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Pathophysiology > Chapter 13_2 flashcards > Flashcards

Chapter 13_2 flashcards

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1
Q

Anemia of Acute Blood Loss: Definition

A

Precipitous drop in RBCs due to hemorrhage (e.g., trauma, internal bleeding). Rapid development of NCNC anemia.

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2
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Anemia of Acute Blood Loss: Pathophysiology

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Loss of RBCs & plasma volume -> tissue hypoxia. Compensatory mechanisms: sympathetic nervous system, RAAS, ADH. Reticulocytosis if marrow responds. Hemodilution can occur as fluid shifts into vasculature.

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3
Q

Anemia of Acute Blood Loss: Signs & Symptoms (Volume Dependent)

A

<15% loss: Orthostatic hypotension, anxiety. 15-30% loss: Tachycardia, vasoconstriction, decreased urine output, restlessness. 30-40% loss: Worsening tachycardia (>120bpm), weak pulse, cool/pale skin, hypotension, oliguria. >40% loss: Profound shock, confusion, severe hypotension, scant/no urine.

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4
Q

Anemia of Acute Blood Loss: Diagnosis

A

CBC: NCNC anemia, high reticulocyte count. Hypotension. FOBT if GI bleed suspected. Imaging (CT) for occult internal bleeding. Blood type/crossmatch.

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5
Q

Anemia of Acute Blood Loss: Treatment

A

Stop bleeding (hemostasis). Restore blood volume (IV normal saline initially, then blood transfusion). Treat shock. Investigate/treat underlying cause (e.g., endoscopy for GI bleed).

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6
Q

Anemia of Chronic Blood Loss: Definition & Common Causes

A

Slow, gradual blood loss (e.g., GI tract - peptic ulcer, colon cancer; or excessive menstrual loss - menorrhagia). Often subtle and asymptomatic.

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7
Q

Anemia of Chronic Blood Loss: Pathophysiology

A

Major problem: Iron-deficiency anemia due to gradual depletion of body’s iron stores as RBCs (and their iron) are lost and not recycled.

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8
Q

Anemia of Chronic Blood Loss: Diagnosis

A

CBC: Microcytic hypochromic anemia (MCHC). Low serum iron, low ferritin, high TIBC. FOBT. Endoscopy/colonoscopy if GI bleed suspected.

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9
Q

Anemia of Chronic Blood Loss: Treatment

A

Remedy source of bleeding. Iron replacement therapy (oral ferrous sulfate or parenteral iron). Transfusion if Hgb very low (<7 g/dL).

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10
Q

Hemolytic Anemia: General Definition & Causes

A

Decreased RBC mass due to premature erythrocyte destruction outpacing bone marrow production. Causes: Hemoglobinopathies, medication side effects (cephalosporins, penicillins, NSAIDs), autoimmune disorders, hereditary spherocytosis, transfusion reactions, HDN.

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11
Q

Hemolytic Anemia: Intravascular vs. Extravascular

A

Intravascular: Occurs within circulating blood. Extravascular: Splenic destruction, lysis in reticuloendothelial system, or mechanical destruction (e.g., prosthetic valves).

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12
Q

Hemolytic Anemia: Autoimmune Types

A

Warm Agglutinin Syndrome: IgG antibodies destroy RBCs at any temperature. Cold Agglutinin Syndrome: IgM antibodies destroy RBCs at low temperatures.

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13
Q

Alloimmune Hemolysis: Definition & Examples

A

Antibodies formed against antigens on foreign RBC surfaces. Examples: Transfusion reactions, Hemolytic Disease of the Newborn (HDN).

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14
Q

Hemolytic Anemia: Signs & Symptoms

A

General anemia symptoms (fatigue, pallor, SOB, tachycardia) PLUS: Chills, jaundice (from hyperbilirubinemia), dark urine (urobilinogen), splenomegaly.

