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Mini 3 Physio, Anatomy, etc. > Physio > Flashcards

Physio Flashcards

1
Q

Tetrodotoxin (TTX)

A

Blocks vg Na channels (puffer fish)

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2
Q

Ciguatoxin

A

Lowers AP threshold (causing more AP firings)

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3
Q

Dendrotoxin

A

Blocks vg K channels (longer duration of AP)

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4
Q

Multiple sclerosis

A

Demyelination of CNS

Less AP conduction rate

Sensory abnormalities and motor problems

Smaller length constant and greater time constant

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5
Q

Botulism

A

Cleaves any SNARE protein preventing release of ACh

Skeletal muscle weakness and paralysis

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6
Q

Tetanus

A

Cleaves synaptobrevin

Tetanus

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7
Q

LEMS = Lambert-Eaton Myasthenic Syndrome

A

Ab formed against vg Ca++ channels at NMJ = skeletal muscle weakness

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8
Q

Curare

A

Binds N1/Nm receptor blocking ACh binding on motor end plate

Treatment = block ACh esterase

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9
Q

Neostigmine

A

Blocks acetylcholinesterase = enhancing ACh

Used to improve skeletal muscle function in myasthenia gravis

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10
Q

Hemicholinium

A

Blocks choline re uptake into NMJ

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11
Q

Poliomyelitis

A

Affects lower motor neurons of SOmatic nervous system = paralysis

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12
Q

Duchenne muscular dystrophy

A

Degeneration of skeletal and cardiac muscle = paralysis and death

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13
Q

Muscle hypertrophy

A

Increase in muscle fiber size due to increased activity or pharmacological agents

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14
Q

Lidocaine

A

Blocks vg Na channels (no depolarization = no AP)

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15
Q

Nerst Equation

A

Eion= 60/z x log ([ion]out/[ion]in)

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16
Q

K+ Em

A

-95mV

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17
Q

Cl-

A

-91mV

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18
Q

Ca2+

A

+132mV

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19
Q

Na+ Em

A

+65

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20
Q

What happens when spinal cord is severed above L1 in micturition reflex

A

Input from higher centers is eliminated, lower bladder capacity, frequent voiding and loss of voluntary control.

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21
Q

Lumbar center for bladder controlled via

A

Sympathetic;

Filling; beta 2 on detractor muscle via hypogastric nerve
Alpha 1 on IUS via hypogastric nerve for contraction

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22
Q

Sacral center for bladder controlled via

A

Parasympathetic

Voiding; M3 on detrusor for contraction via pelvic nerve
M3 on IUS for relaxation via pelvic nerve

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23
Q

Pudental nerve is:

A

Controlled by somatic NS and causes contraction via N1 receptor

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24
Q

Length constant equation

A

Lambda = square root of rm/ri

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25
Q

Time constant equation

A

T = rm x Cm

26
Q

Ejection Fraction

A

EF = SV/EDV x 100

27
Q

Two equations for MAP

A

MAP = CO x TPR

MAP = 1/3PP + diastole

28
Q

Pulse pressure equation

A

PP =systolic - diastolic

29
Q

Flow of vasculature equation (Q)

A

Q = deltaP / R

30
Q

Phasic contraction, what muscle and examples

A

Single unit smooth muscles

Stomach/intestines and esophagus and bladder

31
Q

Tonic contraction, what muscle and examples

A

Constant stimulation over time

Multi unit smooth muscle

Sphincters and blood vessels and airways

32
Q

Ca2+ sources for contraction of smooth muscle (5)

A 
Leak channels
DHP receptors (vg) - primary source
P2X receptor (ligand gated) ECM Ca2+ influx 
RyR receptors (LG)
IP3 Ca2+ release from SR
33
Q

Ca2+ lowering mechanisms for smooth muscle (3)

A

Call membrane Ca2+ ATPase
Na+/Ca2+ exchanger
SR membrane Ca2+ ATPase

34
Q

Players involved in SM contraction:

A

NO troponin

Light chain myosin
Calmodulin (CAM) –> Ca2+-CAM binds to myosin light chain kinase activating MLCK

35
Q

Latch state of smooth muscle

A

Slow myosin ATPase activity allowing a low level of smooth muscle tone utilizing minimal ATP (latch bridges)

