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2024 - Élo - LMCC > Internal Medicine > Flashcards

Internal Medicine Flashcards

1
Q

How to differentiate between primary hyperparathyroidism and familial hyperparathyroid syndromes?

A

Urinary calcium excretion (24-hour urinary calcium or calcium-to-creatinine ratio) should be measured to differentiate between familial hypocalciuric hypercalcemia

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2
Q

In your approach to the etiology of hypercalcemia what should you measure first?

A

PTH for PTH mediated hypercalcemia:
o Elevated - Primary hyperparathyroidism - Excess PTH from autonomous benign adenomas
o Mid- upper normal - Primary hyperparathyroidism likely or familial hyperparathyroid syndromes.
o Low-normal low (non-PTH mediated hypercalcemia)

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3
Q

What do tumors make that are not measured by PTH assays?

A

PTH-RP

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4
Q

____ have 1-alpha hydroxylase and convert 25 (OH)-vit. D3 to 1,25 (OH)2 D3 to increase calcium absorption in gut.

A

Granulomas (sarcoidosis, TB)

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5
Q

In patients with elevated 1,25-dihydroxyvitamin D3, what should be ordered?

A

Chest radiograph

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6
Q

The presence of low serum levels of PTH, PTHrp, and low or normal vitamin D metabolites suggests some other source for the hypercalcemia, name them.

A
  • Immobilization – disturbance of resorption/formation balance
  • Recovery phase of acute renal failure - Acute release of Ca++ from soft tissue deposits
  • Thiazide diuretics
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7
Q

Labs for hypercalcemia?

A

Ionized calcium, calcium, phosphorus, chloride, and PTH levels + PTH-RP, lytes (r/o renal disease), 24hr urine calcium (r/o FHH), vitamin D (r/o vitamin D deficiency), albumin (r.o albumin deficiency)

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8
Q

How do you calculate a corrected calcium?

A

Get a corrected calcium – calcium is 40% protein bound. A simple formula to correct the serum calcium for albumin is: add 0.2 mmol/L to serum Ca++ for every 10 grams of albumin below 37 g/L

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9
Q

Imaging for hypercalcemia?

A

Imaging: neck/thyroid U/S, sestamibi scan (99mTc scan), CT scan

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10
Q

Treatment in acute hypercalcemia?

A
  1. Increase Urinary Ca2+ Excretion: FLUID, FLUID, FLUID! Isotonic saline (4-5 L) over 24 h ± loop diuretic (e.g. furosemide but only if hypervolemic (urine output >200mL/h). Calcitonin
  2. Decrease GI Ca2+ Absorption - Corticosteroids are potent inhibitors of 1a-hydroxylase
  3. Diminish Bone Resorption - bisphosphonates
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11
Q

Treatment of last resort for acute hypercalcemia and when is it indicated?

A

Indication: severe malignancy-associated hypercalcemia and renal insufficiency or heart failure

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12
Q

Treatment in chronic hypercalcemia?

A

Oral bisphosphonates protect bone from progressive calcium loss but do not decrease serum calcium levels.

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13
Q

What is primary hyperparathyroidism?

A

Primary Hyperparathyroidism: Elevated PTH level or serum calcium OR high normal PTH level in the setting of elevated serum calcium

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14
Q

Etiology of primary hyperparathyroidism?

A

Etiology: 80-90% have parathyroid adenoma, 10-20% have parathyroid hyperplasia, less than 1% have carcinoma

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15
Q

Initial medical treatment of hypercalcemia (1° HPTH)

A

Medical—IV NS fluids, furosemide & parathyroidectomy. In acute settings: bisphosphonates and prednisone

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16
Q

Treatment of parathyroid hyperplasia?

A

Neck exploration removing all parathyroid glands and leaving at least 30 mg of parathyroid tissue placed in the forearm muscles (nondominant arm, of course!)

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17
Q

Treatment of parathyroid adenoma?

A

Surgically remove adenoma (send for frozen section) and biopsy all abnormally enlarged parathyroid glands (some experts biopsy all glands)

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18
Q

What is secondary hyperparathyroidism?

