Brainscape's Knowledge GenomeTM

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


See full index

Yr3 Revision > MET3 Revision: Endocrine II > Flashcards

MET3 Revision: Endocrine II Flashcards

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

State the 4 grades of hypertensive retinopathy

A

Grade 1 – silver (copper) wiring
Grade 2 – arteriovenous nipping
Grade 3 – flame shaped haemorrhages + exudates
Grade 4 - papilloedema

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

Name a cardiac cause of secondary hypertension [1]

A

Coarctation of the aorta(differential BP between upper and lower limb and arms; radio-radial delay)

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

Name three renal causes of secondary hypertension [3]

A
  • CKD
  • Glomerulonephritis
  • Renovasculardisease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Name 4 endocrine causes of secondary hypertension [4]

A
  • Conns
  • Cushings
  • Phaeochromocytoma
  • Acromegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Conn’s syndrome refers to an adrenal adenoma producing too much aldosterone.

What are the two options that this could be caused by? [2]

Which is more likely? [2]

A

Solitary aldosterone producing adenoma
* 2/3rds

Bilateral adrenocortical hyperplasia
* 1/3rd

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

You suspect a ptx with Conns syndrome; how would you expect their blood gas to appear after investigation? [1]

A

Hypokalaemic alkalosis (XS aldosterone causes increased K+ secretion and Na+ absorption)

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

You suspect a patient has Conn’s syndrome due their refractory BP.

Name a differential diagnosis that is more common cause of this [1]

A

Renal artery stenosis

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

Apart from investigating electrolytes, what further tests (and results) would you conduct for a ptx suspected to have hyperaldosteronism? [4]

A

Hyperaldosteronism investigations:
- Plasma renin: suppressed
- Elevated serum aldosterone
(these tests are conducted together: paired renin/aldosterone level)
- CT adrenals
- Adrenal vein sampling to differentiate unilateral from bilateral adrenal disease

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

What are clinical presentations of Conn’s syndrome? [6]

A
  • Often asymptomatic
  • cramps
  • muscle weakness
  • hypotonia
  • reduced reflexes
  • Hypertension (often have resistant HTN or severe HTN)
  • 40-60 years old
  • Hypokalaemic (but NOT always present, so can’t rely on this for diagnosis)

often the signs are due to hypokalaemia

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

What is the management of unilateral adrenal adenoma? [1]
What is the management of bilateral adrenal hyperplasia? [2]

A

Unilateral adrenal adenoma: Surgery (laparoscopic adrenalectomy)

Bilateral adrenal hyperplasia: aldosterone antagonist
- eplerenone
- spironolactone

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

What is the 10% rule for phaeochromocytoma? [4]

A

 10% extra adrenal
 10% malignant
 10% familial (endocrine neoplasia syndromes)
 10% bilateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Presentation of phaeochromocytomas? [5]

A

Classic triad:
* Tachycardia
* Sweating
* Episodic headache

Others:
* Tremor
* Anxiety
* Palpitations
* Hypertension
* Tachycardia

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

*

Why does prescribing beta blockers worsen symptoms for patients with phaeochromocytoma? [2]

A

Inhibits B2 receptor action (vasodilatation);

Causes unparalleled action of A1 and A2 receptors (vasoconstriction)

Can cause severe hypertensive crisis

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

Which drugs would you prescribe for symptoms of phaeochromocytoma? [2]

What is an alternative management? [1]

A

Always give alpha blockers first (otherwise can cause hypertensive crisis; then beta blockers)

Alpha blockers:
Doxazosin
Phenoxybenzamine

Beta blockers (if heart disease or tachycardic)
Propranolol
Atenolol

and / or

Surgical resection of the lesion
(Patients have their symptoms controlled medically before surgery to reduce the anaesthesia and surgery risks)

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

Initial tests for diagnosing phaeochromocytoma include? [4]

A
  • Elevated plasma free metanephrines (breakdown products of the catecholamines epinephrine (adrenaline) and norepinephrine)
  • Elevated 24-hour urine catecholamines (not as accurate as measuring metanephrines)
  • Image adrenals (CT/MRI)
  • MIBG (radionucleotide scan of Iodine-123)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the treatment options for acromegaly [3]

A
  • 1st line: trans-sphenoidal surgery

Medical management of acromegaly:

  • Somatostatin analogues: Octreotide
  • Growth hormone receptor antagonist:: Pegvisomont
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the MoA of Pegvisomont? [1]

A

Used to treat acromegaly: GH Receptor antagonist

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

What is the role of calcitonin? [2]
Where is it produced? [1]

A

Lowers Ca2+ & P levels by:
- Inhibits Ca2+ absorption by intestines
- Inhibits Ca2+ reabsorption in kidney
- Promotes osteoblasts, inhibits osteoclasts

Secreted by C cells of thyroid

20
Q

Hypercalcaemia has what effect on urine and thirst? [1]

