Midterm 1 Flashcards
(114 cards)
1
Q
Explain the role of pathophysiology in the diagnosis and treatment of disease.
A
- the study of psychological changes in the body as a result of disease of injury
- molecular > cellular > tissue/organ > system
- need to understand the cellular level before what’s happening at the tissue level
2
Q
Describe the common cellular changes
A
- temporary: returns to normal function
- permanent: doesn’t return to normal function
- atrophy: shrinking
- hypertrophy: growing
- hyperplasia: multiplying cells
- metaplasia: one mature cell type replaced by a diff mature cell type
- dysplasia: cells vary in size, shape, nuclear size, mitotic rate (function abnormally)
- neoplasia: uncontrolled/abnormal growth (tumors)
3
Q
Compare the two types of cell death
A
- atoposis: programmed, self destruction by enzymatic digestion, debris engulfed by phagocytes
- necrosis: injury or disease to cell death
4
Q
Define common terms used in pharmacology
A
the study of medications or chemical compounds that interact with some part of the body in order to produce a certain affect
5
Q
Define and describe the Phases of Drug-Effect, including the details of each phase
A
- pharmaceutical: how the drug progresses from the administered state to being dissolved in solution
- enteral: oral, sublingual, rectal (includes GI system)
- parenteral: injections (IV, SC, IM), inhalation, transdermal)
- pharmacokinetic phase: the effect of the drug on the body
- absorption: affecting factors -> administered route, blood supply
- distribution: affecting factors -> concentration absorbed, blood flow to tissue, % drug bound to plasma protein
- metabolism: primarily in liver, inactivation by enzymes, preparation for excitation, determines half life
- elimination: primarily kidneys, bile, sweat, saliva, respiration during exercise
- pharmacodynamics: effect of drug on body
- therapeutic action: stimulation or inhibition of function
- potency: strength of drug at a particular dose (effects x axis)
- efficacy: maximum effect that can be achived (effects y
6
Q
Define pharmacokinetics and draw a graph of drug concentration vs. time
A
7
Q
Define and compare potency vs. efficacy using pharmacodynamics graph
A
- potency: strength of drug at a particular dose (effects x axis)
- efficacy: maximum effect that can be achived (effects y axis)
8
Q
Describe a drug’s therapeutic action
A
stimulation or inhibition of function
9
Q
Differentiate the types of adverse effects of therapeutic action
A
- indications: approved uses for which the drug has been proven effective
- off-label uses: uses which has shown effectiveness but not original approved purpose
- contraindications: circumstances under which the drug should not be taken
- side effects: unwanted actions, usually mild
- adverse effects: more serious side effects
10
Q
Summarize factors that influence blood levels of a drug
A
- age
- genetic factors
- food and fluid intake
- health status
- liver and kidney function
- circulation and cardiovascular function
- body weight and proportion to fat
- activity level
11
Q
pathology
A
the lab study of cells and tissue changes associated with disease
12
Q
pathogenesis
A
the events involved in the development of a disease
13
Q
etiology and the types
A
the study of the cause(s) of a disease
- idiopathic: the cause is unknown
- iatrogenic: a treatment/procedure/error caused disease
- predisposing factors: risk factors/ behaviours that promote a development of a disease
- prophylaxis: measures taken to preserve health/prevent onset or progression of disease
14
Q
characteristics of a disease
A
- onset can be acute or insidious
- the disease itself can be acute or chronic
- can have signs (you cant feel) and symptoms (can feel)
- can be classified based on remissions and exacerbations
15
Q
stages of a disease
A
- incubation period
- subclinical period: no symptoms
- prodromal period: non specific symptoms
16
Q
disease prognosis
A
the probability for recovery vs other outcomes (based on avg outcomes)
17
Q
non communicable disease of communicable disease (and the types)
A
- non communicable: not spread from person to person
- communicable: spread from person to person
- epidemic:higher than normal or expected number of cases of an infection disease within a given area
- pandemic: higher numbers around the world
- endemic: regulaury found within a population or certain area
18
Q
dose
A
the precise amount of active ingredient in the medication
- combined with inactive substance that helps fill out the medication (improves effectiveness)
19
Q
Describe a drug’s index
A
- the ratio between toxic dose and minimum effective dose
- toxicity is drug specific: chemical properties, routes and rates administered, rates of absorption
- need to determine minimum effective dose
20
Q
Explain the movement of water between body compartments
A
- hydrostatic pressure drives filtration: mainly in capillaries
- osmotic pressure drives osmosis: across all cells (water moves from high [solute] to low [solute]
21
Q
Describe the causes and effects of dehydration.