A

Increased overall PTH production from calcium wasting caused by renal failure or decreased GI calcium absorption, rickets or osteomalacia; calcium levels are usually low

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19
Q

Etiology of secondary hyperparathyroidism?

A

Etiology: severe renal disease or low vitamin D levels

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20
Q

Why does renal disease cause hypercalcemia?

A

The failing kidneys are unable to reabsorb calcium (↓ CA) and unable to excrete phosphorous, which accumulates (↑ PHOS). Renal failure also leads to decreased conversion of 25-vitamin D to 1,25- vitamin D (decreased production of 1 alpha hydroxylase), which further decreases calcium absorption in the gastrointestinal tract.

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21
Q

Management of secondary hyperparathyroidism?

A

Management: Correct calcium and phosphate. If not on dialysis – vitamin D supplementation. If on dialysis then calcimimetrics or phosphate binders – subtotal parathyroidectomy if doesn’t respond to medical therapy

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22
Q

What is tertiary hyperparathyroidism?

A

Autonomous PTH production not responsive to the normal negative feedback due to elevated Ca2+ levels

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23
Q

Etiology of tertiary hyperparathyroidism?

A

Etiology: long term secondary hyperparathyroidism or renal transplant

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24
Q

Management of tertiary hyperparathyroidism?

A

Management: parathyroidectomy

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25
Q

Risk factors of hyperparathyroidism

A

Risk Factors: prior cancer, radiation exposure, renal disease, vitamin D deficiency, medications (calcium, lithium, thiazides), FHx, MEN-I and MEN-IIa

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26
Q

MEN1

A

Hyperparathyroidism, pituitary adenoma, pancreas neuroendocrine tumors

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27
Q

MEN2A

A

Medullary thyroid cancer, hyperparathyroidism, pheochromocytoma

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28
Q

Indications for parathyroidectomy

A

Symptomatic primary hyperparathyroidism due to effects of PTH on bone or kidneys, asymptomatic primary hyperparathyroidism with specific lab criteria

Lab Criteria: elevated Ca2+, marked hypercalciuria, Cr clearance <30% normal, bone density reduction with T score <2.5, <50 years old

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29
Q

Contraindications for parathyroidectomy

A

Familial hypocalciuric hyperkalemia

30
Q

Complications of parathyroidectomy?

A

Recurrent/superior laryngeal nerve injury (hoarseness), post-operative hypocalcaemia (perioral numbness or numbness in fingers or toes, Chvostek sign), infection, bleeding

31
Q

What is hungry bone syndrome?

A

Hungry bone syndrome is the constellation of hypocalcemia, hypophosphatemia, and hypomagnesemia after successful parathyroidectomy due to the sudden withdrawal of excess PTH

32
Q

Definition of hypocalcemia?

A

Definition: total corrected serum Ca2+ <2.2 mmol/L

33
Q

Symptoms and signs for hypocalcemia?

A
  • Hypocalcemia is frequently asymptomatic.
  • Paresthesias: perioral, hands, and feet
  • Hyperreflexia
  • ECG changes
  • Tetany
  • Laryngospasm (with stridor)
  • Chvostek’s sign
  • Trousseau’s sign
34
Q

Tetany is a hallmark of hypocalcemia

A
  • Sensory symptoms consisting of paresthesias of the lips, tongue, fingers, and feet
  • Carpopedal spasm, which may be prolonged and painful
  • Generalized muscle aching
  • Spasm of facial musculature
35
Q

What is Chvostek’s sign?

A

Chvostek’s sign is a twitching of the facial muscles

36
Q

What is Trousseau’s sign?

A

Trousseau’s sign is carpal muscle spasm caused by obstruction to blood flow to the arm by a blood pressure cuff (kept at above systolic pressure for at least two minutes).

37
Q

Initial investigations of hypocalcemia?

A

Initial investigations: PTH, PO43-, Mg2+, Urine Ca2+, creatinine

38
Q

4 main categories of causes of hypocalcemia?

