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Patho > Heme > Flashcards

Heme Flashcards

1
Q

Process of gas transport in anemia

A

Decreased red cell mass sensed by kidney, increased erythropoietin by bone marrow stem cells

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2
Q

Process of gas transport in hypoxia

A

Decreased arterial o2 sat sensed by kidney, stim bone marrow stem cells to inc EPO and red cells

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3
Q

Process of gas transport in polycythemia Vera

A

Inc red cell mass sensed by kidney, dec EPO and rbc produc by bone marrow

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4
Q

Anemia

Definition

A

Dec 10% of rbcs in blood or in quality/quantity of hb. Impaired rbc produc, blood loss, inc rbc destruction

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5
Q

Morphology of rbc in anemia

A

Anisocytosis (various sizes)

Poikilocytosis (various shapes)

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6
Q

What index refers to rbc size

A

MCV

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7
Q

Common anemia symptoms

A

Fatigue, weakness, dyspnea, pallor

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8
Q

Megaloblastic anemia

What its characterized by

A

Macrocytic, normochromic
MCV >100.
Defective dna synthesis (def vit b12 or folate), needed for nuclear maturation/DNA synthesis

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9
Q

Pernicious anemia

Patho behind it

A

Lack of IF from parietal cells, less b12 absorp and less nuclear maturation/dna synthesis. Congenital/adult onset/autoimmune antibodies

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10
Q

Pernicious anemia
__ onset
___ manifestations
__ ___

A

Slow
Neurologic
Nerve demyelination

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11
Q

Pernicious anemia

Evaluation/tx

A

Parietal cell/IF absorption
Gastric biopsy
Total achlorhydria
Vit b12 replacement

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12
Q

Sickle cell anemia
Genetic defect of what
Cells charac by

A

Hgb synthesis

Hb instability/insolubility. Vascular occlusion, severe anemia, painful episodes

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13
Q

Sickle cell anemia
Tx
Prognosis

A

Tx- stem cell transplant

Prognosis- death if no/unsuccessful transplant

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14
Q

Microcytic hypochromic anemias

Related to disorders of what

A

Iron metabolism, porphyrin and heme synthesis, globin synthesis

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15
Q

Which is most common anemia worldwide, what its due to

A

Iron deficiency anemia, pregnancy and chronic blood loss

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16
Q

Patho behind iron deficiency anemia

A

Nutritional deficiency, chronic blood loss, metabolic/functional deficiency. Insufficient iron delivery or use in BM

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17
Q

Iron def anemia
Hb:
Causes what

A

7-8 g/dl

Brittle, thin, coarse ridged, spoon shaped nails. Red, sore, painful tongue

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18
Q

Iron deficiency anemia
Serum ferritin:
Tx

A

1 mcg/l. 8-10 mg of storage iron/kg. Most sensitive

Rule out/find blood loss. Iron replacement tx (ferrous)

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19
Q

Sideroblastic anemia

Due to what

A

Altered mitochondrial metab, iron deposits, dysfunctional hb synthesis in BM

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20
Q

Sideroblastic anemia
Clinical issues
Eval
Tx

A

Inc iron in tissues, spleno/hepatomegaly.

Ringed sideroblasts in BM. Pyroxidine tx

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21
Q

Thalassemia
What happens
Assoc w

A

Inc rbc destruction resulting in dec RBC survival rates

Assoc w mutant genes that suppress rate of globin chain synthesis. AS or B.

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22
Q

Thalassemia tx

A

Blood transfusions. Splenectomy. Chelation therapy. BM transplant. Genetic counseling

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23
Q

Aplastic anemia

What happens

A

Pancytopenia. Dec all 3 blood cell types. BM failure/suppression in production. Pure red cell aplasia. Faconi anemia- genetic alt/predisposition, defects in DNA repair

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24
Q

Aplastic anemia patho

A

BM lesion, hypocellular, fat. Autoimmune or HSCs

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25
Q

Aplastic anemia
__ onset
Symptoms

A

Slower: wbc or plt related

Pallor, weakness

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26
Q

Aplastic anemia

Eval/tx

A

BM bx- high fat content
BM/peripheral blood stem cell transplant
Immunogenic tolerance

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27
Q

Hemolytic anemia

What happens

A

Premature/accel destruction of RBCs and BM compensation

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28
Q

Hemolytic anemia

Causes

A

Inherited/acquired RBC/immunologic.
Blood vessel or lymphoid tissues
Autoimmune hemolytic anemias
Immunohemolytic anemia- mediated by drugs

