high load with maximized force

A

Isotonic

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74
Q

How does warfarin inhibit clotting?

A

It binds competitively to enzymes responsible for post-translational modification of relevant factor —> changes inhibit Ca+2 from binding to the factors

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75
Q

What is the equation for Poiseuille’s Law for resistance? Which is the most important value?

A

R = 8nL/(pi*r^4)

n = viscosity 
L = length
r = radius (most important)

*Can plug into Q=deltaP/R

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76
Q

Fraction of blood ejected from ventricle

A

Ejection fraction

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77
Q

How does the stretch-activation reflex work?

A
  • no hormonal influence
  • dissension —> stretch-activated channels —> local depolarization (Na+, Ca+2, and Mg+2) —> voltage-gated Ca+ channel opening
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78
Q

What substances are required to activate prothrombin?

A

Ca+2
Activated factor X
Platelet phospholipids (from release reaction)

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79
Q

What are some factors that can change compliance of vessels?

A
  • Change in V or
  • Sympathetic stimulation
  • Age
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80
Q

At what steps of the intrinsic clotting cascade is Ca+2 required?

A
  • Activation of Factor IX
  • Activation of Factor X
  • Activation of prothrombin
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81
Q

Where are platelets formed? Where are they found in the body?

A

Formed in bone marrow from megakaryocytes; always in circulation

82
Q

What are the 3 sets of machinery involved in the first step of hemostasis?

A
  1. Neurogenic - pain response/reflex
  2. Myogenic - smooth muscle contraction (fast)
  3. Humoral - local substance release (slower)
83
Q

What would happen to MAP and flow (CO) if you increased contractility?

A 
MAP = increased
CO = increased
84
Q

What would happen if you eliminated complete neural input to the heart? What does this indicate?

A

The heart rate would increase — indicates that the PARASYMPATHETIC system has a dominant effect

85
Q

What would happen to MAP and flow (CO) if you increased TPR?

A 
MAP = increased
CO = decreased
86
Q

Subthreshold oscillation that occurs with a frequency of 3-4 cycles per min in the smooth muscles of the body and antrum of the stomach (peristaltic waves); caused by pacemaker cells

A

base electrical rhythm (BER) or slow wave frequency

87
Q

What does activation of beta-1 receptors by EPI in the heart do?

A

Increases the activity of funny channels —> increases time to depolarization —> increases HR

88
Q

Why does the AV node have a slower rate of electrical activity than the SA node?

A

It has a less stable membrane

89
Q

Fibrous structure that supports the heart valves, electrically separates the atrium and ventricle, and acts as the base

A

Annulus fibrosis

90
Q

What is the equation for cardiac output?

A

CO = HR * SV

91
Q

the filling pressure of the heart at the end of diastole (tension at the muscle at EDV)

A

Preload

92
Q

What happens when these is loss of primary hemostasis?

A

The body is unable to plug up normal nicks/dings and it leads to thrombocytopenic purpura

93
Q

Muscle plasma membrane (contains many myofibrils)

A

Sarcolemma

94
Q

Contains thick and thin filaments

A

A band

95
Q

What happens during the different phases of the ventricular AP?

A

0: opening of voltage-gated Na+ channels

1 (peak): inactivation of Na+ channels and activation of some K+ channels

2 (plateau): slow+prolonged opening of voltage-gated Ca+2 channels (LTCCs) AND closure of potassium channels

3: opening of K+ channels
4: sustained open state of potassium channels

96
Q

Puts in covalent bonds into the fibrin polymers of a clot to strengthen them

A

Fibrin Stabilizing Factor (Factor XIII)

97
Q

What is the equation for stroke volume?

A

SV = EDV - ESV

98
Q

The % change in volume per unit pressure change. Equation?

A

Distensibility

D*V = C

99
Q

ATP utilization via stimulation of skeletal muscle has what affect on: pO2, pCO2, pH, K+, adenosine?

