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192 Cards in this Set
- Front
- Back
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what are neuroendocrine/oxytocin messengers? |
hormone released from axon teminal |
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what is a autocrine messenger? |
action on the same call (paracrine on neighbouring cell) |
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what 4 types of hormones are there? |
peptide, steriod, derived from tyrosine, eicosanoids |
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an example of a hormone derived from tyrosine? |
TH's and catecholamines |
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how are peptide homones made? |
from DNA and made as a pre hormone (hydrophobic chain present) then a pro hormone and then a hormone |
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can steroid hormones be stored? |
no, they diffuse out |
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how do peptide hormones have their effect? |
receptor on cell surface and signal transduction and physiological response |
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how do steroid hormones have their action? (and THs) |
nuclear or cytosolic in location (as synthesised from DNA) and act on intracellular receptors |
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what are dynamic/provocative tests used to asses? |
the integrity of the feedback loop a stimulation test tests for hyposecretion |
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What are the anatomical names for the anterior and posterior pituitary lobes? |
anterior: adenohypophysis posterior: neurohypophysis |
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what is the anterior and posterior lobe of the pituitary formed from? |
anterior: ectodermal upgrowth posterior: neuroectodermal downgrowth |
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what are the arteries and veins called supplying the pituitary gland in development? |
the hypophyseal arteries and veins |
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What are the 3 cell bodies and neurone pathways from the hypothalamus to the anterior pituitary? |
1) arcuate nucleus 2) ventomedial nucleus 3) preoptic nucleus factors all released along portal vessels to capillary bed of adenohypophysis |
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what are the cell bodies present in the posterior pituitary that are the neuronal pathways from the hypothalamus? |
paraventricular (PVN) and supraoptic (SON) nuclei and neurones carrying OXYTOCIN AND ADH along neurones to capillary bed |
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What are the hormones secreting cells of the anterior pituitary? |
ACIDOPHILS: -somatotrophs(GH) -Mammotrophs (Prolactin) BASOPHILS: -Corticotrophs (ACTH) -Thyrotrophs (TSH) CELLS SECRETING GLYCOPROTEINS: -Gonadotrophs (FSH&LH) CHEMOPHOBES (immature hormones?) |
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what do coricotrophs release? |
corticotropin or ACTH and inhibits GnRH release |
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What does TSH do? |
stimulates the synthesis of Thyroid hormones and the size and number of thyroid follicular cells |
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Definition of Tropic? |
affecting the activity of an endocrine |
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Definition of Trophic? |
promotes growth, tissue integrity |
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What does GnRH (Gonadotropin releasing hormone) do? |
release of LH and FSH |
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What is the effect of Somatostatin? |
inhibits the release of TSH and GH reduce gastric acid secretions (gastrin, secretin and histamine) inhibits insulin and glucagon |
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What is the effect of the hypothalmic hormone dopamine? |
inhibits the release of prolactin |
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What 6 hormones are hypothalamus produced hormones? where do they all act? |
GnRH GHRH (GH releasing hormone) SS TSH Dopamine CRH (cortioctrophin releasing hormone)
at the anterior pituitary |
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What organ does GH act on? |
The liver and IGF-1 |
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What organ does ACTH act on? |
Adrenal cortex to produce cortisol |
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what are the posterior pituitary hormones? |
ADH Oxytocin |
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What is the stimulation and action of AVP/ADH? |
stim: inc. body fluid osmolality (dec. blood volume/pressure and stress)
Actions: BVs: vasconstrict and V1 Kidney: inc. perm at DCT and CD to water and urea Stimulates ACTH release |
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What is the stimulation and action of oxytocin? |
stimulated by: suckling and cervical stimulated
Actions: expression of breast milk, contraction of uterine SM, maternal behaviour
CLINICAL: induces labour |
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What are the potential problems associated with pituitary tumours? |
hyposecretion: squash other cells hypersecretion visual disturbances |