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29
Q

Immunohemolytic anemia

What causes it

A

Drugs: pcn, cephalosporins, quinidine, a methyldopa

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30
Q

Models of hemolytic anemia

A

Hapten (pcn, hemolysis by coomplement, IgG)
Immune complex formation (quinidine, hemolysis by complement)
Autoimmune (a methyldopa, phagocytosis on normal rbc antigens)

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31
Q

Hemolytic anemia
What you see clinically
Eval

A

Jaundice, inc bilirubin

BM studies and bone tests

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32
Q

Anemia of chronic disease

Seen in which diseases

A

Mild-mod anemia

AIDS, RA, SLE, hepatitis, renal failure, and malignancies

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33
Q

Anemia of chronic disease

Patho behind it

A

Dec RBC lifespan. Ineffective BM response to EPO. Altered iron metabolism

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34
Q

Relative polycythemia

Causes, what you see

A

Dehydration, diarrhea, vomit, diuretics.

Fluid loss leads to relative inc rbc cts and hb/hct values

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35
Q

Absolute polycythemia

What happens

A

Abn of BM stem cells, polycythemia Vera

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36
Q

Secondary polycythemia

Cause and what happens

A

Inc in EPO in response to chronic hypoxia/tumors, most common. Also occurs w abn hb and inc affinity for o2

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37
Q

Polycythemia Vera

Patho

A

Inc in all blood cells and splenomegaly. Inc sensitivity to GFs

38
Q

Polycythemia Vera

Stage 1 and 2

A

Pre dx but symptomatic

Initial remission w tx

39
Q

PV
Stage 3
Stage 4

A

3- myeloid metaplasia (myelofibrosis)
4- acute leukemia
Hypervolemic

40
Q

Polycythemia Vera
Minimize risk of what
Prevent progression to what
Tx

A

Thrombosis
Myelofibrosis and acute leukemia
Phlebotomy

41
Q

Mono

Background

A

Acute self limiting infec of B lymphocytes transmitted by saliva

42
Q

Mono
Patho
Viruses

A

Caused by Epstein Barr virus 85%. B cells have ebv receptor site. Other viruses may resemble IM.. CMV, hepatitis, influenza, HIV

43
Q

Mono

Symptoms

A

Fever, sore throat, swollen cervical nodes, inc lymphocyte ct, atypical lymphocytes (activated)

44
Q

Mono
__ complic are infrequent
>50% what
At least 10%

A

Serious
Lymphocytes
Atypical lymphocytes

45
Q

Leukemia

What it is

A

Malignant disorder of blood forming organs, excessive accum of leukemic cells. Genetic translocation between 9 and 22.

46
Q

Acute leukemia

What happens

A

Presence of undifferentiated/immature cells. Usually blasts. Progressive neoplasm

47
Q

Chronic leukemia

What happens

A

Slow onset, predominant cell is mature but doesnt function normally

48
Q

ALL

What happens

A

> 30% of lymphoblasts in BM/blood. Most common in kids

49
Q

AML

What happens

A

Abn prolif of myeloid precursors. Immature blast replacement of normal cells

50
Q

CML

What it is

A

Myeloproliferative disorder, polycythemia Vera

51
Q

CLL

What it is

A

Accum of B lymph, failure to develop into plasma cells

52
Q

Malignant lymphoma

Begin as what

A

Malignant transformation of a lymphocyte and proliferation of lymphocytes, history ties, and derivatives in lymphoid tissues

53
Q

Malignant lymphoma
Injury to what
Categories

A

DNA of lymphocyte

Hodkins/non Hodgkins

54
Q

Hodgkin lymphoma

Cells, what happens to them

A

Progression of one group of lymph nodes to another. Reed sternberg cells in lymph nodes. Necessary for dx but not spec to Hodgkin

55
Q

Non Hodgkin lymphoma

Linked to what causes

A

Chromosome translocation, viral and bacterial infec, enviro agents, immunodeficiencies, and autoimmune disorders

56
Q

Non Hodgkin lymphoma

Patho

A

Clonal expansion of B/T/NK cells

Changes in proto oncogenes and tumor suppressor genes contribute to immortality and inc in malignant cells

57
Q

Clinical diff w non-Hodgkin
Nodal involvement
Extranodal involvement
Extent

A

Mult periphery nodes. Mesenteric nodes common. Noncontinguous. Common extranodal. Rarely localized

58
Q

Hodgkin lymphoma
Nodal involvement
Extranodal
Extent

A

Localized to single axial group (cervical, mediastinal). Mesenteric rarely involved. Orderly spread and contiguous. Rare extranodal. Often localized

