Endocrine System Flashcards
what is diabetes insipidus
excess dilute urine = extreme thirst
how is concentrated urine produced
-hypothalamus produces vasopressin (ADH) + stores in pituiltary gland
-ADH is release when H20 in body is too low
-ADH retains H20 in body by reducing H20 lost in kidneys
= concentration urine
how is dilute urine produced in diabetes insipidus
-reduced prod of ADH
-kidneys don’t retain as much water
-too much water released from body causing extreme thirst/polyuria
-more dilute urine
how do you tx lack of vasopressin
with vasopressin or desmopressin
how do you tx if kidneys dont respond to ADH
Thiazide diuretic
desomepressin
-more potent and longer duration of action than vaso
-no vasoconstrictor effect
-s/e; hyponatraemia and nausea
inappropriate ADH production
-more ADH - body stores too much water - dilutes salt conc in blood - hyponatraemia
-tx; fluid retention, demeclocycline (blocks renal tubular effect of ADH), tolvaptan - if used rapidly can cause osmotic demyelination (vaso antagonist)
what are the two types of corticosteroids and the difference
-mineral corticosteroids = high fluid retention low anti-inflammatory effect
-glucocorticoids = low fluid retention and high anti-inflammatory effect
mineral corticosteroid with most activity
1)fludrocortiosne
3) 2) hydrocortisone
fludrocortisone tx and side effects
-used for postural hypotension
-s/e:
-> water and sodium retention - hypertension
-> Odema
-> hypokalaemia
-> hypocalcaemia
most potent glucocorticoids
dexamethasone and betamethasone
then prednisolone, prednisone, deflazlort
glucocorticoids s/e
-diabetes
-osteoporosis
-avascular necrosis of femoral head and muscle
wasting
-gastric ulceration and perforation
corticosteroid s/e more detail
-report blurred vision and visual disturbance (MHRA)
-psychiatric reactions (seek help and stop)
-adrenal suppression (prolonged use = acute adrenal atropy or abrupt stop = acute adrenal insuff, hypotension or death)
-infections due to immunosupression - chicken pox, measles
-insomina
-children = stunt growth
-skin thinning
-prolonged = cushing syndrome
most common corticosteroid s/e
CORTICOSTEROID USE
-cushing syndrome
-osteoporosis
-retardation of growth
-thin skin
-immunosuppression + insomnia
-chorioretinopathy
-oedema
-striae
-emotional disturbance
-rise in BP
-obesity
-increased hair growth (hirsutism)
-diabetes mellitus (hypogly)
-ulcers (peptic)
-suppression (adrenal)
-electrolyte imbalance (hypokal)
managing s/e of corticosteroids
-lowest effect dose for min period
-single dose morning
-if 2DY course = AD
-short courses
-local tx rather than systemic
when corticosteroids gradual withdrawal
-40mg+ predn OD 1WK
-repeat evening doses
- >3wk tx
-recently repeated course
-taking short course within 1yr of stopping longterm therapy
topical steroid potency
-mild = hydrocortisone
-moderate = clobetasone
-potent = bethamethasone
-v.potent = clobetasol
adrenal insufficiency + tx
-due to Addison’s disease or congenital adrenal hyperplasia
-tx - hydrocortisone
- also can use fludrocortisone if primary
-can lead to adrenal crisis (severe dehydration, hypokalaemia shock, altered consciousness, seizures, stroke, cardiac arrest) tx hydrocortisone
description of diabetes
-persistent hyperglycaemia
-causes/types
-> deficient insulin secretion (type1)
-> resistance to action of insulin (type2)
->pregnancy (gestational)
->medications (steroids secondary)
driving + diabetes mellitus
-all drivers tx = insulin must inform DVLA
-drivers should be assessed on awareness of hypoglycaemia = capability of bringing their vehicle to a safe controlled stop
diabetes group 1 drivers
-adequate awareness of hypoglycaemia
- no more than 1 episode of severe hypoglycaemia while awake in 12MT
diabetes group 2 drivers
-must report all episodes of severe hypoglyc incl sleep
-full awareness of hypoglyc
-no episodes in 12MT
-most use blood glucose meter = sufficient memory to store 3MT of readings
-visual impairment inform DVLA x drive
DVLA advice diabetes mellitus
-if insulin tx must carry glucose metere + blood glucose strips
-check conc no more than 2hr before driving and every 2hr while driving
-readings >5mmol/l
-if <5 = snack
hypoglyc while driving
-<4mmol/l
-driver should:
-> safely stop
->turn off car and move from drivers seat
-> eat/drink sugar source
->wait until after 45min blood gluc has returned to normal before driving
-> x drive if hypoglyc awareness
type 1 diabetes mellitus + features
-insulin deficiency - destroyed beta cells in islet of langerhans
-most commonly before adulthood
-typical features:
->hyperglycaemia >11mmol/l
->ketosis
->rapid weight loss
->BMI <25
-> <50yr
-> FH of autoimmune disease
blood glucose monitoring
3 meals always
-QD before each meal + before bed
-5-7 walking
-4-7 fast BG before meals
-5-9 90 mins after eating
- >5 driving
insulin regimens type 1
-always receive insulin therapy
-multiple daily inj basal-bolus insulin regimen (1st line)
-bipharic mixture
-continous SC insulin infusion
multiple daily inj basal-bolus insulin regimen type 1
-basal (long/intermediate acting) OD/BD AND
-bolus (short/rapid acting) before meals
-first line basal = DETEMIR BD
-2nd line basal = glargine OD
bipharic mixture insulin regimen type 1
short acting mixed with intermediate insulin inj 1-3 times a day
continuous SC insulin infusion (insulin pump) insulin regimen type 1
adults = suffer disabling/uncontrolled hypoglyc
insulin requirements for more insulin
infection
stress
trauma
insulin requirements for less insulin
-physical activity
-intercurrent illness
-less food intake
-impaired renal function
-thyroid disorders
-coeliac disease
-addisons disease
insulin administration
-inactivated by GI enzymes - given SC
-inj into body area = SC fat (abdomen - fast outer thigh/buttocks - slower)
-rotate inj site - lipohypertropy can occur due to repeatedly inj same small area - erratic absorption of insulin
types of short acting soluble insulin
-human + bovine/porcine
-inj 15-30 before food
-onset 30-60mins
-peak action 1-4hr
-duration up ro 9hr