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1. Based on the history, what would you expect to see in her CBC?
RBC count is low
2. When do you consider a person anemic?
when Hgb and/or Hct in the peripheral blood is below the lower limit of 95% of
the persons reference interval in terms of his/her age, sex, and geographical
3. How do you classify anemia? What are the important parameters that you
should consider in making the morphological classification of anemia?
according to size and morphology (microcytic, normocytic, macrocytic)
o based on the MCV( mean corpuscular volume)
according to shape (hypochromic, normochromic, hyperchromic)
o based on MCH (mean corpuscular Hemoglobin)
according to Hgb content
o based on MCHC (mean corpuscular Hemoglobin concentration)
4. What morphological changes will you see in the peripheral blood smears in
patients with anemia? What other tests will you request for ?
morphological changes
o anisocytosis
o poikilocytosis
o central pallor
other tests
o reticulocyte count
o osmotic fragility
o folic acid test
o serum iron levels
o electrophoresis
o Hams test
o sucrose hemolysis test
o total iron binding capacity
o serum ferritin
o Cobalamine test
5. What are the symptoms of anemia?
pallor, easy fatigability and mild dyspnea
difficulty in concentrating, insomnia, dizziness
aggravated by exercise

6. What is the most common cause of anemia for this particular patient?
iron deficiency anemia

1. The patients condition is an abnormality of what tissue or body system?
What type of cells does the disease involve?
Diagnosis: acute lymphoblastic leukemia
o an abmnormality of the hematologic and lymphatic systems.
o elevation of white blood cells and lymphoblasts
2. What can explain the proliferation of immature cells in the blood? The high
WBC count? The low platelet count? The low hemoglobin and hematocrit?
proliferation of immature cells in blood
WBC count
platelet count
Hgb & Hct

early lymphoid precursors that proliferate

and replace the normal hematopoietic cells
of the bone marrow.
increased production of immature white
blood cells resembling lymphoblasts
decreased pdtn and sequestration of
blood clots
RBC hemolysis, normocytic anemia

3. Aside from the CBC findings, what other simple laboratory tests can be
abnormal in the patients condition?
fibrinogen and fibrin degradation tests
marrow examination
i mmunochemistry, cytochemistry, and cytogenetic markers
lactic dehydrogenase or uric acid determination
4. Can you explain the enlargement of the liver and the spleen? Can other
organs be enlarged in this condition?
infiltration of leukemic cells into the above mentioned organs due to increased
WBC count

Are there special stains useful in the diagnosis of cases such as this
acid phosphatase


What accounts for the prolonged PTT?

presence of Lupus anticoagulant in the plasma of SLE patients

What is the mechanism of action of the substance in No. 1?

platelet-associated binding of antibodies against 2GPI (or prothrombin)
binding causes platelet activation for coagulation
o in vitro, inhibits normal assembly of the coagulation system
o in vivo, causes prothrombic action

Is Lupus associated with bleeding since Lupus Anticoagulant is present?

No, it is only associated with bleeding only when Lupus is accompanied with
severe thrombocytopenia or acquired Factor II deficiency. Lupus also increases
the risk of anemia, bleeding, blood clotting and vessel inflammation.

What does D-dimer measure?

presence of fibrin degradation products brought about by ongoing thrombosis
and fibrinolysis.

What is the significance of positive D-dimer?

positive D-dimer indicates high levels of fribrin degradation products, which
subsequently indicate excessive thrombosis and fibrinolysis

What are the underlying conditions in this patient that has led to DIC?
sepsis and malignancy (pulmonary carcinoma)
inflammatory responses to bacteria in the blood which may cause endothelial

1. What is your diagnosis? Basis for your diagnosis?
Poststreptococcal Glomerulonephritis
o based on URTI development, moderate to high grade fever which is
often caused by bacterial infection
2. Give your differential diagnoses.
Immune-mediated disease
congestive heart failure
liver failure (cirrhosis, hepatitis, etc.)
3. What other laboratory/ancillary tests could or should be done for the
urine culture
comprehensive metabolic panel (CMP)
creatine clearance urine and blood test
4. Discuss the pathophysiology behind your diagnosis.
severe inflammation damages glomeruli, resulting in a significant decrease in
GFR. This subsequently causes uremic symptoms involving salt/water
retention, eventually causing the edema and hypertension

1. What is the significance of increased number of non-crenated RBC,
especially in first tube?
increased levels of non-crenated RBC in the first tube denotes traumatic tap
2. Interpret CSF analysis report.
CSF protein
CSF glucose
WBC count (neutrophils)
3. What is your preliminary diagnosis?
Bacterial meningitis
4. Would a CSF lactate test be of any value?
Yes, as CSF lactate would be increased in a case of Bacterial meningitis.
Moreover, it can determine the etiology of decreased CSF glucose levels by
differentiating bacterial from viral CNS infections. It may also serve to monitor
severe head injuries.
5. What

additional tests would you request for?

