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HES 311 > Midterm 1 > Flashcards

Midterm 1 Flashcards

1
Q

Pathophysiology

A

study of the physiological changes in the body as a result of disease or injury

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2
Q

leading causes of death in canada

A
  1. cancer
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3
Q

Males life expectancy at birth

A

79 years

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4
Q

Females life expectancy at birth

A

84 years

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5
Q

Health adjusted life expectancy males

A

69 years

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6
Q

Health adjusted life expectancy females

A

70 years

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7
Q

ethology definition

A

the study of the causes of disease

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8
Q

common etiological factors

A

Genetics
- Congenital defects
- Microorganisms (viruses, bacteria)
- Immune dysfunction
- Metabolic dysfunction
- Degenerative changes
- Burns, radiation, other trauma, inflammation
- Other environmental factors
- Nutritional deficiencies or excess

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9
Q

Idiopathic

A

cause of disease is unkown

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10
Q

iatrogenic

A

treatment, procedure/ error that caused the disease

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11
Q

predisposing factors

A

risk factors/behaviours that promote the development of disease

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12
Q

prophylaxis

A

measures taken to preserve health and prevent onset or progression of disease

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13
Q

Disease onset can be _ or _

A

acute or insidious (gradual)

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14
Q

disease itself can be _ or _

A

acute or chronic

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15
Q

diseases can be classified by

A

stages, states, and periods

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16
Q

incubation period

A

time between infection and onset of symptoms

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17
Q

subclinical state

A

disease in it’s earliest stages

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18
Q

prodromal period

A

feels mild symptoms but infection not yet progressed to fullest

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19
Q

Clinical manifestations of disease

A

signs/symptoms

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20
Q

disease can be classified based on

A

remissions and exacerbations

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21
Q

Some diseases have symptoms triggered by

A

precipitating factors

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22
Q

disease prognosis

A

probability of recovery vs other outcomes

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23
Q

prevalence

A

all cases (new and pre-existing)

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24
Q

Incidence

A

limited to new cases only

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25
Q

Morbidity

A

state of being unhealthy

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26
Q

mortality

A

number of deaths that occur

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27
Q

NCD

A

not spread from person to person

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28
Q

Communicable diseases

A

infections that can be spread from person to person

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29
Q

epidemic

A

higher than normal (or expected) number of cases of an infection disease within a given area

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30
Q

pandemic

A

higher numbers around the world

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31
Q

endemic

A

disease regularly found among particular population or in certain area

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32
Q

cellular changes can be

A

temporary or permanent

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33
Q

examples of how cellular changes can happen

A
  • hormones, environment
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34
Q

what can changes in DNA lead to

A
  • permanent changes in structure and function, tissue damage, tumors
  • damage due to changes in metabolic processes, ATP production, pH
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35
Q

atrophy cell changes caused by

A

not enough use of cells
- cells get squashed and small

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36
Q

hypertrophy cell changes caused by

A

overuse of cells
- large cells

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37
Q

hyperplasia cell changes caused by

A

increase in cell division
- increased number of cells in a tissue

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38
Q

metaplasia

A

one mature cell type replaced by a different mature cell type

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39
Q

dysplasia

A

cells vary in size, shape (mitotic rate)

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40
Q

Neoplasia

A

uncontrolled/abnormal growth

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41
Q

benign neoplasm

A

noncancerous uncontrolled cell growth

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42
Q

malignant neoplasm

A

cancerous uncontrolled cell growth

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43
Q

what are the two ways in which cell death occurs

A
  1. apoptosis
  2. Necrosis
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44
Q

apoptosis

A

Programmed cell death
- self-destruction by enzymatic digestion
- debris engulfed by phagocytes

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45
Q

what are the steps of apotosis

A
  1. elimination of unwanted cells
  2. cell shrinks
  3. nuclear fragmentation (units leave cell)
  4. apoptotic bodies (dead fragments)
  5. phagocytosis of apoptotic bodies (no inflammation)
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46
Q

Necrosis

A

Injury or disease lead to cell death

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47
Q

steps of necrosis

A
  1. always pathological
  2. cell enlargement
  3. loss of membrane integrity
  4. leakage of content
  5. inflammation
  6. nuclear degeneration
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48
Q

pharmacology

A

study of medications or chemical compounds that interact with some part of the body (molecules, cells, tissues, systems) in order to produce a certain effect
- examining a drugs action, dosage, therapeutic use, and adverse effects

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49
Q

drug terminology

A
  • each drug has at least 3 names
    (chemical name based on its chemical structure)
  • generic name= usually shortened chemical name used by health professionals
  • brand/trade names given by pharmaceutical companies
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50
Q

drug dose

A

precise amount of active ingredient in the medication

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51
Q

How can we make a drug more convenient to use and improve its effectiveness at getting to its target in the body

A

combining it with inactive substances that help fill out the medication

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52
Q

3 phases of drug action

A
  1. pharmaceutical
  2. pharmacokinetic
  3. pharmacodynamic
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53
Q

goal of drug action

A

get the drug from its point of entry to target tissue

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54
Q

pharmaceutical phase

A

how the drug progresses from the state in which its being administered to being dishevel in solution

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55
Q

two type of routes drug is administered through

A

Enteral and Parenternal

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56
Q

Enteral routes of drug administration

A

oral, sublingual, rectal

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57
Q

Paranteral routes of drug administration

A

Injections (intravenous (iv), subcutaneous (sc), intramuscular),
Inhalation (lungs and nasal), Transdermal

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58
Q

4 subphrases of the movement of drug through the body in the Pharmacokinetic phases

A
  1. Absorption
  2. Distribution
  3. Metabolism
  4. Elimination
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59
Q

Pharmacokinetics: Absorption

A

Passive diffusion vs active transport vs pinocytosis
*oral drugs must first past thought the metabolism

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60
Q

Administration routes of drugs

A
  • IV is the most effective
  • intramuscular vs subcutaneous
  • oral: GI contents, drug coating, blood supply
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61
Q

Pharmacokinetic: distribution phase-factors that could effect distribution

A
  • concentration absorbed
  • blood flow to tissue
  • % drug bound to plasma protein
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62
Q

Pharmacokinetic: metabolism

A
  • primarily in the liver
  • inactivation by enzymes
    *prepares for excretion
  • determines the half life of a drug
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63
Q

what determines the half life of a drug

A

metabolism

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64
Q

pharmacokinetic phases:
- Elimination

A

Primarily done by kidneys
- bile, feces, saliva, sweat, respiration

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65
Q

aerobic exercise effects on pharmacokinetics

A
  • decrease the absorption after oral administration and increases absorption after intramuscular and subcutaneous administration
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66
Q

therapeutic action:

A

stimulation or inhibition of function

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67
Q

graph of drug effect vs dose

A
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68
Q

drug potency

A

strength of a drug at a particular dose
- concentration needed to produce 50% of the maximum effect

