Angeles University Foundation Angeles City Case Analysis Group 1 BSMT 3A DIMLA, Mary Kimberly PARTOLAN, Mark Jadrian SALINAS, March Tracy TORRES, Kristensen January 7, 2010 CASE 2 From a rural hospital in Barangay Ilang-Ilang, this 71-year old woman was transferred to a tertiary hospital complaining of shortness of breath and showing evidence of pulmonary edema. There was no history of chest pains, nausea, vomiting or diaphoresis. Her admission diagnosis was Congestive Heart failure (acute exacerbation), Myocardial Infarction (subendocardial), DM and HTN. Medications included Lasix, morphine, nitroglycerin, and Procardia. Laboratory tests were significant for increased CK, 544 U/L (21-215) with a CKMB of 29.2 ng/mL (0-4), which is a relative index of 54. During the first few days of her hospital stay, blood glucose ranged from 201 to 365 mg/dL (70-110); creatinine ranged from 1.9 to 3.7 mg/dL (0.6-1.0); and BUN ranged from 31 to 46 mg/dL (5-25). Admission urinalysis was significant for: glucose 100 mg/dL; blood moderate; protein >300 mg/dL (<90); WBCs 2-5/hpf; RBCs 10-20/hpf; epithelials/lpf few squamous, few renal; casts/lpf 5-10 granular, 0-1 WBC. After aggressive treatment of the she received intravenous nitroglycerin and insulin. The discharge diagnosis was status postsubendocardial MI, triple-vessel cardiac disease, CHF, renal insufficiency, HTN, and DM. She was scheduled to return to the hospital eventually for a triple vessel coronary bypass. What renal condition do the urinalysis data suggest? Explain. Do the analyses on blood correlate with this? Explain. What is the pathophysiology behind the renal condition in the first question? Explain. Gender: Female Age: 71 Symptoms: Shortness of breath Pulmonary edema *no chest pains *no nausea *no vomiting Diagnosis: CHF (Congestive Heart Failure) MI (Myocardial Infarction)

HTN (Hypertension) DM (Diabetes Mellitus) Medications: Lasix – CHF Morphine –pain killer Nitroglycerin –vasodilator Procardia –antiaginal, antihypertensive Insulin –DM Blood Chemistry Results: CK -554u/l CKMB -29.2u/L Glucose - 201 to 365 mg/dL (70-110) Creatinine- 1.9 to 3.7 mg/dL (0.6-1.0) BUN- 31 to 46 mg/dL (5-25) Urinalysis Results: Chemical: Glucose: 100mg/dl Blood (moderate) Protein- >300 mg/dL (<90) Microscopic: RBC 10-20/hpf WBC 2-5/hpfb Epithelial. Cells (few) Renal Cell (few) Granular Cast (5-10/lpf) Leukocyte Casts (0-1/lpf) Patient Diagnosis: Chronic Glomerulonephritis Terminologies Cardiac markers (CKMB) are biomarkers measured to evaluate heart function. They are often discussed in the context of myocardial infarction, but other conditions can lead to an elevation in cardiac marker level. Blood urea nitrogen (BUN) test is a measure of the amount of nitrogen in the blood in the form of urea, and a measurement of renal function. Pulmonary edema is fluid accumulation in the lungs. It leads to impaired gas exchange and may cause respiratory failure. Congestive Heart failure (CHF) is a condition in which a problem with the structure or function of the heart impairs its ability to supply sufficient blood flow to meet the body's needs. The phrase is often wrongly used to describe other cardiac-related illnesses, such as myocardial infarction (heart attack) or cardiac arrest.

Hypertension is a chronic medical condition in which the blood pressure is elevated. It is also referred to as high blood pressure or shortened to HT, HTN or HPN. The word "hypertension", by itself, normally refers to systemic, arterial hypertension. Diabetes mellitus often referred to as diabetes—is a condition in which the body either does not produce enough, or does not properly respond to, insulin, a hormone produced in the pancreas. Furosemide (INN) or frusemide (former BAN) is a loop diuretic used in the treatment of congestive heart failure and edema. It is most commonly marketed by Sanofi-Aventis under the brand name Lasix. Morphine is an extremely potent opiate analgesic psychoactive drug, is the principal active ingredient in Papaver somniferum, is considered to be the prototypical opioid. In clinical medicine, morphine is regarded as the gold standard, or benchmark, of analgesics used to relieve severe or agonizing pain and suffering. Nitroglycerin is also used medically as a vasodilator to treat heart conditions, such as angina and chronic heart failure. Nifedipine (brand name Adalat, Nifedical, and Procardia) is a dihydropyridine calcium channel blocker. Its main uses are as an antianginal (especially in Prinzmetal's angina) and antihypertensive, Guide Questions: What renal condition do the urinalysis data suggest? Explain. Do the analyses on blood correlate with this? Explain. What is the pathophysiology behind the renal condition in the first question? Explain. CHRONIC GLOMERULONEPHRITIS. Based on the urinalysis test results of the patient, there is a high elevation of protein (proteinuria) and glucose level, a moderate amount of blood (hematuria) has been also detected accompanied by granular and cellular cast. in which these findings are assumed to be the primary urinalysis test result of this renal condition. YES it correlates. According to the blood test assessment, the level of Blood Nitrogen Urea (BUN) and creatinine are markedly increased, this may result to a decreased glomerular filtration rate. When GFR is impaired, less creatinine is excreted by the glomerulus causing serum levels to rise. While the concentration of urea nitrogen in the blood reflects glomerular filtration and urine-concentrating capacity. Because urea is filtered at the glomerulus, blood urea nitrogen (BUN) levels increase as glomerular filtra-tion drops. Because urea is reabsorbed by the blood through the permeable tubules, the BUN rises in states of dehydration and acute and chronic renal failure when passage of fluid through the tubules is slowed. BUN also varies because of altered protein intake and protein catabolism and therefore is a poor measure of GFR. The application of this principle is useful for monitoring progressive changes in renal function. Serum creatinine and BUN are elevated in chronic glomerulonephritis and other related renal conditions. PATHOPHYSIOLOGY OF CHRONIC GLOMERULONEPHRITIS: Chronic glomerulonephritis occurs when there is slow, progressive destruction of the glomeruli of the kidney, with progressive loss of kidney function. Damage to the glomeruli affects the kidney's ability to filter fluids and wastes properly. This leads to blood and protein in the urine called microscopic hematuria and proteinuria. The inflammation causes blood and protein to leak into the urine. As protein levels in the blood fall, excess fluid accumulates in the body.

Tests show protein, blood cells, and kidney cells in the urine, while a high concentration of the body's waste products of metabolism (such as urea and creatinine) may be found in the blood. Creatinine is a substance that is produced by muscle and released into the blood at a relatively constant rate. Laboratory tests for serum creatinine provide an indicator or glomerular filtration rate (GFR). When the GFR is damaged a reduced amount of creatinine is being emit by the the glomerulus that causes the serum creatinine levels to increase. BUN reflects the GFR, because the urea is being filtered to glomerulus, when the BUN elevates the GFR drops, because the urea is being reabsorbed by the blood through the permeable tubules, the BUN rises in chronic renal failure when passage of fluid through the tubules is slowed. BUN also varies because of altered protein intake and protein catabolism and therefore is a poor measure of GFR. Casts (accumulations of cellular precipitates) originate in the renal tubules, from which they take their shape. They are cylindrical with distinct borders. All casts have a precipitated microprotein matrix and arise primarily from the ascending limb of the distal tubule. Granular Cast, indicates that the patient occur glomerulonephritis. The type of cast identified suggests the disease process occurring in the kidney. White blood cells (WBCs) in the urine (a condition termed pyuria) are primarily indicative of urinary tract infection, particularly when bacteria are present. Glomerulonephritis and nephrotic syndrome also may demonstrate pyuria, but usually in combination with proteinuria, red cells, and casts. The finding of WBC casts reflects a kidney infection, because these casts are not formed in the bladder or prostate. Chronic glomerulonephritis usually causes only very mild or subtle symptoms, it goes undetected for a long time in most people. Edema may occur. High blood pressure is common. The disease may progress to kidney failure, which can cause itchiness, fatigue, decreased appetite, nausea, vomiting, and difficulty breathing. Questions Which of the following is not a symptom of Chronic Glomerulonephritis hypertension edema oliguria hypotension All are types of immune mechanisms which contributes to glomerular injury except: a. Deposition of circulating soluble antigen-antibody complexes b. Formation of antibodies specific against the glomerular basement membrane c. Streptococcal release of neuramidase, which alters IgG with binding of anti-IgG to the glomerulus. d. none of the above Chronic Glomerulonephritis includes primary urinalysis results except: a. hematuria b. proteinuria c. granular cast d. oval fat bodies Other significant test for Chronic Glomerulonephritis includes: serum creatinine creatinine clearance both a and b none of the above

Reduction in nephron mass from the initial injury reduces the GFR then leads to: hypertrophy hyperfiltration of the remaining nephrons both a and b none of the above Which of the following best describes Chronic Glomerulonephritis: Occurs primarily in children following viral respiratory infections. Disruption of podocutes in certain areas of glomeruli associated with heroin and analgesic abuse. Deposition of IgA on the glomerular membrane resulting from increased levels of serum IgA Marked decrease in renal function resulting from glomerular damage precipitated by other renal disorder. Which of the following is not a cause of Chronic glomerular injury: Insulin-dependent diabetes mellitus lupus erythematosus Hypercholesterolemia None of the above Chronic Glomerulonephritis can be caused by: mercury non-steroidal anti-inflammatory analgesics HIV All of the above First indicator of renal disorder is: protein glucose blood abnormal sediment The most significant and the only one that can be found in a cast: WBC RBC Renal epithelial Squamous epithelial Chronic glomerulonephritis Chronic glomerulonephritis is the advanced stage of a group of kidney disorders, resulting in inflammation and slowly worsening destruction of internal kidney structures called glomeruli. Causes, incidence, and risk factors: Chronic glomerulonephritis occurs when there is slow, progressive destruction of the glomeruli of the kidney, with progressive loss of kidney function. In some cases, the cause is found to be a specific attack to the body's immune system, but in most cases, the cause is unknown. Iit is generally thought that a still-unidentified abnormality of the immune system is to blame. Damage to the glomeruli affects the kidney's ability to filter fluids and wastes properly. This leads to blood and protein in the urine.

