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Mistakes > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Toxic Thyroid Adenoma

A

The hyperplastic thyroid cells autonomously produce thyroid hormone without TSH

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2
Q

Neonatal thyrotoxicosis

A

Got it from her mama (Graves Dz)

Transplacental anti-TSHr Ab
Self-resolves in 3 months (when maternal Ab is gone)

In the meantime, give methimazole & beta blocker

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3
Q

PTH-Independent Hypercalcemia

A

Malignancy
Vitamin D Toxicity
Extrarenal conversion of 25-hydroxyVitD to 1,25 (Sarcoid)

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4
Q

PTH-Dependent Hypercalcemia

A

Primary Hyperparathyroidism
Familial Hypocalicuric Hypercalcemia
Lithium

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5
Q

Why do Addison’s patients get hyperpigmentation?

A

Cosecretion of Melanocyte-stimulating hormone with ACTH

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6
Q

Why do Addison’s patients get vitiligo?

A

Autoimmune destruction of melanocytes

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7
Q

Hyponatremia in endocrine patient

A

Addison’s

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8
Q

Pubertal gynecomastia treatment

A

Reassurance

Resolves in most patients within a few months to 2 years

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9
Q

Werdnig-Hoffman Syndrome

A

AR Disorder

Degeneration of anterior horn cells & cranial nerve motor nuclei.
Floppy Baby (but not botulism)
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10
Q

Baby appears normal at first

Weeks later, develops:
Apathy
Weakness
Hypotonia
Large tongue
Umbilical hernia
A

Congenital hypothyroidism

Familial or sporadic

Most commonly thyroid dysgenesis (Aplasia, hypoplasia or ectopic gland)

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11
Q

Elderly patient has severe thyrotoxicosis

Before radioactive iodine, what do you give them?

A

Methimazole or PTU

Essentially debulk, since radioactive iodine will transiently worsen the hyperthyroidism

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12
Q

Main substrates for gluconeogenesis

A

Gluconeogenic amino acids (from breakdown of muscle)
Main ones: Alanine & Glutamine
Lactate (from anaerobic glycolysis)
Glycerol 3-phosphate (from triacylglycerol in adipose)

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13
Q

Precocious puberty

A

Development of secondary sex characteristics before the age of:

8 in girls
9 in boys

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14
Q

Central precocious puberty

A

FSH is high
LH is high

GnRH is activated

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15
Q

Peripheral precocious puberty

A

FSH is low
LH is low

Gonads or adrenals release excess sex hormones

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16
Q

Clinical features of PCOS

A

Oligo-ovulation
Clinical or biochemical hyperandrogenemia
Polycystic ovaries on imaging
No evidence of another diagnosis

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17
Q

Clinical features of nonclassic CAH (21-hydroxylase Deficiency)

A

Oligo-ovulation
Hyperandrogenemia
Increased 17-hydroxyprogesterone levels

Presents later than infancy (nonclassic)
Teens to twenties

Girls:
Acne
Irregular menses
Hirsutism

Boys:
Precocious puberty

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18
Q

Clinical features of Ovarian/Adrenal tumors

A

Older age
Rapidly progressive symptoms
Increased androgen levels (>3x normal level)

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19
Q

Hyperprolactinemia

A

Amenorrhea
Galactorrhea
Increased prolactin levels

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20
Q

Cushing Syndrome

A

Cushingoid features (moon facies, buffalo hump)
Nonsuppressible dexamethasone suppression test
Increasd 24h urinary free cortisol

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21
Q

Acromegaly

A

Excessive growth
Increased GH
Increased IGF-1

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22
Q

Pathophys of 21-hydroxylase deficiency

A

Neither cortisol nor aldosterone are made
Pituitary increases ACTH to rectify low levels of cortisol
Adrenals undergo hyperplasia
Build-up of 17-hydroxyprogesterone is diverted to androgen synthesis

Meanwhile, aldosterone deficiency causes salt wasting, though hyponatremia is variable

Additionally, androgen excess impairs hypothalamic sensitivity to progesterone

Rapid GNrH secretion
Hypersecretion of LH & FSH
Increased gonadal steroid production

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23
Q

Most common thyroid epithelial malignancy

A

Papillary Thyroid Cancer

Second place is Follicular Thyroid Cancer

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24
Q

Follicular Thyroid Cancer

A

Peak incidence age 40 - 60
Firm thyroid nodule (Cold on scintigraphy)
Often discovered incidentally

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25
Q

FNA of suspected Follicular Thyroid Cancer

A

Useless

Cytologic findings are indistinguishable between follicular thyroid cancer and benign follicular adenomas

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26
Q

How do we tell the difference between Follicular Thyroid Cancer or Benign Follicular Adenomas?

