Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2a diseases > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the main pancreatic disease?

A

Diabetes Mellitus (DM)

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

What are the two types of DM?

A
  • Type 1 (Autoimmune destruction of pancreatic B cells, resulting in lack of insulin secretion).
  • Type 2 (decrease in insulin sensitivity).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is diabetes mellitus?

A
  • Chronic hyperglycaemia due to insulin dysfunction.

- Glucose cannot be moved from bloodstream into cells effectively, leading to them being starved of energy.

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

What is the clinical presentation of type 1 diabetes?

A
  • Hyperglycaemia
  • Polydipsia
  • Polyuria
  • Weight loss
  • Blurred vision
  • Nausea and vomiting
  • Usually diagnosed in the young.
  • Can present with diabetic ketoacidosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the clinical presentation of type 2 diabetes?

A
  • Usually asymptomatic, and picked up by screening.

- Screening should be carried out when risk factors are present.

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

What is the pathophysiology of type 1 diabetes?

A
  • Hyperglycaemia due to insulin deficiency.
  • Insulin deficiency occurs as a result of pancreatic B-cell destruction (usually caused by autoimmune mechanisms)
  • If no evidence of autoimmune destruction, the disease is referred to as idiopathic type 1 DM.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the pathophysiology of type 2 diabetes?

A
  • Multifactorial disorder
  • Increase in insulin resistance, often accompanied by deficit in insulin secretion.
  • Leads to chronic hyperglycaemia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the aetiology of type 1 diabetes?

A
  • HLA-DR3/4 (human leukocyte antigen) is affected in >90% of type 1 diabetic patients.
  • This abnormality causes autoimmune disease, often including the attack of islet cells (mainly B cells) of the pancreas.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the aetiology of type 2 DM?

A
  • Multifactorial
  • There is an element of genetic susceptibility, but not as strong as in type 1 DM.
  • No HLA link established.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the epidemiology of type 1 DM?

A
  • Onset younger (<30)

- Usually patients will be skinny.

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

What is the epidemiology of type 2 DM?

A
  • Onset older (>30)
  • Patients are usually overweight.
  • More common than type 1 DM generally speaking.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the diagnostic tests for type 1 DM?

A
  • Plasma glucose test (random, fasted, 2 hour etc.).
  • HbA1c. This will provide a measurement of the average plasma glucose over the last 2-3 months.
  • C peptide. This will go down in type 1 DM and remain the same/increase in type 2 DM.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the diagnostic tests for type 2 DM?

A
  • Plasma glucose test (random, fasted, 2 hours etc.).
  • HbA1c. This will provide a measurement of the average plasma glucose over the last 2-3 months to see if it is chronically raised.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What clinical test can be done to tell the difference between type 1 and type 2 DM?

A
  • C peptide test.
  • C pep will be low in type 1 DM
  • C pep will be normal/raised in type 2 DM.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the treatment for type 1 DM?

A

1st line:

  • Basal-bolus insulin
  • Pre-meal insulin IF NEEDED
  • Metformin (a biguanide) IF NEEDED.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the treatment for type 2 DM?

A
  • First line: Diet and exercise changes.
  • If no change, prescribe metformin (biguanide).
  • Add SGLT2 inhibitor if CV risk is high (canagliflozin)
  • Potentially use sulfonylurea (glimepiride) if metformin not tolerated.
  • Give aspirin (non-selective COX inhibitor) or clopidogrel (P2Y12 antagonist) to reduce risk of CVD. Both aspirin and clopidogrel are antiplatelet drugs.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the potential complications of type 1 and 2 DM?

A
  • Diabetic ketoacidosis (body cannot use glucose as fuel due to lack of insulin, so begins to use lipids and peptides instead. This produces ketones, which are released into the blood. High levels of ketones are toxic.)
  • Diabetic nephropathy (chronically high glucose levels do damage to kidneys).
  • Diabetic neuropathy (high glucose levels -> neurological damage, causing lack of sensation in feet/hands.)
  • Diabetic retinopathy (damage to retinal blood vessels, which if severe enough can lead to vision defects.)
  • Hyperosmolar hyperglycaemic nonketotic coma (caused by extremely high glucose levels, similar to ketoacidosis, but with the absence of high ketone levels).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the 4 main thyroid disorders I need to be aware of?

