Visayas Community Medical Center : Department of Internal Medicine

Visayas Community Medical Center

Osmena Blvd, Cebu City

Grand Rounds Protocol:

Obesity As A Risk Factor For Chronic Kidney Disease

Date: Dec 7, 2009                                                                                             Reactor: Dr. German Mayo
Time: 8:30am                                                                                                     Presentor: Francis Cortes
Venue: Conference Room

A 43-year old morbidly obese Caucasian male was referred for evaluation of his chronic renal failure. He had been hypertensive with well controlled blood pressure with a body mass index of 46 and a baseline serum creatinine of 4.3 mg/dl (estimated glomerular filtration rate of 16 ml/min). He had failed all conservative attempts at weight reduction and hence was referred for a gastric by-pass surgery. Following the bariatric surgery he had approximately 90 lbs. weight loss over 8-months and his serum creatinine stabilized to 4.0 mg/dl.

Obesity is an important and potentially preventable risk factor for chronic renal failure (CRF). The incidence of diabetes and hypertension, two primary etiological factors for chronic renal failure, is significantly higher with obesity. Both diabetes and hypertension together account for approximately 70% of end-stage renal disease (ESRD). Because of the high rates of ESRD and death, it is of the utmost importance to identify potentially preventable causes or CRF.

There are few studies investigating the pathophysiology of obesity and its early effects on kidney structure and function. Clinical as well as laboratory animal studies have suggested the role of glomerular hypertension due to renal vasodilatation and increase in hydrostatic pressure leading to increased glomerular wall stress and increased tubular sodium absorption. The other proposed mechanism of excessive tubular sodium re-absorption include increased intra-renal pressures caused by the excess accumulation of adipose tissue in the viscera with compression of the loop of Henle and vasa recta leading to sluggish flow in the renal tubules and vasa recta and thus causing an increase in the tubular sodium re-absorption. Obesity is associated with increased levels of acute phase reactants, and cytokines as well as reactive oxygen species.

Obesity appears to be an independent risk factor for renal failure. Targeting obesity is beneficial not only for better control of hypertension and diabetes, but also possibly helps stabilization of chronic kidney failure.

Objectives:

1.) To Discuss the Growing Epidemiology of Obesity and its relationship to Diabetes Mellitus & Hpn

2.) To Discuss the Hemodynamic Changes in Obesity and its role on Chronic Kidney Disease

3.)To Discuss Obesity Glomerulosclerosis its prevalence and outcome

4.) To Discuss Preventable Measures in avoiding Obesity related CKD

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Medical Grand Rounds
Visayas Community Medical Center

Presentor: Carla B. Cabrera   Date: November 9, 2009
Reactors:    Maria Rosan Trani, M.D.   Time: 8:30 am
   Ruel Dejano, M.D.   Venue: VCMC Conference Room

Athletic Heart
“A Case of Having Too Much Heart”

Objectives:

1.   To briefly discuss the hemodynamics of exercise
2.   To discuss the impact of sports and training on cardiac structure and function
3.   To enumerate the electrocardiographic alterations associated with athlete’s heart
4.   To discuss the clinical significance of the changes in athletes heart and differentiate it from a pathological Cardiomyopathy

   More and more people are participating in athletics, particularly aerobic sports such as cycling and running. This can lead to cardiovascular adaptations that — while physiological — may be difficult to distinguish from disease. This pattern of changes is commonly referred to as athlete’s heart syndrome.

During intensive, prolonged endurance- and strength-training, the body signals the heart to pump more blood through the body to counteract the oxygen deficit building in the skeletal muscles. Long-term athletic conditioning is associated with cardiac morphologic changes, including increased left ventricular (LV) cavity dimension, wall thickness and mass. Although increased, it usually remains within the accepted upper normal limits, and different in most cases from changes seen in patients with structural cardiac diseases, such as cardiomyopathies.

Hypertrophic cardiomyopathy is a primary cardiac disease, for which the most characteristic morphologic feature is a hypertrophied non-dilated left ventricle in absence of cardiac or systemic disease itself capable of producing left ventricular hypertrophy. The prevalence of this disease in the general population is estimated to be 0.2%. The differential diagnosis of athlete's heart and hypertrophic cardiomyopathy is of crucial importance, because sudden death may be the initial clinical event in young athletes with hypertrophic cardiomyopathy, often in relation to exertion.

Although the athletic heart experiences structural changes that are common with some cardiac disease, 80% of people affected by athletic heart syndrome show a decrease in such structural changes and in bradycardia with detraining, thus, no treatment is required for people with AHS. In some cases, 3 months of deconditioning are required in order to distinguish AHS from cardiomyopathy. This may be met with resistance since training is an integral part of an athlete's life.

Case: A 21-year-old man was referred to a cardiologist because of abnormal ECG findings. He has no symptoms and no significant medical history. He is a professional soccer player of African origin, 185 cm, 74 kg. Physical examination is unremarkable, blood pressure was 130/70 mmHg. There is no family history of premature cardiac disease or premature cardiac death. Patient later on diagnosed with athletic heart syndrome.