A

Follicular Thyroid Cancer invades the tumor capsule and/or blood vessels

This is a finding on examination AFTER excision

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27
Q

How does Follicular Thyroid Cancer metastasize?

A

Hematogenously to distant tissues

Bone
Lung

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28
Q

Serum calcitonin elevation

A

Medullary Thyroid Carcinoma
Secreted by the parafollicular cells of the thyroid

MEN2

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29
Q

Path findings of Papillary Thyroid Cancer

A

Large cells
Ground glass cytoplasm
Pale nuclei w/ inclusion bodies & central grooving
Grainy, lamellated calcifications (Psammoma Bodies)

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30
Q

Hurthle Cells

A

Large polygonal cells
Eosinophilic cytoplasm
Large quantities of mitochondria

Seen in Follicular Thyroid Cancer
Also seen in Benign Thyroid Adenomas
Also seen in Hashimoto’s Thyroiditis

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31
Q

Patient presents with hyperthyroid symptoms
Undergoes contrast CT
Develops delirium, GI upset, agitation or seizure

A

Thyroid storm. The Iodinated contrast agent induced it!

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32
Q

What can trigger thyroid storm?

A 
Iodine overload
Surgery
Trauma
Infection
Childbirth
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33
Q

What can thyroid storm lead to?

A 
Cardiac arrhythmias
CHF
Seizures
Hypotension
Shock
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34
Q

Metabolic Syndrome

A

Hypertension
Impaired fasting glucose
Dyslipidemia

Overweight w/ central fat distribution (increased waist-to-hip ratio)

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35
Q

Steroids have been suppressing a patient’s HPA Axis
The patient discontinues the steroids
How long does it take for them to start secreting CRH & ACTH again?

A

6 - 12 months

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36
Q

Cortisol and ACTH levels in Central adrenal insufficiency

A

Morning:
Cortisol Low
ACTH Low

Aldosterone Normal

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37
Q

Cortisol and ACTH levels in Primary adrenal insufficiency

A

Morning:
Cortisol Low
ACTH High

Aldosterone Low

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38
Q

In DKA, why are potassium levels often high?

A

Extracellular shift of K (driven by plasma tonicity)
Loss of insulin-dependent potassium uptake

Hyperkalemia results despite total body potassium deficit

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39
Q

Why does DKA result in a total body potassium deficit?

A

Potassium loss in the urine (glucose-induced osmotic diuresis)
Renal elimination of potassium ketoacid salts

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40
Q

When you give insulin to a DKA patient, how do you avoid hypokalemia?

A

Monitor potassium closely

Add potassium to IV fluids once serum K < 5.2

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41
Q

Severe (often) Refractory Hypotension
Vomiting
Abdominal Pain
Fever

A

Adrenal crisis

Primary or due to suppression with steroid use

Treat with hydrocortisone or dexamethasone & aggressive fluid support

Do not wait for lab confirmation

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42
Q

In a patient receiving >20mg/day of prednisone, how soon do you see HPA suppression?

A

3 weeks

Increase doses of glucocorticoids during acute stressors (like surgery). They won’t naturally upregulate, so you have to give a “stress dose”

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43
Q

In a patient receiving 5 - 20mg/day of prednisone, how bad is their HPA suppression?

A

Variable

Pre-op evaluation with early-morning cortisol level is necessary to determine risk

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44
Q

Hypercalcemia of Thiazide use

A

Mild (<12mg/dL)

Rarely symptomatic

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45
Q

Difference between hypercalcemia of malignancy & primary hyperparathyroidism

A

Malignancy = Severe & Rapid Onset

Primary Hyperparathyroid = Gradual increase

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46
Q

How does sarcoidosis lead to hypercalcemia?

A

Extrarenal production of 1,25-dihydroxyvitamin D

Associated with hyperphosphatemia

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47
Q

Hypercalcemia with normal phosphorous

A

Osteolytic malignancies (Breast Cx, MM)

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48
Q

MEN1

A 
Primary Hyperparathyroidism (Hypercalcemia)
Pituitary tumors (Prolactin, visual defects)
Pancreatic tumors (Gastrinoma)
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49
Q

MEN2A

A

Medullary Thyroid Cancer (Calcitonin)
Pheochromocytoma
Parathyroid hyperplasia

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50
Q

MEN2B

A

Medullary Thyroid Cancer
Pheochromocytoma
Mucosal neuromas / Marfanoid habitus

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51
Q

Patient needs a thyroidectomy and their mama died on the table during the exact same procedure.

