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Unit 2: LGS > Week 2 > Flashcards

Week 2 Flashcards

1
Q

What are motor neurons?

A

-innervates multiple fibers on same muscle

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2
Q

Motor unit

A

is when an alpha motor unit innervates 1 muscle fiber ??????

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3
Q

Patellar reflex response

A
  • 0 through 4

- 2 is considered normal

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4
Q

Patellar reflex response 0-2

  • what is reaction
  • normal
  • abnormal
A
  • 0: no reaction; 1: somewhat diminished, very small, no movement at joint; 2: average small movement
  • normal if equal reaction seen bilaterally
  • abnormal if reaction not seen bilaterally; problem in lower motor unit, disconnect from sensory nerve on
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5
Q

Patellar reflex response 3-4

  • what is reaction
  • normal
  • abnormal
A
  • 3: brisker than avg, medium movement at joint, but normal; 4: very brisk, hyperactive, large movement at joint with clonus
  • normal if equal reaction seen bilaterally; just really brisk due to hyper-reflexion
  • abnormal if reaction not seen bilaterally; problem in upper motor unit, disconnect from brain on down
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6
Q

What can cause hyper-reflexion?

A
  • clinical manifestations that cause hyper activity

- hyperthyroidism, pre-clampsia (hypertension in pregnancy)

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7
Q

Why is reflex necessary?

A

-protect joints from hyperextension

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8
Q

What is clonus?

A

-reflex constant–continued firing

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9
Q

What causes the patellar reflex?

A

-The stretch reflex

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10
Q

Stretch reflex location (4) and nerve root that corresponds

A
  • Patellar: L2-4
  • Achilles: S1
  • Biceps: C5-6
  • Triceps: C6-7
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11
Q

Static response

A

-steady-state; causes tone

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12
Q

Dynamic response

A

-velocity of change in muscle response

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13
Q

What kind of response is used in stretch reflex?

A

-dynamic response

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14
Q

Outline the stretch reflex

A

-stimulus–stretch patellar tendon–passive stretch of muscle spindles–sensory 1a neurons distorted–receptor potential generated–action potential sent through sensory fiber–alpha motor neuron discharged–contraction of extrafusal fibers (EPSP/IPSP)–muscle spindle unloads–sensory fibers start firing–gamma motor neuron activated–intrafusal fiber shorten–sensory 1a neurons stop sending signal–extrafusal muscle relaxes

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15
Q

EPSP

  • stand for
  • function
  • cause
A
  • excitatory response
  • depolarization
  • contraction
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16
Q

IPSP

  • stand for
  • function
  • cause
A
  • inhibitory response
  • inhibition of motor unit
  • leads to relaxation
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17
Q

Intrafusal fibers

A
  • smaller; contract at end but not in center
  • innervated by gamma motor neurons
  • shortening causes 1a sensory neurons to stop firing leading to relaxation
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18
Q

Extrafusal fibers

A
  • larger
  • innervated by alpha motor neuron
  • connected to interneuron
  • contraction leads to contraction of effector muscle; same with relaxation
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19
Q

Afferent fibers in muscle spindles

A
  • 1a: dynamic; signals for stretch reflex to occur

- II: static; causes muscle tone

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20
Q

Counterstrain technique

  • used on
  • nick name
  • type of technique
  • how it works
A
  • strained muscle: stretch reflex over stimulated
  • fold and hold
  • passive and indirect
  • bends patient to passively shorten extrinsic fibers causing muscle spindle to unload, activating gamma motor neuron, contracting intrafusal fibers, stopping sensory 1a neurons, allowing for fibers to relax; must hold for 90 seconds to reset gamma neurons
  • body to be returned to normal position slowly to ensure that gamma neurons are not re-triggered and normal reflex remains
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21
Q

Golgi tendon reflex

  • what does it do?
  • fiber
  • other name
A
  • senses tension and will force muscle to relax when muscle can no longer hold tension
  • uses 1b fiber
  • Inverse myotatic reflex
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22
Q

Inverse myotatic reflex

A

-tension too great–golgi organ stimulates sensory 1b fiber–generates IPSP (relaxation) on agonist AND EPSP (contraction) on anatagonist–contraction stops–muscle relaxes

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23
Q

Muscle energy

  • used on
  • type of technique
  • how it works
A
  • tense muscle that needs to be relaxed
  • active and direct
  • uses isometric contraction (tension) to activate golgi organ to stimulate 1b fiber causing relaxation of agonist
  • needs active motion because golgi body only responds to tension
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24
Q

