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Pathophysiology > module 5 Heme > Flashcards

module 5 Heme Flashcards

1
Q
  1. Blood is comprised of …% plasma, and …% formed elements.
  2. Plasma contains …% water, …… % proteins, and …. % other solutes.
  3. Formed elements is made of 99% of what? <1% of what, and <1% of what?
A
  1. 55% plasma, 45% formed elements
  2. 91% water, 7% proteins, and 2% other solutes like gas etc.
  3. erythrocytes, platelets, and leukocytes
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2
Q
  1. Erythropoesis is under …….. control. Which hormone triggers it?
  2. What produces erythropoetin, and what is its target?
  3. Name a few possible triggers for erythropoetin release.
  4. What 2 organs are responsible for breaking down blood cells?
A
  1. hormonal, erythropoetin
  2. kidneys. Target is bone marrow
  3. decreased rbc’s, blood flow, hemoglobin synth, hemorrhage, increase O2 consumption
  4. spleen and liver
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3
Q
  1. What is O2 bound to in rbc’s?
  2. What is hemoglobin composed of? How many O2 per hemeglobin molecule?
  3. Rbc’s last for about ……. days then they start to get stuck in the …………., and break down into what?
  4. What happens to heme of broken down rbc? Which protein carries Fe to the liver and bone marrow? What protein binds unconjugated bilirubin?
  5. What happens to globin when rbcs break down?
  6. What is responsible for engulfing the old rbc and breaking it down?
A
  1. the heme groups of hemoglobin.
  2. 4 polypeptide chains (a1, a2, B1, B2). Each chain has a heme group. 4.
  3. 120 days, spleen, Heme and globin
  4. Heme breaks into Fe2+ (ferrous iron), which gets recycled and protopoferin 9 which becomes unconjugated bilirubin. Transferin transports Fe. Albumin transports protoporferin 9.
  5. breaks into the 4 polypeptide chains and gets recycled by the body.
  6. macrophage
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4
Q
  1. unconjugated bilirubin in the blood is ………… ………… ………… . What is it bound to?
  2. When does bilirubin become conjugated? Is it water soluble? What does it become next, and where does it go?
A
  1. not water soluble. albumin

2. in the liver with glucuronic acid. Yes. Bile. Goes to colon (makes brown poo), and kidney (makes yellow pee)

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5
Q
  1. The coagulation pathway is only effective in ……………………..? What are the 3 steps?
  2. What does vasospasm achieve?
  3. What important factor is part of platelet plug formation, and what does it do?
  4. What happens in fibrin clot?
  5. What kind of deficiencies happen in clotting?
  6. What over-the-counter medication inhibits TXA2?
A
  1. Small caliber vessels. Vasospasm, platelet plug formation, fibrin clot
  2. decreases blood loss by slowing the flow. Greater contact time for blood to clot around wound.
  3. Von Willebrand factor (vwf) triggers platelet release of thromboxane a2 (TXA2), make platelets stick together forming plug.
  4. pulls wound edges together and stabilize platelet plug.
  5. lack vwf, lack of TXA2, or factor 8.
  6. Aspirin (anticoagulant)
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6
Q
  1. What is fribinolysis?
  2. What are the enzymes that cause clot break down.
  3. In the body’s tug-o-war between clotting and fibrinolysis, which process is generally favored?
A
  1. the process of breaking down fibrin clots
  2. tissue platinogen activator (t-PA), or u-PA (both made by endothelial cells) converts plasminogen to plasmin (breaks down clots).
  3. fibrinolysis unless there is a tissue injury that needs clotting.
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7
Q
  1. In its broadest sense, what is anemia?
  2. Anemia is defined by reduction in what substances? What do each of these cause?
  3. What is hematocrit?
  4. Is anemia a disease?
  5. What are the defining Hg or Hct levels in men and women?
A
  1. Functional inability of the blood to supply the tissues with adequate oxygen for proper metabolic function
  2. Hemoglobin (Hg) concentration, • Hematocrit (Hct) concentration,• Red blood cell (RBC) count. All cause decreased O2.
  3. the ratio of the volume of red blood cells to the total volume of blood
  4. Not a disease, rather an expression of an underlying disorder
  5. Men Hg = <13g/dL, Hct = <41%. Women Hg = <12g/dL, Hct = <36%
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8
Q
  1. How do we classify anemia (4)?
  2. Anemia due to hemolysis or bleeding is characterized by …………. .
  3. What is MCV? MCHC?
  4. In what two ways can we approach anemia?
  5. What 3 things would the kinetic approach see in anemia?
  6. What 2 ways would the morphological approach see anemia?
A
  1. rbc size (microcytic), color (relates to Hg), shape, decreased production vs. increased rbc loss.
  2. reticulocytosis (new rbcs in the flow)
  3. Mean Corpuscular Volume, Mean Cell Hemoglobin Concentration
  4. kinetic classification, or morphological (appearance of cell)
  5. Decreased rbc production (nutrient lack, bone marrow disorder or suppression)

