Heme/Onc Flashcards
Normal Hgb
Males: 14-18 g/100ml
Females: 12-16 g/100ml
Normal Hct
Males: 40-54%
Females: 37-47%
Normal TIBC
250-450 ug/dl
High TIBC indicates..
increased need for iron
Normal serum iron
50-150 ug/dl
normal MCV
80-100 um3
normal MCHC
26-34 pg
normal MCHC
32-36%
thalassemia:
- H/H
- MCV
- MCHC
- TIBC
- serum ferritin
- alpha or beta chains
H/H low
MCV low
MCHC low
TIBC normal
ferritin normal
alpha or beta chains decreased
iron deficiency anemia:
- H/H
- MCV
- MCHC
- RBC
- Serum iron
- serum ferritin
- TIBC
- RDW
H/H low
MCV low
MCHC low
RBC low
serum iron low
serum ferritin low
TIBC high
RDW high
Pernicious anemia (B12 deficiency):
- H/H
- MCV
- MCHC
- RBC
- serum B12
- Anti-IF (intrinsic factor) and anti-parietal antibody test
H/H low
MCV high
MCHC normal
RBC low
serum B23 low (<200 pg/ml)
Anti-IF and anti-parietal cell antibody test
folate deficiency:
- H/H
- MCV
- MCHC
- serum folate
- RBC folate
H/H low
MCV high
MCHC normal
serum folate decreased
RBC folate <100 ng/ml
alcoholism:
- H/H
- MCV
H/H low
MCV high
liver failure:
- H/H
- MCV
H/H low
MCV high
anemia of chronic disease
- H/H
- MCV
- MCHC
- serum iron
- TIBC
- serum ferritin
H/H low
MCV normal
MCHC normal
serum iron low
TIBC low
serum ferritin high (>100ng/ml)
sickle cell disease
- H/H
- MCV
- peripheral smear
H/H low
MCV normal
peripheral smear shows classic distorted sickle-shaped RBCs and Howell-Jolly bodies
renal failure
- H/H
- MCV
H/H low
MCV normal
blood loss
- H/H
- MCV
H/H low
MCV normal
most common cause of anemia
iron deficiency anemia
iron deficiency anemia: causes
blood loss
inadequate iron intake
impaired iron absorption
iron deficiency anemia: S/Sx
Usually slow in onset
As Hct falls:
- Pica: unusual food cravings
- dyspnea, pallor
- weakness, mild fatigue with exercise
- headache
- palpitations, tachycardia, postural hypotension
- koilonychia (spoon-shaped nails)
iron deficiency anemia: treatment
Oral iron 325mg TID for 3-6 months after restoration of normal lab values
Parenteral iron (iron dextran or sodium ferric gluconate) can be given if GI absorption of iron seems to be the problem
anemia of chronic disease: categories
Associated with chronic inflammation, infection, renal failure, malignancy
Anemia of inflammation
-chronic inflammatory conditions such as RA or IBD interfere with hepcidin activity
Anemia of organ failure
-liver or kidney failure suppress erythropoietin activity and therefore the bone marrow is not properly stimulated for erythropoiesis
Anemia of older adults
-anemia that is found in those over age 85 where any other cause is completely lacking
anemia of chronic disease: management
Manage underlying cause
Nutritional support
Severe symptoms:
-transfusion
-recombitant erythropoietin (epoetin alfa or darbopoetin)
Sickle cell anemia
Type of hemolytic anemia
Mutation that causes unstable hemoglobin which denatures under stressors such as hypoxia or acidosis, leading to deformation of the RBC into a sickle shape, and then hemolysis
Results in chronic anemia
sickle cell anemia: signs
Signs of disease develop in infancy or childhood
Delayed growth and development
Increased susceptibility to infections
Hct 20-30% at baseline
Jaundice
hepatosplenomegaly
non-healing ulcers on the legs
retinopathies
cardiomegaly
sickle cell crisis
When exposed to triggers, sickling is influenced by expression of the gene
The rate of sickling overwhelms the spleen’s ability to compensate and painful vaso-occlusive events occur
sickle cell crisis: treatment
Identify precipitating factor
IV hydration: priority
Supplemental O2
Generous analgesia
Transfusion with careful monitoring for iron overload
sickle cell crisis: prevention
Appropriate vaccination
Avoidance of physiologic stress
Hydroxyurea (500-700mg PO daily)
What offers about an 80% cure rate for sickle cell anemia
bone marrow transplant
Immune thrombocytopenic purpura
Formerly “idiopathic”
Results from autoimmune destruction of platelets with or without suppression of thrombopoiesis
Immune thrombocytopenic purpura: diagnosis
Diagnosis of exclusion
bone marrow analysis
low platelet count with other causes ruled out
Immune thrombocytopenic purpura: Symptoms
spontaneous bruising
petechial rash
spontaneous bleeding from the nose, gums, or vagina
Immune thrombocytopenic purpura: labs
Plt <20 or too low to measure
Immune thrombocytopenic purpura: treatment
Treatment is not universal, and some patients are not treated at all and the condition resolves on its own in about 1-2 months
