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Q4 Heme Flashcards

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1
Q

Loss of plasma can cause a falsely ______ Hgb/Hct, and excess plasma/fluids can cause a falsely _______ Hgb/Hct.

A

Elevated
Decresed

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2
Q

Anemia definition in M and F

A

F = Hgb <11.9 and Hct <35%
M = <13.6 and <40%

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3
Q

What are the 4 main pathologies of anemia?

A

Blood loss (bleeding/hemorrhage)
Impaired erythrocyte production
Increased “ breakdown
Combination of these 3 factors.

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4
Q

What is the normal SaO2 and SvO2 concentration and % offloaded at tissues?

A

SaO2 (arterial leaving lungs) is usuallly 100% and then SvO2, returning TO lungs is usually ~75% - usually ~ 24% offload.

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5
Q

How does the body compensate for anemia?
??

A

Dilation of peripheral vessels to decrease SVR (increased NO). This increases CO through decreasing after load and increasing the PREload through increased venous return. Heart rate and contractility increases.

When the volume of RBCs decreases, there is an increased in velocity.
Decreases fluid viscosity for faster flow.

Increased HR and SV (SNS Stim via chemoreceptors to hypoxia)
Increased RR and depth.
Activation of RAAS - Na and H2O retention and more erythropoietin.

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6
Q

What changes happen to the heart in chronic anemia?

A

LV hypertorphy and valvular dysfunction.

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7
Q

As CO/Hgb decreases, DO2 (delivery of O2 to the tissues) ________
As CO/Hgb decreases, arterial saturation ______
As CO/Hgb decreases, Mixed venous sat _______
As CO/HGB decreases, O2 extraction ratio (%) _______

A

Decreases
Decreases
Decreases
Increases

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8
Q

When you have a L shift, there is _____ temp, 2,3DPG, H+ and CO. Blood is more _________ (Acidotic/basic). There is a natural L-shift in the ______ and the RBC holds _____ affinity to O2.
When there is a R shift, Temp, 2,3GPD, H+ ______. Blood is more _____. A natural R shift occurs in _____ where RBC holds _____ affinity to O2.

A

Decrease
Basic (Decrease in H+)
Lungs
More
Increase
Acidotic (increase in H+)
Tissues
Less

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9
Q

Patients who are altitude acclimated have a natural ____ shift and increased _____.

A

Right
2,3DPG
This means they easily release O2 to the tissues so they can survive in low O2 environments.

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10
Q

The amount of O2 that dissolves in plasma is ________. Why is this important?

A

VERY LOW. This means we need Hgb to carry it to the tissues. If we are low in Hgb, the O2 can’t get to the tissues any other way.

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11
Q

What does Anisocytosis mean?

A

A high degree of anisocytosis means there is a lot of variability between cell sizes
A low degree of anisocytosis means there is not much variability, all cells are mostly the same size.

Another term for this is RDW.

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12
Q

What does it mean if someone has a low MCV?

MCH?

A

MCV is average size of RBCs.
Low MCV means microcytic.

MCH is mean corpuscular hemoglobin or average Hgb content in an RBC.

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13
Q

Iron Deficiency Anemia (IDA) is _____cytic and _____chromic.
___ MCV
___ MCH/MCHC
____ RDW

A

MICROcytic/HYPOchromic.

Low
Low
Variable

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14
Q

Pernicious Anemia
___ MCV (____Cytic)
____ MCH/MCHC
____RDW

A

HIGH - MACRO
Variable (usually normal)
Variable (usually high)

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15
Q

For pernicious anemia, DNA is not able to split (deficiency in components) so cells get stuck, but the cytocytic content gets bigger while waiting for cell to split.

A
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16
Q

Initial fluid replacement for Class I, II, III and IV hemorrhage?

A

I - crystalloid
II - Crystalloid (750-1500ml)
III+IV - Crystalloid and blood. (1500->2000ml).

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17
Q

3 major types of anemia involving low production of Erythrocytes.

A

Megaloblastic (Macrocytic/Normochromic) Anemia (PA, Folate deficiency anemia and medication related)
Microcytic/HYPOchromic Anemias (IDA)
Normocytic/normochromic (anemia of chronic disease, aplastic anemia)

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18
Q

Patho Phys of Megaloblastic (macrocytic-normochromic) anemia

A

Vit B12/IF (PA) and Folate are needed to perform DNA synthesis. When they are absent, the cell takes longer than normal to divide. These then larger than normal cells die prematurely.

