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Cheatography

Repro/Endocrine Review Cheat Sheet (DRAFT) by

USMLE- Uworld Review

This is a draft cheat sheet. It is a work in progress and is not finished yet.

Cushings Disease

Decreased ACTH
Exogenous glucoc­ort­icoids
 
Adrenal Tumor
Increased ACTH
High dose dexame­thasone
Increased ACTH
Ectopic ACTH suppre­ssion
 
High dose dexame­thasone
Decreased ACTH
Cushings Diseas­e(P­itu­itary Adenoma)
 
CRH Stimul­ation
Increase ACTH/C­ortisol
Cushings Diseas­e(P­itu­itary Adenoma)
 
CRH Stimul­ation
No change ACTH/C­ort­isol*
Ectopic ACTH secretion.
*Dexam­eth­asone should suppress ACTH and cortisol- if it doesn't then ectopic cause
**CRH should increase ACTH- if it doesn't then ACTH is being secreted from ectopic cause

Congenital Adrenal Hyperp­lasia

Deficiency
Build-up
BP
Sex Hormones
Presen­tation
17a-hy­dro­xylase
Minera­loc­ort­icoids (Aldos­terone)
Increased
Decreased
XY: Atypical Genitalia, undesc­ended testes
       
XX: no secondary sexual charac­ter­istics
21-hyd­rox­ylase
Proges­terone
Decreased
Increased
XY: salt wasting or precocious puberty
 
17-hyd­rox­ypr­oge­sterone
   
XX: virili­zation
11B-hy­dro­xylase
11-deo­xys­terone
Increased (because 11-deo­xyc­ort­ico­sterone has weak minera­loc­ort­icoid proper­ties)
Increased
XY: severe HTN or precocious puberty
 
11-deo­xyc­ortisol
   
XX: virili­zation
3B-hyd­rox­yst­eroid dehydr­ogenase
Pregne­nolone
Decreased
Decreased
XY:adrenal insuff­ici­ency, ambiguous genitalia
 
17-hyd­rox­ypr­egn­enolone
   
XX:adrenal insuff­ici­ency, ambiguous genitalia
 
DHEA

Heavy Menses

Adenom­yosis
Endome­triosis
Leiomyoma (Fibroids)
Endome­trial Hyperp­lasia
Endome­trial Cancer

Male Genitalia

DHT
External Male Genitalia+ Prostate
Testos­terone
Internal Male Genita­lia­(SEED= Seminal Vesicles, Epidid­ymis, Ejacul­atory Duct, Ductus Deferens)
*if female internal genitalia is present in a male then think Anti Mullerian Hormone deficiency
Estrogen
Breast develo­pment
Aromatase
Converts testos­ter­one­--> estrogen

Vaginitis

If there is vaginal inflam­mation
Think Tricho­mon­iasis or Candida vaginitis
Bacterial vaginosis
fishy odor, clue cells(­squ­amous epithelial cells), (+) whiff test
Due to antibiotic use
Treat with metron­idazole
Trichm­oniasis
frothy, yellow­-green discharge, motile tricho­monads,
Due to hx of STIs
Treat with metron­idazole
Candida
cottage cheese, pseudo­hyphae
Due to OCP use, antibi­otics, immuno­sup­pre­ssion, diabetes
Treat with flucon­azole

Ovarian Tumor

Struma Ovarii
Germ cell tumor
 
Associated with thyrot­oxi­cosis (since it can secrete thyroid hormone)
 
Gross: Oily cystic mass
 
Micros­copic: thyroid follicles filled with colloid and surrounded by ovarian storm

Ducts

Parame­son­ephric
form internal female genitalia (fallopian tubes, uterus, upper vagina, cervix)
Mesone­phric
In females= degenerate to form Gartner duct
 
In males= epidid­ymis, seminal vesicles, ductus deferens, ejacul­atory ducts

Genital Ulcers

Painful
Painless
Chancroid (H.Duc­reyi)
Chlamydia
HSV
Syphilis

Staging/ Gleason Score

High Gleason score
poorly differ­ent­iated
Higher Staging
metastasis

Lymph Nodes

Para-A­ortic
Ovaries/ Testes
Superf­icial Inguinal
Scrotum
Deep Inguinal
Glans Penis

Anorexia and Amenorrhea

Due to hypoth­alamic suppre­ssion of GnRH

Hypert­ension in Pregnancy

Think Pre-Ec­lam­psia/ Eclampsia
New-onset HTN
 
Protei­nuria
 
End-organ dysfun­ction
 
(+ seizures in eclampsia)

Vaginal Bleeding during Pregnancy

Placenta Accreta (Painful)
Due to absence of endome­trial decide basalts
 
Or previous uterine scarring (prior C-section)
Molar Pregnancy (Painful)
 
