case study- group 5-sem 4
TRANSCRIPT
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MPHA 4305 -SBT V
Case Study 5
Group 5
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Group Members:Lau Li Wenn BPM 1109 1317
Lee Suo Ying BPM 1109 1311
Lau Wai Hoong BPM 1109 1146
Lee Soo Mei BPM 1109 1044
Lee Yee Ling BPM 1109 1036Lee Ming Keat BPM 1109 1310
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Case History 1
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A 44-year-old man who had lost his job because of
absenteenism, presented to his physician complaining of
loss of appetite, fatigue, muscle weakness, and emotional
depression.
The physician examination revealed a somewhat enlarged
liver that was firm and nodular, and there was a hint of
jaundice in the sclerae and a hint of alcohol in his breath.
The initial laboratory profile included a hematologicalanalysis that showed that he had an anemia with enlarged
red blood cells (macrolytic). A bone marrow aspirate
confirmed the suspicion he had a megaloblastic anemia
because it showed a greater than normal number of redand white blood cell precursors, most of which were larger
than normal. Further analyses revealed that his serum folic
acid level was 1.2ng/mL (normal 2.5 to 20), his serum B12
level was 253 ng/mL (normal 200-900), but his serum iron
level was normal.
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Patient Background
Gender : Male
Age : 44 years old
Symptoms: loss of appetite
fatigue
muscle weakness Emotional depression
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Physical examination:
Enlarged liver (firm & nodular)
Hint ofjaundice in the sclerae Hint ofalcohol in his breath
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Initial laboratory profile
Hematological Analysis:
Anemia with enlarged RBC ( Macrocytic )
Bone Marrow Aspirate: no.RBC& WBC precursor >normal
Size LARGER than normal
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Serum level of
Folic acid : 1.2ng/mL ( normal 2.5-20 )
B12 : 253 ng/ml (normal 200-900) Iron : NORMAL
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Diagnosis:
Megablastic Anemia
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What is megaloblastic anemia?
Enlargement of the red blood cells, and thus
they are dysfunctional
Common causes are, Vitamin B12 and folic
acid deficiency results from
Malabsorption
Dietary deficiency
Gastric diseases
Liver diseases
Medication
Alcoholism
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What is the cause of megaloblastic anemia in this
patient? What is its correlation with alcoholism?
I. Deficiency of folic acid (which may cause byliver disease or alcoholism)
Liver disease:
Cell necrosis, which decreases the livers abilityto metabolize and excrete bilirubin, thusunconjugated bilirubin in the blood lead to
jaundice.
Interfere with the production and metabolism ofred blood cells, thus abnormal RBC are produced
Impairs with the absorption and also diminishhepatic storage of folic acid
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Alcoholism:
Interfere with the enterohepatic cycle
Decrease the absorption of folic acid, becauseusually alcoholism will lead to malnutrition
and thus to the deficiency of many nutrients.
Why deficiency of nutrients?
Poor diet
Intestinal malabsorptionDecrease hepatic uptake
Increase body excretion, mainly via urine
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Alcoholism Liverdisease
Folic aciddeficiency
Megaloblasticanemia
Jaundice
Failed in the
production
of normal
RBC
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Case History 2
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Patient is, a malnourished-appearing woman in
her second trimester of pregnancy, presents to
the local health clinic for her regular checkup.She is a multiparous, 22-year-old woman who
ran away from home when she was 16. She has
a 7-year history of excessive alcohol intake and
has been using cocaine frequently for 3 years.She lives with her boyfriend and her 19-month-
old daughter. During both pregnancies, T.J. lost
8 to 10 Ib during the first trimester secondary
to nausea, vomitting, and aneroxia. Her onlycomplaints are dyspnea on exertion,
palpitations, and diarrhea.
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Pertinent laboratory values include the following:
Hct, 25.5% (normal, 40 to 44%); MCV 112m3
(normal, 76 to 100); MCH, 34 pg (normal, 27 to33);RBC, 1.1 X 106 /mm3(normal, 3.5 to 5.0);
folate, 30ng/mL (normal, in RBC 140 to 960);
serum vitamin B12, 250 pg/mL (normal, 200 to
1,000); reticulocytes, 1% (normal, 0.5 to 1.5);platelets, 75,000/mm3 (normal 130,000 to
400,000); WBC count, 2,000/mm3 (normal, 3,200
to 9,800 ) with hypersegmented PMN; LDH, 450
U/L (normal, 50 to 150); and bilirubin, 1.5 mg/dl.
Normal, 0.1 to 1).
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Patient Background
Name : T.J. Gender: Female
Age : 22 years old
Malnourished-appearing
Stage of pregnancy : 2nd trimester
Has 19-month-old daughter
Excessive alcohol intake ( 7 years)
Cocaine administration (3 years)
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In both pregnancies:
lost 8-10 Ib in 1st trimester (Nausea,
vommitting & anorexia)
Symptoms:
Dsypnea on exertion, palpitations &
diarrhea
P i l b l
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Pertinent laboratory value:
Blood Serum level Normal Range
Hct 25.5% 40-44% Less
RBC 1.1 X 106 /mm3 3.5-5.0 /mm3 Less
Folate 30 ng/mL 140-960 ng/mL Less
Platelets 75,000 /mm3 130,000-400,000/mm3 Less
WBC(Hypersegmented
polymorphonuclear
leukocytes)
2,000/mm3
3,200-9,800 /mm3
Less
MCV 112 m3 76-100 m3 Greater
MCH 34 pg 27-33 pg Greater
LDH 450 U/L 50-150 U/L Greater
Vitamin B12 250 pg/mL 200-1000 pg/mL Normal
Recticulocytes 1% 0.5-1.5% Normal
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Diagnosis?
