Resident Report 4/27 -Hypogonadism

Teaching Pearls:

  • Clinical manifestations include low energy, low libido, erectile dysfunction, hot flashes, etc
  • Primary hypogonadism in males
    • Low total testosterone levels and elevated LH and FSH
  • Secondary hypogonadism
    • Low total testosterone levels and normal to low LH and FSH levels
  • In males, elevated prolactin levels lead to decreased production of LH and FSH
    • Decreased LH leads to decreased testosterone production from Leydig cells
    • Decreased FSH leads to decreased spermatogenesis from seminiferous tubules
  • Elevated prolactin levels could result from medication use
    • Dopamine is secreted by the hypothalamus and leads to inhibition of prolactin secretion
    • Antipsychotic medications exert its effect by blocking dopamine receptors on lactotrophs, leading to increased prolactin secretion.
  • Work-up:
    • Check TSH, total and free testosterone, FSH and LH, and prolactin level

Intern Report 4/26 – Digoxin Toxicity

  • Teaching Points:
    • Clinical Manifestations
      • Neurologic
        • Can present with confusion, lethargy, coma, etc
        • Vision abnormalities can be seen
          • Patients can develop yellow vision
      • Cardiac
        • Most dangerous side effects
        • Classically produces an arrhythmia that could range from atrial tachycardia with AV delay, Bradycardia, junctional rhythm, alternating right and left AV nodal delay, ventricular arrhythmia
        • Alternating right and left BBB is one of the more specific arrhythmias for dig toxicity, although it’s not commonly seen.
      • Gastrointestinal
        • Patients often present with nausea/vomiting and abdominal pain
        • Most common side effects of digoxin toxicity
        • Rare complications include acute mesenteric ischemia
    • Elevation of digoxin level does not correlate with clinical manifestations
    • Digoxin toxicity commonly occurs in decompensated heart failure patients undergoing aggressive diuresis
      • Leads to hypokalemia and low magnesium levels, which potentiates digoxin toxicity.
    • Hyperkalemia is a poor prognostic indicator for acute digoxin toxicity
      • Studies have shown that for patients with K >5.5, mortality was significantly higher
      • Patients with K<5, mortality was much less.
    • Primary treatment of patients with acute digoxin toxicity and hyperkalemia is Digoxin-specific¬†antibody fragment (Fab)
      • It is generally recommended that you do not aggressively treat the hyperkalemia with agents such as calcium gluconate, bicarb, insulin/glucose as Fab will cause potassium to be lowered.
      • Giving these agents could actually cause hypokalemia

Resident Report 4/25 – NPH

Teaching Points:

  • Clinical Manifestations of Normal Pressure Hydrocephalus
    • Gait Abnormalities
      • One of the first clinical signs of NPH
      • Occurs early on in the disease
      • Typically have “magnetic gait” in which their feet appeared stuck to the ground
      • Wide based gait with externally rotated feet
      • Most likely to respond to large volume lumbar taps
    • Cognitive impairment
      • Patients clinically appear more apathetic, similar to a depressed patient
    • Urinary incontinence
      • Also can occur early on in the disease progression
  • Diagnosis
    • Clinical Manifestations as listed above
    • Imaging – MRI Findings
      • Presence of ventriculomegaly in the absence of sulcal enlargement.
      • Non-obstructing hydrocephalus
      • Presence of ventriculomegaly and increased sulcal size suggestive of generalized senile atrophy (hydrocephalus ex vacuo)
    • Lumbar Puncture with normal opening pressure
      • Other etiologies ruled out with CSF studies
    • Spinal Tap Test
      • Perform large volume spinal tap (30-50cc CSF drainage)
      • Have patient ambulate a certain distance, then turn around and ambulate back, before and after spinal tap test
      • Measure changes in mobility, steps, and timing of ambulation, along with MOCA/MMSE
      • If lumbar test shows significant improvement, patient is likely to respond to VP shunting.

Intern Report 4/12 – AH

Teaching Points:

  • Clinical Manifestations
    • Patients present with worsening jaundice, abdominal distension, tender hepatomegaly with nausea and vomiting.
    • Many patients actually stop alcohol intake over the last several weeks due to their pro-inflammatory state of feeling malaise.
    • Amount of alcohol intake is the biggest risk factor to developing alcoholic hepatitis.
    • On average, patients present within their 4-5th decade in life. On average they drink about 100-120g EtOH daily for 10-20 years
      • Each standard EtOH drink – 14 grams
    • Patients may present with AST:ALT ratio >2, which is more specific for alcoholic liver disease.
      • AST can also be elevated in non-liver pathology, including cardiac, renal, rhabdo.
      • AST and ALT would should not be higher than 300-400 if this is solely due to alcohol-related liver disease.
  • Diagnosis includes assessing patient’s clinical history, laboratory data, and exclusion of other causes of hepatitis
    • Exclude viral hepatitis and drug-induced
    • Patients can present with leukocytosis with neutrophilic predominance, fevers, and abdominal discomfort
      • Important to exclude infections such as spontaneous bacterial peritonitis.
    • Liver biopsy notable for neutrophilic inflammation of hepatocytes, whereas all other causes of viral hepatitis is due to mononuclear infiltration.
  • Treatment
    • Most important intervention includes alcohol cessation.
    • Supportive care as patients can have multiple electrolyte abnormalities
    • Nutritional support with protein 1-1.5g/kg body weight
      • >90% of patients with AH have significant protein-calorie malnutrition
    • Medical Therapy for those with severe AH (DF>32) includes glucocorticoids (Prednisolone)¬†but the evidence is rather weak.
    • Treatment – prednisolone 40mg daily for 4 weeks with a 2-3 week taper.
    • Associated with increased risk of infections and GI bleed.