If treatment is given, it focuses on:
-mitigation of bleeding complications
-High dose steroids (e.g.Prednisone 1mg/kg/day) to elevate platelet count
-IV gamma globulin
-Consider platelet transfusion, but these transfused platelets are generally subject to the same immune attack
-splenectomy may be considered in patients who are either unresponsive to steroid treatment, have frequent relapses, or cannot be tapered off steroids after a few months
heparin-induced thrombocytopenia: mechanism
Immune system forms antibodies against heparin when it is bound to platelet factor 4 (PF4) and has a cascading effect:
1. The IgG antibodies form a complex with heparin and PF4
2. The tail of the antibody binds to a protein on the surface of the platelet
3. This results in platelet activation and the formation of platelet microparticles, which initiate the formation of blood clots
4. The platelet count falls as a result, leading to thrombocytopenia
heparin-induced thrombocytopenia: what lab do you send if suspected?
PF4 ELISA
heparin-induced thrombocytopenia: presentation
Hallmark: decrease in platelet count by 30-50% within 5-10 days following expsure to heparin
heparin-induced thrombocytopenia: management
Stop the heparin if platelet counts are dropping within 5 days of administration of heparin
-hold warfarin, because of the high risk of warfarin necrosis
-start alternative AC: bivalirudin, argatroban, fondaparinux (to treat the clots formed during HIT)
Disseminated intravascular coagulation
Acquired condition that results in thrombocytopenia but also involves the clotting cascade being inappropriately activated either locally or systemically
Disseminated intravascular coagulation: causes
Always secondary to something else, so treat the cause
-sepsis
-malignancy, often acute leukemia
-retained products of conception
-liver disease
-massive trauma
-extensive burns
-shock
Disseminated intravascular coagulation: mechanism
- Inappropriate activation of the clotting cascade and platelet activation
- Tons of microvascular clotting
- As DIC progresses, clotting factors and platelets are exhausted and spontaneous bleeding begins
- The organs and body where clotting occurred become ischemic then infarct, which further accelerates the process
- The bleeding results in massive anemia, further starving organs of oxygen
Disseminated intravascular coagulation: labs/Dx
-Presence of a known trigger
-low RBCs
-Prolonged PT and aPTT (reflect underlying consumption and impaired synthesis of the coagulation cascade)
-low fibrinogen (reflecting exhaustion of the finite supply of it)
-rapidly declining platelet count
-elevated FDP
-elevated D-dimer d/t the body trying to stop the massive clotting
-schistocytes on peripheral blood smear
Disseminated intravascular coagulation: management
Treat the trigger
Establish baseline Plt, PT, PTT, D-dimer, fibrinogen
Transfuse:
- platelets for thrombocytopenia
- FFP to replace clotting factors
- cryoprecipitate to maintain fibrinogen levels
Disseminated intravascular coagulation: Platelet transfusion goals
> 20 in most patients
50 in patients with GI or CNS bleeding
Disseminated intravascular coagulation: cryoprecipitate transfusion goals
Fibrinogen >80-100
Disseminated intravascular coagulation: Fresh frozen plasma transfusion goals
PT, PTT <1.5x normal
Disseminated intravascular coagulation: PRBC transfusion goals
Hgb >8
Von Willebrand Disease: diagnosis
vWF activity assay
platelet function assay
Von Willebrand Disease: treatment
DDAVP
more severe bleeding: Factor VIII (Humate P)
Von Willebrand Disease: Type I
mild to moderate bleeding, often never diagnosed
Treatment: DDAVP, only use Factor VIII if bleeding is severe
Von Willebrand Disease: Type II
Moderate to severe bleeding can occur
Treatment: combo of DDAVP and Factor VIII for any type of bleeding
Von Willebrand Disease: Type III
severe bleeding to even minor trauma
Treatment: always Factor VIII regardless of the severity of bleeding
acute leukemia
Rapid increase in the number of immature blood cells
Immediate treatment is required because of the rapid progression and accumulation of blasts, which then spill over into the blood stream and spread to other organs
chronic leukemia
Excessive buildup of relatively mature, but still abnormal, white blood cells
Typically takes months or years to progress
What happens if CML is left untreated?