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15
Q

Hemolytic Anemia: Diagnosis

A

CBC (anemia), elevated reticulocyte count. Increased bilirubin, methemoglobin. Peripheral smear: anisocytosis, poikilocytosis, spherocytosis (misshapen/damaged RBCs). Hgb electrophoresis, bone marrow exam, autoantibody tests.

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16
Q

Hemolytic Anemia: Treatment

A

Depends on cause. Folic acid & iron replacement. Corticosteroids. Immunosuppressive drugs, splenectomy (for autoimmune cases). Transfusions in emergencies.

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17
Q

Hemoglobinopathy: Definition (as cause of hemolytic anemia)

A

Inherited disorder of Hgb structure leading to RBC destruction. Abnormal Hgb carries O2 inefficiently, blood undergoes frequent hemolysis. Examples: Sickle Cell Anemia, Thalassemia.

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18
Q

Sickle Cell Anemia (SCA): Definition & Genetics

A

Inherited hemoglobinopathy (Hgb S) mainly in African, Middle Eastern, Mediterranean descent. Autosomal recessive. Homozygous (SCA disease) vs. Heterozygous (SCA trait - milder/asymptomatic unless stressed).

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19
Q

SCA: Etiology

A

Genetic mutation causing valine substitution for glutamic acid in beta Hgb chain -> Hgb S. RBCs distort to sickle shape under hypoxia, stress, dehydration, infection.

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20
Q

SCA: Pathophysiology

A

Hgb S is fragile. Sickled RBCs are destroyed by immune system (hemolysis, shortened lifespan 10-20 days) -> severe hemolytic anemia. Sickled cells occlude capillaries -> vaso-occlusive crises, ischemia, organ damage.

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21
Q

SCA: Vaso-Occlusive Crises

A

Extremely painful episodes of ischemia due to sickled RBCs blocking blood flow. Common sites: chest, abdomen, long bones, joints. Triggered by cold, hypoxia, infection, dehydration, stress, exertion, pregnancy.

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22
Q

SCA: Clinical Manifestations

A

Anemia symptoms. Jaundice, gallstones (from hyperbilirubinemia). Severe pain during crises. Acute chest syndrome (pulmonary infarction). Increased infection risk (splenic dysfunction). Growth retardation, osteomyelitis, stroke (children). Hand-foot syndrome. Priapism. Renal necrosis. Retinal damage.

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23
Q

SCA: Diagnosis

A

Newborn screening for Hgb S. Hgb electrophoresis (differentiates homozygous/heterozygous). CBC (anemia), peripheral smear (sickle cells), reticulocytosis.

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24
Q

SCA: Treatment

A

Vaso-occlusive crisis: Oxygen, hydration, pain meds (opiates), prophylactic antibiotics. Hydroxyurea (increases Hgb F, reduces crises). Folic acid supplements. Blood transfusions (risk iron overload -> chelation). Bone marrow transplant (curative but donor challenge). Gene therapy (CRISPR-Cas9) experimental.

