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Core conditions > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is type 2 diabetes?

A

A condition where a combination of insulin resistance and reduced insulin production cause persistently high blood sugar levels.

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2
Q

Pathophysiology of type 2 diabetes

A

-Repeated exposure to glucose and insulin makes the cells in the body resistant to the effects of insulin.
-More and more insulin is required to stimulate the cells to take up and use glucose.
-Over time, the pancreas becomes fatigued and damaged by producing so much insulin, and the insulin output is reduced.

-A high carbohydrate diet combined with insulin resistance and reduced pancreatic function leads to chronic hyperglycaemia which leads to microvascular, macrovascular and infectious complications.

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3
Q

Risk factors for type 2 diabetes

A

non-modifiable= older age, ethnicity (black african or carribean, south asian), family history

modifiable= obesity, sedentary lifestyle, high carbohydrate (particularly sugar) diet

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4
Q

Presentation of type 2 diabetes

A

Tiredness, polyuria, polydipsia, unintentional weight loss, opportunistic infections (e.g. oral thrush), slow wound healing, glucose in urine, acanthosis nigricans (associated with insulin resistance)

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5
Q

What is HbA1c?

A

A blood test that reflects the average glucose level over the previous 2-3 months.

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6
Q

HbA1c for pre-diabetes

A

48mmol/mol or above

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7
Q

HbA1c for type 2 diabetes

A

48mmol/mol or above (sample is typically repeated after 1 month to confirm diagnosis)

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8
Q

Management of type 2 diabetes

A

-a structured education program
-low-glycaemic-index, high fibre diet
-exercise
-weight loss (if overweight)
-antidiabetic drugs
-monitoring and managing complications

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9
Q

First-line medical management of type 2 diabetes

A

metformin

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10
Q

How does metformin work?

A

Lowers glucose by inhibiting hepatic gluconeogenesis and opposing the action of glucagon.

Metformin increases insulin sensitivity and decreases glucose production by the liver.

Class of medication = biguanide

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11
Q

Second-line for type 2 diabetes

A

Sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor

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12
Q

What drug is recommended for type 2 diabetic patients with a QRISK score above 10%, making them fall into the ‘high risk’ category for cardiovascular disease?

A

SGLT-2 inhibitors

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13
Q

Drug classification of metformin?

A

Biguanide

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14
Q

Notable side effects of metformin?

A

-gastrointestinal symptoms, including pain, nausea and diarrhoea
-lactic acidosis (secondary to acute kidney injury)

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15
Q

What suffix do SGLT-2 inhibitors end with?

A

-gliflozin

Examples= empagliflozin, canagliflozin, dapagliflozin and ertugliflozin

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16
Q

How doe SGLT-2 inhibitors work?

A

SGLT-2 inhibitors block the action of the sodium-glucose co-transporter 2 protein, causing more glucose to be excreted in the urine.
Loss of glucose in the urine lowers the HbA1c, reduces the blood pressure, leads to weight loss and improves heart failure.

They can cause hypoglycaemia when used with insulin or sulfonylureas.

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17
Q

Side effects of SGLT-2 inhibitors

A

-increased urine output and frequency
-genital thrush due to lots of sugar passing through the urinary tract
-diabetic ketoacidosis

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18
Q

What is Pioglitazone?

A

A thiazolidinedione.
It increases insulin sensitivity and decreases liver production of glucose.

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19
Q

Side effects of Pioglitazone

A

-weight gain
-heart failure
-increased risk of bone fractures
-a small increase in the risk of bladder cancer

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20
Q

What are Sulfonylureas?

A

Sulfonylureas stimulate insulin release from the pancreas.

Gliclazide is the most common sulfonylurea.

Notable side effects= weight gain and hypoglycaemia

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21
Q

What are incretins?

A

Incretins are hormones produced by the gastrointestinal tract. They are secreted in response to large meals and act to reduce blood sugar by:
-increasing insulin secretion
-inhibiting glucagon production
-slowing absorption by the gastrointestinal tract

Incretin examples= DPP-4 (dipeptidyl peptidase-4) inhibitors and GLP-1 (glucagon-like peptide-1) mimetics

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22
Q

Describe DPP-4 inhibitors

A

-Incretin
-DPP-4 inhibitors block the action of DPP-4, allowing increased incretin activity.
Examples= sitagliptin and alogliptin
-side effects= headaches

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23
Q

Describe GLP-1 mimetics

A

-Incretins

-GLP-1 mimetics imitate the action of GLP-1.

