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AMC MCQ - You Can Do It!!!!!❤️❤️ > ENDOCRINOLOGY by Dr Cinitia > Flashcards

ENDOCRINOLOGY by Dr Cinitia Flashcards

1
Q

Hypothyroidism (Hashimoto Thyroiditis) CLINICAL FEATURES

A

Bilateral, firm, rubbery goitre

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2
Q

Hypothyroidism (Hashimoto Thyroiditis) FIRST INVESTIGATION (3):

A
  1. TSH
  2. US If nodule
  3. CT Scan if goitre is causing compression
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3
Q

Hypothyroidism (Hashimoto Thyroiditis) BEST INVESTIGATION (3):

A

1.Antithyroglobulin (TgAb)
2.Antithyroid peroxidase Ab (TPO)
3.Biopsy: Chronic lymphocytic thyroiditis

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4
Q

Hypothyroidism (Hashimoto Thyroiditis) TREATMENT

A
  1. Tx if TSH>7.
    Monitor tx at 3m, 6m, 1y. You start with low dose and you increase it progressively.
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5
Q

Myxedema coma CLINICAL FEATURES

A

Hypotension, hypoventilation, hypoglycaemia, hyponatraemia

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6
Q

Myxedema coma TREATMENT

A

IV Levothyroxine + IV hydrocortisone

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7
Q

Congenital hypothyroidism CLINICAL FEATURES

A

Macroglossia, harsh cry, dry skin, umbilical hernia

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8
Q

Congenital hypothyroidism FIRST INVESTIGATION

A

Neonatal Heel prick TSH is (NEXT) if hypotonic kid with large open ant fontanelle

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9
Q

Congenital hypothyroidism TREATMENT

A

Start thyroxine before 2 weeks of age

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10
Q

Subclinical hypothyroidism CLINICAL FEATURES

A

High TSH and normal T3, T4

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11
Q

Subclinical hypothyroidism FIRST INVESTIGATION

A

TSH

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12
Q

Subclinical hypothyroidism TREATMENT

A
  • TSH 5-10: Review TSH in 3 months
  • TSH>10: Levothyroxine
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13
Q

Sick Euthyroid Syndrome CLINICAL FEATURES

A

Decrease conversion from T4 to T3 so T3 will be low and T4, TSH, and reverse T3 could be normal or even high

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14
Q

Hyperthyroidism CLINICAL FEATURES

A

Fine tremor, proximal myopathy, frozen shoulder

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15
Q

Hyperthyroidism FIRST INVESTIGATION

A
  1. TSH
  2. Radioactive iodine uptake: -
    Low uptake: Thyroiditis -
    High uptake:
    Homogeneous (Graves), heterogenous (multiple- toxic multinodular goitre, single area-toxic adenoma)
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16
Q

Hyperthyroidism TREATMENT (4)

A

1.Carbimazole (Agranulocytosis)
2.Propylthiouracil (Risk of liver dx)
3.Surgery
4.Radioactive iodine (If CIs to surgery)

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17
Q

Graves Disease FIRST INVESTIGATION

A

TSH

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18
Q

Graves Disease BEST INVESTIGATION

A

TSH receptor antibody, anti- TPO

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19
Q

Graves Disease TREATMENT

A

The management of Graves’ disease according to RACGP guidelines involves three primary treatments:

  1. Antithyroid Medications:
    • Drugs: Carbimazole (preferred) and Propylthiouracil (PTU).
    • Duration: 12-18 months.
    • Side Effects: Rash, gastrointestinal discomfort, agranulocytosis, hepatotoxicity.
  2. Radioactive Iodine Therapy:
    • Procedure: Oral administration of I-131.
    • Advantages: Permanent resolution of hyperthyroidism.
    • Disadvantages: Permanent hypothyroidism, potential exacerbation of Graves’ orbitopathy, concerns about fertility and small increased risk of malignancy.
  3. Thyroidectomy:
    • Indications: Severe Graves’ orbitopathy, large goitres, rapid control needed.
    • Advantages: Permanent resolution, may improve orbitopathy.
    • Risks: Surgical risks including hypoparathyroidism and nerve injury.

