Condyloma

1. microbe?

3. histology?

Warty Neoplasm of Sqamous epithelium 

a. vulva/vagina/cervix

Virus: HPV (6, 11)

histology: koilocytic change

a. "Raisin-like" nuclei 

Lichen Sclerosis

features?

complications?

Epidermis (thinning) with Dermis (fibrosis)

Features:

1. Leukoplakia with paper-thin vulvar skin

"Parchmet-like"

Complication:

*risk for squamous cell carcinoma

Lichen Simplex Chronicus

presentation?

complications?

Hyperplasia of vulvar epithelium due to chronic irritation and scratching

Presentation:

Leukoplakia with thickening of vulvar skin

"leather-like"

*no risk for squamous cell carcinoma

Vulvar Carcinoma

presentation?

2 etiologies:

a. ages? 

Squamous cell carcinoma

presentation

1. Leukoplakia + Biopsy confirmation

Etiologies:

1.   HPV (16, 18, 31, 33)

a. women in 40s

2. Long standing Lichen sclerosis

a. 70+ post menopausal women

Extra-mammary Pagat disease

presentation?

location?

what can it look like?

stains to differentiate? 

Malignant epithelial cells in epidermis 

Presentation

Erythematous, itchy, ulcerated skin 

location:

1. breast = cancer

2. Vulva = no cancer

Looks like Melanoma* 

1. Pagat-Disease (PAS & Keratin +)

a. (-) S100

2. Melanoma (S100 +) 

b. (-) PAS and Keratin

Adenosis

*associated with?

*high risk for?

Persistance of columnar epithelium in upper 1/3 vagina

a. not replaced by squamous epithelium

associated: DES exposure in utero

Risk: clear cell adenocarcinoma

Embryonal Rhabdomyosarcoma (Sarcoma botryoides)

Age?

classic presentation?

malignant cell? 

stains?

Malignant proliferation of *immature skeletal muscle

occur: Child < 5 yrs old

presentation:

a. *Grape-like mass protruding from the vagina or penis

malignant cell: Rhabdomyoblast

a. cytoplasmic cross-striations 

b. (+) stain:  Desmin (muscle cell) + Myoglobin 

Vaginal Carcinoma

*Metastasis of Vaginal carcinoma? 

Lower 2/3? 

Upper 1/3?

Carcinoma of Squamous vaginal lining 

associated: HPV (16,18)

Metastasis: Lymph nodes

 lower 2/3: inguinal nodes

upper 1/3: Iliac nodes

Cervical Carcinoma

classic pt?

common presentation?

risk factors? (3)

classic pt: Middle-aged women (40s)

Presentation

1. Vaginal Bleeding 

2. Post-coital bleeding

Risk factors:

1. HPV (E6 & E7) 

2. smoking 

a. carcinogens passed in urine- touch epithelium of cervix

3.* immunodeficiency (can't remove HPV)

Cervical Carcinoma Metastasis? 

leading to?

Local

Metastasis: Bladder

a. invades anterior uterine wall into bladder

lead to: hydronephrosis

a. ureter block

b. renal failure

*Bitemporal hemianopsia is often present

prolactin inhibits GnRH (and thus LH/FSH)

men: impotence

women: amenorrhea and galactoriea

Tx: Dopamine Agonist (Bromocriptine)

*dopamine inhibits prolactin secretion

1. Paraythyroid

2. Pituitary (prolactin or GH)

3. Pancreatic Endocrine tumor 

*autosomal dominant

1. medullary carcinoma of thyroid (calcitonin)

a. congo-red stain

2. pheochromocytoma

3. parathyroid tumor

*Autosomal Dominant

*ret gene mutation

1. medullary carcinoma of thyroid (calcitonin)

a. congo-red stain

2. pheochromocytoma

3. marfanoid habitus / Mucosal neuromas

a. oral/intestinal ganglioneuromatosis 

*autosomal dominant

*ret gene mutation

HPV immunization vaccine?

lasts for how long?

Quadrivalent 6,11 (condyloma)

16,18 (CIN, VAIN, VIN) - dysplasia of lower genital tract

*5 yrs (Pap smears still necessary because there are more HPV subtypes)

Leiomyoma vs. Leiomyosarcoma

1. onset?

2. due to?

3. gross?

4. other? 

