PT 663 exam 2

what are front casters?

small wheels in front which allow for easy change in directions

what are push rims

point of contact of strokes and change in direction

what is a rear wheel

provide stability and point for manual propulsion

what are wheel locks/breaks?

brakes on wheel or at the push handles

what are the characteristics of leg rests

can be elevating, swing-away or permanent; typically length via push-pins

what are footplates

flip up for storage and transfers, down for support for feet

how to estimate the levels of assistance

Low severity: independent → Mod A

• mild (3/5) unilateral or bilateral weakness

• mild cognitive defects

• mild sensory impairments

• able to follow some single step commands

• receptive to verbal and/or tactile cues

high severity: Min A → Max A 2x

• significant (<3/5) unilateral or bilateral weakness

• severe cognitive deficits

• severe sensory impairments

• low level of arousal

• significant motor planning deficits

• unable to follow single step commands

• impaired motor planning

what is the environmental set up for a pivot transfer?

• have all equipment nearby

• clear path

• transfer surface as close as possible (45-65 degree angle)

• Maybe remove arm rests/swing leg rests

• Squat-pivot: equal height surfaces or higher to lower

what are key points for providing a pivot transfer?

1. systems screen to familiarize impairments

2. estimate level of assistance required

3. identify appropriate technique

4. proper positioning for guarding (anterior/lateral approach)

5. transfer toward the stronger side

6. points of contact: posterior hips/low back, mid back, ischial tuberosities

what is postural control?

controlling of the bodies position in space for the purposes of orientation and stability

• postural orientation: posture, ability to maintain an appropriate alignment between body segments, body and the environment of the task

• postural stability: balance, ability to control COM in relationship to BOS

what is static, dynamic, and functional balance

static

• ability to maintain the center of gravity within BOS while standing/sitting still

dynamic

• maintaining upright position while COM and BOS are moving, and COM is moving outside BOS

functional

• ability to perform daily movement tasks requiring balance, may involve static and dynamic balance

how can postural orientation impact stability?

diseases could impact an individuals ability to maintain normal postural orientation, changing the position of the COM over the base of support

• or they do not have the motion to adjust for balance

how is postural orientation used to regain postural stability

arms/legs/trunk moved to correct a shift in COM over BOS

what is the center of mass? center of gravity?

COM: point at the center of the total body of mass (3D)

• just anterior to L2

COG: vertical projection of COM in 2D plan, usually on ground

• average location of the GRF

• standing is never truly static - COP and COM are rarely aligned

• muscles activate to align COP with COG

how does the position of COM impact stabilty?

• higher (away from surface): less stable

• lower (closer to surface): more stable

what is the relationship between BOS and COG

• when within BOS: increased stability

• outside of BOS: decreased stability

what is the limit of stability?

boundaries which the body can maintain stability without changing the base of support

• static balance concept

dynamic stability limit

interaction between the position and velocity of COM. boundaries of the combined COM velocity and position possible without the need to change BOS

• Greater velocity + greater shift in COM

what is the goal of the postural control system?

postural orientation and stability

• controls COM/COP through muscle control

• controlling/adjusting BOS if needed

what is a steady state task? reactive? proactive?

steady state:

• ability to control COM relative to BOS in predictable conditions

reactive:

• require ability to recover a stable position following an unexpected perturbation

proactive:

• ability to activate muscles for control of COM in advance of a potentially destabilizing movement

feed forward and feedback processes in postural control

Feed forward: anticipatory

• postural responses made prior to a voluntary movement

Feedback: compensatory/reactive

• sensory feedback from unexpected external perturbations triggers postural responses

what are the sensory systems involved in balance?

• vision

• somatosensory

• vestibular

why is balance tested?

• to determine risk of falling

• determine what areas of postural control are affected/remediable

• quantify deficits and justify need for therapeutic intervention to measure changes

which populations have an elevated risk of falling?

• older adults

• physically/neurologically comprimised children and adults

what contributes to high fall risk in older adults

sensory

• vision decrease

• vestibular decrease

• little to no change in somatosensory

musculoskeletal

• muscle strength decrease with age

• bone strength decrease

• changes in motion/flexibility

cognition/cognitive

• slowed with aging/disease

how do we determine a fall risk?

• balance performance measures assess balance, not fall risk

• cut off scores are generally determined retrospectively

what is usual vs best performance?

clinic tends to be the “best performance”

• internal and external environment (rushing, dark, not focused, etc)

• encouragement and cues

• control vs lack of control

what is dual task?

interplay between postural control limitations and environmental task limitations

• cognitive load

• physical load

• combined

what may balance interventions address?

structure/function:

• motion, force, energy, control

activity/task specific movement

• sitting/standing

• single or dual tasks

• simple or complex

• static or dynamic

• closed or open environments

what are the principles of balance training

• appropriate postural orientation

• improving task performance

• optimal challenge

• changing environment

• cognitive load

• sensory challenges

• speed

what is ventilation?

bulk flow of air into and out of lungs

• occurs down a pressure gradient

• P_in (inside alveoli) and P_out (outside of body)

how does air get into the lungs in ventilation?

