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BMS200 > wk 12, lec 2 > Flashcards

wk 12, lec 2 Flashcards

1
Q

what is the main cause of babeosiosis

A

babesia microti

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2
Q

what is babesiosis

A
  • Parasitic infection from protozoa babesia from small rodents
    o Babesia microti
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3
Q

most common way to get babesiosis and risk factors

A
  • Tick bite; US summer
    o Risks: if older, asplenia and immunosuppressed
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4
Q

where does the babesia microti invade

A
  • B. microti invades RBCs and alters morphology
    o Increases spleen clearance of RBC, splenomegaly, hemolytic anemia
    o Systemic inflammation: TNF-alpha and IL-6 (lung symptoms)
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5
Q

symptoms of babesisosis

A
  • Symptoms: fatigue, malaise, fever, chill, sweat, headache, cough, N/V, neck stiff
    o Minority are symptomatic
    o Severe- hospital- hemolytic anemia, splenomegaly, infarction, respiratory distress, kidney injury, heart failure
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6
Q

diagnosis of babesiosis

A

microscope blood smear or PCR for B. microti DNA in blood

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7
Q

treat babesiosis

A

macrolide antibitoics and antiparasite agents

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8
Q

3 diseases of hyper coagulability

A
  • Virchow’s triad and pathological coagulation
  • Inherited disorders of the (anti)-coagulation cascade
  • Polycythemia vera
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9
Q

2 diseases of hypocoagulability

A
  • Von Willebrand’s disease
  • Acquired thrombocytopenias
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10
Q

is Disseminated intravascular coagulation (DIC) hyper or hypo coagulability

A

both

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11
Q

virchows triad

A
  1. Hypercoagulability of blood
  2. Abnormal blood flow (stasis or turbulent)
  3. Injury to vessel wall/ endothelium
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12
Q

shear stress in virchows triad: what happens if decrease

A
  • Shear stress (friction of fluid flow) increases NO, prostacyclin and tPA release (vasodilate and prevent clots)

o In decreased shear stress (i.e. stagnant flow or irregular/ narrow blood vessels) there’s less of these factors –> platelet adhesion + coagulation

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13
Q

inherited hyper coagulable conditions

A

o Protein C or S deficiency
o Antithrombin deficiency
o Prothrombin mutation (excessive activation)
o Factor V Leiden- activated protein C resistance (most common)

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14
Q

what happens in Factor V Leiden- activated protein C resistance (most common)

A

 Factor V is resistant to inactivation by protein C = excess acitivity in final common pathway

 Homozygous is bad; fair bit are heterozygous

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15
Q

what are the sign in Factor V Leiden- activated protein C resistance

A

DVT in legs or pelvis, led edema and pain, clot can travel to lung and cause pulmonary embolism

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16
Q

what does a mutation in prothrombin causing excessive activation increase risk of and what is the mechanism

A

 Increase risk of venous thromboembolism
 More conversion of prothrombin to thrombin

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17
Q

2 acquired conditions increasing coagulation

A

o Anti-phosholipid antibody syndrome (APS)
o Estrogen containing OCP (birth control)

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18
Q

what does o Estrogen containing OCP (birth control) increase

A

increase FII (prothrombin), FI (fibrinogen), VII, X, XII, VIII

leads to clotting

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19
Q

o Anti-phosholipid antibody syndrome (APS) - what happens?

A

 Antibodies to protein C, S? endothelial damage?
 Venous or arterial thrombi

leads to increased clotting

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20
Q

Acquired thrombocytopenia (hypocoagulability) due to

A
  • Due to hypersplenism, destruction of platelet by autoantibodies (drugs, viral, idiopathic), destruction of platelets by excessive intravascular coagulation, pancytopenia (low RBC, WBC, platelets) from myelodysplastic syndromes (blood cell cancer) and leukemia
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21
Q

what is the most common isolated thrombocytopenia?