Other than thyroid storm, what are you worried about?

A

MEN2A or MEN2B

A pheochromocytoma can be asymptomatic at time of diagnosis, but cause fatal intraoperative hypertension

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52
Q

What tests should every patient with medullary thyroid cancer get?

A

Plasma metanephrine assy
RET mutation testing (Chromosome 10)

We’re looking for MEN2A or MEN2B cuz pheos suck, especially during surgery

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53
Q

What is Medullary Thyroid Cancer?

A

Calcitonin-producing tumor
Parafollicular C cells in Thyroid

Oft associated with Pheochromocytoma as part of MEN2A or MEN2B

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54
Q

Patient with hyperinsulinism, but low insulin & C-peptide levels

A

Non-beta cell mesenchymal tumor
Secretes IGF II

Measure serum IGF II for diagnosis

If not, then they are injecting themselves

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55
Q

Necrotic migratory erythema

Elevated blood glucose levels

A

Glucagonoma

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56
Q

Differentiating Solfonylurea use from Beta Cell Tumor

A

Sulfonylurea Use - Proinsulin level often <20% of insulin

Confirm with serum levels of sulfonylurea

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57
Q

Patient with primary hyperaldosteronism is given a diuretic. What do we worry about?

A

Diuretic-induced hypokalemia

Oft do not have peripheral edema due to spontaneous diuresis (aldosterone escape)

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58
Q

Screening test for primary hyperaldosteronism

A

Early morning:
Plasma Aldosterone Concentration
Plasma Renin Activity

Primary Hyperaldo:
Ratio > 20
Plasma Aldosterone > 20

You can only do this test after drugs that alter this ratio (potassium-sparing diuretics) are held for 4 weeks

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59
Q

What drugs alter the Aldosterone/Renin Activity ratio?

A

Spironolactone
Eplerenone
Amiloride
Triamterene

Hold these for 4 weeks before attempting to measure the ratio.

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60
Q

Confirmation test for primary hyperaldosteronism

A

Salt loading
Document inability to suppress serum aldosterone

Then, abdominal CT

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61
Q

Most sensitive test for differentiating adrenal adenoma vs bilateral adrenal hyperplasia (in the absence of a discrete unilateral adrenal mass on imaging)

A

Adrenal venous sampling

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62
Q

Paraneoplastic syndromes from lung cancer

A

SIADH

Lambert-Eaton

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63
Q

Treatment for thyroid storm

A

Beta Blockers (propranolol) for symptoms
Thionamides (PTU) to block new synthesis
Iodine solution to block release of existing hormone
Give the iodine at least 1h after PTU, to present excess incorporation of iodine into thyroid hormone
Glucocorticoids to decrease peripheral conversion of T4 to T3

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64
Q

Amenorrhea with increased TSH

A

Hypothyroidism

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65
Q

Amenorrhea with increased Prolactin

A

Hyperprolactinemia

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66
Q

Amenorrhea with increased LH

A

Premature ovarian failure

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67
Q

Most feared side effect of PTU and Methimazole

A

Agranulocytosis

Occurs within 90 days of treatment
Patient complains of fever and sore throat shortly after beginning treatment

Discontinue the antithyroid agent
Measure WBC
If WBC < 1, discontinue the drug & give a broad spectrum antibiotic with pseudomonal coverage
If WBC <1.5, it probably isn’t the drug causing it

Routine WBC testing to monitor is not cost effective

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68
Q

What serum level of prolactin is diagnostic of a prolactinoma

A

> 200 ng/mL

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69
Q

Calculate Corrected Calcium

A

Measured Calcium + 0.8 (4 - serum albumin)

Low albumin will lower the measured calcium incorrectly

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70
Q

Prokinetic agents (GI)

A

Metoclopramide
Erythromycin
Cisapride

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71
Q

Metabolic abnormalities from hypothyroidism

A

Hyperlipidemia
Hyponatremia
Asymptomatic CK elevations (<10x normal)
Asymptomatic serum transaminase elevations

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72
Q

Hyperlipidemia of hypothyroidism

A

Either cholesterol alone (due to decreased LDL surface receptors and/or decreased LDL receptor activity) or both cholesterol and triglycerides (due to decreased lipoprotein lipase activity)
May take months to resolve despite adequate treatment of hypothyroidism

Statins increase risk of myopathy in poorly-controlled hypothyroidism. Give with caution in these patients.