A

Causes polyuria and polydipsia

21
Q

Give three differential diagnoses for polyuria and polydipsia [3]

A

DM
Diabetes insipidus
Hypercalcaemia

22
Q

How should you manage acute hypercalcaemia? [1]
What drug should you prescribe if Ca2+ remains elevated? [1]

A
  1. Give IV saline alone
  2. If Ca still high - give bisphosphinates; pamidronate: prevent bone resorption by inhibiting osteoclast activity
23
Q

Describe dosing of pamidronate for acute hypercalcaemia [1]

Name 2 SEs [2]

A

Single dose of (4mg) will will normalise serum Ca2+ levels with a week

SEs:
- Bone pain
- Decresed PO4-
- Myalgia
- N & V
- Ca2+ decreasing

24
Q

Describe the causes of [3]

Primary hyperparathyroidism
Secondary hyperparathyroidism
Tertiary hyperparathyroidism

A

Primary hyperparathyroidism:
- is caused by uncontrolled parathyroid hormone production by a tumour of the parathyroid glands
- this leads to a raised blood calcium (hypercalcaemia)

Secondary hyperparathyroidism:
- is where insufficient vitamin D or chronic kidney disease reduces calcium absorption from the intestines, kidneys and bones.
- this result in low blood calcium (hypocalcaemia).
- The parathyroid glands react to the low serum calcium by excreting more parathyroid hormone.
- The serum calcium level will be low or normal, but the parathyroid hormone will be high.

Tertiary hyperparathyroidism:
- when secondary hyperparathyroidism continues for an extended period, after which the underlying cause is treated
- hyperplasia (growth) of the parathyroid glands occurs as they adapt to producing a higher baseline level of parathyroid hormone
- Then, when the underlying cause of the secondary hyperparathyroidism is treated, the baseline parathyroid hormone production remains inappropriately high.
- In the absence of the previous pathology, this high parathyroid hormone level leads to the inappropriately high absorption of calcium in the intestines, kidneys and bones, causing hypercalcaemia. Treatment is surgically removing part of the parathyroid tissue to return the parathyroid hormone to an appropriate level.

25
Q

State the most likely cause of:

Primary hyperparathyroidism [2]
Secondary hyperparathyroidism [2]
Tertiary hyperparathyroidism [1]

A

Primary hyperparathyroidism
* Solitary adenoma (80%)
* Hyperplasia (20%)

Secondary hyperparathyroidism
* Vit D deficiency (reduced intake)
* CKD - difficulty making Vit D

Tertiary hyperparathyroidism
- Secondary hyperparathyroidism

26
Q

If you investigate raised hypercalcaemia and find PTH to be undetactable, what would this indicate? [1]

Give three causes of the above [3]

A

Malignancy: PTH related Peptide (PTHrP) causes the increased Ca2+ levels, but itself is undetectable

E.g. squamous cell lung cancers; breast, renal cell carcinomas

27
Q

How would you investigate for hypercalcaemia if PTH is high? [1]

How would you investigate for hypercalcaemia if PTH is low? [1]

A

PTH high: indicates hyperparathyroidism
- USS
- SestaMibi Scan
- Parathyroid venous sampling

PTH low: indicates cancer:
- test for PTH related Peptide (PTHrP) - but can’t measure this - so do local body signs of cancer and further tests

28
Q

Give differential diagnosis of primary hyperparathyroidism [3]

A

Thiazide like diuretics [1]
Lithium [1]
Tertiary hyperparathyroidism [1]

29
Q

What blood tests would you use to investigate primary hyperparathyroidism

A
  • Ca2+ and PTH raised
  • ALP raised (due to bone activity)
    *
30
Q

Describe a radiographical sign of hyperparathyroidism [1]

A

Pepper pot skull: extensive resorption bone in the skull in combination with cystic areas of osteopenia are termed pepper pot skull.

31
Q

What are clinical presentations of Conn’s syndrome? [4]

A
  • Often asymptomatic
  • Hypertension: often have drug resistant or severe HTN
  • 40-60 years old
  • Hypokalaemic (but NOT always present) - therefore signs of hypokalameia
32
Q

How do you treat hyperparathyroidism?
- Surgically? [1]
- Therapeutically? [1]

A

Parathyroidectomy
Cinacalcet directly lowers parathyroid hormone levels by increasing the sensitivity of the calcium sensing receptors to activation by extracellular calcium, resulting in the inhibition of PTH secretion. Indicated in patients with:
- Chronic renal failure
- Tertiary hyperparathyroidism

33
Q

When is cinacalcet indicated for treatment of hypeparathyroidism? [2]
What is the MoA? [1]

A
  • Used for patients with chronic renal failure and tertiary hyperparathyroidism
  • Increases the sensitivity of parathyroid cells to Ca2+ thereby causing less PTH secretion
34
Q

Acute severe hypercalcaemia is a MEDICAL EMERGENCY.
State how you would treat a ptx suffering from acute severe hypercalcaemia [4]

