1st test endocrine

Question 1

Wolfram Syndrome

Answer 1

rare
progressive
degenerative 
transmited AR
DNA

central diabtes insipidus
DM
optic atrophy - blindness
neurosensorila deafness
neuro/psch alterations

Question 2

neurohipofisis

Answer 2

post pituitary
connected to hypothalamus via axons
secretes vasopressin and oxytocin

Question 3

Nephrogenic Diabetes Insipidis

Answer 3

ADH is okay but its afunctional

rec is messed up

poor response of renal tube cells

Question 4

classification in NDI

Answer 4

primary
familiar congenital (AD X linked)

Question 5

secondary NDI

Answer 5

tubulointersticial nephroamties
polycystic kidney, distal tubular acidosis, cistinosis, idiopathic hypercalciuria, renal amyloidosis
secondary tubularintersiticail nefropathy

litio
demeclocicline

Question 6

DIC

Answer 6

altered conservation of body water as a consequence of inadequate ADH
large V of water eliminated in urine

poliruia
compensatory [plidipsia

Question 7

psycogenic polydipsia or primary polidipsi

Answer 7

increased ingestion of water more than necessary –> physiological suppression of ADH due to over hydration and hypotony –> polyuria (sudden 10-12L), nicturia, polydipsia

hipoosmotic polyuria

hypovolemia and hypotension

hypertonic dehydration

astenia with sleep disorder

hipernatremia

Question 8

PP seen in

Answer 8

young women
psychiatric px
fenotiazide (dry mouth) takers
hypothalamic lesions alteraing thirst center

Question 9

normal urine

Answer 9

50cc/hr

Question 10

cause of primary DIC

Answer 10

immunolocial

Question 11

secondary cause of DIC

Answer 11

tumor
qx
trauma
IC tumor = 3rd cause
craneofaringeoma in kids
lung breast CA metastasis in adults
supraselar germinomas
intraselar GI tumors via metastasis
toxoplasmosis, herpes simplex, AIDS, 
qx
truma
Lawrence Moon Biedel Synrome

linfocitic hipofifis (infiltariotn)??

Question 12

phases of DIC from head trauma

Answer 12

polyuria 4-5 days
secondary to transsphenoidal qx

2-3d after qx -> polyuria
this alters ADH liberation

oliguria 4-5d
(cell degeneration with liberation of preformed hormone into circulation)

polyuria and polydipsia (compensatory)
neurosecretory cell death causes Permanent ADH deficit

Question 13

cx of Lawrence Moon Biedel syndrome

Answer 13

obesity, mental deficit, pigmental rhinitis…

Question 14

dx DI

Answer 14

<1010 urine density
urine and serum electrolytes (one high one low)

hypernatremia

plasma osmolarity > 350 mOsm/L

urine osmolarity (lower)

prueba de depuracion aquosa - remove all diuretics, solutions, ingestion - (doesn’t have - oliguria - anuria) if they do will have polydipsia from IC liquid –> coma (2-4hr)

Question 15

what is endocrinology

Answer 15

• Branch of internal medicine that studies regulatory functions of hormones

Question 16

anatomy of hypothalamus

Answer 16

• Weight = 4gr

- 0.3-04cm

Question 17

tx DI

Answer 17

desmopresin - agonist of ADH uniting with V2 rec of acuoporin –> tubular water reabsorption
VO/SC/Spray
1-2mg every 6hr, px responds within days
something about falcemics?

hydration

clorpropamid - increases ADH action - psychiatric use

carbamacepine - increases ADH liberation (high doses) > 1200mg/day

Question 18

irrigation of hypothalamus?

Answer 18

?

- Primary capillary plexus Hypophysary arteries ant branches

Question 19

limits of hypothalamus

Answer 19

• optic chiasm (ant)
  
  • thalamus/3rd ventricle (sup)
  • mamillary bodies (post),
  • infundibulo tallo-hipofisario (int)

Question 20

ADH is also produced where

Answer 20

adenohipofisis

periventricular nucleus

Question 21

SSIADH

Answer 21

excessive persistend ADH secretion , not responding to inhibition -

retain water
low plasma osmolarity - dilution, high urine osmolality

edematized
oliguria

water retained

hyponatremia
nypoosmolarity

Question 22

2 connections of hypothalamus hypofisis

Answer 22

1. Sistema porta hipotalámico-hipofisario.
   
   • Originates in eminencia media.
   • retrógrado & anterógrado flow
   • parvocelulare hypothalamic neurons (parvo = small [short axón -magnocelulares]) secrete hormones that reach AP
2. Neuronas hipotalámicas magnocelulares send axons to NP.

    ○ Porta-hipotalamo-hipofisario = anterior (circulatory)
        • Eminencia media is where portal system is formed
    ○ Neuronas neurohipofisarias magnocelularesPosterior from hypothalamic neuronal axonal connection

Question 23

MC of SSIADH

Answer 23

change personality irritable confusion hallucinate nausea vomit, extrapyrimadial signs
convulsion crisis, altered consciousness

Question 24

DX criteria of SIADH

Answer 24

TABLE… fundamental

complentary
uricemia < 4mg/dL
BUN < 10mg/dL
FENa > 1%

Question 25

functions of hypothalamus can be

Answer 25

endocrine or non endocrine

Question 26

tx of SIADH

Answer 26

``` hydration - hypertonic saline ADH blockers (carbonate litium) loop diuretic ``` vaptan (conivaptan, tolvaptan, relcovaptan)

Question 27

endocrine function of hypothalamus

Answer 27

``` 1. parvocelular neurons secrete liberating facors or inhibitory that act at AP. Magnocelular neurons (supraóptico & paraventricular nuclei) send axons to NP, store these products ```

Question 28

ADH does what

Answer 28

retains water reabsorbs Na+ secretes K+

Question 29

no endocrine function of hypothalmsu

Answer 29

Based in nuclei that regulate sleep, thirst, T, appetite, libido, weight.

Question 30

hyperprolactinemia

Answer 30

incrased prolactin plasma levels > 20ng/mL in men too much produced or liberated and systemic effects >25ng/mL in wommen 2 separate occations amenorrea,/oligomenorrea galactrea produced in lactotrope cells

Question 31

What is hypothalamus?

Answer 31

- The hypothalamus controls the anterior and posterior pituitary's release of hormones differently.  

Question 32

substances that stimulate prolactine/etiology of hiperprolactinemia

Answer 32

``` TRH striadol GnRH AVP oxytocin Serotonin AcH glutamate ``` ``` physiological : stimulation of pezon sex sleep ovulation pregnancy neonatal life ovulation lactancy ingesting AAs exercise emotional stress and physical Trauma qx Hipoglucemia IAM Convulsiones del lóbulo temporal Síncope Venopunción Deshidratación Dolor ``` DRUGS

Question 33

sub that inhibit prolactin

Answer 33

``` dopamine opoid GABA GAP somatostanina, ......... ```

Question 34

first cuase of non tumoral hipoerprolactinemia from drugs EXAM

Answer 34

cause 25-100ng/dl metoclopramida, risperidona, fenotiazina à >200ng/mL) if MC change tx - stop for 3 days , reread levels to see if secondary to drug Si la medicación no puede ser descontinuada y el inicio de la hiperprolactinemia no coincide con el inicio de la terapia, se recomienda MRI de hipófisis en busca de prolactinoma.

