Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
88 Cards in this Set
- Front
- Back
|
lifespan of platelets
|
about 4 days
|
|
|
normal platelet count
|
150,000- 400,000/ml^3
|
|
|
hematopoiesis
|
blood cell production
|
|
|
what happens in the body as a compensatory response to platelet depletion?
|
liver lets out thrombopoietin which produces megakaryocytes which turn into platelets (thrombocytes)
|
|
|
where is red bone marrow found?
|
in flat and irregular bones, ends of long bones, pelvic bones, vertebrae, sacrum, sternum, ribs, flat cranial bones and scapulae
|
|
|
blood cells (white, red, platelets) make up what percent of blood?
|
45%
|
|
|
plasma makes up what percent of blood?
|
55%
|
|
|
erythropoiesis- what stimulates it? what controls it? what is required for it?
|
stimulated by hypoxia; controlled by erythropoietin; requires protein, folate, cobalamin, riboflavin and pyridoxine
|
|
|
hemolysis; usually occurs where?
|
destruction of RBCs; usually occurs in bone marrow, liver and spleen
|
|
|
reasons for change in platelet number?
|
age; altitude; menstruation; season; exercise
|
|
|
thrombocytopenia
|
decrease in platelet count
|
|
|
main complication of thrombocytopenia
|
increased bleeding
|
|
|
some causes of thrombocytopenia
|
certain bacterial/viral infections (AIDS); parasites (malaria); autoimmune disorders (lupus); hypersplenism; depressed bone marrow functions or malignancies
|
|
|
thrombocythemia
|
increase in platelet count; usually in those over 50; can lead to spontaneous clotting
|
|
|
spleen (functions of)
|
hematopoiesis during fetal dvlpmt; filtration of old RBCs; immunologic; storage for RBCs and platelets
|
|
|
causes of anemias
|
blood loss
impaired production of erythrocytes increased destruction of RBCs |
|
|
where are most of the WBCs found?
|
bone marrow (90%)
|
|
|
leukopenia; causes
|
decrease of circulating WBCs; antibiotics, radiation, chemo, genetic blood diseases, infections, tumors, etc
|
|
|
leukocytosis; most common cause?
|
increase in circulating WBCs; acute infection
|
|
|
other causes of leukocytosis
|
malignancy; hemolytic anemia; exercise; labor; pain; cold; menstruation; stress
|
|
|
mild anemia is indicated by
|
Hb 10-14 g/dl
may be asymptomatic palpitations, dyspnea, diaphoresis |
|
|
moderate anemia is indicated by
|
Hb 6-10 g/dl
symptoms may appear with rest as well as activity very exhausted all the time |
|
|
severe anemia is indicated by
|
Hb <6 g/dl
multiple body systems involved need transfusions/treatment ASAP |
|
|
manifestations of anemia
|
pallor, jaundice (hemolysis and increased concentration of bilirubin), pruritis (increased bile salts b/c of increased serum bilirubin), increased HR and SV, systolic murmurs and bruits, peripheral edema, ascites cardiomegaly
MI and CHF in extreme cases |
|
|
always give what before a blood transfusion?
|
Benadryl/Tylenol to avoid anaphylaxis and fever
|
|
|
what is given post-op to decrease fluid excess?
|
Lasix
|
|
|
polycythemia; reasons?
|
increased RBC count; causes sluggish flow;
may be a compensatory response to anemia; may be due to: high altitude; people with cardioresp. problems with low tissue O2 perfusion; tumors; antibiotics; cigarette smokers |
|
|
normal hemoglobin range?
|
12-17 g/dl
|
|
|
most common cause for increase in hemoglobin?
|
dehydration
|
|
|
where does iron absorption occur?
|
in the duodenum
|
|
|
etiology of iron deficiency anemia
|
inadequate dietary intake
malabsorption blood loss hemolysis |
|
|
manifestations of iron deficiency anemia
|
pallor
glossitis (inflamm. of tongue) cheilitis (inflamm. of lips) headache paresthesias burning of tongue |
|
|
how much blood must be lost from upper GI tract for stools to turn black?
