clin path 2 Flashcards by Madison Warner

microchromic microcytic in anemia pattern

external chronic hemorrhage
iron deficiency

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where can bilirubin be conjugated in the dog?

kidneys and hepatocyte
normal for dog to have a little bilirubin in urine

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hemolytic anemia bilirubin metabolism

macrophages on overdrive killing RBCs
hepatocytes cannot keep up and conjugate all the bilirubin
causes increase in unconjugated bilirubin in blood

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fasting hyperbilirubinemia

fats bind to hepatocytes and block bilirubin metabolism
increased unconjugated biliruben
in large animals

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functional cholestasis

accumulation of bile
endotoxin interferes with excretion of conjugated bilirubin
increased conjugated bilirubin

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obstructional cholestasis

bile cannot be excreted (blocked bile duct)
increased conjugated bilirubin
no anemia or regeneration

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intravascular hemolysis

Site of RBC destruction: Blood vessels

Initiating processes:
* Antibodies > MAC
* RBC infectious agents
* Oxidative injury

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extravascular hemolysis

Site of RBC destruction: Macrophages (sinusoidal capillaries)

Initiating processes
* Antibodies > Opsonization
* RBC infectious agents
* Oxidative injury
* Old age markers

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ghost cells

intravascular hemolysis
from RBC + MAC= MAC formation
loss of hemoglobin via MACs = ghost cells

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spherocytes

extracellular hemolysis
no central palor
from destruction of RBC via antibodies, opsonization
mostly used in dog (cats/horses normal RBC look like spherocytes)

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hemoglobinemia

free hemoglobin in blood
can be from ruptured RBCs

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causes of hemolytic anemia

immune mediated hemolytic anemia(IMHA)
infectious hemolytic anemia
oxidative hemolytic anemia
fragmentation hemolysis

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immune mediated hemolytic anemia

antibodies target self RBCs

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how do antibodies to self RBCs form in IMHA?

Autoimmune:
Primary (nonassociative or Idiopathic) or
Secondary (associative)
* Infection
* Neoplasms
* Drugs

Alloimmune

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primary (nonassociative) IMHA clinical signs

Dogs&raquo_space; Cats
Young to middle aged
Predisposed breeds

History & Physical Examination:
-megaly
* Lymphadenomegaly
* Splenomegaly
* Hepatomegaly

Vomiting & diarrhea (V/D)
Polyuria & polydipsia (PU/PD)
Fever

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IMHA mechanism

antibodies (IgG) against RBCs
opsonization and agglutination
complete or partial phagocytosis of RBCs
aggregates of RBCs
biliruben, hemoglobin degredation products (AAs, biliruben, iron,), spherocytes, ghost cells

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IMHA blood smear

agglutination of RBCs, clumps
not rouleaux (chains of RBC, normal in horses)

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infectious hemolytic anemia (associative)

Pathogenesis
* Direct RBC lysis
* Innocent bystander
* Expose hidden antigens > IMHA

Signalment
* Cat, Cattle&raquo_space;> Dog, Horse
* Variable

History & Physical Examination
* Similar to idiopathic IMHA
* -megaly
* Lymphadenomegaly
* Splenomegaly
* Hepatomegaly

Vomiting & diarrhea (V/D)
Polyuria & polydipsia (PU/PD)
Fever

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diagnosing infectious hemolytic anemia

blood smear!!
check for parasites on RBCs

diagnosing infectious hemolytic anemia

blood smear!!
check for parasites on RBCs

oxidative hemolytic anemia (associative)

Pathogenesis
* Toxin ingestion, drug administration
* Oxidative RBC injury

Signalment
* Dogs, cats, horses, sheep

History & Physical Examination
* Toxin/drug exposure
* Hemolytic anemia
* Chocolate brown blood

oxidative hemolytic anemia caused by injury to iron of hemoglobin causes what clinical finding?

methemoglobinemia
blood is brown

oxidative hemolytic anemia caused by injury to globin of hemoglobin causes what clinical finding?

heinz bodies

oxidative hemolytic anemia caused by injury to RBC membranes causes what clinical finding?

