Hypertension

First, some definitions...

• Normal blood pressure: systolic <120 mmHg and diastolic <80 mmHg
• Prehypertension: systolic 120 to 139 mmHg or diastolic 80 to 89 mmHg
• Hypertension:
• Stage 1: systolic 140 to 159 mmHg or diastolic 90 to 99 mmHg
• Stage 2: systolic ≥160 or diastolic ≥100 mmHg

Primary (Essential) Hypertension 

Pathogenesis - poorly understood for but the following have been implicated in primary HTN

• Increased sympathetic neural activity
• Increased Ang II and mineralcorticoid activity
• Genetic predisposition
• Reduced nephron mass

Risk Factors 

• Excess Na or ETOH intake
• Obesity and weight gain
• Physical inactivity
• dyslipidemia
• Depression
• Vitamin D deficiency

Secondary causes of HTN

• Medications - chronic NSAIDs, oral contraceptives and antidepressants. 
• Primary renal disease - vascular and glomerular
• Hyperaldosteronism - the presence of primary mineralocorticoid excess, primarily aldosterone, should be suspected in any patient with the triad of hypertension, unexplained hypokalemia, and metabolic alkalosis.
• Cushing's syndrome
• Hyper/Hypothyroidism and Hyperparathyroidism
• Obstructive sleep apnea
• Coarctation of the aorta

When should you start working up secondary causes of HTN?

It is not cost effective to perform a complete evaluation for secondary hypertension in every hypertensive patient. Thus, it is important to be aware of the clinical clues that suggest secondary hypertension. Clinical clues include...

• Severe or resistant hypertension. Resistant hypertension is defined as the persistence of hypertension despite concurrent use of adequate doses of three antihypertensive agents from different classes, including a diuretic.
• An acute rise in blood pressure developing in a patient with previously stable values.
• Age < 30 years of age in non-obese, non-black patients with a negative family history of and no other risk factors (obesity, HLD) for hypertension.
• Malignant or accelerated hypertension (patients with severe hypertension and signs of end-organ damage such as retinal hemorrhages or papilledema, heart failure, neurologic disturbance, or acute kidney injury). 
• Proven age of onset before puberty.

Tests to order and Physical Exam findings

• BMP to look at the BUN and CR and assess for primary renal disease
• US of the renal vasculature to search for RAS or Fibromuscular Dysplasia 
• On physical exam, carotid, abdominal, or femoral bruits suggest atherosclerotic disease and possible renal artery stenosis, diminished femoral pulses and/or a discrepancy between arm and thigh blood pressures suggest aortic coarctation or significant aortoiliac disease
• Screening for primary aldosteronism begins with a paired, morning measurement of the plasma aldosterone concentration (PAC) and plasma renin activity (PRA) to determine whether the patient has an elevated or high-normal PAC, suppressed PRA, and elevated PAC/PRA ratio
• If the patient is showing clinical clues for pheochromocytoma (episodic headache, sweating, and tachycardia) then measuring fractionated metanephrines and catecholamines in a 24-hour urine collection is the intial step. 
• For Cushing disease workup, UptoDate recommends two first-line tests should be abnormal to establish the diagnosis of Cushing's syndrome. First line tests include...late night salivary cortisol, urinary cortisol, and the low-dose dexamethasone suppression tests
• Sleep study for OSA
• TSH and PTH levels

Acute Pancreatitis

Introduction -The most common cause of pancreatitis is gallstones. The second most common cause if alcohol. Pancreatitis can be divided into two categories. 

1. Edematous acute pancreatitis, which is characterized by acute inflammation of the pancreatic parenchyma and peripancreatic tissues, but without recognizable tissue necrosis
2. Necrotizing acute pancreatitis, which is characterized by inflammation associated with pancreatic parenchymal necrosis and/or peripancreatic necrosis

Clinical Features - Most patients with acute pancreatitis have acute onset of persistent, severe epigastric abdominal pain. In approximately 50 percent of patients, the pain radiates to the back. Approximately 90 percent of patients have associated nausea and vomiting which may persist for several hours.

Diagnosis - The diagnosis of acute pancreatitis requires the presence of two of the following three criteria

1. Acute onset of persistent, severe, epigastric pain often radiating to the back
2. Elevation in serum lipase or amylase to three times or greater than the upper limit of normal
3. Characteristic findings of acute pancreatitis on imaging (focal or diffuse enlargement of the pancreas on contrast-enhanced abdominal CT or MRI is suggestive of acute pancreatitis. Check out the image below...P is for pancreas and it is quite large in that picture)

