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Blood Flashcards

1
Q

When do palmar creases loses their pink color?

A

Hg below 4 g/dL

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2
Q

What symptom is an under-appreciated manifestation of severe anemia?

A

Shortness of breath

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3
Q

When can anemia precipitate dramatic symptoms?

A

Circulation already compromised from vascular disease

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4
Q

What conditions can lead to anemia with a low MCV in a man?

A

GI bleed
Celiac sprue
Thalassemia (very low MCV)

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5
Q

What should you think about with newly unusually heavy menses?

A

Thrombocytopenia, hypothyroidism

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6
Q

What unusual manifestation may be seen in iron deficiency anemia?

A

Pagophagia: compulsive for ice or iced drinks (a form of pica)

(Seen especially in women and children with iron-deficiency anemia)

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7
Q

What lab finding may be seen in hemolysis?

A
  1. Elevated indirect bilirubin
  2. Low serum haptoglobin
  3. Increased plasma lactate dehydrogenase (LDH)
  4. Spherocytes on peripheral smear
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8
Q

What is haptoglobin, and how is it affected in hemolytic anemia?

A

Haptoglobin: plasma protein that binds free hemoglobin and causes it to be sequestered in the spleen

Decreased in hemolytic anemia, as more Hg is released into plasma, which is bound by haptoglobin and cleared.

(Decrease may be small in autoimmune hemolytic anemia because hemolysis occurs primarily in the spleen).

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9
Q

What nutrient needs to be supplemented in hemolytic anemia?

A

Folate (can become deficient due to rapid turnover in bone marrow to make up for hemolysis)

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10
Q

What types of cells are seen on smear in microangiopathic hemolytic anemia?

What are some main elements on the differential diagnosis for this type of anemia?

What is the mechanism of hemolysis?

A

Smear: Schistocytes and helmet cells

Causes:

  1. Thrombotic thrombocytopenic purpura (TTP)
  2. Disseminated intravascular coagulation (DIC)
  3. Malignant hypertension

Mechanism: Shearing of RBC (and damaging platelets) due to fibrin strands deposited in small arterioles, which results from activation of the coagulation cascade

(Can result from anything leading to widespread endothelial injury, including drugs, infection, and fibrinoid necrosis due to malignant HTN)

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11
Q

What type of cardiac disease can lead to hemolysis?

A

Dysfunctional valve disease (heavily calcified or artificial valves)

(Called Waring Blender syndrome)

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12
Q

What types of diseases can show autoimmune hemolytic anemia?

A
  1. Lymphoproliferative diseases

2. Collagen vascular diseases (especially SLE)

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13
Q

What type of hemolytic anemia shows a relatively small decrease in haptoglobin?

A

Autoimmune hemolytic anemia

(Hemolysis occurs primarily in spleen, so little hemoglobin released into blood, so there is little for serum haptoglobin to bind to).

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14
Q

What type of hemolysis has “warm” antibodies? What type of Ig is this? Where does hemolysis occur?

How about “cold” antibodies?

A

Warm:

  • Seen in autoimmune hemolytic anemia.
  • Mainly IgG
  • Hemolysis occurs in spleen (and RES)

Cold:

  • Associated with certain infections (e.g. mycoplasma pneumonia, mono)
  • Mainly IgM
  • Hemolysis occurs in cold-exposed areas of circulation
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15
Q

What is a common cause of hemolytic anemia combined with immune thrombocytopenia (ITP) in younger patients? Older patients?

A

Younger: SLE
Older: Lymphoproliferative disorder

(This combination is called “Evans syndrome)

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16
Q

What is suggested by hemolytic anemia in associated with leukopenia, thrombocytopenia, and venous thrombosis?

A

Paroxysmal nocturnal hemolgobinurea

(In PND, acquired defects in hematopoietic stem cells means these cells are more sensitive to complement, leading to intravascular hemolysis and hemoglobinuria)

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17
Q

Where does venous thrombosus tend to occur in PNH?

What is a potential mechanism?