A
causes:
- insufficient fluid intake
- sweating
- vomiting
- diarrhea
- excess excretion (urine)
net results:
- isotonic dehydration: water = electrolyte loss
- hypertonic dehydration: electrolyte < water loss
- hypotonic dehydration: electrolyte > water loss
test: skin turgor test (pull the skin on back of hand)
22
Q
Explain the causes and signs of hyponatremia
A
- decr [Na+] in blood
- water intoxication
- losing more Na+ than water
effect: - fluid imbalance ( swelling of cells - water moves into cell)
- skeletal muscle cramps, weakness, fatigue
- nausea/ vomiting, diarrhea
- headache, concussion, seizures
23
Q
Discuss the causes and signs of hypokalemia
A
- decr [k+] in blood
- k+ loss or inadequate intake or more k+ entering cells
effects: - muscle cramping, weakness
- cardiac dysrhythmia and cardiac arrest
- alkalosis (incr pH)
24
Q
what electrolytes are higher in interstitial fluid, plasma, and intracellular fluid
A
- interstitial fluid: Na+,Cl-
- plasma: Na+, Cl-, proteins
- intracellular fluid: k+, proteins
25
what regulates water and electrolytes
1. thirst: osmoreceptors measures blood osmolarity
2. kidneys: regulates fluid and electrolyte intake
- directly regulated
- hormone regulated: ADH (water levels), aldosterone (Na+, water levels), Atrial natriuretic peptide (Na+, water levels)
26
water percentages in each compartments
body is made up of 60% water
- 2/3 fluid is inside the cells (intracellular fluid)
- 1/3 fluid is outside the cells (extracellular fluid)
- ECF: interstitial fluid + blood plasma
- fluid moves between cells to keep the electrolytes balanced (homeostasis) --> the water moves to where there is incr [solute] b/c of osmolarity
27
causes of edema
1. high local BP: incr hydrostatic P = incr net fluid movement into interstitial space
- congestive heart failure (pulm edema)
- severe hypertension (lower extremity swelling)
- incr blood volume
2. decr osmotic P in blood: incr net fluid movement into interstitial space (d/t lower plasma protein [])
- kidney disease
- malnutrition or absorption
3. blocked or missing lymphatic vessels: fluid and protein not filtered into lymphatic drainage for return to circulation
- tumor blocking
- lymph node removal
4. incr capillary permeability: excess flow of fluid and proteins into interstitial fluid
- inflammatory response
- infection
- allergy reaction
28
Explain the causes and signs of hypernatremia.
- incr [Na+] in blood
- gaining more Na+ than water or losing more water than Na+
effects:
- fluid imbalance ( water moves out of cells)
- incr thirst, decr urine output
- headache, agitation, seizures, coma
29
Discuss the causes and signs of hyperkalemia.