Increased rbc destruction (inherited or acquired hemolytic anemias like sickle cell or thalessemia)

Blood Loss from tumor, trauma, or chronic

  1. Cell size and cell color. Micro/macrocytic normochromic
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9
Q
  1. What would cause microcytic rbcs, and what is the MCV size?
  2. What are the values for normocytic rbcs?
  3. What would cause macrocytic rbcs, and what is the MCV size?
A
  1. reduced iron, heme, or globin. MCV<80

2. 80

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10
Q
      1. O2 deficit leads to
A
  1. Diminished cell metabolism and reproduction
  2. Tachycardia and peripheral vasoconstriction,
  3. Fatigue, pallor (pale face), dyspnea, tachycardia,
  4. Decreased regeneration of epithelial cells
  5. Digestive tract becomes inflamed and ulcerated, leading to stomatitis
  6. Inflamed and cracked lips
  7. Dysphasia
  8. Hair and skin may show degenerative changes.
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11
Q
  1. Decreased O2 from anemia causes (5)

2. Decreased volume from anemia causes (4):

A 
1. Exertional dyspnea 
• Dyspnea at rest
• Fatigue
• Bounding pulses
• Lethargy, confusion
  1. • Fatigue
    • Muscle cramps (can’t unclench)
    • Postural dizziness and Syncope (fainting from lack of O2 to brain)
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12
Q
  1. What is another name for macrocytic-normochromic anemia, and what is the common name for this?
  2. What causes the cells to be so big?
  3. What causes pernicious anemia?
  4. Name the 2 substances that act as coenzymes to DNA maturation:
A
  1. Megaloblastic anemia. Pernicious anemia or folate deficient
  2. defective DNA synthesis in rapidly dividing stem cells caused by lack of B12 or folate
  3. Autoimmune against parietal cells that make intrinsic factor required for B12 absorption. Results in deficient B12
  4. B12 and Folate
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13
Q
  1. What are the symptoms of pernicious anemia (macrocytic normochromic)?
      1. What are the 3 diagnostic tests for pernicious anemia?
  3. What is the treatment for pernicious anemia?
A 
1. Hg= 7-8g/dL.  
• Difficulty walking
• Loss of appetite
• Abdominal pain
• Weight loss
• Sore tongue
• Neurologic manifestations
  1. Methylmalonic acid and homocysteine level (maturation of dna)
  2. Blood work test for antibodies against parietal cells
  3. Schilling test (academic and research). No longer done.
  4. lifelong high dose B12 replacement (parentarel. injection)
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14
Q
  1. Is folate deficiency pernicious anemia?
  2. Where does folate absorption occur?
  3. What symptoms differ between folate def and pernicious? Where does folate deficient anemia present?
  4. What is treatment for folate deficient anemia
A
  1. No. Similar symptoms, but methylmalonic acid is normal in folate deficient anemia
  2. small intestine
  3. Folate deficient lacks neurological symptoms. Does get cheilosis (mouth fissures), and stomatitis (ulcerations). Normally presents on skin
  4. daily oral administration of folate
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15
Q
  1. What type of anemia is Microcytic Hypochromic, and what disorders does it relate to?
  2. Is iron deficient anemia the most common type?
  3. Name some reasons that iron deficient anemia occurs:
A
  1. Iron deficient anemia. Disorders of iron metabolism, porphyrin, heme, and globin synthesis
  2. yes
  3. blood loss occult or overt, menstruation, pregnancy, rapid growth in children, inadequate iron in diet, too much cow’s milk in infancy
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16
Q
  1. Name the common symptoms of iron deficient anemia:
  2. Name the tests for iron deficient anemia:
  3. What is the treatment of iron def. anemia?
A
  1. Pallor, fatigability, weakness, dizziness,
    irritability, Glossitis (smooth tongue), Restless Legs, Angular stomatitis (cracking of corners of mouth), Koilonychia (spoon-shaped nails)
  2. blood smear

