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479 Cards in this Set
- Front
- Back
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What causes skin differences?
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Four basic layers and adnexal structures
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What are the four basic layers of organization?
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Epidermis, Papillary dermis, Reticular dermis, and subcutaneous tissue (hypodermis)
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What are the major adnexal structural units?
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Pilar (hair), eccrine, and apocrine units
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What layer are the adnexal structures found in?
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Dermis
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What layer does edema and swelling occur in?
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Papillary dermis
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What is the life span of the epidermis?
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21 days
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What do keratinocytes accumulate?
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Keratin and Melanin
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Do keratinocytes get closer together or father apart the further up they go?
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Farther apart
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What property of skin allows up to keep from absorbing things?
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Squamous property
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Do melanocytes stay at the basal layer or do they move up?
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Melanocytes stay at the basal layer
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What do melanocytes make?
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Melanosomes
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What do melanosomes make?
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Dopa
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What does dopa secrete?
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Melanin
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Where is the melanin located?
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Keratinocytes
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What increases melanosome production?
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Sun exposure
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What does a melanocyte look like?
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Nucleus with a halo arround it
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What is a sign of excess keratin?
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Dandruff
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What are Rete pegs?
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Invaginations of the epidermis into the dermis
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Where is the vasuclar plexus located?
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The papillary dermis
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Where are Meissner's corpuscles located?
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Papillary dermis
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What do Meissner's corpuscles do?
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Touch receptors
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Where are Meissner's corpuscles most numerous?
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Hands and feet
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What is the papillary dermis?
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A coat for the epidermis; supplies nutrients for rapidly growing keratinocytes
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Is the papillary dermis fine and delicate or rigid?
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Fine and delicate
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What does the reticular dermis do?
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Serves as a cushion and stable platform for the epidermis and papillary dermis; skin layer where the adnexal structures are located
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Where are adnexal structures housed?
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Reticular dermis
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What are Pacinian corpuscles?
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Pressure receptors
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Where are Pacinian corpuscles found?
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Deep in the dermis
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What is subcutaneous tissue?
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loose and dense connective tissue consisting of adipocytes and fibroconnective tissue
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What does the subcutaneous tissue connect?
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Connects the reticular dermis with fascia of underlying tissue
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What is significant about the subcutaneous layer?
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Major layer of skin where aging is most effective; there is progressive loss of sub-q tissue as aging progresses
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Where are eccrine glands located?
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Mid to lower reticular dermis
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Where are apocrine glands located?
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Deep dermis and often at junction of reticular dermis and sub-q tissue (axilla, scalp, perineum)
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Macule?
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flat area of color change; <1cm diameter; ex--freckle
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Patch?
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Larger, flat, non-palpable lesion; >1 cm; ex---cafe-au-lait spot
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Papule?
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Discrete, solid, raised lesion; <1 cm diameter; ex---nevus
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Nodule?
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Larger, discrete, rounded, raised solid lesion; ex---rheumatoid nodule
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Plaque?
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raised, flat-topped lesion; >1 cm diameter; ex---psoriasis
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Wheal?
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Transient edematous erythematous plaque; ex---hives or urticaria
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Vesicle?
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Fluid-filled lesion; <0.5 cm diameter; ex---herpes
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Bulla?
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larger fluid-filled lesion; ex---friction blister
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Pustule?
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Vesicle like lesion filled with purulent exudate; ex---folliculitis
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Erosion?
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Partial or complete loss of the epidermis; scratching
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Ulcer?
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loss of epidermis and part of dermis
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Fissure?
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Thin, linear erosion or ulceration; ex--cheilitis
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Scale?
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Hyperkeratosis; ex---dry skin
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Crust?
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Dried serous and serosanguinous exudate; ex--impetigo
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Lichenification?
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Accentuation of skin markings with thickening of the skin
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Atrophy?
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Decrease in amount of epidermis, dermis, or sub-q tissue
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Verrucous?
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Wart-like surface
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What is Lentigo Senilis or Solar Lentigo?
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Benign, discrete hyperpigmented macule occuring on chronically exposed skin in adults
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Where is Lentigo Senilis usually seen?
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On the back of the hands and the forehead
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What causes Lentigo Senilis?
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Increased melanin pigment in keratinocytes
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Is there an increase in the number of melanocytes in Lentigo Senilis?
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No
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What does the term Lentigo by itself mean?
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Proliferation of melanocytes
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What is Lentigo Senilis usually referred to?
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"Liver spots"
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What is vitiligo?
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A decrease in number or absence of mealnocytes
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What is melasma?
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Hypermelanosis characterized by development of blotchy, brown macules in a symmetrical distribution
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Where is melasma usually seen on the body?
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Cheeks, forehead, and less frequently on upper lip and neck
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Who usually gets melasma?
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Women--most commonly pregnant women; also ones taking BCP and menopause
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What is the "Mask of Pregnancy?"
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Melasma
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What are feckles?
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Increased production of melanin
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What exaggerates freckles?
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Sun exposure
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What is Acanthosis Nigricans?
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Hyperpigmentation in the flexural regions (axillae, skin folds of neck, groin, and anogenital regions)
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Is Acanthosis Nigricans benign or malignant?
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Both
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Who is usually diagnosed with benign Acanthosis Nigricans?
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Usually children or adolescents
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What is the inheritance for benign Acanthosis Nigricans?
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Autosomal Dominant
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What is benign Acanthosis Nigricans usually associated with?
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Obseity and endocrine abnormalities
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Who is usually diagnosed with malignant Acanthosis Nigricans?
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Middle aged and older individuals
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What does Acanthosis Nigricans usually occur in assoication with?
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Adenocarcinoma
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What are Nevocelluar Nevi?
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Benign neoplasms of the melanocytes
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Where do nevocellular nevi usually occur?