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Visayas Community Medical Center

Department of Internal Medicine

Cebu City

Presentor: Dr. Julie Cinchez
Reactors:     Dr. Matthew Yap & Dr. Dennis Entera
Date: August 3, 2009; 8:30am
Venue: VCMC Conference Room



                ESJ is a 21/M, admitted for abdominal distention. 5 months PTA, patient noted changes of bowel habits, LBM 3-4x/ day, sought consult with a physician and was treated as amoebiasis.

4 months PTA, noted crampy abdominal pain, with constipation. (+) weight loss, ~ 30%. Consult w/ a physician, colonoscopy done revealing an obstructing nodular, hard to biopsy,rectal mass 7-10 cm from anal verge with circular ulcers with erythema scattered at rectum. Biopsy done revealed chronic non- specific colitis, negative for malignancy. Advised colostomy but refused due to financial constraints.

3 weeks PTA, noted gradual abdominal distention,(+) flatus, (-) BM. Consulted w/ a physician, ctscan of abdomen done showed rectal thickening and lymphadenitis of the omentum, CEA also taken, 3.86(<3.4-4.3) was normal. Was then advised admission.

                On admission, vital signs were stable, patient’s abdomen was noted to be distended, tympanitic with absent bowel sounds. DRE revealed a firm mass 4-5 cm from the anal verge, non tender w/ fecal material on examiner’s finger. Patient was then scheduled for surgery (plan: miles procedure) w/ FS.

On the 4^th hospital day, patient underwent anoscopy, FS, exploratory laparotomy, transverse loop colostomy. Frozen section showed severe chronic colitis w/ few atypical cells seen infiltrating the lamina propria suspicious for malignancy. Post op diagnosis was TB enteritis. Biopsy later revealed poorly differentiated adenocarcinoma w/ omentum and mesenteric lymph node metastasis.

Colorectal cancer is second only to lung cancer as a cause of cancer death in the United States: 153,760 new cases occurred in 2007, and 52,180 deaths were due to colorectal cancer. The incidence rate has remained relatively unchanged during the past 30 years, while the mortality has decreased particularly in females. Colorectal cancer generally occurs in persons >= 50 years old.

Objectives:

¨ To review Colorectal Carcinoma as to its:

¤ Incidence

¤ Pathogenesis

¤ Etiology/Risk factors

¤ Screening Recommendations

¤ Survival Rate

¤ Treatment options

Visayas Community Medical Center

Department of Internal Medicine

Grand Rounds Protocol

Presentor: Dr. Shoji S. Mantilla Venue: VCMC Conference Room

Reactor: Dr. Albert Rafanan Date: July 6,2009

Time: 8:30am

Title: “Doctor, why can’t I stay awake?”

Topic: Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) is a common sleep apnea caused by obstruction of the airway. It is characterized by pauses in breathing during sleep. These episodes, called apneas (literally, "without breath"), each last long enough that one or more breaths are missed, and occur repeatedly throughout sleep. In obstructive sleep apnea, breathing is interrupted by a physical block to airflow, despite the effort to breathe.

Common signs of obstructive sleep apnea include unexplained daytime sleepiness, restless sleep, and loud snoring (with periods of silence followed by gasps). Less common symptoms are morning headaches; insomnia; trouble concentrating; mood changes such as irritability, anxiety and depression; forgetfulness; increased heart rate and/or blood pressure; decreased sex drive; unexplained weight gain; increased urination and/or nocturia; frequent heartburn or Gastroesophageal reflux disease; and heavy night sweats.

Prognosis of OSA has a strong association with several diseases, particularly those related to the heart and circulation. A number of cardiovascular diseases -- including high blood pressure, heart failure, stroke, metabolic syndrome, and heart arrhythmias -- have an association with obstructive sleep apnea. This link may be because both cardiovascular illnesses and sleep apnea are associated with obesity and its consequences. However, large cohort observational studies have suggested that OSA itself may lead to incident cardiovascular disease. At this time, however, evidence of a clear causal relationship with any of these health problems is still weak. Some studies have found no significant independent risk for heart disease from obstructive sleep apnea. Likewise, whether treating obstructive sleep apnea decreases the incidence of any of these disorders remains to be proven.

Objectives: Review of the following:

Physiology of Sleep
Evaluation of Sleep
Definition of Obstructive Sleep Apnea (OSA)
Prevalence of OSA
Pathophysiology of OSA
Complications of OSA
Medical Treatment of OSA
Surgical Treatment of OSA

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Visayas Community Medical Center

Department of Internal Medicine

Cebu City

Presentor: Dr. Nino JN Doydora Venue: Conference Room

Reactor: Dr. Mitzie Montebon-Chua Date: June 1, 2009 at 8:30am

Cryptococcal Meningitis

GL, a 42 year old female was admitted to this institution for headache, associated with febrile episodes.

She was diagnosed with SLE in 2006 and was then maintained on prednisone 20 mg OD. She is non hypertensive but recently has been diagnosed with diabetes mellitus and was on metformin 500 mg TID.

More than 2 weeks prior to admission, patient was hospitalized at CVGH due to pneumonia and was treated with Cefuroxime and Ciprofloxacin, discharged improved after 5 days confinement. Her prednisone was increased to 30 mg OD upon discharged.