eccentrocytes
most common in horses
pinched off piece of membrane, flat clear area on side of RBC

fragmentation hemolysis

Pathogenesis * Fragile RBCs * Microangiopathy (diseased small blood vessels) Inciting conditions * Iron deficiency * Hemangiosarcoma * Thrombus * Disseminated intravascular coagulation (DIC) (fibrin strands in vessels breaks RBCs apart) * Heart valve disease Signalment, History & Physical Examination= variable

blood smear of fragmentation hemolysis

acanthocytes, keratocytes, schistocytes

oxidative hemolytic anemia blood smear

ecentrocytes, heinz bodies

bicytopenia

at least 2 cells from bone marrow are decreased

pancytopenia

many cells from bone marrow are decreased (platelets, RBCs, WBCs)

myelosuppression

suppressed marrow production of cells decreased hematopoetic precursors

myelotoxin

damages bone marrow/precursors

myelophthisis

marrow is replaced with something else generalized marrow hypoplasia

non regenerative anemia criteria

no reticulocytes no evidence of acute hemorrhage no evidence of hemolysis marrow hypoplasia (selective erythroid or generalized marrow hypoplasia)

anemia of chronic disease (ACD)/ anemia of inflammatory disease (AID)

iron sequestration (hepcidin lets iron stay stuck in macrophage, GI tract) mild to moderate anemia (NOT severe) normocytic (sometimes microcytic), normochromic cause: almost any disease nonregenerative selective: erythrocytes

myelosuppressive agents/toxins

Selective erythroid hypoplasia * Viruses: **FeLV** * Drugs: rhEPO * Idiopathic: **Autoantibodies** Generalized marrow hypoplasia * Viruses: **FeLV, parvovirus** * Bacteria: Ehrlichia spp * Drugs: **Chemotherapy**, azathioprine, estrogen, trimethoprim-sulfamethoxazole (TMS), methimazole * Toxins: Plants * Idiopathic: Autoantibodies | dont memorize list, just know meds can lead to marrow damage

non regenerative vs regenerative IMHA

non regenerative: precursor immune related anemia (PIMA)

polycythemia

too many cells = erythrocytosis

relative hemoconcentration erythrocytosis

RBC mass is increased relative to the plasma PCV is normal but free water is lost (less plasma) so PCV % increases dehydration lab: * increased total protein (hyperalbuminemia, hyperglubulinemia) * hypernatremia, hyperchloremia * increased USG (specific gravity = concentrated urine) * azotemia (increased waste products, not producing as much urine)

relative redistribution erythrocytosis

RBC mass is increased relative to the plasma due to **excitment**, spleen squeezes out extra RBCs short term lab: * mild neutrophilia * mild lymphocytosis * mild hyperglycemia * mild thrombocytosis * NO hyperproteinemia

Primary absolute erythrocytosis

polycythemia vera RBC neoplasia

secondary absolute erythrocytosis

**increased EPO** appropriate (hypoxia, need more RBC) * low FiO2 * R to L shunt inappropiate * EPO secreting tumor

Fibrinogen

produced in liver soluable protein in plasma function: * fibrinogen > Fibrin (insoluable) * hemostasis * inflammation

4 stages of hemostasis

1. vasoconstriction 2. **p**rimary hemostasis = **p**latelets, von Willebrand factor (vWF) 3. secondary hemostasis= coagulation cascade (Tissue factor, **converts fibrinogen to fibrin)** 4. thrombus and antithrombotic events (shut off coagulation)

edothelial cells of blood vessel

have all the maincomponents of hemostasis

PP:Fib ratio in normal animal horse and ruminant | plasma protein: fibronogen

ruminant: 10-15 PP:fib horse: 15-20 PP:fib

dehydration PP:Fib ratio horse and ruminant

ruminant: >15 PP:fib horse: >20 PP:fib **increased PP:fib ratio**

inflammation PP:Fib ratio horse and ruminant

ruminant: <10 PP:fib horse: <15 PP:fib **decreased PP:fib ratio** increased fibrinogen