A 
pO2 - decreased
pCO2 - increased
pH - decreased
K+ - increased (due to multiple APs)
adenosine - increased (byproduct of ATP usage)
100
Q

The term used for when the aorta distends (systole) and contracts (diastole) to propel blood after the aortic valve closes

A

Windkessel Effect

101
Q

What is the effect of epinephrine on muscle?

A

BOTH alpha-1 and beta-2 present in muscle; epinephrine has a higher affinity for beta-2

Low doses: binds to beta-2 and dilates
High doses: binds to alpha-1 (which has faster conducting fibers) and constricts

102
Q

What does the Frank-Starling Law state?

A

The more blood the heart gets during filling, the more it ejects (ESV does not change)

103
Q

What is the difference between the intrinsic and extrinsic pathways of the clotting cascade?

A

Extrinsic has component that are outside the blood and is the first one to be activated while the intrinsic components are all circulating in the blood in inactivated form and are activated by the extrinsic pathway

104
Q

Flow of blood from the heart

A

Cardiac output

105
Q

What are the roles of troponin and tropomyosin?

A

Tropomyosin covers 7 actins linked end-to-end and Troponin blocks the binding site for myosin. When Ca+2 binds troponin, troponin moves tropomyosin unblocks the myosin binding site on actin

106
Q

What happens to compliance and pressure as a patient ages?

A

Compliance decreases and small volume changes lead to higher changes in pressure; increased pulse pressure (despite little change in MAP)

107
Q

What is released during the release reaction of platelets?

A
  • Ca+2 - part of clotting cascade
  • Serotonin - vasoconstriction
  • ADP - increases platelet aggregation
  • Enzymes that act on platelet phospholipids to produce thomboxane A2 - vasoconstriction and platelet aggregation
108
Q

What is true about troponin/tropomyosin in smooth muscle?

A

Tropomyosin is located on actin but troponin is NOT

109
Q

What are the INTRINSIC mechanisms that cause arteriolar vasodilation?

A
  • hyperpolarization of smooth muscle by opening K+ channels
  • reduction of intracellular Ca+2 by increasing SR Ca+2 uptake
  • direct inhibition of smooth muscle contractile proteins via inhibition of myosin crossbridge
110
Q

In a parallel arrangement, which segment has the largest flow?

A

The segment with the smallest resistance

111
Q

What is the renin-angiotensin cascade?

A

Liver makes angiotensin
Kidneys make renin

In circulation: angiotensinogen clipped by renin to produce angiotensin I —> ACE (in capillaries of the lung) removes 2 nucleotides from angiotensin 1 to make angiotensin II

112
Q

How does contractility affect SV?

A
  • sympathetic stimulation (EPI)
  • increased tension/force (rate and amount)
  • decreases time of contractile period
113
Q

Lie between the longitudinal and circular smooth muscle layers of GI muscle; intrinsically control smooth muscle contractions (synapses with vagus nerve)

A

Myenteric or Auerbach’s plexus

114
Q

What is the role of the parasympathetic system on the cardiovascular system?

A

It is not involved in BP regulation/cardiovascular system

115
Q

What is the equation for ejection fraction?

A

EF = SV/ESV

116
Q

What are the sizes of different lesions caused by loss of hemostasis?

A
  • petechiae (small)
  • purpura (medium)
  • ecchymoses (large)
117
Q

What causes the pressure gradient that moves food through the small intestines?

A

Higher frequency of BER contractions in earlier parts of the intestine (duodenum)

118
Q

What is the equation for pulse pressure?

A

PP = Psys - Pdia

119
Q

What happens during the different phases of the pacemaker AP?

A

0: rapid opening of voltage-gated Ca+2 channels (LTCC) —> rapid depolarization
3: reopening of potassium channels + closing of calcium channels —> repolarization
4: K+ permeability decreases + F-type Na+ (and some K+) “leaks” through (funny) channels + Ca+2 is moving through T channels (subthreshold depolarization)

120
Q

Why are arteries good at storing pressure?

A

They have low compliance —> small volume change = large pressure change

121
Q

What is the slow step of myosin cycling in the absence of actin? What does actin do?

A

M-ADP-P —> M + ATP

Actin is an activator of myosin ATPase and accelerates this step

122
Q

What are some factors that can affect CO via SV? What type of effects are these?