|
50-75 ml (at least)
|
|
|
cobalamin; dietary sources of it
|
vitamin B12; RBC maturation
red meats, especially liver |
|
|
folic acid; dietary sources of it
|
RBC maturation
green leafy vegetables; liver; meat; fish; legumes; whole grains |
|
|
iron; dietary sources of it
|
hemoglobin synthesis
liver and muscle meats; eggs; dried fruits; legumes; dark green leafy vegetables; whole grain and enriched bread and cereal; potatoes |
|
|
vitamin B6; dietary sources of it
|
hemoglobin synthesis
meats (esp. pork and liver); wheat germ; legumes; potatoes; cornmeal; bananas |
|
|
amino acids; dietary sources of it
|
synthesis of nucleoproteins
eggs; milk/milk products; poultry; fish; legumes; nuts |
|
|
vitamin C; dietary sources of it
|
conversion of folic acid to its active forms; aids in iron absorption
citrus fruits; leafy greens; strawberries; cantaloupes |
|
|
drug therapy for iron defeciency anemia; recommendations for taking it/how to take it
|
iron preparations 150-200 mg/day
best absorbed as ferrous sulfate in an acidic environment (ie take with OJ) may be given IV or IM take for 2-3 months |
|
|
side effects of iron preparations
|
may cause heartburn, constipation, diarrhea (if so, adjust dose and type)
|
|
|
when should iron be taken?
|
1 hour before meals
|
|
|
Z-track techniques of giving iron
|
make sure you pull air into the syringe before injecting so that the residual iron doesn't stain the skin
don't massage 2 ml or less |
|
|
the large, abnormal RBCs that are caused by cobalamin and folic acid deficiencies?
|
megaloblasts
|
|
|
cobalamin deficiency (why?)
|
intrinsic factor is not being secreted by the gastric mucosa, which is required for B12 absorption
pernicious anemia most common cause |
|
|
etiology of cobalamin deficiency
|
pernicious anemia cause by absence of intrinsic factor and therefore decreased HCl
|
|
|
manifestations of cobalamin deficiency?
|
tissue hypoxia
sore tongue anorexia N/V abd. pain weakness, paresthesias impaired thought processes |
|
|
pernicious anemia
|
when gastric mucosa is not secreting IF because of antibodies being directed against the parietal cells and/or IF itself
|
|
|
initial treatment for those with cobalamin deficiency anemia
|
1000 mg daily for 2 weeks (parenterally), then weekly, then monthly
Nascobal is treatment of choice protect from injury, burns, trauma |
|
|
causes of folic acid deficiency
|
poor nutrition
malabsorption syndromes drugs ETOH (alcohol) abuse and anorexia dialysis |
|
|
manifestations of folic acid deficiency
|
dyspepsia
smooth, beefy red tongue absence of neurological findings |
|
|
replacement therapy for folic acid deficiency
|
1 mg/day
dietary supplements |
|
|
aplastic anemia- etiology of
|
congenital (30% of children)
acquired- exposure to ionizing radiation, chemicals, bacteria, viruses, etc |
|
|
manifestations of aplastic anemia
|
fatigue
dyspnea susceptible to infection bleeding |
|
|
what is aplastic anemia?
|
pancytopenia (decreased RBCs, WBCs, platelets)
|
|
|
collaborative care for aplastic anemia
|
bone marrow transplant
immunosuppression blood replacement Dextran, albumin, LR (volume expanders) |
|
|
is decreased Hct and Hb an early or late sign of acute blood loss? why?
|
late; first, the patient may have postural hypotension, and to compensate, the blood will move into the intravascular space to make up for the loss; THEN, Hct and Hb will decrease
|
|
|
manifestations of blood loss of:
10% 20% 30% 40% 50% |
10% - none
20% - tachycardia with exercise; slight postural hypotension 30% - postural hypotension; tachycardia with exercise (put HOB down) 40% - decreased BP and CO at rest; rapid, thready pulse; cold, clammy skin 50% - shock and potential death |
|
|
etiology of thrombocytopenia?
|
platelet count < 150,000
inherited acquired- decreased platelet production, increased platelet destruction |
|
|
3 types of thrombocytopenia
|
Immune Thrombocytopenia Purpura
Thrombotic Thrombocytopenia Purpura Heparin Induced Thrombocytopenia with Thrombosis Syndrome |
|
|
immune thrombocytopenia purpura
|
abnormal destruction of platelets (immune, get it? it attacks its own)
autoimmune disease platelets coated with antibodies destroyed by macrophages in the spleen |
|
|
who is ITP most common in?
|
women age 20-40
|
|
|
thrombotic thrombocytopenic purpura
|
not very common
is an enhanced agglutination of platelets, which forms microthrombi that deposit in arterioles and capillaries--- this is why the platelets are reduced, because they're all being used up; results in end organ damage b/c vessels are being clogged up hemolytic anemia neurological abnormalities fever (even in absence of infection) renal abnormalities (causes kidney failure) |
|
|
heparin induced thrombocytopenia and thrombosis syndrome
|
immune response to heparin causes platelet destruction and vascular endothelial injury
platelet aggregation is promoted, which causes decreased circulating platelets, which causes thrombocytopenia |
|
|
manifestations of thrombocytopenia
|
most are asymptomatic
bleeding (epistaxis, gingival) pettechiae ecchymoses prolonged bleeding after IMs, IVs S/S of shock |
|
|
what do lab values of PT and PTT look like in thrombocytopenia?