- incr [k+] in blood
- k+ build up in extracellular fluid or more k+ exit cells
effects:
- tingling, numbness
- muscle cramping, weakness, paralysis
- cardiac dysrhythmia, cardiac arrest
- acidosis (decr pH)
30
way for acid base balance
1. buffer system: HC03- system
2. resp system: regulation of co2 levels
3. kidneys: variable excretion/reabsorption of H+ and HC03-
31
acidosis vs alkalosis
1. acidosis:
- resp acidosis: d/t incr co2
- metabolic acidosis: d/t decr HC03-
2. alkalosis:
- resp alkalosis: d/t decr co2
- metabolic alkalosis: d/t incr HC03-
32
resp acidosis
- incr co2
- causes: anything effecting us to expire air
- compensation:
- resp: kidneys reabsorb HC03- and excrete H+
- met: incr rate and depth of breathing
33
metabolic acidosis
- decr HC03-
causes:
- excess HC03- loss from diarrhea
- incr buffering
- hyperkalemia
- kidney disease or failure
compensation:
- resp: hyperventilation to expel c02
- met: kidneys reabsorb HC03- and excrete H+
34
resp alkalosis
- decr co2
causes:
- hyperventilation
compensation:
- resp: rebreathing (breathing in the air you just expired)
- met: kidneys excrete HC03- and reabsorb H+
35
metabolic alkalosis
- incr HC03-
causes:
- excess HCL loss from stomach
- hypokalemia
- excess ingestion of antacids
compensation:
- resp: hypoventilation to incr co2 levels
- met: kidneys excrete HC03- and reabsorb H+
36
summary of ROME
1. resp:
- incr PCo2 = decr pH (acidosis)
- decr PCo2 = incr pH (alkalosis)
2. met:
- incr HC03- = incr pH (alkalosis)
- decr HC03- = decr pH (acidosis)
37
Summarize the different causes and types of pain
1. nociceptive pain: identifiable issue causing damage
- somatic pain: within the sin or deeper (well localized)
- visceral pain: within or around the organs (poorly localized)
2. neuropathic pain: dysfunction of the NS, no identifiable tissue damage (pain preserved without a stimulus)
38
Describe the physiological pathway of pain
carried by afferent fibres:
1. A-delta fibres (larger, myelinated): low pain threshold
- mechanical and thermal receptors
- Sharp and well localized pain sensations
2. C fibres (small, unmyelinated): high pain threshold
- thermal mechanical and chemical receptors
- doll throbbing aching burning pain poorly localized
39
Explain the gate-control theory in relation to pain control
pain stimuli can be inhibited by:
- afferent impulses from touch stimuli coming into the SC at the same time as the pain stimuli (stimulates IN that inhibit nociceptors 1st order afferent neuron)
- descending signals from the brain (release endorphins directly onto nociceptor first order a freight neurons or indirectly via IN)
40
Describe the various characteristics of pain as discussed in class
41
Compare acute and chronic pain
Chronic:
- lasts more than 3 months
- maybe become an issue of the nerve hypersensitivity
- localized within CNS
- mix of excitatory and inhibitory systems
42
Summarize the components of pain management
- ultimate goal is to remove the cause of pain
- the 4 P's
43
Apply and analyze how physical activity can affect and be affected by different types of pain
- desensitization the sensitized nervous system
- exercise is an anti-inflammatory
- helps to visualize the movement first
- find enjoyable exercise
44
Describe inflammation
- defense mechanism
- caused by stimulus (pathogen, physical damage)
- can be acute or chronic
- Goal: respond to stimul > remove cause > remove damage > repair tissue > restore balance
- warmth and redness d/t incr blood flow to area
45
Compare acute and chronic inflammation
46
Summarize the process of acute inflammation response
1. Initiation and amplification: Chemical mediators released into blood inside of injury by resident immune cells, more immune cells are recruited to area
2. Destruction: utilization of injury and debris removal by chemical mediators in immune cells
3. Termination: cytokines and chemokines end of the inflammatory process
47
Pain threshold
- level of stimulation needed to activate the pain pathway and she will proceed with a signal to the brain
48
pain tolerance
- ability to withstand pain
- modulated by endorphins
- depends on genetics
49
pain and perception response
