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6010 Advance Patho Test 5 COMPLETE ☑️ > Module 10: Alterations Of RBC’s, Platelets, WBC’s And Lymphoid/Hemostatic Function (b) > Flashcards

Module 10: Alterations Of RBC’s, Platelets, WBC’s And Lymphoid/Hemostatic Function (b) Flashcards

1
Q

Anemia

-Definition

A
  1. Reduction in total number of erythrocytes in the circulating blood OR in the quality or quantity of hemoglobin
    - Impaired Erythrocytes production
    - Acute or chronic blood loss
    - Increased erythrocytes destruction
    - Combination of all the above
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2
Q

Anemia

-Classifications

A
  1. Etiology
  2. Morphology — Mainly based on MCV -macrocytic, microcytic, normocytic
  3. Hemoglobin content —Identified by ending in “chromic”

Other Descriptors

  • Anisocytosis — RBCs are present in various sizes (RDW) — Accelerated RBC destruction
  • Poikilocytosis — RBCs are present in various shapes (Peripheral blood smear) — Possible Blood borne cancers — Ex: SICKLE CELL
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3
Q

Anemia

-Manifestations

A
  1. MAJOR physiologic manifestation is HYPOXIA TEST

2. Classic Sx’s of anemia — Fatigue, weakness, dyspnea, and pallor

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4
Q

Anemia

-Compensatory Mechanisms

A
  1. CV Function — Increased preload, HR, & Stroke volume; reduced Afterload —Vasodilation is hypoxia induced — Lower blood viscosity
  2. Respiratory Function — Dyspnea
  3. Nervous System Function — myelin degeneration & Parasthesias
  4. GI Function — Pain, N/V anorexia
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5
Q

Normochromic-Macrocytic Anemias **

-Info

A
  1. Megaloblastic anemias — RBCs are unusually large
  2. Defective DNA synthesis — D/t deficiencies in vitamin B12 or folate
  3. DNA synthesis is altered while RNA processes occur at normal rate — Results in unequal growth of nucleus and cytoplasm
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6
Q

Normochromic-Macrocytic Anemias **

-Vitamin B12 Deficiency Anemia

A
  1. Pernicious anemia is MOST COMMON subtype — Results from lack of INTRINSIC factor from gastric parietal cells
    -Main Cause is: Atrophic Gastritis
    —Autoimmune forms — Parietal cell antibodies — Intrinsic factor antibodies
    -H. Pylori infection destroys parietal cells
    -Prolonged PPI and H2 blocker use — Gastric acid is needed to cleave Vit B12
    -Gastrectomy — Loss of gastric parietal cells
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7
Q

Normochromic-Macrocytic Anemias **

-Pernicious Anemia (Vit B12) Clinical Manifestations

A
  1. Weakness/Fatigue
  2. NEUROLOGIC Sx’s from nerve demyelination — NOT reversible even w/ Tx
  3. Paresthesias of feet and fingers — difficulty walking
  4. Loss of appetite, abdominal pain and weight loss
  5. Sore tongue that is smooth and BEEFY RED — Secondary to atrophic glossitis
  6. Often unrecognized in older adults d/t subtle slow onset and presentation (Develops over 20-30 yrs)
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8
Q

Normochromic-Macrocytic Anemias **

-Folate Deficiency Anemia

A
  1. Folate is essential vitamin for RNA and DNA synthesis
  2. Absorption of folate occurs in UPPER SMALL INTESTINE; self dependent
  3. Common in alcoholics and individuals w/ chronic malnourishment —Folate is stored in the liver
  4. Associated with FETAL NEURAL TUBE DEFECTS
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9
Q

Hypochromic-Microcytic Anemias

-Definition/Info

A
  1. Characterized by red cells that are abnormally small and contain reduced amounts of hemoglobin
    R/T
    -Disorders of iron metabolism
    -Disorders of porphyrin and heme synthesis
    -Disorders of globin synthesis
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10
Q

Hypochromic-Microcytic Anemias

-Iron-Deficiency Anemia

A
  1. Most common type of anemia worldwide
  2. Highest risk — Older adults, women, infants — Black females living in urban poverty HIGHEST RISK
  3. Associated w/ cognitive impairment in children
  4. Iron deficiency anemia and folate deficiency anemia are two LEADING causes of anemia in pregnancy
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11
Q

Hypochromic-Microcytic Anemias

-Iron-Deficiency Anemia Causes

A
  1. Inadequate dietary intake
  2. Chronic blood loss — Most Common in developed countries
  3. Chronic parasitic infections — Developing countries
  4. Metabolic or functional iron deficiency
  5. Menorrhagia — Excessive bleeding during menstruation

Ask Pt’s :: Any blood in stool?