A
  • Graves disease
  • Hashimoto’s thyroiditis
  • Hypothyroidism
  • Thyroid cancer/ malignancies.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is Grave’s disease?

A

HYPERthyroidism due to the pathological stimulation (immune system disorder) of TSH receptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the difference between primary and secondary hyperthyroidism?

A

Primary hyperparathyroidism - Disease is directly within the thyroid, leading to increased T3/T4 secretion (unrelated to TSH levels)

Secondary hyperparathyroidism - Thyroid gland is being overstimulated by excessive TSH hormones.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How will a person with Grave’s syndrome present clinically?

A
  • Rapid heart beat
  • Tremor
  • Diffuse palpable goitre (swollen thyroid gland).
  • Audible bruit over thyroid gland (audible pulse over thyroid due to vascular proliferation).
  • Eye problems: Bulging eyes, and lid retraction.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the pathophysiology of Grave’s disease?

A
  • Thyroid stimulating immunoglobulins bind to TSH receptors on the thyroid, leading to excess T3 and T4 (thyroxine) production.
  • T4 receptors on the pituitary are stimulated due to elevated T4 levels, leading to suppression of TSH secretion.
  • Therefore, Grave’s disease causes high thyroid hormone levels, with low TSH.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the aetiology of Grave’s disease?

A
  • Unclear.
  • There is an element of genetic influence.
  • It is an autoimmune disease, and associated with other autoimmune diseases such as parnicious anaemia and myasthenia gravis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the epidemiology of Grave’s disease?

A
  • The most common cause of hyperthyroidism.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the diagnostic tests for Grave’s?

A
  • Thyroid hormone tests. High T3 and T4

- TSH test. Lower than normal TSH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the potential treatments for Grave’s disease?

A
  • Antithyroid drugs (carbimazole usually, else propylthiouracil). These will be taken in one of two ways:
  • Block and replace. Prolonged treatment using the drug, along with levothyroxine to replace the lost thyroid hormone.
  • Titration. Gradual reduction in the dose of anti-thyroid, until the naturally produced thyoid hormones are at the right level again.
  • Also give a B blocker (atenolol or propanolol) to treat symptoms such as tachycardia, tremor and anxiety. If contraindicated give CCB (verapamil).
  • Thyoidectomy (partial or complete)
  • Radioactive iodine. Taken up by thyroid, and will subsequently kill some of the thyroid, reducing hormone production.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the most common complication of grave’s disease?

A

Thyroid storm (same as thyrotoxic crisis).

  • This is a hypermetabolic state induced by the presence of excessive thyroid hormones.

Hyperthyroidism can also cause atrial fibrillation, and a subsequent irregularly irregular heartbeat.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is Hashimoto’s thyroiditis?

A

HYPOthyroidism due to aggressive destruction of thyroid cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How will a person with Hashimoto’s disease present clinically?

A
  • Rapid enlargement of the thyroid gland, which can cause dyspnoea and/or dysphagia due to pressure changes.
  • The hypothyroidism will cause fatigue, cold intolerance, slowed movement, decreased sweating. (decreased metabolic activity).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the pathophysiology of Hashimoto’s disease?

A
  • Autoimmune disease.

- Causes aggressive destruction of thyroid cells, and thyroid fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the aetiology of Hashimoto’s disease?

A
  • Unknown
  • Autoimmune, with some genetic relation.
  • Can be triggered by iodine insufficiency, infection, smoking and stress.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the epidemiology of Hashimoto’s disease?

A
  • More common in places with lower iodine intake/ iodine deficiency in diet.
  • Approx. 15x more likely in women.
  • The most common cause of HYPOthyroidism.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What investigations are required for diagnosis of Hashimoto’s thyroiditis?

A
  • TSH levels will usually be raised (negative feedback).

- Thyroid antibodies will be present.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What treatments are available for Hashimoto’s disease?

A
  • Thyroid hormone replacement (levothyroxine).

- Resection of obstructive goitre to relieve symptoms (dyspnoea and dysphagia.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the potential complications of hypothyroidism?

A
  • Hyperlipidemia. (Blood contains too many lipids, such as cholesterol and triglycerides.). This can increase risk of cardiovascular disease over time.
  • Myxoedema coma. A form of endocrine emergency (20-50% mortality), usually caused by extreme (and untreated) hypothyroidism. Treated with thyroid replacement (levothyroxine) and hydrocortisone (to protect against potential adrenal insufficiency).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is Hashimoto’s encephalopathy?

