Endocrinology Flashcards
(38 cards)
What is type 1 diabetes?
When the pancreas stops being able to produce insulin - autoimmune destruction of beta cells leading to insulin deficiency
Causes of T1DM?
May be genetic component - HLA 6 predisposition
Viruses - Coxsackie B virus and enterovirus.
What is glucagon?
A hormone that increases blood sugar levels. It is produced by the alpha cells in the Islets of Langerhans in the pancreas.
It is a catabolic hormone (a breakdown hormone). It is released in response to low blood sugar levels and stress.
What is glycogen?
The stored form of glucose in muscle and liver cells
What is glycogenolysis?
The breakdown of glycogen into glucose in the liver
What is gluconeogenesis?
Conversion of proteins and fats into glucose in the liver
What is ketogenesis?
When there is insufficient supply of glucose, and glycogens stores are exhausted, such as in prolonged fasting.
The liver takes fatty acids and converts them to ketones.
Ketones are water soluble fatty acids that can be used as fuel. They can cross the blood brain barrier and be used by the brain.
Sx of T1DM
Polyuria
Polydipsia
Wgt loss
Ketoacidosis (fruity breath smell)
Excessive tiredness
Polyphagia
Ix for T1DM
Normal glucose levels - 11.1 plasma glucose
Patient has DM if:
Fasting glucose - >5.5 - 7 plasma glucose
HbA1c - 6.5% / 48 mmol/mol
Tx of T1DM
- Basal bolus regime - a combination of a background, long acting insulin given once a day, and a short acting insulin injected 30 minutes before the intake of carbohydrates (i.e. at meals).
- Insulin pump - small devices that continuously infuse insulin at different rates to control blood sugar levels. The pump pushes insulin through a small plastic tube (cannula) that is inserted under the skin. The cannula is replaced every 2 – 3 days.
DKA Sx
Diabetes Sx + confusion, vomiting, dehydration
DKA Tx
If px alert - insulin injection
If px confused - Fluid replacement with IV 0.9% sodium chloride + insulin
Hypoglycaemia acute Tx
IV dextrose and intramuscular glucagon.
Macrovascular complications of DM
Coronary artery disease
Peripheral ischaemia causes poor healing, ulcers and “diabetic foot”
Stroke
Hypertension
Microvascular complications of DM
Peripheral neuropathy
Retinopathy
Nephropathy
What is the pathophysiology of T2DM?
Insulin resistance, where the body’s cells become less responsive to the effects of insulin. This resistance results in impaired glucose uptake by cells.
T2DM RF
Genetics
Obesity
Physical inactivity
Age
Race/ethnicity
Tx of T2DM
1st line → Metformin
If Hba1c is >58 then add:
2nd line → DPP4i or SGLT2-i or sulfonylurea or pioglitazone (based on individual factors and drug tolerance)
If not effective then add:
3rd line → insulin (triple therapy)
What is the mechanism of action of sulfonylureas?
Plus give an example.
Stimulate the pancreas to release more insulin by binding to specific receptors on pancreatic beta cells.
Example - gliclazide
What is the mechanism of action of DPP-4 Inhibitors?
Plus give an example.
DPP-4 is an enzyme that breaks down incretins, hormones that stimulate insulin release and reduce glucagon secretion.
DPP-4 inhibitors block the action of DPP-4, increasing the levels of incretins.
Example - sitagliptin
What is the mechanism of action of SGLT-2 Inhibitors?
Plus give an example.
SGLT-2 is a protein responsible for reabsorbing glucose in the kidneys, allowing it to be excreted in the urine.
SGLT-2 inhibitors block the action of SGLT-2, leading to increased urinary glucose excretion.
Example - dapagliflozin
Define thyrotoxicosis aka thyroid storm
Abnormal and excessive quantity of thyroid hormones in the body.
Describe step by step release of TSH into blood?
Hypothalamus detects low T3 and T4 levels in blood = releases TRH (thyrotropin-releasing hormone) = stimulates anterior pituitary gland = release of TSH into blood = acts on thyroid gland = inc. release of T3 and T4 into blood
What is Graves disease?
Autoimmune condition where TSH receptor antibodies cause primary hyperthyroidism. TSH antibodies are abnormal antibodies that mimic TSH and stimulates TSH receptors on thyroid to release T3 and T4.
