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Block 2 > Blood > Flashcards

Blood Flashcards

1
Q

Mediators of increased vascular permeability

A

histamine and serotonin
C3a and C5a
leukotriene C4, D4, E4

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2
Q

Mediators of vasodilation

A

histamine
prostaglandins

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3
Q

Mediators of chemotaxis, leukocyte recruitment and activation

A

TNF, IL-1
chemokines
C3a, C5a
leukotriene B4

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4
Q

Macrophage activator

A

interferon-gamma

macrophages are responsible for development of ceseating granuloma in TB infections

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5
Q

Mediators of fever

A

IL-1, TNF
prostaglandins

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6
Q

Mediators of pain

A

prostaglandins
bradykinin

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7
Q

Mediators of tissue damage

A

lysosomal enzymes of leukocytes,
reactive oxygen species (ROS)

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8
Q

Acute vs chronic inflammation

histology

A

Acute:
- neutrophils
- fibrin

Chronic:
- lymphocytes
- plasma cells
- macrophages

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9
Q

Types of necrosis and the organs typically involved

A

Liquefaction necrosis: brain
- tissue is completely digested and transformed into viscous liquid

Fat necrosis: pancreas
- release of pancreatic enzymes

Coagulative necrosis: liver, spleen, intestine
- underlying architecture of organ is preserved

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10
Q

Granulation tissue

A
  • fibroblasts
  • endothelial cells
  • may be inflammatory cells in the background as well
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11
Q

Hypersensitivity reactions 1-4

A

ACID:
Type I: Allergy

Type II: Cytotoxic
- where it binds

Type III: Immune Complex
- where it lands

Type IV: CD4 effector or Delayed
- everywhere it meets

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12
Q

Type I hypersensitivity

A

Immediate hypersensitivity:
- Th2, IgE antibody, mast cells, eosinophils
- mast cell-derived mediators (granulation) = immediate hypersensitivity reaction (minutes)
- rapid reaction: IgE antibodies are already bound to Fc-epsilon receptor on surface of mast cells
- cytokine-mediated inflammation = late phase reaction (2-24hr after repeat exposure)
- eosinophil recruitment = chronic allergic inflammation, major cause of tissue damage

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13
Q

Type II hypersensitivity

A

Antibody-mediated hypersensitivity:
- own cells (cell surface or extracellular matrix antigens) treated as encapsulated bacteria; get tagged with antibodies (IgG mostly) to be attacked by complement system (lysis) or leukocytes (phagocytosis)
- complement- and Fc receptor-mediated recruitment
- activation of leukocytes (neutrophils, macrophages) ==> opsonization and phagocytosis of cells
- abnormalities in cellular function (hormone/NT receptor signaling)
- usually tissue-specific <- issue is on what type of cell the binding event occurs (ex: hemolytic anemia)

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14
Q

Type III hypersensitivity

A

Immune complex-mediated hypersensitivity:
- immune complexes of circulating soluble antigens and IgG/IgM antibodies deposited in vascular basement membrane
- complexes are unable to be cleared; that is where inflammation occurs
- complement- and Fc receptor-mediated recruitment and activation of leukocytes
- tissue damage secondary to impaired blood flow
- vasculitis, nephritis, arthritis

Serum sickness:
- Deposition in the vasculature of the skin can produce hives through the production of C3a and C5a of the complement system which then activate local mast cells.
- A fever response is caused by release of IL-1 and IL-6 from blood monocytes that have taken up the immune complexes.

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15
Q

Type IV hypersensitivity

A

Delayed, T cell-mediated hypersensitivity:
- sensitization stage of 1-2 weeks
- takes 1-3 days to develop after re-exposure
- CD4+ (Th1, Th17) T-cells (cytokine-mediated inflammation) activate macrophages ==> inflammation
- CD8+ T-cells (T cell mediated cytolysis) direct target cell lysis and inflammation

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16
Q

TNF-a
IL-1

A

inflammatory cytokines that induce gene expression of adhesion molecules on endothelial cells, thereby recruiting leukocytes

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17
Q

tryptase

A

protease that causes tissue damage

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18
Q

leukotrienes C4, D4, E4

A

slow reacting substances of anaphylaxis; cause bronchoconstriction

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19
Q

leukotriene B4

A

chemotactic for neutrophils

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20
Q

bradykinin

A

pain

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21
Q

prostaglandin D2

A

promotes vasodilation and vascular leakage

also bronchoconstriction?