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69
Q

Drug efficacy

A

maximum effect that can be achieved by a drug

(the affect of the drug on the receptor once its bound

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70
Q

potency axis

A

x axis

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71
Q

efficacy axis

A

Y axis

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72
Q

Pharmacodynamics graph

A

the concentration of drugs effect

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73
Q

pharmacokinetics graph

A

the time it takes to be concentrated

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74
Q

pharmacokinetics/pharmacodynamics

A

the time it takes to have an effect

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75
Q

drug indications

A

approved uses for which the drug has been proven effective

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76
Q

off-label uses=

A

uses for which the drug has shown some effectiveness but originally approved purpose

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77
Q

contraindications

A

circumstances which the drug should not be taken

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78
Q

side effects

A

unwanted or intended actions, usually mild

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79
Q

adverse effects

A

serious side effects

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80
Q

adverse side effects examples

A

hypersensitivity
idiosyncratic reaction
iatrogenic effect
teratogenic effect
interactions

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81
Q

iatrogenic effect

A

state of ill health caused by medical treatment

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82
Q

teratogenic effect

A

drugs that can cause birth defects

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83
Q

idiosyncratic reaction

A

drug reactions that are adverse and cannot be explained by known mechanisms of action of the drug

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84
Q

therapeutic index

A

ration between toxic dose and minimum effective dose

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85
Q

toxicity is drug specific meaning:

A
  • chemical properties
  • routes and rates of administration
  • rates of absorption, biotransformation and excretion
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86
Q

how do we avoid drug toxicity

A

need to determine the minimum effective dose, the amount that will produce the desired effect and minimize potential toxic effects

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87
Q

importance of regular dosing

A
  • maintain desirable blood level
  • reach effective blood levels quickly
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88
Q

factors influencing blood levels of a drug

A
  • age
  • genetic factors
  • food and fluid intake
  • health status, presence of other diseases, chronic or acute
  • liver and kidney function
    (absorption, metabolism, excretion)
  • circulation and cardiovascular function
  • body weight and proportion of fat tissue
  • activity level and exercise
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89
Q

3 phases of drug action

A

pharmaceutical, pharmacokinetic, pharmacodynamic

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90
Q

Dose vs Concentration vs Time (half life graph) explained

A

it takes half the time too reach it’s maximum concentration?

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91
Q

concentration effect: potency and efficacy effects

A

potency: amount of drug needed to produce and effect
efficacy: drugs capacity to produce and effect

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92
Q

iatrogenic effect is due to

A

an error in dosage

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93
Q

antagonistic interactions of a drug

A

one substance blocks or reduce the effect of another drug

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94
Q

potentiating drug interactions

A

one substance can increase the effects of another

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95
Q

synergistic drug interactions

A

two substances work together to produce a stronger effect

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96
Q

therapeutic index

A

ratio between toxic dose and minimum effective dose

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97
Q

fluid balance in the body (fluid gained or lost)

A

2.2 intake + 0.3 metabolic production - 2.5 L/day=0

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98
Q

electrolyte balance explained

A
  • electrolytes are kept at a specific concentration inside and outside cells
  • maintenance of homeostasis (rather than equilibrium) is essential for normal function
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99
Q

osmolarity

A

measure of solute

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100
Q

Blood plasma contains

A
  • Proteins (albumin)
  • Na+
  • Ca2+
  • Cl-
  • HCO3-
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101
Q

Interstitial fluid contains

A
  • Ca2+
  • Na+
  • Cl-
  • HCO3-
  • Proteins (K+, K+, Mg2+, intracellular fluid)
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102
Q

how are water and electrolyte levels regulated

A
  • thirst
  • kidneys
    (hormones and direct regulation)
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103
Q

thirst components

A
  • osmoreceptors in the hypothalamus (measure blood osmolarity)
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104
Q

kidney fluid and electrolyte regulation explained

A

varying the amounts that are excreted and reabsorbed

  • direct + hormone
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105
Q

hormones that act on kidneys

A
  • ADH
  • aldosterone
  • atrial natriuretic peptide
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106
Q

ADH effect

A

regulates water level

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107
Q

aldosterone

A

regulates NA+ and water level

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108
Q

Atrial Natriuretic Peptide

A

regulates Na+ and water levels

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109
Q

how does water move between compartments

A

filtration and osmosis

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110
Q

what drives filtration at capillaries

A

hydrostatic pressure

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111
Q

what drives osmosis across cells

A

osmotic pressure

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112
Q

osmotic pressure causes water to move from

A

low solute to high solute

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113
Q

Largest method of water gain

A

Food and drink 2.2 L/day

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114
Q

Largest method of water loss

A

Urine 1.5L/day

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115
Q

body weight water found in

A

2/3rds fluid inside cells
1/3rd fluid outside cells
blood plasma

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116
Q

extracellular fluid

A

interstitial fluid + blood plasma

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117
Q

sodium is found in high concentration,

A

outside or cells

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118
Q

sodium is found in low concentration

A

inside our cells

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119
Q

potassium high amounts

A

inside cell

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120
Q

potassium low amounts found

A

outside cell

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121
Q

most important electrolyte

A

sodium

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122
Q

To keep our electrolyte charge, that means that

A

maintenance of homeostasis is more important than equilibrium

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123
Q

difference between blood plasma and fluid around cells is

A

protein content

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124
Q

osmolarity

A

measure of solute concentration

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125
Q

Hydrostatic pressure

A

forces fluid out : Net filtration

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126
Q

Osmotic pressure

A

draws water in to area of higher solute

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127
Q

why is total blood solute higher than solute in cells

A

due to the amount of proteins

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128
Q

where is fluid excess located edema

A

fluid in the interstitial compartment

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129
Q

edema types

A
  • isotonic : rention of isotonic fluid (same osmolarity)
  • hypotonic: retention of hypotonic fluid (low osmolarity)
  • hypertonic: retention of hypertonic fluid (high osmolarity)

*depending on the cause of edema

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130
Q

edema consequences

A

swelling within the tissues (localized or generalized)
- functional impairment
- pain
- impaired circulation

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131
Q

4 causes of edema

A
  1. high local blood pressure
  2. decreased osmotic pressure in the blood
  3. blocked or missing lymphatic vessels;l
  4. increased capillary permeability
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132
Q

high local blood pressure: edema cause

A

increase hydrostatic pressure
- increased net fluid movement into interstitial space
phatalogiclal states:
- severe hypertesion
- increased blood volume

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133
Q

decreased osmotic pressure in the blood

A
  • increased net fluid movement into interstitial space
    due to lowered plasma concentration
    pathalogical states:
  • kidney disease: excess protein excretion
  • malnutrition or malabsorption
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134
Q

blocked missing lymphatic vessel

A

fluid and protein not filtered out into lymphatic vessel of drainage- causes localized edema
- pathological states:
tumor blocking
lymphatic drainage

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135
Q

isotonic dehydration

A

water and electrolyte loss

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136
Q

hypertonic dehydration

A

more water lost than electrolyte

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136
Q

hypotonic dehydration

A

more electrolytes lost than water

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137
Q

how can you test for dehydration

A

skin turgor test

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138
Q

acute pain

A

fast, localized,
- from injury: can be mechanical and thermal
- travels along pathway of A-delta myelinated fibres