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73
Q

Mechanism of hyponatremia in hypothyroidism

A

Decreased free water clearance

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74
Q

Anemia of hypothyroidism

A

Normocytic

Normochromic (due to decreased RBC Mass)

75
Q

Anemia of chronic autoimmune thyroiditis

A

Pernicious anemia

Some can have macrocytosis without megaloblastic anemia

76
Q

Preferred initial therapy for primary hyperaldosteronism (nonsurgical)

A

Spironolactone
However, it is a progesterone and androgen receptor antagonist. Decreased libido & gynecomastia in men. Breast tenderness, menstrual irregularities in women.

Eplerenone is a very selective mineralocorticoid antagonist without these side effects, and is alternate therapy.

77
Q

Common side effects of pregabalin

A

Drowsiness
Weight Gain
Fluid Retention

78
Q

Initial treatment for diabetic neuropathy

A 
Tricyclics (Amitriptylline) - Avoid in patients > 65 for anticholinergic effects, avoid in patients with pre-existing cardiac disease due to conduction abnormalities
Dual SSRIs (duloxetine)
Anticonvulsants (Pregabalin, Gabapentin)
79
Q

Indication for FNA of thyroid nodule

A

Normal or high TSH
Cold nodules
Thyroid cancer family history
Suspicious thyroid ultrasound findings

80
Q

Indication for radionuclide scan of thyroid nodule

A

Low TSH

Hot nodules are almost always benign, can be treated for hyperthyroidism

81
Q

What is the most common cause of Primary Adrenal Insufficiency in developed countries?

A

Autoimmune Adrenalitis

Can occur in isolation or in association with other autoimmune syndromes (hypothyroidism, vitiligo)

82
Q

Key differences between Primary Adrenal Insufficiency and Central Adrenal Insufficiency

A

Primary has hyperpigmentation & hyperkalemia

83
Q

Who should be screened for diabetes?

A

BP > 135/80
All patients >= 45 years

Anyone with BMI >25 & risk factors

84
Q

Risk factors for diabetes in patients > 25

A 
Physical inactivity
First degree relative with diabetes
High-risk race/ethnicity (nonwhite)
Women whose birth weight >= 9 lb
History of gestational DM
Hypertension or prior cardiovascular disease
Dyslipidemia (low HDL &amp; high triglycerides)
History of PCOS
History of glucose intolerance
85
Q

Screening tests for diabetes

A

Fasting plasma glucose
2h OGTT
HbA1C

86
Q

How does pregnancy increase thyroid hormone production

A

Estrogen leads to increased Thyroxine Binding Globulin synthesis. More thyroxine is bound, so more is made.

hCG shares an alpha subunit with TSH, so stimulates TSH receptors

87
Q

Management of pregnant patient with baseline hypothyroidism

A

Increase replacement thyroxine dose

88
Q

Euthyroid sick syndrome

A

TFT changes in the setting of severe unrelated illness

Commonly:
Low total & free T3
Normal T4 & TSH

T4 & TSH may decrease further with continued illness.
Thyroid hormone supplementation not helpful

89
Q

Subacute (Granulomatous or De Quervain’s) Thyroiditis

A

Hyperthyroidism
Suppressed TSH

Elevated ESR & CRP
Low radioiodine uptake

Follows acute viral illness
Associated with painful, tender goiter

90
Q

DKA vs Hyperosmolar Hyperglycemic State

A 
DKA:
Type 1
Rapid Onset
Hyperventilation &amp; abdominal pain
Anion gap metabolic acidosis
Serum ketones
Osmolality < 320
Hyperosmolar Hyperglycemic State:
Type 2
Gradual onset
Less hyperventilation &amp; abdominal pain
Normal anion gap, normal bicarb
No (or small) serum ketones
Osmolality > 320
91
Q

Common precipitating factors for Hyperosmolar Hyperglycemic State in DMII patients

A 
Infection
Glucocorticoids
Thiazides
Pentamidine
Atypical Antipsychotics
Interruption of insulin therapy
Trauma or acute illness (stroke, MI)
92
Q

Subclinical hypothyroidism

A

Elevated TSH
Normal T4

T3 stays normal until late stages of hypothyroidism

93
Q

Riedel’s (Fibrous) Thyroiditis

A

Inflammatory disorder

Fibrosclerosis of:
Thyroid
Surrounding Tissues
Often remote nonthyroidal structures (eg retroperitoneum)

Most patients have a hard goiter
Hypothyroidism (Subclinical or overt) may be seen

94
Q

Manifestations of hypocalcemia

A 
Perioral tingling/numbness
Muscle cramps
Tetany
Carpopedal spasms
Seizures
QT Prolongation (sometimes)

