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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
FNA of suspected Follicular Thyroid Cancer
Useless Cytologic findings are indistinguishable between follicular thyroid cancer and benign follicular adenomas
26
How do we tell the difference between Follicular Thyroid Cancer or Benign Follicular Adenomas?
Follicular Thyroid Cancer invades the tumor capsule and/or blood vessels This is a finding on examination AFTER excision
27
How does Follicular Thyroid Cancer metastasize?
Hematogenously to distant tissues Bone Lung
28
Serum calcitonin elevation
Medullary Thyroid Carcinoma Secreted by the parafollicular cells of the thyroid MEN2
29
Path findings of Papillary Thyroid Cancer
Large cells Ground glass cytoplasm Pale nuclei w/ inclusion bodies & central grooving Grainy, lamellated calcifications (Psammoma Bodies)
30
Hurthle Cells
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
31
Patient presents with hyperthyroid symptoms Undergoes contrast CT Develops delirium, GI upset, agitation or seizure
Thyroid storm. The Iodinated contrast agent induced it!
32
What can trigger thyroid storm?
``` Iodine overload Surgery Trauma Infection Childbirth ```
33
What can thyroid storm lead to?
``` Cardiac arrhythmias CHF Seizures Hypotension Shock ```
34
Metabolic Syndrome
Hypertension Impaired fasting glucose Dyslipidemia Overweight w/ central fat distribution (increased waist-to-hip ratio)
35
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?
6 - 12 months
36
Cortisol and ACTH levels in Central adrenal insufficiency
Morning: Cortisol Low ACTH Low Aldosterone Normal
37
Cortisol and ACTH levels in Primary adrenal insufficiency
Morning: Cortisol Low ACTH High Aldosterone Low
38
In DKA, why are potassium levels often high?
Extracellular shift of K (driven by plasma tonicity) Loss of insulin-dependent potassium uptake Hyperkalemia results despite total body potassium deficit
39
Why does DKA result in a total body potassium deficit?
Potassium loss in the urine (glucose-induced osmotic diuresis) Renal elimination of potassium ketoacid salts
40
When you give insulin to a DKA patient, how do you avoid hypokalemia?
Monitor potassium closely | Add potassium to IV fluids once serum K < 5.2
41
Severe (often) Refractory Hypotension Vomiting Abdominal Pain Fever
Adrenal crisis Primary or due to suppression with steroid use Treat with hydrocortisone or dexamethasone & aggressive fluid support Do not wait for lab confirmation
42
In a patient receiving >20mg/day of prednisone, how soon do you see HPA suppression?
3 weeks Increase doses of glucocorticoids during acute stressors (like surgery). They won't naturally upregulate, so you have to give a "stress dose"
43
In a patient receiving 5 - 20mg/day of prednisone, how bad is their HPA suppression?
Variable Pre-op evaluation with early-morning cortisol level is necessary to determine risk
44
Hypercalcemia of Thiazide use
Mild (<12mg/dL) | Rarely symptomatic
45
Difference between hypercalcemia of malignancy & primary hyperparathyroidism
Malignancy = Severe & Rapid Onset | Primary Hyperparathyroid = Gradual increase
46
How does sarcoidosis lead to hypercalcemia?
Extrarenal production of 1,25-dihydroxyvitamin D | Associated with hyperphosphatemia
47
Hypercalcemia with normal phosphorous
Osteolytic malignancies (Breast Cx, MM)
48
MEN1
``` Primary Hyperparathyroidism (Hypercalcemia) Pituitary tumors (Prolactin, visual defects) Pancreatic tumors (Gastrinoma) ```
49
MEN2A
Medullary Thyroid Cancer (Calcitonin) Pheochromocytoma Parathyroid hyperplasia
50
MEN2B
Medullary Thyroid Cancer Pheochromocytoma Mucosal neuromas / Marfanoid habitus
51
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?
MEN2A or MEN2B A pheochromocytoma can be asymptomatic at time of diagnosis, but cause fatal intraoperative hypertension
52
What tests should every patient with medullary thyroid cancer get?
Plasma metanephrine assy RET mutation testing (Chromosome 10) We're looking for MEN2A or MEN2B cuz pheos suck, especially during surgery
53
What is Medullary Thyroid Cancer?
