Chapter 23 hematology Flashcards
anemia
decrease in the number of erythroctes
decreas in the quality of oxygen transferred
dehydration =
hemoconcentration
fluid retention=
hemodilution
cause for anamia
impared erythrocyte production
decrease in the erythrocyet production
acute/ chronic blood loss
combination of the above
classiied based on
- their shape, size or substance
cause
clinical manifestation of anamia
fever
fatoque
pallor
trachycardia
dyspenia
hyotension
macrocytic megaloblastic anamia
large stem cellas that mature into erythrocytes that are large in size
1. Pernicious anamia
2. folate deficiency anamia
pernicious anamia is caused by
decreased in VB12
clinical maniufestations
- weakness
-fatique
- difficulty in walking
- abdonmianl pain
- loss of appetite
- sour smooth beefy tongue
- weight loss
Folate deficiency anamia
caused by the deficiency of falic acid
clinicalmanifestation
- same as pernicious
- more GI symptoms
-stomatitus and ulcrs of mouth
- cheritosis= scales and fissures of mouth
Microcytic hyperchromatic anamia
causes iron deficiency anemia
iron deficiency is caused by
loss of blood
- increased demand for iron
- problems with absorption
clinical manifestation of iron
fatigue = nails become spoon-shaped
pallor = dry sources of the mouth
dyspnea( shortness of breath)=red sour punctured tongue
Leukocytes = white blood cells
function affected if there are too many or too few WBC
- normal WBC count is 4500-11000
Leukocytosis
is a high WBC count
- normal protective physiologic response to physiologic stressors
Causes of leukocytosis
invasion of pathigens
- emotional stress
-Temperature change
leukopenia
decrease in WBC count
not normal or beneficiation
predisposes to infections
leukopenia cause
- radiation
- shock
- autoimmune disease
- immunodeficiency
- medications
neutrophilia
immature neutrophils are realeased from the bone marrow when there is an infection
neutropenia
decrease in circulating neutrophils
cause
- prolonged severe infection
- decreased production of neutrophils
- abnormal neutrophils distribution
reduced survival;
infectious mononucleosis
acute self-limiting infection of B-lymphocytes
Pathology and clinical manifestation of Infectious mononucleosis
Patho
- Epstein-Barr virus affect the B-lymphocyte
- atypical lymphocytes develop
- immunocompetent (self-limiting acute viral infection)
immunocompromised ( uncontrolled proliferation of B-cells can occur)
Clinical Manifestation
-fever
-sore, swollen throat (pharyngitis)
- fatigue
-enlargement of spleen and liver
- lymphadenopathy: swollen cervical lymph nodes
-splenic rupture caused by spleen enlargement
Leukemia
-a malignant disorder of blood and blood-forming cells
Patho
- overcrowding of bonemarrow
- excessive proliferation of malignant cells
classified into two
- Acute
- chronic
Acute Leukemia
sudden onset
undifferentiated cells
- Acute myelogenous leukemia
- too many myelogenous or lymphoblastic that are to WBC - Acute lymphocytic Leukemia
- too many immature WBC in the Blood marrow
Chronic leukemia
progressive
differentiated and mature cells
1. Chronic Mylengenous Leukemia
- roo many mature WBC in the bonemarrow
2. Chronic Lymphatic Leukomia
- slow-growing cancer where too many immature lymphocytes are found
clinical manifestation of Leukemia
-fever
-petechiae
- fatigue, anemia
- weight loss
bone pain
infections
welling of the liver, lymph nodes, and spleen
headache, vomiting, blurred vision, and hearing disturbances
lymphadenopathy
enlargments of lymph nodes
can be focal or general
Malignant lymphomas
a diverse group of neoplasms that develop from the proliferation of malignant lymphocytes in the lymphoid system
what are the two main categories of magilant lymphomas
- Hodgkin lymphoma
- non-Hodgkin lymphoma
Hodgkin lymphoma
trigger is unknown
B-cell that has not undergone successful immunoglobulin gene rearrangement
painless
what is the hall mark of hodgkin
Reed Sternberg cells
- magilantly trnasformed B-cellls
- present in lymp nodes
Non-Hodgkin lymphoma
- real classification based on B,NK, and T neoplasms
- Burkitt lymphoma and lymphoblastic lymphoma
patho of non-hodgkin lynmphoma
-clonal expansion of NK, B, and T cells
- chromosome translocation which leads to activation of oncogenes
- tumor suppressors may be inactivated by deletion or mutation of chromosome
- spreads in a very unpredictable way
- not present in RS cells
Burkitt Lymphoma
- Bcell
- tumor grows on the jaw and facial bones
Types
- linked to EBV
- sporadic
- immunodeficiency related
treatment is aggressive and multidrug regimens
Lymphoblastic lymphoma
T-cell
- clone of immature T cells that become malignant in the thymus
- painless lymphadenopathy of the neck, chest
- treatment is combined with chemotherapy
Multiple Myeloma ( plasma cell Magilancy)
- slow proliferation of tumor cell masses in the bone marrow
clinical manifestations
- hypercalcemia
-renal failure
- anemia
- bone lesions
- pain everywhere
disorders of platlets
thromboctopena
- decrease in platlets
thrombocythemia
- increase in platlets
thromboctopenia
patho?
classification ?
- decrease in platlets
normal is 150,000- 400,000
patho
- decreased platlet production
- increased consumption
- conge ital or acquired
classified as
1. heparin- induced thrombocytopenia
2. Immune thrombocytopenia purpura n
Immune thrompbocytopenia purpura
clinical manifestations?
- occurs secondary to an illness
- immune system attacks platlets
can be acute or chronic
acute ITP is commonly seen in children
clinical manifestations
- purpura/pectinate scattered on the body
- bleeding from mucosal sites
Heparin- Induced Thrombocytopenia
- drug related cause of thrombocytopenia
patho
- immune meditated adverse drug reaction
- IgG antibodies target heparin which decreases platlets activation cycle which decreases platlete consumption and eventually platlets level drop
50% drop after heparin administration
Disseminated Intravascular coagulation (DIC)
pathos?
Cause?
clinical manifestation?
- clotting and hemmorage both occur simultaneously
Patho
- widespread activation of coagulation, resulting in formation of fibrin clots in medium and small vessels throughout the body
- widespread clotting leads blockage of blood vessels and organ failure
- leads to consumnrtion of platlets
Cause
- sepsis
- endothelial damage/ tissue factor as the main initiator of DIC
clininical manifestation
- bleeding from venipuncture sites
- purpura, pectechie, and hematromas
symetric cyanosis of the fingers and toes —clotting
hemphilia
- bleeding disorderes
joint bleeding
A VIII
B IX
CXI
