Endocrinology and diabetes

Question 1

What are the mechanisms and causes of diabetes insipidus?

Answer 1

antidiuretic hormone is produced by the hypothalamus and secreted by the posterior pituitary gland.
==»VASOPRESSIN
ADH stimulates water reabsorption from the collecting ducts in the kidneys

Diabetes insipidus is caused by
=> lack of antidiuretic hormone
=> lack of response to antidiuretic hormone

Question 2

What are the features of diabetes insipidus

Answer 2

• Polyuria (>3L of urine per day)
• Polydipsia
• Dehydration
• Postural hypotension

Question 3

What are the different types of diabetes insipidus?

Answer 3

Nephrogenic diabetes insipidus
-> When the collecting duct of the kidney doesn’t respond to ADH

Cranial diabetes insipidus
-> When hypothalamus doesn’t produce ADH for the pituitary gland

Question 4

What is the investigation for diabetes insipidus?

Answer 4

water deprivation test

Question 5

What are the management shown in the water deprivation test?
1. low water deprivation
2. high water deprivation

Answer 5

1. need to give ADH (desmopressin) and measure urine osmolality over 2-4 hrs
2. Rule out diabetes insipidus and don’t need to give desmopressin

Question 6

What the results of Craninal and nephrogenic diabetes insipidus will show in the water deprivation test?

Answer 6

Craninal diabetes insipidus
- Low water deprivation
- high after desmopressin

Nephrogenic diabetes insipidus
- Low water deprivation
- Low after desmopressin

Question 7

Management of diabetes insipidus

Answer 7

• stopping lithium (if there’s any)
• Desmopressin for Craninal DI
• monitor sodium -> risk of hyponatremia
• plenty of water, high-dose of desmopressin, thiazide diuretics and NSAIDs for Nephrogenic DI

Question 8

What is alsdosterone and what does it do?

Answer 8

Mineralocorticoid steroid hormone

stimulates from the adrenal glands. works to:
- increase Na reabsorption from distal tubule
- increase potassium secretion from distal tubule
- Increase hydrogen secretion from the collecting ducts

Question 9

What is the differences of primary and secondary hyperaldosteronism?

Answer 9

Primary hyperaldosteronism
- when adrenal glands producing too much aldosterone. causing low renin level
-> (H) aldosterone & (L) renin

Secondary hyperaldosteronism
- too much renin which release excessive aldosterone
-> (H) aldosterone & (H) renin

Question 10

What are the investigations that is use to find hyperaldosteronism?

Answer 10

Aldosterone-to-renin ratio (ARR)

Blood pressure (2nd most in hypertention)
potassium level (hypokalaemia)
Blood gas (alkalosis)
CT
Renal artery imaging
Adrenal vein sampling

Question 11

Management of hyperaldosterone

Answer 11

Eplerenone

Spironolactone

Surgical removal - if its adrenal adenoma
percutaneous renal artery angioplasty (treat renal artery stenosis)

Question 12

What will the result of TSH and T3 T4 shows in the following conditions:
1) Primary hyperthyroidism
2) Secondary Hyperthyroidism
3) Primary hypothyroidism
4) Secondary hypothyroidism

Answer 12

1) Low TSH, High T3 &T4
2) High TSH, High T3 &T4
3) High TSH, low T3 &T4
4) Low TSH, low T3 &T4

Question 13

How does triiodothyronine (T3) and thyroxine (T4) produced?

Answer 13

The hypothalamus releases thyrotropin-releasing hormone (TRH).
TRH stimulates the anterior pituitary to release thyroid-stimulating hormone (TSH).
TSH stimulates the thyroid gland to release triiodothyronine (T3) and thyroxine (T4).

Question 13

1) Cause of primary hyperthyroidism

2) Cause of primary hypothyroidism

Answer 13

1) GIST
G – Graves’ disease
I – Inflammation (thyroiditis)
S – Solitary toxic thyroid nodule
T – Toxic multinodular goitre

2)
Hashimoto’s thyroiditis
Iodine deficiency
Treatments for hyperthyroidism

Question 14

1) What does anti-thyroid peroxidase (anti-TPO) use for? and what it can indicates?

2) What imagining are use to diagnose thyroid nodules or hyperthyroidism or thyroid cancer?

Answer 14

1) They are antibodies against the thyroid gland and use to present and raise in grave’s disease and Hashimoto’s thyroiditis

2)
Ultrasound - throid nodules and distinguish between cystic and solid nodules

Radioisotope scans - investigate hyperthyroidism and thyroid cancer

Question 15

1) What is the pathophysiology of Type 1 diabetes and what it can commonly lead to?

2) What is the triad of symptoms of hyperglycemia?

3) What is the normal range of blood glucose concentration?

Answer 15

1) Where pancreas stop producing insulin which makes the cells of the body can’t absorb glucose from the blood and use it as fuel. leading the cell thought there’s not enough glucose level and hence glucose level keep rising and cause hyperglycemia

2) polyuria, polydipsia, weight loss

3) 4.4 – 6.1 mmol/L

Question 16

1) what is the 3 features of diabetic ketoacidosis

2) why DKA will lead to those 3 feature

Answer 16

1) Ketoacidosis
dehydration
potassium imbalance

2) Ketoacidosis: without insulin, liver start producing ketones as fuel. glucose and ketones level increase, kidney produce bicarbonate to counteract the ketone acids in blood to maintain pH, but over time bicarbonate used up –> ketoacidosis

Dehydration: hyperglycemia overwhelm the kidneys which the glucose in the urine draws water out by osmotic diuresis –> polyuria –> severe dehydration –> polydipsia

without insulin, potassium is not added or stored in cells, leading to total body potassium is low

Question 17

1) presentation and symptoms of DKA

2) What are the criteria to diagnosis DKA

Answer 17

1) Polyuria
Polydipsia
Nausea and vomiting
Acetone smell to their breath
Dehydration
Weight loss
Hypotension (low blood pressure)
Altered consciousness

2) Hyper glycaemia (glucose >11mmol/L)
Ketosis (ketones >3mmol/L
acidosis (pH <7.3)

Question 18

Treatment for DKA

Answer 18

F – Fluids – IV fluid resuscitation with normal saline (e.g., 1 litre in the first hour, followed by 1 litre every 2 hours)
I – Insulin – fixed rate insulin infusion (e.g., Actrapid at 0.1 units/kg/hour)
G – Glucose – closely monitor blood glucose and add a glucose infusion when it is less than 14 mmol/L
P – Potassium – add potassium to IV fluids and monitor closely (e.g., every hour initially)
I – Infection – treat underlying triggers such as infection
C – Chart fluid balance
K – Ketones – monitor blood ketones, pH and bicarbonate

Question 19

Long term and short term complication for diabetes

Answer 19

Short term:
Hypoglycaemia
Hyperglycaemia (and diabetic ketoacidosis)

Long term:
macrovascular–>
Coronary artery disease is a significant cause of death in diabetics
Peripheral ischaemia causes poor skin healing and diabetic foot ulcers
Stroke
Hypertension

microvascular–>
Peripheral neuropathy
Retinopathy
Kidney disease, particularly glomerulosclerosis

infection-related –>
Urinary tract infections
Pneumonia
Skin and soft tissue infections, particularly in the feet
Fungal infections, particularly oral and vaginal candidiasis