Question 35

increased prolactin due to hypothalamic damage

Answer 35

``` tumors granulomatouse and infiltrative diseases cranial RT vascular cause seccion of tallo ``` also alterations of hypofisis

Question 36

hyperprolactinemia from hypothyroidism

Answer 36

due to increased TRH --> secrete effect on lactotrope cells (more sensibile) decrease sensibility of lactrotoope cells to dopamine increased VIP decrease in PRL wasting in circulation o aclaramiento renal (hipometabolic state lowers GFR) - more in plasma hypofisiary hyperplasia (like puberty )

Question 37

most cells in pituitary are...?

Answer 37

????

Question 38

polyscystic ovary syndrome - PRL

Answer 38

hyperandrogen and estrogen --> lots of estradiol which stimulates prolactin liberation increase number and size of lactotropes decrease of dopamine hypothalamus increased transcriptionfor PRL resistence to dopamine acction

Question 39

adrenal deisease PRL

Answer 39

increased transcription increased lactotrophe cell differentiation PRL increased secretion

Question 40

liver disease PRL

Answer 40

cirrhosis decreased hepatic circulation of PRL increases steroidogenesis - more estrogen/estradiol decreased hypothalamic dopamine (dad)

Question 41

Renal disease PRL

Answer 41

rests action nof dopamine | resists.....PRL

Question 42

isiopathic hyperprolactimea

Answer 42

microprolactinomas? 20% of cases MRI cortes ateration /inactivation of dopamine rec

Question 43

lesions of thorax wall PRL

Answer 43

``` toractomy masectom trauma mammoplasty dermatitis burns herpes zoster breast cyst nipple piercing ``` any stimulation of 4,5,6 intercostal nerve increases neuronal afferent stimulation postsynaptic increased serotonin liberation with stimulates TRH --> PRL increase

Question 44

ectopic production of PRL

Answer 44

``` hypernefroma renal adenoCA bronchogenic CA uterine fibroma ovaric teratioma gonadotroma ovaric dermoid cyst Hodgkin linfoma and T cell linfoma ``` macroprolactinoma and med form before??

Question 45

MC of hiper PRL

Answer 45

increases hypothalamus of dopamine and beta-endorphins rec of PRL in GnRH cells down regulation of GnRH (hypogonadism, galactorrea, hirsutism) decreasd ovarian secretion of estradiol and progesterone (no LH, FSH for steroidogenesis at ovary_ decreased testosterone decreased 5alfa-reductase (converts dihydro..to testosterone) 1. Galactorrea: 80% hiperprolactinémicas, 30% hiperprolactinémicos. 2. Hipogonadismo hipogonadotrópico. Hay ↓FSH, ↓LH, debido a que: a. Neuronas de GnRH tienen receptores para PRLà ↓liberación de GnRH. b. ↑PRL à ↑DA + ↑β-endorfinas en hipotálamo à ↓liberación de GnRH. ``` women Hipoestrogenismo à ¾ Amenorrea / oligomenorrea. ¾ ↓libido. ¾ ↓lubricación vaginal à Dispareunia ¾ Osteopenia/osteoporosis: ↓densidad ósea (-25% lumbar), irreversible ¾ Irritabilidad ¾ Oleadas de calor. Infertilidad. ``` ``` men Hipoandrogenismo: PRL à ↓actividad 5α-reductasa à ↓dihidrotestosterona. ¾ Disfunción eréctil. ¾ ↓libido. ¾ Oligospermia à infertilidad. ¾ ↓volumen eyaculado. ¾ Ginecomastia. ¾ Osteopenia/osteoporosis. ``` la mujer. ¾ PRL à ↑producción ovárica de andrógenos y adrenal de DHEA-S (sulfato de dehidroepiandrosterona). ¾ PRL à ↓síntesis hepática de SHBG à ↑proporción de esteroides sexuales libres (biológicamente activos) en plasma.   Presentación clínica 2. Prolactinemia >200ng/mL. 3. Clínica: galactorrea, hipogonadismo hipogonadotrópico, hirsutismo, efecto de masa (neuroftálmicos, hipopituitarismo).

Question 46

sampling in hiperPRL

Answer 46

2 separate occasions 1-2 hour after waking up discart other causes (meds, liver, preg, renal failure, mammillary stimulation, sex) macroprolactinemia in asymptomatic px (no galactorrea but elevated levels - sim hormones?) drugs 1:100 dilution

Question 47

dx evaluation of hiperprolactimea

Answer 47

hipofisary macroadeoma measure PRL below 200 1:100 dilution - discart hook effect if above ya tu sabe if below 200 - pseudoprolactinoma (something else compressing, dopamine e obstructed) more than 200 - macroprolatinoma1) Tomar muestra adecuadamente: ¾ 2 muestras separadas por 20-40 minutos >1h después de haber despertado, sin tener sexo (coito, manipulación de mamas) o ejercicio. ¾ Diluir muestra 1:100 para evitar efecto hook. ¾ Excluir mediante historia clínica y examen físico: embarazo, uso de fármacos; mediante laboratorio: hipertiroidismo (T4 libre, TSH), IR (creatininemia), IH (transaminasas y fosfatasa alcalina). Si nada de lo anterior es evidente o prolactinemia >100ng/mL: 2) MRI de hipófisis antes y después de administrar gadolinio. ¾ Si se confirma adenoma hipofisario à û Evaluar función hipofisaria û Campimetría visual computarizada (en particular si es un macroadenoma). ¾ Si no se confirma adenoma hipofisario à hiperprolactinemia idiopática.  

Question 48

tx of hiperprolactinmeia

Answer 48

dopamine agonsits Tx de elección. Se unen a D2 en superficie de lactotropas normales y tumorales y producen inhibición de PRL, como lo haría la DA, restauran función gonadal y causan regresión tumoral en 80-90%. Se deben usar de por vida. a) Bromocriptina. Aprobada por FDA. b) Cabergolina. Aprobada por FDA. La más potente y se da 1-2x/semana. c) Quinagolida. d) Lisurida. e) Pergolida. qx - if px wont take drugs, 1. Tumorectomía transesfenoidal, indicada en: ¾ Intolerancia/resistencia a los agonistas de DA. ¾ No deseo de consumir agonistas DA por largo tiempo. ¾ Crecimiento de prolactinoma a pesar del uso de estos. ¾ Deseo de embarazo por parte de la paciente (aunque la mayoría no crece durante el embarazo: indicación relativa). ¾ Prolactinomas con componente quístico. ¾ Preferencia del paciente. ¾ No mejoría de los campos visuales tras 1-3 meses de agonistas DA 1. Agonistas de DA. Tx de elección. Se unen a D2 en superficie de lactotropas normales y tumorales y producen inhibición de PRL, como lo haría la DA, restauran función gonadal y causan regresión tumoral en 80-90%. Se deben usar de por vida. a) Bromocriptina. Aprobada por FDA. b) Cabergolina. Aprobada por FDA. La más potente y se da 1-2x/semana. c) Quinagolida. d) Lisurida. e) Pergolida. Tumorectomía transesfenoidal, 2. Radioterapia hipofisaria. Fallo en tx médico y quirúrgico. 150-200 rads/día, 5x/semana por 5 semanas. Dosis total: 4,500-5,000rads. Alta probabilidad de desarrollar hipopituitarismo.  

Question 49

tx if drugs and qx don't work for hiperPRL

Answer 49

2. Radioterapia hipofisaria. Fallo en tx médico y quirúrgico. 150-200 rads/día, 5x/semana por 5 semanas. Dosis total: 4,500-5,000rads. Alta probabilidad de desarrollar hipopituitarismo.

Question 50

2 types of hypothalamic cells

Answer 50

hypofisiotropic hypothalamic (liberators and inhibitors) vs neurohipofisiary hypothalamic (oxytosin and AVP/ADH)

Question 51

liberators do what?

Answer 51

induce hormonal secretion

Question 52

hypothalamic liberating hormones

Answer 52

TRH --> TSH and prolactin CRH --> ACTH/corticotropin secretion @ suprarenal gland and proopiomelanocortin peptides (MSH, beta-endorphin) GnRH --> LH and FSH (gonadotropins) @ genitals and Prolactin GHRH/somatocrinin --> GH/somatotropin in pulses @ all organs

Question 53

GH secretion is increased by

Answer 53

exercise starvation (hypoglycemia) Sleep

Question 54

relationship between dopamine prolactin and TRH

Answer 54

Prolactin is under tonal dopamine inhibition, and excess TRH levels suppress dopamine.  Thus, prolactin levels will increase as dopamine decreases.  

Question 55

hypothalamic nucleus/region for TRH

Answer 55

paraventricular (medial portion)

Question 56

hypothalamic nucleus/region for CRH

Answer 56

paraventricular (anterior portion)

Question 57

hypothalamic nucleus/region for GnRH

Answer 57

arcuate-preoptic (ant)

Question 58

hypothalamic nucleus/region for GHRH

Answer 58

arcuate

Question 59

Hypopfisis cell populations that produce for TSH

Answer 59

tirotrope cells

Question 60

Hypopfisis cell populations that produce | Prolactin

Answer 60

lactotrope cells

Question 61

Hypopfisis cell populations that produce | ACTH

Answer 61

corticotrope cells

Question 62

Hypopfisis cell populations that produce | FSH and LH

Answer 62

gonadotrope cells

Question 63

Hypopfisis cell populations that produce | GH

Answer 63

somatotrope cells

Question 64

melanocyte inhibiting factor inhibits

Answer 64

release of MSH

Question 65

which are the hypothalamic inhibiting hormones

Answer 65

dopamine (DA) - prolactin release inhibiting hormone - inhibits liberation of Prolactin and lactropes and TSH somatostatin (SS) - inhibits liberation of PRL, TSH, GH

Question 66

region/hypothalamic nucleus for dopamine

Answer 66

arcuate

Question 67

region/hypothalamic nucleus for somatostatine

Answer 67

supraquiasmatic periventricular region (ant)

Question 68

lactancy hormone that stimulates milk ejection

Answer 68

oxytocin

Question 69

what do AVP/ADH do

Answer 69

stimulate reabsorption of water

Question 70

non endocrine functions of the hypothalamus

Answer 70

○ Thirst, temperature, sexual desire, etc thorugh hypothalamic nuclei

Question 71

anterior pituitary hormones are produced by what

Answer 71

parvocellular hypothalamic neurons

Question 72

anterior pituitary hormones

Answer 72

``` ACTH LH, FSH GH TSH Prolactin MSH ```

Question 73

weight of pituitary gland

Answer 73

0.5-0.9gr

Question 74

blood flow of pituitary gland

Answer 74

very vascularized | 0.8ml/gr/min

Question 75

Situations in which Pituitary can double size:

Answer 75

- Pregnancy - Puberty (especially girls) - Primary hypothyroidism - Primary hypogonadism

Question 76

% gland of adeno vs neurohipofisis

Answer 76

75% adeno 25% neuro

Question 77

embryological origin of adenohipofifis

Answer 77

Bolsa de Rathke (evaginación del techo de la orofaringe primitiva).