Resident Report 4/11 – Ca oxalates

Teaching Points:

  • Calcium oxalate crystals
    • Seen in patients with ethylene glycol toxicity, leading to renal failure
    • Urine microscopy notable for envelope-shaped or dumb bell shaped crystals
  • Uric Acid crystals
    • Seen in high uric acid excretion states (tumor lysis syndrome)
    • Urine microscopy notable for rhomboid shaped crystals
  • Struvite crystals
    • Seen in urine infections with bacteria that produce basic pH
    • Examples include ureaplasma urealyticum infections
    • Formation of magnesium ammonium phosphate crystals
    • Urine microscopy notable for coffin-shaped crystals
  • Cystine crystals
    • Seen in patients with cysteinuria
    • Urine microscopy notable for hexagon-shaped crystals

Resident Report 4/7 – NM diseases

Teaching Points:

  • Wound Botulism is due to a bacterial toxin that disturbs the transmission of acetylcholine to bind to nicotinic/muscarinic receptors.
  • Majority of patients get botulism primary from foodborne illnesses, only a small percentage get botulism from wounds.
  • Wound botulism can also be commonly seen in patients who use black tar heroin (skin poppers). Injection of material into subcutaneous and/or muscle tissue provides the ideal environment for anaerobic bacteria – Clostridium botulinum.
  • Clostridium botulinim can produce 8 different strains of toxin – A – H
  • Clinical Manifestations
    • Patients present initially with bulbar symptoms and occasionally ocular abnormalities (diplopia, disconjugate eye movement, pupillary defects)
    • Also present as a symmetric descending paralysis complicated respiratory drive
    • Check history for evidence of skin popping
    • Wound botulism is more likely to cause fever and leukocytosis compared to other forms of botulism.
    • Patients with foodborne botulism typically present first with GI symptoms prior to onset of neurologic abnormalities
  • Diagnosis
    • Important to suspect this in a patient with evolving neurologic deficits
    • Important to obtain wound culture for those who perform skin popping.
    • Diagnosis made by injecting mice and observing clinical manifestation. Then you reinject a second mouse with patient’s serum and antitoxin. If second mouse lives, that’s the diagnosis.
  • Treatment
    • Supportive care including close airway monitoring (intubation if needed)
    • Botulinum heptavalent antitoxin
    • Monitor clinical status – typically a prolonged course of recovery as new axons grow from neurons to develop new neuromuscular junctions for function.
  • Differential Diagnosis
    • Myasthenia Gravis
      • fluctuating weakness worse with repetition/activity
      • Initially involves the bulbar muscles, ptosis
      • Classically associated with thymomas (~80%)
    • Lambert Eaton Syndrome
      • No bulbar involvement. Proximal muscle involvement, ptosis.
      • Improves with repetition
      • Classically associated with small cell lung CA
    • Guillan Barre Syndrome
      • ascending paralysis, sensation intact although patients complain of vague symptoms.
      • Preceding viral URI or GI symptoms
      • Presence of autonomic symptoms such as hyper/hypotension, fluctuating temperatures, urinary incontinence/retention, brady/tachycardia, etc
    • Tick paralysis
      • Very similar presentation to GBS except no autonomic symptoms
      • Often times a tick can be found on the patient’s skin.

Resident Report – 4/6 HyperCA with MM

Teaching Points

  • Symptoms of hypercalcemia include constipation, delayed reflexes, lethargy, confusion
  • Etiologies for hypercalcemia (top 2) include:
    • Primary hyperparathyroidism
    • Malignancy
  • Hypercalcemia secondary to malignancy can arise by different mechanisms:
    • PTHrP
      • Many of your solid tumors
      • Non-Hodgkin’s lymphoma
    • Bone Disease
      • Breast cancer
      • Multiple myeloma
    • Increased production of active Vitamin D
      • Hodgkin’s lymphoma
  • Management of hypercalcemia of malignancy includes the following:
    • IV fluids for immediate effect
      • Many patients with high calcium levels are dehydrated.
      • This is due to hypercalcemia causing nephrogenic DI picture.
    • Calcitonin
      • Works within hours
      • Prone to tachyphylaxis
    • Bisphosphonates
      • Takes up to 48 hours before effect is seen
      • Pamidronate or Zolendronate
      • Caution in use for renal failure
    • Lasix
      • Only used in the setting of symptomatic hypervolemia.
  • Diagnosis of Multiple Myeloma includes the following:
    • M-spike
    • Bone marrow biopsy with >10% plasma cells
    • Clinical manifestations based on the CRAB criteria:
      • HyperCalcemia – 25%
      • Renal dysfunction – 50%
      • Anemia – 75%
      • Bone involvement – 50%