This condition may develop after survival of the acute phase of rapidly progressive glomerulonephritis. In about one-quarter of people with chronic glomerulonephritis there is no prior history of kidney disease, and the disorder first appears as chronic kidney failure. Glomerulonephritis is among the leading causes of chronic kidney failure and end stage kidney disease. Causes include: * Diabetic nephropathy/sclerosis * Focal segmental glomerulosclerosis * IgA nephropathy (Berger's disease) * Lupus nephritis * Membranous glomerulonephritis * Mesangial proliferative disorder * Nephritis associated with disorders such as amyloidosis, multiple myeloma, or immune disorders, including AIDS Symptoms: This condition causes high blood pressure (hypertension) and chronic kidney failure. Specific symptoms include: * Blood in the urine (dark, rust-colored, or brown urine) * Foamy urine Chronic kidney failure symptoms that gradually develop may include the following: * Decreased alertness o Drowsiness, somnolence, lethargy o Confusion, delirium o Coma * Decreased sensation in the hands, feet, or other areas * Decreased urine output * Easy bruising or bleeding * Fatigue * Frequent hiccups * General ill feeling (malaise) * Generalized itching * Headache * Increased skin pigmentation -- skin may appear yellow or brown * Muscle cramps * Muscle twitching * Nausea and vomiting * Need to urinate at night * Seizures * Unintentional weight loss Additional symptoms that may be associated with this disease: * Blood in the vomit or stools * Excessive urination * High blood pressure * Nosebleed

Signs and tests: Because symptoms develop gradually, the disorder may be discovered when there is an abnormal urinalysis during a routine physical or during an examination for another, unrelated disorder. It may be discovered as a cause of high blood pressure that is difficult to control. Laboratory tests may reveal anemia or show signs of reduced kidney functioning, including azotemia. Later, signs of chronic kidney failure may be apparent, including edema . Tests that may be done include: * Chest x-ray * Kidney or abdominal CT scan * Kidney or abdominal ultrasound * IVP * Urinalysis A kidney biopsy may show one of the forms of chronic glomerulonephritis or scarring of the glomeruli. This disease may also alter the results of the following tests: * Albumin * Abdominal MRI * Anti-glomerular basement membrane * BUN * Complement component 3 * Complement * Creatinine clearance * Renal scan * Total protein * Uric acid, urine * Urine concentration test * Urine creatinine * Urine RBC * Urine specific gravity * Urine protein Treatment: Treatment varies depending on the cause of the disorder, and the type and severity of symptoms. The primary treatment goal is control of symptoms. High blood pressure may be difficult to control, and it is generally the most important aspect of treatment. Various medications may be used to attempt to control high blood pressure. Corticosteroids, immunosuppressives, or other medications may be used to treat some of the causes of chronic glomerulonephritis. Dietary restrictions on salt, fluids, protein, and other substances may be recommended to help control of high blood pressure or kidney failure. Dialysis or kidney transplantation may be necessary to control symptoms of kidney failure and to sustain life. The outcome varies depending on the cause. Some types of glomerulonephritis may get better on their own.

If nephrotic syndrome is present and can be controlled, other symptoms may be controlled. If nephrotic syndrome is present and cannot be controlled, end-stage kidney disease is likely. The disorder worsens at widely variable rates. Complications: * Nephrotic syndrome * Acute nephritic syndrome * Chronic renal failure * End-stage renal disease * Hypertension * Malignant hypertension * Fluid overload -- congestive heart failure, pulmonary edema * Chronic or recurrent urinary tract infection * Increased susceptibility to other infections

I. SUMMARY OF THE CASE The 49 year old male presented in E.R. was complaining of abdominal pain accompanied by nausea, vomiting, some coughing which is non-productive and a slightly erythematous rash on the toes of both feet. He was experiencing these in the past 5 months and was getting worst in the last two days. The patient medical history show the he was diagnosed with AIDS last year, disseminated tuberculosis and was an intravenous drug abuser. On admission, the patient is taking in some medications and this includes: INH (Isonicotinic Acid Hydrazide) - It is prescribed for prophylaxis for those who have been exposed to

tuberculosis and is used in combination with other agents in the treatment of tuberculosis caused by mycobacteria sensitive to the drug. Adverse effect: Rashes

RIFAMPIN - an antituberculosis agent, it works by killing or stopping the growth of tuberculosis bacteria. Adverse effects: reddish orange discoloration of body fluids including urine,

BACTRIM DS – antibiotic that treat different types of infection caused by bacteria, used to treat ear infections, urinary tract infections, bronchitis, traveler's diarrhea, and Pneumocystis carinii pneumonia. Adverse effects: nausea, vomiting, abdominal pain and allergic skin reactions such as rash and urticaria, Cough and pulmonary infiltrates

He is also taking in Megace, Flucon, MS Contin, Morphine Elixir The patient’s abdomen x-ray showed multiple air- fluid levels in the small bowel. The patient was then admitted for observation and treatment of the ileus. The results Urinalysis are as follows: Color- amber pH- 7.0 Specific Gravity- 0.020 Glucose- negative Bilirubin- negative Ketone- negative Blood- negative Nitrite and leukocyte esterase- negative Urobilinogen- normal Protein- 30mg/dl

He was discharged after 3 days in stable condition and continued taking in Bactrim DS, INH, Rifampin and Diflucan.

II. ANSWER TO GUIDE QUESTIONS

1. Are there any significant findings in the urinalysis?

Yes, the positive urine protein may indicate a renal disease. The result of the Urinalysis of the patient is 30mg/dL which is trace to 1+. Normal urine contains very little protein; usually, less than 10mg/dL or 100mg/24 hours is excreted and clinical proteinuria is indicated at >30mg/dL.

2. How would you characterize the casts and cells that may be observed in the urine if microscopic analysis

was performed?

Hyaline casts may appear + sulphonamide crystals due to administration of Bactrim.

3. What pathophysiologic picture is illustrated by the urinalysis in this case?

This is a possible case of Focal Segmental Gloerulosclerosis, secondary to narcotic abuse. The patient’s urine protein which is 30mg/dL is considered normal since clinical proteinuria is indicated at >30mg/dL of urine protein, but it still depends upon the severity of the disease. We have concluded that this is a possible case of FSGS probably because the disseminated tuberculosis of the patient was just starting to affect the urinary system that is why only trace up to 1+ protein is present.

AMBER COLORED URINE is due to Rifampin, while nausea, vomiting, abdominal pain and allergic skin reactions such as rash and urticaria are the most common adverse effects of Bactrim DS associated with the Gastrointestinal Tract. Cough and pulmonary infiltrates are also adverse effect of Bactrim DS related with Respiratory. Side effects generally are more common and more severe in patients with AIDS. Side effects generally are more common and more severe in patients with AIDS. Hypersensitivity reactions may be more likely in patients with HIV infection, with opportunistic infections.

ILEUS; an obstruction of the intestine can cause ABDOMINAL PAIN due to contractions of intestinal muscle and distension of intestine. This Abdominal Pain may worsen due to COUGHING. Patients with ILEUS may also report NAUSEA AND VOMITING. One probable cause of ileus is the USE OF CERTAIN DRUGS, such as NARCOTIC PAIN DRUGS or high blood pressure medicine.

DISSEMINATED TUBERCULOSIS (TB) is a contagious bacterial infection that has spread from the lungs to other parts of the body through the blood or lymph system. Disseminated disease develops in the small number of infected people whose immune systems do not successfully contain the primary infection. Since the patient was diagnosed with ADIS, therefore he is immune compromised.