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Face
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What are the 3 types of Nevocellular Nevi?
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Junctional, Compound, and Intradermal
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Where do we find junctional nevi?
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At the dermal/epidermal junction
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What are junctional nevi normally called?
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"Beauty spot" or "mole"
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Are junctional nevi macules or papules?
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Macules
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What is the compound nevus?
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Raised and dome shaped--benign
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Where is the compound nevus found?
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In the dermis
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What is special about an intradermal melanocytic nevus?
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No longer have cell proliferation at the dermal/epidermal junction
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What is specific about a tan/whitish color intradermal nevus?
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Not as much blood supply
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Do intradermal melanocytic nevus usually go away?
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Yes
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Are intradermal melanocytic nevus associated with malignancy?
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No--80-90% of melanomas arise de novo--not assoicated with a nevus
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What kind of nevus has an increase risk for melanoma?
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Congenital nevus
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What is malignant melanoma?
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Malignant neoplasm derived from cells capable of forming melanin
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Where does malignant melanoma usually occur?
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Skin on any part of the body; can occur in the eye and rarely in mucous membranes of the genitalia, anus, and oral cavity
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Who usually gets malignant melanoma?
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Adults
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Does melanoma originate de novo or with an assoicated lesion?
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Usually de novo
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What is melanoma in situ?
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"Malignant Lentigo"; hasn't descended into the dermis...remains in the epidermis
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Do melanomas frequently metastasize?
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Yes
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What is the most common site for melanoma in females?
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Legs
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What is the most common site for melanoma in males?
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Trunk
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What are the characteristics of malignant melanoma?
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Asymmetrical, Irregular vague borders, variations in pigment, and maculopapular "chaos"
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How is melanoma removed?
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Excisional biopsy--DO NOT shave
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What do macular areas of melanoma correspond with?
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The radial growth phase
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What do papular areas of melanoma correspond to?
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Nodular aggregates of malignant cells in the vertical phase of growth
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What is melanoma survival rate based on?
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Dependent on stage--Metastatic to any lymph node is at least stage 3 while mestatic to any distant site is stage 4
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What are the Breslow standards for malignant melanoma?
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A Breslow level of 0.75-1.5 mm is associated with an 80% 5-year survival rate
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What is Fibroepithelial Polyps (FEP)?
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Skin tags, acrochrodon, fibroma molle, squamous papilloma
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Where do FEP's usually occur?
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Occur on neck and groin--usually in older adults
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What are Epithelial Inclusion Cysts (EIC)?
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Obsturction of a hair follice
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Where do EIC's usually occur?
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Face and upper trunk
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What is Benign Fibrous Histiocytoma?
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Benign soft tissue neoplasm seen in adults, frequently on the legs of young-middle aged women
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What is another name for Benign Fibrous Histiocytoma?
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Dermatofibroma
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How does Benign Fibrous Histiocytoma usually present?
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Small tan-brown papules; can be tender
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What is the malignant superficial variant of benign histiocytoma termed?
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Dermatofibrosarcoma Protuberans
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Does malignant superficial variant bengin histiocytoma usually metastasize?
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No but it is locally aggressive
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What is the malignant neoplasm of benign histiocytoma termed?
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Malignant Fibrous Histiocytoma
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What is Seborrheic Keratosis?
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Round, flat, elevated lesions
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Where is Seborrheic Keratosis usually seen?
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Trunk, proximal extremities, face, and neck
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Who usually gets Seborrheic Keratosis?
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Middle aged or older individuals
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What are the characteristics of benign adnexal tumors?
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Symmetrical, small, superficial, and vertical in orientation
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What are the characteristics of malignant adnexal tumors?
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Assymetrical, large, deep, and wide
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What are the 3 types of malignant adnexal tumors?
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Sebaceous carcinoma, eccrine carcinoma, and apocrine carcinoma
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Where is the sebaceous carcimona the most common?
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In the eye
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What is Actinic Keratosis?
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A precancerous skin condition present on sun exposed areas of the skin-usually appears white and flaky due to excess keratin
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Who is most affected by Actinic Keratosis?
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Individuals with extensive prlonged sun exposure
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What are some conditions that place an individual at increased risk for actinic keratosis?
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Fair skin, old scars, organ transplantation, and albinism, and genetic syndromes
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Who is usually affected by Actinic Keratosis?
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Middle aged and elderly
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Where is Actinic Keratosis most likely to appear?
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face, forehead, neck and back of hands
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What does Actinic Keratosis look like?
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Red-brown macules or minimally elevated papules with overlying scales
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How is actinic keratosis best thought of?
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As incompletely developed or nascent squamous cell carcinoma (SCC 1/2 grade)
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What is the progression from Keratosis to Invasive squamous cell carcinoma?
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Keratosis-Squamous cell carcinoma in situ-Invasive squamous cell carcinoma
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What is squamous cell carcinoma?
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A malignat proliferation of epidermal keratinocytes--has the potential for metastasis
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Does squamous cell carcinoma frequently cause death?
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No--very rarely
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What is the second most common cutaneous malignancy?
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Squamous cell carcinoma
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What does squamous cell carcinoma usually look like?
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Small firm skin colored or red nodules with indistinct margins
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What does the surface of squamous cell carcinoma look like?
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Can be granular and bleed easily or it can be smooth, verrucous, or papillomatous
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What is Keratoacanthoma?
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A rapidly growing neoplasm on sun exposed areas
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What usually happens to Keratoacanthoma?
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It usually involutes and goes away
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What kind of growth do we see with Keratoacanthoma?
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Endo and exo growth--"crater-like"
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What is basal cell carcinoma?
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A malignant skin neoplasm that has the potential for local invasion and destruction
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Does basal cell carcinoma usually mestastasize?
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No--very seldom
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What is the most common cutaneous neoplasm?
