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ISBM > Exam #2_Semester 2 > Flashcards

Exam #2_Semester 2 Flashcards

1
Q

core of body

A
  • includes head, thorax, and abdomen
  • is the regulated variable
  • area of the core can change (very beneficial for temp maintenance)
  • maintained at 37 C
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2
Q

location of accurate body temp and why

A

tympanic membrane / infrared sensing on temporal lobe
- b/c shares arterial blood supply with hypothalamus and HT is center of regulatory activities that aim to maintain core temp

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3
Q

conduction

A

transfer of heat from hot object (body) to cooler object though direct contact (accounts of 40% of heat loss)

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4
Q

convection

A

heat loss from skin to air; due to air moment across skin

- air closest to skin is warmed through convection and then replaced by cooler air

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5
Q

sweat - hypo-osmotic (hypotonic) secretion from sweat glands

A

Sweat is hypo-osmotic (derived from ECF – 295 mmol/l; sweat is about half = 150 mmol/l))

We lose more water per volume than solute (fluid loss from EC compartment is main issue); however solute (electrolyte) loss is also occurring

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6
Q

mechanisms by which body produces heat

A

basal metabolic rate (75 kcal/hr)

extreme muscular activity (15-fold inc over basal rate) - not sustainable / energentically costly

shivering (3-5-fold inc over basal rate) - involuntary, can maintain longer

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7
Q

non-shivering thermogenesis

A

means of generating heat metabolically without shivering

involves uncoupling of the ETC and ATPsynthase activity in brown fat

Thermogenin acts as an inner mitochondrial membrane proton channel that serves to reduce the proton gradient across this membrane.

Cellular adenylate charge drops as a result and an increase in cellular metabolic activity follows producing heat.

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8
Q

brown fat

A

unique adipose tissue that expresses uncoupling protein (thermogenin) under control of thyroid hormone

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9
Q

thermoreceptors

A

have both cold and warm receptors in skin; increase or decrease firing frequency depending on skin temp
- poorly adapting receptors - provide constant input

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10
Q

preoptic anterior hypothalamus (POAH)

A

heat loss center

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11
Q

posterior hypothalamus

A

heat gain center

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12
Q

cost of a fever

A

each 1 degree C elevation:

  • 13% inc. in O2 consumption
  • inc. caloric requirement
  • inc. fluid requirment
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13
Q

factors effecting cardiac output

A

Cardiac factors:

  • HR (beats/min)
  • contractility: targeted by inotropic agents

Coupling factors
- preload and afterload

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14
Q

preload

A

diastolic filling of ventricles (inc. beneficial up to a point)

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15
Q

treatment used to target preload

A

diuretics

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16
Q

treatment used to target contractility of myocardium

A

positive inotropic agents

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17
Q

afterload

A

aortic pressure (inc. detrimental to cardiac output)

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18
Q

compliance

A

change in volume for a given change in pressure (veins are more compliant)

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19
Q

chronotropic

A

effect rate of the heartbeat

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20
Q

inotropic

A

effect the force of the heartbeat (can be positive or negative)

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21
Q

SNS receptors

A

adrenergic receptors mediating response of Norepi

act though g proteins (2nd messenger systems)

beta 1: Gs, inc. cAMP, PKA, phosphorylation

  • inc. cardiac contractility
  • dec. SM contractility of vasculature

alpha 1: Gq, inc. IP3

  • dec. cardiac contractility
  • inc. SM contractility of vasculature
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22
Q

cardiac cycle

A

Cardiac cycle is composed of the electrical, mechanical, pressure & volume events that occur in the heart during one contraction (includes contractile and relaxation events)

Electrical→contractile→pressure→volume

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23
Q

systole

A

onset and duration of ventricular contraction (contractile period)
- ends with closure of aortic valve

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24
Q

diastole

A

relaxation of the ventricular myocardium (atrial contraction), longer duration than systole but variable
- begins with end of systole and ends at onset of next systolic period

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25
Q

lactoferrin

A

protein synthesized in response to IL-1

  • binds free iron (Fe2+)
  • bacterial growth is dependent on availability of free Fe and, thus, is inhibited
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26
Q

pressure regurgitation

A

pressure increase in LV so high that it can transduce through the A-V valve (mitral) and register as LA pressure increase (even higher than when atria contract!)
- ends with aortic valve opens

