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patho > Week 7 Hematopoietic Function > Flashcards

Week 7 Hematopoietic Function Flashcards

1
Q

What are the effects of anemia

A
  1. initial symptom: tissue hypoxia
    - pallor, weakness/increased fatigue (not enough oxygen), claudication, increase respiratory rate (bringing in more oxygen by hyperventilating
  2. compensation by the cardiovascular system: increased heart rate (getting little RBCs to lungs to get new oxygen), blood vessel dilation, and increase stroke volume
  3. Renal compensation: increase RBC count and increase circulating volume (salt and water retention) (doing its best to hold onto volume)
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2
Q

Explain hemolytic anemia

A
  • premature destruction of RBCs
  • if destruction occurs in the blood vessels its usually because of defective valves, transfusion reaction
  • if destruction occurs outside of the blood vessels its because destruction in liver and spleen due to congestion or organ injury
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3
Q

Explain the types of hemoglobinopathies (the hemoglobin is broken)

A
  1. sickle cell disease (normocytic, normochromic)
    - when exposed to stressors, they change their shape and stick together. You must change the conditions (dehydration, etc.) to fix. They are having an ischemic injury all over their body and its painful
    - they can hold oxygen still when not sickled
  2. thalassemia (microcytic, hypochromic)
    - alpha or beta chain is broken
    - too small and pale colored
    - these do not hold oxygen correctly
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4
Q

What is another name for pernicious anemia

A

vitamin B12 deficiency

occurs when stomach is damaged or removed because you lose the intrinsic factor and B12 doesn’t make it to your body

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5
Q

What can B12 deficiency lead to and why?

A

permanent neurologic damage

losing intrinsic factors (in the stomach) the body will destroy B12 and doesn’t make into your body. You need it for healthy nerve fibers

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6
Q

What does chronic blood loss lead to

A
  • iron deficiency (you’ll lose iron first to make RBCs)
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7
Q

Explain polycythemia and the three types of polycythemia

A

Definition: increased RBC count and hematocrit greater than 50%

  1. primary polycythemia or polycythemia vera: neoplastic disease where you make too much of all three cell types
    - high risk for clots due to increase platelets
    - have blood drawn off
  2. Secondary:
    - body’s normal response to hypoxia or hypoxemia
    - kidney’s respond by increasing erythropoietin release (because the kidneys just know you don’t have enough RBCs)
    - overabundance due to secondary disease state
  3. relative polycythemia:
    - loss of plasma volume (dehydration)
    - looks like you’re dehydrated but if you add fluid you’ll be find
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8
Q

What are factors that would increase hypercoagulability

A
  1. increased platelet function with diseases such as:
    - polycythemia vera
    - splenectomy
    - chronic inflammation
    - endothelial damage (atherosclerosis)
  2. increased clotting activity:
    - hyper viscosity syndromes (polycythemia)
    - hypoestrogenic states; oral contraceptive use
    - prolonged bed rest (blood flow returning to the heart is sluggish)
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9
Q

What are the two key elements required for successful clotting

A
  • functional and plentiful platelets (too few or they don’t function correctly
  • functional and plentiful coagulation proteins
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10
Q

What is thrombocytopenia

A

low platelets; less than 100,000

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11
Q

What are the two different types of thrombi

A

arterial: defects in proteins involved in hemostasis (atherosclerosis because arteries are getting the plaques)
venous: variety of clinical disorders or conditions (DVT, fat emboli)

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12
Q

What are the causes of platelet bleeding disorders

A
  1. idiopathic or immune thrombocytopenic purpura (ITP)
    - platelets life cycle is shortened for whatever reason
  2. thrombotic thrombocytopenic purpura (TTP)
    - platelets are over stimulated and clumping together (clots) but now you’ve used up all of your platelets so you’re going to bleed easily
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13
Q

What are reasons that platelets won’t work together

A
  • drugs, disease, or certain surgery

- aspirin, NSIADs most common

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14
Q

What are some clotting factor inherited disorders

A
  • hemophilia A (factor VIII deficiency)

- von willebrand disease

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15
Q

what electrolyte do you need to have to have successful coagulation

A

calcium

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16
Q

Explain disseminated intravascular coagulopathy

A
  • a systemic activation of the coagulation cascade
  • excessive systemic clotting develops with depletion of platelets and clotting factors, ultimately resulting in excessive bleeding
  • similar to TTP, except this time the problem is with coagulation
17
Q

Explain the three types on nonneoplastic disorder of leukocytes

A
  1. neutropenia: abnormally low number of neutrophils (<1500)
    - never normal
    - often acquired from meds, radiation, severe infection, immune disorders, malignancies
  2. aplastic anemia: pancytopenia (pan = all over); a reduction or absence of all three blood cell types resulting from failure of bone marrow
    - pale
    - fatigue
    - SOB
    - purpura and petechiae (low platelets)
    - increase risk of infection (low WBC)
  3. infectious mononucleosis: epstein-barr virus infects B lymphocytes (kissing disease)
    - 90% of humans and persisting for the lifetime of the person
    - enlarged lymph nodes, liver and spleen, malaise, fever
18
Q

Explain the different types of acute leukemias

A
  1. acute lymphocytic leukemias (ALL)
    - these don’t mature fully; they’re being made, but never maturing
    - most frequently in children
  2. acute myelogenous leukemia
    - older adults
    - overproducing WBC but they’re not purposeful and the body just thinks you don’t have enough so they overshadow the other types
19
Q

What are the common complications with acute leukemias

A
  • leukostasis: increases blood viscosity then emboli
  • hyperuriemia: increase in metabolites due to chemotherapy
  • tumor lysis syndrome: necrosis of malignant cells leads to release of electrolytes
20
Q

Explain the different types of chronic leukemias

A
  1. chronic lymphocytic leukemia (CLL)
    - most common adult leukemia
    - primarily B cells
    - lymphadenopathy is most common finding
  2. chronic myelogenous leukemia
    - infections, fever, and weight loss
    - chronic phase may be asymptomatic
    - accelerated phase (6-12 months; may be when you experience symptoms)
    - terminal blast phase (3 months)
21
Q

What differentiates chronic leukemias from acute

A
  • the type of leukocytes that are not maturing

- these cells make it to maturity but they are not functional

22
Q

Explain the difference between myelogenic and lymphogenic cells

A
  • Myeloid = neutrophils, monocytes, basophils, eosinophils

- Lymphoid = B cells, natural killer cells, T cells

23
Q

what are the different types of lymphomas

A
  1. Hodgkin’s (17%)
    - abnormal B lymphocyte
    - often localized
  2. non-hodgkin’s lymphoma (83%)
    - rarely localized
    - abnormal T cells or B cells
    - due to infection with HIV, EBV, H. pylori, or HVC
    - multiple peripheral nodes
24
Q

What are the two classifications of immunodeficiency states

A
  1. primary (congenital or inherited)
  2. secondary (acquired later in life):
    - malnutrition
    - infection
    - neoplastic disease (lymphoma)
    - immunosuppressive therapy
25
Q

What are hypersensitivity disorders related to immune response

A

excessive or inappropriate activation of the immune system

26
Q

What are sources of the antigen for hypersensitivity disorders related to immune response

A
  1. allergy:
    - produces over dramatic response or hypersensitivity to environmental antigens
  2. autoimmunity:
    - antigen is located on own cell (cells made by your body)
    - something that caused your own immune system to see something in your body and think “that doesn’t look right” and attacks itself
  3. alloimmunity:
    - an immune reaction to tissues of another individual
    - antigen is located on a cell (but it did not originate from you)
27
Q

Explain Type 2 hypersensitivity - cytotoxic

A
  • antigen is on a cell
  • IgG or IgM
  • your immune system is doing damage
  • seen on red or white blood cells
28
Q

Explain type 3 hypersensitivity - immune complex

A
  • immune system damages surrounding tissue trying to get the antigen out
  • big cause of vasculitis
29
Q

explain type 4 hypersensitivity

A
  • delayed reaction
  • hypersensitivity not necessarily an allergy
  • typically TB test, allergic contact dermatitis
30
Q

What are the two types of transfusion reactions

A
  1. acute: typically ABO incompatibility; can be life threatening leading to renal failure, DIC, shock
  2. delays: due to previous exposure to RBC component; can cause mild fever, jaundice
31
Q

What are the different tissue sources for organ rejection

A
  1. allogenic - human to human
  2. autologous - from yourself; blood drawn to give it back to yourself
  3. syngeneic - twins
32
Q

Explain hyperacute, acute and chronic when relating to organ rejection

A
  • hyperacute = immediate reaction; organ dies; body does not accept it
  • acute = antibodies against the graft; will lose in weeks or later
  • chronic = body eventually catches on to the fact that you have a structure that does not have the same nametag and now your body is attacking it
33
Q

Explain graft versus host disease

A

the graft is fighting the host

you put a fully functional immune system into a non functioning immune system and it will start attacking the host

patho (10 decks)

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