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Basal cell carcinoma
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Where do most basal cell carcinomas occur?
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Head and neck-usually in hair bearing areas
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What are the types of basal cell carcinoma?
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Nodular, sclerosing or morpheaform, pigmented basal cell carcinoma, and superficial basal cell carcinoma
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What is the nodular type BCC?
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Dome shaped papule with telangiectasia; surface may be crusted
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What is the sclerosing or morpheaform type BCC?
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Yellowish-whitish or pearly white plaque with poorly defined margins--difficult to dianose
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What type of surgery is done for sclerosing or morpheaform BCC?
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Mohs surgery
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What is the pigmented basal cell carcinoma?
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Dark irregular pigmentation--may be confused with melanoma
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What is superficial BCC?
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Occurs on NON-EXPOSED location; red, scaly plaque with elevated rolled edges
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What is sclerosing BCC commonly referred to as?
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"Rodent ulcer"
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What is the characteristic cell involved in Langerhans Histiocytosis?
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Immature dendritic cell (Langerhan cell) which has the presence of Birbeck granules
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What is the name of the multifocal multisystem Langerhans Histiocytosis?
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Letterer-Siwe Disease
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Who usually gets Letterer-Swie Disease?
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Children under 2
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What is the name of the mulitfocal unisystem langerhans histiocytosis?
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Hand-Schuler-Chrisitan Disease
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What is the name of the unifocal and multifocal unisystem langerhans cell histiocytosis?
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Eosinophilic granuloma
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What are the two basic forms of Eosinophilic granuloma?
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Bone lesion (unifocal) and pulmonary lesion (multifocal)
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What is Mycosis Fungoides?
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A T cell lymphoma specifically in the dermis
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What are the types of Mycosis Fungiodes?
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Mycosis fungoides and mycosis fungoides d' emblee
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What is mycosis fungoides?
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A chronic proliferative lymphoma occuring over years
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What is mycosis fungoides d' emblee?
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A nodular eruptive variant
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What are Sczary cells?
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A leukimic phase of mycosis fungoides with malignant T cells
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What is Sczary syndrome?
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A diffuse erythema and scaling of the entire body
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What are the three phases of mycosis fungoides?
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Chronic dermatitis, patch stage, and plaque stage
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What is epidermaltrophism?
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An infiltrate of atypical lymphocytes accumulating beneath the epidermal layer creating microabscesses
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What is Mastocytosis?
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Rare clonal neoplasm with variable clinical presentations
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What the Urticaria Pigmentosa?
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Multiple oval red-brown scaling papules
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Who does Urticaria Pigmentosa mostly affect?
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Children
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What are the signs and symptoms of Mastocytosis?
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Flushing reaction in response to certain food and alcohol, pruritis and nosebleeds
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What are the signs and symptoms of Mastocytosis due to?
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The release of histamine
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Is Mycosis Fungoides more common in men or women?
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Twice as common in men
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What is Ichthyosis?
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Genetic disorders resulting in hyperkeratosis--fish scale apperance
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What is the autsomal dominant form of Icthyosis?
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Ichthyosis vulgaris
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What is the autosomal recessive form of Icthyosis?
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Lamellar Ichthyosis
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What is characteristic of Icthyosis?
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Fish-like scales
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What is urticaria associated with?
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Allergic reaction
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What does eczema look like?
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Red, papulovesicular lesions; "boiling over" apperance; may ooze or crust
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Who does eczema most commonly affect?
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Children
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What is Erythema Multiforme?
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Hypersensitivity reaction to drugs, infections, malignancy, and collagen vascular diseases
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What is the characteristic clinical appearance on erythema multiforme?
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"Target" lesions
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What is the severe, systemic febrile form of erythema multiforme?
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Stevens-Johnson Syndrome
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What is Psoriasis?
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Pink plaque; well demarcated; many different clinical presentations
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How is the epidermal layer affected in psoriasis?
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Increased turn over; 8-9 days
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What is Lichen Planus?
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Inflammatory skin condition of mucous membranes and oral cavity
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How does lichen planus present?
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Multiple plaques that are symmetrical
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Where do you see lichen planus?
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Extremities, wrists, elbows, glans penis
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What is Discoid Lupus Erythematosus?
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Malar erythema across bridge of nose; "Butterfly rash"; coin like plaques
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What organ is most affected by lupus?
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Kidneys
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What is atrophy?
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Decreased in cell or organ size
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What is hypertrophy?
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Increase in cell or organ size
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What is hyperplasia?
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Increase in number of cells
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What is metaplasia?
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Replacing one cell type with another
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What is an example of physiologic atrophy?
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Decrease in size of embryological structures-thyroglossal duct, notochord; decrease in thymus during childhood
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What is an example of pathologic atrophy?
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Disuse, aging, lack of nutrition
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What are some causes of cell injury?
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Hypoxia, chemicals, infections, genetic conditions, nutritional causes
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What are examples of reversible cell injury?
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Hydropic
Fatty Hyaline Degeneration (Mallory bodies) Inclusions and deposits |
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What are some examples of irreversible cell injury?
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Necrosis and apoptosis
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What is coagulative necrosis?
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Decrease in blood flow; membrane remains for a little bit
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What is liquefactive necrosis?
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Due to an infection; cell membrane is gone
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What is caseous necrosis?
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Usually due to fungal infections; looks like cheese
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What is fibronoid?
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Necrosis in small arterioles
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What is normal apoptosis?
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Due to embryogenesis, hormone dependent, tumor cell death
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What is pathological apoptosis?
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Following duct obstruction, effect of cyctotoxic T cells, some viral diseases
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What are examples of dystrophic calcification?
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Necrosis and normal serum calcium
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What are examples of metatstatic calcification?
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Normal tissue and hypercalcemia
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What are the characteristics of acute inflammation?