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22
Q

late phase response of allergy

A

T-cell response mediated by cytokines
- treat with glucocorticoid (Prednisone)

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23
Q

C3, C4, C5

A

complement proteins, but also anaphylatoxins that drive mast cell involvement

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24
Q

Erythropoietin (EPO)

A
  • produced in kidneys
  • major hormone regulator of erythropoiesis
  • promotes the proliferation, differentiation, survival of erythroid precursors
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25
Q

Iron deficiency anemia vs. anemia of chronic disease

A

Iron deficiency anemia:
- microcytic, hypochromic anemia
- low serum ferritin and iron
- can be due to loss of blood through GI bleeds

Anemia of chronic disease:
- can be normocytic or microcytic
- high serum ferritin
- chronic inflammation => increase in cytokines and hepcidin => reduced iron release from macrophages, reduced RBC synthesis from low erthropoietin levels, reduced RBC survival

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26
Q

Heme synthesis pathway

A

Occurs in liver and erythroid progenitor cells of bone marrow

First and rate-limiting step: ALA synthase
- glycine + succinyl CoA ⇒ ALA
- requires PLP (vit B6) cofactor
- regulated via: feedback inhibition (heme/hemin), repression of ALA synthase gene, inhibition of ALA synthase transport from cytosol to mitochondria

Last step: ferrochelatase
- last reaction ⇒ heme
- regulated by iron availability in bone marrow

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27
Q

Heme synthesis deficiencies

A

Vitamin B6 deficiency:
- Vit B6 (PLP) cofactor is requred for ALA synthase

Lead-induced anemia:
- lead binds to sulfhydryl groups in ALA dehydratase and ferrochelatase

Porphyrias: occur when body has problems making heme
1. AIP: acute intermittent porphyria
2. PCT: porphyria cutanea tarda
3. EPP: erythropoietic protoporphyria

28
Q

Acute intermittent porphyria (AIP)

A

Pathology:
- defect in porphobilinogen (PBG) deaminase (3rd reaction in pathway)
- porphobilinogen ==> hydroxymethylbilane

Symptoms:
- neurocognitive: fever, muscle weakness, intellectual disability, limb/head/neck/chest pain
- visceral: abdominal pain, vomiting/constipation
- second most common porphyria

Labs:
- PBG and 5-ALA accumulate in plasma and urine
- urine turns red after being left out

Treatment:
- IV hemin and glucose (negative feedback on ALA synthase)

“An Insane Person Peed Blue Dye”

29
Q

Porphyria cutanea tarda (PCT)

A

Pathology:
- deficiency in uroporphyrinogen decarboxylase (UDC) (5th reaction)
- uroporphyrinogen III ==> coproporphyrinogen III
- hepatic
- autosomal dominant
- precipitated by: alcohol, hepatic iron overload, sunlight exposure

Symptoms:
- photosensitivity due to porphyrin accumulation
- light-sensitive blistering, rash, increased hair growth
- most common porphyria

Labs:
- uroporphyrinogen III accumulates in urine

Treatment:
- sun avoidance, sunscreen
- decrease iron load
- chloroquine or hydroxychloroquine treat underlying cause

“People Can Tell U Drink Constantly”

30
Q

Erythropoietic protoporphyria (EPP)

A

Pathology:
- deficiency in ferrochelatase (last step)
- protoporphyrin IX ==> heme
- autosomal dominant

Symptoms:
- hemolytic anemia
- extreme photosensitivity w or w/o blistering

Labs:
- accumulation of protoporphyrin IX in RBC, plasma, feces (NOT urine)

Treatment:
- physical sun blocks
- exchange transfusion
- hematin

“Easily Produces Pebbly Fingers”

31
Q

Heme degradation syndromes

A
  • Neonatal jaundice
  • Gilberts syndrome
  • Crigler-Najjar syndrome
  • Dubin-Johnson syndrome
32
Q

Neonatal jaundice

A

Pathology:
- Deficiency in bilirubin glucuronyl-transferase ==> increased unconjugated (indirect) bilirubin
- UDP glucuronyl transferase (UGT) activity is low at birth
- Rate of bilirubin production is increased due to shorter lifespan of RBCs
- Decreased bacteria in intestine ⇒ increased enterohepatic circulation

Symptoms:
- yellow skin
- toxic encephalopathy (kernicterus)

Treatment:
- phototherapy with blue light: converts unconjugated bilirubin into water soluble isomer
- phenobarbital: induces bilirubin metabolizing enzymes
- blood transfusion to prevent brain damage

33
Q

Gilberts syndrome

A

Pathology:
- glucuronosyltransferase deficiency
- mild increase in unconjugated (indirect) bilirubin

Symptoms:
- generally benign, very mild jaundice during illnesses
- 5-10% of population

34
Q

Crigler-Najjar syndrome

A

Pathology:
- glucuronosyltransferase deficiency
- very high unconjugated bilirubin
- autosomal recessive

Symptoms:
- profound jaundice
- brain damage in infants

Treatment:
- Type I (more severe): phototherapy, liver transplantation
- Type II (still severe but less so): phenobarbital to increase expression of UGT1A1

35
Q

Dubin-Johnson syndrome

A

Pathology:
- mutation in MRP2 gene
- autosomal recessive
- inability of hepatocytes to secrete conjugated bilirubin out of ER after it’s formed ==> mildly increased conjugated bilirubin

