Exam 3 - Anemia: Blood Loss & Inadequate Erythropoiesis Flashcards
what are some examples of traumatic & underlying pathology causing blood loss?
traumatic – HBC, animal attack, & abuse
underlying pathology – gi parasites, inflammation/neoplasia in the gut, drug induced (ulcer or diffuse bleeding), or coagulopathy
trauma causing acute gi bleeds likely affect what organs?
spleen, liver, major vessels, & cardiac
what ectoparasite commonly causes anemia in puppies & kittens?
fleas
what gi parasites can be causes of gi bleeding?
whips & hooks
what primary coagulopathy problems can cause acute bleeding? secondary problems?
primary – IMTP or DIC, platelet disorder
secondary – clotting factor problem or DIC, factor disorder
what are the main categories of mechanisms causing acute gi bleeds?
- trauma
- parasites
- ulcers
- coagulopathy
what are the main categories of mechanisms causing chronic gi bleeds?
- addison’s – atypical or typical, cortisol deficiency
- parasites
- ulcers
- coagulopathy – primary or secondary
what primary coagulopathy problems can cause acute bleeding? secondary problems?
primary – slower onset of decreased platelets, thrombocytopathia
secondary – hepatic dysfunction
in primary coagulopathies caused by platelet disorders, what are the 2 general pathologies?
either decreased number of platelets or function of platelets
what 4 mechanisms are usually involved in primary coagulopathies?
- destruction
- consumption – DIC or hemorrhage
- production problem
- sequestration – splenic
what are the 3 most common primary coagulopathies?
- immune-mediated thrombocytopenia
- rickettsial – consider geographic factors
- paraneoplastic
what is the most severe primary coagulopathy? what about mild-moderate?
- immune-mediated – no other etiology will usually decrease platelets below 10,000-20,000
- rickettsial, consumption, & sequestration
what factors are affected in secondary coagulopathies?
II, VII, IX, & X
what is the most common secondary coagulopathy caused by a toxicity?
anticoagulant rodenticides – affects vitamin k dependent factors
what is expected in the clinical presentation of an animal with a primary coagulopathy?
mucosal surfaces affected!!!
skin – petechiae & ecchymoses
gi, urinary, nasal, cns, & lungs (rare)
what is expected in the clinical presentation of an animal with a secondary coagulopathy?
large cavities affected!!!!
peritoneum, hemothorax, pericardium, & mediastinum
what are the key differences between primary & secondary coagulopathy?
primary – platelet disorder
secondary – factor disorder
what medications can be responsible for large bleeds?
NSAIDS, steroids, & new antibiotics (platelet disorders)
what clinical signs are associated with acute blood loss?
collapse, acute lethargy, extreme thirst prior to anemia to restore volume, & tachypnea in an attempt to increase oxygenation
what clinical signs are associated with chronic blood loss?
weight loss with a good appetite, lethargy, melena from gi or nasal/upper airway bleeding from swallowing blood, & pica which is often indicative of iron deficiency
why can a CBC appear normal in an animal with an acute bleed?
can take up to 48-72 hours to manifest on the CBC as fluid will move from the interstitium to replace deficit
what abnormalities may be seen on a CBC of an animal with an acute bleed?
may be normal or decreased
often not regenerative because it’s too early
platelets may be normal to mildly decreased
what abnormalities may be seen on a CBC of an animal with a chronic bleed?
often low HCT/PCV – variable in severity, but the more chronic, the lower it can go without altered perfusion
low or normal total solids, anisocytosis early on
+/- microcytic hypochromic
should be regenerative if chronic & marrow is working
what abnormalities may be seen on a chemistry panel of an animal with an acute bleed?
panhypoproteinemia
increased BUN:Cr ratio
+/- increased bilirubin with cavitary bleeding – reabsorption of blood
what abnormalities may be seen on a chemistry panel of an animal with a chronic bleed?
panhypoproteinemia
increased BUN:Cr ratio
microcytosis with anemia strongly suggests what 2 things?
iron deficiency anemia & external blood loss
microcytosis without anemia often suggests what things?
breed specific – akitas
portosystemic shunts or other hepatic disease
what may be seen on urinalysis & fecal exams in a patient with suspected blood loss?
hematuria – urinalysis
fecal – hooks or whips
what may be seen on endoscopy in an animal with blood loss?
ulcers, inflammatory enteropathy, or neoplasia
what therapy must be used on a patient with a platelet or clotting disorder?
blood transfusion – correct the underlying disorder
what therapy must be used on a patient with a gi bleed or ulcer?
must give a proton pump inhibitor twice daily at 1mg/kg – omeprazole
also, histamine 2 receptor antagonists – famotidine, but can develop intolerance if given chronically
what 6 pathologies are given as causes of inadequate erythropoiesis?