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139
Q

chronic pain general overview

A
  • slow, diffuse, prolonged
  • existing stimuli, chemical
  • pathway is the slow unmyelinated C fibres
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140
Q

chronic pain details

A
  • lasting more than 3 months
  • may become a nerve hypersensitivity issue
  • may be localized within the CNS (no peripheral stimulus input)
  • may be a mix of excitatory and inhibitory systems
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141
Q

chronic pain pathology involves not on the foot stuck on the accelerator

A

but also a dysfunction with the brake

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142
Q

current research about chronic pain

A

chronic inflammation of the nervous system due to malfunctioning glial cells as a cause of chronic pain

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143
Q

chronic pain ideal combo treatment

A
  • exercise
  • fish oil
  • neuromodulation
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144
Q

pain management types of treatment

A
  • pharmacological treatment (medication)
  • analgesics
  • anesthetics
  • non pharmacological treatment
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145
Q

analgesics

A

decreased pain perception

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146
Q

anesthetics

A

don’t block the pathway but block out ability to sense it: block the pain sensation

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147
Q

pain management is

A

multidisciplinary
- prevention
- psychological
- physical
- pharmaceutical

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148
Q

neuromodulation

A

transcranial magnetic stimulation
- uses electromagnetic coil to deliver a magnetic pulse that stimulates nerve cells in specific regions of the brain
- shown to be effective treatment for chronic depression and chronic neuropathic pain

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149
Q

what type of exercise can help with chronic pain

A
  • exercise that helps desensitize the sensitized nervous system
  • exercise is anti-inflammatory
  • helps visualize the movement first
  • find enjoyable exercise
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150
Q

two types of defence mechanisms in the body

A
  1. innate immunity :
  2. adaptive immunity :
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151
Q

adaptive immunity

A

specific diseases -> immune response
*all defences overcome injury or disease

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152
Q

innate immunity

A

nonspecific defences-
* fluids
*barriers like skin and mucous in the membrane
*phagocytosis: cellular elimination

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153
Q

inflammation

A

important defence mechanism of the body
- immunovascular responsec

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154
Q

how is inflammation caused

A

by a stimulus
- pathogen
- physical damage

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155
Q

how do we respond to inflammation stimuli

A

restore the balance by removing the cause, remove the damage, repair tissue

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156
Q

5 cardinal signs of acute inflammation

A
  1. pain: due to chemical mediators
  2. heat: increased
  3. redness
  4. swelling
  5. loss of function
  • can be localized vs systemic
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157
Q

Acute inflammation response overview

A
  1. initiation and amplification
    - chemical mediators released into the blood and at site of injury by resident immune cells, immune cells recruited to area
  2. destruction
    - neutralization of the injury and debris removal by chemical mediators and immune cells that were just released
  3. termination
    cytokines and chemokine will end the inflammatory process (anti-inflammatories)
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158
Q

local action of chemical mediators

A
  • pain response
  • vascular reposes: vasodilation and increased capillary permeability
  • cellular response: attract immune cells to site of injury
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159
Q

cytokines:

A

immune cell proteins that coordinate the immune response: some are pro- inflammatory and some are antiinflammatory

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160
Q

chemical mediators

A

Cause pain response, allow blood flow, chemical mediator release, draw the immune cells to site of injury

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161
Q

cells involved in the inflammatory response

A

platelets- release blood-clotting proteins at wound site
mast cells- secrete chemical mediators
neutrophils- migrate to the site and secrete factors that kill pathogens, phagocytosis to remove
macrophages- secrete cytokines, phagocytosis to remove pathogens and debris

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162
Q

when are platelets cells involved

A

if there a physical tear

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163
Q

resident immune cells

A

live and wait for wounds

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164
Q

neutrophils,

A

first responders in the blood

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165
Q

macrophages

A

contribute to chemical mediator release

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166
Q

chemical mediators in the inflammatory response

A
  • mast cells
  • macrophages
  • platelets
  • plasma proteins
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167
Q

histamine

A

vasodilation and increased capillary permeability

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168
Q

prostaglandins

A

vasodilation and increased capillary permeability, pain, fever

169
Q

leukotrienes

A

vasodilation and increased capillary permeability, chemo taxis

169
Q

cytokines

A

fever, chemotaxis, recruit more WBC

170
Q

platelets

A

activating factor: clotting and blood vessel repair

171
Q

plasma proteins

A

bradykin- vasodilation
complement system- vasodilation and increased permeability
C-reactive proteins (CRP)- scretion of more cytokines, complement system, chemotaxis
prothrombin and fibrinogen - blood clotting

172
Q

exudate

A

interstitial fluid collected in the area of inflammation

173
Q

types of exudate

A
  • serous:classic white fluid
  • fibrinous: thick and sticky, higher cell fibrin content
  • purulent: thick yellow and green colour, higher WBC and debris, microrganisms: suggest bacterial infection
  • hemorrhagic: blood vessels damaged
174
Q

abscess

A

pocket of prudent exudate in a solid tissue

175
Q

how is Advil used to treat inflammation

A

it inhibits the enzymes involved with the inflammatory response

176
Q

how is prednisone used to treat inflammation

A

suppresses the immune response, inhibiting inflammation

177
Q

non-pharmaceutical treatments to inflammation

A
  • compression
  • cold: causes vasoconstriction to reduce sensory nerve transmission
  • hot: promotes circulation in order to promote healing
  • elevation
  • rest: avoid further trauma
178
Q

elements of healing (3 r’s)

A
  • resolution: damaged cells recover
  • regeneration: damaged cells are a type that can divide by mitosis and can be replaced by identical cell type
  • replacement: damaged cells replaced by connective tissue, loss of function in this area
179
Q

scar tissue=

A

cross linking of collagen

180
Q

steps of from injury to healing

A
  1. injury 2. acute inflammation 3. release of chemical mediators : causing
    - increased BF, vasodilation, chemotaxis, nerve ending irritation, capillary permeability (edema) 4. prep for healing 5. healing
    - scar tissue firbrosis
    - regeneration
    - resolution
181
Q

acute inflammation: what type of immune cells infiltrate

A

neutrophils

182
Q

chronic inflammation: what type of immune cells inflitrate

A

monocytes, macrophages, lymphocytes

183
Q

pro-inflammatory cytokines

A

CRP: c-reactive peptide
IL-6: interleukin 6

184
Q

chronic inflammation is typically

185
Q

chronic inflammation can result from

A
  • acute inflammation that is unable to resolve
  • low level exposure to an irritant or foreign material
  • autoimmune disorders
  • inflammatory and biochemical inducers causing oxidative stress and dysfunction
186
Q

non pharmacologic treatment of chronic inflammation

A
  • nutrition :avoid sugar, refined carbs, trans fats, hydrogenated oils. avoid alcohol consumption, consume grains, whole foods, veg and fish
  • aerobic & resistance exercise:
    promotes meetabolically healthy tissues
    anti-inflammatory benefits
  • sleep quality & quantity
  • stress reduction
187
Q

how is the acid-base balance regulated- 3 methods

A

1) buffer systems in the blood
2) respiratory system: regulate CO2 level
3) kidneys: variable excretion/reabsorption of H+ and HCO3-

