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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

severed pituitary stalk

A

-increased prolactin
-decreased all other anterior hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

reproduction

A

Sex determination, puberty, pregnancy, menopause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

maintaining homeostasis

A

-TSH, PTH, Cortisol, Vasopressin, Insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

adenohypophysis

A

-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
Q

adrenocorticotropic hormone

A

-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
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

28
Q

LH and FSH

A

-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
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

30
Q

prolactin

A

-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
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!!

32
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

33
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

34
Q

hypofunction disorders- tx

A

-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
Q

hyperfunction disorders

A

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