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Pathophysiology Exam 2 > Lecture 17 > Flashcards

Lecture 17 Flashcards

1
Q

Pernicious Anemia

A

B12 and/or folate deficiency

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2
Q

Folate (B9)

A
  • Needed for DNA synthesis and cell division
  • Absorbed in duodenum and jejunum
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3
Q

What are the causes of B12 deficiency?

A

Nutritional deficiency (rare), gastrectomy (removal of a part or all of stomach), Atrophic gastritis (thin and inflamed stomach lining), Intestinal blind loop, parasite, ileal resection (removal or portion of ileum), Crohn’s Disease

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4
Q

What are the causes of folate deficiency?

A

Nutritional deficiency, malabsorption syndromes (Celiac disease, tropical sprue, jejunal resection), drugs, alcohol, pregnancy, lactation

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5
Q

Intrinsic Factor (IF)

A
  • Secreted by gastric parietal cells
  • Vitamin B12 binds
  • Absorbed in ileum and transported to bone marrow
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6
Q

Hemoglobin

A
  • 4 subunits: each with heme group
  • each heme group: iron atom capable of binding oxygen molecule
  • Humans have four functional alleles (alpha1 and alpha 2)
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7
Q

HbA

A

2 alpha and 2 beta globin chains; made by RBCs

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8
Q

HbA2

A

2 alpha and 2 delta chains

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9
Q

HbF

A

2 alpha and 2 gamma chains

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10
Q

Transferrin

A

Glycoprotein that binds and transports iron from gut and transported to marrow (delivered to developing RBCs/Hb)

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11
Q

What happens to iron after RBCs reach their lifespan?

A

120 days: ingested by macrophages -> iron extracted from Hb and recycled to plasmin transferrin

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12
Q

Iron Deficiency Anemia

A
  • Chronic blood loss (iron deficiency) or impaired absorption (celiac sprue, malabsorption of fats, chronic diarrhea)
  • Iron stores completely depleted (hypochromic microcytic anemia: small (microcytic) and pale (hypochromic) RBCs)
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13
Q

Normochromic Normocytic Anemia

A
  • RBCs normal color and size but decreased number
  • Results from nutritional deficiency and abnormalities in erythropoietic growth factor production (Cytokines)
  • Chronic inflammation increases synthesis and release of hepcidin
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14
Q

Hepcidin

A

hormone produced in liver that regulates iron metabolism by binding to ferroportin and inhibiting it (causes retention of iron within enterocytes, hepatocytes, macrophages due to decrease in blood iron levels)

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15
Q

Ferroportin

A

Protein that facilitates export of iron from cells to bloodstream

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16
Q

Hemochromatosis

A

hereditary disease of intracellular accumulation of iron in organs (liver iron deposits: cirrhosis and liver cancer)

17
Q

HFE

A

-Hepatocyte membrane protein
- Regulation of hepcidin production

18
Q

What happens if there is a defect in HFE?

A

Poor regulation of hepcidin -> mucosal transfer or iron -> plasma transferrin -> iron overload

19
Q

Divalent Metal Transporter (DMT1)

A

Transports ferrous iron (Fe2+

20
Q

Hemojuvelin (HJV)

A

membrane bound and soluble protein receptor (HFE2) -> juvenile hemochromatosis

21
Q

Thalassemia

A
  • interruption of alpha and beta globin chain formation by RBCs
  • Alpha and beta forms
  • Genetic (autosomal recessive)
  • Major: homozygous
  • Minor: heterozygous
  • Trait: alpha form when combination of 2 genes deleted
  • Form depends on alpha globin subunit, number of genes, and type of inheritance
22
Q

Hemolytic Anemia

A

Caused by premature destruction of RBCs (and decrease in Hb)

23
Q

Hemolysis

A

Breakdown of RBS (release of Hb into bloodstream)

24
Q

What happens if Hb has missing beta chains?

A
  1. Extra alpha chains collect in RBCs
  2. Damage cell membrane
  3. Hemolysis and anemia
    - Blood transfusions are only treatment
    - Iron chelation therapy: removes excess iron
25
Q

Sickle Cell Anemia

A

Inherited recessive defect of Hb synthesis (point mutation in B chain)

26
Q

Sick Cell Disease

A
  • Homozygous
  • No HbA synthesized (all B chains are S chains that combine with normal alpha chains) -> HbS
  • Hypoxia -> HbS polymerized and assumes sickled shape
27
Q

Sickle Cell Trait

A
  • Heterozygous
  • Normal and abnormal Hb (codominance)
28
Q

Aplastic Anemia

A
  • pancytopenia due to decrease in bone marrow
  • idiopathic or drug/radiation/viral infections
  • Damaged stem cells can produce: progeny expressing neoantigens (novel antigens from mutations recognized by immune cells) -> autoimmunity, clonal population with decrease proliferative capacity
29
Q

Pancytopenia

A

Decreased RBCs, WBCs, platelets in blood

Pathophysiology Exam 2 (8 decks)

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