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Pathology > MIDTERM > Flashcards

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.

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2
Q

Physiology Definition

A

Way in which something functions

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3
Q

Physiology Definition

A

Way in which something functions

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4
Q

Pathology definition

A

Abnormality or Malfunction

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5
Q

Pathophysiology definition

A

Study of the process that is associated with disease or injury

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6
Q

Cell

A

Functional unit of an organism

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7
Q

Tissue

A

By selected adhesion, differntiated cells of similar properties form tissues

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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
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9
Q

Organ Definition

A

Different types of tissues formed together

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10
Q

Organ System

A

Different oragsn working together to perform a common function

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11
Q

Chromosomes

A

Structurs that contains a person’s genes, carry dna within a cell

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12
Q

DNA

A

Carrier of genetic information

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13
Q

Gene

A

Segments of DNA that code for specific proteins in one or more types of cells

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14
Q

Totipotent

A

Stem cells that can divide into all cell types in an organism and can form an organ.

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15
Q

Pluripotent

A

Stem cells that can divide in most cell types of an organism but cannot create own organ by self.

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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

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17
Q

Cell Homeostasis

A

Maintained by regulation and by the exchange of materials and energy with its surroundings

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18
Q

Ischemia

A

Lack of blood flow

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19
Q

Hypoxia

A

Low O2 in tissues

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20
Q

Anoxia

A

Complete absensce of O2 in tissues

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21
Q

Hypoxemia

A

Low O2 than normal in blood

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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)

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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.

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24
Q

Two examples of endotoxins

A

Tetanus and Botulism

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25
Q

Exotoxin

A

A toxin released by a living bacteria cell into its surroundings.

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26
Q

Three Examples of Exotoxins

A

E. Coli, Salmonella, Sepsis

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27
Q

How can we reduce oxygen toxicity during exercise?

A

Avoid prolonged and intense exercise

Avoid exhaustive exercise

Promote moderate, regular long-term aerobic exercise to prevent DNA damage

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28
Q

Physical Stress Theory

A

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

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29
Q

Nutritional Factors

A

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.

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30
Q

Physical agents & Irradiation injury and effects

A

Extremes of physical agents can result in serious side effects. This can include:

  • Temperature: Hypothermia (Frostbite and Frostnip) and Hyperthermia (Burns)
  • Electricity
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31
Q

Reversible Cell Injury Mechanism

A

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

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32
Q

Atrophy

A

Shrinkage of cells

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33
Q

Examples of Atrophy

A

Muscle wasting, bone loss, cachexia, loss of brain tissue, or spinal atrophy in spinal cord injury

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34
Q

Hypertrophy

A

Increase in cell size and organ size

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35
Q

Hyperplasia

A

Increase in number of cells -> organ size

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36
Q

Example of hyperplasia

A

Pure hyperplasia: Endometrial thickness and Callus

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37
Q

Metaplasia

A

Change in cell morphology and function. One adult cell type to another.

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38
Q

Example of Metaplasia

A

Smokers – Changes from Ciliated pseudostratified columnar to stratified squamous epithelium

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39
Q

Dysplasia

A

Increase in cell numbers, altered cell morphology and loss of histologic organization

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40
Q

Example of Dysplasia

A

Neoplasia (Cancer)

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41
Q

What if we do not remove the injury?

A

Not removing the injury/stressor leads to cell death!

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42
Q

Apoptosis

A

Programmed Cell Death (Natural and Needed)

Due to self-generated signals within the cell

Does NOT require energy!

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43
Q

Necrosis

A

Cell death due to extreme external conditions

Caused by toxins, infection, trauma

Damaging or harmful

REQUIRES ENERGY

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44
Q

Types of Necrosis

A
  • Coagulative (Dry Gangrene)
  • Liquifactive (Wet Gangrene)
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45
Q

Coagulative (Dry Gangrene)

A

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

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46
Q

Liquefactive (Wet Gangrene)

A

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

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47
Q

Where does coagulative necrosis normally occur?

A
  • Ischemia
  • Liver
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48
Q

Where does liquefactive necrosis occur typically?

A
  • Bacteria
  • Brain
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49
Q

What type of necrosis is this?

A

Coagulative (dry gangrene)

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50
Q

What type necrosis is this?

A

Liquefactive (Wet gangrene)

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51
Q

Inflammation

A
  • Reaction acheived by chemical mediators (cell and plasma derived) through vascular and cellular responses
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52
Q

Examples of Acute Inflammation

A

Scratch to minor cut injury

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53
Q

Examples of Chronic Inflammation

A

OA, Strain and Stain

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54
Q

Acute Inflammatory Reaction

A
  • 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.
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55
Q

Where is serotonin released from in the blood?

A

Platelets

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56
Q

Where is histamine released from in blood?