It will progress to an acute form that appears like AML with a proliferation of blast cells and becomes fatal
What causes CML?
Overproduction of the myeloid cell d/t chromosomal abnormality called the Philadelphia chromosome
CML: presentation
Fatigue
bone pain
splenomegaly
leukocytosis in the absence of obvious infection; WBC often >150
thrombocytosis
Anemia is not usually present
Mature myeloid cell types (neutrophils, basophils, eosinophils, monocytes) predominate
CML: diagnosis
bone marrow biopsy with genomic testing will reveal bcr/abl genotype
CML: treatment
Often affects the old, so usually just monitor
Treatment:
-tyrosine kinase inhibitors (e.g. imatinib)
-hydroxyurea
-bone marrow transplant (curative)
CML: Management if it transforms to an acute phase
Rising numbers of immature forms in peripheral blood
Tyrosine kinase inhibitors are augmented with a myelosuppressive agent (chemo, radiation) to determine response
blast crisis
Final phase in the evolution of CML
Rapid progression, short survival (behaves like acute leukemia)
Blast crisis: diagnosis
> 20% blasts in the blood or bone marrow
Presence of an extramedullary proliferation of blasts
Based on symptoms and the blast cell percentage, not on the total WBC count
Blast crisis: presentation
Hyperviscosity of the blood, resulting in decreased tissue perfusion
CNS:
-reduced cerebral blood flow can lead to stroke-like symptoms
Cardiopulmonary system:
-acute respiratory failure
-congestive heart failure
-MI
Additional end organ damage
-renal failure
-priapism
-limb ischemia
-bowel infarction
Blast crisis: most effective means of treatment
Urgent hematology consult for consideration of leukopheresis
Myelodysplastic Syndrome
A variety of acquired clonal disorders of the hematopoietic stem cell
Results in cytopenias and hypercellular bone marrow
MDS: biggest risk factor
DNA damage
-hydrocarbons
-ionizing radiation
-alkylating chemo agents
MDS: Diagnosis
Excluding other causes of cytopenias and:
-bone marrow aspiration
-cytogenics
-flow cytometry
MDS: Treatment
Supportive care with blood products and hematopoietic growth factors:
-erythropoetin
-romiplostim
-granulocyte colony stimulating factor (Neupogen)
MDS: complications with therapy
iron overload from multiple blood transfusions
acute leukemia: presentation
Blast cells >20%
Profound fatigue
Fevers
Spontaneous bleeding
Occasionally infiltration of organs with leukemic cells (chloroma) - forms a solid tumor
Remission rates from 50-85%
Long term survival ~ 40%
AML: labs, Dx
Leukocytosis
Severe anemia
Thrombocytopenia
Blasts
-Auer rods present in blasts
Diagnosis: cryogenic testing of a bone marrow aspiration
AML: malignant cell
myeloblast
AML: Treatment
Induction: High-dose Cytarabine (HiDAC) and an anthracycline (usually daunorubicin)
-stops massive proliferation of myeloblasts
-goal: remission
Consolidation:
-goal: remove myeloblasts that may remain in undetectable amounts in the bone marrow
If AML recurs, consider bone marrow transplant, which can be curative
APML: Presentation
Extremely rapid development and fatality, sometimes in less than a week
Fatigue
Bone pain
Night sweats
Bleeding/petechiae
APML: malignant cell
promyelocyte
APML: treatment
all-trans-retinoic acid (ATRA)
ALL: malignant cell
lymphoblast
ALL: mechanism
Lymphocytes have a role in the defense of the CNS, so leptomeningeal spread of ALL to the CNS is common
ALL: treatment
Intrathecal chemo
Cranial radiation
More difficult to treat in adults than children
ALL: labs
Atypical lymphocytes
Pancytopenia with circulation blasts (immature/poorly differentiated cells)
-Neutropenia
-Anemia
-Thromobocytopenia
CLL: malignant cell
B cell lymphocytes
CLL: labs
lymphocytosis
