• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/32

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

32 Cards in this Set

  • Front
  • Back
primary and secondary osteoarthritis.
Primary variants of OA occur as localized or generalized syndromes
versus
Secondary OA has a known underlying cause
major etiologies of osteoarthritis
Obesity
Repetitive motion
Occupation
Sports
Trauma
Genetic factors
physiology of normal cartilage
Functions include:
Movement across joint
Distribution of weight across the joint
Stabilization of the joint
Easily compressed
pathologic changes associated with osteoarthritis.
Increased production and activity of proteases
Matrix metalloproteinases (MMPs)
Chondrocytes undergo apoptosis
clinical presentation of osteoarthritis.
Typically affects knees, hips, hands
-Pain with motion
Due to activation of nociceptive nerve endings within the joint
Joint stiffness
Crepitus
Limited ROM
key features of RA and osteoarthritis
Age of Onset
Joints Involved
Symptoms
Systemic symptoms
signs and symptoms of RA
Joint involvement tends to be symmetrical
-Joint pain and stiffness
Tends to be worse in AM; usually lasts >1 hr after getting up in AM
Joint swelling/warmth/tenderness
-proximal interphalangeal (PIP) and metacarpophalangeal (MCP) joints
extra-articular manifestations of RA
Rheumatoid nodules
-Vasculitis
Role of CD4+ Helper T Cells in RA pathophysiology versus Role of B Lymphocytes
Promote cytokine release
TNF-alpha, IL-1, IL-6
Produce receptor activator of nuclear factor κβ ligand (RANKL)
B lympocytes on the other hand Form antibodies called rheumatoid factors (RF)
Laboratory Findings of RA
CBC
Anemia (normocytic, normochromic)
Thrombocytosis
Neutropenia
-the presence of ≥4
Uric Acid overproducers versus underexcretors
Overproduction of Uric Acid:
-Deficiency of HGPRT
~10-20% of patients
Underexcretion of Uric Acid :
-~80-90% of patients
-Organic acids compete with urate for excretion
Decreased kidney function
Diuretics
-24 hour urine sample to distinguish b/n the two
clinical manifestations of acute gouty arthritis
Predisposition to great toe (Low temperature and poor solvent )
Epidemiology of gout
Increasing age
SCr, BUN
Male gender
Postmenopausal women
Blood pressure
Body weight (obesity)
Alcohol intake
Meat/fish intake
Tophaceous gout
Deposits of urate in soft tissues
risk factors for SLE
Genetics
Hormonal and immunologic
Environmental
T/F.SLE is a chronic inflammatory disease
True
T/f.Most patients with ANAs do not have SLE; but most people with SLE do have ANAs
True
T/F. SLE Onset can be acute OR insidious
True
-Disease course characterized by exacerbations and remissions.
Signs and symptoms of SLE includes arthritis, arthralgia, myositis
True
three methods of bacterial spread to the bone
Hematogenous Osteomyelitis
Contiguous Spread Osteomyelitis
Vascular Insufficiency
most common organisms involved in the development of osteomyelitis
Staphylococcus aureus:Long bones, vertebrae
S. aureus:Femur, tibia, cranium, mandible
S. aureus:Feet
Likely Pathogen of osteomyelitis in IVDA or hemodialysis
S. aureus, Pseudomonas aeruginosa
Risk of AOM greatest in young children (< 3 years)
ET is shorter, less rigid, and more horizontal
Key elements in the diagnosis of AOM
Acute (abrupt) onset of signs and symptoms
Middle ear inflammation and erythema of the tympanic
Presence of middle ear effusionmembrane
Most Prevalence pathogen of Acute Otitis
Streptococcus pneumoniae
A Certain diagnosis of AOM
Certain diagnosis = rapid onset + middle ear effusion + middle ear inflammation
4 primary factors involved in the pathogenesis of acne
Increased sebum production
Sloughing of keratinocytes
Bacterial growth & colonization
Inflammation
5 different acne lesions
Acne Vulgaris( No inflammation present)
Papules( inflammation present)

Pustules (inflammation present)

Nodules (cysts)
Open Comedones versus Closed Comedones
Blackheads”
Plugs of material open to skin surface in a dilated hair follicle
versus “Whiteheads”
Plugs of material open to skin surface in a closed hair follicle
Etiology of Acne
Factors that DO affect acne
Genetics
Climate
Stress
Physical activity
Factors that DO NOT affect acne
Diets high in fat
Poor hygiene
Psoriasis etiologies
Immunologic Mechanisms
-Activation of T-cells
4 different types of psoriasis.
Psoriasis vulgaris (plaque-type)-(Auspitz sign)

Guttate(Teardrop shaped ,mostly in children )
Pustular
Erythrodermic(Affects all body surfaces (i.e., hands, nails, trunk, extremities)
)