- affected by age, family traditions, prior experience, fear/anxiety
- individualized and subjective
- diff responses to stimulus
50
endorphin
Neurotransmitter that helps reduce pain
51
key points of reconceptualizing pain
1. pain level is not proportionate to tissue injury
2. pain is modulated by many factors
3. the relationship between pain and the state of the tissues becomes less predictable as pain persists
52
describe the signs of acute inflammation
1. pain:
- pressure on nerves
- chemical mediators (nociceptors)
2. heat /redness:
- incr blood flow to area
3. swelling:
- edema (incr capillary permeability)
4. loss of function:
- pain or inflammation
- injury itself
All is localized or systemic
53
Summarize the process of healing from inflammation and the factors that affect it
- Chemical mediators are released into the blood at the side of the injury by resident immune cells
- Actions of the mediators:
- pain response: bind to nearby nociceptors
- vascular response: Vasco dilation and increase capillary density
- cellular response: attractive nuisance to the side of injury via chemotaxis
54
cytokines
Proteins that coordinate any response
- a pro inflammatory and anti-inflammatory
55
cells that are involved in inflammatory response
- platelets: release blood clotting proteins at the wound site if needed ( only physical tear)
- mast cells: secrete chemical mediators
- neutrophils: migrate to the site and secrete factors that kill pathogens and phagocytosis to remove pathogens and debris
- macrophages: secrete cytokines and phagocytosis to remove pathogens and debris
56
exudate and the characteristics
- interstitial fluid collected in the area of inflammation
1. serous: classic edema (watery, fluid plus small amounts of protein and white blood cells)
2. fibrinous: repairing tissue damage (thick and sticky higher cell in fibrin content)
3. purulent: suggests bacterial infection -> like puss (thick and yellow green color, higher white blood cells and debris, may contain microorganisms)
4. hemorrhagic: blood vessel damage
- abscess: pocket of purulent exudate in solid tissue
57
Non-pharmaceutical treatments of acute pain/inflammation
- compression: fluid build up
- cold: vasoconstriction, first 24 hrs
- hot: promotes circulation, after 24 hrs
- elevation
- rest and avoid further trauma
58
potential fates of healing
1. resolution: damaged cells recover
2. regeneration: damage cells are a cell type that can divide by mitosis and be replaced by identical cell types
3. Replacement: damage cells replaced by connective tissue (scar tissue= collagen crosslinking), loss of function in area
59
Non-pharmaceutical treatment of chronic inflammation
1. nutrition: anti-inflammatory versus inflammatory foods
2. Aerobic and assistance exercise
3. Sleep quality/quantity
4. stress reduction
60
Describe and compare the different types of pathogens
- microorganism that can cause a disease
1. bacteria
2. viruses
3. fungi
4: Protozoa
5. prions
61
Describe the different modes of transmission of infectious disease
1. direct contact
2. indirect contact
3. droplets
4. aerosol
5. vector borne
62
Summarize the physiology of infection in terms of time course
1. incubation period: growing the organism
2. prodromal period: signs and symptoms
3. acute period: symptoms
63
List the components of the immune system and the purpose of each
1. organs and tissues
- bone marrow, spleen, thymus gland, tonsils
- lymph nodes and vessels
2. cells:
- leukocytes
3. molecules/chem mediators:
- cytokines
- antibodies (immunoglobulins- adaptive system)
64
Explain the innate and acquired immune response in terms of the components and steps involved for each
65
Summarize the four types of immune system pathologies
1. hypersensitivity reactions: immune system overreacts to cause damage instead of hypersensitivity
2. autoimmune conditions: cant distinguish between self-and non-self antigens
3. immunodeficiency: consequences of a defect in one or more components of the immune system
4. immunocompromised condition: leaves the body vulnerable to infection d/t an issue with the normal functioning of the system
66
Use Allergic Asthma to explain the basis of a hypersensitivity reaction
- chronic inflammation of the airways
