intro Flashcards

1
Q

The glands

A

-hypothalamus- within brain -> releasing hormones -> effect pituitary gland
-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
Directly innervated by hypothalamic neurons via the pituitary stalk:
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

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3
Q

primary organ/problem** vs secondary vs tertiary

A

PRIMARY:
-the distal organ that actually has the disease
-primary problem is in the target organ/peripheral endocrine gland
-ex. decrease T4 production -> dysfunction in thyroid gland itself -> primary hypothyroidism

2ndary problem
- pituitary problem
-ex. hypo functioning of the pituitary gland -> no stimulation to thyroid gland to produce T4 -> secondary hypothyroidism

Tertiary problem
- hypothalamus problem (rare)

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4
Q

endocrinology

A

Endocrinology: “to set in motion”
-endocrine = ductless
-works elicit cellular responses and regulate physiologic processes through feedback mechanisms

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5
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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6
Q

Posterior pituitary hormones

A

1) oxytocin
2) Vasoactive peptide (AVP)/ antidiuretic hormone (ADH)
-AVP/ADH deficiency = diabetes insipidus (DI) -> lots of dilute urine and extreme thirst
-excessive or inappropriate AVP production = hyponatremia if water intake is not reduced in parallel with urine output

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7
Q

Hypothalamus Hormones

A

TRH, CRH, GnRH, GHRH, Somatostatin, Dopamine

(The Coolest Girls Get Sick D*ck)

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8
Q

What are the anterior pituitary hormones?

A

TSH, FSH, LH ,ACTH , MSH , Growth Hormone and Prolactin

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9
Q

What are the thyroid hormones? T3 and T4 repress…..

A

T3 and T4

T3 and T4 repress TSH
-NEGATIVE feedback
- -increase in hormone from target organ (ex. T4) -> sends signal to pituitary and hypothalamus to decrease stimulating hormones (decrease TSH and TRH)

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10
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
-Insulin synthesis requires ongoing gene transcription but at the translational level is controlled by the glucose & amino acid levels

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11
Q

physiology: what type of binding, receptor types, and what is the Hypothalamic- pituitary relationship

A

Selective binding
- regulation of gene function and enzyme action

Receptors
- membrane
- nuclear

Hypothalamic- pituitary relationship -> middle man
-varying degrees of control
-negative feedback control mechanism

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12
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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13
Q

hormone flow chart

A

-somatostatin - inhibits GH and TSH
-IGF*- part of GH that affects the tissues and long bones
-GH- affects glucose
-TSH can affect prolactin

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14
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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15
Q

What factors stimulate growth vs what leads to epiphyseal closure

A

stimulate growth:
-GH
- IGF-I
- thyroid

epiphyseal closure:
- sex steroids

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16
Q

Factors involved in short stature

A

-GH deficiency,
-hypothyroidism
- Cushing’s syndrome,
-precocious puberty,
-malnutrition or chronic illness
- genetic abnormalities

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17
Q

reproduction

A

Sex determination, puberty, pregnancy, menopause

18
Q

What factors involved in maintaining homeostasis?

A

-TSH
- PTH
- Cortisol**
- Vasopressin
- Insulin

19
Q

hyperfunction

A

OVERSECRETION of hormones
-produced by a certain set of cells

Causes:
-tumors (benign (MOST) or malignant)* MC
-hyperplasia of endocrine gland
-ectopic secretion of hormones by other tumors

-ex. lung cancer -> increase ADH (malignant)

20
Q

hypofunction

A

Under stimulation from pituitary or abnormal tissue response

tx: replacement of hormone or hormone stimulating drugs

21
Q

hormone secretion, transport, and degradation

A

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
-frequency of dosing and the time required to reach steady state are closely linked to RATE of hormone decay

22
Q

The circulating level of a hormone is determined by:

A
  • rate of secretion and its circulating half life
    -half life important for achieving physiologic hormone replacement
23
Q

hypothalamo- pituitary axis

A

adenohypophysis = anterior pituitary
-portal vascular system: blood vessels connect hypothalamus and anterior pituitary

Neurohypophysis- neuronal control; posterior pituitary

Cyclical release of hormones:
-pulsatile release of hormones
-circadian rhythms- it matters when you do the blood draw (morning vs night) for ACTH, GH, prolactin
-month long rhythms with superimposed circadian rhythms: LH, FSH

24
Q

If pituitary stalk is severed what increases and what decreases?

A

Pituitary stalk is severed:
- prolactin release INCREASES because it is regulated by INHIBITORY STIMULI
- release of all other anterior pituitary hormones DECREASE because it is regulated by POSITIVE FEEDBACK

25
Q

hypothalamus

A

-receives input from virtually all other areas of the CNS
-regulation of most anterior pituitary hormones depends on stimulatory signals: + feedback
-prolactin: inhibitory stimuli

Hypothalamic abnormalities (tumors and encephalitis and other inflammatory lesions):
-neurohormones- synthesized in different centers within hypothalamus
- some disorders affect only one neurohormone, whereas others affect several
-under section or over secretion of neurohormones can result

26
Q

anatomy of pituitary gland

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
-expanding intrasellar pathologic processes -> central mass effects and endocrinologic impact

27
Q

Where is the pituitary gland located? + what is the sella contiguous to

A

-located within the sella turcica (bone)

Sella is Contiguous to:
- cavernous sinuses
- cranial nerves
-optic chiasm

Contents of the CS are:
-internal carotid artery
-CN III and IV
- first and second divisions of CN V and VI

28
Q

anterior lobe/Adenohypophysis

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

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

29
Q

melanocyte stimulating hrmones

A

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

30
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

31
Q

adrenocorticotropic hormone

A

-ACTH aka corticotropin
CRH is primary stimulator of ACTH release
-CRH-ACTH-cortisol axis is a central component of the response to stress -> ADH too plays a role in stress

Role of ACTH:
-induces the adrenal cortex to release cortisol, several weak androgens, DHEA
-without ACTH, adrenal cortex ATROPHIES and cortisol release virtually ceases >
-hydrocortisone (a synthetic form of cortisol): when administered as a med -> causes a decrease in the body’s own production of cortisol through negative feedback mechanisms

note aldosterone - NOT STIMULATED by ACTH -> renin and volume control

32
Q

TSH

A

-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

33
Q

LH and FSH

A

-control the production of the sex hormones
-these are NOT life threatening if hyper or hypo

Stimulated by:
- gonadotropin releasing hormone (GnRH)

Suppressed by:
- estrogen and testosterone

Women: LH and FSH stimulate
- ovarian follicular development
- ovulation

Men:
- FSH acts on sertoli cells and is essential for spermatogenesis
-LH acts on Leydig cells of the testis to stimulate testosterone

34
Q

growth hormone

A

-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

35
Q

prolactin

A

-produced in the cells called lactotrophs
-pituitary doubles in size during pregnancy -hyperplasia- increasing in cell and hypertrophy of lactotrophs

Function:
- stimulating milk production
-release also during sexual activity and stress

36
Q

why is prolactin sometimes a sensitive indicator of pituitary dysfunction?

A
  • prolactin hormone is most frequently produced in excess by pituitary tumors *
    -often first hormone to become deficiency from infiltrative disease or tumor compression of the pituitary
37
Q

other anterior pituitary hormones

A

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!!

38
Q

neurohypophysis

A

-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

39
Q

approach to the patient

A

-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

40
Q

hypofunction disorders- tx

A

Replacement of the peripheral endocrine hormone!!!!
-regardless of whether the defect 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

41
Q

hyperfunction disorders

A

-radiation therapy
- surgery
- drugs that suppress hormone production
-receptor antagonist