Partial Mole- has fetal tissue
 
Complete Mole- NO fetal tissue
Ectopic Pregnancy (Mild Pain)
Abruptio Placentae (Painful)
Placenta Previa (Painless bleeding)

Cervicitis (PID)

Neisseria Gonorr­hoeae
Chlamydia Tracho­matis
*if antibiotic coverage remains incomplete then can lead to infert­ility

Combin­ation Therapy

Buserelin and Bicalu­tamide
Buserelin- continuous stimul­ation of pituitary gland to down-r­egulate GnRH--> decrease LH-->d­ecrease testos­terone
 
Bicalu­tamide- helps prevent the initial testos­terone surge effect from the buserelin admini­str­ation
Leuprolide and Flutamide
Leupro­lid­e-long acting GnRH antago­nist- causes a transient increase in LH-->t­est­ost­erone levels
 
Flutam­ide­-co­mpe­titive testos­terone receptor blocke­r-c­oun­teracts the initial surge of testos­terone

Drugs for pregnancy termin­ation

Mifepr­istone
-partial proges­terone agonis­t--­>causes placental separation and uterine contra­ction
Misopr­ostol
E1 agonis­t--> stimulates uterine contra­ctions
Methot­rexate
Folic acid antago­nis­t--­>de­stroys prolif­erating fetal cells

Mullein Agencies vs Androgen Insens­itivity

Mullein Genesis
Stage 4: breast; Stage 4: pubic hair
AIS
Stage 4: breast; Stage 2: pubic hair

Phases of Meiosis

Female
Prophase I until ovulation
 
Metaphase 2 until fertil­ization

Postme­nop­ausal bleeding

Think Endome­trial Hyperp­lasia or Cancer

Testicular Torsion

Has absent cremas­teric reflex

Physio­logic Changes in Pregnancy

Increase CO
Increase Plasma Volume
Decrease SVR
Increase Response Tidal Volume
Decrease FRC
Increase GFR
Chronic hypove­nti­lation (-->re­spi­ratory alkalosis)

Congenital Rubella

I heart ruby earrings:
I("e­ye")­--> cataracts
Heart-­->PDA
Ruby--> Rubella (envel­oped, single­-st­randed, positi­ve-­sense RNA virus)
Earrin­gs-­-> sensor­ineural hearing loss
 

Hypogl­ycemic Episodes

More common with Sulfon­ylureas:
Inhibits K+ channel to allow for Ca2+ influx

SGLT-2 Inhibitors (-glif­ozin)

decrease renal absorption of glucose and sodium

Insulin (Endog­enous vs Exogenous)

Endogenous
insulin+C-peptide
endope­pti­dases in secretory granules cleave proinsulin into insulin and C-peptide
   
Sulfon­ylureas and Meglit­inides are the only ones that stimulate endogenous insulin production
   
Insulin producing tumors
Exogenous
insulin only

Congenital Hypoth­yro­idism

high TSH; low T4
Initially asympt­omatic because of the presence of material thyroxine
 
Need levoth­yroxine treatment otherwise can lead to neuroc­ogn­itive dysfun­ction

SIADH

Think Euvolemic Hypona­tremia

Neonatal Hypogl­ycemia

Mother had gestat­ional diabet­es-­-> hyperg­lycemia in mother­-->­hyp­erg­lycemia in baby-> so baby was producing high levels of insulin to counteract high glucos­e--> pancreatic B cell hyperp­lasia since it is working extra-­-> once born then not receiving high levels of glucose from mother but still producing a lot of insuli­n=n­eonatal hypogl­ycemia

MEN Syndromes

MEN 1
Pituitary (Usually a Prolac­tinoma)
 
Pancreas (Usually Zollinger Ellison syndrome)
 
Parath­yroid
 
Men 2A
Parath­yroid
 
Medullary thyroid carcinoma
 
Pheoch­rom­ocytoma
 
MEN 2B
Medullary thyroid carcinoma
 
Pheoch­rom­ocytoma
 
Oral Gangli­one­uromas

SIADH

Think Euvolemic Hypona­tremia

TBG Deficiency

low total T4, normal free T4, normal TSH

Adrenal Gland Secretions

Adrenal Cortex
Zona Glomer­ulosa
Aldost­erone
 
Zona Fasiculata
Cortisol
 
Zona Reticu­laris
Sex Hormones
Adrenal Medulla
 
Catech­ola­mines

Ketone Bodies

Can't be utilize by RBCs since they lack mitoch­ondria

Sympto­matic Relief of Thyrot­oxi­cosis

B-blockers

Diabetes

Type 1
Due to autoimmune response against beta cells-­-> loss of insulin production
 
More suscep­tible to DKA
 
Younger patients
Type 2
Due to insulin resistance
 
Older patients
 
Pancreatic islet amyloid deposition

Antihy­per­lip­idemic drugs

Statins
Primarily lowers choles­terol
Ezetimibe
Lowers choles­terol and LDL
Fibrates
Lowers trigly­cerides
Niacin
Lowers trigly­ceride and LDL, Increases HDL
Bile acid resins
Lowers LDL

