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USMLE Endocrine > Endocrine Pathology > Flashcards

Endocrine Pathology Flashcards

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USMLE® Step 1 flashcards
1
Q

What is osmotic demyelination syndrome a result of?

A

SIADH being corrected too quickly

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2
Q

How is SIADH treated?

A
  • Fluid restriction
  • Salt tablets
  • IV hypertonic saline
  • Diuretics
  • ADH antagonists (e.g. conivaptan, tolvaptan, demeclocycline)
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3
Q

What does the body respond to water retention with?

A
  • Decreased aldosterone
  • Increased BNP and BNP
  • Increased urinary Na+ secretion
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4
Q

What are the different causes of SIADH?

A

HELD

  • Head injury/CNS disorders
  • Ectopic ADH (e.g. SCLC)
  • Lung disease
  • Drugs (SSRIs, carbamezpine, cyclophosphamide)
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5
Q

What is diabetes inspidus characterised by?

What is the urine osmolarity?

A
  • Large amounts of dilute urine

- Urine osmolarity usually <300mOsm/kg

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6
Q

What are the 2 types of Diabetes Inspidus?

A
  • Central DI (decreased ADH release)

- Nephrogenic DI (ADH resistance)

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7
Q

What are the possible causes of primary polydipsia (excessive water intake)?

A
  • Psychiatric illness

- Hypothalamic lesions affecting thirst centre

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8
Q

What are causes of central DI?

A
  • Idiopathic
  • Tumours (e.g pituitary)
  • Infiltrative diseases (e.g sarcoidosis)
  • Trauma
  • Surgery
  • Hypoxic encephalopathy
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9
Q

Hoe is central DI treated?

A

Desmopressin

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10
Q

What are the causes of nephrogenic DI?

A
  • Hereditary (ADh receptor mutation)
  • Drugs (lithium, demeclocycline)
  • Hypercalcemia
  • Hypokalemia
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11
Q

In what type of DI is desmopressin effective?

A

Central (causes a significant increase in urine osmolarity ~ 50%)

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12
Q

How is Nephrogenic DI treated?

A
  • Underlying cause treated
  • Low solute diet
  • HCTZ (diuretic)
  • Amiloride (diuretic)
  • Indomethacin (NSAID)
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13
Q

What are the different causes of hypopituitarism?

A
  • Empty Sella syndrome (atrophy/compression, often idiopathic)
  • Sheehan syndrome (Infarct, postpartum)
  • Pituitary apoplexy (hemorrhage)
  • Brain injury
  • Radiation
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14
Q

What are the symptoms/signs of Sheehan syndrome?

A
  • Ischemic infarct of pituitary following postpartum bleeding; pregnancy-induced pituitary growth increases susceptibility to infarction
  • Presents w. failure to lactate, absent menstruation
  • Cold intolerance
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15
Q

What are the causes of empty sella syndrome?

A
  • Atrophy or compression of pituitary
  • Often idiopathic, associated w. idiopathic intracranial hypertension
  • Common in obese females
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16
Q

How can hypopituitarism be treated?

A
  • HRT (corticosteroids, thyroxine, sex steroids, GH)
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17
Q

What is the most common cause of death in gigantism?

A

HF

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18
Q

What are the signs of acromegaly?

A
  • Large tongue w. deep furrows
  • Deep voice
  • Large hands and feet
  • Coarsening of facial features w ageing
  • Frontal bossing (forehead enlarged)
  • Diaphoresis (excessive sweating)
  • Impaired glucose tolerance (insulin resistance)
  • Hypertension
  • Possible colorectal polyps and cancer
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19
Q

How is acromegaly diagnosed?

A
  • Increased serum IGF-1
  • Failure to suppress serum GH following oral glucose tolerance test
  • Pituitary mass seen on brain MRI
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20
Q

How is acromegaly treated?

A
  • Pituitary adenoma resection
  • Treat with octreotide (somatostatin analog) (if not cured)
  • Pegvisomant (GH receptor antagonist)
  • Dopamine antagonist (cabergoline)
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21
Q

What are rarer causes of DM?

A
  • Unopposed secretion of GH and epinephrine

- Patients on glucocorticoid therapy

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22
Q

What are small vessel diseases due to in DM?

A

diffuse thickening of basement membrane

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23
Q

What are the diagnostic cutoffs for fasting plasma glucose?

A

> 126 mg/dL after fasting for > 8 hours

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24
Q

Describe the 2 hour oral glucose tolerance test

A

> 200 mg/dL 2 hours after consumption of 75g of glucose in water

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25
Q

What is required to diagnose diabetes from a random plasma glucose?

A

> 200mg/dL and presence of hyperglycemic symptoms

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26
Q

What is found on histology in type 2 DM?

A

Islet amyloid polypeptide (IAPP) deposits

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27
Q

What is found on histology in type 1 DM?

A

Islet leukocyte infiltrate

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28
Q

What destroys Beta cells in type 1?