Leiomyoma

1. Pre-menopausal women (20-40)

2. Estrogen related (*grow w/ prego and shink w/ menopause)

3. Multiple, well-defined, white-whirly masses

4. asymptmatic 

Leiomyosarcoma

1. Post-menopausal women 

2. De-Novo*

3. Single lesion w/ necrosis & Hemorrhage

multiple follicular cysts due to hormone imbalance

**LH:FSH > 2

excess LH-> Theca Cells produce Excess Androgen -> Hirsuitsm

*excess androgen enters Adipose-> converted to Estrone

*high amounts of estrone shunts down FSH in pituitary.

(No FSH, can't convert androgen to estradiol and follicle degenerates)

Classic presentation of Polcystic ovarian disease?

can develop?

Obese women with infertility

(lots of adipose to convert androgen to estrone)

*oligomenorrhea

*hirsutism

*High circulating estrone levels -> endometrial carcinoma

(who's key risk factor is excess estrogen)

develop:

1. Type II DM (insulin resistance) 

2. Endometrial Carcinoma (high estrone)

*EC major risk factor is high estrogen

Endodermal sinus tumor (yolk sac)

high yield characteristics

#1 germ cell tumor in kids

AFP elevation

Schiller-duval bodies 

Leydig-cell tumors (sex-cord stromal cells)

*hisutism or virilization in women

PTH main action?

(4)

Bone resorptionmoa?

Overall effect: increase serum Ca & lower P

1. increase bone resorption of Ca & P 

2. Inc. Kidney Ca reabsorption (@dct)

3. inhibit kidney P reabsorption (@pt)

4. activate Vitamin D in kidney (1a-hydroxylase)

Bone resorption

osteoblasts (PTH receptors) -> inc. RANK-Ligand and M-CSF -> stimulate osteoclast maturation

Regulation:

low ca: inceased pth*

low Mg: decreased pth*

*lower MG: diarrhea, diuretics, aminogclycosides, alcohol abuse

Hyper-aldosteronism (Conn Syndrome) 

Metabolic Sx

Physical Sx

Hyper-Na leading to HTN + hypo-K and alkalosis 

Hypokalemic metabolic alkalosis --> weakness/parestesias 

Long acting insulin?

Short acting insulin?

Best to reduce post-meal hyperglycemia?

1. NPH, glargine, detemir.

2. Regular, lispro, aspart.

3. Lispro and aspart. 

1. Zona Glomerulosa (Conns Syndrome)

a.Excess Aldosterone (HTN, Hypokelemia)

b. Parasthesias/weakness from low K+

2. Zona Fasiculata (Cushings)

a.  Excess Cortisol

3. Zona Reticulata (Androgen Excess)

a.Hirsutism & Virulization

hCG

1. Structurally similar to

hCG similar to: TSH, LH, and FSHa 

a. can stimulate TSH receptor -> hyperthyroidism

Stroma Ovarri Teratomas or Seminomas

Signaling Pathways: Steroid Receptor

1. Cytosolic?

2. Nuclear?

Cytosolic : "VET CAP"

- Vitamin D

- Estrogen

- Testosterone

- Cortisol

- Aldosterone

- Progesterone

Nuclear

a. Thyroid Hormone (T3/T4)

Hypothalamus Hormones

Stimulatory? (4)

Inhibitory? (3)

Stimulatory

1. TRH -> TSH/Prolactin

2. CRH -> ACTH

3. GhRH -> GH

4. GnRH -> FSH/LH

Inhibitory

1. Dopamine -| Prolactin

2. Somatostatin -| GH, TSH

3. Prolactin -| GnRH

Most common Tumors

1. Adrenal Gland

2. Adrenal Medulla

3 Tumor in children

1. Adrenal Indidentaloma

2. Pheochromocytoma

3. Neuroblastoma

Etiologies of Cushings

1. Endogenous

2. Exogenous

*Unaffected by Dexamethasone supression test?