rbc indices

serrum ferritin

serum iron saturation/transferrin

bone marrow iron stain (prussian blue)

  1. oral iorn dsalts (may caue constipation: take w/ vitamin C)
17
Q
  1. What is anemia of chronic disease?
  2. What is the morphology of this kind of anemia?
  3. What is a morphological sign that would appear on a smear for uremic patients?
  4. what is a treatment?
A
  1. anemia caused by kidney disease resulting in low erythropoietin and low reticulocyte count
  2. normochromic normocytic
  3. burr cells or echinocytes
  4. daily administration of erythropoetin, maintain iron level, and watch Hg levels for dialysis patients (11-12g/dL)
18
Q
  1. How do platelet dysfunctions manifest?
  2. Are platelet disorders congenital or acquired?
  3. What is the most common inherited bleeding disorder?
  4. What type of inherited disorder is this?
A
  1. Petechiae
    Purpura
    Mucosal bleeding
    Gingival bleeding
  2. both
  3. Von Willebrand Disease. Can be fully lacking or partially lacking of VWF
  4. autosomal dominant
19
Q
  1. What is the role of Vitamin K?
  2. where is this synthesized and who would lack it?
  3. What medications antagonize vitamin K?
  4. Name 2 anticoagulant drugs:
  5. Name one thrombolytic agent:
A
  1. necessary for synthesis and regulation of prothrombin 2 and other procoagulant factors/proteins
  2. Synth in gut. Newborns lack it, as well as those with compromised gut microflora or those w/ malabsorption, or biliary disease.
  3. warfarin, and some antibiotics
  4. warfarin or heparin
  5. plasminogen activators
20
Q
  1. What kind of disorder causes a broad range of hemostasis disorders, including defects in coagulation, fibrinolysis, and platelet number and function?
  2. Describe disseminated intravascular coagulation:
  3. What is the cause of DIC?
  4. What are clinical signs and symptoms?
A
  1. liver disease
  2. Complex, acquired disorder in which clotting, and hemorrhage simultaneously occur. Patient bleeds out.
  3. infection of gram - bacteria, cancer/leukemia, trauma, pregnancy, transfusion reaction
  4. Bleeding from venipuncture sites, arterial lines, Purpura, petechiae, and hematomas, Symmetric cyanosis of the fingers and toe
21
Q
  1. What is the disease caused by inherited deficiency of factor 8? Factor 9?
  2. It is due to which kind of inheritance?
  3. Can female experience this disease?
  4. What kind of problems do hemophiliacs suffer?
A
  1. Hemophilia A, hem B
  2. sex-linked X recessive
  3. mildly
  4. joint bleeds, mucosal bleeding, uncommonly CNS bleeds

Pathophysiology (11 decks)

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