Intro Flashcards

1
Q

The glands

A

-hypothalamus- within brain -> releasing hormones -> effect pituitary gland
-hypothalamus is part of diencephalon
-pituitary- you can see it -> trophic hormones act on distal target organs
-thyroid- TRH (hypothalamus) -> TSH (pituitary)
-parathyroid- 4 small glands
-pancreas- islets of langerhans
-adrenals
-gonads

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2
Q

posterior pituitary gland

A

-has stored* hormones
-anterior- originates from the gut
-Directly innervated by hypothalamic neurons via the pituitary stalk -> its a continuation of it
Posterior pituitary secretion of
-Vasopressin (antidiuretic hormone; ADH)
-Oxytocin
-Both are very sensitive to neuronal damage by lesions that affect the pituitary stalk or hypothalamus
-neuroendocrine stimulation releases stored hormones

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3
Q

primary organ/problem**

A

-the distal organ that actually has the disease
-primary problem is in the target organ
-2ndary problem- pituitary problem
-tertiary problem- hypothalamus problem
-ex. decrease T4 production -> dysfunction in thyroid gland itself -> primary hypothyroidism
-ex. hypo functioning of the pituitary gland -> no stimulation to thyroid gland to produce T4 -> secondary hypothyroidism
-ex. primary thyrotoxicosis
-ex. adisons disease- primary

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4
Q

severed pituitary stalk

A

-increased prolactin
-decreased all other anterior hormones

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5
Q

endocrinology

A

-to set in motion
-glands and their hormones
-endocrine- ductless
-exocrine- from a cell into the blood system
-elicit cellular responses and regulate physiologic processes through feedback mechanisms
-paracrine effect- exert an effect on cells on the organ from which they were released
-autocrine effect- on the same cell type

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6
Q

different mechanisms of cell signaling (she brushed over this)

A

-intracrine- within cell
-autocrine- from within cell to outside -> back in
-paracrine- local
-endocrine- general circulation
-neuroendocrine

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7
Q

the hormones

A

-hypothalamus- GnRH, thyrotropin releasing hormone, cortisol RH, somatostatin, GHRH

-pituitary:
-anterior- GH, ACTH, TSH, FSH, LH, prolactin
-posterior- vasoactive peptide (AVP) or antidiuretic hormone (ADH); oxytocin
-AVP deficiency causes diabetes insipidus (DI);
-excessive or inappropriate AVP production- hyponatremia if water intake is not reduced in parallel with urine output

-thyroid- T3 & T4 (active)

-adrenals-
-mineralocorticoids
-norepinephrine

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8
Q

basic genetics of hormones (she brushed on this…dont really study)

A

The synthesis of peptide hormones and their receptors occurs through a classic pathway of gene expression ->

Transcription → mRNA → protein → posttranslational protein processing → intracellular sorting, membrane integration, or secretion ->

Have regulatory DNA elements ->

-Control by other hormones also necessitates the presence of specific hormone response elements
-TSH repressed by the thyroid hormones
-Insulin synthesis requires ongoing gene transcription but at the translational level is controlled by the glucose & amino acid levels

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9
Q

physiology

A

-selective binding- regulation of gene function and enzyme action
-hypothalamic- pituitary relationship -> middle man
-varying degrees of control
-negative feedback control mechanism
-increase in hormone from target organ (ex. T4) -> sends signal to pituitary and hypothalamus to decrease stimulating hormones (decrease TSH and TRH)
-receptors- membrane and nuclear

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10
Q

hormones to target organs image

A

-cortisol- most important hormone*- you can not live without it -> controls BP and glucose
-every cell needs T4 for metabolism
-FSH & LH - affect testes and ovaries
-prolactin- produces breast milk itself

-ADH -> kidneys
-oxytocin -> breasts and uterus

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11
Q

hormone flow chart

A

-somatostatin - inhibits GH and TSH
-IGF*- part of GH that affects the tissues and long bones - made in liver
-GH- affects glucose
-TSH can increase prolactin

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12
Q

hyperthyroidism

A

-increase T4
-tachycardia, sweating, diarrhea, anxiety, tremors
-increased metabolism

-constipation, depressed, gained weight, myxedema, slower movements

-problem is in the thyroid?, pituitary?, hypothalamus?

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13
Q

growth functions

A

-Stature
-GH deficiency, hypothyroidism, Cushing’s syndrome, precocious puberty, malnutrition or chronic illness, or genetic abnormalities
-Many factors (GH, IGF-I, thyroid hormone) stimulate growth, whereas others (sex steroids) lead to epiphyseal closure

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14
Q

reproduction

A

Sex determination, puberty, pregnancy, menopause

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15
Q

maintaining homeostasis

A

-TSH, PTH, Cortisol, Vasopressin, Insulin

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16
Q

hyperfunction

A

-over secretion of hormones
-often due to tumors (benign (MOST) or malignant)
-hyperplasia of endocrine gland
-ectopic secretion of hormones by other tumors
-produced by a certain set of cells
-ex. lung cancer -> increase ADH (malignant)

17
Q

hypofunction

A

-under stimulation from pituitary or abnormal tissue response

18
Q

hormone secretion, transport, and degradation

A

-circulating level of a hormone is determined by its rate of secretion and its circulating half life
-stored in secretory granules
-releasing factors or neural signal -> ion channels -> secretion of hormone
-transport and degradation- affect the rapidity with which its signal decays
-half life important for achieving physiologic hormone replacement
-frequency of dosing and the time required to reach steady state are intimately linked to rate of hormone decay

19
Q

hypothalamo- pituitary axis

A

-adenohypophysis
-portal vascular system
-neurohypophysis- neuronal control
-pulsatile release of hormones
-circadian rhythms- it matters when you do the blood draw (morning vs night)
-month long rhythms with superimposed circadian rhythms- LH, FSH

20
Q

hypothalamus

A

-receives input from virtually all other areas of the CNS
-regulation of most anterior pituitary horomones depends on stimulatory signals- + feedback
-prolactin is regulated by inhibitory stimuli
-if pituitary stalk is severed - prolactin release increases -> whereas release of all other anterior pituitary hormones decrease
-hypothalamic abnormalities (tumors and encephalitis and other inflammatory lesions)
-neurohormones- synthesized in diff centers within hypothalamus -> some disorders affect only one neuropeptide, whereas others affect several
-under section or over secretion of neurohormones can result

21
Q

anatomy

A

Lateral view of the brain showing the relationship of the hypothalamus to the median eminence and the pituitary gland
-pituitary gland enlargement >10 -> optic chiasm pressure -> visual field defects
-located within the sella turcica
-comprises antomically and functionally distinct anterior and posterior lobes
-sella is Contiguous to vascular and neurologic structures -> Including the cavernous sinuses, cranial nerves, and optic chiasm [contents of the CS are: internal carotid artery, CN III and IV, first and second divisions of CN V and VI]
-expanding intrasellar pathologic processes -> central mass effects and endocrinologic impact

22
Q

anterior lobe

A

-Hypothalamic neural cells synthesize specific releasing and inhibiting hormones
-These are secreted into the portal vessels of the pituitary stalk
-Superior and inferior hypophyseal arteries

23
Q

melanocyte stimulating hrmones

A

-Addison disease
-melanocytes are in vicinity -> darker skin
-ACTH but also melanocytes

24
Q

pituitary gland

A

-peripheral endocrine organ functions are controlled to varying degrees by pituitary hormones
-functions vary from minimal to extensive control
-master gland/middle man
-hypothalamic-pituitary axis (HPA)- negative feedback system
-pituitary tumors cause characteristic hormone excess syndromes
-hormone deficiency may be inherited or acquired

25
adenohypophysis
-Specialized portal vascular system regulates synthesis and release of the 6 major peptide hormones of the anterior pituitary -Hypothalamic-pituitary axis: -Thyrotropin releasing hormone [TRH → TSH] -Corticotropin releasing hormone [CRH→ACTH] -Gonadotropin releasing hormone [GnRH → FSH; LH] -Growth hormone releasing hormone [GRH → GH] -Dopamine/TRH → Prolactin
26
adrenocorticotropic hormone
-ACTH -aka corticotropin -CRH is primary stimulator of ACTH release -induces the adrenal cortex to release cortisol, several weak androgens, DHEA -CRH-ACTH-cortisol axis is a central component of the response to stress -> ADH too plays a role in stress -you must slowly taper exogenous cortisol -> can cause crisis -> die -without ACTH, adrenal cortex atrophies and cortisol release virtually ceases > -hydrocortisone- gradual decrease due to negative feedback of the hormone while supplementing it -aldosterone - NOT STIMULATED by ATCH -> renin and volume control
27
TSH
-regulates the structure and function of the thyroid gland -stimulated synthesis and release of thyroid hormones -synthesis and release stimualted by the hypothalamic hormone -> thyrotropin (TRH) -suppressed by negative feedback
28
LH and FSH
-control the production of the sex hormones -these are not life threatening if hyper or hypo -synthesis and release of LH and FSH are stimulated by- gonadotropin releasing hormone (GnRH) -and suppressed by- estrogen and testosterone -in women -> LH and FSH stimulate- ovarian follicular development and ovulation -in men, FSH acts on -> sertoli cells and is essential for spermatogenesis -LH acts on leydig cells of the testis to stimulate testosterone -LH surge after ovulation -FSH increase gradually
29
growth hormone
-stimulates somatic growth and regulates metabolism -synthesis and release of GH- major stimulator -> GHRH -major inhibitor- somatostatin -GH controls synthesis of insulin like growth factor 1 (IGF1 AKA somatomedin C) which largely controls growth -produced by many tissues, the liver is the major source
30
prolactin
-produced in the cells called lactotrophs -pituitary doubles in size during pregnancy -hyperplasia- increasing in cell and hypertrophy of lactotrophs -major function stimulating milk production -release also during sexual activity and stress -may be a sensitive indicator of pituitary dysfunction -hormone most frequently produced in excess by pituitary tumors -often first hormone to become deficiency from infiltrative disease or tumor compression of the pituitary
31
other anterior pituitary hormones
-can cause hyperpigmentation of the skin: -Pro-opiomelanocortin (POMC, - gives rise to ACTH) α- and β- melanocyte-stimulating hormone (MSH) -Significant clinically in disorders in which ACTH levels are markedly elevated (i.e. Addison's disease, Nelson syndrome) -endogenous opiods: -encephalins -endorphins- bind to and activate opioid receptors the CNS -exercise!!
32
neurohypophysis
-POSTERIOR PITUITARY -comprises of axons originating from neuronal cell bodes located in the hypothalamus -> antidiuretic hormone- AKA arginine-vasopressin (AVP) or ADH -oxytocin- uterine contraction and breast milk ejection -pulsatile fashion
33
approach to the patient
-hx and PE -look for manifestation of hyper or hypo functioning- 1st step -measurements and endocrine testing -quantitative hormone measurements and clinical context -biochemical testing- immunoassay (plasma/serum; urine), mass spectroscopy (various forms of chromatography and enzymatic methods), broad range (circadian rhythm, dynamic test necessary) -imaging- CT, MRI, US, thyroid scan -screening
34
hypofunction disorders- tx
-replacement of the peripheral endocrine hormone -regardless of whether the dect is primary or secondary (an exception is GH replacement for pituitary dwarfism) -if resistance exists- drugs that reduce resistance can be used (metformin or thiazolidinedione for type 2 diabetes mellitus) -hormone stimulating drugs
35
hyperfunction disorders
-radiation therapy, surgery, drugs that suppress hormone production -receptor antagonist