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SA DX & TX I > Exam 3 - Anemia: Blood Loss & Inadequate Erythropoiesis > Flashcards

Exam 3 - Anemia: Blood Loss & Inadequate Erythropoiesis Flashcards

1
Q

what are some examples of traumatic & underlying pathology causing blood loss?

A

traumatic – HBC, animal attack, & abuse

underlying pathology – gi parasites, inflammation/neoplasia in the gut, drug induced (ulcer or diffuse bleeding), or coagulopathy

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2
Q

trauma causing acute gi bleeds likely affect what organs?

A

spleen, liver, major vessels, & cardiac

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3
Q

what ectoparasite commonly causes anemia in puppies & kittens?

A

fleas

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4
Q

what gi parasites can be causes of gi bleeding?

A

whips & hooks

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5
Q

what primary coagulopathy problems can cause acute bleeding? secondary problems?

A

primary – IMTP or DIC, platelet disorder

secondary – clotting factor problem or DIC, factor disorder

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6
Q

what are the main categories of mechanisms causing acute gi bleeds?

A
  1. trauma
  2. parasites
  3. ulcers
  4. coagulopathy
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7
Q

what are the main categories of mechanisms causing chronic gi bleeds?

A
  1. addison’s – atypical or typical, cortisol deficiency
  2. parasites
  3. ulcers
  4. coagulopathy – primary or secondary
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8
Q

what primary coagulopathy problems can cause acute bleeding? secondary problems?

A

primary – slower onset of decreased platelets, thrombocytopathia

secondary – hepatic dysfunction

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9
Q

in primary coagulopathies caused by platelet disorders, what are the 2 general pathologies?

A

either decreased number of platelets or function of platelets

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10
Q

what 4 mechanisms are usually involved in primary coagulopathies?

A
  1. destruction
  2. consumption – DIC or hemorrhage
  3. production problem
  4. sequestration – splenic
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11
Q

what are the 3 most common primary coagulopathies?

A
  1. immune-mediated thrombocytopenia
  2. rickettsial – consider geographic factors
  3. paraneoplastic
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12
Q

what is the most severe primary coagulopathy? what about mild-moderate?

A
  1. immune-mediated – no other etiology will usually decrease platelets below 10,000-20,000
  2. rickettsial, consumption, & sequestration
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13
Q

what factors are affected in secondary coagulopathies?

A

II, VII, IX, & X

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14
Q

what is the most common secondary coagulopathy caused by a toxicity?

A

anticoagulant rodenticides – affects vitamin k dependent factors

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15
Q

what is expected in the clinical presentation of an animal with a primary coagulopathy?

A

mucosal surfaces affected!!!

skin – petechiae & ecchymoses
gi, urinary, nasal, cns, & lungs (rare)

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16
Q

what is expected in the clinical presentation of an animal with a secondary coagulopathy?

A

large cavities affected!!!!

peritoneum, hemothorax, pericardium, & mediastinum

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17
Q

what are the key differences between primary & secondary coagulopathy?

A

primary – platelet disorder

secondary – factor disorder

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18
Q

what medications can be responsible for large bleeds?

A

NSAIDS, steroids, & new antibiotics (platelet disorders)

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19
Q

what clinical signs are associated with acute blood loss?

A

collapse, acute lethargy, extreme thirst prior to anemia to restore volume, & tachypnea in an attempt to increase oxygenation

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20
Q

what clinical signs are associated with chronic blood loss?

A

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

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21
Q

why can a CBC appear normal in an animal with an acute bleed?

A

can take up to 48-72 hours to manifest on the CBC as fluid will move from the interstitium to replace deficit

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22
Q

what abnormalities may be seen on a CBC of an animal with an acute bleed?

A

may be normal or decreased

often not regenerative because it’s too early

platelets may be normal to mildly decreased

23
Q

what abnormalities may be seen on a CBC of an animal with a chronic bleed?

A

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

24
Q

what abnormalities may be seen on a chemistry panel of an animal with an acute bleed?

A

panhypoproteinemia

increased BUN:Cr ratio

+/- increased bilirubin with cavitary bleeding – reabsorption of blood

25
Q

what abnormalities may be seen on a chemistry panel of an animal with a chronic bleed?

A

panhypoproteinemia

increased BUN:Cr ratio

26
Q

microcytosis with anemia strongly suggests what 2 things?

A

iron deficiency anemia & external blood loss

27
Q

microcytosis without anemia often suggests what things?