-smudge cells are often present
CLL: Presentation
Immunosuppression is the biggest clinical factor
Liver and spleen are often enlarged
Occasionally, signs of autoimmune hemolytic anemia
CLL: treatment
Ibrutinil - has tyrosine kinase inhibition effects
Rarely, CLL can transform a lymph node into an aggressive large B-cell lymphoma, called a…
Richter Transformation
Lymphomas: Presentation, labs
Lymphadenopathy
Normal CBC
Lymphomas: Diagnosis, Staging
lymph node biopsy
Staging:
- Stage I: disease localized to single lymph node or group
-Stage II: more than one lymph node group involved; confined to one side of the diaphragm
-Stage III: lymph nodes or the spleen involved; occurs on both sides of the diaphragm
-Stage IV: liver or bone marrow involvement
Diffuse Large B-Cell Lymphoma (DLBCL): presentation
Type of Non-Hodgkins Lymphoma
Aggressive tumor which can arise in any part of the body
First sign: rapidly growing mass in a lymph node
Sometimes associated with “B symptoms” (e.g. fever, weight loss, night sweats)
Diffuse Large B-Cell Lymphoma (DLBCL): What viral infections are associated?
EBV
CMV
HIV
Diffuse Large B-Cell Lymphoma (DLBCL): treatment
lymph node resection
chemo (R-CHOP or R-EPOCH, Rituximab)
Radiation
Bone marrow transplant in recurrent disease
Cutaneous T-Cell Lymphoma (CTCL)
Type of Non-Hodgkin’s Lymphoma
Caused by a mutation of T-cells (unlike most NHL which are generally B-cell related)
Cutaneous T-Cell Lymphoma (CTCL): Presentation
Generalized erythroderma with lichenification (thick, leathery)
Lymphadenopathy
Atypical T-cells seen in the blood (called Buttock Cells)
Most CTCLs are mistaken for something else, so if the dermatologic condition does not resolve in the usual period of time, CTCL should enter the differential
Cutaneous T-Cell Lymphoma (CTCL): treatment
Biologic therapy (monoclonal antibodies)
Chemotherapy
Radiation
Hodgkin’s Lymphoma: prevalence
A type of lymphoma with a bimodal distribution of prevalence (first in the 20s, second in the 50s)
Hodgkin’s lymphoma: presentation
painful, tender lymph node, usually in one of the cervical chains and spreads in a predictable fashion along lymph node groups
More common in males, average age is 32 years
Hodgkin’s lymphoma: diagnosis
Biopsy to confirm diagnosis, showing Reed-Sternberg cells (giant lymphocytes with multiple or bilobed nuclei)
- differentiates from non-hodgkin’s lymphoma
CT, X-rays, ultrasound, MRI to locate and stage the disease
Hodgkin’s lymphoma: treatment
Excision of an affected node
Chemo: ABVD, Stanford V, BEACOPP
Plasma Cell Myeloma (aka multiple myeloma)
Disease of plasma cells which infiltrate the bone marrow, causing bony destruction and paraprotein formation
Plasma Cell Myeloma (aka multiple myeloma): presentation
C = hypercalcemia
R = renal failure
A = anemia
B = bony lesions, which cause characteristic “moth-eaten” or “punched out” appearance to large bones (e.g. skull, pelvis, femurs)
Plasma Cell Myeloma (aka multiple myeloma): diagnosis
proton electrophoresis of urine or blood (SPEP, UPEP) to identify the pathognomonic “Bence-Jones” protein
Serum and urine assessment for monoclonal protein
Serum-free light chain assay
Bone marrow aspiration for increased plasma cells
Plasma Cell Myeloma (aka multiple myeloma): treatment
Incurable; goal is remission and treat symptoms
Lenalidomide (Revlimid): immunomodulator
Bortezomib (Velcade): proteasome inhibitor
Bone marrow transplant: given as a rescue after a toxic dose of chemotherapy is given to eradicate plasma cells
Orthopedic procedures to help with pathologic fractures
Oncologic complications: tumor lysis syndrome - labs
hyperuricemia
hyperkalemia
hyperphosphatemia
hypocalcemia