- anemia of chronic inflammatory disease – CKD
- lack of erythropoietin – CKD
- precursor immune mediated anemia
- marrow infiltration – neoplastic or infectious (viral, fungal)
- toxicities
- pure red cell aplasia
what is the common characterization associated with anemia of inflammatory disease?
normocytic, normochromic non-regenerative anemia that is moderate in severity at the most
what mechanism causes anemia of inflammatory disease?
inappropriate iron handling – ferritin levels are high but there is low iron binding (low TIBC)
what common endocrinopathy causes an anemia of inflammatory disease?
hypothyroidism
why is a bone marrow examination usually not warranted in a patient with an anemia of inflammatory disease?
typically, not a bone marrow problem – would expect to see erythroid hypoplasia & Fe in the marrow
what are the key differences in the iron profiles between anemia of inflammatory disease & iron deficiency anemia?
inflammatory disease – decreased TIBC (low iron binding capacity), increased ferritin, but plenty of iron in the bone marrow
iron deficiency – increased TIBC, decreased ferritin, & iron deficiency in the marrow
what anemia is associated with chronic kidney disease? what is the mechanism?
normocytic, normochromic non-regenerative anemia
EPO deficiency – lack of production
what is precursor immune mediated anemia?
same concept as IMHA but at the level of the bone marrow only – can see very severe anemias in a relatively stable patient
what is key in diagnosing precursor immune-mediated anemia?
lack of other cytopenias
bone marrow examination is required for diagnosis
when would you use PCR for diagnosing an infiltrative disorder causing an anemia?
FeLV or ehrlichia
what drugs can cause toxicities resulting in an anemia?
immunosuppressants, antibiotics, estrogen, methimazole, & fenbendazole
what lab abnormalities are commonly seen in patients with anemia due to infectious processes or toxicities?
bicytopenia or pancytopenia
what are some fungal, chronic, & neoplastic processes that can cause anemia?
fungal – histoplasmosis
viral – FeLV
chronic – chronic ehrlichia
neoplasia – lymphoma, multiple myeloma, histiocytic sarcoma
what is seen on bone marrow examination that is nearly pathognomonic for pure red cell aplasia?
lack of erythroblasts, adequate myeloid & megakaryocytic lines, adequate iron & EPO
what is the mechanism of pure red cell aplasia?
selective erythroid hypoplasia in marrow that may be a primary or secondary immune-mediated process with other cell lines are not affected
what is another name for pure red cell aplasia?
primary failure erythropoiesis
what are the steps for deciding treatment for inadequate erythropoiesis?
- identify primary cause – anemia of inflammatory disease vs. CKD vs. primary marrow disorder
- if bone marrow exam is needed – do it, bicytopenia or pancytopenia or very chronic anemia
- treat based on bone marrow, Fe panel if needed
steroids often needed for PIMA or pure red cell aplasia
what is the indication for EPO supplementation?
reserved for anemia with CKD
what are the disadvantages of using epogen for EPO supplementation?
more likely to see adverse effects – formation of anti-EPO antibodies causing a severe anemia & you have to dose more often
what are the advantages of using Aranesp for EPO supplementation?
less likely to see adverse effects & you don’t have to dose as often
what should be monitored when using EPO supplementation for an anemic patient?
CBC weekly for the 1st 4-6 weeks
PCV/TS every 2 weeks after
why can treatment be discouraging for PIMA?
can take a very long time for the anemia to resolve if at all
what therapy is often used for PIMA?
steroids – same as IMHA
multiple immunosuppressives – cyclosporine & steroids
cobalamin – helps with normal RBC maturation
