MIDTERM Flashcards
1
Q
WHO - Health Definition
A
A state of complete physical, mental and social well-being and not merely the absence of disease or infirmity.
2
Q
Physiology Definition
A
Way in which something functions
3
Q
Physiology Definition
A
Way in which something functions
4
Q
Pathology definition
A
Abnormality or Malfunction
5
Q
Pathophysiology definition
A
Study of the process that is associated with disease or injury
6
Q
Cell
A
Functional unit of an organism
7
Q
Tissue
A
By selected adhesion, differntiated cells of similar properties form tissues
8
Q
Tissue membranes - Types
A
- Mucous: Line digestive, respiratory, urinary and reproductive
- Serous: pericarium, peritoneal, pleural
- Cutaneous: Skin
- Synovial: Inside joint cavities produce fluid
9
Q
Organ Definition
A
Different types of tissues formed together
10
Q
Organ System
A
Different oragsn working together to perform a common function
11
Q
Chromosomes
A
Structurs that contains a person’s genes, carry dna within a cell
12
Q
DNA
A
Carrier of genetic information
13
Q
Gene
A
Segments of DNA that code for specific proteins in one or more types of cells
14
Q
Totipotent
A
Stem cells that can divide into all cell types in an organism and can form an organ.
15
Q
Pluripotent
A
Stem cells that can divide in most cell types of an organism but cannot create own organ by self.
16
Q
ICF Model vs Nagi Model
A
ICF: Funtional Impairment, Activity restrictioins, participant limitations, contextual factors (environmental, personal)
Nagi: Disease (Pathology) -> Impairment -> Functional Limitation -> Disability
17
Q
Cell Homeostasis
A
Maintained by regulation and by the exchange of materials and energy with its surroundings
18
Q
Ischemia
A
Lack of blood flow
19
Q
Hypoxia
A
Low O2 in tissues
20
Q
Anoxia
A
Complete absensce of O2 in tissues
21
Q
Hypoxemia
A
Low O2 than normal in blood
22
Q
What happens with decresed blood flow?
A
Decreased O2 changes metabolism from **aerobic to anerobic metabolism **
Decreased ATP synthesis changes cell membrane permeability and can lead to intracellular movement of ions and fluids. Leads to cell swelling.
**Increased buildup of CO2 **
Can result in cell death (Ex: Stroke and MI)
23
Q
Endotoxin
A
A toxin that is present inside a bacterial cell and is released when the cell disintegrates. Sometimes responsible for characteristic symptoms of a disease.
24
Q
Two examples of endotoxins
A
Tetanus and Botulism
25
Exotoxin
A toxin released by a living bacteria cell into its surroundings.
26
Three Examples of Exotoxins
E. Coli, Salmonella, Sepsis
27
How can we reduce oxygen toxicity during exercise?
Avoid prolonged and intense exercise
Avoid exhaustive exercise
Promote moderate, regular long-term aerobic exercise to prevent DNA damage
28
Physical Stress Theory
Avoid single high load
Minimize repeated moderate level stress, repetitive forces, and low and sustained load over long time
Controlled increase of physical stress would be beneficial in minimizing or preventing cell injury
29
Nutritional Factors
In normal liver: Hepatocytes produces lipoproteins (made up of cholesterol, triglycerides, phospholipids, and proteins) that transport fat molecules in plasma.
Fatty liver: Disaggregation of ribosomes from RER causes decreased protein synthesizes that leads to excessive accumulation of fats in hepatocytes resulting in decreased lipoproteins in the circulation.
30
Physical agents & Irradiation injury and effects
Extremes of physical agents can result in serious side effects. This can include:
- Temperature: Hypothermia (Frostbite and Frostnip) and Hyperthermia (Burns)
- Electricity
31
Reversible Cell Injury Mechanism
Ionic shifts across cell membrane with **increased sodium and calcium influx into cell **
Increased cell volume (swelling) into cytosol – mitochondria and ER
- Decreased energy production – Decreased ATP and **increased Lactic Acid (due to anerobic metabolism)
- Increased acidity of cell (pH)** - slow down of metabolism and causes more cellular damage
Plasma membrane blebs and detaches from cell membrane
Ribosome detaches from ER in severe cases – decreased protein synthesis
32
Atrophy
Shrinkage of cells
33
Examples of Atrophy
Muscle wasting, bone loss, cachexia, loss of brain tissue, or spinal atrophy in spinal cord injury
34
Hypertrophy
Increase in cell size and organ size
35
Hyperplasia
Increase in number of cells -> organ size
36
Example of hyperplasia
Pure hyperplasia: Endometrial thickness and Callus
37
Metaplasia
Change in cell morphology and function. One adult cell type to another.
