Internal Med- Endo + Neuro Flashcards
25-year-old man concerned about some “bizarre symptoms” that he has been. He tells you that approximately 6 months ago, he began to experience the following symptoms: headaches, visual defects, weight gain, an appearance of his forehead growing, enlarging hands and feet (he could no longer get his gloves and shoes on), and increased sweating. On examination, mental status is normal, and the apical impulse is felt in the fifth intercostal space, midclavicular line. His blood pressure is 170/ 105 mm Hg. He does have a protruding brow, and three discrete visual field defects are noted (two in the left eye and one in the right eye). His tongue appears enlarged, and he is sweating profusely.
Acromegaly
Etiology of acromegaly
pituitary adenoma that secretes excessive amounts of Growth Hormone; rarely, they are caused by non-pituitary tumors that secrete GHRH
occurs if growth hormone (GH) hypersecretion begins in childhood, before the closure of the epiphyses
Gigantism
Acromegaly involves growth hormone GH hypersecretion beginning in adulthood; a variety of bony and soft tissue abnormalities develop
Whats the difference in Acromegaly vs Gigantism
- Gigantism occurs if growth hormone (GH) hypersecretion begins in childhood, before the closure of the epiphyses
- Acromegaly involves growth hormone GH hypersecretion beginning in adulthood; a variety of bony and soft tissue abnormalities develop
Dx studies for acromegaly
- GH test 2 hour after glucose load
- Increased IGF-1
- MRI/CT shows a pituitary tumor
Tx of acromegaly
Pituitary tumor removal
a 25-year-old male presents complaining of extreme weakness, 20-lb weight loss, lightheadedness, and dizziness. On physical exam, he appears ill, and his blood pressure is 90/70 mm Hg. He has dark skin and hyperpigmented creases on his palms. Serum sodium is low, potassium is elevated; urea level and serum calcium are both elevated as well.
Addisons dz (adrenal insufficiency)
What causes addisons disease
autoimmune factors (70% of cases), infections, or disease within the adrenal gland. This causes a decrease in cortisol secretion and increased ACTH
ADDison’s disease = ADrenal Down or “ADD” hormone to treat ADDison’s
What are the electrolyte findings of primary adrenal insufficiency
HYPERkalemia and HYPOnatremia
What are the secondary causes of adrenal insufficiency?
Deficient secretion of ACTH by the pituitary gland which may be isolated or occur in conjunction with other pituitary hormone deficiencies. ACTH and cortisol levels both are low.
- Secondary factors include a pituitary adenoma or discontinuation of steroid use
Primary or secondary
PITUITARY FAILURE which results in ↓ Cortisol, ↓ ACTH (from pituitary failure), and normal aldosterone with little or no ACTH response with the administration of CRH
Secondary adrenocortical insufficiency
Initial dx for chronic adrenal insufficiency
8 AM serum cortisol + plasma ACTH along with an ACTH stimulation test (should be high dose)
- Elevated ACTH with low cortisol is diagnostic of primary adrenal insufficiency, particularly in patients who are severely stressed or in shock
- Low ACTH and low cortisol suggest secondary or tertiary adrenal insufficiency
What are common lab findings associated with adrenocortical insufficiency
- WBC count with moderate neutropenia, lymphocytosis, and total eosinophil count over 300/μL
- Low serum Na+ (aldosterone causes sodium reabsorption and potassium excretion => low aldosterone = sodium excretion and potassium reabsorption)
- Elevated K+ (aldosterone causes sodium reabsorption and potassium excretion => low aldosterone = sodium excretion and potassium reabsorption)
- Low fasting blood glucose (due to lack of cortisol => cortisol stimulates gluconeogenesis)
What is expected of cortisol levels after giving cosyntropin in a pt with suspected adrenocortical insufficiency
- Cortisol levels are low or fail to rise after giving cosyntropin (ACTH1-24) stimulation test (confirmatory)
Addisons aka primary adrenal insufficiency tx
Steroids + mineralcorticoids
Hydrocortisone or Prednisone + fludrocortison (mineral)
Tx for adrenal crisis
Emergent IV saline, glucose, steroids
Cushing syndrome is caused by
Cushy = too much cortisol→ d/t ACTH excess → Pituitary adenoma
High cortisol, low K+, high BP
Why does cushing disease cause a decrease in potassium?
Cortisol, at high levels, acts like a mineralocorticoid (aldosterone), stimulating the absorption of sodium and excretion of potassium at the collecting tubules. Hence, any disorder involving an excess of mineralocorticoids will cause hypokalemia
Sx of cushings
- Fat redistribution (buffalo hump, moon facies), pigmented striae, obesity, skin atrophy, weight gain, easy bruising, elevated glucose, infections, cataracts, and hirsutism
Why do people gain weight with Cushings?