- response to something in the environment that causes more inflammation
Results:
- local inflammatory response
- bronchospasm
Trigger>dendritic cell>Helper T cells>cytokine> mast cells and eosinophils>more cytokines and leukotrienes
67
Explain the general mechanism of autoimmune disorders
1. immune system forms antibody to self antigens
2. autoantibodies attack self antigens and immune complex deposit
3. inflammation and tissue damage occur
68
Give an overview of Lupus and explain how it is considered an autoimmune disorder
- etiology unknown
some trigger>causes cell damage and/or death>immune system reacts and forms antibodies>inflammation
69
Explain the causes and effects of immunodeficiency
- primary: inherited defect in immune system
- secondary: induced as a consequence of a disease, treatment or malnutrition
70
Give an overview of HIV and AIDS (what they stand for) and how it is considered an immunodeficiency
- HIV: human immunodeficiency virus
- AIDS: acquired immunodeficiency syndrome (complications that arise from the virus)
HIV> T helper cells, dendritic cells, macrophages>HIV enters cells and inserts RNA onto immune cells> whenever immun cell is activated, it produces more of the virus
71
Summarize the exercise considerations for people living with HIV
- people with AIDS and HIV are often asymptomatic
- improve CVD risk, BC, muscle function, psychological symptoms and other outcomes of HIV
72
Summarize the trajectory of bone density changes across lifespan for male and female and explain factors that affect it
1. genetics
2. hormones
3. PA
4. nutrition
73
Define osteoporosis and summarize the etiology and risk factors
- critically low bone mass and density with loss of bony matrix and mineralization
1. primary: age related (higher in older females)
2. secondary: d/t another disorder or issue
Risk factors:
- genetics
- age
- sex
- menopause
- sedentary life
- nutrition
74
Explain the pathophysiology of osteoporosis
1. decr in estrogen -> incr osteoclast and decr osteoblast
2. chronic inflammation -> cytokines incr osteoclast
3. age related decline -> decr in stem cells
4. modifiable factors: nutrition, PA, alcohol, medication
75
Summarize the signs, symptoms, treatment and prevention of osteoporosis
symptoms:
- spontaneous fractures
- back pain from compression
- abnormal curvature os spine with loss of height
treatment:
- dietary supplements
- pharmaceuticals: promote bone formation
- estrogen replacement therapy for postmenopausal females
76
Define osteoarthritis and describe it's risk factors, signs/symptoms and treatment
- mechanical degeneration/inflammation within synovial joint
- breakdown of cartilage
risk factors:
- age, genetics, obesity, joint injury, inflammation
symptoms:
- asymmetric , <4 joints
- beginning and end of day stiffness, incr with activity
- pain with movement, weight bearing
- limited ROM
- localized inflammation
- enlarged joints
treatments:
- exercise , phsyio
- pharmaceuticals
- hyaluronic acid or corticosteroid injections
- surgery
77
Explain the pathophysiology of osteoarthritis
78
Define rheumatoid arthritis and describe it's risk factors, signs/symptoms and treatment
- chronic inflammatory disease - autoimmune
- exacerbations and remissions
- slow onset, bilateral joints
risks:
- genetics, sex (females higher), environmental hazards
symptoms:
- 3+ joints, symmetrical
- finger joints
- morning stiffness
- limited ROM
- joint deformities
- potential blood markers
treatments:
- treat to target (disease modifying anti-rheumatic drugs)
- multidisciplinary therapy
- all exercise
79
Explain the pathophysiology of rheumatoid arthritis
80
bacteria
- single cell organisms
- rigid cell wall
- contains DNA/RNA
- can survive and divide outside a living hos
81
viruses
- small intracellular parasite
- protein coats the DNA/RNA
- requires a living host to replicate, but can remain dormant outside for a bit
82
fungi
- found everywhere
- eukaryotic single cells (yeasts) or chains of cells (molds)
- produce spores and become airborne
- only certain are pathogenic
- allergies
83
Protozoa
- parasites
- complex eukaryotic organisms
- can live independently
84
prions
- no genetic material