If fall in calcium levels is rapid (like in surgical patients), a modest reduction can cause severe symptoms

95
Q

Causes of Primary Hypoparathyroidism

A

Post-Surgical (most common)
Autoimmune
Congenital absence/maldevelopment of parathyroids (DiGeorge Syndrome)
Defective CaSR on parathyroids
Non-autoimmune destruction of parathyroids (Infiltrative diseases: Hemochromatosis, Wilson’s, Irradiation)

96
Q

Most common nonsurgical cause of hypoparathyroidism

A

Autoimmune hypoparathyroidism

97
Q

Drugs that cause Vitamin D deficiency by inducing P450 system

A

Phenytoin
Carbamazepine
Rifampin

98
Q

Causes of calcium precipitation with phosphate in peripheral tissues

A

Renal Failure
Rhabdomyolysis
Phosphate Administration
Acute pancreatitis (calcium soaps in abdominal cavity)
Diffuse Osteoblastic Metastases (Prostate & Breast Cx)

99
Q

Hypocalcemia & Hyperphosphatemia in the presence of normal renal function

A

Hypoparathyroidism

Most likely post-surgical or autoimmune

Non-autoimmune & Defective CaSR possible too

100
Q

Necrolytic Migratory Erythema

A

Erythematous papules/plaques on face, perineum, extremities

Lesions enlarge & coalesce over 7 - 14 days

Central clearing, blistering, crusting, scaling at borders

Seen with glucagonoma

101
Q

Glucagonoma Presentation

A

Necrolytic Migratory Erythema
Diabetes (easily controlled w/ oral agents & diet)
GI Symptoms
Weight Loss
Neuropsych (Ataxia, dementia, proximal weakness)
Association with venous throbmosis

102
Q

Glucagonoma Diagnosis

A

Hyperglycemia
Glucagon > 500
Normocytic, normochromic anemia (either anemia of chronic disease or glucagon’s direct effect on erythropoiesis)
Abdominal imaging (CT or MRI) to localize tumor and/or metastases

103
Q

Carcinoids

A

Slow-growing tumors in distal small intestine, proximal colon & lung

Secrete:
Histamine, serotonin, VIP

104
Q

Where do carcinoids metastasize?

A

Liver

In these cases, the liver can’t metabolize the histamine, serotonin & VIP via first-pass metabolism. This leads to carcinoid syndrome

105
Q

Carcinoid Syndrome

A 
Flushing
Secretory diarrhea
Bronchospasm
Cardiac valvular abnormalities
Niacin Deficiency
106
Q

Niacin Deficiency

A

Pellagra:

Dermatitis
Diarrhea
Dementia

107
Q

Why does Carcinoid Syndrome lead to Niacin Deficiency?

A

Tryptophan is shunted to serotonin and none is left for niacin synthesis

108
Q

Rapid-onset hirsutism (with or without virilization)

A

Androgen-secreting neoplasm (ovaries or adrenals)

109
Q

Primary ovarian androgens

A

Testosterone
Androstenedione
Dehydroepiandrosterone

110
Q

Primary adrenal androgens

A

Testosterone
Androstenedione
Dehydroepiandrosterone
Dehydroepiandrosterone-sulfate (DHEAS)

111
Q

How can you tell the difference between ovarian or adrenal origin of an androgen-secreting neoplasm?

A

DHEAS is normal if the origin is ovarian

DHEAS is elevated if the origin is adrenal

112
Q

Most common cause of short stature & pubertal delay in adolescents

A

Constitutional growth delay

Normal birth weight and height
From 6 months - 3 years, heigh growth velocity slows
3 years old, child develops normal velocity
Follows growth curve at 5th - 10th percentile
Bone age is delayed too
Puberty & adolescent growth spurt are delayed, but eventually occur.
Patient will reach normal adult height

113
Q 
Painless muscle weakness (progressive)
Weight Gain
Bone Loss
Hypertension
Hirsutism
A

Hypercortisolism (Cushing Syndrome)

114
Q

Myopathy in Cushing Syndrome

A

Proximal weakness

Atrophy due to catabolic effects of cortisol on skeletal muscle

115
Q

Hypercalcemia Symptoms

A

Abdominal Pain
Constipation
Polydipsia

116
Q

Medications that increase the risk of Milk-Alkali Syndrome

A

Thiazide Diuretics
ACE Inhibitors
ARBs
NSAIDs

117
Q

Milk-Alkali Syndrome

A 
Hypercalcemia
Hypophosphatemia
Hypomagnesemia
Metabolic Alkalosis
AKI
118
Q

Chronic Autoimmune (Hashimoto) Thyroiditis

A

Hypothyroid features
Diffuse goiter

TPO Antibody
Variable radioiodine uptake

119
Q

Painless Thyroiditis

A

Variant of Hashimoto

Mild, brief hyperthyroid phase
Small, nontender goiter
Spontaneous recovery (also called silent thyroiditis)

TPO Antibody
Low radioiodine uptake

120
Q

How does infection precipitate DKA?

