P1 Spring Organs 2011-01-18 (Blood)

Front 1

What can low albumin levels cause?

Back 1

edema, due to low osmotic (pulling) pressure in blood

Front 2

Equation for hematocrit?

Back 2

volume of packed RBCs / total blood volume

Front 3

Name three things that can cause a higher hematocrit?

Back 3

-increase in elevation
-dehydration
-overactive stem cells (eg pathological polycythemia)

Front 4

Name two things that can cause a lower hematocrit?

Back 4

-anemia (loss of rbcs)
-overhydration

Front 5

Features of a reticulocyte?

Back 5

-has hemoglobin
-does not have a nucleus
-is not yet biconcave (TF: still immature)
note: TF means therefore

Front 6

What does a reticulocyte index < 1 indicate?

Back 6

bone marrow anemia (cant produce many reticulocytes)

Front 7

What does a reticulocyte index > 1 indicate?

Back 7

-anemia (loss of rbcs)
-chronic anemia (continual production of reticulocytes and continual loss of mature rbcs)

Front 8

Blood types of baby and mom in erythroblastosis fatalis?

Back 8

baby: Rh+
mom: Rh-

Front 9

Factors needed in erythropoesis?

Back 9

-healthy bone marrow
-erythropoetin (and relatively healthy kidneys)
-vitamin B12
-folic acid
-iron
-low oxygen? (me)

Front 10

When is epo generally used?

Back 10

For patients with ESRD (end stage renal disease), no kidneys = no erythropoetin produced

Front 11

What is transferrin?

Back 11

Transport form of iron (as it goes mainly to the bone marrow).

Front 12

What is ferretin?

Back 12

Storage form of iron (in liver and heart)

Front 13

Types of anemia where you have low numbers of RBCs?

Back 13

-Spherocytosis
-Hemorrhagic anemia
-Aplastic anemia
-Pernicious anemia
("SHAP")

Front 14

Type of anemia where you have low amount of hemoglobin?

Back 14

Iron deficiency anemia (low iron = low hemoglobin)

Front 15

Type of anemia where you have abnormal hemoglobin (and low numbers of RBCs)

Back 15

Sickle cell anemia

Front 16

What causes microcytic hypochromic anemia?

Back 16

Low amount of iron (less hemoglobin results in fainter color and smaller cells)

Front 17

What causes megaloblastic anemia?

Back 17

Low vitamin B12 and/or folic acid results in macrocytes

Front 18

What are the features of a macrocyte?

Back 18

-large, spherical RBC
-not biconcave, not flexible
-ruptures easily in tight capillaries
-seen in megaloblastic anemia (and pernicious anemia)

Front 19

What is pernicious anemia? Cause?

Back 19

A form of megaloblastic anemia, due to lack of intrinsic factor that is needed to absorb vit B12 from the stomach (into the blood stream, so it can travel to the bone marrow)

Front 20

What is vitamin B12 and folic acid used for?

Back 20

They aid in the maturation of RBCs, and are needed anywhere there is rapidly growing cells, such as during pregnancy.

Front 21

What is aplastic anemia?

Back 21

"Bone marrow anemia".
Unable to produce enough RBCs because bone marrow is busted (eg due to radiation, chemo typically).

Front 22

Where do old RBCs get recycled?

Back 22

In the liver and spleen.

Front 23

What causes jaundice?

Back 23

When biliruben (which comes from the porphyrin in heme) isn't excreted properly by the liver (into the bile and pooh).

Front 24

Treatment for pernicious anemia?

Back 24

B12 shot (straight into bloodstream so no stomach involvement).

Front 25

Which type of anemia can cause infection and excessive bleeding?

Back 25

Aplastic anemia (bone marrow anemia) (due to lower WBCs and platelets, not just low RBCs)

Front 26

Features of spherocytosis?

Back 26

-Hereditary
-Spherical shaped RBCs
-Rupture easily
(me: similar to macrocytes of megaloblastic anemia, but cause is hereditary).

Front 27

Cause of sickle cell anemia?

Back 27

Hereditary, sixth position of beta chain in hemoglobin there's a valine (should have glutamic acid).
Get HbS, which sickles the cell under low oxygen tension.

Front 28

What does anemia (in general) cause other than fatigue, weakness, pale skin, and dizziness?

Back 28

Possible heart failure, due to the increased cardiac output, due to faster blood return to heart (inc venous return), due to the decrease in blood viscosity.

Front 29

Types of polycythemia?

