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Physiology > phys review session #2 > Flashcards

phys review session #2 Flashcards

1
Q

ALS (Leu gherings)
-state physiologic cause

A

-caused by the degeneration of upper and lower motor neurons
-descending tracts become physically hardened

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2
Q

ascending pathways

A

go to spinal chord > synapse in 1st, 2nd, 3rd order neurons > post central gyri is final destination

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3
Q

what is the primary somatosensory cortex?

A

post central gyri

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4
Q

descending pathways

A

*talking motor

go to 2 neurons > then precentral gyrus > then to affected tissue

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5
Q

isotonic muscle contractions

A

-load remains constant as muscle changes
*eccentric and concentric
concentric= muscle shortens
eccentric= muscle lengthens

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6
Q

isokinetic contractions

A

-constant motion
-velocity remains constant as the muscle fibers shorten

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7
Q

isometric muscle contraction

A

-constant length
-muscle length remains constant as tension increases

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8
Q

what do bones function as

A

levers

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9
Q

what do joints function as

A

fulcrums

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10
Q

skeletal muscles provide _____ to _____ bones

A

force, move

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11
Q

what do muscle receptors do?

A

they provide afferent info needed to control skeletal muscle activity

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12
Q

function of muscle spindles

A

monitor muscle LENGTH

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13
Q

what do golgi tendon organs do?

A

detect changes in TENSION- found in tendons of muscle

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14
Q

stretch reflex

A

local negative feedback mechanism to sense and resist changes in muscle length when an additional load is applied

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15
Q

muscle spindle structures

A

-distributed throughout skeletal muscle
-each spindle innervated by efferent neuron
*intrafusal-y motor neuron
*extrafusal-a motor neuron

-afferent sensory endings
*annulospiral endings=central portion of INTRAFUSAL fibers
*secondary (flower spray) endings= ends of INTRAFUSAL fibers

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16
Q

hemiplegia

A

one side of motor cortex damaged

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17
Q

paraplegia

A

thoracic spinal chord damaged

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18
Q

decebrate and decorticate posturing (rigidity) caused by?

A

severe brain injuries
-descending motor tracts that control flexor muscles = destroyed
-descending motor tracts that control extensor muscles = spared

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19
Q

where will sensory info terminate?

A

post central gyrus

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20
Q

where will appropriate motor response originate?

A

pre central gyrus

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21
Q

NT released by pregang neurons of ANS

A

ACh to stimulate post gang neuron

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22
Q

what NT do sympathetic post gang neurons release?

A

norepinephrine

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23
Q

what NT do parasympathetic post gang neurons release?

A

Ach

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24
Q

nitric oxide

A

released by parasympathetic fibers in the penis, causes vasodilation and allows for erection

*binds to g coupled protein receptor

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25
Q

cholinergic receptors

A

bind to ach

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26
Q

muscarinic receptors

A

-Cardiac, smooth muscle, glands
-Bind ACh from parasympathetic postganglionic fibers
-GPCR’s that activate 2nd messenger pathways
-Excitatory or inhibitory

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27
Q

what is the motor unit of muscle contraction?

A

motor neuron and all the fibers it innervates

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28
Q

patellar tendon reflex

A

Stretching of muscle spindle of the quadriceps femoris results in contraction

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29
Q

cross extensor reflex
*type of withdrawal reflex

A

The crossed extensor reflex is a withdrawal reflex. The reflex occurs when the flexors in the withdrawing limb contract and the extensors relax, while in the other limb, the opposite occurs.

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30
Q

flexor withdrawal reflex

A

The flexor reflex is initiated by cutaneous receptors, involving an entire limb. This is exemplified by pulling the hand back from a hot object, via flexing of the arm

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31
Q

Parkinson’s disease

A

a progressive disorder that is caused by degeneration of nerve cells (dopaminergice fibers) in the part of the brain called the substantia nigra, which controls movement.

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32
Q

smooth muscle cross bridge cycle

A

-thin filaments lack troponin
-contraction relies on thick filaments (myosin-linked regulation)
-activation occurs when calcium binds to calmodulin
-this activates myosin light chain kinase (phosphorylates myosin)
-calcium is reduced and kinase is inactivated and myosin dephosphorylated
-smooth muscle relaxes

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33
Q

skeletal muscle contraction

A

-actin= where binding sites for myosin are; when tropomyosin blocks these sites the muscle is relaxed

-When Ca2+ binds to troponin, tropomyosin shifts away from binding site
-Once complex shifts, actin/myosin bind at cross-bridges
-Myosin heads “move” and muscle contracts results

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34
Q

nicotinic receptors

A

-on postganglionic cell bodies of all autonomic ganglia
-Receptors are Na+ & K+ channels
-Results in net depolarization and action potential.
-Excitatory

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35
Q

adrenergic receptors

A

Alpha (α) receptors:
α1 – excitatory
α2 -inhibitory
Beta (β) receptors:
β1 – excitatory
b2-inhibitory

*bind to epi and norepinephrine

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36
Q

propranolol- beta blockers

A

Competitive antagonists that block the receptor sites for epinephrine (adrenaline) and NE on adrenergic beta receptors.

