Martin: Transfusion Medicine Flashcards
1
Q
RBC membrane contains what?
A
- Proteins: Rh antigens
- Carbs: ABO system
2
Q
What are the primary and secondary response to immunization to RBC antigens?
In other words, how do we develop antibodies to antigens that we DON’T have?
A
1. Primary response: Occurs after 1st immune exposure to a “foreign” protein Ag (days or weeks after exposure)
2. Secondary (anamnestic) response: occurs upon a repeat exposure to a “foreign” protein Ag (noticed much quicker after such exposure); For example, during a transfusion.
3
Q
For most Blood Group Antigens, but not ABO, what type of AB develop during a primary and secondary response?
A
- Primary response = a sustained high concentration of IgM + Ab and some IgG after days or weeks
- Secondary response = transient rise in IgM and a sustained IgG
4
Q
What antigens make up ABO system?
A
- 1. H
- 2. A
- 3. B
5
Q
What antigens make up the following blood types:
- O blood
- A blood
- B blood
- AB blood
A
- 1. O blood = H Ag only
- 2. A blood = H + A
- 3. B blood = H + B
- 4. AB blood = H + (A+B)
6
Q
What is a secretor, in blood bank terms?
A
Someone with “Se” allele, which allows them to make ABO antigens in their secretions and plasma.
7
Q
Roughly 80% of the population carries at least one allele called “Se.”
What is this allele?
A
“Se” => produces H antigen on “type 1 chains” (long carb-rich chains).
- Once the H antigen is made, then the person can make either A or B antigens (or both) on the type 1 chains
8
Q
What is the MC type of blood?
Least common?
A
- Most common: Type O (45%)
- Least common: AB
9
Q
Antigens & Antibodies in person with Type O blood.
A
- Antigens = H
- Antibodies =
- Anti-A
- Anti- B
- Anti- AB
10
Q
Antigens & Antibodies in person with Type A blood.
A
- Antigens = H + A
- Antibodies = Anti-B
11
Q
Antigens & Antibodies in person with Type B blood.
A
- Antigens = H + B
- Antibodies = Anti-A
12
Q
Antigens & Antibodies in person with Type AB blood.
A
- Antigens = H/A/B
- Antibodies = None
13
Q
What are Subtypes of
A
14
Q
What are the 2 steps in Blood Typing?
A
- “Front/forward typing” = determines which antigens are on the patient’s RBC by mixing patients blood with anti-A/B/D antibodies
-
“Back/reverse typing” = test for isohemagglutinins (antibodies against ABO antigens they do NOT have), like Anti-A/anti-B.
- Serum or plasma that was separated from the pts RBC is mixed with two different red cells from the laboratory (A and B cells)
15
Q
ABO subtypes exist and pose what problem?
A
Can cause compatability issues when transfusing a patient.
16
Q
What disease can alter expression of ABO antigens on the RBC?
A
- 1. Leukemia = ↓ Ag
- 2. “Acquired B” = Intestinal obst → ↑ bowel permeability, bacterial
polysaccharides into circulation abs = orbed by grp A cells
- 2. Gastric or pancreatic cancer = bld grp specific soluble substances (BGSS) in serum neutralizes antisera used in forward grouping.
17
Q
What is Bombay phenotype?
What is the problem with this phenotype?
A
- Rare blood type (Oh/ h/h) where patient lacks H antigen. Thus, RBC has NO antigens.
- Antibodies: anti-A, Anti-B, Anti-AB and Anti-H Ab.
- Problem
- Can donate to ANYONE
- Can ONLY receive Bombay blood.
18
Q
What happens when a patient with Bombay phenotype receives a blood transfusion?
A
Anti-H IgM Ab (more common than IgG) activates compliment system => intravascular hemolysis of RBC => acute hemolytic transfusion reaction.
19
Q
What is a complication in mothers with Bombay phenotype?
A
Hemolytic disease of the newborn can occur (Oh, h/h)
20
Q
Type O blood can donate blood to who?
A
All types.
21
Q
Type A blood can donate blood to who?
A
- Type A
- Type AB
22
Q
Type B blood can donate blood to who?
A
- Type B
- Type AB
23
Q
Type AB blood can donate blood to who?
