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Phase 2 v2 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is type 1 diabetes?

A
  • Metabolic disorder characterised by absolute insulin deficiency, leading to hyperglycaemia.
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2
Q

What is type 2 diabetes?

A
  • A progressive disorder associated with decreased insulin secretion and increased insulin resistance. Leads to poor glycemic control (hyperglycaemia).
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3
Q

What is the clinical presentation of type 1 diabetes?

A
  • Peak presentation at 10-14 YO (young).
  • Polyuria/polydipsia.
  • Weight loss.
  • Excessive tiredness.
  • For many patients, the first presentation will be DKA.
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4
Q

What is the main risk factor for developing type 1 diabetes?

A
  • Genetics. Presence of HLA-DR3/4 predisposes someone to type 1 diabetes.
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5
Q

What is the clinical presentation of type 2 diabetes?

A
  • Often asymptomatic at presentation and picked up on by screening.
  • Can present with polyuria/polydipsia, but this is usually in more advanced hyperglycaemia.
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6
Q

What are the risk factors for type 2 diabetes?

A
  • Age (older).
  • Obesity.
  • FH of type 2 diabetes.
  • Non-white.
  • Gestational diabetes.
  • Pre-diabetes (HbA1c between 42 and 47).
  • Dyslipidaemia (raised cholesterol).
  • CVD (peripheral/coronary artery disease).
  • Stress.
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7
Q

What are the investigations for diabetes mellitus (including ones used for the most common complications)?

A
  • HbA1c > or = 48mmol/mol.
    A repeat confirmatory test will be needed unless the patient has severe symptoms/the HbA1c is extremely high.
  • Fasting lipid profile. Raised LDL common in diabetics.
  • Urine ketones should be tested if the patient is symptomatic. This could show raised ketones, which increase risk of future diabetic kidney disease (CKD).
  • C-peptide. Used to differentiate between type 1 and 2 diabetes (not used routinely). High or normal in Type 2, low in type 1.
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8
Q

What are the key differences between type 1 and 2 diabetes mellitus?

A
  • Type 1 in younger, type 2 in older.
  • Type 1 associated with BMI<25, type 2 associated with BMI>25.
  • C-pep. Raised/normal in type 2, low in type 1.
  • Acanthosis nigricans. Associated with insulin resistance, so therefore is associated with type 2 diabetes not type 1.
  • DKA absent: Type 2.
  • More gradual onset: type 2.
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9
Q

How is type 1 diabetes monitored by the doctor?

A
  • HbA1c check every 3-6 months. Aim for HbA1c > 48.
  • Annual screenings for: Diabetic retinopathy, BP, Foot examination (Peripheral vascular disease, peripheral neuropathy).
  • ACR (albumin:creatinine ratio). Used to monitor the kidney function in a patient with diabetes.
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10
Q

How is type 1 diabetes monitored by the patient?

A
  • Regular capillary glucose monitoring.
  • Should be done at least 4 times a day.
  • If the patient has severe symptoms, or a neurological cognitive disorder that prevents them from manually monitoring their glucose, consider giving them a real-time capillary glucose monitor.
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11
Q

How are diet and exercise managed in type 1 diabetes?

A
  • Diet. Individualised diet plan to patient with aim to maintain a healthy glucose level.
  • Exercise. Exercise should be advised, but appropriate precautions taken.
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12
Q

What medication is used to treat type 1 diabetes?

A
  • Basal-bolus insulin.

This involves basal (slow acting) insulin at regular intervals, and extra bolus (fast acting) insulin prior to meals and exercise.

  • Consider use of an insulin pump if adherence is poor.
  • Consider adding metformin (a biguanide) if BMI>25.
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13
Q

What are the main potential complications of type 1 diabetes?

A
  • DKA.
  • Hypoglycaemia.
  • Retinopathy.
  • Diabetic kidney disease (A type of CKD).
  • Diabetic neuropathy.
  • CVD (hypertension, peripheral vascular disease etc.)
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14
Q

How are exercise and diet managed in type 2 diabetes?

A
  • Increase physical activity.

- Low fat, reduce calorie intake.

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15
Q

What are the different stages of glucose management for type 2 DM?

A

1st line: diet and lifestyle advice.

2nd line: add metformin (a biguanide).

3rd line: Start another diabetic medication (e.g. canagliflozin, a SGLT2 inhibitor).