Question 78

embryological origin of neurohipofisis

Answer 78

Evaginación del hipotálamo ventral y del piso del 3° ventrículo

Question 79

irrigation of adenohipofisis

Answer 79

Arteria hipofisaria superior + sistema porta hipotalámico (0.8ml de sangre/g de tejido)

Question 80

irrigation of neurohipofisis

Answer 80

Arteria hipofisaria media + Arteria hipofisaria inferior

Question 81

Venous drainage of pituitary glland

Answer 81

cavernous senos --> sup and inf petrous senos --> yugular veins --> SVC --> RA

Question 82

pituitary cell types

Answer 82

* Nulas - don’t secrete hormones, do secrete NTs | * Secretory - classified in 5 types

Question 83

cx of somatotropic cells

Answer 83

@ lateral portions acidofiles 50%

Question 84

function of somatotropic cells in skeletal muscle

Answer 84

increases muscle mass increases AA capitation decreases proteolysis decreases glucose capitation (CONTRAREGULATOR) --> hyperglucemiant

Question 85

function of somatotropic cells in adipose tissue

Answer 85

``` decrease capitation of glucose increase lipolysis (degradation of TGs/FAs) -increases activity of hormonosensible/GH lipase ```

Question 86

function of somatotrpic cells in liver

Answer 86

increase protein synthesis increases gluconeogenesis (formation of glucose from lactate, pyruvate, glycerol, AAs) increases IGF-1 synthesis (somatomedine C) --> which in turn increases bone lineal growth , muscle and visveral growth

Question 87

what is IGF-1

Answer 87

a cofactor that helps GH functions/efficacy = NECESSARY

Question 88

cx of lactotrpic cells

Answer 88

acidofiles posterior 10-25%

Question 89

function of lactotropic cells

Answer 89

in mammary glands increase milk production during lactancy decreases GnRH (FSH LH) --> amenorrea

Question 90

cx of corticotropic cells

Answer 90

basophils | 15-20%

Question 91

function of corticotropic cells

Answer 91

@ adrenal cortex increase growth, development, vascularization increase LPL capitation which increases synthesis and adrenal secretion of glucocorticoids (cortisol) and sex steroids (androgens and estrogens) increases melanin synthesis stimulate mineralocorticoids, sex hormones increase CyP450 : cholesterol --> pregnenolone decrease GnRH and GH

Question 92

cx of gonadotropic cells

Answer 92

basophiles anterior 10-15%

Question 93

function of LH in women

Answer 93

theca cells: make androgens - testosterone and androstenedione by theca cells in ovaries that by diffusion pass to granulouse cells (through aromatase converts androgens to estrogens) ovaric follicle: rupture causing ovulation

Question 94

function of LH in men

Answer 94

Leydig intersticial cells of testicle: synthesis and secretion of testosterone decreases hypothalamic secretion of GnRH and pituitary secretion of FSH and LH by RAN

Question 95

function of FSH in w0men

Answer 95

acitmates aromatase androstenedione --> estrone (E1)in adipocytes testosterone --> estradiol (E2) growth and follicular development dominant foliculo selection production of inhibine by granous cells in ovaries which cause less secretion of FSH from pituitary

Question 96

estrogen byexcellence

Answer 96

estradiol

Question 97

function of FSH in men

Answer 97

proliferation of seminiferous tubes principal determinant of testicular volume spermatogenesis production of inibine thru sertoli cells in the testicle --> decreases pituitary FSH secretion

Question 98

cx of tirotropic cells

Answer 98

anterolateral anteromedial 10%

Question 99

function of tirotropic cells in thyroid

Answer 99

stimulate vascularity and thyroid growth stimulate production of T3 and T4 morphological changes causing pseudopod formation increases iodine trapping and bone reabsorption (that's why hyperthyroidism causes early osteoporosis) decreases colloid, fotitias of IC colloid stimulates tiroglobulin hydrolysis 6. Iodine metaoblism phases stimulation 7. Increases mRNA of tiroglobulin and thyroid peroxidase 8. Increases 5' deyodase I (T4-->3 peripheral) 9. Glucose captation, O2 consumption and CO2 production +

Question 100

hormones that share alfa subunits

Answer 100

LH FSH TSH

Question 101

80% of somatomelina C / IGF-1 produced where?

Answer 101

liver but it acts in the muscle =

Question 102

how can IGF-1 lead to microsomal children

Answer 102

mothers pancrease stimulates insulin also stimulating IGF-1

Question 103

which homones are glucoproteins

Answer 103

TSH LH FSH share homology

Question 104

which are somatotropins

Answer 104

PRL | GH

Question 105

irrigation of hypothalamus

Answer 105

thru superior hypophyseal artery

Question 106

TFs involved in development of adenohipofisary cells

Answer 106

5. POU1F1 (Pit-1): lactotropas, somatotropas y tirotropas. 6. Prop-1: gonadotropas. (promiscuous) 7. T-pit: corticótropas.

Question 107

TSH also stimulates

Answer 107

estrogen

Question 108

ADH nucleus

Answer 108

is a nonapeptide that is synthesized predominately in the supraoptic nucleus of the hypothalamus, and secreted from the posterior pituitary upon stimulation of these cell bodies. 

Question 109

primary stimulus for ADH secretion

Answer 109

``` The primary stimulus for antidiuretic hormone (ADH) secretion is an increase in serum osmolarity.  A loss of intracellular water from hypothalamic osmoreceptor neurons bathed by hyperosmolar blood will stimulate ADH release.  Other factors that increase ADH secretion include: • Pain/stress • Hypoglycemia • Nausea • Volume contraction • Nicotine and opiates • Angiotensin II ```

Question 110

2 primary functions of ADH

Answer 110

* Regulate serum osmolarity * Maintain (increase) blood pressure Antidiuretic hormone also increases the permeability of the inner medullary collecting duct to urea.  This increases the osmotic gradient created by the countercurrent multiplier, facilitating the production of concentrated urine (i.e. increasing urine osmolarity). - Increases water reabsorption in renal colector tubules - Modualtes BP by increasing SM arterial tone Stimulates liberation of ACTH by hypofisary corticotrope cells

Question 111

oxytocin nucleus

Answer 111

Oxytocin is a nonapeptide that is primarily produced by the paraventricular nuclei within the hypothalamus, and secreted from the posterior pituitary

Question 112

how does oxytocin travel to posterior pituitary

Answer 112

Like ADH, oxytocin travels to the posterior pituitary via carrier proteins called neurophysins. 

Question 113

stimulus for oxtocin secretion

Answer 113

The major stimulus for oxytocin secretion is suckling.  Other positive stimuli include dilation of the cervix and orgasm, Bconfidence , memory, conection and empathy.

Question 114

effects of oxytocin

Answer 114

The primary effects of oxytocin are milk ejection @ lactation and uterine contraction @ labor.

