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Pathology > Damjanov chapter 6 > Flashcards

Damjanov chapter 6 Flashcards

1
Q

In adults, where is the hematopoietic bone marrow confined to? What are the first signs of hematopoiesis in the embryo? What later are the sites for fetal hematopoiesis?

A

Axial skeleton: sternum, ribs, vertebrae, and pelvic bones;
yolk sac;
liver and spleen

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2
Q

The hematopoietic bone marrow comprises of the ____ and the _____

A

Hematopoietic cells and bone marrow stroma

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3
Q

What are sinusoids?

A

Bv’s with fenestrated walls that allow newly formed blood cells to enter the circulation

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4
Q

With aging, hematopoietic elements ____ in number, and the ____ become more numerous, replacing up to _____ of the total hematopoietic bone marrow in the elderly

A

decrease; fat cells; 70%

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5
Q

Adult bone marrow has 25 to 500 million what? What is their marker and what do they resemble?

A

Pluripotent SC’s!!

Small lymphocytes and marker is CD34

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6
Q

What stimulates RBC precursors, platelet production, neutrophil precursor differentiation?

A

EPO, thrombopoietin, G-CSF

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7
Q

Four requirements for normal hematopoiesis:

A
  1. Proteins (unusual dietary habits, eating disorders, malabsorption problematic, as is increased demand during pregnancy or childhood)
  2. Iron (need for Hb)
  3. Vitamin B12 (need to make THF as well as MMA for the spinal cord)
  4. Folic acid (issues with inadequate intake, absorption, or utilization)
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8
Q

Shelf life of RBC’s is what? Where can old RBC’s be destroyed?

A
  1. 120 days

2. Spleen by splenic macrophages or in the blood vessels

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9
Q

After intravascular hemolysis, what does Hb bind? Where does the Hb go? What can happen to a part of the Hb?

A

Albumin; liver;
can be oxidized into MetHb, which is degraded into globin and oxidized heme, or ferriheme, which binds to hemopexin to go to the liver

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10
Q

Arneth index:

A

a curve based on the number of segments of neutrophilic nuclei (left shift indicates younger PMNs, whereas right shift indicates more aging PMNs)

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11
Q

Aging platelets are _____ by what, and may be ____ where?

A

phagocytosed; splenic or hepatic phagocytic cells;

consumed at sites of minor endothelial cell injury, activating intravascular coagulation

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12
Q

Tissue derivatives of monocytes act as what? Macrophages produce ____ and many other biologically active substances

A

Antigen-presenting cells;

cytokines

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13
Q

Platelets are essential for ____ but they also secrete what?

A

Clotting; mediators of inflammation

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14
Q

How can you shift the O2 sat curve to the left?

A
  1. Increase pH of blood into alkaline range
  2. Reducing the PCO2
  3. Reducing the temp
  4. Decreasing concentration of 2,3-BPG
  5. Increasing Hb F and decreasing HbS
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15
Q

Increased amounts of methemoglobin can lead to what?

A

Possible cyanosis due to drugs and toxins

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16
Q

PMNs are efficient at fighting bacteria because (4 things)

A
  1. High mobiity (can exit blood vessels and reach site of infection quickly)
  2. Sensitivity to chemotactice stimuli (made by bacteria and injured tissue cells)
  3. Phagocytic capacity (can ingest bacteria and facilitated by opsonins)
  4. Bactericidal activity (use O2-dependent and O2-independent enzymatic mechs)
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17
Q

Eosinophils more prominent if an infection is _____; react most prominently to what?

A

long-lasting; parasites;

alson with allergies, autoimmune diseases, and skin diseases

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18
Q

T lymphocytes, B lymphocytes, and NK cells approximate percentages in circulating blood?

A

10-15, 70-80, 10-15

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19
Q

Platelets released from the BM are carried to where?

A

Spleen, their primary reservoir

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20
Q

Platelets contain what? 4 things

A
  1. Mitochondria (generate energy; glycogen in cytoplasm)
  2. Granules (alpha granules with vWF, fibrinogen, factor V, PDGF, TGF-beta; dense granules with ADP)
  3. Cytoskeleton
  4. Plasma membrane:
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21
Q

In defective primary hemostasis, what is prolonged? What about in secondary hemostasis?

A

Bleeding time;

PTT and aPTT

22
Q

Some physical findings for a hematologic disease?