Acute renal failure develops soon after
Oncologic complications: tumor lysis syndrome - treatment
aggressive IV hydration before, during, and after chemo to maintain urine output and prevent the buildup of cellular materials from destroyed cancer cells
Allopurinol
Rasburicase
NaHCO3 infusions during chemo to alkalinize the urine
Severe: consult nephrologist to determine if emergent HD is needed
thalassemia minor: etiology
Heterozygous; has only one copy of the beta thalassemia gene
thalassemia major: etiology
Homozygous; has two genes for beta thalassemia and no normal beta-chain gene
thalassemia major: presentation
Normal presentation at birth d/t protective effects of fetal hemoglobin
Anemia develops within the first few months of life and becomes progressively severe
Other findings in early life:
- failure to thrive
- feeding difficulties d/t easy fatigue and lack of oxygen
- bouts of fever
- diarrhea
- hepatosplenomegaly and jaundice
- maxillary enlargement
folate deficiency: cause
inadequate intake or malabsorption of folic acid (needed for RBC production)
folate deficiency: S/Sx
fatigue
dyspnea on exertion
pallor
headache
tachycardia
anorexia
glossitis
** no neurological signs ** – differentiates B12 from folate deficiency
folate deficiency: management
folate 1mg PO daily
foods high in folic acid: bananas, peanut butter, fish, green leafy vegetables, iron-fortified breads and cereals
Pernicious anemia (B12 deficiency): management
B12 (cyanocobalamin) 100mg IM daily x 1 week, then x1/month and lifelong monitoring
Von Willebrand Disease
genetic disorder that results in the reduced ability to create blood clots, caused by deficiency or mutation in von Willebrand factor and clotting factor VIII
Von Willebrand Disease: S/Sx
frequent, prolonged, severe episode of bleeding
easy bruising
leukemias: S/Sx
may be asymptomatic
fatigue
weakness
anorexia
generalized lymphadenopathy
weight loss
leukemias: labs, Dx
CBC with subnormal RBCs and neutrophils
elevated ESR
peripheral blood smear to distinguish acute and chronic leukemia
bone marrow aspiration to confirm Dx
leukemias: treatment
chemotherapy
- allopurinol to reduce tumor lysis syndrome in high-risk patients
- bone marrow transplant
- control symptoms
lymphomas: management
radiation
chemotherapy
bone marrow transplant
immune thrombocytopenia purpura: other considerations
thrombocytopenic precautions
- avoid constipation (increase fiber, laxatives, etc)
- no flossing
- no shaving
- hold pressure for 5 mins or more for cuts, line insertion, etc.
heparin- induced thrombocytopenia purpura
- stop the heparin
- argatroban (Acova), lepirudin (Refludan) - reverse HIT while offering AC properties
How to differentiate ITP from SLE? They both have thrombocytopenia
bone marrow analysis
Patients with which selective immunoglobulin deficiency have a high risk of reaction when receiving blood products?
IgA
risk for anaphylaxis
Which immunoglobulin deficiency is associated with repeated infections?
IgM
IgG
Schistocytes
RBC fragments
Result of mechanical destruction (fragmentation hemolysis) of a normal RBC when there is damage to the blood vessel and a clot begins to form
Often seen when there is something implanted in circulation (balloon pump, VAD, mechanical valve, etc.)
Always pathological
Suggests some degree of hemolysis
Howell-Jolly bodies
Nuclear remnants in the cityplasm
Generally indicate splenic dysfunction
Dohle bodies
Rough endoplasmic reticulum remnants in neutrophils
Seen in infections and inflammatory conditions
Bands
Abnormal cells
Cell undergoing granulopoiesis, derived from a myelocyte, and leading to a mature granulocyte
Seen in infections
What does a “shift to the left” mean?
There is a greater than normal count of neutrophils and the presence of immature neutrophils such as bands and metamyelocytes
Blasts
Unipotent stem cells
Seen in the peripheral blood
Usually indicates a leukemia or severe myelodysplastic syndrome
hemachromatosis
iron overload
hemachromatosis: causes
primary causes: gene mutation of hepcidin common in Celtic, English, and Scandinavian people
secondary causes: excessive blood transfusions, too much iron supplementation
results of hemachromatosis
cirrhosis
bronzing of the skin
systolic CHF, arrhythmias
endocrine problems
How is hemachromatosis diagnosed?
Ferritin >300 in males and post-menopausal females, >200 in premenopausal females
TIBC very low
genetic testing if the cause is thought to be primary
How is hemachromatosis treated?
Phlebotomy to reduce ferritin
Primary hemachromatosis can be treated with chelating agents such as Deferasirox (Exjade)
hemolytic anemia
due to increased RBC destruction (usually prematurely), faster than the body’s ability to replace them
All of the hemolytic anemias cause..
hyperbilirubinemia
hemolytic anemia: labs
low haptoglobin
high LDH (lactate dehydrogenase)
Elevated LFTs with normal GGT
Carcinoid crisis
Rare and extremely dangerous manifestation that occurs in patients with neuroendocrine tumors
Sudden onset of hemodynamic instability
carcinoid crisis: treatment
octreotide to control symptoms
glucocorticoids to abort the episode
Carcinoid crisis: S/Sx
diarrhea
flushing
wheezing
bronchospasm
hypotension refractory to IV fluids
Thrombotic thrombocytopenic purpura
Results in blood clots forming in small blood vessels throughout the body
Results in low platelet count, low RBCs due to their breakdown, and often kidney/heart/brain dysfunction
Thrombotic thrombocytopenic purpura: known triggers
bacterial infections
certain medications
autoimmune diseases such as lupus
pregnancy
Triggers form an autoantibody against vWF, which in turn prevents proper platelet adhesion
Thrombotic thrombocytopenic purpura: labs/Dx
thrombocytopenia
normal or slightly elevated PT/PTT
normal FDP
Thrombotic thrombocytopenic purpura: presentation
fever
AMS
acute renal failure
hemolytic anemia
Thrombotic thrombocytopenic purpura: When to start treatment
High mortality – presumptive diagnosis of TTP is made and therapy is started even when only hemolytic anemia and thrombocytopenia are seen.
Thrombotic thrombocytopenic purpura: treatment
Transfusion is contraindicated as it fuels the coagulopathy
Treatment of choice: plasmapheresis
-Rituximab is often given to augment treatment
-steroids are also helpful
Thrombotic thrombocytopenic purpura: monitoring
Monitor levels:
-lactate dehydrogenase
-platelets
-schistocytes
TTP is a rare complication of which medication?
clopidogrel (Plavix)
Neoplasm that arises from the endocrine and nervous systems
Commonly in GI tract, lung, pancreas
Most common small bowel tumor
neuroendocrine tumor
most common primary malignancy affecting the duodenum and jejunum
adenocarcinoma
Management for pulmonary nodules based on size
> 4mm or high risk: serial chest CTs
<6mm: serial chest CTs not required if low risk
<1 cm: intermediate probability of being malignant; serial chest CTs
> 1cm: intermediate probability of being malignant; evaluate by PET
-Positive PET: excise nodule
-Negative PET: serial chest CTs
Pulmonary nodules: criteria for low probability of malignancy
small size
higher density
discrete and smooth border
benign pattern of calcification
- popcorn calcification
- central calcification
- diffuse homogenous calcification
- concentric calcification
Peutz-Jeghers syndrome is a hereditary disorder that increases risk for several cancers, especially…
ovarian
endometrial
breast
colorectal
liver
lung
testicular
familial adenomatous polyposis is associated with what types of cancer
papillary thyroid cancer
adrenal carcinomas
CNS tumors
multiple endocrine neoplasia type 1 (MEN1) is associated with what disorders
pitutary adenomas
primary hyperparathyroidism
GI tumors
Von Hippel-Lindau (VHL) is associated with what types of cancer
RCC
end-lymphatic sac tumors
pheochromocytomas
angiomatosis
hemagioblastomas
form of intrinsic hemolytic anemia caused by a defect in the RBC membrane, resulting in small spherical erythrocytes that lack central pallor on a peripheral smear
spherocytosis
spherocytosis: labs
increased indirect bilirubin
increased reticulocyte count
+ osmotic fragility test
spherocytosis: S/Sx
anemia
jaundice
splenomegaly
sickle cell crisis: triggers
Dehydration (most common)
Hypoxia
Infections
High altitudes
Physical or emotional stress
Acidosis
Surgery
Blood loss
advanced ovarian cancer: treatment
surgical debulking, followed by cisplatin or carboplatin plus paclitaxel chemotherapy regimen
Von Willebrand Disease: S/Sx
easy bruising
mucosal bleeding
prolonged bleeding after minimal trauma
severe bleeding after major surgery
Women: menorrhagia is a common presenting complaint
Plasma Cell Myeloma (aka multiple myeloma): S/Sx
bone pain (most common presenting symptom)
renal failure
anemia
hypercalcemia
pathologic fractures
weakness
infection (often pneumococcal)
spinal cord compression
Glucose-6-phosphate deficiency
Most commonly affects African Americans and persons of Mediterranean descent
Hemolytic anemia results from oxidative stress that is induced by sulfonamides, quinine, primaquinine, dapsone, and fava beans
Glucose-6-phosphate deficiency: S/Sx
Typically asymptomatic until they encounter a triggering agent, then present with jaundice, back pain, dark urine, fatigue
Glucose-6-phosphate deficiency: labs
Hgb: low
Retics: high
Unconjugated bilirubin: high
Drug of choice for DVT prophylaxis for bed ridden patients
LMW Heparin
Most common cause of thrombocytopenia
idiopathic thormbocytopenic purpura
acute chest syndrome
Major complication of sickle cell disease
May be the result of trigger vasooclusion d/t pneumonia, asthma, hypoventilation
Characterized by:
-fever
-pleuritic chest pain
-low oxygen saturation
-multilobar infiltrates
malignancy-associated hypercalcemia: management
Goal: restore a eucalcemic state while inhibiting bone resorption
- IV hydration with NS to provide resuscitation and re-establish renal perfusion with calciuresis
- bisphosphonates given within 24 hours if no improvement
- calcitonin as an adjuvant to inhibit osteoclastic bone resorption
Henoch-Schonlein purpura
IgA vasculitis
Characterized by:
-purplish rash
-abdominal pain
-glomerulonephritis
adrenal insufficiency: diagnosis
ACTH stimulation test
-cosyntropin (Cortrosyn), a form of synthetic ACTH, is given IV push and cortisol levels are drawn at 0, 30, and 60 minutes
-cortisol levels normally rise to >20mg/dL
-If the levels fail to rise by >5-10% of the baseline, the test is diagnostic for adrenal insufficiency
hemolytic uremic syndrome: presentation
renal failure
neurologic abnormalities
hemolytic anemia
thrombocytopenia
hemolytic uremic syndrome: labs/Dx
FDP normal
thrombocytopenia
hemolytic uremic syndrome is most often associated with…
diarrheal illness caused by a Shiga toxin-producing E. coli
protein C deficiency is a disorder associated with increased risk for…
VTE
neutropenic fever
Sign of severe infection in patients with ANC<1000
Rapidly fatal if left untreated
neutropenic fever: management
Urine, sputum, blood cultures
Empiric broad-spectrum ABx as soon as possible
Neutropenic isolation precautions
Private room with positive pressure air ventilation
SVC syndrome
partial or complete obstruction of blood flow through the SVC
SVC syndrome: causes
Most common: tumor
infection
thrombus
SVC syndrome: S/Sx
Develop slowly
Cough
Face or neck swelling
Feeling of fullness in your upper body
Upper extremity swelling
SOB, cyanosis
Chest pain
Horner’s syndrome
SVC syndrome: management
Treat underlying cause
SVC syndrome: diagnosis
xray
CT
venography