Management

• Fluid replacement - Up to Date recommends aggressive hydration at a rate of 5 to 10 mL/kg per hour of isotonic crystalloid solution (NS or LR) to all patients with acute pancreatitis. Fluid management needs to be reassessed frequently during the hospital stay. Monitor the vital signs, keep HR <120 and MAP between 65-89 and monitor the BUN as both the BUN at the time of admission and the change in 24 hours since admission can predict mortality. Watch the urine output (should be >0.5 to 1 cc/kg/hour) and try to achieve a reduction in hematocrit with a goal of 35 to 44 percent
• Pain control - Abdominal pain is often the predominant symptom in patients with acute pancreatitis and should be treated with analgesics. Hydromorphone and Fetanyl are recommended. I remember while studying for the boards that Merperidine was recommended over Morphine because it is believed that Morphine will cause contraction of the Sphincter of Oddi which would exacerbate the pancreatitis. However, Merperidine has a very short half life and can be cumbersome to manage the patient's pain adequately. 
• Nutrition - In mild pancreatitis, in the absence of nausea or vomiting, oral feeds can be initiated as soon as the pain is decreasing and inflammatory markers are improving (about 24-48 hours). A low fat, soft diet is recommended. In moderately severe to severe pancreatitis, oral feeding is frequently not tolerated. Patients usually require enteral or parenteral feeding.  Early enteral nutrition (within 24 to 48 hours) should be initiated when a patient is transferred to the ICU, or has the development of organ failure, or systemic inflammatory response syndrome (SIRS) persisting for 48 hours. Enteral feeding requires the placement of a jejunal feeding tube beyond the ligament of Treitz. The reason it needs to be beyond the ligament of Trietz is to avoid the duodenal release of cholecystokinin, the hormone that will activate the pancreas. A feed that is high protein and low fat is best to avoid little activation of the pancreas. 

Upper GI Bleed

The Common Internal Medicine posts continue. I have two patients with upper GI bleeds (UGIB) on my census this week. One patient has a large antral ulcer and another patient has a varicele bleed from cirrhosis of the liver.

Introduction - An upper gastrointestinal bleeding includes hemorrhage originating from the esophagus to the ligament of Treitz. Peptic ulcer bleeding causes more than 60 percent of cases of upper gastrointestinal bleeding, whereas esophageal varices cause approximately 6 percent. Other etiologies of upper gastrointestinal bleeding include arteriovenous malformations, Mallory-Weiss tear, gastritis and duodenitis, and malignancy.

Management 

Triage the patient - Patients with acute upper gastrointestinal (GI) bleeding commonly present with hematemesis or melena. The very first thing you should do when evaluating a patient with an UGIB is ask if they are hemodynamically stable and order a type and cross in case the patient will need a transfusion.

General Support - The patient recieve supplemental oxygen and be kept NPO for 24 hours or as long as an active bleed is occuring. If hemodynamic instability is occurring or suspected, the patient should have two large bore IV catheters or a central line for rapid fluid resuscitation.

Fluid Resuscitation - Patients with active bleeding should receive intravenous fluids, about 500 mL of normal saline or lactated Ringer's solution over 30 minutes, while being typed and cross-matched for blood transfusion.

Blood Transfusion - The decision on whether to transfuse or not depends on the patient's medical history. Do they have and co-morbid condition such as unstable angina that make them more susceptible to hypoxemia. Up to Date recommends that you should try to keep the patient's hemoglobin > 7, including patients with stable CAD. In patients with unstable CAD, the recommendation is > 9. However, patients with active bleeding and hypovolemia may require blood transfusion despite an apparently normal hemoglobin. In one of my patients, he became tachycardiac with a HR of 120 and so we transfused two PRBC eventhough his hemoglobin was >7. One should also avoid over transfusing (Hg>10) the patient as it may precipitate the bleeding.

Medications 

Acid suppression - Patients admitted to the hospital with acute upper GI bleeding are typically treated with a proton pump inhibitor (PPI). We started my patients on IV Protonix for 72 hours. PPIs may also promote hemostasis in patients with lesions other than ulcers secondary to the neutralization of gastric acid which leads to the stabilization of blood clots.

Prokinetics - The goal of using a prokinetic agent (erythromycin and metoclopramide) is to improve gastric visualization at the time of endoscopy by clearing the stomach of blood, clots, and food residue. We suggest that erythromycin be considered in patients who are likely to have a large amount of blood in their stomach, such as those with severe bleeding.  Erythromycin is a motilin agonist and will promote gastric motility. My patient with an antral ulcer may have benefited from this as the endoscope report read that "stomach difficult to fully visualize due to the large amount of blood".

Octreotide - Somatostatin, or its analog octreotide, is used in the treatment of variceal bleeding and may also reduce the risk of bleeding due to nonvariceal causes. In patients with suspected variceal bleeding, octreotide is given as an intravenous bolus of 20 to 50 mcg, followed by a continuous infusion at a rate of 25 to 50 mcg per hour. My patient with a varicele bleed and cirrhosis is on octreotide.
Octreotide is not recommended for routine use in patients with acute nonvariceal upper GI bleeding, but it can be used as adjunctive therapy in some cases, such as when the patient needs to be stabilized before an endoscopy. My patient with an antral ulcer is currently not on octreotide.

