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PARASCI_L8
Endocrine Disorders
Question | Answer |
---|---|
complex syndrome involving metabolic dysfunction, sexual immaturity and growth retardation | hypopituatarism |
enlargement of thyroid gland | goitre |
thyroid hormone secretion insufficient for metabolic needs, thyroid gland enlarges to compensate, & overcome mild - moderate impairment | simple goitre |
affects regional groups of people where soil and food iodine are low | enemic goitre |
developing brain major target, crosses blood-brain barrier in foetal development, affects growth & development, metabolism, body temperature and heart rate | triiodothyronine (t3) |
regulates many of the body's metabolic functions, basal metabolic rate can increase by 60-100% when large amounts of T4 present, principle function to stimulate O2 consumption, generates body heat | thyroxine (t4) |
metabolic imbalance due to increased secretion of T4 and T3 stimulating protein, lipid and carb metabolism, | Hyperthyroidism |
Autoimmune disorder increasing t4 production manifesting as hyper-metabolism, toxic goitre, exopthalmos | graves disease |
extreme & life threatening form of graves disease, hyperthermia 41C<, tachycardia, heart failure, delirium, coma | thyroid storm (thyrotoxic crisis) |
hypothalamic, pituatary or thyroid insufficiency,/resistance to thyroid hormone. | hypothyroidism |
autoantibodies destroy thyroid gland tissue, can lead to goitre | chronic autoimmune thyroiditis (Hashimotos thyroiditis) |
severe adult hypothyroidism: non pitting oedema seen in facial puffiness and thick tongue | Myxedema |
untreated congenital hypothyroidism; thyroid gland non-funcitonal or absent | cretinism |
characteristic orange-peel skin with oedematous appearance | pretibial myxedema |
acute hypothyroidism causing hypotension, hypoglycaemia, hypothermia and LoC | Myxedema coma |
excessive glucocorticoids due to tumore or large amounts of glucorticoids administered in chronic inflammatory conditions | cushing syndrome |
deficiency in adrenocortical secretions | addisons disease |
secretes digestive juices | acini |
secretes hormones into blood | islets of langerhans |
secretes insulin and amylin | beta cells |
secretes glucagon | alpha cells |
promote glucose uptake by target cells & glucose storage, prevents fat & glycogen breakdown, inhibits gluconeogenesis | insulin |
maintains BGL between meals/fasting, exerts main action in liver, increases plasma glucose via glycogenolysis & gluconeogenesis | glucagon |
90-95% of sufferers, more common in younger people but can occur at any age | Type 1A immune-mediated diabetes mellitus |
much less common, no autoimmune involvement | Type 1B idiopathic diabetes mellitus |
hyperglycaemia with insulin resistance- no destruction of beta cells | Type 2 diabetes mellitus |
glucose intolerance during pregnancy of women with no history of diabetes | gestational diabetes |
excessive hunger | polyphagia |
excessive thirst | polydipsia |
excessive urination | polyuria |
sudden onset, cool, pale moist skin, normal RR, breath odour, weak rapid pulse, uncoordinated headache, irritable, poor conc. seizures | hypoglycaemia |
slower onset, warm, feverish, red & dry skin, deep and rapid breathing, possible kussmaul breathing, possible acetone breath, tachycardic, nausea & vomiting, abdo pain, hypotension, decreased LoC | hyperglycaemia |
insulin inhibits lipolysis, & release of free fatty acids, insufficient insulin -> hyperglycaemia and lipid mobilisation -> ketosis occurs fatty acids released and converted to ketones, | diabetic ketoacidosis |
hyperglycaemia pulling water from body cells (incl brain) | hyperglycaemia hyperosmolar state |
Kussmaul respiration, nausea & vomiting, abdo pain, fatigue, thirst, sweet smelling breath, confusion, drowsiness, hypotension, tachycardia | Symptoms of DKA |
Usually present dehydrated with stupor or in coma, unconscious, polyuria (weeks), profound dehydration, hypotension (later), tachycardia | symptoms of HHS |
disorder of water metabolism; deficient ADH secretion or renal resistance to ADH | diabetes insipidus |
deficiency of ADH acute onset | neurogenic diabetes insipidus |
resistance of renal tubules to ADH | nephrogenic diabetes insipidus |
caused by excessive fluid intake, primary polydipsia, | psychogenic diabetes insipidus |
metformin (glucophage), chloropropamide, Glycburide (diabeta), Glipizide (glucotriol) | Oral meds for type 2 diabetes |
actrapid (humalog/novalog), long acting (levemir/lantus), premixed (regular insulin + NPH) | Insulin meds for type 1 diabetes |