Brainscape's Knowledge GenomeTM

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


See full index

Yr3 Revision: Condensed Notes > Endocrine II > Flashcards

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

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
6
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
7
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
8
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
9
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
10
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
11
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
12
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
13
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
14
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
15
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
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

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

Give differential diagnosis of primary hyperparathyroidism [3]

A

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
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
25
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

26
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

27
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.

28
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
29
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

30
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
31
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)

32
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)
33
Q

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

A

Adrenal vein sampling

34
Q

Which symptom would differentiate between a patient is suffering from thyrotoxicosis as opposed to malignancy? [1]

A

Increase in appetite

35
Q

Name and explain drugs may you suspect of a patient’s DH, who is displaying symptoms of thyrotoxicosis [3]

A

Amiodarone (treats afib): high levels of iodine
Lithium: can mimic iodine
ARVs

36
Q

What type of Ig are the anti TSH receptor antibodies? [1]

A

IgG

37
Q

Asides from TSHR-Ab, which other antibodies would you potentially test for in a ptx presenting with thyrotoxicosis? [1]

A

Thyroid Stimulating Immunoglobulin (TSI)

38
Q

Describe basic overview of toxic multinodular goitre [1]

A

Multiple autonomous nodules develop that are capable of producing and secreting thyroid hormones.

39
Q

Describe the structure of the goitre seen in Grave’s disease [1]

A

Diffuse smooth goitre with a bruit

40
Q

Which autoimmune diseases are commonly associated with Graves disease? [5]

A
  • Vitiligo (pale white patches on skin)
  • Addison’s disease
  • Pernicious anaemia
  • Myasthenia gravis
  • Type 1 DM
41
Q

What is the main risk factor for Grave’s eye disease? [1]

A

Smoking

42
Q

AEs of carbimazole? [3]

A

AGRANULOCYTOSIS - results in a severely low white blood cell count (leukopenia) - most commonly neutropenia: can lead to sepsis

Rash

Arthralgia

Hepatitis

Vasculitis

43
Q

Signs of hypothyroidism?

A

BRADYCARDIC:
* Bradycardia
* Reflexes relax slowly
* Ataxia (cerebellar)
* Dry, thin hair/skin
* Yawning/drowsy/coma
* Cold hands +/- temperature drop * Ascites
* Round puffy face
* Defeated demeanour
* Immobile +/- Ileus (temporary arrest of intestinal peristalsis)
* Congestive cardiac failure

44
Q

How do you investigate for hypothyroidism? [4]

A

Thyroid function tests:
- High TSH; low T3/T4 (primary)
- Low TSH; low T3/T4 (secondary)

Thyroid antibodies (e.g. anti-TPO-Ab in Hashimotos)

Cortisol to ensure patient has a normal ACTH/cortisol reserve.
- Sometimes profound hypothyroidism can infiltrate tissues such as the adrenal gland and disrupt cortisol reseves. If thyroxide is given in these conditions it may trigger Addinsonian Crisis

Anaemia:
- Usually normochromic and normocytic
- May be macrocytic (sometimes due to pernicious anaemia)
- Or microcytic (in women, due to menorrhagia or undiagnosed coeliac disease)

45
Q

Treatment for hypothyroidism?

A

ORAL LEVOTHYROXINE (T4)
- Aim is normal TSH conc. which will be achieved by levothyroxine - but don’t give too much so as to completely suppress TSH as this carries risk of AF and osteoporosis

46
Q

Describe what a thyroid crisis is [1], how it occurs [1], and features? [3]

A

Rare, life threatening condition in which there is a rapid deterioration of thyrotoxicosis (RAPID T4 INCREASE)
Features include hyperpyrexia, tachycardia, extreme restlessness
and eventually delirium, coma and death

Usually precipitated by stress, infection, surgery or radioactive
iodine therapy in an unprepared patient

47
Q

Treatment for thyroid crisis / storm? [4]

A
  • ORAL CARBIMAZOLE
  • ORAL PROPRANOLOL
  • ORAL POTASSIUM IODIDE (to block acutely the release of thyroid hormone from gland)
  • IV HYDROCORTISONE (to inhibits peripheral conversion of T4 to T3)
48
Q

Describe the features of a myxoedema coma [5]

A
  • hypothermia
  • cardiac failure (bradycardia)
  • hypoventilation
  • hypoglycaemia
  • hyponatraemia
  • myxoedema (thickened, swelling of skin)
49
Q