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What common pituitary tumours are there? |
GH-secreting prolactinoma ACTH-secreting (cushings disease) |
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Give an example of a suppression test |
When suspecting hyper secretion Oral glucose tolerance test: high [glucose] suppresses GH release failure to lower GH secretion suggests a GH tumour |
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what are the S/S of a prolactinoma and what is the treatment? |
S/S: loss of fertility, libido, watery milk from nips treatment: Dopamine-R agonist (inhibits prolactin)
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What are the S/S of Acromegoly and what is the treatment? |
S/S enlarged hands and feet and lower jaw due to XS GH TREATMENT: surgical removal and radiotherapy, SS analogues inhibit GH release (Dopamine-R agonists as some adenomas have dopamine-R which when activated inhibit GH) |
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What is Cushings Syndrome? |
XS Glucocorticoid main cause: ACTH secreting anterior pituitary tumour |
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what are the consequences of having ADH deficiency? |
diabetes insipidus |
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What two hormones are produced by the thyroid gland? |
Tri-iodothyronin (T3) Thyroxine (T4) |
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what is the thyroid gland made form in embryology? |
an endodermal downgroth of the floor of the pharynx between anterior 2/3 and post 1/3 of the tongue, grows from the foramen cecum |
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where are cysts and ectopic thyroid tissue often found? |
along the thyroglassal duct |
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What is the epithelium of the thyroid gland? |
cuboidal? |
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what cells produce calcitonin in the thyroid? |
parafollicular c cells |
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what is the colloid in the histology of the thyroid gland? |
it is the centre of the tube surrounded by cuboidal epithelium it has the hormone in it |
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where are the parathyroid gland situated? |
on the posterior surface of the thyroid gland and secrete parathyroid hormones (have chief cells- can form parathyroid adenoma which disrupts Ca2+ metabolism) |
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What is T4 and T3 made from? |
Tyrosine +I2-->MIT or DIT
DIT+DIT =thyroxine T4 MIT +DIT =Tri-iodotyronine T3 |
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What makes rT3? |
DIT+MIT (as opposed to MIT+DIT)=rT3 antagonist at T3-R |
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What does the transport of Iodine into the lumen depend on? |
Sodium-Iodine symporter on the basal membrane Pendrin (transports Iodine to lumen) |
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What enzyme oxidises The I-? |
Thyroid peroxidase (catalyst for producing MIT&DIT) |
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The cold temperature in the neonate stimulates what hormone? |
TRH-->TSH--->T3/T4 |
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How does Stress affect the levels of TRH and TSH? |
directly inhibits TRH and releases SS from the hypothalamus and inhibits TSH
thus inhibiting T3/T4 |
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What does T4 and T3 bind to in the plasma? |
Thyroxine binding globulin (TBG) 70% Transthyretin 10% Albumin 20% |
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When T4 and T3 reach their organs what occurs? |
T4 can be converted to T3 (4-5x more potent) or to rT3 (no action) |
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What are the actions of thyroid hormones? |
increase metabolism and BMR and metabolism of CHOs, proteins, fats, stimulate growth and development and synergistic with actions of SNS and cetcholamines (beta adrenocepots, inc. HR) |
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Where is the T3-R in the cell? |
within the nucleus |
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what happens to the levels of rT3 in times of stress? |
it is increased and T3 is decreased, this lowers the metabolic rate |
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What T3, T4 and TSH levels would you expect to see in hypothyroidism with:
primary failure of thyroid gland
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dec. T3/T4 Inc.TSH
GOITRE |
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What T3, T4 and TSH levels would you expect to see in hypothyroidism with:
Secondary hypothalmic or anterior pituitary failure |
dec. T3/T4 dec. TSH
NO GOITRE |
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What T3, T4 and TSH levels would you expect to see in hypothyroidism with:
Lack of dietary Iodine? |
dec. T3/T4 inc. TSH
GOITRE |
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what drugs can cause hypothyroidism? |
lithium |
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What T3, T4 and TSH levels would you expect to see in hyperthyroidism with:
Abnormal levels of Thyroid stimulating Immunoglobulins (Graves Disease) |