A
- Type AB
24
Q
What is the Rh (Rhesus) System?
A
NOT naturally-occuring antibodies made d/t exposure of a antigen during pregnancy or transfusion. 5 most important antigens are
- D (Rhesus factor/Ag)
- “d”= absence of D
- C = co-dominant with c
- E = co-dominant with e
25
1. **Rh (+) =**
2. **Rh (-) =**
What is the most common?
1. **Rh (+)** = has D antigen\* (MC)
2. **Rh (-)** = lacks D antigen
26
1. Do Rh (-) people develop anti-D Ab?
2. If so, what type of Ig are they?
3. What problem can develop if Ab develop?
1. Antibodies **only** develop if **pt is exposed to D+ RBC**, like in transfusions and during pregnancy if mom is D- and baby is D+ (hence, NOT naturally occuring Ab)
2. **IgG** anti-D Ab
3. IgG anti-D Ab can cross placenta and **Newborn Hemolytic Disease (Hydrops fatalis):**
1. Occurs if mom is Rh(-) and bb is Rh(+) or if dad and bb are _both_ (Rh+):
2. 1st pregnancy: Mom is exposed to Rh(+)/D+ RBC when baby is delivered and develops IgG anti-D Ab.
3. 2nd pregnancy: IgG anti-D Ab =\> cross placenta =\> attack bbs RBC if the 2nd bb is also Rh(+)/D+.
27
Test to determine if **mom** has **anti-D IgG Ab?**
**Indirect Coombs Test:**
1. Mix **moms serum** + **D+ RBC**
2. **(+)** = mom has anti-D+ IgG aB
1. RBC will agglutinate
3. **(-)** = mom does NOT have anti-D IgG aB
1. RBC do NOT agglutinate
28
What is **RhoGAM?**
What findings will be seen after administration?
**RhoGAM** = _anti-D Ig_ medication that prevents _Rh immunization_ in pregnancy or obstretrical complication, a condition where Rh(-) mom develops Ab after exposed to Rh(+) blood.
Transatory increase of passively transferred Ab in the patients blood will cause positive serology testings results.
29
1. What are other antigens on the RBC?
2. When are they tested for?
3. How do AB against these antigens develop?
1. Kell, Duffy, Kidd, MNS, Lewis, MNS
2. Only tested when patient has ABNL screening tested
3. Ab only develop during pregnancy or transfusion (thus, NOT natural. ONLY natural are A/B antibodies)
30
1. What is the **Kell antigens on the surface of RBC?**
2. What is their importance?
3. Most common phenotype?
1. Antigens =
* **1. K = kell**
* **2. k= cellano**
2. 2nd in immunogenicity (2nd most targeted antigens, D).
3. MC phenotype = **kk** (91%)
31
What alloantibodies develop to **Kell antigens?**
When does this cause a problem?
**Anti-K _IgG_ alloantibody**.
* No Kell antigen =\> Anti-K IgG AB develop during transfusion/pregnancy with blood containing that antigen.
* Can cause
* **1. HDN**
* **2. Hemolytic transfusion rxn**
32
Kell system **McLeod phenotype i**s associated with what diseases (2)?
1. **Chronic compensated hemolytic anemia** = presence of acanthocytes on blood smear.
2. **Chronic granulomatous disease (CGD)** = Lack K Ag on neutrophil/monocytes membrane =\> deficiency of NADH-oxidase =\> no H2O2 to destroy microbes = \> increase risk of bacterial infections.
33
What are the **Duffy Antigens?**
**Duffy glycoprotein** = receptor for malarial parasite Plasmodium vivax.
Antigens =
* 1. Fya = Duffy(a)
* 2. Fyb = Duffy (b)
34
What is the MC **Duffy** phenotype in African-Americans?
What does this imply?
**Fy (a-,b-)** = resistant to Plasmodium vivax infection
35
What antibodies are produced against **Duffy antigens?**
What problems can they cause?
**IgG** =\> cause _HDN_ & _hemolytic transfusion rxn_
36
What are the **MNS antigens?**
## Footnote
**-** Antibodies?
- Exhibits what effect?