A
  1. Loss of calcium from the circulation
  2. Decreased vitamin D production or action
  3. Decreased parathyroid hormone production or action
  4. Low magnesium
39
Q

Ddx for loss of calcium from the circulation

A
  • Hyperphosphatemia (e.g., renal insufficiency)
  • Pancreatitis
  • Radiocontrast agents (EDTA)
  • Osteoblastic metastases
  • Rhabdomyolysis
40
Q

Ddx for decreased vitamin D production or action

A
  • Kidney injury
  • Rickets
  • Malabsorption
  • Neonatal
  • Alterations in vitamin D metabolism as occur with certain drugs (eg, phenytoin, phenobarbital, rifampin)
  • Lack of sunlight
41
Q

How does pancreatitis cause hypocalcemia?

A

When lipolytic products released from the inflamed pancreas chelate calcium

42
Q

What is rickets?

A

Mutation in the gene encoding the 1-alpha-hydroxylase enzyme - needed to convert inactive vitamin D to the active form calcitriol

43
Q

Hypoparathyroidism is characterized by ____ and _____

A

Hypoparathyroidism is characterized by hypocalcemia and hyperphosphatemia

44
Q

What else should you treat concurrently with hypocalcemia?

A

Treat concurrent hypomagnesemia

45
Q

Treatment of mild and symptomatic hypocalcemia? (ionized Ca2+ >0.8 mmol/L)?

A
  • Calcium supplementation - 1500-2000 mg of elemental calcium/d
  • Calcitriol 0.25 μg/d (especially in renal failure or hypoparathyroidism)
46
Q

Treatment of acute or symptomatic hypocalcemia (ionized Ca2+ <0.7 mmol/L)?

A

IV calcium gluconate 1-2g over 10-20 min followed by slow infusion for tetany

47
Q

If PTH recovery not expected in hypocalcemia, what is the treatment?

A

Requires long-term therapy with calcitriol and calcium •

48
Q

Should you treat asymptomatic hypocalcemia?

A

No

49
Q

Definition of fever?

A

Oral temperature >38.3°C

50
Q

Definition of fever of unknown origin?

A

>38.3°C for > 3 wks duration

51
Q

Fever in children under 2 must be a ____ temperature for accuracy

A

Rectal

52
Q

Fever DDx

A
  1. Infectious causes
    - Upper and lower respiratory tract infections
    - Gastrointestinal infections
    - Urinary tract infections
    - Meningitis
    - Endocarditis
    - Skin infections
    - Bacteremia
  2. Malignant: leukemia, lymphoma, myelodysplastic syndromes, metastatic cancer
  3. Autoimmune and inflammatory disorders
    - Vasculitis, RA
    - IBD, sarcoidosis
    - Endocrine (thyroid disease)
  4. Post-surgical
  5. Allergic reaction, EtOH withdrawal, transfusion reaction
  6. Drug induced: overdose or side effect
  7. Environmental: heat stroke
53
Q

Hyperthermia DDx

A
  • Drugs (e.g.atropine)
  • Blood transfusion reaction
  • Infection/sepsis
  • Medical disorder (e.g.thyrotoxicosis)
  • Malignant hyperthermia
54
Q

Fever occurs when the body’s _____ (located in the hypothalamus) resets at a higher temperature, primarily in response to an infection. Elevated body temperature that is not caused by a resetting of the temperature set point is called _____.

A

Thermostat
Hyperthermia

55
Q

The cause of an acute (ie, duration ≤ 4 days) fever in adults is highly likely to be ____. When patients present with fever due to a noninfectious cause, the fever is almost always _____.

A

Infectious
Chronic or recurrent

56
Q

Investigations for fever?

