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Physiology > Exam 1 (Cardio) > Flashcards

Exam 1 (Cardio) Flashcards

1
Q

Effect of BoTX

A

Affect synaptic transmission via disruption of SNARE proteins.

Cause flaccid paralysis and autonomic symptoms, affecting peripheral cholinergic fibers.

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2
Q

Effect of TeTX

A

Affect synaptic transmission via disruption of SNARE proteins.

Mainly taken up by inhibitory neurons in the spinal cord resulting in lethal spastic paralysis.

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3
Q

EPSP

A

Excitatory Postsynaptic Potentials

Release Ach or glutamate. Increase probability of AP

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4
Q

IPSP

A

Inhibitory Postsynaptic Potentials

Release glycine or GABA. Reduce probability of AP occurring. Allow for CHLORIDE to rush in and RMP gets stuck at 65 (Cl- potential)

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5
Q

Sarin gas works by…

A

Inhibiting AChE and causing death via overstimulation

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6
Q

Cardiac E-C coupling vs Skeletal vs Smooth

A

CARDIAC: AP –> L-type Ca2+ into T-tubules –> Ca2+ activation of DHPR –> RYR activation –> Ca2+ release from SR –> cross-bridge formation

SKELETAL: AP travels into T-tubules –> voltage based activation of DHPR –> RYR activation –> Ca2+ release from SR –> cross-bridge formation

SMOOTH: Some stimulation (AP to voltage gated Ca2+ channel; Hormone or NT to IP3 or Ligand gated Ca2+ channel) –> Ca2+ influx –> Ca2+ binding to calmodulin –> Myosin kinase activation–> contraction –> myosin phosphatase –> relaxation

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7
Q

3 general requirements for re-entry of excitation

A

(1) GEOMETRY for a conduction loop
(2) SLOW or DELAYED conduction
(3) UNIDIRECTIONAL conduction block

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8
Q

alpha receptors

A

Located on vascular smooth muscle; causes vasoconstriction.

Coronary and cerebral vessels have little sympathetic vasoconstrictor innervation.

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9
Q

beta-1 receptors

A

primary adrenergic receptor on cardiac muscle; stimulates heart rate and contractility

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10
Q

beta-2 receptors

A

primarily located on vascular smooth muscle; causes vasodilation

secondary adrenergic receptor on cardiac muscle; stimulates heart rate and contractility

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11
Q

venous pressure

A

5

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12
Q

right atrial pressure (mean)

A

2

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13
Q

right ventricle pressure (systolic)

A

25

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14
Q

right ventricle pressure (end-diastolic)

A

2

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15
Q

Pulmonary artery pressure (systolic)

A

25

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16
Q

Pulmonary artery pressure (diastolic)

A

10

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17
Q

Pulmonary artery pressure (mean)

A

15

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18
Q

Pulmonary wedge pressure

A

Indirect measurement of left atrial pressure

6

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19
Q

Left atrial pressure (mean)

A

6

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20
Q

left ventricle pressure (systolic)

A

120

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21
Q

left ventricle pressure (diastolic)

A

6

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22
Q

Brachial artery pressure (mean)

A

95

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23
Q

Renin-Angiotensin- Aldosterone mechanism

A

Used for long-term regulation of blood pressure

Low arterial pressure –> baroreceptors (or sometimes directly sensed in renal arterioles) –> Renin release from renal JGA converts Angiotensinogen to Angiotensin I –> ACE in endothelial cells of the lungs and kidneys converts Angiotensin I to ANGIOTENSIN II

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24
Q

Angiotensin II Function

A
  • vasoconstriction of renal and systemic vessels
  • stimulates aldosterone release from adrenal cortex, leading to increased Na+ reabsorption in kidney
  • Acts on hypothalamus to stimulate thirst and ADH
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25
Q

Poiseuille’s Law (and the 2 associated laws) Don’t include constant values.

A

Used to determine flow

F= P/R

F= [(P1-P2) x r^4]/ L x viscosity

R = (L x viscosity)/ r^4

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26
Q

Laplace relationship

A

Used to determine wall tension

T= (Pxr)/ wall thickness

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27
Q

Cardiac Output

A

Heart rate x Stroke Volume

28
Q

Viscosity

A

Slipperiness

Shear stress/ shear rate …. or…. pressure/velocity

29
Q

Reynold’s number

A

Indicates likelihood of turbulent flow (NR > 3000)

Reynolds Number (NR)= [density(velocity)diameter]/viscosity

30
Q

a, c, and v waves (CARDIAC CYCLE)

A

a- pressure from atrial contraction

c- mitral valve bulging back into atria during ventricular contraction

v- caused by filling and emptying of atria (begins during isovolumic relaxation)

31
Q

physiological splitting

A

aortic valve closes slightly before pulmonic valve (exaggerated during inhalation)

32
Q

persistent splitting

A

caused by right bundle branch block

increases split between aortic valve and pulmonary

33
Q

paradoxical splitting

A

caused by left bundle branch block

pulmonary valve closes before aortic

34
Q

1st heart sound

A

closing of mitral (bicuspid) and tricuspid valves

35
Q

2nd heart sound

A

closing of aortic and pulmonary valves

36
Q

3rd heart sound

A

Pathological

Caused by rapid filling of a dilated ventricle (usually during cardiomyopathy)

37
Q

4th heart sound

A

A strong contraction of the atria, physiologically associated with athletes and children.