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16
Q

When is metformin contraindicated?

A
  • If GFR < 30.
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17
Q

What medications are given to control high BP in DM?

A
  • ACEI (ramipril) or ARB (losartan).
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18
Q

What medications are given to those at high risk of CVD with type 2 DM? How are they determined to be at high risk of CVD?

A
  • High intensity statins (atorvastatin).

- High risk determined using the QRISK3 scoring system.

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19
Q

What should happen on a diabetic “sick day”?

A
  • All diabetic medications should be stopped until they are better.
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20
Q

How should type 2 diabetes medication be managed during pregnancy?

A
  • Metformin is safe.

- All other DM type 2 drugs should be stopped.

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21
Q

What are the potential complications of type 2 DM?

A
  • Diabetic kidney disease (CKD).
  • Diabetic retinopathy.
  • Peripheral neuropathy.
  • CVD.
  • Congestive heart failure.
  • Stroke.
  • DKA is still possible in type 2 diabetes, but more common in type 1.
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22
Q

What are the different classes of medications used to treat type 2 diabetes?

A
  • Biguanides.
  • GLP-1 agonists.
  • SGLT2 inhibitors.
  • DPP-4 inhibitors.
  • Sulfonylurea.
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23
Q

What is DKA and what is the criteria?

A

Diabetic ketoacidosis.

It is an acute metabolic complication of diabetes, and the criteria is:

  • Hyperglycaemia.
  • Ketonaemia (high ketones).
  • Metabolic acidosis (low bicarbonate).
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24
Q

Which type of diabetes does DKA occur in?

A
  • Can occur in both, but more common in type 1.
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25
Q

What is the clinical presentation of DKA?

A
  • Diagnosis of diabetes/signs of diabetes (polydipsia/polyuria, tiredness, weight loss etc.).

DKA:

  • Nausea/vomiting.
  • Hyperventilation.
  • Abdominal pain.
  • Reduced consciousness/coma.
  • “Pear drop” smell in breath.
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26
Q

What are the risk factors for DKA?

A
  • Inadequate insulin therapy.
  • Poor adherence to/missed dose of insulin therapy.
  • Infection.
  • MI.
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27
Q

What is the pathophysiology of DKA?

A
  • Reduced insulin.
  • Increased levels of counter-regulatory hormones (GH, glucagon, cortisol, adrenaline).

This causes:

  • Hyperglycaemia.
  • Volume depletion (low BP).
  • Lipolysis (increased levels of FFA/ketones in blood).
  • Hyperkalaemia (reduced uptake of potassium by the cells).
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28
Q

How is DKA treated?

A
  • Saline IV (to restore blood volume).

- Fixed rate insulin infusion.

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29
Q

What are the potential complications of DKA?

A
  • Fixed rate insulin infusion can cause hypokalaemia. Add K supplementation to the saline.
  • Fixed rate insulin can cause hypoglycaemia. Prevent this by properly monitoring capillary glucose during treatment.
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30
Q

What is HHS?

A

Hyperosmolar hyperglycaemic state.

Metabolic state characterised by:

  • Hyperglycaemia.
  • High serum osmolality.
  • Volume depletion (low BP)
  • THERE IS NO SIGNIFICANT KETOACIDOSIS.
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31
Q

What are the key clinical presentations of HHS?

A
  • Develops over days/weeks.
  • Exacerbated diabetic symptoms (polydipsia, polyuria, weight loss etc).
  • KEY SYMPTOM: ACUTE COGNITIVE IMPAIRMENT.
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32
Q

What are the common causes of HHS?

A
  • Inadequate diabetic medication.
  • Missed doses/poor treatment adherence.
  • MI.
  • Dehydration (e.g. care home patient).
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33
Q

What is the pathophysiology of HHS?

A
  • Caused by decreased levels of insulin, but not to the same level as in DKA.
  • This means that whilst levels are low enough to cause hyperglycaemia, they are NOT LOW ENOUGH TO CAUSE LIPOLYSIS (KETOACIDOSIS).
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34
Q

What are the investigations for HHS?

A
  • Blood glucose - elevated.
  • Blood ketones - NO CHANGE.

There will potentially be a slight acidosis on ABG, but not to the same extent as seen in DKA.

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35
Q

What is the treatment for HHS?

A

SAME AS DKA.