-Examples= exenatide and liraglutide

-They are given as subcutaneous injections

-Liraglutide can also be used for weight loss in non-diabetic obese patients.

-Side effects= reduced appetite, weight loss, gastrointestinal symptoms, including discomfort , nausea and diarrhoea.

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24
Q

What are the different types of insulin

A

Rapid-acting insulins (e.g., NovoRapid) start working after around 10 minutes and last about 4 hours.

Short-acting insulins (e.g., Actrapid) start working in around 30 minutes and last about 8 hours.

Intermediate-acting insulins (e.g., Humulin I) start working in around 1 hour and last about 16 hours.

Long-acting insulins (e.g., Levemir and Lantus) start working in around 1 hour and last about 24 hours or longer.

Combinations insulins contain a rapid-acting and intermediate-acting insulin. In brackets is the ratio of rapid-acting to intermediate-acting insulin:

Humalog 25 (25:75)
Humalog 50 (50:50)
Novomix 30 (30:70)

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25
Q

What are the key complications of type 2 diabetes?

A

-infections (preiodontitis (gum disease), thrush and infected ulcers)
-diabetic retinopathy
-peripheral neuropathy
-autonomic neuropathy
-chronic kidney disease
-diabetic foot
-gastroparesis (slow emptying of the stomach)
-hyperosmolar hyperglycaemic state)

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26
Q

What drug is used as first-line to manage hypertension in patients of any age with type 2 diabetes?

A

ACE inhibitors

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27
Q

ACE inhibitors are started in type 2 diabetics with ………. when the albumin-to-creatinine ratio (ACR) is above 3 mg/mmol (as opposed to 30 mg/mmol in patients without diabetes).

A

Chronic kidney disease

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28
Q

……. are started in type 2 diabetics with chronic kidney disease when the albumin-to-creatinine ratio (ACR) is above 30 mg/mmol (in addition to the ACE inhibitor).

A

SGLT-2 inhibitors

29
Q

… (e.g., sildenafil or tadalafil) may be used for erectile dysfunction.

A

Phosphodiesterase‑5 inhibitors

30
Q

What type of drugs are used to help with gastroparesis?

A

Prokinetic drugs

31
Q

4 drugs options for neuropathic pain (e.g. diabetic neuropathy)

A

Amitriptyline – a tricyclic antidepressant
Duloxetine – an SNRI antidepressant
Gabapentin – an anticonvulsant
Pregabalin – an anticonvulsant

32
Q

What is Hyperosmolar Hyperglycaemic State?

A

Hyperosmolar hyperglycaemic state (HHS) is a rare but potentially fatal complication of type 2 diabetes.
It is characterised by hyperosmolality (water loss leads to very concentrated blood), hyperglycaemia and the absence of ketones, distinguishing it from ketoacidosis.
It presents with polyuria, polydipsia, weight loss, dehydration, tachycardia, hypotension and confusion.
It is a medical emergency with high mortality.
Treatment is with IV fluids and careful monitoring.

33
Q

What is type 1 diabetes?

A

Type 1 diabetes is a condition where the pancreas stops being able to produce adequate insulin. Without insulin, the cells of the body cannot absorb glucose from the blood and use it as fuel. Therefore, the cells think there is no glucose available. Meanwhile, the glucose level in the blood keeps rising, causing hyperglycaemia.

34
Q

Type 1 diabetes may present with the classic triad of symptoms of hyperglycaemia…

A

-polyuria
-polydipsia
-weight loss (mainly through dehydration)

Alternatively, patients may present with diabetic ketoacidosis

35
Q

What is the ideal glucose concentration in the body?

A

4.4-6.1 mmol/L

36
Q

Where and what produces insulin?

A

Insulin is a hormone produced by the beta cells in the Islets of Langerhans in the pancreas. It is an anabolic hormone (a building hormone).

37
Q

How does insulin act to reduce blood sugar levels?

