Pathophysio Disorders Part 1 Flashcards
Benign papillomas
Exaggeration of normal skin composition
Only invades kin and mucous membrancous
Most resolve within 5 years
Viral infection
Verrucae (warts)
Common infection of skin and mucous membrane
Vesicles and erythema become pustules, ulcers, crusts then heal
Herpes simplex
Type 1- above the waist
Type 2- below the waist
Acute, localized, inflammatory
Normally within dermatosomal segment
Stays latent in dorsal root ranglia
eruption of vesicles and erythematous bases
Herpes Zoster- shingles
Can cause infection
often erythematous macules or plaques with peripheral scaling and central clearing
Superficial fungal infection
Fungal infection found in immunoimpaired people
Mucocutaneous candidiasis
Fungal infection found in infants and bed ridden patients
Intertrigo
Acute, contagious
vesciles, pustules, yellowing crusts
bacterial infection
Impetigo
Bacterial STD
3 stages-lesion, rash, goes to brain
Syphilis
Excessive growth of keratinocytes/ keratin
looks like a fish!
congenital ichthyosis
hyperkeratosis
stimulation by pressure
corns, calluses
most common skin cancer
basal cell carcinoma
rare, highly malignant, skin cancer
melanoma
Diffuse, punctate, macular rash
Begins on trunk, spread to arms/ legs
Swollen lymph nodes
Can cross placenta
Rubella- 3 day (german) measles
Herpes 6 and 7
5-15 months- maculopapular rash on trunk
spreads to appendages- high fever, inflamed tympanic membranes
no swollen lymph nodes
roseola infantum
Macular, blotchy rash
begins onf face, spreads to appendages
high temp, photosensitivity, macules may hemorrhage
highly communicable
Measles
Skin lesions in 3 stages: macule, vesicle, granular scab
All 3 forms visible by 3rd day
Chicken pox- varicella
Systemic reactions to toxins produce by alpha beta-hemolytic streptococci
normally with strep throat
pink punctate skin rash
high fever, strawberry tongue
scarlet fever
superficial, partial thickness burn
1st degree burn
Epidermis and part of dermis (partial thickness)
SubQ structure stay intact (full thickness)
2nd degree burn
Full thickness burn
extends into subcutaneous tissue
vasculature involvment
third degree burn
full thickness beyond dermis
muscle and bone involving
4th degree burn
lateral curvature of the skin
resolves when patient bends to affected side
non-structural scoliosis
lateral curavture of the spine
fails to correct on forced bending against curavture
vertebral rotation
structural scoliosis
Bone resoprtion rate greater than formation
osteoclasts outpace osteoblasts
cancellous lost faster than cortical
osteoporosis
Deficit in mineraliation of osteoid
Vitamin D deficiency prevents normal calcium and phosphorus maintenance
Rickets (children) Osteomalacia (adults)
Progressive slow metabolic disorder
excessive bone resorption follow by excessive bone formation
overproduction of cancellous bone
fragility leads to deformities and fractures
Paget Disease
Soft tissue trauma due to unyielding structure of inert tissues
decreae compartment size, increased compartment content
all cause pressure- ischmia and pain
Compartment syndrome
Common, severe X-linked
Muscle cells lack dystrophin
Duchenne Muscular Dystrophy
inherited, autosomal dominant, face and shoulder affected
facioscapulohumeral muscular dystrophy
Chronic, autoimmune diseaes of neuromuscular function
voluntary muscle weakness and fatigue
Ach receptor antibodies
Myasthenia Gravis
Pain syndrome, chronic muscle pain
unkown etiology
Fibromyalgia syndrome
Degenerative, progressive, non-inflammatory disease
Loss of articular cartilage
More prevelant with age
Osteoarthritis
Systemic inflammatory disease
characterized by inflammation in joint cavity
stimulate edema, neovascularization, synovial proliferation
rheumatoid arthritis
Agglutination due to mismatch ABO blood types
Type II hypersensitivty rxn
transufion rxn
Rh- mother with Rh+ fetus
type II hypersensitivty rxn
hemolytic disease of the newborn
antibodies form to ach receptor on motor end plates of muscles
no effect cells
loss of motor end plate function
types II hypersensitivity rxn
Myasthenia Gravis
similar to myasthenia Gravis but with effector cells
- Body develops autoantibodies directed towards autoreceptors in thyroid gland
- Build up receptors and enhance normal function of thyroid gland (hyperthyroidism)
Graves Disease
Donor tissue - antigen for which recipient has preformed antibodies
Revascularization of new tissue - antibodies attach
Effects and complement mediate lysis of donor tissue
Inflammation, thrombosis & hemorrhage - 48 till donor tissue death
hyperactue graft reaction
Caused by persistent low-grade infection
Interaction of soluble exogenous antigen with soluble antibody
Immune complex deposited in glomerular capillary wall
Damage to glomerular basement membrane
Proteinuria, hematuria, hypertension, oliguria
Immune complex glomerulonephritis
Autoimmune, connective tissue, collagen vascular or inflammatory disorder
Development of antibodies against nuclear antigens
Anti-nuclear and anti-DNA autoantibodies attach - deposit on collagen-rich tissues
Systemic lupus erythematosus
Rapid type IV
Soluble antigen triggers T cells - release cytokines - activate basophils - move to infected area - skin swelling in 24 hrs
Cutaneous basophil hypersensitivity
Hapten penetrates skin - becomes immunogenic
Activation of CD4+ cells - inflammatory response and attraction of effector cells
- epidermal phenomenon - peaks in 48-72 hrs
Contact hypersensitivity
Person with tuberculosis antibodies is exposed to tuberculin in a TB test
Dermal phenomenon
Tuberculin-type hypersensitivity
Primary defense against intracellular infections
Protective - eventually causes tissue destruction
Antigen not degraded in macrophages
Lymphocytes create inflammatory response
Granulomatous hypersensitivity
Autosomal recessive or X-linked recessive
Possible defective expression of MHC
Possible mutation to RAG1 & RAG2
SCID
X-linked
Mutation of WASP gene - cytoplasmic signaling
Deficiency of platelets, non-functional T cells
Trouble mounting immune responses
Wiskott-Aldrich Syndrome
thymic hypoplasia
T cell development affected due to deletion on chromosome 22
Normal B cells
Normally found with other developmental disorders
DiGeorge Syndrome
Autosomal recessive T-cell disorder
Selective deficiency of cell-mediated immunity against Candida albicans
Persistent or recurrent severe skin, nail and mucous membrane infections
Other B and T cell functions are normal
Chronic Mucocutaneous Candidiasis
failure of IgA lymphocytes to become plasma cells
Autosomal dominant or recessive
Prone to respiratory, GI and genitourinary infections
IgA deficiency
B cells unable to complete maturation
Mutation of btk gene
Increase in T cells
Prone to recurrent bacterial infections
Bruton X-linked agammaglobulinemia
Infant slow to acquire normal Ig levels
Normalcy achieved usually by age 4
Transient hypogammaglobulinemia
