Endocrinology Flashcards

1
Q

What triggers parathyroid hormone release?

A

Low serum calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where does PTH act?

A

Kidneys - Increased calcium reabsorption
Kidneys - increased hydroxylation of vitamin D (indirectly GIT)
Bone - increased bone resorption (resorption > formation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is a normal serum calcium level?

A

1.1mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Vitamin D deficiency biochemistry

A

HIGH PTH
LOW Ca2+
LOW PO4-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Hypoparathyroidism biochemistry

A

LOW PTH
LOW Ca2+
HIGH PO4-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pseudohypoparathyroidism biochemistry

A

HIGH PTH
LOW Ca2+
HIGH PO4-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pseudopseudohypoparathyroidism

A

Has all the clinical features of pseudoHPT but without the biochemical changes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hypercalcaemia (malignant) biochemistry

A

LOW PTH
HIGH Ca2+
Normal PO4-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Primary Hyperparathyroidism Biochemistry

A

HIGH PTH
HIGH Ca2+
LOW PO4-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Tertiary Hyperparathyroidism Biochemistry

A

HIGH PTH
HIGH Ca2+
HIGH PO4-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why might total calcium be low but the Pt. is not actually hypocalcaemic?

A

If low serum albumin, low total calcium but NORMAL ionised calcium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the consequences of Hypocalcaemia?

A
Pins and needles
Muscle Spasms
Seizures
Long QT interval
Basal Ganglia calcification
Cataracts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Signs for Hypocalcaemia

A

Chvostek’s and Trousseau’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the causes of Hypocalcaemia?

A

Vitamin D Deficiency
Hypoparathyroidism
Pseudohypoparathyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the causes of hypoparathyroidism?

A

Syndromes (Di George)
Genetics
Surgical (injury to parathyroid gland)
Radiation (cancer treatment)
Autoimmune Disease
Infiltration (haemochromatosis or Wilson’s - metal deposits)
Magnesium deficiency - Mg required to release PTH from cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Definition of pseudoparathyroidism

A

A resistance to parathyroid hormone resulting in hypocalcaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does Pseudoparathyroidisim present?

A
Short stature
Obesity
Round face
Mild learning difficulties
Subcutaneous ossification
Short 4th metacarpal
Other hormone resistance (diabetes etc)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What may give a false hypercalcaemia result?

A

Remember to correct for albumin
Tourniquet may have been left on too long
Old sample - haemolysis of RBCs releases Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the symptoms of Hypercalcaemia?

A
Thirst
Polyuria
Nausea
Constipation
Confusion
Coma
Renal Stones
Short QT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the main causes of hypercalcaemia?

A

Malignancy (bone mets, myeloma, lymphoma, PTHrP)

Primary Hyperparathyroidism

21
Q

Examples of other causes of hypercalcaemia

A
Thiazide diuretics
Thyrotoxicosis
Sarcoidosis
FHH
Immobilisation
Milk-alkali syndrome
Adrenal Insufficiency
Phaeochromocytoma
22
Q

Why does granulomatous disease cause hypercalcaemia?

A

In granulomas, macrophages gather and produce their own vitamin D.

23
Q

What are the consequences of Hypercalcaemia?

A

Bones, Stones, Groans and Moans

24
Q

What is the main cause of primary hyperparathyroidism?

A

Benign Adenomas of the parathyroid (80%)

25
Q

What causes tertiary hyperparathyroidism?

A

Renal failure resulting in decreased production of vitamin D.

26
Q

What percentage of ingested glucose goes to the liver?

A

40%

27
Q

What glucose transporter is found on the surface of Beta Cells?

A

GLUT2

28
Q

What glucose transporter is found on the surface of other cells?

A

GLUT4

29
Q

Result of Insulin

A

Decrease hepatic glucose output
Increase glucose uptake via GLUT4
Suppresses lipolysis and muscle breakdown

30
Q

Definition of Diabetes Mellitus

A

A disorder of carbohydrate metabolism characterised by chronic hyperglycaemia.

31
Q

How does diabetes mellitus cause mortality and morbidity?

A

Diabetic Ketoacidosis
Hyperosmolar hyperglycaemic coma
Micro/Macrovascular tissue complications

32
Q

What is the main side effect of treatment of diabetes mellitus?

A

Hypoglycaemia

33
Q

What are the types of diabetes?

A
Type 1
Type 2 (inc gestational and medication induced)
Maturity onset diabetes of youth (MODY) 
Pancreatic diabetes
Endocrine (acromegaly/Cushing's)
Malnutrition related
34
Q

Biochemistry for Diabetes diagnosis

A

Symptoms + Random Glucose >11
Fasting Glucose >7
HbA1c >48

35
Q

Why is there no weightloss in type 2 diabetes?

A

The low levels of insulin are protective against catabolism, preventing muscle/weight loss

36
Q

What are the principles of diabetes treatment?

A

Control Symptoms
Prevent acute emergencies e.g. DKA
Identify and prevent microvascular complications
HbA1c >50 (as low as possible without insulin or sulfonylureas)

37
Q

What are the symptoms of type 1 diabetes?

A
Nausea
Vomiting
Fatigue
Polyuria
Polydipsia
Weight loss
38
Q

What are the symptoms of type 2 diabetes?

A
Frequent UTIs
Polyuria
Polydipsia
Dehydration
Fatigue
39
Q

What are the treatments for type 2 diabetes?

A
Weight loss
Diet
Exercise
Manage BP and cholesterol
Metformin, Sulfonylureas, Insulin.
40
Q

What is Addison’s Disease?

A

Primary adrenocortical insufficiency

41
Q

What is the aetiology of Addison’s Disease?

A

Autoimmune
Disseminated Tuberculosis
Adrenal Mets (rare)

42
Q

Pathogenesis of Addison’s Disease

A

Lack of glucocorticoid and mineralocorticoid production in the adrenal cortex.

43
Q

How advanced does adrenal damage have to be before clinical signs manifest? (Addison’s Disease)

A

90% destroyed

44
Q

How does Addison’s disease present?

A

Tiredness, lethargy, weakness
Anorexia, nausea, vomiting and diarrhoea
Prominent weight loss

45
Q

Biochemistry of Addison’s Disease

A
LOW Na+
HIGH K+ 
HIGH Urea
Up to 50% Hypoglycaemic
Circulating antibodies may be found (against adrenal tissue)
46
Q

What is the test for Addison’s disease?

A

Synacthen test

Inject ACTH - no rise in plasma cortisol = Addison’s

47
Q

What is the treatment for Addison’s Disease?

A

Synthetic Hormone replacement

Hydrocortisone and fludrocortisone

48
Q

What must patients on hydrocortisone do when they are unwell?

A

Increase their dose of hydrocortisone