Flexion reflex

A

stimulus occurs–EPSP interneurons stimulate alpha motor neuron to activate flexion of muscles on limb stimulus occurred AND– IPSP interneurons activate alpha motor neurons to inhibit antagonist extensor muscles–causes one or more joints to flex

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25
Q

Cross extension reflex

A
  • coupled to flexion reflex

- interneurons invoke opposite pattern of activity in contralateral side of spinal chord; extension of opposite limb

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26
Q

Iso metric movement

A

-same length; different tone

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27
Q

Iso tonic movement

A

-same tone; different length

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28
Q

Types of skeletal muscle

A

Type I and II

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29
Q

Type I

  • name
  • characteristics
  • examples
A
  • slow twitch
  • smaller, slower, decreased force
  • ex: posture, long distance running, writing
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30
Q

Type II

  • name
  • characteristics
  • examples
A
  • fast twitch
  • larger, bigger, more explosive
  • ex: squat, sprint
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31
Q

Recruitment

A

Slow: first to be used, low energy, high endurance
Intermediate: medium energy, medium endurance
Fast: last to be used, high energy, low endurance

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32
Q

How to regulate strength on contraction in skeletal muscles

A

spatial and temporal recruitment

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33
Q

Spatial

A

-increasing amount of motor neurons used–causing more fibers to be contracted

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34
Q

Temporal

A

-increasing amount of action potentials to fiber to cause increased movement

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35
Q

Tetanus

A

-continuous contraction of skeletal muscle–caused by increase in twitch without relaxation–full force movement

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36
Q

Relationship between length and force

-difference between skeletal and cardiac muscle

A
  • increase in length allows for increased amount of actin/myosin crossbridge formation which causes increased tension and increased force of contraction
  • skeletal muscle can be over stretched leading to no tension; cardiac cannot be over stretched
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37
Q

How does body try to prevent overstretching of muscle

A

tendon, only allows for muscle to be stretched so far unless it is ruptured

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38
Q

Relationship between velocity and force

-what counter velocity

A

The less load, the higher velocity able to be produced leading to increased force of contraction
-after load: load muscle has to work against making it slower

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39
Q

passive muscle movement

A

-allows for tone to exist which keeps muscles connected and in place

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40
Q

Muscle Types

A
  • Type I
  • Type II a
  • Type II b
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41
Q

Type I

  • type-why?
  • Kind of Respiration
  • Myoglobin-low/high; why?
  • What does it look like?-why?
  • Nutrient preference
  • Fatigue
A

• Slow twitch muscle fibers - b/c they have slow speed of contraction b/c smaller muscle fibers; dec. ATP hydrolysis
• Oxidative - means it undergoes aerobic metabolism to prod. It’s energy (TCA & ETC cycle meaning it takes longer and prod. More ATP)
• Gets more oxygen by having more myoglobin (1 unit) which pulls oxygen from blood; also inc. conc. Of capillaries which allows greater fusion to occur
• Vascularized - Look more red
• Prefer fats as their fuel source b/c you don’t want to use up all of blood glucose and these don’t have a lot of glycogen to begin w/
-Fatigue resistant

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42
Q

Type II a

  • type
  • respiration; why?
  • fatigue
  • ex
A

• Fast twitch
• use oxidative and glycolysis: unique b/c they can be resistant to fatigue; bigger diameter in muscle but don’t fatigue as easily (ex: ocular muscles)
-Intermediate Fatigue
-eye muscles

43
Q

Type II b

  • type-why?
  • Kind of Respiration
  • Myoglobin-low/high; why?
  • What does it look like?-why?
  • Nutrient preference
  • Fatigue
A

• Fast twitch - use glycolysis which is quicker to make ATP
-Anaerobic- do not use oxygen
• Low myoglobin; look kinda whitish
• glycogen (fast glycolytic) is a polymer of glucose which makes G1 P which then makes G6P which will then go into glycolysis
• Fatigue easily b/c of high lactic acid production

44
Q

Fatigue

A
  • depletion of fatty acids & glycolysis which will increase metabolites such as lactic acid and inorganic phosphate this will decrease sensitivity to calcium binding to troponin meaning calcium can’t bind and actin and myosin can’t bind so no cross-bridging can form so no tension
45
Q

What occurs with exercise training?

A

-Increase in the oxidative capacity of exercising muscles - mitochondrial number will increase

46
Q

What happens if PDH is decrease?

A

-Pyruvate cannot be turned into Acetyl-CoA; leading to decrease in TCA, ETC and increase in lactic acid

47
Q

How regular exercise increases oxidative capacity of exercising muscles

A

-More time spent training=more mitochondrial content, but it plateaus after 4/5 days of steady exercise

48
Q

What occurs with detraining? Retraining?