III. SAMPLE TEST PAPER

1. This is the most indicative of renal disease among the routine chemical tests performed on urine:

a) Protein b) Glucose

c) pH d) Blood

2. Normal levels of protein present in urine daily: a) 5mg/dL b) 10mg/dL

c) 15mg/dL d) 20mg/dL

3. The amber color urine was caused by which of the following medications that the patient is taking in? a) INH b) Bactrim DS

c) Rifampin d) Flucon

4. With the given Physical and Chemical results, Microscopic Analysis should be requested.

a) Statement is TRUE b) Statement is FALSE

5. What Renal disorder is related to the case of the patient?

a) Acute Glumerulonephritis b) Focal Segmental

Glomerulosclerosis

c) Alport Syndrome d) Good Pasture Syndrome

6. Among which of the following Renal Disease may resemble with your answer in number 5?

a) Nephrotic Syndrome b) Minimal Change Disease

c) Either d) Neither

7. Focal Segmental Glomerulosclerosis is often associated with the following conditions seen in the patient except:

a) Cough b) AIDS

c) Narcotic abuse of drugs d) NIL

8. What are the cast or cells that may be present if Microscopic Analysis is performed? a) Fatty Cast b) Hyaline Cast c) Waxy Cast d) RBC Cast

9. The cause of proteinuria based on the origin of Protein:

a) Pre renal b) Renal

c) Post Renal d) NIL

10. Clinical proteinuria is indicated in which of the following protein levels in urine?

a) >10mg/dL b) >20mg/dL

c) >30mg/dL d) >40mg/dL

ANSWERS:

1. A) Protein 2. B) 10mg/dL 3. C) Rifampin 4. A) TRUE 5. B) Focal Segmental Glomerulosclerosis 6. C) Either 7. A) Cough 8. B) Hyaline Cast 9. B) Renal 10. B) >30mg/dL

IV. PERTINENT INFORMATION

FOCAL SEGMENTAL GLOMERULOSCLEROSIS FSGS affects only certain numbers and areas of glomeruli, and others remain normal. Symptoms may be similar to the nephritic syndrome and minimal change disease owing to damaged podocytes. Immune deposits, primarily immunoglobulins M and C3, are a frequent finding and can be seen in undamaged glomeruli. FSGS is often seen in association with abuse of heroin and analgesics and with AIDS. Moderate to heavy proteinuria and microscopic hematuria are most consistent urinalysis findings. Focal Segmental Glomerulosclerosis is a disease that attacks the kidney’s filtering system (glomeruli) causing serious scarring. FSGS affects only certain numbers and areas of glomeruli, and others remain normal. Symptoms may be similar to the nephritic syndrome and minimal change disease owing to damaged podocytes. FSGS is often seen in association with abuse of heroin and analgesics and with AIDS. Moderate to heavy proteinuria and microscopic hematuria are most consistent urinalysis findings. Primary UA results: Proteinuria Microscopic hematuria Macroscopic or microscopic hematuria Other Significant test: Drugs of abuse HIV tests Genetic testing

Etiology: Disruption of podocytes in certain areas of glomeruli associated with heroin and analgesic abuse and AIDS. Clinical course: May resemble nephritic syndrome or minimal change disease The individual components of the name refer to the appearance of the kidney tissue on biopsy: FOCAL—only some of the glomeruli are involved (as opposed to diffuse) SEGMENTAL—only part of an entire glomerulus is involved (as opposed to global) GLOMERULOSCLEROSIS—refers to scarring of the glomerulus (a part of the nephron) The important risk of intravenous drug use as a pathogenic factor of renal disease and shows a rarity of renal disease in homosexual or bisexual men with AIDS. The patient’s complaint matches the side effects of the Bactrim DS he is taking which is more common in AIDS patients. This includes vomiting, nausea, urticaria, rashes and systemic lupus erythematous. There are no significant findings in the urinalysis; amber colored urine may be due to his medications. If microscopic analysis is performed, crystalluria may be observed as a side effect. If crystalluria is observed in the urinalysis, the patient will experience irritation of the kidney. However, crystals observed in urinalysis are usually insignificant. Kidney damage under a microscope showed diffuse glomerular membrane increased, with minimal glomerular sclerosis. The number of occurrence ranging from segmental glomerular sclerosis, which is characterized by a thick cytoplasm containing vacuoles of epithelial cell proliferation, capillary wall collapse, or because of protein deposition (hyaline degradation) and to the capillaries disappear, cavity foam cells (lipid filled with mononuclear cells). Glomerular cysts are usually expanded, tubular damage is extensive. Focal Segmental Glomerulosclerosis (FSGS) is a disease that attacks the kidney’s filtering system (glomeruli) causing serious scarring. FSGS is one of the many reasons of a disease known as Nephrotic Syndrome, which occurs when valuable protein in the blood leaks into the urine (proteinuria).

V. REFERENCES Susan King Strasinger, Urinalysis and Body Fluids, 2008 Amy M. Karch, Lippincott’s Nursing Drug Guide, 2009 http://www.drugs.com/sfx/bactrim-side-effects.html www.medicinenet.com/abdominal_pain/article.htm en.wikipedia.org/wiki/Abdominal_pain http://www.medcohealth.com/medco/consumer/ehealth/ehsarticle.jsp?packageTemplate=HE+article+XML+template&ltSess=y&currentPage=%2Fconsumer%2Fehealth%2Fehsarticle.jsp&com.broadvision.session.new=Yes&articleID=97666 en.wikipedia.org/wiki/Bowel_obstruction www.answers.com/topic/ileus www.health-care-clinic.com/family-health/i/ileus.htm www.health-care-clinic.com/family-health/i/ileus.htm http://en.wikipedia.org/wiki/Focal_segmental_glomerulosclerosis http://www.ich.ucl.ac.uk/gosh_families/information_sheets/focal_segmental_glomerulosclerosis/image1.jpg http://www.91sqs.com/attachments/2007/07/2446_200707141110261.jpg http://www.nephcure.org/fsgs-facts.htm http://www.tcmwell.com/TCM_News/hiv/The-performance-of-HIV-infection---Urinary-system.html Angeles University Foundation Angeles City College of Allied Medical Professions Medical Technology Department Post Prelim Conference in Clinical Microscopy Case 7

Submitted By: GROUP 10 Torres, Chelzylyn M. Bacani, Fernando, Ocampo, Toni Jerico Savellano, Lara Mikee Submitted To: Ms. Crizelda Liwanag, RMT Mrs. Eloisa Q. Singian, RMT 7 January 2010 Angeles University Foundation Angeles City Group 7 Dimaun, Joy Sandoval, Noel Santos, Marjorie Soliman, Lea Case Jessica is a 20-year old woman admitted to R/O appendicitis, pancreatitis, pyelonephritis, abdominal abscess, or ruptured viscus. She came to the ER complaining of severe abdominal pain or what is called an “acute abdomen”. Because she was 36 weeks’ (estimated) IUP, a low C-section was performed and the child was delivered. Her appendix was found to be ruptured and it was removed at the same time. Blood cultures were positive for E.coli, sensitive to Cefotan (cefotetan disodium) and to gentamicin, which she was given. The urinalysis, obtained two days postsurgery, was as follows: glucose negative, bilirubin small; ketones 40 mg/dL; specific gravity 1.025; blood negative; pH 6.5; protein 30 mg/dL; urobilinogen 1.0 EU/dL; nitrite negative; leucocyte esterase trace; color orange; WBCs 5-10/hpf; RBCs 0-2/hpf; epithelial cells 1+/hpf; bacteria 1+/hpf; bacteria 1+; casts 1-5 granular. Ictotest negative. C&S was not requested on this urine.

Questions: 1. What aspects of the urinalysis do you find significant? Microorganisms (bacteria, trichomonads, yeast) In health, the urinary tract is sterile; there will be no microorganisms seen in the urine sediment. Microorganisms are usually reported as "none," "few," "moderate," or "many" present per high power field (HPF). Bacteria from the surrounding skin can enter the urinary tract at the urethra and move up to the bladder, causing a urinary tract infection (UTI). Leukocyte esterase: Normally negative. Leukocytes are the white blood cells (or pus cells). This looks for white blood cells by reacting with an enzyme in the white cells. White blood cells in the urine suggests a urinary tract infection. WBC up to 5/HPF are commonly accepted as normal. Greater numbers (pyuria) generally indicate the presence of an inflammatory process somewhere along the course of the urinary tract (or urogenital tract in voided specimens). Granular casts almost always indicate significant renal disease. However, granular casts may be present in the urine for a short time following strenuous exercise. Granular casts that contain fine granules may appear grey or pale yellow in color. Granular casts that contain larger coarse granules are darker. These casts often appear black because of the density of the granules. 2. What pathophysiologic aspects of this case are illustrated by the urine microscopic examination? The acute pyelonephritis of the patient is the result of the bacterial invasion (e.coli) from the ruptured appendictis of the patient Appendicitis Appendicitis is a condition characterized by inflammation of the appendix. Reginald Fitz first described acute and chronic appendicitis in 1886,