A

Contractility (via sympathetic activity)
Preload (via EDV)
Afterload (via arterial pressure)

Inotropic effects

123
Q

What are the effects on epinephrine on arterioles?

A

BOTH alpha-1 and beta-2 are present in arterioles so it’s tissue-dependent

124
Q

What happens when there is no ATP?

A

Muscle becomes stiff because all cross bridges are attached (rigor mortis)

125
Q

Second membrane system that encases each individual myofibril

A

Sarcoplasmic reticulum

126
Q

The amount of blood in the ventricle after contraction and before filling

A

end systolic volume (ESV)

127
Q

Why are veins good at storing volume?

A

20x more compliant than arteries —> need to have much more volume to cause small pressure change

128
Q

What kind of channels activate cardiac muscle?

A

Ionotropic

129
Q

The enzyme that makes the post-translation modification that allows Ca+2 to bind to clotting factors requires what?

A

Vitamin K

130
Q

Sound of the mitral valve closing

A

1st heart sound (LUB)

131
Q

Describe the sequence of cardiac muscle activation?

A

Beta-1 receptor in gap junction stimulated —> increased cAMP —>PKA activated —> T-tubule depolarized —> L type Ca+2 Channel opens (LTCC) —> influx of Ca+2 into sarcolemma —> RyR2 channel activated (voltage-gated) —> Ca+2 efflux from the sarcoplasmic reticulum —> activation of cardiac muscle

132
Q

What is the role of the parasympathetic system on the heart?

A

Decreases heart rate and contractility via the vagus nerve

133
Q

What are some factors that can affect CO via HR? What type of effects are these?

A

Parasympathetic/sympathetic activity

Chronotropic effects

134
Q

What is the equation for CO using MAP?

A

CO = MAP/TPR

*MAP = Paorta - PRA

135
Q

What is the dominant regulator of contractility?

A

Increases/decreases in sympathetic activity

136
Q

acts on kidney and promotes Na+2 retention; also affects anything that carries sodium out of the body (sweat glands, tear glands, etc.)

A

Aldosterone

137
Q

Carries the depolarization from the sarcolemma to the interior of the muscle

A

t (transverse) tubules

138
Q

End of one Z line to the next Z line

A

Sarcomere

139
Q

What is associated with the latch state of smooth muscle?

A

A drop in Ca+2

140
Q

What is the equation for Reynold’s number for determining turbulent flow?

A

Nr = pDV/n

p = density
D = diameter
V = velocity
n = viscosity

The hight Reynold’s #, the more turbulent

141
Q

In a parallel arrangement, what are the equations for total flow, total change in pressure, and total resistance?

A

Qt = QA + QA + QA

*Pt = PA =PB = *PC

1/(RT = RA + RB + RC)

142
Q

Where is renin produced?

A

Juxtaglomerular cells in glomeruli of the kidneys

143
Q

What calcium channels are located in the skeletal muscle? Cardiac?

A

Skeletal - Rhy1 receptors

Cardiac - Rhy 2 receptors; requires extracellular calcium

144
Q

How much blood tends to pool in the venous system do to gravity?

A

About 500ml on average

145
Q

What regulates myosin activity in smooth muscle?

A

Phosphorylation of constituent myosin light-chain subunits (indirectly regulated by Ca+2)

146
Q

What factors affect venous return?

A
  • vis a tergo
  • skeletal muscle pumps
  • valves
  • respiratory pump (thoracic cavity pressure)
  • rapid ejection of ventricles (base moves down and increase atrial volume)
  • venomotor tone
147
Q

What are the neurotransmitters involved in smooth muscle control?

A

Excitatory - Ach

Inhibitory - ATP, VIP, NO, EPI

148
Q

Describe the crossbridge movement of myosin along actin.

A

Myosin head bound to actin angled —> +ATP —> head pivot straight and releases actin —> +Ca+2 —> head binds to actin straight —> -ADP —> head (staying bound) powerstroke to an angle

149
Q

Contains only thin filaments

A

I band

150
Q

How are platelets made and what are they composed of?