Muscles are used to increase volume (expand thorax) → decreases pressure

• P_in < P_out

• air flows in until P_in = P_out

how does air get out of the lungs during ventilation?

muscles relax which decreased volume → Increases pressure

• P_in > P_out

• air flows until P_in = P_out

Thorax typical volume

the chest wall generally wants to expand/have a large volume

• when collapsed (non-pathologically) it will bounce back to an expanded position

at rest, what is the equilibrium pressure for the lung

can expand with external forces, but wants to maintain a small equilibrium volume

when the lung and thorax are coupled what happens to the equilibrium

chest wall wants to expand + lung wants to collapse

• they pull against each other, creating a 3rd pressure

• intrapleural pressure: often negative at rest

what is the expanding vs collapsing pressure

pressure between the opposing forces of the chest wall and the lungs

• Expanding pressure: negative

• Collapsing pressure: positive

what is the functional residual capacity?

resting volume of the lung and chest wall (they are equal and opposite)

what is total lung capacity?

maximal volume of chest wall and lung with expanding pressure

what is residual volume

minimum volume of coupled chest wall and lung with collapsing pressure

what is the transmural pressure?

pressure keeping the alveoli open - difference between the alveolar pressure and intrapleural pressure

• typically positive at rest (+5: pulling open)

transmural pressure during ventilation

inspiration

1. chest wall pulls lungs open → more negative intrapleural pressure + expands lung which creates negative alveolar pressure (larger intramural pressure)

2. peak inhalation: alveolar pressure at equilibrium → intramural pressure = to intrapleural pressure

expiration

1. positive pressure in alveolus (+1) drives air out, intramural pressure is gradually decreasing

2. goes back to equilibrium

what is minute ventilation

Tidal volume x respiratory rate

• Tidal volume = 450ml

• RR = 12

• Minute ventilation = 450 × 12 = 5.4 L/min

• BUT, some stay in the conducting zone

what is the conducting zone? how does it impact ventilation?

anatomic dead space where gas exchange does not occur (about 150 ml)

• we never get all of the air in our lungs out, so some of the “used” air remains

  • 450 ml of fresh air

  • 300 ml of fresh air got into alveoli (because the last 150 is stuck in dead space)

what is alveolar ventilation?

(Tidal volume - dead space volume) x respiratory rate

• (.45 - .15) x 12 = 3.6L/min

how does gravity act on the lungs?

• weight of the lungs with gravity has more expansive pressure on alveoli in the apex of the lung

• alveoli in the base of the lung expand less due to gravity, which allows for greater room for expansion with breathing, allowing for more air intake in the base

What is the inspiratory reserve volume

between top of tidal volume and top of maximal inhalation

what is vital capacity?

difference between maximal inhalation to bottom of maximal exhalation

expiratory reserve volume

amount of exhalation below tidal volume

what is total lung capacity

residual volume + vital capacity

what is functional reserve capacity?

difference between end of tidal volume and residual volume

what is reserve volume on a spirometer graph?

volume that cannot be expired from lungs

Measures of air flow

obtained during max exhalation as quickly as possible

• FVC: forced vital capacity

• FEV₁: volume of air exhaled in 1 second

  • more impacted by obstructive diseases than FVC

• FEV₁/FVC

what is pneumothroax?

collapsed lung

• air in the thoracic cavity between the lung and chest wall (sucks air in due to negative pressure

weakness (high spinal cord injury) of respiratory muscles

C3 or above

• paralysis of diaphragm

• requires mechanical ventilation

weakness (low spinal cord injury) of respiratory muscles

strong diaphragm, weak intercostals and abdominals

• upper chest paradoxical pattern

• the chest wall collapses as the diaphragm lowers (since they cannot resist that motion)

• only the abdomen can expand

impact of asthma on ventilation

impact on airway diameter

• bronchospasm → decreased diameter and increased resistance to airflow

• increased pressure gradient required to maintain flow → increased muscle effort

• increased work of breathing

how does dynamic compression impact ventilation?

airway diameter changes during breathing

• increased diameter during inspiration

• decreased diameter during expiration

• occurs in forced exhalations

emphysema and ventilation

increased compliance

• more stretchy and has a larger resting position

  • takes less pressure to increase the same amount of volume

• decreased elastic recoil of lung

• elevated FRC - decreases mechanical advantage of diaphragm (less room for movement in contraction)

• have to use muscle to exhale (due to decreased elasticity)

• increased work of breathing

pulmonary fibrosis and ventilation

decreases compliance

• need more muscular effort to expand the lung

• an increase in tissue stiffness

• lower FRC (low lung volume, low diameter, increased resistance)

• increased air pressure for the same lung volume

what is surfactant and surface tension in the alveoli?