  • Saline IV.
  • Fixed rate insulin infusion.
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36
Q

What are the potential complications of HHS? How are they treated?

A
  • Hypokalaemia (due to insulin administration). Give potassium supplementation with the saline.
  • Hypoglycaemia (due to too much insulin). Avoid by closely monitoring blood glucose during treatment.
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37
Q

What is Grave’s disease?

A
  • Autoimmune thyroid condition associated with primary hyperthyroidism.
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38
Q

What is the clinical presentation of Grave’s disease?

A
  • Sweating/heat intolerance.
  • Weight loss.
  • Palpitations.
  • Tremor.
  • Goitre (swollen thyroid).
  • Orbitopathy (bulging eyes).
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39
Q

What are the risk factors for development of Grave’s disease?

A
  • FH.
  • Female (6:1)
  • Smoking
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40
Q

What is the pathophysiology of Graves disease?

A

TSH receptor antibodies are produced (TRAb).

These stimulate the TSH receptors, causing:

  • Hypersecretion of thyroid hormones (T3/4).
  • Hypertrophy/hyperplasia of the thyroid gland (goitre).
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41
Q

What are the investigations used for Grave’s disease?

A
  • TSH test. Will be low in Grave’s disease (negative feedback).
  • T3/4 testing. Will be high.
  • Potential use of TRAb testing. This test is highly sensitive, so useful if diagnosis is questionable.
  • IMAGING IS NOT ROUTINELY USED.
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42
Q

What is the treatment for Grave’s disease?

A

1st line is radioactive iodine.

If contraindicated (pregnant) or not wanted, consider:

  • Carbimazole (an anti-thyroid drug).
  • Surgery (Throidectomy) and T3/4 replacement with levothyroxine post-surgery.

B-blockers (atenolol) used for symptomatic relief until the mainstay treatments begin to take affect. CCB if B-blockers contraindicated (e.g. in asthma).

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43
Q

What is a thyroid storm and its associated symptoms? What disease is it associated with?

A

Associated with Grave’s disease.

Refers to a severe, acute attack of hyperthyroidism. Symptoms:

  • Volume depletion (due to lots of vomiting and sweating).
  • Congestive heart failure.
  • Confusion.
  • Nausea/vomiting.
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44
Q

What is the treatment for a thyroid storm?

A
  • Supportive therapy (IV fluids for volume depletion, cooling for raised temperature).
  • Carbimazole (high dose anti-thyroid drug).
  • B-blockers (e.g. atenolol).
  • Iodine (To reduce T3/4 secretion).
  • Hydrocortisone (corticosteroids - these reduce T3 to T4 conversion).
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45
Q

What is Hashimoto’s thyroiditis?

A
  • An autoimmune thyroid condition associated with raised TPO (Thyroid perioxidase) antibodies and hypothyroidism.
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46
Q

What is the clinical presentation of Hashimoto’s thyroiditis?

A
  • Cold intolerance.
  • Weight gain.
  • Depression.
  • Tiredness.
  • Muscle weakness.
  • Goitre (enlarged thyroid gland).
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47
Q

What are the risk factors for Hashimoto’s thyroiditis?

A
  • Female (7:1)
  • Middle aged (peak at 40-60)
  • FH
  • Other autoimmune conditions
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48
Q

What is the pathophysiology of Hashimoto’s thyroiditis?

A
  • Antibodies (primarily antithyroid perioxidase antibodies/ TPO antibodies) are produced.
  • These antibodies attack the thyroid, causing goitre and hypothyroidism.
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49
Q

What are the key investigations used in Hashimoto’s thyroiditis?

A
  • TPO antibody testing. If positive, highly suggestive of Hashimoto’s thyroiditis.
  • T3/4. Low.
  • TSH. Raised (negative feedback).
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50
Q

What is the treatment for Hashimoto’s thyroiditis?

A
  • Levothyroxine (thyroid hormone replacement).
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51
Q

What are the 4 types of thyroid cancer and which are the two most common?

A
  • Papillary thyroid carcinoma. Most common (80%)
  • Follicular thyroid carcinoma. Second most common (10%)
  • Anaplastic thyroid carcinoma.
  • Medullary thyroid carcinoma.
52
Q

What is the typical clinical presentation of thyroid cancer?

A
  • Usually presence of an asymptomatic thyroid nodule in a female in her 30s or 40s.
53
Q

What are the risk factors for thyroid carcinoma?