A
  • Effects brain function

- Associated with Hashimoto’s thyroiditis, but relationship unclear.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Other than Hashimoto’s disease, what are the 3 broad categories of hypothyroid disease?

A
  • Primary
  • Secondary
  • Transient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the clinical presentation of hypothyroidism?

A

Symptoms relate to reduced metabolic activity.

  • Insidious (slow) onset.
  • Tiredness/ lethargy
  • Intolerance of cold
  • goitre (swelling of thyroid gland)
  • Slowing of intellectual activity.
  • Constipation
  • Deep hoarse voice
  • Puffy face, hands and feet.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What do the different classifications of thyroid disease mean?

A
  • Primary. Means disease directly associated with the thyroid gland.
  • Secondary. Means disease associated with the pituitary or hypothalamus.
  • Transient. Means it is temporary hypothyroidism (eg after birth, or after withdrawing from treatment for a short time.)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the pathophysiology of primary hypothyroidism?

A
  • Aggressive destruction of the thyroid cells due to cellular/antibody mediated immune processes.
  • Antibodies bind and block TSH receptors on thyroid, leading to inadequate T3/4 production and secretion.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the pathophysiology of secondary hypothyroidism?

A
  • Reduced release or production of TSH due to issues with either the hypothalamus (TRH) or the pituitary (TSH).
  • This results in reduced T3/4 release from the thyroid.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the pathophysiology of transient hypothyroidism?

A
  • Sudden deficit of T3/4 leading to raised TSH levels (-ve feedback) as the thyroid tries to re-establish normal T3/4 levels.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the aetiology of hypothyroidism?

A

Primary:

  • Hashimotos thyroiditis (autoimmune)
  • Iodine deficiency
  • Congenital defects

Secondary:

  • Isolated TSH deficiency
  • Hypopituitarism (due to neoplastic infection/tumour of pituitary).
  • Hypothalamic disorder (neoplasm, severe head trauma).

Transient:
- Caused by withdrawal from thyroid therapies., such as iodine supplementation withdrawal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the diagnostic tests used to diagnose hypothyroidism?

A
  • Low free serum T4 levels.
  • TSH will be normal/high in primary hypothyroidism.
  • TSH will be low in secondary hypothyroidism.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What treatments are given for primary and secondary hypothyroidism?

A

Primary - Thyroid hormone replacement therapy (Levothyroxine), and potential resection of the obstructive goitre.

Secondary - Still give thyroid hormone replacement (levothyroxine) but also treat the underlying cause.

Transient - Will often resolve on its own. If due to treatment withdrawal, consider restarting treatment/ re-establishing a higher dose.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the 5 common classifications of thyroid cancer?

A
  • Papillary
  • Follicular
  • Anaplastic
  • Lymphoma
  • Medullary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What thyroid cancers usually present as asymptomatic thyroid nodules (hard and fixed)?

A
  • Papillary thyroid cancer
  • Follicular thyroid cancer
  • Anaplastic thyroid cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What thyroid cancer presents as a rapidly growing mass in the neck?

A
  • Thyroid lymphoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What thyroid cancer causes diarrhoea, flushing episodes and itching?

A
  • Medullary thyroid cancer.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is a papillary thyroid cancer?

A
  • A cancer of the thyroid gland which exhibits papillae (small rounded processes) amongst it’s cells histologically.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is a follicular thyroid cancer?

A
  • Cancer of the follicular cells of the thyroid (cells responsible for T3/4 production and secretion.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is an anaplastic thyroid cancer?

A
  • A very aggressive, rapidly proliferating cancer.

- Consists of cells that have little to no resemblance to normal cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is a thyroid lymphoma?

A

Cancer of the thyroid originating from leukocytic cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is a medullary thyroid cancer?

A

Cancer that starts in the “C” cells of the thyroid. These are the cells that produce calcitonin (related to calcium management in the body).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the pathophysiology of a papillary thyroid cancer?

A
  • Tends to spread locally within the neck.

- Could compress the trachea.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the pathophysiology of a follicular thyroid cancer?

A
  • Greater likelihood to metastasise and spread to the lungs and bones than a papillary thyroid cancer.
  • Still may infiltrate neck
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the pathophysiology of an anaplastic thyroid cancer?

A
  • Dedifferentiation of follicular thyroid cells, and rapid proliferation of those cells.
  • Dedifferentiation means that these cancer cells no longer uptake iodine or contribute to T3/4 synthesis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the pathophysiology of thyroid lymphoma?

A
  • Originates from leukocytic cells.

- Almost always will be non-hodgkins (Reed-Sternberg cells are NOT present in non-hodgkins).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is the pathophysiology of medullary thyroid cancer?

A
  • Cancer of the parafollicular calcitonin producing cells (“C-cells”).
  • Medullary cancer results in large amounts of calcitonin production (affects calcium regulation - hypocalcaemia).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is the epidemiology of thyroid cancers?

A
  • 70% of thyroid cancer is papillary, and this is 3x more common in women. Also more likely to occur in young people.
  • 20% of thyroid cancer is follicular. Occurs in middle ages and more common for people with iodine deficiency.
  • Lymphoma, anaplastic and medullary thyroid cancers are far less common.
  • Thyroid lymphoma is associated with Hashimoto’s thyroiditis (an inflammatory hypothyroid disease, so makes sense!).
61
Q

What investigations are conducted to diagnose thyroid cancers?

A
  • Fine needle aspiration, then histological assessment of the biopsy.
  • Calcitonin can be measured by blood test. If serum calcitonin is high, probably medullary cancer.
62
Q

What are the treatment options for thyroid cancer?

A
  • Total thyroidectomy
  • Radioactive iodine administration.
  • External radiotherapy. (Palliative care to reduce symptoms).
  • Prophylactic central lymph node dissection (a preventative measure to reduce chance of cancer spreading).
63
Q

What is the main disease of hypercortisolism?

A

Cushing’s syndrome

64
Q

What is Cushing’s syndrome?

A

Persistently and inappropriately elevated circulating glucocorticoid (cortisol).

65
Q

What is the clinical presentation of Cushing’s syndrome?

A
  • Obesity (with fat distribution being central “pot belly”)
  • Plethoric complexion (red faced)
  • Rounded “moon face”
  • Thin skin
  • Bruising
  • Striae (around abdomen especially)
  • Hypertension
  • Pathological fractures.
66
Q

What is Cushing’s DISEASE?

A
  • When the elevated glucocorticoid levels are attributed to inappropriate ACTH secretion from the pituitary (secondary hyperglucocorticoid disease).
  • Caused by presence of a benign adenoma of the pituitary gland.
  • Cushing’s disease is a subtype of cushing’s syndrome.
67
Q

What is the pathophysiology of Cushing’s syndrome?

A
  • Many features occur due to the catabolic effect cortisol has on protein. (Such as thin skin, easy bruising, striae).
  • Excessive alcohol intake can mimic the clinical and biochemical signs of Cushing’s syndrome. However, these symptoms will resolve when alcohol intake is reduced. (Pseudo-cushing’s).
68
Q

What is the aetiology of Cushing’s syndrome?

A

ACTH-dependant Cushing’s (secondary):

  • Excessive ACTH from pituitary (Cushing’s disease).
  • ACTH producing tumour
  • Too much ACTH being administered to patient.

ACTH-independent Cushing’s (primary):

  • Excess glucocorticoid administration (MOST COMMON CAUSE)
  • Adrenal adenomas
  • Adrenal carcinomas
69
Q

What does ACTH stand for?

A

(AdrenoCorticoTrophic Hormone)

70
Q

What is the epidemiology of Cushing’s syndrome?

A
  • 1/100,000
  • Higher incidence in patients with diabetes.
  • 2/3 of Cushing’s cases are Cushing’s disease (secondary hyperglucocorticoid) rather than Cushing’s syndrome.
71
Q

How is Cushing’ syndrome investigated and subsequently diagnosed?

A

CONFIRM RAISED CORTISOL LEVELS:

  • 48 hour low dose dexamethasone. For a normal patient, this will result in less ACTH being released (-ve feedback) by the pituitary, and as a result less cortisol will be released by the adrenal glands.
  • However, a cushing’s syndrome patient will have raised cortisol levels, as the increased level of cortisol will not impact upon their cortisol production.

This is established by monitoring the cortisol levels.

ESTABLISHING THE CAUSE OF CUSHINGS SYNDROME:

  • Carry out an MRI of both the renal system (adrenal glands for primary disease/ACTH-independent disease) and the pituitary.(for secondary disease/ ACTH dependant disease).
72
Q

How is Cushing’s syndrome treated?

A
  • For tumours, surgical removal. This is first line for all types of Cushing syndrome where it is possible.
  • Otherwise, cortisol synthesis inhibition. (Drugs include metyrapone and ketoconazole).
73
Q

What are the potential complications of Cushing’s syndrome?

A
  • Hypertension
  • Obesity (Increase in circulating FFA (free fatty acids) leading to lipid accumulation in both the liver and skeletal muscle).
  • Potential death
74
Q

Does Cushing’s syndrome normally get better?

A

No, rarely enters remission.

75
Q

What is Acromegaly?

A

Overgrowth of all organ systems due to excess GH.

76
Q

What is the clinical presentation of acromegaly?

A
  • Slow onset (timeline only usually established by using old photos).
  • Larger hands/feet.
  • Large tongue
  • Prognathism (protruding jaw).
  • Interdental separation
  • Spade-like hands (widened fingers).
77
Q

What is the difference between gigantism and acromegaly?

A
  • Gigantism occurs when GH secretion is high in younger people whose long bone epiphyses have not yet fused. This leads to them having tall stature along with large hands and feet.
  • Acromegaly occurs when GH secretion is high in older people after their long bone epiphyses have already fused. As a result there is no change in stature, just an increase in hand and feet size.
78
Q

What is the pathophysiology of acromegaly?

A
  • GH acts directly upon many tissues such as the liver, muscle, bone and fat.
  • GH also acts indirectly, as it affects the levels of insulin-like growth factor (IGF-1) which also contributes to managing growth and development.
  • Excess of either hormone causes excess growth of many different organ systems.
79
Q

What is the aetiology of acromegaly?

A
  • Normally as a result of excessive GH secretion by a pituitary tumour.
  • GH can be secreted by other tumours too such as hypothalamic and specific lung cancers, but this is far rarer.
80
Q

What is the epidemiology of acromegaly?

A
  • 1/200,000
  • Average age of DIAGNOSIS is 40, but disease has often been present long before then due to the insidious progression pattern.
81
Q

What are the commonly used investigations to diagnose acromegaly?

A

2 Components:

Glucose tolerance test (GOLD STANDARD)x:

  • Patient is given a high glucose content drink
  • Normally, GH would drop in response to this. If it doesn’t drop sufficiently, person has acromegaly.

IGF-1 test:
- IGF-1 stays a lot more constant throughout the day than GH does, so provides a much better average to go off when trying to determine whether a person has too much GF/IGF-1 or not than GH alone.

82
Q

What are the treatment options for acromegaly?

A
  • Transsphenoidal resection surgery (removal of pituitary tumour). IF POSSIBLE THIS IS 1ST LINE.
  • IF SURGERY NOT POSSIBLE SOMATOSTATIN ANALOGUES ARE FIRST LINE (Again, somatostatin inhibits GH production). 2 examples of SSA are Octreotide and Ianreotide.
  • Dopamine agonists (Bind to D2 receptors and restrict GH secretion). Often given as dual therapy with SSAs.

2nd line:
- GH receptor antagonists (Due to -ve feedback loops, suppress GH secretion) For example, pegvisomant.

83
Q

What are the potential complications of acromegaly?

A
  • Hypertension
  • Diabetes
  • Untreated adenoma can impact optic chiasm (Blindness/ vision impairment).
  • Acromegaly patients are at a significantly higher risk of colorectal cancer.
84
Q

What is Conn’s syndrome?

A
  • Same thing as primary hyperaldosteronism.

- Means that aldosterone levels are high INDEPENDENTLY of the RAAS system.

85
Q

What is the clinical presentation of Conn’s syndrome?

A
  • Hypertension (possibly low urine output)

- Hypokalaemia (aldosterone increases K excretion, but increases Na and water retention).

86
Q

What is secondary hyperaldosteronism?

A
  • This is where aldosterone levels are high due to high renin levels (so DEPENDANT on the RAAS system).
87
Q

What is the pathophysiology of Conn’s syndrome?

A
  • Aldosterone stimulates sodium reabsorption and potassium excretion in the distal tubules.
  • Therefore, hyperaldosteronism will cause increased sodium reabsorption, and increased potassium excretion.
  • If sodium reabsorption increases, so does water reabsorption.
88
Q

What is the aetiology of Conn’s syndrome?

A
  • Potentially an adrenal adenoma secreting excess aldosterone.
89
Q

What are the diagnostic tests for Conn’s syndrome?

A
  • Plasma aldosterone (high)

- Renin (should be low - if normal or high suggests secondary hyperaldosteronism).

90
Q

What are the treatment options for Conn’s syndrome?

A

For an adenoma:
- Surgical removal

For adrenal hyperplasia:
- Aldosterone antagonist (usually spironolactone).

91
Q

What is hypoadrenalism?

A
  • The adrenal glands do not produce adequate levels of adrenal hormones.
92
Q

What is Addison’s disease?

A
  • Primary adrenal insufficiency.
93
Q

What is the pathophysiology of Addison’s disease?

A
  • Autoimmune destruction of the adrenal cortex, leading to less cortical products (cortisol AND aldosterone).
  • Negative feedback stimulates excess ACTH, leading to melanocyte stimulation and HYPER PIGMENTATION (differentiates Addison’s from secondary hypoadrenalism).
94
Q

What is the clinical presentation of Addison’s disease?

A
  • Insidious onset.
  • Non-specific symptoms (lethargy, depression, anorexia, weight loss, weakness, fatigue).
  • Postural hypertensions

The 4 T’s:

  • Thin
  • Tanned (hyperpigmentation)
  • Tired
  • Tearful
95
Q

What is the aetiology of Addison’s disease?

A
  • Organ specific autoantibodies in 90% of cases.
96
Q

What are the diagnostic tests for Addison’s disease?

A
  • Morning serum cortisol, and ACTH levels should be taken at the same time.
  • Raised ACTH with low serum cortisol is a strong indicator of Addison’s disease (primary adrenal insufficiency).
97
Q

What is the treatment for Addison’s disease?

A
  • Hormone replacement (hydrocortisone) and mineralocorticoid (fludrocortisone).
98
Q

What is an adrenal crisis and how is it treated?

A
  • Acute medical emergency caused by a lack of cortisol.
  • IV hydrocortisone immediately if suspected.
  • Saline for hypotension/ dehydration if required. If glucose is low, 5% dextrose.
  • Treat underlying cause if possible.
99
Q

What is secondary adrenal insufficiency?

A
  • Reduction of adrenal cortex stimulation.
  • Less cortisol (but not less aldosterone) due to low ACTH.
  • Low ACTH means there is NO PIGMENTATION (differentiates this disease from Addison’s).
100
Q

What are the symptoms of secondary hypoadrenalism?

A
  • Same as Addison’s but without the pigmentation:
  • Tired
  • Teary
  • Thin
  • NOT Tanned
101
Q

What is the aetiology of secondary adrenal insufficiency?

A
  • Hypothalamic-pituitary disease.

- Long-term steroid therapy. This can lead to suppression of the HPA (hypothalamic-pituitary-adrenal) axis.

102
Q

What investigations are used to diagnose secondary adrenal insufficiency?

A
  • Serum cortisol + ACTH.

- Both cortisol and ACTH being low will indicate secondary adrenal insufficiency.

103
Q

What is the treatment for secondary adrenal insufficiency?

A
  • Hormone replacement (just hydrocortisone, as aldosterone has not been affected).
  • Try to taper off the hydrocortisone if condition improves.
104
Q

What are the symptoms of hyperkalaemia?

A

“MURDER”

M-Muscle weakness
U-Urine- oliguria, anuria
R-Respiratory distress
D-Decreased cardiac contractility
E-ECG changes (Tall, tented T waves and prolonged PR interval)
R-Reflexes- hyperreflexia, or areflexia (flaccid)

105
Q

What are the signs on an ECG of hyperkalaemia?

A
  • Tall, tented T waves

- Sometimes loss of P waves

106
Q

What is the aetiology of hyperkalaemia?

A
  • Renal impairment (most common). Leads to potassium retention in the nephron.
  • Can also caused by use of potassium sparing diuretics (drugs that increase water loss but not potassium loss).
107
Q

What investigations are used to diagnose hyperkalaemia?

A
  • Usually, routine blood test that finds raised potassium.

- Sometimes, ECG. Will show tall, tented T waves and sometimes absence of P waves.

108
Q

What is the treatment for hyperkalaemia?

A
  • Restriction of dietary potassium.

- Loop diuretics.

109
Q

What is the main potential complication of hyperkalaemia?

