- Over 90% of hypercalcemia is caused by primary hyperparathyroidism or malignancy.
- Malignancy etiologies could be due to bone metastasis and/or PTHrP
- Granulomatous diseases can cause hypercalcemia by expressing 1a-hydroxylase, which induces production of active Vitamin D.
- Severe hypercalcemia (over 13mg/dL) is usually associated with malignancy and is most commonly seen in the inpatient setting
- Mild to moderate hypercalcemia (11-13mg/dL) is usually seen in patients with primary hyperparathyroidism. It is most commonly seen in the outpatient setting.
- Metastatic tumors to the hypothalamus/pituitary space are usually caused by lung or breast cancer
- Management of hypercalcemia
- IV Fluids to improve GFR immediately for calcium excretion.
- Calcitonin intermediate onset of 4-6 hours. Be aware of tachyphylaxis
- IV bisphosphonates, onset 24-48 hours (pamidronate, zolendronate)
- A normal to high level of PTH in a patient with hyperparathyroidism almost always suggests primary hyperparathyroidism as the etiology.
- V1 receptors are present in the blood vessels whereas V2 receptors are present in the collecting tubule. Activation of V2 receptors causes aquaporin channels within the membrane to allow reabsorption of water.
- The hypernatremia from Diabetes insipidus may be masked until the patient is unable to satisfy their thirst or if they are unable to access water (for example, outpatients with DI usually don’t have hypernatremia because they can obtain free water from the most powerful sensing mechanism – thirst)
- The etiologies for hypernatremia include poor water intake (inability to access water) versus diabetes insipidus.
- Central DI will respond appropriately to ddAVP whereas nephrogenic DI will have a suboptimal response
- Nephrogenic DI can be caused by electrolyte abnormalities (hypercalcemia, hypokalemia), medications (lithium, demeclocycline, etc), and genetic factors
- Prolactin levels will INCREASE with pituitary stalk compression due to the lack of inhibition from hypothalamic dopamine, while all other anterior pituitary hormones (FSH, LH, ACTH, TSH, GNRH) would decrease.
A Very Special Thank you to Dr. Crapo for joining us!!! Also a special thank you to Dr. Kevin Ku for bringing in yummy bagels!
http://stanfordmedicine25.stanford.edu/the25/nvwf.html for a good description of the jugular venous waveform
||Acute or subacute
|Jugular Venous Waveform
||Slow Y Descent
||Steep Y wave
We went over a fascinating case of MSSA endocarditis in the setting of immunosuppression. Below are some of the clinical pearls:
- Modified Duke Criteria for infective endocarditis
- Major criteria
- Positive blood cultures
- Typical microorganism from two separate blood culture
- Single positive blood culture for Coxiella burnetii
- Persistently positive blood cultures
- Echocardiogram findings of vegetation
- New valvular regurgitation
- Minor criteria
- Predisposing heart condition or IVDU
- Fever >38C
- Vascular phenomena
- Major arterial emboli
- Septic pulmonary infarcts,
- Mycotic aneurysm
- intracranial hemorrhage
- conjunctival hemorrhages
- Janeway Lesions
- Immunologic phenomena
- Osler nodes
- Roth spots
- Rheumatoid factor
- Clinical Diagnosis
- 2 Major criteria OR
- 1 major and 3 minor criteria OR
- 5 minor criteria
2. Surgical Indications for treatment of endocarditis:
- Valve dysfunction causing heart failure
- Para-valvular involvement causing abscess, fistula or heart block
- Difficult to treat organisms (fungal)
- Persistent bacteremia
- Recurrent septic emboli with vegetations despite appropriate antibiotic therapy
3. Most common bacteria associated with endocarditis
- Viridans streptococci
- Staphylococcus (MRSA or MSSA)
Thanks to Zach, one of the Stanford ophthalmology residents, for teaching us about the eye today at morning report! Here are some of the highlights:
- Eye Pain: Usually related to pathology with the ANTERIOR segment of the eye. If pain resolves with topical anesthetic, think about dry eyes/external irritant.
- Photophobia: Usually caused by ciliary body spasm
- Inflammation from outside to inside:
- Blepharitis: Eyelid inflammation
- Conjunctivitis: Bacterial/viral/allergic
- Scleritis/Episcleritis: Can be associated with collagen vascular disease (RA common)
- Keratitis: Corneal inflammation, HSV classic cause
- Iritis: Inflammation of the Iris
- Uvea = Ciliary body + Choroid + Iris
- Anterior Uveitis
- Posterior Uveitis
- Retinitis: Pt’s may report flashing lights
- Retinal Detachment is classically described as a curtain over the eyes
- Cherry red spot is seen in central retinal artery occlusion
Great session with our pulmonary critical care attendings Dr. Friedenberg and Dr. Gohil. This is our safe environment to practice rapid response/code scenarios and receive feedback which we do monthly. Thanks to everyone who participated!
- ABCDEFG: ABCs…don’t ever forget glucose! Make sure to check the fingerstick glucose during codes. It’s quick, easy, and can save lives!
- During a code, no “air orders” and make sure to close the loop
- As the code leader, be concrete with your instructions and delegation of tasks
- Carry your code cards and take a look at the H’s and T’s when you are stuck
- Remember that patients who are altered and unable to protect their airways are not good candidates for BIPAP, these patients often just need intubation
- Post-intubation codes: Remember that sedation, hypotension from decreased preload/positive pressure ventilation, air-trapping from hyperventilation, and ventilator dysynchrony can lead to post-intubation code situations.