and it has been recognized as one of the most common causes of

severe acute abdominal pain worldwide. Symptoms Signs and symptoms of acute appendicitis can be classified into two types, typical and atypical. The typical history includes pain starting centrally (periumbilical) before localizing to the right iliac fossa (the lower right side of the abdomen); this is due to the poor localizing property of visceral nerves from the mid-gut, followed by the involvement of somatic nerves as the inflammation progresses. The pain is usually associated with loss of appetite and fever, although the latter isn't a necessary symptom. Nausea or vomiting may occur, as well as drowsiness and malaise. Atypical symptoms may include pain beginning and staying in the right iliac fossa, diarrhea and a more prolonged, smoldering course. If an inflamed appendix lies in contact with the bladder, there is frequency of urination. With post-ileal appendix, marked retching may occur. Tenesmus or "downward urge" (the feeling that a bowel movement will relieve discomfort) is also experienced in some cases. Causes On the basis of experimental evidence, acute appendicitis seems to be the end result of a primary obstruction of the appendix lumen. Once this obstruction occurs the appendix subsequently becomes filled with mucus and swells, increasing pressures within the lumen and the walls of the appendix, resulting in thrombosis and occlusion of the small vessels, and stasis of lymphatic flow. Rarely, spontaneous recovery can occur at this point. As the former progresses, the appendix becomes ischemic and then necrotic. As bacteria begin to leak out through the dying walls, pus forms within and around the appendix (suppuration). The end result of this cascade is appendiceal rupture (a 'burst appendix') causing peritonitis, which may lead to septicemia and eventually death. Pyelonephritis Pyelonephritis is an ascending urinary tract infection that has reached the pyelum (pelvis) of the kidney (nephros in Greek). If the infection is severe, the term "urosepsis" is used interchangeably (sepsis being a systemic inflammatory response syndrome due to infection). It requires antibiotics as therapy, and treatment of any underlying causes to prevent recurrence. It is a form of nephritis. It can also be called pyelitis. Diagnosis The presence of nitrite and leukocytes (white blood cells) on a urine dipstick test in patients with typical symptoms are sufficient for the diagnosis of pyelonephritis, and are an indication for empirical treatment. Formal diagnosis is with culture of the urine; blood cultures may be needed if the source of the infection is initially doubtful. Causes Most cases of "community-acquired" pyelonephritis are due to bowel organisms that enter the urinary tract. Common organisms are E. coli (70-80%) and Enterococcus faecalis. Hospital-acquired infections may be due to coliforms and enterococci, as well as other organisms uncommon in the community (e.g. Klebsiella spp., Pseudomonas aeruginosa). Most cases of pyelonephritis start off as lower urinary tract infections, mainly cystitis and prostatitis. Pathology Acute pyelonephritis is an exudative purulent localized inflammation of the renal pelvis (collecting system) and kidney. The renal parenchyma presents in the interstitium abscesses (suppurative necrosis), consisting in purulent exudate (pus): neutrophils, fibrin, cell debris and central germ colonies (hematoxylinophils). Tubules are damaged by exudate and may contain neutrophil casts. In the early stages, glomeruli and vessels are normal. Gross

pathology often reveals pathognomonic radiations of hemorrhage and suppuration through the renal pelvis to the renal cortex. Chronic infections can result in fibrosis and scarring. Sample Test Paper It is an infection of the kidney, and the ureters, the ducts that carry the urine away from the kidney? Appendicitis Pyelonephritis Kidney stone NOTA Exams and test for pyelonephritis? Blood cultures Urine culture Both nota Medications for pyelonephritis? amoxicillin cephalosporin Both nota The following are other possible complication of pyelonephritis, exept? Kidney failure perinephric abscess Sepsis nota The following are symptoms of pyelonephritis except? Back pain Abdominal apin Fatigue aota These are urination problems of pyelonephritis? Blood in the urine Cloudy or abnormal urine color Increased urinary frequency or urgery AOTA What is the probable cause of acquiring pyelonephritis in this case? E. coli Staphylococcus Both NOTA Positive results for pyelonephritis? Leukocyte Bacteria Both Nota A positive bilirubin and urobilinogen may lead to? liver damage heart failure convulsion aota Presence of WBC in the urine indicates what? Infection Heart problems No need to worry nota References: http://library.med.utah.edu/WebPath/TUTORIAL/URINE/URINE.html http://en.wikipedia.org/wiki/Urinary_cast http://en.wikipedia.org/wiki/Appendicitis http://en.wikipedia.org/wiki/Pyelonephritis

group 4

CLINICAL MICROSCOPY

[Year]

[Type the document title] [Type the document subtitle]

Robin Christian G. Cao

Johanna Selina D. Lim

Jennie Q. Lingad

Anna Kamille C. Suyat

[ T Y P E T H E C O M P A N Y A D D R E S S ]

Group 4

Cao, Robin Christian G.

Lim, Johanna Selina D.

Lingad, Jennie Q.

Suyat, Anna Kamille C.

Case 6

With a medical history of HTN, IDDM and CHF, this 57-year old woman was attending a

social event until the early morning hours, had been walking around complaining of shortness of

breath, and suddenly collapsed with a blood-tinged discharge coming from her mouth. She

was rushed to the ER in a private car and on arrival was unresponsive to verbal or painful stimuli,

and showed agonal respirations with a weak radial pulse. The impression was respiratory arrest,

acute pulmonary edema, R/O MI. Subsequent laboratory work did not support the diagnosis of

acute MI, suggesting instead acute pulmonary edema. Her admission urinalysis produced the

following results:

Urinalysis Results

Physical Examination

Color Amber

Appearance Hazy

pH 5.5

Specific Gravity 1.010

Chemical Examination

Protein 100 mg/dL

Glucose 250 mg/dL

Bilirubin and Ketones Negative

Urobilinogen Normal

Nitrite and Leukocyte Esterase Negative

Microscopic Examination

White Blood Cell 20-50/hpf

Red Blood Cell 0-2/hpf

Epithelial Cell Few/hpf

Bacteria 1+/hpf

Casts TNTC granular/lpf

Blood Small

Questions:

What urinalysis results do you find significant?

What pathophysiology of this case is most closely related to the urinary sediment

findings? Answers:

Significant Findings

o Color : Amber

o Protein :100 mg/dL

o Glucose : 250 mg/dL

o WBC : 20-50/hpf

o Bacteria :1+/hpf

o Cast :Granular TNTC/LPF

This is a case of pulmonary edema secondary to left sided heart failure base on the

patient signs and symptoms and history of IDDM, CHF and Hypertension.

Pathophysiology

o The decreased in cardiac output in heart failure patients results in an "unloading"

of high-pressure baroceptors in the left ventricle, carotid sinus, and aortic arch.

This unloading leads to the generation of afferent signals to the central nervous

system that stimulate cardioregulatory centers in the brain which stimulate the

release of anti-diuretic hormone from the posterior pituitary. Antidiuretic hormone

(ADH) is a powerful vasoconstrictor that increases the permeability of the renal

collecting ducts, leading to the reabsorption of free water. These afferent signals

to the CNS also activate efferent sympathetic nervous system pathways that

innervate the heart, kidney, peripheral vasculature, and skeletal muscles.

Sympathetic stimulation of the kidney leads to the release of renin, with a

resultant increase in the circulating levels of angiotensin II and aldosterone. The

activation of the renin-angiotensin-aldosterone system promotes salt and water

retention and leads to vasoconstriction of the peripheral vasculature, myocyte

hypertrophy, myocyte cell death, and myocardial fibrosis. While these

neurohormonal mechanisms facilitate short-term adaptation by maintaining

blood pressure, and hence perfusion to vital organs, these same neurohormonal

mechanisms are believed to contribute to end-organ changes in the heart and

the circulation, and to the excessive salt and water retention in advance heart

failure.

In summary the cause of the concentrated urine which causes the amber color is

the release of Anti-diuretic hormone by the posterior pituitary and the activation

of renin-angiotensin-aldosterone pathway which lead to water reabsorption.

Amber Urine

o Amber colored urine is normal in the presence of dehydration this is due to the

increase in the concentration of urobilinogen which is a pigment that gives the

urine its color. When a person is well hydrated this urobilinogen is diluted resulting

to a yellow or sometimes colorless color of the urine. In our case where there is no

presence of fluid loss (dehydration) the principle that cause the amber colored

urine is the same (that it is due to a concentrated urine) but the mechanism that

cause this is different (no fluid loss or dehydartion). This mechanism is best

explained with the understanding of the pathopysiology of heart failure (disease

of the patient)

Proteinuria

o The presence of proteinuria is caused by the hypertension that is caused by the

vasoconstricting effect of angiotensin II and sodium retention by the aldosterone.

Hypertension causes proteinuria by altering the glomeruli and post glomeruli

structure this is due to ischemia or direct damage to this structure because of the

increase in pressure. These changes in turn allow the protein to pass through

resulting to proteinuria.

Glucosuria

o Glucosuria is caused by the patient IDDM. Glucosuria occurs when the

concentration of glucose in the urine is greater in the amount of glucose that the

kidney can reabsorb back in the circulation.

Pyuria and Bacteria +1

o Pyuria and bacteria +1 may signify urinary tract infection. Since the patient is a

female and has history of IDDM she is most prone to the development of UTI.

Granular Casts

o The presence of granular cast that is TNTC signify that this patient has a long

standing UTI. This is due to the fact that granular cast are found on patient with

pyelonephritis, viral infection, and chronic lead poisoning. Since the patient

doesn’t have history of viral infection and chronic lead poisoning the most

probable cause of the granular cast are pyelonephritis (type of UTI).

o Granular cast may also be pathologic or non pathologic. The origin of the

granules in nonpathologic conditions appears to be from the lysosomes excreted

by RTE cells during normal metabolism. Increased cellular metabolism occurring

during strenuous exercise accounts for the transient increase of granular casts. In

disease states, granules may represent disintegration of cellular casts and tubule

cells or protein aggregates filtered by the glomerulus.

