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Internal Medicine > Step Up - Endocrine > Flashcards

Step Up - Endocrine Flashcards

1
Q

Provide the four most common causes of hyperthyroidism and a brief description of each.

A

1) Graves disease - 80% of cases, autoimmune disease, thyroid-stimulating IgG. Diffuse involvement.
2) Plummer disease - 15% of cases, hyperfunctioning areas result in low TSH and atrophy of normal part of thyroid gland
3) Toxic thyroid adenoma - 2% of cases, single nodule
4) Hashimoto thyroiditis and subacture thyroiditis - can cause transient hyperthyroidism

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2
Q

Describe the characteristics of the thyroid gland in the following diseases: Graves, subacute thyroiditis, plummer disease, hashimoto’s thyroiditis, toxic adenoma.

A

1) Graves - diffusely enlarged, nontender, bruit may be present
2) Subacute thyroiditis - diffusely enlarged, tender
3) Plummer disease - bumpy, irregular, asymmetric
4) Hashimoto’s - bumpy, irregular, asymmetric
5) Toxic adenoma - single nodule, atrophic gland

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3
Q

Provide 5 symptoms of hyperthyroidism.

A

Nervousness, insomnia, irritability, hand tremor, hyperactivity, tremor, excess sweating, heat intolerance, wt loss, increase appetite, diarrhea, palpitations, muscle weakness

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4
Q

How is hyperthyroidism diagnosed (3)? How is true hyperthyroidism differentiated from conditions that increase TBG?

A

1) Dx:
a) Serum TSH - low
b) T4 and free T4 should be elevated
c) May test T3, but not necessary
2) Radioactive T3 uptake - in hyperthyroidism TBG saturated with T4, thus uptake is low. In states of increased TBG, uptake will be high.

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5
Q

Outline the treatments for hyperthyroidism and provide the indications for each (5).

A

1) Thionamides - Methimazole or PTU - inhibits synthesis and conversion of T4 to T3
2) B - blockers - for acute management of adrenergic symptoms (palpitation, sweating…)
3) Sodium Ipodate - rapidly lowers T3 and T4, appropriate for acute management
4) Radioiodine 131 - destroys thyroid follicular cells. Contraindicated in pregnancy due to cretinism risk.
5) Surgery - for those refractory to medical managment or those who prefer surgery. Significant SE.

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6
Q

Describe the clinical features of thyroid storm (3). How is it treated (4)?

A

1) Hx of hyperthyroidism
2) precipitating factor - infection, DKA…
3) F, tachy, psychosis, GI upset
4) Tx: IV fluids, cooling blankets, PTU Q2H, B-blockers, dexamethasone (stop T4 to T3 conversion).

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7
Q

What are the two most common cause of primary hyperthyroidism? What causes secondary hypothyroidism? What are the clinical findings of secondary hypothyroidism?

A

1) Hashimoto disease, Iatrogenic (radiation, thyroidectomy, lithium)
2) Secondary - cause by deficits in pituitary (tertiary caused by deficit in hypothalamus)
3) Secondary: low TSH and T4

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8
Q

Provide 5 symptoms of hypothyroidism.

A

Symptoms: fatigue, weakness, lethargy, heavy menstuation, weight gain, cold intolerance, constipation, slow mentation, dull expression, muscle weakness, arthralgias, depression, diminished heart sounds

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9
Q

Provide 5 signs of hypothyroidism.

A

Signs: dry skin, course hair, hoarseness, nonpitting edema, carpal tunnel, slow relaxation of reflexes, loss of lateral portion of eyebrows, bradycardia, goiter, URTI

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10
Q

How is hypothyroidism diagnosed (3)? What lab abnormalities may exist (2)

A

1) TSH level - most sensitive. High in primary, low in secondary causes
2) T4 level low, may be normal in subclinical cases.
3) High antimicrosomal antibody in Hashimoto’s
4) Lab abnormalities: normocytic anemia, high LDL and low HDL.

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11
Q

What is the treatment for hypothyroid, how long is it maintained?

A

1) Levothyroxine (T4)

2) Treated indefinitely

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12
Q

Describe the causes, features, diagnosis and treatment of subactue (viral) thyroiditis

A

1) Cause - viral illness
2) Transient hyperthyroidism, euthyroid, then hypothyroid as thyroid is inflammed and leaks all stored T4. Thyroid enlarged and painful.
3) Dx: Radioiodine uptake low, low TSH due to T4 and T3 suppression.
4) Tx: NSAIDs for pain, self-limited

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13
Q

Provide 5 characteristics of a solitary thyroid nodule that is suggestive of malignancy.

A

malignant characteristics: nodule fixed in place, no movement on swallowing, firm consistency, irregular, solitary, Hx of radiation therapy, vocal cord paralysis, cervical adenopathy, elevated serum calcitonin, Fam Hx

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14
Q

Describe the work-up for thyroid nodules (3).

A

1) FNA - reliable for all thyroid cancers except follicular
2) Thyroid Scan - if FNA indeterminate. Cold nodules more likely to be malignant.
3) Thyroid U/S - differentiates solid from cystic, most cancer are solid.

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15
Q

Describe the 4 types of thyroid cancers, their prevalence, and relevant clinical features.

A

1) Papillary carcinoma - 70-80% of cases, slow growing, Hx of radiation, positive iodine uptake
2) Follicular carcinoma - 15% of cases, slow growing but more malignant (hematologic spread), most are radioiodine sensitive
3) Medullary carcinoma - 2-3% of cases, C cells, 2nd most malignant
4) Anaplastic carcinoma - 5%, highly malignant

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16
Q

What is the treatment for papillary, follicular, medullary, and anaplastic thyroid tumors?

A

1) Papillary - lobectomy or thyroidectomy, iodine ablation
2) Follicular - thyroidectomy, iodine ablation
3) Medullary - thyroidectomy
4) Anaplastic - Palliative chem/rad.

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17
Q

What size is used to differentiate micro from macro-adenoma? What are clinical features of pituitary adenomas (3)? How are they diagnosed? How are they treated?

A

1) 1.0cm
2) Features
a) Hypersecretion of prolactin, GH, ACTH, TSH
b) Hypopituitarism - lack of GH or LH/FSH
c) Mass effect - headache, visual distrubance
3) Dx - MRI
4) Transsphenoidal surgery

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18
Q

What are the hormones of the anterior pituitary gland (6)?

A 
GH
Prolactin
LH/FSH
ACTH
TSH
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19
Q

Provide 3 common causes for hyperprolactinemia

A

Causes: prolactinoma (pituitary adenoma), medications, pregnancy, renal failure, suprasellar mass lesions, hypothyroidsm, idiopathic

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20
Q

What are the clinical features of prolactinemia in men (8) vs. women (7)?

A

Men: hypogonadism, low libido, infertility, impotence, galatorrhea, gynecomastia, headache, visual field disturbance
Women:
a) pre-menopausal: menstrual irregularities, infertility, low libido, dysparunia, osteoparosis, galactorrhea
b) post-menopausal: mass effect - headache and visual disturbance

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21
Q

How is prolactinemia diagnosed (3)? How is it treated (3)?

A

1) Dx: high serum prolactin, do pregnancy and TSH test as they are on DDx, MRI/CT for cranial mass
2) Tx: treat underlying cause, if prolactinoma - treat with Bromocriptine or Cabergoline, surgery if refractory to therapy.

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22
Q

What hormone is involved in acromegaly? What are common clinical features (3)? How is it diagnosed (3)? What is the appropriate treatment?

A

1) GH
2) features
a) growth promotion - large hands/feet/head, organomegaly, enlarged jaw
b) Metabolic disturbances - glucose intolerance
c) Parasellar manifestation - headache, visual fields, HTN, sleep apnea
3) Dx: high IGF-1, GH not suppressed with glc load, MRI
4) Transsphenoidal resection

23
Q

What are the features of diabetes insipidus (3)? What are the two types? How are they differentiated? How are they treated?

A

1) features: polyuria (5-15L), thirst and polydipsia, hypernatremia
2) Types:
a) Central - low ADH secretion
b) Nephrogenic - kidney non-responsive to ADH
3) Dx:
- water deprivation: if concentrated urine produced, then primary polydipsia
- Desmopressin test: if urine concentrates, then Central DI
4) Tx:
a) Central - DDAVP, treat underlying cause
b) Nephrogenic - Na restriction, and thiazide diuretics.

24
Q

What are the clinical features of SIADH (5)? How is it diagnosed, what are common lab abnormalities seen (3)? How is it treated?

A

1) Features: hyponatremia -> lethargy, weakness, coma, seizures, death.
2) Dx: Dx of exclusion
Labs: hyponatremia, concentrate urine, low BUN and creatinine
3) Tx: typically water restriction, NS or hypertonic saline if severe

25
Q

What is the risk of rapidly correcting hyponatremia in SIADH?

A

Central Pontine Myelinolysis

26
Q

What is the typical cause of hypoparathyroidism? What are some common clinical features (4)? How is it diagnosed (3)? How is it treated (2)?

A

1) Thyroid surgery
2) features: arrhythmia, paresthesia, rickets or osteomalacia, prolonged QT interval
3) Dx: low serum Ca, high serum Phos, low serum PTH
4) Tx: Calcium and vit D supplementation

27
Q

What are the clinical features of hyperparathyroidism (4)? How is it diagnosed (2)? How is it treated (2)?