A

Systemic release of insulin counterregulatory hormones (Catecholamines, Cortisol)

Excess glucagon causes hyperglycemia, ketonemia, osmotic diuresis

Renal net loss of potassium, but acidosis and decreased insulin activity leads to increased serum levels despite decreased total body stores

121
Q

Mechanism of fatigue in hyperthyroidism

A

Chronic sympathetic hyperstimulation

122
Q

Acute Thyrotoxic Myopathy

A

Severe Muscle Weakness (proximal or distal)
Without bulbar or respiratory muscle involvement

Weeks to months after onset of hyperthyroidism

Objective findings: Muscle atrophy

Treatment of hyperthyroidism improves the myopathy

123
Q

Primary (Testicular) Hypogonadism in Men - Causes

A

Congenital (Klinefelter, Cryptorchidism)
Drugs (Alkylating Agents, Ketoconazole)
Orchitis (Mumps), trauma, torsion
Chronic kidney disease

124
Q

Secondary (Pituitary/Hypothalamic) Hypogonadism in Men - Causes

A 
Gonadotroph Damage:
Tumor
Cranial trauma
Infiltrative diseases (hemochromatosis)
Apoplexy
Gonadotroph Suppression:
Exogenous androgens
Hyperprolactinemia
DM
Morbid Obesity
125
Q

Combined Primary/Secondary Hypogonadism in Men - Causes

A

Hypercortisolism

Cirrhosis

126
Q

Low LH & Low Testosterone

A

Central Hypopituitarism

127
Q

Low TSH & Low Thyroxine

A

Central Hypothyroidism

128
Q

Central Hypopituitarism & Central Hypothyroidism

A

Nonfunctioning Pituitary Adenoma

Usually arises from gonadotropin-secreting cells (Gonadotrophs) in pituitary gland. These usually secrete LH & FSH, but now only secrete the common alpha-subunit (minimal clinical symptoms)

129
Q

Ways Sheehan Syndrome can present

A

Failure of postpartum lactation
Secondary Adrenal Insufficiency (hypotension & anorexia)
Amenorrhea & Central Hypothyroidism

130
Q

Management of Sheehan Syndrome

A

Replacement of deficient hormones

No effective treatment to restore lactation exists

131
Q

Precocious Puberty with normal bone age

A

Isolated Breast Development - Premature Thelarche
Isolated Pubic Hair - Premature Adrenarche

Reassurance is appropriate
Ultrasound adrenals and ovaries/testes to look for source.

132
Q

Precocious Puberty with advanced bone age

A

High LH - Central Precocious Puberty. Get a contrast MRI to rule out intracranial process. 80% of cases are idiopathic.
Low LH - Peripheral Precocious Puberty (Gonadotropin independent)

If the LH is not initially high, do a GnRH Stimulation test to determine the appropriate LH category.

133
Q

Treatment for Idiopathic Gonadotropin Dependent (central) Precocious Puberty

A

GnRH Agonist Therapy (prevent premature epiphyseal plate fusion, maximize adult height potential)

Make sure you’ve done a contrast MRI first to rule out intracranial tumor. Treatment for that would usually be resection.

134
Q

Danazol

A

Testosterone derivative
Progestin-like effects

Used in combination with GnRH agonists & progestins to treat endometriosis

135
Q

Further evaluation for Gonadotropin Independent (peripheral) Precocious Puberty beyond a low LH

A

Ultrasound of adrenals, ovaries/testes to look for peripheral source

136
Q

Untreated hyperthyroidism can lead to

A

Bone loss (Increased osteoclastic bone resorption)
Osteoporosis
Cardiac Tachyarrythmias
AFib

137
Q

Does myopathy occur in hypothyroidism or hyperthyroidism?

A

Both!

