week 20

explain core temp and skin temp and their changes

core temp remains stable and protects the functions of the internal organs

skin temp rises and falls with the surrounding temperature

What is considered a fever for adults and children

adults: 99.9F

children: 100.4F

How does body temp change throughout the day?

it is lowest in the morning and increases throughout the day and late afternoon

• this must be taken into account when determining if someone has a fever or not

How does sex, age, weight, and height affect body temp?

sex: higher temp in women

age: body temp decreases with age (little old ladies be cold)

weight: higher temp with higher weight

height: lower temp with taller height

explain heat exchange with the environment:

conduction, convection, radiation, and evaporation

conduction: tranfer heat through direct contact

convection: lose heat through movement of air or water (like an oven)

radiation: transfer heat through electromagnetic waves

evaporation: lose heat through water evaporation (sweating)

explain the idea behind a basal/resting metabolic rate

heat is produced by your metabolism literally doing nothing special like exercising, just by keeping your organs functioning

this is why you burn calories throughout the day even when you are watching tv on the couch

metabolic rate is proportional to _____

how does infancy, pregnancy, and gender affect metabolic rate?

proportional to body surface area

metabolic rate is highest in infancy (to sustain growth)

metabolic rate is high in pregnancy (to sustain fetal growth)

metabolic rate is higher in males even if they are the same height and weight as a female

metabolic rate and catecholamines, thyroxine, and progesterone

catecholamines: pheochromocytoma (weight loss and heat intolerance)

thyroxine

• hyperthyroidism: weight loss, heat intolerance

• hypothyroidism: weight gain, cold intolerance

progesterone: increase in body temp after ovulation

explain the thermic effect of food

metabolic rate and body heat increase when you digest

fats and proteins increase it more than sugars/carbs do

explain heat production during external work and exercise

skeletal muscle becomes the main source of heat, and can increase metabolic rate up to 10 fold

working muscles can warm the blood by 1-2F

which one goes with what?

adrenergic and cholinergic

vasodilation and vasocontriction

adrenergic: vasoconstriction (you tense up with adrenalin)

cholinergic: vasodilation

explain the regulation of cutaneous blood flow when you are hot vs cold

hot = vasodilation → so more blood goes to the surface of skin and can be cooled by radiation

cold = vasoconstriction → so the warm blood stays in the core of the body (not the periphery) and keeps us warm

explain the two segments of the eccrine glands and their functions

bottom/deep part: coil (subdermal) that produces the primary secretion

top part: duct (in the dermis and epidermis) which reabsorbs the sodium and chloride ions that were in the primary secretion so they aren’t all lost to the sweat

swaet glands are innervated by the post-ganglionic ______ neurons

cholinergic sympathetic

explain the relationship of acclimation to heat, swaeting, aldosterone, and salt levels

more acclimated = more sweat BUT more aldosterone so = more salt reabsorption

less acclimated people will lose more salt with their sweat than acclimated people

skin thermoreceptors: describe them, what types, what’s more?

these are the free nerve endings in the skin that sense temperature in the environment

hot and cold receptors

there are more cold receptors than hot so we are more sensitive to cold

explain thermal sensing and how the skin thermoregulators work in tandem with the hypothalamic temperature-sensitive neurons

skin thermoreceptors sence a change in ambient temp and send info to the hypothalamic temperature-sensitive neurons so they can keep the core temp steady even as the environmental temp changes

explain chemical thermogenesis

brown adipose tissue (not white) produces heat and activates lypolysis → then this activates the mitochondria uncoupling protein 1 (UCP1) and there is uncoupling of the electrochemical proton gradient of electrochemical proton gradient and ATP synthesis → energy dissipates as heat

exaplin the shivering thermogenesis

you have an increase in basal skeletal muscle tone → involuntary clonic rhythmic contractions → mote neurons innervated

this can impair voluntary movements like talking or fine motor function becuase the shivering takes over

what is the hierarchy of the thermoregulatory response?

1st: behavioral responses (go inside, take off or put on clothes, etc.)

2nd: autonomic responses (swaeting, shivering, vasodilation or constriction

3rd: endocrine responses: hormones

explain fever, chills, and crisis

pyrogens (IL-1, IL-6, TNF, IFN) all increase the set point, so then we have fever and our set point threshold is higher so our body thinks that its normal is now too cold so we try to get warm and vasoconstrict → makes our skin cold so we shiver

then with crisis: we have the resolution of the fever, so the set point goes down, now our core knows that we are too hot and we get vasodilation and sweating (“fever breaks”)

What are the 3 major medications that she went over for fever?

corticosteroids (decrease the pyrogenic cytokines at the beginning)

antipyretics

dantrolene (inhibits shivering and heat production)

dome-shaped, smooth topped, hairless

pink, tan, brown, or sometimes black

often has a history of recent rapid growth

1/3rd of pts are children

are benign but there can be a histologic similarity to melanoma

spitz nevus

develpment of a clearing around a preexisting nevus, sometimes preceded by faint arythema

tx: reassurance, excision if suspicious

halo nevus

aquired, asymptomatic and benign

dark-blue to gray-black sharply-defined papule

common on the dorsa of hands or feet, buttocks, back, csalp, or face

blue nevus

light brown pigmented macula ranging from a few cm to >15cm

distinctive: many dark brown small macules or papules scattered throughout the pigmented background

nevus spilus

discrete, stuck-on appearance, greasy, warty, brown grey or tan; benign

seborrheic keratosis

what is it called when you have many seborrheic keratoses that appear abruptly? What does that indicate?

sign of leser-trelat

concerned for: onternal malignancy (GI commonly)

a subtype od seborrheic keratosis

multiple tiny black lesions, some enlarging to more then a cm

seen in darly pigmented pts

dermatosis papulosa nigra

very common, fibrous reaction to trauma or bite

assymptomatic

variable color: skin colored to pink to tan to dark brown

dimple sign: lateral compression with thumb and index finger produces a depression or dimple

dermatofibroma

skin tags found commonly in middle aged and eldery females or obese pts

commonly found in intertriginous areas, neck, axilla, breasts, and eyelids

tx: scissor excision

acrochordons

rapidly developing hemangioma arising at site of minor trauma

bright red to violaceous, smooth, dome-shaped nodule

bleeds spontaneously or after minor trauma

tx: surgical excision

pyogenic granuloma

pale, yeloow, donut shaped, umbilicated papules

common on the face: forehead, cheeks, lower lid, and nose

sebaceous hyperplasia (tumors of enlarges sebaceous glands)

sweat duct tumor

1-2mm flesh colored papules

usually see multiple

common on lower lids (can also be on face, axilla, chest, vulva, etc.)

syringomas

occur at puberty

common on face

pink to skin colored papules

trichoepithelioma

white to yellow, keratin-containing epidermal cysts

located on eyelids, cheek, forehead, and sites of trauma

milium

benign vascular tumor

pale patch the first month and enlarges rapidly by the first year

red-purple, soft to firm

most go away by age 5

strawberry nevus

deep, vascular malformation composed of capillary, lymphatic, and venous tissue

cavernous hemangioma

vascular capillary malformations that do not undergo spontaneous involution

irregularly shaped red to violaceous patch present at birth

does not cross midline; dermatomal

port wine stain

port wine stain that does cross dermatomes

can affect the eye and forehead (and brain)

Sturge-weber syndrome

port wine stain with enlargement of extremity

klippel-trenaunay-weber syndrome

common and asymptomatic bright red domes papules

principally on the trunk

cherry angiomas

rough, adherent, scaly papules

arise in areas of dermatoheliosis (sun exposed regions)

premalignent potential; may develop into SCC

can develop a cutaneous horn

actinic keratosis

if you see “rolled borders” think ____

basal cell carcinoma (there are several types)

what type of basal cell carcinoma?

pearly papule or nodule with telangiectasia and a rolled border

nodular basal cell carcinoma

what type of basal cell carcinoma?

large ulcer with rolled borders

ulcerating basal cell carcinoma

what type of basal cell carcinoma?

waxy, white, indistinct, worst prognosis

sclerosing (cicatricial) basal cell carcinoma

what type of basal cell carcinoma?

red scaly plaque, pearly white border, resenbles eczema or psoriasis, least aggressive

superficial basal cell carcinoma

sharply demarcated, pink to red, scaling papules or plaques

most often caused by UVR or HPV infection

squamous cell cacinoma in situ (superficial); aka Bowden’s disease

indurated erythematous hyperkeratotic scaly papules

occur on face, tips of ears, preauricular areas, scalp, dorsal hands, forearms, and lower lips

invasive squamous cell carcinoma

mole present since birth

highly pigmented with hair growth in the lesion

can be small (<1.5cm) to medium (1.5-2cm) or giant (>20cm)

giant is correlated with a higher lifetime risk of melanoma

congenital nevus

What are the ABCDEs of melanoma?

assymetry

border irregularity

color variation

diameter >6mm

evolving (changing over time)

What are the risk factors of melanoma?

“MMRISK”

more than 5 atypical moles

more than 50 common moles

red hair or freckling

inability to tan

sunburn

kindred (family hx)

longitudinal pigmented streak that extends from the proximal or lateral nail fold

hutchinson’s sign

location: palms, soles, terminal phalages, nail beds, and mucous membranes

poor prognosis

acral lentiginous melanoma

history: chronic, relapsing

symptoms: itchy

PE: ill-defines, greasy yellow with fine white scale

distribution: scalp, nasolabial folds, eyebrows, central chest (not on the elbows, knees or nails)

seborrheic dermatitis

history: arthritis/joint pain

symptoms: usually not itchy

PE: sharpy demarcated, deep red, with thick white scale, nail findings

distribution: typically affects scalp, elbows, knees, rarely affects the face

psoriasis

What workup should we do for a pt with seborrheic dermatitis?

HIV testing if new onset and severe

which one is this?

KOH: septate, branching hyphae

KOH: spaghetti and meatballs

branching: tinea corporis

spaghetti: tinea versicolor

usually occurs in the spring and fall

PE: hearld patch (a single plaque usually on the trunk) then 2-21 days later you get a generalized eruption in christmas tree pattern

pityriasis rosea

multiple, 1-2cm, scattered scaly salmon pink papules in a general distribution sparing the palms and soles; tear drops

tests: ASO titer and throat culture (VDRL to r/o syphilis and KOH to r/o tinea)

erruptive guttate psoriasis

starts in the summer and seems to go away in the winter

PE: sharply marginated, hyper or hypopigmented, scaly rounf or oval macules of varying sie

seen on upper trunk, arms, neck, axillae, and abdomen

tinea versicolor (what we think the boys have)

clinical: thick silvery white scaly plaques

seen on extensor suraces (elbows and knees) and scalp

family history and joint pain

nail findings: onycholysis, pitting, and oil spot

psoriasis

What is the koebner phenomenon and what does it go with?

the induction of new psoriasis skin lesions following a local trauma or injury to the skin

triggers: physical trauma, mechanical, allergic, or chemical

• like a tattoo or surgical incision

What is auspitz sign and what does it go with?

this is when a scale of psoriasis is scraped, you see pinpoint bleeding

confluent erythematous scaly patches and plaques with irregular configuration

most common cutaneous lymphoma

a clonal proliferation of T cells

can have a patch, plaque, or tumor stage

mycosis fungoides

purple, polygonal, pruritis, planar (flat), papules

wickham’s striaw (white lacy discoloration in mouth)

lichen planus

What test should you order if you suspect lichen planus?

hepatitis C

dermatophyte infection via autoinoculation or animal contact

PE: small to large scaly sharp marginated annular plaques and central clearing

most commonly caused by trichphyton rubrum

tinea corporis

what is the presnetation of dermatophytosis (fungus) after application of topical steroids?

tinea incognito

what should we think when we see distal/lateral subungal onychomycosis?

T. rubrum

What occurs in places where opposing skin surfaces rub against eachother like arm pits, groin, lips, under breasts, etc.

erythematous patches or plaques that are mirror images

intertrigo

Which type of intertrigo?

caused by trichophyton rubrum

PE: bilateral annular plaques with advancing border and central clearing that spares the scrotum and penis

tinea cruris (jock itch)

Which type of intertrigo?

PE: deep pink to red color and well defined boarders that often involve the penis and scrotum

usually see psoriasis elswhere on the body

inverse psoriasis

Which type of intertrigo?

PE: beefy red colored lesions with satellite pustules seen beyond the border

occurs in skin folds where occlusion from clothing produces warm, moist conditions

candidiasis

Which type of intertrigo?

caused by corynebacterium minutissimum

predisposing factors: excessive sweating, obesity, ppor hygeine, diabetes, old age

diagnosis: can be made by shining a wood’s ligh on the area: you see a coral-red fluorescence produced by bacteria

erythrasma

Which type of intertrigo?

caused by repetitive rubbing and scratching

PE: local thickened plaques that are poorly demarcated

lichen simplex chronicus (is eczematous)

common in lower extremities

common in patients with chronic venous insuficiency (obesity, DVT history, HTN, etc.)

associated wit varicose veins, edema, hyperpigmentation, and ulcerations

erythema, scaling, hyperpigmentation in the medial supramalleolar region

can form crust, lichenification (thickening), sclerosis, and ulceration

stasis eczema

pruritis sweelings; whela/hive; can progress to anaphylaxis

tx: epinephrine

urticaria

swelling of tongue, lips, face, neck, and lower airway

two subtypes:

• C1-esterase deficiency

• ACE inhib or NSAID use

tz: icatibant (bradykinin inhib), ecallantide (kallikrein inib), C1 esterase inhib

angioedema

usually 2’ to HSV infection

targetoid lesions, low grade fever, malaise

can be minor (no mucosal involvement and no systemic signs) or major (severe mucosal involvement and systemic signs)

Erythema multiforme

Erythema multiforme is associated with ___ and should be treated ____

can be HSV related, treat with acyclovir

SJS vs TEN: what are the percentages of body involvement for each?

SJS: <10%

TEN: >30%

drug-specific CD8+ cytotoxic cell mediated rxn; can have genetic predisposition (HLA)

diagnosis: clinical, +Nikolsky sign, keratinocyte necrosis, mucous membrane involvement (pain with swallowing)

SJS/TEN (need to know % skin involvement to differentiate)

broken skin barrier leads to staph aureus infection

+ Nikolsky sign

symptoms: bullse then epidermis desquamates leaving skin similar to a brun; mucous membranes are spared

tx: IV antibiotics and supportive care

staphylococcal scaled skin syndrome

associated with wound packing or tampon use

hypotension

symptoms: fever 102+, desquamative rash on the palms and soles, hypotension, multisystem organ involvement 3+ systems

toxic shock syndrome (the shock is where the hypotension comes from)

autoimmune; IgG abs against desmoglein 3

+Nikolsky sign, IgG deposits in a reticular pattern allong the dermal epidermal junction

tx: admit, plasmaphersis and IVIG, tx fluid and electrolyte inbalances

pemphigus vulgaris

usually has a clear drug trigger, associated with HLA genes, delayed type IV hypersensitivity

symptoms: extensive skin rahs, fever 101.3+, visceral organ involvement, liver injury common, facial edema, rarely do you have mucosal involvement or skin detachment

drug reaction wiht eosinophilia and systemic symptoms (DRESS)

What are the key differences between SJS/TEN and DRESS?

SJS/TEN: mucosal involvment and skin detachment

DRESS: rare to have mucosal involvment or skin detachment

risk factors: asplenia, complement deficiency, croding (prisons or dorms)

symptoms: HA, fever, altered mental status, n/v, neck stiffness, petechial/purpuric rash

meningococcemia

How do we treat meningococcemia?

IV 3rd gen cephalosporine and IV vancomycin

cause: due to breaking skin integrity (staph aureus, strep, clostidum, anaerobes)

signs and sympt: excruciating pain out of proportion, systemic septic signs, subq emphysema and crepitus

necrotizing fasciitis

latent VZV in trigeminal ganglion reactivates → vesicular rash in a dermatomal distribution

diagnosis: Hutchinson’s sign

herpes zoster ophthalmicus (opthamic emergency)

endemic to southeastern and south-central US

acute febrile tick-borne illness caused by Rickettsia rickettsia (think summer months)

symptoms: triad of fever, HA, petechial or maculopapular rash starting at the wrise and ankles

Rocky Mountain Spotted fever

How do we treat Rocky mountain spotten fever?

doxycycline (even in kids, benefits > risk)

common in children; asian population

symptoms: conjunctivitis, rash (palms and soles), adenopathy, strawberry tongue, hand and feet edema, and fever > 5 days

high risk of coronary artery vasculitis, including aneurysms and thrombosis if untreated

Kawasaki disease

What conditions requires immediate surgical debridement?

necrotizing fascitis

How do we treat kawasaki disease?

aspirin, supportive care, IVIG, need an echo

cause: paramyxovirus

symptoms: cough, conjunctivitis, corya, and koplik spots; maculopapular erythematous rash that starts on the face and spreads to the trunk and extremities

complications: encephalitis, blindness, and subacute sclerosing panencephalitis

measles (rubeola)

How do we treat measles?

contact health officials, supportive care, vitamin A