Symptoms:
- usually asymptomatic
- moderate jaundice

36
Q

```

Platelet disorders

A
  • Bernard-Soulier disease
  • Glanzmann thrombasthenia
  • Gray platelet syndrome
  • idiopathic thrombocytopenia purpura (ITP)
  • thrombotic thrombocytopenia purpura (TTP)
37
Q

Bernard-Soulier syndrome

A

Pathology:
- autosomal recessive
- deficiency of GPIb receptor for vWF ==> impaired platelet adhesion to vWF

Symptoms:
- epistaxis, mucosal bleeding, easy bruising

Labs:
- thrombocytopenia
- giant platelets on smear
- prolonged bleeding time
- normal PT and PTT
- decreased platelet aggregation to ristocetin (induces binding of vWF and GPIb)
- ADP aggregation, epinephrine aggregation, collagen aggregation

Treatment:
- supportive
- platelet transfusion

38
Q

Glanzmann Thrombasthenia

A

Pathology:
- autosomal recessive
- deficiency/abnormality of platelet GIIb/IIIa (fibrinogen receptor) ==> platelets unable to aggregate

Symptoms:
- mucocutaneous microhemorrhages, epistaxis, petechiae/purpura

Labs:
- normal platelet morphology on smear
- absent platelet aggregation to ADP, collagen, epinephrine
- normal aggregation to ristocetin

Treatment:
- platelet transfusions

39
Q

Platelet Storage Pool Disease (Gray Platelet Syndrome)

A

Pathology:
- autosomal recessive
- deficient platelet granule contents: alpha, delta, or both
- decreased platelet secretion
- decreased secondary wave of platelet aggregation

Symptoms:
- mild, lifelong bleeding symptoms

Labs:
- gray appearing platelets in smear due to absence of alpha granules
- prolonged bleeding time
- normal PT and PTT
- normal ristocetin
- no second wave in ADP and epinephrine aggregation; impaired collagen aggregation

Treatment:
- anticipating and preventing risks of bleeding

40
Q

Idiopathic/Immune thrombocytopenic purpura (ITP)

A

Pathology:
- autoantibodies (usually IgG) directed against GpIIb/IIIa or GpIb bind to platelet surface
- platelets being destroyed

Symptoms:
- easy bleeding, petechiae, epistaxis
- acute ITP: self limited, seen in children after viral infections
- chronic ITP: tends to affect women between 20-40

Labs:
- large platelets on smear <- megakaryotes stimulated due to platelets being destroyed
- increased bleeding time
- normal PT and PTT
- coagulation factors unaffected

Treatment:
- Prednisone (immune suppressant)
- splenectomy

41
Q

Thrombotic thrombocytopenic purpura (TTP)

A

Pathology:
- ADAMTS13 (protease) deficiency ==> abnormally large vWF multimers that activate platelets
- vWF multimers remain attached to endothelial cells ==> platelet adhesion, aggregation, microvascular thrombosis
- usually due to acquired antibodies

Symptoms:
- occurs primarily in adults
- skin and mucosal bleeding
- classic pentad: thrombocytopenia, microangiopathic hemolytic anemia, neurologic impairment, fever, renal dysfunction

Labs:
- erythroid progenitors (nucleated RBCs) and schistocytes, thrombocytopenia
- increased bleeding time
- normal PT and PTT
- coagulation factors unaffected

Treatment:
- plasma exchange using FFP
- corticosteroids

42
Q

ITP vs. TTP

A

ITP: disorder of platelet destruction governed by platelet autoantibodies

TTP: disorder of platelet consumption and microthrombi formation resulting in organ ischemia

43
Q

Aspirin

A
  • irreversibly inhibits platelet cyclooxygenase (normally induces platelet activation)
  • normal platelet count
  • Low dose aspirin is good: it irreversibly inhibits platelet and endothelial cell TXA2 synthesis
  • Endothelial cells can synthesize new enzyme and produce PGI, but platelets cannot recover
44
Q

Hypocoagulation (bleeding) disorders

A
  • von Willbrand deficiency
  • Disseminated intravascular coagulation (DIC)
  • Hemophilia A & B
  • Vitamin K deficiency
45
Q

von Willebrand deficiency

A

Pathology:
- Types 1-3 vWF deficiency: 1 = slight decrease, 2 = qualitative, 3 = absent
- vWF binds to exposed collagen at site of injury => GpIb receptors on platelets bind to vWF => activation of GpIIb/IIIa => platelets crosslink
- vWF is carrier protein for FVIII

Symptoms:
- primary hemostasis impairment
- secondary hemostasis impairment (prolonged PTT that may not see mixing correction)
- mucosal bleeding, superficial bleeding

Treatment:
- Desmopressin (vasopressin)

46
Q

Disseminated intravascular coagulation (DIC)

A

Pathology:
- Systemic activation of clotting cascade ⇒ increased consumption of clotting factors and platelets ⇒ exhaustion of clotting factors