- transmitted by protein particles (prions) that can self propagate
- symptoms are neurodegenerative
85
reservoir
the source carrying the infection
86
leukocytes involved in adaptive immune response
1. antigen presenting cells:
- dendritic cells
2. B lymphocytes:
- recognizing specific antigens that have invaded the body before
3. T lymphocytes:
- recognize specific antigens that presented by the dendritic cells
- turns into
87
what happens during an innate immune response
88
steps of the initiation of the adaptive immune response
89
difference between osteoclasts, osteoblasts, osteocytes and osteogenic cells
- osteoclasts: breakdown bone (resorption)
- osteoblasts: create new bone tissue
- osteocytes: bone remodeling and maintaining health
- osteogenic cells: stem cells to create and repair bone
90
bone structure
- compact bone: cortical, dense outer region
- spongy bone: trabecular, deep and mesh like
- red bone marrow: site of hematopoiesis
- yellow bone marrow: found in long bones of adults (adipose tissue)
91
exercise prescription for osteoporosis
-goal: prevent fractures
- 150 min/wk mod-vig aerobic exercise
- weight bearing
- progressive resistance training (2d/wk, 8-12 reps)
- challenge balance and felx
- spine sparing strategies
92
Describe the types of fractures and be able to identify fractures according to classification (14)
1. complete: bone is broken to form 2+ pieces
2. incomplete: partially severed (ex-greenstick fracture)
3. open (compound fracture): skin is broken, higher risk of infection
4. closed: skin not broken
5. simple: single break, bone ends maintain alignment
6. comminuted: multiple fracture lines and bone fragments
7. compression: bone crushed into smaller pieces and collapses
8. spiral: angles around the bone
9. transverse: across the bone (horizontally)
10. longitudinal (linear): along the axis of the bone (ex-stress fracture)
11. oblique: at an angle with respect to the diaphysis
12. impacted: one end forced into the other at the location of the break (ex-compression)
13. stress: repeated excessive stress
14. pathologic: weakness in bone structured/t conditions, causes spontaneous fractures
93
Summarize the signs, symptoms and variable treatment of fractures
signs/symptoms:
- pain, swelling, bruising, inability to move joint
- misaligned, shortened, deformed
treatments:
- immediate immobilization
- surgery if needed
- exercise to maintain ROM, muscle mass, circulation
94
Explain the steps of the physiology of bone healing
1. hematoma formation:
- bone break > bleeding from surrounding vessels > clot forms > fibrin mesh forms to seal off site
2. inflammatory phase:
- inflammatory response d/t cell damage/necrosis
- growth of granulation tissue within fibrin mesh
- fibroblast/chondroblasts migrate and from the procallus (fibrocartilaginous callus)
3. reparative phase:
- osteoblasts generate new bone over the procallus creating new bone
4. remodeling:
- response to mech stress
- remodeled by osteoblast/clasts
- excessive callus removed and more compact bone laid down
95
Summarize the factors that affect bone healing
- age (younger kids)
- extent of damage
- prolonged inflammation
- systemic factors (aging , circulatory, diabetes, nutrition, smoking)
- complications
96
Describe potential short- and long-term complications of bone healing
short term:
- broken ends can damage surrounding tissue
- compartment syndrome (bleeding or edema > incr pressure > impaired blood supply, potential necrosis)
- ischemia d/t cast compression (not enough blood flow)
- infection (most common in surgical intervention)
- osteomyelitis (when bacteria enters the bone)
long term:
- healing abnormalities:
- malunion: bones don't heal in alignment
- delayed union: takes longer to heal
- nonunion: failure to heal
- mobility complications:
- joint stiffness
- instability
- side effects of long term immobilization:
- pressure injury
- deep vein thrombosis (blood clots)
97
Define concussion, list common causes and summarize the 2 main types of concussion-related injuries
- mild traumatic brain injury induced by biomechanical forces
- no obvious brain trauma (functional damage)
common causes:
- motor vehicle accident
- contact sport