Question 115

adverse effects of oxytocin

Answer 115

* Hyponatremia and seizures (due to anti-diuretic properties similar to antidiuretic hormone) * Subarachnoid hemorrhage * Uterine rupture in pregnant patients

Question 116

irrigation of hypothalamus

Answer 116

MCA of ICA

Question 117

function of thyroid hromones

Answer 117

``` Thyroid hormones: • induce central nervous system maturation during growth • increase basal metabolic rate • increase cardiac output • promote bone growth ```

Question 118

what stimulates TRH

Answer 118

cold

Question 119

what inhibits TRH

Answer 119

stress

Question 120

what inhibits TSH

Answer 120

DA, SS, cortisol, GH, T3 y T4 thyroxine

Question 121

TSH does what

Answer 121

stimulates T3 and T4 secretion from thyroid and - neg feedback to decrease TRH and TSH @ thyroid increase growth and vascularity, capitation of I- inorganic, increases oxidation of Inorganic I- creating more reactive yodant species (EIRs) 4) ↑Incorporación de EIR en residuos tirosina de la tiroglobulina[4] à ↑formación de yodotirosinas: MIT[5] y DIT[6]. increases formation of thyroid peroxidase 6) ↑Acoplamiento de yodotirosinas: MIT + DIT = T3, DIT + DIT =T4. 7) ↑formación de la gota de coloide. 8) ↑Liberación de T3 y T4.

Question 122

what increases TSH

Answer 122

TRH and estradiol

Question 123

difference between types of hypothyroidism

Answer 123

a. Primary: damage to thyroid gland: ↑TSH + ↓T3 y T4. b. Central: ↓TSH (o inapropiadamente normal) + ↓T3 y T4. Secundary: damage/disfunción of tirotrpic cells that makeTSH. Terciario: damage /disfunción to hypothalamic neuronas that produce TRH. 2° y 3° son bioquímicamente indistinguibles. ``` - Pirmary = @ thyroid gland ○ High tsh ○ Low T4 - Secondary ○ Both low - Tertiary ○ Both low ```

Question 124

90% of T3 in circulation comes from

Answer 124

T3 circulante (forma biológicamente activa) se deriva de la T4.

Question 125

feedback of increased cortisol

Answer 125

less hypothalamic secretion of CRH and hypofisary secretion of ACTH (por RAN)

Question 126

what increases ACTH

Answer 126

CRH and AVP Stress, trauma , int. qx, infections, hypoglicemia (similar to GH contraregulatory hormones)--> ACTH and catecolamines @ adrenal gland

Question 127

cortisols effect on hormones

Answer 127

AVP, ↓CRH, ↓ACTH, ↓GnRH.

Question 128

what is cortols made from

Answer 128

cholesterol and needs cytochrome p450

Question 129

cx of cortisol

Answer 129

- Catabolic - hyperglucemic - Anabolic only I liver --> + cytocrome p450 - Antiinflammatory - Immunosuppressor

Question 130

different types of hypoadrenalism

Answer 130

c. Primary (Addisons disease): damage to adrenals ↑ACTH + ↓cortisol + hiperpigmentación of skin and mucus due to RAN deficit). d. Central: ↓ACTH (o inapropiadamente normal) + ↓cortisol. Secundary: damage/disfunción in corticotropas cells that produce ACTH Terciary: damage/disfunción hipotalámic neurons that produce CRH. Primary Adrenal Insuff - ACTH up - Low cortisol Secondary @ corticotrope cell lesion - Both down Hypofisis trurmor of ACTH - Both up Adrenal tumor that secretes cortisol - Low ACTH - High cortisol

Question 131

circadian rhythm of cortisol secretion

Answer 131

- Different quantitites @ different times - máxima @6:00-8:00am; - mínima @12:00am.

Question 132

how to know if there is a loss of cortisol circadian rythm

Answer 132

- Para determinar si hay pérdida de este ritmo circadiano (propio del Síndrome de Cushing Endógeno) se mide cortisolemia @8:00am (5-25μg/dL) y @4:00pm (suele estar al 50% respecto a 8:00am, es decir, 2.5-12.5μg/dL)

Question 133

GnRH pulse

Answer 133

Hipotálamo produce GnRH en pulsos de 60/90-120 minutosà sistema porta va a gonadotropas adenohipofisarias à ↑FSH (end) y ↑LH. (beginning)

Question 134

different types of masculine hypogonadism

Answer 134

primary (hypergonadotropic) damage , testicular dysfunction - ↑FSH + ↑LH + ↓testosterona + ↓inhibina. Central (hypogonadotropic) - ↓FSH + ↓LH + ↓testosterona + ↓inhibina ...secondary - damge corticotropes that produce FSH and LH ...tertiary - damage to hypothalamic neurons that produce GnRH

Question 135

aromatase

Answer 135

- Testosterone to estradiol (E2) -↓hipotalámic secretion of GnRH and pituitary FSH y LH (por RAN), when secreción is >200pg/mL during >40-50h will be ↑secreción hipotalámica of GnRH (por retroalimentación positiva [RAP]) à↑↑↑LH (pico de LH) à ovulación. ○ Estradiol negative feedback vs LH, FSH, GnRH - Androstenediona à estrona (E1). ¾ Also pulsatilie - If > 200mg/dl > 40-50hr --> negative feedback - more than this time --> postiive feedback --> dominant follicular rupture --> primary oocyte = OVULATION ¾ Andrógenos à ↓secreción hipotalámica de GnRH e hipofisaria de FSH y LH (por RAN). ¾ Inhibina? - Can only inhibit FSH - not LH

Question 136

feminine hypogonadism

Answer 136

1. Primary (hipergonadotrópic): damage disfunción of ovary: ↑FSH + ↑LH + ↓estradiol + ↓inhibina. 2. Central (hipogonadotrópico): ↓FSH + ↓LH + ↓testosterona + ↓inhibina Secundario: damage/disfunción en corticotropas productoras de FSH y LH. ¾ Terciario: damage/disfunción de hipotalámic neurons that produce GnRH.

Question 137

where is the Kiss1 gene

Answer 137

``` in hypothalamus (núcleos anteroventral periventricular [AVPV] y arcuato), placenta and oncocytes --> produces 145 AA protein that is cleabed into 4 peptides: (Kisspeptines - ligands of Kiss1-R (GPR54 linked to G protein expressed in productor neurons of GnRH) ○ Discovered in philadelphia - hersheys kisses ``` - Kp54 (metastine), Kp14, Kp13, Kp10

Question 138

function of kisspeptins

Answer 138

Sex steroids increase Kiss1 gene expresion in AVPV nucleus and degrease it inn arcuate nucleus --> LH peak Stimulate GnRH liveration Initiate puberty ¾ Regulation of ovulation (neuroendocrine) ¾ Initiation, maintenance, and regulation of fertility

Question 139

3 circulation forms of prolactin

Answer 139

3. native PRL (de 23.5 kDa). the one that is normally secreted in 6-14 pulsos during the day(60% while sleeping). 4. Big-PRL (de 50kDa).co secreted in small quantities 5. Big-Big-PRL (de 150kDa). also cosecreted in small quantities

Question 140

macroprolactina

Answer 140

all 3 PRL + 1 IgG immunoreactive low biological activity

Question 141

dx macroprlactinemia

Answer 141

measure prolactin precipitación inpolietilenglicol o cromatografía . gel

Question 142

when to suspect macroprolactinemia

Answer 142

Suspect macroprlactinemia? - fem, high prolactin, no drugs that stimualte , no galactorrea - at expense of macroprolactins, also inhibit GnrH in asymptomatic px with hyperprolactinemia

Question 143

inhibitors of PRL secretion

Answer 143

``` Dopamina[1][2] Somatostatina GABA (ácido γ-aminobutírico). GAP (péptido asociado a GnRH) Calcitonina. ```

Question 144

stimulators of PRL secretion

Answer 144

``` Estradiol[3] TRH GnRH AVP Oxitocina VIP Serotonina Bombesina ``` ``` Galanina Histamina Neuropéptido Y Sustancia P Angiotensina II Neurotensina Péptido histidina-metionina ```

Question 145

Physiological factors that liberate PRL (date night)

Answer 145

``` stimulación de las mamas Coito, especialmente en mujeres Sueño Ovulación Embarazo Vida neonatal Lactancia Ingesta de aminoácidos Ejercicio ```

Question 146

ACTH does what @ adrenals

Answer 146

increases growth and development of adrenal cortex increases adrenal capture of lipoproteins (cholesterol is substrate for adrenal steroidogenesis) increases activity for CyP450scc, enzyme that transforms (cutting lateral chain) cholesterol --> pregnenolone increases stimulation of MSH alfa-R --> which increases synthesis of melanin by melanocytes

Question 147

action of kisspeptines in hypothalamus

Answer 147

increases secretion of GnRH to begin puberty neuronendocrine control of ovulation initiation, maintenance, metabolic regulation of fertility

Question 148

Prolactin function

Answer 148

stimulates production of maternal milk during latency

Question 149

differentiating types of hyperthyroidism

Answer 149

``` Hyperthyroidism - Primary ○ Low TSH ○ High T4 - With levated TSH and T4 ```

Question 150

Hipergonadotropic Hipogonadism

Answer 150

- High LH and FSH | - Low estradiol , low testosterone

Question 151

Hipogonadotropic Hipogonadism

Answer 151

- Both low

Question 152

cx of hypofisary adenoma

Answer 152

- Benign tumors of hypofisial gland - 10-15% of IC neuplasias - 3rd cause + Fc - 90% of hypofisial neoplasias

Question 153

% of hipofisary adenomas that are prolactinoma

Answer 153

45% □ Inhibit GnRH can call a combined syndrome

Question 154

epi cx of prolactinoma

Answer 154

○90% Micro in women, 60% macro in men ○ 3rd decade women ○ Men older (Son 8 veces más frecuentes en mujeres y se suelen diagnosticar entre 20-40 años.