Endogenous

a. Pituitary Adenoma

b. Small Cell Lung Cancer (Ectopic)

c. Adrenal Adenomas

Exogenous

a. Ectopic glucocorticoid Use

High Dose Dextramethasone

a. only lowers ACTH/Cortisol if pituitary adenoma (vs. Ectopic ACTH tumor)

*adrenal adenoma/carcinoma will have low ACTH regardless

Key differences

1. Primary and Secondary Adrenal Insufficiency

2. Primary and Secondary Hyperaldosteronism

1. Addison's -

Primary: Hyperpigmentation (high ACTH secretion; contain MSH)

Secondary: No hyperpigmentation

b. No Hyperkalcemia (aldosterone can still function via RAA)

2. Conn's Syndrome

- Primary: Low Renin

a. Tumor

- Secondary: High Renin

a. kidney percieves low volume

Adrenal medulla Tumors with Urine Elevations

1. VMA

2. HVA

1. Pheochromocytoma

a. VMA = breakdown of NE

b. associated : MEN 2a/2b, Neurofibromatosis

2. Neuroblastoma (#1 in children)

a. HVA = breakdown of Dopamine

b. associated: N-myc oncogene overexpression

c. Bombesin (Tumor Marker)

major functions of Thyroid hormone?

a. synthesized location?

1. Brain Maturation

2. Bone Growth

3. BMR increase

a. Increase Na-K+ ATPase*

4. Beta-Adrenergic Effects

a. increase B1 expression*

5. Increase: Glycogenolysis, gluconeogenesis, lipolysis

TH production: follicular cells of thyroid

a. peroxidase enzyme

1. Blood Pressure (A1-receptor upregulation)

2. Decrease Bone Formation

3. Anti-inflammatory / immunosuppression

a.* inhibit LT and PG synthesis

b. Inhibit Leukocyte adhesion -> neutrophilia

c. Block Histamine release

d. reduce eosinophils

e. block IL-2

4. Inc. Insulin Resistance (diabetogenic)

5. Inc. Gluconeogenesis, Lipolysis, proteolysis

6. help mature fetal  lung

*regulated: CRH, ACTH

*Stress stimulates secretion

Sheehan Syndrome

1. pathophysio

2. key signs

Pregnancy related ischemic infarct of Anterior Pituitary

a. High Estogen during prego stimulates Pituitary growth & vascularization

b. birthing results in blood loss/hypotension, infarcting the anterior pituitary 

Signs:

1. Failed Lactation (no prolactin)

2. Loss Of Pubic Hair (no LH)

can also have hypothyroidism (TSH) / hypocortisolism (ACTH)

Diabetes Insipidus

1. signs?

2. lab values?

3. Vasopressin Admin?

With no ADH (Central or Nephro) the collecting tubules are impermeable to water, causing water loss via urine. 

Features: 

1. Polyuria

2. Polydyspia

3. normal blood glucose (vs. Diabetes mellitus)

4. Very Dilute urine*

Vasopressin Administration

a. Central: Urine Concentrates

b. Nephrogenic: urine still dilute

ADH is responsible for maintaining water balance by regulating water absorption in collecting tubule of kidney. 

a. Normally acts on V2 receptors and insert aquaporins to serve as water channel

 1. Central DI

2. Nephrogenic DI

Etiologies?

treatment?

Central D.I.

Due to: head trauma 

tx: Desmopressin (ADH analog)

Nephrogenic D.I.

Due to: Lithium, Demeocycin

1.  Hydroclorothiazie 

2. Indomethacin

3. amiloride

SIADH 

1. due to?

2. features?

3. *associated

4. treatment

SIADH 

a. excess ADH leads to excess water reabsorption

Lab:

Plasma: Low Sodium & Osmolality

Urine: Inc. concentration, Sodium

body fluid volume: Normal

*low Na can causes cerebral edema and seizures

*associated:

1. Small Cell Lung Carcinoma (ectopic ADH)

2. Cyclophosphamide

Treatment: Demeclocycline 

Graves Disease

1. features

2. histology

*Auto-ab vs. TSH (stimulatory effect)

Features:

1. Hyperthyroidism

2. Exopthalmos

3. Pretibial myxedema

*both due to inc. GAG deposition which uptakes water

4. Diffuse Goiter

a. constant TSH stimulation -> growth

Histology

Scalloped Appearance of Colloid Follicle

Lab:

High Total & Free T4

Low TSH

Hyperthyroidism

Features?

Etiologies? (3)

Features

a. Heat Intolerance (Inc. BMR)

b. Weight loss DESPITE inc. appetite

c. Hyperactivity

d. Diarrhea*

e. Hypocholesterolemia

f. Hyperglycemia (gluconeogenesis, glycogenolysis)

1. Graves

2. Thyroid Storm

3. Toxic Multi-nodular goiter

Thyroid deficiency in neonates/infants

Features

a. MR

b. Course Facial Features

c. Short stature/bone abnormalities (thyroid req. for growth)

d. umbilical hernia

Hashimoto Thyroiditis

Asociated?

