Endocrine flashcards
Type 1 Diabetes
RF
Pathology
Symptoms
Investigations
Treatment
When the body has impaired ability to produce insulin due to autoimmune destruction of beta cells leading to hyperglycemia.
RF - Family history, HLA DR3 and DR4, Environmental infection (e.g. viral). (most common in 10-14 years and more common in europe)
PATHOLOGY
Autoimmune destruction of pancreatic beta cells –> leads to absolute insulin deficiency
- Hyperglycemia
- Low cellular glucose (less intake by muscles and adipose)
- Increased counter regulatory hormones –> leading to increased gluconeogenesis and glycogenolysis
SYMPTOMS
- Weight loss (lean patient)
- Polyuria
- Polydipsia
- Glycosuria
- Nocturia
Investigations
- Fasting plasma glucose - >7
- Random plasma glucose - >11.1
- Oral glucose tolerance test - > 11
- HbA1C - > 48 mmol/L or >6.5% (pre diabetes >42mmol/mol)
TREATMENT
Basal bolus insulin
Diabetic Ketoacidosis
RF
Pathology
Symptoms
Investigations
Treatment
Main complication of type 1 diabetes (due to poor management). Characterised by hyperglycemia, ketonaemia and metabolic acidosis
RF - pancreatitis, inadequate/inappropriate insulin treatment
PATHOLOGY
Absolute insulin deficiency + effect of counter regulatory hormones (increased lipolysis and gluconeogenesis) –> leads to excess free fatty acids being converted to ketone bodies.
Symptoms
DEHYDRATION
Polyuria
Polydipsia
Tachycardia
Delirium
Vomiting
Abdominal pain
Kussmaul’s breath - deep laboured breathing
(Fruity pear drop breath)
Investigations
Serum ketone - elevated
RPG - >11.0
Venous blood gas (metabolic acidosis) - pH <7.3 (or HCO3- <15mmol)
Treatment
1st line
Rehydration with IV fluids FIRST
then insulin infusion
(can give potassium to replenish K+ stores)
(can give glucose to prevent hypoglycemia)
Type 2 diabetes
RF
Pathology
Symptoms
Investigations
Treatment
A progressive disorder characterised by peripheral insulin resistance and partial insulin deficiency (amyloid deposits in the pancreas)
RF - Family history, obesity, hypertension, low physical activity (genetic link in T2DM is stronger than HLA link in T1DM)
PATHOLOGY
There is peripheral insulin resistance due to decreased GLUT 4 expression (on the liver, adipocytes and muscle) + pancreas pathology (removal, pancreatitis, amyloid deposits causing minor destruction)
–> Leads to hyperglycemia with increased insulin demand from a depleted beta cell population
SYMPTOMS
Typically an obese, hypertensive and older patient with:
- Polydipsia
- Polyuria
- Glycosuria
- Acanthosis nigricans –> dark pigmented skin folds due to insulin resistance)
INVESTIGATIONS
- Fasting plasma glucose - >7
- Random plasma glucose - >11.1
- Oral glucose tolerance test - > 11
- HbA1C - > 48 mmol/L or >6.5%
TREATMENT
First line - Lifestyle modifications (diet and exercise)
First line drug treatment
- Metformin
If HbA1C is above agreed threshold,
Other drugs include
- Sulphonylureas e.g. Gliclazide
- DPP4 inhibitors e.g. Gliptins
- SGLT 2 inhibitor e.g. Gliflozin
What are the functions and side effects of the 4 possible drugs for T2DM?
Metformin - (A biguinide)
- Reduces gluconeogenesis and increases glucose uptake by increasing insulin sensitivity
- Side effects of diarrhoea, abd pain, renal disease, heart failure, lactic acidosis
Sulphonylurea (Gliclazide)
- Stimulates insulin release by binding to beta cell receptors
- Side effect of hypoglycemia, hunger, weight gain
DPP4 inhibitors (Sitagliptin)
- DPP4 inhibition blocks incretin degradation which stimulates the release of insulin by beta cells
- GI side effects: Constipation, diarrhoea, vomiting, gastritis
SGLT 2 inhibitors (Empagliflozin)
- Prevents kidney from reabsorbing glucose via Cotransporter
- Side effects include: UTI, nausea, constipation, polyuria
Hyperosmolar hyperglycemic state
RF
Pathology
Symptoms
Investigations
Treatment
Main complication of type 2 diabetes. A state of hyperglycemia, hyperosmolality and volume depletion often precipitated with infection.
PATHOLOGY
- Due to elevations in serum glucose (due to insulin deficiency) and hyperosmolality (water loss leads to concentrated blood) –> there is excessive gluconeogenesis due to increased counter regulatory hormones.
SYMPTOMS
- Dehydration
- Cognitive impairment (disorientation, decreased consciousness, coma)
- Polyuria, polydipsia, glycosuria
INVESTIGATIONS
- Increased serum osmolality
- RPG > 11.1
- Serum ketones will not be elevated (eliminates DKA)
TREATMENT
- Intravenous fluid replacement (saline) FIRST
Followed by intravenous insulin
Hypoglycemia
RF
Pathology
Symptoms
Investigations
Treatment
Abnormally low blood glucose levels that have the potential to cause harm
- Mostly due to side effects of using drugs that treat diabetes.
