February 5th - MHH - Polyuria and Diabetes Insipidus

Today at Morning Report, Endocrine consults presented a patient in her third trimester with polyuria and polydipsia.  Here is a general approach to a patient with polyuria, and info on DI

In general, polyuria is defined as at least 3L of urine a day. The frequency of urination does not matter as much as the total amount.  Patients with polyuria will commonly also have polydipsia (to compensate, as long as their thirst center is intact) and will have nocturia.





The basic causes to know for rotations and the boards are:
Diabetes Mellitus
Diabetes Insipidus (Central and Nephrogenic)  - and their multiple causes
Primary/Psychogenic Polydipsia
Diuretic Use (esp in those using it for weight loss)
Hypercalcemia
Medications (either directly or by causing a nephrogenic DI)
Post-ATN or Post-Obstrutive Uropathy

Your exam in these patients may show signs of dehydration, although this is not as common when the patient has an intact thirst mechanism. A Good neurologic examination is essential with the variety of causes of central DI.  Further examination is directed mostly to other causes of Central/Nephrogenic DI or primary polydipsia (i.e. skin findings with sarcoid, amyloid infiltration, lymph nodes with systemic lymphoma, etc)

For the boards, a key topic is being able to identify and contrast Central Diabetes Insipidus, Nephrogenic Diabetes Insipidus and Primary Polydipsia

Central Diabetes Insipidus occurs from inadequate secretion of vasopressin. 
Causes: There are familial/inherited forms, but this is not as common as other causes - tumors of the CNS (including lymphoma and mets), trauma, granulomatous disease (TB/Sarcoid), infections (meningitis) and Sheenhan Syndrome. 

Nephrogenic Diabetes Insipidus occurs from renal insensitivity to vasopressin. 
Causes: This is commonly an inherited disorder, but can be secondary to medications (esp Lithium, Ampho B), systemic conditions (amyloid, Sjogrens, sickle cell disease, pregnancy), or electrolytes (HyperCA and HypoK)

Primary Polydipsia is simply increased water intake, usually psychogenic in nature (but can also be seen with lesions that affect the thirst center of the brain - sarcoid is a commonly tested one. 

Labs: Basic workup should include ruling out causes listed above, if not already obvious.  The best test to do initially is a BMP and Urine Osmolarity.  Patients will not be hypernatremic if they have an intact thirst mechanism, so don't rule out any of the above three if the patient has access to water, and takes in an amount to offset their urine output.  Undiagnosed DM and secondary osmotic diuresis can be ruled out with the glucose on the chemistry.  The electrolytes are also very important - both Hypercalcemia and Hypokalemia can not only cause polyuria, but in most cases, will make the symptoms worse as they interfere with the kidneys ability to concentrate urine.  Therefore, check these labs and correct as needed. 

Urine Osmolarity will be low in patients with Both forms of DI - generally <200. This is usually also the case with Primary Polydipsia. This is the general first step, although it makes sense because of very dilute urine. 

The other test that is done is the much heard about water deprivation test.  Patients are to be started on this protoco , and are instructed to not drink for about 2 hours before coming to the clinic or hospital for testing. During the time frame, the patient is not given access to fluids -> dehydration -> maximum stimulus for Vasopressin Secretion. Basic labs are drawn, and both Urine Volume/osm are measured every 2 hours. During this time frame, patients with Primary Polydipsia will be able to concentrate their urine. Therefore, in patients with Primary Polydipsia, the Urine osm will rise during the test.  In patients with both Central and Nephrogenic DI, the urine osm does not change much, yet the serum sodium may increase. 

So, now with no change in urine osm, the patient has either Central or Nephrogenic DI. How to tell apart - the patient is given desmopressin and we see what happens to the Urine Osm. Those patients with Central  DI will have at least a 50% increase in the Urine Osm after this medication, whereas patients with nephrogenic DI will have none or a slight increase (<10%) in their urine Osm. In those with primary polydipsis, the urine osm will increase at least 50% as well. 