Symptomatic Treatment: Beta-blockers for initial symptom control.

These options should be discussed with patients to tailor treatment based on individual preferences and clinical features oai_citation:1,RACGP - Thyroid disease Long term management of hyperthyroidism and hypothyroidism oai_citation:2,RACGP - Evaluating and managing patients with thyrotoxicosis oai_citation:3,RACGP - Hyperthyroidism in a hypothyroid patient.

Same than above + Tx of vision threatened:
1. IV Methylprednisolone
2. Oral high dose prednisolone

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20
Q

Hyperthyroidism in pregnancy TREATMENT

A
  1. Propylthiouracil in 1st trimester
  2. Carbimazole in 2nd/3rd trimester
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21
Q

Subacute thyroiditis (De Quervains) CLINICAL FEATURES

A

Pain/Tenderness, fever

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22
Q

Subacute thyroiditis (De Quervains) FIRST INVESTIGATION

A
  1. TSH
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23
Q

Subacute thyroiditis (De Quervains) BEST INVESTIGATION

A
  1. ESR>50mm/Hr

The best investigation for subacute thyroiditis (De Quervain’s thyroiditis) as per the RACGP guidelines is the measurement of C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR). Elevated levels of these markers indicate inflammation, which is characteristic of subacute thyroiditis. Additionally, thyroid function tests typically show suppressed TSH levels with elevated free T4 and free T3 during the hyperthyroid phase, and reduced or absent uptake on a radionuclide thyroid scan supports the diagnosis.

For more detailed information, you can refer to the RACGP article on managing thyrotoxicosis here oai_citation:1,RACGP - Evaluating and managing patients with thyrotoxicosis oai_citation:2,RACGP - Thyroid disease Long term management of hyperthyroidism and hypothyroidism.

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24
Q

Subacute thyroiditis (De Quervains) TREATMENT

A
  1. Analgesia: NSAIDs
  2. Severe: Oral prednisolone.
  3. If constitutional symptoms: BB
    NOT antithyroid medication
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25
Q

Thyroid Storm CLINICAL FEATURES

A

Anxiety, weight loss, hyperpyrexia, tachycardia

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26
Q

Thyroid Storm TREATMENT

A

Hospital admission: IV saline, IV steroids

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27
Q

Thyroid Nodule CLINICAL FEATURES

A

Moves with swallowing, can cause compression.

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28
Q

Thyroid Nodule FIRST INVESTIGATION

A
  1. TSH -TSH Normal or
    High: Next: US. Next: FNA -TSH
    Low: Next T3 & T4. Next: Radioisotope scan and US. If cold nodule: FNA
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29
Q

Thyroid Nodule BEST INVESTIGATION

A
  1. FNAC
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30
Q

Retrosternal Goitre CLINICAL FEATURES

A

Compression

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31
Q

Retrosternal Goitre FIRST INVESTIGATION

A
  1. X-ray

Retrosternal goitre refers to an enlarged thyroid gland that extends into the chest cavity behind the sternum. Using an X-ray as the first investigation is recommended for several reasons:

  1. Initial Assessment of Size and Position:
    • Overview of Goitre: An X-ray provides a quick and initial assessment of the size and position of the goitre. This helps in understanding how much of the thyroid has extended into the chest cavity.
    • Tracheal Deviation or Compression: X-rays can show if the goitre is causing any displacement or compression of the trachea, which is critical for assessing potential breathing issues.
  2. Accessibility and Simplicity:
    • Widely Available: X-rays are widely available in most medical settings and can be performed quickly, making them an accessible first step in investigation.
    • Non-Invasive: The procedure is non-invasive, straightforward, and doesn’t require special preparation, making it easy to perform on most patients.
  3. Guidance for Further Imaging:
    • Determining Need for Advanced Imaging: Based on X-ray results, clinicians can determine if further imaging studies like CT scans or MRIs are necessary. These advanced imaging techniques are more detailed but also more resource-intensive and less readily available.
  4. Identifying Complications:
    • Secondary Findings: An X-ray can also help identify other potential issues, such as the presence of calcifications within the goitre or signs of compression of nearby structures, guiding the urgency and nature of subsequent investigations.

