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Endocrine > Endo Patho Anki > Flashcards

Endo Patho Anki Flashcards

1
Q

The main functions of the thyroid gland are brought by the two main parenchymal cell types: 1. […] 2. […]

A

The main functions of the thyroid gland are brought by the two main parenchymal cell types: 1. Follicular cells –> T3 and T4 thyroid hormones 2. Parafollicular C cells –> Calcitonin

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2
Q

Normal thyroid weighs about […] generally heavier in which gender? […]

A

Normal thyroid weighs about 20-25g generally heavier in which gender? women!

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3
Q

Clinical consequences of enlargement of thyroid (goiter)? […]

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Clinical consequences of enlargement of thyroid (goiter)? 1. Breathing difficulty (compression on trachea) 2. Stridor (compression on trachea) 3. Swallowing difficulty (compression on esophagus) 4. Hoarseness of voice (recurrent laryngeal nerve compression) Think of it as DDD; dysphonia, dysphagia and dyspnoea. Mass effect!! Stridor = breathing sound due to large airway obstruction, usually worse

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4
Q

Main functions of thyroid hormone: 1. […] 2. […]

A

“Main functions of thyroid hormone: 1. Basal metabolic rate (BMR) - Heart rate - appetite - catabolism - protein synthesis 2. Growth and maturation - esp of CNS (deficient children will be short and have mental deficiency) (aka ““cretinism””)”

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5
Q

[…] is secreted by thyroid gland which is stimulated by […] secreted by anterior pituitary gland which is stimulated by […] secreted by hypothalamus

A

Thyroid hormone is secreted by thyroid gland which is stimulated by Thyroid stimulating hormone (TSH) secreted by anterior pituitary gland which is stimulated by Thyrotropin releasing hormone (TRH) secreted by hypothalamus

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6
Q

Thyroid hormone is secreted by […] which is stimulated by Thyroid stimulating hormone (TSH) secreted by […] which is stimulated by Thyrotropin releasing hormone (TRH) secreted by […]

A

Thyroid hormone is secreted by thyroid gland which is stimulated by Thyroid stimulating hormone (TSH) secreted by anterior pituitary gland which is stimulated by Thyrotropin releasing hormone (TRH) secreted by hypothalamus

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7
Q

Primary disease of thyroid is defined by […] Secondary disease of thyroid is defined by […]

A

Primary disease of thyroid is defined by disease occuring at thyroid itself - (TSH high T3 and T4 low (or vice versa)) Secondary disease of thyroid is defined by disease caused by malfunctioning of pituitary gland or hypothalamus - (TSH low, T3 and T4 low (or vice versa))

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8
Q

Calcitonin function: […]

A

“Calcitonin function: reduces calcium level in blood by 2 mechanisms: major: inhibiting osteoclast in bones, or minor: inhibit calcium tubular reabsorption ““importance of this role in humans is unclear, as patients who have very low or very high levels of calcitonin show no adverse effects.”””

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9
Q

2 categories of pathologies for thyroid diseases: 1. […] 2. […]

A

2 categories of pathologies for thyroid diseases: 1. Function abnormality (physiology) 2. Goiter (anatomy)

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10
Q

some signs and symptoms of (name 6 each) Hyperthyroidism […] Hypothyroidism […]

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some signs and symptoms of (name 6 each) Hyperthyroidism - tachycardia - increased appetite - weight loss - heat intolerance - diarrhea - irritability (or nervousness or tremor)- warm and sweaty Hypothyroidism - bradycardia - decreased appetite - weight gain - cold intolerance - constipation - mental slowness - dry and cool If you need help just compare the following: 1. HR 2. Weight 3. Cold/ Hot

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11
Q

Biochemical test for thyroid function: checking the levels of 1. […] 2. […]

A

Biochemical test for thyroid function: checking the levels of 1. TSH (used to distinguish primary vs secondary thyroid disease) 2. free T4 Mainly the above. But also total T4, T3, autoantibodies.

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12
Q

Example of Primary Hyperthyroidism 1. […] 2. […] 3. […] 4. […] Primary Hypothyroidism 1. Hashimoto thyroid (autoimmune destruction of thyroid gland) - aka chronic lymphocytic thyroiditis) 2. Iatrogenic - thyroidectomy - Radiation therapy (eg. for cancer) - drugs especially iodide/ 131-I therapy 3. Congenital/Developmental - eg. hyperplasia, dysgenesis

A

Example of Primary Hyperthyroidism 1. Graves disease (autoimmune that stimulates T3 T4 production) - ophthalmapathy sign - autoantibodies - aka toxic diffuse goiter 2. Toxic multinodular goiter - MNG (thyroid gland that contains autonomously functioning thyroid nodules) 3. Toxic adenoma - eg. follicular adenoma 4. Exogenous thyroid hormone/ iatrogenic - eg. post-surgical Primary Hypothyroidism 1.

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13
Q

2 types of goiter and some examples: 1. […] 2. […]

A

2 types of goiter and some examples: 1. Diffuse - Graves disease - simple goiter due iodine deficiency - Dequervain’s thyroiditis (aka subacute granulomatous thyroiditis or giant cell thyroiditis) 2. Localised/Nodular - multinodular goiter (nodular hyperplasia) - Dequervain thyroiditis (thyroiditis) - Hashimoto’s disease (thyroiditis) - neoplastic

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14
Q

2 examples of benign thyroid neoplasms: […] 2 examples of well differentiated malignant thyroid follicular cells: - Papillary type carcinoma (#1) - Follicular carcinoma - Hurthle cell carcinoma 1 example of poorly/un- differentiated maligant thyroid follicular cells: - Poorly differentiated carcinoma (insular) - Anaplastic carcinoma 2 examples of non-follicular maligant thyroid neoplasm - Medull

A

2 examples of benign thyroid neoplasms: - Follicular adenoma - Hürthle cell adenoma 2 examples of well differentiated malignant thyroid follicular cells: - Papillary type carcinoma (#1) - Follicular carcinoma - Hurthle cell carcinoma 1 example of poorly/un- differentiated maligant thyroid follicular cells: - Poorly differentiated carcinoma (insular) - Anaplastic carcinoma 2 examples of non-follicu

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15
Q

4 etiological causes/ classifications of thyroid diseases 1. […] 2. […] 3. […] 4. […]

A

4 etiological causes/ classifications of thyroid diseases 1. Congenital anomalies 2. Hyperplasia (diffuse and nodular goitre) 3. Thyroiditis and Immune disorders (Hashimoto, Dequervain, Graves) 4. Neoplasms (adenoma, carcinoma, lymphoma) Similar concept to all other diseases: Infection, Autoimmune, Congenital, Metabolic, Neoplasm

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16
Q

Most common causes of Hyperthyroidism - […] - […] - […] Hypothyroidism - […] - […]

A

Most common causes of Hyperthyroidism - Graves disease (85%) - Multinodular goitre - Adenoma Hypothyroidism - Hashimoto thyroiditis (60%) - Iatrogenic

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17
Q

4 examples of congenital thyroid diseases 1. […] - Embryogenal vestige - can be complicated with infection/malignancy - Moves up when pt protrude tongue!! - Treatment: surgical excision 2. […] 3. […] 4. […]

A

4 examples of congenital thyroid diseases 1. Thyroglossal duct cyst - Embryogenal vestige - can be complicated with infection/malignancy - Moves up when pt protrude tongue!! - Treatment: surgical excision 2. Abnormal development of thyroid gland (aplasia/agenesis or hypoplasia) 3. Ectopic thyroid tissue (located at abnormal position) 4. Thyroid dyshormongenesis (not common) When asked about congen

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18
Q

Thyroid hyperplasia is commonly due to? […]

A

Thyroid hyperplasia is commonly due to? abnormal iodine availability or usage (it could also be due to ingestion of goitrogens, substances that interfere with thyroid hormone synthesis) A low amount of thyroxine (one of the two thyroid hormones, T4) in the blood, due to lack of dietary iodine to make it, gives rise to high levels of thyroid stimulating hormone (TSH), which stimulates the thyroid g

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19
Q

What is the pathogenesis for diffuse and multinodular goitre? […]

A

What is the pathogenesis for diffuse and multinodular goitre? Impaired synthesis of thyroid hormones (low iodine levels/iodine deficiency/goitrogens/congenital enzyme defects/AR) –> compensatory increase in TSH –> hypertrophy and hyperplasia of follicular cells –> enlargement of thyroid gland (diffuse goitre) –> recurrent hyperplasia and involution –> nodular enlargement (multinodular goitre)

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20
Q

MNG is an evolution from […], with extreme and irregular enlargements. What is the clinical significance of MNG? - […] - […] - […] - […] - […]

A

MNG is an evolution from simple goitre, with extreme and irregular enlargements. What is the clinical significance of MNG? - Commonest cause of goitre - May mimic neoplastic disease - Mass effects: compression of trachea, RLN (hoarseness), difficulty swallowing - Cosmetic issues - Toxic goitre –> hyperthyroidism

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21
Q

The commonest type of goitre is […]