Of NOTE:  On Boards, some other lab info/approaches may be given to differentiate the conditions.  With a low urine osm, and without the use of the water deprivation test, desmopression may be administered to see what happens to the urine osm.  If it changes >50%, then it is central DI.  Also, on various board review materials, they mention measuring ADH during the deprivation test. This is usually not done much clinically. You should be aware that with the water deprivation test - a rising plasma osm with no change in ADH is Central, and a rising ADH with no change in urine osm is Nephrogenic.  This makes sense, and may be presented on boards - but is not usually the way to diagnose this clinically. 

Treatment:
Central DI: Usually get intranasal Desmopressin lifelong
Nephrogenic DI:  Treat the underlying disorder/change medications.  Treatment is also thiazide Diuretic +/- K-sparing diuretic (The cause voume contraction sensed by the kidneys, and the resulting autoregulatory decrease in GFR will help decrease Urine Output)

Reference:
Image Courtesy of www.operationalmedicine.org

February 2nd - MHH - Mesenteric Ischemia and Ischemic Bowel Disorders

Today at Hermann, a case was presented regarding a patient with post-prandial abdominal pain (and also history of coronary artery disease and PVD).  The diagnosis was Mesenteric Ischemia (aka "Intestinal Angina")

Housestaff frequently interchange the different ischemic diseases of the bowel, and I've hear the term "ischemic colitis" to describe the clinical scenario above. Here is a review of the different ischemic disorders involving the bowel.


There are essentially 4 ischemic disease that affects the mesentery - acute and chronic mesenteric ischemia, mesenteric thrombosis and ischemic colitis. Keep in mind, that each of these has a variety of causes (see below).

Mesenteric Ischemia
In almost all of the causes, the presentation is similar - post prandial abdominal pain, weight loss and "fear of eating." Most of these symptoms occur indolently, yet depending on the cause, this symptoms can present more acutely.  The symptoms simply occur from a supply/demand mismatch, and the SMA is the usual site of involvement.  Overall, these patients DO NOT present with blood in the stool/diarrhea.... that is unless there is another overlapping cause that leads to gut infarction. This overlapping cause is usually caused by severe hypovolemia, cardiogenic shock or sepsis.

On exam, the classic presentation is that the patient's complaint of pain is out of proportion to the exam.  In fact, the way that patients describe pain - one may suspect that they would have peritoneal signs, but they are essentially non-tender during the exam.  (Remember, however, that this would not be the case if there was gut infarction that resulted from an overlapping cause).  In all patients, Auscultation of the abdomen may reveal a bruit. 

   Acute Mesenteric Ischemia - These patients usually present acutely, and are the highest risk of developing infarction of the bowel.  There are a variety of causes, but in all - patients have poor perfusion of the colon - usually at the area of the SMA

Embolic Disease: Common causes of this include atrial fibrillation, or a mural clot post myocardial infarction.This is sometimes seen after vascular surgery as well. Emesis is usually present.

Mesenteric Arterial Thrombosis: Usually causes by rupture of an atherosclerotic plaque. Patients present usually when precipitated by low-flow states.  These cases commonly develop gut infarction/necrosis rapidly. 

Non-occlusive disease: Hypotension from a variety of causes (MI, Sepsis, etc), vasopressors, cocaine and Digoxin

Workup of Acute Mesenteric Ischemia:  CBC (may have elevated white count, and usually hemoconcentration occurs), Amylase usually elevaed.  Can have a lactic acidosis. KUB (to rule out other causes) may have findings later in the disease course (especially c/w SBO). CT may be helpful, but mostly to rule out other causes of abdominal pain.  Diagnosis is usually done via angiography, which is currently preferred over MRA. 