- syndrome secondary to sepsis, obstetric disasters, malignancies, leukemia, snake bites, heat stroke, brain injury, transfusion reaction, etc.

Symptoms:
- clotting and bleeding can dominate
- prolonged PT and PTT
- D-dimer positive (fibrin degradation product)
- low factors V & VIII, low platelets, low fibrinogen (clot)

Treatment:
- treat underlying cause

47
Q

Hemophilia A & B

A

Pathology:
- X-linked deficiencies
- Hemophilia A = factor VIII deficiency
- Hemophilia B = factor IX deficiency
- inhibitors can develop after previous exposure (mixing study would be positive)

Symptoms:
- prolonged PTT, mixed study negative (corrects)
- hemarthrosis (hemophilia of joint spaces, deep tissue)

Treatment:
- replacement of deficient factor
- prophylaxis, on demand therapy

48
Q

Vitamin K deficiency

A

Pathology:
- malnutrition, alcohol use disorder
- vitamin K-dependent factors are deficient: factors II, VII, IX, X

Symptoms:
- PT affected more than PTT

49
Q

Hypercoagulation (clotting) disorders

A
  • Factor V Leiden mutation
  • prothrombin mutation
  • protein C & S deficiency
  • antithrombin III deficiency
50
Q

Factor V Leiden mutation

A
  • autosomal dominant
  • point mutation abolishes binding site for protein C => factor V resistant to degradation => increased risk for venous thrombosis
  • common (> 1%)
51
Q

Prothrombin mutation

A
  • autosomal dominant
  • G20210A mutation causes increased prothrombin (factor II) expression => hypercoagulation
  • common
52
Q

Protein C & S deficiency

A
  • normally, protein C complexes with protein S to inhibit factors V and VIII => degradation of thrombus
  • both vitamin K-dependent <- would expect protein C/S levels to be low in a patient on warfarin
  • if pt with low protein C is started on warfarin, increased risk of clotting => superficial necrosis of skin (breasts)
  • rare
53
Q

Antithrombin III deficiency

A
  • too little or abnormal antithrombin III produced => decreased inhibition of coagulation
  • rare
54
Q

Type and screen test vs Type and crossmatch test

A

Used prior to blood transfusions

Type and screen: performed when blood may be needed
- front type: using reagent anti-A/anti-B Abs to type for antigens on RBC
- back type: using reagent A and B RBC type for matching Ab in plasma

Type and crossmatch: performed with blood is definitely needed
- blood units are reserved and tested for ABO and Rh compatibility

55
Q

Hemolytic Disease of Newborn (HDN)

A

Pathology:
- Rh(D) negative mom is exposed to Rh(D) positive fetal cells, stimulating mom to make anti-Rh(D) IgG antibodies
- first pregnancy is stimulus for immunization; often not affected

Symptoms:
- fetal RBCs attacked by mom’s anti-Rh(D) antibodies ==> fetal anemia
- baby can be born with jaundice (high bilirubin) and anemia

Treatment:
- Rh(D) negative mom should receive pooled IgG anti-Rh(D) at 28wks and within 72hr postpartum
- if fetal anemia develops: transfusion of washed group O RBC intrauterine to baby
- if fetus born with anemia and jaundice: neonatal exchange transfusion (removal of whole blood and replacement with group O Rh- RBC and AB plasma)

56
Q

Coombs test

A

Direct antiglobulin test:
- detects antibodies already bound to blood RBCs
- pt’s blood sample is directly used and washed, then incubated with Coomb’s reagent (C3, antihuman Ab) ==> RBCs agglutinate
- positive DAT = pt’s RBCs have auto IgG antibodies and/or C3 on them
- ex: to detect hemolytic anemia

Indirect antiglobulin test:
- detects serum antibodies that might bind to RBCs
- recipient serum is combined with donor blood sample ==> recipient Igs form complexes with donor RBCs ==> C3 added to agglutinate targeted RBCs
- cross-match testing, maternal serum testing

57
Q

Mixed lymphocyte reaction (blood test)

A

To ensure bone marrow donor is a match with recipient:
- mix blood mononuclear cells from 2 persons (donor and recipient) in tissue culture
- bone marrow recipient APC presents MHC I/II, which is recognized by donor T lymphocytes
- MHC I would stimulate CD8+ CTL proliferation
- MHC II would stimulate CD4+ helper T cell proliferation
- measure lymphocyte proliferation in vitro ==> less proliferation of T cells is good

58
Q

List the

Transfusion reactions:

A
  • acute hemolytic transfusion reaction (AHTR)
  • delayed hemolytic transfusion reaction (DHTR)
  • febrile non-hemolytic transfusion reaction (FNHTR)
  • allergic and anaphylactic transfusion reaction