A
  • Mitochondrial content is decreased

- Mito content will increase, but it is harder than detraining

49
Q

Long/low impact exercise vs Short/high impact exercise

A
  • consistent mild exercise leads to steady state mitochondrial content; still beneficial because still allows for oxygen content systemically
  • with high exercise intensity the higher the increase in mitochondria content
50
Q

What kind of respiration does increased mitochondrial content push muscles towards?

A
  • aerobic metabolism meaning muscles will prefer fatty acids
  • Lots of acetyl co-A from fatty acid break down which goes to TCA which produces NADH meaning inc. of NADH into ETC
51
Q

What happens to NADH/NAD ratio with increased lipolysis?

A

-stays lows b/c even though more NADH being produced in TCA it is immediately going back into ETC; therefore muscle keeps using more and more fats

52
Q

How is creatine made?

A

-glycine and arginine in kidney will synthesize guanidino acedate (intermediate)–combines with S-adenosyl methionine in liver and is methylated
into creatine and arthinine (used in urea cycle)

53
Q

What does creatine do? How is it used?

A
  • stores high energy phosphate bond through formation of phosphocreatinine
  • Skeletal & cardiac muscles & neurons use phosphocreatine as an energy source (only for emergency demands bc only lasts for a couple of seconds)
54
Q

Importance of creatine kinase

A

-Creatine kinase will transfer phosphate from phosphocreatine to ADP to make ATP, turning it into creatinine which will be excreted in kidneys

55
Q

Kidney dysfunction and creatinine

A
  • elevated serum creatinine means there is low glomular filtration rate
  • elevated serum creatine means there can be damage to neuron, skeletal/cardiac muscles; if patient presents without heart/neuro systems then it will be damage to muscle–can also be seen with color of urine because of damaged myoglobin urea
56
Q

Hormones used to regulate metabolism during exercise

A

Epinephrine
Insulin
Glucagon
Cortisol

57
Q

Epinephrine regulating metabolism during exercise

A
  • produced from adrenal medulla which has affect on glycogenolysis in liver and skeletal muscles;
  • in liver glycogenolysis usually depends on glucagon levels
  • in skeletal muscle there is not receptors for glucagon and so glycogenolysis depends on cellular AMP levels
  • this is a sympathetic response, protein hormone
58
Q

Insulin regulating metabolism during exercise

A
  • regulates fuel metabolism
  • produced from beta cells of the endocrine pancreas
  • main stimulus of insulin production: inc. blood glucose (so right after eating) (anabolic bc cell will have a lot of sugar to make things)
59
Q

Glucagon regulating metabolism during exercise

A
  • regulates fuel metabolism; antagonist of insulin
  • produced from alpha cells of the endocrine pancreas
  • main stimulus of insulin production: decreased blood glucose (catabolic)
60
Q

Cortisol regulating metabolism during exercise

A
  • steroid hormone produced from adrenal cortex;
  • stimulated by stress, fight-flight, anger, anything that requires an emergency need so needs more glucose meaning it’ll increase glucagon production which will inc. glycogenolysis and gluconeogenosis to make more glucose
61
Q

2 processes that lead to production of glucose

A

Glycogenolysis and glyconeogenosis

62
Q

Fuel used by skeletal muscle

A
  • Glycogenolysis: Type II b
  • Blood borne fatty acid: beta oxidation, Type I
  • Blood borne glucose: to maintain glucose homeostasis in the blood 80-100 (neurons)
63
Q

Which cell will glycogenolysis stop at G6P?

A

-skeletal muscle, G6p will go into glycolysis

64
Q

Glycogenolysis

A
  • biochemical breakdown of glycogen to glucose
  • activated by low blood sugar
  • Rate limiting enzyme is glycogen phosphorylase–activated by AMP levels in muscles (epinephrine) and glucagon in liver
  • Glycogen storage is used up within 2 minutes and causes build up of lactic acid bc it is anaerobic; need to rest and allow for muscles to take in more glucose before starting exercise again
65
Q

Fatty Acid beta oxidation

A
  • occurs in mitochondria
  • end product is acteyl-Coa
  • rate limiting enzyme is Acetyl Co-A carboxylase bc it turns on malonyl CoA which inhibits fatty acid oxidation
  • high AMP will keep ACC low, turns off malonyl coA allowing for CPT1 to bring fatty acid into mitochondria where it will be broken down into acteyl CoA
66
Q