A

Immune thrombocytopenia (ITP)

  • Most common isolated thrombocytopenia (isolated= no underlying disease or drug)
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22
Q

what happens in adults vs kids in immune thrombocytopenia

A
  • Kids: virus or vaccination; usually resolves
  • Adults: chronic and doesn’t resolve
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23
Q

immune thrombocytopenia- what are there no deficiencies in what are there low levels of

A
  • No deficiencies in coagulation factors
  • Platelets destroyed in spleen; splenectomy (removal) helps
  • Deficit in platelet production (cytotoxic t cells attack megakaryocytes and inadequate TPO)
  • Autoantibodies to platelet antigens- GP Ib/IX
  • Overactive Th1 and Th17
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24
Q

removal of what can help immune thrombocytopenia

A

splenectomy

because there are too many platelets getting destroyed in the spleen

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25
Q

features of immune thrombocytopenia

A

o Mucocutaneous bleeding= purpura and petechia, epistaxis (nose bleed), gingival bleeds

o menorrhagia, prolonged bleeds in surgery, low platelet counts that increase risk of intracranial bleeds, conditions that increase bleeding risk (NSAID, antiplatelet drug, older, high BP)

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26
Q

how to treat immune thrombocytopenia

A

splenectomy to reduce platelet destruction and glucocorticoids to increase platelet count

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27
Q

most common inherited bleeding disorder?

A

von willebrand disease

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28
Q

3 types of von willebrand disease

A

Tyoe 1 vWD Mild, autosomal dominant, vWF deficit

Type 2 vWD Mild- moderate, autosomal dominant,lots of vWF in circulation but doesn’t function effectively

Type 3 vWD Severe, autosomal recessive, severe vWF deficit (looks like thrombocytopenia & hemophilia)

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29
Q

what does vWF do for clotting

A
  • vWF stabilized VII, forms multimers for platelet adhesion to subendothelial matrix (bind GP Ib/IX and GP IIb/IIIa), made in basement membrane of endothelial cells and platelet granules
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30
Q

in von willebrnad disease what are there deficits in

A

vWF,
- defects in platelet function, but normal platelet count
o mucosal bleeding, bruising, epistaxis, menorrhagia, prolonged bleeds

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31
Q

how to treat von willebrand disease

A
  • treat with vasopressin (casuse vWF release from endothelial cells)
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32
Q

Disseminated intravascular coagulation (DIC) - what happens to get the clotting then the bleeding

A
  • widespread activation of coagulation cascade  form microthrombi and subsequent hemorrhage from consumption of clotting factors and platelets

o fibrin and fibrin degradation products are deposited, vessels occluded then loss of fibrin and consumption of platelets lead to hemorrhage (bleed)

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33
Q

what can Disseminated intravascular coagulation (DIC) be secondary to

A
  • secondary disorder to infection, trauma, malignancy, sepsis, burns
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34
Q

symptoms of Disseminated intravascular coagulation (DIC)

A

dyspnea, cyanosis, respiratory failure, coma, convulsions, oliguria, renal failure, microangiopathic hemolytic anemia

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35
Q

acute vs chronic effects in Disseminated intravascular coagulation (DIC)

A

o acute= hemorrhage
o chronic= thrombosis

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36
Q

what type of disorder is polycythemia vera

A

hyper coagulability

  • myeloproliferative disorder (too many RBCs, WBCs, platelets)
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37
Q

things that cause polycythemia’s vera

A

chronic myelogenous leukemia, essential thrombocytosis, myelofibrosis , clonal stem cell disorder
o Other causes: COPD, renal artery stenosis, OSA, chronic pulmonary disease

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38
Q

where is the a mutation in that causes polycythemia’s vera

A
  • Mutation in autoinhibitory region of JAK2 tyrosine kinase
    o Part of cascade for EPO and TPO
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39
Q

what is high in polycythemia’s vera

A
  • Asymptomatic high Hb or hematocrit
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40
Q

why is there neurologic symptoms and what are they in polycythemia’s vera

A
  • Neurologic symptoms b/c hyperviscosity
    o Headache, vertigo, tinnitus, visual, TIA, hypertension, venous or arterial thrombosis (cardiac, cerebral), DVT, gout (increase uric acid)
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41
Q

key symptoms in polycythemia’s vera

A
  • Erythromelalgia (burning hands and feet and erythema)
  • Pruritic after warm shower (mast cell and histamine)
  • Plethoric (ruddy complexion, cyanosis)
  • Splenomegaly and hepatomegaly
42
Q

treatment of polycythemai vera

A

phlebotomy (blood draw) and hydroxyurea (for cancer) to decrease RBC count and thrombotic events