Hypothyroid myopathy or Thyrotoxicosis

In hypothyroid myopathy, CK can be elevated for years before clinical symptoms of hypothyroid appear.
ESR/CRP may be normal

138
Q

Manifestations of hypothyroid myopathy

A

Any of the above:

Asymptomatic CK Elevation
Myalgias
Muscle Hypertrophy
Proximal Myopathy
Rhabdomyolysis
139
Q

Methimazole Adverse Effects

A

Agranulocytosis
1st Semester Teratogen
Cholestasis

140
Q

PTU Adverse Effects

A 
Hepatic Failure (Black Box Warning!)
ANCA Vasculitis
141
Q

Radioiodine Ablation Adverse Effects

A

Permanent Hypothyroidism
Worsening of ophthalmopathy
Possible radiation side effects

142
Q

Surgical Thyroidectomy Adverse Effects

A

Permanent Hypothyroidism
Potential RLN Damage
Potential Hypoparathyroidism

143
Q

Typical manifestations of Acromegaly

A

Coarsening of facial features
Pharyngeal Crowding
Hand/Feet Enlargement

144
Q

What causes acromegaly?

A

Excessive growth hormone secretion
Often from a pituitary somatotroph adenoma

GH induces the liver to produce IGF-1, which causes excessive growth of bone & soft tissues

145
Q

Cardiac manifestations of Acromegaly

A

Concentric Myocardial Hypertrophy
Diastolic Dysfunction
LV Dilation & Global Hypokinesis

Combined with concurrent HTN, OSA & valvular heart disease, can lead to heart failure & arrhythmias.

146
Q

Anti-thyroid peroxidase autoantibodies

A

Painless (silent) thyroiditis

Does not require specific therapy, but beta blocker may be useful for symptomatic control

147
Q

The effect of respiratory alkalosis on calcium homeostasis

A

Hydrogen ions dissociate from albumin
Calcium ions bind in their place
Ionized calcium is lower, though total body stores are constant
Symptoms of hypocalcemia manifest (paresthesias, hypercoagulability, etc)

148
Q

Sequellae of Radioactive Iodine Therapy for Graves

A

Resolution of hyperthyroidism in 6 - 18 weeks
Permanent hypothyroidism in most patients
Worsening of Graves ophthalmopathy

149
Q

Increased IL-6

A

Multiple Myeloma

150
Q

Thyroiditis: Differentiating endogenous thyroid hormone release vs exogenous/factitious thyrotoxicosis

A

High Thyroglobulin - Endogenous release

Low Thyroglobulin - Exogenous use

151
Q

Features of isolated premature adrenarche

A 
Body Odor
Oily Hair/Skin
Acne
Pubic Hair (pubarche)
Axillary hair
Elevated DHEAS, but low Testosterone
152
Q

Euthyroid (Normal TSH) states that increase TBG

A

Estrogens (Pregnancy, OCPs, HRT)
Hepatic Dysfunction (acute hepatitis)
Medications (Tamoxifen)

153
Q

Euthyroid (Normal TSH) states that decrease TBG

A 
Hormonal abnormalities (Cushing's, glucocorticoids)
Hypoproteinemia (Nephrotic Syndrome, Starvation)
Medications (Niacin, high-dose androgens
154
Q

Indications for BRCA Testing

A

FamHx Ovarian Cancer at any age

FamHx Breast Cancer <= 50 in first-degree relative

155
Q

Typical presentation of Thyroid Lymphoma

A

Rapidly enlarging, firm goiter
Compressive symptoms (Dysphagia, Hoarseness)
Systemic B Symptoms (Fever, night sweats, weight loss)

Gland is frequently fixed, and doesn’t move up when swallowing.

More frequent in patients with Pre-existing Hashimoto’s

156
Q

Pemberton Sign

A

When a thyroid lymphoma has retrosternal extension and compresses veins.

The sign is when the patient lifts their arms over their head and venous distension worsens due to compression of subclavians.

157
Q

Positive TPO Antibodies

A

Hashimoto’s Thyroiditis

Treat with levothyroxine even if the patient is asymptomatic. It reduces titers of TPO antibodies, and reduces the risk of miscarriage

158
Q

Primary treatment for papillary thyroid cancer

A

Surgical resection

159
Q

After surgically removing papillary thyroid cancer? who gets adjuvant therapy?

A

Patients at increased risk of recurrence (large tumors, extrathyroidal invasion, lymph node metastasis, incomplete resection)

Radioiodine ablation & suppressive doses of thyroid hormone

160
Q 
Patient 3 - 4 months old
Hypoglycemic (often with seizures)
Lactic acidosis
Hyperuricemia
Hyperlipidemia
Doll-like face
Rounded cheeks
Thin extremities
Short stature
Protuberant abdomen
A

G6PD deficiency

Type 1 Glycogen Storage Disease
Von Gierke Disease

Glycogen builds up in organs and causes damage

161
Q

Diarrhea (Smelly, Floating)
Weight Loss
Bone Pain

A

Steattorhea & Malabsorption
Chylomicron-mediated Vitamin D absorption is interrupted
Hypocalcemia & Hypophosphatemia
Secondary hyperparathyroidism leads to osteomalacia

162
Q

What can cause Vitamin D deficiency?