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25
Thalassemia: Definition & Genetics
Inherited Hgb synthesis defect (alpha or beta chain missing/variant). Common in Mediterranean, African, SE Asian descent. Autosomal recessive. Minor (heterozygous, carrier, mild/no symptoms) vs. Major (homozygous, moderate/severe disease, e.g., Beta thalassemia major/Cooley's anemia).
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Thalassemia: Pathophysiology
Deficient Hgb chain synthesis -> reduced Hgb & RBC production. Unaffected chains accumulate -> interfere with RBC maturation -> defective RBCs destroyed (hemolysis) in marrow/spleen. Heinz bodies (pathological polypeptide fragments) form in RBCs. Exaggerated erythropoiesis -> bone marrow expansion/osteopenia.
27
Thalassemia: Clinical Manifestations
Anemia symptoms. Severe forms: Early childhood symptoms, require frequent transfusions. Bone pain, bone deformities ('chipmunk cheeks', 'hair-on-end' skull on x-ray). Hepatosplenomegaly (protuberant abdomen). Iron overload (hemochromatosis) from hemolysis/transfusions. Jaundice, dark urine, gallstones.
28
Thalassemia: Diagnosis
CBC: Microcytic hypochromic anemia. Hgb electrophoresis (identifies abnormal Hgb, e.g., Hgb A2 in beta thalassemia). Iron studies (to differentiate from iron deficiency). Genetic testing. X-rays (bone changes).
29
Thalassemia: Treatment
Asymptomatic trait: No treatment, genetic counseling. Severe forms: Transfusions, infection prevention (immunizations), splenectomy (increases infection risk), iron chelation, folic acid. Enhancement of Hgb F (Luspatercept). Bone marrow transplant, gene therapy (experimental).
30
Hereditary Spherocytosis: Definition & Genetics
Familial hemolytic disorder from lack of RBC membrane proteins -> fragile, spherical RBCs. Autosomal dominant. Most common in Northern European descent.
31
Hereditary Spherocytosis: Pathophysiology & Complications
Spherocytic RBCs sequestered/destroyed in spleen -> splenomegaly. Complications: Aplastic crisis (rapid Hgb drop), megaloblastic crisis (folate deficiency), hemolytic anemia, cholecystitis/cholelithiasis, severe neonatal hemolysis.
32
Hereditary Spherocytosis: Treatment
Blood transfusions, splenectomy. Lifelong folic acid supplementation (1mg/day) to prevent megaloblastic crisis.
33
Blood Transfusion Reactions: Hemolytic Type (Acute)
Recipient antibodies attack donor RBC antigens (usually ABO incompatibility due to clerical error). Rapid intravascular hemolysis. Symptoms (fever, chills, flushing, nausea, IV site burning, chest tightness, restlessness, back/joint pain, tachycardia, tachypnea) appear quickly. Severe: hypotension, bleeding, hemoglobinuria, shock, renal failure.
34
Blood Transfusion Reactions: Nonhemolytic Febrile & Minor Allergic
Nonhemolytic febrile: From cytokines in stored blood. Fever, chills, malaise 1-6 hrs post-transfusion. Minor allergic: From donor plasma proteins. Urticaria.
35
Blood Transfusion Reactions: Anaphylactic
Rare, often in IgA deficient patients with anti-IgA antibodies. Rapid onset (<10mL transfused) of dyspnea, flushing, urticaria, abdominal pain, bronchospasm, hypotension, facial/tongue edema.
36
Blood Transfusion Reactions: Treatment
Stop transfusion immediately. Saline IV. Hemolytic: Support renal function (diuretics). Anaphylactic: Epinephrine, corticosteroids, antihistamines, vasopressors. Febrile/Allergic: Acetaminophen, antihistamines, steroids.
37
Hemolytic Disease of the Newborn (HDN): Mechanism
Maternal antibodies attack fetal/neonatal RBC surface antigens (A, B, or RhD). ABO incompatibility (IgM, usually mild postnatal hemolysis, jaundice). Rh incompatibility (can cause severe erythroblastosis fetalis).
38
Erythroblastosis Fetalis (Box 13-4)
