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1 CEP > Lectures 11-15 > Flashcards

Lectures 11-15 Flashcards

1
Q

How many tests would you carry out for diabetes?

A

In the presence of symptoms, 1 is enough.

Without symptoms, 2 are required

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2
Q

In type 1 diabetes, what might low insulin levels cause?

A

High blood glucose levls
increased lipolysis (and hence DKA)
increased protein degradation

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3
Q

What are the types of insulin? What examples of them might there be?

A

Meal time insulin - aspart

Longer acting insulin - Zinc

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4
Q

What allows the body to produce more insulin at mealtimes?

A

The incretin effect

stimulates endocrine cells, GLP-1 release

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5
Q

What binds iodine to tyrosine residues in thyroglobulin molecules?

A

thyroperoxidase

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6
Q

What enzyme forms T3 from T4?

A

deiodinase

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7
Q

How does TSH increase T3 production?

A

It binds to the TSHR’s on the basolateral membrane of the thyrocytes, causing an increase in Na/I symporters on the membrane, increasing the iodine presence within the cell

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8
Q

How would you test for thryoid function?

A

TSH and T4/T3 levels

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9
Q

What are the 3 main causes of Hyperthyroidism?

A

Graves’
Toxic nodular goitre
Thyroiditis: inflammation

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10
Q

What causes Grave’s disease?

A

pathogenic antibodies bind to TSH receptors on thyrocytes

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11
Q

What causes neonatal hyperthyroidism?

How is it treated?

A

TSH-R antibodies cross the placenta.
Antithyroid drugs
Surgical removal of thyroid
radioiodine therapy

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12
Q

What is the main classification of antithyroid drugs?

A

Thioamides

they block iodine incorporation through inhibition of thyroperoxidases

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13
Q

What might be a complication of antithyroid drugs?

A

Argranulocytosis

Liver disease with propylthiouracil

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14
Q

What are the complications of a total thyroidectomy?

A

hypothyroidism
Hypoparathyroidism (- Ca levels)
Recurrent laryngeal nerve damage

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15
Q

What might cause hypothyroidism?

A

Hashimoto’s hypothyroidism (autoimmune)
iodine deficiency
silent thyroiditis

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16
Q

What is cretinism?

A

congenital hypothyroidism, causing stunted mental and physical growth

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17
Q

How would the presence of thryoid nodules be investigated?

A

Serum TSH, T3/T4
Assessment of thyroid size (imaging)
Assessment of thyroid pathology

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18
Q

How would an ultrasound scan be useful for investigating thyroid pathology?

A

differentiates between cystic and solid nodules

19
Q

What are the phases of insulin release?

A

1 - within 2 minutes of food ingestion, lasts 10-15 minutes

2 - sustained until normoglycaemia restored

20
Q

What are the subunits of the insulin receptor?

A 
2 alpha (extracellular)
2 beta (transmembrane, tyrosine kinase)
21
Q

How are pre-diabetic treated?

A

Nicotinamide (DNA repair)

22
Q

Who would be prescribed Metformin?

A

diabetics with a BMI over 25

23
Q

What are the 3 main dosal regimes of insulin?

A 
Short acting (3x daily) + and intermmediate/long acting one
pre-mixed short + intermmediate insulins 2x daily
continuous infucion
24
Q

What are the 3 main complications of insulin therapy?

A

Hypoglycaemia
Allergy
lipodystrophy

25
Q

What is diabetes type 2 caused by?

A

A loss of 1st phase insulin secretion, and hence insulin resistance

26
Q

How does Metformin work?

A

It is a hypoglycaemic agent. Reduces gluconeogenesis in the liver.
Activates AMP-activated protein kinase, decreasing gene expression.
Increases Glucose uptake in muscles.

27
Q

How do sulphonoureas work?

A

They bind to SUR’s on B cells (a part of K(ATP) channels), causing the depolarisation of the membrane, increasing insulin secretion

28
Q

Who shouldn’t be given sulphonoureas?

A

Pregnant or breastfeeding women

29
Q

What do thiazolidinediones do?

A

bind to transcription factors, increasing lipogenesis, decreasing gluconeogenesis and increasing glucose uptake

30
Q

What are the two forms of drugs based on the incretin effect?

A

Inhibitors of DP-4

GLP-1 agonists

31
Q

How do SGLT2 inhibitors work?

A

increase glucose and Na+ loss in the proximal tubule

32
Q

How does PTH increase calcium levels?

A

Stimulates osteoclasts to release calcium into plasma (and reabsorption in Distal CT)
Ultimately activates Vitamin D (via 1-alpha hydroxylase) which causes Ca2+ absorption in the GIT, and reabsorption in the proximal tubule

33
Q

Where does Vitamin D come from?

A

UV light converts 7-dehydroxycholesterol in the skin to Vitamin D3, which is then converted into calcidiol in the liver, which is then converted to 1,25 dihydroxy VD3 in the kidney

34
Q

Which of PTH or Calcitonin is more important?

A

PTH

35
Q

What is FGF23?

A

It is produced by osteocytes, and responds negatively to phosphate, it increases renal excretion of phosphate and suppresses renal synthesis of 1,25D3

36
Q

What are osteocytes?

A

Found in the calcified matrix, with long processes contacting other osteocyes and osteoblasts

37
Q

What are osteoblasts?

A

bone forming cells

38
Q

What are osteoclasts?

A

bone reabsorbing cells
attached to bone by integrins
They can sometimes dig the Howship’s Lacuna

39
Q

What are the different forms of hyperparathyroidsm caused by?

A

primary - PT tumour
secondary - renal disease, decreased activation of Vitamin D
tertiary - PT hyperplasia

40
Q

What is Rickets caused by?

A

Vitamin D/Calcium deficiency.
lack of mineralisaiton
osteoid at growth plates are weak, so the growth plate expands to compensate.

41
Q

What is the difference between rickets and osteomalacia?

A

Rickets - affects growing bones

Osteomalacia - affects adult bones

42
Q

Name 2 types of antithyroid drugs

What enzymes do they target?

A

Propylthiouracil - deiodinase

Carbimazole - thyroperoxidase

43
Q

What is the active form of carbimazole?

A

Methimazole

1 CEP (8 decks)

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