A
  • MI causing death.
110
Q

What is the clinical presentation of hypokalaemia?

A
  • Usually asymptomatic
  • Muscle weakness
  • Increased risk of arrhythmia
  • Polyuria
111
Q

How does the ECG of a patient with hypokalaemia look?

A
  • T wave flattening/ inversion.

- Presence of a U wave (wave after T, representing repolarisation of the purkinjee fibres.

112
Q

What is the pathophysiology of hypokalaemia?

A
  • Excessive loss of potassium through the kidneys in response to aldosterone therapy or diuretic therapy.
  • Aldosterone directly inhibits potassium reabsorption in the kidneys (due to Na K pumps being up-regulated).
113
Q

What are the investigations used for hypokalaemia?

A
  • Routine bloods show low K

- ECG. Flat/ inverted T waves and potentially prominent U waves.

114
Q

What is the treatment for hypokalaemia?

A

Treat underlying cause

  • Withdrawal of harmful medication.
  • Increase dietary potassium/ give a potassium supplement if required.
  • Check magnesium levels, as these are closely related.
115
Q

What are the complications of hypokalaemia?

A

Cardiac arrhythmia and sudden death.

116
Q

What is syndrome of inappropriate ADH secretion?

A

Continued secretion of ADH despite:

  • plasma hypotonicity (less solute concentration than cells).
  • normal plasma volume.
117
Q

What are the symptoms of syndrome of inappropriate ADH secretion?

A

If mild:

  • Nausea
  • Headache
  • Irritability
  • Mild hyponatraemia

If severe:

  • Fits
  • Coma
  • Severe hyponatraemia
118
Q

What is the pathophysiology of syndrome of inappropriate ADH secretion?

A
  • Impaired free water excretion secondary to inappropriate secretion of ADH.
119
Q

What is the aetiology of syndrome of inappropriate ADH secretion?

A
  • Disordered hypothalamic-pituitary secretion of ADH.
  • Ectopic ADH production.

Neurological:

  • Trauma
  • Tumour
  • Infection

Pulmonary:

  • Small cell cancer
  • Mesothelioma
  • CF
120
Q

What investigations are used to diagnose syndrome of inappropriate ADH secretion?

A
  • FBC (low osmolality of electrolytes)

- Check how concentrated urine is (often still highly concentrated despite low osmolality of serum electrolytes).

121
Q

What treatment is given to patients with syndrome of inappropriate ADH secretion?

A

1st line:

  • Reduce fluid intake.
  • Treat underlying cause.

2nd line or if disease is more severe:
- Tolvaptan (ADH receptor antagonist).

122
Q

What is diabetes insipidus?

A

The hyposecretion of or insensitivity to ADH.

123
Q

What is hyposecretive DI called?

A

Cranial diabetes insipidus.

124
Q

What is insensitivity DI called?

A

Nephrogenic diabetes insipidus.

125
Q

What is the clinical presentation of diabetes insipidus?

A
  • Polyuria

- Compensatory polydipsia

126
Q

What is the pathophysiology of cranial DI?

A
  • Disease of the hypothalamus (site of ADH production) resulting in insufficient ADH production.
127
Q

What is the pathophysiology of nephrogenic diabetes insipidus?

A
  • Depends on the aetiology

- Can be disruption of channels/damage to the kidneys, resulting in reduced response to ADH.

128
Q

What is the aetiology of cranial DI?

A
  • Neurosurgery.
  • Trauma.
  • Tumour.
  • Infiltrative disease of the hypothalamus.
  • Idiopathic.
129
Q

What is the aetiology of nephrogenic DI?

A
  • Hypokalaemia
  • Hypercalcaemia
  • Drugs
  • Renal tubular acidosis
  • Sickle cell
  • Prolonged polyuria
  • CKD
130
Q

What are the diagnostic tests used to confirm DI?

A

Urine volume
- Confirm there is polyuria (>3L every 24 hours)

Water deprivation test:

  • Deprive patient of fluid for 8 hours.
  • Measure serum and urine osmolality, and urine volume hourly.
  • For a patient with DI, the urine will remain dilute despite dehydration.
131
Q

What testing is done to tell the difference between cranial/central DI and nephrogenic DI?