(Non diabetic cause - liver failure, Addison’s disease)
SYMPTOMS
- Irritability
- Tremor
- Dizziness
- Hunger
- Falls and dislocation
INVESTIGATIONS
Fingerstick measurement of glucose to confirm diagnosis (<3.9mmol/L)
TREATMENT
IV Dextrose
(If no IV access then IM glucagon)
(Sometimes patient is awake and can swallow, they can treat with 15g fast acting carbohydrates e.g. Sweets, sugary soft drinks, jellies)
Examples of Monogenic diabetes
1) Maturity onset diabetes of the young –> Autosomal dominant gene defect altering beta cell function and insulin secretion –> T2DM in young people (<25 years)
2) Maternally inherited diabetes and deafness (MIDD) - mutation in mitochondrial DNA leading to loss of beta cell mass
3) Permanent neonatal diabetes - mutation in Kir 6.2 and SUR 1 subunits.
4) Latent autoimmune diabetes of adults (LADA)
- T1DM beginning in adulthood.
Hyperparathyroidism
RF
Pathology
Symptoms
Investigations
Treatment
Excess parathyroid hormone is secreted from the parathyroid gland
RF - Multiple endocrine neoplasia 1 (MEN 1), female, >50-60 years
PATHOLOGY
Primary (most common) –> Usually a parathyroid adenoma - Parathyroid gland over secreting PTH despite normal serum calcium –> leads to hypercalcemia
(Hyperparathyroidism leading to hypercalcemia)
Secondary –> Occurs due to a physiological response to a decrease in calcium e.g. Vitamin D deficiency, CKD (hypocalcemia leading to hyperparathyroidism)
Tertiary –> After a prolonged period of secondary hyperparathyriodism - In response to chronic PTH secretion, glands become hyperplastic and secrete PTH autonomously (Hyperparathyroidism regardless of high calcium)
SYMPTOMS
Bones, stones, groans, moans
Bones - Painful bones - osteitis fibrosa cystica
Stones - Kidney stones
Groans - Constipation
Moans - Depression, myalgia, anxiety (psychedelic moans)
INVESTIGATIONS
1st line - Serum calcium and PTH
Primary - High PTH, High Calcium, Low phosphate, High ALP
Secondary - High PTH, Low calcium, High phosphate
Tertiary - All high
Dexa scan - for bone density
ECG - Shows a short QT interval in Hypercalcemia
TREATMENT
Primary - Parathyroidectomy (removal of parathyroid adenoma)
If its secondary or tertiary, treat the cause
e.g. Bisphosphonates to prevent bone resorption
Rehydrate to prevent kidney stones
What cancers can lead to hyperparathyroidism?
Squamous cell lung cancer, breast cancer and renal cancer.
They secrete a protein called parathyroid hormone related protein (PTHrP) –> which shares structural similarities with PTH and can mimic its actions in the body
Complication of hyperparathyroidism
Severe hypercalcemia - treat with IV fluids and bisphosphonates
Hypoparathyroidism
RF
Pathology
Symptoms
Investigations
Treatment
Deficiency of parathyroid hormone synthesis or secretion
RF - Thyroid surgery, parathyroid surgery, hypomagnesaemia
PATHOLOGY
Primary
Parathyroid gland failure e.g. DI George syndrome
Secondary
Destruction of parathyroid gland due to surgery, radiation
Vitamin D deficiency
Hypomagnesaemia (required for production and release of PTH)
SYMPTOMS
- Paraesthesia, laryngospasm
(CATs go Numb)
- Convulsions, arrhythmia, tetany, numbness
– Chvostek’s sign (tapping on cheek causes twitching of facial muscle)
– Trousseau’s sign - upon inflating BP cuff above systemic pressure –> Carpopedal spasm (fingers come together)
INVESTIGATION
First - Serum calcium and PTH
Low PTH, Low calcium, High phosphate
ECG - Long QT interval (hypocalcemia)
TREATMENT
1st line - Oral calcium supplements and vitamin D3
Briefly what is pseudoparathyroidism
Body does not respond to PTH due to resistance (mutation in G alpha subunit of the receptor)
Results in short stature and short 4th/5th Metacarpal
Hypercalcemia
RF
Pathology - Main causes
Symptoms
Investigations
Treatment
Mostly caused by Primary hyperparathyroidism or malignancies
(Also caused by excess Vitamin D or calcium supplementation)
SYMPTOMS
- Bones, stones, groans, moans
Bones - Painful bones - osteitis fibrosa cystica
Stones - Kidney stones
Groans - Constipation
Moans - Depression, myalgia, anxiety (psychedelic moans)
INVESTIGATION
1st line - Serum PTH
ECG - Short QT interval
TREATMENT
IV fluids (rehydration) and IV bisphosphonates
- Surgical removal of parathyroid adenoma
2 checks to do when talking blood samples/investigating them.
Ensure that tourniquet is not on for too long (Concentration of electrolytes may be higher due to pooling below the tourniquet)
Ensure that sample is not old and haemolysed
Hypocalcemia
RF
Pathology - Main causes
Symptoms
Investigations
Treatment
Caused by:
- Hypoparathyroidism
- CHRONIC KIDNEY DISEASE
- Hypomagnesaemia
(Vitamin D deficiency)
SYMPTOMS
- Paraesthesia, laryngospasm
(CATs go Numb)
- Convulsions, arrhythmia, tetany, numbness
– Chvostek’s sign (tapping on cheek causes twitching of facial muscle)
– Trousseau’s sign - upon inflating BP cuff above systemic pressure –> Carpopedal spasm (fingers come together)
INVESTIGATIONS
Long QT interval on ECG.
Serum PTH and calcium
*Check for history of neck surgery - may point to parathyroid injury
TREATMENT
- Oral calcium and Adcal (Vit D3) supplements
(Severe - calcium gluconate)