38
Example of Metaplasia
Smokers – Changes from Ciliated pseudostratified columnar to stratified squamous epithelium
39
Dysplasia
Increase in cell numbers, altered cell morphology and loss of histologic organization
40
Example of Dysplasia
Neoplasia (Cancer)
41
What if we do not remove the injury?
Not removing the injury/stressor leads to cell death!
42
Apoptosis
Programmed Cell Death (Natural and Needed)
Due to self-generated signals within the cell
**Does NOT require energy!**
43
Necrosis
Cell death due to extreme external conditions
Caused by toxins, infection, trauma
Damaging or harmful
**REQUIRES ENERGY**
44
Types of Necrosis
- Coagulative (Dry Gangrene)
- Liquifactive (Wet Gangrene)
45
Coagulative (Dry Gangrene)
Several days after cell death
Localized death of body tissue. Due to prolonged ischemia, inadequate O2, or lack of blood flow
Morphology: Firm and architecture is maintained
Microscopic: Outline of the cell is preserved but no nucleus
46
Liquefactive (Wet Gangrene)
Within hours of cell death
**Pyogenic bacteria** causes death of neurons releases lysozomes that liquefy the area, usually in CNS
Morphology: Liquid Form (may have pus)
Microscopic: Inflammatory cells with a lot of Neutrophils
47
Where does coagulative necrosis normally occur?
- Ischemia
- Liver
48
Where does liquefactive necrosis occur typically?
- Bacteria
- Brain
49
What type of necrosis is this?
Coagulative (dry gangrene)
50
What type necrosis is this?
Liquefactive (Wet gangrene)
51
Inflammation
- Reaction acheived by chemical mediators (cell and plasma derived) through vascular and cellular responses
52
Examples of Acute Inflammation
Scratch to minor cut injury
53
Examples of Chronic Inflammation
OA, Strain and Stain
54
Acute Inflammatory Reaction
- Initial Vasoconstriction due to Serotonin
- Overridden by histamine and other VDs (bradykinin and postaglandins) creates vasodialation. Leading to formation of exudate and transudate and in some cases effusion.
55
Where is serotonin released from in the blood?
Platelets
56
Where is histamine released from in blood?
Mast Cells
57
Exudate
- **High protein content**, and may contain some RBC and WBC
- Inflammation due to contraction of endothelial cells and the leakage of plasma fluid with proteins and other substances through this gap formed between endothelial cells
- **Protein leave, water follows. Cells contract to open up pathway for water to leave.**
58
Transudate
- **Low protein content**, few cells
- Plasma leaks to extravascular area mainly due to **increased hydrostatic** and decreased oncotic pressures
59
Effusion - Exudate or Transudate?
Can be either and is typically when fluid moves into anatomical spaces such as pleural, pericardial or peritoneal cavities or joint spaces.
60
What type of cellular response occurs in exudate inflammation?
Cellular responses include Leukocyte adhesion, margination, diapedesis and chemotaxis to the pathogen or the damaged cell/tissue. They also help with phagocytosis and releases growth factors that promotes the healing process.
61
Types of Exudates
Sanguineous
Serous
Catarrhal
62
Sanguineous
Mostly referred
Appearance: Blood-tinged yellow or pink; prescence of RBCs
Significance: Expected for 48-72 hours after injury or trauma to the microvasculature. A sudden increase may precede wound dehiscence (rupture or seperation)
63
Serous
Mostly PT candidate
Appearance: Thin, clear ywlloe or strawcolored; contains albumin and immunoglobulins
Significance: Occurs in the early stages of most inflammations; common with blisters, joint effusion with RA, viral infection; expected for up to 1 week after trauma or surgery. A sudden increase may indicate a draining seroma (pocket of serum within tissue/organ)
64
Catarrhal
Mostly a PT candidate
Appearance: Thin, clear mucus
Significance: Seen with inflammatory process within mucous membranes (Ex: Upper respiratory infection)
65
Pathogens, damaged cells and leukocytes can release ____. Such as _____ and ____ that can increase _________, promote _____ and increase ____________ from the _________.
