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Skin, Lymph, Blood > Dr. Singh - Hematopathology : RBC And Bleeding Disorders > Flashcards

Dr. Singh - Hematopathology : RBC And Bleeding Disorders Flashcards

1
Q

How to access for anemia

A

You look at Hemoglobin (12-16) or you look at Hematocrit (36%-48%)
For women ranges

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2
Q

How to measure the properties of RBCs

A

MCV(mean corpuscular volume) = Hct/RBC
MCH = Hgb/RBC
MCHC = Hgb/Hct

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3
Q

Low MCV

A

Microcytic Anemia

Volume of each cell is smaller

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4
Q

high MCV

A

Macrocyclic anemia

Volume of each RBC is larger

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5
Q

Low MCH

A

Hypochromic (lighter in color in middle is larger)

Low amounts of hemoglobin in each RBC

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6
Q

Polychromatic cells

What are they and how to confirm

A

They are Reticulocyte with a small RNA in them, they look more purple in color and slightly bigger then the RBCs
- confirm with supravital stain that stains the RNA inside it

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7
Q

Normal or low Reticulocytes seen and anemia

A

The BM has a problem and does not make more RBCs, RBCs have low Hcrit and Hgb

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8
Q

Anemia with many reticulocytes seen

A

There is a problem in the periphery causing the RBCs to not survive or function
BM produces more RBCs

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9
Q

Anisocytosis

A 
Elevated RDW (distribution of size in RBCs)
**** FE+3 deficiency anemia**** can cause this
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10
Q

Acute Blood Loss causes what to happen immediately and overtime

A

No difference in MHV and all other properties
- BP down, pulse up

OVERTIME :
- blood left pulls fluid from body = Hct and Hgb goes down (6-7hr later)

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11
Q

Chronic Blood loss

A

Very mild and gradual sx
- pt can come in with 5.5 hgb and feel fine due to body compensation
EX: heavy menstrual cycle, GI bleeds

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12
Q

Hemolytic Anemias what is it generally and 7 types

A 
Peripheral destruction 
= high BM production of reticulocytes
1. G6PD deficiency 
2. Hereditary Spherocytosis 
3. Hemolytic anemia from trauma 
4. Immunohemolytic anemia
5. Paroxysmal Npcturnal Hemoglobinuria 
6. Sickle Cell
7. Thalassemia
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13
Q

Hereditary spherocytosis is what

A

Inherited mutation in RBC cytoskeleton spectrin
Small pieces on the plasma membrane bud off over time and makes the RBC small and round (small dark cell)
= high risk of hemolysis

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14
Q

Hereditary spherocytosis causes hemolytic anemia how

A

They are inflexible and unable to bend trough the vessels + MAINLY the spleen M eat them
= splenomegally + hypersplenism (many M made)

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15
Q

Hereditary spherocytosis TX

A

Take the spleen out

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16
Q

Hereditary spherocytosis on blood smear

A

Round and dark with no central pallor
Have Howell Jolly bodies if spleen is removed (DNA inclusions that the spleen normal removes) = a dot that is dark and small the RBCs

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17
Q

Hereditary spherocytosis SX

A

Anemia (normal MCH, high MCHC, low MCV)
Jaundice
Splenomegaly
Can be mild

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18
Q

Hereditary spherocytosis what can be life threatening

A

A Parvovirus B19 which attached Proerythrooblasts can cause an aplastic crisis, with extremely low RBCs extremely anemic

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19
Q

G6PD deficiency is transmitted how and in what populations usually

A

X- linked + homozygous carriers can have SXs
Sub-Saharan Africa
Mid East
Mediterranean

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20
Q

G6PD deficiency is what

A

G6PD makes NADPH which gives its electrons to make GSH (glutathione which is important to reduce free radicals)

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21
Q

G6PD deficiency causes hemolytic anemia how and when

A

When the conditions in body makes a lot of free radicals (a few days after, not immediately after:

  1. Stress
  2. Drugs (anti-malaria….)**
  3. Foods like favs beans (favism)
  4. Infections
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22
Q

Heinz bodies

A

Oxidative damaged proteins in the cells that climb together

Chopped out by the spleen

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23
Q

G6PD deficiency is found in the aftercare Middle East and Mediterranean for what reason

A

Protects them from Plasmodium falciparum infection

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24
Q

Sickle Cell Anemia is caused how

A

They have a B-chain mutation = HgS (normal HgA + HgB)