A

Intra-abdominal vessels (including portal and hepatic veins)

Complement against platelets may make them prone to aggregration

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18
Q

What are common causes of drug-induced hemolytic anemias?

A
  1. Penicillin
  2. Cephalosporins
  3. Methyldopa (for HTN)
  4. Quinine
  5. Sulfonamides (e.g. TMP-SMX, sulfadiazene (for Toxo), sulfasalazine (for RA), zonisamide (antiepileptic))
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19
Q

What causes a delayed hemolytic transfusion reaction?

A

Antibody response against minor antigens (e.g. Kidd, Duffy, Kell) that may lead to extravascular immune hemolysis days-to-weeks after transfusion.

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20
Q

What reactions does B12 catalyze?

A
  1. 5-methyltetrahydrofolate to tetrahydrofolate (the active form)
  2. Homocysteine to methionine
  3. Methylmalonic acid to succinic acid
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21
Q

Other than macrocytosis, what else is seen on blood smear in megaloblastic anemia?

A

Multisegmental polymorphonuclear leukocytes (PMNs)

The delayed maturation seen in RBCs also affects granulocytes

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22
Q

In what condition can a non-megaloblastic macrocytosis be seen?

A

Hypothyroidism

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23
Q

What are some causes of B12 deficiency?

A
  1. Long-standing strict veganism
  2. Pernicious anemia (lack of intrinsic fracture production due to autoimmune destruction of parietal cells)
  3. Ileal disease (e.g. Crohn’s, celiac) or resection
  4. Gastrectomy / gastric bypass
  5. Small intestinal bacterial overgrowth (SIBO, due to bacteria competing for B12)
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24
Q

What lab changes are seen in B12 deficiency?

Which is the most reliable test?

A

Decreased B12, elevated MMA, elevated homocysteine

Elevated MMA is the most reliable test

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25
Q

What neurological changes can be seen in B12 deficiency?

A
  1. Subacute combined degeneration (damage to dorsal columns and lateral corticospinal tracts)
  2. Personality changes and dementia
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26
Q

What types of conditions in folate deficiency associated with?

A
  1. Alcoholism
  2. Increased demand (e.g. pregnancy)
  3. Increased bone marrow turnover (e.g. hemolytic anemia)
  4. Impaired absorption (e.g. celiac ds)
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27
Q

What can impair folate absorption?

A

Anticonvulsants, estrogens, alcohol

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28
Q

What two factors make alcoholics prone to folate deficiency?

A
  1. Poor nutrition

2. Alcohol inhibits deconjugation of polyglutamate forms of folic acid found in food (but not folate supplements)

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29
Q

What are three key factors that affect the hemoglobin dissociation curve, and how do they do so?

A
  1. pH: Acidity leads to right shift, decreased affinity
  2. Temperature: Higher temperature leads to right shift, decreased affinity
  3. 2,3-DPG: Higher levels lead to right shift, decreased affinity
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30
Q

What consequences can oxidative damage of RBC’s have?

A
  1. Denaturation of RBC proteins that form Heinz bodies, which distort cell architecture and leads to RBCs being cleared by the spleen).
  2. Oxidation of iron in heme to methemoglobin (which cannot bind oxygen)
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31
Q

What pathway protects RBCs against oxidative damage?

A

Pentose phosphate shunt (which requires glucose-6-phosphate dehydrogenase) generates NADPH, which forms oxidized glutathione that can eliminate free radicals

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32
Q

What can be seen on blood smear with damage of RBCs due to oxidative stress?

A
  1. Heinz bodies (clumps of denatured proteins)

2. Bite cells (areas where Heinz bodies have been removed)

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33
Q

What is the mechanism of acute episodes of hemolytic anemia in G6PD deficiency?

A

G6PD is part of the pentose phosphate shunt, which is required to generate glutathione that helps RBCs deal with oxidative stress.

Triggers of oxidative stress, including infection, some drugs (antimalarials, sulfa drugs, some antibiotics), and some food (fava beans), can lead to episodes.

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34
Q

What can lead to a false-negative in a test for G6PD deficiency?