Reference:

o Robbins and Cotrans Pathologic Basis of Disease 7th Edition

o Harrisons Principle of Internal Medicine 17 Edition

o Henry’s Clinical Diagnosis and Management by Laboratory methods 21st Edition o Oxford handbook of Clinical diagnosis 1st Edition

Case #5: An 82 year old woman with an history of HTN treated with Vasotec (enapril maleate), and of NIDDM, was seen in the outpatient clinic complaining of a blister on her lower lip that she said she had been developing slowly over a year. The blister was diagnosed as a mucocele (a mucus cyst), and an

appointment was made to have it biopsied and excised at a future date. In the course of her examination, a routine urinalysis (without the microscopic) was requested and the urine was found to be significant for nitrite positive; and leukocyte esterase moderate. The results prompted the request for a urine C&S. The urine C&S subsequently indicated a colony greater than 100,000 CFU/ml with an identification of E. coli.

What aspect of the urine sediment do you find significant? - Pus cells and bacteria (Caused the Nitrite and Leukocytes Esterase test in the urine to be positive.)

There are certain types of bacteria (e.g. E. coli) which have the ability to reduce nitrate, a normal constituent of urine, to nitrite, which does not normally appear in the urine. Therefore, Nitrites in the urine can be an early warning that a urinary tract infection might exist.

A positive LE test result is most frequently accompanied by the presence of bacteria. The LE detects the presence of esterase in the granulocytic white blood cells (neutrophils, eosinophils, and basophils) and monocytes. Neutrophils are the leukocytes most frequently associated with bacterial infections.

What diagnosis would you give this case? - Urinary tract infection

The presence of a single type of bacteria (E. coli) growing at high colony counts (greater than 100,000 colony forming units (CFU)/ml) indicates a Urinary Tract Infection.

What type of treatment do you think this patient was given for the condition shown here - Antibiotic therapy with the correct dosage relating to her age.

Antibiotic Age Route Dosage

Trimethoprim-Sulfamethoxazole (TMP-SMX

Adult ORAL or IV 160 mg-800 mg/ 12 hours for 10 to 14 days 8 to 10 mg/kg/day

Nitrofurantoin (Furadantin, Macrodantin

Adult ORAL 50 to 100 mg four times daily for seven days

Amoxicillin Adult ORAL 250 mgs/ 8 hrs or 500 mgs/12 hours.

What results will be expected upon performing the microscopic examination of the patient's urine? - Urine microscopic exam will be, pus cells ranging from many to TNTC (too numerous to count) and bacteria.

References: http://www.labtestsonline.org/understanding/analytes/urine_culture/test.html

http://www.testsymptomsathome.com/TEC06.asp

http://adam.about.com/reports/000036_7.htm

http://kidney.niddk.nih.gov/kudiseases/pubs/utiadult/

http://adam.about.com/reports/000036_7.htm

http://www.labtestsonline.org/understanding/analytes/urine_culture/test.html

http://www.testsymptomsathome.com/TEC06.asp

http://kidney.niddk.nih.gov/kudiseases/pubs/utiadult/

http://www.drugs.com/mtm/sulfamethoxazole-and-trimethoprim.html

http://en.wikipedia.org/wiki/Nitrofurantoin

http://www.drugs.com/pdr/amoxicillin.html

http://www.rxlist.com/vasotec-drug.htm

Angeles University Foundation

College of Allied Medical Professions

Department of Medical Technology

In Partial Fulfillment of the requirement in

Clinical Microscopy

(Case Analysis)

Submitted by:

Group 5

Garcia, Vixienne Geia

Natividad, Justine Lorenz

Nicdao, Jan Kevin

BSMT III-A

Submitted to:

Ms. Crizelda Liwanag

Submitted on:

January 7, 2010

Sample Test Paper:

1. NIDDM stands for:

a. Non-Identifiable Diabetes Mellitus

b. Non-Insulin Dependent Diabetes Mellitus

c. Non-Insulin Deficient Diabetes Mellitus

2. In the case, the old woman was complaining of a blister on her lower lip, which was later

diagnosed as a mucocele. A mucocele is a/an:

a. Allergy

b. Mucus cyst

c. Mole

3. An excision and a/an ____ were scheduled on a future date for the mucocele.

a. Chemotherapy

b. Biopsy

c. Aspiration

4. Which of the following was used to treat the patient’s history of HTN?

a. Vasotec

b. Amoxicillin

c. Nitrofurantoin

5. The significant results of the requested Routine Urinalysis is/are:

a. Leukocyte esterase (many); nitrite (+)

b. Leukocyte esterase (few); nitrite (-)

c. Leukocyte esterase (moderate); nitrite (+)

6. The results in #5 prompted for a/an:

a. C&S

b. Repeat test

c. None; the tests were sufficient in diagnosis

7. Women tend to have higher LE values due to:

a. Vaginal contamination

b. Difference in sexual activity

c. Men and women have same range values

8. In the nitrite reaction, which is normally found in the urine?

a. Nitrite

b. Nitrate

c. Both

9. The C&S results indicated:

a. >100,000 CFU/ml of E.coli

b. <100,000 CFU/ml of E.coli

c. 100,000 CFU/ml of E.coli

10. The diagnosis of the case was:

a. HTN

b. UTI

c. NIDDM

Answer Key:

1. NIDDM stands for:

a. Non-Identifiable Diabetes Mellitus

b. Non-Insulin Dependent Diabetes Mellitus

c. Non-Insulin Deficient Diabetes Mellitus

2. In the case, the old woman was complaining of a blister on her lower lip, which was later

diagnosed as a mucocele. A mucocele is a/an:

a. Allergy

b. Mucus cyst

c. Mole

3. An excision and a/an ____ were scheduled on a future date for the mucocele.

a. Chemotherapy

b. Biopsy

c. Aspiration

4. Which of the following was used to treat the patient’s history of HTN?

a. Vasotec

b. Amoxicillin

c. Nitrofurantoin

5. The significant results of the requested Routine Urinalysis is/are:

a. Leukocyte esterase (many); nitrite (+)

b. Leukocyte esterase (few); nitrite (-)

c. Leukocyte esterase (moderate); nitrite (+)

6. The results in #5 prompted for a/an:

a. C&S

b. Repeat test

c. None; the tests were sufficient in diagnosis

7. Women tend to have higher LE values due to:

a. Vaginal contamination

b. Difference in sexual activity

c. Men and women have same range values

8. In the nitrite reaction, which is normally found in the urine?

a. Nitrite

b. Nitrate

c. Both

9. The C&S results indicated:

a. >100,000 CFU/ml of E.coli

b. <100,000 CFU/ml of E.coli

c. 100,000 CFU/ml of E.coli

10. The diagnosis of the case was:

a. HTN

b. UTI

c. NIDDM

Research Information:

Hypertension is a chronic medical condition in which the blood pressure is elevated. It is also referred to as high blood pressure or shortened to HT, HTN or HPN. The word "hypertension", by itself, normally refers to systemic, arterial hypertension. Hypertension can be classified as either essential (primary) or secondary. Essential or primary hypertension means that no medical cause can be found to explain the raised blood pressure. It is common. About 90-95% of hypertension is essential hypertension. Secondary hypertension indicates that the high blood pressure is a result of (i.e., secondary to) another condition, such as kidney disease or tumours (adrenal adenoma or pheochromocytoma). Persistent hypertension is one of the risk factors for strokes, heart attacks, heart failure and arterial aneurysm, and is a leading cause of chronic renal failure. Even moderate elevation of arterial blood pressure leads to shortened life expectancy. At severely high pressures, defined as mean arterial pressures 50% or more above average, a person can expect to live no more than a few years unless appropriately treated. Beginning at a systolic pressure (which is peak pressure in the arteries, which occurs near the end of the cardiac cycle when the ventricles are contracting) of 115 mmHg and diastolic pressure (which is minimum pressure in the arteries, which occurs near the beginning of the cardiac cycle when the ventricles are filled with blood) of 75 mmHg (commonly written as 115/75 mmHg), cardiovascular disease (CVD) risk doubles for each increment of 20/10 mmHg.

VASOTEC® (Enalapril Maleate) is the maleate salt of enalapril, the ethyl ester of a long-acting angiotensin converting enzyme inhibitor, enalaprilat. Enalapril maleate is chemically described as (S)-1-[N-[1-(ethoxycarbonyl)-3-phenylpropyl]-L-alanyl]-L-proline, (Z)-2-butenedioate salt (1:1). Enalapril maleate is a white to off-white, crystalline powder with a molecular weight of 492.53. It is sparingly soluble in water, soluble in ethanol, and freely soluble in methanol. Enalapril is a pro-drug; following oral administration, it is bioactivated by hydrolysis of the ethyl ester to enalaprilat, which is the active angiotensin converting enzyme inhibitor. VASOTEC is indicated for the treatment of hypertension. It is effective alone or in combination with other antihypertensive agents, especially thiazide-type diuretics. The blood pressure lowering effects of VASOTEC and thiazides are approximately additive.

Diabetes mellitus type 2 or type 2 diabetes (formerly called non-insulin-dependent diabetes mellitus (NIDDM), or adult-onset diabetes) is a disorder that is characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency. Traditionally considered a disease of adults, type 2 diabetes is increasingly diagnosed in children in parallel to rising obesity rates due to alterations in dietary patterns as well as in life styles during childhood. Unlike type 1 diabetes, there is very little tendency toward ketoacidosis in type 2 diabetes, though it is not unknown. One effect that can occur is nonketonic hyperglycemia which also is quite dangerous, though it must be treated very differently. Complex and multifactorial metabolic changes very often lead to damage and function impairment of many organs, most importantly the cardiovascular system in both types. This leads to substantially increased morbidity and mortality in both type 1 and type 2 patients, but the two have quite different origins and treatments despite the similarity in complications.