A

Malabsorption
Intestinal bypass surgery
Celiac sprue
Chronic liver or kidney disease

163
Q

What can cause Osteomalacia

A

Vitamin D deficiency (malabsorption, intestinal bypass surgery, celiac sprue, CKD or chronic liver disease)
Renal tubular acidosis (Proximal, Type 2)
Inadequate calcium intake

164
Q

Paget’s disease of the bone

A

Accelerated focal bone remodeling:
Increased osteoclast activity
Rapid disorganized osteoblast activity

Normal serum calcium, phosphorous and PTH
Markers of bone resorption (c-telopeptide, n-telopeptide) and bone formation (alk phos, osteocalcin) are high

165
Q

C-Telopeptide

N-Telopeptide

A

Markers of bone resorption

166
Q

Osteocalcin

Alkaline Phosphatase

A

Markers of bone formation

167
Q

Lytic bone lesions

A

Metastatic Breast Cancer
Renal Cell Carcinoma
Multiple Myeloma

168
Q

Difference between thyrotoxicosis of painless (silent) thyroiditis & Grave’s disease on scintigraphy

A

Painless thyroiditis - Radioiodine uptake is decreased

Graves - Radioiodine uptake is increased

169
Q

Positive Prussian Blue stain in urine

A

Hemosiderin is present

This indicates hemolysis

170
Q

After getting an antibiotic for a UTI, a dude gets dark pee that stains prussian blue positive

A

G6PD. He’s hemolyzing after getting a sulfa drug

171
Q

Hypothyroid patient becomes pregnant

A

Increase her levothyroxine dose

Increased thyroxine-binding globulin requires more thyroid hormone, but she can’t produce it on her own.

Increase by 30% at the time pregnancy is detected, then adjust every 4 weeks based on TSH

172
Q

Risks of maternal hypothyroidism

A

Gestational hypertension
Preeclampsia
Premature delivery
Postpartum hemorrhage

173
Q

Refeeding syndrome

A

Insulin increases for the first time in forever
Phosphorous, potassium & magnesium flood into the cells and out of the serum
Arrhythmias & cardiopulmonary failure result
Also seizures & wernicke encephalopathy

174
Q

Hypopituitarism

A

Central Adrenal Insufficiency
Hypogonadotropic Hypogonadism
Central hypothyroidism

T4 is low
Cortisol is low
Aldosterone is normal (controlled by RAAS)

175
Q

Most important initial step in managing Hyperosmolar Hyperglycemic State

A

Fluid resuscitation to save them from the osmotic diuresis.

176
Q

Low calcium
High phosphate
High PTH

A

Secondary hyperparathyroidism
Caused by chronic renal failure retaining phosphate, which binds to circulating calcium.
That binding interferes with formation of 1,25 vitamin d
Less calcium is absorbed

177
Q

Metformin: Things to know

A

First agent for most DMII patients
Weight neutral
Low risk of hypoglycemia
Lactic acidosis is a life-threatening complication

178
Q

Sulfonylureas: Things to know

A

Generally added if metformin fails on its own

Weight gain & hypoglycemia are main side effects

179
Q

Thiazoledinediones: Things to know

A

Used if unable to tolerate metformin or sulfonylureas
Side effects: Weight gain, edema, CHF, Bone fracture, bladder cancer
Low risk of hypoglycemia when used alone or with metformin
Can be used in renal insufficiency

180
Q

DPP4 Inhibitors: Things to know

A

Low risk of hypoglycemia
Weight neutral
Can be used in renal insufficiency

181
Q

GLP-1r Agonists: Things to know

A

Possible second agent if metformin fails alone
Especially good if weight loss is desired
Low hypoglycemia risk when used alone or with metformin
Associated with acute pancreatitis

182
Q

When do you just observe a prolactinoma?

A

When it is asymptomatic and < 10mm

183
Q

When do you use dopamine agonists (Cabergoline, Bromocriptine) to treat a prolactinoma?

A

When it is symptomatic and < 3cm

184
Q

When do you resect a prolactinoma?

A

When it is symptomatic and >= 3cm

OR

When it increases in size while on dopamine agonist treatment

Mistakes (8 decks)

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