inc. T3/T4 dec.TSH
GOITRE |
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What T3, T4 and TSH levels would you expect to see in Hyperthyroidism with:
secondary to XH hypothalmis/ant. pit secretion |
inc. T3/T4 inc. TSH
GOITRE |
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What T3, T4 and TSH levels would you expect to see in hyperthyroidism with: |
Inc. T3/T4 dec. TSH
GOITRE |
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What two types of goitre are there? |
Diffuse: overstim of the thyroid gland (TSH or TSI (graves) Nodular: one area of enlargement (tumour) |
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What are the S/S of hypothyroidism? |
weight gain, dry skin, hoarse voice, menstrual changes, cold intolerance, dec. HR/BP, depression, poor memory
DEC BMR
NEONATE: dwarfism, mental retardation |
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What should you test for if you suspect hashimoto's in hypothyroidism? |
Thyroid antibodies |
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How do you manage hypothyroidism? |
synthetic hormones Leuothyroxine (T4) Liothyronine (T3) |
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What is Graves' disease? |
form of hyperthyroidism, thyroid stimulating antibodies are produced which bind to TSH receptors on the thyroid gland causing an inc in T3/T4 and a dec. is TSH via neg feedback. GOITRE |
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What are the S/S of hyperthyroidism? |
weight loss, sweating, heat intolerance, palpitations, tremor, nervousness and anxiety |
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How do you test for thyroid tumours? |
the thyroid uptake test (123 I) |
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What are anti-thyroid (thionamides) drugs? e.g. carbimazole and propylthiouracil(PTU) |
Dec. production of THs (inhibit iodination of coupling pieces via TPO) PTU blocks T4 to T3 converting (deiodination) *several weeks for clinical response* |
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What are non selective beta blockers used for in the treatment of thyroid problems? |
dec. action od catecholamines-->relieve the tumour and anxiety |
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What is the use of radioactive Iodine (123 I) in thyroid problems? |
1st line treatment for elderly with nodular goitres and hyperthyroidism (used in relapse) given as a drink (can cause hypothyroidism) |
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What does the outer cortex of the adrenal gland secrete and what is it controlled by? |
steriod hormones and controlled by adenohypphysis |
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what does the inner medulla secrete and what is it controlled by? |
catecholamines (chromatin cells) under nervous control |
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what are the different sections of the adrenal gland derived from? |
cortex: from coelomic mesothelium (mesoderm) medulla: neural crest (neuroectoderm) |
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Is the metal cortex responsive to ACTH? |
YES |
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what is responsible for the gut closure in the foetus? |
corticosteroids |
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What are the 3 zones in the cortex? |
innermost: Zona reticularis Middle: Zona fasciculata outer: zona glomerulosa |
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what structure is filled with blood and passes through from the cortex to the medulla? |
sinusoids |
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what do the different layers of the cortex secrete? |
Zona glmoerulosa: mineralocorticoids zona fascilulata: glucocorticoids and gonadocorticoids Zona reticularis: glucocorticoids and gonadocorticoids |
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what are the pale staining cells in the adrenal medulla in groups that have a rich blood supply? |
chromaffin cells |
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What are the arrangements of cells in the 4 different areas of the cortex? |
z.g: columnar/ovoid cells (large round cups) z.f: sinusoid between columns (contains blood) z.r: cells in cords separated by sinusoids, irregular clumps |
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What organelles are only present in the medulla and not the cortex? |
RER, Granules and Mitochondria (petide synth) |
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What organelles are only present in the cortex and not the medulla? |
SER, Lipid droplets, tubular cristae in motochondira (steriod synth) |
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what is the rate limiting step in the synthesis of steroid hormones? |
transport of cholesterol from the outer to the inner mitochondrial membrane |
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What hormones are systhesised in the different parts of the cortex? |
Zona Glomerulosa: ALDOSTERONE Zona Fascilata: CORTISOL Zona Reticularis: Lesterone, Osture, Oestradiol, oestriol |
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Which out of Cortisol and Aldosterone is the most potent mineralocorticoid and the most potent glucocorticoids? |