A

Autoimmune T-cell-mediated destruction of Beta cells (eg due to presence of glutamic acid decarboxylase antibodies)

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29
Q

What is the genetic predisposition to diabetes like in type 1 and type?

A
  • 50% concordence in identical twins in type 1

- 90% concordance in identical twins in type 2

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30
Q

What is the association between type 1 and HLA system?

A

HLA-DR4 and DR3

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31
Q

What are the causes of increased cortisol ?

A
  • Exogenous corticostroids (decreased ACTH, bilateral adrenal atrophy), most common cause
  • Primary adrenal adenoma, hyperplasia, or carcinoma decreases ACTH and atrophy of uninvolved adrenal gland
  • ACTH screting pituitary
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32
Q

What are the findings in Cushing syndrome?

A
  • Incr Cholsterol
  • Incr Urinary free cortisol
  • Skin changes (thinning striae)
  • Hypertension
  • Immunosuppression
  • Neoplasm
  • Growth restriction (in children)
  • Increased Sugar (hyperglycemia, insulin resistance)
  • Moon facies, amenorrhea, buffalo hump, osteoperosis, incr weight (truncal obesity), hirsuitism
33
Q

How is cushing’s diagnosed?

A
  • Increased free cortisol on 24-hr urinalysis

- Increased late night salivary cortisol, and no suppression with overnight low-dose dexamethasone test

34
Q

What is Nelson syndrome?

A

Enlargement of pre-existing ACTH-secreting pituitary adenoma after bilateral adrenalectomy for refractroy Cushing disease
- Presents with increased ACTH (hyperpigmentation), mass effect (headaches, bitemporal hemianopia)

35
Q

How is Nelson syndrome treated?

A
  • Transsphenoidal resection

- Postoperative pituitary irradation for residual tumour

36
Q

What are the symptoms of adrenal insufficiency?

A
  • Weakness
  • Fatigue
  • Orthostatic hypotension
  • Muscle aches
  • Weight loss
  • GI disturbances
  • Sugar/salt cravings
37
Q

How is adrenal insuffficiency treated?

A

Glucocorticoid/ mineralcorticoid treatment

38
Q

What types of hypercortisolemia has decreased ACTH levels?

A
  • Exogenous steroids

- Adrenal tumour

39
Q

What types of hypercortisolemia have increased ACTH levels?

A
  • Pituitary adenoma (Cushing’s)

- Ectopic ACTH secretion

40
Q

How can ectopic and Cushings hypercortisolemias be differentiated?

A
  • Ectopic cause will not have suppressed ACTH after dexamethasone adminstration - Cushings will
  • CRH stimulation test will cause increased ACTH in Cushing’s and no effect in Ectopic
  • MRI can show pituitary tumour
  • CT of chest/abdo pelvis can show ectopic ACTH secreting gland
41
Q

What is MSH a biproduct of?

A

POMC cleavage

42
Q

What are the causes of Addisons disease? (primary adrenal insifficiency)

A
  • Autoimmune adrenalitis (developed world)

- TB (developing world)

43
Q

What is the eitiology behind acute adrenal insufficiency? (adisonian crisis)

A
  • Acute stressors that increase steroid requirements (e.g. infection)
  • In patients with preexisting adrenal insufficiency or on steroid therapy
44
Q

What may acute adrenal insuffciency (addisonian crisis) present with?

A
  • Acute abdomen
  • N/V
  • Altered mental status
  • Shock
45
Q

What is Waterhous-Friderichsen syndrome?

A

Bilateral adrenal hemorrhage often due to meningococcemia

- May present with w acute adrenal insufficicnecy, fever, petechiae, sepsis

46
Q

Why does hyperpigmentation not occur in secondary and tertiary adrenal insufficiency?

A

Decreased ACTH is the cause of secondary adrenal insufficiency
- Decreased CRH and then ACTH in the case of tertiary

ACTH is thr hormone responsible for the hyperpigmentation

47
Q

Why is there no hyperkalemia in secondary and tertiary adrenal insufficiency?

A

Adrenal gland is functioning and intact so aldosterone sysnthesis is and therefore intact RAAS and no hyperkalemia

48
Q

What is tertiary adrenal insufficiency most commonly due to?

A

Abrupt cessation of chronic steroid therapy

Tertiary from Treatment

49
Q

What are the levels of aldosterone and renin in primary hyperaldosteronism?

A
  • Aldosterone increased

- Renin decreased (treatment resistant)

50
Q

What can secondary hyperaldosteronism be due to?

A
  • Renovascular hypertension
  • Juxtaglomerular cell tumours (renin-producing)
  • Edema (cirrhosis, HF, Nephrotic syndrome)
51
Q

What are examples of neuroendocrine tumours?

