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Medical Conditions I > Exam II > Flashcards

Exam II Flashcards

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USMLE® Step 1 flashcards
0
Q

What does cardiac muscle rely on for muscle contraction?

A

Relies heavily on entrance of extracellular calcium for muscle contraction

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1
Q

What does skeletal muscle rely on for energy?

A

ATP is important for muscle contraction and relaxation

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2
Q

What are characteristics of smooth muscle?

A

Found in arteries, GI tract
Controlled by autonomic nervous system
Able to undergo cell proliferation (regenerate)

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3
Q

What factors go into strength?

A

A factor of the number of motor units recruited and their firing frequency

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4
Q

Slow oxidative fibers make up what type of muscles?

A

Endurance and postural muscles

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5
Q

Fast glycolytic muscles are for?

A

More anaerobic activities and fatigue quick

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6
Q

What is the process of skeletal muscle contraction?

A
  • Contraction initiated by increase in intracellular calcium
  • Actin and myosin filaments slide over each other
  • cross-bridges activated by ATP
  • ATP also necessary to break linkage of myosin and actin
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7
Q

The process of smooth muscle contraction

A
  • Filaments are not in parallel, but cross obliquely
  • Actin attached to dense bodies
  • Contraction initiated by increase in intracellular calcium
  • Anatomy of smooth muscle allows larger tension range; can contract even when organ distended
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8
Q

What are some age-related muscle changes?

A
  • Sarcopenia: age-related decreases in strength
  • Gender differences:
    - Males: peaks in the 2nd & 3rd decade remains for 45-50
    - Females: lose earlier
  • Age: accounts for only 30% of changes
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9
Q

UAE strength is maintained __________ than LE strength.

A

More

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10
Q

Changes in motor fibers & motor units over time

A
  • Decline in the number and size of muscle fibers
  • Decreased motor unit firing rates
  • 1% loss of motor units per year starting after the 20s
  • Loss in fast twitch muscle fibers
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11
Q

Changes in structural muscles

A
  • increased connective and fat tissue within muscle (don’t contract)
  • increased membrane thickness–> decreased nutrient delivery
  • decreased protein synthesis
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12
Q

Characteristics of connective tissue

A
  • most abundant tissue in the body
  • connects, binds, supports tissue
  • consists of cells & extracellular matrix
  • 2 main types
    • connective tissue proper
    • special
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13
Q

Characteristics of Connective Tissue Proper: loose

A
  • soft and pliable: secretes extracellular matrix

- Example: Fibroblasts- produce collagen, elastin, and reticular fibers

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14
Q

Characteristics of Connective Tissue Proper: reticular

A

Provides internal scaffold for soft organs, capillaries, nerves, and muscles

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15
Q

Characteristics of Connective Tissue Proper: Dense

A
  • Attaches structures, provides strength

- Found in tendons & ligaments

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16
Q

Characteristics of Specialized Connective Tissue types

A
  • Bone
  • Cartilage
  • Hematopoietic & lymphatic tissues
  • Blood cells
  • Adipose tissue
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17
Q

Characteristics of Connective Tissue Extracellular Matrix

A
  • Supportive matrix
  • 3 types of fibers
    • collagen
    • elastin
    • reticular fibers
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18
Q

Characteristics of Collagen

A

Tough; serves as structural framework for skin, ligaments, & tendons

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19
Q

Characteristics of Elastin

A

Stretchable; found in tissues that must deform & return to original shape (example: arteries)

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20
Q

Characteristics of Reticular fibers

A

Thin, flexible network in organs that need to change form or volume

Example: bladder, uterus

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21
Q

Characteristics of Collagen Class Type I

A

Thick bundles common in the body

Form mature scars, tendons, and bones

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22
Q

Characteristics of Collagen Class Type II

A

Thin supporting tissue

Forms cartilagenous tissue

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23
Q

Characteristics of Collagen Class Type III

A

Thin elastic tissue

More prevalent in infants –> turns into type I

Contributes to wound healing & fresh scars

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24
Q

Characteristics of Collagen Class Type IV

A

Forms basement membrane

Where cells attach

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25
Q

What type of collagen is articular collagen and what are some examples?

A

Type II

Examples: joint surfaces, bone apophyses, epipheseal plates, costal cartilage, fetal skeleton

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26
Q

What type of collagen is fibrocartilage collagen and what are some examples?

A

Type I

Examples: tendon insertion, ligament insertion, meniscus, disk

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27
Q

What type of collagen is elastic collagen and what are some examples?

A

Type III

Examples: Trachea, Earlobe, ligamentum flavum

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28
Q

What type of collagen is Fibroelastic collagen and what are some examples?

A

Type II

Example: Meniscus

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29
Q

What is tendon structure and function?

A
  • connect muscle to bone
  • dense bands of fibrous connective tissue
    - cross bridges (strength)
    - bundles parallel to tendon axis (stretch)
    - surrounded by sheath (lubricate)
  • handle large unidirectional forces; provide strong flexible support
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30
Q

What are tenocytes?

A

Collagen producing cells that constitute tendons

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31
Q

What is the Tendon Healing Sequence?

A
  1. Hemostasis & inflammation (3 days typically)
  2. Proliferation: within 2 weeks immobilization –> random deposition of collagen
  3. Maturation/Remodeling: begins 3 weeks; immature Type III collagen to Type I & fibers re-align
    - collagen diameter is smaller (reducing tensile strength)
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32
Q

A healed tendon is __________.

A

Remarkably different from normal

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33
Q

Surgery precautions for tendons

A
  • Main concern post-op is protect healing tissues
  • Max muscle forces avoided until at least 8 weeks post-op
  • Significant weakness persists
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34
Q

What is ligament structure and function?