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Short duration, edema, and neutrophils
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What are the cardinal signs of acute inflammation?
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Rubor, tumor, calor, dolor, and functio leasa
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What is chemotaxis?
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Movement of cells; cells coming toward other cells
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What endogenous factors are involved in chemotaxis?
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Complement components, leukotrienes, and chemokines
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What are the steps in phagocytosis?
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Opsonization, engulfment, and degradation
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What are the outcomes of acute inflammation?
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Resolution, fibrosis, abscess, and chronic inflammation
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What cells are involoved in chronic inflammation?
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Mononuclear cells, lymphocytes, plasma cells, and eosinophils
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What is characteristic of chronic inflammation?
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Granuloma formation
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What is dysplasia?
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Disorderly but non neoplastic growth
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What is neoplasia?
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Cancerous growth
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What is the difference between ischemia and hypoxia?
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Ischemia is the decrease in O2 and nutrients where as hypoxia is the decrease in O2
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How do you tell the difference between atrophy and hypoplasia?
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If the blood vessels are of normal size but the organ is smaller, that is atrophy; if the blood vessels and organ are both small, that is hypoplasia
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What are some ways atrophy is pathologic?
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Disuse
Denervation Decreased blood supply Nutrition Loss of endocrine stimulation Aging Pressure |
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Is atrophy an active or passive process?
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Active process
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What are examples of physiologic hyperplasia/hypertrophy?
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Estrogen stimulation of endometrium, hormonal changes in pregnancy, removal of 1/2 liver, excercise
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What are examples of pathological hyperplasia/hypertrophy?
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Increased workload on the heart
Chronic renal failure Removal of a kidney |
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What is squamous metaplasia?
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Transformation of different epithelium into stratifed squamous epithelium
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What are some causes of squamous metaplasia?
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Cigarette smoke, bladder stones, and ducts lodged with caliculi, chronic acid reflux, trauma to muscle or bone
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What is a precursor to esophageal cancer?
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Barrett's esophagus
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What is the mechanism of metaplasia?
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Represents a "reprogramming" of stem cells
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Is metaplasia a phenotypic change?
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No
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Is metaplasia a precursor to cancer?
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No--but the place where metaplasia has taken place has an increased risk of developing neoplasm
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What happens when cells are injured?
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Depletion of ATP
Generation of reactive O2 species Defects in membrane permeability Increased intracellular calcium Loss of calcium homeostasis |
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What are the targets for cell injury?
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Aerobic respiration
Cell membranes Protein synthesis Nucleus |
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What are the classes of cell injury?
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Reversible and irreversible
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What is reversible cell injury?
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Changes in ion concentration and influx of water
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What is irreversible cell injury?
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Cell death.....necrosis and apoptosis
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What are examples of reversible cell injury?
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Hydropic change
Fatty change Hyaline degenration Inclusions and deposits |
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What changes on the subcellular level of reversibly injured cells?
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Endoplasmic reticulum
Mitochondria Plasma membrane Nucleus |
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Is fatty liver a reversible or irreversible process?
|
Reversible
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What are reversible changes in hypoxia most likely due to?
|
Decrease in cell membrane transport systems
Decrase oxidative phosphorylation Decreased prtoein synthetic functions Altered cytoskeletal elements |
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What are signs seen in hypoxia?
|
Cell swelling, blebs
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What is karyolysis?
|
Fades away
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What is Pyknosis?
|
Hard and dark nucleus; chromatin is really tight and clumped
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|
|
What is Karyorrhexis?
|
Random breakup of nucleus
|
|
|
When are morphological changes usually seen in cells?
|
6-12 hours after cell death has occurred
|
|
|
What is a repurfusion injury?
|
When restoring blood flow to the ischemic/hypoxic tissue had bad effects
|
|
|
What can happen in a reperfusion injury?
|
Production of oxygen free radicals
Complement system becomes activated which further activates inflammation Cytokines are generated causing vasoconstriction |
|
|
What are free radicals?
|
Reactive molecular species that contain a single unpaired electron
|
|
|
How are free radicals formed?
|
Iron and copper catalyzed Haber-Weiss reaction
|
|
|
What causes free radical formation?
|
Radiation
Drugs Oxidation-Reduction Reactions Iron and Copper contribute electrons Nitrous Oxide |
|
|
What is the worst free radical and causes the most damage?
|
Hydroxyl radical
|
|
|
How do free radicals cause damage to cells?
|
They combine with other molecules disrupting structure and function
|
|
|
What things do free radicals injure that are important to cells?
|
Membranes, Proteins, and DNA
|
|
|
What is an example of chemical injury?
|
Carbon tetrachloride
|
|
|
What problems can carbon tetrachloride cause?
|
Damage to the ER
Lipid accumulation in hepatocytes Plasma membrane damage--allows for influx of calcium |
|
|
What is the main target of carbon tetrachloride?
|
Liver
|
|
|
How is free radical damage prevented?
|
Antioxidants (Vit A & E)
Sequestration of molecules that cause free radical formation (iron and copper) Detoxifying enzymes (SOD, catalase, GPX) |
|
|
What enzymes would in indicative of a myocardial infarct?
|
Creatinine Kinase and Troponin
|
|
|
What enzymes would be indicative of liver damage?
|
AST and ALT
|
|
|
What enzymes would be indicative of pancreatic damage?
|
Lipase and amylase
|
|
|
What are morphologic changes in cell injury?
|
Cell swelling
Accumulated products in cytoplasm Loss of specialized structure Surface blebs |
|
|
What nuclear changes are seen in cell injury/necrosis?
|
Karyolysis, karyorrhexis, pyknosis
|
|
|
What type of necrosis retains a little bit of the cell membrane?
|
Coagulative necrosis
|
|
|
What is an example of coagulative necrosis?
|
Myocardial infarct
Gangrene |
|
|
What type of necrosis destroys the entire cell membrane?
|
Liquefactive necrosis
|
|
|
What is an example of liquefactive necrosis?
|
Abscess
|
|
|
Does liquefactive necrosis require bacteria to be present?
|
Yes--except for brain lesions
|
|
|
What is an example of enzymatic fat necrosis?
|
Acute pancreatitis
|
|
|
What is an example of caseous necrosis?
|
Tuberculosis
|
|
|
Where is a pale or white infarct seen?
|
Heart
|
|
|
Where is a red or hemorrhagic infarct seen?
|
Lungs
|
|
|
What is gangrene?
|
Gradual ischemia of distal extremities, especially the foot and leg
|
|
|
Can gangrene be considered a type of liquefactive necrosis?
|
Yes--usually starts as coagulative necrosis and then progresses, once it becomes infected, to liquefactive
|
|
|
What are the two types of gangrene?
|
Wet and dry
|
|
|
What is dry gangrene?
|
Black-brown, mummified appearance
|
|
|
What is wet gangrene?
|
Bacterial superinfection of necrotic material
|
|
|
What is saponification?
|
Fatty acids combined with calcium
|
|
|
Where is saponification seen?
|
Fat necrosis--pancreatitis
|
|
|
What is responsible for caseous necrosis?
|
Usually due to myocbacterial and fungal infections
|
|
|
What is the typical appearance of caseous necrosis?
|
"Cheesy"
|
|
|
What is fibrinoid necrosis?
|
Special type of necrosis occurring in the arterial walls
|
|
|
What usually causes fibrinoid necrosis?
|
Extreme hypertension or immune complex deposition in artery walls
|
|
|
What does fibrinoid necrosis usually look like?
|
Bright pink color
|
|
|
Is apoptosis physiological or pathological?
|
Both
|
|
|
Is necrosis physiological or pathological?
|
Always pathological
|
|
|
What are three reasons we need apoptosis?
|
Proper in utero development, involution of hormonally active tissues (menstrual cycle and lactation), destruction of cells that represent threat
|
|
|
What are caspases?
|
Cysteine proteases--enaymes responsible for alerations characteristic of apoptosis
|
|
|
What are the three types of caspases?
|
Interleukins
Initiators Executioners |
|
|
What are the initiator caspases?
|
Initiate signal for death but don't actually kill (caspase 2, 8, 9)
|
|
|
What are the executioner caspases?
|
The ones that cause apoptosis (3, 6, 7)
|
|
|
What are the two initiation pathways of apoptosis?
|
Extrinsic and Intrinsic
|
|
|
What is the extrinsic pathway of apoptosis?
|
Death receptor initiated pathway; members of the tumor necrosis factor receptor family
|
|
|
What is the intrinsic pathway of apoptosis?
|
The mitochondrial pathway; replacement of anti-apototic proteins in mitochondria
|
|
|
What is another way to initiate apoptosis besides the intrinsic and extrinsic pathways?
|
Receipt of negative signals--free radicals, uv damage, etc.
|
|
|
Does apoptosis involve inflammation?
|
No
|
|
|
Does necrosis involve inflammation?
|
Yes
|
|
|
Apoptosis or Necrosis--Hypoxia, toxins, cell swelling, coagulation, disruption, random, diffuse, atp depletion, membrane injury, free radical damage, inflammation
|
Necrosis
|
|
|
Apoptosis or Necrosis--Physiologic or pathologic, single cells, chromatin condensation, internucleosomal, gene activation, endonuclease, no inflammation
|
Apoptosis
|
|
|
What is heterophagy?
|
Uptake by endocytosis--phagocytosis vs. pinocytosis; extracellular
|
|
|
What is autophagy?
|
Removal of damaged organelles during cell injury, remodeling, or atrophy; intracellular
|
|
|
What are heterophagy and autophagy?
|
Lysosomal catabollism
|
|
|
What is the cell's response to injury in apoptosis?
|
Lysosomal catabolism
Hypertrophy of SER Mitochondrial alterations Cytoskeletal abnormalities |
|
|
What does intracellular accumulations signal to the cell?
|
Damage or adaptation to stress
|
|
|
What things accumulate in the cell during injury?
|
Lipids
Proteins Metals Exogenous and Endogenous Pigment |
|
|
How does fat accumulation usually begin?
|
As small droplets of lipid (microvesicular) and then progresses into a single large droplet (macrovesicular)
|
|
|
What are two diseases characterized by microvesicular fat only?
|
Reyes syndrome and acute fatty liver in pregnancy
|
|
|
What is another lipid besides fat that can accumulate intracellularly?
|
Cholesterol
|
|
|
What does alpha-1-antitrypsin do?
|
Inhibits elastase
|
|
|
What is A1AT disease?
|
Production of abnormally folded A1AT in heptaocytes; protein collects in cytoplasm and results in liver and lung damage
|
|
|
What metals can accumulate in the cell?
|
Iron and Copper
|
|
|
What are conditions in which iron accumulates?
|
Aplastic anemia
Sickle cell anemia Thalassemias Bone Marrow Transplant |
|
|
What is hemochromatosis?
|
AR disorder of iron absorption; increased uptake in GI tract; deposition in various organs resulting in toxicity
|
|
|
What is Wilson's disease?
|
AR disease of copper toxicity
|
|
|
What types of exogenous pigments accumulate in cells?
|
Carbon particles or soot
Tattoos |
|
|
What types of endogenous pigments accumulate in cells?
|
Iron, billirubin, lipofuscin
|
|
|
What is dystrophic calcification?
|
Deposition of calcium in necrotic or traumatized tissue with normal calcium levels
|
|
|
What are examples of dystrophic calcification?
|
Fat, caseous, and coagulation necrosis
Athersclerosis |
|
|
What is metastatic calcification?
|
Occurs in normal tissue with high calcium levels
|
|
|
What are examples of metastatic calcification?
|
Hypersecretion of PTH
Destruction of bone tissue Vit D poisoning Milk-alkali syndrome |
|
|
Is dystrophic calcification localized or systemic?
|
Localized
|
|
|
Can metastatic calcification affect any tissue/organ or is it localized?
|
It can affect any organ
|
|
|
What are the most common site for metastatic calcification?
|
GI, kidneys, and lungs
|
|
|
What is hyaline?
|
An adjective describing a glassy pink appearnace
|
|
|
Is hyaline intracellular or extracellular?
|
Can be both
|
|
|
What is hyalin?
|
A noun; refers to a substance that has a hyaline appearance
|
|
|
Is hyalin intracellular or extracellular?
|
Intracellular
|
|
|
What is the definition of acute inflammation?
|
The rapid delivery of defensive devices to the site of injury
|
|
|
What are the components of the acute inflammatory response?
|
Increased blood flow
Changes in the microvasculature Loss of plasma proteins and blood cells |
|
|
What is the Lewis Triple Response?
|
Transient vasoconstriction
Arteriole dilation Fluid loss |
|
|
What vessels are involved in actue inflammation?
|
Capillaries
Venules Lymphatics |
|
|
Are neutrophils long or short lived?
|
Short lived--they only live a few hours
|
|
|
Are macrophages long or short lived?
|
Long lived--they live a few days
|
|
|
What are the hallmarks of acute inflammation?
|
Arteriole dilation
Increased permeability Fluid into vascular space |
|
|
What are the likely mechanisms for increased vascular permeability?
|
Histamine
Bradykinin Formation of endothelial gaps |
|
|
When does immediate sustained reaction occur in response to injury?
|
Burns, lytic bacterial infection--leakage starts with injury and last for several hours to days
|
|
|
What vessels are affected by immediate sustained reaction?
|
Venules, capillaries, and arterioles
|
|
|
When does the delayed prolonged reaction occur in response to a direct injury?
|
Mild to moderate thermal injury, X-rays, UV light (sunburn)--2-12 hours after injury lasting for hours to days
|
|
|
What vessels are affected by the delayed prolonged reaction?
|
Capillaries and venules
|
|
|
What do E-selectins do?
|
Rolling and adhesion to activated endothelium
|
|
|
What do E-selectins bind with?
|
Sialylated CHO groups on Lewis type antigens on leukocytes
|
|
|
What are E-selectins induced by?
|
TNF and IL-1
|
|
|
What do P-selectins do?
|
Involved in rolling
|
|
|
Where are P-selectins found?
|
Endothelial cells and platelets
|
|
|
What do P-selectins bind to?
|
Sialylated CHO group on Lewis-type antigens on leukocytes
|
|
|
What is responsible for redistributing P-selectins to the cell surface?
|
Histamine, thrombin, platelet activating factor
|
|
|
What are L-selectins found?
|
Lymphoctes, neutrophils and other leukocytes
|
|
|
What does L-selectins bind with?
|
CD34 on endothelium
|
|
|
Where are ICAM-1 and VCAM-1 found?
|
Endothelial cells
|
|
|
What do ICAM and VCAM bind to?
|
Integrins on leukocytes
|
|
|
What induces ICAMS and VCAMS?
|
TNF and IL-1
|
|
|
Where are LFA-1 and MAC-1 found?
|
Many cell types
|
|
|
What do LFA-1 and MAC-1 bind to?
|
ICAM-1 on endothelial cells
|
|
|
Where is VLA-4 found?
|
Many cell types
|
|
|
What does VLA-4 bind to?
|
VACM-1 on endothelial cells
|
|
|
What are the steps in leukocyte delivery to the site of injury?
|
Margination, rolling, and adhesion
Transmigration across the endothelium Migration in interstitial tissues |
|
|
What is chemotaxis?
|
Unidirectional migration of leukocytes in response to a diffusion gradient of a chemical attractant
|
|
|
What is chemokinesis?
|
Increased frequency or velocity of locomotion of leukocytes
|
|
|
In what direction do cells move?
|
Stretch out forward and pull back end up
|
|
|
In a tissue sample that is taken 1 week after cell injury, what cell types will be present?
|
Macrophages--no neutrophils!
|
|
|
What type of receptors are involved in leukocyte activation?
|
Toll like receptors, Seven-a-helical, and mannose receptors
|
|
|
What are the steps in phagocytosis?
|
Opsonization
Engulfment Killing and degradation |
|
|
What chemical mediators are preformed in secretory granules?
|
Histamine, serotonin, and lysosomal enzymes
|
|
|
Where is histamine found?
|
Mast cells, basophils, platelets
|
|
|
Where is serotonin found?
|
Platelets
|
|
|
Where are lysosomal enzymes found?
|
Neutrophils and macrophages
|
|
|
What are the newly synthesized chemical mediators?
|
Prostaglandins, leukotrienes, platelet activating factors, activated oxygen species, nitric oxide, and cytokines
|
|
|
Where are the newly synthesized chemical mediators usually found?
|
Mostly leukocytes
|
|
|
What chemical mediators are released from plasma?
|
Factor XII (Hageman factor) and complement
|
|
|
What does Factor XII stimulate?
|
Kinin system/Coagulation
|
|
|
What are C3a and C5a? What do they do?
|
Anaphylatoxins--cause histamine release and increase vascular permeability and vasodilation
|
|
|
What forms the membrane attack complex?
|
C5-C9
|
|
|
What does the membrane attack complex do?
|
Causes lysis of bacteria and cells
|
|
|
Which complement pathway involves C1, C2, C4?
|
Classical pathway
|
|
|
Which complement pathway involves C3?
|
Alternative pathway
|
|
|
Wha is the Hageman factor?
|
Factor XII
|
|
|
What activates the Hageman factor?
|
Collagen, basement membrane, platelets, and HMWK
|
|
|
What does Factor XIIa activate?
|
Kinin cascade
|
|
|
What does the activation of the kinin cascade cause?
|
Conversion of Prekallikrein to Kallikrein
|
|
|
What does bradykinin do?
|
Increase vascular permeability
Smooth muscle contraction Arteriole dilation |
|
|
What does Kallikrein activate?
|
Plaminogen which converts to plasmin
|
|
|
What does plasmin activate?
|
C3 which converts to C3a
|
|
|
What activates Fibrin?
|
Plasmin
|
|
|
What does fibrin form that causes increased vascular permeability?
|
Fibrin split products
|
|
|
What does cyclooxygenase produce?
|
Prostaglandins
|
|
|
What does lipooxygenase produce?
|
Leukotrienes
|
|
|
What do prostaglandins produce?
|
Prostacyclin and Thromboxane
|
|
|
What does prostacyclin do?
|
Inhibits platelet aggregation and causes vasodilation
|
|
|
What does thromboxane do?
|
Causes vasoconstriction; produces platelet aggregation
|
|
|
What do leukotrienes do?
|
Vasoconstriction, bronchospasm, and increased permeability
|
|
|
What is the difference between specific granules and azurophil granules?
|
Azurophil granules cause a lot more damage and are larger
|
|
|
What does platelet activating factor do?
|
Produces cardinal signs of inflammation
|
|
|
What are the important cytokines in inflammation?
|
TNF and IL-1
|
|
|
What are important chemokines?
|
Platelet 4 and Eotaxin
|
|
|
What does nitric oxide do?
|
Relaxes smooth muscle and decreases platelet aggregation
|
|
|
What are the three types of Nitric Oxide?
|
Endothelial, Neuronal, and Inducible NOS
|
|
|
Where does inducible NO play a role?
|
In monocytes and macrophages by TNF and IL-1
|
|
|
What is the central player in starting the coagulation, fibrinolytic, complement, and kinin cascade?
|
Hageman Factor
|
|
|
What is a chemotactic agent for neutrophils?
|
LTB4
|
|
|
What are the major cell players in inflammation?
|
PMNs, eosinophils, lymphocytes, macrophages, basophils, mast cells and platelets
|
|
|
What is an abcess?
|
Localized collection of pus
|
|
|
What is cellulitis?
|
Diffuse edematous spreading inflammation within solid tissues
|
|
|
What is an ulcer?
|
Defects in the surface of an organ or tissue
|
|
|
What are the hallmark cells of inflammation?
|
Neutrophils
|
|
|
What do neutrophils function to do?
|
Phagocytize bacteria and debris
|
|
|
What kind of granules do neutrophils contacin?
|
Specific and azurophil granules
|
|
|
What are the specific chemotrractants for eosinophils?
|
Eotaxins 1 and 2
|
|
|
What do eosinophilic granules contain?
|
Major basic protein
|
|
|
Are basophils circulating or resident?
|
Circulating
|
|
|
Are mast cells resident or circulating?
|
Resident
|
|
|
What is contained in the alpha granules in platelets?
|
Fibrinogen, platelet factor 4, and platelet derived growth factor
|
|
|
What is contained in the delta granules in platelets?
|
ATP, Histamine, and Serotonin
|
|
|
What is Chediak-Higashi syndrome?
|
Defects in locomotion and lysosomal degranulation
|
|
|
What is pemphigus?
|
Autoimmune disease with antibodies directed against the desmosomes of the squamous epithelium
|
|
|
What is the most common form of pemphigus?
|
Pemphigus vulgaris
|
|
|
What type of hypersenstivity reaction is pemphigus vulgaris?
|
Type 2
|
|
|
What layers of skin does pemphigus vulgaris affect?
|
Just the epidermis
|
|
|
Do the blisters form above or below the basal layer?
|
Above the basal layer--suprabasal bullae
|
|
|
What type of antibodies does pemphigus vulgaris have?
|
Antibodies against 3-desmoglein--IgG to desmosomes
|
|
|
What might you see on a histo slide signaling pemphigus vulgaris?
|
Net-like deposit
|
|
|
Are the bullae of pemphigus vulgaris likely to rupture?
|
Yes
|
|
|
Who is normally affected by bullous pemphigoid?
|
Older people
|
|
|
Are the bulla in bullous pemphigoid smaller or larger than pemphigus vulgaris?
|
Smaller fluid filled blisters
|
|
|
Where does bullous pemphigoid typically occur?
|
At the dermal/epidermal junction
|
|
|
What type of hypersensitivity is bullous pemphigoid?
|
Type 2
|
|
|
Are the bullae of bullous pemphigoid likely to rupture?
|
No
|
|
|
What does bullous pemphigoid typically affect?
|
The hemidesmosomes
|
|
|
Is bullous pemphigoid acantholytic or nonacantholytic?
|
Nonacantholytic--sub epidermal
|
|
|
What is pemphigus?
|
Autoimmune disease with antibodies directed against the desmosomes of the squamous epithelium
|
|
|
What is the most common form of pemphigus?
|
Pemphigus vulgaris
|
|
|
What type of hypersenstivity reaction is pemphigus vulgaris?
|
Type 2
|
|
|
What layers of skin does pemphigus vulgaris affect?
|
Just the epidermis
|
|
|
Do the blisters form above or below the basal layer?
|
Above the basal layer--suprabasal bullae
|
|
|
What type of antibodies does pemphigus vulgaris have?
|
Antibodies against 3-desmoglein--IgG to desmosomes
|
|
|
What might you see on a histo slide signaling pemphigus vulgaris?
