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73 Cards in this Set

  • Front
  • Back
Prolactinoma
MOST COMMON tumor of pituitary

amenorrhea/oligomenorrhea, impotence, galactorea, gynocomasteam visual complaints (bc this is a macroadenoma so its so big it pushed on the optic chiasm)
Cushing's Dz
due to ant. pituitary tumor
overproduce ACTH

over produce cortisol = steroid man
Acromegaly
due to ant pituitary adenoma that over produced Growth Hormone AFTER adolescence

outgrow shoes, gloves & hats, dev course facial features
Gigantism
due to ant pituitary adenoma that over produced Growth Hormone PRIOR to puberty

tall and large but proportional
PCOS
over produced LH!
NOT assoc. w/ pituitary adenoma
acne, hirsutism, infertility

LH:FSH ratio is 2:1 or more
Menopause
ovarian failure

no estrogen or progesterone = no negative feedback so high FSH

FSH:LH ratio is 2:1

hot flashes and osteoporosis
SIADH
excess ADH produced by posterior pituitary

excess water reabsorption from the kidney = hyponatremia, cerebral edema with maybe hypertension
What else can produce high SIADH?
Small cell lung cancer

head trauma-damage to hypothalamus or post. pituitary
Panhypopituitarism aka pituitary cachexia or simmonds dz
1-pituitary tumor-nonfunctional
2-postpartum pituitary necrosis-Sheehan's Syndrome

decreased TSH, GH, ACTH, LH and FSH
Pituitary Dwarfism
congenital def in Growth hormone

short and proportionately small
Diabetes Insipidus (central)
caused by ADH def secondary to decreased secretion by the posterior pituitary-usually head trauma wherein the post. pituitary or hypothalamus are damaged

polyuria & polydipsia

*nephrogenic DI is due to lack of kidney response to ADH but cause similar symptoms
Conn's Syndrome
adrenal adenoma that overproduces aldosterone

too much aldosterone=hypernatremia=severe HTN (headache) & hypokalemia->muscle weakness
Cushing's Syndrome
due to ANY cause for increased glucocorticoids

screen: 24 hour urine test bc levels flucuate throughout the day

confirm:dexamethasone suppression test
5 caused of Cushings Syndrome
1-adrenal adenoma
2-adrenal carcinoma
3-Cushing's Dz-pit ACTH producing adenoma
4-small cell lung cancer-paraneoplastic production of ACTH
5-prolonged use of glucocorticoids-steroids
Pheochromocytoma
excess NE +/- Epi secretion ( tumo rof the adrenal medulla)

sporadic HTN,paroxysmal hyperhidrosis, and episodic aggressive behavior changes

Best screen:24 hour urinary VMA (also use 24 hr metanephrines and normetanepthrines or 24 hr catacholamines
Neuroblastoma
malignant tumor of adrenal gland or sympathetic ganglia or both produces excess norepi

neural crest in origin

peak age <3 yo

presenting sign-enlarging abdomen & HTN can occur. later symptoms are due to metastisis
Addison's Dz
autoimmune but can be bc invasion of mycobacterium tuberculosis or histoplasma capsulatum

decreased aldosterone production=excess Na loss through kidney=hypotension

hyperkalemia=muscles weakness and cardiac arrhythmias

decreased neg feedback on ant pit =over produce POMC=increase ACTH and MSH(why JKF so tan bc excess melanin)
Graves Dz (diffuse toxic goiter)
young females
MOST COMMON cause of HTN in US

ANTI-TSH antibodies
exopthalmos, dermopathy (pre tibial fat pad)

1st line management: radioablation with sodium iodine
Plummers Dz (nodular toxic goiter)
post menopausal women, multiparous females-risk increased with degree of parity (aka more kids higher risk)

due to; reactivation of subsequent hyperactivity of isolated nests of cells within the thyroid gland

often no HYPERthyroid symp just recurrent fatigue, tired & malaise-bc rest of the gland is inadequately stimulated due to to resulting low TSH levels
Diffuse Simple Goiter (iodine def)
any age-in regions of world iwth no iodized salt or with out crustaceans

hypothyroid symptoms

treat:iodine
Hashimotos ThryoidItis
t cell disorder with ANTI-MICROSOMAL antiboides-gradually and progressively destruct the gland

constipation, fatigue,dry skin, coarse hair, swollen legs, cold intolerence, weight gain

treat: levothyroxine
Riedels (FIbrous) Thyroiditis
elderly
chronic use of migrain meds -weird
fibrosis and bc nonfunctional
treat:levothyroxine
DeQuervain's throiditis
probably viral & usually follows a viral URI