Using an X-ray as the first investigation for retrosternal goitre is recommended due to its ability to provide an initial overview of the goitre’s size, position, and effect on surrounding structures. It is a widely available, non-invasive, and simple tool that helps guide further diagnostic steps if needed.

For more detailed guidelines, you can refer to the RACGP website:
- RACGP - Goitre

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32
Q

Retrosternal Goitre BEST INVESTIGATION

A

CT of neck and upper chest

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33
Q

Retrosternal Goitre TREATMENT

A

Total thyroidectomy

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34
Q

Thyroid Cancer CLINICAL FEATURES (4)

A

-Hoarseness
-Psammoma bodies: PapillaryThyroid Ca
-Follicular cells: always do excisional biopsy bc it’s hard to diff between non and carcinoma. - Parafollicular C cells (secrete calcitonin): Medullary thyroid Ca. MEN2.
-Rapidly growing: Anaplastic

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35
Q

Thyroid Cancer FIRST INVESTIGATION

A
  1. TFT
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36
Q

Thyroid Cancer BEST INVESTIGATION

A
  1. FNAB
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37
Q

Hyperparathyroidism CLINICAL FEATURES

A

HyperCalcaemia (Stones, polyuria, hypoPh, constipation, psych disturbance)

38
Q

Hyperparathyroidism FIRST INVESTIGATION

A
  1. Ca

The first investigation for suspected hyperparathyroidism, according to the RACGP guidelines, is:

Serum calcium levels.

If the serum calcium is elevated, the next step would typically be to measure parathyroid hormone (PTH) levels to confirm the diagnosis of primary hyperparathyroidism. Elevated calcium levels in conjunction with elevated or inappropriately normal PTH levels would suggest primary hyperparathyroidism.

39
Q

Hyperparathyroidism BEST INVESTIGATION

A
  1. PTH
40
Q

Hyperparathyroidism TREATMENT

A

Qx for Ca<0.25, nephrolithiasis, bone erosions, reduction in bone mass, reduction of Cr clearance.

41
Q

Diabetes Mellitus Type 1 FIRST INVESTIGATION (2)

A

Urine Dipstick for sugar.
Other: Abs against Hashimoto

42
Q

Diabetes Mellitus Type 1 BEST INVESTIGATION

A

FSB

43
Q

Diabetes Mellitus Type 1 TREATMENT (4)

A
  1. Admission
  2. Insulin
  3. Follow up w/ HbA1c e/3m (<7%)
  4. Vaccine for Pneumococcal, Influenza, and dTPa
44
Q

Diabetes Mellitus Type 2 FIRST INVESTIGATION

A

RBG≥11.1

45
Q

Diabetes Mellitus Type 2 BEST INVESTIGATION

A

FBG:
- If ≥7: DM
- If 5.5-6.9->OGTT. If
OGTT≥11.1: DM, if 7.8-11
Retest in a year, if <7.8 with
FBG 6.1-6.9 retest in a year, OGTT≤7.7 Retest in 3 years - HbA1c: ≥6.5: DM, 6-6.4: retest in 1y, ≤5.9 retest in 3
years

Here’s a more organized version of your notes:

  • FBG ≥ 7.0 mmol/L: Diagnosis of Diabetes Mellitus (DM).
  • FBG 5.5-6.9 mmol/L: Requires an Oral Glucose Tolerance Test (OGTT).
    • OGTT ≥ 11.1 mmol/L: Diagnosis of Diabetes Mellitus (DM).
    • OGTT 7.8-11.0 mmol/L: Retest in 1 year.
    • OGTT < 7.8 mmol/L:
      • If FBG is 6.1-6.9 mmol/L: Retest in 1 year.
      • If OGTT ≤ 7.7 mmol/L: Retest in 3 years.
  • HbA1c ≥ 6.5%: Diagnosis of Diabetes Mellitus (DM).
  • HbA1c 6.0-6.4%: Retest in 1 year.
  • HbA1c ≤ 5.9%: Retest in 3 years.
46
Q

Diabetes Mellitus Type 2 TREATMENT (5):

A

1.Lifestyle modifications for 3-6m
2.Metformin
3.Metformin+Sulfonilurias or acarbose
4.Insulin (If HbA1c>9%)
5.Follow-up with HbA1c e/3m (<7) except in risk of hypoglycaemia (7-8)
- Pioglitazone - bladder Ca
- Rosiglitazone-HF

47
Q

Diabetic Nephropathy TREATMENT (2)

A

Annual screening for albuminuria
Photocoagulation

48
Q

Diabetic Retinopathy FIRST INVESTIGATION

A

Screening e/2y.
- If nonproliferative dx: e/1y
- If proliferative dx: Urgent referral
- If vitreous
hemorrhage: Same day referral

49
Q

Diabetic Retinopathy TREATMENT

A

Photocoagulation

50
Q

Diabetic Neuropathy FIRST INVESTIGATION

A
  1. Check Vitamin B12 levels (Metformin can decrease them)
51
Q

Diabetic Neuropathy TREATMENT

A
  1. Amitriptyline
  2. Gabapentin/Pregabalin
52
Q

Diabetic Ketoacidosis CLINICAL FEATURES

A

MCC: Infections, HypoK, HypoNa, ketones

53
Q

Diabetic Ketoacidosis FIRST INVESTIGATION

A

MCC: Infections, HypoK, HypoNa, ketones

54
Q

Diabetic Ketoacidosis BEST INVESTIGATION

A

Ketones in serum or urine

55
Q

Diabetic Ketoacidosis TREATMENT (2)

A
  1. Rehydration (NS IV 15-20mL/kg)
  2. Short acting insulin IV
56
Q

Hypoglycaemia CLINICAL FEATURES

A

Early dumping: 30 mins-1hr: Tx diet
Late dumping:1-3 hrs after meals

57
Q

Hypoglycaemia TREATMENT

A

Conscious:
-<1yr: Milk, >1yr something sweet Unconscious: If Glucose<3
-Children: 10% dextrose
-Adults: 50% Dextrose
Next: IM Glucagon

58
Q

Hyperglycaemic hyperosmolar nonketotic Coma CLINICAL FEATURES

A

Glucose >33 with normal ketones

59
Q

Hyperglycaemic hyperosmolar nonketotic Coma TREATMENT (2)

A
  1. Rehydration (NS 0.45%)
  2. Insulin with caution

**1. Fluid Replacement:
- Goal: Correct dehydration, which is the main problem in HHNC.
- Method: Large amounts of IV fluids are given, usually starting with saline. This helps restore the fluid balance and lower blood sugar levels gradually.

**2. Insulin Therapy:
- Goal: Reduce high blood glucose levels.
- Method: Insulin is given, usually at a low dose, through an IV. This helps to bring down the blood sugar levels without causing a rapid shift in electrolytes.

Note: Monitoring and managing electrolytes (like potassium) and addressing the underlying cause (like infection) are also crucial parts of treatment. 2)

60
Q

Addison’s dx CLINICAL FEATURES

A

Hypotension, weakness, fatigue, HypoNa, HyperK

61
Q

Addison’s dx FIRST INVESTIGATION

A

Cortisol level

62
Q

Addison’s dx BEST INVESTIGATION

A

Short synacthen stimulation test

The best investigation for diagnosing Addison’s disease, according to RACGP guidelines, is the Short Synacthen Stimulation Test (SST).