59
Q

Macrocytic normochromic anemias

A

Megaloblastic
Pernicious
Sickle cell

60
Q

Microcytic hypochromic anemias

A

Iron deficiency
Sideroblastic
Thalassemia

61
Q

Normocytic normochromic anemias

A

Aplastic
Hemolytic
Anemia of chronic disease

62
Q

What pulm/cv manifestations happen in PE

A

Inc dead space vent and right heart hypoxic vasoconstriction

63
Q

Virchows triad

A

Endothelial injury, hypercoagulability, abn blood flow

64
Q

Steps of thrombosis 4

A

Propagation (accum plt and fibrin)
Embolization (dislodge)
Dissolution (fibrinolytic activity)
Organization (inflam, fibrosis, EC SMS ingrowth) and recanalization

65
Q

What happens with cardiac/arterial thrombi

A

Begin at site of injury (plaque)/turbulence (bifurcation), retrograde growth.

66
Q

3 ways cardiac thrombi occur

A

MI to mural thrombus. RHD to MV Stenosis to LA dilation w afib augmenting atrial blood stasis to mural thrombus. Atherosclerosis.

67
Q

What happens in venous thrombi

What are they predisposed to

A

Local congestion, pain, swelling, rarely embolism. Edema and impaired venous drainage predisposes to infection from slightl trauma and varicose ulcers

68
Q

Deep venous thrombi come from where, what they do

A

Larger veins above knee. Embolization, asymptomatic, realize later. Stasis and hypercoag leads to CV failure and pro coag factors

69
Q

Thrombocytopenia
Ct is what
When spontaneous bleed happens
Often secondary to what

A

<100k. 10-15k/mm3.

Congenital/acquired conditions in which plt count or survival decreases

70
Q

What is ITP

A

Autoimmune increased plt destruction

71
Q

What is TTP

A

Revise this couldn’t read slide

72
Q

DIC
Not what
What happens

A

Not a primary disease. Activation of thrombin in microcirculation. Causes diffuse circulatory insufficiency in brain, heart, lung, kidneys. Ischemia, microinfarcts, and hemolysis occur.

73
Q

DIC

Multiple thrombi lead to what

A

Rapid consumption of plt and coagulation proteins. Consumptive coagulopathy.

74
Q

DIC

Acute v chronic

A

Acute- bleeding diathesis

Chronic- thrombotic complications

75
Q

What happens clinically in DIC

A

Shock, hypotension, inc in FDPs

76
Q

What is patho behind DIC

A

Activated thrombin > body’s antithrombin. Thrombin doesnt stay localized. Widespread ischemia, infarction, and organ hypoperfusion. Activating plasmin (fibrinolytic) leads to FDP and d dimer increase

77
Q

9 steps of DIC coag

A

Suppress normal control of homeostasis. Induce TF release. Fibrin clot. Fibrinolysis. Diminished fibrinolysis. Consumption of plt and clotting factors.

78
Q

Inflammatory states

A

Atherosclerosis, obesity, dm 2, tumors

79
Q

Anti plt refers to what

A

Preventing the plt from being activating and releasing alpha granules that have clotting mechanisms

80
Q

Anticoags refer to what

A

Prevent plt from binding together

81
Q

Cox leads to what

Adp causes what

A

Cox- plt activation

Adp- plt binding together and activation

82
Q

What % of blood contains plt

A

Less than 1%

83
Q

What is included in intrinsic pathway of regulation

A

Thrombin cleaves fibrinogen to fibrin

84
Q

Which 3 factors inhibit plt agg

A

Prostacyclin, no, and adp

85
Q

What does AT3 do

A

Binds thrombin, inhibits clot formation. In the endothelium

86
Q

What does tissue factor pathway inhibitor do

A

Tissue factor needed for clot formation. Inhibit it, no clot.

87
Q

Thrombomodulin- what does it do

A

Activates protein c which causes inhib of factors 5 and 8, cleaves it to inactivate. 5 and 8 in intrinsic pathway. Inhibits clot

88
Q

What factors favor thrombosis

A

Exposiure of collagen and VWF

89
Q

What can activate endothelium

A

Ht, shear stress, turbulent flow, bacterial infection.

90
Q

What can cause abn blood flow

A

Turbulence, stasis, disrupt laminar flow, prev diluting of clotting factors, retard in flow.
Plt activ by atherosclerotic plaques, aneurysms, mi, mv stenosis

91
Q

What happens in HIT

A

PF4 released from a granules in plt, forms complex w heparin. IgG antibodies attack this complex and activate plt. Overall decrease in plts

92
Q

What happens TTP

A

Plts aggregate and occlude arterioles and capillaries. VWF exposed. Can be acute or chronic is relapsing. Acute is ideopathic.

Patho (11 decks)

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