* **4 important antigens:** M, N, S and s
* **Antibodies**: Anti-M **_IgM_** antibodies, but non-hemolytic
* **Dosage effect** = react more strongly with homozygous cell, than hetero
37
* What are **Kidd antigens?**
* What antibodies develop to antigens?
* What problems does it cause?
* Antibodies exhibit ____ phenomenon.
1. **Antigens** = Jka/Kidd (a) and Jkb/Kidd (b)
2. **Antibodies** = anti-Jka **IgG ab** and anti-Jkb **IgG ab** = common, but low titers and weak, so they disappear quickly.
3. Causes
* **Delayed Hemolytic Transfusion reactions**: (+) compliment =\> rapid hemolysis. Then, Ab disappear and reappear when transfusion with Kidd
4. **Dosage phenomenon**
38
What blood type is the **universal recipient/donor?**
* **Universal recipient:** AB+
* **Universal donor:** O-
39
What is the MC complication of **transfusions**?
**Febrile nonhemolytic reaction** = inflammatory reaction where Ab react to antigens on donor leukocytes that occurs due to pyrogenic cytokines that develop in products during storage , causing:
* _Fever (1C or \>)_, _chills,_ _HTN_ ± dyspnea **within 6 hours** of a transfusion of red cells or platelets.
40
**_Febrile non-hemolytic reaction_**
1. DDx
2. What increases risk?
3. Treatment?
4. Prevention?
1. DDx
1. Hemolytic transfusion reaction
2. TRALI
2. Storage age of the product
3. Tx = Symptoms are short-lived;
1. Treat with antipyretics
2. NO ASA
4. Prevention:
1. pre-medicate with anti-pyretic,
2. pre-storage leukocyte reduction,
3. plasma reduction or wash PC
41
**RBC** only last ___ days
**Platelets** only last ___ days
**Plasma** may be frozen and stored for ___ year.
* Red blood cells only last **42** days
* Platelets only last **5** days
* Plasma may be frozen and stored for **1** year.
42
Other complications to **transfusions**
1. **Allergic reaction**
2. **Hemolytic reactions** (acute and delayed)
3. **Transfusion-realted acute lung injury (TRALI)**
4. **Infectious reactions**
43
**_Allergic reaction d/t transfusion_**
1. Who is this more likely to occur in?
2. How does it occur?
1. **Previously sensitized recipients (**MC in people with **_IgA deficiency)_**
2. **IgG Ab** recognize **IgA** in infused blood =\> **allergic reaction**
1. **Uticarial allergic reactions** can occur when recipients **_IgE Ab_** recognize allergen in blood.
44
What are symptoms of Allergic reaction to transufion?
SX: pruritis, urticaria, erythema, & cutaneous flushing.
* If upper airway=\> laryngeal edema (hoarse + stridor + lump in throat)
* if lower airway =\> bronchonstriction (wheeze, tightness, dyspnea)
*
45
**_Allergic reaction during transfusions_**
1. DDx
2. Tx
3. Prevention
1. **DDx** = drug reaction, allergy to tape/latex
1. If dyspnea, R/O TRALI and volume overload
2. **Treatment =**
1. intubate and O2 prn
2. IV antihistamine
3. do NOT have to DQ transfusion.
3. **Prevention**
1. Premedicate with antihistamine
2. Cant ID Ag, so cant select Ag- neg products, except in IgA deficiency.
46
Treatment/prevention of a **_severe_** anapylactic reaction?
1. Treatment = same as allergic reaction + **EPI,** **diphenhydramine** (if _cutaneous_ sx) and **Aminophylline** (if _bronchospasm_)
2. Prevention =
1. IgA def pt have anti-IgA ab, so give products with NO IgA.
2. Pre-med with antihistamine/ steroids
47
**_Acute Hemolytic Reactions due to transfusions_**
* Caused by?
* Most common cause?
* **Pre-formed IgM Ab** react to donor cells, causing compliment-mediated _intravascular hemolysis_ within **24 hours** of tranfusion.
* **MCC** = Human error (problem in patient ID/ tube labeling), causing RBC incompatability
48
**_Acute Hemolytic Reactions due to transfusions_**
1. IgM Ab that react to donor antigens cause what?
2. Symptoms?
3. Tests?
* Cause _complement-mediated intravascular hemolysis_ & _hemoglobinuria_.