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27
Q

Dicrotic Notch

A

result of the closing aortic valve at very beginning of diastole
- small increase in aortic pressure

28
Q

isovolemic contractile period (ICP)

A

period between mitral valve closure and aortic valve opening where pressure rapidly builds (0→80 mm Hg; in systole) but LV volume is not changing
- occurs at onset of systole

29
Q

rapid ejection phase

A

dramatic drop in LV volume resulting from the opening of the aortic valve and continued inc. in LV pressure

  • Initial ejection is faster, followed by a slower ejection phase near end of systole
  • period b/t ICP and IRP
30
Q

isovolemic relaxation period (IRP)

A

begins when the aortic valve closes, and encompasses a span of time when there is no volume change in LV (large dec. in pressure)

  • A-V (mitral) valves not open yet since LA pressure still lower than the LV pressure
  • occurs at onset of diastole
31
Q

stroke volume (SV)

A

EDV - ESV
EDV = end diastolic vol
ESV = end systolic vol

32
Q

ejection fraction (EV)

A

SV (EDV-ESV) / EDV

  • percentage of blood ejected per contraction
  • important measure of cardiac function
33
Q

what is the myocardium always working against

A

pressure in aorta

34
Q

cardiac glycosides

A

appropriate tx for CHF
• Inhibit Ca extrusion indirectly by inhibiting the Na/K-ATPase pump and thus diminishing the Na+ gradient needed to power this anti-port mechanism (inc. in intracellular Na)
• Positive inotropic agents – maintain higher levels of myoplasmic free Ca2+ levels, resulting in greater force generation and a raise in dP/dT (rate of force generation)

35
Q

sinus rhythm of the heart

A

electrical activity determines rate of heart

- emanating from the sino-atrial node (located at the junction of the RA and superior Vena Cava)

36
Q

Ca-channel blockers - effect on myocardium

A

Decreased plateau phase duration = dec. overall AP duration = decreased force generated

  • negative inotropic effects
  • dose dependent (more blocker = greater dec in force)
37
Q

maximum diastolic potential

A

moment of peak polarity (hyper polar) in nodal cell - not maintained
- point of regulation: can make this even more hyper polarized = longer distance to achieve threshold = slow HR

38
Q

compliance

A

change in vol. that occurs with incremental change in pressure (vessels ability to stretch)
- decreased with age

39
Q

transmural pressure (TP)

A

difference in pressure existing across the wall (pressure inside vascular structure v. pressure outside vascular structure)
- positive TP must be present for flow to occur through vessel

40
Q

critical closing pressure

A

internal pressure at which a blood vessel collapses and closes completely

  • consequence of drop of pressure in vasculature
  • transmural pressure (TP) has dropped to 0 – no patency
  • if blood pressure falls below critical closing pressure, then the vessels collapse
41
Q

why does blood continually flow through capillaries during both systole and diastole

A

aortic compliance
- elastic recoil of aorta (due to compliance) during diastole results in continuous flow of blood through the capillaries during both systole and diastole

42
Q

mean arterial pressure (MAP)

A

Arterial pressure is constantly changing

  • MAP is average pressure integrated across an entire cardiac cycle
  • this is what we are talking about when we discuss ΔP (change in MAP) - driving force
  • regulated variable!

MAP = diastolic pressure + 1/3 pulse pressure

43
Q

pulse pressure

A

systolic pressure - diastolic pressure

44
Q

MAP - how to estimate

A

MAP = diastolic pressure + 1/3 pulse pressure

45
Q

basal tone

A

non-neurologically (or hormonally) dictated contractile activity within the vasculature (SM contraction creates tone)
- creates passive resistance

46
Q

resting sympathetic tone

A

always level of resistance above basal tone imparted by SNS on the vasculature

  • creates active resistance
  • Norepi response
47
Q

oncotic pressure

A

osmotic pressure due to presence of protein within vasculature or EC space
- remains constant in vasculature

48
Q

hydrostatic pressure

A

pressure created by fluid inside vasculature

- decreases as vessel diameter decreases (less fluid)

49
Q

specific permeability

A

relative ease with which a substance moves out of the capillaries

  • decreases as molecular weight and radius of molecule increases
  • large molecule = lower permeability
50
Q

