Endocrine Flashcards

1
Q

Patients with thyroid nodules should be evaluated for what?

A

Malignancy (family history, radiation exposure in childhood, cervical LND), Compressive symptoms (hoarseness, difficulty swallowing), functional status

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2
Q

What is the definitive diagnosis for tyroid cancer?

A

Fine needle aspiration (FNA) however the goal of this clinical assessment is to determine who requires this invasive procedure

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3
Q

What is the initial testing to evaluate thyroid nodule?

A

Serum TSH level, and thyroid ultrasound

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4
Q

What are the suspicious ultrasound findings?

A

Internal vascularity, microcalcifications, hyperechoic, large size

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5
Q

Patients with low TSH, what is the next test and clinical assessment?

A

Iodine 123 scintigraphy

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6
Q

What is the next step in a patient who has no cancer risk factors or suspicious ultrasound findings however has normal or elevated TSH?

A

FNA

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7
Q

When can CT scan of the neck be chosen for diagnosis?

A

Retrosternal goiter in patients with compressive symptoms

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8
Q

What is the primary modality for initial staging of thyroid cancer?

A

Ultrasound of the neck and cervical lymph nodes

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9
Q

Total thyroidectomy is recommended for which patients?

A

Four large papillary thyroid cancer’s, extra thyroid tumor extension, distant metastasis, history of head or neck radiation exposure

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10
Q

Which patients can be managed with simple thyroid lobectomy?

A

Papillary cancer is less than 1 cm microcarcinoma with no lymph node involvement

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11
Q

When is radioactive iodine used?

A

Adjunct therapy for thyroidectomy patience with race for metastasis such as does with very large tumors invasive tumors or lymph node involvement

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12
Q

Non-functioning pituitary adenoma most commonly arises from what type of cells?

A

Gonadotrophin secreting cells (gonadotrophs)

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13
Q

How would the patient present physically and labs who has a nonfunctioning pituitary adenoma?

A

Suppressed LH and FSH, amenorrhea, blurred vision, dyspareunia, increased alpha subunits headaches, mass effect

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14
Q

What are alpha subunits?

A

Dysfunctional cells in most gonadotroph adenomas secrete primarily a common alpha subunit

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15
Q

What is the preferred therapy for most non-functional pituitary adenoma’s? What are the effects that can be expected after?

A

Transphenoidal surgery; Patients may experience rapid relief of associated neurologic symptoms end it may also regain normal gonadal function after resection

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16
Q

What can explain the mild increase in prolactin and nonfunctional pituitary adenoma’s?

A

If a large would be able to compress the pituitary stock and black normal hypothalamic inhibition of prolactin secretion, leading to mild increase in prolactin levels

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17
Q

How can patients with pituitary adenomas be treated for their amenorrhea?

A

Estrogen and progesterone

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18
Q

What is a growth hormone producing add a noma and how can you be treated?

A

Acromegaly. Octreotide hey somatostatin analog ask on somatostatin receptors in the pituitary to inhibit the release of growth hormone

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19
Q

Increased urinary cortisol level, nonsuppressible high dose of dexamethasone suppression test, and undetectable ACTH levels are suggestive of what?

A

Cushing’s syndrome secondary to an adrenal etiology

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20
Q

What is the ideal imaging for adrenal glands?

A

CT scan and MRI have equal sensitivity and specificity for adrenal tumors however you CT scan for less cost for the more MRI as sometimes more useful for for the characterization of adrenal tumors

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21
Q

What is inferior petrosal sinus sampling used for?

A

Differentiate between ACTH production, pituitary versus ectopic

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22
Q

What is the Definition of failure to thrive?

A

Weight below 5th percentile or downtrending weight percentile’s crossing two percentiles 50th 25th 10th

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23
Q

What are the causes of FTT?

A

Inadequate intake, inadequate calorie absorption (cystic fibrosis, celiac disease), increase calorie requirement (hyperthyroidism, congenital heart disease)

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24
Q

What is the first step in patients with FTT?

A

Thorough history and physical examination

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25
Q

What is the most common etiology for FTT?

A

In adequate calorie intake secondary to psychosocial stressors

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26
Q

What are the example of psychosocial stressors that can cause in adequate caloric intake?

A

Poverty (lack of access to food) lack of knowledge of appropriate feeding techniques (excessive water to formula powder ratio), poor parental/child relationship (neglect, abuse)

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27
Q

What is the hormone that induces maternal insulin resistance? And when is it secreted during gestation?