* **Symptoms**: _Fever_, _hypOtension_, and flank pain appear rapidly.
* Can progress to _DIC_, shock, acute renal failure, and death.
* **Test**: (+) direct Coombs test
49
Mortality and DDx of **Acute Hemolytic Transfusion Reaction**
1. Mortality depends on amount of RBC transfused
2. DDx= **AIHA**
50
Treatment and prevention of **AHTR**
**Treatments**
1. DQ and verify ID (another patient may be getting a wrong product.
2. If severe, CV support, fluid resucittaiton, presso
**Prevent** = Properly ID patients!
51
**_Delayed Hemolytic Reactions due to transfusions_**
* Caused by?
* Most common cause?
* **Caused by** = _IgG_ antibodies from prior tranfusion/exposure to foreign protein antigens =\> _extravascular hemolysis_ tht occurs \>24 hours - 2 weeks after transfusion
* **MCC** = prior blood transfusions
52
**_Delayed Hemolytic Reactions due to transfusions_**
* Associated labs and tests?
* Ab to antigens like Rh, Kell and Kidd can cause what?
* DHTR can cause _____ in what sickle cell patients
* **Labs/tests**
1. (+) Direct Coombs test
2. Hemolysis: ↓ haptoglobin, ↑ LDH, rise in unconjugated Hgb
3. ↓ H&H
4. Detection of new RBC Ab\*\*\*\*\*
* **(+) compliment =\> severe and fatal reactions.**
* **Sickle cell crisus**
53
**_DHTR_**
1. Treatment
2. Prevention
1. **Most tolerate well, observe patient**
1. If extravascular hemoslsis occurs =\> IVIG
2. **Prevention** = detect RBC AB via serology
54
What is **Transfusion-related acute lung injury (TRALI)?**
Severe, often fatal complication that occurs **within hours of tranfusion** where factors in transfused blood activate **MHC-I Ag on neutrophils** in the lungs that occurs MC in
1. Patients with lung disease
2. Multiparous women.
3. High levels of donor antibodies (fresh frozen plasma and platelets)
55
What is the pathogesnsis of **TRALI**?
“Two hit” hypothesis.
1. 1st hit = priming event that leads to neutrophils in lungs
2. 2nd hit =
* Transfused AB recognize antigens on **neutrophils** via **MHC Class 1 antigens**, which are most often found on **multiparous women**
56
Clinical Presentation of **TRALI**
1. **Sudden onset respiratory failure**, during or soon after a transfusion.
2. CXR = **non-cardiogenic pulmonary edema (d**iagnostic and resolves in 48-96 hours)
3. **NO** ABNL breath sounds and **NO** signs of cardiac failure.
57
**Treatment and prevention of TRALI**
**Treatment** =
1. Antipyretic and fluids to tx HTN and fever
2. Supportive
**Prevention** =
1. _↓ lipid mediators_ by _pre-storage leukocyte reduction_ or ↓ storage time of cellular components, esp _platelets_
58
**Bacterial contamination** is much more common in _platelet/RBC_ preparations. Why?
**Platelets:** platelets (unlike red cells) must be stored at _room temperature;_ which favors growth of bacteria
59
Most **bacterial infections** transmitted through transfusions are \_\_\_\_\_, indicating what?
**Skin flora,** indicating that contamination occur when product was obtained from donor.
60
**Bacterial contamination** during transfusion depends on what?
**Type and storage of what you are tranfusiing.**
1. **Yersenia entercolitica** and pseudomonas = in PC
2. **Staph, strep, E.coli** and **serratia** = platelets
61
Symptoms of infection due to transfusion
* **Fever, chills, hypotension**: resemble symptoms seen in hemolytic/ non-hemolytic transfusion reactions.
62
Viral infection via blood products has decreased.
However, when can it occur and what viruses are more commonly transmitted?
1. When the donor is acutely infected, but the virusDNA/RNA cannot be detected.
2. HIV, hepatitis C, and hepatitis B.
63
To donate blood, how old do you have to be and what requirements do you have to meet?
1. **16 YO.**
2. **Weight/Hb** level requirments must be met
64
What are reasons you can be denied being able to give blood?