A
  • Rehydrate with IV 0.9% saline fluids - to prevent stones
  • Furosemide: loop diuretic that increases Ca2+ excretion
  • Give bisphosphonates (to prevent bone resorption by inhibiting osteoclasts) after rehydration e.g. IV PAMIDRONATE
  • Measure serum U&E’s daily and serum Ca2+ 48hrs after initial treatment
  • Can give glucocorticoid steroids e.g. ORAL PREDNISOLONE in myeloma, sarcoidosis and vitamin D excess
35
Q

What is the name of this sign? [1]
When does it occur? [1]
What does it indicate? [1]

A

Trousseau sign: hypocalcemia
The hand adopts a characteristic posture when the sphygmomanometer cuff is inflated above the systolic blood pressure within 3 minutes.

36
Q

What is the name of this sign? [1]
How do you illicit this sign? [1]
What does it indicate? [1]

A

Chvostek’s Sign: - indiactes hypocalcaemia

  • This clinical sign refers to a twitch of the facial muscles that occurs when gently tapping an individual’s cheek, in front of the ea
37
Q

How do you treat ptx with hypocalcaemia:

With < 1.9 Ca2+, no symptoms? [2]
With < 1.9 Ca2+, symptoms? [2]

A

 < 1.9 with no symptoms
-  Oral calcium supplements
-  If due to severe vitamin D def, treat with high dose vit D (Calcitriol)

 < 1.9 with symptoms
-  IV calcium gluconate

38
Q

State 5 causes of hypocalcaemia [5]

A

 Thyroid / parathyroidectomy
 Severe vitamin D deficiency
 Magnesium deficiency (PPI induced - PPIs needed for PTH to work)
 Pancreatitis
 Cytotoxics

39
Q

What pathology is this a sign of? [1]

Explain

A

Pseudohypoparathyroidism is a rare genetic metabolic bone disease caused by a defect in the GNAS1 protein that leads to a decreased response to PTH.

Patients present with characteristic findings of short 4th and 5th metacarpals, round facies, short stature, and symptoms of hypocalcemia.

40
Q

How does renal artery stenosis cause HTN? [2]

A
  • Atherosclerosis or fibromuscular dysplasia most causes narrowing of the renal arteries
  • The chronic ischemia produced by the obstruction of renal blood flow leads to adaptive changes in the kidney which include the formation of collateral blood vessels and secretion of renin by juxtaglomerular apparatus
41
Q

What are the radiological investigations of suspected Conn’s syndrome and phaeochromocytoma? [1]

A

Use MIBG scan: Iodine-123

42
Q

[] is used to diagnose patients with primary hyperaldosteronism (Conn’s syndrome) when the adrenal CT scan does not show a tumor

A

Adrenal vein sampling is used in patients with primary hyperaldosteronism (Conn’s syndrome) when the adrenal CT scan does not show a tumor

43
Q

State the overarching causes of hypocalcaemia [8]

A
  • Secondary to increased serum phosphate levels: CKD
  • Severe vitamin D deficiency
  • Reduced PTH production:
    Primary hypoparathyroidism
    & Secondary hypoparathyroidism
  • Radiation
  • Hypomagnesaemia - Mg is required for PTH secretion
  • Pseudohypoparathyroidism: failure of target cell response to PTH due to owing to a mutation in the Gs alpha-protein (GNAS1), which is coupled to the PTH receptor
  • Pseudopseudohypoparathyroidism: Same phenotypic defects as pseudohypoparathyroidism e.g. short stature; but without any abnormalities of Ca2+ metabolism
  • Drugs: Calcitonin - decreases plasma Ca2+ and phosphate; Bisphosphonates - reduce osteoclast activity resulting in reduced Ca2+
  • ACUTE PANCREATITIS
44
Q

Describe the causes of primary and secondary hypoparathyroidism [2]

A

Primary hypoparathyroidism:
- caused by autoimmune DiGeorge syndrome (Congenital familial condition in which the parathyroid glands fail to develop;
- idiopathic hypoparathyroidism

Secondary hypoparathyroidism
- After parathyroidectomy or thyroidectomy surgery. most common cause)

45
Q

Clinical presentation of hypocalcaemia? [6]

A
  • Increase excitability of muscles and nerves
  • Parathesiae (numbness and tingling) around the mouth and in the extremities, followed by cramps, tetany
  • Convulsions and death if untreated
  • Chvostek’s sign: (tapping over the facial nerve in the region of the parotid gland causes twitching of the IPSILATERAL facial muscles
  • Trousseau’s sign: carpopedal spasm induced by inflation of sphygmomanometer cuff to a level above systolic blood pressure
  • papilloedema and a prolonged QT on ECG (severe hypocalcaemia)
46
Q

How would differentiate unilateral from bilateral adrenal disease? [1]

A

Adrenal vein sampling

Yr3 Revision (37 decks)

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