A
  • Bone to bone
  • Dense bands of fibrous connective tissue
    - Long sheets or short thick strips
  • Bundles of collagen fibrils are parallel to long axis of ligament
    - Cross linkages
    - Crimping (allows to stress & move out of line)
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35
Q

Ligaments are ________ organs.

A

Sensory

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36
Q

Ligament healing is variable depending on…..

A

The injury and involved tissue

Example: ACLs tend not to heal well

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37
Q

Ligament healing sequence

A
  1. Hemostasis & inflammation
  2. Proliferation
  3. Maturation/Remodeling (months to years)

End result: a ligament that is morphologically & biomechanically inferior
-leads to ligamentous laxity

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38
Q

What is disk structure and function?

A
  • Functions to withstand pressure & tension
  • 3 zones
    • Outer annulus fibrosis: type I & concentric rings
    • Fibrocartilaginous inner annular fibrosis (Type II)
    • Visco-elastic nucleus pulposis (Type II & water)
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39
Q

Disk changes across the lifespan: Newborn

A
  • Annulus well vascularized
  • With weight-bearing, vascularization changes & by age 5, only outer annulus is vascularized (thus healing only occurs in annulus)
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40
Q

Disk changes across lifespan: adult –> aging nucleus

A
  • decreased proteoglycan content
  • water binding ability decreases
  • less able to accommodate compressive loads
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41
Q

Disk changes across the lifespan: Annulus

A
  • composition changes to Type I collagen

- Thick & disorganized fibers lessen metabolite transfer

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42
Q

Disk disease progression

A

Nucleus less able to absorb water –> dehydration –> nucleus thick & fibrous –> fissures form in annulus –> disk begins to collapse –> reduced load bearing capacity –> altered passage of nutrients & wastes

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43
Q

Risk factors for herniation

A
  • Early morning (during the night no weight bearing so taller & more water in nucleus)
  • Lifting of heavy loads
  • Torsional stress
  • Strenuous exercise
  • Smoking
  • Genetics
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44
Q

Characteristics of intervertebral disk healing

A
  • evidence exists that the healing of the outer annulus can occur
    - due to increased cell density & blood supply (metabolite transport)
    - can adapt its strength to mechanical demands
  • reduces pain & inflammation & increases function
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45
Q

Elements of bone

A
  • Bone matrix
  • Bone cells
    • Osteoblasts
    • Osteocytes
    • Osteoclasts
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46
Q

What do osteoblasts?

A

Build bone

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47
Q

What are osteocytes?

A

Bone cells that affect blasts and clasts

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48
Q

What are osteoclasts function?

A

Destroy bone

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49
Q

Does a traumatic fracture occur?

A

Sudden impact

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50
Q

How does a stress or fatigue fracture occur?

A
  • Due to rhythmic, repeated, microtrauma

- Partial (called a “reaction”) or complete (called a “fracture”)

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51
Q

How does an insufficiency fracture occur?

A

Due to normal stress on weak bone or bone with insufficient elasticity

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52
Q

How does a pathological fracture occur?

A

In bone affected by neoplasm or other disease

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53
Q

Diagnosis of fracture with radiographs can miss?

A
  • May not detect stress reaction

- 35% of sacral fractures undetected

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54
Q

What is a CT good for in diagnosing a fracture?

A
  • May be better for sacral fractures

- Good for pathological fractures

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55
Q

What are MRIs good for and what’s a con for diagnosing a fracture?

A
  • Can detect stress injuries

- but are expensive

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56
Q

What is the rule about films and diagnosing a fracture?

A

Always need 2 views

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57
Q

7 elements for complete radiograph evaluation of a fracture?

A
  • Anatomic site & extent of fracture
  • Type of fracture
  • Alignment of fracture
  • Direction of fracture
  • Presence of associated abnormalities
  • Special types of fracture
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58
Q

Characteristics of Stage 1 of Bone healing?

A
  • Hematoma development and inflammation
    - Brings fibroblasts, growth factors, & cytokines to the area
    -By the end of week 1 phagocytic cells have removed initial       hematoma & fibrosis is beginning
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59
Q

Characteristics of Stage 2 bone healing?

A
  • Reparative phase
    • soft callus forms around week 2
    • osteoclasts clear necrotic bone
    • bone growth factors facilitate repair
    • hard callus replaces soft callus
    • completed in 6-12 weeks
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60
Q

Characteristics of Stage 3 bone healing

A
  • remodeling phase
    • bone union achieved
    • immature disorganized bone is remodeled into mature bone, adding stability
    • excessive bony callus resorbed
    • bone remodels in response to stress
    • months to years
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61
Q

Factors that impact bone healing

A
  • Age (kids 4-6 weeks, teens 6-8 weeks, adults 10-18 weeks)
  • Bone involved
  • Fracture site and type
  • Treatment required
  • Soft tissue injury
  • Nutritional status (calcium & vitamin D)
  • Co-morbid conditions
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62
Q

Characteristics of the inflammatory process

A
  • a non-specific response
    • immune reactions
    • injury
    • ischemic
  • localized protective response serves to destroy, dilute, or wall off both the injurious agent & the injured tissue
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63
Q

What are the types of inflammation

A

Acute & chronic

Local & systemic

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64
Q

What are the cardinal signs of acute inflammation

A
  • Rubor (redness)
  • Tumor (swelling)
  • Calor (heat)
  • Dolar (pain)
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65
Q

What are secondary signs of acute inflammation

A
  • loss of function

- fever may occur (systemic sign)

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66
Q

There _______ be inflammation without healing, but there _______ be healing without inflammation.

A

Can

Can’t

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67
Q

What is acute inflammation and what is it’s aim?

A
  • Early (almost immediate) reaction of local tissue to injury
  • Aim: remove injurious agent & limit tissue damage
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68
Q

What happens in the vascular stage of acute inflammation

A

Changes in the blood vessels occur

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69
Q

What happens in the cellular stage of acute inflammation

A

Movement of WBCs into the area

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70
Q

What is step 1 of the vascular stage of acute inflammation

A

Rapid vasoconstriction (reduces immediate blood loss)

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71
Q

What is step 2 of the vascular stage of acute inflammation

A

Rapid vasodilation (increased blood flow causes increased heat & swelling)

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72
Q

What is step 3 of the vascular stage of acute inflammation

A

Vessel becomes more permeable

  - Loss of proteins with fluid outflow (exudate) 
  - Produces swelling (edema) in tissue
  - Serves to dilute offending agent
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73
Q

What is step 4 of the vascular stage of acute inflammation

A

Flow stagnates, clotting of blood occurs (aids in confining spread of bacteria)

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74
Q

What is step 1 of the cellular stage of acute inflammation

A

Margination & adhesion (mediators cause WBC to accumulate along vessel endothelium)

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75
Q

What is step 2 of the cellular stage of acute inflammation

A

Emigration (WBCs squeeze out of the vessel)

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76
Q

What is step 3 of the cellular stage of acute inflammation

A

Chemotaxis

-WBCs are guided to the site of inflammation by cytokines, bacterial & cellular debris, & complement fragments

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77
Q

What is step 4 of the cellular stage of acute inflammation

A

Activation & Phagocytosis

-WBCs engulf & destroy pathogens

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78
Q

What is the job of neutrophils in the cellular stage of acute inflammation

A
  • Cause phagocytosis within 90 min & generate toxins to destroy pathogens (especially bacteria)
  • Key to fighting infection
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79
Q

What is the job of eosinophils in the cellular stage of acute inflammation

A

Generate toxins to destroy pathogen (especially parasites) & mediate allergic reactions

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80
Q

What is the job of basophils in the cellular stage of acute inflammation

A

Produce allergic reactions

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81
Q

What is the job of monocytes in the cellular stage of acute inflammation

A

Engulf larger pathogens; predominate cell type 24 hours after injury

AKA phagocytes

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82
Q

What is the role of chemical mediators in acute inflammation

A
  • Derived from plasma & cells
  • Responsible for vascular & leukocyte response
  • Numerous effects on blood vessels, inflammatory cells, & other cells
    - Vasoconstrict
    - Vasodilate
    - Modulate vascular permeability
    - Contribute to chemotaxis
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83
Q

What are characteristics of cell-derived mediator histamine in acute inflammation

A
  • From mast cells; also in basophils & platelets
  • Cause vasodilation & increase permeability
  • One of the 1st mediators of inflammatory response
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84
Q

What are characteristics of cell-derived mediator arachidonic acid metabolites in acute inflammation

A
  • Found in cell membrane phospholipids
  • Synthesizes prostaglandins via cyclooxygenase (COX) enzyme
  • Corticosteroids & NSAIDS block arachidonic acid production
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86
Q

What are characteristics of cell-derived mediator platelet activating factor in acute inflammation

A
  • Induces platelet activity

- Activates cells (including endothelial cells & leukocytes

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87
Q

What are characteristics of plasma-derived mediator coagulation/fibrolytic system in acute inflammation

A

aids in blood clotting

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88
Q

What are characteristics of cell-derived mediator cytokines in acute inflammation

A
  • Many kinds exist and have a number of inflammatory effects
  • IL-1
    • Contributes to fever
    • Alters blood chemistry, including increasing coagulation factors
    • Increases number of neutrophils
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89
Q

What are characteristics of plasma-derived mediator kinin enzymatics in acute inflammation

A
  • Causes increased capillary permeability

- Cause pain

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90
Q

What are characteristics of plasma-derived mediator proteins in the complement system in acute inflammation

A
  • Cause vasodilation and capillary permeability
  • Promote leukocyte activation, adhesion, & chemotaxis
  • Augment phagocytosis
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91
Q

What is RICE or PRICE Treatment?

A 
Protection
Rest 
Ice
Compression
Elevation
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92
Q

What is the etiology of chronic inflammation?

A
  • Repeated acute microtrauma & overuse
  • Persistence of the offending agent (asbestos, surgical suture)
  • repeated bouts of the acute inflammation
  • Recurrent infections
  • Low-grade responses that fail to evoke an acute response
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93
Q

What are the 3 phases of tissue healing?

A
  • Inflammatory
  • Proliferative
  • Remodeling & maturation
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94
Q

What is the purpose of the Inflammatory phase of tissue healing?

A

Sets the stage for healing

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95
Q

What is the purpose of the Proliferative phase of tissue healing?

A

Fill in the wound gaps

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96
Q

What is the purpose of the Remodeling & Maturation phase of tissue healing?

A

Restore tissue properties

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97
Q

What is the purpose of the Inflammatory phase of wound healing?

A
  • Begins: instantaneously with cell injury
  • Prepares wound for healing
  • Hemostasis (vasoconstriction; blood clotting through platelet activation & aggregation)
  • Vasodilation (increases vascular permeability)
  • Migration of phagocytic cells
  • Macrophages also release growth factors that stimulate growth, etc.
  • Ends: 10 days post-injury
  • MOST activity completed by 72 hours
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98
Q

What is a manifestation of local inflammation?

A

Production of exudate (fluids, plasma proteins, cellular debris)

Examples: serous, hemorrhagic, fibrinous, & purulent exudate

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99
Q

What is Serous Exudate?

A

watery fluids low in protein content due to plasma entering inflammatory site (manifestation of local inflammation)

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100
Q

What is hemorrhagic exudate?

A

Leakage of RBC (manifestation of local inflammation)

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101
Q

What is fibrinous exudate?

A

Large amounts of fibrinogen & form a thick, sticky mesh work like a blood clot (manifestation of local inflammation)

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102
Q

What is purulent exudate?

A

Pus composed of degraded WBC, proteins, & tissue debris (manifestation of local inflammation)

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103
Q

What are characteristics of tissue repair?

A
  • Overlaps the inflammatory process
  • Attempt to maintain/regain normal tissue structure & function
  • 2 forms
    • Regeneration
    • Replacement
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104
Q

What is the purpose of regeneration tissue repair?

A

injured cells are replaced with same type of cells with no evidence of previous injury

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105
Q

What is the purpose of replacement tissue repair?

A

injured cells replaced with connective tissue (scar)

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106
Q

Characteristic of regeneration of Labile cells and examples?

A
  • Constant state of renewal

- Examples: cells lining GI tract, blood cells, basement membrane of skin

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107
Q

Characteristic of regeneration of Permanent cells and examples?

A
  • Unable to divide & reproduce
  • Examples: Neurons & Cardiac cells
  • Replaced with fibrous scar tissue
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108
Q

Characteristic of regeneration of Stable cells and examples?

A
  • renewed slowly; capable of renewal after tissue loss

- Example: liver cells

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109
Q

The Proliferation & migration flow chart

A

Endothelial cells proliferate –> Establish vascular network –> Form new capillaries –> Granulation tissue formed –> Cells proliferate to fill wound bed –> continued cleaning of wound –> Epithelial cell migration –> Wound covered

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110
Q

Characteristic of Remodeling & maturation tissue contraction

A
  • Epithelial cell migration causes wound shrinkage

- Fibroblasts –> myofibroblasts

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111
Q

What are the 2 patterns of chronic inflammation?

A
  • Nonspecific chronic inflammation

- Granulomatous inflammation

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112
Q

What are clinical manifestations of chronic inflammation?

A
  • Pain
  • Fibrosis
  • Decreased joint mobility
  • Decreased nutrition
  • Retention of metabolites & tissue fluid
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113
Q

What is the goal of remodeling and maturation tissue regeneration?

A
  • Goal is to restore normal tissue structure and function by generating new sin cells
  • Often involves replacement by scarring as well (occurs when the wound depth is below epidermis)
114
Q

Characteristics of scar tissue development

A
  • 2 step processes
    • Angiogenesis
    • Fibrinogensis
  • As scar matures, vascular degeneration occurs resulting in pale, largely avascular scar
  • “closing the gap” trumps function of scar
115
Q

What is angiogensis of scar tissue development?

A

sprouting new capillaries

116
Q

What is fibrinogenesis of scar tissue development?

A

activated fibroblasts result in collagen synthesis, forming scar tissue

117
Q

What are characteristics of remodeling of scar tissue?

A
  • Synthesis of collagen by fibroblasts & lysis by collagenase enzymes
  • Fibers acquire a more organized pattern; reorients tissue for strength
118
Q

Scar tissue has ______ tensile strength.

A

reduced (20-30%)

119
Q

Scar tissue and how PT affects it.

A
  • Influenced by PT interventions
  • Stress on the scar helps induce reorganization
  • What can we do to stress the scar?
120
Q

What is a Keloid scar?

A

Mass caused by excessive scar production; African-Americans have increased tendency

121
Q

What is wound healing primary intention and when does it occur?

A
  • Healing following a non-infected laceration or surgical incision
  • Seen in wounds with minimal tissue loss and have eges closely approximated
  • Heals with no infection and little to no scarring
122
Q

What is wound healing secondary intention and when does it occur?

A
  • Seen in deep or large wounds
  • Healing proceeds from “the bottom” upward & from the edges of intact tissue
  • Scarring is more extensive
  • Infected primary may heal by secondary
123
Q

What is wound healing Tertiary intention and when does it occur?

A
  • Intentional delay of closure or re-opening of previously closed wound
  • Used for infected wounds to allow cleansing
  • Want granulation of deeper tissue before superficial tissue closes
124
Q

What is resolution in outcomes of tissue healing?

A

recovery of cells-no need for replacement

125
Q

What is regeneration in outcomes of tissue healing?

A

replacement of dead cells with healthy duplicates

126
Q

What is fibrous tissue repair/scar tissue formation in outcomes of tissue healing?

A

replacement of dead cells with non-functional scar tissue

127
Q

What is persistent infection in outcomes of tissue healing?

A

development of an abscess or granuloma

128
Q

What is chronic inflammation in outcomes of tissue healing?

A

continuous inflammatory response

129
Q

What are factors that affect wound healing?

A
  • Malnutrition
  • Blood flow & oxygen delivery
  • Impaired inflammatory & immune response
  • Wound separation, infection, & foreign bodies
  • Age
130
Q

What are the properties of the immune system?

A
  • Protects the body against foreign substances
  • Distinguishes self from non-self, attacking the “non-self”
  • When working well, prevents infection & disease
  • When not working well, localized or systemic infection or disease
131
Q

What are the characteristics of the regulation of the immune response?

A
  • Self-regulation is an essential property of the immune system
  • Regulation not well understood
  • Exposure to foreign antigens can lead to excessive tolerance & infection
132
Q

What is the term for inadequate immune response?

A

Immunodeficiency

133
Q

What is terms for excessive immune response?

A

Allergic reaction or autoimmune disease

134
Q

What does tolerance mean?

A

The ability of the immune system to be non-reactive to self-antigens (pregnancy, blood transfusion)

135
Q

What are the central organs involved in Immune Response?

A
  • Immune cell production & maturation
  • Bone marrow: B-cells
  • Thymus: T-cells
136
Q

What is the job of peripheral lymphoid organs involved in Immune Response and what are some examples?

A
  • Trap & process antigens & promote interaction with mature immune cells
  • Examples: spleen, tonsils, & appendix
137
Q

What is an antigen?

A
  • Any foreign substance in the body that does not have the characteristic cell surface markers
  • Leads to the immune response
138
Q

What is an Epitope?

A
  • Immunologically active site on antigen
  • Like a receptor
  • Unique shape
  • Recognized by antibody
139
Q

What is a major histocompatability complex?

A
  • Consists of unique cell markers that inform the body of what belongs
  • Inherited: influence one’s predisposition to disease
  • Provide cell to cell communication
  • Determine how a person responds to antigens
140
Q

What are the WBCs in the innate immunity?

A
  • Granulocytes
    • Neutrophils
    • Basophils
    • Eosinophils
  • Monocytes –> macrophages
  • Natural killer (NK) cells
141
Q

What are the WBCs in acquired immunity?

A
  • Lymphocytes
    • B cells
    • T cells
    • NK cells
142
Q

What are characteristics of innate (Non-specific) Immunity?

A
  • Lacks memory, non-adaptive
  • Defenses in place before infection occurs
  • Rapid response (but not variable)
  • Includes
    • Epithelial barriers that block entry
    • Phagocytic cells
    • Natural Killer cells
  • Doesn’t require exposure
143
Q

What are the exterior defense of innate immunity?

A

skin and body orifices provide defense

144
Q

What is the function of phagocytes in innate immunity?

A

readily kill and ingest antigens

145
Q

What is the function of soluble (inflammatory mediators) in innate immunity?

A

complement system (proteins) coat pathogens so they can be more easily phagocytosed

146
Q

What is the function of NK cells in innate immunity?

A

Kill viruses, tumor cells, others

147
Q

What are characteristics of Acquired (Adaptive) immunity?

A
  • Specific
  • Recognizes & reacts to specific pathogens
  • Have a “memory”
  • Many different antigen receptors involved
  • Active & passive forms
  • 2 types
    • Humoral
    • Cell-mediated
148
Q

What are characteristics of passive adaptive immunity?

A
  • Transfer of protective antibodies against an antigen from another person
  • Short-term protection (weeks to months)
  • Example: mother to baby via breast milk, hepatitis vaccine
149
Q

What are characteristics of Active adaptive immunity?

A
  • Develops after exposure to antigen
  • Long-lasting due to memory cells
  • Examples: vaccination with inactive virus (mumps, measles, polio), tetnus every 10 years
150
Q

What are characteristics of humoral (antibody-mediated) adaptive immunity?

A
  • Mediated by molecules in blood produced by B lymphocytes

- Principle defense against extracellular microbes

151
Q

What are characteristics of cell-mediated adaptive immunity?

A
  • Mediated by specific T-lymphocytes
  • Defends against intracellular microbes (viruses)
  • HIV attacks these
152
Q

What are characteristics of Immunoglobins?

A
  • Produced by B-lymphocyte-plasma interaction
  • “Y” shaped
  • Forked ends bind with antigen
  • Tail determines class
153
Q

What are factors affecting immunity?

A
  • Age
  • Nutrition
  • Pollution & chemicals
  • Surgery & anesthesia
  • Trauma & illness
  • Medications
  • Sleep
  • Stress
  • Psychosocial situations
154
Q

Developmental aspects of immunity in Infants

A

Protection of newborn against antigens occurs through transfer of maternal antibodies

155
Q

Developmental aspects of immunity in Elderly

A
  • Decline in immune responsiveness (cell-mediated & humoral responses)
  • Difficult time mounting an infection –> more susceptibility
  • Risk of reactivation of dominant infection
  • Higher prevalence of autoimmune
  • Higher incidence of cancer
  • Vaccination less effective
  • Elders need to have full cycle of meds
156
Q

What is primary immunodeficient disease?

A
  • Defect in T or B cells or lymphoid tissue
  • Increase one’s risk of infection, autoimmunity, or cancer
  • Rare
157
Q

What is secondary immunodeficient disease?

A
  • Due to underlying or previous disease
  • Use of medications & medical treatments for other conditions can cause immunosuppression
  • Chemo
  • Corticord steriods
158
Q

What are hypersensitivity disorders?

A

exaggerated or inappropriate response to an antigen

159
Q

What is immediate hypersensitivity disorder?

A

occur within minutes of exposure

160
Q

What is late phase hypersensitivity disorder?

A

persistent symptoms for hours to days after allergen is removed

161
Q

What is delayed hypersensitivity disorder?

A

occur after days due to increased sensitization

162
Q

What is immediate, allergic, anaphylactic hypersensitivity disorder?

A

normally harmless substance causes response in susceptible people

163
Q

What is cytotoxic hypersensitivity disorder?

A

body tissue recognizes self as foreign or reaction between exogenous pathogen & endogenous tissue

164
Q

What is immune complex hypersensitivity disorder?

A

accumulation of antigen-antibody complexes in tissue –> inflammation

165
Q

What is cell-mediated immunity hypersensitivity disorder?

A

a delayed response (transplant)

166
Q

What is auto-immune disease and what is it etiology?

A
  • Body fails to distinguish self from non-self
  • Immune system response attacks the body tissue
  • Etiology: genetic, hormonal, & environmental combo
167
Q

What is iso-immune disease?

A
  • Organ & tissue transplantation
  • Body recognizes the tissue as non-self
  • Goal: prevent rejection through matching
168
Q

Skeletal Changes that occur in the lifespan?

A
  • Max bone density achieved by age 30
  • Many factors influence skeletal development
  • Affects the cartilage, bone surface or bone itself
169
Q

How is nutrition important in bone building?

A

It is key to building up to peak bone mass (vitamin D & calcium the most important)

170
Q

What effect does exercise have on bone density?

A

More stress increases bone density

  • running>walking
  • swimming is bad for bone density
171
Q

What are characteristics of alkaline phosphatase?

