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What is the leading cause of death in the US?
Coronary heart disease
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condition in which fatty material collects along the walls of the arteries. this material thickens, hardens (plaques) and may eventually block arteries---??
atherosclerosis
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LDL is considered______(good/bad) cholesterol.
transports cholesterol _____(to/from) cells
BAD
transports to cells
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HDL is considered ______(good/bad) cholesterol.
transports _____(to/from) cells
GOOD
transports from cells
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Are the following risks non-modifiable or modifiable?
1. age (above 40)
2. genetics
3.gender
4.obesity
5. high fat diets
6. smoking
7. sedentary lifestyle
8.diabetes
9. hypertension
10. heavy alcohol consumption
1-3 non
4-10 modifiable
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when do cardiac conditions affect men? (early/late)
when do cardiac conditions affect women? (early/late)
affect men early
affect women late
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course of CAD:
C-reactive proteins
elevated C-reactive proteins
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course of CAD:
WBCs/lipids
WBCs and lipids accumulate at site
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course of CAD:
muscle cells
smooth muscle cells multiply
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course of CAD:
thrombus
thrombus formation creates obstruction
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HDL and LDL levels for norms
HDL: greater than 60
LDL: less than 100
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chest pain is also called...?
myocardial infarction
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MI is caused by?
decreased O2 to myocardium as a result of obstructed arteries
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what is the stable subtype of CAD?
chest pains with physical exertion or emotional stress
most common
predictable
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what is the unstable type of CAD?
unexpected
usually occurs at rest
can be severe and prolonged
may procede a MI
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what is the variant type of CAD?
spontaneous and nearly always occurs at rest
due to vasospasm at rest
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signs and symptoms of CAD
chest tightening
can be felt anywhere between belly button and jaw
sweating, loss of breath, palor, nausea
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treatment of CAD
usually subside with rest
coronary vasodilators
if it persists seek medical attention
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what is the primary cause of a MI?
atherosclerosis
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what are the 3 primary mechanisms of MI?
1. thrombus obstructs pathway
2. vasospasm leads to total obstruction
3. embolus flows thru coronary a. before it lodges in smaller branch
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signs and symptoms of MI
angina greater than 20 mins
sweating, loss of breath, palor, fear and nausea
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what is a silent heart attack?
no symptoms
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treatment of MI
CPR
rest, O2 therapy, beta blockers, ace inhibitors, surgeries
if blood can be restored within 20-30 mins prevents damage
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co-morbidities of MI
- stroke
- CHF
- pulmonary embolism
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what is a cardiac dysrhythmia?
deviation from hearts normal beat cycle
caused by interference in hearts conduction system
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types of cardiac dysrhythmias?
- SA node
- AV node
- atrial conduction abnormalities
- ventricular conduction abnormalities
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signs and symptoms of cardiac dysrhytmias
- angina
- fainting
- SOB
- sweating
- similar to all other cardiac conditions
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purposely destroying a dysfunctional area of the heart causing the abnormal rhythm
cardiac ablation
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whats another name for asystole?
cardiac arrest
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why does asystole occur?
loss of consciousness due to lack of O2 to brain
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causes of pneumonia
- infection
- aspiration
- organisms such as bacteria, fungi, virus
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course of pneumonia
depends on type and how soon treatment is started
can be very fatal in very old or very young
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type of pneumonia:
inflammation of alveolar wall and leakage of cells, fibrin, and fluid into alveoli causing consolidation
lobar pneumonia
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type of pneumonia:
inflammation and purulent exudate in alveoli often arising from prior pooled secretions or irritations
bronchopneumonia
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type of pneumonia:
interstitial inflammation around alveoli
interstitial pneumonia
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clinical features of lobar pneumonia
high fever
cough with rusty sputum
rales progressing to absence of breath
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clinical features of bronchopneumonia
mild fever
cough with yellow-green sputum
dyspnea
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clinical features of interstitial pneumonia
variable fever and headache
aching muscles
nonproductive hacking cough
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clinical features of Legionnaires
cough may be severe
diarrhea
nausea,vomitting, GI issues
headaches, muscle aches, chest pain, SOB
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clinical features of pneumocystis
difficulty breathing
nonproductive cough
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co-morbidities of pneumonia
- lung abcess
- ARDS
- sepsis
- respiratory failure
- pleural effusion
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causes of tuberculosis
- oral droplets
- coughing, forced respiratory movements
- bacteria
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who are most easily infected with tuberculosis?