1) Histamine
2) IL-1
3) TNF
4) Fever
5) Macrophages and monocytes
6) C-Reactive Protein
7) Liver
66
Hemostasis Steps
* Primary - Blood Clotting (Platelets, promote serotonin and histamine)
* Secondary - Coagulation cascade through intrinsic and extrinsic pathway (Enzyme thrombin converts circulating fibrinogen to fibrin resulting in fibrin polymers to stabilize bloodclot; Thrombin also activates more platelets for more blood clot formation)
* Fibrin Remodeling - To prevent too musch blood clot, body activate fibrinolytic system (TPA is released and changes plasminogen to plasmin which splits fibrin)
* Plasmin also activates complement factor which can activate Hageman Factor
* Hageman Factor creates Bradykinin and can convert plasminogen to plasmin)
67
Complement Proteins
* MAC - C5b-C9 (Makes pore on cell and causes lysis)
* C1b and C3b - Opsonization - Tag! - Promote phagocytosis
* Promote vasodilation and Increase permeability of blood vessels to allow leukocytes and plasma to go to the infected area
68
Cardinal Signs
Redness
Edema
Heat
Pus Formation
Pain
Loss of Function
69
PT Intervention - Acute Inflammation
Pain Control (Cold Therapy)
Exercise: Protect the joint
Limit movement (Compression causes irritation of joints)
Avoid overstretching (during edema) that can cause hypermobility (once swelling is reduced)
NSAIDs and Corticosteroids – Ligament/Joint laxity (protect joint from excessive loads)
During Remission – careful but proceed with stretching
Diet: Decrease refined CHO and Omega-6 Fatty Acids, Increase Omega-3 FA.
70
Leukopenia – what is it and why it is important?
- Decreased WBCs
- Worst prognostic factor during systemic infections (Use PPE with patients – We won’t see as PTs)
71
Use of NSAIDs, Corticosteroids and COX-2 inhibitor - Benefits vs Risks
Benefit:
Generally, they help with pain control
Risks:
NSAIDS and Corticosteroids – stomach ulcer
Cox-2 inhibitor: heart attack due to increased VC and platelet aggregation effect
72
What are the differences between granulation tissue and granuloma?
Granulation Tissue:
Endothelial cells – angiogenesis
Fibroblasts – newly formed collagens with proteoglycans
Red “beefy” wound
Scar Formation
Granuloma:
Microscopic <2 mm diameter
Macrophages are surrounded by lymphocytes
Aggregated macrophages forms large cells
Why? Try to seal the area to avoid spread of infection
Ex: Lungs – TB, Suture, RA
73
How should a PT approach a patient with granulation tissue?
- Stretching skin too much
- Friction over tissues
- Pressure on area
74
Explain the difference between repair and regeneration
Repair: Laying down connective tissues or glial scarring (CNS). This is the only type of healing for permanent cells and is associated with tissues that have damaged extracellular matrix/basement membrane.
Regeneration: Regrowth of tissues and can be seen in labile and stable cells as long as the basement membrane is intact.
75
Extracellular matric - structures and functions
Collagen: Most abundant protein in your body, mainly serves a structural role
Laminin: Structural significance and overall maintenance/survival of tissue
Integrin: Help to integrate the outside of the cell to the inside
Fibronectin: promotes cell to cell adhesion, cell to basement membrane attachment and clot stabilization
Proteoglycan: Withstands compressional forces through hydration and swelling pressure to the tissue
76
How many types of Collagen are their?
7
77
Collagen 3 - Location, Mechanical and Wound Healing
Location: Found in **blood vessels, skin**, uterus, and GI tract
Mechanical: Thin filaments -> strong but pliable
In wounds healing: Collagen III is synthesized first that results in the formation of fresh scars
78
Collagen I - Location, Mechanical, Wound Healing
Location: **Bone, Tendon**, Ligament and Skin
Mechanical: Thick bundles -> very strong -> helps to build tensile force when it is stretched
In wound healing: laid down in the later stages of wound healing. Helps with formation of mature scar.