CSF culture for Neisseria meningitides
CT or MRI scans at latter stages
electrolyte monitoring for severe cases

1. Discuss the pathology involved in SLE.
multi-organ autoimmune disease caused by anti-nuclear autoantibodies (ANA)
to DNA and histones
lesions are due to immune complex deposition within connective tissues
clinical features:
o vasculitis
o glomerulonephritis
o polyarthralgia
o malar rash
o coronary artery disease
2. What clinical specimens can be used and what laboratory procedures
should be requested in order to diagnose the case?
serum tests for ANA & it subtypes (Anti-dsDNA, Anti-Smith, Anti-histone)
detection of ANA via indirect immunofluorescence
tests for complications in associated organs
o urinalysis
3. Explain the presence of anemia, leucopenia, proteinuria, and hematuria in
the patient.

antibodies targeted against RBCs and WBCs

nephrotoxicity caused by glomerulonephritis
destruction of the glomerulus in glomerulonephritis

4. What reaction type of synovial effusion does this patient have?

non-erosive arthritis caused by type III immune-mediated tissue injury
5. What

are the expected findings in the synovial fluid analysis of this patient?
gross: clear, viscous
microscopic: few WBCs
chemical: low complement. content

1. What is your clinical impression?
acute myocardial iInfarction and unstable angina
o hx of characteristic chest pain
o distinguishing electrocardiographic changes
o typical pattern of serum cardiac enzyme risk
2. What other laboratory test/s would you request to establish diagnosis? Give
reasons why you will request such test/s?
o relatively specific for diagnosis of AMI
cardiac enzymes, Creatine Kinase (CK-MB) and Troponin (I and T)
o CK-MB: not found in normal myocardium, indicates muscle injury, gold
standard biochemical marker for AMI
o Troponin (I and T): highly specific for myocardial injury.
3. What is the significance of lipid profile in relation to present condition of
the patient?
indicates total cholesterol level
o NV: ~163 mg/dl
o patient's is 250.16 mg/dl, denoting high blood cholesterol
4. What are the possible reasons why he has elevated SGOT and SGPT levels?
biochemical markers for the diagnosis of acute myocardial infarction, though
they are markers for muscle injury in general.

1. Does the HBsAg (+) status denote a previous HBV infection? In what
manner did the infant acquire the infection?
Viral infection was via from his Hepa-B(+) positive mother
2. What probably was the status of the mother with regards to HV serum
markers during pregnancy and partuition?
chronic Hepa-B.
3. Is the child infectious? What additional tests can help quantify the childs
infectivity? Under what circumstances can he infect others?
Child is an asymptomatic carrier, but may experience complications in later
life such as cirrhosis or hepatic carcinomas.
quantitative measures of infectivity include determining antigen levels in his
4. What

biochemical tests are used for follow up?


5. What do the levels of SGOT and SGPT signify at present? At what stage in
HBV clinical course would the child and mother probably be at present?
SGOT and SGPT levels indicate varying increases during the prodromal phase
of acute viral hepatitis, and precedes the rise in bilirubin level.
Mother and child would be clinically icteric at this stage.
6. Are follow-up tests for HBV serum markers indicated? What would you
recommend as tests to determine in the future the childs status as to
activity of HBV infection, infectivity or recovery? Would you recommend
future testing for sufficiency of liver function with regards to possibility of
cirrhosis and neoplasm?

1. What kind of BTR did the patient experience?
acute hemolytic transfusion reaction
2. What are the signs and symptoms associated with this kind of BTR?
intravascular hemolysis, hemoglobinemia, hemoglobinuria, fever,
hypotension, tachypnea, tachycardia, pain at infusion site


3. What substance is responsible for red discoloration of patients urine?

hemoglobin released from intravascular hemolysis and filtered via kidneys
4. What blood bank procedures should be done during the investigation of this
kind of BTR?
post-transfusion re-blood typing, crossmatching, Du variant testing.
5. What do you mean by massive bleeding and massive blood transfusion?
massive bleeding:
o loss of circulating blood volume of nearly 50% within at least 3 hours or
150 ml/min
massive blood transfusion:
o transfusion of at least 50% of the patients blood volume within 24
hours or replacement of 10 units of blood within a 24 hour period
6. Is the administration of Diphenyhydramine indicated in this case?
No, because dephenhydramin is indicated only for patients allergic to the
7. Patient developed liver and renal damage and died after four days. What
could have been the clinical course prior to her demise?
renal dysfunction and failure brought about by immune complexes from RBC
tissue factor released from the lysed erythrocytes may initiate DIC and lead to
subsequent death
8. How could this BTR be prevented?
proper labeling and storage of donor blood
crossmatching of donor and patient for compatibility
per-unit transfusions
history of previous transfusions and/or complications or blood bank antibody
vital signs pre and post-transfusion