Treatment of Acute Mesenteric Ischemia: This is an emergency, as it can rapidly progress to bowel infarction and gangrene   During angiography, thrombolytics can use used with ischemic disease.  Some may need angioplasty or stents afterwards if there is atherosclerotic disease.  Less emergent cases can be treated with Heparin or LMWH.  If there are any signs of infarction (peritonitis, acidosis, lactic acid up) - then emergent surgery is needed

Chronic Mesenteric Ischemia - Over 90% of patients with this have atherosclerotic disease as the cause.  They usually have more chronic symptoms, and although they rarely get gut infarction, they have a high risk of emboli/thrombosis which can lead to infarction.  Think of this as the cause of abdominal pain in a patient with risk factors for coronary artery disease (esp Smoking, DM, HTN, Dyslipidemia) and/or have a history of CAD/MI/CVA/PVD. 

Workup of Chronic Mesenteric Ischemia: Mostly done to rule out other causes (i.e. liver disease, pancreatitis, biliary disease, nephrolithiasis, etc).  Angiography is the gold standard for diagnosis.

Treament of Chronic Mesenteric Ischemia: Stenting of the SMA.  If this is not possible, endarterectomy or bypass can be performed

Mesenteric Venous Thrombosis -  Usually presents acutely, but can be chronic.  Causes by other things you would think of causing venous thrombosis - hypercoaguable states (esp Factor V Leidin, Protein C/S, PNH), pancreatitis, cirrhosis and sickle cell disease. 

Patients present very similarly to those with mesenteric ischemia - post-prandial abdominal pain, "fear of food" and weight loss. The exam is the same as well - essentially non-tender although the patient complains of a lot of pain.  Bruits are not usually heard. 

Workup: Rule out other causes of abdominal pain.  CT scan is the test of choice. Once imaging shows findings c/w a thrombosis - then workup the cause.

Treatment: Consists of heparin/LMWH then long-term coumading. Thrombolysis for emergent cases. Surgery is signs of infarction/peritonitis develop. 

Ischemic Colitis (aka Colonic Ischemia - confusing huh?)
These Patients have a non-occlusive cause of their disease. Unlike the above causes, which invariably affect the SMA, this disease usually affects the IMA.  Especially involved is the so called "watershed area" of the splenic flexure.  Any area distal from the splenic flexure, however, can be involved. 

There are multiple causes of this - mostly post-operative, low-flow states, hypercoaguable states, vasospastic drugs (cocaine), vasculitis and history of radiation exposure.   Embolism post MI or from Afib is RARELY the cause. 

These patients present very different from mesenteric ischemia.  The presentation is almost always acute, with pain on the left side of the abdomen.  These are the patients that present with a sequence including strong urge to defecate  then diarrhea without blood then diarrhea with blood.  Low grade fever may be present, as well as nausea and emesis.  They are usually very tender on physical exam.

Workup: KUB to r/o other causes, as well as labs to investigate pancreatitis, infectious causes, and other mimics.  Colonoscopy is diagnostic (will show mucosal hemorrhage). 

Treatment: Supportive care - fluids, NPO and antibiotics if severe.  Patients can progress to gangrene of the gut, and will need immediate surgical resection. 

January 26th - LBJ - Nephrotic Syndrome

Today at LBJ, a case of nephrotic syndrome was presented.  Although the exact diagnosis for this patient is not known (biopsy results pending), for boards you should know the basic causes of nephrotic syndrome - as well as further work-up and treatment










Lab findings/Diagnosis: The classic necessary finding in nephrotic syndrome is proteinuria (usually at least 3+ on urine dipstick, but a 24-hr urine protein of >3grams or a spot Urine Protein/Cr ratio >3 is more specific). Patients will also have hypoalbuminemia, dyslipidemia (LDL and TG), HTN and hypogammaglobulinemia. There is usually not as much inflammation as in patients with nephrotic syndromes, with some exceptions - but in most patients there will not be hematuria or dysmorphic RBCs/RBC casts.  While pending biopsy, serologic workup can be performed (you'll see why below) including HIV, ANA, anti-DS DNA, Complement Levels, RPR, Hepatitis Panel and Serum Protein/Urine Protein Electrophoresis with IF. Remember to get a good review for all OTC medications taken as well. Workup in most adult patients will require a biopsy for ultimate diagnosis unless the cause is obvious (i.e. diabetic). 


