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Endocrinology Flashcards

1
Q

What triggers parathyroid hormone release?

A

Low serum calcium

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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)

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3
Q

What is a normal serum calcium level?

A

1.1mmol/L

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4
Q

Vitamin D deficiency biochemistry

A

HIGH PTH
LOW Ca2+
LOW PO4-

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5
Q

Hypoparathyroidism biochemistry

A

LOW PTH
LOW Ca2+
HIGH PO4-

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6
Q

Pseudohypoparathyroidism biochemistry

A

HIGH PTH
LOW Ca2+
HIGH PO4-

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7
Q

Pseudopseudohypoparathyroidism

A

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

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8
Q

Hypercalcaemia (malignant) biochemistry

A

LOW PTH
HIGH Ca2+
Normal PO4-

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9
Q

Primary Hyperparathyroidism Biochemistry

A

HIGH PTH
HIGH Ca2+
LOW PO4-

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10
Q

Tertiary Hyperparathyroidism Biochemistry

A

HIGH PTH
HIGH Ca2+
HIGH PO4-

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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.

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12
Q

What are the consequences of Hypocalcaemia?

A 
Pins and needles
Muscle Spasms
Seizures
Long QT interval
Basal Ganglia calcification
Cataracts
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13
Q

Signs for Hypocalcaemia

A

Chvostek’s and Trousseau’s

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14
Q

What are the causes of Hypocalcaemia?

A

Vitamin D Deficiency
Hypoparathyroidism
Pseudohypoparathyroidism

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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

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16
Q

Definition of pseudoparathyroidism

A

A resistance to parathyroid hormone resulting in hypocalcaemia

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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)
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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+

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19
Q

What are the symptoms of Hypercalcaemia?

A 
Thirst
Polyuria
Nausea
Constipation
Confusion
Coma
Renal Stones
Short QT
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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
What causes tertiary hyperparathyroidism?
Renal failure resulting in decreased production of vitamin D.
26
What percentage of ingested glucose goes to the liver?
40%
27
What glucose transporter is found on the surface of Beta Cells?
GLUT2
28
What glucose transporter is found on the surface of other cells?
GLUT4
29
Result of Insulin
Decrease hepatic glucose output Increase glucose uptake via GLUT4 Suppresses lipolysis and muscle breakdown
30
Definition of Diabetes Mellitus
A disorder of carbohydrate metabolism characterised by chronic hyperglycaemia.
31
How does diabetes mellitus cause mortality and morbidity?
Diabetic Ketoacidosis Hyperosmolar hyperglycaemic coma Micro/Macrovascular tissue complications
32
What is the main side effect of treatment of diabetes mellitus?
Hypoglycaemia
33
What are the types of diabetes?
``` Type 1 Type 2 (inc gestational and medication induced) Maturity onset diabetes of youth (MODY) Pancreatic diabetes Endocrine (acromegaly/Cushing's) Malnutrition related ```
34
Biochemistry for Diabetes diagnosis
Symptoms + Random Glucose >11 Fasting Glucose >7 HbA1c >48
35
Why is there no weightloss in type 2 diabetes?
The low levels of insulin are protective against catabolism, preventing muscle/weight loss
36
What are the principles of diabetes treatment?
Control Symptoms Prevent acute emergencies e.g. DKA Identify and prevent microvascular complications HbA1c >50 (as low as possible without insulin or sulfonylureas)
37
What are the symptoms of type 1 diabetes?
``` Nausea Vomiting Fatigue Polyuria Polydipsia Weight loss ```
38
What are the symptoms of type 2 diabetes?
``` Frequent UTIs Polyuria Polydipsia Dehydration Fatigue ```
39
What are the treatments for type 2 diabetes?
``` Weight loss Diet Exercise Manage BP and cholesterol Metformin, Sulfonylureas, Insulin. ```
40
What is Addison's Disease?
Primary adrenocortical insufficiency
41
What is the aetiology of Addison's Disease?
Autoimmune Disseminated Tuberculosis Adrenal Mets (rare)
42
Pathogenesis of Addison's Disease
Lack of glucocorticoid and mineralocorticoid production in the adrenal cortex.
43
How advanced does adrenal damage have to be before clinical signs manifest? (Addison's Disease)
90% destroyed
44
How does Addison's disease present?
Tiredness, lethargy, weakness Anorexia, nausea, vomiting and diarrhoea Prominent weight loss
45
Biochemistry of Addison's Disease
``` LOW Na+ HIGH K+ HIGH Urea Up to 50% Hypoglycaemic Circulating antibodies may be found (against adrenal tissue) ```
46
What is the test for Addison's disease?
Synacthen test | Inject ACTH - no rise in plasma cortisol = Addison's
47
What is the treatment for Addison's Disease?
Synthetic Hormone replacement | Hydrocortisone and fludrocortisone
48
What must patients on hydrocortisone do when they are unwell?
Increase their dose of hydrocortisone

Phase 2a (1 decks)

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