|
can be WNL!!!!
|
|
|
what platelet count means there will be spontaneous bleeding?
|
< 20,000
|
|
|
treatment for ITP
|
steroids
immunosuppressive therapy splenectomy (if unresponsive to steroids) transfusion |
|
|
how low must platelet count be in order to use immunosuppressive therapy?
|
<30,000
|
|
|
what do the steroids do for thrombocytopenia?
|
suppress phagocytic response of splenic macrophages (so they don't destroy the platelets); alters spleens recognition of platelets and increases the life span of platelets; depresses antibody formation and decreases capillary fragility and bleeding time
|
|
|
treatment for TTP
|
steroids
plasmapheresis splenectomy |
|
|
treatment for HITTS
|
discontinuing heparin
plasmapheresis protamine sulfate thrombolytics/surgery |
|
|
coumadin may be restarted for those with HITTS when platelet count is back up to what?
|
100,000
|
|
|
HITTS is usually noticed at what point?
|
when baseline platelet count has fallen 50% or more or if a thrombus forms while on heparin therapy
|
|
|
disseminated intravascular coagulation (DIC)
|
DIC leads to the formation of small blood clots inside the blood vessels throughout the body. As the small clots consume coagulation proteins and platelets, normal coagulation is disrupted and abnormal bleeding occurs from the skin (e.g. from sites where blood samples were taken), the gastrointestinal tract, the respiratory tract and surgical wounds. The small clots also disrupt normal blood flow to organs (such as the kidneys), which may malfunction as a result.
|
|
|
causes of DIC
|
always has an underlying cause, ie cancer, trauma, infections, etc
|
|
|
manifestations of DIC
|
bleeding, pallor, pettechiae, oozing blood, hematomas, occult hemorrhage, weakness, malaise, fever, tachypnea, hemoptysis, orthopnea, tachycardia, hypotension, GI bleeding, distension and bloody stools, hematuria, vision changes, dizziness, headache, change in mental status, bone and joint pain, cyanosis, gangene
|
|
|
2 main differences in DIC and thrombocytopenia
|
neurological changes in DIC DO exist!
PTT and PT INCREASE in DIC, and not in thrombocytopenia |
|
|
Hodgkin's disease
|
12% of all lymphomas
REED-STERNBERG CELLS found |
|
|
etiology of Hodgkin's
|
infection with Epstein-Barr virus
genetic predisposition exposure to occupational toxins normal structure of lymph nodes is destroyed by hyperplasia of monocytes and macrophages arises in single location and spreads along adjacent lymphatics infiltrates other organs |
|
|
where can the Reed-Sternberg cells be found?
|
in the lymph OR marrow
|
|
|
manifestations of Hodgkin's disease
|
enlargement of CERVICAL, AXILLARY OR INGUINAL nodes
nodes are moveable, nontender weight loss fatigue fever chills night sweats tachycardia cough dyspnea stridor dysphagia anemia hepatomegaly/splenomegaly |
|
|
what are the B symptoms of Hodgkin's? (poorest prognosis)
|
fever, night sweats, weight loss, pruritis
|
|
|
stages of Hodgkin's?
|
Stage I: single lymph node or single extranodal site
Stage II: two or more lymph nde regions on same side of diaphragm or localized involvement of an extranodal site and one or more lymph node regions on the same side of the diaphragm (above or below) Stage III: involvement of lymph node regions on both sides of the diaphragm; may include a singe extranodal site, spleen or both Stage IV: diffuse or disseminated disease of one or more extralymphatic organs or tissues with or without associated lymph node involvement |
|
|
non-Hodgkin's lymphoma- etiology
|
can originate outside of lymph nodes (primarily of B or T cell origin)
spread can be unpredictable majority have a widely disseminated disease at diagnosis! MOST COMMON HEMATOLOGIC CANCER!!!!!!!!!!!!!!!!! |
|
|
manifestations of non-Hodgkin's
|
painless lymph node enlargement
other symptoms depend on where disease has spread |
|
|
treatment of non-Hodgkin's
|
radiation (SOMETIMES)
watchful waiting (LOTS OF RELAPSES) chemotherapy |
|
|
side effect of therapy for Hodgkin's and non-Hodgkin's
|
pancytopenia
|