A

The commonest type of goitre is MNG Dont forget that MNG can be mistaken for cancer!! Simple goitre is usually missed

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22
Q

Name 4 examples of thyroiditis - (AI) […] - (AI) […] - (Other thyroiditides) […] - (Other thyroiditides) […]

A

Name 4 examples of thyroiditis - (AI) Hashimoto thyroiditis - (AI) Graves disease - (Other thyroiditides) DeQuervain thyroiditis - (Other thyroiditides) Riedel thyroiditis googled:

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23
Q

Clinical presentation of DeQuervain thyroiditis (aka subacute granulomatous thyroiditis) - Usually seen after […] - usual women 30-50yo - short history - self limiting - usually not clinically apparent - systemic symptom (fever, malaise, etc.) - this goitre is TENDER. (most goitre not tender) Gross morphology: - Patchy - firm, pale and yellowish areas with intervening normal parenchyma. - Enlarg

A

“Clinical presentation of DeQuervain thyroiditis (aka subacute granulomatous thyroiditis) - Usually seen after viral infection (MCQ uses URTI as example) - usual women 30-50yo - short history - self limiting - usually not clinically apparent - systemic symptom (fever, malaise, etc.) - this goitre is TENDER. (most goitre not tender) Gross morphology: - Patchy - firm, pale and yellowish areas with i

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24
Q

Riedel thyroiditis is characterized by […] is commonly mistaken for […]

A

“Riedel thyroiditis is characterized by extensive fibrosis of thyroid and surrounding structures is commonly mistaken for thyroid carcinoma VERY RARE. Hard and FIXED. ““A rider with his thick biker jacket”””

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25
Q

Hashimoto thyroiditis is […] Most commonly seen in - […] - […] Outline the pathogenesis of Hashimoto thyroiditis […] […]

A

Hashimoto thyroiditis is immune mediated cytotoxic destruction of thyrocytes. Caused by both cellular and humoral immunity. See below. Most commonly seen in - women (common risk factor for all AI diseases) - 45-65yo Outline the pathogenesis of Hashimoto thyroiditis Immune mediated cytotoxic destruction of thyrocytes Sensitization of CD4+ Th cells to thyroid antigens –> CD8+ T cell mediated cell d

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26
Q

Hashimoto thyroiditis complications (IMPT!!!) - […] - […] - […]

A

Hashimoto thyroiditis complications (IMPT!!!) - hypothyroidism - risk of other autoimmune diseases (eg. DM type 1, SLE, Sjogren syn) - B cell lymphoma of thyroid (e.g MALT)

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27
Q

Name some examples of autoantibodies to TSH receptors (TRAb)in Graves Disease. Which one is the most specific? 1. […] 2. […] 3. […]

A

Name some examples of autoantibodies to TSH receptors (TRAb)in Graves Disease. Which one is the most specific? 1. Thyroid stimulating immunoglobulin (TSI) (most specific for Graves) 2. Thyroid growth stimulating immunoglobulins (TGI) 3. TSH-binding inhibitor immunoglobulin (TBH) Additional ones might be autoantibodies like anti-TPO and anti-thyroglobulin, which are seen in Hashimoto as well

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28
Q

Graves Disease T3/T4 level: […] TSH: […] Presents as diffuse goitre +/- bruit Clinical triad: - Hyperthyroidism - Infiltrative ophthalmopathy (protruding eyes) - Infiltrative dermopathy (pretibial myxoedema) - only minority Pathogenesis: autoantibodies to TSH receptor (TRAbs) - e.g. TSI thyroid stimulating immunoglobulin - TSI most specific for Graves’ - Mimics actions of TSH → increased relea

A

Graves Disease T3/T4 level: High TSH: Low (due to negative feedback) Presents as diffuse goitre +/- bruit Clinical triad: - Hyperthyroidism - Infiltrative ophthalmopathy (protruding eyes) - Infiltrative dermopathy (pretibial myxoedema) - only minority Pathogenesis: autoantibodies to TSH receptor (TRAbs) - e.g. TSI thyroid stimulating immunoglobulin - TSI most specific for Graves’ - Mimics actions

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29
Q

Difference between graves and hashimoto disease in terms of morphology. (IMPT!!!) […]

A

Difference between graves and hashimoto disease in terms of morphology. (IMPT!!!) - Hashimoto is pale due to lymphocyte infiltrate. - Graves is reddish, like a steak because of hyperplasia/vascularity

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30
Q

2 most common maligancy in thyroid 1. […] 2. […]

A

“2 most common maligancy in thyroid 1. Papillary Thyroid carcinoma (PTC) 2. Follicular Thyroid carcinoma (FTC) PTC is MOST common, and thankfully has the BEST prognosis among the thyroid carcinomas. Also well known for LYMPHATIC spread. Other keywords include RET, BRAF and its distinctive histo features that is a must know: - Finely dispersed chromatin (orphan annie eye or ground glass apperance-

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31
Q

Clinical presentation of benign neoplasms of thyroid 1. […] 2. […] 3. […]

A

Clinical presentation of benign neoplasms of thyroid 1. solitary painless nodule (classically single nodule) 2. usually COLD nodules 3. rarely hyperfunctioning A cold nodule is a thyroid nodule that does not produce thyroid hormone

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32
Q

Microscopically MIFC is similar to follicular adenoma except for […]

A

Microscopically MIFC is similar to follicular adenoma except for capsular/vascular invasion.

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33
Q

Prognosis of thyroid follicular carcinoma: MIFC: […] Widely invasive: […]

A

Prognosis of thyroid follicular carcinoma: MIFC: GOOD!! (unless vascular invasion) Widely invasive: moderate

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34
Q

A Hürthle cell is often associated with […] as well as […].

A

A Hürthle cell is often associated with Hashimoto’s thyroiditis as well as oncocytic change. (Hürthle cell adenoma and Hürthle cell carcinoma, a subtype of follicular thyroid cancer)

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35
Q

Papillary carcinoma high risk group: […]

A

Papillary carcinoma high risk group: 1. 20-40 or children 2. exposed to ionising radiation

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36
Q

clinical presentation for thyroid papillary carcinoma (PTC) 1. […] 2. […] 3. […]

A

clinical presentation for thyroid papillary carcinoma (PTC) 1. painless nodule (cold) 2. enlarged cervical lymph nodes due to lymphatic spread (unlike follicular carcinoma) 3. BAD - hoarseness, cough, dysphagia

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37
Q

Prognosis for papillary carcinoma: […]

A

Prognosis for papillary carcinoma: v good! Follicular carcinoma also quite good.

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38
Q

(IMPT!!!) Diagnosis of follicular carcinoma (FTC) defined by: […] Diagnosis of papillary carcinoma (PTC) defined by: […]

A

“(IMPT!!!) Diagnosis of follicular carcinoma (FTC) defined by: Capsular or vascular invasion Diagnosis of papillary carcinoma (PTC) defined by: Nuclear features even in absence of papillae - Finely dispersed chromatin (orphan annie eye or ground glass apperance) - Nuclear grooves (coffee bean appearance) - Pseudoinclusions (it looks like there’s cytoplasm in the nucleus, or ““trapped””) - Oval and

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39
Q

Poorly differentiated carcinoma aka insular carcinoma spreads mainly by […] - […] - […] - […] Micro histology: - […]

A

Poorly differentiated carcinoma aka insular carcinoma spreads mainly by lymphatics and blood vessels - Invasive - May co-exist with well differentiated carcinomas (PTC, FTC) - Prognosis is between WDTC and anaplastic TC Micro histology: - Growth in large islands

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40
Q

Thyroid Medullary carcinoma refers to NET of the […] Clinical indications - […] (most impt!) - […] - […] - look out for […]

A

Thyroid Medullary carcinoma refers to NET of the parafollicular C cells Clinical indications - Raised serum calcitonin (most impt!) - paraneoplastic syndrome - mass - look out for MEN syndrome (very associated with family history!) The MEN (multiple endocrine neoplasia) syndromes are conditions which cause overactivity and enlargement in certain endocrine glands. MEN syndromes are usually (but not

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41
Q

Thyroid carcinoma spread (IMPT!!!) PTC: […] FTC: […]

A

Thyroid carcinoma spread (IMPT!!!) PTC: Lymphatic (to lymph node) FTC: Blood (to bone) PTC lymph, FTC Blood

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42
Q

Thyroid lymphoma usually arises in the background of which disease? […] Red flag: […]

A

Thyroid lymphoma usually arises in the background of which disease? Hashimoto thyroiditis!!! Red flag: Recent enlargement in elderly patients Recall that thyroid lymphomas are a complication of Hashimoto

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43
Q

forms of calcium in the body […]

A

forms of calcium in the body - bound to albumin - ionized - complexes Therefore TOTAL calcium might not be the amount of calcium that’s active only 1% of body calcium is in circulation, and only ~50% of this 1% is active (ionised)

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44
Q

Name the important hormones that affect calcium regulation […]