A
  • Head/neck irradiation (e.g. previous chemo in that area).

- Female (2:1).

54
Q

What are the investigations used for thyroid carcinoma?

A

1st line: TSH test. This is usually normal in thyroid cancer, and rules out the possibility of hyperthyroidism.

GOLD STANDARD: Fine needle biopsy. This shows both if thyroid carcinoma is present, and the type of thyroid carcinoma.

USS neck may be used to look at the dimensions of the tumour and lymph node involvement.

55
Q

What is the treatment for thyroid carcinoma?

A

Same treatment for both follicular and papillary carcinoma (90% of all thyroid cancer):

- Total thyroidectomy/partial thyroidectomy.
AND
- Radioactive iodine
AND
- Levothyroxine (to replace T3/4).
56
Q

What is cushing’s syndrome?

A
  • The clinical manifestation of pathological hypercorticolism from ANY SOURCE (e.g. cushing’s disease).
57
Q

What is the clinical presentation of cushing’s syndrome?

A
  • Facial plethora (“moon face”)
  • Abdominal striae + central obesity.
  • Hypertension.
  • Diabetes mellitus.
  • Mood changes (e.g. depression).
  • Bitemporal hemianopia (due to pressure on the optic chiasm by a pituitary tumour/cushing’s disease).
58
Q

What are the risk factors of cushing’s syndrome?

A
  • Use of high dose glucocorticoids (exogenous cushing’s). THE MOST COMMON CAUSE OF CUSHING’S SYNDROME OVERALL.
  • Pituitary adenoma/cushing’s disease.
    CAUSES 80% OF ENDOGENOUS CUSHING’S SYNDROME.
  • Adrenal adenoma.
    CAUSES 15% of ENDOGENOUS CUSHING’S SYNDROME.
59
Q

What is the pathophysiology of cushing’s syndrome?

A
  • Increased levels of cortisol causes the clinical manifestation.
  • Severity of symptoms directly correlates with degree of cortisol excess.
60
Q

How are the causes of cushing’s disease classified?

A

Exogenous cushing’s syndrome:
- This is caused by the patient taking high doses of corticosteroids.

ACTH-independent (primary) cushing’s syndrome:
- This is caused by too much cortisol secretion despite suppressed ACTH. (direct problem with the adrenal gland.)

ACTH-dependant (secondary) cushing’s syndrome:
- Too much cortisol secretion due to raised levels of ACTH. Usually caused by cushing’s disease (pituitary adenoma).

61
Q

What are the investigations used to diagnose Cushing’s disease?

A

First line: Dexamethasone suppression test. If cortisol is still high after dexamethasone admission, this is suggestive of Cushing’s syndrome.

THEN: ACTH measurement:

  • ACTH high - ACTH-dependant cushing’s (cushing’s disease).
  • ACTH low - ACTH-independent cushing’s (adrenal adenoma).
62
Q

What is the treatment for cushing’s disease?

A

FOR CUSHINGS DISEASE:
- Laproscopic adenectomy of the pituitary adenoma. (usually done transsphenoidally).

FOR ADRENAL ADENOMA:
- Unilateral adrenalectomy.

GIVE GLUCOCORTICOID REPLACEMENT THERAPY POST SURGERY.

63
Q

What is acromegaly?

A
  • Chronic disease caused by excess GH secretion from the pituitary.
64
Q

What is the clinical presentation of acromegaly?

A
  • Usually insidious onset, therefore retrospective diagnosis.
  • Jaw enlargement.
  • Nose enlargement.
  • Arthropathy.
  • Large hands/feet (spade-like extremities).
  • Mood disorders (depression).

Pituitary tumour can cause bitemporal hemianopia (due to proximity to the optic chiasm).

65
Q

What is the pathophysiology of acromegaly?

A
  • Increased levels of GH secreted from the pituitary.
  • Stimulates increased levels of IGF-1 secretion from the liver.
  • IGF-1 is actually the hormone responsible for most of the manifestations seen in acromegaly, not directly caused by GH.
66
Q

What are the investigations used for acromegaly?

A
  • IGF-1. This is used as oppose to GH as it stays at a more constant level throughout the day, so is more reliable.
  • If pituitary tumour is suspected cause, MRI brain.
67
Q

What is the treatment for acromegaly?

A

1st line: Transsphenoidal pituitary adenectomy.