188
Q

hypokalemia:

A

decreased K+ in the blood(increased pH)
- caused by alkalosis
- causes muscle cramping and weakness

189
Q

hyperkalemia

A

increased K+ in blood
- caused by acidosis
- causes tingling and numbness

190
Q

hyponatremia

A

losing more water Na+ than water or gaining more water than Na+
- muscle cramps, weakness

191
Q

hypernatremia

A

increased Na+ in the blood
- increased thirst, decreased urine

192
Q

acidosis

A
  • respiratory acidosis: increased CO2
  • metabolic acidosis: decrease in HCO3- (excess acid present)
193
Q

alkalosis

A
  • respiratory alkalosis: decreased CO2
  • metabolic alkalosis: increased HCO3- (excess acid loss from the blood)
194
Q

respiratory acidosis compensation (too much CO2)

A

metabolic: kidneys reabsorb HCO3- and excrete H+
respiratory: increase rate and depth of breathing

195
Q

metabolic acidosis (too much HCO3) compensation

A

respiratory: hyperventilation to expel more CO2
metabolic: kidneys reabsorb HCO3- and excrete H+

196
Q

respiratory alkalosis (decreased PCO2) compensation

A

Metabolic: kidneys excrete HCO3- and reabsorb H+
Respiratory: rebreathing= paper bag

197
Q

metabolic alkalosis (increased HCO3- out)

A

Respiratory: hypoventilation to increase CO2 level in blood
Metabolic: kidneys excrete HCO3- and reabsorb H+

198
Q

ROME acronym

A

Respiratory Opposite
- increase in PCO2=decrease pH
- decrease in PCO2=increase in pH
Metabolic Equal
- increase in HCO3-=increase in pH
- decrees in HCO3-= decrease in pH

199
Q

our experience of pain can be described by what two components

A
  1. sensory component
  2. affective & cognitive component
200
Q

Nociceptive pain

A

arises from an identifiable tissue, causing tissue damage
- thermal, mechanical, chemical
* somatic pain: with the skin or deeper
* within or around organs: sympathetic nervous system fibres, detect pain stimulus

201
Q

neuropathic pain

A

caused by dysfunction of the nervous system
- often no indentifiable tissue damage
- can present in many different ways

202
Q

pain threshold:

A

level of stimulation needed to activate the pain pathway and achieve a perceivable signal to the brain

203
Q

pain tolerance

A

ability to withstand pain- intensity and Time
*70% of pain tolerance is due to genetics
- modulated by endorphins (increased with pain tolerance)
- modulated by fatigue, stress, mental health (decreased pain tolerance)

204
Q

pain perception and response

A
  • affected by age, culture, family traditions, prior experience, fear or anxiety , personality
205
Q

enorphin

A

neurotransmitters that help reduce pain (increase the pain threshold)
- endogenous opioids

206
Q

is pain cut and dry

207
Q

3 key points for reconceptualizing pain

A
  1. pain level is not proportionate to tissue injury
  2. pain is modulated by many factors
    (somatic, psychological, social domains)
  3. the relationship between pain and the state of the tissue becomes less predictable as pain persists
208
Q

Pain receptor: nociceptor

A

responds to extreme thermal, mechanical, or chemical stimuli

209
Q

what type of fibres are the pain stimuluses carried by

A
  1. A-delta fibers
  2. C fibers
210
Q

C fibers

A

(small unmyelinated
- high threshold thermo, mechano, chemo receptors (dull, throbbing, aching, burning pain, poorly localized)

211
Q

A- delta fibers

A

(larger, myelinated)
- low threshold pain (mechanical and thermal)
- transmits sharp well localized pain sensations

212
Q

pain stimuli can be inhibited by

A
  • afferent touch stimuli coming into the spinal cord at the same time as pain stimuli: stimulates interneurons that inhibit the nociceptor 1st order afferent neuron
  • descending signals from the brain: release endorphins directly onto nociceptor 1st order afferent neutrons or indirectly via interneurons
213
Q

endogenous opioids also known as

A

endorphins

214
Q

Gate Control Theory: Pain control : gate open

A
  1. painful stimulus
  2. substance p release
  3. pain stimulus sent to brain
  4. RAS alert
  5. Pain is percieved
215
Q

Gate control: Gate closed

A

painful stimulus inhibited!

  • activates an interneuron releasing endorphin >enkephalin< which is an endogenous opioid. this causes an inhibition of release of substance P

Block the release of substance P
1. put pressure on muscle: to distract the brain with mechanical stimuli in area of painful stimuli

  1. allow endorphins to block the pain
216
Q

enkephalin

A

blocks substance P, allows for serotonin to kick in

217
Q

reticular formation

A

can directly inhibit nociceptor
- activates interneuron
through serotonin inhibiting substance P
-> reducing the amount of neurotransmitter released and reducing the firing rate of second order afferent

218
Q

Referred pain

A

brain interprets organ pain in the skin of the area of the organ

219
Q

acute pain

A

fast, localized
A-delta myelinated fibers
short term

220
Q

chronic pain

A

slow, diffused, prolonged
slow unmyelinated C fibers

221
Q

chronic pain

A
  • last no more than 3 months
  • may become an issue of nerve hypersensitivity
  • may be localized within the CNS
  • mix of excitatory and inhibitory systems
222
Q

chronic pain pharmacological treatments

A
  • analgesics
  • anesthetics
223
Q

chronic pain management non pharmacological treatments

A

multidisciplinary
- prevention, psychological, physical, pharmaceutical

224
Q

neuromodulation

A
  • transcranial magnetic solution
    uses a coil to deliver magnetic pulses stimulating nerve cells in specific regions of the brain to help with chronic pain
225
Q

chemotaxis

A

migration of cells in response to a chemical stimulus

226
Q

Possible threats on our body

A
  • microorganisms
  • toxins
    allergens
  • our own cells that have turned into tumour
227
Q

immune system is designed to protect us from threats in which 3 steps

A
  1. prevent entry
  2. prevent spread/growth
  3. removal of threat
228
Q

infectious disease caused by

A

pathogens (microorganisms that invade, multiply, and cause damage)
- this includes bacteria, viruses,protozoa, prions

229
Q

infection

A

a pathogen has reproduced in the hosts body

230
Q

bacteria

A

prokaryotic single cell organisms, rigid cell wall
- contain DNA, RNA
- survive and divide outside living host
- named based on their shape and characteristics

231
Q

viruses

A

small intracellular parasite
a protein coats with a core that contains DNA or RNA
requires a living hosts to replicated

231
Q

fungi

A

found everywhere in the environment
- eukaryotic (single celled yeast) or chains of cells (mold)
- can produce bigger spores that become airborne (inhalation=allergic reaction_
- only certain fungi are pathogenic
worse for people who are immunocompromised