Mutation is GAG ——> GTG (Glu—> Val)

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25
Q

Sickle Cell Anemia Ss and SS and Ss

A

Heterozygous = SC trait
Homozygous SS = SC disease/anemia
Homozygous Ss = no SC

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26
Q

The populations that have a high chance of having Sickle Cell Anemia (HgS) can also be found to have what other hemoglobin modifications

A
  1. HgbC

2. B-thalassemia

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27
Q

Sickle Cell Anemia have RBCs that prefer and especially under what conditions

A

Polymerization

  • Hypoxia
  • ICF dehydration
  • Low pH = low O2 affinity
  • sluggy blood
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28
Q

Sickle Cell Anemia polymerization can cause what to happen

A

The polymerizartion causes hemolysis of the RBCs and that causes occlusion of small vessels causing more hypoxia in certain areas

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29
Q

Sickle Cell Anemia RBC 2 main properties

A
  1. Dense long polymer inside

2. Sticky surface from membrane damage

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30
Q

Sickle Cell Anemia SX

A
  1. Acute resp distress
  2. Acute chest syndrome
  3. Asymptomatic bone necrosis (marrow emboli can happen)
  4. Infarction of spleen (severe infection from capsular bacteria)
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31
Q

SC disease has what kind of hemoglobin

SS disease has what kind of hemoglobin

A

HgS + HgC = milder

HgS only = Sickle Cell Anemia

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32
Q

SC disease does what tho RBC

A

NO polymerization, the HgC crystallizes instead
They look like misshaped blobby RBCs (poikilocytes) + cells with pallor around the edge no in the center(Target cells)
Same risks and complications as SS only less severe

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33
Q

Sickle Cell Anemia TX

A
  1. Hydroxyurea : increase HgF

2. CRISPR gene editing

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34
Q

Thalassemia locations its found

A

Around Mediterranean Sea and some of Africa and Middle East

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35
Q

B- Thalassemia MAJOR what happens

A

The HgA aggregate and form clumps inside the RBCs (due to no normal HgB) + (hypochromic)

  1. Spleen hemolysis = hemolytic anemia
  2. Ineffective making of RBCs in BM = hemolysis in the BM (hypoproliferative)
  3. High Erythropoietin = BM expands
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36
Q

HgA and HgB are made from how many genes

A

A : 2 chr having 2 alleles = 4

B : 2 chr having 1 alleles = 2

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37
Q

B- Thalassemia is what

A

You can have 2HgA + 1 HgB = MINOR/ Trait
OR
2HgA + 0 HgB = MAJOR

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38
Q

Ineffective erythropoiesis can cause what to happen

A
  1. BM expands

2. Increased FE is taken into body = Fe overload (hyperchromatosis)

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39
Q

B- Thalassemia MINOR what happens

A 
Mild
Mycrocytic anemia (confused itch Fe deficient anemia)
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40
Q

Microcytic anemia from B- Thalassemia minor vs Fe deficiency

A

B-th Minor : high Ferritin, normal or high Fe levels, normal transferrin
Fe D: low ferritin, Transferrin, Fe levers

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41
Q

a- Thalassemia different types and severity

A
  1. aaaa = normal
  2. a*aaa= asymptomatic carrier
  3. aaaa= asymptomatic a-thal minor (mild microcytic anemia)
  4. aaa*a= HbH disease symptomatic and microcytic+hemolytic anemia, splenomegally)
  5. aaaa = fetal hydrops no life
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42
Q

a- Thalassemia with HbH disease what happens

A

Only 1 normal a-globin ——> you get 4HbB tetramer = HbH
It has highh affinity for O2 and cant deliver properly
= anemia and splenomegaly

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43
Q

a- Thalassemia with all 4 a-globins gone causes

A

Fetal hydrops = Hb Bart’s disease

  1. Rely on embryonic Hb that is BAD at delivering O2 = fetal hypoxia + anemia
  2. heart try’s to compensate = edema and effusion
  3. Liver and spleen try to compensate = enlarge
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44
Q

Paroxysmal Nocturnal Hemoglobinuria (PNH) happens how

A

RBC have CD55 + CD59 on membrane to —I complement

  1. Mutation in the PIGA gene = no CD55/59
  2. MAC complexes form on RBCs = blood urine
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45
Q

PNH is transferred how

A

Acquired on X-chr on hematopoietic stem cells so it effects all blood cells
= can lead to not just hemolytic anemia, however also WBCs involved can cause AML + MDS