A
  • Non-specific marker of metabolic activity in bone tissue
  • Adults<children
  • Levels increased with fracture & metabolic bone diseases
  • Mainly in liver
172
Q

What is serum calcium used for and what do high levels mean?

A
  • Used to screen for or monitor calcium regulation disorders (parathyroid gland or kidneys) or diseases of the bone
  • Higher because calcium is being pulled out of bone
  • Cancer can cause high serum calcium
173
Q

What are risk factors for osteoporosis?

A
  • Ethnicity (Caucasian & Asian)
  • Genetics
  • Climatic/environmental (less change in climate)
  • Hormonal factors
  • Diet
  • Exercise/activity
  • Body type
  • Prolonged immobilization
  • Alcohol, tobacco, & anti-coagulant use (synergistic)
174
Q

What is the pathogenesis of osteoporosis?

A
  • Between 35 & 40 years old bone resorption>bone formation
  • Bone matrix deteriorates
  • Trabecula thin
  • Bone fibrils become more longitudinally arranged
  • Bone becomes filled with more fat tissue
175
Q

What are most common spots and causes of primary osteoporosis?

A
  • Hormonal changes
  • Women
  • Hip, spine, and radius
  • Cancellus bone because highly vasculized
176
Q

What are the most common spots and causes of secondary osteoporosis?

A
  • Aging process regardless of hormones
  • Cancellous & cortical bone
  • More femur fractures
  • Pelvis, humerus, tibia (long bone fractures)
177
Q

What are the effects of Osteoporosis?

A
  • Postural abnormalities
  • Increased fracture risks
  • Pain
  • Functional consequences (balance, chest, reaching)
  • Shortened stature
  • Respiratory compromise
  • Increased satiety
178
Q

How is osteoporosis diagnosis?

A
  • Bone mineral density (BMD) testing
  • Radiographs
  • Laboratory tests
179
Q

What is a bone mineral density test?

A
  • Dual Energy X-ray Absorptiometry (DEXA)
  • Measure of mineral content in bone
  • Recommended for every woman >65 y.o. & postmenopausal<65 with fracture history
  • Hip & spine main bones
180
Q

What is a T-score?

A
  • Standard deviation from peak bone mass
  • Can tell bone is weak
  • Disadvantage: not age matched
181
Q

What is a Z-score?

A

-Number of standard deviations as compared to mean value for others at the same age and gender

182
Q

Is a radiographic analysis good for detecting osteoporosis?

A

Bad way to tell because someone has to lose 30-50% of bone mass for it show up

183
Q

What is the treatment for osteoporosis?

A
  • Begins with prevention
  • then
    - Medications
    - Calcium & vitamin D
    - Estrogen replacement
    - Lifestyle changes
    - Exercise
    - Total body vibration
    - No smoking
    - Limit alcohol intake
184
Q

What is Vertebroplasty?

A

Insertion of cement into vertebral body

185
Q

What is kyphoplasty?

A

Insertion of small balloons into vertebral body

186
Q

What is osteomalacia?

A
  • Progressive disease

- Lack of mineralization of new bone matrix –> softening of bone without loss of matrix

187
Q

What is Paget’s disease?

A
  • 2nd most common metabolic
  • Leads to abnormal bone remodeling
    - Increase bone resorption due to activated osteoclasts
    - Excessive, disorganized bone formation
    - Soft bone deposition
188
Q

What is clinical presentation of Paget’s disease?

A
  • Change in bone shape, size, & direction
  • Postural abnormalities
  • Fatigue, lightheadedness, stiffness
  • Can impact nervous system
  • Varus
  • Rickets
189
Q

What is hematology?

A

Form & structure of blood & blood-forming tissue

190
Q

What are the 2 main components of blood?

A
  • Plasma
  • Formed elements
    • RBC
    • WBC
    • Platelets
191
Q

What are the 3 main characteristics of RBCs?

A
  • Thin (helps with oxygen delivery)
  • Flexible (get into small areas)
  • Biconcave (increase surface area)
192
Q

What is anemia?

A

Diminished oxygen-carrying capacity of blood

193
Q

What does anemias generally result from…..

A
  • Decreased erythrocyte production
  • Increased erythrocyte destruction
  • Blood loss
  • Combination of above factors
194
Q

What does hypoxia lead to?

A
  • Fatigue
  • Weakness
  • Dyspnea
  • Angina
  • Tachycardia –> ventricular hypertrophy
  • Pallor
  • Headache & fainting
195
Q

What is hemoglobin?

A

Concentration of the oxygen-carrying pigment of the erythrocytes

196
Q

What is hematocrit?

A

percentage of total blood volume occupied by RBCs

197
Q

What are the goals of treatment of anemia?

A
  • Alleviate or control the cause
  • Reduce symptoms
  • Prevent complications
198
Q

What are guidelines for PT in the treatment of anemia?

A
  • Seek physician approval before treating patient with anemia
  • Expect fatigue & decreased exercise tolerance
    - Monitor VS & O2
  • Know the cause of the anemia & the patient’s co-morbidities
199
Q

What does leukocytosis mean?

A

Increase in WBCs

200
Q

What does leukopenia mean?

A

Decrease in WBCs

201
Q

What does Neutropenia mean?

A

Decrease in neutrophils (most common of leukopenia)

202
Q

What is the pathogenesis of disorders of WBCs?

A

Suppression of bone marrow, damage to cells, removal of cells from circulation

203
Q

What is leukemia?

A
  • Neoplasm of blood forming
  • Replaces normal bone marrow with malignant clone of lymphocyte or myelogenous cells
  • Acute or chronic forms
204
Q

What are symptoms of leukemias?

A
  • Anemia
  • Infection
  • Bleeding tendencies
  • Bone pain
205
Q

What are ways of diagnosis of leukemias?