A

Human placenta lactogen; second and third trimesters; insulin resistance and sure as they are sufficient supply of glucose for fetal development.

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28
Q

What patient are at risk for gestational diabetes mellitus GDM?

A

Inadequate pancreatic function

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29
Q

What are the complications that are associated with GDM?

A

Obstetric (preeclampsia) and Neonatal ( hypoglycemia polycythemia)

30
Q

When a patient screamed at for GDM?

A

Patient with risk factors for undiagnosed pre-gestational type two diabetes obesity prior macrosomic and spent our screen as early as the initial prenatal visit. Patient without risk factors are screamed at 24 and 228 weeks gestation

31
Q

What is the approach for screening GDM?

A

Two-step approach: glucose challenge test (GCT) then 3-hour glucose tolerance test (GTT)

32
Q

What is the indication for second step for the two-step approach screening?

A

GCT: Blood glucose level greater or equal to 140 mg over deciliter is an indication for second step

33
Q

How is GM diagnosed?

A

GTT: Fasting blood glucose levels measured one, two, three hours after 100g Glucose load;
When two or more of GTT values are elevated

34
Q

Why is hemoglobin A-1 C level a less sensitive screening test for diabetes and pregnant women?

A

Because it is a lower than normal in pregnant women do to physiologic increases in red blood cell mass and cell turnover

35
Q

What should be monitored in patients with abnormal GTT?

A

Fasting less the 95. postprandial glucose levels At one hour less than 140 at two hours less than 120

36
Q

What are the consequences for poor maternal glycemic control? What should be done to prevent this?

A

Fetal hyperglycemia and hyper-insulinemia, resulting in macrosomia;
Severe maternal hyperglycemia can cause chronic uteroplacental insufficiency and fetal growth restriction; Insulin

37
Q

How would a patient with thyroid Lymphoma present?

A

Chronic lymphocytic infiltration; Mild goiter over years, preexisting Hashimoto thyroiditis, mildly enlarged thyroid gland difficulty swallowing that rapidly worsens, swelling in front of neck growing rapidly recently, fever, night sweats and weight loss, positive Pemberton’s test

38
Q

What is Pemberton’s test?

A

Consist of having a patient rates his arms over his head for up to 60 seconds, the presence of facial plethora or an engorgement of the neck veins is suggestive of thyroid obstruction symptoms

39
Q

What is colloid goiter?

A

Cause for thyroid enlargement in adolescent girls who have normal thyroid function test and negative anti-thyroid antibodies

40
Q

How may patients with Familial Hypocalciuric Hypercalcemia (FHH) present?

A

Asymptomatic hypercalcemia, high normal PTH, low urinary calcium excretion, mildly serum calcium

41
Q

What are the effects of mutated calcium sensor receptor in FHH?

A

Defective calcium sensing receptor causes decreased sensitivity to calcium and higher calcium concentration’s are required to suppress PTH release. Concurrently defective CaSRcauses increased reabsorption of calcium in renal tubule’s

42
Q

What can untreated primary hyperparathyroidism lead to?

A

Osteoporosis, nephrolithiasis, chronic kidney disease

43
Q

FHH and PHPT can’t be differentiated by what?

A

Urinary calcium excretion. FHH is associated with lower urinary calcium levels (less than 100mg/24hrs), PHPT causes increased reabsorption of calcium, net excretion is increased due to accelerated bone turnover (Greater than 300)

44
Q

Diagnosis of FHH is confirmed by what?

A

Testing for CaSR mutations

45
Q

How would a patient with Nelsons syndrome present? Labs and imaging?

A

Tanned patient with bitemporal hemianopsia, history significant for bilateral adrenalectomy for Cushing’s disease; Extremely high ACTH and pituitary adenoma with suprasellar extension on MRI

46
Q

How does craniopharyngioma present?

A

Occur in children can also occur in adults. Present with visual field defect’s and hypopituitarism. Diabetes insipidus is more common compared to Mass Effect

47
Q

Describe the relationship between bitemporal hemianopsia and brain tumors?

A

Brain tumors usually do not present with bitemporal hemi of naps here except for parasellar and intrasellar meningiomas

48
Q

How would a patient with DKA presents?

A

Abdominal discomfort, nausea/vomiting, hyperglycemia with metabolic acidosis and a positive ketones

49
Q

How can DKA be precipitated?

A

Not taking the appropriate dosage of insulin along with some type of stressed like concurrent illness

50
Q

What is the initial management for DKA? How should a risk of hypokalemia be avoided?