2nd line (if surgery unsuccessful/not possible): Use a somatostatin analogue (SSA) such as octreotide.

68
Q

What are the most common complications of acromegaly?

A
  • Hypertension.
  • Cardiac complications (LVH, IHD, cardiomyopathy)

Complications are all directly due to excess GH/IGF-1.

69
Q

What is Conn’s syndrome also called? What is it?

A
  • Primary aldosteronism.

- It refers to high levels of aldosterone with primary (kidney) cause.

70
Q

What is the clinical presentation of Conn’s syndrome?

A

Hypertension.
Polyuria/nocturia.

Hypokalaemia (Not present often in clinical practice, but highly indicative if it is). Symptoms of hypokalaemia include:

  • AF
  • Muscle weakness.
  • Tingling.
  • Cramps.
71
Q

What is the pathophysiology of Conn’s syndrome?

A
  • Excessive production of aldosterone irrespective of the negative feedback cycle in the RAAS system. This causes:
  • Increased sodium resorption.
  • Increased loss of potassium and H+ (if prolonged can cause hypokalaemia and/or metabolic acidosis).
  • Renin and angiotensin (I and II) are down-regulated due to the negative feedback loop present in RAAS.
72
Q

What are the investigations used in Conn’s syndrome?

A

1st line:

  • Aldosterone:renin ratio.
  • Raised ratio indicative of PA (primary aldosteronism).
  • May also do a plasma potassium test. Hypokalaemia is rare in patients with Conn’s, but highly indicative if they do.

GOLD STANDARD/confirmatory if the R:A ratio was raised:

  • Fludrocortisone suppression test.
  • If aldosterone remains high despite fludrocortisone being given over multiple days, highly suggestive of primary aldosteronism (Conn’s syndrome).

(Fludrocortisone would suppress aldosterone secretion in normal patients).

73
Q

What is the treatment for Conn’s syndrome?

A

1st line: Laparoscopic unilateral adrenoectomy + spironolactone (Potassium-sparring diuretic).

2nd line (if surgery not possible/unsuccessful): Just spironolactone.

74
Q

What is the MOA for spironolactone in Conn’s syndrome?

A

Acts as a potassium sparring diuretic/ ARB:

  • Competitively binds to angiotensin receptors on the Na/K channels at the distal convoluted tubule, and blocks them.
  • Increases excretion of sodium and water by decreasing Na resorption (reducing BP).
  • Spares potassium (because potassium is no longer being exchanged for sodium in the distal convoluted tubule).
75
Q

What are the complications of Conn’s syndrome?

A

Complications associated with hypokalaemia/hypertension:

  • Heart failure.
  • MI.
  • Stroke.
  • AF.
  • Impaired renal function.
  • Potentially hyperkalaemia can occur (due to spironolactone, a potassium sparring diuretic).
76
Q

What is carcinoid syndrome?

A
  • Presence of a carcinoid tumour that secretes serotonin.
77
Q

Where are carcinoid tumours most typically found?

A
  • Midgut.
  • Lungs.
  • Pancreas.
78
Q

What is the clinical presentation of carcinoid syndrome?

A
  • Flushing.

- Diarrhoea.

79
Q

What are the tests used to confirm carcinoid syndrome?

A
  • Urinary 5-HIAA over 24 hours. (5-HIAA is a metabolite of serotonin).
  • CT scan to find the carcinoid tumour and any metastases.
80
Q

What is the treatment for carcinoid syndrome?

A
  • Somatostatin analogue (e.g. octreotide).
81
Q

What is hypercalcaemia of malignancy?

A

Hypercalcaemia caused by a cancer. It is the most common cause of hypercalcaemia in an inpatient setting.

82
Q

What are the symptoms of hypercalcaemia?

A
  • Neuropsychiatric changes (e.g. fatigue, mood disturbance, coma).
  • GI disturbances (e.g. loss of appetite, nausea, constipation).
  • Muscle weakness.
  • Polyuria/polydipsia.
  • Bone pain.
83
Q

What are the investigations used in hypercalcaemia of malignancy?

A
  • ECG. Assess for shortened QT interval.
  • Adjusted serum calcium. Elevated.
  • Serum PTH. Can be used to assess for PTH-dependant hypercalcaemia.
84
Q

What is the treatment for hypercalcaemia of malignancy?