A

Mast Cells

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57
Q

Exudate

A
  • 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.
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58
Q

Transudate

A
  • Low protein content, few cells
  • Plasma leaks to extravascular area mainly due to increased hydrostatic and decreased oncotic pressures
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59
Q

Effusion - Exudate or Transudate?

A

Can be either and is typically when fluid moves into anatomical spaces such as pleural, pericardial or peritoneal cavities or joint spaces.

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60
Q

What type of cellular response occurs in exudate inflammation?

A

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.

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61
Q

Types of Exudates

A

Sanguineous
Serous
Catarrhal

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62
Q

Sanguineous

A

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)

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63
Q

Serous

A

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)

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64
Q

Catarrhal

A

Mostly a PT candidate
Appearance: Thin, clear mucus
Significance: Seen with inflammatory process within mucous membranes (Ex: Upper respiratory infection)

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65
Q

Pathogens, damaged cells and leukocytes can release ____. Such as _____ and ____ that can increase _________, promote _____ and increase ____________ from the _________.

A

1) Histamine
2) IL-1
3) TNF
4) Fever
5) Macrophages and monocytes
6) C-Reactive Protein
7) Liver

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66
Q

Hemostasis Steps

A
  • 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)
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67
Q

Complement Proteins

A
  • 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
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68
Q

Cardinal Signs

A

Redness
Edema
Heat
Pus Formation
Pain
Loss of Function

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69
Q

PT Intervention - Acute Inflammation

A

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.

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70
Q

Leukopenia – what is it and why it is important?

A
  • Decreased WBCs
  • Worst prognostic factor during systemic infections (Use PPE with patients – We won’t see as PTs)
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71
Q

Use of NSAIDs, Corticosteroids and COX-2 inhibitor - Benefits vs Risks

A

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

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72
Q

What are the differences between granulation tissue and granuloma?

A

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
Q

How should a PT approach a patient with granulation tissue?

A
  • Stretching skin too much
  • Friction over tissues
  • Pressure on area
74
Q

Explain the difference between repair and regeneration

A

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
Q

Extracellular matric - structures and functions

A

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
Q

How many types of Collagen are their?

A

7

77
Q

Collagen 3 - Location, Mechanical and Wound Healing

A

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
Q

Collagen I - Location, Mechanical, Wound Healing

A

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
Q

Collagen II - Location, Mechanical

A

Location: Cartilage and Physis (growth plate)
Mechanical: Thin filaments -> in articular cartilage withstands shear force at surface and compressive/tensile forces at base

80
Q

Collagen IV - Location, Mechanical

A

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
Q

Collagen VII - Location, Mechanical

A

Location: Found in anchoring filaments (lymphatics)
Mechanical: Helps open lymph vessels

82
Q

What is the most comon type of collage in tissue?

A
  • Collagen III (Later turns into Collagen I)
  • Skin, Bone, Tendon, Ligaments
83
Q

Angeiogenesis

A

Growth and proliferation of new blood vessels (capillaries)

84
Q

Granulation tissue

A

Connective tissue and microscopic blood vessels that form over the wound during healing, “beefy red”

85
Q

What are the 4 stages of healing?

A

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
Q

Venous Insufficeny

A

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
Q

What is this?

A
  • Lipodermatosclerosis
  • Thicker skin and discoloration; tight skin
88
Q

What is this?

A
  • Hemosiderin
  • Dark Skin
89
Q

Aterial insufficency

A

Intemittent claudication

Hair loss

Initially pain occurs with activity

As it progresses:
Resting pain
Burning pain with elevation
Ulcers can develop

90
Q

What is this?

A
  • 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
Q

Neuropathic Wounds - Causes and Changes

A

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
Q

What is this?

A

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
Q

What are the 5 Stages of Pressure Ulcers? What tissues are involved?

A

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
Q

Factors that influence healing

A

Physiologic variable (age, vascular sufficiency)

General Health

Presence of comorbidities

Drug Use

Nutrition

Local or Systemic Infection

Type of Tissue

Medical Treatment

95
Q

Scarring - Normal vs Abnormal

A

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
Q

What are some of the earliest sensory impairments associated with Diabetes Mellitus?

A

Neuropathy: numbness, tingling, pain, weakness, spasms, atrophy

97
Q

Venous vs Arterial Wound

A

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
Q

What is this?

A

Keloid Scarring

99
Q

What is this?

A

Hypertrophic Scarring

100
Q

Lung - Repair or Regenerate?

A

Pneumonia - Regen (Cell loss but maintenance of extracellular matrix)

Abestosis - Repair (Cell loss and destruction of ECM)

101
Q

Heart - Repair or Regen

A
  • Repair (Permanent cells; Take 8-12 weeks following MI to form a dense connective tissue
102
Q

Why do MCLs heal faster than ACLs?