children
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course of tuberculosis
anorexia, night sweats, fatigue, weight loss set in
cough gets more productive and severe
sputum more purulent
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if tuberculosis is untreated what happens?
disease destroys large portion of lungs and other organs
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what are the 2 stages of tuberculosis?
primary and secondary
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primary tuberculosis subtype
bacteria into lungs and causes inflammation
tubercle forms
caseation necrosis occurs in middle of tubercle
6-8 weeks infection complete although disease not active
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secondary tuberculosis subtype
considered active infection stage after years of infection
bacteria multiply spread into lungs and other areas
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tests for TB
skin test, blood test, sputum test
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does primary tuberculosis display symptoms?
no!
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secondary tuberculosis clinical features
gradual onset
systemic signs appear first
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signs and symptoms of tuberculosis
weight loss, anorexia, fatigue
night sweats
prolonged cough that becomes more severe
purulent sputum with blood
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co-morbidities of tuberculosis
- collapsed lung
- organ failure
- joint damage
- meningitis
- death
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cause of CF
genetic
mutated 7th chromosome
autosomal recessive
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what ethnicity does CF affect most?
whites
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what is the course of CF?
lifespan is increasing
chronic cough increases over time
respiratory failure is common cause of death
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CF and lungs
mucus obstructs bronchioles which causes air trapping
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CF and prancreas
exocrine ducts become blocked
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other organs involved with CF
small intestine
bile ducts of liver
salivary and sweat glands
reproductive organs
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tests for CF
sweat analysis
stool analysis
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clinical features of CF
- salty skin
- cant gain weight
- abdominal distention
- inability to meet growth landmarks
- fatigure--endurance issues
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co-morbidities of CF
- diabetes
- osteoporosis
- chronic infection
- cirrhosis
- collapsed lung
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cause of asthma
actual cause is unknown
children with sedentary lifestyle
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course of asthma
depends on severity
cause reversible bronchial obstruction
chronic asthma causes irreversible damage in lungs when severe and frequent
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extrinsic asthma
childhood onset
acute
type 1 hypersensitivity
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instrinsic asthma
adult onset
triggered by infections, aspirin, exercise, cold
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what happens in both types of asthma
bronchioles and bronchi constrict
increased mucus and edema
obstruction, hypoxia
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clinical features of asthma
- cough, dyspnea
- wheezing
- hypoxia
- thick mucus
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co-morbidities of asthma
- GERD
- obesity
- depression
- sinusitis
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causes of COPD
chronic exposure to lung irritants
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what is the most common cause of COPD
smoking!
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course of COPD
irreversible and progressive damage to lungs
results in hypoxia
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alveolar walls and septae are destroyed leading to permanently inflated alveolar air spaces, smoking is a cause
describes...?
emphysema
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fibrosis and thickening of bronchi wall occurs from constant irritation from smoking or exposure to industrial pollution. oxygen levels are low and during coughing episodes cyanosis occurs.
describes...?
chronic bronchitis
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irreversible abnormal dilation of the bronchi caused by recurrent inflammation and infection in the airways, indilated areas, large amounts of fluid constantly collect and become infected
bronchiectasis
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clinical features of emphysema
- gradual onset
- dyspnea on exertion then with rest
- barrel chest
- anorexia and fatigue
- clubbed fingers
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clinical features of bronchiectasis
- chronic cough with purulent sputum
- rales
- dyspnea
- hemoptysis
- weight loss
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clinical features of chronic bronchitis
- SOB
- productive cough
- cough more severe in morning
- systemic edema
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OT treatment of respiratory conditions
- ADL's
- patient education
- energy conservation techniques
- breathing strategies
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PT treatment of respiratory conditions
- breathing exercises
- strengthening and endurance exercises
- postural drainage
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in general: diabetes is caused from what?
deficiency of insulin from beta cells of islets of langerhans in pancreas
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what does insulin do?