79
Collagen II - Location, Mechanical
Location: Cartilage and Physis (growth plate)
Mechanical: Thin filaments -> in articular cartilage withstands shear force at surface and compressive/tensile forces at base
80
Collagen IV - Location, Mechanical
Location: Basement Membranes; CNS- Blood Vessels; PNS - Only in Schwann Cells
Mechanical: Helps in stability (tensile strength) of the BM and a vital collagen during regeneration
Allows selective permeability
81
Collagen VII - Location, Mechanical
Location: Found in anchoring filaments (lymphatics)
Mechanical: Helps open lymph vessels
82
What is the most comon type of collage in tissue?
- Collagen III (Later turns into Collagen I)
- Skin, Bone, Tendon, Ligaments
83
Angeiogenesis
Growth and proliferation of new blood vessels (capillaries)
84
Granulation tissue
Connective tissue and microscopic blood vessels that form over the wound during healing, “beefy red”
85
What are the 4 stages of healing?
1) Hemostasis and Degeneration (Platelets and fibrin; Growth Factor Release)
2) Inflammatory (Elastase and collagenase break down area; Cardinal Signs)
3) Proliferation and Migration (Stimulate epithelial cells, fibroblasts and vascular endothelial cells; wound contraction - collagen, elastin and proteoglycans)
4) Remodeling and Maturation (Collagen; 70-80% tensile strength of original skin; still at risk for injury)
86
Venous Insufficeny
Location: Distal lower leg; Medial Malleolus
Pulse: Normal or Decreased
Pain: Mild, comfortable with legs elevated, aching pain in dependent position
Temperature: Normal:
Edema: Often marked edema
Appearance: Irregular, dark pigmentation (hemosiderin), fibrotic, granualtion, shallow
87
What is this?
- Lipodermatosclerosis
- Thicker skin and discoloration; tight skin
88
What is this?
- Hemosiderin
- Dark Skin
89
Aterial insufficency
Intemittent claudication
Hair loss
Initially pain occurs with activity
As it progresses:
Resting pain
Burning pain with elevation
Ulcers can develop
90
What is this?
- Aterial Ulcer
Location: Distal lower leg, toes, feet; Lateral malleolus, anterior tibial area
Pulse: Absent or decreased
Pain: Painful especially when elevated
Temperature: Cool
Edema: Often marked edema
Appearance: Irregular, smooth edges, minimum to no granulation, deep
Gangrene: Black, gangrenous skin adjacent to ulcer
91
Neuropathic Wounds - Causes and Changes
Cause: Diabetes, Improper foot care, mechanical – shear and friction
Changes:
Sensory: Numbness, tingling, pain
Motor: Weakness, spasms, atrophy
Autonomic: Impaired thermoregulation, no sweating to dry skin
92
What is this?
Diabetic Ulcer
Location: Distal lower leg, toes, feet; Lateral malleolus, anterior tibial area; Plantar Aspect of foot, Metatarsal heads
Pulse: May be present or decreased
Pain: No
Temperature: Normal or increased
Edema: Mild or none
Appearance: Callus, usually round
Gangrene: May develop, infection common (sepsis)
93
What are the 5 Stages of Pressure Ulcers? What tissues are involved?
Stage 1: Non-blanchable erythema (abnormal redness) of intact skin
Stage 2: Partial thickness skin loss with exposed dermis
Epidermis and dermis
Stage 3: Full thickness skin loss
Epidermis, dermis, subcutaneous fat
Stage 4: Fill thickness and tissue loss
Unstageable Full thickness: Obscured full thickness skin and tissue loss
Tunneling or caves
94
Factors that influence healing
Physiologic variable (age, vascular sufficiency)
General Health
Presence of comorbidities
Drug Use
Nutrition
Local or Systemic Infection
Type of Tissue
Medical Treatment
95
Scarring - Normal vs Abnormal
Abnormal:
Keloid: Grow larger, appear worse, invades surrounding tissues (out of wound boundary), often painful
Hypertrophic: Typically pink in color, stay within the wound boundary, generally resolves in 12 to 24 months. **Type III collagen.** Raised collagen but within boundaries. Common in burns.
Hypotrophic scar: Not enough scar to cover the damaged area
Contracture: caused by excessive contraction. Excessive shrinking of scar, leads to atrophy and functional impairment
Normal:
Normal tissue healing process that aims to decrease wound area and closes off wound
96
What are some of the earliest sensory impairments associated with Diabetes Mellitus?