A

Name the important hormones that affect calcium regulation - PTH - Vit D - Calcitonin - Thyroid hormones - Adrenal hormones - Prostaglandins - Osteoclast activating factor In decreasing importance

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45
Q

PTH is produced by the […] and degraded mainly in the […]

A

PTH is produced by the parathyroid gland and degraded mainly in the kidney

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46
Q

PTH is cleaved within circulation to form 2 fragments, the C and N terminal. […] activity at N terminal […] activity at C terminal

A

PTH is cleaved within circulation to form 2 fragments, the C and N terminal. Biological (attaches to receptors) activity at N terminal Immunological activity at C terminal

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47
Q

PTH secretion is controlled by - […] - […] - […]

A

PTH secretion is controlled by - ionised calcium concentration - 1,25 dihydroxyvitamin D - magnesium (as a cofactor)

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48
Q

Actions of PTH (IMPT!!!!) Bone - […] Kidney - […] and - […] - […]

A

Actions of PTH (IMPT!!!!) Bone - stimulate bone resorption to mobilize its calcium and phosphate Kidney - increase distal nephron calcium reabsorption and - phosphate excretion at proximal tubule - Promotes formation of 1,25-dihydroxyvitamin D from 25-OHD TLDR, PTH increases Ca2+ Increased Ca2+ absorption in intestines is mediated via the 1:25 dihydroxyvitamin D produced in the kidneys

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49
Q

Name 5 examples that causes hypercalcemia 1. […] 2. […] 3. […] 4. […] 5. […] 6. […] 7. […] 8. […]

A

Name 5 examples that causes hypercalcemia 1. HyperPTH (pri, ter) 2. Malignancy (Multiple myeloma, humoral hypercalcaemia of malignancy, met to bone, eroding the bones) 3. Vitamin D excess (sarcoidosis, vit D intoxication) 4. Milk alkali syndrome 5. Immobilisation 6. Familial hypocalciuric hypercalcaemia 7. Endocrine disorders 8. Drugs Hyperparathyroid AND Malignancy most common

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50
Q

“Clinical features of hypercalcaemia (““stones, bones, moans (psychiatric), groans (abdominal)”” - Renal (stones, thirst, polyuria) - Bones - GI (e.g anorexia, abdominal pain) - Neurological (eg. fits, confusion, irritability) - Cardiac (eg. arrythmia) What are the clinical features of hypocalcaemia then? […]”

A

“Clinical features of hypercalcaemia (““stones, bones, moans (psychiatric), groans (abdominal)”” - Renal (stones, thirst, polyuria) - Bones - GI (e.g anorexia, abdominal pain) - Neurological (eg. fits, confusion, irritability) - Cardiac (eg. arrythmia) What are the clinical features of hypocalcaemia then? SAME! Interestingly, hypocalcaemia give the SAME symptoms as hypercalcaemia can deduce becaus

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51
Q

Is hypercalcaemia a medical emergency? […] Outline the treatment approaches for hypercalcemia: - (urgent treatment) […] - […] - […] - […]

A

Is hypercalcaemia a medical emergency? YES! Outline the treatment approaches for hypercalcemia: - (urgent treatment) serum adjusted calcium >3.5mmol/L - rehydrate with IV saline - Biphosphonates - treat with underlying cause (eg. surgical removal of parathyroid nodule)

52
Q

What are the differential diagnosis for these lab parameters? high calcium low phosphate –> […] high calcium high phosphate –> […] low calcium high phosphate –> […] low calcium low phosphate –> […]

A

What are the differential diagnosis for these lab parameters? high calcium low phosphate –> Primary Hyperparathyroid Maligancy high calcium high phosphate –> Malignancy (primary/secondary) / hypervitaminosis D low calcium high phosphate –> Hypoparathyroidism / Renal failure low calcium low phosphate –> Vitamin D deficiency

53
Q

Primary hyperparathyroidism prevalence: […] Aetiology: […]

A

“Primary hyperparathyroidism prevalence: 1 in 1000 Aetiology: Parathyroid adenoma, hyperplasia, carcinoma Read all the slides below. ““Humoral hypercalcemia of malignancy (HHM) is caused by the oversecretion of parathyroid hormone-related peptide (PTHrP) from malignant tumors.”””

54
Q

Name some mechanisms by which malignancies cause hypercalcemia 1. […] (malignancy erodes the bone and dumps the calcium into blood) 2. […] (releases cytokines osteoclast activating factor which promotes osteoclast activity) 3. […] (parathyroid hormone related peptide is released, acting like PTH)

A

Name some mechanisms by which malignancies cause hypercalcemia 1. Tumors with bony metastasis (malignancy erodes the bone and dumps the calcium into blood) 2. Multiple Myeloma (releases cytokines osteoclast activating factor which promotes osteoclast activity) 3. Tumors without bony metastases (humoral hypercalcemia of maligancy aka HHM) (parathyroid hormone related peptide is released, acting lik

55
Q

Name the key differences between hyperparathyroidism and malignancy […]

A

Name the key differences between hyperparathyroidism and malignancy Malignancy has higher degree of hypercalcaemia (met to bones), shorter duration, rapid rate of increase of calcium, renal stones are uncommon and plasma PTH is low/undetectable (suppressed by hypercalcaemia) Plasma PTH is high for hyperPTH (duh) so that is a defining difference!! i.e when u r not sure of whats the cause of the hyp

56
Q

Investigation of the cause of hypercalcemia - can measure patient’s […]

A

Investigation of the cause of hypercalcemia - can measure patient’s PTH levels

57
Q

Clinical features of hypocalcemia […]

A

Clinical features of hypocalcemia - neurological - CVS - Cataracts How is this same as hypercalcaemia???? Ok la roughly i guess LOL

58
Q

Treatment of hypocalcemia involves prescribing: […]

A

Treatment of hypocalcemia involves prescribing: Oral calcium Vitamin D supplements

59
Q

name 4 causes of hypocalcemia - […] - […] - […] - […] - rare causes (eg. acute pancreatitis, where there is saponification etc of fat and calcium)

A

“name 4 causes of hypocalcemia - hypoparathyroidism (needs all 4 glands to be non-functioning) - vitamin D deficiency (Malabsorption, inadequate diet, poor exposure to sunlight) - renal disease (decrease in vit D enzyme 1a hydroxylase) - pseudohypoparathyroidism (receptor-ligand failure mimicking hypoparathyroidism, thats why ““pseudo””) - rare causes (eg. acute pancreatitis, where there is saponi

60
Q

Investigation of hypocalcemia involves measuring patient’s […]

A

Investigation of hypocalcemia involves measuring patient’s PTH levels Same as hypercalcaemia.

61
Q

The adrenal glands can be found on top of each kidney. Each adrenal gland has 2 regions that carry our seperate functions: Adrenal Cortex: […] Adrenal Medulla: […]

A

The adrenal glands can be found on top of each kidney. Each adrenal gland has 2 regions that carry our seperate functions: Adrenal Cortex: secretes aldosterone, cortisol, sex hormones (SALT SUGAR SEX!) Adrenal Medulla: secretes epinephrine (80%) and norepinephrine (20%) SALT SUGAR SEX! SALT SUGAR SEX!! SALT SUGAR SEX!!! corresponds to Zona glomerulosa (outer), Zona fasciculata and Zona reticularis

62
Q

The adrenal glands can be found on top of each kidney. Each adrenal gland has 2 regions that carry our seperate functions: […]: secretes aldosterone, cortisol, sex hormones (SALT SUGAR SEX!) […]: secretes epinephrine (80%) and norepinephrine (20%)

A

The adrenal glands can be found on top of each kidney. Each adrenal gland has 2 regions that carry our seperate functions: Adrenal Cortex: secretes aldosterone, cortisol, sex hormones (SALT SUGAR SEX!) Adrenal Medulla: secretes epinephrine (80%) and norepinephrine (20%) SALT SUGAR SEX! SALT SUGAR SEX!! SALT SUGAR SEX!!! corresponds to Zona glomerulosa (outer), Zona fasciculata and Zona reticularis

63
Q

Cortisol regulation pathway […] produces Corticotropin-releasing factor (CRF/ CRH), which stimulates the […] to produce Adrenocorticotropic hormone (ACTH), which stimulates the […] to produce cortisol Cortisol exhibits negative feedback on BOTH ant pit and hypothalamus

A

Cortisol regulation pathway Hypothalamus produces Corticotropin-releasing factor (CRF/ CRH), which stimulates the anterior pituitary gland to produce Adrenocorticotropic hormone (ACTH), which stimulates the Adrenal cortex to produce cortisol Cortisol exhibits negative feedback on BOTH ant pit and hypothalamus

64
Q

Cortisol regulation pathway Hypothalamus produces […], which stimulates the anterior pituitary gland to produce […], which stimulates the Adrenal cortex to produce cortisol Cortisol exhibits negative feedback on BOTH ant pit and hypothalamus

A

Cortisol regulation pathway Hypothalamus produces Corticotropin-releasing factor (CRF/ CRH), which stimulates the anterior pituitary gland to produce Adrenocorticotropic hormone (ACTH), which stimulates the Adrenal cortex to produce cortisol Cortisol exhibits negative feedback on BOTH ant pit and hypothalamus

65
Q

Cushing disease is the disease where a person has high levels of […] Cushing syndrome is […]

A

Cushing disease is the disease where a person has high levels of ACTH (that leads to high cortisol) Cushing syndrome is the set of symptoms that present similarly to cushing’s disease - excess cortisol Cushing disease = pituitary ACTH secreting adenoma Cushing syndrome = set of symptoms similar to cushing disease (excess cortisol)

66
Q

Causes of cushing’s syndrome/ adrenal hyperactivity: most common: […] others: - […] - […] - […]

A

Causes of cushing’s syndrome/ adrenal hyperactivity: most common: Iatrogenic others: - Cushing’s disease (pituitary ACTH secreting adenoma) - adrenal cortical tumor (adenoma, carcinoma) - ectopic ACTH secretion, EAS (paraneoplastic syndrome)(eg. Small cell carcinoma of lung) TLDR, either iatrogenic or tumour.