Cortisol: roughly equal at both (but higher than aldosterone for glucocorticoid potency so used as anti-inflam) Aldosterone: v.v.v. potent mineralocorticoid (na+ retention) |
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What is a mineralocorticoid? |
a steroid hormone that influences salt and water balance (aldosterone) |
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what is the action of aldosterone? |
acts on DCT and CD to promote NA+ retention and K+ elimination in urine. secreteion stimualted by inc. plasma [k+] and RAAS independent of ACTH |
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What are androgens? |
DHEA and sulphated DHEA and adrostenedione decreased release below 21 yrs and 50% in women (axillary hair and libido) ?men? related by ACTH but no feedback on CRH /ACTH |
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What is the body response to stress in the adrenal gland? |
Hypothalamus synthsises CRH Ant. pit produces ACTH acts on adrenal cortex to produce cortisol (neg feedback look) to go to target cell |
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when are cortisol levels at their highest? |
in the morning |
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What is cortisol transported with in the blood? |
bound to transotin (cBG) and Albumin
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What does cortisol act via and where to regulate gene expression in target tissues |
via Glucocorticoid-R (GR) an intracellular receptor |
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What are the actions of cortisol? |
metabolic, anti-inflam, adaptive for stress |
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What are the metabolic effects of cortisol? |
opposite of insulin! Muscle and Adipose: dec. glucose uptake inc. fat and protein breakdown and dec. synth. liver: inc. gluconeogenesis and glycogen synth. |
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What are the anti-inflammatory and immunosuppressive effects of cortisol? |
stimualte production of lipocotin 1 which inhibits PLA2 (AA-->PGs and TPXs SO dec. inflam. mediators) dec. T Lymphocytes, ILs, cytokines, NO produciton stabalises lysosomes
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Other than cortisol what also helps aid in 'stress response'? |
SNS and adrenaline (inc. CO and ventilation and diversion of blood to heart and muscle) |
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what can prolonged cortisol elevation do? |
muscle wasting, hyperglycaemia, GI ulcers (inc. PGs in gut) and imparied immune response |
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What are the signs and symptoms of Cushing's Disease? |
trunkal obesity, buffalo hump (altered fat dep.) acne (XS androgens) thin arms and legs, purple straie (breakdown of protein) poor wound healing (loss of collagen)
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Cushing's syndrome is often due to an ACTH secreting anterior pituitary tumour causing cushing disease, how could you identify the location of this tumour? |
adrenal:inc. cortisol dec. ACTH Pituitary: inc. cortisol inc. ACTH ectopic : inc. cortisol inc. ACTH (tumour cells have impaired responsiveness from neg feedback) high dose DEX will suppress pituitary ACTH but not affect adrenal or ectopic ACTH source |
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What will the CRH stimulation test distinguish the difference between when diagnosing cushing's disease and where the tumour is? |
Normal CRH:inc. ACTH so inc, cortisol ectopic: no change piuitary inc.inc. CTH, inc.inc. cortisol |
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What is the treatment for bushings disease? |
if ant pit: MRI Adrenal: CT/MRI Bronchial (ectopic): CXR ACTH-sec tumour: octreoscan (TM) surgery, radiotherapy, drugs to inhibit steriodogenesis |
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What is Conn's syndrome? |
primary hyperaldosteronism Na+ and water retention and K+ loss (hypokalaemia) due to a tumour |
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What is conn's associated with? |
hypertension (1% of pt's with hypertension have Conns) |
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What is the treatment for conns syndrome? |
surgery and alsoterone receptor antagonist (spirolactone-K+ sparing dieuretic) |
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What is Addison's Disease? |
Adrenal Insufficiency v. rare and chronic failure of the adrenal glands primary insufficiency: gradual destruction of adrenal tissue |
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What happens to aldosterone, cortisol, androgen and ACTH in addison disease? |
dec. aldosterone, cortisol, androgens inc. ACTH |
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What are the S/S for addison disease? |
postural hypertension, muscle weakness, hyponatraemia, hyperkalaemia, weightloss, nausea and vomiting |
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what is the treatment for addisons disease? |
life long hormone replacement glucocorticoid: hydrocortisone (mimic daily changes) mineralocorticoid=fludrocotisone (daily) |
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What are secondary adrenal insufficiencies? |
lack of ACTH production (tumour/damage to pit.)