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Question 1:
T.J is not taking any presciption
medications. What factors make T.J. at
risk for folate deficiency???
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1. Pregnancy
Increased need for folic acidRequire more folate to meet the needs of her
developing baby.
If she dont have sufficient folate intake, she
may become folate deficient and her unborn
baby may develop a neural tube defect.
This happens when unborn baby's nerves and
spinal cord do not develop properly in the firstmonths of pregnancy.
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2. Malnutrition
Poor dietary intake of folic acid
(does not eat enough foods that contain
folic acid)
Diets lacking of fresh fruits andvegetables, or consistently overcook food
Imbalance and unhealthy diet
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Inadequate dietary intake of folic acid
interferes with the absorption of folate.
Drinking too much alcohol can reduce T.J.
body's ability to absorb and use folate.
3. Chronic Alcoholism
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Question 2
Which laboratory values support thediagnosis of folate deficiency ? How
should T. J be treated and monitored?
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The folate concentration in the RBC is only 30ng/mL, which is much lower than the normal
range. The Vitamin B12 is at normal range.
The MCV or MCH has increased in the patients,with folate deficiency, indicates the patient
diagnosed with megaloplastic anemia. The platelets count are low, and the white blood
cells count are low with hypersegmentedpolymorphonuclear leukocytes.
Hypersegmented polymorphonuclear leukocytesare the earliest and most specific signs ofmegaloblastic anemia.
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Treatment
Oral folic acid therapy can be given,
because it is inexpensive and stable.
15mg daily for 4 months due to themalabsorption states.
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Monitoring the Condition
Around 10 days after starting treatment, the
blood test is taken to check whether the levels
has started to rise.
Approximately 8 weeks is required for anotherblood test to confirm the treatment has been
successful.
The blood test is taken again after the treatment
has finished.
C t d 3
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Case study 3
A 65-year-old woman presents to the medical out-patient
department with a history of fatigue. She has in the last few months
been undergoing adjuvant cytotoxic chemotherapy for a node-positive resected breast cancer. The patient is pale, but no other
abnormalities are noted. Her full blood count shows a haemoglobin
level of 9.8 g/dL with a mean corpuscular volume of 86 fL; other
haematological indices and serum transferrin are normal. Her faecal
occult blood is negative. She is started on oral iron sulphate andgiven weekly injections of erythropoietin 40 000 U subcutaneously.
Three months later, her haemoglobin level has risen to 13.5 g/dL,
but she presents to the Accident and Emergency Department with
acute-onset dysphasia and weakness of her right arm. Her supine
blood pressure is 198/122mmHg. Her neurological deficit resolves
over 24 hours and her blood pressure settles to 170/96 mmHg. She
has no evidence of cardiac dyshythmias or of carotid disease on
ultrasonic duplex angiography, and her serum cholesterol
concentration was 4.2 mmol/L.
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Summary Gender: woman
Age: 65 yrs old
History: fatigue
Therapy received before: adjuvant cytotoxic
chemotherapy : node-positive resected breastcancer.
Haemoglobin level: 9.8 g/dL with a mean
corpuscular volume of 86 fL
other haematological indices and serum transferrin:
normal
faecal occult blood: negative
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Treatment: oral iron sulphate & inject erythropoietin
40 000U (SC) weekly.
Haemoglobin level after 3 months: risen to 13.5 g/dL
Accident & emergency department: due to acute-
onset dysphasia and weakness of her right arm.
Supine blood pressure: 198/122mmHg.
After 24 hours, blood pressure- 170/96 mmHg,
neurological deficit resolves
Cardiac dyshythmias / carotid disease in ultrasonicduplex angiography- negative
Serum cholesterol conc.4.2 mmol/L
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Question 3
What led to this patients acute neurological episode? Does she
require further therapy?
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Question 3
The 65-year-old woman is diagnosed for a
node-positive resected breast cancer. She
had been undergoing cytotoxic
chemotherapy in the last few months.
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1) Filgrastim (granulocyte colony-stimulating
factor; G-CSF).
2) Sargramostim (granulocyte-macrophage
colony-stimulating factor; GM-CSF).
Both stimulate the production of neutrophils
and accelerate the recovery of neutrophils
after cancer chemotherapy.
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4) Oprelvekin (interleukin-11 [IL-11]) increases
the number of peripheral platelets. It is usedfor the treatment of thrombocytopenia
patients after had cancer chemotherapy.
5) It reduces the need for platelettransfusions.
Common adverse effects of IL-11 are
fatigue, headache, dizziness, and fluidretention.
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Serum cholesterol concentration= 4.2mmol/L.
Total Cholesterol [mmol/L (mg/dl)]
a) Risk indicated if greater than 4.5
b) Desirable: =240)
The first steps in treating high cholesterol
levels are regular physical activity andhealthy eating.