You are on page 1of 12

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:

o 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.
SCRIPT IN CM

Scene 1: at AUFMC Emergency Room

Attending Physician: Does your mother suffered from any chest pains?
Daughter: No.
AP: Nausea…vomiting?
Daughter: No, what she always complains about is her having shortness of breath
AP: From what we have of your mother’s previous record in Ilang-Ilang Rural hospital,
she’s been showing evidence of pulmonary edema. But we need series of tests to confirm
it and to know exactly the reason why your mother is here. Don’t worry iha, your mother
will be fine.

(exit….)

Scene 2: (this scene should portray a medtech asking the sample specimen needed for the
lab) Remember: Proper identification of the medtech and the patient should be evident.

Medtech: Goodmorning maam! I’m ________________, the medtech in charge for this
particular sample collection. I’m here to collect a urine sample from the patient. Are
you ____________________ (patient’s complete name w/ middle name)
Patient: yes, I am.
Daughter: They need your urine sample again.
Mother: But I don’t need to pee right now. It’s hard for me nowadays…
MT: Sorry for the inconvenience maam, but we have already a solution for that.
(showing a geriatric bag or “wee-wee” bag). For this you will pee as you like and it
would be just fine.
Daughter: would it be good for her?
MT: It would be very convenient. I’ll be back in time..(exits..)

Scene 3: at the CM section of the hospital laboratory

Medtech doing a Urinalysis( might be physical or microscopic)

Interpretation of results and reporting it to the doctor

(showing MT and doctor together)

Scene 4: at the patient’s room

Doc: Goodmorning..are you feeling better?


Mother: I’m not gonna die, am I doc?
Doc: Well, according to what we observed, you madam, is suffering from a congestive
heart failure and shortness of breathing indicates a sign of myocardial infarction. You
also have diabetes and a high blood pressure.
Do you have any history of Diabetes and CHF in your family?
Mother: I guess we do, both in my father’s side…
Doc: So I would suggest that you take up morphine, lasix, nitroglycerin and Procardia as
medications. Would that be ok to all of you?
Daughter: Doc, in my mother’s condition, would she undergo a surgery soon?
Doc: That depends on her but for now I’ll just recommend these medications.
Daughter: Ok..then so be it.

Scene 5: ipapakita ditto yung results ng case analysis natin…


References:

Urinalysis and Body Fluids, 5th edition by Susan King Strasinger


http://www.auburn.edu/~deruija/renal_part4/sld006.htm
http://prosono.ieasysite.com/patho_notes_renal_disease.pdf
http://www.nlm.nih.gov/medlineplus/ency/article/000495.htm
http://www.columbianephrology.org/Teachingframe.htm
http://en.wikipedia.org/wiki/Procardia
http://en.wikipedia.org/wiki/Morphine
http://en.wikipedia.org/wiki/Nephritic_syndrome
http://en.wikipedia.org/wiki/Cardiac_marker
http://en.wikipedia.org/wiki/CK
http://en.wikipedia.org/wiki/BUN
http://en.wikipedia.org/wiki/Mi
http://en.wikipedia.org/wiki/Lasix
http://en.wikipedia.org/wiki/Pulmonary_edema
http://www.nlm.nih.gov/medlineplus/ency/article/003586.htm
Questions

Which of the following is not a symptom of Chronic Glomerulonephritis


a. hypertension
b. edema
c. oliguria
d. 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:


a. serum creatinine
b. creatinine clearance
c. both a and b
d. none of the above

Reduction in nephron mass from the initial injury reduces the GFR then leads to:
a. hypertrophy
b. hyperfiltration of the remaining nephrons
c. both a and b
d. none of the above

Which of the following best describes Chronic Glomerulonephritis:


a. Occurs primarily in children following viral respiratory infections.
b. Disruption of podocutes in certain areas of glomeruli associated with heroin and
analgesic abuse.
c. Deposition of IgA on the glomerular membrane resulting from increased levels of
serum IgA
d. 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:


a. Insulin-dependent diabetes mellitus
b. lupus erythematosus
c. Hypercholesterolemia
d. None of the above

Chronic Glomerulonephritis can be caused by:


a. mercury
b. non-steroidal anti-inflammatory analgesics
c. HIV
d. All of the above

First indicator of renal disorder is:


a. protein
b. glucose
c. blood
d. abnormal sediment

The most significant and the only one that can be found in a cast:
a. WBC
b. RBC
c. Renal epithelial
d. 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

You might also like