Glycolysis

A
  • Hexokinase will usually trap glucose from blood in cell by adding a phosphate but type II fibers have low hexokinase which limits their ability to use glucose from blood and instead forces them to use their glycogen
  • acetyl co A cannot be converted back to pyruvate immediately, only through formation of ketone bodies. However, acetyl-CoA can be converted back to fat
67
Q

Blood glucose level maintenance

A
  • liver
  • will make glucose through stimulate glycogenolysis by breaking down glycogen into G6P which is then broken down into glucose (muscle cannot go all the way back to glucose because does not have enzyme to break down g6p to glucose)
  • Can also make glucose from gluconeogenesis (glucose made from pyruvate, glycerol, AA (alanine), lactate)
68
Q

Blood glucose level and exercise

A
  • basal level: mid level demand for glucose, 75% made from glycogenolysis, 25% from gluconeogensis
  • 40 min exercise: high level demand for glucose, increase in glycogenolysis and gluconeogenesis but total amnt sugar made from gluconeogenesis is at 23%
  • 240 minutes of exercise: high level demand for glucose, cannot keep up, glycogenolysis drops down, gluconeogenesis tries to compensate by elevating but can only provide for 45% glucose
69
Q

Muscle recruitment

A
  • Type 1 is recruited more b/c its smaller than type II and does not fatigue as easily,
  • Type 2 will be recruited b/c need bigger muscles
70
Q

Coordinated training

A
  • repetitive motion

- uses type I to not fatigue easily, don’t need a lot of force

71
Q

Lower intensity/endurance

A
  • want type I muscles that do not fatigue easily

- walk, bike, ride, long distance

72
Q

Strength training

A
  • want type II muscles because need more energy
  • uses more mitochondria because more muscles are needed to contract to make motion
  • weight lifting
73
Q

How to delay muscle soreness

A
  • caused by lactic acid build up

- best way is to stretch type II muscle

74
Q

Protocol for patient exercise

A
  • beginners: low intensity, long amount of time

- advanced: high intensity, short amount of time

75
Q

Can you train to recruit different types of fibers

A

yes, recruit different fibers at different times

76
Q

Cardiac muscle metabolism

A
  • aerobic
  • fatty acid/lactate (RBC and skeletal muscle)
  • lactate oxidized to pyruvate to acetyl CoA to TCA/ETC
  • utilizes very little glucose bc need to maintain blood glucose homeostasis
77
Q

Cardiac ischemia

  • how is it caused
  • what is serious consequence
A
  • lack of blood flow to myocardium due to blockage of coronary arteries which decreases perfusion and oxygen delivered to myocardium
  • infarct: cell death, longer blood flow is locked the more cell death that occurs
78
Q

How metabolism changes in ischemic heart?

A

-Blockage of blood flow = less oxygen = cardiac muscles will switch to anaerobic metabolism of blood glucose leading to production of lactic acid

79
Q

Reprofusion injury

A

-When O2 is re-introduced then myocardium will be able participate in fatty acid oxidation (aerobic) which will go into TCA = Inc. NADH = build up of NADH and acetyl CoA = block PDH = anaerobic metabolism despite presence of oxygen which will increase lactic acid production which will lower pH and damage myocardium even more

80
Q

GABA

A
  • is the chief inhibitory neurotransmitter in the central nervous system.
  • role is reducing neuronal excitability throughout the nervous system
  • Excessive amounts lead to inhibition of muscle contraction
  • Its release is increased with alcohol
81
Q

Alpha 2 receptors

A
  • in the presynaptic cleft
  • inhibits sympathetic activity
  • agonists of these receptors will reduce sympathetic output
82
Q

NMDA

A
  • glutamate receptor/ excitatory
  • needs binding of glycine and glutamate; as well as depolarization
  • opens ion channel to Na,Ca, K;
  • blocked by magnesium and needs multiple stimulation to be activated
  • receptor for neuropathic pain
83
Q

Glutamate neurotransmitter

A

mediates the majority of excitatory synaptic transmission throughout the central nervous system

84
Q

Crystal meth

A

stimulant, induce hallucination, most addictive drug, blocks re-uptake neurotransmitters and increases neurotransmitter release

85
Q

Succinylcholine

  • used for?
  • how?
  • side effects?
  • duration?
  • contraindication
A
  • used for rapid intubation– depolarizing paralytic
  • Induces action potential causing contraction of all muscles in body; leading to relaxation and does not allow for re-polarization which inhibits muscles being able to contract again
  • cells can be ruptured with all muscles contracting at the same time; will see increase in K creating an increase in the T-wave
  • 2 minutes to take effect; lasts 15-20 minutes
  • 1 in 2000 have a gene that does not allow for metabolization of this drug and can lead to uncontrolled Ca release and malignant hyperthermia
86
Q