Neuropathy: numbness, tingling, pain, weakness, spasms, atrophy
97
**Venous vs Arterial Wound**
Venous: **Pulse - Normal or Decreased**, **Pain - Mild;** **Comfortable with legs elevated**, **Temp - Normal**, Edema - Often, Appearacnce: Irregular, dark pigment
Arterial: Pulse - **absent or decreased**,** Pain - ****Yes especially when elevated**, **Temp - Cool**, Edema - Often, Appearance: Irregular, smooth edges, deep; Gangrene: Black
Other sign (A): Intermittent claudification, hair loss, pain with acitivity
98
What is this?
Keloid Scarring
99
What is this?
Hypertrophic Scarring
100
Lung - Repair or Regenerate?
Pneumonia - Regen (Cell loss but maintenance of extracellular matrix)
Abestosis - Repair (Cell loss and destruction of ECM)
101
Heart - Repair or Regen
- Repair (Permanent cells; Take 8-12 weeks following MI to form a dense connective tissue
102
Why do MCLs heal faster than ACLs?
Extraarticular ligaments (MCL): Heal like other tissues
Intraarticular ligaments (ACL): Matric metalloproteinases are highly active and in large amounts that affects clotting and hematoma formation
103
How would you provide a better healing environment for someone with a ligament injury?
Early mobilization
Avoid too little or too aggressive loads
Decreased pain to reduce the use of NSAIDs in the first two-weeks to promote the normal COX 1- related prostaglandin production
104
Bone healing and repair – cells and callus and their impact on physical therapy practice
**Weight-bearing exercises promote mechanical loading. They provide mechanical loading to activate Osteocytes that signals Osteoblasts to promote bone formation. **
Soft callus – often does not withstand external forces and better to offloaded. Type 3 Collagen.
Hard callus – Indicates better withstanding of external forces. Thus, weight-bearing is often promoted when hard callus is noticed in imaging. Type 1 Collagen.
105
What should the therapist observe when evaluating a patient with a fracture?
Observe for atrophy, stiffness, DVT, ROM, edema, erythema
106
**Neoplasia - Modifiable and Non modifiable risk factors**
**Modifiable: 95% other factors **
Virus
Chemical Agents
Radiation
Drugs
Smoking
Hormones
Excessive Alcohol
Diet and Nutrition
**Non-Modifiable: 5-10% Genetic, Age, Sex**
107
Neoplasm - Primary
Site where cancer first developed
Ex: Lung Cancer in Lungs
108
Neoplasm - Secondary
Cancer devloped and metastisised to a different location
109
Benign
Not cancerous or malignant
Can become harmful as it grows
**Well differentiated cells**
110
Malignant
- Non encapsulated
- Invasive
- Rapid
- Poorly differentiated
- Metastisis
111
**Carcinoma in situ**
Cancer within the basement membrane that has not spread beyond the basement membrane. Abnormal growth could become cancerous, if goes into tissue & or blood stream (travel to different parts of the body)
- Begnign Cancer
112
Metastasis
- Cancer spreads to different parts of the body
- Generally occurs in blood or lymph vessels
113
Explain the difference between well differentiated and poorly differentiated
Well differentiated Cell: Similar to cells in the area
Poorly differentiated (anaphylasia): Very abnormal, only share some features
114
Encapsulation
Cancer cell growth that is contained within a capsule
115
Explain the difference between invasive and non invasive
Invasive: Unencapsulated cancer that spreads to surrounding tissues
Non-Invasive: Stays within same tissue
116
Cancer - CAUTION Mneomic
**C**hange in bowel or bladder habits
**A** sore that does not heal
**U**nusual bleeding or discharge
**T**hickening or lump in the breast or elsewhere
**I**ndigestion or difficulty in swallowing
**O**bvious change in a wart or mole
**N**agging cough or hoarseness
117
**Cancer - ABCDE rule**
A – Assymetry
B – Borders
C – Color
D – Diameter
E - Evolution
118
Cachexia - Effects
- Decreased survival
- Increased complications of surgery, radiotherapy, and chemotherapy
- Weakness, anorexia, chronic nausea
- Psychological distress in patient and family
119
Cancer related fatigue – Documentation process
Initial visits and at intervals
120
**Exercise modifications to acutely radiated tissue**
**Acutely radiated (Less than 2 hours of radiation)** – No soft tissue mobilization and no exercise within two hours of radiation
Skin inspection and AROM after two hours of radiation
121
Exercise recommendations adults with chronic conditions including cancer
150 mins of moderate level aerobic activity and at least 2 days of strengthening exercise
122
What is this?