An oral mucocele, is a clinical term that refers to two related phenomena: mucus extravasation phenomenon, and mucus retention cyst. The former is a swelling of connective tissue consisting of

collected mucin due to a ruptured salivary gland duct usually caused by local trauma, in the case of mucus extravasation phenomenon, and an obstructed salivary duct in the case of a mucus retention cyst. The mucocele is a bluish translucent color, and is more commonly found in children and young adults.

A urinary tract infection (UTI) is a bacterial infection that affects any part of the urinary tract. The main causitive agent is Escherichia coli. Although urine contains a variety of fluids, salts, and waste products, it usually does not have bacteria in it. When bacteria get into the bladder or kidney and multiply in the urine, they cause a UTI. The most common type of UTI is a bladder infection which is also often called cystitis. Another kind of UTI is a kidney infection, known as pyelonephritis, and is much more serious. Although they cause discomfort, urinary tract infections can usually be quickly and easily treated with a short course of antibiotics.

Angeles University Foundation Angeles City, Pampanga Clinical Microscopy Case Study Analysis Group 6 Alagdon, Edsel Gomez, Paul Arvin Laus, Abigail BSMT 3-A Ms. Crizelda Liwanag January 7, 2010 Case 10: A 32-year old woman with a long history of IDDM has been checking her blood sugar at home daily and administering her own insulin. On a rainy Sunday night, she was admitted through the ER after 2 days of vomiting, upper abdominal pain, and right jaw pain. Her admission diagnosis was Diabetic Ketoacidosis and dehydration. The admission urinalysis (no microscopic) was significant for glucose >1000 mg/dL and ketones >80 mg/dL. Her condition was resolved with fluid and electrolyte therapy and insulin drip. Guide Questions and Answers: 1. What urinalysis results correlate with the diagnosis of DKA? Color Colorless Odor Strong, sweet smell pH Decreased Protein Increased

Glucose Increased Specific Gravity Increased Ketones Present 2. Explain. The color of the urine appears to be diluted, but the specific gravity is high due to the increased glucose content. Excretion of ketone bodies in the urine is responsible for the sweet smell of the urine. The production of ketone bodies increases the acidic nature of the urine. The presence of sugar in the blood leads to its excretion in to urine. Ketones in the urine mean the body is burning fat to get energy. 3. What results should be expected from the microscopic examination? In patients with diabetes mellitus, fatty casts are observed during microscopic examination of the urine. 10-item Sample Test Paper: 1. The urinalysis was significant because of: a. Increased amount of glucose b. Decreased amount of ketones c. Presence of low specific gravity d. Increased pH 2. What sediment constituents may be seen from the microscopic examination? a. RBC casts b. WBC c. Fatty casts d. Bacteria 3. What may be the cause of the woman having diabetic ketoacidosis on her case? a. Failure to administer insulin b. High insulin intake c. Drinking lots of electrolytes d. Low glucose level 4. Which will show a correct urinalysis results for Diabetic ketoacidosis? a. Odor – normal; pH – 7; protein – increased; glucose – normal; spec. gravity – normal; ketones – negative b. Odor –strong sweet; pH – decreased; protein – increased; glucose –increased; spec. gravity –increased; ketones - present c. Odor – normal; pH – decreased; protein – increased; glucose –increased; spec. gravity – normal; ketones - negative d. Odor –foul; pH – decreased; protein – increased; glucose – increased; spec. gravity – normal; ketones - negative e. 5. In the patient’s case, insulin level is low with type 1 Diabetes. What is the other name for this type? a. Insulin Sufficient Diabetes mellitus b. Adequate insulin diabetes mellitus c. Non-insulin dependent diabetes mellitus d. Insulin dependent diabetes mellitus 6. The insulin level of the patient is low because of: a. Excessive urination and sweating b. Her immune system destroys some beta cells in the pancreas c. Her kidney is swelling d. High glucose level 7. What organ of the body is responsible for the insulin problem in type 1 diabetes? a. Kidney b. Pancreas c. Spleen d. gallbladder 8. In the absence of glucose, most cells use this to produce ATP for energy production: a. Fatty acids b. Sucrose c. Protein d. Cells don’t use energy at all 9. Fatty acid breakdown causes: a. Bad cholesterol production b. Release of glucose c. Fatty acid accumulation

d. Ketone production and accumulation 10. It is a condition among Diabetes patients wherein insulin deficiency or resistance causes the pulling of fluid body tissues leading to polyuria and dehydration a. Hyperglucosemia b. Polyuria c. Hyperglycemia d. Metabolic acidosis Answer Key: 1. A 2. C 3. A 4. B 5. D 6. B 7. B 8. A 9. D 10. C Pertinent Information: Autoimmune diseases are diseases that occur because of the body’s immune system attacking its own cells and rendering a function useless as is the case in diabetes. In diabetes, the killer T cells of the body attack the insulin producing cells of the pancreas; thereby, shutting down the production of insulin. When the production of insulin is affected, the body cannot control the amount of sugar in the blood and this sugar is even excreted in the urine. The liver then starts to produce ketone bodies as a response to the low insulin level, which the body is fooled into thinking that, it is because of a low intake of glucose. The production of ketone bodies then increases the acidic nature of the blood, because ketones are created from fatty acids and the adipose stores in the liver. At a certain pH level that indicates high acidity, the tissues of the body start to die and the breath of diabetes patient has a sweet, alcoholic smell that emergency room doctors immediately recognize as the symptom of diabetic ketoacidosis. This condition is potentially fatal if not treated on time. The presence of sugar in the blood leads to its excretion into urine, which is due to the overloading of certain binding proteins in the kidneys that send back glucose into the blood in normal circumstances. Urine that usually contains glucose and sugars has a sweet, fruity smell. However it is an indication that you need to rush to the emergency room before ketoacidosis occurs and a possible coma. References: Diabetes Mellitus: A Guide to Patient Care by Lippincott Williams and Wilkins Nutrition and Diagnosis-related Care by Sylvia Escott-Stump Urinalysis and Other Body Fluids by Susan King Strasinger Handbook of Disease by Lippincott Williams and Wilkins Principles of Anatomy and Physiology by Gerard Tortora Angeles University Foundation AY 2009 – 2010 Clinical Microscopy: Case Study No. 3

Group 2 Garcia, Tiffany Verzil Geronimo, Jerome Nogoy, Princess May Ramos, Jayson BSMT 3 – A Ms. Crizelda D. Liwanag/Eloisa Q. Singian Instructors January 7, 2010

Summary Patient: Man, 46 years old Urinalysis results: Bilirubin: large Color: amber Casts: granular, 1-5/lpf WBC: 1-5/hpf Ictotest: positive

Blood Chemistry Results: Total Bilirubin: 32.1 mg/dL (0-1.5) Conjugated Bilirubin 22.2 mg/dL (0-0.4) ALP: 299 U/L (37-107) AST: 302 U/L (8-42) ALT: 46 U/L (3-96) LD: 272 U/L (100-190) Total Protein: 4.9 g/dL (6.4-8.2) Albumin: 2.1 m/dL (3.4-5.0)

Accompanied Signs and Symptoms: Diarrhea (entire previous month) Gas and Nausea (previous 3 wks) Jaundice Patient Diagnosis: Liver Cirrhosis Hepatocellular Carcinoma Obstructive Jaundice Guide Questions: What urine results correlate with the diagnosis? Explain.

Color: amber o The patient’s urine color is caused by the presence of the abnormal pigment Bilirubin due to the

blockage of the hepatic portal vein which carries the bile pigment to the GIT. The presence of this pigment in the urine, significantly in an increased level coincides with the diagnosis of the patient’s liver diseases such as that of jaundice, cirrhosis and hepatocellular carcinoma.

Ictotest: positive o Indicates the presence of Bilirubin which is correlated with liver damage and jaundice. This test is

requested to further identify if the amber colored urine is caused by early stages of liver diseases.

Bilirubin: large o Bilirubin resulted in high level in the urinalysis result due to the damaged integrity of the liver

and the blockage of the porta of hepatis (the liver’s portal vein), thus, the blood containing the pigment cannot reach the gastrointestinal tract. The patient, having been diagnosed to have liver cirrhosis at first - which is the onset of his history of alcoholism, wherein the liver is injured due to massive alcohol consumption by blocking the normal metabolism of protein, fats and carbohydrates – and further became hepatocellular carcinoma due to malignancy and severe damage of the liver cells is confirmed to possess these diseases.

How do the blood analyses correlate with this? Explain.

Total Bilirubin and Conjugated Bilirubin – high o Due to the blocked portal vein of the patient, direct bilirubin aggregated, escaped from the liver,

and ended up in the blood. Increased direct bilirubin usually means that the liver is obstructed, thus, correlated to hepatic carcinoma and jaundice.

o Total Bilirubin is also increased due to cirrhosis of the patient. Liver Enzymes:

ALP: 299 U/L (37-107) o Alkaline Phosphatase, high. Elevated ALP detects diseases involving the biliary system of our

body. Since the patient has a liver disease, this enzyme is expected to rise because of the damage of the oragan’s cells. This marker is intended to be sensitive upon the deterioration of the liver’s cells, as in cirrhosis and carcinoma, wherein it is leaked out in the blood.

o It is elevated due to the excessive alcohol consumption, which indicates shedding of the liver, cirrhosis – the patient showed history of alcoholism.