Hyperthyroid symptoms followed by hyporthyroid symptoms

transient and temporary

NSAIDS
Sick Euthyroid Syndromes
due to sever illness, physical trauma, physiologic stress

treat the underlying cause

many variants but all have NORMAL TSH
follicular adenoma
single, palpable, thyroid nodule

female

>45 y/o

hyperthyroid signs
Carcinomas of thyroid
females>males

painless mass

euthryoid-NORMAL thyroid levels

cold nodules-radioactive iodine injected and nodule shows no activity
4 types of thyroid carcinoma
Papillary
Follicular
Ananplastic
Medularry
Papillary CA
Most common and best pronosis so yay :)

females in their 20's

fingerlike projections & ground glass appearance of nuclei

assoc w/ prior radiotherapy of the neck
Follicular CA
middle aged
poorer prognosis
Anaplastic CA
elderly
VERY aggressive & very poor prognosis
Medullary CA
Late middle aged/ early elderly

tumor of parafollicular C cells (part of the MEDULLA of the thryoid gland)

C cells make calcitonin (encourage Ca deposition in the bone)

tumor makes high calcitonin=hypocalcemia
5 roles of Parathyroid hormone
1-activate osteoclasts-increasing serum Ca
2-Increase renal tubular re-absorption of Ca=increase serum Ca
3-Increase Vit D conversion to 1,25 dihydroxyvitamin D in kidneys-increase serum calcium & phosphorous
4-increase renal phosphate excretion-DECREASE serum phosphate-lose massive amts by this
5-increase GI absorption of Ca=increase serum Ca
Primary hyperparathyroidism
due to pathology of the parathyroid gand

hi PTH
hi Ca
lo
PO4
Secondary hyperparathyroidism
due to low calcium with resulting response of activity by parathyroid gland

ex:Chronic renal failure-so kidneys will not reabsorb CA=loss Ca in urine= PTH increased in response so

hi PTH
lo Ca-bc kidney failed
hi PO4-bc kidney failed
Hypoparathyroidism
lack of parathryoid activity

ex: accidental parathyroid removal with thyroidectomy

lo PTH--> lo Ca & Hi PO4
Pseudohypoparathyroidism
PTH receptors are non functional so parathyroids ar enormal but tissues can't respond

inherited rather than acquired

hi PTH but no respone so lo Ca & lo PO4

several types: 1a is also known as Albright's -features: short stature, obesity, and short hand bones
Pseudopseudohypoparathryoidism
AD but INTERESTING BC-inherit gene from DAD get this but inherit gene from mom and get pseudohypoparathhyroidism type 1A

PTH receptors are fine but 2nd messanger system is defective= response to PTH slow but possible-Ca and PO4 equilibrate slowly

features: short stature, obesity, and short hand bones
Primary Diabetes
1-Type 1
2-Type 2
3-gestational
4-MODY
Secondary Diabetes-
hemochromatosis,chronic pancreatitis, pancreatic Ca
Hallmarks of all diabetes
hyperglycemia, polyphagia, polyuria, polydipsia, increased infections, blurred vision
Type 1 DM
not common- ANTI ISLET CELL Ab destroy beta islet cells

juvenile onset-lean body-no insulin

KETOACIDOSIS RISK-lack of insulin + stress = extreme over activation of HSL=explosive lipolysis and consequent ketoacidosis

HLA DR3 & DR4
Type 11 DM
very common & growing in kids

hypoosmolar nonketotic coma risk-glucose levels reach super high levels and pull water into vasculature thereby dessicating (drying out) the brain = coma

women>men

No HLA connection or autoantibodies

OBESE
Chronic Complications of DM
neuropathy, atheroscleroiss (MI, PVD, stoke, AAA, mesenteric ichemia) retinopathy, nephropathy
Gestational Diabetes
Beta cell reserve is inadequate for increased demands of preggo

exacerbated by human placental lactogen, product of the placenta which causes mild insuline resistance