Metastasis from primary melanoma
123
What is this?
Multiple Myeloma
Cancer of plasma cells in bone marrow
124
What is this?
- Chondrosarcoma
- Malignant tumor composed of cartilage-producing cells
- **Second most common** malignancy of bone
125
What is the most common malignancy of bone?
Osteosarcoma
126
Innate vs adaptive immunity
Innate (Natural/Non Specific)
- First line of defense
Adaptive (Aquired or Specific):
Immunologic memory
- Memory B and T cells
Pathogen-specific
- Active (Long Term, produce antibodies)
- Passive (Milk, Placenta)
127
Neutrophils
* First line of defense
* Phagocytosis
* Degranulation
* Causes fever
* Cooperation with the immune response by phagocytosis but does not turn on the immune response – Free Antigen
128
Macrophages
* Eats things bigger than what Neutrophils can
* Second line of defence from the bloodstream
* Phagocytosis
* Filter debris created by Neutrophils
129
Esinophils
* Eat things bigger than what Neutrophils and Macrophages can
- Death by cytotoxicity (granules)
* Phagocytosis – kills parasites
130
Basophils
Releases **Heparin (anticoagulant) and Histamine (Vasodialation) **
Increases blood supply to the area
Flushes out pathogens
Helps recruit more
**Allergy Reaction **
131
Mast Cells
Produce whole body **Allergy and Anaphylaxis** response
Produce cytokines
132
B Lymphocytes
Humoral Immunity
Plasma Cells
- Produce specific antibodies
Memory Cells
- React when they encounter the same pathogen
133
T Lymphocytes
* Cell Mediation
* Memory Cells
- Quickly change to cytotoxic cell when reactivated
* Suppressor or Regulator T cells
- Peripheral tolerance
* Helper T Cells
- MHC-II
134
What is epitope?
Point of attachment of the antigen
135
Antibodies - types and roles
* Produced by Plasma Cells
* IgM (First secreted and primary initial response)
* IgG (most abundant, antibody in the blood and tissue fluids)
- Isotype switching
* IgA - (Breast Milk, prevents colonization at the site of entry on mucosal surfaces)
* IgG and IgD goe back to plasma cells and become their antigen receptors
136
MHC - I and II
MHC (recognition self vs nonself)
- **MHC I - Cytotoxic T Cell - CD 8+**: Cell Mediated Immunity (Cytotoxic, directly kills antigen by perforin, granzyme. Creates a pore and results in apoptosis). On all cells, self anitgen.
- **MHC II - Helper T Cell - CD 4+**: Cell mediated and humoral; Immunity against intracellular and extracellular pathogens, stimulate B cells to produce antibodies, help NK cells to kill, Neutrophil recruitment, down regulate the adaptive immune system. Adaptive immunity
137
Types of hypersensitivity
Type I, II, III, IV HS
138
Type 1 HS
*** IgE Mediated
- Mast Cells or Basophils
* Atopy – Nuts, Bees **
* Sensitization (B cell comes and produces IgE and then goes onto Mast cells, Basophils and Esonophils that then when second exposure release granules and kill cells) and Exposure
139
Type II HS
* ** Antibody mediated cytotoxicity **
* IgM or IgG attach to **target and cell surface**
140
Type III HS
* **Immune Complex Mediated**
* Circulates in blood and depositis in tissues
* Circulating antigen (soluble)
141
What is the difference bwteeen type II and type III HS?
