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Flashcards in UW - Med/Endocrine Deck (58)
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1
Q

What results from elevated GH in acromegaly?

A

Stimulates hepatic production of IGF1

2
Q

What should be measured when there is clinical suspicion of acromegaly?

A

IGF1 - if elevated do oral glucose suppression test (if inadequate suppression of GH, rule in acro)

3
Q

What is neuroleptic maligant syndrome (NMS) and how do you treat?

A

Recent onset of confusion, fever, muscle rigidity, diaphoresis, and CK of 50k, following treatment by dopaminergic antagonist

Tx = dantrolene (muscle relaxant) and bromocriptine/amantadine as 2nd line

4
Q

What should you suspected in someone who is hyperthyroid presenting with mild fever and sore throat?

A

Consider agranulocytosis as a result of Tx w/ PTU or methimazole, making patient susceptible to infection (stop medication immediately)

5
Q

What is the most common thyroid malignancy?

A

90-95% are epithelial and >70% of these are PAPILLARY

6
Q

What is the purpose of the cosynotropin test?

A

ACTH synthetic analog, if it causes a rise in cortisol (>20micrograms in 1 hr) when administered, primary AI can be ruled out. Small rise in cortisol = primary AI

7
Q

What are the initial screening tests for supsected AI (primary/central)?

A

Simultaneous basal early-morning cortisol, adrenocorticotropic hormone (ACTH), and Cosyntropin test

8
Q

What will occur if propranalol is given to a patient with pheochromocytoma?

A

Rapid increase in blood pressure, as a result of unopposed alpha-adrenergic activity

9
Q

What complication are patients with Hashimoto’s Thyroiditis at a higher risk of developing?

A

60x increased risk of thyroid lymphoma

10
Q

What is the main treatment for Grave’s disease and contraindications to this treatment?

A

Radioactive Iodine Therapy - but not w/ pregnancy or very severe opthalmopathy

11
Q

Why is hypertension and hypokalemia more severe w/ ectopic ACTH secretion?

A

High levels of cortisol are produced –> saturate 11-betaHSD (enzyme that converts to inactive cortisone) –> now also bind mineralocorticoid-R causing HTN and HoK+

12
Q

What are the major causes of osteomalacia?

A

Vit. D deficiency as a result of malabsorption, intestinal bypass surgery, celiac sprue, Chronic liver or kidney disease, renal tubular acidosis, inadequate calcium intake

13
Q

What does negative ANA ab rule out?

A

SLE

14
Q

How can you differentiate thyroiditis from Grave’s disease?

A

Thyroiditis - thyrotoxicosis from leakage of thyr hormones into circulation from inflammatory dmg to foliccles, w/ reduced radioactive iodine uptake, often in post partum period (increased rad Iod uptake in Grave’s)

15
Q

What is Osteitis fibrosa cystica (von Recklinghausen disease of bone) and its associated clinical features?

A
  1. Osteoclastic resorption of bone –> replacement w/ fibrous tissue (brown tumor) and bone pain
  2. caused by hyperparathyroid from PT carcinoma
  3. Xray - subperiosteal resorption of bone on radial aspect of middle phalanges, distal clavicular tapering, salt/pepper appearance on skull, bone cysts, and brown tumors of long bones
16
Q

What are the diagnostic criteria for PCOS?

A

> 2-3 of: Androgen excess (hirsituism, acne, androgenic alopecia), Olig/anovulation, Polycystic ovaries on US
AND exclusion of other hyperandrogenic conditions

17
Q

What useful test can be done in suspected PCOS?

A

72 hr oral glucose tolerance test (fasting blood glu and HbA1c if OGTT not feasible)

18
Q

What is the purpose of tight glucose control in diabetes?

A

Decrease incidence of microvascular complications like retinopathy, neuropathy and nephropathy

19
Q

What clinical signs are consistent w/ Grave’s disease?

A

Insomnia, fatigue, weight loss, lid lag, tremor

A-fib from increased sensitivity of beta-adrenoreceptors to sympathetic stimuli

20
Q

What is the reason for the hemolysis due to G6PD deficiency? Clinical features associated with this?

A

Hemolysis precipitated by infections or meds that increase OXIDATIVE STRESS (especially sulfa, or fava beans)

Heinz bodies form in RBC membrane

21
Q

What ion imbalance is prone to occur in patient’s who are hospitalized long term, like after complicated surgery? Which patients are at more risk and how can you treat?