232
Q

protozoa

A

parasites (pathogenic protozoa)
complex eukaryotic organisms
- unicellular motile
ex. pin worms, tape worms, amoebas, malaria

236
Q

prions

A

infection transmitted by protein particles that are able to self-propagate
(induces protein into brain, misfiled, non functional, neurodegeneration)
-do not contain genetic material

  • symptoms cause death (neuro-degenerative)
236
Q

reservoir

A

source carrying the infection

236
Q

infection modes of transmission

A

direct contact
indirect contact
droplets
aerosol
vector-borne

236
Q

infection steps

A

reservoir, portal of exit, mode of transmission, portal of entry, susceptible victim

237
Q

physiology of infection, PERIODS

A

incubation period. prodromal period, acute period

237
Q

8 steps of infection

A
  1. pathogen enters host
  2. pathogen colonizes to appropriate site
  3. pathogen reproduces rapidly
  4. prodromal signs appear
  5. acute signs present
  6. decreased reproduction and death of pathogens
  7. recovery- signs subside
    *can have chronic infection : mild signs but destructive
  8. total recovery
237
Q

components of the immune system

A
  • organs and tissues
  • cells
  • molecules / chemical mediators
237
Q

organs and tissues of the immune system

A

bone marrow, slpeen, thymus glands, tonsils, lymph nodes and vessels

237
Q

immune system cells

A

leukocytes (WBCs)

237
Q

molecules/chemical mediators of the immune system

A

cytokines
- complement system
- anti bodies
- chemical mediators: histamine, bradykinin, prostaglandin, leukotrienes

238
Q

what is the compliment system

A

group of small proteins in the blood. that complement the immune response

238
Q

innate immune response

A

defence mechanism:
- physical & chemical barriers, inflammatory response
*FAST
*NO MEMORY

immune cells: non-specific
*distinguish between what should and shouldn’t be in the body

molecular components: non-specific, chemical mediators involved in an inflammatory response

239
Q

Adaptive immune response

A

defence mechanism: Kill compromised cells (antibody tags antigen)
*Initial response takes a few weeks
*immunologic memory: stronger and faster response each time the pathogen is present
- immune cells are specific for each invader
certain cells have antigens- ID

  • molecular components: antibodies and chemical mediators
240
Q

Leukocytes involved in the INNATE immune response: explained

A

all cells differentiated from myeloid progenitor:
- found circulating the in the blood within tissues at all times
- natural killer cells also part of the innate immune response: target cells infected with virus + cancer cells
—-> TRIGGERING APOTOSIS

241
Q

which cells are the link between the innate and adaptive immune repsonse

A

dendritic cells

242
Q

types of leukocytes involved in the adaptive immune response

A
  • antigen presenting cells: dendric cells
  • B lymphocytes
  • T lymphocytes
243
Q

what do B lymphocytes do

A

recognize specific antigens that have invaded the body before *AKA MEMORY
and
secrete antibodies

244
Q

what do T lymphocytes do

A

recognize specific antigen that is presented by the dendritic cells
turn into:
- helper T cells: secreting cytokines to help coordinate the immune response
- cytotoxic T cells: kill target cells that present a specific antigen

245
Q

during an innate immune response,

A

local neutrophils & macrophages:
- do phagocytosis
secrete chemical mediators that
- trigger inflammatory response
- trigger release of other chemical mediators
- recruit more immune cells
(basophils, eosinophils, neutrophils, macrophages, dendritic cells)
+ natural killer cells
(if the pathogen is a virus or tumour)
- apoptosis of viral-infected abnormal cells

246
Q

initiation of the adaptive immune response

A
  1. dendritic cell pahgocytizes a pathogen for the first time
  2. breaks up the pathogen in to small peptides
  3. travels to lymph node and presents an antigen to T cells
  4. T cells mature and reproduce
  5. antigen- specific B cells develop and reproduce, target specific pathogen: turn into plasma cells once exposed to antigen : plasma cells secrete antibodies
    *memory B cells reproduce for next time
    *antibodies attach to the pathogen to mark it for destruction
247
Q

Acute exercise effect on immune response

A
  • leukocytes: higher number of natural killer cells, T cells, immature B cells
  • increased antipathoden activity
  • enhanced blood redistribution to target tissues
  • increased activity of antioxidant enxymes
248
Q

chronic exercise effect on immune system

A
  • increase T cell proliferative capacity
  • increased phagocytosis and cytotoxic activity
  • increased production of anti-inflammatory mediators
  • increased cell energy production
249
Q

hypersensitivity reactions

A

immune system overreacts to damage instead of protection
- ex allergic reactions

chronic inflammation in the airways
- trigger
- dendritic cells
- helper T cells
- cytokines
- mast cells & eosinophils
– more cytokines & leukotrienes

RESULT:
- local inflammatory response
- bronchospasm (smooth bronchioles contract) increased mucus secretion

250
Q

autoimmune conditions

A

immune system can’t distinguish between certain self and non self antigens
- it forms antibodies
- autoantibodies attack self-antigens and immune complexes
- inflammation and tissue damage occur

251
Q

immunodeficiency

A

consequence of a defect in one or more components of the immune sytesm
- primary
INHERITED defect in the immune system
- secondary (acquired)
induced as a consequence of disease, treatment, or malnutrtion

  • when immune cell is activated it produces more virus that leaves the cell, infects more immune cells
252
Q

immunocompromised condition

A

any condition that leaves your body vulnerable to an infection, because of an issue with the normal functioning of the immune system,

253
Q

ethology of autoimmune disorders is

A

unknown
- likely genetics, environmental

254
Q

autoimmune disorders steps

A
  • trigger
  • cell damage or death
  • immune system reacts and forms antibodies
  • inflammation
255
Q

how to keep an infection live HIV chronic

A

anti-retroviral therapy:

256
Q

exercise considerations for people living with immunodeficiencies like HIV

A

exercise can improve risk,

257
Q

how does age related decline contribute to osteoporosis

A
  • decline in stem cells that produce osteoblasts
  • decline in growth factors involved in promotion of bone formation
258
Q

considerations of modifiable factors

A
  • diet
  • physical inactivity
  • alcohol intake
  • medication
259
Q

OPG

A

osteoprotergerin (secreted by osteoblasts and other tissues)
- A decoy receptor: blocks the action of RANKL by binding to it. Causes RANK L to not be able to bind to its receptor on osteoclast precursor cell so osteoclast differentiation is inhibited

260
Q

control of bone remodeling

A

RANKL binds to it’s receptor->osteoclast differentiation and activation

261
Q

estrogen role in control of bone remodelling

A

inhibits expression of RANK-L
increases production of OPG
- inhibits osteoclast formation

262
Q

secondary osteoporosis can be caused by (etiologies)

A

-disease: endocrine or high cortisol
- excessive alcohol use: inhibits OB, increased pro-inflammatory cytokines, impaired vitamin absorption
- prolonged steroid use
- female athlete triad: intense training, poor nutrition, low estrogen/menstrual dysfunction