A
  • GI system - Carcinoid, gastrinoma
  • Pancreas - Insulinoma, glucagonoma
  • Lungs - SCLC
  • Thyroid - Medullary carcinoma
  • Adrenals - Pheochromocytoma
52
Q

What do neuroendocrine tumours share a common biologic function through?

A

Amine precursor uptake decarboxylase (APUD)

53
Q

How may neuroendocrine tumours be treated?

A
  • Surgery

- Somatostatin analogs (octreotide)

54
Q

What is the most common tumour of the adrenal medulla in children < 4 yrs old?

A

Neuroblastoma

55
Q

What cells does neuroblastoma originate from?

A

Neural crest cells

56
Q

What is the most common presentation of neuroblastoma?

A
  • Abdominal distension
  • Firm, irregular mass
  • Mass can cross midline
  • opsoclonus-myoclonus syndrome (dancing eyes-dancing feet)
57
Q

What can differentiate between neuroblastoma and Wilms tumour?

A
  • Wilms tumour is unilateral cannot cross midline and is smooth
  • Neuroblastoma is irregular mass that can cross midline
58
Q

What is more likely to develop hypertension neuroblastoma or pheochromocytoma?

A

Pheochromocytoma

59
Q

What can be found in urine in neuroblastoma?

A

HVA and VMA (catecholamine metabolites)

60
Q

What can be seen on histology in neuroblastoma?

A

Homer-Wright rosettes (neuroblasts surrounding a central lumen)
- Bombesin and NSE +ve

61
Q

What oncogene is amplified in neuroblastoma?

A

N-myc oncogene

62
Q

What are the symptoms/signs of pheochromocytoma?

A

EPISODIC hyderadrenergic symptoms (5 Ps)

  • Pressure (hypertension)
  • Pain (headache)
  • Perspiration
  • Palpitations (tachycardia)
  • Pallor

May secrete EPO -> polycythemia

63
Q

What is the rule of 10s in relation to pheochromocytoma?

A

10%:

  • Malignant
  • Calcify
  • Bilateral
  • Kids
  • Extra-adrenal (bladder wall, organ of Zuckerkandl)
64
Q

What substances can be found in urine and plasma of pheochromocytoma patients?

A
  • HVA (Homovanillic acid)

- VMA (vanillylmandelic acid)

65
Q

What is pheochromocytoma positive for?

A
  • Chromogranin
  • Synaptophysin
  • NSE
66
Q

How is pheochromocytoma treated?

A
  • Alpha1 blockers (phenoxybenzamine)
  • Beta blockers
  • Tumour resection
67
Q

What does somatostatin in somatostatinoma cause a decrease of (in relation to hormones)?

A
  • Decreased secretin ]
  • CCK
  • Glucagon
  • Insulin
  • Gastrin
  • Gastric inhibitory peptide
68
Q

What will stomatostatinoma present with?

A
  • Diabetes/glucose intolerance
  • Steatorrhea
  • Gallstones
  • Achlorydia (lack of HCl)
69
Q

What are the 6 Ds associated with glucagonoma?

A
  • Dermatitis (necrolytic migratory erythema)
  • Diabetes (hyperglycemia)
  • DVT
  • Declining weight
  • Depression
  • Diarrhoea
70
Q

What is the treatment of glucagonoma?

A

Octreotide/soamtostatin analog and surgical resection

71
Q

What are the symptoms associated with carcinoid syndrome?

A

5-HT in systemic circulation

  • Episodic flushing
  • Diarrhoea
  • Wheezing
  • R sided valvular heart disease (e.g tri regurg, pulmonic stenosis)
  • Niacin deficiency (pellegra)
72
Q

What can be seen on histology in carcinoid tumour?

A
  • Prominent rosettes
  • Chromogranin A positive
  • Synaptophysin positive
73
Q

How is a carcinoid tumour treated?

A
  • Surgical resection
  • Somatostatin analog
  • Tryptophanhydroxylase inhibitor (e.g. telotristat) for symptom control
74
Q

What do neuroendocrine cells secrete in carcinoid tumours and how can this enter systemic circulation to cause carcinoid syndrome?

A

5-HT - can bypass hepatic first pass metabolism and enzymatic breakdown from MAO in lung by metastasising to the liver

75
Q

What is the rule of 1/3 in relation to carcinoid tumours?

A
  • 1/3 metastasise
  • 1/3 present with 2nd malignancy
  • 1/3 are multiple
76
Q

What is Zollinger-Ellison syndrome due to?

A

Gastrin-secreting tumour (gastrinoma) of duodenum or pancreas
- Causes acid hypersecretion -> recurrent duodenal and jejunal ulcers

77
Q

What can ZE syndrome present with?

A
  • Abdo pain (peptic ulcer disease, distal ulcers)

- Diarrhoea (malabsorption)

78
Q

How can Zollinger Ellison syndrome be diagnosed?

A

Positive secretin stimulation test:

- Increased gastrin levels after administration of secretin, which normally inhibits gastrin release

USMLE Endocrine (8 decks)

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