NR 507
Week 3 – Part 1, 2 & 3
Case Study Discussions and Quiz
, NR 507 Week 3 TD and Quiz
PART 1:
A 17-year-old African American from the inner city complains of severe
chest and abdominal pain. Upon examination the attending physician
performs and EKG, chest x-ray, and an abdominal and chest clinical
examination and finds nothing. Assuming, she is drug seeking he sends her
home. She comes back to the ER four hours later and now you see the
patient. She explains that she was running track this past afternoon at school
and that despite being very hot (100 F) she pushed on. Afterwards, she starts
feeling extensive pain in her chest and abdomen. She has jaundiced eyes,
her blood pressure is 98/50, pulse is 112, T = 99.9 F, R = 28. The pain seems
out of proportion to the physical findings.
What is your list of differential diagnoses in this case and explain how
each of these fits with the case patient as described above. Be sure to list
at least three (3) pertinent differential diagnoses. Indicate which of these
you would select as the most likely diagnosis and explain why.
Now, as she is in the ER she begins to exhibit stroke like features. ? Does
this change your differential?
How do you treat this patient now? Are they any preventative actions
that could have been taken?
1. Sickle Cell Crisis. Sickle cell disease (SCD), which is an inherited autosomal
recessive disorder, that originates from a genetic mutation in the hemoglobin (Hgb)
beta globin gene to the formation of the abnormal erythrocyte Hemoglobin S (HbS),
which replaces the normal Hgb (Peres de Olivera, Leão Santos, de Lourdes Silva,
Quadros Dias, de Silveria, & de Azevedo Guimarães, 2017). Another name for HbS is
sickle hemoglobin; this type of hemoglobin (Hgb) responds to dehydration and lack
of oxygen by “hardening” and stretching into long, crescent, sickle cell shaped
erythrocytes (McCance, Huether, Brashers, & Rote, 2013). Depending on ones
genetic inheritance of SCD, the disease can take 3 forms: Sickle cell anemia, sickle
cell-Hb C disease, or sickle cell-thalassemia disease (McCance et al., 2013). Sickle
cell trait is where one carries the sickle cell gene but typically does not have any
complications of the actual disease. SCD has a tendency to affect certain people who
originate from central Africa, parts of India, the Mediterranean, and the Near East
(McCance et al., 2013). As of 2013, 1 in 500 African American children and 1 in
36,000 Hispanic American kids are born with sickle cell anemia (McCance et al.,
2013).
, Extensive sickling of cells, also referred to as sickle cell crisis, can cause a
number of acute clinical manifestations. Crisis is typically triggered by stress, cold,
hypoxemia, and/or decreased plasma osmolality or volume (McCance et al., 2013).
When sickling occurs, sickle cells clog vessels, some of which can cause hypoxemia
and others that can cause much worse, such as a splenic or hepatic infarct and even an
MI or CVA; these are just a few of many serious complications that can occur (Ward,
Simpson, & Verhovsek, 2016). Clinical manifestations of crisis include jaundice,
fatigue, pallor, and severe pain that may not match physical findings (McCance et al.,
2013). Treatment during crisis includes oxygen, hydration via intravenous fluids,
analgesics, and as long as blood counts are acceptable, some patients may receive
hydroxyurea (McCance et al., 2013).
While in the ER, if the patient began exhibiting stroke like symptoms, it would
not change my differential. CVA is a possible serious complication of SCD. I would
immediately get the patient to CT in order to confirm CVA and distinguish between
hemorrhagic or embolism. If the patient were positive for CVA, I would treat
according to the type of infarct. Preventative actions so that the patient did not end up
back in the ER in sickle cell crisis and possibly positive for a CVA would be
education. The previous provider should have never sent the patient home, had he
recognized the signs and began treatment then, the patient may not be experiencing
her current complications.
2. Thalassemia. This is an inherited autosomal recessive disease that impairs synthesis
rates in 2 chains, the alpha and beta chains, within Hb A (McCance et al., 2013). Beta-
thalassemia affects Italians, Greeks, Sephardic Jews, and sometimes Arabs (McCance et
al., 2013). Alpha- thalassemia affects Cambodians, Vietnamese, Laotians, and Chinese
(McCance et al., 2013). African Americans are affected by both Alpha- and Beta-
thalassemias (McCance et al., 2013). Clinical manifestations can range from
asymptomatic or minor, such as microcytic-hypochromic hemolytic anemia, bronzing
of the skin, hyperplasia of bone marrow, and mild splenomegaly to severe with
complications such as severe anemia, significant cardiovascular complications,
enlarged liver and spleen, destruction of red blood cells, spinal issues, lower extremity
weakness, and bone marrow hyperplasia that can cause deformities, especially to the
face (McCance et al., 2013). If children who have alpha- or beta-thalassemia are left
untreated, they will likely die by the time they are 6 years old (McCance et al., 2013).
This diagnosis was listed because some of the clinical manifestations match those of the
patient, however the patient’s presentation does not fully fit this differential.
3. Acute Pancreatitis. Pancreatitis is inflammation of the pancreas and can be a serious
health issue. Acute pancreatitis typically develops related to bile or pancreatic duct
obstruction or by obstructing outflow of its digestive enzymes (McCance et al., 2013).