converts sugar, starch and other foods into energy
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cause of type 1 diabetes
immune system destroys beta cells which leads to no insulin production and a build up of sugar in the blood stream
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cause of type 2 diabetes
beta cells become resistant to insulin and pancreas is unable to produce enough to overcome this resistance
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cause of gestational diabetes
placenta builds up an enzyme that is resistant to insulin
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acute complications of diabetes
- hypoglycemia (excess of insulin)
- diabetic ketoacidosis (low insulin levels, high blood sugar)
- hyperosmolar hyperglycemic nonketotic coma (insulin deficit)
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chronic complications of diabetes
- microangiopathy (rupture of small vessels and capillaries)
- macroangiopathy (obstruction of large arteries
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2 subtypes of diabetes:
initial and progressive
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initial stage of diabetes
- decreased glucose
- hyperglycemia
- glucosuria
- polyuria
- polydipsia
- polyphagia
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progressive stage of diabetes
- (more in type 1)
- excess of ketones from lack of glucose
- ketonuria
- dehydration
- dehydration can lead to diabetic coma
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Type 1 diabetes:
other names and risk factors
- IDDM, juvenile diabetes
- genetic
- environmental (viruses)
- low vitamin d
- more common in whites
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Type 2 diabetes:
other names and risk factors
- NIDDM, mature onset
- weight, inactivity
- genetic
- increased age
- high LDL/triglycerids
- low HDL
- being black, mexican, indian
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gestational diabetes risk factors
- over age of 25
- if you've had type 2 or prediabetes
- being overweight before pregnancy
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diabetes insipidus
- inability to regulate fluid
- inefficiency of production/regulation of ADH
- polyuria and polydipsia
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what are the 3 p's of diabetes?
polyuria
polydipsia
polyphagia
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clinical features of diabetes
- weight loss
- fatigue
- nausea
- glucosuria
- possible neuropathy
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levels for diabetes
70-100 mg/dL normal
100-126 mg/dL prediabetes
anything over 126 mg/DL = diabetes
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co-mobidities of type 1 and 2 diabetes
- cancer
- wound healing
- cardiovascular issues
- neuropathy
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co-morbidities of gestational diabetes
- hypoglycemia
- jaundice
- type 2 diabetes
- preeclampsia
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treatment for diabetes
- healthy diet
- monitor blood sugar
- meds
- physical activity
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OT treatment for diabetes
- ADLs
- patient education
- adaptive equipment
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PT treatment for diabetes
- exercise program
- pt education
- wound care
- muscle strengthening and mobility
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what causes burns?
- direct contact with heat
- chemicals
- radiation
- electricity
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who is most commonly burned?
white men
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course of burns
depends on severity, cause of burn, areas impacted
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what is the rule of 9's?
- head and each arm 9%
- each leg 18%
- ant/post surface of trunk each 18%
- groin 1%
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superficial partial thickness burns
- formerly 1st degree
- damage to epidermis and upper dermis
- red dry skin painful to touch
- heal well without scar
- (mild sunburn)
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deep partial thickness burns
- formerly 2nd degree
- damage to epidermis and part of dermis
- area becomes red, blistered, and painful, skin appears waxy
- burn heals by regenerating from edges
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full thickness burns
- formerly 3rd and 4th degree
- destroys all skin layers
- initially may be painless due to nerve destruction
- skin can be black white yellow brown
- these require grafts
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mechanism of injury of burns
- scald
- flame
- direct contact
- electrical
- chemical
- non-accident
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healing phase of scars:
phase 1
- (less than 1 week)
- body removes dead/dying skin
- body fights infection
- body sends skin repairer cells
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healing phase of scars:
phase 2
- (few weeks)
- body makes collagen fibers to form scar tissue
- body creates new blood vessels in burned area
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healing phase of scars:
phase 3
- (months to years)
- scar tissue matures
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PT/OT intervention for burns
- exercises for joint mobility
- gaining function thru ADLs
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co-morbidities
- inability to sweat
- change in skin strength, color, sensation
- need for skin rehydration
- shock
- pain
- respiratory problems
- infection
- metabolic needs
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what is osteoarthritis?
wear and tear
DJD resulting in pain, stiffness, loss of function
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does OA affect other organs?
NO!
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what is the primary form of OA?
obesity and aging
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what is the secondary form of OA?
injury or abuse
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what is the genetic component of OA?
