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RBC - Coggle Diagram

- - - - IMHA
- - - - 24-72 hrs
      - HCT and plasma prot conc dec
    - - eventually becomes regener
        
        macrocytic, hypochromic
  - - - ani adapts = clin signs not evident until HCT very low
      - microcytic normochromic or microcytic hypochromic
    - - becomes non-regener
  - - - intravasc scavenged by haptoglobin
        
        Hgb/haptoglobin complex taken up by hepatocytes
        
        Hgb degraded sim to extravasc heolysis
        
        plasma discolored - pink to red (Hgb-emia)
        
        hemoglobinuria
      - extravascu
        
        icterus
  - - - regener, normocytic/normochromic OR macrocytic/hypochromic
      - spherocytes
      - pos Coombs test
      - agglut
      - ghost c
      - inflamm leukogram
        
        leukocytosis, neutrophilia w/ regener left shift, monocytosis
      - Hgb-emia/Hgb-uria
  - - - Mycoplasma
        
        M. haemofelis
        
        M. haemocanis
        
        M. wenyonii (cattle), M. ovis (sheep/goats), M. haemolamae (llama/alpacas)
      - Anaplasmosis
      - Babesiosis
        
        B. canis
        
        B. gibsoni
      - Others: Theileriosis, Cytauxzoonosis
  - - - exogenous
      - endogenous
    - - macrocytic, hypochromic
      - lg #s Heinz
      - ghost, Heinz, eccentrocytes
    - - feline
        
        caused by: acetominophen, onion/garlic, proglylene glycol, zinc (pennies), methylene blue, propofol
      - canine
        
        caused by: onion/garlic, acetaminophen, Zn toxicity, propylene glycol, propofol, benzocaine, naphthalene
      - equine
        
        caused by: red maple leaf, onion/garlic
      - ruminant
        
        caused by: Brassica (kale, rape, cabbage), onion/garlic, copper toxicosis, selenium defic
- - - - retics appear in circu 2-3 d following stim and produc peak in 7-10 d
    - - same c, vis diff
      - retic = RBCs w lg blue mats of RNA and mitoch stained w new methylene blue
      - polyhcromatophil
        
        lg, pink/blue RBC vis w Wright's
        
        polychromasia supports retic for regener
    - - COUNT is better bc quant
      - do not use retic %
    - - anemia + inc retics = regener
        
        most common causes of regener anemia = hemorr (RBC loss) and hemolysis (RBC destruc)
      - anemia + norm/dec retic = non-regener
  - - - VERY recently released from BM
    - - released 3-4 wks prior
    - - dogs only have aggreg
      - cats have aggreg and punctate
      - rum have aggreg + basophilic stippling (= regener)
      - horses do not release retics into periph blood in regener anemias
        
        may see inc MCV but need serial CBCs to monitor response to anemia
- - - - assoc w/ underlying conditions: inflamm, infec, neoplasia, metab dz
      - alt iron kinetics, dec EPO produc, dec BM response to EPO, dec RBC lifespan
    - - mild to mod dec in RBC indices
      - normocytic, normochromic, non-regener
  - - - maj cause is dec EPO produc
      - uremic inhib of erythropoiesis, shortened RBC survival, inflamm, disordered iron-hemostasis
    - - mod to severe normocytic, normochromic non-regener
  - - - damage to hematopoietic precursors in BM
        
        drugs, chem, toxins, estrogen, infec agents
    - - bicytopenia or pancytopenia in periph blood
      - normocytic, normochromic non-regener
  - - - caused by immu-medi destruc of erythroid precursors in BM
    - - severe normocytic, normochromic non-regener
      - norm leukocyte and plt #s
      - mk dec in eythroid precursors
  - - - neoplasia
        
        myelophthisis
        
        "crowding out" of hmpt c in BM space by popu of neoplastic c -> disrupt BM microenviron
      - myelofibrosis
        
        idiopathic replacement of BM space by fibrous tis
    - - 1+ cytopenias
      - normocytic, normochromic, non-regener
- - - - but CANNOT use as indicator of regener
- - - - progen c responsi for produc of c that reside in BM and circu in blood
      - pluripotent stem c
        
        c that produce all or most c lines
      - progenitor c pool
        
        committed to producing 1+ c lines
      - prolif pool
        
        rapid prolif but committed to 1 c line
      - matur pool
        
        c no longer have capacity to divide
    - - Epo is produced by c in renal cortex that have abil to sense blood on
      - inc amts of Epo are produced by c in response to renal hypoxia
    - - rubriblast -> prorubricyte -> rubricyte -> metarubricyte -> reticulocyte -> erythrocyte
      - as RBC dev they become sm w/ more Hgb
      - process takes 5 d from seq of rubriblast to retic
      - once in circu, retic take ~1 d to mature to RBC (so total matur is ~6 d in health)
      - w inc Epo, retics can be released early and show up in circu in 2-3 d (evidence of regener)
  - - - func of Hgb
        
        trnspt O2 from lungs to tis
        
        trnspt CO2 from tis to lungs
        
        buffer H+
    - - Fe absorbed from intes
        
        transpt of intraluminal Fe to intes enterocyte is medi by DMT1
        
        export of Fe from enterocyte to blood is medi by ferroportin
        
        Fe is trnspt in blood bound to transferrin
        
        hepcidin is neg regu of Fe metab
    - - dogs = 120 d
      - horse = 145 d
      - cat = 70 d
      - cow = 130 d
    - - RBC lysed and Hgb degraded to heme and globin
        
        globin further degrade into aa
        
        heme is degraded to Fe and bilirubin
        
        Fe stored as ferritin or hemosiderin or trnspt back to BM bound to transferrin
        
        bilirubin is released into circu -> binds to alb -> trnspt to liver where it is conju and excre in bile
        
        if enough bili present in circu = yellow (icteric) plasma
  - - - reported on CBC as MCV (mean c vol)
        
        MCV WRI = normocytic
        
        MCV > RI = macrocytic
        
        caused by
        
        most common cause is inc # of young RBCs (retics)
        
        poodle macrocytosis (hereditary)
        
        w/o polychromasia in cats = FeLV
        
        hereditary stomatocytosis
        
        c swelling during storage -> rela rare
        
        inc # of lg RBCs
        
        MCV < RI = microcytic
        
        caused by
        
        Fe defic anemia
        
        hepatic failure/portosys shunt
        
        Akita and Shiba Inu dogs norm have sm RBCs than other dog breeds
        
        inc # of sm RBC
        
        anisocytosis = variation in RBC size (RDW)
    - - calc value
        
        WRI = normochromic
        
        *> RI = hyperchromic
        
        almost always artifact
        
        < RI = hypochromic
        
        Fe defic
        
        regener response
    - - dogs = biconcave discs w central pallor
      - cat, horse, cow, sheep = discoid, no central pallor
      - llama, camel, bird, reptile = elliptical
- - - - loss of body fl (dehyd)
        
        diag by evidence of dehyd on PE, prot conc varia by if inc = supportive of dehyd
        
        most common cause of erythrocytosis in domestic ani
      - splenic contract
        
        most apparent in horse
        
        prot conc norm, may see Epi leukogram, HCT typ normalizes w/in few hrs
  - - - primary
        
        polycythemic vera
        
        rare chronic myeloprolif disorder
      - secondary inappropriate
        
        renal ischemia or Epo producing tumor = Epo inc (w/o hypoxemia)
      - secondary appropriate
        
        sys hypoxemia due to lung dz, cardiac dz, or high latitudes = inc Epo produc
- - - - hyperglobulinemia or hypofibrinogenemia
  - - - won't disperse w saline = pos