Acute pancreatitis can occur from direct cellular injury related to a viral infection, drugs,
alcohol, genetic disorders, abdominal trauma, and peptic ulcer disease (McCance et al.,
2013). Acute pancreatitis typically affects about 17 in 100,000 Americans and they are
usually between 50 to 60 years of age (McCance et al., 2013). This diagnosis was chosen
based on some of the similar clinical manifestations however, this patient is not
Week 3 – Part 1, 2 & 3
Case Study Discussions and Quiz
, NR 507 Week 3 TD and Quiz
PART 1:
A 17-year-old African American from the inner city complains of severe
chest and abdominal pain. Upon examination the attending physician
performs and EKG, chest x-ray, and an abdominal and chest clinical
examination and finds nothing. Assuming, she is drug seeking he sends her
home. She comes back to the ER four hours later and now you see the
patient. She explains that she was running track this past afternoon at school
and that despite being very hot (100 F) she pushed on. Afterwards, she starts
feeling extensive pain in her chest and abdomen. She has jaundiced eyes,
her blood pressure is 98/50, pulse is 112, T = 99.9 F, R = 28. The pain seems
out of proportion to the physical findings.
What is your list of differential diagnoses in this case and explain how
each of these fits with the case patient as described above. Be sure to list
at least three (3) pertinent differential diagnoses. Indicate which of these
you would select as the most likely diagnosis and explain why.
Now, as she is in the ER she begins to exhibit stroke like features. ? Does
this change your differential?
How do you treat this patient now? Are they any preventative actions
that could have been taken?
1. Sickle Cell Crisis. Sickle cell disease (SCD), which is an inherited autosomal
recessive disorder, that originates from a genetic mutation in the hemoglobin (Hgb)
beta globin gene to the formation of the abnormal erythrocyte Hemoglobin S (HbS),
which replaces the normal Hgb (Peres de Olivera, Leão Santos, de Lourdes Silva,
Quadros Dias, de Silveria, & de Azevedo Guimarães, 2017). Another name for HbS is
sickle hemoglobin; this type of hemoglobin (Hgb) responds to dehydration and lack
of oxygen by “hardening” and stretching into long, crescent, sickle cell shaped
erythrocytes (McCance, Huether, Brashers, & Rote, 2013). Depending on ones
genetic inheritance of SCD, the disease can take 3 forms: Sickle cell anemia, sickle
cell-Hb C disease, or sickle cell-thalassemia disease (McCance et al., 2013). Sickle
cell trait is where one carries the sickle cell gene but typically does not have any
complications of the actual disease. SCD has a tendency to affect certain people who
originate from central Africa, parts of India, the Mediterranean, and the Near East
(McCance et al., 2013). As of 2013, 1 in 500 African American children and 1 in
36,000 Hispanic American kids are born with sickle cell anemia (McCance et al.,
2013).
, Extensive sickling of cells, also referred to as sickle cell crisis, can cause a
number of acute clinical manifestations. Crisis is typically triggered by stress, cold,
hypoxemia, and/or decreased plasma osmolality or volume (McCance et al., 2013).
When sickling occurs, sickle cells clog vessels, some of which can cause hypoxemia
and others that can cause much worse, such as a splenic or hepatic infarct and even an
MI or CVA; these are just a few of many serious complications that can occur (Ward,
Simpson, & Verhovsek, 2016). Clinical manifestations of crisis include jaundice,
fatigue, pallor, and severe pain that may not match physical findings (McCance et al.,
2013). Treatment during crisis includes oxygen, hydration via intravenous fluids,
analgesics, and as long as blood counts are acceptable, some patients may receive
hydroxyurea (McCance et al., 2013).
While in the ER, if the patient began exhibiting stroke like symptoms, it would
not change my differential. CVA is a possible serious complication of SCD. I would
immediately get the patient to CT in order to confirm CVA and distinguish between
hemorrhagic or embolism. If the patient were positive for CVA, I would treat
according to the type of infarct. Preventative actions so that the patient did not end up
back in the ER in sickle cell crisis and possibly positive for a CVA would be
education. The previous provider should have never sent the patient home, had he
recognized the signs and began treatment then, the patient may not be experiencing
her current complications.
2. Thalassemia. This is an inherited autosomal recessive disease that impairs synthesis
rates in 2 chains, the alpha and beta chains, within Hb A (McCance et al., 2013). Beta-
thalassemia affects Italians, Greeks, Sephardic Jews, and sometimes Arabs (McCance et
al., 2013). Alpha- thalassemia affects Cambodians, Vietnamese, Laotians, and Chinese
(McCance et al., 2013). African Americans are affected by both Alpha- and Beta-
thalassemias (McCance et al., 2013). Clinical manifestations can range from
asymptomatic or minor, such as microcytic-hypochromic hemolytic anemia, bronzing
of the skin, hyperplasia of bone marrow, and mild splenomegaly to severe with
complications such as severe anemia, significant cardiovascular complications,
enlarged liver and spleen, destruction of red blood cells, spinal issues, lower extremity
weakness, and bone marrow hyperplasia that can cause deformities, especially to the
face (McCance et al., 2013). If children who have alpha- or beta-thalassemia are left
untreated, they will likely die by the time they are 6 years old (McCance et al., 2013).
This diagnosis was listed because some of the clinical manifestations match those of the
patient, however the patient’s presentation does not fully fit this differential.
3. Acute Pancreatitis. Pancreatitis is inflammation of the pancreas and can be a serious
health issue. Acute pancreatitis typically develops related to bile or pancreatic duct
obstruction or by obstructing outflow of its digestive enzymes (McCance et al., 2013).
Acute pancreatitis can occur from direct cellular injury related to a viral infection, drugs,
alcohol, genetic disorders, abdominal trauma, and peptic ulcer disease (McCance et al.,
2013). Acute pancreatitis typically affects about 17 in 100,000 Americans and they are
usually between 50 to 60 years of age (McCance et al., 2013). This diagnosis was chosen
based on some of the similar clinical manifestations however, this patient is not