Type II is made and attacks that same specific area
142
Type IV HS
* Cell Mediated
* T Cells
* Delayed Immunity
143
Type I HS - Condition
Bee Sting, Nuts, contact w/skin, inhaled
Analylaxis
IgE
144
Type II HS - Conditions
* Cell destruction w/o inflammation (Hemolytic Anemia, Thrombocytopenia, Neutropenia)
* Cellular Destruction (Rheumatic fever: (immune system attacks mitral valve instead of pathogen; Guillan-Barre Syndrome: immune system attacks peripheral nervous system instead of virus)
* Cellular Dysfunction (MG and Thyroid - Graves Disease)
145
Type III HS - Conditions
**Systemic Lupus Erythematosus (SLE) -> DNA (antigens/autoanitgen - own cell)** attacks different systems and organs. Can lead to:
Urticaria, Synovitis in RA, Nephritis, Pleuritis, Pericarditis, Hep B, Malignancy
146
Type IV HS - Conditions
* Local: Dermatitis (Poison Ivy, Latex)
* Systemic: Multiple Sclerosis and Inflammatory Bowel Disease
* Graft versus host disease and transplant rejection
147
Difference between surface antigen vs circulating antigen
Surface Antigen: On surface of cells, involved in **Type II HS**
Circulating Antigen: Antigens circulating in blood, involved in **Type III HS **
148
Histamine
* Vasodilation
* Reaction depends on location IgE is present
* Ex: Whole Body – Anaphylactic Shock (bee sting is #1 cause)
149
Leukotrienes
* Produced by leukocytes, cause tightening of airway muscles and production of excess mucus and fluid
* Contraction of lung smooth muscle
150
Serotonin
Stored in platelets
Vasoconstriction – usually overridden by histamine
151
Prostaglandin
* Lipid compounds made at sites of tissue damage or infection
* Increase vascular permeability
* Contraction of smooth muscles
152
**Anaphylaxis and Anaphylactic shock – clinical signs and symptoms**
Wheezing, Hypotension, Runny Nose, Urticaria, Swelling, Rhinorrhea (clear runny nose with sneezing)
Trigger: Exercise
Type I HS
Epinephrine reverses symptoms
153
Therapist Implications - HS
Be mindful
Ultrasound gels, Lanolin, Lotions, Latex Allergies
Reaction – Immediate and Delayed
Refferal
154
Myasthenia Gravis
* Skeletal Muscle Weakness with activity and improvement w/rest
* Type II HS
* Blocks ACh
155
Myasthenia Gravis - Signs & Symptoms
* Ptosis: Drooping of one or both eyelids
* Diplopia: Blurred or Double Vision
* Dysphagia: Difficulty swallowing
* Dysarthria: Impaired Speech
* **Proximal muscle weakeness and fatigue exaggerated by exertion **
* Respiratory muscle failure in progressive condition
* Severe Quadriparesis
156
Multiple Sclerosis
(Type II – Ig in CNS; Type IV demyelination w/T Cell)
* Fatigue
* Spasticity
* Increased deep tendon reflexes
* Positive Babinski’s sign and clonus
157
Guillian Barre
* Type II
* Muscle wekness due to paralysis
158
Guillian-Barre Syndrome - Signs & Symptoms
First tingling and weakness in one or both legs
Spreads to arms and trunk (“Stocking-glove” pattern numbness)
Comes quickly and worsens over hours or days
**Pricking or pins and needles sensations in the hands and feet
Coordination problems and unsteadiness
Diminished deep tendon reflexes **
159
Systemic Lupus Erythematosus
Type III
**Senstivity to sunlight
Skin Reash - A "butterfly" rash**
Fever with no other cause
Mouth Sores
160
Ankylosing Syndrome
Type III
Early
- Scaroilitis
- Muscle Spasms in the paravertebral area
- **Intermittent low back pain (insidious and non-traumatic) **
Late
- Constant low back pain
- Spinal deformities
- Decreased chest expansion
- **Anklyosis – SI and Spine**
161
What is this?
Dermatomyosisits
| Type III
162
Signs and Symptoms – Dermatomyositis
- Red scaly thickening of the skin over bony prominences of extensor surfaces (elbows, knuckles, knees)
- Patchy, red skin rash on the face and around the eyes (Heliotrope Rash)
- Periorbital edema (puffy eyelids)
What do you do?