Calcitonin-producing tumor Parafollicular C cells in Thyroid Oft associated with Pheochromocytoma as part of MEN2A or MEN2B
54
Patient with hyperinsulinism, but low insulin & C-peptide levels
Non-beta cell mesenchymal tumor Secretes IGF II Measure serum IGF II for diagnosis If not, then they are injecting themselves
55
Necrotic migratory erythema | Elevated blood glucose levels
Glucagonoma
56
Differentiating Solfonylurea use from Beta Cell Tumor
Sulfonylurea Use - Proinsulin level often <20% of insulin Confirm with serum levels of sulfonylurea
57
Patient with primary hyperaldosteronism is given a diuretic. What do we worry about?
Diuretic-induced hypokalemia Oft do not have peripheral edema due to spontaneous diuresis (aldosterone escape)
58
Screening test for primary hyperaldosteronism
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
59
What drugs alter the Aldosterone/Renin Activity ratio?
Spironolactone Eplerenone Amiloride Triamterene Hold these for 4 weeks before attempting to measure the ratio.
60
Confirmation test for primary hyperaldosteronism
Salt loading Document inability to suppress serum aldosterone Then, abdominal CT
61
Most sensitive test for differentiating adrenal adenoma vs bilateral adrenal hyperplasia (in the absence of a discrete unilateral adrenal mass on imaging)
Adrenal venous sampling
62
Paraneoplastic syndromes from lung cancer
SIADH | Lambert-Eaton
63
Treatment for thyroid storm
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
64
Amenorrhea with increased TSH
Hypothyroidism
65
Amenorrhea with increased Prolactin
Hyperprolactinemia
66
Amenorrhea with increased LH
Premature ovarian failure
67
Most feared side effect of PTU and Methimazole
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
68
What serum level of prolactin is diagnostic of a prolactinoma
>200 ng/mL
69
Calculate Corrected Calcium
Measured Calcium + 0.8 (4 - serum albumin) Low albumin will lower the measured calcium incorrectly
70
Prokinetic agents (GI)
Metoclopramide Erythromycin Cisapride
71
Metabolic abnormalities from hypothyroidism
Hyperlipidemia Hyponatremia Asymptomatic CK elevations (<10x normal) Asymptomatic serum transaminase elevations
72
Hyperlipidemia of hypothyroidism
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.
73
Mechanism of hyponatremia in hypothyroidism
Decreased free water clearance
74
Anemia of hypothyroidism
Normocytic | Normochromic (due to decreased RBC Mass)
75
Anemia of chronic autoimmune thyroiditis
Pernicious anemia Some can have macrocytosis without megaloblastic anemia
76
Preferred initial therapy for primary hyperaldosteronism (nonsurgical)
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
Common side effects of pregabalin
Drowsiness Weight Gain Fluid Retention
78
Initial treatment for diabetic neuropathy
``` 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
Indication for FNA of thyroid nodule
Normal or high TSH Cold nodules Thyroid cancer family history Suspicious thyroid ultrasound findings
80
Indication for radionuclide scan of thyroid nodule
Low TSH Hot nodules are almost always benign, can be treated for hyperthyroidism
81
What is the most common cause of Primary Adrenal Insufficiency in developed countries?
Autoimmune Adrenalitis Can occur in isolation or in association with other autoimmune syndromes (hypothyroidism, vitiligo)
82
Key differences between Primary Adrenal Insufficiency and Central Adrenal Insufficiency
Primary has hyperpigmentation & hyperkalemia
83
Who should be screened for diabetes?