  • SST assesses the adrenal glands’ ability to produce cortisol in response to synthetic ACTH (Synacthen). In Addison’s disease (primary adrenal insufficiency), the adrenal glands are damaged and cannot produce adequate cortisol, leading to a poor or absent response to Synacthen.
  • A baseline cortisol level is measured.
  • Synthetic ACTH (Synacthen) is administered.
  • Cortisol levels are measured again 30 and 60 minutes later.
  • A low cortisol response confirms the diagnosis of Addison’s disease.

This test is preferred because it is specific, reliable, and directly assesses adrenal function oai_citation:1,Islamic Prayer Times Today, Salat Time, Namaz Timings | IslamicFinder oai_citation:2,Pakistan Prayer Times, Salah (Salat), Azan Time & Namaz TimeTable | IslamicFinder.

63
Q

Addison’s dx TREATMENT

A
  1. IV line with fluids
    - Dx made: Hydrocortisone
    - No Dx: Dexamethasone
64
Q

Hyperaldosteronism CLINICAL FEATURES

A

Hypertension, HyperNa, HypoK. Renin low if primary. Renin high if secondary

  • High Aldosterone: Too much aldosterone hormone.
  • Low Potassium: Aldosterone causes potassium loss, leading to low levels.
  • High Sodium: Sodium may be high due to retention by aldosterone.
  • Low Renin: In primary hyperaldosteronism, renin (a hormone that regulates aldosterone) is low.

These changes help the body retain sodium and water, but at the cost of losing potassium.

65
Q

Hyperaldosteronism FIRST INVESTIGATION

A

Plasma aldosterone and renin.
- Next: Adrenal CT if primary

66
Q

Hyperaldosteronism TREATMENT (2)

A
  1. Spironolactone/Amiloride
  2. Surgery to remove adenoma
67
Q

Cushing Syndrome CLINICAL FEATURES

A

Hyperglycaemia, Hypertension, amenorrhoea, weakness, obesity, HyperNa, HypoK

68
Q

Cushing Syndrome FIRST INVESTIGATION (3)

A
  1. 24-hour cortisol
  2. Early morning cortisol levels following a low dose dexamethasone suppression test
  3. ATCH
69
Q

Cushing Syndrome BEST INVESTIGATION

A
  1. High dose dexamethasone suppression test. 2. Cranial CT/MRI
70
Q

Cushing Syndrome TREATMENT

A

Surgery. Give steroids if ACTH is supressed

The treatment of Cushing syndrome, according to RACGP guidelines, depends on the underlying cause of the excess cortisol production. Here’s a simplified overview:

  • First-line treatment for Cushing syndrome caused by an adrenal tumor, pituitary adenoma (Cushing’s disease), or ectopic ACTH-secreting tumor.
  • Adrenalectomy: Surgical removal of the adrenal tumor.
  • Transsphenoidal Surgery: For pituitary adenomas, this surgery involves removing the tumor through the nasal passages.
  • Resection of Ectopic Tumors: If the source of excess ACTH is outside the pituitary (like in the lungs), the tumor is surgically removed.
  • If surgery is not an option or as a pre-surgical treatment, medications can be used to lower cortisol levels:
    • Ketoconazole, Metyrapone, or Mitotane: These drugs inhibit cortisol production.
    • Pasireotide: A drug used particularly for Cushing’s disease that inhibits ACTH release from the pituitary.
  • Used when surgery is not completely effective or if the tumor cannot be removed. This is more commonly applied in cases of pituitary adenomas.
  • Hypertension, diabetes, and osteoporosis should be managed according to standard treatment guidelines, as these are common complications of Cushing syndrome.
  • Regular monitoring of cortisol levels is essential after surgery to ensure that the treatment is effective and to manage potential adrenal insufficiency.