Shortening velocity, phosphorylation and Ca2+ levels kept low

Only occurs in multi unit SM

36
Q

Max shortening velocity

A 
Slow fibers (I) myosin w low ATPase activity
Fast fibers (II) myosin w high ATPase activity
37
Q

Major pathway to form ATP

A

Oxidative fibers

Glycolysis fibers

38
Q

Type I skeletal muscle

A

Slow oxidative fibers

Dark
Recruited first
Smallest in diameter
Fatigue resistant (standing

39
Q

Type IIa Skeletal Muscle

A

Fast-oxidative-glycolytic fibers

Grey
Fast fatigue resistant (walking and running)

40
Q

Type IIb Skeletal Muscle

A

Fast-glycolysis fibers
White
Largest in diameter, recruited last (galloping and jumping)
Fast fatiguable

41
Q

Passive tension (preload)

A

Force generated by stretching connective tissue

No stimulation by somatic muscles

42
Q

Active tension (Afterload)

A

Force generated by contractile protein

With stimulation, cardiac/skeletal/smooth

43
Q

Supraventricular tachycardia and cause

A

HR > 100 beats/min, crammed QRS

Abnormal electrical conduction at SA or AV node

Beta blocker

Wolf Parkinson White Syndrome

44
Q

First degree AV block and cause

A

Long PR interval, with everything else normal

AV disease, high vagal tone (athletes), MI

Beta blocker, AcH inhibitor

45
Q

Second degree AV block and causes

A

Mobitz type I
Elongated PR interval with a drop in QRS, not consistent
AV node disease
Benign

Mobitz type II
Normal PR interval with a QRS ratio (count P waves)
His-Purkinje disease

Pacemaker

46
Q

Third degree AV block

A

Complete heart block
Atria and ventricles beat at own rate
Congenital

Pacemaker

47
Q

Atrial fibrillation

A

No clear pattern, No clear P waves, incomplete ventricle filling

48
Q

Lub sound

A

Start of systole when AV valve closes

49
Q

“Dub” sound

A

End of systole when AOrtic valve closes

50
Q

Starling equation

A

Net fluid movement = Kf x (Pc + #IF) - (Pif + #c)

Net force same without Kf

51
Q

Cardiogenic Shock

A

Inability of heart to pump sufficiently

Heart failure

Lower SV, lower CO –> decrease in MAP

52
Q

Hypovolemic Shock

A

Inadequate blood volume

I.e. Hemorrhage

Lower blood volume —> decrease MAP

53
Q

Anaphylactic/Septic Shock

A

Immunological response resulting in vasodilation

I.e. Allergic rxn (histamine)

Decrease central venous volume, decrease peripheral vascular tone NS TPR —-> decrease MAP

54
Q

Neurogenic Shock

A

Fall in sympathetic nerve activity of increase in parasympathetic activity due to trauma, etc.

Decrease TPR and peripheral vascular tone —> decrease in MAP

55
Q

Phase I of Valsalva

A

Aortic pressure: increase in pressure, mild increase SV

HR: decrease to compensate

56
Q

Phase II in Valsalva

A

Aortic Pressure: less blood flow to heart therefore reducing EDV, SV, CO, and systolic BP

HR: increase to compensate

57
Q

Phase III of Valsalva

A

Aortic pressure: released causing re-expansion of aortic and pulmonary vessels = fall in systolic BP, and relieve of compression in veins causing them to expand and fill w blood reducing amount going to heart

HR: slight increase

58
Q

Phase IV of Valsalva

A

Aortic pressure: expanded vessels are filled w blood and increase blood to heart increasing CO

HR: decrease, MAP back to normal

59
Q

Capacity Equations: (4)

A 
TLC = IRV + ERV + RV + TV
VC = TV + IRV + ERV
FRC = VC + ERV
IC = IRV + TV
60
Q

Minute Ventilation

Alveolar Ventilation

A

MV = TV x RR

AV = (TV-DS) x RR

61
Q

Transpulmonary Pressure

A

Pressure difference bw alveolar pressure and intrapleural pressure

62
Q

Airway resistance equation (Poiseulle’s Law)

A

R = 8nl/pie r^4

Mini 3 Physio, Anatomy, etc. (7 decks)

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