Clinical:  Patients can present with HTN, Foamy Urine, Edema (starts in dependant areas - such as periorbital, scrotum and legs - but patients can eventually get anasarca/pleural effusion/ascites), infections (due to low gamma globulins), and thrombosis (Lower extremity, pulmonary embolism and renal ven thrombosis due to loss of AT-3).  How does renal vein thrombosis present? -Acute abdominal pain + sterile pyuria should clue you in to this entity


Like the causes of glomerulonephritis, one can think of causes of nephrotic syndrome in two categories: Those that are systemic diseases, and those that cause more specific changes on biopsy


The systemic diseases that cause nephrotic syndrome:
1) Diabetes Mellitus - the most common!  Remember the A1c can be normal in those patients that have developed some element of renal insufficiency.  These patients usually do not need a renal biopsy to diagnose, and this is usually a clinical diagnosis.  Patients should be placed on an ARB/ACEI and a low protein diet.  Patients that do not have good glycemic control, uncontrolled HTN, and keep spilling protein will get progressive decrease in GFR. This is usually not too rapid, and occurs over a number of years. 


2) SLE - Can also present with a more "nephritic" component. Remember, SLE can affect the kidney in a variety of ways...


3) Multiple Myeloma - Patients will present clinically with: high globulin gap, bone pain, anemia, renal failure, hypocalcemia.  They might not have frank nephrotic syndrome on presentation, and might just has +1 protein in their urine. Still, a work-up for this must be done for patients with nephrotic syndrome (SPEP/UPEP with IF)


4) Amyloidosis - usually caused by light chain deposition, or from AL forms.  On the boards, these patients will have other clues/findings (such as restrictive heart failure, neuropathy, etc)


The Renal "Causes" of nephrotic syndrome
1) Minimal Change Disease - In adults, the causes can be Idiopathic or caused by NSAIDS or  Hodgkin's Lymphoma.  Biopsy shows "effacement of foot processes" Treat with steroids +/-  cytotoxic agents (such as cyclophosphamide) 


2) Membranous Nephropathy - There are MULTIPLE causes for this on biopsy. 
    Drugs: NSAIDS, Gold
    Autoimmune Disease: SLE
    Cancer: Solid tumors, especially HCC, RCC, Colon and Lung
    Infections (HCV, HBV, HIV, Malaria)
       These patients usually have the underlying condition treated/removed first, and if
     severe disease, get  steroids +/- cytotoxic agents


3) Focal Segmental Glomerulosclerosis - has MULTIPLE causes as well
     Idopathic (esp with h/o HTN), Sickle Cell Disease, Heroin use, Obesity.
     Steroids are usually given to treat, but most end up needing Dialysis


Overall, patients with nephrotic syndrome should be placed on ACEI/ARB and diuretics as needed.  Good BP control is essential.  Many patients need to be on medications for dyslipidemia.  A word about anticoagulation - these patients are "hypercoaguable", so do they all need treatment?  Usually when inpatient - only DVT prophylaxis is given.  Life-long treatment is usually given to patients with one thrombotic event. Prophylactic treatment to prevent an occurance of a thrombosis is not usually done, except in some cases of membranous nephropathy.

January 25th - MHH - Scleroderma

At MHH, a case of CREST Syndrome was presented - here is a brief overview of scleroderma - subtypes, lab findings, and management. 

For internal medicine boards, you should be familiar with the systemic forms of scleroderma (as opposed to those which only dermatologists treat)




The first is Limited Systemic Sclerosis (used to be called "CREST" syndrome - which is a good way to remember the salient features)

These patients will have findings that go along with the CREST letters - Calcinosis, Raynaud's phenomenon, Esophageal Dysmotility, Sclerodactyly and Telangiectasias.  These patients usually only have skin changes in their extremities distal to the wrist, and mostly in the upper extremities.

