Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

pathophysiology > Blood and Coagulation > Flashcards

Blood and Coagulation Flashcards

1
Q

hypoalbuminemia

A

drugs bound to serum proteins to a various drug and only a free drug is pharmacologically active. can lead to a significant increase in free drug concentration - not enough albumin

consequence- drug toxicity - recommend lowering the dose - based on where the albumin is synthesized and what the organ is affected (liver)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what explains feeling tired all the time and walking up the stairs is hard

A

low hemoglobin levels, o2 capacity is reduced - anemia from a ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

RDW high. what does that mean?

A

the higher the red blood cell distribution width the more variable the size of the RBC - means the body is trying to make more blood cells trying to compensate for RBC - RBC has no mitochondria which reflects the release of large immature RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

MCV

A

mean corpuscular volume - determines the average red blood cell size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

MCH

A

mean corpuscular hemoglobin - hemoglobin value x 10 divided by the RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

MCHC

A

Mean corpuscular hemoglobin content: hemoglobin x 100 divided by the HCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Normochromic

A

normal MCH or MCHC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

hypochromic

A

low MCH/MCHC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

microcytic

A

low HCT and low MCV or small red cell anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

macrocytic

A

low HCT and high MCV or large RBC anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

normocytic

A

low HCT (hemocrit, volume of RBC in blood) and normal MCV – or normal RBC anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

anemias

A

group of diseases characterized by a decrease in HB or RBC resulting in reduced oxygen-carrying capacity of the blood
results from inadequate RBC production, increased RBC destruction or hemolysis or blood loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

hyproliferative

A 
anemia class
marrow damage
iron deficiency
decreased deficiency
decreased stimulation 
inflammation
metabolic disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

maturation disorders

A

anemia class

cytoplasmic defects - thalassemia (less O2 carrying, heme messed up), iron deficiency, sideroblastic (ucleated erythroblasts (precursors to mature red blood cells) with granules of iron accumulated in the mitochondria surrounding the nucleus)

nuclear maturation defect- folate deficiency, vitamin b12 deficiency, refractory anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

hemorrhage/hemolysis

A

anemia class

blood loss, intravascular hemolysis, autoimmune disease, hemoglobuinopathy, metabolic/membrane defect,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

normocytic normochromic anemia

A

destruction or sudden loss of red cells: hemolytic anemia/acute blood loss

disorders of erythropoietin (produced in kidneys) production/efficacy

chronic diseases: chronic infections (HIV, hepatitis B/C, bacterial endocarditis, or osteomyelitis) autoimmune disease (RA, Crohns, systemic lupus erythematoses), lymphomas, chronic liver or renal disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

erythropoieten (EPO

A

differentiation into erythrocytes is dependent on EPO as it speeds of the stages of pro erythroblasts
EPO is synthesized by the kidney and released into the blood stream as a response to hypoxia (lack of o2) upon reaching the bone marrow, EPO stimulates RBC progenitors via transmembrane receptors - glycoprotein made of 166 amino acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

microcytic hypochromic anemia

A

deficiency in Hb synthesis - iron deficiency or poor iron utilization, or chronic blood loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Macrocytic Normochromic Anemia

A

megoblasts are distinct cells that express a biochemical abnormality of retarded DNA synthesis resulting in unbalanced cell growth. may affect all hematopoietic cell lines.

caused by B12 or folate deficiencies and hemolytic anemias (RBC destroyed faster than they can be made)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

why are hemolytic anemias macrocytic

A

early appearance of large quantity of reticulocytes (immature RBC larger than normal cells bc normal cells shrink after time ) in peripheral circulation (reticulocytosis) indication of increased RBC production. DNA synthesis is impaired. the larger red cells are always associated with insufficient numbers of cells and often also insufficient hemoglobin content per cell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

mild anemia

A

no clinical symptoms and may be found on accident. healthy patients may acclimate to very low Hb conc if anemia is developed slowly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

anemia symptoms

A

fatigue, dizziness, irritability, weakness, vertigo, shortness of breath, chest pain, decreased exercise tolerance, neurologic symptoms in vitamin B12 deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

anemia rapid onset symptoms: … why?