A

1) Features
a) Stones
b) bones
c) groans - muscle pain, gout, PUD
d) psych overtones - depression, fatigue
2) Dx
a) Labs - high Ca, high PTH, low phos, chloride/phosphous ratio > 33.
b) Xrays - subperiosteal bone resorption
3) Tx
a) Surgery
b) Medical - Lasix to promote calciuria

28
Q

What are the four most common causes of cushing syndrome?

A

1) Iatrogenic - steroid administration
2) ACTH-secreting pituitary adenoma (Cushing’s disease) - Androgen excess common
3) Adrenal adenoma
4) Ectopic ACTH production - typically SCC of lung

29
Q

Describe the clinical features of cushing’s syndrome (5)

A

Features: central obesity, hirsutism, moon facies, ‘buffalo hump’, striae on abdo, lanugo, acne, easy bruising, HTN, glucose intolerance, hypogonadism, masculinization in females (in ACTH dependent forms), proximal muscle wasting, weakness, osteoporosis, depression, mania, infection risk increased

30
Q

How is Cushing’s Syndrome diagnosed (4)?

A

1) Low dose dexamethasone test - positive if morning cortisol >5.
2) High-dose dexamethasone test - determines etiology. Pituitary tumors will be suppressed by large dose.
3) Alternatively, 24hr urine free cortisol test
4) MRI/CT area of interest

31
Q

How is Cushing’s syndrome treated (2)?

A

1) Taper dose if iatrogenic cause

2) Surgery for other etiologies if possible.

32
Q

Where do pheochromocytomas typically originate from? What cell line do they arise from? What are the clinical features (6)?

A

1) 90% of cases from adrenal medulla
2) Arise from chromaffin cells
3) Features: HTN, severe headache, tachycardia, palpitations, anxiety. Lab abnormalities: high glc, high lipids, low K.

33
Q

What tests are used to diagnose pheochromocytoma (2)? How is it treated (3)?

A

1) Dx: Urine catecholamine degradation products - metanephrine, vanillylmandelic acids. MRI/CT for localization.
2) Tx: Surgical resection. a- and b-blockade prior to surgery for BP and HR control.

34
Q

What are the two most common causes of primary hyperaldosteronism? What are the clinical features (4)?

A

1) Causes: adrenal adenoma, bilateral adrenal hypertrophy

2) Clinically: high BP, headache, polydipsia, absence of pitting edema

35
Q

How is primary hyperaldosteronism diagnosed (3)? How is it treated (2)?

A

1) Dx: aldosterone-renin ratio >30, saline infusion test and monitor aldosterone response, CT/MRI
2) Tx: if adenoma, resect. If bilateral hypertrophy, spironolactone.

36
Q

What is MEN Syndrome? Describe the associated tumors in MEN type 1 (hint: 3Ps), MEN type 2a (hint: MPH), and MEN type 2b (hint: MMMP).

A

1) Autosomal dominant disease, increased likelihood of developing multiple endocrine tumors.
2) MEN type 1: Parathyroid hyperplasia, Pancreatic islet cell tumor, Pituitary tumor
3) MEN type 2a: Medullary thyroid carcinoma, pheo, hyperparathyroidism
4) MEN type 2b: Mucosal neuromas, medullary thryoid carcinoma, marfan-like body, pheo

37
Q

What are the common causes of primary (2) and secondary (1) adrenal insufficiency? What are the clinical features of adrenal insufficiency (5)?

A

1) Primary: Addison’s, TB
2) Secondary: long-term steroid therapy (low ACTH)
3) Clinically: low cortisol (N/V, wt loss, hypoglycemia, hyperpigmentation (primary only)). Low aldosterone (primary only, hyponatremia, hyperkalemia)

38
Q

How is adrenal insufficiency diagnosed (3)? How is it treated ()?

A

1) Dx:
a) low plasma cortisol, low plasma ACTH (in secondary)
b) ACTH test - cortisol does not respond effectively (does not differentiate primary from secondary).
c) CT/MRI if secondary/tertiary
2) Tx:
a) Primary - supplement glucocorticoid (hydrocortisone, prednisone) and mineralocorticoid (fludrocortisone)
b) secondary - replace glucocorticoid, no mineralocorticoid needed.

39
Q

What is the most common cause of congenital adrenal hyperplasia? What are the clinical features (2)? How is it diagnosed? How is it treated (2)?

A

1) 21-hydroxylase deficiency (AR disease)
2) Features - virilization of females (ambiguous genitals), salt wasting (low aldosterone)
3) Diagnosis - high serum 17-hydroxyprogesterone
4) Tx: provide mineralo- and glucocorticoid supplementation (reduces high ACTH). Surgically correct genitals.

40
Q

Discuss the onset, age of onset, body habitus, ketosis, antoantibodies, endogenous insulin, HLA association, and genetic factors assosicated with type 1 DM.