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12
Q

Hypochromic-Microcytic Anemias

-Iron-Deficiency Anemia Clinical Manifestations

A
  1. Fatigue, weakness, SOB
  2. Pale earlobes, palms, and conjunctivae
  3. Brittle, thin, coarsly ridged and spoon-shaped nails — Concave or KOILONYCHIA **
  4. Red, sore, painful tongue — Severity of tongue pain coincides w/ severity of anemia
  5. Angular stomatitis — Dryness and soreness in corners of the mouth
  6. Symptomatic when Hgb is 7-8g/dl
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13
Q

Hypochromic-Microcytic Anemias

-Sideroblastic Anemia

A
  1. Group of disorders caused by defect in mitochondrial heme synthesis
    —Altered mitochondrial metabolism causes ineffective iron UPTAKE and results in dysfunctional hemoglobin synthesis
  2. Ringed sideroblasts in bone marrow are diagnostic
  3. Clinical manifestations — Hemochromatosis & Splenomegaly & Hepatomegaly
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14
Q

Normochromic-Normocytic Anemias

-Definition/Info

A
  1. Characterized by RBCs that are relatively normal size and hemoglobin content, but INSUFFICIENT NUMBER
  2. Least frequent w/ no common cause
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15
Q

Normochromic-Normocytic Anemias

-Aplastic Anemia

A
  1. Pancytopenia — Reduction or absence of ALL 3 types of blood cells (Ex: WBC, RBC, and PLT)
  2. Most aplastic anemias are AUTOIMMUNE disorders — Some d/t chemical exposure to benzene, arsenic, chemotherapy drugs
  3. Pure RBC aplasia — Only RBCs are affected
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16
Q

Normochromic-Normocytic Anemias

-Aplastic Anemia Patho

A
  1. AUTOIMMUNE destruction of hematopoietic stem cells or their progenitors at various stages of differentiation by CYTOTOXIC T-CELLS
  2. Clinical Findings — Characteristic lesion is a hypo cellular bone marrow that has been REPLACED WITH FAT
  3. Clinical Manifestations
    - Hypoxemia, pallor — occasionally brownish pigmentation of the skin
    - Weakness w/ FEVER and dyspnea w/ rapidly developing signs of HEMORRHAGING if PLT’s are affected
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17
Q

Normochromic-Normocytic Anemias

-Post-Hemorrhagic Anemia

A
  1. Acute blood loss from vascular space

2. Manifestations depend on severity of blood loss — If blood loss exceeds 2 liters, Shock sets in

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18
Q

Normochromic-Normocytic Anemias

-Hemolytic Anemia

A
  1. Accelerated destruction of RBCs — Congenital vs acquired
  2. Autoimmune hemolytic anemias
    —Autoantibodies against antigens normally on surface of erythrocytes
19
Q

Normochromic-Normocytic Anemias

-Autoimmune Reactive Antibody Types

A
  1. Warm-Reactive Antibody Type — IgG which binds at normal body temp 40 degrees C
  2. Cold agglutinin Type — IgM — Optimally binds at 31 degrees C — Can occur after Infections — Ex: Mono, mycoplasma PNA, TB
    —Occurs in lower temp areas — Ex: Fingers, toes, and ears — Can lead to gangrene
  3. Cold Hemolysin Type — IgG Occurs in children <10 yrs old — Intravascular hemolysis s/p exposure to cold — IgG auto-antibodies
    —Linked with Mums, measles, varicella, mycoplasma PNA
20
Q

Normochromic-Normocytic Anemias

-Drug-Induced Hemolytic Anemia

A
  1. Result from allergic reaction against foreign antigens

—Ex Meds: Penicillin, Cephalosporins (90%), hydrocortisone

21
Q

Normochromic-Normocytic Anemias

-Anemia of Chronic Disease (Inflammation)

A
  1. Seen in — AIDS, RA, SLE, Hepatitis, renal failure, & Malignancies
  2. Pathological Mechanisms TEST
    - Decreased erythrocytes life span
    - Suppressed production of erythropoietin
    - Ineffective bone marrow response to erythropoietin
    - Altered iron metabolism
  3. During inflammation, Neutrophils release LACTOFERRIN to bind to iron to reduce it’s availability for bacteria
22
Q