- REFER IF NOT CURRENTLY DIAGNOSED, monitor disease progression
163
**Difference between Autograft, Isograft, Allograft, and Xenograft**
Autograft: Same person
Isograft: From another individual with same genotype
Allograft: Cadaver
Xenograft: Different species
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**HIV vs AIDs**
HIV
A virus that may cause infection
Lentivirus that selectively target cells of the immune system
AIDs
Condition brought on by late stage HIV, specifically when CD4 cells decrease to <200cells/cubic mm of blood
Susceptible to opportunistic infections
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HIV Transmissioin
Body Fluids (Pre-seminal and semen, Vaginal, Rectal, Breast Milk)
High Risk Behaviors (Unprotected sex, Having sex with 6 or more partners in a year, Sexual activity with someone with known HIV or IV drug use)
Men having sex with men
Injection drug users
Non-disclosures
Two woman with one man
STDs increase risk for HIV
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Pathogenesis
Chronic infection involving slow degradation of immunity that ultimately leads to AIDs
HIV virus -> CD4, Macrophage, B Cells, Dendritic cells, microglial cells ->
Convert RNA to DNA ->
Integrates with cell genome ->
Assembly (protease), create more virus particles
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HIV risk reduction strategies
Obtain testing for HIV if engaged in high risk behaviors
Protection during sex
Protect/”safe” use of needles
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**Standard precautions - HIV**
PPE
Wash hands immediately if contaminated by blood or other fluids
Prevent needle or scalpel sticks
Keep ventilation devices
People with open wounds should not treat patients
Extra cautions for pregnancy
Exposure followed by evaluation
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**Recommended Exercise guidelines for HIV**
Pain with peripheral neuropathy – Can use TENS
Progressive resisted exercise – 3x a week for 6 weeks
Moderate Exercise (70-80% HR)
Borg's RPE Scale (No higher than 14)
Monitor Vitals
**Early Hiv - No limitations with good vitals
Symptomatic and Advanced HIV - Constant or interval aerobic exercise for at least 20 minutes, 3x a week for 4 weeks, Prolonged recovery period, No exercise with inflammatory myopathies and myositis **
Only need to wear gloves if they have a cut.
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Radiation Toxicity
Fatigue
Decrease aerobic endurance
Radiation fibrosis
Radiation dermatitis
Hair loss
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Radiation Therapy - Exercise Implications
No direct treatment to acutely radiated tissues
Individualized
Vital signs – monitor
RPE should not exceed 15-17
Regular moderate exercise than inactivity
Self paced walk
**No exercise within two hours of chemo **
Global stretching – careful
Soft tissue mobilization – not during acute and sub acute phase of radiation (4 months)
Careful around immobile area
AROM – first line of exercise
AROM to the end range is advised for 18 to 24 months post radiation
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Modifiable indicator of mortality and predictor of survival
Cardiorespiratory fitness: is a modifiable indicator of long-term mortality and health care professionals should encourage patients to maintain high levels of fitness
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Pre-school ages (3-5)
-Everyday throughout day
- Active play through physical activity
Children and Adolescents (6-17)
- 60+ moderate to vigorous daily
- Variety
- At least 3 days a week
- Vigorous activity
- Activity to strengthen muscle and bones
Adults (18-64 yr)
- At least 150 min mod
- At least 2 days a week strength train
Older adults (65+ yr)
- At least 150 min mod
- At least 2 days a week strength train
- Activities for balance
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Different types of fat and the most harmful fat
Brown fats – specialized, thermoregulation, convert energy from food into heat
- Infants – more sensitive to cold
White fat – storage for tri-glycerol – long term reservoir for energy
Ectopic fat – MOST HARMFUL abnormal lipid droplets in no-fat cells (heart, pancreas, liver, and skeletal muscle
- Obese people become insulin resistant -> cannot uptake and store excess energy -> ectopic fat
- **In SM, kills skeletal muscle cells **
- In diabetes – low strength and impaired function
- Excess Ectopic is called visceral
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What are the complications associated with obesity?
NTs and Glucose act on adipocytes and produce adipokines
Complications:
Metabolic syndrome
High BP
Heart disease
Cancer
High Cholesterol
Atheroclerosis
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**Body fat assessment techniques**
Waist circumference: measures abdominal fat
- Increases health risk
- >35 inches for women
- >40 inches for men
BMI: Most common measure
- Overweight 25-29.9 kg/m2
- Obesity (Class 1) 30-34.34.9 kg/m2
Waist-Hip Ratio
- Highly significant with association with MI
- 85%+ Women
- 90%+ Men
- Apple vs Pear Shape
Body Adipose Index
- Strong predictor of BMI
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**Most common body fat measurement**
BMI
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Strongest predictor of health risk
**Waist to hip ratio**
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What is the difference between heparin and histamine?
Heparin is local reaciton
Histmaine can be WHOLE BODY