A

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
Q

How would you provide a better healing environment for someone with a ligament injury?

A

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
Q

Bone healing and repair – cells and callus and their impact on physical therapy practice

A

**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
Q

What should the therapist observe when evaluating a patient with a fracture?

A

Observe for atrophy, stiffness, DVT, ROM, edema, erythema

106
Q

Neoplasia - Modifiable and Non modifiable risk factors

A

**Modifiable: 95% other factors **

Virus

Chemical Agents

Radiation

Drugs

Smoking

Hormones

Excessive Alcohol

Diet and Nutrition

Non-Modifiable: 5-10% Genetic, Age, Sex

107
Q

Neoplasm - Primary

A

Site where cancer first developed
Ex: Lung Cancer in Lungs

108
Q

Neoplasm - Secondary

A

Cancer devloped and metastisised to a different location

109
Q

Benign

A

Not cancerous or malignant
Can become harmful as it grows
Well differentiated cells

110
Q

Malignant

A
  • Non encapsulated
  • Invasive
  • Rapid
  • Poorly differentiated
  • Metastisis
111
Q

Carcinoma in situ

A

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
Q

Metastasis

A
  • Cancer spreads to different parts of the body
  • Generally occurs in blood or lymph vessels
113
Q

Explain the difference between well differentiated and poorly differentiated

A

Well differentiated Cell: Similar to cells in the area
Poorly differentiated (anaphylasia): Very abnormal, only share some features

114
Q

Encapsulation

A

Cancer cell growth that is contained within a capsule

115
Q

Explain the difference between invasive and non invasive

A

Invasive: Unencapsulated cancer that spreads to surrounding tissues

Non-Invasive: Stays within same tissue

116
Q

Cancer - CAUTION Mneomic

A

Change in bowel or bladder habits
A sore that does not heal
Unusual bleeding or discharge
Thickening or lump in the breast or elsewhere
Indigestion or difficulty in swallowing
Obvious change in a wart or mole
Nagging cough or hoarseness

117
Q

Cancer - ABCDE rule

A

A – Assymetry

B – Borders

C – Color

D – Diameter

E - Evolution

118
Q

Cachexia - Effects

A
  • Decreased survival
  • Increased complications of surgery, radiotherapy, and chemotherapy
  • Weakness, anorexia, chronic nausea
  • Psychological distress in patient and family
119
Q

Cancer related fatigue – Documentation process

A

Initial visits and at intervals

120
Q

Exercise modifications to acutely radiated tissue

A

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
Q

Exercise recommendations adults with chronic conditions including cancer

A

150 mins of moderate level aerobic activity and at least 2 days of strengthening exercise

122
Q

What is this?

A

Metastasis from primary melanoma

123
Q

What is this?

A

Multiple Myeloma
Cancer of plasma cells in bone marrow

124
Q

What is this?

A
  • Chondrosarcoma
  • Malignant tumor composed of cartilage-producing cells
  • Second most common malignancy of bone
125
Q

What is the most common malignancy of bone?

A

Osteosarcoma

126
Q

Innate vs adaptive immunity

A

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
Q

Neutrophils

A
  • 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
Q

Macrophages

A
  • Eats things bigger than what Neutrophils can
  • Second line of defence from the bloodstream
  • Phagocytosis
  • Filter debris created by Neutrophils
129
Q

Esinophils

A
  • Eat things bigger than what Neutrophils and Macrophages can
  • Death by cytotoxicity (granules)
  • Phagocytosis – kills parasites
130
Q

Basophils

A

Releases **Heparin (anticoagulant) and Histamine (Vasodialation) **

Increases blood supply to the area

Flushes out pathogens

Helps recruit more

**Allergy Reaction **

131
Q

Mast Cells

A

Produce whole body Allergy and Anaphylaxis response

Produce cytokines

132
Q

B Lymphocytes

A

Humoral Immunity

Plasma Cells
- Produce specific antibodies

Memory Cells
- React when they encounter the same pathogen

133
Q

T Lymphocytes

A
  • Cell Mediation
  • Memory Cells
  • Quickly change to cytotoxic cell when reactivated
  • Suppressor or Regulator T cells
  • Peripheral tolerance
  • Helper T Cells
  • MHC-II
134
Q

What is epitope?

A

Point of attachment of the antigen

135
Q

Antibodies - types and roles

A
  • 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
Q

MHC - I and II

A

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
Q

Types of hypersensitivity

A

Type I, II, III, IV HS

138
Q

Type 1 HS

A

*** 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
Q

Type II HS

A
  • ** Antibody mediated cytotoxicity **
  • IgM or IgG attach to target and cell surface
140
Q

Type III HS

A
  • Immune Complex Mediated
  • Circulates in blood and depositis in tissues
  • Circulating antigen (soluble)
141
Q

What is the difference bwteeen type II and type III HS?