A

Aggressive IV fluid support with normal Saline and continuous insulin. Potassium should be monitored and added to IV fluids if Potassium levels are less than 5.2

51
Q

What indicates on going keto acidosis? For how long should I V insulin be continued for?

A

Anion gap with low bicarbonate. IV insulin should be given until anion gap is normalized

52
Q

During the treatment in DKA with IV insulin what is a good indicator of possible hypoglycemia as a complication? What should be done to prevent hypoglycemia?

A

Persistently elevated anion gap with blood glucose less than 200; Insulin dose should be half the end of patients to receive IV fluids with 5% dextrose

53
Q

How was the sodium concentration of IV fluids determine?

A

By finding the corrected serum sodium. If less than 135 should use normal Saline,
If greater than 135 should use half normal saline

54
Q

How do you calculate corrected serum sodium?

A

[(Measures sodium +0.016) times (glucose -100)]

55
Q

What should be done for a patient who had DKA with insulin infusion and the ion gap has normalized along with glucose less than 200?

A

Subcutaneous insulin should be given now and insulin infusion should be stopped in two hours

56
Q

What is the criteria for transition from intravenous insulin to subcutaneous insulin?

A

Glucose less than 200 able to eat and 2/3: serum anion gap less than 12, bicarbonate less than 15, Venus pH greater than 7.3

57
Q

What is the management for DKA and HHS as a pertains to IV fluids?

A

Hi Flo normal Saline is initially recommended

Add dextrose 5% when serum glucose is less than or equal to 200

58
Q

What is the management for DKA and HHS as a pertains to Insulin?

A

Initial continuous IV insulin fusion. Switched to SQ basal bolus if reach criteria. Overlap SQ and IV insulin by 1-2 hours

59
Q

What is the management for DKA and HHS as a pertains to Potassium?

A

Add IV potassium of serum K+ is less than or equal to 5.2

Hold insulin for serum K+ less than 3.3

60
Q

Explain what consists in a patient who is converted to SQ insulin?

A

Combination of long acting insulin basal insulin (glargine, detemir), rapid acting insulin bolus insulin (regular lispro aspart) with meals and correction insulin for hyperglycemia on sliding scale

61
Q

What is the management for DKA and HHS as a pertains to Bicarconate?

A

Consider for patients with severe acidosis (pH less than 6.9) Which can result in decreased cardiac contractility and systemic vasodilation

62
Q

What is the management for DKA and HHS as a pertains to phosphate?

A

Consider for Serum phosphate less than 1mg/dL, cardiac dysfunction or respiratory depression. Monitor serum calcium frequently

63
Q

When a patient with diabetes given high intensity Staten that supposed to moderate intensity Statin?

A

ten-year ASCVD risk equal to or greater than 7.5 will result in high intensity

64
Q

What are the guidelines for Statin therapy?

A

ASCVD, LDL greater than 190, diabetes above age of 40, 10yr risk getter than 7.5

65
Q

What is diabetic retinopathy screening indicated for type one and type two patients? This method mimics what other screening test for diabetic patient?

A

Type 1 beginning 3 to 5 years after original diagnosis, type 2 at the time of diagnosis; Same method is used for nephropathy

66
Q

What is the preferred medication for treating hypertension in patients who are diabetic? What other instance with diabetes should this medication be used?

A

ACEi, Diabetes with Nephropathy

67
Q

What is the difference between physiologic gynecomastia and pseudo gynecomastia? How should it to be differentiated?

A

Pseudogynecomastia are deposits of fat in overweight or obese boys. It’s able to be differentiated by the presence of palpable mass

68
Q

What are the major causes for primary ovarian insufficiency (POI)? What is the treatment?

A

Fragile X syndrome, turner syndrome, autoimmune oophoritis, anticancer drugs pelvic radiation, galactosemia; Estrogen therapy with progestin if intact uterus

69
Q

What is a common gynecological complication associated with cancer treatment (chemotherapy and radiation therapy)?

A

POI

70
Q

What therapy can be used in postmenopausal osteoporosis however it hasn’t been proven to alleviate rapidly loss of bone mass in POI patients?

A

Bisphosphonates and calcitonin as second line agent

71
Q

What is Raloxifene why can it be use for postmenopausal osteoporosis? What are some of the drawbacks?

A

Selective estrogen modulator; Stimulates as your receptors on bone cells to improve density however is antagonistic on other estrogen response of sales and therefore would worsen Hypoestrogen symptoms