- falling down stairs
- domestic violence
1. coup-contrecoup injury:
- from impact causes brain to hit on opposite side of skull
- results in stretching and shearing of neurons
2. torque (rotational) injury:
- head neck or twist causing brain to rotate
- results in stretching and shearing of neurons
98
Describe the pathophysiology, diagnosis, symptoms and treatment of concussion
symptoms:
- somatic: nausea, headache, dizziness, sensitivity to light
- cognitive: concentration, memory issues
- mood: emotion, anxiety, depression
- sleep: too much/ to little
treatments:
- early mild-mod PA reduces time-to-symptom-free
- avoid activity that causes excess brain movement
- rehabilitation with support
- avoid repeated concussion (Chronic Traumatic Encephalopathy)
99
Link concussion to the pathogenesis of Chronic Traumatic Encephalopathy as a possible consequence
- repeated concussion
1. damage d/t misfolding of structural protein (tau protein)
2. clustering and buildup around blood vessels
3. neuronal death
4. brain atrophy
5. dementia
100
Define and characterize Spinal Cord Injury
- obstructs the transmission of neural messages through the spinal cord > loss of somatic and autonomic control
1. tetraplegia:
- C1-T1 ( loss function of all limbs)
2. paraplegia:
- T2-onwards (lost function of lower limbs)
3. complete: loss of all sensory and motor function
4. incomplete: some functions remain
101
Describe the pathophysiology of SCI in terms of the 2 phases and sub-classification
1. primary injury:
- sudden trauma to spine > acute SC compression, shearing stress, severing (incomplete /complete) > acute impact to neurons, glial cells, and neural parenchyma
2. secondary injury:
- primary triggers secondary injury (biochemical/metabolic and mech changes in neural tissue)
102
Explain briefly how the ASIA Scale is used to classify the type of SCI
103
Summarize the systemic effects of SCI in relation to autonomic dysregulation
1. cardiovascular: issues with regulation of HR and BP
2. pulmonary: ventilation severely impaired in injuries above C5
3. bowel and bladder functioin, sexual function (sacral)
4. thermoregulation (sacral)
5. hyperreflexia: d/t control disinhibition of spinal reflex arcs > inappropriate activation of the stretch reflex
6. autonomic dysreflexia
104
Explain the side effect of autonomic dysreflexia in relation to an undetected stimulus (e.g. full bladder)
- uncontrolled SNS response to an afferent stimulus below SC 1
- result: widespread vasoconstriction below level of injury > incr BP > baroreceptors sense and send signals to medulla > parasympathetic response (above injury) > decr HR and vasodilation
- can be life threatening
- sudden acute hypertension, bradicardia
105
Summarize the considerations for exercise in SCI and apply the PA Guidelines for adults with SCI
- maintaining/building strength
- maintaining general health and fitness
- consider autonomic limitations, medication
- consider potential comorbidities:
- respiratory complications
- CVD
- pressure injuries, joint contractures, osteoporosis
106
colles fracture
- distal radius fracture with dorsal angulation and impaction
107
abnormal curvatures of the spine
- side effect of osteoporosis or arthritis
1. lumbar lordosis: spine curves inward at lower back
2. kyphosis: hunch back, rounded upper back
3. scoliosis: S or C shaped sideways, genetic
108
Describe the etiology, pathogenesis, diagnosis and treatment of Multiple Sclerosis
109
Summarize and apply the exercise considerations for Multiple Sclerosis
110
Describe the etiology, pathogenesis, diagnosis and treatment of Parkinson's Disease
111
Summarize and apply exercise considerations for Parkinson's Disease
112
skeletal muscle disorders
1. disuse atrophy
- if not being innervated everyday they start to atrophy
- degeneration d/t SCI immobilization
2. muscular dystrophies
- genetic
- progressive degeneration of skeletal muscle fibres (necoris)
- muscle fibres replaced by adipose and CT
113
NMJ disorders
- durg/toxin induced
1. Myasthenia gravis:
- autoimmune
- attack on the nicotinic ACH receptors
- well controlled and not progressive
- lower density of receptors on motor end plate (lower response and fatigued muscles)
114