BP > 135/80 All patients >= 45 years Anyone with BMI >25 & risk factors
84
Risk factors for diabetes in patients > 25
``` 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 & high triglycerides) History of PCOS History of glucose intolerance ```
85
Screening tests for diabetes
Fasting plasma glucose 2h OGTT HbA1C
86
How does pregnancy increase thyroid hormone production
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
Management of pregnant patient with baseline hypothyroidism
Increase replacement thyroxine dose
88
Euthyroid sick syndrome
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
Subacute (Granulomatous or De Quervain's) Thyroiditis
Hyperthyroidism Suppressed TSH Elevated ESR & CRP Low radioiodine uptake Follows acute viral illness Associated with painful, tender goiter
90
DKA vs Hyperosmolar Hyperglycemic State
``` DKA: Type 1 Rapid Onset Hyperventilation & abdominal pain Anion gap metabolic acidosis Serum ketones Osmolality < 320 ``` ``` Hyperosmolar Hyperglycemic State: Type 2 Gradual onset Less hyperventilation & abdominal pain Normal anion gap, normal bicarb No (or small) serum ketones Osmolality > 320 ```
91
Common precipitating factors for Hyperosmolar Hyperglycemic State in DMII patients
``` Infection Glucocorticoids Thiazides Pentamidine Atypical Antipsychotics Interruption of insulin therapy Trauma or acute illness (stroke, MI) ```
92
Subclinical hypothyroidism
Elevated TSH Normal T4 T3 stays normal until late stages of hypothyroidism
93
Riedel's (Fibrous) Thyroiditis
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
Manifestations of hypocalcemia
``` 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
Causes of Primary Hypoparathyroidism
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
Most common nonsurgical cause of hypoparathyroidism
Autoimmune hypoparathyroidism
97
Drugs that cause Vitamin D deficiency by inducing P450 system
Phenytoin Carbamazepine Rifampin
98
Causes of calcium precipitation with phosphate in peripheral tissues
Renal Failure Rhabdomyolysis Phosphate Administration Acute pancreatitis (calcium soaps in abdominal cavity) Diffuse Osteoblastic Metastases (Prostate & Breast Cx)
99
Hypocalcemia & Hyperphosphatemia in the presence of normal renal function
Hypoparathyroidism Most likely post-surgical or autoimmune Non-autoimmune & Defective CaSR possible too
100
Necrolytic Migratory Erythema
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
Glucagonoma Presentation
Necrolytic Migratory Erythema Diabetes (easily controlled w/ oral agents & diet) GI Symptoms Weight Loss Neuropsych (Ataxia, dementia, proximal weakness) Association with venous throbmosis
102
Glucagonoma Diagnosis
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
Carcinoids
Slow-growing tumors in distal small intestine, proximal colon & lung Secrete: Histamine, serotonin, VIP
104
Where do carcinoids metastasize?
Liver In these cases, the liver can't metabolize the histamine, serotonin & VIP via first-pass metabolism. This leads to carcinoid syndrome
105
Carcinoid Syndrome
``` Flushing Secretory diarrhea Bronchospasm Cardiac valvular abnormalities Niacin Deficiency ```
106
Niacin Deficiency
Pellagra: Dermatitis Diarrhea Dementia
107
Why does Carcinoid Syndrome lead to Niacin Deficiency?
Tryptophan is shunted to serotonin and none is left for niacin synthesis
108
Rapid-onset hirsutism (with or without virilization)
Androgen-secreting neoplasm (ovaries or adrenals)
109
Primary ovarian androgens
Testosterone Androstenedione Dehydroepiandrosterone
110
Primary adrenal androgens
Testosterone Androstenedione Dehydroepiandrosterone Dehydroepiandrosterone-sulfate (DHEAS)
111
How can you tell the difference between ovarian or adrenal origin of an androgen-secreting neoplasm?
DHEAS is normal if the origin is ovarian | DHEAS is elevated if the origin is adrenal
112
Most common cause of short stature & pubertal delay in adolescents
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
``` Painless muscle weakness (progressive) Weight Gain Bone Loss Hypertension Hirsutism ```
Hypercortisolism (Cushing Syndrome)
114
Myopathy in Cushing Syndrome
Proximal weakness Atrophy due to catabolic effects of cortisol on skeletal muscle
115
Hypercalcemia Symptoms
Abdominal Pain Constipation Polydipsia
116
Medications that increase the risk of Milk-Alkali Syndrome
Thiazide Diuretics ACE Inhibitors ARBs NSAIDs
117
Milk-Alkali Syndrome
``` Hypercalcemia Hypophosphatemia Hypomagnesemia Metabolic Alkalosis AKI ```
118
Chronic Autoimmune (Hashimoto) Thyroiditis
Hypothyroid features Diffuse goiter TPO Antibody Variable radioiodine uptake
119
Painless Thyroiditis
Variant of Hashimoto Mild, brief hyperthyroid phase Small, nontender goiter Spontaneous recovery (also called silent thyroiditis) TPO Antibody Low radioiodine uptake
120
How does infection precipitate DKA?