A

1st line:

  • IV saline.
  • Calcitonin.
  • Alendronic acid (biphosphonates).
85
Q

What are the SIGNS of hypocalcaemia? (5 listed).

A
  • Trousseau’s sign +ve (inflation of BP cuff produces hand/wrist flexion).
  • Chvostek’s sign +ve (tapping of facial nerve causes facial twitching/spasm).
  • ECG will show prolonged QT interval.
  • Hyperpigmentation.
  • Nail changes.
86
Q

What are the SYMPTOMS of hypocalcaemia?

A
  • Muscle spasms/cramps.

- Tingling fingers/toes.

87
Q

What is a serious complication of hypocalcaemia?

A

Seizure.

88
Q

What is the treatment for hypocalcaemia?

A
  • Calcium gluconate (Calcium supplementation).
89
Q

What are the causes of hypercalcaemia?

A

CHIMPANZEES:

C - Calcium supplements
H - HyperPTH
I - Iatrogenic (thiazide diuretics).
M - Multiple myeloma.
P - PTH tumour.
A - Alcohol.
N - Neoplasm (Other cancers).
Z - Zollinger-ellison syndrome.
E - Excess vit. D
E - Excess vit. C
S - Sarcoidosis.
90
Q

What are the signs of hyperkalaemia?

A

ECG - “Go, go tall, go long, go far”:

  • Absent P waves.
  • Tall tented T-waves.
  • Wide QRS complex.
  • Long PR interval.
91
Q

What are the symptoms of hyperkalaemia?

A
  • Muscle weakness.
  • Oliguria.
  • Weak pulse.
92
Q

What are the common causes of hyperkalaemia? (3 given)

A
  • High K+ intake.
  • Thiazide diuretics (K+ sparring).
  • Renal disease (Reduced K+ excretion).
93
Q

What is the treatment for hyperkalaemia?

A
  • Calcium gluconate to protect the cardiac membrane.

- Insulin + glucose to increase K+ absorption by cells.

94
Q

What is the most important risk of hyperkalaemia?

A
  • Life-threatening cardiac arrhythmia.
95
Q

What is Addison’s disease?

A
  • Primary adrenal insufficiency.

- Results in deficiency in both cortisol and aldosterone.

96
Q

What is the clinical presentation of Addison’s disease?

A

“Thin, tanned, tired, tearful”.

  • Fatigue.
  • Weight loss.
  • Hyperpigmentation (due to high levels of ACTH in response to low cortisol).
  • Anxiety.
97
Q

What are the risk factors for Addison’s disease?

A
  • Female.

- Other autoimmune diseases (e.g. DM1, coeliac, RA).

98
Q

What are the investigations used for Addison’s diseasse?

A
  • Morning cortisol levels - Low.
  • Plasma ACTH - Raised.
  • Can use high dose ACTH test: In Addison’s high dose ACTH will have no effect on the raised cortisol levels.
99
Q

What is the treatment for Addison’s disease?

A
  • Hydrocortisone (replaces cortisol).

- Fludrocortisone (replaces aldosterone).

100
Q

What is the main serious complication of Addison’s disease?

A
  • Adrenal crisis. Severe drop in blood pressure, circulatory failure.
  • Give saline and IV hydrocortisone immediately.
101
Q

What is the most common electrolyte imbalance seen in Addison’s disease?

A
  • Hyponatraemia and hyperkalaemia.
102
Q

What is the most common cause of secondary adrenal insufficiency? How does it cause secondary adrenal insufficiency?

A
  • Glucocorticoid treatment.
  • Causes HPO axis suppression (reduced CRH from hypothalamus, reduced ACTH from the anterior pituitary).
  • This decreases the production of cortisol.
103
Q

What are the symptoms of secondary adrenal insufficiency?

A

“Tired, thin, tearful BUT NOT TANNED!”

  • Fatigue
  • Anorexia/ weight loss
  • Anxiety

There is no tan as ACTH is decreased rather than increased as seen in Addison’s.

104
Q

What are the investigations used in suspected adrenal insufficiency?

A
  • Serum cortisol - Low.
  • Serum ACTH - Low.
  • ACTH stimulation test. Cortisol increases, suggesting secondary adrenal insufficiency as oppose to primary (Addisons).
105
Q

What is the treatment for secondary adrenal insufficiency?

A
  • Taper of corticosteroid therapy.

- Must be gradual to reduce the risk of adrenal crisis.