Question 155

MC of prolactinoma in men

Answer 155

disfunción eréctil, disminución volumen testicular y del eyaculado, oligospermia, ginecomastia., glactorrea, low libido, infertility, azoospermia

Question 156

what is prolactinoma

Answer 156

○ Tumor of lactotrope cell line mostly in adenohipofifsis ' ○ Cosecretion of hormones and PRL level hyperprolactinemia --> decreased secretion GnRH --> decreased LH and FSH

Question 157

pseudoprolactinoma

Answer 157

effecto de tallo - too much prolactin from compression of tallo macroadenomas even if they aren't prolactinomas cause hyperprolactinemia < 200ng/mL due to effecto de tallo

Question 158

MC of prolactinoma in women

Answer 158

amenorrea, oligomenorrea, disminución lubricación vaginal, dispareunia, oleadas de calor, osteopenia/osteoporosis. Falla en menarquia, regular period with short lutea fase, infertility, low libidio, galactorrea i. Inhhibition of GnRH

Question 159

MC of prolactinoma common to both sexses

Answer 159

decresed libido, infertlility e. Reduction of bone mass and osteoporosis

Question 160

mass effect MC of prolactinoma

Answer 160

i. Loss of vision ii. Headache iii. Convulsions iv. Hydrocefaly v. Unilateral exoftalmo vi. Paralysis of craneal nerves ○ Neurological/oftalmological ○ Headache, IC HTN, convulsions, apoplejia, compression of quiasm

Question 161

Hook Effect - de cancho

Answer 161

results in elevated PRL levels which interfere with immunoradiometric ensayo and arrojan a abnormally low cifra (20-200ng/ml) what would lead one to believe its a nonsecreting macroadenoma to aboid this sample should be diluted 1:100 if there is a pituitary macroadenoma and prolactinemia < 200 if its still in 20-200 range its a pseudo prolactinoma i. >200ng/dl ii. Interference with radioimmunoensayo iii. Low PRL

Question 162

before samplimg for prolactinoma what is important to consider

Answer 162

i. Take prolacin 1-2hr at wake up to aboid false + ii. 2 separate elvated tests iii. Discard hyperprolactinemia (pregnancy meds 25-100ng/ml, hypothyroidism, renal insuff, or hepatic insuff)

Question 163

hipofisial adenoma 20%

Answer 163

somatotropoma ○ High GH ○ Gigantism , acromegaly

Question 164

hipofisial adenoma 10-12%

Answer 164

corticotropoma ○ High ACTH ○ Cushingnhibit GnRH ® So these we cause combined sydrome

Question 165

hipofisial adenoma 1-2%

Answer 165

tirotropoma ○ High TSH | ○ Bocio and hyperthyroidism

Question 166

hipofisial adenoma 15%

Answer 166

gonadotropoma ○ High FSH, LH ○ No clinical syndrome

Question 167

hipofisial adenoma 5-10%

Answer 167

tumor of celulas nulas

Question 168

what is hypopituitarism

Answer 168

○ Low hormonal secretion (2 or more) ○ Can be total Syndrome --> decrease/absence of 1 or more hormones of pit. Gland

Question 169

mechanisms for hypopituitarism

Answer 169

``` § Tumor compresses hypothalamus - decreasing § Compressing pit. Gland § Compression of THH § Decrease of pit. Irrigation § Necrosis of hipofisis ```

Question 170

what is combined syndrome

Answer 170

- Combined syndrome of hypersecretion of 1 hormone associated to decrease in secretion of 1 o more adenohipofisial hormones

Question 171

microadenoma

Answer 171

< 10mm

Question 172

what is corticotropoma

Answer 172

hypersecretion of ACTH --> hyperproduction of adrenal cortisol --> decreased GnRH --> decreased LH, FSH, GH

Question 173

examples of microadenomas

Answer 173

prolactinoma | corticotropoma

Question 174

macroadenoma

Answer 174

> 10mm ○ More in adults ○ Mechanical compression of hypothalamus, hypofisis, infundibulo, portal vessels --> focal pituitary necrosis ○ (craniofaringioma in kids)  

Question 175

neurological MC of hypopituitarism??

Answer 175

1. Cefalea. 4. Epilepsia del lóbulo temporal. 7. Alteración de conciencia (somnolencia, estupor y coma). 2. Parálisis de NC III, IV, VI (compresión senos cavernosos). 5. Rinorrea de LCR (si destruye piso de silla turca). 8. Defectos de campos visuales (hemianopsia bitemporal; por compresión del quiasma óptico). 3. Hidrocefalia obstructiva (compresión 3° ventrículo). 6. Obstrucción vía aérea nasal. 9. Disminución agudeza visual y ceguera (compresión del nervio óptico y de las cintillas).

Question 176

hipofisial apoplejia

Answer 176

Spontaneous Infarto/hemorrage of hypophysary adenoma (10-15%) clinically in 66%.

Question 177

local consequences of hipofisial apoplejia

Answer 177

Signos de irritación meníngea: cefalea, Kernig, Brudzinski. Parálisis ocular, diplopía, proptosis, defectos de campos visuales. Alteración de la conciencia Alteración de autorregulación simpática Dolor facial Hidrocefalia obstructiva

Question 178

systemic consequences of hipofisial apoplejia

Answer 178

``` Hipopituitarismo: 1. Insuficiencia suprarrenal secundaria aguda: hipotensión y choque. 2. Hipotiroidismo central. 3. Hipogonadismo secundario.   Silla turca vacía ```

Question 179

wermer syndrome

Answer 179

(Múltiple Endocrine Neoplasia 1, las 3 P). HAD, coexistence of 2/3of the following: 1. Pituitary adenoma. a. In 60% of NEM1, generally prolactinomas (60%), somatotropomas y corticotropomas, y generally are macroadenomas. 2. Primary Hiperparatiroidism (from hiperplasia or multiple adenomas). a. Initial clínica-bioquímica presentation. b. 60-90% of NEM1. 3. pancreáticos y duodenales neuroendocrinos tumors: insulinomas, glucagonomas, gastrinomas, VIPomas, somatostatinomas.  

Question 180

gigantism vs acromegaly

Answer 180

excessive secretion of GH that if before closure of hipofisis is gigantism (prominent lineal growth of long bones) if after closure = acromegaly (exaggerated growth of bland tissues, bones of hands, feet, mandible, internal viscera)

Question 181

etiology of gig/acro

Answer 181

somatotropoma 1. Somatotropoma productor de GH (99%). 65% son macrosomatotropomas. 2. Secreción ectópica de GH: in pancreatic and lung cancer ``` 3. excessive secretion of GHRH Eutópica: gangliocitoma o hypothalamic coristoma . b. Ectópica: Tumores islotes pancreáticos. ¾ Carcinoides bronquial, intestinal o tímico. ¾ CA microcítico de pulmón. ¾ CA medular de tiroides. ¾ Feocromocitoma. ¾ Adenoma adrenal. ```

Question 182

general MC of gig/acro

Answer 182

``` Fatiga Intolerancia al calor Ganancia de peso Diaforesis Hiperhidrosis palmoplantar ```

Question 183

osteomegalia in gig/acro

Answer 183

Prognatismo: aumento de espacios interdentales maloclusión. Dedos engrosados y elongados (acropaquia)[1]. Rasgos faciales grotescos[2]. Crecimiento de manos y pies[3] Tórax en tonel[4]

Question 184

Dermatolomegalia ig/acro

Answer 184

Engrosamiento cutáneo por depósito de glucosaminoglucanos. Hipersecreción sebácea: piel oleosa, acné, quistes sebáceos. Hipertricosis (50%). Cutis verticis gyrata[6] Hiperpigmentación (40%) Papilomas Acantosis nigricans[5] (10%) Moluscos fibrosos

Question 185

organomegalia acro/gig

Answer 185