Cortisol stimulates fat and carbohydrate metabolism for fast energy and stimulates insulin release and maintenance of blood sugar levels. The end result of these actions can be an increase in appetite”
Dx of cushings
- Gold standard test → Twenty-four-hour urine test: A test in which urine is collected for 24 hours to measure the amounts of cortisol. A higher than normal amount in the urine may be a sign of disease in the adrenal cortex
- Dexamethasone suppression test
Tx of cushings
Cushing’s disease (pituitary/secondary) is treated with transsphenoidal surgery
- Cushing syndrome (primary) ectopic or adrenal tumors: the tumor is removed - ketoconazole is given in inoperable patients
- Iatrogenic steroid therapy - begin gradual steroid withdrawal to prevent Addisonian crisis
5-year-old male complaining of an unabated thirst that began three weeks ago. He is constantly drinking and goes to the bathroom around five times a night. He has lost five pounds over the last few weeks. The patient is on lithium for bipolar disorder. His BP is 115/70. The patient’s labs are significant for serum Na of 145 mEq/L (normal: 135-145). Urine osmolality is 185 mOsm/kg, and urine specific gravity is 1.004 (normal: 1.012 to 1.030).
Diabetes insipidus
What causes diabetes insipidus
deficiency of or resistance to vasopressin (ADH), which decreases the kidneys’ ability to reabsorb water, resulting in massive polyuria
2 types of diabetes insipidus
Central → no ADH PRODUCTION
Nephrogenic → ADH produced, but kidney doesnt RECOGNIZE it
MCC for central diabetes insipidus
- No ADH production most common type: idiopathic, autoimmune destruction of posterior pituitary from head trauma, brain tumor, infection, or sarcoidosis
MCC for nephrogenic diabetes insipidus
- Partial or complete insensitivity to ADH: caused by drugs (Lithium, Amphoterrible), hypercalcemia and hypokalemia affect the kidney’s ability to concentrate urine, acute tubular necrosis
Dx of diabetes inspidius
Serum osmolality (concentration) is high (unable to stop the secretion of water into the kidneys so blood becomes more concentrated) and urine osmolality is low because it is so dilute
- Water deprivation test – simplest/most reliable method - continued production of dilute urine despite water deprivation
-
Desmopressin stimulation test:
- Central: reduction in urine output indicating a response to ADH
- Nephrogenic: continued production of dilute urine (no response to ADH) because kidneys can’t respond
Tx of diabetes inspidius
- Central = desmopressin/DDAVP
- Nephrogenic = sodium and protein restriction, HCTZ, indomethacin
11-y/o girl brought to you by her mother who reports weight loss along with increased thirst and urination. The patient has felt tired and nauseous. On examination her weight is below the 5th percentile, she looks thin, and her skin is pale. her blood pressure is 100/70 and her pulse is 104 bpm. Her respirations are deep at a rate of 28 breaths/minute. Her breath smells fruity.
DM type I
Etiology of DM type I
Autoimmune- HLA-DR3/4/O antibodies. Islet cell antibodies
Sx of DM I
- Polyuria, polydipsia, polyphagia, fatigue, and weight loss
- Often first recognized as diabetic ketoacidosis:
- Symptoms: Fruity breath, nausea, vomiting, dehydration
Tx of DM type I
Insulin
What is the Dawn phenomenon
Normal glucose until 2-8 am when it rises. Results from decreased insulin sensitivity and a nightly surge of counter-regulatory hormones during nighttime fasting
- Treat with bedtime injection of NPH to blunt morning hyperglycemia, avoiding carbohydrate snack late at night
What is the somogyi effect
Nocturnal hypoglycemia followed by rebound hyperglycemia due to a surge in growth hormone
- Treat with decreased nighttime NPH dose or give bedtime snack
DKA tx
- Diabetic ketoacidosis (DKA) should always be handled in a hospitalized setting, usually an intensive care unit, and often with an endocrinologist’s consultation, if appropriate.
- TREAT WITH FLUIDS! Patients with DKA are always dehydrated and need large-volume IV fluid resuscitation, usually isotonic fluids such as normal saline. If the corrected serum sodium level is high, this can be reduced to half-normal saline. Insulin should always be administered by an IV pump to guard against accidental overdose.