Glucose Transp­orters

GLUT-4
Insulin Depend­ent­--> expression increases with insulin concen­tration
 
Muscle cells, Adipocytes
GLUT 1,2,3,5
Insuli­n-I­nde­pen­den­t--> does NOT increase with insulin concen­tration
 
Brain, Kidney, Intestine, RBCs, Liver

Bone Formation/ Loss

PTH--> osteob­las­t--­>Bone formation
PTH-->­RAN­K(o­ste­obl­ast­s)+­RAN­K-L­/NFkB-L (osteo­cla­sts­)--­>net bone loss
OPG-bind compet­itively to RANK-L to prevent bone loss

Insulin Drugs

Long-a­cting (Glargine, detemir, degludec)
mimic regular insulin
Short-­acting (Lispro, aspart, glulisine)
mimics postpr­andial insulin

Permissive Effect of Cortisol on Ne/Epi

Cortisol indirectly acts Ne/Epi receptors to upregulate them--> this then makes them available for the the catech­ola­mines to bind to them
 

Turner syndrome (45, XO)

Widely spaced nipples
Ovarian dysgenesis (streak ovaries)
Horseshoe kidney
Short
Webbed neck
Coarct­ation of aorta
Aortic Dissection
Bicuspid Aortic valve
Cystic Hygroma in neck

Klinef­elter (47, XXY)

Decreased inhibin levels
Learning disabi­lities
Gyneco­mastia
Small, firm testes
Tall

Edwards syndrome

Hypertonia
Clenched fists
Rocker bottom feet

Down syndrome

Upslanting palpebral fissures
Epicanthal folds
Single palmer crease

Drugs and common AE

Levoth­yroxine
Atrial fibril­lation
PTU, methim­azole
Agranu­loc­ytosis (Nuetr­openia)
 
PTU- Hepato­toxic (But preferred drug in last two trimes­ters)
 
Methim­azo­le-­Ter­ato­genic in FIRST trimester
Sulfon­yureas
Hypogl­ycemia
HIV HAART therapy
Lipody­strophy
B-Blockers
Mask Hypogl­ycemic episodes
Estrogen
ischemic stoke (therefore don't give in migraines since they already have an increased baseline for an ischemic stroke)
Metformin
Lactic acidosis (CI in renal insuff­ici­ency)
Tamoxifen
Gyneco­mastia
Glucoc­ort­icoids
Osteop­orosis
GLP-1 agonists (exena­tid­e/l­ira­glu­tide)
Weight loss
Trazadone
Priapism
Bile acid resins (Chole­sty­ramine, Choles­tipol, Colese­velam)
Hypert­rig­lce­ridemia

Intrac­ellular Pathways

Pathway
Hormones
Bind activated receptors to DNA to modify transc­ription
Steroid and thyroid hormones
Adenylyl cyclase converts ATP to cyclic amp--> activates protein kinase A
PTH, ACTH, TSH, ADH(V2), glucagon
Bind G protein coupled receptor that activate PLC
GnRH, TRH, Ang II, AHDH(V1)
PLC activates PIP3--> DAG+IP3 to then activate PKC
GnRH, TRH, Ang II, AHDH(V1)
JAK-STAT Pathway
GH

Familial Hyperl­ipo­pro­tei­nemia (Type 1)

deficiency of LPL or Apo C-2:
Hypert­rig­lyc­eri­demia
 
recurrent acute pancre­atitis
 
milky appearing retinal vascul­ature (lipemia retinals)
 
yellow populates on extensor surfaces (eruptive xanthomas)

Keep-i­t-S­imple Concepts

PTH
increase Ca+ (Primary regulator of PTH-if low then PTH increases to increase Ca2+ levels)
 
decrease PO4-
 
increase Vitamin D (by upregu­lating 1-a-hy­dro­xylase)
Ca2+
Calcitonin
counte­racts Ca2+
Insulin
decreases glucose (blood­str­eam­--> adipose tissue­/sk­eletal muscle)
 
counte­racts glucagon
Glucagon
increases glucose (adipose tissue­/sk­eletal muscle­-->­blo­ods­tream)
Vitamin D
increase Ca+
 
increase PO4-
Leydig cells
LH-->s­ecrete testos­terone
Sertoli cells
FSH-->­spe­rma­tog­enesis and increase inhibin
 
increases glucose by glycog­eno­lysis and glucon­eog­enesis in the liver

Neiman­n-Pick vs Tay-Sachs

Neiman­n-Pick
Hepato­meg­aly­/Sp­len­omegaly
Tay-Sachs
NO hepato­meg­aly­/sp­len­omegaly