Dantrolene

  • used for
  • how
  • side effects
A
  • used to treat malignant hyperthermia
  • binds to rynaidine receptor subtype 1 causing decrease in release of Ca from SR; eventually allowing for decrease in Ca in cell and relaxation of muscle
  • if given improperly, will cause muscle weakness
87
Q

Celecoxib

  • what is it
  • contraindications
A
  • NSAID; selective for Cox 2 inhibition
  • cannot be given to patients with high risk of clots bc. vasodilation would be inhibited and only cox 1 which has thrombolitic effect would be left; therefore this could lead to higher chances of clot forming
88
Q

Cox 1

A
  • converts arachadonic acid into prostaglandin which leads to inflammatory response in damaged tissue
  • increased thrombilitic effect due to platelet aggregation
  • allows for proliferation of protective lining in GI
89
Q

Cox 2

A
  • converts arachadonic acid into prostaglandin which leads to inflammatory response in damaged tissue
  • allows for vasodilation
90
Q

Atopic individual

  • NSAIDS?
  • Alt. treatment
A
  • person who is hyperallergic
  • cannot take NSAID due to risk of exacerbating asthma
  • For patients with minor injury use RICE protocol for inflammation and acetaminophen for pain
91
Q

How does NSAID effect asthmatics?

A

inhibition of COX-1 enzyme, leads to decrease in production of thromboxane and some anti-inflammatory prostaglandins, which results in the overproduction of pro-inflammatory leukotrienes to cause severe exacerbations of asthma and allergy-like symptoms

92
Q

Naproxen vs Ibuprofen

A

-both are non-selective cox inhibitors
-N: half life of 14-16 hrs
I: half life of 4-6 hrs
-If naproxen is taken by asthmatic individual will take longer amount of time to get rid of and cause asthma symptoms for longer amount of time

93
Q

Depomedrol

  • type
  • effect
  • contraindications
A
  • glucocorticoid (steroid), can cause elevated sugar
  • used only for inflammation
  • diabetics, especially if uncontrolled
94
Q

Ibuprofen

  • type
  • effect
  • contraindications after surgery
A
  • NSAID; non-selective COX inhibitor
  • pain and inflammation
  • cannot be bloody surgery bc med is anticoagulant (due to inhibition of COX1)
  • can cause GI problems (treat with PPI)
  • metabolized in kidney
95
Q

Hydrocodone

  • type
  • effect
  • side effect
A
  • opioid
  • analgesic only, does not reduce inflammation
  • can cause constipation and CNS depression
96
Q

Acetaminophen

A
  • analgesic/antipyretic
  • will not help with inflammation
  • metabolized in liver
97
Q

Indomethacin

A
  • NSAID
  • very potent–good for chronic pain cause can be given in smaller dosage
  • aceitic acid derivative
98
Q

Diclofenac

A
  • NSAID
  • aceitic acid derivative
  • enteric coated (protects gut)
99
Q

NSAID induced nephritis

A
  • due to taking NSAID chronically
  • stop NSAID and side effects should reverse
  • if patient still needing pain relief try Diclofenac (topical/injectable) or Acetaminophen and RICE
100
Q

Cyclobenzaprine

A
  • muscle relaxant
  • no definitive MOA;
  • metabolized in the liver (good for patients with kidney failure)
101
Q

Tramadol

A
  • mixed drug; can be used for pain or depression
  • mild opoiod effects, blocks re-uptake of serotonin and nor-epi
  • alpha 2 agonist effects
  • effects modulation of ascending pain signal making it more dull
102
Q

Kidney failure side effects

A
  • anemia–lack of EPO being able to create RBC
  • Increased BUN/creatinine
  • decreased GFR
  • hypoalbuminemia: bc peeing protein out
  • NO NSAIDS
103
Q

How do capsaicin, arnica, tiger balm, icy hot, and bio-freeze work?

  • how applied? how often?
  • how long to reach efficacy?
  • contraindications
A
  • Neuromascaraders: distract brain from pain by introducing hot/cold sensation
  • topical; need to be put on a couple times a day
  • takes two weeks to reach full effect
  • surgery–can have blood thinning properties
104
Q

NSAID

A
  • nonsteroidal anti-inflammatory drug
  • Ibuprofen: non selective
  • Celecoxib: cox 2 selective
  • Diclofenac: aceitic acid derivative; low load of toxicity
  • Indomethacin: aceitic acid derivative; very potent

Unit 2: LGS (5 decks)

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