43
Q

impaired ____ in megaloblastic anemia

A

DNA synthesis

44
Q

what are the 2 causes of megaloblastic anemia

A

b12 and folate deficiencies

45
Q

what are b12 and folate needed for and therefore their deficiency causes ,megaloblastic anemia

A

o B12 and folate needed to synthesize thymidine

46
Q

b12 vs folate deficiency causing megalobakstic anemia

A

o B12 deficiency: inadequate diet, pernicious anemia, inflammation in ileum, SIBO

o Folate deficiency: inadequate diet, malabsorption, folate antagonist drugs (methotrexate)

47
Q

symptoms of megaloblastic anemia

A

o Symptoms of deficiency of b12 and foalte: weakness, fatigue, sore tough, cheilosis

48
Q

what do RBCs look like in megaloblastic anemia ? what happens to RBC precursors?

A
  • RBCs and precursors are large and oval shaped – marrow looks hypercellular
    o Impaired nuclear maturation and cytosol accumulation
    o Delay in maturation of blasts
49
Q

hemolysis in megaloblastic anemia?

A

mild or absent

50
Q

platelet and leukocyte count in megaloblastic anemia

A

lower

51
Q

diagnosis of megaloblastic anemia

A

smear of peripheral blood and b12 and folate levels, test for b12 deficiency neuropathy

52
Q

pernicious anemia cause

A

autoimmune attack on parietal cells

53
Q

what do parietal cells do

A

o which secrete gastric acid and intrinsic factor in stomach and are needed for B12 absorption

54
Q

what is pernicious anemia associated with

A

thyroiditis

(autoimmune)

55
Q

onset and findings in pernciisous anemia

A
  • slow onset anemia, neurological findings (degenerate spine), paresthesia
56
Q

the absorption of what vitamin is effected in pernciisous anemai

A

b12

57
Q

what does pernicious anemia increase risk of

A
  • increased risk of gastric carcinoma if untreated

bc stomach acid affected

58
Q

treatment of pernicious anemai

A
  • treat: good prognosis with B12 supplementation
59
Q

cause of folate defieicny anemia

A
  • Decreased intake or increased requirement (i.e. pregnancy, malignancy)
60
Q

symptoms of folate defieincy anemia

A
  • Same as pernicious anemia symptoms but without neurological symptoms
    o Rule out
61
Q

treatment of folate deficiency anemai

A

supplement folate DUH!

62
Q

2 types of autoimmune hemolytic anemias (AIHA)

A

warm antibody hemolytic anemia
cold agglutinin disease

63
Q

what is the innocent bystander effect in autoimmune hemolytic anemias (AIHA)

A

: innocent bystander damage (antibodies directed to a medication or foreign substance attack RBCs b/c molecule get stuck to RBC)

64
Q

IgG or IgM in warm antibody hemolytic anemia and cold agglutinin disease

A

warm= igG

cold= igM

65
Q

temperature in warm antibody hemolytic anemia

A

 Antibody binds at 37 degree Celsius

66
Q

IgG in warm antibody hemolytic anemia

A

 RBCs removed in liver or spleen by macrophages with Fc receptors- usually IgG

67
Q

warm antibody hemolytic anemia and cold agglutinin disease- which is extravascular and intravascular hemolysis?

A

intravascular= cold
extravascular= warm

68
Q

3 mechanisms of extravascular hemolysis in warm antibody hemolytic anemia

A
  • Phagocytosis
  • Fragmentation
  • Cytotoxicity (ADCC)
69
Q

what can warm antibody hemolytic anemia be secondary to

A

HIV, viral vaccines and esp drugs

70
Q

cold agglutinin disease temperature

A
71
Q

cold agglutinin disease and IgM

A
72
Q

cold agglutinin disease is what type of hemolysis and what is activated

A

 Intravascular hemolysis (complement activation)

73
Q

cold agglutinin disease can be secondary to

A

 Secondary viral infections: EBV, CMV or mycoplasma infection

74
Q

what test is done to diagnose Autoimmune hemolytic anemias (AIHA) (cold and warm)