1. Receipient of dura mater graft
2. Transfusion of blood or blood components within the previous 12 months, or human-derived clotting factors within the previous 12 months
3. Incarceration under certain circumstances
4. Getting a piercing or tattoo with nonsterile materials within the previous 12 months
5. Certain medications
6. Pregnancy
7. **Needle use for not anything prescirbed**
8. **HIV+**
9. **Hep since 11YO**
10. **Babesiosis, Chagas, CJD, cCJD**
65
Who is responsible for all aspects of donor selection and donor safety?
**Blood bank medical director**
66
How are specimans collected and what must the speciman include?
1. Collected at beside
2. Must include the time + date + initial of phlebotomist.
3. Each patient must have a permenant and unique ID
67
What are common tests performed prior to **transfusions**?
* **1. Blood type testing** (Forward/front typing = mix pts RBC + antibody =\> agglutination will indicate presence of antigen on RBC)
* Example: Pt RBC + anti-A ab: if agglutination occurs, pt is A(+).
* **2. Type and screen (T&S)**
* **3. Cross match**
68
What is performed in a **Type and Screen (T&S) test?**
When is it performed?
1. **Determine ABO + Rh of patients RBC**
2. **Antibody screening test** = screen for Ig Ab to rare antigens via _Indirect Antiglobulin Test (IAT/ Indirect Coombs test),_ which will only be present if prior exposure.
1. If (+), perform _Ab indentification_ to ID specific antibodies.
3. Perform when transfusing
69
What is a **Type** and **Crossmatch test (type and cross)?**
* Match donor blood to patients
70
How is a **Antibody Screen** done?
* Purpose
* How is test performed
* When is it performed
**_Indirect Antiglobulin Tests/ Indirect Coombs Test_**
**_Purpose_**: detects antibodies freely floating in patient to rare antigens, which only develop if prior exposure.
**_Test_**:
1. Mix **patients serum** (which contains Ig Abs) + **Reagent RBC/foreign RBC** (RBC with many antigens)
1. **(+)** =\> RBC agglutinate due to presence of antibodies. Next, perform other tests to determine the specific Ab present.
2. **(-)** =\> RBC do not agglutinate and NO Ab are present.
**When is it performed?**
1. Before blood transfusion to detect if a reaction will occur
2. Prenatal testing of PG women
71
What is a **Direct Coombs test?**
* Purpose
* How is test performed
* When is it performed
* **Purpose**: Test used to detect Ab/compliment proteins that are attached to RBC, which can destroy and cause anemia.
* **Test**:
* 1. Mix **pts RBC** + anti-human AB
* 2. (+) = \> agglutination occurs
* **When is it performed?**
* Detect AI hemolytic anemia
* Transfusion reaction W/U
72
What test is done if ABNL Ig are detected in the **T&S?**
1. **Antigen detection test =** determine specific antibody present in patient, not made by the patient.
2. Test =
1. Commercial anti-sera + patients cells
2. Confirms whether patient has antigens on cells.
73
What is the purpose of **IAT**?
What antibodies are detected at room temperature, 37 degrees and AHG?
Checks for **hemolysis** and **agluttination** against screening cells.
1. **Room temp** = Cold IgM Abs
2. **37 degrees** = warm Abs
1. IgG
2. Rh
3. Kell, Kidd, Duffy
3. **AHG** = Warm IgG Abs that coat RBC membrane
74
What is the MC autoAB?
Benign cold **IgM** agglutinin.
75
What is **Cold Agglutinin Disease?**
* **Intravascular hemolysis** that occurs in cold weather, which can activate **compliment** =\> cause **life-threatening hemolyic anemia** due to **Mycoplasma pneumonia** or **EBV** (infectious mono)
76
How is **Type and Crossmatching/Compatability testing** done?
**No agglutination or hemolysis = compatable!**
77
Who can receive donor **A** PC?
1. **A**
2. **AB**
78
Who can receive **donor B packed cells?**
1. B
2. AB
79
Who can receive donor AB blood?
