Blood (unfinished) Flashcards
Erythropoiesis is the
process of forming RBC’s
What is erythropoietin
A hormone that is synthesized and released by the _____that communicates with the _____ ________ to say-
A hormone that is synthesized and released by the kidneys that communicates with the bone marrow to say- “produce more RBCs, we need more RBCs”
Steps of erythropoiesis:
Begins with an ________ _______.
Then _________ accelerates the cell’s differentiation, becoming a committed _________.
Then the committed proerythroblast becomes a _________, where the _______ ______ and is ______.
Then it becomes a __________ with ___ ______- reticulocyte leaves bone marrow and enters the bloodstream. Finally, it becomes an erythrocyte, and hemoglobin synthesis ceases.
Begins with an erythroid progenitor. Then erythropoietin accelerates the cell’s differentiation, becoming a committed proerythroblast. Then the committed proerythroblast becomes a normoblast, where the nucleus shrinks and is reabsorbed. Then it becomes a reticulocyte with no nucleus- reticulocyte leaves bone marrow and enters the bloodstream. Finally, it becomes an erythrocyte and hemoglobin synthesis ceases.
Between which cells does erythropoietin act?
Between the erythroid progenitor and committed proerythroblast
When does the nucleus shrink and get reabsorbed?
Normoblast
A reticulocyte is an immature RBC- it typically represents less than 1% of RBCS, so if you see more in the blood, what does that mean?
The pt. is trying to compensate for reduced RBC by releasing these “baby RBC’s” from the bone marrow
Reticulocytes are an index..
of suspicion for ANEMIA, regardless what’s causing that anemia
Why are reticulocytes an index of suspicion of anemia? (FYI)
The BM is responding to the demand of RBCs and is kicking out more of those reticulocytes earlier, so the BM is compensating for tissue hypoxia, which is why you see an increase of reticulocytes- it’s not a fully functioning adult, but can still differentiate into an erythrocyte in the blood stream.
Erythropoiesis is a negative feedback loop:
Erythropoiesis is a negative feedback loop: If there’s a drop in O2 sat., the kidneys will sense the low oxygen levels due to reduced blood flow to kidneys, so kidneys release _________ (___);
EPO goes to bone marrow and stimulates the production of _____(erythrocytes); blood goes back to the kidneys, kidneys detect adequate O2 levels and turn off EPO stimulation.
Erythropoiesis is a negative feedback loop: If there’s a drop in O2 sat., the kidneys will sense the low oxygen levels due to reduced blood flow to kidneys, so kidneys release erythropoietin (EPO)
; EPO goes to bone marrow and stimulates the production of RBCs (erythrocytes); blood goes back to the kidneys, kidneys detect adequate O2 levels and turn off EPO stimulation.
What is hemostasis
local control of bleeding
Hemostasis- platelet plug
◦ Platelet plug (primary hemostasis; _______ _____ ____) prolonged bleeding if there are low platelet count
prevents further bleeding
Hemostasis: Platelet plug inhibition
◦ ___ much ______ → _______ _____ _____ to tissue and/or ______ because it _____ the blood vessel
◦ _______ neighbor cells release _________ & ____ _____for ___________ (to keep the vessel from closing)
◦ Too much clotting → reduced blood flow to tissue and/or embolus because it occludes the blood vessel
◦ Undamaged neighbor cells release prostaglandin & nitric oxide for vasodilation (to keep the vessel from closing)
Hemostasis: Blood Clot
◦ Formed as plug traps circulating RBCs & macrophages
◦ Stabilized by _______
◦ Formed as plug traps circulating RBCs & macrophages
◦ Stabilized by fibrinogen
Hemostasis: Clot retraction and dissolution, AKA _______
◦ Clot “______,” pulling together edges of the damaged vessel
◦ Clot _______ over time (________ → plasmin dissolves fibrin meshwork for phagocytosis)
◦ Replaced with_______ tissue
AKA fibinolysis
◦ Clot “tightens,” pulling together edges of the damaged vessel
◦ Clot dissolves over time (plasminogen → plasmin dissolves fibrin meshwork for phagocytosis)
◦ Replaced with normal tissue
What would happen if we didn’t have platelet plug inhibition?
The clot would continue to grow deeper into that vessel and we could have problems with ischemia due to the size of the clot
Anemia is defined as
Too few red blood cells &/or abnormal Hemoglobin
What are the 3 mechs. of anemia?
RBC production disorder, increased RBC loss from bleeding, and increased RBC destruction
Anemia mech: RBC production disorder
- Inadequate ___, ____ _____, Vit ____, ______, or _______– there will be a deficiency in ____ if any of these things are reduced (ex: _____ disease)- a RBC needs these things to form
- ______ ______ disease (e.g., _______,______ _____)
- Inadequate iron, folic acid, Vit B12, globulin, or erythropoietin – there will be a deficiency in RBCs if any of these things are reduced (renal disease
- Bone marrow disease (e.g., leukemia, radiation exposure)
Anemia mech: what was the second one again?