|
Net-like deposit
|
|
|
Are the bullae of pemphigus vulgaris likely to rupture?
|
Yes
|
|
|
Who is normally affected by bullous pemphigoid?
|
Older people
|
|
|
Are the bulla in bullous pemphigoid smaller or larger than pemphigus vulgaris?
|
Smaller fluid filled blisters
|
|
|
Where does bullous pemphigoid typically occur?
|
At the dermal/epidermal junction
|
|
|
What type of hypersensitivity is bullous pemphigoid?
|
Type 2
|
|
|
Are the bullae of bullous pemphigoid likely to rupture?
|
No
|
|
|
What does bullous pemphigoid typically affect?
|
The hemidesmosomes
|
|
|
Is bullous pemphigoid acantholytic or nonacantholytic?
|
Nonacantholytic--sub epidermal
|
|
|
What is pemphigus?
|
Autoimmune disease with antibodies directed against the desmosomes of the squamous epithelium
|
|
|
What is the most common form of pemphigus?
|
Pemphigus vulgaris
|
|
|
What type of hypersenstivity reaction is pemphigus vulgaris?
|
Type 2
|
|
|
What layers of skin does pemphigus vulgaris affect?
|
Just the epidermis
|
|
|
Do the blisters form above or below the basal layer?
|
Above the basal layer--suprabasal bullae
|
|
|
What type of antibodies does pemphigus vulgaris have?
|
Antibodies against 3-desmoglein--IgG to desmosomes
|
|
|
What might you see on a histo slide signaling pemphigus vulgaris?
|
Net-like deposit
|
|
|
Are the bullae of pemphigus vulgaris likely to rupture?
|
Yes
|
|
|
Who is normally affected by bullous pemphigoid?
|
Older people
|
|
|
Are the bulla in bullous pemphigoid smaller or larger than pemphigus vulgaris?
|
Smaller fluid filled blisters
|
|
|
Where does bullous pemphigoid typically occur?
|
At the dermal/epidermal junction
|
|
|
What type of hypersensitivity is bullous pemphigoid?
|
Type 2
|
|
|
Are the bullae of bullous pemphigoid likely to rupture?
|
No
|
|
|
What does bullous pemphigoid typically affect?
|
The hemidesmosomes
|
|
|
Is bullous pemphigoid acantholytic or nonacantholytic?
|
Nonacantholytic--sub epidermal
|
|
|
What is pemphigus?
|
Autoimmune disease with antibodies directed against the desmosomes of the squamous epithelium
|
|
|
What is the most common form of pemphigus?
|
Pemphigus vulgaris
|
|
|
What type of hypersenstivity reaction is pemphigus vulgaris?
|
Type 2
|
|
|
What layers of skin does pemphigus vulgaris affect?
|
Just the epidermis
|
|
|
Do the blisters form above or below the basal layer?
|
Above the basal layer--suprabasal bullae
|
|
|
What type of antibodies does pemphigus vulgaris have?
|
Antibodies against 3-desmoglein--IgG to desmosomes
|
|
|
What might you see on a histo slide signaling pemphigus vulgaris?
|
Net-like deposit
|
|
|
Are the bullae of pemphigus vulgaris likely to rupture?
|
Yes
|
|
|
Who is normally affected by bullous pemphigoid?
|
Older people
|
|
|
Are the bulla in bullous pemphigoid smaller or larger than pemphigus vulgaris?
|
Smaller fluid filled blisters
|
|
|
Where does bullous pemphigoid typically occur?
|
At the dermal/epidermal junction
|
|
|
What type of hypersensitivity is bullous pemphigoid?
|
Type 2
|
|
|
Are the bullae of bullous pemphigoid likely to rupture?
|
No
|
|
|
What does bullous pemphigoid typically affect?
|
The hemidesmosomes
|
|
|
Is bullous pemphigoid acantholytic or nonacantholytic?
|
Nonacantholytic--sub epidermal
|
|
|
What is pemphigus?
|
Autoimmune disease with antibodies directed against the desmosomes of the squamous epithelium
|
|
|
What is the most common form of pemphigus?
|
Pemphigus vulgaris
|
|
|
What type of hypersenstivity reaction is pemphigus vulgaris?
|
Type 2
|
|
|
What layers of skin does pemphigus vulgaris affect?
|
Just the epidermis
|
|
|
Do the blisters form above or below the basal layer?
|
Above the basal layer--suprabasal bullae
|
|
|
What type of antibodies does pemphigus vulgaris have?
|
Antibodies against 3-desmoglein--IgG to desmosomes
|
|
|
What might you see on a histo slide signaling pemphigus vulgaris?
|
Net-like deposit
|
|
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Are the bullae of pemphigus vulgaris likely to rupture?
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Yes
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Who is normally affected by bullous pemphigoid?
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Older people
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Are the bulla in bullous pemphigoid smaller or larger than pemphigus vulgaris?
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Smaller fluid filled blisters
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Where does bullous pemphigoid typically occur?
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At the dermal/epidermal junction
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What type of hypersensitivity is bullous pemphigoid?
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Type 2
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Are the bullae of bullous pemphigoid likely to rupture?
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No
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What does bullous pemphigoid typically affect?
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The hemidesmosomes
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Is bullous pemphigoid acantholytic or nonacantholytic?
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Nonacantholytic--sub epidermal
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What does dermatitis herpatiformis have a major association with?
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Celiac disease
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What antibodies in celiac disease can cross react with regions of the dermal papillae?
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Anit-gliadin antibodies
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Where does dermatitis herpatiformis typically occur?
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At the dermal/epidermal junction
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What type of hypersensitivity reaction is dermatitis herpatiformis?
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3
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Where do the blisters of dermatitis herpatiformis typically sit?
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In the dermal papillae
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Where do you typically see dermatitis herpatiformis on the skin?
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In the extensor areas
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