A

1) Onset - sudden
2) Age of onset - young (less than 20)
3) Body Habitus - thin
4) Ketosis - common
5) Autoantibodies - present typically
6) Endogenous Insulin - low or absent
7) HLA - Yes (HLA-DQ/DR)
8) Genetic factors - 50% concordance in twins

41
Q

Discuss the onset, age of onset, body habitus, ketosis, antoantibodies, endogenous insulin, HLA association, and genetic factors assosicated with type 2 DM.

A

1) Onset - gradual
2) Age of onset - adults
3) Body Habitus - obese
4) Ketosis - rare
5) Autoantibodies - absent
6) Endogenous Insulin - low, normal, or high
7) HLA - No
8) Genetic factors - 90% concordance in twins

42
Q

How is diabetes diagnosed (4)?

A

1) 2 fasting BG >7
2) Single random BG >11.1, with symptoms
3) OGTT with 2-hr PP BG>11.1
4) HgB A1C >6.5%

43
Q

Discuss the Dawn and Somogyi effect wrt DM. When should evening insulin be increased?

A
  • both result in morning hyperglycemia
    1) Dawn - morning hyperglycemia due to physiologic noctural release of GH
    2) Somogyi - morning hyperglycemia due to reflexive mechanisms created by noctural hypoglycemia.
  • measure BG at 3am. If high, then Dawn effect, and increase evening insulin
44
Q

Describe the general outpatient approach to treating diabetic patients (10).

A

1) HbA1c every 3 months, goal is less than 7.
2) Pts should measure BG at home, before meals and at HS
3) Screen for urine protein, ACEi if positive
4) Check urea and creatinine
5) Eye screening yearly
6) Check feet each visit
7) Statin if LDL >100
8) ACEi or ARB if BP >130/80
9) Daily aspirin if >30yo
10) pneumococcal vaccine

45
Q

What are the symptoms of DM (7)?

A

1) Polyuria - glc induced osmotic diuresis
2) Polydipsia
3) Fatigue
4) Wt loss
5) Blurred vision
6) Fungal infections - candida
7) Numbness and tingling - stocking, glove

46
Q

Provide 4 oral hypoglycemic drugs that are used in the treatment of DM2. What are there mechanisms of action?

A

1) Sulfonylureas - stimulate pancreas to produce more insulin
2) Metformin - increases insulin sensitivity
3) Acarbose - decreases gut glc uptake
4) Thiazolidinediones - increase insulin sensitivity in muscle and fat tissue.

47
Q

What is the time of onset and duration of action for the commonly used insulins: lispro, regular, and NPH?

A

1) Lispro - onset 15 min, duration 2-4hrs
2) Regular - onset 30-60 mins, duration 4-6hrs
3) NPH - onset 2-4 hrs, 18-28hrs

48
Q

What is considered good control of diabetes wrt HbA1c, fasting BG, and postprandial BG?

A

1) HgA1c - less than 7%
2) Fasting less than 7
3) PP less than 10

49
Q

Describe the macrovascular complications of DM. What are the target ranges for treatment (2)? How do the macrovascular complications manifest (3)?

A

1) Increased rate of arthrosclerosis - CAD is most common cause of death in DM patients.
2) Targets: BP less than 130/80, LDL less than 100
3) Manifestations
a) CAD - increased risk MI and CHF
b) PVD
c) Stroke

50
Q

Describe the 3 microvascular complications of DM. How are they monitored and prevented/treated?

A

1) Diabetic nephropathy - starts with microalbuminuria (30-300 mg/day), risk of progression to proteinuria and ESRD, treat with ACEi
2) Diabetic retinopathy - both nonproliferative and proliferative retinopathy occur. Risk of blindness, retinal detachment, vitrious hemorrhage. Annual eye screening, laser photocoagulation
3) Diabetic neuropathy - tight sugar control important for prevention. NSAIDs, gabapentin, TCAs for tx.

51
Q

What lab abnormalities are seen in DKA (4)?

A

1) Hyperglycemia, often >25
2) AG metabolic acidosis
3) Ketonemia - b-hydroxybutyrate
4) Other electorlyte imbalances - Na, K, Mg, phos

52
Q

How is DKA treated (3)?

A

1) IV insulin - close AG and correct met. acidosis
2) Fluids - NS, then D5NS once BG = 14.
3) KCL IV
- dont give bicarb

53
Q

What is hyperosmolar hyperglycemic nonketotic syndrome? Who does it affect? What are the features? How is it treated?

A

1) severe hyperglycemia with dehydration due to osmotic diuresis
2) Affects elderly DM2 patients
3) No acidosis or ketosis as there is a small amount of insulin present. BG often >45
4) Tx: fluid replacement, IV insulin, D5NS at BG=14.

54
Q

What test can differentiate hypoglycemia from insulinoma from surreptitious insulin injection?

A

C-peptide level (only present in endogenous insulin)

Internal Medicine (9 decks)

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