Severe HDN if Rh-positive fetus & Rh-negative mother (previously sensitized to Rh antigen). Maternal IgG anti-Rh antibodies cross placenta, attack fetal RBCs -> severe hemolysis, anemia, heart failure, hepatosplenomegaly, hyperbilirubinemia (kernicterus). RhoGAM given to Rh-neg mothers post-delivery to prevent sensitization.
39
Anemia Due to Lead Poisoning: Mechanism
Lead impairs Hgb synthesis, destabilizes RBC structure (-> hemolysis), shortens RBC lifespan. Toxic to neurological system (esp. children). Can cause iron-deficiency anemia by interfering with iron metabolism.
40
Lead Poisoning: Symptoms & Treatment
CNS: Irritability, behavioral changes, developmental delays, learning disabilities. Diagnosis: Blood lead levels. Treatment: Chelation therapy (EDTA, succimer, D-penicillamine) if lead >45 mcg/dL. Prevention is key.
41
Red Blood Cell Maturation Defects: General Causes
Deficiency of nutrients for RBC synthesis (protein, iron, B12, folic acid) or bone marrow dysfunction (e.g., aplastic anemia, lack of EPO).
42
Iron-Deficiency Anemia: Definition & Prevalence
Most common anemia worldwide. Due to inadequate iron for Hgb synthesis. High prevalence in women of childbearing age, older adults, underdeveloped countries.
43
Iron-Deficiency Anemia: Common Causes/Risk Factors
Inadequate intake (vegetarian diet, food insecurity), excessive menstrual blood loss (menorrhagia), GI blood loss (peptic ulcer, colon cancer, NSAID use), pregnancy/lactation, growth spurts, malabsorption (celiac, IBD, bariatric surgery), achlorhydria (older adults, PPI use).
44
Iron-Deficiency Anemia: Pathophysiology
Iron loss > absorption -> depletion of iron stores (ferritin) -> impaired Hgb synthesis -> microcytic, hypochromic RBCs. Severe: decreased RBC production.
45
Iron-Deficiency Anemia: Specific Signs & Symptoms
General anemia symptoms PLUS: Hair loss, cheilitis (cracked mouth corners), glossitis (smooth red tongue), koilonychia (spoon-shaped nails), PICA (craving nonfood substances).
46
Iron-Deficiency Anemia: Diagnosis (Box 13-5)
CBC: Low Hgb, Hct, MCV (microcytic), MCHC (hypochromic). Low serum iron, low serum ferritin, HIGH TIBC. Peripheral smear: small, pale RBCs. FOBT (for GI bleed).
47
Iron-Deficiency Anemia: Treatment
Oral iron (ferrous sulfate) + Vitamin C (enhances absorption). Parenteral iron if malabsorption/intolerance. Correct underlying cause.
48
Vitamin B12 Deficiency: Role of B12 & Consequences of Deficiency
B12 (cobalamin) needed for DNA synthesis in RBCs and normal myelin synthesis. Deficiency -> megaloblastic anemia, neurological dysfunction (subacute combined degeneration - numbness, weakness, gait issues; mental changes - depression, memory loss).
49
Vitamin B12 Deficiency: Common Causes/Risk Factors
Dietary lack (vegetarian/vegan, poor nutrition, alcohol use disorder), malabsorption (pernicious anemia, gastric atrophy/achlorhydria in elderly, gastric bypass, H. pylori, celiac/IBD, metformin use).
50
Pernicious Anemia: Specific Cause of B12 Deficiency
Autoimmune destruction of intrinsic factor (IF) in stomach. IF is essential for B12 absorption. Common in older adults.
51
Vitamin B12 Deficiency: Diagnosis (Box 13-6)
CBC: Low Hgb/Hct, HIGH MCV (megaloblastic), normal MCH/MCHC, low reticulocytes. Low serum B12. Elevated tHCy AND MMA levels. Pernicious anemia: IF antibodies, parietal cell antibodies, high gastrin.
52
Vitamin B12 Deficiency: Treatment
Correct underlying cause if possible. Parenteral B12 (hydroxocobalamin injections). High-dose oral B12 for some. Ensure adequate folic acid.
53
Folic Acid Deficiency: Consequence
Megaloblastic anemia (similar to B12 deficiency). Folic acid needed for DNA synthesis.
54
Folic Acid Deficiency: Risk Factors
Pregnant/lactating women, alcohol use disorder, chronic NSAID use, certain drugs (phenytoin, methotrexate), older adults (malnutrition), malabsorption (celiac, IBD), chronic inflammatory disorders.
55