  • septic transfusion reaction
  • transfusion-associated circulatory overload (TACO)
  • transfusion-related acute lung injury (TRALI)
  • post-transfusion purpura (PTP)
  • transfusion-associated graft vs. host disease (TA-GVHD)
59
Q

Acute hemolytic transfusion reaction (AHTR)

A

Pathology:
- preformed RBC antibody (pt has hx of transfusions) reacts with donor RBC
- complement activation => membrane lysis => release of free Hb, IgM

Symptoms:
- intravascular hemolysis < 24hr after transfusion
- fever, hypotension, shock, pink/red urine
- 40% mortality
- negative DAT (direct antibody test) due to all incompatible cells hemolyzed; positive urine hemoglobinuria, schistocytes

Treatment:
- stop transfusion, support BP
- protect kidneys: IV fluids, diuretics

60
Q

Delayed hemolytic transfusion reaction (DHTR)

A

Pathology:
- new alloantigen develops in pt post-transfusion
- no complement activation; instead, cells destroyed via phagocytosis (reticuloendothelial system) ==> extravascular hemolysis

Symptoms:
- progressive anemia 3 days-3wk after transfusion
- may present with fever, jaundice, dark urine
- positive DAT, positive new antibody

Treatment:
- transfusion of antigen-free RBCs

61
Q

Febrile non-hemolytic transfusion reaction (FNHTR)

A

Pathology:
- cytokines released from donor lymphocytes accumulate in bag during storage ==> antibodies in recipient plasma react

Symptoms:
- temperature increase of >1C (fever may be only symptom)
- often accompaniesd by chills / rigors

Treatment:
- increased risk due to previous alloimmunization to HLA
- prevention: leukoreduction (remove WBCs), premedicate with acetaminophen

62
Q

Allergic and anaphylactic transfusion reaction

A

Allergic:
- pts develop urticaria (hives), flushing, pruritus (itching)
- due to recipient IgE reacting to donor plasma proteins
- Tx: stop transfusion, give antihistamine, may restart once symptoms resolve

Anaphylactic:
- pts develop urticaria, wheezing low BP
- due to recipient IgA reacting to donor plasma proteins
- Tx: stop transfusion, start epinephrine, antihistamines, corticosteroids
- Prevention: wash donated RBCs/platelets

63
Q

Septic transfusion reaction

A

Pathology:
- bacteria in donor blood
- higher risk in platelet transfusions (platelets stored in room temp)

Symptoms:
- fevers, rigors, drop in BP, increase in HR

Treatment:
- broad spectrum abx until organism identified

64
Q

Transfusion-associated circulatory overload (TACO

A

Pathology:
- transfusion ==> expansion of intravascular volume ==> pulmonary edema
- increased risk in those with heart failure, renal insufficiency

Symptoms:
- acute hypertension (increase in blood volume)
- jugular venous distension (backup of blood from heart into veins)
- elevated brain natriuretic peptide
- usually NO fever
- CXR: pulmonary edema

Treatment:
Prevention: decrease rate of transfusion (slowly over 4hr)

65
Q

Transfusion-related acute lung injury (TRALI)

A

Pathology:
- donor anti-HLA antibodies and/or anti-neutrophil antibodies passed onto recipient ==> recipient granulocytes release proinflammatory mediators ==> increased vascular permeability ==> pulmonary endothelium damage, fluid extravasion into lungs
- usually FFP or platelets

Symptoms:
- within 6hr of transfusion: fever, tachycardia, hypotension, hypoxemia (low blood O2)
- CXR: new bilateral infiltrate

Treatment:
- supportive
- prevention: no FFP from any female donors

66
Q

Post-transfusion purpura (PTP)

A

Pathology:
- previously sensitized recipients (hx of transfusion, pregnancy) produce platelet-specific alloantibodies which may be autoreactive ==> thrombocytopenia
- within 2wks of transfusion

Symptoms:
- purpura (bruising)
- thrombocytopenia (10,000 platlets/uL)
- mucosal bleeding (GI bleeding) common

67
Q

Transfusion-associated graft versus host disease (TA-GVHD)

A

Pathology:
- different HLA antigens between donor (graft) and recipient (host)
- functionally active immune cells must be present in donor blood product
- host incapable of rejecting donor immune cells
- high risk for immunocompromised recipients

Symptoms:
- onset 3-30 days after transfusion
- rash (trunk => extremities), fever, watery diarrhea, elevated LFT (liver enzymes), pancytopenia
- bone marrow failure
- > 90% mortality within 1-3wk of symptom onset

Treatment:
- prevention: irradiation of products (inactivates donor lymphocytes)

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