Endocrinology Flashcards

1
Q

What is type 1 diabetes?

A

When the pancreas stops being able to produce insulin - autoimmune destruction of beta cells leading to insulin deficiency

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2
Q

Causes of T1DM?

A

May be genetic component - HLA 6 predisposition

Viruses - Coxsackie B virus and enterovirus.

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3
Q

What is glucagon?

A

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.

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4
Q

What is glycogen?

A

The stored form of glucose in muscle and liver cells

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5
Q

What is glycogenolysis?

A

The breakdown of glycogen into glucose in the liver

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6
Q

What is gluconeogenesis?

A

Conversion of proteins and fats into glucose in the liver

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7
Q

What is ketogenesis?

A

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.

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8
Q

Sx of T1DM

A

Polyuria
Polydipsia
Wgt loss
Ketoacidosis (fruity breath smell)
Excessive tiredness
Polyphagia

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9
Q

Ix for T1DM

A

Normal glucose levels - 11.1 plasma glucose

Patient has DM if:

Fasting glucose - >5.5 - 7 plasma glucose

HbA1c - 6.5% / 48 mmol/mol

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10
Q

Tx of T1DM

A
  1. 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).
  2. 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.
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11
Q

DKA Sx

A

Diabetes Sx + confusion, vomiting, dehydration

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12
Q

DKA Tx

A

If px alert - insulin injection
If px confused - Fluid replacement with IV 0.9% sodium chloride + insulin

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13
Q

Hypoglycaemia acute Tx

A

IV dextrose and intramuscular glucagon.

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14
Q

Macrovascular complications of DM

A

Coronary artery disease

Peripheral ischaemia causes poor healing, ulcers and “diabetic foot”
Stroke

Hypertension

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15
Q

Microvascular complications of DM

A

Peripheral neuropathy

Retinopathy

Nephropathy

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16
Q

What is the pathophysiology of T2DM?

A

Insulin resistance, where the body’s cells become less responsive to the effects of insulin. This resistance results in impaired glucose uptake by cells.

17
Q

T2DM RF

A

Genetics
Obesity
Physical inactivity
Age
Race/ethnicity

18
Q

Tx of T2DM

A

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)

19
Q

What is the mechanism of action of sulfonylureas?
Plus give an example.

A

Stimulate the pancreas to release more insulin by binding to specific receptors on pancreatic beta cells.

Example - gliclazide

20
Q

What is the mechanism of action of DPP-4 Inhibitors?
Plus give an example.

A

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

21
Q

What is the mechanism of action of SGLT-2 Inhibitors?
Plus give an example.

A

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

22
Q

Define thyrotoxicosis aka thyroid storm

A

Abnormal and excessive quantity of thyroid hormones in the body.

23
Q

Describe step by step release of TSH into blood?

A

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

24
Q

What is Graves disease?

A

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.

25
Q

Causes of hyperthyroidism

A

G - Graves’ disease MC
I - Inflammation (thyroiditis)
S - Solitary toxic thyroid nodule
T - Toxic multinodular goitre

26
Q

Hyperthyroidism Sx

A

Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Insomnia
Diarrhoea
Sexual dysfunction

27
Q

Sx specific to Graves’ disease

A

Diffuse goitre (without nodules)

Exophthalmos

Pretibial myxoedema - skin condition caused by deposits of glycosaminoglycans under the skin on the anterior aspect of the leg

Thyroid acropachy - hand swelling and finger clubbing

28
Q

Ix for hyperthyroidism

A

Bloods:
TSH level (primary = low, secondary = high)
Free T4 and T3 (high)
TSH receptor antibodies (+ve)

29
Q

Hyperthyroidism Tx

A

1st line: Carbimazole
if high dose - levothyroxine can be added

2nd line: Propylthiouracil

Radioactive iodine - drinking a single dose of radioactive iodine. The thyroid gland takes this up, and the emitted radiation destroys a proportion of the thyroid cells.
requires long-term levothyroxine

30
Q

Side effects of taking carbimazole and propythiouracil?

A

Carbimazole: acute pancreatitis

Both: Agranulocytosis, with a dangerously low white blood cell counts. Agranulocytosis makes patients vulnerable to severe infections. A sore throat is a key presenting feature of agranulocytosis.

31
Q

Pre-cautions of radioactive iodine use

A

Women must not be pregnant or breastfeeding and must not get pregnant within 6 months of treatment

Men must not father children within 4 months of treatment

Limit contact with people after the dose, particularly children and pregnant women

32
Q

Sx of thyrotoxicosis

A

Presentation of hyperthyroidism with fever, tachycardia and delirium.

33
Q

Tx of thyrotoxicosis

A

Propylthiouracil - preferred tx

34
Q

Describe Hashimoto’s thyroiditis

A

Autoimmune condition causing inflammation of the thyroid gland. It is associated with anti-thyroid peroxidase (anti-TPO) antibodies and anti-thyroglobulin (anti-Tg) antibodies.

35
Q

Causes of hypothyroidism?

A

Hashimoto’s thyroiditis MC
Iodine deficiency *
Lithium
Pituitary adenomas

36
Q

Sx for hypothyroidism + specific sx in Hashimoto’s?

A

Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention (including oedema, pleural effusions and ascites)
Heavy or irregular periods
Constipation

Hashimoto’s - initially cause a goitre, after which there is atrophy (wasting) of the thyroid gland.

37
Q

Ix of hypothyroidism?

A

Bloods:
TSH level (primary = high, secondary = low)
Free T4 and T3 (low)

38
Q

Tx of hypothyroidism

A

Oral levothyroxine (T4)