Back 29

-Primary polycythemia (aka pathological polycythemia)
-Secondary polycythemia (aka physiological polycythemia)

Front 30

Result and cause of pathological polycythemia?
Any altered levels?

Back 30

Result: An increase in number of RBCs, normal/low erythropoetin levels
Cause: Overactive stem cells

Front 31

Result and cause of physiological polycythemia?
Any altered levels?

Back 31

Result: An increase in number of RBCs, high erythropoetin levels
Cause: High altitude (normal)

Front 32

What is diapedesis?

Back 32

When reticulocytes squeeze out of the bone marrow, and into blood vessels.

Front 33

Whats the structure of a hemoglobin (Hb) molecule?

Back 33

4 peptides (2 alpha chains, 2 beta chains)
There's one heme in each peptide that has a porphyrin ring that holds an iron that carries one oxygen molecule.

Front 34

Most common type of anemia?

Back 34

Iron deficiency anemia

Front 35

List the results of iron deficiency anemia.

Back 35

-microcytic hypochromic cells (due to low Hb)
-learning problems in kids
-dysfunctional enzymes that use iron (cytochromes, catalase, peroxidase, etc).

Front 36

Where does intrinsic factor come from?

Back 36

Secreted by parietal cells in the stomach lining (gastric mucosa).

Front 37

What is the end result of all anemias?

Back 37

Low oxygen in the tissues (and brain?).

Front 38

Tests for anemia?

Back 38

Reticulocyte index:
For aplastic anemia check to see if RI is < 1.
For all other anemia check to see if RI is > 1.
me: my guess is hematocrit could give you a general idea.

Front 39

What can sickle cell anemia cause (besides fewer RBCs)?

Back 39

Vasoocclusive crisis (pain and possible stroke due to RBCs stuck in capillaries).

Front 40

List the granulocytes and agranulocytes.

Back 40

granulocytes: basophils, eosinophils, neutrophils (grandpa BEN), monocytes.
agranulocytes: lymphocytes

Front 41

List 5 differences between neutrophils and macrophages

Back 41

Neutrophils:
Destroys bacteria in blood or tissue.
One time use, then inactive.
Kills 3-20 bacteria.
Only kills bacteria.
Short lifespan (1 day?)

Macrophages:
Destroys bacteria in tissue only (ineffective in blood as a monocyte).
Multiuse.
Kills ~100 bacteria at a time.
Kills bacteria, some parasites, and old/damaged cells.
Longer lifespan (months?).

Front 42

What increases both vasodilation and vasopermeability during an infection?

Back 42

-Toxins
-Clotting factors
-Inflammatory mediators
All of which can be released from tissues/cells during infection.
IBLV these also act as chemoattractants for neutrophils and macrophages.

Front 43

List the first line defenders of the reticuloendothelial system (be specific).

Back 43

The following fixed (tissue) macrophages:
Alveolar macrophages (lungs)
Histiocytes (skin)
Tissue macrophages (lymph nodes)
Kupffer cells (liver)
("AHTK!!")

Front 44

Events that occur during inflammation (basic)?

Back 44

1. Increased vasodilation (causing redness)
2. Increased vasopermeability (plasma leaks into tissue causing swelling)
3. Clotting of interstitial fluid
4. Migration of neutrophils and monocytes

Front 45

During inflammation, activated macrophages release what growth factors?
Where do these go, and what do they do?

Back 45

Activated macrophages release:
TNF
IL-1
G-CSF, M-CSF, GM-CSF
They go to the bone marrow, to produce more granulocytes (mainly neutrophils) and moncytes

Front 46

What do eosinophils do?

Back 46

-Anti parasite (schistosomiasis, trichinosis)
-Weakly phagocytic

Front 47

What do mast cells and basophils release, and under what condition?

Back 47

-Release heparin and histamine when allergen crosslinks IgE on its surface
-Important in allergic reactions

Front 48

What does a high eosinophil count suggest?

Back 48

Parasitic infection

Front 49

List the cells that have IgE receptors.

Back 49

-Basophils
-Eosinophils
-Mast cells
-Monocytes/macrophages
-Platelets

Front 50

What cells do asthma drugs target?
Where?

Back 50

Mast cells, in the lungs

Front 51

What is leukopenia, and what cell count signifies that a patient has leukopenia?

Back 51

Low WBC count (< 2500 cells/mcl)

Front 52

What is a normal WBC count?

Back 52

4500-10,000 cells/mcl

Front 53

List the causes of leukopenia.