``` Laringomegalia y apnea del sueño Parotidomegalia Nefromegalia Hepatomegalia Macroorquidismo   Cardiomegalia (15%) asociada a ICC/ cardiomiopatía hipertrófica. ```

Question 186

endocrinological metabolopathies in acro/gig

Answer 186

``` HTA (25%) Intolerancia a glucosa (50%) DM (25%) Hiperfosfatemia[7] Hipocalcemia por hipercalciuria[8] Nefrolitiasis Hipopituitarismo[9] Hiperprolactinemia[10] ```

Question 187

neuropathy in acro/gig is due to

Answer 187

comprisive effect

Question 188

neuroatropathies in acro/gig

Answer 188

Neuropatía periférica por compresión de nervios periféricos por osteomegalia. Compresión de médula espinal. Síndrome del túnel carpiano Artropatía.

Question 189

dx of gig/acro

Answer 189

Medir IGF-1 (somatomedina C, (+: >1ng/mL) o GH (+: >1ng/mL) en sangre a los 0, 30, 60, 90, 120 minutos. 2) MRI de hipófisis con gadolinio à a. adenoma hipofisario: evaluación hormonal + campimetría visual computarizada b. No adenoma hipofisario: GHRH en plasma, MRI de tórax, TAC de abdomen.

Question 190

tx of gig/acro

Answer 190

1) Extirpación transesfenoidal. Cura 70% de microadenomas y 50% de macroadenomas. 2) Análogos de la somatostatina: lanreótido, octreótido. Inhiben síntesis de GH hasta en un 90% por somatotropas y reducen tamaño tumoral. 3) Pegvisomant. Bloquea unión a GH-R. 4) Agonistas dopaminérgicos: bromocriptina, cabergolina, quinagolida, lisurida y pergolida a dosis mayores que las usadas para prolactinomas. 5) Radioterapia hipofisaria, con el riesgo de producir hipopituitarismo. Tx dura 6 meses a 20 años, pero normaliza los niveles en 90% de casos.  

Question 191

Etiology of CUshing syndrome

Answer 191

deberse a: ¾ Exógeno. Forma más frecuente. Por el uso a dosis excesivas o prolongadas de glucocorticoides (estados inflamatorios crónicos). Endógeno. Por tumor productor de ACTH,

Question 192

endogenous causes of Cushing are classified into

Answer 192

ACTH dependent (excess produced due to tumor which increases cortisol production by suprarenals) and ACTH independent (excess cortisol produced by adrenal hyperplasia/tumor) Cortisol causes RAN on ACTH

Question 193

ej of ACTH dependent causes

Answer 193

§ Corticotropoma hipofisario (“Enfermedad de Cushing”). 68% de casos de síndrome de Cushing endógeno en adultos. Secreción ectópica de ACTH por tumor extrahipofisario. 12% de casos de síndrome de Cushing endógeno en adultos.

Question 194

acute presentation of ACTH dependent causes of cushing

Answer 194

CA de pulmón 75%.

Question 195

chronic presentation cushing (ACTH dependent)

Answer 195

v Carcinoides bronquial, intestinal o del timo. v Tumores de células de los islotes pancreáticos, especialmente insulinomas. v CA medular del tiroides. v Feocromocitoma. § Síndrome de secreción ectópica de CRH por tumor extrahipotalámico. <1% de los casos de síndrome de Cushing endógenos en adultos. v CA medular del tiroides. v Carcinoide bronquial. v CA de próstata metastásico.

Question 196

ej of ACTH independent causes of cushing

Answer 196

§ Adenoma/CA productor de cortisol. | § Hiperplasia micronodular/macronodular.

Question 197

general MC of cushing

Answer 197

Obesidad centrípeta Cefalea Psicopatías Miastenia proximal

Question 198

cutaneuous MC of cushing

Answer 198

``` Estrías purpúricas >1cm de diámetro @ abdomen, flancos, MS, MI. Adelgazamiento cutáneo. Fragilidad capilar (equimosis o moretones espontáneos o por traumas mínimos) Hiperpigmentación (en ACTH dependiente). Cara redonda. Acné. Hirsutismo. Plétora Acantosis nigricans Micosis Pobre cicatrización ```

Question 199

endocrinological metabolic MC of cushing

Answer 199

``` Alcalosis hipocalémica Retraso de crecimiento óseo Oligomenorrea/amenorrea. Alteración libido/ disfunción eréctil. HTA (80%) Intolerancia a glucosa y DM Hipercalciuria con Nefrolitiasis ``` Leucocitosis neutrofílica. Osteopenia/osteoporosis. Hiperlipidemia. Poliuria.

Question 200

dx of cushing

Answer 200

confirm biochemically dx of cushing (confirm endogenous hiperorisolism) distinguish between ACTH dependent vs independent distinguish between corticotropoma vs ectopic secretion

Question 201

how to biochemically confirm cushing

Answer 201

a. Cortisol libre en orina de 24h 2-4x mayor del límite superior. b. Prueba de Nugent: supresión con 1mg de dexametasona: ¾ 1° día de la prueba: 1mg VO de dexametasona a las 11pm. ¾ 2° día de la prueba: medir cortisolemia @ 8am y si es <1.8 μg/dL se excluye. c. Medir cortisol salival a las 11pm: >145 ng/dL (>4nmol/L). d. Cortisolemia >1.8 μg/dL @12nm con paciente dormido (no tiene aplicabilidad clínica). e. Prueba de dexametasona-CRH.

Question 202

how to distinguish between ACTH dependent vs independent

Answer 202

Determinar ACTH en plasma: a. ACTH bajo à ACTH independiente à hacer TAC de suprarrenales. ACTH normal (10 pg/mL) /alto à ACTH dependiente

Question 203

how to distinguish between corticotropoma and ectopic secretion

Answer 203

MRI de hipófisis con gadolinio à (neg) à MRI de tórax + TAC de abdomen + perfil hormonal: ¾ Insulinemia à insulinoma. ¾ Catecolaminas en suero y orina de 24h + metanefrinas à feocromocitoma. ¾ Ácido 5-OH-indol-acético en orina de 24h à tumor carcinoides. ¾ Calcitonina à CA medular de tiroides.

Question 204

tx for cushing

Answer 204

1. Extirpación transesfenoidal. Cura 80%, 10-30% tiene recurrencia à 30-50% no son curados. 2. Radioterapia hipofisaria. 40% son curados (85% si son <18años). El 60% no es curado pero está protegido contra el síndrome de Nelson (crecimiento excesivo de un corticotropoma + defectos de campos visuales + hiperpigmentación cutánea [cuando tx inicial es adrenalectomía bilateral]) 3. Mitotane (adrenolítico: destructor de adrenales) + inhibidor de la síntesis adrenal de cortisol. 80% se cura. 4. Inhibidores de enzimas adrenales de la síntesis del cortisol (ketoconazol, metirapona). 5. Adrenalectomía bilateral total.  

Question 205

10% of prolactinomas cosecrete

Answer 205

GH

Question 206

cx of macroprolactinoma in men

Answer 206

estos producen prolactinemia >200ng/mL).

Question 207

dx evaluation of prolactinoma

Answer 207

1) Tomar muestra adecuadamente: ¾ 2 muestras separadas por 20-40 minutos >1h después de haber despertado, sin tener sexo (coito, manipulación de mamas) o ejercicio. ¾ Diluir muestra 1:100 para evitar efecto hook. ¾ Excluir mediante historia clínica y examen físico: embarazo, uso de fármacos; mediante laboratorio: hipertiroidismo (T4 libre, TSH), IR (creatininemia), IH (transaminasas y fosfatasa alcalina). Si nada de lo anterior es evidente o prolactinemia >100ng/mL: 2) MRI de hipófisis antes y después de administrar gadolinio. ¾ Si se confirma adenoma hipofisario à û Evaluar función hipofisaria û Campimetría visual computarizada (en particular si es un macroadenoma). ¾ Si no se confirma adenoma hipofisario à hiperprolactinemia idiopática.

Question 208

psychopharmacological drugs that cause hyperprolactinemia

Answer 208

drugs psychodrugs - decrease tono hypothalamic of dopamine Fenotiazinas (40-90%, clorpromazina y demás) Butirofenonas (haloperidol y demás, 40-90%) Risperidona (100%). Antidepresivos (IMAO, tricíclicos, IRSS) Benzodiacepinas Sulpirida Amoxapina

Question 209

antiHTN drugs that cause hyperprolactinemia

Answer 209

``` Antihypertensives Metildopa y reserpina (disminuyen producción DA)   Verapamilo Clonidina Labetalol Atenolol ```