Dx of DM
- Random blood glucose level of > 200 mg/dL + diabetic symptoms
- 2 separate fasting (8 hours) glucose levels of > 126 mg/dL
- 2-hour plasma glucose of > 200 on an oral glucose tolerance test (3-hour GTT is the gold standard in GDM)
- Hemoglobin A1c of > 6.5%
How often should A1c be checked
Hemoglobin A1c
- Represents mean glucose level from the previous 8-12 weeks (approx lifespan of an RBC)
- Useful to gauge the “big-picture” overall efficacy of glucose control in patients (either Type 1 or Type 2) to assess the need for changes in medication/insulin levels
What is the tx goal of A1c
- Treatment goal of A1c < 7.0%
Tx goal of DM with finger stick glucose monitoring
- seful for insulin-dependent (either type 1 or 2) diabetics to monitor their glucose control and adjust insulin doses according to variations in diet or activity
- Treatment goals: < 130 mg/dL fasting and < 180 mg/dL peak postprandial
Dx of DM type II
random glucose > 200 x two
fasting glucose > 126 x two
A1c of > 6.5%
MC Tx of DM
MC = Metformin decreases hepatic glucose production and peripheral glucose utilization, decreases intestinal glucose absorption (these are reasons it leads to weight loss)
- Side effects: Lactic acidosis, GI side effects, initiation is contraindicated with eGFR <30 mL/min and not recommended with eGFR 30 to 45 mL/min, discontinue 24 hours before contrast and resume 48 hours after with monitoring for creatinine, stop if creatinine is > 1.5
Dx criteria for prediabetes
- A1C 5.7 - 6.4
- Fasting glucose 100 - 125
- 2-hour oral glucose tolerance test 140-199
What are the glucose goals and mgmt of DM
- A1C < 7.0 % check every 3 months if not controlled and 2x per year if controlled
- Preprandial glucose 80-130 mg/dL (60-90 if pregnant)
- Peak postprandial (1 to 2 hours after beginning of the meal) blood glucose < 180 mg/dL
- Annual dilated eye exams, ACEI if microalbuminuria, annual foot examination
-
Blood pressure
- ACC/AHA blood pressure targets - the target for patients with comorbidities is < 130/80
- JNC 8 treatment targets: Reduce BP to < 140/90 mm Hg for everyone < 60 including those with a kidney disorder or diabetes
Bone remodeling disorder that results in formation of unorganized mosaic of woven lamellar bone that is less compact and weaker than normal bone
Pagets disease of bone
What areas does pagets dz of bone MC affect
Pelvis, skull, spine, and legs
RF of pagets dz of bone
Family history
Sx of Pagets dz of bone
Symptomless for long periods of time; When symptoms occur its bone deformities, broken bones, pain in affected area
Dx of Pagets dz of the bone
Xray → Lytic lesions and thickened bone cortices; Bone bx may be done to r/o malig
What are common lab findings in pagets dz of bone
Increase alk phose and osteoclastic and osteoblastic activity
Tx of Pagets dz of bone
Bisphosphonates and calcitonin; Surgery may correct bone deformities, decompress impinged nerves, reduce fractures
Catecholamine secreting adrenal tumor
Pheochromocytoma
Sx of pheochromocytomas
Associated with neurfibromatosis type 1 and Von Hippel-lindau dz
5 Ps → pressure, pain (HA), perspiration, palpitations, palllor
Dx of pheochromocytoma
24hr catecholamines including metabolites
MRI or CT of abd to visualize tumor
Tx of pheochromocytoma
Tx w/ complete adrenalectomy; Preop tx with nonselective a blockade (phenoxybenzamine or phentolamine followed by bblockers to control HTN
MC type of noncancerous tumor in the pituitary gland
Pituitary microadenomas ; less than 1cm in diameter
Macroadenomas are larger than 10mm
Sx of pituitary adenoma
Diminished temporal vision, or bitemporal hemianopsia
Prolactinoma sx
Amenorrhea, galactorrhea, HA;
Location of mass at sella turcica → Mass presses on optic chiasm affecting visition loss
Corticotroph adenoma secretes
ATCH → Overproduction = Cushings syndrome
Study of choice to look for sellar lesions/tumors
MRi
Tx of pituitary tumors
Dopamine agonists → Cabergoline, bromocriptine
Ultimate tx = Transsphenoidal resection of pituitary tumor
MC risk of thyroid cancer
Radiation exposure; MC female 40-60
Sx of thyroid cancer
Hoarse voice; solitary cold nodule on thyroid uptake scan
Thyroid cancer MC type
Papillary carcinoma
Dx of thyroid cancer
US → All lesions>1cm should be biopsied
Smaller lesions can be reevaluated if continues to gro
High risk of malignancy for thyroid cancer found on US
Microcalcifications, solid cold nodule, irregular nodule margins, nodule that is taller than it is wide
To evaluate thyroid malignany, what dx study is done
Thyroid uptake scan; Cancerous does not take up iodine (cold nodule)
Noncancerous will take up iodine (hot nodule)