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19
Q

What does Vit B12 (cobalamin) do?

A

It works with methionine synthase to activate folate for Neucleic acid synthesis.
5.10 Methylene TH4

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20
Q

Folate is Vit ____

A

B9

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21
Q

B9 and B12 are found exclusively in ____

A

Foods.

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22
Q

B12 mostly in foods of animal origin.

A
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23
Q

2 causes of B12 deficiency

A

Lack of dietary intake (Vegans)
Pernicious anemia (lack of IF and ability to properly absorb B12)

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24
Q

Key difference between folate (B9) deficiency and B12 deficiency is:

A

B12 has anemia AND neurological symptoms due to demyelination (peripheral neuropathy)

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25
Two types of PA
Congenital - IF deficiency. B12 must bind with IF in order to be absorbed in the GI tract. Autoimmune - gastritis - destroys parietal cells that create IF.
26
If someone has macrocytic-normochromic erythrocytes on smear, what anemias could they have?
PA, Vit B12 or Folate deficiency anemia
27
What is the only way to distinguish vit B12 deficiency r/t dietary deficiency or issues with absorption?
Gastric biopsy.
28
Would oral B12 supplementation be an adequate tx for PA? Why or why. Not?
No. Because in PA, IF is lacking, so B12 cannot be absorbed through the GI tract. It must be given as a shot.
29
What chronic illnesses could lead to vit B9 (folate) deficiency?
Alcoholism (interferes with folate metab in liver) Celiac disease and IBD Pregnancy
30
What is an example of microcytic-HYPOchromic anemia?
IDA.
31
What type of anemia is IDA?
Microcytic-HYPOchromic
32
What is the most common nutritional deficiency in the world?
IDA
33
4 causes of IDA
Dietary deficiency Impaired absorption Increased requirement Chronic blood loss
34
Iron is needed for____
Hgb synthesis.
35
What stage of IDA do symptoms appear?
Stage 3 - when the microcytic/HYPOchromic erythrocytes are released into circulation and replace normal onesie.
36
Which lab tests can show iron storage values?
Serum ferritin or transferrin
37
T/F; Iron replacement therapy corrects IDA right away.
False. Usually takes abut 1-2mmonths to see effects.
38
What type of anemia is common in hospitalized individuals? 4 main causes?
Anemia of chronic disease (normocytic/normochromic) Infections Cancer Autoimmune (RA, SLE, IBD) CDK/Inflammatioin
39
Someone with RA or solid tumor cancer or CKD is most likely to develop which anemia?
Anemia of chronic disease.
40
What causes the anemia in anemia of chronic disease?
Decreased erythropoietin production from stressed kidneys Impaired iron utilization - sequestered in macrophages - IL6 decreases activity of the pump that allows iron back out into circulation when needed. RBCs die prematurely Decreased response of bone marrow to erythropoietin
41
What does it mean to have “sequestered” iron? How does chronic disease affect this?
Used iron normally circulates until it is picked up and stored by machrophages until needed again. Macrophages have ferroportin transporters that release iron back into the blood stream when it’s needed again. During inflammatory states, IL-6 causes an increase in hepatocyte hepcidin secretion. Hepcidin decreases the Ferroportin pump activity leaving the iron molecules in the macrophage. Iron levels will appear normal, but they are “sequestered” in the macrophage and not in circulation where it can be used.
42
Acute blood loss anemia would appear as ________ cytic, ___chromic.
Normo Normo
43
How can you distinguish ACD and IDA?
ACD will fail to respond to iron replacement therapy.
44
What type of anemia is aplastic anemia? (AA)
Normocytic/normochromic.
45
What is unique about AA compared to other anemias?
Since it results from decreased bone marrow production, ALL cells are affected (Pancytopenia). Low RBC, neutrophils and thrombocytes are all present.
46
Which anemia causes pancytopenia?
AA.
47
What is the patho Phys theory behind AA?