Problem: headache, associated with febrile episodes

Patient’s headache was noted <2 weeks after discharge and was characterized to be bi-frontal, occasionally radiating to the occipital area and nape; it was described as dull, not aggraviated with bright light and was temporarily relieved by paracetamol PO. Patient decided to seek consult with AP and was referred to a neurologist for further evaluation. She was then advised for admission for further work-up.

At the ER, she was noted to be conscious, coherent, ambulatory with no headache noted. She has been taking paracetamol PO RTC q4H. BP was 110/80, HR 76, RR 19, afebrile with a weight of 69 kg. There was no papilledema noted on fundoscopic exam. There was no nuccal rigidity. Negative for Kernig’s and Brudzinsky’s signs. No focal neurologic deficit noted. She was then schedule for lumbar tap. Opening pressure was 18cmH2O while closing pressure was 17.5 cm H2O. CSF examination revealed: clear, colorless fluid with WBC 0-2, protein 139 (elevated), CSF glucose 42 and random blood sugar was 263 with CSF/Serum glucose ratio of 0.16. CSF was negative in India Ink, gram stain, AFB smear and KOH mount while positive for Cryptococcal Latex Agglutination System Test (CALAS).

Patient was then started on amphothericin B at 0.7mg/kg/day IV drip. Prednisone was increased to 30 mg OD, she was also given initially metformin and sitaglyptin but later switched to insulin for better glycemic control. She is now on her 13^th day of IV treatment. The plan is to complete 14 days of amphothericin B therapy and she will be given fluconazole PO as home medication.

Cryptococcus Meningitis (CM) has an incidence rate of 1 in 200,000 in the general population (US data). However, it occurs at ~10% in patients with HIV AIDS. In this condition, the leptomeningis is infected with Cryptococcus sp which usually presents as sub-acute type of meningitis. Predisposed to this condition are those with HIV/AIDS, lymphoreticular malignancies, organ transplantation patients, and those on corticosteroid therapy.

Objectives:

· To review Cryptococcus meningitis as to its:

o Etiology and pathophysiology

o Clinical manifestations

o Diagnosis and differential diagnoses

o Treatment options and follow up

· To review local studies on cryptococcal meningitis

· To discuss the prognosis, outcome and survival of patients diagnosed with Cryptococcus meningitis

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Visayas Community Medical Center

Department of Internal Medicine

Cebu City

Presentor: Dr. Nino JN Doydora Venue: Conference Room

Moderator: Dr. Edgar Molleno Date: October 6, 2008

Reactor: Dr. Ronald Eullaran Time: 8:30am

DERMATOMYOSITIS

A 45 year old female was admitted for (3 weeks) rashes (on her hands, face and neck) associated with body malaise; it was noted after she ate shrimp. She claims to be allergic to seafoods and some vegetables. She was seen by a local physician who gave her loratadine 5mg + bethamethasone 250 mcg (Claricort) 1 tablet once a day which she took for a week with mild resolution of rashes. She sought second opinion and her medication was shifted to loratadine 10 mg OD and prednisone 10 mg OD. Persistence of rashes associated with body malaise prompted admission. She was eventually referred to a rheumatologist who saw her with resolving rashes. Weakness of the proximal muscles was noted; with difficulty in combing hair, changing clothes, going up the stairs. Primary impression was Dermatomyositis. It was further supported by elevated total (creatinine kinase) CK of 3,275 u/l. She was given hydrocortisone IV and EMG-NCV studies were done and suggested pathology involving the proximal muscles of both upper and lower limbs –suggesting “myopathy”. After 5 days. Total CK was repeated and was 1,249 u/l. Her muscle strength continued to improve from the initial examination of 2/5 (motor strength) and has improved to 4/5 in all four extremities. She was then discharged, improved; to continue prednisone at 1mg/kg/day and to follow-up with AP monthly for the next 2 months.

Polymyositis (PM) and dermatomyositis (DM) are uncommon systemic diseases characterized by inflammatory and degenerative changes in the muscles (polymyositis) or in the skin and muscles (dermatomyositis). Occurring one in every 100,000 in the general population, the female to male ratio is 2:1. These diseases may appear at any age but occur most commonly from age 40 to 609, in children, from age 5 to 15. The most specific skin signs are Gottron’s papules over the knuckles and a periorbital heliotropic rash. Manifestations include symmetric weakness, some tenderness and later atrophy, principally of the proximal limb girdle muscles. Complications can include visceral involvement and cancer. Diagnosis is by clinical findings and abnormalities on muscle tests, which may include muscle enzymes, MRI, electromyography, and muscle biopsy. The cause is an autoimmune reaction to muscle tissue in a genetically susceptible individual. Treatment is with corticosteroids, sometimes combined with immunosuppressants of IV immune globulin. The most recent therapy undergoing trials involve the use biologics in DM.

Objectives:

· To review Dermatomyositis as to its:

o Etiology

o Pathophysiology

o Clinical manifestations

o Diagnosis and deifferential diagnoses

o Treatment options

· To discuss prognosis, outcome and survival of patients diagnosed with dermatomyositis