67
Q

Clinical features of Cushing’s syndrome? (IMPT!!!!) - […] - […] - […] - […] - […] - […] - […] - […] - […] - […] - […] - […] - etc

A

Clinical features of Cushing’s syndrome? (IMPT!!!!) - central obesity (lemon on a stick appearance) - dorsocervical fat pad (buffalo hump) - plethoric facies/ peripheral sustenance (moonface) - purple abdo striae, hirsutism - muscle atrophy/ wasting - hypertension - glucose intolerance - menstrual dysfunction - muscle weakness - bruising - osteoporosis - cataracts - etc Physical features: Central

68
Q

What are the 3 ways to diagnose cushing’s syndrome? (IMPT!!!!) 1. […], negative if […] 2. […], negative if […] 3. […]

A

What are the 3 ways to diagnose cushing’s syndrome? (IMPT!!!!) 1. DST 0.5mg, 6-hourly for 48 hrs (8 times), negative if cortisol <50 nmol/L 2. Overnight DST 1mg at 11pm, negative if <140nmol/L cortisol at 8am next day 3. Urinary free cortisol (meaning unbound cortisol in the urine) DST = Dexomethasone Suppression Test If cortisol level falls below the indicated value, it means successful suppressi

69
Q

Conn’s syndrome is […] Causes of Conn’s: 1. Adrenal aldosterone producing adenoma (APA) 2. Idiopathic hyperaldosteronism with bilateral adrenal hyperplasia (BAH) What are the biochemical imbalances you will look for to confirm? […]

A

Conn’s syndrome is aka primary hyperaldosteronism: the disease where excess production of the hormone aldosterone by the adrenal glands resulting in low renin levels. Often it produces few symptoms Causes of Conn’s: 1. Adrenal aldosterone producing adenoma (APA) 2. Idiopathic hyperaldosteronism with bilateral adrenal hyperplasia (BAH) What are the biochemical imbalances you will look for to confir

70
Q

Pheochromocytoma is […] Major component of […]. Also part of […] and […]. Symptoms and Signs (deduce): 1. Hypertension (intermittent/sustained/paroxysms superimposed) 2. Headache 3. Sweating 4. Palpitations and tachycardia Treatment with? Phenoxybenzamine (a-adrenergic non-selective blocker) Diagnostic testing for pheochromocytoma is normally looking for metanephrines(metabolite of epineph

A

Pheochromocytoma is a rare tumor of adrenal medulla. It results in the release of too much epinephrine and norepinephrine Major component of MEN Type IIa and IIb. Also part of VHL and NF-1. Symptoms and Signs (deduce): 1. Hypertension (intermittent/sustained/paroxysms superimposed) 2. Headache 3. Sweating 4. Palpitations and tachycardia Treatment with? Phenoxybenzamine (a-adrenergic non-selective

71
Q

Pheochromocytoma is a rare tumor of adrenal medulla. It results in the release of too much epinephrine and norepinephrine Major component of MEN Type IIa and IIb. Also part of VHL and NF-1. Symptoms and Signs (deduce): 1. […] 2. […] 3. […] 4. […] Treatment with? Phenoxybenzamine (a-adrenergic non-selective blocker) Diagnostic testing for pheochromocytoma is normally looking for metanephrin

A

Pheochromocytoma is a rare tumor of adrenal medulla. It results in the release of too much epinephrine and norepinephrine Major component of MEN Type IIa and IIb. Also part of VHL and NF-1. Symptoms and Signs (deduce): 1. Hypertension (intermittent/sustained/paroxysms superimposed) 2. Headache 3. Sweating 4. Palpitations and tachycardia Treatment with? Phenoxybenzamine (a-adrenergic non-selective

72
Q

Clinical features of glucocorticoid (cortisol) deficiency - […] - […] - […] - […] mineralcorticoid (aldosterone) insufficiency - […] - […] - […] - […]- […]

A

Clinical features of glucocorticoid (cortisol) deficiency - weakness - hypoglycemia - weight loss - GI discomfort mineralcorticoid (aldosterone) insufficiency - sodium wasting - hypovolemia - postural hypotension - hyperkalemia- Pigmentation (only for primary. not secondary. biochem about melanin production) All can deduce!!

73
Q

Insulin Tolerance Test is used for testing which hormones? 1. […] 2. […] 3. […]

A

Insulin Tolerance Test is used for testing which hormones? 1. ACTH 2. Cortisol 3. Growth Hormone (and i suppose all those in these 2 hormone’s axis. like GRH and CRH) An insulin tolerance test (ITT) is a medical diagnostic procedure during which insulin is injected into a patient’s vein, after which blood glucose is measured at regular intervals. This procedure is performed to assess pituitary fun

74
Q

Hurthle (oncocytic) cell change: […]

A

Hurthle (oncocytic) cell change: Large Eosinophilic Granular (because of increase in mitochondria, can mimic neoplasm)

75
Q

“Papillary Thyroid Carcinoma - most common thyroid malignancy, thankfully best prognosis among the thyroid carcinomas - lymphatic spread - molecular markers: RET, BRAF Most common variants of papillary carcinoma of thyroid (PTC): 1. Classical 2. Follicular 3. Encapsulated 4. Worst: Tall cell variant Microscopic: Presentation of classical PTC: - Branching of well formed papillae with fibrovascular

A

“Papillary Thyroid Carcinoma - most common thyroid malignancy, thankfully best prognosis among the thyroid carcinomas - lymphatic spread - molecular markers: RET, BRAF Most common variants of papillary carcinoma of thyroid (PTC): 1. Classical 2. Follicular 3. Encapsulated 4. Worst: Tall cell variant Microscopic: Presentation of classical PTC: - Branching of well formed papillae with fibrovascular

76
Q

Addison’s disease = […] Logically, effects would mimic that of: […] & […] Diagnosis of Addisons? - Short Synacthen test Diagnosis of Ddx for Addisons? - Long Synacthen test

A

Addison’s disease = primary adrenal insufficiency (decreased production of cortisol and aldosterone) Logically, effects would mimic that of: Hypocortisolism & Hypoaldosteronism Diagnosis of Addisons? - Short Synacthen test Diagnosis of Ddx for Addisons? - Long Synacthen test Short Synacthen test: The test is based on the measurement of serum cortisol before and after an injection of synthetic ACTH

77
Q

Addison’s disease = primary adrenal insufficiency (decreased production of cortisol and aldosterone) Logically, effects would mimic that of: Hypocortisolism & Hypoaldosteronism Diagnosis of Addisons? - […] Diagnosis of Ddx for Addisons? - […]

A

Addison’s disease = primary adrenal insufficiency (decreased production of cortisol and aldosterone) Logically, effects would mimic that of: Hypocortisolism & Hypoaldosteronism Diagnosis of Addisons? - Short Synacthen test Diagnosis of Ddx for Addisons? - Long Synacthen test Short Synacthen test: The test is based on the measurement of serum cortisol before and after an injection of synthetic ACTH

78
Q

Aetiology of adrenal insufficiency: Primary: […] Secondary: Clinical features of primary insufficiency? - Hypocortisolism: hypoglycaemia, weight loss, GI disturbances, weakness - Hypoaldosteronism: hypovolaemia, postural hypotension, hyperkalaemia and hyponatraemia - (Hyper)Pigmentation (ACTH overproduction) - Vitiligo sometimes seen in autoimmune adrenalitis Clinical features of secondary insuf

A

Aetiology of adrenal insufficiency: Primary: Secondary: Clinical features of primary insufficiency? - Hypocortisolism: hypoglycaemia, weight loss, GI disturbances, weakness - Hypoaldosteronism: hypovolaemia, postural hypotension, hyperkalaemia and hyponatraemia - (Hyper)Pigmentation (ACTH overproduction) - Vitiligo sometimes seen in autoimmune adrenalitis Clinical features of secondary insufficien