A

1) It causes cells to absorb glucose from the blood and use it as fuel.
2) It causes muscle and liver cells to absorb glucose from the blood and store it as glycogen in a process called glycogenesis.

38
Q

Where and what produces glucagon?

A

Glucagon is a hormone produced by the alpha cells in the Islet of Langerhans in the pancreas.

It is a catabolic hormone (a breakdown hormone).

39
Q

How does glucagon work?

A

Glucagon is released in response to low blood sugar levels and stress and works to increase blood sugar levels. It tells the liver to break down stored glycogen and release it into the blood as glucose in a process called glycogenolysis. It also tells the liver to convert proteins and fats into glucose in a process called gluconeogenesis.

40
Q

What are ketones and what is ketogenesis?

A

Ketogenesis is the production of ketones which occurs when there is insufficient glucose supply and glycogen 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.
People in ketosis have a characteristic acetone smell to their breath.

41
Q

How can ketone levels be measured?

A

-urine dipstick
-in blood using a ketone meter

42
Q

The … buffer ketone acids in healthy people, so the blood does not become acidotic.

A

Kidneys

43
Q

What is diabetic ketoacidosis?

A

When type 1 diabetes causes extreme hyperglycaemic ketosis, this results in life-threatening metabolic acidosis.

44
Q

What are the 3 key features of diabetic ketoacidosis?

A

-ketoacidosis
-dehydration
-potassium imbalance

45
Q

Describe ketoacidosis

A

Without insulin, the body’s cells cannot recognise glucose, even when there is plenty in the blood, so the liver starts producing ketones to use as fuel. Over time, there are higher and higher glucose and ketones levels. Initially, the kidneys produce bicarbonate to counteract the ketone acids in the blood and maintain a normal pH. Over time, the ketone acids use up the bicarbonate, and the blood becomes acidic. This is called ketoacidosis.

46
Q

Why does dehydration happen in diabetes?

A

High blood glucose levels (hyperglycaemia) overwhelm the kidneys, and glucose leaks into the urine. The glucose in the urine draws water out by osmotic diuresis. This causes increased urine production (polyuria) and results in severe dehydration. Dehydration results in excessive thirst (polydipsia).

47
Q

Describe potassium imbalance in diabetes

A

Insulin normally drives potassium into cells. Without insulin, potassium is not added to and stored in cells. The serum potassium can be high or normal as the kidneys balance blood potassium with the potassium excreted in the urine. However, total body potassium is low because no potassium is stored in the cells. When treatment with insulin starts, patients can develop severe hypokalaemia (low serum potassium) very quickly, leading to fatal arrhythmias.

48
Q

Presentation of diabetic ketoacidosis

A

Leads to…

Hyperglycaemia
Dehydration
Ketosis
Metabolic acidosis (with a low bicarbonate)
Potassium imbalance

Patients present with symptoms of these abnormalities:

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

49
Q

Treatment of diabetic ketoacidosis

A

FIG-PICK:
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

50
Q

Long term management of type 1 diabetes

A

Subcutaneous insulin
Monitoring dietary carbohydrate intake
Monitoring blood sugar levels upon waking, at each meal and before bed
Monitoring for and managing complications, both short and long term

51
Q

What is basal-bolus regime?

A

A basal-bolus regime of insulin involves a combination of:

Background, long-acting insulin injected once a day
Short-acting insulin injected 30 minutes before consuming carbohydrates (e.g., at meals)

52
Q

What is lipodystrophy?

A

Injecting into the same spot can cause lipodystrophy, where the subcutaneous fat hardens.

53
Q

What are the advantages and disadvantages of insulin pumps?

A

The advantages of an insulin pump are better blood sugar control, more flexibility with eating and less injections.

The disadvantages are:

Difficulties learning to use the pump
Having it attached at all times
Blockages in the infusion set
A small risk of infection

54
Q

What does HbA1c measure?

A

Measures glycated haemoglobin, which is how much glucose is attached to the haemoglobin molecule. This reflects the average glucose level over the previous 2-3 months (red blood cells have a lifespan of about 4 months). It is measured every 3 to 6 months to track the average sugar levels. It is a lab test.

