Endo patio Flashcards
Predisposing factors for Type 1 diabetes
- Autoimmune diseases : Coeliac, Addisons, pernicious anaemia
- HLA - DR3 + DR4
- Identical twins
- Enterovirus, cocksackie B virus, vitamin D deficiencies
Predisposing factors for T2 diabetes
- Metabolic syndrome
- High cholesterol
- Gestational diabetes
- Obesity
- Genetics:
- Ethnicities e.g Asian/african
- Environment = poor diet, low birth weight, PCOS, history of GDM,
Describe how a diagnosis of diabetes is established
Type 1:
- DKA can be first presentation of type 1 diabetes
- In T1D aiming for 4-7mmol
- Presentation = polydipsia, polyuria, respiratory respirations,
Investigations
- Auto antibodies
- Blood glucose concentration
- VBG : Acidosis in DKA
- Blood ketones
- C peptide
- HbA1c
Diagnosis = Hyperglycaemia ( >11) typically with one of following : Weight loss, ketosis, BMI < 25, family/personal history of autoimmune disease, age < 50
Is a clinical diagnosis
How T2DM diag osed
Persistent hyperglycaemia characterised by
- HbA1c > 48
- Fasting glucose > 7mmol
- Random glucose > 11
Clinical features
- Polydipsia, polyuria, blurred vision, weight loss, fatigue, recurrent infections
- Acanthosis nigoracans = skin condition -> dark pigmentation ( insulin resistance)
Explain why ketoacidosis develops in untreated or uncontrolled type 1 diabetes
In DKA :
- Lack of insulin due to autoimmune mediated destruction of beta cells
- Impaired glucose uptake into the cells
- Free fatty acids -> ketones
- Ketones acidify the blood stream
Explain the term peripehrla neuropathy caused by diabetes
Hyperglycaemia -> damages nerves -> loss of sensation
What is hypoglycaemic shock -
- Hypoglycaemia
- Increased insulin which lowers BGC
- Tremor, palpitations, anxiety, sweatign, huner, dizziness, weakness, altered MS, confusion, seizures
- Emergency treatment:
- If conscious - Fast acting carb followed by slower acting
- Unconcious - 20% 100ml dextrose + 1mg IM glucagon
- Need rapid corrections
Ketoacidosis
- Lack of insulin -> BGC remains high as impaired glucose uptake into cells
- Dehdyration, Hypotension, kussmaul breathing, ketotic breath,r educd consciousnes,s coma,
- Emergency treatment: Iv fluids (0.9% slaine), IV insulin (0.1units/kg/hr), K+ monitoring, IV dextrose once BGC stabilised to <14. IV 10% dextrose at rate 125ml/hour
- Need slow correctiosn to prevent cerebral oedema
What is this?
Figure 1 Insulitis. The human islet (centre) is infiltrated with mononuclear cells: macrophages and CD8+ and CD4+ T lymphocytes
List the causes of hypoparathyroidism and hyperparathyroidism
Physiology
- Parathyroid glands + chief cells produce PTH in response to hypocalcaemia
- PTH = Increases osteoclast, increase VD, increased Ca2+ absorption in gut + kidneys
Hypoparathyroidism
- Iatrogenic post surgical removal of part of gland e.g tumour removal
- Congenital disease
- Idiopathic
- Psuedohypoparathyrodisim = resistance to PTH hormone
Hyperparathyroidism
- Primary = uncontrolled PTH from PT glands due to tumour ( adenoma is most common) -> hypercalcaemia
- Secondary = insufficient vitamin D or chronic renal failure -> reduced absorption of Ca2+ -> hypocalcaemia
- PT glands respond by increasing excretion of PTH = hyperplasia
- Serum Ca2+ = normal/low but PTH = high
Hypoparathyroidism
Complications in Hypoparathryoidism
- Muscle twitches, cramping, spasms, pARaesthesia, depresison, cataracts, prolonged QT itnerva;
Complications in Hyperparathryodiism
- Renal stones
- Painful bones
- Abdo symptoms. - constipation, nausea, vomtiing
- Psychiatric - fatigue, depression, psychosis
- ECG changes - flat T waves, QT shrotening, PR prolongation
Is trace glycosuria nromal in pregnancy
Yes - trace glycosuria is common in pregnancy due to the increased GFR and reduction in tubular reasbroption of filtered glucose.
How can excessive alcohol lead to polyuria
ADH suppression in posterior pituitary gland subsequently leading to polyuria