Net filtration pressure (NFP)

A

pressure generated that determine fluid movement and exchange
- the starling forces

51
Q

hypoproteinemia

A
  • low levels of protein within plasma (blood in vasculature) impacts oncotic pressure
  • radical shift in starling forces – huge shift of positive NFP – driving fluid out of vasculature
  • malnourishment (low protein) – distended stomachs (Kwashiorkor)
52
Q

flow-limited distribution

A

exchange of nutrients and wastes across capillaries is limited by flow of the blood

  • diffusion is efficient
  • exchange is limited by rate of blood flow
  • occurs in healthy situation
53
Q

diffusion-limited distribution

A

results in greater distance between capillary and cell, resulting in decreased efficiency of diffusion

  • occurs in peripheral edema (expanded ISF)
  • exchange is limited by rate of diffusion
  • occurs in unhealthy situation
54
Q

auto-regulation

A

blunted response of flow to pressure changes (mainly from 60-140mmHg)

  • intrinsic mechanism that limits flow in the face of increasing pressures – results in more constant flow in these organs
  • less effect of SNS on pressure / flow in these organs
  • kidney, brain, liver, heart
55
Q

reactive hyperemia

A
  • occlude flow for brief period, when flow is resumed it is at an elevated level that tapers off back to baseline
  • Increase in flow (hyperemia) is a consequence of the reactivity of the vasculature (vasodilate to allow transient inc. in flow)
  • effect of local metabolites (adenosine, K+, etc.)
56
Q

rectifying current

A

K current (inward) involved in plateau and maintaining the resting membrane potential

57
Q

role of lymphatics

A

Present in all tissues except bone, cartilage, CNS and epithelium

Serves to return fluid from the ECF to the circulatory system

Nutrient absorption in the GI tract

58
Q

drivers of lymphatic flow (4)

A

o Increased capillary hydrostatic pressure (HP) (exercise)
o Increased capillary permeability (leakiness)
o Increased ISF [protein], which increases ISF / tissue oncotic pressure, drawing fluid into the ISF
o Decreased capillary oncotic pressure

59
Q

effect of taking a deep breath

A

reduces several pressures that increase VR

Intra-thoracic pressure (ITP) drops as we inhale (intra-thoracic volume increases = dec. in ITP)
• RA pressure (RAP) drops with drop in ITP
• Pressure in jugular vein (JVP) drops too

Results in transient, large increase in SVCF (superior vena cava flow) = increase in venous return

60
Q

what happens to BP when you stand and why

A

large inc. in pressure below myocardium and large dec. in pressure above myocardium
- gravity has large impact on fluid volume - plays a huge role in transmural pressures

61
Q

what effect does walking have on venous pressures and why

A

phasic contraction of skeletal muscle drops venous pressures since muscles pump fluid back into central portion of vasculature system

62
Q

What drives delivery of O2 to the heart?

A

entirely driven by blood flow

  • heart has high A-V O2 difference, meaning that it utilizes a lot of O2
  • heart is an aerobic organ
63
Q

factors that influence oxygen consumption of the myocardium (heart)

A

Ventricular wall tension
• Increased wall thickness→increased wall tension→increased O2 consumption

Heart rate:
• More quickly heart is contracting = greater O2 requirement

Velocity of fiber shortening (dP/dt)
• Greater velocity
• Hint: can think about catecholamines driving O2 requirement for myocardium (they inc. HR and force of contraction (dP/dt))

Peak tension developed

64
Q

phospholamban

A

protein that typically decreases rate at which SERCA pump re-sequesters free Ca+2
- phosphorylated = less inhibition of SERCA and greater rate of re-sequestration

65
Q

two effects of Ach on heart rate

A

Ach binds M2 receptors (activate Gi and dec cAMP)

  • diminished If (inward cAMP dependent Na current) by reducing conductance of HCN channels (slows phase 4)
  • activated Ach-activated K channels and K efflux occurs, causing further hyper-polarization (further from threshold)

OVERALL: dec. HR

66
Q

factors that influence arterial blood pressure

A

physical factors:

  • blood volume
  • vessel compliance (dec. with age)

physiological factors:

  • cardiac output (HR x SV)
  • peripheral resistance

ISBM (7 decks)

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