How do you treat a patient presenting with myxoedema coma? [3]

A
  • IV/ORAL T3
  • IV fluid
  • IV corticosteroids (until the possibility of coexisting adrenal insufficiency has been excluded)
  • Glucose infusion
  • Gradual rewarming
50
Q

Explain the 5 main types of thyroid carcinoma [5]

A

Papillary (70%):
* Most common, well differentiated
* Young people, local spread and good prognosis
* Arise from thyroid epithelium
* Lymph node metastasis predominate
* Usually contain a mixture of papillary and colloidal filled follicles
* Histologically tumour has papillary projections and pale empty nuclei

Follicular (20%):
* Middle age, spread to lung/bone, usually good prognosis
* 3x more likely in women
* Well differentiated, arise from thyroid epithelium
- Follicular adenoma: Usually present as a solitary thyroid nodule. Malignancy can only be excluded on formal histological assessment.
- Follicular carcinoma: Capsular invasion seen microscopically, and without this finding the lesion would be a follicular adenoma. Vascular invasion predominates unlike papillary which is lymph-node predominant

Anaplastic (< 5%):
* Very undifferentiated and arise from thyroid epithelium
* Aggressive, local spread but poor prognosis

Lymphoma (2%)
* Can be associated with Hashimoto’s

Medullary cell (5%):
* C cells derived from neural crest and not thyroid tissue
* Serum calcitonin levels often raised
* Both lymphatic and haematogenous metastasis are recognised, nodal disease is associated with a very poor prognosis.

51
Q

Which is the most common type of thyroid carcinoma? [1]

A

Papillary (70%)

52
Q

General treatment of thyroid carcinomas? [4]

A
  • Administer lots of LEVOTHYROXINE (T4) to keep TSH reduced as this is a growth factor for the cancer!
  • Iodine 131 ablation
  • Thyroidectomy
  • Chemotherapy helps to reduce risk of spread and treats micro-metastases that have been undetected
53
Q

What are the three stages of De Quervain’s thyroiditis? [3]

A

De Quervain’s thyroiditis, also known as subacute thyroiditis, is a condition causing temporary inflammation of the thyroid gland. There are three phases:

Thyrotoxicosis
Hypothyroidism
Return to normal

54
Q

De Quervain’s thyroiditis usually occurs after what? [1]

A

A viral infection

55
Q

Describe the initial thyrotoxic phase of De Quervain’s thryoiditis [3]

A
  • Excessive thyroid hormones
  • Thyroid swelling and tenderness
  • Flu-like illness (fever, aches and fatigue)
  • Raised inflammatory markers (CRP and ESR)
56
Q

TOM TIP: The MHRA issued a warning in 2019 about the risk of [] in patients taking carbimazole.

In your exams, look out for a patient on carbimazole presenting with symptoms of []

A

TOM TIP: The MHRA issued a warning in 2019 about the risk of acute pancreatitis in patients taking carbimazole.

In your exams, look out for a patient on carbimazole presenting with symptoms of pancreatitis (e.g., severe epigastric pain radiating to the back).

57
Q

TOM TIP: Both carbimazole and propylthiouracil can cause agranulocytosis, with a dangerously low white blood cell counts. Agranulocytosis makes patients vulnerable to severe infections.

[] is a key presenting feature of agranulocytosis. In your exams, if you see a patient with a sore throat on carbimazole or propylthiouracil, the cause is likely agranulocytosis. They need an urgent full blood count and aggressive treatment of any infections.

A

TOM TIP: Both carbimazole and propylthiouracil can cause agranulocytosis, with a dangerously low white blood cell counts. Agranulocytosis makes patients vulnerable to severe infections.

A sore throat is a key presenting feature of agranulocytosis. In your exams, if you see a patient with a sore throat on carbimazole or propylthiouracil, the cause is likely agranulocytosis. They need an urgent full blood count and aggressive treatment of any infections.

58
Q

How do you adapt a pregnant women’s dose of levoythroxine due to their pregnancy? [1]

A

In pregnancy, anyone already on levothyroxine treatment should increase their dose. Thyroid doses should be adjusted in steps of 25-50mcg. In pregnancy, the increase in thyroid replacement is typically 20-50%, which normally equates to 25mcg-50mcg increase.

Yr3 Revision: Condensed Notes (46 decks)

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