Hematology Flashcards
Common clotting pathway starts at
factor 10
extrinsic is cause by
trauma
factor 10 uses ___ to make _____
prothrombin
thrombin
Thrombin changes ____ to _____
fibrinogen to fibrin
Protein __ & ___ need vitamin ___
C & S need K
Vitamin is involved with which factors
2, 7, 9, 10
What factors are in the intrinsic pathway?
12, 11, 9, 8
what factors are in the extrinsic pathway
7
What factors are in the common pathway?
5, 2(prothrombin & thrombin), 1 (fibrinogen & fibrin), 13, Protein C, S
Partial prothrombin time
intrinsic + common, 12, 11, 9, 8, 10
Prothrombin time
extrinsic + common, 7 & 10
Bleeding time measures
platelet function
TT measures
common pathway
Lifespan of RBC?
120 days
RBC come from
common myeloid progenitor which came from hemocytoblast
To mature a RBC we need
B9, B12
RBC is made in the
bone marrow, leaves when its a reticulocyte
Heme has how many alpha chains?
2
each iron hold onto __ oxygen, making __ in total for each heme
1, 4
Iron is absorbed in the
duodenum
folate is absorbed in the
jejenum
B12 is absorbed in the
Ileum
hepcidin
regulates iron, increases iron when needed, during infection it inhibits iron absorption from food
Hepcidin is induced by
IL-6 and LPS (infection & inflammation)
Hepdicin is inhibited
EPO
EPO is released by
the kidneys because they can detect how much oxygen is in the blood
Anemia means
low O2 carrying capacity, not low O2
Types of hereditary hemolytic anemias:
pyruvate kinase deficiency G6PD deficiency abnormal membraine (spherocytosis) Abnormal heme ( alhpa & beta thalassemia), sickle cell anemia
Types of acquired hemolytic anemias:
alloimmune, drug induced, autoimmune
Spherocytosis key features:
autosomal dominant
defective spectrin
splenomegaly
G6PD deficiency
viral infection, fave beans, sulfa drugs, quinin
heinz bodies
Sickel cell
hypoxia, dehydration, acidosis, vaso-occlusive, aplastic crisis, splenomegaly
alpha thalassemia
HbH beta 4, south east asia
hydrochromic cells, target cells
hydrops fetalis
hard time passing through the spleen
beta thalassemia
HbA, HbF
mediterranean & US, hypochromic cells, target cells
hard time passing through the spleen
Glutathione is
powerful antioxidant that takes hydrogen peroxide and makes water uses NADPH
G6PD is needed
to help RBC makes NADPH which is needed by glutathione to reduce hydrogen peroxidse and reuse glutathione
Heinz bodies are
denature globin chains that are stuck to the inside of the RBC because the globin & heme bond was attacked
Bite cells are
heinz bodies that were bitten by the macrophages in the spleen to get the bodies out
bilirubin in the liver gets
changed from unconjugated to conjugated
Conjugated bilirubin travels from the liver
to the gallbladder, mixes with bile and enters the SI
urobilinogen is made
in the Si and goes to the kidney
Spleen macrophage takes heme and makes
unconjugated bilirubin
ALL Leukemia
Children
fever, petechiae, eccymoses, CNS infiltrate
good prognosis
Lymphoblasts
AML leukemia
any age
fever, petechiae, ecchymoses, lymphadenopathy (splenomegaly)
depending on type
Auer robs in myeloblasts
CML leukemia
young adults
fever, night sweats, splenomegaly
poor Philidelphia chromosome (better prognosis if present) this gene encodes a protein with high tyrosine kinase activity
CLL leukemia
elderly
insidious, few symptoms, low Ig levels, infections
Fair
lymphocytes
predominate
Hairy cell leukemia
hepatosplenomegaly
poor
pancytopenia
TRAP
Non-pitting edema
Lymphatic obstruction - keeps the proteins in the interstitium and retains water
-usually CHF, followed by renal complications
Pitting edema
increased in hydrostatic pressure or decreased oncotic protein pressure
There is no protein in the interstitial to retain fluid
venous insufficiency