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46
Q

PMS pt can also have

A

AML and MDS

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47
Q

PNH Sx

A
  1. Wake up and have blood in urine since at night blood pH lowers and MAC form more easily
  2. Thromboembolism (portal, cerebral, hepatic)
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48
Q

PNH TX

A
  1. Eculizamab ——I C5–>C5a

= prone to get Neisseria infection (esp Neisseria meningitis)

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49
Q

Immunohemolytic anemia can happen in what 3 ways

A
  1. Idiopathic = autoimmune hemolytic anemia
    WARM Ab
  2. Idiopathic = Chronic hemaggulutinin disease
    COLD Ab
  3. Mismatched blood transfusion (hemolytic D of newborn)
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50
Q

Coombs test : indirect and direct

A

I : test Ab in plasma

D : test Ag on RBCs

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51
Q

WARM hemolytic anemia

A

IgG : more active in hot temps
Bind to RBCs to opsonizing them in spleen or phagocytoced
- Autoimmune or drug related

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52
Q

COLD hemolytic anemia

A

IgM : stronger affinity at low temps
Usually on nose and fingertips (Raynaud phenomena)
IgM makes C3b opsonizing cells removed then by spleen and liver and BM

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53
Q

WARM Hemolytic Anemia looks like what on blood smear

A

Kinda like hereditary spherocytosis
Round dark small cells
(RBC have Ab damage and condenses the cell)

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54
Q

Hemolysis from RBC trauma

A
  1. Mechanically : prosthetic heart valve (causes laser cells that look similar to SS)
  2. Microangiopathic hemolytic anemia : DIC, TTP/HUS-> thrombosis
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55
Q

Megaloblastic anemia what is it

A

Big cells of blood cells of many types (large N)

  • NO Folate or B12 effects DNA of RBCs and other cells
  • increased erythropoietin makes BM to increase synthesis however cant due to DNA impairment = hypercellularity in BM, still low reticular count in periphery
56
Q

Megaloblastic anemia looks like what under blood smear

A
  1. Low Hb, low Hct,

2. High MCV macrocytic (when lymphocyte is not larger then the RBCs on the smear you know)

57
Q

How does B12 help make DNA

A

B12+ Methyl THF ——> 5,10-methylene THF polyglutamate

58
Q

Pernicious anemia is what

A

Autoimmune disorder attacking the parietal cells of the IF itself

  • seen in older adults usually
  • lymphocytes attacked
59
Q

Stomach cells that you see with Precarious an

A

Goblet cells are seen which should only be in the intestines
You see an accumulation of lymphocytes below the mucosa

60
Q

Megaloblastic anemia SX

A
  1. Atrophic glossitis : on tongue removed papillae and easy infection (when B12)
  2. Gait or balance issues —> spinal demyelination in posterior and later nerves, taste, smell and visual changes, dementia
  3. Anemia
  4. Gastric problem (if B12)
61
Q

Pernicious anemia DX

A
  1. Megaloblastic anemia
  2. Low B12
  3. IF Abs
  4. HIGH Homocysteine + HIGH MM Co-A
62
Q

Folate Deficiency happens how

A
  1. Pregnancy —> Neural tube defects
  2. Marrow hyperplasia
  3. Methotrexate
  4. X absorption = sprue
  5. Infancy, poor diet, alcoholism
63
Q

Folate Deficiency DX:

A
  1. Megaloblastic anemia
  2. Low red cell folate measured
  3. HIGH Homocysteine
64
Q

Fe deficiency anemia on blood smear

A
  1. Microcytic
    2 hypochromic : low Hb
  2. Hypoproliferative (due to low Fe)
  3. ANISOCYTOSIS
65
Q

When Fe comes into body where does it go

A
  1. Marrow : stored as ferritin OR put into HgB on RBCs

2. Blood : by binding to Transferrin which carries it to the marrow

66
Q

Hepcidin does what

A

BLOCKS FERROPORTIN from bringing Fe into the blood from the mucosa cells that it was stored in = this Fe gets pooped out

67
Q

What can mess with the role of Hepcidin

A

High inflammation in the gut ——> high levels of Hepcidin = low Fe absorption even when the body needs it

68
Q

Fe deficiency anemia causes

A
  1. Diet
  2. X absorption = sprue
  3. Increased requirements
  4. Chronic Blood loss
69
Q