A

They are pinched off pieces of the cytoplasm of megakaryocyte; no nucleus or intracellular structures; full of granules

151
Q

What is the main factor affecting ESV?

A

Contractility

152
Q

What is the equation for mean arterial pressure?

A

MAP = Pdia + 1/3PP

153
Q

What would a VWF deficiency result in?

A
  • deficit in platelet adhesion
  • easily bruised
  • worsened by aspirin
154
Q

What is the frequency of the intestinal BER?

A

12/min in the duodenum
8/min in the ileum

*Intestines have their own set of pacemakers

155
Q

Sound of turbulent flow anywhere but the heart

A

Bruit

156
Q

What is secreted by healthy endothelial cells that causes vasoconstriction?

A

Endothelin

157
Q

What is a characteristic of smooth muscle myoactin ATPase?

A

It is about 1/10th slower than in cardiac/skeletal muscle (does not decrease force though!)

158
Q

What does the phosphorylation of phosphalomban do?

A

Relaxation of muscle occurs faster.

It DECREASES PL’s inhibition of Ca+2-ATPase —> increased influx of Ca+2 back into the SR —> decreased duration of contraction

159
Q

Insertion of fibrin to make a strong clot

A

Coagulation

160
Q

Inactive precursor of thrombin; always in circulation

A

Prothrombin

161
Q

What are the functions of the ANP (atrial natriuretic peptide)?

A

Decreases BP:

  • blocks Ach release from preGSNs
  • inhibits alpha-1 receptors (decreased sensitivity to NE)
  • inhibits renin synthesis
  • inhibits Pressor area in medulla
  • inhibits aldosterone
  • inhibits renal Na+ retention
162
Q

What is the flow of each ion during systole (small/negligible, in, out)?

A 
Na+ = in
K+ = small
Ca++ = out

Makes the membrane more positive (depolarization)

163
Q

What is a characteristic of parasympathetic innervation of the heart (vagus) that is not seen in sympathetic innervation?

A

The diastolic potential is more negative in parasympathetic innervation where as there is no change in sympathetic innervation

164
Q

Describe the pacemaker activity of smooth muscle/

A

Smooth muscle cells are part of a functional syncitium (via electrical gap junctions) and function as a “single unit”

165
Q

Why can’t cardiac muscle twitch?

A

Because of the prolonged duration of L type Ca+2 channel current

166
Q

What are unique characteristics of smooth muscle actin and myosin filaments?

A
  • disordered distribution; interspersed throughout cell
  • Actin: inserts into dense bodies (scattered) and dense plaques (attached to cell membrane)
  • not bipolar but “side-polar” cross-bridges; eliminates issue with extreme overlap
167
Q

What causes platelets to adhere to a site of injury?

A

bind to Von Willibrand factor (produced by epithelial cells) —> complex binds to exposed collagen —> platelets sticking —> Release Reaction

168
Q

Strong, fibrous, cabling that forms the body of a clot

A

Fibrin

169
Q

In a series arrangement, what are the equations for total flow, total change in pressure, and total resistance?

A

Qtotal = QA = QB = QC

*Ptotal = *PA + *PB + *PC

Rtotal = RA + RB + RC

170
Q

What effect does increased contractility have on the Frank-Sterling curve?

A

It shifts it up because SV is higher so EDV is also higher

171
Q

What if the mechanism of action of fibrin?

A

Fibrin monomers spontaneously polymerize —> long chains of fibrin polymer —> anchor to surface of platelets and tissue —> form cabling system —> stabilized by Factor XIII

172
Q

What are desmasones made up of?

A

Adhering

173
Q

What is the mechanism of the Frank-Sterling Law?

A

More stretch leads to more overlap in sarcomere so during contraction which leads to greater force of contraction

174
Q

What occurs during the flight-or-fight response?

A
  • pressor activation of heart, veins, and arterioles
  • dilation of vessels to brain, heart, and skeletal muscle (EPI)
  • inhibition of NTS so its unresponsive to baroreceptors
175
Q

What is the flow of each ion during diastole (small/negligible, in, out)?