263
Q

are pro inflammatory cytokines good or bad

264
Q

An osteoporotic bone has

A
  • lower trabecular number and thickness
  • increased trabecular spacing and cortical thinning + expansion of bone marrow cavity
265
Q

an osteoporotic can be caused by

A
  • increased bone resorption
  • decreased bone formation
  • increase osteoclasts
266
Q

signs and symptoms of osteoporosis

A

spontaneous fractures
back pain (from compression fractures of vertebrae)
abnormal curvatures of spine with loss of height (stooped posture)

267
Q

treatment of osteoporosis

A
  • dietary supplements : Vitamin D, Ca 2+
  • pharmaceuticals : promote bone formation/inhibit resorption
  • estrogen replacement therapy for post-menopausal females
268
Q

how does physical activity help with osteoporosis prevention

A
  1. anti-inflammatory effects
  2. mechanical loading of bone
    (stimulates osteoblast differentiation and promotes osteocyte survival)
269
Q

how much of a bones mass and improved fracture risk does PA have

A
  • 5-10% difference in peak bone mass
  • 25-50% difference in hip fractiure risk
270
Q

therapeutic goal

A

prevents bone loss and prevents falls: preventing fractures

272
Q

synovial joints

A

move freely within their ROM
- lined with articular cartilage and chondrocytes and extracellular matrix, synovial membrane, outer fibrous joints

272
Q

ACSM and Osteoporosis canada exercise recommendations

A
  • at least 150mins/week mod-big aerobic exercise
  • emphasis on weight-bearing activities, not high impact

Progressive resistance training for all major muscle groups:
- at least 2d/week
- exercise intensity at 8-12 RM
- spine sparing strategies : posture, strength and flexibility in core muscles and spinal extensors

273
Q

chondrocytes

A

maintain the cartilage
- secrete different enzymes to balance breakdown of old and production of new cartilage

274
Q

extracellular matrix

A

collagen- structure support
proteoglycans - provide elasticity and high tensile strength

276
Q

synovial membrane contents

A

inner lining of joint
- forms loose connective tissue
- blood vessels
- cells that clear debris and cells that secrete synovial fluid

277
Q

outgrows fibrous joint capsule

A

attaches to bone
reinforces with ligaments

278
Q

menisci

A

pads of fibrocartilage which helps stabliize and is a extra shock absorber

279
Q

bursae

A

between tendons and ligaments
- fluid filled sacs providing extra cushioning

280
Q

osteiarthritis

A

considered a disease of mechanical degeneration + inflammation within a synovial joint
- degeneration of articular cartilage, friction and damage, inflammation, pain

*localized to the affected joint
- result of something that causes increased release degradative enzymes by chondrocytes
- favours cartilage breakdown

281
Q

osteoarthritis risk factors

A

age
genetics
obesity
join injury
inflammation

282
Q

osteoarthritis steps

A
  • chondrocytes triggered to release degradative enzymes
  • breakdown of cartilage
  • small cartilage pieces break of into joint space
  • synovium cells remove debris, immune cells recruited, cytokine secretion, inflammation of synovium
  • cracks form, synovial fluid enters and cracks widen
    (no longer have smooth even surface)
  • bone is exposed and rubs against articulating bone
  • bone eburnation (looks polished)
  • osteophytes and cysts develop
283
Q

osteoarthritis results with

A

narrowed joint space with decreased ROM
inflammation in and around the join and surrounding tissues

284
Q

osteoarthritis signs and symptoms

A
  • asymmetric joints, often weight bearing
  • beginning and end of day stiffness, increases with activity
  • pain with movement/weight bearing
  • limited ROM
  • localized inflammation
  • enlarged joint: can harden as osteophytes develop
285
Q

osteoarthritis treatment

A
  • exercise physiotherapy
  • pharmacological: anti inflammatories
  • hyaluronic acid or corticosteroid injections
  • survey
286
Q

rheumatoid arthritis

A
  • chronic inflammatory disease: autoimmune
    characterize by exacerbations and remissions : progressive joint damage
287
Q

describe the onset of inflammatory disease

A

slow onset, usually with symmetric (bilateral join involvement)
* often begins in small joints of fingers

288
Q

describe the severity of rheumatoid arthritis

A

severity varies based on # of joints implicated, degree of inflammation, rapidity of progression

289
Q

rheumatoid arthritis risk factors

A

genetics:
sex: 3:1
environmental hazards
infections
autoimmune

290
Q

rheumatoid athritis - pathophysiology

A

autoimmune response
- inflammation of the synovial membrane: vasodilation, capillary permeability, immune cells recruited, cytokine release

  • cytokines trigger synovial cells to proliferate
  • forms panes (thickened and inflamed synovial membrane with granulation scar tissue)
  • panes releases proteolytic enzymes and cytokines
  • destruction of cartilage
291
Q

with inflammation , ___ usually comes along

A

vasodilation
increased capillary permeability
immune cells recruited
cytokine release

292
Q

what happens when immune cells fail to recognize self

A

produce autoantibodies

293
Q

rheumatoid arthritis signs and symptoms

A

3+ joints affected often symmetrically.
- often begins in the fingers
- chronic morning stiffness lasts for at least an hour (stiffness improves throughout the day)
- limited range of motion, pain with movement
- joint deformities with disease progression
- blood markers: elevated blood CRP and rheumatoid factor
- possibility of systemic symptoms: fever, fatigue, loss of appetite

309
Q

fracture

A

complete or partial break in bone

310
Q

types of fractures

A
  • complete or incomplete
  • open or closed
  • number of fracture lines
  • direction of fracture lines
311
Q

complete fracture

A

bone is broken in two pieces

312
Q

incomplete fracture

A

bone is partially severed
- more common break in children because of their softer bone

313
Q

greenstick fracture

A

incomplete fractureo

314
Q

open fracture/compound

A

skin is broke
bone fragments may protrude through skin
usually more damage to soft tissue surrounding bone
higher risk of infectionc

315
Q

closed fracture

A

skin is not broken through

316
Q

number of fracture lines: simple

A

single break, bone ends maintain alignment and position

317
Q

comminuted fracture

A

multiple fracture lines and bone fragments

318
Q

compression fracture

A

bone is crushed into smaller pieces and collapses

319
Q

transverse fracture line

A

across the bone

320
Q

spiral fracture line

A

angles around the bone

321
Q

longitudinal fracture line

A

along the axis of the bone

322
Q

oblique fracture line

A

at an angle with respect to diaphysis

323
Q

impacted fracture

A

one end force into the other at the location of the break
-><-

324
Q

stress fracture

A

repeated excessive stress

325
Q

pathologic bone

A

weakness in bone structure due to other conditions

326
Q

coles fracture

A

distal radius fracture
with dorsal angulation(upwards)
- like a dinner for

327
Q

fractures treatment

A
  • immediate immobilization
  • survey if needed
    (insertion of rods, plates, pins, realignment)
  • exercise to maintain range of motion, muscle mass, and circulation
328
Q

broken bone healing process 4 steps

A
  1. hematoma formation
  2. inflammatory phase
  3. reparative phase
  4. remodelling phase
329
Q

hematoma formation

A
  • bone break
  • bleeding from the blood vessels in and around/bone and surrounding tissues
  • clot forms in the medullary cavity, under periosteum and between bone fragments
  • fibrin mesh forms, seal off fracture site and act as scaffolding in steps
330
Q

inflammatory response and reparative phase

A

inflammatory response due to cell damage/necrosis and presence of debris at the cite (infiltration of immune cells)
- growth of new tissue within the fibrin mesh network
- new capillaries infiltrate the area
- fibroblasts and chondroblast migrate here, form the pro callus (3 weeks post injury)