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
Mechanism of fatigue in hyperthyroidism
Chronic sympathetic hyperstimulation
122
Acute Thyrotoxic Myopathy
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
Primary (Testicular) Hypogonadism in Men - Causes
Congenital (Klinefelter, Cryptorchidism) Drugs (Alkylating Agents, Ketoconazole) Orchitis (Mumps), trauma, torsion Chronic kidney disease
124
Secondary (Pituitary/Hypothalamic) Hypogonadism in Men - Causes
``` Gonadotroph Damage: Tumor Cranial trauma Infiltrative diseases (hemochromatosis) Apoplexy ``` ``` Gonadotroph Suppression: Exogenous androgens Hyperprolactinemia DM Morbid Obesity ```
125
Combined Primary/Secondary Hypogonadism in Men - Causes
Hypercortisolism | Cirrhosis
126
Low LH & Low Testosterone
Central Hypopituitarism
127
Low TSH & Low Thyroxine
Central Hypothyroidism
128
Central Hypopituitarism & Central Hypothyroidism
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
Ways Sheehan Syndrome can present
Failure of postpartum lactation Secondary Adrenal Insufficiency (hypotension & anorexia) Amenorrhea & Central Hypothyroidism
130
Management of Sheehan Syndrome
Replacement of deficient hormones No effective treatment to restore lactation exists
131
Precocious Puberty with normal bone age
Isolated Breast Development - Premature Thelarche Isolated Pubic Hair - Premature Adrenarche Reassurance is appropriate Ultrasound adrenals and ovaries/testes to look for source.
132
Precocious Puberty with advanced bone age
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
Treatment for Idiopathic Gonadotropin Dependent (central) Precocious Puberty
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
Danazol
Testosterone derivative Progestin-like effects Used in combination with GnRH agonists & progestins to treat endometriosis
135
Further evaluation for Gonadotropin Independent (peripheral) Precocious Puberty beyond a low LH
Ultrasound of adrenals, ovaries/testes to look for peripheral source
136
Untreated hyperthyroidism can lead to
Bone loss (Increased osteoclastic bone resorption) Osteoporosis Cardiac Tachyarrythmias AFib
137
Does myopathy occur in hypothyroidism or hyperthyroidism?
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
Manifestations of hypothyroid myopathy
Any of the above: ``` Asymptomatic CK Elevation Myalgias Muscle Hypertrophy Proximal Myopathy Rhabdomyolysis ```
139
Methimazole Adverse Effects
Agranulocytosis 1st Semester Teratogen Cholestasis
140
PTU Adverse Effects
``` Hepatic Failure (Black Box Warning!) ANCA Vasculitis ```
141
Radioiodine Ablation Adverse Effects
Permanent Hypothyroidism Worsening of ophthalmopathy Possible radiation side effects
142
Surgical Thyroidectomy Adverse Effects
Permanent Hypothyroidism Potential RLN Damage Potential Hypoparathyroidism
143
Typical manifestations of Acromegaly
Coarsening of facial features Pharyngeal Crowding Hand/Feet Enlargement
144
What causes acromegaly?
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
Cardiac manifestations of Acromegaly
Concentric Myocardial Hypertrophy Diastolic Dysfunction LV Dilation & Global Hypokinesis Combined with concurrent HTN, OSA & valvular heart disease, can lead to heart failure & arrhythmias.