Stages of Fe Deficiency anemia

A
  1. Ferritin Fe stores in BM decrease
  2. Ferritin Fe stores decrease even more and RBC start becoming hypochromic
  3. Sx of Fe deficiency start, no Fe stores in BM, anemia
70
Q

Fe Deficiency anemia SX

A
  1. Koilonychia : fragile nails with vertical stripes
  2. Alopecia : hair loss
  3. Atrophic glossitis (like pernicious anemia)
  4. Angular cheilitis (side of mouth skin is irritated and raw looking)
71
Q

Fe study of Fe Deficiency anemia shows what

A
  1. Low FE, ferritin, hepcidin
  2. High TIBC (total iron binding capacity)
  3. Marrow has less stained Fe
72
Q

What can look like Fe Deficiency anemia

A 
Anemia of chronic disease : 
1. Inflammation (immune disease, pernicious anemia) 
2. Malignancy 
3. Infection 
= THEY HORDE FE (won’t let them go)
73
Q

Reason anemia of chronic disease take Fe and does not give it

A
  1. Cytokines = hepcidin increases

2. Erythropoietin decreases for some reason

74
Q

What do you see in the anemia of chronic disease blood

A
  1. Low Fe in serum
  2. Low TIBC
  3. High ferritin (not from high Fe only from inflammation)
  4. A lot of Fe stained in the tissues in BM
75
Q

Aplastic Anemia is what and what do you see in BM

A

Only fat almost
Panocytopenia (all cells are low)
thrombocytopenia
Anemia

76
Q

Aplastic Anemia is caused usually because of what

A
  1. Drugs (chemotherapy, adverse reaction to NSAIDS or AB)
  2. Irradiation
  3. Viral infection
  4. Rare inherited Fanconi anemia (DNA repair defect, new stem cells destroyed by body, or new stem cells cant make right blood cells)
77
Q

Aplastic Anemia SX

A
  1. Bruising
  2. Anemic -> fatigue
  3. Febrile (low Granulosites)
  4. Leukopenia
78
Q

Aplastic Anemia BLOOD SMEAR

A

Normocytic + LIKE NO reticulocytes

79
Q

Aplastic Anemia DX how

A

Go to BM and see to rule out any other disorder (you should see mostly fat, no cells)

80
Q

Pure red cell aplasia happens when

A
  1. Autoimmune problem (usually thymoma) —> Myasthenia gravis

2. Parvovirus B19 infection (especially when the patient has hemolytic anemia)

81
Q

Myelophthisic anemia is what

A

Something is taking up space in the BM , preventing blood cells from maturing and being made

  1. Cancer (neuroblastoma)
  2. Necrosis
  3. Fibrosis
  4. Inflammation
82
Q

Myelophthisic anemia causes what and what do you see on the blood smear

A

Very abnormal cells if they manage to escape from the BM = LEUKOERYTHROBLASTOSIS : immature erythroid and myeloid cells

  1. Blast forms
  2. Early precursor cells
  3. Hypechromatic RBCs
  4. Abnormal shaped cells
83
Q

Stages of fixing a vascular injury

A
  1. Vasoconstriction : to direct blood away from the injury
  2. Platelet plug
  3. Coagulation cascade and stabilize plug
  4. Fibrolysis
84
Q

Primary disorder is caused by what and what are the common SX

A

Platelets dysfunction (vWF), vessel wall disfunction

  • skin and superficial bleeding
  • petechiae and eccymoses
  • immediate bleeding
  • Autosomal D = not as serious
85
Q

Secondary disorder is caused by what and what are the common SX

A

Coagulation disorder

  • deep bleeds in muscles and joints and tissues
  • Hematomas, hemarthroses (F8 deficiency)
  • Delayed bleeding
  • AR or X-linked - more serious
86
Q

Tertiary disorder is caused by what and what are the common SX

A

Fibronolysis factors are elevated

  • wounds and GI/GU tract bleeding
  • delayed bleeding
  • hematuria an menorrhagia
  • autosomal recessive
87
Q

How to see wall abnormalities

A

You have to look at History and PE

88
Q

How to see reduced platelets

A

CBC

89
Q

How to see function of platelets

A

Platelet function test, morphology

90
Q

How to see clotting factor abnormalities

A

PTT and PT

91
Q

Vessel wall disorders can happen from

A
  1. Aging : more fragile BVs
  2. Infections
  3. Ehlers Danlos
  4. Scurvy
  5. Cushing syndrome (high corticosteroids) or other steroids
  6. Hereditary Hemorrhagic telangiectasia (skin and GI mucosal bleeding)
  7. Perivascular amyloid : can happen in myeloma (periorbital bruising, raccoon eye from amyloid deposition)
92
Q