Presentation?

Lab/histology?

inc. risk for?

Auto-immune destruction of thyroid

Associated: HLA-DR5

Presentation: 

1. Hypothyroid (weight gain, fatigue, constipation)

Lab:

a. Lymphocyte + plasma cell infiltrate with germinal centers

b. Anti-microsomal & anti-thryoglobulin antibodies

c. Hurthle Cells (eosinophilic cells lining follicles)

Complications: B-cell lymphoma (marginal zone)

Subacute Thyroiditis (De Quervains)

unique feature?

histology?

Granulomatous thyroiditis following a viral infection

a. increased ESR

b. reduced iodine uptake

c. *Thyroid Tenderness/pain

Histology

a. cellular iniltrate with occasional multinucleated giant cells!

Explain the different end results in tall stature of a 6 y/o (98th percentile) due to

1. Excess GH

2. Precocious Puberty 

1. Gigantism

a. does not lead to premature epiphysis closure

b. becomes a giant

2. Precocious Puberty

a. Sex hormones promote both bone growth and epiphyseal plate closure

b. Precocious puberty may result in ultimately shorter stature than their peers

c. Develop secondary sexual characteristics at young age

Papillary Carcinoma of Thyroid

highly associated?

*Histology? (3)

Most common thyroid tumor

a. associated with childhood radiation

Histology

a. Psammoma bodies 

b. Ground-Glass nuclei ("orphan annie")

c. nuclear grooves

Medullary Carcinoma of Thyroid 

1. neoplasm?

2. stain?

3. associated?

4. mutation?

Neoplasm of Parafollicular C-cells

a. Calcitonin secretion

b. AMYLOID stroma (Congo-Red Stain)

Associated:

1. MEN 2a

2. MEN 2b

*If RET mutation found must do prophylactic thyroidectomy

*Mostly in Tail of Pancreas

Alpha: Glucagon

1. Peripheral Location

Beta: Insulin

1. Central Location

Delta: Somatostatin

1. Interspersed

Glucose uptake into cells

1. Insulin not required?

a. Receptors?

2. Insulin Required

1. a. GlUT-1: RBCs / BRAIN

b. GLUT-2: B Islet Cells / Liver/ Kidney/ Small Intestines

2. a. GLUT-4: Adipose / Skeletal muscle

Diabetic Ketoacidosis

complication of?

mechanism?

Signs?

Labs?

Type I DM complication

a. Stress (ex. infection) causes SANS response

b. Glucagon -> Lipolysis-> Free FA -> Ketone body in liver

*No Insulin to manage the excess glucose in blood

Triad:

a. Kussmaul respiration (Deep/rapid)

b. Fruity Breath (exhaled acetone)

c. High Ketones

labs:

a. High Hyperglycema (>300)

b. Anion-gap Metabolic Acidosis

c. Hyperkalemia

I. insulin stimulates K+ uptake (no insulin in type 1 DM)

II. acidosis causes H-K exchange -> hyper-K

Hyper-osmolar non-ketotic coma

1. complication of?

2. features?

3. ketones?

Type II DM complication

High glucose levels act osmotically causing life-threatening diuresis

Features

1. Hypotension

2. Coma 

*Ketones are Absent (vs. DKA)

a. small amount of circulating insulin prevents KA

Androgen Insensitivity vs. 5-a-reductase deficiency

a. defect

b. presentation

c. labs

Androgen Insensitivity Syndrome (46, XY)

a. Defective Androgen Receptor

b. Phenotypic Female (uterus, uterine tubes absent)

c: Elevated Testosterone, LH, Estrogen

5a-Reductase deficiency

a. Testosterone cant be converted to DHT

b. ambiguous genitalia until puberty

c. Normal Genitalia at puberty 

d. Normal Tesosterone, LH, Estrogen

Oogenesis

arrested stages + stage of ovum development?

no fertilization?

fertilization? 

Primary oocyte (Diploid 4N)

a. Meiosis I (arrested in Prophase until ovulation)

Secondary Oocyte (Haploid 2N)

a. Meiosis II (arrested in Metaphase until fertilization)

No fertilization:

Secondary Oocyte degenerates

Ferilization:

Ovum creation a. Haploid (N)

Important actions

1. Testosterone (3)

2. DHT (3)

Testosterone

1. Differentiation of wolfian ducts

(Seminal Vesicles, Epididymus, Ejaculatory ducts, ductus deferanns)

2. Epiphyseal closure

3. Spermatogenesis in sertoli 

DHT (active ; via 5-a-reductase)

1. Differentiation 

(Penis, scrotum, prostate)

2. Baldness

3. Prostate Growth

Menopause 

signs?

test to menopause?