79
Q

Aetiology of adrenal insufficiency: Primary: Secondary: […] Clinical features of primary insufficiency? - Hypocortisolism: hypoglycaemia, weight loss, GI disturbances, weakness - Hypoaldosteronism: hypovolaemia, postural hypotension, hyperkalaemia and hyponatraemia - (Hyper)Pigmentation (ACTH overproduction) - Vitiligo sometimes seen in autoimmune adrenalitis Clinical features of secondary insuf

A

Aetiology of adrenal insufficiency: Primary: Secondary: Clinical features of primary insufficiency? - Hypocortisolism: hypoglycaemia, weight loss, GI disturbances, weakness - Hypoaldosteronism: hypovolaemia, postural hypotension, hyperkalaemia and hyponatraemia - (Hyper)Pigmentation (ACTH overproduction) - Vitiligo sometimes seen in autoimmune adrenalitis Clinical features of secondary insufficien

80
Q

is Hashimoto thyroiditis painful? painless goitre What colour is the goitre? (IMPT!!!) pale ( bc full of lymphocytes) Biochemistry profile? - T3/T4 Down - TSH Up - Autoantibodies Anti-TPO, anti-TSH, anti-Tg Microscopic appearance? - […] - […] - Thyroid follicles - […], […]

A

is Hashimoto thyroiditis painful? painless goitre What colour is the goitre? (IMPT!!!) pale ( bc full of lymphocytes) Biochemistry profile? - T3/T4 Down - TSH Up - Autoantibodies Anti-TPO, anti-TSH, anti-Tg Microscopic appearance? - Fibrosis - Immune cell infiltrates (immune cells; lymphocytes, plasma cells, reactive lymphoid follicles) - Thyroid follicles - Atrophic, Hurthle (oncocytic) cell chan

81
Q

What is the clinical triad of Graves Disease? (IMPT!!!) 1. Hyperthyroidism 2. Infiltrative ophthalmopathy/exophthalmos (infiltration by mononuclear inflammatory cells, oedema, accumulation of extracellular matrix e.g. glycosaminoglycans) 3. Infiltrative dermopathy/pretibial myxoedema (only in minority) High risk group: 20-40yo women with family history (AI so always females more at risk!!) Clinica

A

What is the clinical triad of Graves Disease? (IMPT!!!) 1. Hyperthyroidism 2. Infiltrative ophthalmopathy/exophthalmos (infiltration by mononuclear inflammatory cells, oedema, accumulation of extracellular matrix e.g. glycosaminoglycans) 3. Infiltrative dermopathy/pretibial myxoedema (only in minority) High risk group: 20-40yo women with family history (AI so always females more at risk!!) Clinica

82
Q

Morphology of benign thyroid adenomas: Gross: - […] - […] - […] - Orange-brown colour: […] Microscopic (all about the same with each other): - Intact surrounding capsule (desmoplastic capsule) - Follicles uniformed, distinct from surrounding parenchyma - Macrofollicular, microfollicular and mixed follicle sizes - Monotonous cells - uncommon Cystic change or haemorrhage - Hurthle cell chang

A

Morphology of benign thyroid adenomas: Gross: - Rounded, encapsulated, well demarcated - Intact capsule (no invasion into thyroid parenchyma) - Bulging from the cut surface - Orange-brown colour: Hurthle cell adenoma (HCA) Microscopic (all about the same with each other): - Intact surrounding capsule (desmoplastic capsule) - Follicles uniformed, distinct from surrounding parenchyma - Macrofollicul

83
Q

Morphology of benign thyroid adenomas: Gross: - Rounded, encapsulated, well demarcated - Intact capsule (no invasion into thyroid parenchyma) - Bulging from the cut surface - Orange-brown colour: Hurthle cell adenoma (HCA) Microscopic (all about the same with each other): - […] - […] - […] - […] - uncommon […] - Hurthle cell change (in HCA) What is the important thing to note for thyroid

A

Morphology of benign thyroid adenomas: Gross: - Rounded, encapsulated, well demarcated - Intact capsule (no invasion into thyroid parenchyma) - Bulging from the cut surface - Orange-brown colour: Hurthle cell adenoma (HCA) Microscopic (all about the same with each other): - Intact surrounding capsule (desmoplastic capsule) - Follicles uniformed, distinct from surrounding parenchyma - Macrofollicul

84
Q

Causes of thyroid carcinomas: Genetic: FTC: […] PTC: […] Medullary CA: […] Anaplastic CA: […] Environmental: […] […]

A

Causes of thyroid carcinomas: Genetic: FTC: RAS family mutations PTC: RET gene&raquo_space; RET/PTC rearrangements, BRAF mutations Medullary CA: MEN2 syndrome (worst prognosis associated with RET mutations) Anaplastic CA: p53 mutations Environmental: Ionising radiation Longstanding MNG

85
Q

2 types of thyroid medullary carcinoma - 80% sporadic - 20% familial MEN2 mutations/ familial/ RET is the worst prognosis Gross morphology: 1. Solitary (sporadic) or bilateral (MEN/ familial) 2. Necrosis and haemorrhage 3. Invasion beyond thyroid Microscopic morphology: 1. […] 2. […] 3. […] 4. […] 5. […]

A

“2 types of thyroid medullary carcinoma - 80% sporadic - 20% familial MEN2 mutations/ familial/ RET is the worst prognosis Gross morphology: 1. Solitary (sporadic) or bilateral (MEN/ familial) 2. Necrosis and haemorrhage 3. Invasion beyond thyroid Microscopic morphology: 1. Epithelioid or spindled cells 2. Salt and pepper chromatin 3. Architecture has nests, trabeculae and follicles 4. Amyloid (Co

86
Q

Anaplastic carcinoma Risk group: elderly Differentiation? UNDIFFERENTIATED Prognosis: V v v bad. survival in months Microscopy: - […] - […] - […] - […]

A

Anaplastic carcinoma Risk group: elderly Differentiation? UNDIFFERENTIATED Prognosis: V v v bad. survival in months Microscopy: - Highly pleomorphic cells - Giant tumour cells - Spindle cells (sarcomatoid features) - Small anaplastic cells

87
Q

MNG (multinodular goitre) is a progression from simple goitre, where there is […] Clinical significance: - […] - […] - […] - […] Microscopic morphology: - Pseudopapillae - crowded columnar cells as seen in simple goitre - Cystic change - Haemorrhage

A

MNG (multinodular goitre) is a progression from simple goitre, where there is an extreme irregular enlargement. Clinical significance: - Can mimic neoplastic disease - Commonest goitre - Mass effects (compression): Dyspnoea, Dysphonia and Dysphagia - Hyperthyroidism (possible, though normally euthyroid) Microscopic morphology: - Pseudopapillae - crowded columnar cells as seen in simple goitre - Cy

88
Q

MNG (multinodular goitre) is a progression from simple goitre, where there is an extreme irregular enlargement. Clinical significance: - Can mimic neoplastic disease - Commonest goitre - Mass effects (compression): Dyspnoea, Dysphonia and Dysphagia - Hyperthyroidism (possible, though normally euthyroid) Microscopic morphology: - […] - […] - […]

A

MNG (multinodular goitre) is a progression from simple goitre, where there is an extreme irregular enlargement. Clinical significance: - Can mimic neoplastic disease - Commonest goitre - Mass effects (compression): Dyspnoea, Dysphonia and Dysphagia - Hyperthyroidism (possible, though normally euthyroid) Microscopic morphology: - Pseudopapillae - crowded columnar cells as seen in simple goitre - Cy

89
Q

HLA associations: Graves disease: […] Hashimoto’s disease: […]

A

“HLA associations: Graves disease: HLA-DR3 and HLA-B8 Hashimoto’s disease: HLA-DR3 and HLA-DR5 ““DR3 B8 Graves, DR3 DR5 Hashimoto, DR4 RA”””

90
Q

Pheochromocytoma is a rare tumor of adrenal medulla. It results in the release of too much epinephrine and norepinephrine Major component of MEN Type IIa and IIb. Also part of VHL and NF-1. Symptoms and Signs (deduce): 1. Hypertension (intermittent/sustained/paroxysms superimposed) 2. Headache 3. Sweating 4. Palpitations and tachycardia Treatment with? […] (a-adrenergic non-selective blocker) Di

A

Pheochromocytoma is a rare tumor of adrenal medulla. It results in the release of too much epinephrine and norepinephrine Major component of MEN Type IIa and IIb. Also part of VHL and NF-1. Symptoms and Signs (deduce): 1. Hypertension (intermittent/sustained/paroxysms superimposed) 2. Headache 3. Sweating 4. Palpitations and tachycardia Treatment with? Phenoxybenzamine (a-adrenergic non-selective

91
Q

Aetiology of adrenal insufficiency: Primary: Secondary: Clinical features of primary insufficiency? - Hypocortisolism: […] - Hypoaldosteronism: […] - […] - […] Clinical features of secondary insufficiency? - No symptoms of aldosterone insufficiency - No hyper-pigmentation (no ACTH this time) - May have other conditions: Hypogonadism/ hypothyroidism etc