Back 53

-HIV
-Chemotherapy
-Radiation
-Some chemicals (benzene)

Front 54

What is agranulocytosis?
Causes?

Back 54

Low granulocytes (basos, eosins, neutros).
Same causes as leukopenia.

Front 55

What is leukemia?

Back 55

An increase in abnormal WBCs

Front 56

List the common types of leukemia.

Back 56

-ALL (acute lymphocytic leuk)
-CLL (chronic lymphocytic leuk)
-AML (acute myelogenous leuk)
-CML (chronic myelogenous leuk)

Front 57

Differentiate between myelogenous and lymphocytic?

Back 57

Lymphoid cells are B and T cells.
Myeloid cells are basos, eosins, neutros, monocytes, erythrocytes, platelets.

Front 58

List symptoms of leukemia.

Back 58

-Pain
-Fractures
-Infection, anemia, bleeding
-Swollen/tender lymph nodes (lymphocytic leuk)
-Metabolic starvation
-Death

Front 59

What occurs during a mismatch blood transfusion?

Back 59

-Recipient Abs attach to donor Ag on donor RBCs
-Donor RBCs agglutinate/clump
-Donor RBCs are hemolyzed by recip WBCs

Front 60

What are the results of a mismatch blood transfusion, and why?

Back 60

-Pain, fever, jaundice, kidney failure, possibly fatal.
-Due to the release of hemoglobin by hemolyzed donor RBCs.

Front 61

How can you detect a mismatch blood transfusion?

Back 61

Hemoglobin in the urine.

Front 62

What blood type is the universal recipient?
Why?

Back 62

AB+
Has no anti A or anti B Abs.
Rh+ can receive Rh+ or Rh-

Front 63

What blood type is the universal donor?
Why?

Back 63

O-
Type O has no A or B Ag on its surface.
Even though type O contains anti A and anti B Abs, they are not in sufficient amount to cause a reaction in the recipient.

Front 64

List the most common blood types in order.

Back 64

O (47%)
A (41%)
B (9%)
AB (3%)

Front 65

Difference between CdE and cDe?
Why?

Back 65

CdE is Rh-
cDe is Rh+
xDx is positive, xdx is negative

Front 66

Why is an initial exposure to a mismatch OAB blood type serious, but not to Rh?

Back 66

People already have OAB Abs soon after birth due to exposure to food/meat or bacteria, but the formation of Rh Abs require direct exposure to blood.

Front 67

Can an Rh+ receive Rh- blood?

Back 67

Yes, its the other direction thats the problem.

Front 68

How much mistyped donor blood is required to cause jaundice in the recipient?

Back 68

400ml or more of mistyped blood

Front 69

List the symptoms of erythroblastosis fatalis.

Back 69

-Anemia
-Enlarged liver and spleen (trying to produce more RBCs)
-Immature RBCs (erythroblasts, nucleated)
-Biliruben in brain (kernicterus)
-Jaundice? (me)
-Possible death

Front 70

Erythroblastosis fetalis treatment? Prevention?

Back 70

Treatment: Rh- blood transfusion to fetus/neonate.
Prevention: Give mom Rh+ Abs to immediately kill any fetal Rh+ that enters mom.

Front 71

How do platelets reinforce the fibrin plug?

Back 71

Platelets release factor 13a (fibrin stabilizing factor).

Front 72

List the causes of platelet aggregation?

Back 72

-Thromboxane A2 and ADP (both produced by platelets)
-Thrombin
-Collagen (attracts and activates platelets)

Front 73

Where is prothrombin produced and what stimulates its production?

Back 73

-produced in liver.
-thrombin stimulates liver to make more prothrombin

Front 74

How does aspirin affect coagulation?

Back 74

It prevents formation of thromboxane A2

Front 75

How does vitamin C affect coagulation?

Back 75

Vit C is necessary for formation of collagen, and collagen attracts and activates platelets during platelet plug formation.

Front 76

What's a natural anticoagulant?

Back 76

Heparin + antithrombin 3

Front 77

Where does heparin come from?

Back 77

Secreted by mast cells and basophils (they also secrete histamine btw).

Front 78

List fibrin clot formation steps.

Back 78

1. prothrombin → thrombin (via prothrombin activator 10a and ca+)
2. fibrinogen → fibrin (via thrombin)
3. fibrin → loose fibrin mesh (with ca+)
4. loose fibrin mesh → tight fibrin mesh (with fibrin stabilizing factor 13a)

Front 79

List everything thrombin does.