55
Q

Long term complications of type 1 diabetes

A

-Chronic high levels cause damage to the endothelial cells of blood vessels. This leads to leaky, malfunctioning, vessels that are unable to regenerate.
-High glucose levels also cause immune system dysfunction and create an optimal environment for infectious organisms to thrive.

Macrovascular complications include:

Coronary artery disease is a significant cause of death in diabetics
Peripheral ischaemia causes poor skin healing and diabetic foot ulcers
Stroke
Hypertension

Microvascular complications include:

Peripheral neuropathy
Retinopathy
Kidney disease, particularly glomerulosclerosis

Infection-related complications include:

Urinary tract infections
Pneumonia
Skin and soft tissue infections, particularly in the feet
Fungal infections, particularly oral and vaginal candidiasis.

56
Q

what are the short term complications?

A

-hypoglycaemia
-hyperglycaemia (and diabetic ketoacidosis)

57
Q

What is diabetes insipidus?

A

Diabetes insipidus (DI) is a disorder characterised by polydipsia, polyuria and formation of inappropriately hypotonic (dilute) urine.

2 types= central/cranial DI and nephrogenic DI.

58
Q

Diabetes insipidus occurs due to: (2)

A

-a lack of antidiuretic hormone (cranial diabetes insipidus)
-a lack of response to antidiuretic hormone (nephrogenic diabetes insipidus)

59
Q

Where is antidiuretic produced and what secretes it?

A

-produced in the hypothalamus
-secreted by the posterior pituitary gland

60
Q

Function of antidiuretic hormone?

A

-it is also known as vasopressin
-It stimulates water reabsorption from the collecting ducts in the kidneys

61
Q

What is primary polydipsia?

A

Primary polydipsia is when the patient has a normally functioning ADH system but drinks excessive amounts of water, leading to excessive urine production. This is not diabetes insipidus.

62
Q

What is nephrogenic diabetes insipidus?

A

When the collecting ducts of the kidneys do not respond to ADH.

63
Q

Causes of nephrogenic diabetes?

A

-idiopathic
-medications, particularly lithium (used in bipolar affective disorder)
-genetic mutations in the ADH receptor gene
-hypercalcaemia
-hypokalaemia
-kidney disease (e.g. polycystic kidney disease)

64
Q

What is cranial diabetes insipidus and what causes it?

A

-when the hypothalamus does not produce ADH for the pituitary gland to secrete it.

Causes:
-idiopathic
-brain tumours, injury, surgery, infections e.g. meningitis or encephalitis
-genetic mutations in the ADH gene
-Wolfram syndrome (a genetic condition also causing optic atrophy, deafness and diabetes mellitus)

65
Q

Presentation of diabetes insipidus

A

-polyuria (3 litres or more per day)
-polydipsia
-dehydration
-postural hypotension

66
Q

What do investigations show in diabetes insipidus?

A

-low urine osmolarity (lots of water diluting the urine)
-high/normal serum osmolality (water loss may be balanced by increased intake)
-more than 3 litres on a 24-hour urine collection

67
Q

Describe the water deprivation test in primary polydipsia, cranial DI and nephrogenic DI

A

-aka desmopressin stimulation test
-patient avoids all fluids for up to 8 hours before test, then urine osmolarity is measured
-if urine osmolarity is low, synthetic ADH (desmopressin) is given and osmolarity is measured again over 2-4 hours

-in primary polydipsia-> water deprivation causes urine osmolarity to be high and this rules out diabetes insipidus

-in cranial DI, the patient lacks ADH. The kidneys are still capable of responding to ADH. Initially the urine osmolarity remains low as it continues to be diluted by the excess of water lost in the urine. After desmopressin is given, the kidneys respond by reabsorbing water and concentrating the urine. The urine osmolality will be high.

-in nephrogenic diabetes insipidus, the patient is unable to respond to ADH. The urine osmolality will be low both before and after the desmopressin is given.

68
Q

What is the management for diabetes insipidus?

A

Cranial DI-> desmopressin (synthetic ADH) to replace the absent ADH. Risk of hyponatraemia.

Nephrogenic DI-> ensuring water access, high-dose desmopressin, thiazide diuretics, NSAIDs

69
Q
A

Core conditions (15 decks)

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