A

Aetiology of adrenal insufficiency: Primary: Secondary: Clinical features of primary insufficiency? - Hypocortisolism: hypoglycaemia, weight loss, GI disturbances, weakness - Hypoaldosteronism: hypovolaemia, postural hypotension, hyperkalaemia and hyponatraemia - (Hyper)Pigmentation (ACTH overproduction) - Vitiligo sometimes seen in autoimmune adrenalitis Clinical features of secondary insufficien

92
Q

Aetiology of adrenal insufficiency: Primary: Secondary: Clinical features of primary insufficiency? - Hypocortisolism: hypoglycaemia, weight loss, GI disturbances, weakness - Hypoaldosteronism: hypovolaemia, postural hypotension, hyperkalaemia and hyponatraemia - (Hyper)Pigmentation (ACTH overproduction) - Vitiligo sometimes seen in autoimmune adrenalitis Clinical features of secondary insufficien

A

Aetiology of adrenal insufficiency: Primary: Secondary: Clinical features of primary insufficiency? - Hypocortisolism: hypoglycaemia, weight loss, GI disturbances, weakness - Hypoaldosteronism: hypovolaemia, postural hypotension, hyperkalaemia and hyponatraemia - (Hyper)Pigmentation (ACTH overproduction) - Vitiligo sometimes seen in autoimmune adrenalitis Clinical features of secondary insufficien

93
Q

4 T’s of mediastinal masses: […] […] […] […]

A

4 T’s of mediastinal masses: Thyroid Teratoma (germ cell tumours) T-cell lymphoma (or any other lymphoma) Thymoma (thymus) - but usually no lymph node enlargement

94
Q

Follicular Thyroid Carcinoma (FTC) Morphological defining feature from follicular adenoma […] Subtypes - […] - […] - […]

A

Follicular Thyroid Carcinoma (FTC) Morphological defining feature from follicular adenoma capsular OR vascular invasion Subtypes - minimally invasive (MIFC) - capsular only - encapsulated angioinvasive - vascular - widely invasive (uncommon, obvious but ill-defined) MIFC is similar to follicular adenoma (both grossly and microscopically) except for capsular/vascular invasion.

95
Q

Morphology of benign thyroid adenomas: Gross: - Rounded, encapsulated, well demarcated - Intact capsule (no invasion into thyroid parenchyma) - Bulging from the cut surface - Orange-brown colour: Hurthle cell adenoma (HCA) Microscopic (all about the same with each other): - Intact surrounding capsule (desmoplastic capsule) - Follicles uniformed, distinct from surrounding parenchyma - Macrofollicul

A

Morphology of benign thyroid adenomas: Gross: - Rounded, encapsulated, well demarcated - Intact capsule (no invasion into thyroid parenchyma) - Bulging from the cut surface - Orange-brown colour: Hurthle cell adenoma (HCA) Microscopic (all about the same with each other): - Intact surrounding capsule (desmoplastic capsule) - Follicles uniformed, distinct from surrounding parenchyma - Macrofollicul

96
Q

Cortisol regulation pathway Hypothalamus produces Corticotropin-releasing factor (CRF/ CRH), which stimulates the anterior pituitary gland to produce Adrenocorticotropic hormone (ACTH), which stimulates the Adrenal cortex to produce cortisol Cortisol exhibits negative feedback on […]

A

Cortisol regulation pathway Hypothalamus produces Corticotropin-releasing factor (CRF/ CRH), which stimulates the anterior pituitary gland to produce Adrenocorticotropic hormone (ACTH), which stimulates the Adrenal cortex to produce cortisol Cortisol exhibits negative feedback on BOTH ant pit and hypothalamus

97
Q

60 y/o woman with no significant past medical history presented with neck swelling for 1 year Name 5 structures/organs in the neck. For each of these structures/organs, give an example of a cause for neck swelling - Thyroid –> Hashimoto, Graves, MNG, neoplasms, thyroglossal cyst - Esophagus –> neoplasms - Parotid gland –> neoplasm - Submandibular gland –> neoplasm - Virchow nodule –> abdomina

A

60 y/o woman with no significant past medical history presented with neck swelling for 1 year Name 5 structures/organs in the neck. For each of these structures/organs, give an example of a cause for neck swelling - Thyroid –> Hashimoto, Graves, MNG, neoplasms, thyroglossal cyst - Esophagus –> neoplasms - Parotid gland –> neoplasm - Submandibular gland –> neoplasm - Virchow nodule –> abdomina

98
Q

60 y/o woman with no significant past medical history presented with neck swelling for 1 year Name 5 structures/organs in the neck. For each of these structures/organs, give an example of a cause for neck swelling - […] - […] - […] - […] - […] - etc etc etc Goitre means enlargement of the thyroid gland. What are 5 causes of goitre? Which ones are most common? […] What kinds of radiolog

A

60 y/o woman with no significant past medical history presented with neck swelling for 1 year Name 5 structures/organs in the neck. For each of these structures/organs, give an example of a cause for neck swelling - Thyroid –> Hashimoto, Graves, MNG, neoplasms, thyroglossal cyst - Esophagus –> neoplasms - Parotid gland –> neoplasm - Submandibular gland –> neoplasm - Virchow nodule –> abdomina

99
Q

60 y/o woman with no significant past medical history presented with neck swelling for 1 year Name 5 structures/organs in the neck. For each of these structures/organs, give an example of a cause for neck swelling - Thyroid –> Hashimoto, Graves, MNG, neoplasms, thyroglossal cyst - Esophagus –> neoplasms - Parotid gland –> neoplasm - Submandibular gland –> neoplasm - Virchow nodule –> abdomina

A

60 y/o woman with no significant past medical history presented with neck swelling for 1 year Name 5 structures/organs in the neck. For each of these structures/organs, give an example of a cause for neck swelling - Thyroid –> Hashimoto, Graves, MNG, neoplasms, thyroglossal cyst - Esophagus –> neoplasms - Parotid gland –> neoplasm - Submandibular gland –> neoplasm - Virchow nodule –> abdomina

100
Q

40 y/o housewife complains of progressive weight gain of 20kg in 1 year (nani???), fatique, postural dizziness, loss of memory, slow speech, deepening of her voice, dry skin, constipation and cold intolerance. Gross description? - […] - […] Diagnosis? […]

A

40 y/o housewife complains of progressive weight gain of 20kg in 1 year (nani???), fatique, postural dizziness, loss of memory, slow speech, deepening of her voice, dry skin, constipation and cold intolerance. Gross description? - Diffuse mild enlargement, firm - Cut surface shows pale, tan-coloured, homogenous appearance Diagnosis? Hypothyroidism (possibly Hashimoto’s since its more common, plus

101
Q

40 y/o housewife complains of progressive weight gain of 20kg in 1 year (nani???), fatique, postural dizziness, loss of memory, slow speech, deepening of her voice, dry skin, constipation and cold intolerance. She was diagnosed with hashimoto thyroiditis. Compare the gross of multinodular goitre with hashimoto. Why does hashimoto look so pale? […] What are 2 other autoimmune conditions that can

A

40 y/o housewife complains of progressive weight gain of 20kg in 1 year (nani???), fatique, postural dizziness, loss of memory, slow speech, deepening of her voice, dry skin, constipation and cold intolerance. She was diagnosed with hashimoto thyroiditis. Compare the gross of multinodular goitre with hashimoto. Why does hashimoto look so pale? Lymphocyte infiltrate What are 2 other autoimmune cond

102
Q

40 y/o housewife complains of progressive weight gain of 20kg in 1 year (nani???), fatique, postural dizziness, loss of memory, slow speech, deepening of her voice, dry skin, constipation and cold intolerance. She was diagnosed with hashimoto thyroiditis. Compare the gross of multinodular goitre with hashimoto. Why does hashimoto look so pale? Lymphocyte infiltrate What are 2 other autoimmune cond

A

40 y/o housewife complains of progressive weight gain of 20kg in 1 year (nani???), fatique, postural dizziness, loss of memory, slow speech, deepening of her voice, dry skin, constipation and cold intolerance. She was diagnosed with hashimoto thyroiditis. Compare the gross of multinodular goitre with hashimoto. Why does hashimoto look so pale? Lymphocyte infiltrate What are 2 other autoimmune cond

103
Q

“The pt is a 31 y/o woman who has noted increasing fatigue and a 7kg weight loss withut dieting over the past 4 months. She also has increasing anxiety and nervousness with diarrhea Physical examination shows a diffusely enlarged thyroid gland Her temperature is 37.5, pulse is 103/min, respirations are 28/min, and blood pressure is 140/75 mmHg. What are 3 possible causes of hyperthyroidism? […]

A

“The pt is a 31 y/o woman who has noted increasing fatigue and a 7kg weight loss withut dieting over the past 4 months. She also has increasing anxiety and nervousness with diarrhea Physical examination shows a diffusely enlarged thyroid gland Her temperature is 37.5, pulse is 103/min, respirations are 28/min, and blood pressure is 140/75 mmHg. What are 3 possible causes of hyperthyroidism? Graves