Myeloproliferative RBC Disorders

-Polycythemia

A
  1. Relative Polycythemia — Dehydration — Fluid loss results in relative increase of RBCounts & Hgb and Hct values — Resolves w/ fluid intake
  2. Polycythemia Vera
    - Chronic neoplastic, NONMALIGNANT condition
    - Splenomegaly
    - Donate blood is Tx
23
Q

Myeloproliferative RBC Disorders

-Iron Overload

A
  1. Primary — Hereditary hemochromatosis
    -Common inherited, autosomal recessive disorder of iron metabolism
    -Excess iron deposited in liver, pancreas, heart, joints, endocrine glands, causing TISSUE DAMAGE
    LEADS TO — Bronze skin, Hepatomegaly, DM, Cardiomegaly
    -TX is phlebotomy, DO NOT take vitamin C or Iron

OR
2. Secondary — Cytoblastic anemia, Aplastic anemia, Dietary overload

24
Q

Neutropenia

-Definition/Info

A

Reduction in circulating neutrophils

  1. Primary — Kostmann & box syndrome
    - Congenital — Cyclic neutropenia and neutropenia w/ congenital immunodeficiency diseases — Multiple syndromes
    - Acquired — Hypoplastic anemia, aplastic anemia, leukemia’s, lymphomas, myelodysplastic syndrome
  2. Secondary — Lower count from other disorders —Ex: Immune disorders and drugs — Lupus, Splenomegaly, CA meds
25
Q

Lymphocytosis & Lymphocytopenia

A
  1. Lymphocytosis
    - Acute viral infections — EBV
    - Other causes — Leukemia, lymphomas, some chronic infections
  2. Lymphocytopenia
    —Causes — Immune deficiencies, lymphocyte destruction from drugs, viruses, or radiation — AIDS
26
Q

Infectious Mononucleosis

-Info

A
  1. Acute, Self-limiting infection of B-Lymphocytes transmitted by saliva through personal contact**
  2. Commonly caused by the Epstein-Barr Virus EBV (85%) — B lymphocytes have EBV receptor site
  3. Other viruses that cause IM
    - Cytomegalovirus CMV — Think CMV for IM infection in person >40 yrs old
    - Hepatitis
    - Influenza
    - HIV
27
Q

Infectious Mononucleosis

-Classic Triad

A
  1. Fever, Tonsillar enlargement, & Lymphadenopathy of cervical or auricular lymph nodes (Found 98% of the time together in positive IM)**
  2. Diagnostic is the MONOSPOT qualitative test for heterophilic antibodies 98% specific
28
Q

Leukemia’s

-Info

A
  1. Malignant disorders of the blood and blood-forming organs
  2. Uncontrolled proliferation of malignant leukocytes
    - Overcrowding of bone marrow
    - Decreased production and function of normal hematopoietic cells
  3. Classification
    - Predominant cell of origin — Myeloid or lymphoid
    - Rate of progression — Acute or chronic
29
Q

Leukemia’s

-Acute Vs Chronic

A
  1. Acute Leukemia
    —Presence of undifferentiated or immature cells — Usually BLAST CELLS
    —RAPID onset w/ narrow window in which to treat
  2. Chronic Leukemia
    —Predominant cell is MATURE but does not function normally
    —SLOW progression

SEE PHOTO IN PHONE**

30
Q

Leukemia’s

-Acute Lymphocytic Leukemia (ALL)

A
  1. MOST COMMON childhood leukemia
  2. Greater than 30% lymphoblasts in the bone marrow or blood
  3. Genetic anomaly — PHILADELPHIA CHROMOSOME
    - Reciprocal translocation results in abnormal chromosome — Between chromosomes 9 and 22
31
Q

Leukemia’s

-Acute myelogenous Leukemia (AML)

A
  1. MOST COMMON adult leukemia (Mean age 67 yrs)

Causes

  • Abnormal proliferation of myeloid precursor cells
  • Decreased rate of apoptosis
  • Arrest in cellular differentiation

RISK factors

  • Down syndrome
  • Exposure to radiation, benzene, and chemotherapy
  • Hereditary conditions
32
Q

Leukemia’s

-Clinical Manifestations of ACUTE leukemia’s

A
  1. Fatigue — Anemia
  2. Bleeding — Reduced PLTs
  3. Fever — Infection from decreased healthy WBC’s
  4. Bone pain — Proliferation of lymphoblasts and myeloblasts stretch periosteum of the bone
  5. CNS — Leukemic infiltration — Cerebral bleeding and HA, blurred vision, meningeal irritation
33
Q

