Exocrine Endocrine Stuff 💘 Flashcards
Exocrine parts of pancreas
90% exocrine
Exocrine produces bicarbonate amylase protease lipase .
Produces buffering solution and enzymes to aid digestion
Endocrine parts of pancreas
10% endocrine (lighter regions)
Islets of langerhans
These produce insulin glucagon somatostatin pancreatic polypeptide and ghrelin
Controls hunger sensation and glucose homeostasis
Acinus
Cluster of cells that resemble a many lobed berry
Intercalated ducts
Portion of the exocrine gland that drains from acting’s into larger ducts and eventually the intralobular duct
Helps takes enzymes
Secretes bicarbonate
Bicarbonate secretion from duct cells
Apical And bicarbonate secretion by interaction of the CL & K ion channels and apical cl-/HCO3- exchange
the basal membrane contains sodium potassium pump establishes and out in sodium concentration gradient that serves as a driving force for intracellular accumulation hco3- via na/h exchange
Bicarbonate secretion part 2 (secretin)
Secretin activates potassium and calcium channels via generation intracellular camp.
Activation of basolateral potassium channels hyper-polarizes the cells favoring apical CL efflux through camp activated CL channels.
Favor recycling of chloride that’s taking in to cell by sale by chloride bicarbonate exchange
Cholecystokinin
Responsible for digestion of fat and protein
Produced by i cells and acts on acinus to release digestive enzymes
Secretin
Hormone that regulate water homeostasis and secretions in the stomach and duodenum is produced by S cells and acts on the intercalated ductal cells to release bicarbonate.
Both hormone release is controlled by Vagus nerve
Percentage of each cell type
Alpha 20-25 Beta 70-75 Delta <5 Epsilon <1 Pp cell >1
Delta cells produce
Somatostatin
Epsilon produces
Ghrelin
Pp cells produce
Polypeptides
Insulin synthesis
Preproinsulin targeted by 24aa signal peptide and taken to RER
Single polypeptide cleaved forming proinsulin
Prounsulin folds 3 disulphide bonds form then moves to trans golgi network
Matures ti active form due to endopeptidases releasing c peptide fragment
Packaged into granules and wait for release
Two forms of insulin
Hexameric- inactive storage form. Three folds held together by zinc forming histidine bonds
Monomeric- active form, half life of 6 mins, composed of alpha and beta chains linked via disulphide bridges
Insulin secretion
Glucose sensing and uptake by GLUT2
Causes rise in atp causing depolarisation and k+ flows in
Causes Calcium influx and storages granules release insulin via exocytosis
IRS1
Triggers movement of GLUT 4 glucose receptor to cell surface for glucose uptake
Glucagon synthesis
29aa polypeptide generated by proprotein convertsse 2 cleaving Pro glucagon in alpha cells
Cystic fibrosis
Caused by frameshift mutation in the cystic fibrosis conductance regulator gene.
Affects lungs pancreas liver and intestine
Abnormal transport of chloride and sodium across the epithelium leading thick viscous secretions that block exocrine movement of digestive enzymes
Anterior Pituitary gland nerves and contents
axons from hypothalamus release neurohormones into primary plexus into hypothalamo hypophyseal portal system and it’s endocrine cells produce hormones
Contains chromophobes and chromophils (acidophils and basophils)
Posterior pituitary gland nerves and contents
Axons from hypothalamus release neurohormones directly into arterial system
Contains neural tissue and non myelinated axons
Pituicytes support glial type cells
Thyroid gland
Composed of many follicles
Follicular cells are a single layer of epithelium which surround each folllicle
Centre of follicle is colloid which stores hormones
Para follicular cells are less numerous lighter in colour larger and secrete calcitonin
Parathyroid gland
Two superior and two inferior
Contained within connective tissue capsule
Have chief cells and secretory granules which contain pth
Also have oxyphil cells
Thyroid hormone release
Thyrotropin relaxing hormone produced by neurons in the hypothalamus stimulates release of tsh and prolactin in anterior pituitary
Tsh stimulates thyroid release 83% t4 7% t3
Also produced calcitonin
Thyroid action
Stimulates metabolic rate- increases number and size of mitochondria
Also has positive inotropic and chronotropic effects on heart and important in growth and development in skeletal and nervous system
Thyroid formation
Iodide atoms actively transported across follicular cells and are trapped in colloid and oxidised to iodine by thyroid peroxidase
I2 then attaches to tyrosine molecule iodine+ tyrosine =MIT 2 iodine and tyrosine=DIT
MIT+DIT=t3 DIT+DIT=t4
T3 mainly made in liver and kidney
Congenital hypothyroidism
Absence or ectopic thyroid
All neonates screened this (Guthrie blood spot)
Treated with life long thyroxine
Acquired hypothyroidism
Via iodine deficiency
Decreased t3 and t4 which increase tsh and trh due to lack of negative feedback
Symptoms include decreased metabolic rate
Autoimmune thyroiditis (hashimotos disease)
Associated with thyroid peroxidase and thyroglobulin antibodies
Causes chronic thyroid damage and drip of blood hormone over years
More common in females
Secondary hypothyroidism
Due to something other than gland eg pituitary Tumour (can’t produce tsh)
Hyperthyroidism
Main causes are autoimmune thyroid diseases and toxic nodular goitre
Overproduction of t3&t4 surpassing tsh levels
Thyroid eye disease
Protrusion of eyes
Lid lag (white if eyes above and below iris come visible)
Opthalrhoplegia eyes are not straight
Can cause double vision and increased damage risk
Hyperthyroidism treatment
Inhibit iodide oxidation by thyroid peroxidase
Ptv
Beta blockers to alleviate symptoms
Radioactive iodine if other drugs unsuccessful
Or total thyroidectomy (surgery) (lifelong thyroxine)
Primary hyper parathyroidism
Usually due to a single benign parathyroid adenoma causing overproduction of pth
Symptoms of hypercalcaemia
Treated surgically unless it’s modest then ca levels monitored instead
HPA axis
Negative feedback system
Hypothalamus produces CRH which causes anterior pituitary to release acth
Stimulates adrenal cortex to release cortisol
High levels of cortisol then inhibits ant pituitary and hypothalamus
Adrenal insufficiency
Adrenal glands fail to produce enough cortisol
Primary is problem with adrenal gland
Secondary is problem with pituitary gland
Tertiary problem in hypothalamus
Primary adrenal insufficiency
Secondary tertiary
Aka Addison’s disease
High levels of acth
Acts on melanocytes yo produce more melanin causing hyper pigmentation
In secondary high CRH in tertiary CRH ACTH and cortisol low
Testing for adrenal conditions
If u suspect insufficiency u stimulate to see response
If u suspect over functioning u suppress the gland
Synacthen stimulation test for adrenal insufficiency use ACTH and see if ride in cortisol after 30 mins
For secondary you do insulin stress test
Hypercortisolemia
Aka cushings disease causes protein depletion and poor wound healing and osteoporosis
Due to high acth and low crh
Tested with dexamethasone test-absence of supressuon yo dexamethasone =cushings disease
Prolactin action
Baby sucks on breast stimulates hypothalamus to stimulate pituitary yo produce prolactin producing milk
More it sucks more milk produced
Ghrh
Ghrh>gh>igf1 (liver)> growth and development and stress