secondary adrenal suppression: long term glucocorticoid is (suppresses ACTH levels-->adrenal suppression) |
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What is an example of a secondary adrenal insufficiency? |
congential adrenal hyperplasia (defect in enzyme in prod. of cortisol and aldosterone) |
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What are the levels of aldosterone and cortisol in the secondary adrenal insufficieny, congenital adrenal hyperplasia? |
dec. aldosterone, cortisol and accumulation of androgens as it shifts to the sex hormone pathway. XS ACTH as dec. neg feedback which causes the hyperplasia of the adrenals |
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What is the consequence of Congenital hyperplasia? |
severe: females born with ambiguous genitals children: early pubery females: more muscular |
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how do you treat congenital adrenal hyperplasia? |
hormone replacement: glucocorticoids activate neg feedback loop and plastic surgery
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what two types of cells are there that secrete hormones in the GI tract? |
open type (straight onto surface and are responsice to gut contents) closed type (deep to surface receptive to changes in tissue environment) |
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There are many types of enteroendocrine tumours of the pancreas depending on the cell type: what is: insulinoma gastronoma glucaconoma |
secrete insulin secrete gastrinsecrete glucagon |
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Which part of the pancreas contains the acinar cells and develops first? |
the exocrine part |
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What cells are associated with the endocrine part of the pancreas? |
the islet cells (adjacent to the ducts of the exocrine part) |
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what is the innervation of the pancreas? |
symp: abdominal pelvic splanchnic para: vagus |
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What is the blood supply of the pancreas? |
splenic and superior and inferior pancreaticoduodenal aa veins tributaries of splenic and superior mesenteric portal |
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what is the distribution is the islets around the pancreas? |
Head: 25% unicate process: 25% body 20% tail 30% |
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What do the Alpha cells of the pancreas secrete? |
glucagon (18%)-dense spheres |
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What do the beta cells of the pancreas secrete? |
Insulin (75%)-crystals, loose mem |
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What do the D cells of the pancreas secrete? |
Secretin (3%)- geterogenous, large spheres |
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What makes up pro-insulin? |
a-cain, B-chain and C-peptide |
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What is lost from pro insulin to make insulin? |
C-peptide lost |
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what enzymes cleaves the c-peptide to convert pro insulin to insulin? |
PC1 (at 32,33) PC2 (at 65,66) |
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What enzyme removes two amino acids at the ends of the c-peptide? |
CPH removes 64+65 CPH removes 31+32 |
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What happens to the insulin a c-peptide after the cleavage of the c-peptide has occurred? |
packaged into secretory granules |
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What 3 factors control insulin release? |
Nutrient stimules Potentiators (GLP-1, GIP) Neural control |
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How does nutrient stimulus affect insulin release? |
blood glucose >5mM (inc. ATP:ADP) closes ATP-K+ channels and mem depol. so voltage gates Ca2+ channels open-->insulin release |
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How do potentiators affect insulin release? |
Gut hormones: GLP-1 (glycogen like peptide), GIP (gastrc inhibitory polypeptide) are incretins Glucagon, which is ss inhibits |
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How does neural control affect insulin release? |
Symp. Beta-adrenoceptors via a2 adrenoreceptor dec. Insulin release Parasympathetic: muscarinic: so inc. IR |
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What is the actions of insulin on the liver? |
increase glycogen synth dec. glycogen breakdown dec. gluoconeogenesis
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What are the actions of insulin on the muscle? |
inc. uptake of glucose via GLUT-4 inc. protein synth dec. protein breakdown |
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What are the actions of insulin on adipose tissue? |
inc. uptake of glucose via GLUT-4 inc, lipogenesis dec. lipolysis |
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What type of hormone is glucagon? |
peptide hormone (synthesised as pro glucagon in alpha cells) |
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What stimulates the release of glucagon? |
low BG (<3.5mmol) para+symp. NS Amino Acids *inhibited by high BG, insulin and SS* |
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What are the main actions of glucagon? |
stimulate hepatic glycogenolysis stimulate hepatic gluconeogenesis +lipolysis |
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What is Somatostatin? |
peptide hormone |