In summary, the approach to treating Cushing syndrome involves addressing the root cause (often through surgery), managing cortisol levels with medication if necessary, and treating any associated conditions. Regular follow-up is crucial to monitor the effectiveness of treatment and manage any complications oai_citation:1,Islamic Prayer Times Today, Salat Time, Namaz Timings | IslamicFinder oai_citation:2,United States: Prayer Times | Muslim Pro.

71
Q

Pheochromocytoma CLINICAL FEATURES

A

Headache, palpitations, diaphoresis

72
Q

Pheochromocytoma FIRST INVESTIGATION

A
  1. 24-hour free catecholamines (increased VMA)
73
Q

Pheochromocytoma BEST INVESTIGATION

A
  1. Plasma metanephrines +MRI
74
Q

Pheochromocytoma TREATMENT (3)

A
  1. Alpha Blockers (Phenoxybenzamine)
  2. BB
  3. Qx
75
Q

Adrenal Tumours TREATMENT

A
  • <4cm and benign: Follow up in 3-6m - ≥4cm and suspicious: Adrenalectomy
76
Q

Pituitary Tumour FIRST INVESTIGATION (2)

A
  1. TFT
  2. CT

The first-line investigation for diagnosing a pituitary tumor, according to RACGP guidelines, is Magnetic Resonance Imaging (MRI) of the brain. MRI is the gold standard for visualizing the pituitary gland and identifying any tumors, including their size, location, and impact on surrounding structures. Alongside MRI, hormonal blood tests are crucial to assess the tumor’s functional status by measuring hormone levels such as prolactin, growth hormone, ACTH, and others, depending on the clinical presentation.

For more details, you can visit the RACGP site here.

77
Q

Pituitary Tumour BEST INVESTIGATION

A
  1. MRI
78
Q

Pituitary Tumour TREATMENT

A

-If <1cm: Review in 1y
-If ≥1cm: with visual field symptoms: Transphenoidal resection

79
Q

Hyperprolactinaemia CLINICAL FEATURES

A

Reduced libido, amenorrhoea, erectile dysfunction

80
Q

Hyperprolactinaemia FIRST INVESTIGATION

A
  1. Prolactin:
    - >5000: Prolactinoma
    - <5000: other causes
81
Q

Hyperprolactinaemia BEST INVESTIGATION

A
  1. MRI
82
Q

Hyperprolactinaemia TREATMENT (2)

A

1.Dopamine agonist (Cabergoline, bromocriptine)
2.Surgery

83
Q

Acromegaly CLINICAL FEATURES

A

Spade like hands, frontal bossing, greasy skin, thickened palms, increased shoe size, heteronymous hemianopia

84
Q

Acromegaly FIRST INVESTIGATION

A
  1. IGF-1.
  2. Measurement of GH following OGTT. If GH is no supressed by glucose, acromegaly
85
Q

Acromegaly BEST INVESTIGATION

A

Pituitary MRI

86
Q

Diabetes Insipidus CLINICAL FEATURES

A

Low ADH, HyperNa, HypoK

87
Q

Diabetes Insipidus FIRST INVESTIGATION

A
  1. Plasma Na and osmolality
88
Q

Diabetes Insipidus BEST INVESTIGATION

A

Water deprivation test: - In primary polydipsia osmolarity will go back to normal. Desmopressin administration to see if its central (Osm increases) or nephrogenic

89
Q

Diabetes Insipidus TREATMENT

A

1.Central: Desmopressin
2.Nephrogenic: Solute restriction and thiazides

90
Q

SIADH CLINICAL FEATURES

A

High ADH, HypoNa, concentrated urine. Caused by SSRI, morphine, surgery, etc

91
Q

SIADH FIRST INVESTIGATION

A
  1. Plasma Na and osmolality
92
Q

SIADH TREATMENT (3)

A

1.Water restriction
2.Hypertonic saline if pt is severely symptomatic.
3. Demeclocycline

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