Other findings and complications in these patients include:
-Hyper/hypo pigmentation of skin
-Tight skin around face/paucity of wrinkles/"mouse facies"
-Digital ulcerations and ischemia
-Arthritis
-Lung disease (pulmonary HTN)
-"Watermelon Stomach"/Gastric vascular antral ectasia and GI Bleeding. Bacterial overgrowth and malabsorbtion can occur as well

Lab findings: ANA (>90%)and  anti-centromere staining pattern of ANA (50%)

Treatment:
Raynaud's: Warming of fingers, calcium channel blockers
Digital ulcers: warming of extremities, aspirin, topical nitrates and prostacyclins
Esophageal Dysmotility: Almost all patients are on PPIs. May need Feeding tube placed
Pulmonary HTN: Supplemental Oxygen, Calcium channel blockers, bosenten, prostacyclins

Other category is Diffuse Systemic Sclerosis:

Clinically these patients have skin involvement more proximal to the wrist, and also have involvement of the torso/face.  Although these patients will have some overlap features of the CREST syndrome (especially telangiectasias, "mouse facies" and Raynaud's), in general organ invovlement is more prevalent:

MS: Abnormal nailfold capillaries, arthritis may be present, tendon friction rubs,
        myositis and myalgias
Lungs: Patients can develop interstitial lung disease and pneumonitis
Renal: Scleroderma Renal Crisis (HTN, Renal Failure and hemolytic anemia)
GI: Malabsorbtion, bacterial overgrowth and primary biliary cirrhosis
CV: Fibrosis, Myocarditis, CHF, Pericardial Effusions

Labs: ANA (>90%) and scl-70 (30%)

Treatment:  Patients get treated for systemic sclerosis with steroids when organs are affected (i.e. Heart and Lung).  Cyclophosphamide is used for intersititial lung disease, and other cytotoxic agents are added with heart involvement.   Scleroderma renal crisis is treated with ACEIs.  Arthritis is usually treated with NSAIDS and Acetaminophen.  Remember, steroids are not given to all patients - only when there is some element of systemic involvement, or myositis.

January 22nd - MHH - Lung Cancer

Today at morning report, a 47 year old AAF with significant tobacco use presented with 2 months of worsening dyspnea on exertion.  Although the final pathology was not back, it is likely small-cell lung cancer.

On the boards, the info you'll need to know for Lung Cancer is broad, so here is a quick review.  I would be familiar with staging - although the boards will not likely ask you to stage, they may ask a questions regarding treatment modality. To know this, you need to know the stage.




Risk Factors: Smoking (increases risk about 15x normal. Even 2nd hand smoke exposure increases risk about 2x), asbestos exposure, other heavy metal exposure

Clinical Presentation:  Over 90% of patients with a diagnosis of lung cancer have some sort of symptoms - either from local involvement, paraneoplastic syndromes or metastatic disease.  Local symptoms depend on the location of the lesion.  So the more "central" cancers (i.e. small cell and squamous cell) present with bronchial obstruction, pneumonia, cough, hemoptysis and dyspnea.  The more "peripheral" cancers can present with pleurisy, chest wall pain and pleural effusion. Obviously either can cause dyspnea as well as cough/hemoptysis, and there is some overlap.  Think of lung cancer in a patient with a history of COPD that presents with an "exacerbation" that is different than their usual exacerbation (i.e. more severe, or lasting longer). Also consider with new onset COPD symptoms in an older patient.  Other signs/symptoms include change in voice, Horner's Syndrome, arm paresthesias, SVC syndrome, clubbing, temporal wasting and lymph node enlargement.  Metastatic disease can present with bony pain, headache/AMS, or hepatomegaly.  We'll go over paraneoplastic syndromes in a bit as well.