AST: 302 U/L (8-42) - high o Aspartate Amino Transferase (Serum Glutamate Oxaloacetate Transferase) showed high level. As

a liver enzyme, it is increased in the blood due to its leakage from the destructed cells of the liver. But, as an enzyme involved in other organs such as the heart, and skeletal muscles, it is more sensitive than specific. Still, due to the dramatic increase of ALP, it is confirmed that its increase is due to the lowering profile of the liver. Thus, correlating to the patient’s diagnosis of jaundice and hepatocellular carcinoma.

ALT: 46 U/L (3-96) o Alanine Amino Transferase is, by contrast, normally found largely in the liver. This is not to say

that it is exclusively located in liver, but that is where it is most concentrated, making it specific than only sensitive. It is released into the bloodstream as the result of liver injury. It therefore serves as a fairly specific indicator of liver status of the patient.

LD: 272 U/L (100-190) o Isoenzyme Fractionation detects any LD increase in the serum. Since this enzyme is not that

correlated with most of the hepatic disorders, due to its sensitivity, there can be a strong possibility of liver damage. As the patient’s liver disease in the case is already chronic, great increase in LD suggests that the diagnosis is highly correlated with the result.

Total Protein and Albumin – low o Value of the total protein decreases in the serum is due to the decrease in the level of albumin,

globulin or both. Albumin is low due to the damage in the patient’s liver, wherein the low values indicate the poor capability of the organ to synthesize proteins due to the concluded hepatic profile of the patient.

Pathophysiology: In this case, a long term history of the patient signifies the outcome of the diagnosis. Due to severe alcohol abuse, the liver develops a scar tissue that replaces normal parenchyma, blocking the portal flow of blood through the organ and disturbing normal function. Thus, if the portal vein is clogged, the blood containing the pigment from the disintegration of the hemoglobin will not be able to enter the ducts of the bile and will not be able to reach the GIT, making it a single way directed to the urinary system producing darker color urine and pale colored stool. The pigment that creates the amber color of the patient’s urine is known to be bilirubin, which is not considered a normal constituent. Blockage of the portal vein will result to a pressure into the liver obstructing it and damaging its cells, thus creating jaundice. The patient’s alcohol abuse led to the prior diagnosis of cirrhosis and by then succeeded to hepatocellular carcinoma during the onset of its malignancy. Since the liver is the main organ in damage, protein synthesis is dysfunctional, thus lowering the total protein and albumin levels of the patient’s serum under blood chemistry tests. Enzymes, as known to hasten the synthesis of the proteins intracellularly, due to the patient’s liver disease, leak outside the bloodstream, thus increasing the levels of enzymes extracellularly. Name: ______________________________ Date: _________ Score: ____________ 1. Increased levels of _________ in the urine may be due to liver disease, such as cirrhosis.

a. bilirubin b. rbc c. bacteria

2. The most abundant blood plasma protein and is produced in the liver. Low level of this protein in blood indicates liver disease.

a. globin b. albumin c. fibrinogen

3. Patients with long history of alcoholism may develop ______________.

a. hepatitis b. cirrhosis c. jaundice

4. This type of test is requested to detect early stages of liver disease, such as hepatitis.

a. Ictotest b. AST c. ALP

5. What test is done to diagnose liver or bone disease?

a. ALT b. ALP c. AST

6. The amber color of the urine is due to the presence of ____________in the urine

a. wbc b. cast c. bilirubin

7. What causes the appearance of conjugated bilirubin in the urine?

a. disrupted hemoglobin degradation b. liver damage c. both

8. An enzyme found in high amounts in heart muscle and liver and skeletal muscle cells.

a. ALT b. AST c. ALP

9. This type of jaundice is caused by an interruption to the drainage of bile duct

a. pre hepatic b. hepatic c. post hepatic

10. Its presence helps to determine the cause of clinical jaundice

a. globin b. albumin c. conjugated bilirubin 1. A 2. B 3. B 4. A 5. B 6. C 7. C 8. B 9. C 10. C

References: Strasinger, Susan K. & Di Lorenzo, Marjorie S. Urinalysis and Body Fluids. 5th Edition. F.A. Davis Company, Thailand. 2005 Calbreath, Donald. Clinical Chemistry http://www.medicinenet.com/liver_blood_tests/page2.htm http://www.nlm.nih.gov/medlineplus/ency/article/003470.htm http://www.abcompany.com/docgolob/bloodchemistry.htm http://www.labtestsonline.org/understanding/analytes/bilirubin/faq.html http://digestive.niddk.nih.gov/ddiseases/pubs/cirrhosis/#cause http://en.wikipedia.org/wiki/Gamma-glutamyl_transpeptidase http://en.wikipedia.org/wiki/Cirrhosis http://en.wikipedia.org/wiki/Jaundice#Post-hepatic http://web2.airmail.net/uthman/lab_test.html hoAngeles University Foundation College of Allied Medical Professions Department of Medical Technology CASE ANALYSIS Preliminary term In partial fulfillment of the requirements in Clinical Microscopy Submitted to:

Ms. Crizelda D. Liwanag, RMT, MS Submitted by: Guevarra, Sonny Mungcal, Lilibeth Sarmiento, Norilie Mae Tayag, Joseph John S. Group # 8 Summary of the case Case #8 A urine specimen is obtained from a 14-year-old boy with a history of a sore throat. Three weeks ago he was cultured and treated for a streptococcal throat infection with a single intramuscular dose of penicillin. Two weeks after his initial visit, he showed no abnormal physical findings; however, his urinalysis revealed microscopic hematuria and he was told to rest. Currently he has weakness and anorexia. He woke up with a headache and puffy eyelids and says his urine is dark and there is very little of it. Urinalysis Results: Physical Appearance : color: red (red-brown) clarity: cloudy Chemical Screening : pH 6.0 specific gravity 1.025 protein (strip) 300 mg/dL protein (SSA) 3+ blood large nitrite negative leukocyte esterase negative glucose negative ketones negative bilirubin negative urobilinogen 0.5 EU/dl

Microscopic: red blood cells 10-25/hpf (dysmorphic forms present) white blood cells 0-2/hpf casts 2-5 red blood cell casts/lpf crystals few amorphous urates Guide Questions:

1. What urinalysis findings are abnormal or discrepant? The negative result for leukocyte esterase and the positive result for white blood cells in the microscopic examination give discrepant information. However, this result may be due to the sensitivity of the leukocyte esterase test. The test requires at least 5 WBC/hpf in order to yield a positive result, whereas, the microscopic examination reveals only 0-2 WBC/hpf.

2. What is the significance of dysmorphic red cells in the urine sediment of this patient? Dysmorphic red blood cells are RBC’s that vary in size, have cellular protrusions and are fragmented. These abnormal RBC’s are associated primarily with glomerular bleeding. 3. Proteinuria is an important indication of renal disease. Match the following protein tests (a and b) with the proteins they measure. a. Reagent strip test for protein? b. Sulfosalicylic acid test for protein? _a/b__ albumin _b___ Tamm-Horsfall glycoprotein _b__ plasma globulins

4. What is the significance of red blood cell casts in this patient? The presence of RBC casts in the urine is more specific. This condition shows bleeding within the nephron. RBC casts are primarily associated with the damage of the glomerulus that allows the passage of the cells through the glomerular membrane.

5. Why don't you see bacteria in the microscopic examination of the sediment in this patient? Although there is a presence of white blood cells in the microscopic examination, there are no bacteria seen in the urine. This may be a signal that the renal disease is not of bacterial etiology.

6. What is the likely diagnosis for this patient? The physical signs and symptoms and the medical history of the patient, together with the findings of the urinalysis, constitutes the likely diagnosis for the patient which is acute glomerulonephritis (specifically acute poststreptococcal glomerulonephritis). Sample Test Paper

1. What would be the likely cause of the cloudy urine specimen in the case?

a. Red Blood Cells b. White blood Cells c. Urinary crystals d. Squamous Epithelial Cells

2. The following may cause dysmorphic Red Blood Cells except:

a. Strenuous exercise b. Glomerular bleeding c. Diabetes mellitus

3. To be considered as UTI, bacteria should be accompanied by:

a. WBC’s b. RBC’s c. Bacterial motility d. Abnormal urinary crystals

4. RBC’s are sometimes confused with WBC’s, yeasts and oil droplets. What reagent would be likely used to confirm microscopic hematuria and the dysmorphic RBC’s

a. Sternheimer-Malbin b. 1% acetic acid c. Hansel Stain d. Prussian blue

5. What result in the urinalysis constitutes to glomerulonephritis?

a. Hematuria b. RBC casts c. Proteinuria d. All of the above

6. Red blood cell casts are associated with:

a. Strenuous contact sports b. Proteinuria c. Dysmorphic RBC’s d. Only B and C e. All of the above

7. Post infection glomerulonephritis is associated by recent infection of:

a. Staphylococcus aureus b. Streptococcus agalactiae c. Streptococcus pyogenes d. B and C e. All of the above