A

During a hemolytic episode, older cells with lowest levels of G6PD are preferentially destroyed, making average G6PD levels higher than normal for that person.

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35
Q

What drugs can precipitate acquired methemoglobinemia?

A
  1. Local anesthetics (e.g. benzocaine)
  2. Dapsone (used for leprosy)
  3. Nitrous oxide
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36
Q

What is the classic cause of congenital methemoglobinemia?

A

AR deficiency in cytochrome b5 reductase, the enzyme that converts methemoglobin back to hemoglobin using NADH.

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37
Q

What is used to treat methemoglobinemia?

A

Methylene blue (reduces methemoglobin back to hemoglobin)

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38
Q

What usually causes unexpected bouts of hematuria in young African Americans?

A

Sickle trait (sickling in efferent renal arteriole leads to papillary necrosis).

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39
Q

What is suggested by an abundance of target cells in the peripheral smear?

A

Hemoglobin C or SC disease

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40
Q

What should you think about in familial cases of polycythemia?

A

Hemoglobin variants with increased O2 affinity (and so impaired O2 release in tissues)

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41
Q

What are some causes of normochromic-normocytic anemia resulting from impaired production?

A
  1. Anemia of chronic disease
  2. Pure red cell aplasia
  3. Myelodisplastic syndromes
  4. Myelopthisis (displacement of bone marrow by fibrosis, granulomas, or tumors)
  5. Myelofibrosis (bone marrow malignancy of hematopoietic stem cells)

(All may be microcytic as well)

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42
Q

What platelet counts are associated with bleeding in response to minor trauma? Serious bleeding in response to trauma? Life-threatening spontaneous hemorrhage?

A

Bleeding in response to minor trauma: below 50,000
Serious bleeding in response to trauma: below 20,000
Spontaneous life-threatening hemorrhage: below 10,000

43
Q

What are 10 causes of thrombocytopenia?

A
  1. Viral infections
  2. Autoimmune destruction
  3. Drugs
  4. Alcohol
  5. Chemotherapy
  6. Folate deficiency
  7. Hematologic malignancies
  8. Marrow failure
  9. Hypersplenism
  10. Peripheral consumption (e.g. DIC)
44
Q

What type of bleeding is classically seen in thrombocytopenia?

Hemophilia?

A

Thrombocytopenia: mucocutaneous bleeding and bleeding immediately after trauma (and CNS and GI bleeds at very low levels).

Hemophilia: hemarthrosis, intramuscular, and visceral bleeds, and delayed bleeds after trauma (platelets provide initial hemostasis)

45
Q

How can petechiae and morbilliform rashes easily be distinguished clinically?

A

Morbilliform rashes blanch with pressure, petechiae do not.

46
Q

What conditions are seen with palpable petechiae?

A

Vasculitis

47
Q

What types of infections can lead to clinically significant thrombocytopenia?

A
  1. HIV
  2. Hep. C
  3. EBV
  4. Rickettsial disease (e.g. RMSF)
48
Q

What is suggestive of microantiopathic disease such as TTP and DIC on blood smear?

A

Schistocytes and helmet cells

This will not be seen in ITP

49
Q

How are thrombocytopenia purpura (TTP) and idiopathic/immune thrombocytopenic purpura (ITP) treated?

A

TTP: Plasmapheresis/IVIG
ITP: Steroids

50
Q

What is the mechanism of ITP?

A

IgG against platelets leads to their removal in the reticuloendothelial system (e.g spleen)

51
Q

What can trigger ITP?

A

Antecedent infection (especially in children)

52
Q

What do you make of negative antiplatelet antibodies in a test for ITP?

A

Do not rule out ITP because tests may have false negatives

53
Q

What is the mechanism of TTP?

A

Deficiency (usually acquired) of a metalloprotease that cleaves vWF multimers. These vWF multimers lead to platelet clumping and initiate thrombosis.

54
Q

What is the clinical pentad of TTP?