Immune-mediated Activated T-cells inhibit hematopoietic stem cells. 70% is autoimmune 15% is drugs or ionizing radiation (cancer or bone marrow transplant).
48
Tx for AA
Bone marrow suppression/transplant Immunosupression
49
What is G6PD and what does it do? What happens if it is deficient?
G6PD protects the RBC from damage from oxidative stress (from ROS). Increased oxidative stress can come from certain drugs (sulfa, antimalarials, nitrofurantoins, salicylates), infections or diet (fava beans). Cells die prematurely (mostly in spleen).
50
How does G6PD present in infants?
Acute hemolytic anemia.
51
What types of anemias are associated with Heinz bodies?
G6PD deficiency. The hemoglobin precipitates. Can lead to early cell death. Sometimes Beta Thalassemias (over abundance of alpha chains)
52
Tx during G6PD crisis?
Blood transfusion and iron supplementation.
53
Why does sickle cell happen?
A genetic mutation that replaces glutamate with valine. HgbS
54
What is the most important factor that determines polymerization to sickle shape?
Deoxygenation or hypoxia. This is the main triggering factor for crisis.
55
What should you AVOID in sickle cell patients?
HYPOXIA!!!! Fever, infx, acidosis, dehydration, constricting clothes and exposure to cold.
56
Beta Thalassemia - what?
Mutation in HBB gene - over production of alpha Hgb chains and not enough beta.
57
Which type of thalassemia can affect fetus in utero?
Alpha thalassemias Beta thalassemias only affect born people (fetal gamma Hgb replaced with beta)
58
A patient only has 1 or 2 missing HBA1 and HBA2 genes. They will have these clinical symptoms:
None. They may have HYPOchromic cells.
59
What lab values can indicate hemolysis? What anemia can this happen in?
Elevated iron and bili levels. Thalassemias.
60
T/F: Beta thalassemia major can be cured.
True - only through allogenic stem cell transplant from matched family member.
61
Where does the majority of hemolytic anemia occur? What can be an example of this?
Phagocytosis in the lymphoid system (EXTRAVASCULAR) Minority intravascular - mechanical, parasites, toxic factors. Spherocytes = extravascular hemolysis Schistocytes = intravascular.
62
What are some examples of Congenital hemolytic anemia? Acquired?
G6PD, sickle cell, Thalassemia. Autoimmune, mismatched transfusion, drug induced.
63
What is the classic example of INTRAvascular hemolysis?
Transfusion rxn.
64
What is the difference between relative and absolute polycythemia?
Relative = increase in RBC concentration due to loss of plasma (dehydration) Absolute = total increase in RBC concentration.
65
Things that cause increased erythropoietin secretion and therefore causing ______
Polycythemia. Chronic hypoxia, smoking, COPD. Genetics (PV)
66
What does it mean if there is a JAK2 gene mutation?
JAK 2 increases the activity of erythropoietin (no negative feedback mechanism). Tx is blood letting.
67
Your patient has a thrombotic event, splenomegaly and aquagenic pruritis - what do you suspect?
Polycythemia Vera
68
Viral infections, nutritional deficiencies, Renal failure and AA all result in
SECONDARY (Aquired) Decreased platelet production.
69
HIT, ITP, TTP are all ______
Consumptive coagulopathies.
70
which HIT (type 1 or 2) is less severe and why?
1 is less severe W/in 1-4 days of therapy initiation HIGH doses of heparin. Resolves spontaneously.
71
What is involved in HIT type 2
Heparin, platelet factor 4 and IgG. Hypercoagulable state >5 days after heparin start. Consumptive
72
T/F: 1st line tx for HIT type 2 is to give platelets.
False. This will just fuel the fire. You need to give anticoagulants and only replace platelets if count drops below 20,000 with signs of spontaneous bleeding.
73
ITP
Immune Thrombocytopenic Purpura Viral infx, SLE. Spontaneous resolution 1-2 mo 7-28% convert to chronic (associate with autoantibodies against platelet antigens,
74
TTP
Familial (rare - presents in kids) Acquired (more Common and severe - F in their 30s) Platelet aggregation and microthrombi through out the body - decrease in plasma disintegrin and ADAMTS13 which cleaves vWF.
75
What is the “classic Pentad” of TTP s/s?
Plt <20,000 schistocytes (intravascular hemolytic anemia) Ischemic signs in CNS (memory disturbances, HA, coma) Ischemic kidney signs Fever