screen: Glucola test in 27-28 weeks
MODY-maturity onset diabetes of the young
glucokinase defect-prevents cells from being able adequately phosphorylate the glucose that is made available to them=glucose cannot be used & released back into serum =HYPERGLYCEMIA
MEN's
AD
LIFE LONG risk of dev certain neoplasms of certain endocrine glands
MEN type 1-Wermer's Syndrome
adrenal cortex
pituitary
parathyroid
pancreas
MEN type 2a-Sipple's
adrenal cortex-pheochromocytoma
thyroid medculla
parathyroid
MEN type 2b=MEN type 3
adrenal medulla
thryoid medulla
mucosal neuroms
marfanoid features
Seborrheic Keratosis
at or later than middle age
benign and on the trunk
round, flat , coin like plaques that feel velvety/granular/greasy and often look stuck on
Keratoacanthoma
50 yo male esp caucasian
flesh colored dome shaped nodule with keratine filled plug
may heal spon

face or dosum of hands
Actinic Keratosis
SUN
dysplasia b4 malignancy
some have cutaneous horn
Basal Cell Carcinoma
SUN-esp chronic sun exposure

slow growing and rarely mets

pearly gray with telangiectasias
Squamous cell Carcinoma
SUN
male>female
too much UV= DNA damage= damage langerhans cells=no surviellance=malig can grow and dev

#1 skin tumor on sun exposed sites in older adults
Melanoma
SUN
most are cured by excision
most important sign-change in color
may be pruitic
risk factors-sun, preexiting nevus, genetics, carcinogens
Bowen Dz
genital region
>35 yo
thickened, gray-white plaques
>90% have HPV (16)
possible assoc w/ visceral malignancy
Bowenoid Papulosis
multiple, pigmented papules on external genitialia of MALES

may mimc condyloma acuminatum

<35 yo
rarely transitions to squamous cell CA
Erythroplasia of Queyrat
single or multiple, shiny, red plaque on the glans penis or prepuce
>35 yo
10% tranisition to squamous cell CA
Pemphigus
ANTI KERATINOCYTE Abs
male>female but rare
40-60 yo
the Abs cause a loss of attachement bt keratinocytes and fluid fills within the spaces getting vesicles
Pemphigoid
ANTI EPIDERMAL BASEMENT MEMBRANE Abs

common
tense bullae filled with clear fluid in elderly

heals with a scar

abs dev agaisnt adhesions sites bt basal cells and basement membrane=loss of attachment=fluid fills the area=lifitng the entire cutaneous epithelial layer from its basement membrane= bullae
Impetigo
due to Strep pyogenes or Staph aureus

vesicles/bullae=pustules=rupture= crusted skin lesions

hands or face
Pityriasis (pityriasis rosea)
Rash often preceded by a HERALD PATCH

round to ovale plaques with surrounding scale most often in trunk

CHRISTMAS TREE pattern

self limited-resolves in 2-8 weeks
Rosacea
Chronic dz of nose, forehead, cheeks
>30 yo
females more but males when do get it have it worse

erythema, telangiectasia, superficial pustules, facial flushing

exacerbated by heat, stress, emotional stimuli, alcohol, hot drinks

long standing=tissue overgrowth of nose

increased occurrence of keratitis, iritis, chalazions which may be sight threatening
tinea versicolor
hyper/hypo pigmented scaly patches on trunk

promoted by heat and humidiity

"SPEGHETTI & MEATBALLS" bc a mixture of hypea and spores
Psoriasis
sharply demarkated, erthyematous plaques with thick scale

elbows, knees and scalp
Seborrheic dermatitis
COMMON
Neonates and adults at risk

greasy scales over erythematous patches or plaques

#1 location-scalp=sever dandrugg
cradle cap in infant

VERY COMMON in those w/ parkinsons, CVA or HIV
Eczema
final common expression of atopic dermatitis, contact dermatitis, seborrheic dermatitis and related disorders

erythematous apules and macules and vesicles coalesce to form patches and plaques, may progress to weekping, crusting and or thickened scale
Xanthoma
cholesterol accumulation within the dermis
Capillary hemangioma
2 types
1-ordinary birthmark-salmon patch or stork bite
closely packed capillaries;regress spontaneously

2-strawberrry-dev 1-3 yo and regress by 7
Cavernous Hemangioma-Port Wine stain
face
large, dilated vascular channel
assoc w/ Struge Weber-congenital dz with faulty mesoderm and ectoderm dev=hemangiomas assoc/ w/ meninges= SEIZURES
Cafe au Lait
Light Brown macules with smooth border over ner ve trunks
Vitiligo
ANTI MELANOCYTE Abs
asymp, flat NON pigmented macules
Lentigo
opposite of vitiligo
benign
hyperplasia of melanocytes = small oval tan macules
"Liver Spots"