A 
Na+ = small
K+ = out
Ca++ = small

Makes the membrane more negative (hyperpolarization)

176
Q

What happens to blood pressure when pressure/height is increased?

A

It increases initial but then results to baseline (vessels autoregulate BP via intrinsic mechanisms)

177
Q

What is a normal ejection fraction?

A

50%-67% at rest

178
Q

What are some differences between the motor neuron (pacemaker) AP and ventricular AP?

A

Motor Neuron:

  • brief AP
  • uses funny channels
  • AP over before contraction begins
  • brief refractory period (can tetanize)

Ventricular:

  • prolonged AP
  • AP is as long as contraction
  • longer duration
  • longer refractory period (can’t tetanize)
179
Q

Where are the main baroreceptors located?

A

Between the media and adventitia of the aortic arch and carotid sinus

180
Q

What is a characteristic of smooth muscle contraction?

A

It contracts slowly and topically (prolonged contraction)

181
Q

What are the two main ATPase pump in sarcomere?

A
  • Na+/K+ pump to maintain cell gradient

- Sarcomere pump to pump Ca+2 back into SR

182
Q

Where do the P and D centers project and what function do they have?

A

P —> (+)preGSN —> decreased release of ACh on postGSN —> increased release of NE on heart/veins/arteries

D —> (-)preGSN —> increased release of ACh on postGSN —> decreased release of NE on heart/veins/arteries

183
Q

Opposite reaction of stretch-activation

A

Stress-relaxation

184
Q

Shortage of thrombocytes

A

Thrombocytopenic purpura

185
Q

unconnected/closed gap junctions

A

Hemichannels

186
Q

What is the dominant regulator of heart rate at rest?

A

Vagal stimulation (but sympathetic stimulation contributes as well)

187
Q

Low resistant connections in cardiac muscle made up of connexin

A

Gap junctions

188
Q

Protein in circulation that binds and inhibits thrombin and other activated factors

A

Antithrombin III

189
Q

How does heparin inhibit clotting?

A

It enhances the activity of antithrombin III x1000

190
Q

Protein activated by thrombin-protein thrombomodulin complex that limits clotting

A

Protein C

191
Q

What happens when thrombin binds to thrombomodulin ?

A

Thrombomodulin (receptor on endothelial cells) binds thrombin —> thrombin loses procoagulant activity —> activates protein C —> protein C binds protein S —> inhibits factors VIII and V

192
Q

Clot limiting factor produced by endothelial cells that binds to “VIIa:tissue factor complex”, inhibiting the tissue factor pathway

A

Tissue factor pathway inhibitor (TFPI)

193
Q

What is the inactive form of plasmin?

A

Plasminogen

194
Q

How is plasmin activated? What is it’s role?

A

Activated by tPA produced by endothelial cells

Degrades both fibrin and fibrinogen (anticoagulant; clot buster)

195
Q

How does thrombin overcome the quick action of TFPI?

A

It has a positive feedback on the intrinsic pathway (Factors XI and VIIIa) and extrinsic pathway (Factor V)

196
Q

How doe aspirin work?

A

Aspirin inhibits cyclooxygenase (released from platelets), which normally gives rise to Thromboxane A2 (which causes platelet adhesion/aggregation and vasoconstriction)

Binds irreversibly so it takes days to recover

197
Q

What is the hydrostatic pressure gradient and its equation?

A

Water trying to leave the capillary

Pcap - Pif

198
Q

What is the oncotic pressure gradient and its equation?

A

Water trying to enter the capillaries

  • (PIcap - PIif)
199
Q

What is hydraulic permeability and what is the equation?

A

Permeability of membrane to the water

F = Kf [(Pcap - Pif) - (PIcap - PIif)]

Kf = permeability of capillary to water

200
Q

What occurs when hydrostatic pressure is higher than oncotic?

A

Filtration (fluid out)

201
Q

What occurs when oncotic pressure is higher than hydrostatic?

A

Reabsorbtion (fluid flows in)

BUPA Physiology (3 decks)

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