A
  1. Thrombocytopenic purpura
  2. Microangiopathic hemolytic anemia
  3. Neurologic symptoms (e.g. delirium, hallicinations, stroke, headache)
  4. Fever
  5. Decreased renal function
55
Q

What is the triad of hemolytic-uremic syndrome?

A
  1. Microangiopathic hemolytic anemia
  2. Acute renal failure
  3. Thrombocytopenia
56
Q

What is the cause of hemolytic-uremic syndrome?

A

Shiga-toxin or Shigalike-toxin, most commonly produced by enterohemorrhagic E. coli (e.g. O157:H7), but also Shigella or Campylobacter

Toxin diffusely damages endothelium and triggers thrombosis

57
Q

What is the mechanism of DIC?

A

Damaged endothelium releases “tissue factor,” which drives intravascular coagulation and thrombosis, which consumes coagulation factors and leads to paradoxical bleeding.

58
Q

What are some lab findings in DIC on CBC and coags?

A

CBC: Thrombocytopenia
Coags: Prolonged PT and PTT

59
Q

What labs indicate the fibrinolysis in DIC?

A

Fibrin-split products (FSPs) and D-dimer: elevated

Fibrinogen: varies (decreased by consumption but increased as part of acute phase reaction)

60
Q

What types of things can drigger DIC, in general?

A
  1. Severe infection
  2. Malignancy
  3. Trauma
  4. Toxins
  5. Obstetric emergencies (e.g. eclampsia, placental abortion, postpartum hemorrhage)
61
Q

What types of malignancy are most commonly associated with DIC?

A
  1. PML (promyelocytic leukemia)

2. Mucin-producing adenocarcinomas (lung, breast, stomach, prostate, pancreas, ovary, and biliary tract)

62
Q

What are the most common causes of drug-induced thrombocytopenia?

Out of these, which is the most common and severe?

A
  1. Heparin-induced thrombocytopenia (HIT) is most common and severe
  2. Quinidine and quinine
  3. Penicillins
  4. Thiazide diuretics
63
Q

What are the two types of heparin-induced thrombocytopenia (HIT)?

A

Type 1: Mild thrombocytopenia, begins within two days, self-limited, no bleeding

Type 2: Severe reaction with platelet aggregation and endothelial damage leading to thrombosis and thrombocytopenia, delayed a few days (e.g. 4) after starting heparin

(If someone says HIT without specifying, they generally mean type 2)

64
Q

What is the pathophysiology of heparin-induced thrombocytopenia (type II)?

A

Antibody against heparin-platelet complex leads to platelet aggregation, thrombosis, and thrombocytopenia.

Thrombosis causes most of morbidity/mortality, not bleeding.

65
Q

Is HIT more common with unfractionated or LMW heparin?

A

Unfractionated

66
Q

What is the treatment for HIT (type 2)?

A
  1. Stop heparin and avoid for life
  2. Direct (e.g. argatroban, dabigatran/Pradaxa) or indirect (rivaroxaban/Xarelto, apixiban/Eliquis) thrombin inhibitors
    (Warfarin is NOT given until platelet count has normalized, as this can cause microthrombosis)
67
Q

What types of things can cause petechial and purpurae with normal platelet counts and function?

A
  1. Vasculitis, classically palpable purpurae (e.g. Henoch-Schonlein purpura, HSP)
  2. Capillary damage from infection or toxin
  3. Capillary fragility (e.g. senile purpura, scurvy)
68
Q

What is Henoch-Schonlein purpura?

What is the classic triad of symptoms?

What are some serious complications?

A

An IgA and complement-mediated vasculitis with palpable petechiae and normal/elevated platelets. (Most common in kids but can be seen in adults)

Triad:

  1. Palpable purpura (especially on legs and buttocks)
  2. Arthritis (of large joints)
  3. Abdominal pain

Complications: GI hemorrhage (e.g. due to intussusception), renal disease

69
Q

What is autoerythrocyte sensitization?

A

Recurrent attacks of painful purpura and ecchymoses, especially in the legs, often precipitated by stress, with normal coagulation studies.

Rare and poorly understood

Also known as “painful bruising syndrome”

70
Q

What are senile purpura?

A

Purple ecchymoses, predominantly on dorsal forearms, due to fragile capillaries in older patients.

(Requires no workup other than platelet count, which should be normal)

71
Q

What is the mechanism of petechiae and purpurae in scurvy?

A

Weak connective tissue leads to capillary fragility

72
Q

What causes petechiae/purpura in acute meningococcemia?

A

Endotoxins and cytokines damage endothelium and lead to subcutaneous hemorrhage.

DIC often co-occurs

73
Q

What causes petechiae/purpura in viral hemorrhagic fevers (e.g. Lassa fever, Ebola)?

A

Endothelial damage leading to hemorrhage, as well as likely DIC

74
Q

What is the difference between absolute and relative polycythemia?

A

Absolute: >55% Hct due to increase in RBC mass
Relative: >55% Hct due to decreased plasma volume (hypovolemia)

75
Q

What are causes of absolute polycythemia?

A
  1. Polycythemia vera (RBC neoplasm)
  2. Chronic hypoxia (e.g. cyanotic heart disease, OSA)
  3. High altitude (long-term)
  4. Paraneoplastic syndromes (ectopic EPO, e.g. with RCC, HCC, VHL)
  5. Variant hemoglobin with high O2 affinity
76
Q

What is the cutoff of polycythemia?

A

> 55% Hct

77
Q

What other findings can be seen in polycythemia vera?

A
  1. Splenomegaly
  2. Increased uric acid
  3. Ruddy complexion
  4. Tortuous, engorged retinal veins
78
Q

How can acute pancreatitis lead to elevated hematocrit?

A

Fluid exudate into the abdomen leads to loss of plasma volume

79
Q

What is essential thrombocytosis?

What are some frequently associated findings?

What are some complications?

A

Myeloproliferative disorder with overproduction of platelets.

Associated findings: Mild splenomegaly, leukocytosis, platelet count >500,000

Complications: Arterial thrombosis, paradoxical bleeding with platelets >1 million (alterations in vWF)

80
Q

What are some causes of nonmalignant thrombocytosis?

A
  1. Any inflammatory disease
  2. Post-splenectomy
  3. Iron deficiency anemia
81
Q

What BMP value can be artificially altered in thrombocytosis?

What test can get around this?

A

Pseudohyperkalemia: platets in clotted serum released potassium

Plasma potassium (rather than serum potassium) will show an accurate value

82
Q

What types of infections are seen in neutropenia? Below what ANC?

A

Bacterial and fungcal infections (not viral, treated by lymphocytes instead)

Seen with ANC < 500 (ANC <1,500 counts as neutropenia)

(Agranulocytosis is ANC of essentially zero)

83
Q

What are three types of drugs that can cause agranylocytosis?

A
  1. Antithyroid agents (carbimazole, methimazole, and propylthiouracil)
  2. Psychotropic agents (namely clozapine)
  3. Antibiotics, especially chloramphenicol (rarely used because of this and aplastic anemia), but also penicillin and Bactrim
    (Very rarely with NSAIDs)
84
Q

What are some causes of neutropenia?

A
  1. Medication induced
  2. Infection (viral and severe bacterial)
  3. Autoimmune neutropenia
  4. Hypersplenism (with pancytopenia)
85
Q

What conditions are associated with autoimmune neutropenia?

A

Collagen vascular disease (especially SLE and RA)

86
Q

What are three infectious disease associated with lymphocytosis?

What else can cause it?

A

Infections:

  1. Infectious mononucleosis (EBV)
  2. Cytomegalovirus infections
  3. Pertussis

Other cause: CLL

87
Q

What lab test distinguish leukemoid reactions to infection from chronic myelcytic leukemia (CML)?

A

Leukocyte alkaline phosphatase: High in leukemoid reactions, low in CML

(In CML also see elevated basophils and Philadelphia chromosome)

88
Q

What is leukoerytrhoblastic reaction?

What is it associated with?