A
  • Administer desmopressin (synthetic ADH).
  • If the patient responds normally to the desmopressin, DI is central/cranial and to do with ADH production.
  • If there is little to no change in the patients urine and it remains dilute, DI is nephrogenic and to do with ADH insensitivity.
132
Q

What is the treatment of DI?

A

Central DI:
- Desmopressin

Nephrogenic DI:

  • Treat underlying cause (often renal disease)
  • Maintain adequate fluid intake to prevent dehydration.
  • Can use hydrochlorothiazide or sodium restriction in diet to reduce urine output.
133
Q

What is hyperparathyroidism?

A

Excessive secretion of PTH

134
Q

What are the three types of hyperparathyroidism and what are they?

A

Primary hyperparathyroidism:
- One parathyroid gland produces excess PTH, due to adenoma or hyperplasia of the gland.

Secondary hyperparathyroidism:
- Increased secretion of PTH to compensate for hypocalcaemia.

Tertiary hyperparathyroidism:
- Autonomous secretion of PTH due to chronically high levels of calcium.

135
Q

What is the clinical presentation of primary hyperparathyroidism?

A
  • 70-80% asymptomatic.
  • Bone pain (osteoporosis or osteopenia)
  • Renal calculi
  • Nausea
  • Neuropsychiatric

“Bones, stones, abdominal groans and psychic moans”.

136
Q

What is the clinical presentation of secondary/tertiary hyperparathyroidism?

A
  • CKD signs
  • Muscle cramps
  • Bone pain
137
Q

What is the aetiology of primary hyperparathyroidism?

A
  • Single parathyroid adenoma or hyperplasia.
138
Q

What is the aetiology of secondary/tertiary hyperparathyroidism?

A
  • CKD usually, but can be any condition with hypocalcaemia (e.g. vitamin D deficiency)
  • Tertiary hyperparathyroidism develops from secondary if hypersecretion of PTH is chronic.
139
Q

How common is primary hyperparathyroidism?

A
  • Third most common endocrine disorder.
140
Q

How is each type of hyperparathyroidism investigated/diagnosed?

A

All through blood tests:

Primary - Hypercalcaemia and raised PTH
Secondary - Hypocalcaemia and raised PTH.
Tertiary - Hypercalcaemia and chronically high PTH

To tell the difference between primary and tertiary look at course of disease and symptoms (is there any CKD?).

141
Q

What is the treatment for primary hyperparathyroidism?

A
  • Surgical removal of adenoma.
  • Vit. D supplementation (increase gut absorption of calcium, otherwise this will be down-regulated due to high levels of calcium already in the blood).
  • If osteoporosis is present, consider biphosphonates (alendronic acid).
142
Q

What is the treatment for secondary hyperparathyroidism?

A
  • Vit D and calcium supplementation always.
  • If malabsorption related, treat the GI cause.
  • If CKD related, treat the CKD.
143
Q

What is the treatment for severe secondary/tertiary hyperparathyroidism?

A
  • Partial or total parathyroidectomy with close calcium monitoring afterwards.
144
Q

What is hypoparathyroidism?

A
  • Caused by reduction or absence of PTH, leading to low calcium (hypocalcaemia) and elevated phosphate (hyperphosphataemia).
145
Q

What is the clinical presentation of hypoparathyroidism?

A
  • Increased excitability of muscles and nerves.
  • Numbness around the mouth/extremities.
  • Cramps/convulsions
  • Positive Trousseau sign (occlude blood flow to hand, leading to flexion at the wrist and MCP joints - this is a sign of hypocalcaemia).
  • Positive Chvostek sign (tap the mandible of an individual - their facial muscles twitch. Another sign of hypocalcaemia).
146
Q

What is the pathophysiology of hypoparathyroidism?

A

Normally, PTH stimulates vitamin D activation, which facilitates:

  • intestinal calcium absorption.
  • renal reabsorption of calcium.
  • calcium release from bone.

PTH also inhibits phosphate reabsorption.

ALL OF THESE PROCESSES ARE INHIBITED IN HYPOPARATHYRODISIM.

147
Q

What is the aetiology of hypoparathyroidism?

A
  • Can be transient.

- Most commonly follows anterior neck surgery.

148
Q

What are the investigations used to diagnose hypoparathyroidism?

A
  • Calcium low
  • PTH low
  • Phosphate high
149
Q

What is the treatment for hypoparathyroidism?

A
  • Calcium

- Calcitrol (biologically active form of vitamin D).

Phase 2a diseases (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions