Histo: Endocrine

Front 1

Features and Function

Back 1

- consists endocrine glands and cellular components
- homeostasis and long tem adaptive responses
- use hormones (transport by blood vessels) to control cellular activity and metabolism.

Neuroendocrine system: endocine is slow reposne and nervous is rapid response to stimuli.

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Short/Long range hormonal contro:
1. Autocrine
2. Paracrine
3. Endocine

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1. self regualted of a cell by its own secretory product

2. short range control, among cells close by or in same orgran, hormone sent via intercellular space and local capillary.

3. long range control with vascular distribution to remote sites, hormones identify receptors on target cells generating metabolic or specific receptor-linked responces, effects multiple/distributed target sites.

Front 3

Tropic vs. Trophic

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Tropics: affinity of the hormone to its receptor

Trophic: action of hormone on the target cell (that affects metabolism of target cell)
Types:
- inotropic: influence gating of channels
- metabotropic: influence cell's metabolism (via sencondary messenger systems)

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Hormones molecule types:

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1. proteins & glycoproteins
2. Peptides & polypeptides
3. lipids and steroids

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Extra/intracellular receptors for hormones

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1. peptide/proteins based hormones have extracellular receptors liniekd to target cell via 2ndary messenger systems (cAMP, cGMP, phosphotidylinositol, tyrosine kinase, Ca++)

2. Lipid-based steroid hormones can permeate cell membranes to bind with intracellular cytoplasmic or intranuclear receptors.

Front 6

Feedback inhibition:

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increase in tropic molecules that stimuate secretion/release from a target site of a proudct that in turns down regulates the tropic hormone --> self-limiting feedback for homeostasis in supply and demand.

Front 7

Endocrine-neuroendorines system functions

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1. reproductive physiolog
2. growth and development
3. metabolism (oxidative, glucose, fat, minerals)
4. Electrolyte and fluid balance
5. Blood pressure
6. Fight of flight reactions
7. diurnal or other biorhythms
8. immunologic responses
9. inflammation
10.hematopoeisis

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Histologic Characteristiscs of Endo glands:

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1. solid organs: cells in cords or clumps
2. capillary rich: with sinusoidal or fenestrated endothlium and gland cells polarized toward vascular supply
3. ductless
4. strainig characterisitcs determined by content of cytoplams or secretory granules.
- proteins: basophilic or acidophilic
- lipids: abstance of staining and lacy appearance.

Front 9

Pituitary Gland (hypophysis)
location, structure, tumor, relationship with hypothalamus

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Location: pituitary fossa at the base of brain

bilobed: posterior & anterior lobes

Master gland: its hormones have major controlling influences

Glandular tumor (adenomas) produce endocine and neurological dustubances.

Relationship with hypothalamus:
1. Anterior lobe
- H control production of 6 hormones from anterior lobe via releasing/inhibitory factors (RF/IF)
- RF/IF transported from neuron terminals in H and capillaries into hypophyseoportal vessels to cap in anterior lobe (two cap system).

2. Posterior lobe
- 2 posteror lobe hormones are produced in nuerons of H
- hormones transprot out of H along axon by axoplasmic trnasport and released into p. lobe capillaries.

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Pituitary: Development of Ant. (Adenohypophysis) and Post(neurohypophysis)lobes. .

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Adenohypophysis:
evagination of oral ectoderm, rathke's pouch that loses connection with oral cavity
- Pars distalis + pars tuberalis (extension of pars distalis along the pituitary stalk).


neurohypophysis:
from neural tube but retains connection with hypothalamus by stalk, infundibulum, through which axons of neurons in H each the post. lobe.
- pars intermedia + the neurohypophysis [infundibulum (stalk) + pars nervosa].

Rathke's cysts:
Colloid filled spaces at the interface between adneo and neurohypophysis.

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Adenohypophysis cell types

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3 cell types:
chromophil:
1. acidophil 35%: stain with eosin
2. basophil 15% :stain with hematoxylin)
3. chromophobes 50%: small unstained; reserved precusors for chromophils.

Front 12

Pituitary cell types and hormaones.

Back 12

p. 87

Front 13

Control of anterior lobe hormones

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1. Feedback frmo target organs
- actions of hormone on target organ produce changes that act back on the pituitary.
- negative feedback: demand/supply homeostasis.

2. hypothalamic RF/IF
- H produced with neuron axon terminals ends on capillaries in median eminence of H and RF/IF are secrete into hypothalamic capillaries -> hypophyseoportail veins -> capillaryin adenohypophysis -> cells of adenophypophysis.

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Neurohypophysis:
types of cells, location of H production of hormones, process of hormone release.

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2 cell types: glial (pituicytes) & endothlial cells

Vasopression (ADH): made in supraoptic nucleus of H.

Oxytocin: made in paraventricualr nucleus of H.

Hormones transported from H with neurophysins (transport proteins) along axons into post. pituitary's nerve terminal (Herring bodies)and release.

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Control and actions of Post. Pituitary hormones

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Vasopression (ADH): Osmo-baroreceptors stimulate release to conserve fluid by increase permeability of kidney to collect more water.

Oxytocin: secreted in resposne to suckling of infants causing myoepithelia contraction and milk ejection, stimualte uterine sm mm contraction and reduce postpartum bleeding.

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Pineal Gland
Derivation, location, cell & hormone function, other features.

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Derived from dorsal outpocketing of neural tube, epiphysis

Location: midbrain junction with thalamus, midline reference for shift in skull.

pinealocytes: produce melatonin, catecholamine-serotonin that controls diurnal rhythms, anti gonadotrophic (no melatonin -> precocious puberty); light related function taken over by retina.


brain sand (corpora arenacea): granular calcification that increase with age.

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Pancreas: derivation, structures, cells.

Back 17

Islet of Langerhans:
- lightly encapsulated, well-vascularized cell clusters
- among serous secretory acini of exocrine pancreas
- derived from endoderm of developing gut
- islet is lineage of enteroendocrine cells asso. with gut epithelium.
- beta cell: granules extracted by alcohol
- alpha cells: form cluster at islet perimeter

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Beta cells, secretion, control

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Produce insulin, disulfide-linked polypeptide chains (A&B); reduce blood sugar

1. increase cellular uptake of glucose
2. glucose utilization and storage (glycogen)
3. exerting paracine control of glucagon secretion from alpha cell

CONTROL
Insulin secretion increase when:
- increase blood glucose
- parasympathetic auto.

Insulin secretion decrease:
- increase glucagon
- increase somatostatin
- sympathetic auto.

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1. Alpha cells
2. Delta cells
3. minor cell types

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1. fewer than beta cells, produce glucagon, raise blood sugar, promote glycogen breakdown, depress insulin produce, lipid mobilization from fat (oppo. insulin)
2. produce somatostatin: exerts paracine effects that depress activity of alpha and beta cells
3. produce hormones asso. enteroendocrine activity: vasoactive intestinal polypeptide (VIP), gastrin, CCK.

Front 20

Diabetes Mellitis

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Type I: islet cell destruction from inflammatory infiltration and autoimmune attack

Type II: insulin secretion problem and target cell responsiveness.

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Adrenal (Suprarenal) Gland
derivation, structure, hormones functions.

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Cortex & medulla: two glands of separate embryonic origins

1. cortex: derived from mesoderm, produce adrenocortical steroid from 3 diff. layers

2. Medulla: derived from neuroal crest cells that migrated, produce chromaffin cells *catecholamines)

centripetal blood flow: outside in, cortex to large medullary vein.

medullary production of epinephrine is dependent on cortical steroids.

Cortex layers:

1. Z. Glomerulosa: produces mineralocorticoids (esp. aldosterone), conserve sodium by increaseing recovery from urinary filtrate by distal convoluted tubules. Destruction of adrenal cortex is lethal due to sodium depletion.