Leukemia’s

-Chronic Leukemia’s

A
  1. Chronic Lymphocytic Leukemia (CLL) — COMMON in adults older than 50 yrs (70% Asymptomatic at diagnosis
    —Affects monoclonal B lymphocytes — One single ancestral cell mutated
    —FAMILIAL tendency
  2. Chronic Myelogenous Leukemia (CML) — Usually Dx’d in adults (60 -80yrs old)
    —Philadelphia chromosome is OFTEN PRESENT and BCR-ABL1 causes initiation of CML
34
Q

Leukemia’s

-Chronic Lymphocytic Leukemia manifestations

A
  1. Asymptomatic at time of Dx
  2. Lymphadenopathy is MOST COMMON finding
  3. Increased risk of infection w/ encapsulated bacteria
35
Q

Leukemia’s

-Chronic Myelogenous Leukemia

A

Infections, fever, and weight loss

  1. Chronic Phase — 2-5 years — Sx’s may not be apparent
  2. Accelerated phase — 6-18 months — SPLENOMEGALY is primary sx
  3. Terminal Blast Phase — “BLAST CRISIS” — Survival ONLY 3-6 months
36
Q

Malignant Lymphomas

-Info

A
  1. Neoplasm of malignant lymphocytes in the lymphoid system
  2. Two major categories
    —HODGKIN lymphoma — Linked to EBV**
    —Non-Hodgkin lymphoma
  3. Result from genetic mutations or a viral infection
Leukemia = CA in the bone marrow and blood
Lymphomas = CA is in lymph nodes and other tissues (Thymus & Bone marrow)

SEE PICTURE IN PHONE

37
Q

Malignant Lymphomas

-Hodgkin Lymphoma

A
  1. Proliferation of abnormal B cells (Reed-Sternberg cells) that may be linked to EBV infectionTEST
  2. Reed-Sternberg cells in the lymph nodes
    - Derived from malignant B cells that usually become binucleate
    - Necessary for the dx but not specific to Hodgkin lymphoma
    - Release cytokines — iL10
38
Q

Malignant Lymphomas

-Hodgkin Lymphoma Clinical Manifestations

A
  1. Enlarged PAINLESS neck lymph nodes
  2. Lymphadenopathy, causing pressure or obstruction
  3. Mediastinal mass
  4. Fever, weight loss, night sweats, pruritus, fatigue

Tests
-CXR, Lymphangiography, BIOPSY (GOLD STANDARD)

39
Q

Malignant Lymphomas

-Non-Hodgkin Lymphoma

A
  1. Generic term for a diverse group of lymphomas — B-cell neoplasms make up 80 - 90%
40
Q

Malignant Lymphomas

-Non-Hodgkin Lymphoma Clinical Manifestations

A
  1. Localized or generalized painless lymphadenopathy
  2. Retroperitoneal and abdominal masses w/ Sx’s of abdominal fullness and back pain
  3. Ascites and Leg swelling
  4. Dx Tx — BIOPSY
41
Q

Multiple Myeloma

-Definition/Info

A
  1. Plasma cells proliferate in the bone marrow
  2. Increased osteoclastic bone destruction
  3. Anemia 72%, Bone lesions 80%, Hypercalcemia** MOST CONCERNING, renal failure

Clinical Manifestations

  • Cortical and medullary bone loss
  • Skeletal pain
  • Recurring infections d/t loss of humoral immune response

Tx is mostly supportive — POOR PROGNOSIS

42
Q

Disorders of Platelets

-Thrombocytopenia

A
  1. Platelet count <100,000/mm
  2. Caused by — Hypersplenism, Autoimmune dz, hypothermia, & viral/bacterial infections that cause DIC
  3. Clinical Manifestations — Petechiae and Purpura — Frank bleeding from mucous membranes (epistaxis, hematuria, Menorrhagia, bleeding gums)
43
Q

Disorders of Platelets

-Immune Thrombocytopenic Purpura ITP **

A
  1. IgG antibody targets PLT glycoproteins TEST
  2. One of the MOST COMMON childhood bleeding disorders — s/p viral infections
  3. Manifestations — Petechiae & Purpura, progressing to major hemorrhage
44
Q

Disorders of Platelets

-Essential (Primary) Thrombocythemia

A
  1. PLT count > 400,000/mm
  2. Myeloproliferative disorders of PLT precursor cells — Megakaryocytes in bone marrow are produced in EXCESS
  3. Microvasculature Thrombosis — More concerning

6010 Advance Patho Test 5 COMPLETE ☑️ (6 decks)

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