A

breed specific – akitas

portosystemic shunts or other hepatic disease

28
Q

what may be seen on urinalysis & fecal exams in a patient with suspected blood loss?

A

hematuria – urinalysis

fecal – hooks or whips

29
Q

what may be seen on endoscopy in an animal with blood loss?

A

ulcers, inflammatory enteropathy, or neoplasia

30
Q

what therapy must be used on a patient with a platelet or clotting disorder?

A

blood transfusion – correct the underlying disorder

31
Q

what therapy must be used on a patient with a gi bleed or ulcer?

A

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

32
Q

what 6 pathologies are given as causes of inadequate erythropoiesis?

A
  1. anemia of chronic inflammatory disease – CKD
  2. lack of erythropoietin – CKD
  3. precursor immune mediated anemia
  4. marrow infiltration – neoplastic or infectious (viral, fungal)
  5. toxicities
  6. pure red cell aplasia
33
Q

what is the common characterization associated with anemia of inflammatory disease?

A

normocytic, normochromic non-regenerative anemia that is moderate in severity at the most

34
Q

what mechanism causes anemia of inflammatory disease?

A

inappropriate iron handling – ferritin levels are high but there is low iron binding (low TIBC)

35
Q

what common endocrinopathy causes an anemia of inflammatory disease?

A

hypothyroidism

36
Q

why is a bone marrow examination usually not warranted in a patient with an anemia of inflammatory disease?

A

typically, not a bone marrow problem – would expect to see erythroid hypoplasia & Fe in the marrow

37
Q

what are the key differences in the iron profiles between anemia of inflammatory disease & iron deficiency anemia?

A

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

38
Q

what anemia is associated with chronic kidney disease? what is the mechanism?

A

normocytic, normochromic non-regenerative anemia

EPO deficiency – lack of production

39
Q

what is precursor immune mediated anemia?

A

same concept as IMHA but at the level of the bone marrow only – can see very severe anemias in a relatively stable patient

40
Q

what is key in diagnosing precursor immune-mediated anemia?

A

lack of other cytopenias

bone marrow examination is required for diagnosis

41
Q

when would you use PCR for diagnosing an infiltrative disorder causing an anemia?

A

FeLV or ehrlichia

42
Q

what drugs can cause toxicities resulting in an anemia?

A

immunosuppressants, antibiotics, estrogen, methimazole, & fenbendazole

43
Q

what lab abnormalities are commonly seen in patients with anemia due to infectious processes or toxicities?

A

bicytopenia or pancytopenia

44
Q

what are some fungal, chronic, & neoplastic processes that can cause anemia?

A

fungal – histoplasmosis
viral – FeLV
chronic – chronic ehrlichia
neoplasia – lymphoma, multiple myeloma, histiocytic sarcoma

45
Q

what is seen on bone marrow examination that is nearly pathognomonic for pure red cell aplasia?

A

lack of erythroblasts, adequate myeloid & megakaryocytic lines, adequate iron & EPO

46
Q

what is the mechanism of pure red cell aplasia?

A

selective erythroid hypoplasia in marrow that may be a primary or secondary immune-mediated process with other cell lines are not affected

47
Q

what is another name for pure red cell aplasia?

A

primary failure erythropoiesis

48
Q

what are the steps for deciding treatment for inadequate erythropoiesis?

A
  1. identify primary cause – anemia of inflammatory disease vs. CKD vs. primary marrow disorder
  2. if bone marrow exam is needed – do it, bicytopenia or pancytopenia or very chronic anemia
  3. treat based on bone marrow, Fe panel if needed

steroids often needed for PIMA or pure red cell aplasia

49
Q

what is the indication for EPO supplementation?

A

reserved for anemia with CKD

50
Q

what are the disadvantages of using epogen for EPO supplementation?

A

more likely to see adverse effects – formation of anti-EPO antibodies causing a severe anemia & you have to dose more often

51
Q

what are the advantages of using Aranesp for EPO supplementation?

A

less likely to see adverse effects & you don’t have to dose as often

52
Q

what should be monitored when using EPO supplementation for an anemic patient?

A

CBC weekly for the 1st 4-6 weeks

PCV/TS every 2 weeks after

53
Q

why can treatment be discouraging for PIMA?

A

can take a very long time for the anemia to resolve if at all

54
Q

what therapy is often used for PIMA?

A

steroids – same as IMHA

multiple immunosuppressives – cyclosporine & steroids

cobalamin – helps with normal RBC maturation

SA DX & TX I (59 decks)

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