A

Both nucleoated RBC and immature WBCs seen on peripheral smear

Causes:

  1. Marrow infiltration (myelopthisis)
  2. Myelofibrosis
  3. Severe infection (sepsis, military TB)
89
Q

What conditions is eosiniphilic leukocytosis seen in?

A
  1. Parasitic infestations (worms, not protozoans)
  2. Allergic reactions
  3. Some collagen vascular diseases (e.g. Churg-Strauss syndrome, also known as eosinophilic granulomatosis with polyangiitis)
90
Q

What are hypereosinophilic syndromes?

What three groups can they be divided in to?

A

> 1,500 eosinophils/uL with organ infiltration and dysfunction (e.g pulmonary, cardiac, GI)

Groups:

  1. Primary: Myeloproliferative disorder
  2. Secondary (parasitic infection, CVD, malignancy)
  3. Idiopathic
91
Q

What is associated with monocytosis?

A

TB

92
Q

What three organ systems can be infiltrated with eosinophils and lead to significant morbidity and mortality?

A

Cardiac, pulmonary, and GI

93
Q

What can result from cardiac eosinophilic infiltration?

A

Coronary artery damage can lead to infarction

Myocardium damage can lead to thrombus formation

94
Q

What are two causes of pulmonary eosinophilic infiltration?

A
  1. Chronic eosinophilic pneumonia (direct eosinophilic infiltration
  2. Helminth parasites in the lungs (ascaris, hookworm, Strongyloides)
95
Q

What can result from GI infiltration with eosinophils?

A

Abdominal pain, weight loss, vomiting, diarrhea

96
Q

What are risk factors for DVT?

A
  1. Venous stasis
  2. Endothelial damage
  3. Hypercoagulability
  4. Older age
    (The first 3 are Virchow’s triad)
97
Q

What is the most significant inherited hypercoagulable state?

A

Factor V Leiden (clotting factor resistant to inactivation by protein C).

(Autosomal dominant, seen in 5% of U.S. population and about 25% of DVT/VTE patients)

98
Q

What is an autoimmune disease associated with both venous and arterial thrombosis?

What other complications may be seen in this disease?

A

Antiphospholipid syndrome

Other complications:

  1. Fetal loss and other pregnancy complications
  2. Acute adrenal insufficiency
99
Q

What antibodies are associated with antiphospholipid syndrome?

A
  1. Lupus anticoagulant (misnomer - actually procoagulant, and often absent in lupus)
  2. Anti-cardiolipin
  3. Anti-beta2-glycoprotein
100
Q

What are the most common thrombotic events seen in antiphospholipid syndrome?

A

Venous thrombosis and stroke (MI also seen but less common)

101
Q

What endocrine abnormality is associated with antiphospholipid syndrome?

What are early signs?

What is the test for this?

A

Acute adrenal insufficiency (due to infarction from arterial thrombosis or hemorrhage following adrenal vein thrombosis)

Early signs: back pain and hypotension

Test: ACTH stimulation test (a.k.a. cosyntropin test)

102
Q

What renal disease can lead to a hypercoagulable state?

What is the mechanism?

What particularly type of thrombosis is commonly seen?

A

Nephrotic syndrome, due to loss of antithrombin III in the urine.

Associated with renal vein thrombosis (antithrombin III will be lowest in the renal vein because it has just been lost in the nephron)

103
Q

What can lead to an acquired hemophilia?

How can it be distinguished from congenital hemophilia on labs?

What is the general strategy for treatment?

A

Autoantibodies against clotting factors (most commonly factor VIII/8, which is lost in hemophilia A)

Unlike factor deficiencies, PTT will not normalize on 1:1 mixing with normal plasma

Treatment: immunosuppression

104
Q

What are the most common manifestations of von Willebrand disease (vWD)?

What other clotting factor is affected?

How is it treated, and when is treatment required?

A

Manifestations: mild bleeding diathesis: bruisability, heavy menstrual flow, bleeding after surgery

Factor VIII/8 is also modestly reduced (circulates with vWF)

Trearment: Replacement of vWF or DDAVP (which increases vWF release) prior to surgery / dental procedures

On Rounds Pearls (3 decks)

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