Cessation of Estrogen Production

a. elevated FSH (lose inhibition of estrogen feedback)

signs:

a. Hisutism

b. Hot flashes

c. Vaginal atrophy

d. Osteoporosis

e. CAD 

test: extremely elevated FSH

a. lose (-) feedback for FSH d/t no estrogen

Ashermann Syndrome

due to?

Secondary Amennorrhea 

due to: Loss of basalis (regenerative layer) 

*aggressive dilation and curettage (D&C)

Endometrial Polyp

presents?

*associated? 

Hyperplastic protrusion of endometrium 

Presents: Abnormal urterine bleed

*Arise as SE of Tamoxifen

a. Anti-estrogen (breast)

b. pro-estrogen (endometrium)

Endometriosis 

presentation?

Locations?

treatment?

Endometrial Glands & Stroma outside uterine cavity

a. bleeding/shedding of tissue outside uterus form blood collections, which can cause inflammatory response

Presentation

a. Dysmenorrhea 

b. Dyspareunia (painful sex)

c. Menorrhagia

d. pelvic pain

e. Dyschezia (painful defcation)

*Uterus normal size (vs. adenomyosis)

Locations

a. Ovary (chocolate cyst)

b. soft tissue (gun-powder lesions)

treatment: Danazol

Adenomyosis

presentation?

treatment?

Endometriosis within myometrium

presentation

a. menorrhagia

b. dysmenorrhea

c. pelvic pain

*uterus = enlarged*

treatment: hysterectomy 

Endometrial Hyperplasia 

due to?

presentation?

complication?

Hyperplasia of Endometrial glands 

1. unopposed Estrogen

2.  Post-menopausal vaginal bleeding

complications:

Endometrial carcinoma

predictor: cellular-atypia 

Endometrial Carcinoma 

present?

pathways? (2)

Neoplasm: Endometrial Glands 

a. invasion dictates prognosis

present: Post-menopausal bleeding

Pathways:

1. Endometrial Hyperplasia 

a. unopposed estrogen

b. endometriod histology

2. Sporadic (no precursor lesion)

a. p53 mutation

b. Serous (Papillary) structure w/ psomma body 

Cystadenoma vs. Cystadenocarcinoma

tumor marker?

cyst type?

onset?

types of cancers?

Ovarian Surface Epithelium tumors

a. Ca-125 tumor marker (monitor, not screening)

Cystadenoma

a. Single cyst (Simple, Flat lining)

b. Pre-menopausal women

Cystadenocarcinoma

a. Complex-multiple cysts (Shaggy lining)

b. Post-menopausal women 

Serous (h20 filled)

b. Psmomma bodies

Mucinous (mucin filled)

a. Pseudomyxoma peritonei

Female: Teratoma

1. neoplasm?

2. types? (3)

1. composed of 2-3 germ cell layers 

Types

1. Benign: Mature Teratoma (dermoid cyst)

2. malignant: Immature Teratoma 

a. #1 common is neural ectoderm 

3. Stroma Ovarii: contains functional thyroid tissue

*Hyperthyroidism 

Female: Choriocarcinoma 

1. neoplasm?

elevated in serum?

2. spread

3. Chemotherapy

1. Trophoblasts/Syncytiotrophoblasts

a. mimic placenta (absent villi)

b. elevated b-hCG

2. Hematogenous

a. Primary tumor smaller than mets site

3. Poor response (vs. Gestational form)

Female: Fibromas

1. neoplasm

2. Meigs Syndrome

1. Fibroblasts

2. Triad

a. Ovarian Fibroma

b. Ascitis

c. Pleural effusion (hydrothorax)

*Pulling sensation on groin

Female: Brenner Tumor

1. neoplasm

2. H&E

1. Bladder-like epithelium

a. Urothelium

b. Solid, pale-yellow color

2. "coffee bean" nuclei 

Female: Granulosa-Theca tumor

1. produces?

Presentation (kids, adults, elderly)

Histo?