A

Type II is made and attacks that same specific area

142
Q

Type IV HS

A
  • Cell Mediated
  • T Cells
  • Delayed Immunity
143
Q

Type I HS - Condition

A

Bee Sting, Nuts, contact w/skin, inhaled
Analylaxis
IgE

144
Q

Type II HS - Conditions

A
  • 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
Q

Type III HS - Conditions

A

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
Q

Type IV HS - Conditions

A
  • Local: Dermatitis (Poison Ivy, Latex)
  • Systemic: Multiple Sclerosis and Inflammatory Bowel Disease
  • Graft versus host disease and transplant rejection
147
Q

Difference between surface antigen vs circulating antigen

A

Surface Antigen: On surface of cells, involved in Type II HS

Circulating Antigen: Antigens circulating in blood, involved in **Type III HS **

148
Q

Histamine

A
  • Vasodilation
  • Reaction depends on location IgE is present
  • Ex: Whole Body – Anaphylactic Shock (bee sting is #1 cause)
149
Q

Leukotrienes

A
  • Produced by leukocytes, cause tightening of airway muscles and production of excess mucus and fluid
  • Contraction of lung smooth muscle
150
Q

Serotonin

A

Stored in platelets
Vasoconstriction – usually overridden by histamine

151
Q

Prostaglandin

A
  • Lipid compounds made at sites of tissue damage or infection
  • Increase vascular permeability
  • Contraction of smooth muscles
152
Q

Anaphylaxis and Anaphylactic shock – clinical signs and symptoms

A

Wheezing, Hypotension, Runny Nose, Urticaria, Swelling, Rhinorrhea (clear runny nose with sneezing)

Trigger: Exercise

Type I HS

Epinephrine reverses symptoms

153
Q

Therapist Implications - HS

A

Be mindful

Ultrasound gels, Lanolin, Lotions, Latex Allergies

Reaction – Immediate and Delayed

Refferal

154
Q

Myasthenia Gravis

A
  • Skeletal Muscle Weakness with activity and improvement w/rest
  • Type II HS
  • Blocks ACh
155
Q

Myasthenia Gravis - Signs & Symptoms

A
  • 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
Q

Multiple Sclerosis

A

(Type II – Ig in CNS; Type IV demyelination w/T Cell)
* Fatigue
* Spasticity
* Increased deep tendon reflexes
* Positive Babinski’s sign and clonus

157
Q

Guillian Barre

A
  • Type II
  • Muscle wekness due to paralysis
158
Q

Guillian-Barre Syndrome - Signs & Symptoms

A

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
Q

Systemic Lupus Erythematosus

A

Type III
Senstivity to sunlight
Skin Reash - A “butterfly” rash
Fever with no other cause
Mouth Sores

160
Q

Ankylosing Syndrome

A

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
Q

What is this?

A

Dermatomyosisits

Type III

162
Q

Signs and Symptoms – Dermatomyositis

A
  • 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
Q

Difference between Autograft, Isograft, Allograft, and Xenograft

A

Autograft: Same person

Isograft: From another individual with same genotype

Allograft: Cadaver

Xenograft: Different species

164
Q

HIV vs AIDs

A

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

165
Q

HIV Transmissioin

A

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

166
Q

Pathogenesis

A

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

167
Q

HIV risk reduction strategies

A

Obtain testing for HIV if engaged in high risk behaviors

Protection during sex

Protect/”safe” use of needles

168
Q

Standard precautions - HIV

A

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

169
Q

Recommended Exercise guidelines for HIV

A

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.

170
Q

Radiation Toxicity

A

Fatigue

Decrease aerobic endurance

Radiation fibrosis

Radiation dermatitis

Hair loss

171
Q

Radiation Therapy - Exercise Implications

A

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

172
Q

Modifiable indicator of mortality and predictor of survival

A

Cardiorespiratory fitness: is a modifiable indicator of long-term mortality and health care professionals should encourage patients to maintain high levels of fitness

173
Q
A

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

174
Q

Different types of fat and the most harmful fat

A

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

175
Q

What are the complications associated with obesity?

A

NTs and Glucose act on adipocytes and produce adipokines

Complications:

Metabolic syndrome

High BP

Heart disease

Cancer

High Cholesterol

Atheroclerosis

176
Q

Body fat assessment techniques

A

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

177
Q

Most common body fat measurement

A

BMI

178
Q

Strongest predictor of health risk

A

Waist to hip ratio

179
Q

What is the difference between heparin and histamine?

A

Heparin is local reaciton
Histmaine can be WHOLE BODY

Pathology (7 decks)

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