Question 210

antiemetics that cause hyperprolactinmia

Answer 210

``` Antiemetics Metoclopramida Domperidona Cisaprida   Bloquean receptores D2 de DA en lactotropas ```

Question 211

hormonal prepared drugs that cause hyperprolactinemia

Answer 211

``` hormonal preps Estrógenos. Disminuyen tono dopaminérgico, aumentan # y tamaño de lactotropos y aumentan síntesis de PRL. AO GABA Progesterona Serotonina (5-HT) Testosterona Noradrenalina (NE) Endorfinas TRH ```

Question 212

toxic drugs that cause hyperprolactinemia

Answer 212

``` narcoticsCocaína Morfina y heroína Anfetaminas Metadona Nicotina Cerveza Codeína ```

Question 213

antihistaminic H2 drugs that cause hyperprolactinemia

Answer 213

H2 histamine blockersCimetidina | Ranitidina

Question 214

Miscellanious drugs that cause hyperprolactimeia

Answer 214

``` miscelanious Inhibidores de proteasas (SIDA) Fenitoína (anticonvulsivante) Isoniazida (antituberculoso) Piridostigmina (colinérgico) Medroxalol (antiadrenérgico) ```

Question 215

causes of hyperprolactinemia that are related to damage of hypolathamus or infundible

Answer 215

``` Tumores: a. Craniofaringiomas. b. Germinomas. c. Meningiomas d. Metástasis a hipotálamo. e. Extensión supraselar de AH Enfermedades granulomatosas Enfermedades infiltrativas Radioterapia craneal Vasculopatías. Sección infundibular ```

Question 216

causes of hypofisiopathy that are related to hipofiospathy

Answer 216

Prolactinomas (AH más frecuente). En mujeres suelen ser micro (90%, 100-200ng/mL) y en hombres macro (60%, >200ng/mL). 8x más frecuente en mujeres, edad de dx más frecuente: 20-40 años.   Macro-AH, por “efecto de tallo” (<200ng/mL). Hipofisitis linfocítica. Quiste intraselar. Quiste de hendidura de Rathke. Silla turca vacía Acromegalia (50% de somatotropomas coproducen PRL

Question 217

causes of hyperprolactinemia associated with primary hipothyroidism

Answer 217

Produce híper-PRL en 10-40%. Se da por: 1. ↑TRH hipotalámica à ↑PRL 2. ↑sensibilidad a TRH de lactotropas 3. ↑VIP à ↑PRL. 4. ↓DA hipotalámica 5. ↓metabolismo PRL à ↓eliminación PRL

Question 218

causes of hyperprolacinemia associated with polycystic ovary

Answer 218

Produce híper-PRL en 10-30%. Estado hiperandrogénico o hiperestrogénico (ver atrás)

Question 219

causes of hyperprolactinemia associated with organ failure

Answer 219

Suprarrenal: ↓cortisol à ↑expresión gen PRL. Renal: produce híper-PRL en 20-75%. ↓depuración. Hepática: Produce híper-PRL en 5-20%. ↓depuración hepática, acumulación de estradiol.

Question 220

causes of prolactinemia associated with thoracic wall , medular lesions

Answer 220

Toracotomía, mastectomía, traumatismo, mamoplastía, dermatitis, quemaduras, herpes zoster, brassiere ajustado, quiste mamario, mesotelioma, esofagitis, piercings en pezones, lesión, cirugía o tumor de médula espinal. Por estimulación nervios costales 4°-6° produce galactorrea por estimulación del SNA.

Question 221

causes of prolactinemia associated with ectopic prodcution

Answer 221

``` CA broncogénico (secreción VIP) Hipernefroma AdenoCA renal. Teratoma ovárico Gonadoblastoma Leucemia mielógena aguda Linfoma de Hodgkin y de células T ```

Question 222

causes of prolactinemia associated with - miscellanous

Answer 222

``` Encefalitis Neurofibromatosis Pseudotumor cerebral Seudociesis Porfiria ```

Question 223

causes of prolactinemia associated with macroprolactienmia

Answer 223

Autoanticuerpos anti-“big-big” PRL. Sospechar ante hiperprolactinémicos asintomáticos, pues estas moléculas tienen muy poca actividad biológica.   Se presenta hasta en el 40% de las detecciones de híper-PRL.

Question 224

causes of prolactinemia associated with - idiopathic

Answer 224

20% de los hiperprolactinémicos. Puede ser por mínimas dimensiones. Se piensa en resistencia de lactotropos a la DA o poca actividad de sus receptores. Se normalizan espontáneamente en 30%.

Question 225

for hyperprolactinemia when is transesfenoidal tumorectomy ndicated

Answer 225

¾ Intolerancia/resistencia a los agonistas de DA. ¾ No deseo de consumir agonistas DA por largo tiempo. ¾ Crecimiento de prolactinoma a pesar del uso de estos. ¾ Deseo de embarazo por parte de la paciente (aunque la mayoría no crece durante el embarazo: indicación relativa). ¾ Prolactinomas con componente quístico. ¾ Preferencia del paciente. ¾ No mejoría de los campos visuales tras 1-3 meses de agonistas DA

Question 226

what are somatotropoma

Answer 226

tumor of somatotropes that secrete GH

Question 227

what is cosecreted in 20-25% in somatotropomas

Answer 227

PRL

Question 228

65-80% of somatotrpomas are

Answer 228

macroadeomas

Question 229

MC of somatotropomas

Answer 229

gigantism /acromegaly in 99% | mass effect

Question 230

mass effect in somatotropma

Answer 230

(hipopituitarismo, hiperprolactinemia y neurooftalmopatías

Question 231

< 1% of gigantism and acromegaly is due tu

Answer 231

ectopic secretion of GH excessive secretion of GHRH 1. Eutópica (hipotalámico): gangliocitoma o coristoma. 2. Ectópica: tiroides (CA medular), timo (carcinoide), bronquio (carcinoide), pulmón (CA microcítico), intestino (carcinoide), páncreas (CA de islotes), adrenales (adenoma o feocromocitoma).

Question 232

Dx of somatotropoma

Answer 232

3. Confirmación bioquímica: a. IGF-1 (somatomedina C) elevado. b. Prueba de sobrecarga oral de glucosa midiendo GH (SOG-GH). Medir GH en ayuna y cada 30mins durante 2h después de la sobrecarga con 75g glucosa VO. Confirmación: GH > 1ng/mL por lo menos en 1 de las muestras tomadas post-administración de glucosa. 1. MRI de hipófisis con gadolinio … ¾ Positivo à a. Campimetría visual computarizada. b. Evaluación hipofisaria. ¾ Negativo à c. GHRH en plasma. d. TAC tórax y abdomen.

Question 233

what are corticotropomas

Answer 233

tumors of corticotropas that secrete ACTH producing CUSHINGS disease

Question 234

what is cushings diesase

Answer 234

a state of hypercortisolism due to hyperstimulation of adrenal gland

Question 235

cortico tropoma is responsible for what percent of endogenous cushing in adults

Answer 235

68% 90% are microadinomas

Question 236

biochemical confirmation of corticotropoma

Answer 236

a. Cortisol urinario libre de 24h. Positivo: 2-4x > límite superior. b. Prueba de supresión con 1mg nocturno de dexametasona. Se administra 1mg de dexametasona @11pm del primer día y se mide cortisolemia a la mañana siguiente. Positivo: >1.8μg/dL. c. Cortisol salival @11pm. Positivo: >145ng/dL

Question 237

least frequent AHs 1-2%

Answer 237

tirotropmas

Question 238

most invasice AHs

Answer 238

tirotropmas

Question 239

% of tirotropomas that are macroadenomas

Answer 239

85% are macroadenomas causeing mass effect ontop of hormonal effects (bocio, hiperhyroidism with increased TSH ¾ Cosecretan GH (16%), PRL (11%), LH/FSH (1.4%) y subunidad α[2].

Question 240

hpo vs pan

Answer 240

decreased or no of one or more pit hromes pan is all > 90% of mass

Question 241

causes of hypopituitarism (one or more hormons) 8Is A

Answer 241

direct or indirect ``` tumoral invasion (meningioma, glioma, ) pit infarct infiltration of hipofisis infection in this region injury in this region - postqx, RT, trauma iatrogenic immunological idiopathic isolated - deficit of just one hormone ```

Question 242

types of tumors that cause hipopituitarism

Answer 242

hipofisiary adenoma compression ``` hypothalamic tumor cystic lesion (craneofaringoma, Rathke, aracnoidoceles) ``` metastasis vascular lesions (necrosis) - no cells to produce hormenes

Question 243

adenomas and hipoputuitarism

Answer 243

compress hypothalamus and pituitary and THH (tallo) decrease pit irrigation increase intrasellar pressure prolactinoma (PRL inhibits GnRH) corticotropoma (ACTH inhibits GnRH) so two hormones are down thru RAN down FSH, LH, testerone men, estradiol women

Question 244

pituitary infart

Answer 244

apoplejia don't know if hemorrhage or infart acute both caus epituitary infarct (10-15% adenomas inernal hemorrhage??, autocorrection) local MC:cefalea, meningeal irritation, visual signs, altered conscieness, facial pain (due to increase in ICP - blood irritates calls cytokines and proinfalmmatory factors causing headache by VD) altrered sympathetic regulation obstructive hydrocefaly systemic: hypopituitarism empty silla turca syndrome

Question 245

pathogenesis of apoplejjia

Answer 245

adenoma of pituitary grows fast mass compresses superior pit artery , less perfusion, necrosis can also cause its own vascular anomalies all 3 of these conditions cass perfusion insuff and causes isquemic necrosis --> death of pit cell death

Question 246

pituitary infract, Sheehan syndrome

Answer 246

@ post partum blood loss in labor causes less blood flow up which is already big (pit) due to preg necrosis failed lactancy, failed reinico of menstruation, massive labor hemorrhage (PRL inhibits GnRH - after nipple stimulation) cells dead anyway no PRL or GnRH

Question 247

infiltrations and infections for hipopituitarism

Answer 247