A
  • CBC and differential, blood culture, urine culture, urinalysis, pregnancy test
  • Venous gas (acidosis for sepsis)
  • Stool O&P, C.dif, Gramstain, culture, monospot
  • CRP
  • PT/PTT
  • LFT, TSH
  • Electrolytes with blood urea nitrogen (BUN) and creatinine
  • CXR, Mantoux skin test, sputum culture
  • Lumbar puncture
57
Q

A low WBC count may be just as worrisome as a high one; the WBC count may not be elevated in ______ in the presence of a serious infection. Overwhelming infection can cause bone marrow suppression and a reduced WBC, which may be manifest before the presence of hemodynamic compromise. Many indolent infections may not be associated with elevations in the WBC count.

A

Alcoholic patients, the older adult patients, HIV-infected patients, and other immunocompromised patients

58
Q

Management of fever?

A
  • ABCDEs and GCS, IV fluids, O2
  • Broad spectrum IV abx if sepsis is suspected
  • If temperature is ≥ 41° C, other cooling measures (sponge bath)
  • Treat underlying disease
  • Drugs:
  • Acetaminophen 650 to 1000 mg orally every 6 hours
  • Ibuprofen 400 to 600 mg orally every 6 hours
59
Q

Definition of malignant hyperthermia?

A

Hypermetabolic disorder of skeletal muscle

60
Q

Pathophysiology of malignant hyperthermia?

A

Due to an uncontrolled increase in intracellular Ca2+ (because of an anomaly of the ryanodine receptor which regulates Ca2+ channel in the sarcoplasmic reticulum of skeletal muscle)

61
Q

Anesthetic drugs triggering malignant hyperthermia include:

A
  • All inhalational agents except nitrous oxide
  • Depolarizing muscle relaxants: SCh
62
Q

Clinical features of malignant hyperthermia?

A
  1. Onset: immediate or hours after contact with trigger agent
    - increased oxygen consumption
    - increased ETCO2 on capnograph
    - tachycardia/dysrhythmia
    - tachypnea/cyanosis
    - diaphoresis
    - hypertension
    - increased temperature (late sign)
  2. Muscular symptoms
    - trismus (masseter spasm) common but not specific for MH (occurs in 1% of children given SCh with halothane anesthesia)
    - tender, swollen muscles due to rhabdomyolysis
    - trunk or total body rigidity
63
Q

Clinical features of malignant hyperthermia?

A
  • Non-specific malaise, headache, fatigue
  • Body temp <40.5oC (usually normal) No coma or seizures
  • Dehydration (HR, orthostatic hypotension)
64
Q

Treatment of malignant hyperthermia?

A
  • Rest in a cool environment
  • IV NS if orthostatic hypotension; otherwise replace losses slowly PO
65
Q

What is “water depletion” in heat exhaustion?

A

Heat exhaustion occurs if lost fluid not adequately replaced

66
Q

What is “salt depletion” in heat exhaustion?

A

Heat exhaustion occurs when losses replaced with hypotonic fluid

67
Q

Heatstroke is differentiated from heat exhaustion by presence of the following?

A
  • CNS dysfunction
  • Temperature > 40C
68
Q

Clinical features of classical heat stroke?

A
  • Occurs in setting of high ambient temperatures (e.g. heat wave, poor ventilation)
  • Often patients are older, poor, and sedentary or immobile
  • Dry, hot skin
  • Temp usually >40.5oC
  • Altered mental status, seizures, delirium, or coma
  • May have elevated AST, ALT
69
Q

Clinical features of exertional heat stroke?

A
  • Occurs with high endogenous heat production (e.g. exercise) that overwhelms homeostatic mechanisms
  • Patients often younger, more active Skin often diaphoretic
  • Other features as for classical heat stroke, but may also have DIC, acute renal failure, rhabdomyolysis, marked lactic acidosis
70
Q

Treatment of heat stroke?

A
  • Cool body temperature with water mist (e.g. spray bottle) and standing fans
  • Ice water immersion also effective; monitor body temperature closely to avoid hypothermic overshoot
  • Secure airway because of seizure and aspiration risk
  • Give fluid resuscitation if still hypotensive after above therapy
  • Avoid β-agonists (e.g. epinephrine), peripheral vasoconstriction, and antipyretics (e.g. ASA)

2024 - Élo - LMCC (23 decks)

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