A
  1. Easy fatigability (reduced capacity of blood to carry O2)
  2. Pallor (reduced concentration of Hb in anemia)
  3. Ruddy red face (polycythemia with hypervicous blood and dilation of retinal blood vessels)
  4. Jaundice
  5. Tachycardia (compensatory)
  6. Oral mucosal changes (beefy red tongue in iron deficiency anemia; glossitis with B12, B9 deficiency)
  7. Recurrent infection: leukopenia, aplastic anemia, leukocytes screwed up
  8. Excessive bleeding: hemophilia presents with post-traumatic bleeding, hemarthrosis, or prolonged bleeding after surgeries
  9. Lmyphadenopathy
  10. Splenomeg (can see in leukemia and lymphoma)
23
Q

Mnemonic for causes of splenomeg?

A

SPLENIC: splenitis (inflammation, especially sepsis), portal hypertension, leukemia/lymphoma, erythrocyte disorders, neonatal disorders due to inborn genetic errors, immune disorders, cardiac failure!!!

24
Q

Variation in size of RBCs and presence of several pops of cells are

A

best dectected by calculating RBC distribution width (RDW)

25
Q

Increase in number of neutrophils may be due to? 5 things

A
  1. Increased bone marrow production of neutrophils
  2. Accelerated maturation process
  3. Increased release of neutrophils from BM
  4. Redistribution of neutrophils in circulation
  5. Decreased splenic trapping
26
Q

Causes of neutophilia

A
  1. Acute bacterial infection (appendicitis, pneumonia)
  2. Chronic bacterial infection (chronic suppurative osteomyelitis)
  3. Autoimmune diseases (SLE, dermatomyositis, vasculitis)
  4. Tissue injury/necrosis (MI, trauma)
  5. Metabolic disorders (uremia, gout, acidosis)
  6. Decreased WBC trapping (splenectomy)
  7. Therapy (growth factor therapy, like G-CSF, and steroids)
  8. Myeloproliferative disorders (polycythmia vera, CML, myelofibrosis)
  9. Neoplasms (lymphoma, melanoma)
27
Q

Causes of eosinophilia is what?

A

PARASITE: parasitic infection (protozoan like amebiasis or toxoplasmosis, or metazoan like intestinal worm), allergy (hay fever, asthma, eczema), rx (drug reaction), autoimmune disorders (pemphigus vulgaris, Churg-Strauss), skin diseases, infections (nonparasitic, like fungal or bacterial), tumors (Hodgkins, NH, myeloproliferative disorders, eosinophilic leukemia), eosinophilic syndromes of unknown origin (hypereosinophilic syndrome)

28
Q

Lymphocytosis is what? Lymphocytopenia is what?

A

> 5000/uL (acute infections, chronic infections, noninfectious causes, neoplasia);
<1000/uL (therapy-related, infections, autoimmune diseases, dietary deficiency and metabolic disorders, congenital immunodeficiency disorders)

29
Q

Causes of thrombocytopenia? What is the most common drug-induced immune thrombocytopenia?

A

Reduced production (aplastic anemia, radiation, Vit B12 and folate deficiencies, myelofibrosis, MD syndrome, HIV infection), dilutional, distributional (splenomegaly), immune destruction (SLE, ITP, heparin), consumptive (DIC, TTP, HELLP)

30
Q

Most common inherited bleeding disorder?

A

vWF (increases bleeding time and aPTT)

31
Q

PT used as a clinical test for what?

A
  1. Anticoagulant therapy
  2. Evaluating function of the liver
  3. Screening test for coagulation deficiencies
32
Q

What do you add to test PT? PTT?

A

Phospholipids, tissue factor (factor III), and calcium;

kaolin added to citrated plasma, and later phospholipid and calcium

33
Q

How can you determine if an inhibitor is present, and what would that affect time wise?

A

Mix patient plasma with normal plasma to see if PT or PTT change (examples are anti-facotr VIII or lupus anticoagulant)

34
Q

Thrombin helps make what? Plasmin does what?

A

Make fibrin, which is stabilized factor XIIIa;
convert fibrinogen into fibrin degradation products that can cause platelet dysfuction, as well as mediating fibrinolysis to produce D-dimers

35
Q

What level is elevated in DIC? When is it not elevated? What is FDP elevated in plasma?

A

Fibrin D-dimers; not in DVT or PE;

hypercoag states like DIC, DVT, PE, preeclampsia

36
Q

Reduced serum ___ is a reliable sign of iron deficiency. What does it correlate with?