Thrombocytopenia

A

Low platelets that can be very low (below 150,000) and still have no sx
When it reaches 50,000 you see sx
At 20,000 you have spontaneous dangerous bleeds

93
Q

HIV - associated thrombocytopenia

A
  1. Infection goes to BM and it’s hematopoietic stem cells = no platelet production
  2. Auto-Ab against Platelets made
94
Q

Drug induced thrombocytopenia

A
  1. Myelosuppression : chemo, chloramphenicol, Penicillamine , Gold salts (for aplastic anemia) = no P made
  2. Drug- induced immune thrombocytopenia : Quinidine, Vancomycin, Heparin = destroy P in periphery by drug induced Abs
95
Q

Heparin and drug induced thrombocytopenia

A

Heparin binds to the PF4 complex which then binds to platelets
This causes IgG to come and opsonizing it
- thrombocytopenia + thrombosis

96
Q

Immune thrombocytopenia purpura

A

Autoimmune problem where Ab coat platelets and they can destroyed in the spleen

  • spontaneously (acute or chronic, chronic harder to tx)
  • viral (Hep, HIV)
  • SLE
97
Q

Immune thrombocytopenia purpura SX

A

Petechiae and purpura
CBC = low platelets
Platelet Ab stain can be + or sometimes - : so best thing to do is look at BM and see INCREASED MEGAKARYOCYTES

98
Q

Immune thrombocytopenia purpura TX

A
  • corticosteroids
  • IVIg
  • Anti-CD20 ( Rituximab) -> attacks B-cells
99
Q

Thrombotic microangiopathies : TTP/HUS

A

Non- immune destruction of platelets

  1. Thrombotic thrombocytopenia
  2. Hemolytic Uremic Syndrome
100
Q

Thrombotic thrombocytopenia (TTP) SX

A 
Fever
Thrombocytopenia 
Microangiopathic hemolytic anemia 
Neurological defects
Renal failure 
=PENTAT ****
-more in adults
101
Q

Hemolytic Uremic Syndrome (HUS) SX`

A
  1. Same SX as TTP however more Kidney problems then brain problems
  2. More in kids
102
Q

TTP and HUS happens how

A
  1. An exaggerated platelet plug forms and consumes all platelets
  2. RBCs sheat and burst when they hit themselves against the platelet bumps in the vessels
103
Q

TTP and HUS on Blood smear

A

You see

  • no platelets
  • some uncleared RBC due to mature RBCs getting sheared
  • schistocytes : sheared RBCs
104
Q

What exactly happens in TTP

A

The vWF and platelets make the platelets plug and the PROTEASE is what prevents the plug from growing too big
** ADAMTS13 mutation on protease so body has Abs against it = X protease
= microvascular thrombosis

105
Q

TTP TX

A

Plasma exchange therapy

Exchange all plasma with new plasma what has no ADAMS13 mutation on the protease

106
Q

HUS what exactly happens + initial SX

A

From the shiga- like toxin from E. Coli O157: H7
= bloody Diarrhea
* check if there is thrombocytopenia, Microangiopathic hemolytic anemia, and renal insufficiency = HUS TRIAD**

107
Q

HUS TX

A

To infection and hydrate them

108
Q

No platelet adhesion caused by

A
  1. Bernard Soulier (Gp1b R)

2. vWF factor disease (vWF)

109
Q

No aggregation of platelets

A

Glanszmann thrombocytopenia (Gp2b-3a)

110
Q

No granule (ADP, thromboxane release) =

A

Storage pool disorders, Factor 5, vWF, ADP, thromboxane

111
Q

Acquired platelets function problems

A

Uremic acid : platelets to tank (Uremia)

Aspirin

112
Q

Grey Platelet Syndrome is what

A

X a-granules in the platelets

(They contain , Factor 5, vWF, fibrinogen)= bleeding, big and grey and no granules in platelets blood smear

113
Q

vWF in secondary Hemostasis

A

vWF in circulation binds to F8 and carries it to the platelet plug and then it can convert F10 —> F10a