Antibiotics - Antibiotics are considered in the patient with an UGIB and cirrhosis. Bacterial infections are present in up to 20 percent of patients with cirrhosis who are hospitalized with gastrointestinal bleeding and up to an additional 50 percent develop an infection while hospitalized. The most common infections include spontaneous bacterial peritonitis, UTI, respiratory infections and septicemia. Studies have shown that by giving patients with a varicele bleed and cirrhosis prophylactic antibiotics, you will decrease mortality, hospital stay and recurrence of bleeding. The most common antibiotics used are the fluoroquinolones and ceftriaxone. Ceftriaxone is used on patients with severe cirrhosis or if the patient is in a hospital setting where there is a high resistance to the flouroquinolones. My patient with a varicele bleed and cirrhosis is on 1 gm/day of IV ceftriaxone X 5 days.

Anticoagulants - hold any anticoagulant medication (plavix, aspirin or coumadin) that the patient may be on.

Procedures - upper endoscopy is diagnostic test of choice for patients with UGIB.

Syncope

It is almost the 2 month countdown to the beginning of my Internal Medicine residency. I am looking forward to not being a medical student anymore but, naturally, I am terrified at the idea of being a physician. It has been very busy around here. We are in the process of sorting and packing up our home while trying to go to our everyday jobs as well. Still, I want to stay true to the spirit of my blog and continue to learn and read no matter how busy life gets. I thought that it would be appropriate to start focusing on common Internal Medicine admission problems to prep for the upcoming excitement! Today's topic...Syncope!

Introduction - Syncope is the abrupt and transient loss of consciousness associated with absence of postural tone, followed by complete and often rapid spontaneous recovery.

There are many causes of syncope but one can sort differentials into most likely vs least likely by taking a detailed history. Questions I ask all of my syncope patients include...

• What were you doing before it happened (laying to sitting to standing position? stressful event? Prolonged standing?)?
• Did you have any flushing, lightheadedness diaphoresis or nausea?
• Did you feel any palpitations?
• Did you lose bowel of bladder control?
• Did you have tremors/shaking?
• Were you short of breath?
• Did you have any chest pain?
• Was it witnessed? If so, what did the patient look like or do when they passed out? How long were they unconscious? Were they confused when they woke up? How long were they confused?
• Did the patient experience any auras before they passed out?
• Patients past medical history (panic attacks with hyperventilation, cardiac conditions or diabetes)
• Any new medications (antiarrhythmics or antihypertensives) or illicit drugs/etoh?
• Recent illness?
• Decreased oral intake?
• Has this ever happened before and if so, what was the circumstance?

Physical Exam

• Blood pressure obtained in the supine, sitting, and erect position may detect orthostatic hypotension
• Heat rate - is it tachy, brady or irregular?
• Resp rate - is the patient hyperventilating?
• Cardiac ascultation
• Neurologic findings such as unilateral neurologic defecits

Causes of Syncope

Vasovagal - Vasovagal syncope (also known as neurocardiogenic syncope) is the most common cause of syncope. Vasovagal syncope may be caused by autonomic cardioinhibitory and/or vasodilator responses. It is likely that sensory inputs through vagal afferents, pain pathways, and central pathways to cause inhibition of the sympathetic nervous system and vagal activation. The most frequent mechanism for vasovagal syncope is a cardioinhibitory response and the most common abnormality was prolonged asystolic pauses and bradycardia. 

Situational - Situational syncope refers to syncope associated with specific scenarios.

Some situations  (postmicturition, cough, or post-tussive) appear to trigger a neural reflex causing a vagal response others (eg, straining, squatting) may cause syncope via mechanisms unrelated to neural reflexes. Several forms of situational syncope are associated with gastrointestinal stimuli (swallowing, defecation, visceral pain).

Orthostatic (Postural) - When autonomic reflexes are impaired or intravascular volume is decreased, a significant reduction in blood pressure occurs upon standing, a phenomenon termed orthostatic hypotension. Orthostatic hypotension can cause dizziness, syncope, and even angina or stroke. Many disorders can cause orthostatic hypotension (Parkinsons, dementia with Lewy bodies and Multiple System Atrophy), volume depletion (blood loss or decreased oral intake) and medications (antihypertensives) are all common causes.

Cardiogenic - Cardiac causes of syncope include structural heart disease leading to abrupt episodic drops in cardiac output by various mechanisms and thus, decreased cerebral perfusion. These conditions may include an abnormal heart rhythm (arrhythmia), obstructed blood flow in the heart or blood vessels, valve disease, aortic stenosis, blood clot, or heart failure

Neurologic - Neurologic syncope is the loss of consciousness due to a neurological condition such as seizure, stroke, transient ischemic attack or other rare causes including migraines and normal pressure hydrocephalus.

What tests should you order?

• Orthostatic Blood Pressures
• Echocardiogram when there is previous known heart disease or data suggestive of structural heart disease or syncope secondary to cardiovascular cause
• Immediate EKG monitoring when there is a suspicion of arrhythmia
• Blood glucose
• CBC/CMP
• In hospital monitoring is recommended if patient has structural heart disease and is determined to be at risk for arrhythmia 
• If a neurologic cause is suspected should get CT or head without contrast or EEG if patient had suspected seizure activity 
• Exercise if exercise induced syncope is suspected
• Psychiatric consult if pseudosyncope is suspected
• Tox screen is high suspicion of drug/alcohol abuse