331
Q

reparative phase of bone healing

A

osteoblasts generate new bone over the fibrocartilage model (pro callus)
- the procallus is replaced by bone (bony callus)

332
Q

Bone healing remodeling

A

during the following months in response to mechanical stress on the bone, repaired bone is remodelled by osteoblasts and osteoclast activity
- excessive callus removed and more compact bone laid down

*osteoclasts chisel to make a perfectly shaped bone remodel

333
Q

factors that affect bone healing

A

age:
- kids 1-2 months
- adults 2+ months
extend of damage:
- prolonged inflammation
- complicated breaks
systemic factors:
- aging
- circulatory issues
- anemia
- diabetes
- nutritional deficits
- drugs
- smoking

334
Q

fractures possible complications

A
  • broken ends of the bone damaging surrounding structures
  • compartment syndrome (bleeding)
  • fractures of long bones
    (rare but potential for release of adipose from fracture area to enter the bloodstream)
  • ischemia
  • infection
335
Q

compartment syndrome

A
  • bleeding or edema
  • increased pressure inside limb
  • impaired blood supply
336
Q

what happens when adipose tissue from fractured area enters the bloostream

A

obstruction of blood flow
- in lungs: pulmonary embolism
- in Brain: stroke

337
Q

ischemia in fracture

A
  • due to cast compression
  • due to edema within casted area
  • monitor distal portion of limb for colour temp and feel
338
Q

infection in fractures

A

most common with compound fractures or those that require surgical interventions
- osteomyelitis
bacteria entering the bone
local and systemic manifestations
* can cause pain

339
Q

heal abnormalities : long term fracture complication

A
  • malunion
  • delayed union
  • nonunion
340
Q

malunion

A

healing outside of alignment: causes deformity

341
Q

delayed union

A

more time to heal

342
Q

nonunion

A

failed to heal

343
Q

mobility complications in fracture long term complications

A
  • joint stiffness
  • instability
  • contractures (muscular) limited ROM
344
Q

side effects of long term immobilization in fractures

A

pressure injury
blood clots (deep vein thrombosis)

345
Q

can smoking effect bone healing, how?

A

Yes, smoking causes decreased circulation contributing to non-union

346
Q

lumbar lordosis

A

spine curves inwards at lower back
- common risk, poor posture, pregnancy, central obesity

347
Q

kyphosis

A

“hunchback”
- rounded upper back
- risk of poor postures

348
Q

scoliosis

A

S or C shaped sideways curvature of the spine
- risk factor genetics

349
Q

lumbar lordosis exercise treatment

A
  • build strength in hip extensors and stretch hip flexors
  • build strength in abdominals
350
Q

concussion

A

mild traumatic brain injury induced by biomechanics forces
- direct blow to head or transmitted
- no obvious brain trauma on imaging

351
Q

most common causes of concussions

A
  • motor vehicle accident
  • contact sport
  • falling down stairs
  • domestic violence
352
Q

two main types of concussion

A
  • coup-contrecoup injury
  • torque (rotational) injury
353
Q

coup-contrecoup injury

A

movement of brain hitting one side of skull to other side of skull
[contusion from impact (coup) causes movement of brain to impact opposite side of skull (countrecoup)]
- results in stretching and shearing of neurone

354
Q

torque rotational injury

A

head and neck twists causing brain to rotate
- results in stretching and shearing of neuronc

355
Q

concussion pathophysiology

A
  1. neuron injured due to stretching and shearing
  2. axons leak: resulting in spontaneous AP firing
  3. excess glutamate (excitatory neurotransmitter release)
  4. neurons stimulated EPSP
  5. increase in metabolic activity
  6. increased glucose demand in blood, but decrease in blood to brain
  7. imbalance of nutrient supply and demand (hours to days)
  8. neurons damaged and enter a low metabolic state for short period of time (up to 30 days)
359
Q

glutamate

A

excitatory post synaptic potential

360
Q

GABA

A

inhibitory post synaptic potential

361
Q

concussion symptoms

A

diagnosis based on description and symptoms

362
Q

4 domains of concussion symptoms

A

somatic: nausea, pain, vomitting, vision, sound
cognitive: concentration and memory
mood: emotion
sleep: too much or too little

363
Q

acute concussion symptoms

A
  • confusion
  • memory loss
  • loss of consciousness
364
Q

chronic symptoms

A
  • headache
  • dizziness
  • nausea
  • sensitivity to light noise
  • fatigue
  • vision
  • emotional
  • sleep
365
Q

concussion treatment

A
  • early mild-mod PA can reduce time-to-symptom-free
  • avoid activity that could cause excess brain movement
366
Q

what can repeated concussion lead to

A
  • damage and misfolding of a structural protein: Tau protein (clustering and buildup around blood vessels in brain)
  • neuronal death
  • brain atrophy
  • dementia
367
Q

spinal cord injury (SCI)

A
  • obstructs transmission of neural messages through spinal cord
    —>
    loss of somatic and autonomic control of the trunk, limbs, viscera below the site of injury
368
Q

complete spinal cord injury

A

loss of all sensory and motor function at and below the level of injury

369
Q

incomplete spinal cord injury

A

some function remains

370
Q

somatic nervous system disruption

A

motor and sensory pathways

371
Q

autonomic nervous system disruption

A

SNS&PNS
- won’t pass info from brain and won’t be able to receive feedback

372
Q

tetraplegia

A

C4 Injury and C6 injury

373
Q

paraplegia

A

T6 injury L1 injury

374
Q

primary SCI injury

A
  1. sudden trauma to the spine
  2. acute spinal cord compression: shear, stress, severing and pulling on spinal cord
  3. acute impact to neurons, glial cells and neural parenchyma
375
Q

SCI secondary injury

A
  • primary injury triggers a secondary injury
  • involves cascade of biochemical and metabolic changes within the neural tissues
  • secondary injury is the consequence of these downstream effects (haemorrhage and inflammation)
376
Q

3 phases of a secondary injury

A
  • acute phase
    : hemorrahage, inflammation, ischemia, cell death begins
  • sub acute phase
    : further neurotoxicity, scar tissue formation, undamaged tracts begin to resume function
  • chronic phase:
    continued cell death and scar tissue
    cyst development
378
Q

asia scale Acomplete

A

no sensory or motor function is preserved in the sacral segments S4-S5

380
Q

asia scale incomplete B

A

sensory but no motor function is preserved below the neurological level and include sacral segments S4-S5