76
How do we treat TTP?
Plasma exchange with FFP!! ReplacesADAMMST13 to cleave vWF.
77
Which syndrome is GP-1b involved in and what does it do?
Bernard-Soulier syndrome. It’s used to help bind the RBC to the wall in areas of high shear (arterial). It receives vWF.
78
Von Willebrand Disease and factor _____ go together
VIII
79
vWF travels with ______ in plasma until activated by ________ or_______
VIII platelet Alpha IIB/Beta3 exposed collagen
80
Difference between FVIII deficiency and vWF?
Hard to tell…..
81
Types of vWD
Type 1 - normal vWF quality. - just not enough Type 2 2A - decreased quality (platelet adhesion) 2M - decreased quality (platelet adhesion) 2B - INCREASED platelet binding (plt slightly low due to using up stores) 2N - decreased binding with FVIII (may be confused with hemophilia. Type 3 - absolute quantitative deficit (genetic in kids)
82
Which types of VWD respond to DDAVP therapy?
1, 2A and 2M
83
Which VWD should you NOT give DDAVP in ?
2B - you’ll get excess clotting.
84
Tx for vWD 2B, 2N and type 3
Factor VIII concentrate or VWF concentrate.
85
Difference between Hemophilia A+B?
A is FVIII deficiency B is FIX deficiency
86
Difference between Hemophilia A and vWD 2N?
2N is decreased binding of vWF to FVIII while HemA is low FVIII levels.
87
Why is recombinant FVIIa given to hemophilia patients?
Because long term patients develop antibodies against factors. The recombinant VIIa bypasses other factors that the body has. Become resistant to.
88
Difference between hemophilia A, vWD and Factor V Leiden?
HemA and vWD are hypocoagulable disease while Factor V Leiden is HYPERcoagulable.
89
Look in book on Factor V Leiden.
90
Factor V Leiden and Protein C+S deficiency are hereditary
91
What are Vit K dependent factors?
II, VII, IX, X, protein c +. S
92
2 places we get vit K? How can we become deficient?
Food and GI tract bacteria. Low vit K in diet or lack of GI bacteria- newborn, oral abx, etc.
93
Does liver disease cause a hyper or hypocoagullable state?
BOTH! It’s a mixed bag
94
In liver disease, decreased fibrinogen, increased t-PA and increased NO would cause _______ (bleeding or clotting?)
Bleeding. Also: decreased platelets, decreased plt activation, increased prostacyclin,decreased factor. II, V,VII, X,XI, decreased fibrinogen, increased fibrinolysis, decreased TAFI
95
In liver disease, decreased ADAMTS13, increased factor VIII, decreased plasminogen and increased PAI would cause ____________ (bleeding/clotting?)
Clotting. Also increased vWF, ULvWF, decreased activated proteins C+S, decreased antithrombin, decreased plasminogen.
96
What is the best test to see whether liver disease pts are more prone to clotting or bleeding?
Thromboelastography (TEG)
97
Main cause for DIC?
Sepsis OB and Malignancy are close seconds.
98
Score algorithm for DIC: Platelet count PT prolongation Fibrin degradation products Fibrinogen levels
Plt: >100,000 =0, <100,000 = 1, <50,000 = 2 PT Prolongation: <3s = 0, >3<6s =1, >6s=2 Fibrin deg products: no increase = 0, mod increase = 2,strong increase = 3 Fibrinogen level: >1 = 0, <1 = 1 > or = 5 = consistent with OVERT DIC. <5, not likely DIC, repeat test in 1-2 days.
99
According to the scoring algorithm, what diagnostic test holds the most weight in dx DIC?
Increase of fibrin degradation products (0-3while all other tests are 0-1 or 2)
100
In DIC, what happens to platelets, PT prolongation, Fibrin degradation products and fibrinogen levels?
Platelets decrease, PT increases (prolongs), Fibrin deg products increase and fibrinogen level decreases.
101
Tx for DIC?
Heparin/LMWH
102
Arterial Oxygen Content (CaO2)= (O2 carrying capacity x SaO2) + (dissolved O2) CaO2 = (1.34 x Hb x SaO2) + (PaO2 x 0.0031) This number is usually >75% (only 25% offloaded to tissues) but when the number nears 50%, this is a clear sign that _________
Patient is reaching the limit of their ability to deliver O2 to the tissues. No matter what the Hgb level is, if the CaO2 (arterial O2 content) is <50%, they need blood.
103
determine CaO2: given a hemoglobin of 14, a SaO2 of 95% and a PaO2 of 60, what is the CaO2?
(1.34 x 14 x 0.95) + (60 x 0.0031) = 17.82 + 0.186 = 18.006 mL/dL

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