A

direct and indirect Coombs test

75
Q

what is a positive Coombs test result

A

positive= RBCs agglutination

76
Q

direct Coombs test vs indirect

A
  • Direct coomb’s test (direct antiglobulin test)
    o Wash patients RBCs and look for remaining antibodies bound to RBCs
  • Indirect coomb’s test (indirect antiglobulin test)
    o Patients plasma and expose to standard RBC sample
    o Look for patients antibodies binding RBCs
77
Q

what could cause low and high RBC counts

A

 Low= anemias of RBC destruction (AIHA), hypoproliferative anemias, hypersplenism

 High= high altitudes, chronic hypoxia, polycythemia

78
Q

what is the preferred lab metric to diagnose anemai

A

hemoglobin

79
Q

hematocrit is

A

 % of total blood volume made up by RBCs

80
Q

what decreased hemoglobin and hematocrit concentration

A

 Hemoglobin and hematocruit [ ] is dereased in fluid resuscitation (i.e. IV dilutes blood)

81
Q

MCV

A

 Mean corpuscular volume (MCV)
* RBC size
* Divide hematocrit by total RBC count

82
Q

MCH

A

 Mean corpuscular hemoglobin (MCH)
* Mass of hemoglobin per red cell

83
Q

RDW

A

 RBC distribution width (RDW)
* Variance in RBC size

84
Q

what is anisocytosis

A
  • Anisocytosis= higher RDW (RBC distribution width), more variable size of RBCs
85
Q

what has high and low RDW (RBC distribution width

A
  • IDA has high degree of anisocytosis (variable RBC size)
  • Thalassemia has uniform RBC size
86
Q

total reticulocyte count assesses

A

 Assess RBC production
 Reticulocytes are immature RBCs made in bone marrow then go to blood

87
Q

normal total reticulocyte count

A

1%

88
Q

blood loss does what to total reticulocyte count

A

increases

89
Q

total reticulocyte count can differentiate

A

 Help differentiate hypoproliferative marrow from compensatory marrow response to anemia

90
Q

low total reticulocyte count means and causes

A

 Low= impaired RBC production from nutritional deficiencies, bone marrow infiltration, aplastic anemias

91
Q

Normocytic, normochromic anemia

A

▪ Early iron deficiency
▪ Anemia of chronic illness/disease (ACD)
▪ Acute blood loss
▪ Aplastic anemia or other types of marrow failure
▪ Hemolytic anemias

92
Q

Microcytic, hypochromic anemia

A

▪ Late iron deficiency
▪ Thalassemia
▪ Lead poisoning
▪ Sideroblastic anemia
▪ ACD can also be mildly microcytic, hypochromic
▪ Mnemonic - TAILS

93
Q

Microcytic, normochromic anemia

A

▪ Renal disease

94
Q

Macrocytic, normochromic anemia

A

Megaloblastic =
* Vitamin B12 or folic acid deficiency
* Chemotherapy

▪ Non-megaloblastic:
* Liver disease, alcohol use
* Hypothyroidism
* Myelodysplastic syndromes

95
Q

cell size in vitamin b12 of folic acid deficient

A

microcytic

96
Q

prothrombin time (PT/inR) vs activated partial thromboplastin time (aPTT)- which for extrinsic and intrinsic pathwy

A

PT= extrinsic
aptt= intrsinic

97
Q

factors in prothrombin time (PT/inR) vs activated partial thromboplastin time (aPTT)

A

pt/inr: o Factors I, II, V, VII, X

aPTT: o Factors I, II, V, VIII, IX, XI, XII

98
Q

if prothrombin time is prolonged its because of

A

o Prolonged if deficient (long time to clot)
 Liver disease, hereditary, vitamin K deficiency, warfarin, bile duct obstruction, DIC

99
Q
  • Activated partial thromboplastin time (aPTT) is used to monitor
A

o Monitor heparin therapy

100
Q
  • Activated partial thromboplastin time (aPTT) increases in
A

 DIC, vitamin K deficiency, warfarin, herparin, cirrhosis, congeital clotting deficiencies

101
Q

D dimers are used to test for

A

o *Test for disseminated intravascular coagulation (DIC) (elevated)
 Not specific though; also elevated in malignancy, liver, pregnancy, DTV, MI etc

102
Q

d-dimer are

A

fibrin degradation fragment that is made through fibrinolysis

BMS200 (46 decks)

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