A
  • Blood counts
  • Bone marrow biopsy
  • Initially, leukocyte counts elevated but may be low
206
Q

What are lymphomas?

A
  • Cancer of lymph system
  • 2 groups
    • Hodgkin’s
    • Non-Hodgkin’s
  • Among most curable
207
Q

Prothrombin time, Partial thromboplastin time, & International normalized ratio…… Increased time means ______.

A

Don’t clot well so at risk for bleed

208
Q

What is the international normalized ratio (INR)

A
  • Gold Standard

- PT values used to calculate INR

209
Q

Increased INR means……

A
  • The slower your blood will clot

- Higher risk of bleeding

210
Q

Decreased INR means……

A
  • The quicker your blood will clot

- Higher risk to develop a blood clot

211
Q

What is hypercoagulability?

A

Exaggerated production and/or occurrence of thromboses

212
Q

What are causes of Hypercoagulability?

A
  • Increased platelet function
  • Increased clotting activity
  • Genetic or acquired
213
Q

What are causes of thrombocytopenia?

A
  • Inadequate platelet production
  • Platelet destruction
  • Splenic sequestration of platelets
214
Q

What is thrombocytopenia is associated with….

A
  • Cancer: leukemia metastatic cancer
  • Aplastic anemia
  • Aggressive chemo
215
Q

What are symptoms/signs of throbocytopenia?

A
  • Mucosal bleeding
  • Petechaiae and/or purpura
  • Hematuria
216
Q

What is Von Willebrand disease?

A
  • Autosomal dominant
  • Reduced platelet adhesion
  • Defective clot formation
  • Internal or joint bleeding
217
Q

What are signs and symptoms of localized infection?

A

Swelling

  • red
  • pain
  • heat
  • maybe pus
218
Q

What are signs and symptoms of systemic infection?

A
  • Fever & chills
  • Malaise
  • Sweating
  • Nausea and vomiting
  • Changes in mentation
  • Spasticity
219
Q

What is symptomatology?

A

Collection of signs and symptoms expressed (clinical picture or disease presentation)

220
Q

Mechanisms of infection may be specific

A

Reflect the site of infection

Examples: diarrhea, rash, pneumonia

221
Q

Mechanisms of infection that are non-specific

A

Fever
Headache
Lethargy
Malaise

222
Q

Mechanisms of infection you may see overt signs… What is an example?

A

Chicken pox

223
Q

Mechanisms of infection covert signs…. What is an example?

A

WBC count

224
Q

What is the site of infection?

A

Depends on type of pathogen, portal of entry, & host’s immune defenses

225
Q

What is sepsis & septicemia?

A
  • Infection by microbials in blood

- Can cause death

226
Q

What is an abscess?

A

Localized pocket of infection; can be surgically removed or drained

227
Q

What is an infectious disease?

A

Consequences of microbial invasions

228
Q

What is a host?

A

Any organism capable of supporting another organism’s nutrition & growth

229
Q

What is colonization?

A

Host carries organism, but does not have disease

230
Q

What is an infection?

A
  • Presence & multiplication of living organisms on or within the host
    - Healthy infection
    - Pathogenic infection
231
Q

What is an incubation period?

A

is from pathogen entering host–> appearance of clinical symptoms

232
Q

What is a latent infection?

A

Microorganism has replicated but is dormant or inactive

233
Q

What is the period of communicability?

A

When the infection can be transferred to another person

234
Q

What is virulence?

A

Disease-producing potential (vigorous)

235
Q

What are pathogens?

A

Virulent organisms capable of causing disease

236
Q

What is opportunistic pathogens?

A

Attack vulnerable hosts (weakened immunity illness, or medical therapy)

237
Q

What are nosocomial infections?

A
  • Acquired during hospitalization
  • Tend to be related to invasive procedures
  • Involve drug resistant organisms
  • Increased hospitalization
  • Medicare will not pay for
  • Increase of risk with increase in doctors
238
Q

What are intracellular organisms as infectious agents?

A
  • Grow & multiply only in host cells
  • Require host metabolism for survival
  • Example: Virus
239
Q

What are extracellular organisms as infectious agents?

A
  • Can grow & multiply outside of the cells
  • Can be cultured on artificial media
  • Example: bacteria
240
Q

What are principal pathogens as infectious agents?

A
  • Cause disease, even in people with intact immune systems

- Example: flesh eating bacteria

241
Q

What are opportunistic pathogens?

A

Cause disease only in those with immunodeficiency

242
Q

What are viruses?

A
  • Smallest known organism
  • Protein coat with RNA or DNA
  • Penetrate living cell, replicate with cell’s DNA. create new viruses or latent virus
  • May or may not cause death of host cell
  • Must live off the host & need to be within the cell
243
Q

What is bacteria as a pathogen?

A
  • Single-celled with well defined cell walls

- Can grow independently & reproduce frequently

244
Q

What is Gram (+) Bacteria?

A
  • Easier to treat

- Stains black or purple

245
Q

What is Gram (-) Bacteria?

A
  • Harder to treat because double cell wall

- Stain pink

246
Q

What is a culture?

A
  • Propagation of microorganism outside of the body (not all pathogens are capable of this type of reproduction)
  • Should be done before antibiotic therapy
247
Q

What is serology?

A
  • Study of serum
  • Blood tests to detect infectious disease
  • Antibody titer; assesses rise of antibody level associated with a specific pathogen
248
Q

What is the general treatment for infectious diseases?

A
  • goal is to rid body of pathogen & restore normal physiologic function to damaged tissue
  • Most of the infectious diseases are self-limiting with little or no medical therapy required
249
Q

What is the treatment of viruses?