A

palpitations, tachycardia, angina, breathlessness. body can’t compensate for all of the changes because it is a rapid onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

onset more chronic:

A

fatigue, weakness, headache, dyspnea on exertion, vertigo, faintness, sensitivity to cold, loss of skin tone. allows for compensating mechanisms because onset is not acute. not associated with any CV symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
anemia signs
tachycardia, pale, dec mental acuity, inc intensity of cardiac valve murmurs, diminished vibratory sense or gait abnormal
26
chronic hemolytic anemia
sickle cell - inherited recessive hemoglobinopathy resulting in abnormal hemoglobin hemolobin S
27
sickle cell trait (SCT)
sickle cell syndrome - heterozygous inheritance of one normal b-globin gene producing HbA and one sickle gene producing HbS gene - asymptomatic
28
Sickle cell disease (SCD)
homozygous or compounded heterozygous.
29
sickle cell treatment
decitabine induces HbF inhibits DNA methylation - DNA methylation silences genes chronic transfusions therapy primarily for stroke prevention and amelioration of organ damage - not actually treating the disease hydroxyurea increases production of fetal Hb and not he adult form. HbF interferes with the crystallization of Hb, so RBCs no longer sickle
30
pathophys sickle cell
stresses of ciruclation and repetitive sickle-unsickle cycles lead to RBC fragmentation - severe alteration in membrane structure and function - typical sickled cell survives for about 16 to120 days, whereas the life span of a normal RBC is 120 days reticulocytes Hb S has reduced oxygen affinity which increases its polymerization - when it gives up oxygen : polymerization pulls RBC into a sickle shape - sickled RBC becomes tangled with others that block blood flow resulting in tissue damage and pain from hypoxia - abnormal b-polypeptide chain
31
blood group
classification of blood based on the presence or absence of inherited antigens = carbs present on surface of RBC
32
alloantibodies
all individuals produce antibodies to the carbohydrate antigen that they lack
33
inheritance of ABO blood group
genes determining the A and B phenotypes expressed in mendelian co-dominant manner each coding for glycosyltransferase to a attach a specific carbohydrate
34
issoagglutinins
naturally occuring anti-A and anti-B antibodies - type A produces anti-B and type B produces anti-A isoagglutinin no isoagglutinin found in AB - universal recipient type O produce both anti-A and anti-B - universal donors (cells not recognized by any ABO isoagglutinins)
35
if your blood cells do not stick together in the presence of anti-A or Anti-B
you have O type blood because O type blood produces both antibodies
36
if your blood cells stick in anti-B
you have B type blood because B blood produces anti-A not anti-B
37
Rh system
antigen found on a 30-32 kDa RBC membrane protien with no defined function - - D antigen is Rh positivity - lack D antigen Rh negative - Rh-negative exposed to Rh-positive can allow them to create the anti-D alloantibody
38
Rh negative blood transfusion
should be given Rh-negative so that the patient doesn't have alloimmunization to the D antigen. Rh-positive blood can only be used once in the case of an emergency because after that they will develop the antibody already
39
Rh negative women pregnant with Rh positive baby
Rh antibodies after second pregnancy cross the placenta and attack the blood of Rh-positive fetus = hemolytic anemia in the fetus prevented with Rh immunoglobulin - prevents production of Rh antibodies but it doesn't help if the patient sis already sensitized
40
anti- A serum (agglutination), anti-B serum (agglutination), anti Rh serum (no agglutination)
AB-
41
Rh positive people can donate to _______ and Rh negative people can donate to _______
Rh + donate to RH + | Rh - donate to anyone
42
too little hemostasis
allows excessive bleeding
43
hemostasis (3 steps)
ability to stop blood loss from a damaged vessel 1. vasoconstriction 2. platelet plug formation 3. coagulation
44
too much hemostasis
too much creates a thrombus, blood clot that adheres to the undamaged wall of a blood vessel and stops blood flow
45
platelet plug formation
begins with platelet adhesion to exposed collagen, followed by platelet activation with the local release of cytokines. release of these factors reinforce local vasoconstriction and platelet activation. platelet aggregate to one another to form a loose plug. exposed collagen binds and activates platelets release of platelet factors factors attract more platelets platelets aggregate into platelet plug
46
what prevents the platelet plug from continuing to spread and form
1. intact endothelium prevents platelet adhesion | 2. intact endothelium releases prostacyclin and nitric oxide which prevents platelet adhesion
47
platelet disorders