A
  • Hypercalcemia of Immobilization (unknown cause but most likely from increased osteoclastic bone resorption)
  • Pts w/ chronic renal insufficiency at increased risk, may get hyperCa2+ as early as 3 days post immobile
  • Tx: Hydration and bisphosphonates
22
Q

What patients are at increased risk of pseudogout?

A

HyperPTH, post surgical, hypercalcemia

23
Q

What is euthyroid sick syndrome?

A

“Low T3 syndrome” - drop in total/free T3 w/ normal T4 and TSH levels
-Occurs from decreased peripheral deiodination of T4 -> T3 due to caloric deprivation, elevated glucocorticoid, inflammatory cytokine levels, and inhibitor of 5’-monodeiodinase (from free FAs and certain meds)

24
Q

What is Reidel’s thyroiditis?

A

Inflammatory disease causing fibrosclerosis of thyroid, surrounding tissues and remote non-thyroid structures (retroperitoneum)
-Most have hard goiter

25
Q

What is a major risk factor of untreated hyperthyroidism and why?

A

Rapid bone loss from increased osteoclastic bone resorption –> Increased Serum Ca and Urine Ca

26
Q

What are the causes of hypercalcemia w/ low PTH? Normal/elevated PTH?

A

Low - Malignancy, Vit D tox, granulomatous disease (sarcoid)

N/H - Primary hyperparathyroidism

27
Q

How can you differentiate primary from secondary hyperPTH?

A

PTH levels are much higher in secondary vs. primary

Ca levels are low/normal in secondary

Moderate to severe CKD can increase PTH in secondary via feedback mechanism

28
Q

What are common offending medications for hyperK+?

A

Beta blockers, K+ sparing diuretics (AMILORIDE, Triamterene), ACEI, ATRB, NSAIDs

29
Q

How do diabetic foot ulcers form?

A
  • Chronic unnoticed trauma due to advanced peripheral neuropathy and poor wound healing from microvascular insufficiency
  • Often in association w/ Charcot deformity, common on soles of feet over metatarsel heads and tops of toes
30
Q

What are useful signs of hypercalcemia? What could be the cause in an otherwise healthy patient taking lots of supplements?

A
  • Abdominal pain, constipation, polyuria and polydipsia
  • Likely from excessive Vitamin D intake (megadoses of Vit D or multiple V. D containing products)
  • Could also be from Granulomatous disease (sarcoid) or lymphoma
31
Q

What are the signs of malabsorption?

A

Diarrhea, weight loss, edema and vitamin deficiencies

32
Q

How may a patient w/ hypothyroid myopathy?

A

Fatigue, myalgias, proximal muscle weakness, sluggish ankle reflexes, elevated creatine kinase (CK)

33
Q

What are patients w/ diabetes at risk for post-operatively?

A

Necrotizing surgical wounds (gray dishwater fluid draining) -> urgent surgical exploration

34
Q

How can infection precipitate DKA in patients w/ T1DM?

A
  • Systemic release of insulin counterregulatory hormones (catecholamines, cortisol).
  • Excess glucagon –> Hyperglycemia, ketonemia, osmotic diuresis, increased lypolysis (increased FFA))
  • Diuresis -> renal loss of K+, decrease total body K+
35
Q

What renally acting drug can precipitate hyperosmolar hyperglycemic state (HHS, aka HONC) and why?

A

Thiazide diuretics –> reducing intravascular volume, decreases GFR, and activation of counterregulatory hormones (e.g. cortisol & glucagon which increase glucose production)

36
Q

What are the signs/symptoms of glucagonoma?

A

Diabetes mellitus, necrolytic migratory erythema (NME- erythematous papules or plaques, large painful inflamed bilsters), weight loss, diarrhea, and anemia, serum glucagon >500

37
Q

What is urine 5-hydroxyindoleacetic acid excretion and indicator of?

A

Carcinoid syndrome - diarrhea, weight loss, episodic flushing

38
Q

What are the clinical signs and symptoms of panhypopituitarism?