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37
Q

atropine (anatagonist)

A

-Blocks effects of ACh at muscarinic receptors but not nicotinic receptors.
-Muscarinic junctions are parasympathetic (for this example, glands)
-Use to suppress salivary and bronchiole secretions before surgery without interfering with sympathetic activities (e.g., heart rate).

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38
Q

salbutamol (agonist)

A

Selectively activates β2 adrenergic receptors at low doses, causing dilation of the bronchioles in the treatment of asthma without stimulating the heart.

39
Q

sliding filament mechanism

A

-Thin filaments on side of sarcomere slide inward over stationary thick filaments toward center of A band during contraction
-As thin filaments slide inward, they pull Z lines closer together
Sarcomere shortens
-All sarcomeres throughout muscle fiber’s length shorten simultaneously
-Contraction is accomplished by thin filaments from opposite sides of each sarcomere sliding closer together between thick filaments

40
Q

what are the effects of calcium on the sliding filament theory?

A

increase Ca2+ starts filament sliding

decrease Ca2+ terminates sliding

41
Q

power stroke

A

-Sarcoplasmic reticulum releases Ca2+ into cytosol.
-Myosin, via ATP being hydrolyzed by ATPase is “cocked and ready” in a high energy state.
-Myosin head bind to actin, triggering the release of energy that has it “cocked and ready”.
-Myosin heads swivel toward center of sarcomere (power stroke) into a low energy state
-ATP binds to myosin head and detaches it from actin
-Hydrolysis of ATP transfers energy to myosin head and reorients it to being “cocked and ready”
-Contraction continues if ATP is available and Ca2+ level in sarcoplasm is high.

42
Q

what happens when sarcomere shortens

A

contraction *note this deals with sliding filament theory

43
Q

dicrotic notch

A

a disturbance in aortic pressure curve as a result of the closure of the aortic valve

44
Q

how does heart recieve blood?

A

diastoly

45
Q

systole

A

contracting and emptying

46
Q

diastole

A

relaxation and filling

47
Q

end diastolic volume

A

volume of blood in each ventricle at the end of diastole (~ 135 ml)

48
Q

isovolumetric ventricular contraction

A

Time during ventricular contraction when no blood can leave or enter heart, blood volume remains the same.

49
Q

stroke volume

A

Amount of blood pumped out of each ventricle with each contraction

50
Q

end systolic volume

A

volume of blood remaining in ventricles at the end of systole

51
Q

isometric ventricular relaxation

A

When semilunar valves close, ventricular pressure still exceeds atrial pressure, so all valves are closed. Blood volume remains the same.

52
Q

regions of sarcomere (functional unit in skeletal muscle)

A

A band: thick filaments with portions of thin filaments that overlap on both ends of thick filaments
H zone: Lighter area within middle of A band where thin filaments do not reach
M line: Extends vertically down middle of A band within center of H zone
I band: Remaining portion of thin filaments that do not project into A band

53
Q

T tubules

A

-Local depolarization activates them, triggering the opening of the abutting foot proteins.
-Continuous with sarcolemma – action potential on membrane also spreads down into T-tubule

54
Q

flow of blood through the heart

A

right:
vena cava > r atrium > triscuspid valve > r ventricle > pulmonary valve > pulmonary artery

left:
pulmonary veins > left atrium > mitral valve > left ventricle > aortic valve > aorta

55
Q

what vessels control bp and how?

A

arterioles because they can vasoconstrict and vasodilate due to circular smooth muscle

56
Q

how do you calculate pulse pressure

A

subtract diastolic pressure from systolic pressure

ex: 120/80 = 40 pulse pressure

57
Q

what causes congestive heart failure?

A

Deterioration of the ventricular muscle and remodeling of the heart wall that decreases chamber compliance and efficiency

*decreased vascular compliance

58
Q

precapillary sphincters

A

-surround capillaries
-circular smooth muscle
-Contraction of sphincters reduces blood flow into capillaries.
-Relaxation of sphincters has opposite effect

59
Q

local chemical influences of arteriolar radius

A

Local metabolic changes
Histamine release

60
Q

local physical influences of arteriolar radius

A

-Local application of heat or cold
-Chemical response to shear stress
-Stress on endothelial lining due to friction; Promotes release of NO
-Myogenic response to stretch

61
Q

where is blood flow constant?

A

brain

62
Q

active hyperemia

A

increased blood flow in response to enhanced organ activity.