8. The build up of these substances in the nephron after infection may trigger glomerulonephritis

a. Immune complexes b. M protein c. Streptococcus toxin d. Penicillin given to the patient

9. In the patient’s urinalysis, why is there presence of white blood cells?

a. To fight bacterial infection b. The white blood cells attack the substances which inflames the nephron after a recent infection and

are filtered after c. They pass through the compromised glomerular membrane together with other particles because d. The white blood cells are not reabsorbed back into the blood vessels from the tubules

10. The following produces esterases except

a. Trichomonas

b. Lymphocytes c. Histiocytes

Answer key

1. A 2. C 3. A 4. B 5. D 6. E 7. C 8. A 9. C 10. B

Pertinent Information A urinalysis (or "UA") is an array of tests performed on urine and one of the most common methods of medical diagnosis. Urinalysis has three phases namely; the physical, chemical and microscopic examination. The physical examination includes the determination of the urine color and clarity of urine. In the chemical test, the reagent strip is currently used because it provides simple and rapid means for performing chemical analysis on urine. Tests include pH, glucose, protein, ketones, blood, bilirubin, leukocyte esterase, urobilinogen and specific gravity. The last part of urinalysis, microscopic examination, deals with the determination of urinary sediments. These include RBC’s, WBC’s epithelial cells, casts, bacteria, parasites, yeasts, crystals mucus, spermatozoa and artifacts. Urinary findings in the case Color and Clarity The color of urine may range from colorless to black. These may indicate normal conditions, physical activity, metabolic functions or pathologic conditions.

Urine color Possible Clinical Significance

Colorless Recent fluid consumption

Pale yellow Polyuria or Diabetes

Dark Yellow Concentrated Urine

Yellow green Bilirubin oxidized to biliverdin

Green Pseudomonas infection

Pink/Red Hematuria (RBC’s, hemoglobin and myoglobin)

Brown/Black Methemoglobin, Alkaptonuria, Melanin

Color and clarity are routinely determined at the same time. Clarity refers to the transparency of the urine specimen. Freshly voided normal urine is usually clear.

Clarity Term

Clear No visible particulates, transparent

Hazy Few particulates

Cloudy Many particulates

Turbid Print cannot be seen through urine

Milky May precipitate or clotted

*Clinical Significance of the physical examination The urine specimen is said to be red and cloudy. This may indicate hematuria with many particulates. Protein The presence of proteinuria is often associated with renal disease. Normal urine contains very little protein (<10mg/dL or 100mg per 24hours) is excreted. These proteins are primarily low-molecular-weight serum proteins that have been filtered by the glomerulus and proteins produced from the genitourinary tract. Albumin is the major protein found in normal urine. Normal albumin content is low because majority is not filtered by the glomerulus and the filtered albumin is reabsorbed back into the tubules. Other proteins may include microglobulins, Tamm-horsfall protein and proteins from prostatic, seminal and vaginal secretions. Demonstration of proteinuria does not always signify renal disease. Clinical proteinuria is indicated at >30mg/dL. *Clinical Significance of the protein test in the case The result of the test reveals a large amount of protein present in the blood. This condition may be associated to a renal disease, giving the disability of the glomerulus and tubules to properly filter and reabsorb the proteins Blood Macroscopically, blood may be seen in the urine by means of hematuria (cloudy red urine) or hemoglobinuria (clear red urine). Any amount of blood greater than 5 cells per microliter of urine is significant. In the chemical examination, the test for hemoglobin is the most reliable means for determining blood. Hematuria is closely associated with the renal and genitorurinary disorders in which bleeding is the result of trauma or damage to the organs of these systems. Common causes may include renal calculi, glomerular diseases, tumors and pyelonephritis. On the other hand, hemoglobinuria results from the lysis of the red blood cell in which hemoglobin is released. It may also be a result of intravascular hemolysis and the subsequent filtering of hemoglobin through the glomerulus. Intravascular hemolysis is evident in urine without red blood cells. Another type of protein which may produce a red pigment is myoglobin. Its presence in the urine, myoglobinuria, is indicative of muscular destruction. Myoglobin is a heme containing protein found in the muscle that may react positively with the reagent strip for blood. The diagnosis of myoglobinuria is also based on the patient’s medical history and serum levels of certain enzymes. *Clinical Significance of the blood test in the case The test is required to confirm if the red pigment in blood is caused by blood itself. Other substances such as beets may produce red urine similar to hematuria. Blood gave a large result in the chemical test signifying “true hematuria”.

Leukocyte Esterase The Leukocyte esterase test is a urine test for the presence of white blood cells and other abnormalities associated with infection. White blood cells in the urine, accompanied by bacteria, usually indicate a urinary tract infection. The leukocyte esterase (LE) test detects esterase, an enzyme released by white blood cells specifically granulocytes and monocytes. Positive test results are clinically significant. The LE test is also used to screen for gonorrhea and for amniotic fluid infections. The combination of the LE test with the urinary nitrite test provides an excellent screen for establishing the presence of a urinary tract infection (UTI). Urine sample that tests positive for both nitrite and leukocyte esterase should be cultured for pathogenic bacteria. Normal values for leukocyte esterase are based on the microscopic examination of 0-5 per hpf. Women tend to have a higher number than men because of vaginal contamination. Microscopic Red Blood Cells and Red Blood Cell Casts Red blood cells in the urine sediments appear as smooth, non-nucleated and bi-concave disks and are reported as the average number seen per 10 hpfs. RBC’s shrink and may appear crenated in concentrated urine, due to the loss of water. In dilute solutions, RBC’s may rupture releasing the hemoglobin. Dysmorphic RBC’s have cellular protrusions and are fragmented. They are primarily associated with glomerular bleeding. The number and appearance of dysmorphic RBC’s must also be considered because abnormal urine concentration affects RBC appearance. Dysmorphic cells are also associated with strenuous exercise. The presence of RBC’s in the urine is associated with glomerular membrane or vascular injury within the genitourinary tract. The presence of RBC casts in the urine specifically indicates bleeding within the nephron. RBC casts are associated with glomerulonephritis that allow the passage the passage of cells through the glomerular membrane. RBC casts associated with glomerular damage are usually accompanied by proteinuria and dysmorphic RBC’s. Like dysmorphic cells, RBC cast formation may be triggered by strenuous activities. RBC casts should be accompanied by free standing RBC to prevent inaccurate reporting or misidentification of the casts. White Blood Cells WBC’s are slightly larger than RBC’s. The predominant WBC found in urine sediment is the neutrophil. Neutrophils exposed to hypotonic urine absorb water and swell. Brownian movement of the granules within these cells produces a sparkling appearance known as glitter cells. Presence of eosinophils upon staining indicates drug induced interstitial nephritis, UTI and renal transplant rejection. Pyuria (increase in urinary WBC indicates the presence of inflammation in the genitourinary system. Examples of bacterial infections are pyelonephritis, cystitis, and prostatitis. Pyuria may also be present in nonbacterial disorders such as glomerulonephritis, lupus erythemathosus and tumors. Amorphous Urates Amorphous urates are microspically yellow brown granules and are normal crystals seen in acidic urine. They occur in clumps that may resemble casts. Acute Glomerulonephritis Acute glomerulonephritis is characterized by the sudden appearance of hematuria, proteinuria and red blood cell casts in the urine, edema (most noticeable around the eyes), fatigue and hypertension with or without oliguria. It can follow streptococcal infections. This illness was first recognized as a complication of the convalescence period of scarlet fever in the 18th century. A link between hemolytic streptococci (group A and contains the M protein in the cell wall) and acute glomerulonephritis was recognized in the 20th century. Pathophysiology Poststreptococcal glomerulonephritis follows infection with only certain strains of streptococci, designated as nephritogenic. The offending organisms are virtually always group A streptococci. Acute poststreptococcal glomerulonephritis (APSGN) follows pyodermatitis with streptococci M types 47, 49, 55, 2, 60, and 57 and throat infection with streptococci M types 1, 2, 4, 3, 25, 49, and 12.

APSGN is believed to be an immune-mediated disease, in which an immune complex containing a streptococcal antigen is deposited in the affected glomeruli. The size of glomerular basement membrane (GBM) pores and the molecular size of the streptococcus-Ig complex are also important determinants. The molecular size of the streptococcus-Ig complex is about 15 nm (10 nm for streptococcus group A and 5 nm for immunoglobulin). The GBM pore sizes in children and adults are 2-3 nm and 4-4.5 nm, respectively. Therefore, the immune complex molecule can be more easily rodded into the glomerulus in children than in adults and, thus, may explain the increased frequency of APSGN in children compared to that in adults. Successful management of the secondary complications, until the immune complexes have been cleared from the blood will result in no permanent kidney damage. References: S. K. Strasinger and M.S. Di Lorenzo, Urinalysis and Body Fluids, 4

th ed., 2001

http://emedicine.medscape.com/article/777272-overview http://emedicine.medscape.com/article/240337-overview http://en.wikipedia.org/wiki/Glomerulonephritis http://library.med.utah.edu/WebPath/TUTORIAL/URINE/URINE.html http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=cm&part=A5435 http://medres.med.ucla.edu/Education/Lectures_and_Conferences/IMS_2007_pdf/CCJM%20Proteinuria%202003.pdf