38
Q

Gallop

A

hearing the 1st, 2nd, and 3rd heart sounds

39
Q

Diastasis

A

Middle stage of diastole when passive filling has slowed but the atrial “kick” has not yet arrived.

40
Q

Relative atria pressure before and after birth and how that affects flow (no need for numerical values)

A

Right atria = higher pressure before birth

This allows flow through foramen ovale and keeps blood away from lungs. This decrease is caused by uterine contractions and eventual cord clamping.

After birth, left atria= higher pressure. This closes the foramen ovale

41
Q

What accounts for easier passage of blood into the pulmonary vasculature at birth?

A

With the first breath, alveoli are opened, pulmonary capillaries open and pulmonary vascular resistance drops.

42
Q

What causes decreased flow across the ductus arteriosus (connects pulmonary artery to aorta)? What causes its eventual closing

A

Increased systemic pressures (crying, moving, no placenta). Bradykinin produced in lungs causes its eventual closing.

43
Q

Apgar scale (categories + highest rating)

A

HR, RR, Color, Tone, Irritability (2 points max, so high of 10 points)

44
Q

CPP

A

Cerebral Perfusion Pressure

Mean arterial pressure - Intracranial venous pressure.

A decrease in MAP or an increase in Intracranial pressure can reduce cerebral perfusion pressure and cause ischemia.

45
Q

Agents which serve as vasodilators (especially in the brain)

A

Adenosine (released due to ischemia), K+, NO.

46
Q

Cushing Response

A

An elevation in intracranial pressure causes:

(1) Increased BP (due to sympathetics)
(2) Decreased HR (due to parasympathetics)
(3) Irregular respiration (due to brainstem damage)

47
Q

Autoregulation of pulmonary vessels

A

They DO NOT autoregulate

48
Q

Most important control factor for skin blood flow

A

Neural control (NOT metabolic)

49
Q

Apical skin

A

Present on nose, lips, hands, etc.

  • favors heat loss
  • contains specialized AV anastomoses called glomus bodies which facilitate heat loss
  • vasoconstricted at rest, vasodilates passively
50
Q

Nonapical skin

A
  • Lacks AV anastomoses
  • Exhibits vasodilation as sweat glands via sympathetic release of Ach
  • Also exhibit the usual NE induced vasoconstriction
51
Q

Mean Circulatory Pressure

A

Pmc. The mean pressure that exists in the circulatory system when cardiac output stops. It is the “fullness” of the system.

2 things influence it:

(1) absolute blood volume
(2) venous tone

52
Q

3 main points regarding splanchnic regulation

A

(1) Blood flow usually determined by rate of active transport of solutes across mucosal epithelium. Flow increases due to metabolism and increased O2 demand
(2) Sympathetics are the major neural control and cause constriction
(3) Parasympathetics cause INDIRECT stimulation of intestinal blood flow via increasing motility and glandular secretions

53
Q

Increased tone will cause what change to compliance?

A

Decreased compliance

54
Q

Physical characteristics of an artery

A

TUNICA INTIMA- connective tissue + internal elastic lamina
TUNICA MEDIA- smooth muscle and External Elastic Lamina
TUNICA ADVENTITIA- connective tissue + smooth muscle + vessels and innervation.

55
Q

Physical characteristics of a vein

A

TUNICA INTIMA- connective tissue
TUNICA MEDIA- very little smooth muscle
TUNICA ADVENTITIA- well developed connective tissue + little smooth muscle + vessels

56
Q

Prostacyclins

A

VASODILATOR

Increases cAMP to phosphorylate MLCK, inhibiting its functioning and decreasing actin-myosin interaction

57
Q

Endothelin

A

VASOCONSTRICTOR

Cause release of calcium via IP3, increasing calmodulin functioning therefore contraction.

58
Q

Chemoreceptor functioning

A

Primarily activated by low PO2, but also affected by high PCO2 or low pH.

Primarily involved with regulation of respiration

Cause increased HR and BP (via symp. stimulation and eventual blockage of para.)

59
Q

What organs have strong autoregulation? Weak autoregulation? Little to no autoregulation?

A

STRONG: heart, brain, kidneys, muscle
WEAK: splanchnic circulation
LITTLE: skin, lungs

60
Q

Factors which shift the cardiac function curve

A

Afterload and contractility

61
Q

Factors which shift the vascular (venous) function curve

A

Blood volume and venous tone

62
Q

Ductus venosus

A

Shunts blood from umbilical vein to IVC, bypassing liver

63
Q

Ductus arteriosus

A

Goes from pulm. artery to aorta, bypassing lungs

64
Q

Foramen Ovale

A

Shunt from right atria to left atria

65
Q

Titin connects which 2 parts of the sarcomere?

A

Z-line to M-line

66
Q

How does vagal nerve activity affect heart?

A

(1) increased special conduction and atrial K+ permeability
(2) Inhibits funny channels
(3) Inhibits slow Ca current

67
Q

Rheumatic fever can cause

A

Mitral stenosis

Physiology (12 decks)

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