Endocrinology Flashcards
Viruses linked to causing T1DM
Coxsackie B (COX A causes hand foot and mouth
Enterovirus
Blood glucose range
4.1-6.1 mmol/l
Where is insulin secreted from
Beta cells in Islets of Langerhans (pancreas)
Where is glucagon secreted from
Alpha cells in Islets of Langerhans (pancreas)
Classic triad of hyperglycaemia symptoms
Polyuria, polydipsia, weight loss (dehydration)
What is secondary enuresis
Bed wetting in previously dry child
Associated with T1DM
Important bloods in newly presented T1DM (not in DKA)
FBC UE HBA1C
TFTs, TPO - autoimune thyroid disease
anti-TTG
Insulin antibodies, anti-GAD antibodies, islet cell antibodies - destruction of pancreas
Consequence of injecting insulin into the same spot repeatedly
Lipodystrophy
Subcutaneous fat hardens and prevents normal adsorption
What is Lipodystrophy
Subcutaneous fat hardens and prevents normal adsorption.
Should change site to inject
Most common insulin regime and meaning?
Basul bolus
Basal - long acting such as Lantus (normally in evening)
Bolus - short acting such as Actrapid (before meals)
IV treatment and does of dextrose for a hypo
10% at 2mg/kg as a bolus
Neurological DKA risk
Cerebral oedema
Cause of cerebral oedema in DKA
Rapid correct of dehydration
DKA criteria
BM >11, ketones >3, pH <7.3
2 key DKA treatment principles
Correct dehydration OVER 48 HOURS
Fixed rate insulin infusion
(add potassium)
Test for adrenal insufficiency
ACTH stimulation test (short synacthen)
Caution with adrenal insufficiency patients in other illnesses
Higher steroid demand and increased risk of hypoglycaemia
Addisionian crisis signs and symptoms
Hyperkalaemia, hyponatremia, hypoglycaemia
Reduced GCS, hypotension
Enzymes causing congenital adrenal hyperplasia
21-hydroxylase
11-beta- hydroxylase
Genetic inheritance of congenital adrenal hyperplasia
AR
Congenital adrenal hyperplasia effect on hormone levels
Low cortisol and aldosterone
High androgens
Testosterone hormone type
Androgen
Aldosterone hormone type
Mineralcorticosteroid
21-hydorxylase enzyme function
Progesterone to aldosterone and cortisol
Congenital adrenal hyperplasia pathophysiology
No conversion of progesterone to aldosterone and cortisol as defect in 21-hydorxylase. Extra progesterone gets converted to testosterone
Congenital adrenal hyperplasia symptoms in young babies
Virilised genitalia
Poor feeding, dehydration, vomiting, arrhythmias
Congenital adrenal hyperplasia in boys and girls
F: tall, facial hair, no periods early puberty
M: tall, deep voice, large penis, early puberty
SKIN PIGMENTATION
Skin changes in congenital adrenal hyperplasia
Pigmentation - increased ACTH -> increased melanocyte stimulating hormone
Congenital adrenal hyperplasia management
Cortisol replacement Aldosterone replacement (fludrocortisone)
Growth hormone deficiency presentation
Micropenis, hypoglycaemia, severe jaundice
Poor growth (ESPECIALLY AFTER 2-3 YEARS), short, late puberty
Cause of acquired hypothyroidism
Hashimotos (anti TPO)
Newborn hypothyroidism symptoms
Neonatal jaundice, poor feeding, constipation, increased sleeping, reduced growth
Associated conditions with acquired hypothyroidism
T1DM, coeliacs
Release of growth hormone is from where and mediated by what
GHRH (hypothalamus) -> anterior pituitary
most common mutations in growth hormone deficiency
GH1 or GHRHR (receptor)
Condition that results in underdeveloped pituitary gland
Empty sella syndrome
What is empty sella syndrome
Shrinking of pituitary gland (leads to growth hormone deficiency)
What does growth hormone do?
Acts on liver to release IGF-1
What cell maintains bone
Osteocyte
Cite (citation)=maintains credibility
What cell forms bone matrix
Osteoblast
Blast=build
What cell reabsorbs damaged bone
Osteoclast