Back 79

-Converts fibrinogen → fibrin
-Stimulates liver to produce more prothrombin
-Increases activity of fibrin stabilizing factor 13a
-Promotes aggregation and activation of platelets
-Promotes/activates factors 8-13 (note this includes factor 10, prothrombin activator)

Front 80

What is the rate limiting factor in clot formation?

Back 80

prothrombin activator (10a)

Front 81

Why would liver disease increase bleeding?

Back 81

The liver produces:
-prothrombin
-fibrinogen
-prothrombin activator (10a)
-factors 7 and 9

Front 82

How does prothrombin get near the platelet plug to aid in formation of the fibrin mesh?

Back 82

prothrombin attaches to the platelet membrane.

Front 83

Difference between plasma and serum?

Back 83

Plasma has clotting factors, fibrinogen, and an anticoagulant thats added.
Serum does not have any of these.

Front 84

How does prothrombin activator get produced?

Back 84

via either the intrinsic or extrinsic pathways

Front 85

List the steps of the intrinsic pathway.

Back 85

1. Collagen (blood trigger) activates factor 12
2. 12 activates 11
3. 11 activates 9
4. 9 activates 10 (prothrombin activator)

Front 86

List the steps of the extrinsic pathway.

Back 86

1. Tissue factor (in tissue, not blood) activates factor 7.
2. Factor 7 activates 10 (prothrombin activator).

Front 87

List three things that heparin + antithrombin 3 do.

Back 87

1. Removes thrombin
2. Removes some factors such as prothrombin activator (10a)
3. Inhibits platelet aggregation.

Front 88

What does the fibrinolytic system do, and how?

Back 88

Dissolves blood clots.
Plasminogen is converted to plasmin by tpa released from cells. Plasmin breaks down the fibrin clot.

Front 89

List 5 disorders that cause coagulation defects.

Back 89

1. Vitamin C deficiency (low collagen)
2. Vitamin K deficiency
3. Hemophilia (clotting disorder)
4. Thrombocytopenia (low platelets)
5. Liver failure/disease (low fibrinogen, prothrombin, prothrombin activator, factors 7 and 9)

Front 90

Why does vitamin C deficiency cause bleeding problems if it's just an attractant for platelets?

Back 90

Platelets must adhere to the collagen to form platelet plug.

Front 91

Why does vitamin K deficiency cause bleeding problems?

Back 91

The liver needs vitamin K to make prothrombin (factor 2), as well as factors 7, 9, and 10 (prothrombin activator).

Front 92

Vitamin C deficiency is called _____ ?

Back 92

scurvy

Front 93

What is obstructive jaundice, and what does it cause?

Back 93

Obstructive jaundice leads to vitamin K deficiency, because bile cant be secreted by the liver into the gut. Bile is needed to absorb vitamin K.

Front 94

What types of hemophilia are there, and what is the cause of each?

Back 94

Hemophilia A: nonfunctional clotting co-factor 8.
Hemophilia B: nonfunctional clotting factor 9.
Hemophilia C: nonfunctional clotting factor 11.

Front 95

Difference between a thrombus and an embolism?

Back 95

A thrombus is a stationary blood clot, and an embolism is a thrombus that moved to a new location.

Front 96

What is DVT and why is it dangerous?

Back 96

Deep Venous Thrombosis.
The blood clot in your vein might travel into your right heart and then to your lungs, becoming a pulmonary embolism.

Front 97

Why is a pulmonary embolism dangerous? How can you get rid of it?

Back 97

Can result in pulmonary hypertension, lung failure, and even heart failure.
Tpa (via a catheter) can dissolve the clot usually.

Front 98

Is an arterial embolism dangerous?

Back 98

If it goes to your periphery, not so much, but if it enters an artery to the brain it can cause a stroke.

Front 99

List the causes of DVT.

Back 99

-Inactivity
-Long distance travel (eg economy class syndrome)
-Bedrest
-Surgery
-Drugs (eg birth control)

Front 100

How does warfarin/coumadin work (in general) as an anticoagulant?

Back 100

It interferes with vitamin K which is used by the liver to make coagulation factors.

Front 101

Can heparin, coumadin, or aspirin be clinically used to dissolve clots?

Back 101

No, only to prevent them.
Tpa (tissue plasminogen activator) can be given to dissolve clots.

Front 102

List substances that are derived from the arachidonic acid pathway? Which ones are blocked by aspirin?

Back 102

-Leukotrienes
-Prostaglandins (blocked)
-Prostacyclin (pg12) (blocked)
-Thromboxane A2 (blocked)