Increased RBC loss from bleeding
(if we’re bleeding we’re going to loss RBCs (blood loss leads to anemia)
Anemia mech:: Increased RBC destruction- exs
drugs or transfusion reaction
What’s another mechanism of anemia? What are the clinical manifestations of that?
↓ O2 delivery to cells → clinical manifestations
Tachycardia, murmurs, orthostatic hypotension
Dyspnea, tachypnea
Headache, fatigue, lightheadedness, pallor, intermittent claudication
-cytic
size
-chromic
amount of hemoglobin
macro
lrg RBC size
micro
too small RBC size
hypo
low hemoglobin
Hemolytic Anemia is
normocytic (normal size) and normochromic (normal red color)
Hemolytic Anemia: 2 points
↓ RBC by cell destruction (hemolysis, which is breakdown of RBCs) - ↓ Hgb/Hct
↑ RBC production in bone marrow (compensatory mechanism/adaptive, so inc. reticulocyte count
Causes of hemolytic anemia
Genetic defect;
idiopathic;
severe burn or infection;
DIC;
hemodialysis;
exposure to incompatible blood, drug, or toxin;
malaria; newborn hemolytic disease, transfusion reaction; sickle cell anemia; thalassemia (defective Hgb)
RBC Antigens
Specific antigens on RBC cell membrane
◦ ABO antigens – 2 genes coding for:
A antigen
B antigen
Neither antigen = O
RBC Antigens:
◦ Rh factor on RBC cell membrane=
◦ Rh factor on RBC cell membrane = Rh+;
no factor = Rh-
RBC antigens: Immune response to blood with foreign antigen
Pregnancy/L&D
Blood transfusion
◦ If mismatched blood is given to a patient, which type of hypersensitivity reaction will ensue and what is the pathologic mechanism?
Type 2 hypersensitivity reaction- it’ll lead to cell lysis. (remember, we’re talking about hemolytic anemia; the breakdown of RBCs)
Anemia: Hemolytic (Transfusion Reaction)
Normocytic, normochromic
________-_______destruction of ABO-incompatible RBC
Immediate, ____–_______
**List the manifestations*
WBC transfusion reaction milder
Anemia: Hemolytic (Transfusion Reaction)
Normocytic, normochromic
Immune-mediated destruction of ABO-incompatible RBC
Immediate, life-threatening
WBC transfusion reaction milder
- Fever/chills, N/V
- Flank pain
- Hematuria
- Facial flushing
- Chest/low back/ abdominal pain
- Decrease BP, Increase HR, dyspnea, shock, death
Treatment of hemolytic anemia- transfusion reaction
Rx:
◦ Prevention!
Verify correct patient, correct blood
Full patient assessment to determine a baseline (vitals, & everything) trouble breathing? Pain? BP? n/v?
Monitor them for a full 20 mins
◦ Immediately stop transfusion if the patient is developing a hemolytic transfusion reaction!!!
◦ ↑ fluids to flush kidneys with normal IV solution the more it flushes the less likely they are to go into renal failure
◦ Support ABC
◦ Steroids
Iron deficiency anemia is..
Microcytic (smaller size), hypochromic (less color than normal)
Iron deficiency anemia is the most
common worldwide
Iron deficiency anemia has a ___ development:
Slow development: decreased RBC –> bone marrow increases production of small, HGB-deficient RBCs
Stages of Iron deficiency anemia
Stage 1: Depleted ___ ____
Stage 2: Decreased _______ of ____ to the _____ _____ —> ___ ____ ________
Stage 3: Iron-deficient RBCs circulating (______, _______)
Stage 1: Depleted iron stores
Stage 2: Decreased transport of iron to the bone marrow —> iron deficient erythropoiesis
Stage 3: Iron-deficient RBCs circulating (microcytic, hypochromic)
Causes of Iron deficiency anemia
deficient diet, chronic blood loss, malabsorption disorder, NSAIDS, pica
Manifestations of Iron deficiency anemia
DOE, cold intolerance, HA
Kolionychia- spoon shaped
Cehliosis, stomatitis, glossitis
Dysphagia
brittle/thin/concave nails, maybe mouth sores
pica and leg cramps if severe
burning mouth/glossitis
Iron deficiency anemia Hgb lebels
Hgb less than 8 gm/dL- systemic signs
Hgb less than 5 gm/dL- heart failure, death
Splenomegaly and hepatomegaly/jaundice are common in which anemia
Hemolytic
Decreased Hgb and Hct, decreased serum iron, ferritin (diagnostic), transferrin; increased TIBC indicated
iron deficiency anemia
Kolionychia, or spoon-shaped/concave nails indicate
iron deficiency anemia
Hallmarks of iron deficiency anemia
Pallor of skin, mucous membranes, and palmar creases
Kolionychia (concave, rigid, brittle)
Glossitis (bald fissured appearance due to loss of papillae and flattening)