Diagnosis:  CXR for initial suspicion, followed by CT Scan.  You ideally want to biopsy any lymph nodes first, but can also biopsy the mass.  Bronchoscopy can be used for central lesions that are >4cm.  Open biopsy or IR-guided biopsy if the lesion is peripheral or small.

Classification/Pathology and Subtypes:
Small-Cell Carcinoma
Non-Small Cell Subtypes (includes squamous cell, large cell and adenocarcinoma)
Others: carcinoid and rare pathology (carcinoid is reviewed in one of my earlier posts)

Small Cell Carcinoma
Usually metastasize early, as compared to the non-small cell types. Located more "central" Paraneoplastic syndromes include SIADH, Eaton-Lambert and ectopic ACTH production. 

Staging for Small Cell:
Limited: Can fit within one radiation therapy Port (Confined to one Lymph Node, the Mediastinum and A Supraclavicular LN)

Extended: If it does not fit into one port

Treatment for Small Cell:
Limited: Cisplatin + Etoposide with Radiation

Extensive:  Cisplatin + Etoposide or Carboplatin + Etoposide
If Brain Metastases are Present - Radiation and Steroids (Some give prophylactic cranial irradiation for both stages, although it is more controversial for Limited-Stage Disease)

Non-Small Cell Subtypes:
Squamous Cell - Most likely to cavitate.  Central Lesion. Hypercalcemia
Large Cell - Peripheral. Mets to CNS
Adenocarcinoma - Peripheral.  Seen 50% of the time in non-smokers. Bronchoalveolar carcinoma is a subtype of adenocarcinoma that looks like pulmonary edema/diffuse interstitial infiltrates

Staging for Non-Small Cell:
Stage I: <3cm and no LAD or Mets
Stage II: Hilar LAD or Chest Wall
Stage III: Mediastinal LAD
Stage IV: Mets

Further Workup for Non-Small Cell:
PET Scan
Mediastinoscopy for LN >1cm
CT and MRI of Head usually needed
Bone Scan if symptoms of bone pain or increased Alk Phos
Treatment for Non-Small Cell:
Stage I and II: Sx and Chemo (Debate if radiation is added to this – it may increase mortality).

Stage III: Chemo and Radiotherapy
Stage IV: Chemo for patients with good Performance status

Chemotherapy for Non-Small Cell usually consists of:
Paclitaxel+Carboplatin or

Cisplatin+Etoposide
Adenocarcinoma:  Oral Gefitinib used at times

Here is a chart I made comparing "high-yield" basics for the 4 types:

Paraneoplastic syndromes - the boards like these, so know them cold!
SIADH - Hyponatremia (what are the labs with SIADH? UNa>50 and Uosm>200) - Small Cell
Hypercalcemia and it's multiple symptoms - usually squamous cell
Acromegaly - GH secretion usually from small cell subtype
Cushing's Syndrome - ACTH secretion from small cell subtype
Hypertrophic Pulmonary Osteoarthropathy - New periosteal bone formation - usually adenocarcinoma
Lambert Eaton Syndrome - Proximal Muscle Weakness, autonomic dysfunction (impotence and dry mouth) with areflexia and sparing cranial nerves  The amplitude of action potentials on EMG, and symptoms, improve with repetitive stimulation. This usually occurs with Small Cell Subtypes.  (Remember that Myasthenia has cranial nerve involvement, normal reflexes, and worsening with repeated motion)

January 22nd - MHH - All about the Pituitary

Today at Morning Report a case of a piuitary mass in a patient with history of treated prolactinoma was presented.  Here is an overview of pituitary masses, pituitary disorders, and more on prolactinomas









Pituitary Mass:

Clinical Symptoms: Pituitary masses cause one of two major categories of symptoms - those of mass effect and those of either hypersecretion or hyposecretion of hormones.  Mass Effect from tumor growth can cause headache, seizures, diploplia, blurry vision and/or visual deficits.