381
Q

asia scale incomplete C

A

motor function is preserved below neurological level and more than half the key muscles below neurological level have a muscle grade greater than or equal to 3

382
Q

asia scale incomplete D

A

motor function is preserved below the neurological level, at least half of key muscles below the neurological level have a muscle grade greater or haul to 3

383
Q

asia scale Normal E

A

sensory and motor functions are norma

384
Q

side effect of SCI

A
  • cardiovascular:: HR BP issues loss of NS signals
  • pulmonary: ventilation impaired with injuries abouve C5
  • bowel and bladder function: sexual function all likely affected
  • thermoregualation : harder to regulate below level of SCI
  • hyperreflexia (spasticity) : due to central disinhibition of spinal reflex arcs: leads to inappropriate activation of stretch reflex muscle
  • autonomic dysreflexia
385
Q

autonomic dysreflexia

A

uncontrolled SNS response to an afferent stimulus below SCI level
- widespread vasoconstriction below level of injury
*can be life threatening: sudden acute hypertension along with Bradycardia

386
Q

PA guidelines for adults with SCI

A

STARTING LEVEL
20 mins 2x of aerobic activity
3sets 10reps 2x week strength training activity

ADVANCED LEVEL
30mins 3x week aerobic activity

3sets10reps2xweek strength training activity

387
Q

muscular dystrophies

A

genetic
- progressive degeneration of skeletal muscle fibers (necrosis)
- muscle fibers replaced by adipose and connective tissue

387
Q

skeletal muscle disorders examples

A
  • disuse atrophy
  • muscular dystrophies
  • myasthenia graves
  • amyotrophic lateral sclerosis (lou Gehrig)
388
Q

neuromuscular junction disorders can be

A

drug/toxin induced or genetic

389
Q

gravis

A
  • autoimmune
  • attack on the nicotinic acetylcholine receptors
390
Q

Amyotrophic lateral sclerosis (Lou Gehrig)

A
  • genetic or unknown ethology
    (genetics and environment?)
  • rapidly progressive
  • degeneration of motor neuron’s
    (protein misfolding, neuronal death, neuronal degeneration)
  • affects upper and/or lower MNs,
    (muscle weakness, spasticity, impaired fine motor control, hyporeflexia, brainstem involvement, dysphagia, dysarthria, dysphonia
  • end stage is paralysis, respiratory failure and multiple sclerosis
391
Q

multiple sclerosis

A
  • inflammatory autoimmune disease that effects the conduction of neural impulses
  • chronic degenerative disease
    demyelination of the neuron’s(from interneurons 1A and 1B) within the CNS, scar tissue forms
392
Q

what results from multiple sclerosis

A
  • clumsiness and muscle weakness
393
Q

what ages is onset of multiple sclerosis

A

onset between 15 and 50 years od age

394
Q

Multiple sclerosis etiology

A

unknown
- links to genetics, environment, virus

395
Q

multiple sclerosis symptom details

A
  • demyelination can occur anywhere, in patches within the CNS
  • usually characterized by exacerbations and remissions
  • 80% of diagnoses begin as relapsing-remitting
  • degeneration can be progressive
    *myelin can be repaired
  • variable severity (mild and slow vs fast and progressive)
395
Q

in MS, location of demyelination will determine

A

the symptom type

396
Q

MS- extent of demyelination will determine the

A

symptom severity

396
Q

MS- cerebellum demyelination symptoms

A

loss of balance and ataxia and tremor

397
Q

MS- cranial nerve demyelination symptoms

A

diplopia and loss of vision

398
Q

MS-motor nerve tracts demyelination

A

weakness and paralysis

399
Q

MS- damage to sensory nerve tracts

A

paresthesia, prickling burning sensation

400
Q

multiple sclerosis pathophysiology

A
  1. unknown tigger
  2. activated T cells cross the blood brain barrier
  3. secretes cytokines
  4. immune cells recruited, macrophages
  5. attack oligodendrocytes(cells that form the myelin sheath with CNS)
  6. myelin damaged and breaks down
  7. scar tissue formation, axonal destruction
401
Q

multiple sclerosis diagnosis and treatment

A

Diagnosis: of exclusion
treatment:
- disease modifying drugs, slow down progressions
- pharmaceuticals to treat complications
- physio and exercise to maintain strength and mobility
- occupational therapy to support ADL
- adaptive equipment

402
Q

exercise prescriptions in those with MS

A

shown to improve muscle weakness, bladder and bowel function, fatigue, psychological health, quality of life
considerations for exercise prescription
- physical limitations
- supportive equipment
- variable strength levels

403
Q

cerebral palsy(neuromuscular disorder originating from the brain)

A
  • neurodevelopment condition: something happens during development (pre or post natal)
  • muscles affected depends on what part of the brain is affected
    spastic: upper motor neurons are damaged
    dyskinetic: involuntary movements if basal ganglia is damaged
    ataxic: damage to cerebellum
404
Q

parkinsons disease

A

disease of synaptic transmission
- dopamine is released and reduced via destruction of neurons of the nigrostrital pathway
* progressive and degenerative
* average age of diagnosis: mid 502

405
Q

Parkinson’s disease progression

A

cardinal symptoms-> dementia (sometimes)-> death due to complications

406
Q

in parkinsons patients dopamine neurons in the ____ degenerate

A

nigro-stratial pathway

407
Q

dopaminergic neurons of the substantial nigra normally responsible for

A
  1. allowing signals to be sent to cerebral cortex for movement initiation
  2. fine tuning of signals to prevent unwanted movement
408
Q

explain how the dopamine release is reduced in Parkinson’s disease

A

destruction of neurons of the nigrostriatal pathway (neurons that project from substantial nigra to stratum within basal ganglia)

409
Q

parkinsons disease pathophysiology

A
  1. unknown trigger
  2. degeneration of neurons of the substantial nigra that produce and release dopamine
  3. less dopamine released onto neurons of striatum
  4. imbalance of excitatory and inhibitory neurotransmitters released in striatum
  5. result= not enough voluntary initiation of movement and too much involuntary movement
410
Q

dopamine job

A

neurotransmitter that produces an inhibitory or excitatory stimulus on postsynaptic neurons
> dopamine plays key role in control and fine tuning

411
Q

parkinsons 4 cardinal symptoms

A
  • bradykinesia (slow movement)
  • muscle rigidity (spastic movement)
  • resting tremor
  • postural instability
412
Q

how is Parkinson’s diagnosed

A

diagnosed based on symptoms

413
Q

parkinsons treatment

A

Pharmaceutical treatment:
- dopamine replacement therapy
dopamine cannot cross blood-brain-barrier so, L-dopa (levodopa) given; it’s a precursor so it will be converted to dopamine in the brain
- drugs that inhibit dopamine breakdown so that dopamine that is produced will last longer
Exercise, PT, OT:
- maintain mobility, stability, and posture to delay disability
- exercise to maintain strength, balance, and flexibility
- safe exercise

HES 311 (2 decks)

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