• surface tension causes alveoli to collapse

• surfactant decreases surface tension to keep alveoli open

• loss of surfactant leads to alveolar collapse/atelectasis

what are the defense systems for the lung in the nasal passages

• nose hairs filter larger particles from air

• turbinates trap larger particles

what are the defense systems for the lung in the respiratory zone

• macrophages and immune cells engulf particles and bacteria

what are the defense systems for the lung in the conducting zone

mucocilliary escalator

• mucus traps particles

• cilia sweeps mucus and trapped particles to larger airways and oropharynx

• impaired by smoking, dehydration, lung pathology, anesthesia

what do beta cells do in the pancreas

produce insulin to reduce blood glucose levels

what do alphacells do in the pancreas?

glucagons

• increase blood glucose levels

what does insulin do in the liver?

released with high glucose levels

stimulates glycogen formation (storage of glucose) from the blood

what occurs when theres is low blood sugar

promotes glucagon release

• stimulates glycogenolysis to convert glycogen into glucose

• also gluconeogenesis: nonfuel tissue to usable glucose

what are the goals of counter-regulatory hormones

raise blood glucose levels to prevent hypoglycemia

what is the sequence of glucose

1. hyperglycemia → insulin release

2. Acts on liver to convert glucose to glycogen

3. Binds to receptors on cell membranes to help open glucose transporter channels

what is Glut-4 transporters?

channel, when open, pulls glucose from system into cells

• on fat/muscle cells

what is the function of counter regulatory hormones?

stopes the Glut-4 transporter opening

• more glucose remains in blood stream

what is diabetes mellitus?

disorder of the glucose metabolism

• deficiency of insulin

• inability to use insulin at peripheral sites (insulin resistance)

prevalence of diabetes mellitus in the US?

1/10 individuals have the condition

• more than 1/3 have prediabetes

types of diabetes?

type 1

• 90-95%

• can develop at any age

type 2

• 90-95%

• risk factors: physical inactivity, overweight, diet, family history, age, BP, ethnicity, stress, impaired glucose tolerance

Gestational

• any degree of glucose intolerance with onset or first recognition during pregnancy

pathogenesis of type I DM

genetic predisposition → Immune response against normal beta cells → immune attack (beta cell destruction)

pathogenesis of type 2 DM

genetic predisposition + obesity → insulin resistance (body cannot use insulin in peripheral sites) → body thinks there is not enough insulin (overactive) → exhaustion of beta cells → impaired beta cell function → hyperglycemia

how is diabetes diagnosed?

• HbA1c or A1c: average of blood glucose over 3 months

• fasting plasma glucose

• oral glucose tolerance test

diagnostic measures for diabetic and prediabetic

diabetic

• A1c: >6.5

• Fasting: >126

Prediabetic

• A1c: 5.7-6.4

• Fasting: 100-125

common signs and symptoms of DM

• polyuria: urination

• polydipsia: increased fluid intake

• polyphagia: increased hunger

• weight loss/gain: wasting and cellular starvation

• fatigue: energy loss and catabolism

what is ketoacidosis?

acidic fat by-product called ketone bodies

• moderate to high levels of ketones in urine is a RED FLAG TO EXERCISING (30-80 or more mg/dl)

what glucose levels are concerning, especially for ketoacidosis?

>250

macrovascular long term complications of DM

• cardiovascular diseases (CVD)

• atherosclerosis: fat deposits on BV

• stroke

• peripheral artery disease

microvascular long term complications of DM

• nephropathy

• retinopathy

• neuropathy

MSK impairments commonly associated with DM

• frozen shoulder

what are predictive of DM complications?

chronicity and high uncontrolled blood sugar levels

conventional risk factors for complications

• dyslipidemia

• hypertension

• coagulopathy

vascular disease

• venoconstriction + inflammation + thrombosis

• occur earlier and more extensive in DM

• lead to CAD, stroke, peripheral vascular disease

peripheral vascular disease

• symptoms: cramping while walking, pain relieved by rest, pain at rest, gangrene

• examine: peripheral pulses, skin and nail condition, ankle brachial index

nephropathy

micro-vessels in kidneys over time become more atherosclerosis → renal disease → end stage renal disease → dialysis

retinopathy

DM is second leading cause of adult-onset blindness

• microaneurysms

• blurred vision, specks of blood “floating”

• regular eye checks

peripheral neuropathy (PN) sensory

• 2/3 of individuals

• small + large fiber

• feet > hand, pain, tingling, burning, numbness, complete anesthesia

peripheral neuropathy (PN) motor

• intrinsic foot muscle weakness + deformity → increased risk of ulceration

• charcot neuroarthropathy: destructive loss of protective sensation, foot bone collapse

peripheral neuropathy (PN)

50-75% of people with DM have some form

peripheral neuropathy (PN) autonomic

• skin is dry, cracked, callous formation

• loss of fat pad cushion → ulceration

joint complications of DM

• deformities of toes, midfoot collapse

• limited ROM of ankle, foot, shoulder

• UE disorders: frozen shoulder, carpal tunnel, trigger finger

muscle complications of DM

• wasting in foot and hand

• loss of muscle strength

• high prevalence of rotator cuff tears

function complications of DM

• slow gait speed

• slow 5 x STS

• impaired balance, fall risk

what is the goal of diabetes management?

control/regulate blood sugar levels

• Target HbA1c <7

• Type 1: exogenous insulin (injection or pump)

• Type 2: oral hypoglycemic medication, dietary control, exercise, insulin if needed

PT considerations for patients taking exogenous insulin

they are at a higher risk of hypoglycemia with exercise