104
Q

“The pt is a 31 y/o woman who has noted increasing fatigue and a 7kg weight loss withut dieting over the past 4 months. She also has increasing anxiety and nervousness with diarrhea Physical examination shows a diffusely enlarged thyroid gland Her temperature is 37.5, pulse is 103/min, respirations are 28/min, and blood pressure is 140/75 mmHg. What are 3 possible causes of hyperthyroidism? Graves

A

“The pt is a 31 y/o woman who has noted increasing fatigue and a 7kg weight loss withut dieting over the past 4 months. She also has increasing anxiety and nervousness with diarrhea Physical examination shows a diffusely enlarged thyroid gland Her temperature is 37.5, pulse is 103/min, respirations are 28/min, and blood pressure is 140/75 mmHg. What are 3 possible causes of hyperthyroidism? Graves

105
Q

The pt is a 31 y/o woman who has noted increasing fatigue and a 7kg weight loss withut dieting over the past 4 months. She also has increasing anxiety and nervousness with diarrhea Physical examination shows a diffusely enlarged thyroid gland Her temperature is 37.5, pulse is 103/min, respirations are 28/min, and blood pressure is 140/75 mmHg. What are 3 possible causes of hyperthyroidism? Graves

A

“The pt is a 31 y/o woman who has noted increasing fatigue and a 7kg weight loss withut dieting over the past 4 months. She also has increasing anxiety and nervousness with diarrhea Physical examination shows a diffusely enlarged thyroid gland Her temperature is 37.5, pulse is 103/min, respirations are 28/min, and blood pressure is 140/75 mmHg. What are 3 possible causes of hyperthyroidism? Graves

106
Q

42 y/o lady who noticed a neck lump. On examination, a 4.5cm nodule was detected in the thyroid. What is the most common cause of a thyroid nodule? Dominant nodule of a MNG Gross description: - […] - […] - […] Microscopic description (IMPT!!!) - […] - […] - […] Diagnosis? Thyroid follicular adenoma What is the closest differential diagnosis, and how are they differentiated? Thyroid fol

A

“42 y/o lady who noticed a neck lump. On examination, a 4.5cm nodule was detected in the thyroid. What is the most common cause of a thyroid nodule? Dominant nodule of a MNG Gross description: - Rounded, encapsulated well demarcated nodule - Intact capsule - Focal haemorrhage Microscopic description (IMPT!!!) - Completely encapsulated nodule, no capsular or vascular invasion - Follicles of various

107
Q

42 y/o lady who noticed a neck lump. On examination, a 4.5cm nodule was detected in the thyroid. What is the most common cause of a thyroid nodule? Dominant nodule of a MNG Gross description: - Rounded, encapsulated well demarcated nodule - Intact capsule - Focal haemorrhage Microscopic description (IMPT!!!) - Completely encapsulated nodule, no capsular or vascular invasion - Follicles of various

A

“42 y/o lady who noticed a neck lump. On examination, a 4.5cm nodule was detected in the thyroid. What is the most common cause of a thyroid nodule? Dominant nodule of a MNG Gross description: - Rounded, encapsulated well demarcated nodule - Intact capsule - Focal haemorrhage Microscopic description (IMPT!!!) - Completely encapsulated nodule, no capsular or vascular invasion - Follicles of various

108
Q

42 y/o lady who noticed a neck lump. On examination, a 4.5cm nodule was detected in the thyroid. What is the most common cause of a thyroid nodule? […] Gross description: - Rounded, encapsulated well demarcated nodule - Intact capsule - Focal haemorrhage Microscopic description (IMPT!!!) - Completely encapsulated nodule, no capsular or vascular invasion - Follicles of various sizes (mixed macrof

A

“42 y/o lady who noticed a neck lump. On examination, a 4.5cm nodule was detected in the thyroid. What is the most common cause of a thyroid nodule? Dominant nodule of a MNG Gross description: - Rounded, encapsulated well demarcated nodule - Intact capsule - Focal haemorrhage Microscopic description (IMPT!!!) - Completely encapsulated nodule, no capsular or vascular invasion - Follicles of various

109
Q

A 44 y/o otherwise healthy woman feels a small lump on the left side of her neck. A firm, painless 1.5cm cervical lymph node is also palpable. Gross description: - multifocal pale nodules of varying sizes - poorly circumscribed, invasive borders - matted mass of similarly affected extrathyroidal nodules (cervical LN involvement) Microscopic description: (vvv IMPT!!!! can be 5 mark question) - Fine

A

A 44 y/o otherwise healthy woman feels a small lump on the left side of her neck. A firm, painless 1.5cm cervical lymph node is also palpable. Gross description: - multifocal pale nodules of varying sizes - poorly circumscribed, invasive borders - matted mass of similarly affected extrathyroidal nodules (cervical LN involvement) Microscopic description: (vvv IMPT!!!! can be 5 mark question) - Fine

110
Q

A 44 y/o otherwise healthy woman feels a small lump on the left side of her neck. A firm, painless 1.5cm cervical lymph node is also palpable. Gross description: - multifocal pale nodules of varying sizes - poorly circumscribed, invasive borders - matted mass of similarly affected extrathyroidal nodules (cervical LN involvement) Microscopic description: (vvv IMPT!!!! can be 5 mark question) - Fine

A

A 44 y/o otherwise healthy woman feels a small lump on the left side of her neck. A firm, painless 1.5cm cervical lymph node is also palpable. Gross description: - multifocal pale nodules of varying sizes - poorly circumscribed, invasive borders - matted mass of similarly affected extrathyroidal nodules (cervical LN involvement) Microscopic description: (vvv IMPT!!!! can be 5 mark question) - Fine

111
Q

A 44 y/o otherwise healthy woman feels a small lump on the left side of her neck. A firm, painless 1.5cm cervical lymph node is also palpable. Gross description: - […] - […] - […] Microscopic description: (vvv IMPT!!!! can be 5 mark question) - […] - […] - […] - […] - […] - +/- […] Whats the diagnosis? PTC Name 2 other variants. Which variant has the worst prognosis? - Classical

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A 44 y/o otherwise healthy woman feels a small lump on the left side of her neck. A firm, painless 1.5cm cervical lymph node is also palpable. Gross description: - multifocal pale nodules of varying sizes - poorly circumscribed, invasive borders - matted mass of similarly affected extrathyroidal nodules (cervical LN involvement) Microscopic description: (vvv IMPT!!!! can be 5 mark question) - Fine

112
Q

What is abnormal? […] What hormone has caused this? Where is this hormone produced? […] Gross description: - […] Diagnosis? Adrenocortical adenoma

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What is abnormal? Hirsutism What hormone has caused this? Where is this hormone produced? caused by androgen, which is produced in adrenal cortex (other sources also possible) Gross description: - Encapsulated, pale yellow ovoid nodule in adrenal gland Diagnosis? Adrenocortical adenoma

113
Q

What is abnormal? Hirsutism What hormone has caused this? Where is this hormone produced? caused by androgen, which is produced in adrenal cortex (other sources also possible) Gross description: - Encapsulated, pale yellow ovoid nodule in adrenal gland Diagnosis? […]

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What is abnormal? Hirsutism What hormone has caused this? Where is this hormone produced? caused by androgen, which is produced in adrenal cortex (other sources also possible) Gross description: - Encapsulated, pale yellow ovoid nodule in adrenal gland Diagnosis? Adrenocortical adenoma

114
Q

Thyroid Neoplasms - Overview Benign #1 Follicular adenoma #2 Hurthle cell adenoma Malignant Follicular cell origin 3 categories: well-differentiated, poorly differentiated, undifferentiated Well differentiated → […] prognosis - […] carcinoma → […] spread to bone - […] carcinoma - […] carcinoma → […] spread to local nodes Poorly differentiated - Poorly differentiated (insular) carcinoma

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Thyroid Neoplasms - Overview Benign #1 Follicular adenoma #2 Hurthle cell adenoma Malignant Follicular cell origin 3 categories: well-differentiated, poorly differentiated, undifferentiated Well differentiated → good prognosis - Follicular carcinoma → blood-borne spread to bone - Hurthle cell carcinoma - Papillary carcinoma → lymphatic spread to local nodes Poorly differentiated - Poorly different

115
Q

Thyroid Neoplasms - Overview Benign #1 Follicular adenoma #2 Hurthle cell adenoma Malignant Follicular cell origin 3 categories: well-differentiated, poorly differentiated, undifferentiated Well differentiated → good prognosis - Follicular carcinoma → blood-borne spread to bone - Hurthle cell carcinoma - Papillary carcinoma → lymphatic spread to local nodes Poorly differentiated - Poorly different

A

Thyroid Neoplasms - Overview Benign #1 Follicular adenoma #2 Hurthle cell adenoma Malignant Follicular cell origin 3 categories: well-differentiated, poorly differentiated, undifferentiated Well differentiated → good prognosis - Follicular carcinoma → blood-borne spread to bone - Hurthle cell carcinoma - Papillary carcinoma → lymphatic spread to local nodes Poorly differentiated - Poorly different

