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45 Cards in this Set
- Front
- Back
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PROLACTIN SECRETION
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INCREASES SECRETION:
- ESTROGEN: inhibits PIF/DOPAMINE - SUCKLING: neuroendocrine reflex - SLEEP INHIBITS SECRETION: - PIF/DOPAMINE: tonically secreted PREGNANCY: PRL levels fall after delivery NEONATE: high only immediately after birth MENOPAUSE: falls to pre-puberty levels. |
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PROLACTIN AXNS
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1. mammary gland development: works with estrogen & progesterone (lobuloalveolar growth)
2. milk production 3. maintain milk production after it's been established 3. Physiologic infertility during lactation (lactational amenorrhea) 4. Inhibits progesterone secretion in immature ovarian follicles 5. Faciliates axn of LH/Testosterone in males. 6. CONTROLS PROGESTERONE SECRETION in ovarian follicles |
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HORMONES AFFECTING MAMMARY GLANDS OF PREGNANCY/LACTATION
* estrogen, GH, cortisol, prolactin, oxytocin |
1. Mammogenic: promote cell proliferation
- Lobuloalveolar growth - Ductal growth: 2. Lactogenic: initiate milk production - prolactin, hPL, cortisol, WITHDRAWAL of prog/estrogen 3. Galactokinetic: promote milk-letdown - OXYTOCIN & vasoprssion 4. Galactopoetic: maintain milk production - Prolactin & cortisol **4th mo. of pregnancy: mammary gland is fully developed & ready to lactate. |
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OXYTOCIN & LACTATION
- posterior pituitary - supraoptic & paraventricular nuclei |
- Contracts estrogen-primed uterus
- Inhibited by progesterone - Protects against hemorrhage after expulsion of placenta - terminates corpus luteum fxn @ end of menstrual cycle - amnesic effect NEUROENDOCRINE REFLEX: - Contracts myoepithelial cells surrounding mammary acini & release of milk into nipple *Reflex is blocked by neural lesions/stress/fright *Reflex can also be conditioned to sound of crying baby. |
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SUPPRESSING LACTATION
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- HIV+ mom
- Prolactinoma - Loss of pregnancy after 4 mo. - Galactorrhea: continued milk discharge w/o suckling stim tx w/ D2-R agonist (dopamine) or ergotalkaloids. |
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skin - protects from mechanical trauma & barrier to water loss
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1. EPIDERMIS: resists friction & tangential stress
- adhesions between layers - cross-linked keratin fibers - lamellar bodies 2. DERMO-EPIDERMAL JXN/PAPILLARY DERMIS/RETE RIDGES -increased surface area for interface 3. RETICULAR DERMIS - cushion 4. SUBCUTIS (fat) - allows skin to move freely relative to fascia/mm underneath 5. SEBACEOUS GLANDS - thin lipoidal film resists water loss |
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EPIDERMAL LAYERS:
1. GERMINATIVE/BASAL |
- Adhesions of cells to basal lamina
- Hemidesmosomes connect to intracell. keratin int. filaments - REGENERATE post-trauma - Resistant to apoptosis: lotsa receptors for growth factors (disappear as they move up) |
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EPIDERMAL LAYERS:
2. SPINOUS |
- Desmosomes b/w keratinocytes connect to the rigid keratin int. filmanet network in cytoplasm
* blisters break this desmosomal attch |
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EPIDERMAL LAYERS:
3. GRANULAR |
- Primarily sets up formation of stratum corenum
- make involucrin, lamellar bodies, keratohyaline granules - CROSS-LINKED membrane & int. filmanets = thick, cornified layer - Lamellar bodies exocytose - APOPTOTIC CELLS ARE NOT PHAGOCYTIZED/FRAGMENTED |
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EPIDERMAL LAYERS:
4. STRATUM CORNEUM |
- Dead cells = intact corenocytes
- Phospholipid lamellae are b/w layers of dead corneocytes 2 different compartments: 1. lamellae: hydrophobic 2. corneocytes: hydrophilic = get water & trap it there/prevent loss |
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DERMO-EPIDERMAL JUNCTION
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aka papillary dermis, rete ridges
- WEAKEST point in skin structure - increased surface area for interface = ^ strenght - more ridges in areas of high abrasian |
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PROTECTION AGAINST UV DAMAGE
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#1. MELANIN: heterpolymer transferred from melanocytes to keratinocytes
- MAIN protection against radiation: entire UV & Visible spectrum 2. ANTIOXIDANT ENZYMES: made by keratinocytes in spinous layer - catalases, peroxidases, etc 3. MACROPHAGES/LANGERHANS: phagocytose UV damaged cells - autoimmune dz can occur if langerhans presents self-Ag to T cells. |
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MELANOCYTES:
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- Neural crest cell derivates
- basal/germ layer - no stem cell population (hair follicles have one though) - differences in intensity does NOT mean diff numbers of melanocytes |
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MELANIN PRODUCTION
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MADE IN MELANOSOMES
- Rate-limiting step: tyrosinase changing tyrosine --> DOPA --> tyrosinase is melanosome-bound enzyme - 2 types of melanin - keratinocytes engulf melanosomes on melanocyte dendrites - melanosomes sit on "sunny-side up" of keratinocyte nucleus. **melanin production in linked with Phe & Tyr** |
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MELANIZATION
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1. Melanocortins: MSH (stim)
- source of POMC & MSH is local (skin keratinocytes) 2. MSH binds MC1-R - g-protein linked receptor on melanocytes 3. Binding of MC1-R = ^ eumelanin * loss of fxn of this receptor = ^ risk of melanoma **exposure to UV light: - increases melanocyte prolif, melanosome production, & rate of transfer to keratinocytes |
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SKIN - INNATE IMMUNITY
**keratinocytes participate a lot** |
- barrier
- Sebaceous glands: continuous lipoidal secretions = bacteriostatic & fungistatic - Macrophages & Dendritic APCs - Neutrophils (inflamm) - Cytokines: IL-1, TNFa, chemokines (from UV damaged keratinocytes) - Receptors for foreigners: CD14, TLR, mannose - Defensins & other antibacterial proteins |
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SKIN - ACQUIRED IMMUNITY
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1. LANGERHANS & DERMAL DENDRITIC CELLS
- increase in # @ inflamed sites - BIRBECK GRANULES 2. T-CELLS: - acquire new adhesion molecules (CLA) that lets them EXIT node = sensitized 3. TRAFFICKING: CLA - cutaneous lymphocyte antigen - glycoprotein - recognized by post-cap venule endothelium in lymph nodes. |
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SKIN - THERMOREGULATION
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1. Distinct warmth & cold receptors
2. Eccrine sweat glands: evaporate fluid 3. Vascular dilation & constriction - apical skin: glomus - nonapical skin |
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ECCRINE & APOCRINE SWEAT GLANDS
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ECCRINE: "SWEAT"
- NEURAL CONTROL - STIMULATED BY HEAT - cholinergic sym. fibers APOCRINE: adrenergic fibers - body odor - empty into pilosebaceous units. (sebaceous glands are not under neural conrol) |
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CONTROL OF VASODILATION/CONSTRICTION
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SYMPATHETIC NS (more important) & LOCAL FACTORS
- active vasodilation in non-apical skin = increased blood flow through skin 10x (active vasoconstriction is less effective) |
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APICAL SKIN & HEAT EXCHANGE
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NOSE/LIPS/EARS/HANDS/FEET
- high surface area-to-volume ratio that favors heat loss GLOMUS: digit tips & nailbeds - thoroughfare channel that connects arteriole & venule directly - rapid HEAT LOSS when open - sympathetic control: NE = vasoconstrict (keep you warm) ---> withdrawal of NE = passive vasodilation - resting: tonic sym - partially closed glomus. |
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nonapical skin & heat exchange
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- NO A-V ANASTAMOSE
- SEPARATE CONTROLS: ACTIVE VASODILATION: local control of sweat glands VASOCONSTRICTION: adrenergic (NE). VERY LITLE ACTIVITY AT REST. |
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ALTERATIONS IN BODY TEMPERATURE SET POINT
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FEVER: infxn results in elevation of set point (body tries to reach this set pt)
MENOPAUSAL HOT FLASHES: Depression in set point - body tries to lose heat HYPOTHERMIA: lose ability to thermoregulate due to extreme lowering of set point. |
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PRINCIPAL MODES OF HEAT LOSS FROM BODY
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1. Radiation: NOT in contact
- main contribution to heat loss. 2. Conduction: direct contact (thermal gradient) - clothes insulate us and limit this 3. Evaporation: - humidity decreases ability to lose heat by sweating 4. Convection: air currents |
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MECHANISMS ACTIVATED BY HEAT
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INCREASE HEAT LOSS
- cutaneous vasodilatation - sweating (evap) - increased respiration rate DECREASED HEAT PRODUCTION - anorexia - apathy & inertia - decreased secretion of TSH |
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MECHANISMS ACTIVATED BY COLD
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INCREASE HEAT PRODUCTION
- shivering - hunger - exercise - ^ sns - NE & EPI DECREASE HEAT LOSS - cutaneous vasoconstriction - curliing up - horripilation |
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HYPOTHALAMUS & TEMPERATURE
*evaluates core temp* |
*HYPOTHALAMIC SET POINT*
(PROPORTIONAL CONTROL - not just ON/OFF) ANTERIOR HYPOTHALAMUS - responds to over-warmed blood & peripheral sensation impulses - COOLS YOU DOWN POSTERIOR HYPOTHALAMUS - responds to over-cooled blood & peripheral sensation impulses - KEEPS YOU WARM (warm butt) these signals are integrated in the central processing of hypothalamus |
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PERIPHERAL TEMP. SENSORS & SET POINT
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Skin temperature changes the "set point" level at which sweating or shivering begins.
- anticipatory response: starting to sweat/shiver before the core temperature changes a lot |
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CAUSES OF FEVER
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- inflamm, infxn, toxins, immunity
- activated macros - endogenous pyrogen prodcution: IL1,6,8, TNF - Stimulation of PGE production at level of anterior hypothalamus - Elevated set-pt **Aspirin BLOCKS cyclooxygenase (PGE production) = no elevation of set pt. |
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HYPOTHERMIA
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BODY TEMP BELOW 85 DEGREES
- rate of heat production in each cell is super depressed - sleepiness/coma depresses CNS heat-control mechanisms & prevent shivering |
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HEAT STROKE
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Upper limit to heat loss mechanisms
- 106-108 degrees - sweating diminishes as heat-regulating ability gets depressed - hot body gets even hotter |
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SKIN-SENSATION
(thermoreceptors) |
- SENSORY RECEPTORS IN BOTH EPIDERMIS & DERMIS
THERMORECEPTORS ARE NOT SPREAD EVENLY THROUGHOUT SKIN - unmyelinated C fibers or Ad fibers |
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SKIN - PAIN
(itching) |
receptors for mechanical, thermal, & chemical stimuli
ITCHING: unmyelinated C fibers - lower frequency of impulse stimuli than pain - HISTAMINE = major itch inducer. from mast cells - proteases, neuropeptides, eicosanoids, opioids, GFs, eosinophil products & platelet products (seratonin) induce histamine release |
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VITAMIN D & SKIN
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Photoactivation occurs in BASAL layer of epidermis: 7-dehydrocholesterol is converted to VIT D3.
- need UV-B energy VIT D needed for calcium metabolism & growth factors |
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HAIR TYPES
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LANUGO: fetal/neonate
VELLUS: short, non-pigment, all-over body TERMINAL HAIR: "hairy" eyebrow/eyelash, scalp, groin, etc SEBACEOUS : atrophied hair shaft & hypertrophied sebaceous glands |
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FUNCTIONS OF HAIR
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1. Sensation: mechanoreceptors
- sense stuff above the surface of skin 2. Thermoregulation: goose bumps = erector pilae mm contracting & trapping air 3. Immunity: Langerhans, perifollicular macros, hair matrix cells @ base lack MHC Class I Ags 4. Regenerate epidermis 5. Psychosocial 6. Disperse sweat 7. Protection |
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HAIR CYCLING
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1. ANAGEN: 90% hair
- IGFF1 & FGF7 made by dermal papillae 2. CATAGEN - apoptosis - towards end of catagen, dermal papillae moves up to bulge - restart anagen. 3. TELOGEN - "club" hair: shed/washed off **Cycling is synchronized during fetal dev & neonate - Mostly MOSAIC pattern after (independent) |
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ANDROGENS & HAIR
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ANDROGEN RECEPTORS ON DERMAL PAPILLAE
- ex// beard: classic androgen-dep region ANDROGENIC BALDING: androgen stimulation = synthesis of inhibitory factors & miniature hair follices (5a-reductase type II) |
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NEURAL CONTROL OF HAIR GROWTH
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hair follicles are most richly innervated part of skin, ESPECIALLY THE BULGE
MERKEL CELLS: make neuropeptides, which control & modulate growth cycles |
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TELOGEN EFFLUVIUM vs. ANAGEN EFFLUVIUM
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TELOGEN: increased #s of hair enter telogen too soon
- fever, malnutrition, drugs, pregnancy, anemia, endocrine ANAGEN: - Hair growth is interrupted in anagen - usually due to antineoplastic drugs |
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ANDROGENETIC ALOPECIA
(common baldness) |
Shortened anagen cycles -->gradual change of terminal hair into vellus hair
- occurs due to androgenic stim & other factors |
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HIRSUTISM vs. HYPERTRICHOSIS
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HIRSUTISM:
excessive hair growth in androgen-dep areas in (aging) WOMEN HYPERTRICHOSIS: excessive hair growth for that location, age, gender, race - anagen is extended & vellus --> terminal |
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SWEAT GLAND FXN
(ECCRINE) **lots of soles of feet & not on back ** **decreases with age: old people are more sensitive to temp. extremes |
SECRETION: SNS - ACh release
- ultra-filtrate = plasma-like REABSORPTION: occurs in duct - 2 cell layers thick; acts like syncytium = HYPOTONIC SWEAT EXCRETION: minor |
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CONTROL OF SWEATING
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1. ^ Hypothalamic temperature: induces general sweating
2. Unmyelinated sympathetic C fibers secrete Ach - B-adrenergic stimulates a little - local skin temp & emotional stress also stimulates sweat |
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CONTENTS OF SWEAT
**sweat rate affects content** |
NaCl: secreted by secretory coil in isotonic amounts; reabsorbed by the duct
- increased sweat rate = less reabs of NaCl K+: sweat > plasma Urea: [ ] is highest with a low sweat rate Glucose: ^ with ^ plasma glucose Cl-: CFTR channel in apical duct cell |