Folic Acid: Role in Preventing Neural Tube Defects & Cardiovascular Disease
Prevents fetal neural tube defects (spina bifida, anencephaly) - 400mcg/day pre-conception/early pregnancy. Needed for homocysteine (tHCy) breakdown; high tHCy linked to endothelial injury/arteriosclerosis.
56
Folic Acid Deficiency: Diagnosis (Box 13-7)
CBC: Low Hgb/Hct, HIGH MCV. Low serum folic acid. Elevated tHCy, NORMAL MMA level (differentiates from B12 deficiency).
57
Folic Acid Deficiency: Treatment & ALERT
Oral folic acid (1mg/day). Correct underlying cause. ALERT: Must exclude B12 deficiency BEFORE treating with folic acid alone, as it can mask B12 deficiency's neurological damage while correcting anemia.
58
Aplastic Anemia: Definition & Pathophysiology
Bone marrow failure -> pancytopenia (deficiency of all blood cells: RBCs, WBCs, platelets). Hematopoietic stem cell pool severely reduced; marrow often fatty. Acquired (infections like hepatitis/HIV/EBV, toxins, radiation, drugs, immune disease) or inherited (genetic mutations).
59
Aplastic Anemia: Clinical Presentation & Diagnosis
Symptoms of anemia, leukopenia (infections), thrombocytopenia (petechiae, bleeding). CBC: pancytopenia. Bone marrow exam: severe hypocellularity, predominance of fat. Genetic testing, HLA typing, viral serologies.
60
Aplastic Anemia: Treatment
Blood transfusions (goal: independence from them). Prophylactic antibiotics. Bone marrow transplant (HLA-matched sibling preferred). Immunosuppressive drugs (antithymocyte globulin, cyclosporine). Bone marrow stimulants (filgrastim, epoetin-alfa).
61
Anemia of Chronic Disease (ACD): Mechanism
Develops from chronic disorders (infection, inflammation, cancer, HF, diabetes). Mechanisms: Decreased RBC survival, blunted marrow response to EPO, impaired iron metabolism/recycling.
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ACD: Diagnosis & Treatment
Usually NCNC anemia (can become microcytic). Normal/high ferritin (vs. low in iron deficiency). Treatment: Focus on underlying disease. Recombinant EPO (may need higher doses).
63
Polycythemia: General Description
Opposite of anemia; overabundance of RBCs, making blood viscous, increasing clotting risk.
64
Primary Polycythemia (Polycythemia Vera): Definition & Etiology
Hyperproliferation of ALL blood cells (RBCs, WBCs, platelets) in bone marrow. Etiology unknown; ~30% chromosomal abnormalities (20q/13q deletions, trisomy 9). ~90-95% have JAK2 mutation (tyrosine kinase -> hyperproliferation). Rare, >60 yrs, more men.
65
Primary Polycythemia: Symptoms & Complications
Related to hyperviscosity: Systolic HTN, DVT. Neurological (vertigo, tinnitus, headache, visual issues, TIAs). Organ ischemia, easy bruising/bleeding. Erythromelalgia (painful ischemia/infarction in extremities). Pruritus. Splenomegaly. Hyperuricemia/gout.
66
Primary Polycythemia: Diagnosis & Treatment
CBC: High Hgb (>20g/dL), Hct (>60%), high WBC/platelets. EPO level (normal/low indicates no EPO stimulus). Abdominal US (spleen). JAK2 mutation test. Treatment: Phlebotomy, aspirin/anticoagulants, allopurinol, myelosuppressive agents (hydroxyurea), JAK2 inhibitors (Ruxolitinib).
67
Secondary Polycythemia (Erythrocytosis): Definition & Cause
More common. Hyperproliferation of ONLY RBCs. Caused by prolonged hypoxia (compensatory effort to improve O2 delivery) stimulating EPO. Common in COPD, high altitudes, severe heart/lung disease.
68
Secondary Polycythemia: Symptoms & Diagnosis
Slow onset, may be asymptomatic. Headache, dizziness, weakness, SOB (orthopnea), splenomegaly symptoms, vision changes, skin redness/itching, unexplained bleeding. CBC: High Hgb/Hct (Hgb usually not >17-18 g/dL). HIGH EPO level.
69
Secondary Polycythemia: Treatment
Reverse underlying cause of hypoxia if possible.

Pathophysiology (51 decks)

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