**Only type AB blood**
80
1. When a transfusion is performed, what should you do to make sure an AE does not occur?
2. If it does, what do you do next?
1. **Monitor closely for the first 15 minutes** of transfusion and intermittingly during
2. If AE:
**1. Immediately stop transfusion!**
**2. Immediately report reaction to blood blank.**
3. Retrun bag with attached tubing + paperowrk
4. Send post-transfusion blood sample + urine (not as emergent)
81
When is **transfusion of RBC** indicated? (4)
* 1. ↑ in O2 carrying capacity (someone is hypoxic)
* 2. Hgb \<7 or Hct \<21 in healthy pt WITH acute anemia (bleeding)
* 3. Hgb is 7-9 in pt with cardio/cerebrovascular RF.
* 4. HbS is 30-50% in Sickle cell pts to prevent stroke.
82
**PRBC**
1. What is PRBC?
2. When is it indicated?
3. What are the expected effects?
4. CI?
1. RBC with plasma removed
2. Symptomatic anemia due to increase blood loss, ↓ survival or production
3. Effects: _+1-2g/dL Hb_ and _~3% Hct per_ unit in 24 hr
4. CI = Volume expansion, coagulation deficiency or drug treatable anemia
83
**_Platelets_**
1. When is it indicated?
2. What are the expected effects?
3. CI?
1. Bleeding d/t thrombocytopenia or prophylaxis in severe thrombocytopenia without bleeding (\<10,000 platelets)
2. _6_ pooled platelets in adults =\> **↑ plt count by 30-60,000**
3. CI =
1. Plasma coagulation deficit
2. Rapid plt destruction (ITP or TTP)
84
During **platelet transfusions,** what complication can occur?
* **Complications less likely** bc platelets only have ABO antigens and HLA-1, not Rh or HLA-2. But
* Rh exposure from RBC contamination can occur; may need RHIG
85
How many platelets are **pooled platets (6 single units, creating a 6 pack)?**
**5.5 x 10¹⁰/unit**
**+ fibrinogen + WBC**
86
What are **phersis platelets?**
Platetlets come from a ONE donor, which decreases exposure to single donors and increases platet retention = decreases risk of infections.
87
**_Fresh Frozen Plasma (FFP)_**
1. What does it contain
2. Indication
3. CI
4. Effect
1. All coag factors + 400mg of fibrinogen
2. **Indication** = deficiency of coag factor with or w/o bleeding
1. Prophylatic if PT/PTT are prolonged and pt is at risk of bleeding
2. Documented factor deficiency in bleeding patient
3. Isolated factor def for which factor derivative is not avail.
4. Emergent reversal of Warfarin
5. Tx TTP
3. **CI** = Volume expansion
4. **Effect**: PT/PTT normalize, 1 unit will increase factor level by 20-30%
Once thawed, must used within 24 hours or clotting factors degrade.
88
**_Cyroprecipitate_**
1. What it is?
2. Indications?
**What is it?** Thawed FFP that contain tons of fibrinogen + vWF + factor 8
**Indications** = Fibrinogen \<80 mg/dL with ongoing bleeding
1. Hemophilia A
2. von Willebrand’s disease
3. hypofibrinogenemia DIC
4. Factor 8 def
5. bleeding uremia patient
6. topical glue
89
How is **RhoGAM** administered?
1. 1 full dose (300mg) at 26-28 wks GA or within 72 hours of delivering Rh+ infant
* 1 mini dose (50mg) for termination or ectopic pregnancy before 12 wks GA
2. 1 full IM dose to prevent alloimmunization of 15 mL of Rh + RBCs or 30mL of WB
3. Rh IG _IV_ over 8 hours until full dose is reached
90
What should you do before administering blood and whta is the most important step in a SAFE transfusion?
1. Identification of Patient!!!
2. Verify unit
3. The most important step in safe transfusion is clerical verification!!
91
1. Infusion time: must be completed in \_\_\_
2. Unused units MUST be returned within \_\_\_\_
3. Only _______ can be transfused with blood!!
1. **4 hours**
2. **30 minutes**
3. **NL saline**
92
How are neonates transfused?
quad” packs
93
What is defined as **massive transufions?**
How is it done?
Problems?
Transfusion of RBC that amounts to full blood volume within 24 hrs: 1 unit of FFP for ever 2-3 units of RBCS
Usually 10-12 units in an adult per day
Problems:
1. Coagulopathy
2. Hypothermia
3. Hypocalcemia
94
fuck this lecture