A
  • Various meds & vaccines
  • Effective treatment is difficult, however
    - Replication peaks before symptoms
    - Drugs require intact immune system
    - Able to “hide”
    - Develop drug resistance
250
Q

What are vaccines?

A
  • Stimulate immune system to be prepared to fight virus later on
  • Use of killed or attenuated vaccine effective without causing disease
  • Limitations: vaccines specific to one virus
251
Q

What is the treatment of bacterial infections?

A
  • Depends on the type (Gram + or Gram -)
  • Antibodies
    • Bactericidal (kill the bacteria)
    • Bacteriostatic
      - Inhibit bacterial growth, without killing
      - Require intact immune system
252
Q

What is innate resistance?

A

no transport mechanism to move drug across bacterial cell wall

253
Q

What is acquired resistance?

A
  • Various
  • Spontaneous genetic mutation & other genetic alterations
  • Enzymes that block access to the cell
  • Problems with binding sites on the cell membrane
  • Transporters that pump the antibiotic away from the cell
254
Q

What is the problem of overuse of antimicrobial agents?

A
  • Given in busy clinics to patients infected with viruses
  • Given prophyloctically to surgery patients
  • Given to animals in our food chain for growth & fighting infection
  • Soaps & lotions are increasing in popularity
255
Q

What are examples of carcinogens?

A
  • Tobacco use
  • Viruses
  • Chemical agents
  • Physical agents
  • Drugs
  • Hormones
  • Excessive alcohol consumption
256
Q

What are risk factors for cancer?

A
  • Advancing age
  • Previous CA
  • Lifestyle/behavior
  • Exposure to viruses
  • Hormones
  • Environmental
  • Gender
  • Stress
257
Q

What are characteristics of neoplasm?

A

-Abnormal growth (serves no useful purpose)
-Uncoordinated growth
-Benign or malignant
Primary or secondary

258
Q

What is a benign neoplasm?

A
  • More differentiation of cells; resemble cells of tissue origin
  • Slow growth
  • Non-invasive
  • Contained in fibrous capsule
  • Can disturb function
  • Typically not lethal
  • Can be lethal
259
Q

What is an adenoma?

A

Benign tumor of glandular epithelial cells

260
Q

What is an osteoma?

A

Benign tumor of bone

261
Q

What is a lipoma?

A

Benign tumor of fatty tissue

262
Q

What is a polyp?

A

Projection from mucosal surface

263
Q

What is a cancer in situ?

A

Localized pre-invasive lesion

264
Q

What is a neoplasm malignant?

A
  • Lacks differentiation
  • Grows rapidly
  • Can grow into surrounding tissues & distant sites
  • Fingerlike projections
  • Can cause death
  • 2 categories
    • Solid tumors
    • Hematologic cancer
265
Q

What is a carcinoma?

A
  • Malignant neoplasm derived from epithelial tissue
  • Tend to metastasize through the lymphatic or hematopoetic systems
  • Most common sites:
    • skin, cervix, stomach, large intestine, prostate gland, bronchi, breast
266
Q

What is a sarcoma?

A
  • Malignant neoplasms
  • Connective tissue origin
  • Highly malignant
267
Q

What is osteosarcoma?

A
  • Malignant neoplasms
  • Most common & most malignant bone cancer
  • Most commonly seen in males between ages 15-30
  • Found in the metaphyses of long bones in adolescences
268
Q

What is a lymphoma?

A
  • Malignant neoplasm

- A lymphoid tissue neoplasm

269
Q

What is leukemia?

A
  • Malignant neoplasm

- Abnormal cells of hematological origin that metastasize through invasion & inflitration

270
Q

What is an invasion?

A

Extensive infiltration & invasion of surrounding tissues

271
Q

What is a metastasis?

A
  • Development of (distant) secondary tumor
    - Process involves the breaking off of cells
    - Spreads to other locations in the body (lymphatic, circulatory, directly to surrounding tissues)
272
Q

What are metastasis most common sites?

A
  • Bone
  • Brain
  • Lung (because blood returns here 1st)
  • Liver
  • Lymph nodes
  • Because the most vascularized
273
Q

What are local signs & symptoms of cancer?

A
  • Pain
  • Fracture
  • Shortness of breath
  • Coughing
274
Q

What are systemic signs of cancer?

A
  • Pain
  • Fatigue
  • Cachexia (global wasting of muscle)
  • Hormonal imbalance
  • Anemia
  • Leukopenia
  • Bleeding or non-healing wounds
  • Infection
275
Q

What are paraneoplastic syndromes?

A
  • Manifestations in sites not directly affected by cancer
  • Not explained by local or distant spread of the tumor
  • Can show before the actual diagnosis of cancer is made
276
Q

What are diagnostic methods in oncology?

A
  • Biopsy
  • Blood test
  • MRI
  • CT scan
  • Isotope scan
  • Mammography
  • Ultrasonography
  • Urinalysis
277
Q

What is a biopsy?

A

The single most important diagnostic method for the study of tumors

278
Q

How do you perform a sentinel node biopsy?

A
  • Insert radioactive dye in several places around the tumor
  • Watch the up-take through the lymph
  • sentinel node is the main lymph node that the radioactive dye passes or gathers
279
Q

What are diagnostic imaging for cancer?

A
  • MRI
  • CT
  • Radiographs
  • Nuclear Medicine
280
Q

What is staging & grading diagnostic methods?

A
  • Useful in determining prognosis & selecting treatment
  • Grading: histological or cellular characteristics
  • Staging: extent & spread of disease
281
Q

What is the TNM system?

A

T= Size & local spread of primary tumor
N= Involvement of regional lymph nodes
M= Extent of metastasis
This system helps stage

282
Q

What are the goals of intervention for cancer?

A
  • Cure the cancer
  • Control the cancer
  • Provide palliative care to the cancer patients

Medical Conditions I (3 decks)

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