When you see a pituitary mass, you should order the following:
TSH and FT4
Prolactin
Alpha Subunit (marker produced by GH) and IGF-1
FSH/LH
Cortisol
Estradiol in Females
Testosterone in Men

Specific Symptoms: Will depend on hormone effects, some of which include:
Patients can get S/Sx of hyper/hypothyroidism
Patients may get cushing's disease or adrenal insufficiency (the former is more common)
Acromegaly may result as well
Prolactinoma symptoms (more below)

Treatment: Depends on treating the causes of hormone excess or deficiency.  Surgery is usually used in these cases as well. 


Prolactinoma:


Classified as microadenomas (<1cm) or macroadenomas (>1cm).  Usually macroadenomas cause visual field defects, but microadenomas are more common overall

Symptoms:  In Men - Loss of libido, impotence, loss of peripheral body hairDiagnosis: Imaging (MRI) and Prolactin Levels. You should work these patients up for "pituitary masses" as stated above - importantly obtaining a TSH (to rule out secondary elevated PRL caused by an elevated TRH level OR concurrent hypothyroidism) and cortisol levels, in addition to other hormones. 

                      In Women - Amenorrhea, galactorrhea and hirsutism
                      If the tumor is large enough, compression of nearby cells can lead to deficiency  
                                of other hormones - commonly TSH, GH and ACTH.                   
                      And of course, mass effect symptoms depending on size of tumor
                 

So, in morning report there was some discussion was raised about levels of Prolactin. What is normal? How high of a levels leads you to suspect prolactinoma? What else raises levels of PRL?

Normal:  <25ng in females, <20ng in Males and Children
40-85 ng: Craniophayngomas, Hypothyroidism and Drugs (esp anti-emetics, antipsychotics and TCAs
~50ng: 25% chance of pituitary tumor and ~100ng: 50% chance of pituitary tumor
>150ng: Usually a prolactinoma, and if the level is >200 it is about 100% chance of being a prolactinoma

Other causes of increased prolactin include:
Any pituitary lesion
Hypothalamic Lesions (histiocytosis X, sarcoid, TB, glioma)
Endocrine: Hypothyroidism, Addison's Disease, Glucortocoid Excess, COS
Ectopic production: Bronchogenic carcinoma, RCC
Neurogenic: Post-Seizure, Spinal Cord Lesion, Nursing
Stress (includes vigorous exercise and post-op)
Pregnancy
Chronic Kidney Disease
Drugs (antiemetics, antipsychotics, opiates)

Treatment of Prolactinoma:Medical treatment with dopamine agonists - bromocriptine and cabergoline.  Bromocriptine is not well tolerated due to side effects, including orthostasis, nausea and dizziness. Bromocriptine, however, is the choice of treatment in pregnant patients.  Nonetheless, both medications can both reduce tumor size and prolactin levels. Pergolide was previously used, but withdrawn due to it's association with valvular disease in patients. 


Surgical treatment is done if drug therapy does not help or is poorly tolerated.  Still, drugs are usually given post-operatively.   


Irradiation is given usually only if the lesion is very large or medical/surgical therapy doesn't help much

Other Pituitary Disorders:


Empty Sella Syndrome - This occurs when the CSF compresses the pituitary.  Mostly present in a multiparous women. Can be secondary to irradation or trauma.  Sometimes this  is benign and does not require treatment, other times hormone replacement is needed. 

Pituitary Apoplexy - Infarct and hemorrhage into the pituitary.  Patients will present acutely with signs of meningiitis (i.e. meningismus and headache) as well as nausea/vomiting, altered mental status, visual changes and vertigo.  If you suspect this, order imaging (MRI is better than CT) and if it is present, neurosurgery needs to be called ASAP!  Sometimes steroids are used for minor cases, but patients with severe symptoms need surgical decompression.

Sheehan Syndrome - Postpartum infarct of pituitary with usual decreases in almost all hormones - TSH, ACTH, GH, LH, FSH as well as sometimes causing DI.  Hormone replacement is the treatment of choice. 