1. Estrogen Secreting

Kids: Precocious puberty

Adults: Menorrhagia or metorrhagia

a. Endometrial hyperplasia / carcinoma

*directly related to estrogen excess

Post-menopausal: abnormal uterine bleed 

Histology: *Call-Exner bodies

a. small follicles filled w/ eosinophilic secretions

1. Placenta Previa

2. Placenta Abruption

3. Placenta Accreta

1. Placenta attach to lower uterine segment 

a. Painless 3rd trimester bleeding

b. C-section delivery

2. Premature detachment of placenta from implant site

a. Painful 3rd trimester bleed (abrupt)

b. Still birth

3. Placenta attach to myometrium

a. difficult placenta delivery

b. massive bleeding after delivery 

b-hCG

produced by?

actions?

pathological elevations

1. Syncytiotrophoblasts of placenta

Actions

1. Maintain Corpus Luteum (thus, progesterone) for 1st trimester by acting like LH

2. Pregnancy detection in urine

pathological

a. Hyatidiform moles

b. Choriocarcinoma

c. gestational trophoblastic tumors 

*Medications that have similar composition to b-HCG can be used to induce LH surge

Hyatidiform Mole

features?

lab? 

Complete vs. Incomplete

Growth of abnormal placental tissue 

a. Enlarged Uterus + high b-hCG

b. Pass "grape-like" masses 2nd trim

c. no heart sounds + "snowstorm" ultrasound

Complete

a. 46 chromosome (only paternal)

b. no fetal tissue

c. all villi hydrotrpic

d. Choriocarcinoma

Incomplete

a. 69 chromosome (2 sperm + 1 ovum)

b. some fetal tissue

c. mixed normal and hydrotropic villi

d. 

2 methods of developing of choriocarcinoma

treatment differences? 

Gestational Pathway

a. Molar pregnancy

 *responds to chemo

Germ-cell pathway

*no response to chemo 

Male: Seminoma

present?

histo?

gross?

prognosis?

Germ cell tumor

a. equivalent of female dysgerminoma 

present: Painless testicular mass (vs. embryonal c.)

histo: Fried-Egg appearance 

gross: Homogenous mass w/o hemorrhage or necrosis

prognosis: good 

*responds to radiotherapy

Male: Embryonal Carcinoma

1. neoplasm

2. present?

3. gross

4. elevated in serum?

5. chemotherapy response?

1. immature cells 

a. glandular/papillary morphology

2. Painful testicular mass (vs. seminoma)

3. Heterogenous mass w/ necrosis and hemorrhage 

4. 

pure = b-hCG

mixed: b-HCG + AFP 

5.  Chemo-Irony*

a. possible of turning it into a teratoma!

b-hCG has similar composition with? 

clinical importance?

diseases?

b-hCG similar to FSH/LH and TSH

Paraneoplastic symptoms

1. FSH/LH -> Gynecomastia

2. TSH -> Hyperthyroidism

Disease

1. choriocarcinoma (b-HCG)

Teratoma prognosis: 

females?

males?

F: benign

M: Malignant

PSA levels

1. normal?

2. BPH

3. Prostatic Adenocarcinoma

a. 0-4

b. 4-10

c. >10

1.  Decreased Free PSA (Cancer only makes bound-PSA)

Prostatic Adenocarcinoma

1. neoplasm

2. location

3. presentation

4. labs

5. Grading system

6. Metastasis

1. Prostatic Glands

2. Peripheral, Posterior Prostate

3. Silent (d/t location)

LABS:

PSA > 10 

% Free PSA: decreased (cancer only makes bound PSA)

biopsy: Nuclei w/ dark nucleoli

5. Gleason Grading (Tissue Architecture)

6. Lumbar Spine (+ low back pain)

*Sclerosis of Bone 

*increased Alk Phosph

Explain the connection between Anorexia Nervosa and Amennorhea 

if left untreated?

Amenorrhea due to loss of pulsatile GnRH from Hypothalamus

a. occurs when body fat drops below critical level

b. results in low FSH/LH, and thus, low estrogen

If untreated: lead to osteoporosis

Posterior Pituitary

a. contain?

b. original synthesis location

Neurohypophysis (neuroectoderm origin)

a. ADH

b. Oxytocin

Hypothalamus

a. ADH: Supraptic Nuclei

b. Oxytocin: Paraventricular

*travel to Post. pituitary via neurophysins

POMC

1. cleaved into?