63
Q

reactive hyperemia

A

When blood flow is occluded, chemical changes in tissues dilates arterioles. When flow is returned, blood flow is much higher than normal. (not always a good thing – reperfusion injury)

64
Q

blood supply of heart

A

has to be continuous

65
Q

ischemia

A

lack of blood to heart; coul dbe due to occlusion of coronary artery

66
Q

how to calculate cardiac output

A

heart rate x stroke volume

67
Q

pericardial sac

A

The pericardium is a fibrous sac that encloses the heart and great vessels. It keeps the heart in a stable location in the mediastinum, facilitates its movements, and separates it from the lungs and other mediastinal structures. It also supports physiological cardiac function

68
Q

purpose of pericardial fluid

A

basically frictionless environment for heart to contract and relax

69
Q

QRS complex

A

ventricular depolarization
*atrial repolarization happening at same time but not shown

70
Q

ST segment

A

shows when the ventricle is contracting but no electricity is flowing through it.

71
Q

P wave

A

atrial depolarization

72
Q

T wave

A

ventricular repolarization

73
Q

three groups of plasma proteins

A

Albumins
Globulins
-Alpha (α)
-Beta (β)
-Gamma (γ)
Fibrinogen
-Key factor in blood clotting

74
Q

what percent of a blood sample is made of plasma

A

55%

75
Q

what is plasma made of?

A

plasma proteins, electrolytes, lipids, carbohydrates

76
Q

erythrocytes

A

-Red blood cells (RBCs)
-Contain no nucleus, organelles, or ribosomes
-Structure is well suited to transport respiratory gases
-hemoglobin

77
Q

main function of WBCs

A

immunity

78
Q

hemoglobin

A

-Found only in red blood cells
-Pigment containing iron
-Appears reddish when oxygenated
-Appears bluish when deoxygenated

79
Q

2 parts of hemoglobin

A

-Globin portion
*Protein composed of four highly folded polypeptide chains

-Heme groups
*Four iron-containing nonprotein groups
*Each is bound to one of the polypeptides

80
Q

Erythropoiesis

A

-process of creating RBCs
-occurs in bone marrow
-Pluripotent stem cells (aka hemocytoblasts) in red bone marrow differentiate into the different types of blood cells

**erythropoetin required (mainly from kidneys)

81
Q

leukopoesis

A

-Leukopoiesis occurs varying rates depending on the body’s changing needs
-Granulocyte colony–stimulating factor stimulates increased replication and release of granulocytes
***Especially neutrophils from bone marrow

82
Q

thrombopoetin

A

Hormone produced by liver increases number of megakaryocytes and therefore increases platelet production

83
Q

2 general types of polycythemia

A

-Primary polycythemia= Caused by tumor-like condition of bone marrow *erythropoiesis proceeds at uncontrolled rate
*Increases blood viscosity, TPR
-Reduce oxygen delivery, overwork the heart, increase B.P.

-Secondary polycythemia= Erythropoietin-induced adaptive mechanism to improve blood’s oxygen-carrying capacity in response to prolonged reduced oxygen delivery to the tissues
*Occurs normally in people living at high altitudes

84
Q

how many clotting factors do we have?

A

13

85
Q

intrinsic vs extrinsic coagulation

A

intrinsic= activated by factors within blood stream
extrinsic= activated by tissue damage

86
Q

clotting factors associated with intrinsic and extrinsic coagulation

A

intrinsic= factor 12

extrinsic= tissue factor 3

*both activate factor 10

87
Q

factor 10 function

A

prothrombin > thrombin > fibrinogen > fibrin > proteins that intermesh due to factor 13 and forms clot

88
Q

neutrophils

A

-Phagocytic specialists
-Release web of extracellular fibers called neutrophil extracellular traps (NETs) that contain bacterialcidal compounds
-Can also destroy bacteria by phagocytosis

Functions :
-First defenders on scene of bacterial invasion
-Very important in inflammatory responses
-Housekeeping role

89
Q

dendritic cells

A

professional antigen presenting cells that inform the fight against invasive pathogens while enforcing tolerance to self and harmless environmental antigens. They capture pathogens and receive signals from pathogens that influence the outcome of immune responses.

90
Q

macrophages

A

effector cells of the innate immune system that phagocytose bacteria and secrete both pro-inflammatory and antimicrobial mediators. In addition, macrophages play an important role in eliminating diseased and damaged cells through their programmed cell death.

91
Q

esonophils

A

think allergic rxn and parasites

92
Q

basophils

A

Synthesize and store:
*Histamine=
Release is important in allergic reactions

*Heparin=
Speeds up removal of fat particles from blood after fatty meal

Can also prevent clotting of blood samples drawn for chemical analysis
Used extensively as anticoagulant drug

93
Q

blood types

A

blood group A – has A antigens on the red blood cells with anti-B antibodies in the plasma. blood group B – has B antigens with anti-A antibodies in the plasma. blood group O – has no antigens, but both anti-A and anti-B antibodies in the plasma. blood group AB – has both A and B antigens, but no antibodies.

Physiology (3 decks)

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