116
Q

Thyroid Neoplasms - Overview Benign #1 Follicular adenoma #2 Hurthle cell adenoma Malignant Follicular cell origin 3 categories: well-differentiated, poorly differentiated, undifferentiated Well differentiated → good prognosis - Follicular carcinoma → blood-borne spread to bone - Hurthle cell carcinoma - Papillary carcinoma → lymphatic spread to local nodes Poorly differentiated - […] carcinoma

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Thyroid Neoplasms - Overview Benign #1 Follicular adenoma #2 Hurthle cell adenoma Malignant Follicular cell origin 3 categories: well-differentiated, poorly differentiated, undifferentiated Well differentiated → good prognosis - Follicular carcinoma → blood-borne spread to bone - Hurthle cell carcinoma - Papillary carcinoma → lymphatic spread to local nodes Poorly differentiated - Poorly different

117
Q

Thyroid Neoplasms - Overview Benign #1 […] #2 […] Malignant Follicular cell origin 3 categories: well-differentiated, poorly differentiated, undifferentiated Well differentiated → good prognosis - Follicular carcinoma → blood-borne spread to bone - Hurthle cell carcinoma - Papillary carcinoma → lymphatic spread to local nodes Poorly differentiated - Poorly differentiated (insular) carcinoma →

A

Thyroid Neoplasms - Overview Benign #1 Follicular adenoma #2 Hurthle cell adenoma Malignant Follicular cell origin 3 categories: well-differentiated, poorly differentiated, undifferentiated Well differentiated → good prognosis - Follicular carcinoma → blood-borne spread to bone - Hurthle cell carcinoma - Papillary carcinoma → lymphatic spread to local nodes Poorly differentiated - Poorly different

118
Q

Thyroid Neoplasms - Overview Benign #1 Follicular adenoma #2 Hurthle cell adenoma Malignant […] cell origin 3 categories: […], […], […] Well differentiated → good prognosis - Follicular carcinoma → blood-borne spread to bone - Hurthle cell carcinoma - Papillary carcinoma → lymphatic spread to local nodes Poorly differentiated - Poorly differentiated (insular) carcinoma → blood and lymphati

A

Thyroid Neoplasms - Overview Benign #1 Follicular adenoma #2 Hurthle cell adenoma Malignant Follicular cell origin 3 categories: well-differentiated, poorly differentiated, undifferentiated Well differentiated → good prognosis - Follicular carcinoma → blood-borne spread to bone - Hurthle cell carcinoma - Papillary carcinoma → lymphatic spread to local nodes Poorly differentiated - Poorly different

119
Q

“Papillary Thyroid Carcinoma - most common thyroid malignancy, thankfully […] prognosis among the thyroid carcinomas - […] spread - molecular markers: […] Most common variants of papillary carcinoma of thyroid (PTC): 1. […] 2. […] 3. […] 4. Worst: […] Microscopic: Presentation of classical PTC: - Branching of well formed papillae with fibrovascular cores and lining epithelium - Unifo

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“Papillary Thyroid Carcinoma - most common thyroid malignancy, thankfully best prognosis among the thyroid carcinomas - lymphatic spread - molecular markers: RET, BRAF Most common variants of papillary carcinoma of thyroid (PTC): 1. Classical 2. Follicular 3. Encapsulated 4. Worst: Tall cell variant Microscopic: Presentation of classical PTC: - Branching of well formed papillae with fibrovascular

120
Q

Graves Disease T3/T4 level: High TSH: Low (due to negative feedback) Presents as […] goitre +/- […] Clinical triad: - […] - […] (protruding eyes) - […] - only minority Pathogenesis: […] - e.g. […] - TSI most specific for Graves’ - Mimics actions of TSH → increased release of thyroid hormones

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Graves Disease T3/T4 level: High TSH: Low (due to negative feedback) Presents as diffuse goitre +/- bruit Clinical triad: - Hyperthyroidism - Infiltrative ophthalmopathy (protruding eyes) - Infiltrative dermopathy (pretibial myxoedema) - only minority Pathogenesis: autoantibodies to TSH receptor (TRAbs) - e.g. TSI thyroid stimulating immunoglobulin - TSI most specific for Graves’ - Mimics actions

121
Q

Inflammatory ThyroiditisSubacute granulomatous thyroiditis / DeQuervain thyroiditis Likely due to viral infection / post-viral inflammatory process Pathogenesis: virus-induced tissue damage → cytotoxic T lymphocyte response to thyroid antigens → damage follicular cells Clinicals: Short history (weeks) + self limiting; Pain in the neck + goitre; Recent URTI Morphology: Patchy - firm, pale yellowish

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Inflammatory ThyroiditisSubacute granulomatous thyroiditis / DeQuervain thyroiditis Likely due to viral infection / post-viral inflammatory process Pathogenesis: virus-induced tissue damage → cytotoxic T lymphocyte response to thyroid antigens → damage follicular cells Clinicals: Short history (weeks) + self limiting; Pain in the neck + goitre; Recent URTI Morphology: Patchy - firm, pale yellowish

122
Q

Inflammatory ThyroiditisSubacute granulomatous thyroiditis / DeQuervain thyroiditis Likely due to […] / […] inflammatory process Pathogenesis: […] → […] response to thyroid antigens → damage follicular cells Clinicals: Short history (weeks) + self limiting; Pain in the neck + goitre; Recent URTI Morphology: […] with intervening normal parenchyma Destruction of follicles, neutrophils / mi

A

Inflammatory ThyroiditisSubacute granulomatous thyroiditis / DeQuervain thyroiditis Likely due to viral infection / post-viral inflammatory process Pathogenesis: virus-induced tissue damage → cytotoxic T lymphocyte response to thyroid antigens → damage follicular cells Clinicals: Short history (weeks) + self limiting; Pain in the neck + goitre; Recent URTI Morphology: Patchy - firm, pale yellowish

123
Q

is Hashimoto thyroiditis painful? […] What colour is the goitre? (IMPT!!!) […] Biochemistry profile? - T3/T4 […] - TSH […] - Autoantibodies […] Microscopic appearance? - Fibrosis - Immune cell infiltrates (immune cells; lymphocytes, plasma cells, reactive lymphoid follicles) - Thyroid follicles - Atrophic, Hurthle (oncocytic) cell change

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is Hashimoto thyroiditis painful? painless goitre What colour is the goitre? (IMPT!!!) pale ( bc full of lymphocytes) Biochemistry profile? - T3/T4 Down - TSH Up - Autoantibodies Anti-TPO, anti-TSH, anti-Tg Microscopic appearance? - Fibrosis - Immune cell infiltrates (immune cells; lymphocytes, plasma cells, reactive lymphoid follicles) - Thyroid follicles - Atrophic, Hurthle (oncocytic) cell chan

124
Q

What is the clinical triad of Graves Disease? (IMPT!!!) 1. Hyperthyroidism 2. Infiltrative ophthalmopathy/exophthalmos (infiltration by mononuclear inflammatory cells, oedema, accumulation of extracellular matrix e.g. glycosaminoglycans) 3. Infiltrative dermopathy/pretibial myxoedema (only in minority) High risk group: […] Clinical appearance (in addition to the triad): 1. […] 2. […] 3. […

A

What is the clinical triad of Graves Disease? (IMPT!!!) 1. Hyperthyroidism 2. Infiltrative ophthalmopathy/exophthalmos (infiltration by mononuclear inflammatory cells, oedema, accumulation of extracellular matrix e.g. glycosaminoglycans) 3. Infiltrative dermopathy/pretibial myxoedema (only in minority) High risk group: 20-40yo women with family history (AI so always females more at risk!!) Clinica

125
Q

What is the clinical triad of Graves Disease? (IMPT!!!) 1. […] 2. […] 3. […] High risk group: 20-40yo women with family history (AI so always females more at risk!!) Clinical appearance (in addition to the triad): 1. Thyrotoxicosis 2. Diffuse goitre with or without bruit (vascularisation) 3. Exophthalmos & Pretibial myxoedema Gross morphology: 1. Symmetrical diffuse enlargement 2. Soft reddi

A

What is the clinical triad of Graves Disease? (IMPT!!!) 1. Hyperthyroidism 2. Infiltrative ophthalmopathy/exophthalmos (infiltration by mononuclear inflammatory cells, oedema, accumulation of extracellular matrix e.g. glycosaminoglycans) 3. Infiltrative dermopathy/pretibial myxoedema (only in minority) High risk group: 20-40yo women with family history (AI so always females more at risk!!) Clinica

126
Q

Anaplastic carcinoma Risk group: […] Differentiation? […] Prognosis: […] Microscopy: - Highly pleomorphic cells - Giant tumour cells - Spindle cells (sarcomatoid features) - Small anaplastic cells

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Anaplastic carcinoma Risk group: elderly Differentiation? UNDIFFERENTIATED Prognosis: V v v bad. survival in months Microscopy: - Highly pleomorphic cells - Giant tumour cells - Spindle cells (sarcomatoid features) - Small anaplastic cells

Endocrine (13 decks)

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