2. this explains

polypeptide precusor that is enzymatically cleaved into

1. ACTH

2. MSH 

3. B-endorphin

2. explains hyperpigmentation that occurs with certain diseases

*Melasma (mask of pregnancy)

a. Estogen stimulates increase in MSH-> hyperpigmented

*Addisons

a. low cortisol stimulates high ACTH -> hypermigmented bc MSH also produced

Enzyme Deficiency

17a-hydroxylase

21- Hydroxylase

11b-hydroxylase

labs:

high?

low?

presentation?

17a-Hydroxylase

lab:

 low: cortisol + androgens

high: Mineralcorticoids & Corticosterone

Presentation

*All Phenotypic Females

*Salt retention, HTN

21 Hydroxylase

Lab:

low: Cortisol + Aldosterone

high: Testosterone + 17-OH-progesterone

Presentation

*Girls = Ambiguus genitalia

*Salt Wasting (Hypotension)

11B-hydroxylase

lab

low: Cortisol + aldosterone

high: 11-deoxycortisone & 11-deoxycortisol + Testosterone

Presentation

*Girls = Ambiggus Genitalia

*HTN & Salt Retention

Fetal Lung Maturation 

1. maturation

2. marker?

3. admin to quicken maturation?

1. Cortisol (Fetal & maternal)

2.  Lecithin: Sphingomyelin ratio

a. mature > 1.9

3. Corticosteroids

Synthesis location

1. PTH

2. Calcitonin

1. Chief (principle) cells of parathyroid

2. Parafollicular cells (c cells) of thyroid

Polyuria & Polydispia 

1. what 3 disease possibilities?

2. differentiate

Possibilities

1. D. mellitus

2. D. Insipidus

3. psychogenic Polydipsia

Differentiate

1. High Blood Glucose

2. Serum Na > 142 (due to water loss)

a. water deprivation doesn't increase urine osm

.

3.  Serum Na < 137

a. water deprivation increases urine osm. 

Primary Hyperparathyroidism

1. due to?

2. cardinal features

3. chart location

4. lab?

Parathyroid Adenoma

Cardinal Features:

1. Bone Loss:

*subperiosteal thinning & cystic degeneration

2. Renal Stones

3. Gi Upset (ulcerS)

4. Psychiatric disorders 

"Bones, stones, groans, and psychic moans"

*Chart = Top Right*

Lab

1. Low P (vs. secondary)

2. high Urine cAMP (PTH 2nd signal mech)

3. high Alkaline phosphatase

Secondary Hyperparathyroidism

1. due to?

2. chart location?

High PTH due to renal failure

a. can't excrete P, which binds Ca in plasma and reduces active level

lab:

1. high P (Vs. primary)

2. Low Ca (bound by P)

3. high Alk P

Chart: Top Left

Pancreatic Endocrine tumors

1. VIPoma

2. Gastrinoma

3. Glucagonoma

4. Somatostatinoma

VIPoma (Pancreatic Cholera)

a. Diarrhea with excess Cl loss in stool

b. achlorhydria (vip inhibits gastin)

Tx: Octreotide (somatostain)

Gastrinoma

a. Multiple Ulcers (Jejunum ulcers are highly indicitive)

b. ZE syndrome

Tx: PPIs (Omeprazole)

Glucagonoma (Alpha)

a. Secondary DM & Migratory erythema of skin

Somatostatinoma (Delta)

a. reduced GB contractility (CCK): stone formation

b. steatorrhea

c. Aclorhydria

SRY on Y chromosome induce Testis-Determining Factor (TDF) 

TDF is responsible for gonadal differentiation into Testes containing Sertoli & Leydig

Sertoli: MIF

a. involutes paramesonephric duct (prevent female characteristics)

Leydig: Testosterone transfers Wolfian duct into:

1. Seminferous Tubules

2. Epididymus

3. Ejaculatory duct

4. Ductus Deferens

DHT: Genetic Tubercle & urogenital sinus into:

1. External Genitalia & Prostate

Kallman Syndrome

1. due to

2. features

Absent GnRH secretory neurons in Hypothalamus

due to: defective migration of olfactory placode

features

1. Hypogonadism

2. Anosmia

3. Delayed Puberty

Klinefelter Syndrome

1. Karyotype

2. due to

3. onset of symtpoms

4. lab serum levels

47 XXY

due to: Meiotic Nondysjunction

3. Symptoms Arise At pubery

Features:

1. Tall stature

2. Small Firm Testes

3. Azospermia

4. Gynecomastia

LAB:

increased: FSH/LH

decreased: Testosterone, Sperm Count