114
Q

vWF D not enough of this

A

Type 1 and Type 3(worse has absolutely no vWF = coagulation and platelet disorder )
1C= makes it only it gets rapidly broken down and cleared

115
Q

vWF D qualitative

A 
Type 2 ( 2A no multimer forming)
Defected ligand factors
116
Q

Hemophilia SX

A

Arthrphathy
Hemorrhage in retroperitoneaum or soft tissues
Muscle hematoma

117
Q

Hemophilia A and B

SX

A 
A : F8
B : F9
- deep bleed after trauma
- isolated PTT
- X-linked
118
Q

Hemophilia A and B TX

A

Replacement factor or F8 or F9

119
Q

Plt : N
PT : N
PTT : HIGH

A
  • X F11
  • mild to moderate hemophilia A or B (injury bleeding)
  • mild vWF (spontaneous bleeding)
  • severe vWF, Hemo A/B (Severe spontaneous bleeding)
  • heparin, lupus anticoagulant (no bleeding)
120
Q

Plt : N
PT : High
PTT : N

A

X F7

121
Q

Plt : N
PT : High
PTT : HIGH

A
  1. X F2, F5, F10 (common pathway)
  2. Afibrinogenemia
  3. X F5+F8
122
Q

Plt : LOW
PT : High
PTT : HIGH

A

DIC (Disseminated Intravascular coagulation)

Liver disease

123
Q

DIC (Disseminated Intravascular coagulation)

A
  1. Thrombohemorrhagic disorder (too much spontaneous coagulation formation , thrombi)
  2. Consumptive coagulation (bleeding, no coagulation lefts to fix it)
    = widespread thrombosis all over in tiny vessels
124
Q

DIC (Disseminated Intravascular coagulation) caused by

A

Too much tissue factor released

125
Q

DIC (Disseminated Intravascular coagulation) SX

A
  1. Consumption of all clotting factors
  2. Ischemia tissue damage
  3. Bleeding (X coagulation, + thrombosis activated plasmin = fibrinolysis)
126
Q

DIC (Disseminated Intravascular coagulation) can cause what to happen

A
  1. Black fingers and toes

2. Hemorrhage of the adrenal glands = Waterhouse- Friderichsen Syndrome

127
Q

DIC (Disseminated Intravascular coagulation) DX

A
  1. Low PLT
  2. HIGH PT and PTT
  3. HIGH D-dimes (product of plasmin lysine coagulation factors = fibrinolysis)
128
Q

transfusion screens for what

A
  1. Donor HEP, HIV

2. Blood tested for : HIV, HBV, West Nile, Zika, chagas, syphilis, hcv, htlv

129
Q

How can a donors blood get infected

A

Sometimes especially platelets that are stored at room temperature can get infected by bacteria if contaminated in any way
= recipient gets hypotensive and febrile immediately during trasnfusion

130
Q

Acute immune hemolytic reaction happens how and when

A

If mismatched blood type happens

- by IgM antibodies

131
Q

What does it mean o be A- or B- or AB-

A

You are Rh- and you have Anti- D Ab

Rh+ has no Anti-D Ab

132
Q

Delayed immune hemolytic reaction happens how and when

A

During transfusion or mixing of blood that is Rh+ and Rh-
= makes IgG, so the first time its exposed it is fine only the second time there will be hemolysis and problems
(ESP Rh- mom and Rh+ fetus)

133
Q

2 types of delayed immune hemolytic reaction

A
  1. Rh+ fetus and Rh- mom
  2. IgA deficiency patient getting a blood transfusion
    = uses IgG
134
Q

IgA deficiency patient getting a blood transfusion what happens

A

The pt has Anti-IgA IgG-antibodies that attack any IgA that it gets from any transfusion
= anaphylactic reaction
= you need was the blood before giving it

135
Q

Acute Lung Injury (TRALI)

A

Transfusion related

= inflammation and infiltrates start to accumulate in the lungs of recipient (acute resp failure)

136
Q

Acute Lung Injury (TRALI) SX

A

Difficulty breathing
Fever + Hypotension (mimicking sepsis)
= during or after transfusion

137
Q

Immune modulation (TRIM)

A

Transfusion related
When a pt is being transfused :
1. Immune system is somewhat pro-infammatory state always
2. Immune system is also downregulated from pathogens and things happening in the body that actually need to be taken care of due to being distracted by the transfused entities
** really make sure patient needs a transfusion, PROS over CONS

Skin, Lymph, Blood (9 decks)

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