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What hormones does somatostatin inhibit? |
inhibits glucagon and insulin secretion in paracrine mech. |
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What effect does cortisol have on glycogenolysis? |
none |
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what effect does insulin have on gluconeogenesis? |
dec. |
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what effect does growth hormone have on glycogenolysis? |
none |
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What hormone stimulates and what hormones inhibits hepatic ketogenesis? |
insulin inhibits it, glucagon stimulates |
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when does metabolic acidosis occur? |
in starvation and in T1DM |
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What is a consequence of loss of insulin action? |
ketones increase -metabolic acidosis -nauseas, vomiting, breathlessness, abdo pain
increase glucose-osmotic diuresis -frequncy urinating, dehydration, thirst |
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what is the difference between type one and type two diabetes? |
T1DM: insulin insufficiency T2DM: impaired b-cell function and/or loss of insulin sensitivity |
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What are the values for fasting blood glucose and a random glucose sample that if associated with symptoms is treated as DM |
fasting>= 7.0mmol random >=11.1mmol
if no symptoms must have 2 values |
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what are the characteristics of T1DM? |
autoimmune, progressive destruction of B cells. onset <40, rapid, weight normal or loss tendency to ketosis treat with insulin |
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What are the characteristics of T2DM? |
relative insulin deficient/imparied b-cell function and or insulin resistance onset >40years, gradula and complications usually overweight NO KETONES IN URINE diet, drugs treatment (insulin 20%) |
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what might me a genetic reason someone might have hyperglycaemia? |
downs, prader-willi |
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what is the steps for treatment of diabetic patients (t2dm)?
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1) diet and lifestyle advice 2) Metformin (not for renal impairment) Sulphonylurea (okay if not overweight (fx:weight gain)) 3) dual therapy 4) start insulin (triple therapy 5)intensity insulin regime/+other drugs (thiazolinedions, GLP-mimetics (inhibits glucagon) |
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How does metformin act to help T2DM? |
activates AMP Kinase dec. gluconeogenesis and inc. glucose utilisation |
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How do sulphonylureas act to help T2DM?
what other class of drugs work in the same way? |
stimulate insulin secreteion and block islet b-cell ATP-sensitvie k+ channel
prandial glucose regulators also affect this |
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How do Thiazolidinediones act to help T2DM? |
PPARy agonists 'insulin sensitizers'
tosiglitazone liscense suspended |
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How does Acarbose act to help T2DM? |
a-glucaidase inhibitor delays digestion and absorption of starch and sucrose |
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How do GLP-1 and PP-4 inhibitors act to help T2DM? |
promote insulin release dec. glucagon secretion dec. gastric emptying dec. hepatic glucose glucose production |
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How do Na-Glucose transport 2 ihibitors help in T2DM? |
inhibits renal glucose reabsorption so increases urinary glucose excreted |
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What are the different classifications of insulin? |
short acting (soluble analogues, lispro, aspart) intermediate-acting (complex with protamine, insulin, zinc suspension) long action (insulin zinc suspension) or analogues pre-mixed or biphasic,: mixture of short and intermediate acting |
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what is the basal bolus treatment? |
basal: long acting given less often bolus, short acting to give spikes |
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What are the three acute complications of diabetes? |
hypoglycaemia diabetic ketoacidosis hyperosmolar hypergylcaemia state (HHS) |
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How does hypoglycaemia occur in T1 and T2 DM? |
T1: insulin overdose, XS exercise T2: sulphonylureas, hepatic or renal disease |
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What are the symptoms of hypoglycaemia? |
palpitation, tremours, sweating, loss of concentration, slurred speech, seizures (deficiency of glucose in brain) |
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What is the treatment for acute hypoglycaemia? |
concious: d-glucose, sugary food/drink unconcious: glucose I.V or glucagon (not after alcohol) |
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What is diabetic ketoacidiosis? |
hyperglycaemia and metabolic acidosis MEDICAL EMERGENCY |
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what is the treatment for diabetic ketoacidosis? |
replacement of fluids, electrolytes potassium and bicarbonate replacement insulin and treat underlying cause |
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What is hyperosmolar hyperglycaemic state (HHS)? |
acute complication of diabetes, sever hyper without ketosis (T2D) managed as DKA (less insulin)
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What are the long term secondary complications of diabetes? |
microvascular: retinopathy nephropathy neuropathy macrovascular: metabolic syndrome IHD and Stroke Peripheral Heart Disease
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what occurs in microvascular complications of diabetes long term? |
damages to small vessels by hyperglycaemia ang glycation of proteins |
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What are the classifications of retinopathy? |
background microanyersm pre-proliferative (areas of retina become ischaemic) proliferative (new BVs bleed-->blindness) maculopathy (macula affected) |
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What is nephropathy? |
diabetes long term microvascular complication of damage to the kidney, ends in renal disease ACEi's are protective :) |
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what nerves are often affected in neuropathy? |
cranial, autonomic and PNS , mainly in feet, inc. risk of food ulcers. innapropriate response to stimuli: Causalgia |
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What is the compilation in long term macrovascular complications of diabetes? |
accelerated atherosclerosis (sped up by the diabetes) |
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What is metabolic syndrome? |
macrovascular complication associated with DM, glucose intol dsylipidaemia hypertension abdo obesity |
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What is peripheral vascular disease? |
intermittent claudication (ischaemia), ulceration risk of gangrene , amputation diabetetic foot ulcers poor blood supply |
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how do you manage the microvascular complications associated with DM? |
good glycemic control control of hypertension (ACEi, ATRA, CCB) |
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How do you manage the macrovascular complications of DM? |
good glycemic control control of hypertension control of dislipidaemia (statins) use of anti-platelets (L.D Aspirin, clopidogrel) |
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What is an example of a synergistic hormone action? |
(more than one hormone acting has a greater effect than just one acting) THs on activity of catecholamines (upreg. beta-adrenoceptor expression) |
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What hormones act along with CRH to stimulate ACTH release in a synergistic way? |
AVP/ADH act on ant. pit. -->ACTH -->adrenal cortex -->cortisol -->target cell |
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what hormones does cortisol act permissively on? |
on catecholamine in fight or flight |
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what hormone acts on GH permissively in growth production? |
THs |
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at what age does the amount of lymphoid tissue peak? |
when child goes to school |
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what are the metabolic actions of GH? |
inc. lipolysis inc. amino acid uptake and protein synth inc hepatic glucose output dec. glucose uptake (fat SKm) |
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What are the indirect effects of GH on Growth? |
release of GF, IGF-I, IGF-II from liver growth via IGF-I on cells -stim pretin synthesis and inc cell size, inc cell number and promote skeletal growth |
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Which hormones affect GH? |
insulin: growth promoter sex hormones: inc. at puberty, linear growth, stop bone long by promoting epiphyseal plate closure glucocorticoids (stress and antigrowth) in steroids with children |
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What is the control of GH release? |
hypothalamus->GHRH->ant. pit.-> GH->liver and other tissues ->somatomedins ->growth
SS inhibits ant pit from releasing GH
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What stimulates the levels of GHRH to inc. to stimulate the ant. pit. to produce GH? |
dec. [glucose] dec. [FFA] inc. [amino acids]
stress, sleep and exercise |
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what is the effect of glucocorticoids on GH release? |
initially synergism on metabolism: inc. gluconeogenesis and lipolysis
if high [glucocorticoids] inhibit GH (cushings syndrome and long term use of steroids) |
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What are some of the disurbances that cause a stunted stature? |
pituitary dwarfism (GH deficieny) hypothyroidism (insufficient THs for GH) cushing's syndrome (XS cortisol so inhibits GH) congential adrenal hyperplasia sexual precocity (inc androgens) |
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What are the effects of a growth hormone deficiency in adults? |
psychological XS tirdness osteoporosis, inc adipose, impaired hair growth |
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What ar the disturbances hormonally that can cause accelerated growth (tall stature)? |
gigantism (often due to tumour with XS GH) hyperthyroids -->XS THs-->GH activity sexual precicity (initial access then cones close-short) |
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What is Acromegaly? |
XS GH in Adult coarsinf of facial features enlarged hand and feet headaches, sleep apnoea glucose intolerance irregular or loss of periods |