A
  1. Glucocorticoid deficiency (low ACTH, low cortisol) - fatigue, loss of appetite, hypogycemia, hyponatremia, eosinophilia
  2. Testosterone deficiency (low/normal FSH and LH, low testosterone) - low libido, erectile dysfunction
  3. Hypothyroidism (low TSH, low free T4) - cold intolerance, constipation, bradycardia
39
Q

What are patients w/ mild primary hyperaldosteronism prone to developing?

A

Diuretic induced hypokalemia, also possibly met alk and mild hypernatremia

40
Q

What are the major clinical features that can be present in Amyloidosis?

A
  • Asymptomatic proteinuria or nephrotic syndrome
  • Restrictive cardiomyopathy
  • Hepatomegaly
  • Peripheral neuropathy &/or autonomic neuropathy
  • Visible organ enlargement
  • Bleeding diathesis
  • waxy thickening, easy skin bruising
41
Q

How long after having diabetes mellitus does nephropathy usually occur?

A

10-15 years

42
Q

What symptoms are usually present in diabetic retinopathy?

A
  • Asymptomatic until late stage of disease

- poor night vision, curtain falling (w/ vitreous bleed), floaters (during resolution of vitreous bleed)

43
Q

Which thyroid cancers secrete calcitonin?

A

Medullary carcinoma

44
Q

What distinguishes follicular carcinoma on FNA bx? Pathophysiologically?

A
  • Invasion of tumor capsule and blood vessels is necessary to distinguish from follicular adenoma
  • Early hematogenous spread to lung, brain and bone
45
Q

What is the best way to determine a patients risk for diabetic foot ulcers?

A

Monofilament testing -> measures pressure threshold and sensation on bottom of patient’s foot

46
Q

What calcium and phosphate levels are present in V. D deficiency?

A

Low to low-normal serum phosphate and normal serum calcium

47
Q

How can chronic kidney disease lead to calcium and phosphate and hormone imblanace?

A

Phosphate retention –> excess binds calcium –> secondary rise in PTH (also from excess phos)

Phosphate also interferes w/ production of calcitriol –> decreased intestinal calcium absorption

48
Q

What is a key side effect of triamcinolone? How can you confirm?

A

suppressed endogenous pituitary-adrenal axis and put at increased risk for adrenal insufficiency
-Stress dose of steroids

49
Q

What abdominal exam finding can be seen w/ DKA and how should it be treated?

A
  • Generalized abdominal pain w/ guarding
  • Pt should get serial abdominal physical exams and monitor for improvement of symptoms as the acidosis is corrected (if sx don’t improve w/ correction of DKA consider imaging)
50
Q

What lab finding is indicative of lupus anticoagulant (as in antiphospholipid ab syndrome or SLE)?

A

Prolonged PTT

51
Q

What is the effect of oral estrogen therapies on thyroid function?

A

Increases TBG (via decreased clearance), normal patients will increase thyroxine to saturate extra TBGs, but hypothyroid patients will require more levothyroxine

52
Q

What is the effect of chronic liver disease to thyroid hormones?

A

Decreased TBG production -> decreased total free levels of T3/T4

53
Q

What lab findings are consistent w/ Hashimoto’s thyroiditis?

A

-Elevated TSH, low T4, + anti-thyroid peroxidase Abs

54
Q

What is the primary treatment for PCOS?

A

Weight loss and Combined hormonal contraceptive therapy (metformin only for insulin resistance - T2DM)

55
Q

What is the criteria for diagnosing Behcet’s syndrome?

A

Recurrent oral ulcers + 2 of the following (recurrent genital ulcers; eye lesions - anterior/posterior uveitis; retinal vascularization; skin lesions -erythema nodosum, acneiform nodules and populopustuler lesions, +pathergy test)

56
Q

What is the next step in management for asymptomatic hyperparathyroidism? How do you distinguish from Familial HH?

A
  • Neck imaging in preparation for parathyroidectomy (to decrease risk of future complications)
  • familial hypocalciuric hypercalcemia has low urine calcium in comparison
57
Q

What are the main contraindications for antithyroid drugs (PTU, methimazole)?

A

Allergic reaction (2%) and Agranulocytosis (.3%) in both
Meth- 1st trimester teratogen, cholestasis
PTU-Hepatic failure, ANCA vasculitis

58
Q

What comprises MEN2B disorders?

A

Mucosal neuromas, pheochromocytoma, medullary carcinoma of thyroid (marfanoid)