2. Z. Fasiculata:
Produces glucocorticoids: corticosterone, cortisone
Effects:
- carbohydrate, protein, lipid metabolism
- depression of inflammation and immune response.
- Hematopoeisis

3. Z. reticularis
- Produce androgenic 17-ketosteroid, adrenocortical hyperotrphy can have masculinizing effects in females
- graveyard for aging cortical cells

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Adrenal Medulla

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Derived from neural crest cells

Analogous to postganglionic sympathic neurons; controlled by preganglionic sympathetic fibers

Chromaffin cells
- ability to reduce chromium salts
- extramedullary clusters (paraganglia)
- pheochromocytomas: tumors from chromaffin, removal of benign growth will cure severe hypertension
- E/Norepinephrine: facilitate fight or flight by control patterns of blood flow to muscles, blood pressure, act. hear, glucose

Epinephrine: product of methylation of norepinephrine by 0-methytransferase (dependent on adrenocorticosteroids)

Front 23

Addison's

Cushing's disease

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Addison's disease: adrenocortical degeneration
- not produce enough mineralcorticoids/glucocordicoise
- loss of feedback inhibition and hypertrophy of pituitary basophils (excess ACTH secretion); overporudction of MSH produces hyperpigmentation

Cushing's Disease:
- too much adrenocordical hormones
- basophil tumors with adrenocortilcal hypertrophy form excess of ACTH

Front 24

Thyroid Gland Strucure & function

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Butterfly with two lobes connected by ishmus anterior to trachea.

Two components have separate embryonic origins

Derived from endoderm, originate from base of tongue and migrate to hyroglossal duct

ectopic gladular tissues - source of disorder (hyperthyroidism and tumor)

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Thyroid Gland histo features

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- Extracellular storage of hormones in follicles
- Capillary plexus surround follicle
- Simple cuboidal follicular epithelium around colloids
- Colloid: glycosylated storage form of thyroglobulin contain tyrosine-based triiodothyronin, thyroxin hormones (T3,T4).
- T3, T4: act at mitochondrial level to regualte oxidative metabolims and set metabolic rate, influecne protein and lipid metabolism, active transcription foctors affect DNA transcription.
- States of activity affect: amt of colloid, thickness of follicular epithelium from squamous to columnar.

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Synthesis, Release and Control of Thyroid hormone:

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Synthesis:
1. Iodide ion concentration from blood by pumps in the basal membrane (~20:1
concentration above blood levels)
2. Thyroglobulin synthesis in RER
3. Oxidation of iodide by iodine peroxidases
4. Iodination of tyrosine residues of thyroglobulin at the luminal (apical) border.

Release
1. uptake of colloid at the follicular lumen
2. Degradation of the thyroglobulin complex in lysosomes
3. Release of T3 (triiodothyronine) and T4 (Thyroxin) from the basal region of the cell

Control
- by Thyroid Simulating Hormone (TSH), a product of pituitary basophils that increases hormone synthesis and release.

http://www.colorado.edu/intphys/Class/IPHY3430-200/image/23-9.jpg

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Thyroid: Parafollicular Cells (C-Cells)

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- Located within the basal lamina surrounding
each follicle
- stain intensely with silver but are otherwise difficult to
identify.
- Respond to increases in blood calcium levels by secretion of calcitonin that reduces blood calcium by actions on the kidney, gut, and bone (opposite effects of parathyroid hormone)

Front 28

Parathyroid Glands
cell types and hormones

Back 28

Consist of 4 small bean-sized nodules embedded on posterior surface of thyroid.

Chief cells:
- produce parathyroid hormone (PTH)
- small cells wtih clear cytoplams (look like lymphocutes)

Oxyphils:
- large eosinophic cells in clusters
- regressive form of chief cells
- fatty replacemnet of glandular tissue with aging

Parathyroid hormone (PTH) increase blood calcium:
1. Increasing the activity of osteoclasts. PTH also can liberate calcium from intracellular pools in osteocytes (osteocytic osteolysis).
2. Controlling Ca++ absorption from the gut.
3. Influencing calcium reabsorption by the kidney in exchange for phosphate.

Front 29

Hyperparathyroidism

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Results in excessive removal of bone in addition to derangements in calcium and phosphate metabolism. Loss of bone density and osteoporosis greatly weaken bones making patients subject to fractures.

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Thyroid pathophysiology

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Goiter: thyroid enlargement

Hyperthyroidism: hyerpactivility with reduction of colloid and hpercellularity of follicles

Graves: abnormal immunoglobulin mimics action of TSh to stimulate gland to produce hormone

Iodine deficiency goiter: large amount of colloid, but little active iodinaed hormone, due to lack of active hormone to provide feedback inhibition.

Cretinism: hypothyroidism during pregnancy -> fetal growth and development problems.