A

ferritin;
low total serum iron concentration and reduced transferrin saturation; reduced amounts of hemosiderin in bone marrow macrophages

37
Q

In PBS, smears of patients with iron deficiency anemia, RBCs appear ____ and what else?

A

Pale (hypochromic), vary in size (anisocytosis) and shape (poikilocytosis)

38
Q

Pernicious anemia: think of p’s

A

Parietal cells of the stomach (produce IF and destroyed by antibodies), posterior columns of the spinal cord, proprioception, paraparesis, psychosis

39
Q

Causes of aplastic anemia

A

Primary; secondary (drugs, radiation therapy, toxic chemicals, viral infections, immune disorders, myelofibrosis)

40
Q

Hemolytic anemia clinical and lab findings:

A
  1. Hypoxia
  2. Acute hemolysis (elevated serum LDH, hemoglobinemia, free Hbb binds to haptoglobin to go to liver, hyperbilirubinemia and jaundice follow; hemoglobinuria, hemosiderinuria when renal tubular cells shed)
  3. Chronic hemolysis: get jaundice; potential formation of biliary stones
  4. splenomegaly: could have autosplenectomy and reduced size
  5. Reduced RBC life span and sequestration into liver and spleen
  6. Increased erythropoiesis: also more reticulocytes
  7. Expansion of hematopoiesis can replace fatty bone marrow and you get chipmunk facies and crew cut in skull
  8. Extramedullary hematopoiesis (could be spleen or liver usually)
41
Q

Polycythemia vera would show what?

A
  1. Increased RBC count
  2. High Hct values
  3. High Hb values
  4. Increased total RBC mass
  5. Increased WBC count
  6. Increased platelet count
42
Q

Clnical findings in PV?

A
  1. Increased RBC volume
  2. Hyperviscosity of the blood
  3. Thrombosis
  4. Bleeding tendency
  5. Splenomegaly (pooling of RBCs, WBCs, and platelets in spleen)
  6. Hyperuricemia: uric acid generated in hyperactive bone marrow
  7. Histamine excess: pruritus and peptic ulcer formation
  8. Hypermetabolism
43
Q

In relative polycythemia, red cells mass is ____, but the plasma volume is ____; in contrast to PV in which the volume of RBCs is ____ and the plasma volume _____

A

normal; decreased;

increased; normal

44
Q

In CML, what would you see?

A
  1. Constitutional symptoms
  2. Elevated WBC count
  3. Reduced neutrophil alkaline phosphatase
  4. Reduced RBC count
  5. Variable platelet counts
  6. Hyperuricemia
  7. Splenomegaly
  8. Hypercellular bone marrow
45
Q

Three phases of CML:

A

chronic, stable phase (1-5 years), accelerated (appearance of blast cells and reduced RBC and platelet counts), and then blast crisis (>20%) with potential transition to AML

46
Q

Clinical findings of AML?

A

TAL

47
Q

Clinical features of CLL?

A
  1. Lymphocytosis
  2. Clonal proliferation of lymphocytes (could see CD5 markers, which is aberrant for B cells)
  3. Chromosomal abnormalities (don’t divide readily in culture)
  4. Depressed serum immunoglobulins (could be monoclonal spike of abnormal immunoglobulin, the M protein)
  5. Anemia and thrombocytopenia
  6. Lymphadenopathy and splenomegaly
  7. Signs of hypermetabolism (the B symptoms)
  8. Elevated serum LDH, uric acid, and beta2-microglobulin
48
Q

Clinical symptoms of lymphoma?

A
  1. Lymphadenopathy
  2. Constitutional symptoms: fever, weight loss, night sweats, fatigue
  3. Immunologic disturbances: loss of delayed hypersens, hypogammaglobulinemia, monoclonal globulin production
  4. Rapidly evolving lymphadenopathy with involvement of extranodal sites (extranodal spread can happen with highly aggressive lymphomas)
  5. Extranodal masses: e.g. mycosis fungoides or Burkitt’s in the jaw
49
Q

T/F: alkaline phosphatase is not elevated in lytic lesions of the bones in MM

A

True: meaning that osteoclasts are not activated!!

50
Q

____ stimulates the release of vWF from endothelial cells and is useful for what type of vWF disease?

A

Desmopressin; type 1 vWF

51
Q

Most common causes of platelet dysfunction are what?

A

Aspirin and NSAIDS

Pathology (40 decks)

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