articular cartilage has acclerate breakdown
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course of OA
- progressive
- cartilage becomes stiff and loses elasticity
- loss of cartilage means joint loses ability to be shock absorber
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pathophys of OA
- excessive mechanical stress cause articular cartilage breakdown
- joint becomes rough and worn
- tissue damage releases enzymes which accelerate disintegration of cartilage
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what happens when OA get more progressed/
cysts and bone spurs develop and can break off into synovial cavity
joint becomes more narrow
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diagnosing OA
x-ray, MRI, blood tests
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clinical features of OA
- decreased ROM
- aberrant movement
- muscle atrophy
- crepitus
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clinical features of OA if TMJ involved
mastication as well as opening/closing problematic
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clinical features of OA if hands involved
heberden's node-bony enlargement of DIPs
swelling
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subtypes of OA
inflammatory
erosive
primary
secondary
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inflammatory OA
- seen in middle aged women
- affects PIPs and DIPs
- treated with NSAIDs
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erosive OA
- erosion of cartilage
- seen in hands
- pain, tenderness, swelling
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primary OA
- idiopathic
- seen in older adults
- caused by wear and tear
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secondary OA
- DJD of synovial joints
- seen in younger population
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co-morbidities of OA
- upper limb sprain
- synovial and tendon disorders
- obesity
- ischemic heart disease
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general treatment for OA
- no specific treatment to hault degeneration
- reduce joint pain while maximizing function
rest, diet, minimal stress
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OT treatment of OA
- assistive devices
- alternate ways to perform ADLs
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PT treatment of OA
- increase ROM
- strengthen muscles
- maintenance of joints
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cause of total joint replacement
unknown
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common reasons for hip replacement
- arthritis-most common
- osteonecrosis
- fracture
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common reason for knee replacement
- OA-most common
- RA
- post-traumatic arthritis
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what is RA
- autoimmune, body attacks joints because it thinks they are foreign
- affects joints equally
- pain on both sides of body
- joints become stiff and warm
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pre-op for TJR
- pain
- pay attention to contralateral side
- has advanced arthrosis
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post op for TJR
- pain
- mechanical compression and cryotherapy for pain
- CPM machine to move joint to prevent stiffness
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PT and post op
training for ADLs, gait, transfers, joint mobility
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what is the most important aspect before moving the patient?
weight bearing status!
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recovery from surgery
- continue PT/OT
- scar formation
- recovery usually in 12 weeks
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PT for TJR
- gait
- strengthening
- joint mobility
- ROM
- assistive devices
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OT for TJR
- ADL's/IADL's
- mobility
- adaptive devices
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types of TJR
- metal and plastic (most common)
- ceramic
- metal on metal
- cemented vs non cemented
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posterior approach to hip replacment
- goes thru hip rotators
- most common
- moore or southern
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lateral approach to hip replacement
goes thru glute med and glute min
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anterolateral approach to hip replacement
goes in btwn glute med and TFL
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anterior approach to hip replacement
goes in btwn sartorius and TFL
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unicompartimental knee replacement
partial knee replacement
repair medial, lateral or patellar compartment
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minimally invasive knee replacement
spare quads and have smaller incisions
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hip precautions following replacement
do not flex past 90d
no hip adduction across midline
no hip ER/IR
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knee precautions following replacement
WB status
do not cross legs
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precautions to providing treatment if patient is experiencing:
- nausea
- vomiting
- confusion
- light headedness
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absolute contra-indications for TKA/THR
- severe vascular disease
- sepsis
- infection
- osteomyelitis
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relative contraindications for TKA/THR
- muscular atrophy or neurological disorders
- below 60
- pregnancy
- obesity
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what are some functional limitations resulting from TJR
- gait deviations
- decreased strength
- limited ROM
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co-morbidities of TJR
- thrombophlebitis
- bone fracture
- infection
- disloaction or loosening of joint
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causes of FAS
mother drinking during pregnancy
-
effects of FAS
depend on extent of alcohol consumption
not normal brain functioning
growth,mental or physical deficits
CNS most impacted
-
pathophys of FAS
mother drinks and it goes into bloodstream crossing placenta
babies cannot metabolize alcohol like adults
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tests for FAS
no test to determine
after birth look at abnormal facial features, growth, CNS, motor skills
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clinical features of FAS
- elongated midface
- thin upper lip
- flattened maxilla
- microcephaly
- smooth philtrum
- small palpebral fissure
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birth defects of FAS:
structural
head circumference at or below 10th percentile
deformed brain structures
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birth defects of FAS:
neurological
poor hand/eye coordination/ nystagmus
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birthday defects of FAS:
functional
- cognitive
- executive functioning
- memory
- fine motor deficits
- attention problems
- hyperactivity
- limited social skills
- decreased intelligence
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additional issues associated with FAS
- poor coordination
- decreased muscle tone
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subtypes of FAS
- partial FAS
- alcohol related birth defects
- alcohol related neurodevelopmental disorders
- fetal alcohol effect
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co-morbidities of FAS
- heart defects
- ADHD
- lung and kidney defects
-
treatment for FAS
- medsb
- behavior and education therapy
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