``` infiltrative: amyloidosis sarcoidosis histocitiosis X hemochromatosis (destroynormal tissue that's there) ``` ``` infection: micosis (coccido, crypto) Tb sifilis AIDS pituitary abcess ``` (hipofisisits linfocitica px ej?)

Question 248

cranial injury hipopituitarism

Answer 248

trauma can be direct to brain ``` indirect.....causes of pituitary infarct cerebral edema (compresses) ``` hemorrhage or fracture of cranium (blood irritative ,and proinflammatory) cerebral hypoxia

Question 249

iatrogenic causes of hipopituiraism

Answer 249

qx of pit gland due to hypothalamic lesion cranial RT (gammaknife) - waves destroy the mass/lesion but its not selective just like the surgery

Question 250

hipofisitis --> hypopituitarism can be

Answer 250

primary or secondary

Question 251

primary hipofisitis

Answer 251

linfocitic (1A) granulomatous xantomarous

Question 252

secondary hipofisitis

Answer 252

``` local lesion (germinoma) systemic enf (saroidis) ```

Question 253

isolated hypopituitarism ca n have 3 MC cx

Answer 253

isolated FSH LH down (without corticotropoma, hiperPRL) - kallman syndrome (anosmia --> hipogonadismo hippanotropica??) FSH alone hyperprolactimea TSH down alone (IRC, linfocitic hipofisitis, pseudohipoparatiroidism) ACTH down alone (hipofisitis linfocitic, Sheehan, cranial trauma, Tpit gene mutation)

Question 254

tpit gene

Answer 254

transcription for??

Question 255

empty silla turca cause

Answer 255

partial or toal deficiency in sella diaphragm and LCR infiltrates compresses pit gland

Question 256

clinical empty silla turca

Answer 256

oftalmologica (hemaniopsia bitemporal, blurry, blind, papilledema), neurological (cefalea, increased pressure, convulsions, paraplejias), endrological (hipo) 50%

Question 257

@ def GH

Answer 257

neonates: hipoglicemia, hiperbilirrubinemia, convulsions (confused with kernicterus) short stature - infantile, delayed denticion, facial mcizo hypoplasia, frente oprominente, small mouth, occipital prominence

Question 258

@ def ACTH

Answer 258

tired, less quality sleep, less muscular dislipidemia

Question 259

def gonadotropins

Answer 259

no cx sexuals ni 1 or secondary ``` criptoquidia micropene delayed puberty small testicles little pubic hair gynecomastia ``` adults: less libido less energy, less EPO, less testicle, heat waves, dyspareunia (SSAME AS MENOAPAUSE) amenorrea, dry vaginal, osteopenia

Question 260

TSH def

Answer 260

``` HIPOTHYROIDISM MC weak dry skin palpebral edema adinamia, somnolencia hair falls cold skin thin nails striated bradipsiquia, bradilalia attention deficit memory loss depression, psycosis disfonia ```

Question 261

def ACTH

Answer 261

``` depression weight loss postural hypotension (why) epigastric pain nausea vomit hipoglicemia (no contrareg_ hipnatremia anemia, linfocitosis ```

Question 262

def GH

Answer 262

hipoglicemia induced with insulin GH < 10ng/ml in ALL samples give insulin (0.05-0.15 unidades/kg) to induce hipoglicemia take basal glicemia (84mg/dl ej) 0 measure glicemia, GH, cortisol 0, 15, 30, 45, 60, 90, 120 well done to dx if glicemia is < 40mg/dl or half of what px had a basal if (43 CANT USE) GH should be increasing >10 is no deficit - GH this test measures somatotrope and corticotrope RESRERVES to say px has GH deficit has to be 9 and down (1 at 10 = healthy) cortisol should go up and if not its a def in reserve of corticotrope cells (cut off is = 18, healthy below deficit) In all samples

Question 263

contraregulating hormones

Answer 263

cortisol GH glucagon catecolamines @ hypoglycemia these hormones go up

Question 264

masculine hypogonadism dx

Answer 264

infertile measure serum testosterone at 8 and 11am (nadir times) if < 300ng/dl = confirmation primary or secondary (gonadotripinas ) in primary will be one elevated?? secondary hipo hipo

Question 265

hipogonisms in women

Answer 265

amenorrea measure LH, FSH, E2.... also prolactin E2 down , LH, FSH up - primary (karyotype, precoz menopause, autoimmune ooforitis) = menopause if > 50 E2 down, LH, FSH down secondary hypogonadism MRI hipsifis, evaluate hipo function, central? discart preg and hiperprolactinemia

Question 266

insuff suprarenal dx

Answer 266

measure cortisol 8am (5-25) and 4pm (half) Cortisol in morning @ insuff should be < 3 if < 18 = falla adrenal if > 18mcg/dl = sano if 3-18 - short ACTH stimulation test - inject 250microg of ACTH or 0.25mg - cortisol up N, doesn't if sick (<18 = ADRENAL FAILURE)

Question 267

hormone replacement tx GH

Answer 267

give GH in kids 0.035mg/kg/d SC

Question 268

hormone replacement tx ACTH

Answer 268

give hydrocortisone - 20-30mg/d VO Prednisina 5-7.5mg/d VO Cortisone 25-37.5 mg/d VO

Question 269

hormone replacement tx TSH

Answer 269

levoritoxine - 1.6-1.8mcg/kg/d VO

Question 270

LH FSH

Answer 270

men - testerone esters 250mg C/3wk 2.5-7.5mg/d 5-10 gel/24hr women estrogen 1-2mg/d estrogen and progestogens 25-100ug/24hrs (combined birth control)

Question 271

craneofaringioma

Answer 271

tumors atht originate in remnants of cells from Rathke sac and can cause hipopit in kids most common cause of hipopit in kids 2-3% of IC tumors seen in 2 peaks of life between 2-25yr or > 65yr 25% cause hypothalamic alterations 5% @ hypofisis both @ 70% 25-30% mixed 15% solid 55-60% cystic usually > 1cm = macroadenomas, mass effect --> hipopit highly invasice with hypothalamic extension

Question 272

MC of craneofaringoam

Answer 272

neuro MC - headache, visual camp deficit, hydrocephaly, convulsions ``` hipopituiartism (tumba ADH) - 80% deficit MC delayed puberty DI ``` hyperprolactinemia - tallo effect <100ng/dl

Question 273

dx of craneofaringeoma

Answer 273

MRI of hypofisis with gadolinio - fine, cortes, if small can catch it most are big (cant see calcifications which cystic lesions do become) CT craneo (can see calcifications) Xray (calcification, other lesion, silla turca issues) campimetric deficits altered III, IV, VI less visual acuity measure prolactin in plasma, FSH LH, estradiol, FSH LH testosterone RSH T4 free GH, IGF1 Cortisol ACTH hipoglicemia induced by insulin test (FOR LAS RESERVAS) -

Question 274

tx craniofaringioma

Answer 274

qx | hormone replacement therapy

Question 275

post qx complications for craneofaringioma

Answer 275

DI - 16-66% adrenal insuff 40% panhipopituitarism 23% hipotiroidism 28%