146
Anti-thyroid peroxidase autoantibodies
Painless (silent) thyroiditis Does not require specific therapy, but beta blocker may be useful for symptomatic control
147
The effect of respiratory alkalosis on calcium homeostasis
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
Sequellae of Radioactive Iodine Therapy for Graves
Resolution of hyperthyroidism in 6 - 18 weeks Permanent hypothyroidism in most patients Worsening of Graves ophthalmopathy
149
Increased IL-6
Multiple Myeloma
150
Thyroiditis: Differentiating endogenous thyroid hormone release vs exogenous/factitious thyrotoxicosis
High Thyroglobulin - Endogenous release | Low Thyroglobulin - Exogenous use
151
Features of isolated premature adrenarche
``` Body Odor Oily Hair/Skin Acne Pubic Hair (pubarche) Axillary hair Elevated DHEAS, but low Testosterone ```
152
Euthyroid (Normal TSH) states that increase TBG
Estrogens (Pregnancy, OCPs, HRT) Hepatic Dysfunction (acute hepatitis) Medications (Tamoxifen)
153
Euthyroid (Normal TSH) states that decrease TBG
``` Hormonal abnormalities (Cushing's, glucocorticoids) Hypoproteinemia (Nephrotic Syndrome, Starvation) Medications (Niacin, high-dose androgens ```
154
Indications for BRCA Testing
FamHx Ovarian Cancer at any age | FamHx Breast Cancer <= 50 in first-degree relative
155
Typical presentation of Thyroid Lymphoma
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
Pemberton Sign
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
Positive TPO Antibodies
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
Primary treatment for papillary thyroid cancer
Surgical resection
159
After surgically removing papillary thyroid cancer? who gets adjuvant therapy?
Patients at increased risk of recurrence (large tumors, extrathyroidal invasion, lymph node metastasis, incomplete resection) Radioiodine ablation & suppressive doses of thyroid hormone
160
``` Patient 3 - 4 months old Hypoglycemic (often with seizures) Lactic acidosis Hyperuricemia Hyperlipidemia ``` ``` Doll-like face Rounded cheeks Thin extremities Short stature Protuberant abdomen ```
G6PD deficiency Type 1 Glycogen Storage Disease Von Gierke Disease Glycogen builds up in organs and causes damage
161
Diarrhea (Smelly, Floating) Weight Loss Bone Pain
Steattorhea & Malabsorption Chylomicron-mediated Vitamin D absorption is interrupted Hypocalcemia & Hypophosphatemia Secondary hyperparathyroidism leads to osteomalacia
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What can cause Vitamin D deficiency?
Malabsorption Intestinal bypass surgery Celiac sprue Chronic liver or kidney disease
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What can cause Osteomalacia
Vitamin D deficiency (malabsorption, intestinal bypass surgery, celiac sprue, CKD or chronic liver disease) Renal tubular acidosis (Proximal, Type 2) Inadequate calcium intake
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Paget's disease of the bone
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
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C-Telopeptide | N-Telopeptide
Markers of bone resorption
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Osteocalcin | Alkaline Phosphatase
Markers of bone formation
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Lytic bone lesions
Metastatic Breast Cancer Renal Cell Carcinoma Multiple Myeloma
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Difference between thyrotoxicosis of painless (silent) thyroiditis & Grave's disease on scintigraphy
Painless thyroiditis - Radioiodine uptake is decreased | Graves - Radioiodine uptake is increased
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Positive Prussian Blue stain in urine
Hemosiderin is present | This indicates hemolysis
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After getting an antibiotic for a UTI, a dude gets dark pee that stains prussian blue positive
G6PD. He's hemolyzing after getting a sulfa drug
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Hypothyroid patient becomes pregnant
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
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Risks of maternal hypothyroidism
Gestational hypertension Preeclampsia Premature delivery Postpartum hemorrhage
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Refeeding syndrome
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
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Hypopituitarism
Central Adrenal Insufficiency Hypogonadotropic Hypogonadism Central hypothyroidism T4 is low Cortisol is low Aldosterone is normal (controlled by RAAS)
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Most important initial step in managing Hyperosmolar Hyperglycemic State
Fluid resuscitation to save them from the osmotic diuresis.
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Low calcium High phosphate High PTH
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
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Metformin: Things to know
First agent for most DMII patients Weight neutral Low risk of hypoglycemia Lactic acidosis is a life-threatening complication
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Sulfonylureas: Things to know
Generally added if metformin fails on its own | Weight gain & hypoglycemia are main side effects
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Thiazoledinediones: Things to know
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
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DPP4 Inhibitors: Things to know
Low risk of hypoglycemia Weight neutral Can be used in renal insufficiency
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GLP-1r Agonists: Things to know
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
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When do you just observe a prolactinoma?
When it is asymptomatic and < 10mm
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When do you use dopamine agonists (Cabergoline, Bromocriptine) to treat a prolactinoma?
When it is symptomatic and < 3cm
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When do you resect a prolactinoma?
When it is symptomatic and >= 3cm OR When it increases in size while on dopamine agonist treatment

Mistakes (8 decks)

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