106
Q

What is the main complication of secondary adrenal insufficiency?
How does it present?
How is it treated?

A
  • Adrenal crisis.
  • Hypovolaemia, low BP, tachycardia.
  • Treat with IV saline + hydrocortisone.
107
Q

What is SIADH?

A
  • Inappropriate secretion of ADH (vasopressin).

- Leads to euvolaemic hyponatraemia and production of concentrated urine.

108
Q

Where is ADH produced and secreted from?

A
  • Produced in the hypothalamus.

- Secreted from the posterior pituitary.

109
Q

What is the clinical presentation of SIADH?

A

Symptoms of cerebral oedema:

  • Headache.
  • Nausea/vomiting.
  • Altered mental state.
  • Seizure/coma.
110
Q

What are the investigations used for SIADH?

A
  • Serum osmolality/sodium. Low.

- Urine osmolality/sodium. High.

111
Q

What is the treatment for SIADH?

A
  • Hypertonic saline.
  • Restrict fluid intake.
  • Furosemide (loop diuretics).
  • Tolvaptan (ADH receptor antagonist).
112
Q

What is diabetes insipidus (DI)?

A
  • The inability to concentrate urine, resulting in production of large volumes of unconcentrated urine.
113
Q

What are the two types of DI?

A
  • Central DI. Reduced ADH secretion/production (Hypothalamus/posterior pituitary).
  • Nephrogenic DI. Reduced renal sensitivity to ADH.
114
Q

What is the clinical presentation of DI?

What is it important to rule out before diagnosing DI?

A
  • Polyuria/polydipsia.
  • Dilute (hypotonic) urine.
  • Important to rule out primary polydipsia (high fluid intake, leading to high urine production).
115
Q

What is the main risk factor for central DI?

A
  • Recent head trauma/neurosurgery (could disturb the HP axis).
116
Q

What are the investigations for DI?

A
  • Urine osmolality - Low.
  • 24 hour urine volume >3L.

GOLD STANDARD:
- Water deprivation test. In DI, urine output will remain high and dilute despite water deprivation.

  • ADH stimulation test. If giving ADH (desmopressin) resolves the problems, DI is central. If the problems persist, the DI is nephrogenic.
117
Q

What is the treatment for DI?

A
  • Central DI, give desmopressin (ADH analogue).

- Nephrogenic DI, more difficult. Try to match urine output with fluid intake.

118
Q

What are the two types of hyperparathyroidism?

What are the calcium and PTH levels in each?

A
  • Primary hyperparathyroidism. This is caused by autonomous over production of PTH.
  • Characterised by HIGH calcium and high PTH levels.
  • Secondary hyperparathyroidism. This is when hypocalcaemia stimulates excessive PTH production.
  • Characterised by LOW calcium and high PTH.
119
Q

What is the most common cause cause of primary hyperparathyroidism?

A
  • Parathyroid adenoma (causes 80% of primary hyperparathyroidism).
120
Q

What is the clinical presentation of primary hyperparathyroidism?

A 
- OSTEOPOROSIS HISTORY.
May include:
- Fatigue
- Myalgia
- Anxiety/depression.
121
Q

What are the investigations used for primary hyperparathyroidism?

A
  • Serum calcium. High.
  • Serum PTH. High.
  • CT of parathyroid may reveal an adenoma.
122
Q

What is the treatment for primary hyperparathyroidism?

A
  • Parathyroid surgery.
123
Q

What are the 2 most common causes of secondary hyperparathyroidism?

A
  • CKD.

- Vit. D deficiency.

124
Q

How does secondary hyperparathyroidism present?

A

Symptoms of hypocalcaemia:

  • +ve Chvostek’s and Trousseau’s signs.
  • Muscle cramps.
  • Numb fingers/toes.
  • POTENTIALLY OSTEOMALACIA due to vit. D deficiency.
125
Q

What are the investigations use for secondary hyperparathyroidism?

A
  • Serum calcium. Low.
  • Serum PTH. High.
  • Serum 25-hydroxyvitamin-D. Low if Vit. D deficient.
  • Urea/creatitine raised in CKD.
126
Q

What is the treatment for secondary hyperparathyroidism?

A
  • Vit D./calcium supplementation as appropriate (for both CKD and Vit. D deficiency secondary hyperparathyroidism).

Phase 2 v2 (14 decks)

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