January 15th - LBJ - ASD and Congenital Heart Disease

Atrial Septal Defects are a commonly tested question on boards, and are a very complicated topic.  However, here are the basics you'll need to know for boards. 


Even though it is a congenital heart defect, the various types of ASDs can be asymptomatic until adolescence or adulthood.  Therefore, physical exam features are clues into the presence of the defect before symptoms develop








In general, patients can present with symptoms attributable to atrial fibrillation, right-sided heart failure, and rarely Pulmonary HTN. 




There are 4 types of ASD, each with subtle features to know.  You'll most likely be given a patient with an ostium secundum defect, so know this one well.  A lot of the concepts are also relevant to the other types of ASD, so just remember what makes the others different (which I'll list)


Ostium Secundum - The most common Type of ASD, and the 2nd most common congenital abnormality in adults (the most common being a bicuspid aortic valve)


Exam: Fixed Split S2 and systolic murmur at LUSB. Loud P2 if patient get Pulmonary HTN
EKG: Right Axis Deviation and RBBB
CXR:  Enlarged Right Ventricle, prominent pulmonary vasculature
Diagnosis: Echocardiogram
Treatment: Surgical Closure of the ASD.  This is done in symptomatic patients, and in asymptomatic patients that a have pulmonary: system shunt ratio >2:1. If there is pulmonary HTN, surgical closure usually cannot be done, but percutaneous closure can be done. 
Complications:Patients can get TIA, Strokes, and Eisenmenger's Syndrome


Ostium Primum
Exam: Pansystolic Murmur of MR or TR
EKG: First Degree AV Block, Left Axis Deviation and RBBB
Treatment: Treatment of choice is percutaneous closure


Sinus Venosus - Know patients have anomalous pulmonary venous return, treat with surgery


Coronary Sinus - Know that patients usually have a Left SVC, treat with surgery


Okay, so what else do you need to know for boards regarding congenital heart disease? Here are the very basic minimums to know about most of the congenital diseases in adults that you will encounter on boards:


PFO:
Diagnose with agitated saline and TTE
Evidence to suggest there is an association b/w PFO and migraines and cryptogenic stroke
Some advocate closure of a PFO in those with cryptogenic stroke, but this is controversial


VSD: 
Exam with holosystolic systolic murmur at LLSB, Prolonged Split of S2, as well as murmurs of AR/TR

Diagnose with Echo (suggestive) but need cath to tell difference in O2 Sat b/w Right Atrium and Ventricle

Patients with large VSDs, Significant Shunt, Progressive AR and Volume Overload undergo closure

If left untreated, patients will develop Eisenmenger Syndrome


PDA: 
More common in females, may have history of congenital Rubella infection.

Can present with symptoms of heart failure, and can get pulmonary HTN

Exam wth a Machine-like murmur at LUSB. May have bounding peripheral pulses

Interestingly, if Einsenmeger's occurs there is "differential cyanosis" - only in the lower extremities

Diagnose with Echo, Cath can reveal difference in O2 sat b/w Right Ventricle and Pulmonary Artery

Treatment is closure if the patient has symptoms (but not if the patient has with Pulmonary HTN!)


Coarction of Aorta:
Usually associated with Bicuspid Aortic Valve, and patients can get Mitral Valve disease, as well as LVH

Patients can present with HTN, symptoms of CHF and leg claudication

Exam with a delayed pulse between radial/brachial and femoral areas. Femoral Pulse can be absent. HTN can be present in the Upper Extremities compared to Lower Extremities. Patients usually also have a systolic murmur

CXR with Rib Notching (due to collateral vessels) and a "Figure 3 Sign" (dilated aorta above and below coarcted area)

EKG - LVH

Diagnosis - MRI can visualize best, cath usually done to measure degree and gradient

Treatment - Can do balloon with stenting or surgical repair. Usually done in younger patients, or those with an increased gradient

Outcome - patients have risk for aortic dissection and advanced HTN