1. low numbers - platelet count of 5,000-10,000 is required to maintain vascular integrity in the microcirculation - decreased production - sequestration (enlarged spleen) - increased distruction 2. high number 3. dysfunction
48
decreased in production of low platelet numbers targets which tissue? why does this come about?
targets bone marrow | usually because of an infection compromising the low platelet numbers or drug-induced chemo can depress bone marrow
49
why does an enlarged spleen have low platelet numbers?
spleen is usually a good filter : sequestered means the platelets will get stuck!
50
how does an increased destruction of platelets happen?
immune mediated: antibodies that react with specific platelet surface antigens and result in thrombocytopenia (deficiency in platelets and causes bleeding)
51
petechiae
pinpoint, non-blanching hemorrhage (put pressure on it and it doesn't go away), thrombocytopenia
52
purpura
larger, non-blanching flat patch, thrombocytopenia
53
thrombocytopenia
deficiency in platelets and causes bleeding
54
ecchymosis
larger than purpura, non-blanching hemorrhage
55
heparin
anticoagulant action by accelerating the activity of antithrombin III to inactivate factor 4, 5, 6, 7
56
intrinsic- contact activation
collagen or other factors activates factor 12
57
extrinsic- cell injury
damage exposes tissue factor 3 which activates factor 7
58
if you have a patients with existing clots can heparin lyse those closts
no because it inhibits thrombin preventing activation of plasminogin to plasmin to break down the fibrin polymer
59
conversion of fibrinogen into fibrin and subsequent fibrinolysis
1. fibrinogen converted to fibrin polymer which forms a clot - activated by thrombin 2. fibrin polymer is activated by thrombin, plasminogen, and tpa to activate plasmin which is needed to destroy the fibrin polymer called fibrinolysis
60
heparin induced thrmobocytopenia
- heparin reacts with PF-4 which is normally present on the surface of endothelial cells or released in small quants from the circulating platelets - specific antibodies react with these conjugates to form immune complexes and the complex binds to fragment receptors on the circulating platelets - this releases PF-4 from alpha-granules in platelets - newly released PF-4 binds to additional heparin and the antibody forms more immune complexes, establishing a cycle of platelet activation - as activated platelet are destroyed the number of platelets will decrease and will estaablish thrombocytopenia excess pf-4 binds to heparin-like molecules on endothelial cells which leads to immune-mediated EC injury and increaes thrombosis and disseminated intravascular coagulation
61
heparin induced thrombocytopenia differs from other drug-induced tcp
1. thrmobocytopenia not usually as severe 2. not associated with bleeding by increaes the risk of thrmobosis 50% treamtment: prompt discontinuation of heparin and use of alternative anticoagulats if bleeding risk does not outweigh thrmobotic risk
62
high platelet number
iron deficiency, secondary to inflammation or infection: reactive thrombocytosis, myeloproliferative process (cancer-like)
63
platelet dysfunction (2)
inherited mutations: secretion defects (cant do hemostasis and platelet plug or vasoconstriction - can't have platelet activation - platelet gets activated ad they secrete platelet factors - cant release factors when they do this - function is displaced) acquired: drugs
64
drug induced platelet dysfunction: clopidogrel (plavix
adp induces platelet activation by binding platelet receptor P2Y12 clopidogrel prevents binding ofadenosine diphosphate to platelet P2Y receptor impaired activation of the GPIIb/IIIa complex inhibits platelet aggregation
65
coagulation factors (3)
1. vitamin k-dependent factors: 2,6,9,10 2. contact activation factors: 11 and 12, prekallikrein, high molecular weight kininogen 3. thrombin sensitive factors: 5, 7, 13, fibrinogen
66
coagulation definition
exposed collagen and tissue factor initiates the formation of a fibrin protein mesh to stabilize platelet plug into a clot. fibrin is the end product of a series of enzymatic reactions = coagulation cascade
67
warfarin
inhibits the synthesis of vitamin k dpendent coagulation factors warfarin exerts anticoagulant effect by inhibiting vitamin k epoxide reductase and inhibiting vitamin k quinone reductase limits the gamma-carboxylation of the vitamin-k dependent coagulant proteins
68
coagulation cascade - common pathway
unite pathways to create thrombin that converts fibrinogen into fibrin polymer - active factor 13 will convert fibrin into a cross linked polymer that stabilizes the clot
69
fibrinolysis
as the wall vessel slowly repairs itself the clot disintegrates: thrombin works with a second factor called plasminogen activator tPA to convert inactive plasminogen into plasmin plasmin breaks down fibrin polymers which is a process known as fibrinolysis

pathophysiology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions