clin path 2 Flashcards
microchromic microcytic in anemia pattern
external chronic hemorrhage
iron deficiency
where can bilirubin be conjugated in the dog?
kidneys and hepatocyte
normal for dog to have a little bilirubin in urine
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
fasting hyperbilirubinemia
fats bind to hepatocytes and block bilirubin metabolism
increased unconjugated biliruben
in large animals
functional cholestasis
accumulation of bile
endotoxin interferes with excretion of conjugated bilirubin
increased conjugated bilirubin
obstructional cholestasis
bile cannot be excreted (blocked bile duct)
increased conjugated bilirubin
no anemia or regeneration
intravascular hemolysis
Site of RBC destruction: Blood vessels
Initiating processes:
* Antibodies > MAC
* RBC infectious agents
* Oxidative injury
extravascular hemolysis
Site of RBC destruction: Macrophages (sinusoidal capillaries)
Initiating processes
* Antibodies > Opsonization
* RBC infectious agents
* Oxidative injury
* Old age markers
ghost cells
intravascular hemolysis
from RBC + MAC= MAC formation
loss of hemoglobin via MACs = ghost cells
spherocytes
extracellular hemolysis
no central palor
from destruction of RBC via antibodies, opsonization
mostly used in dog (cats/horses normal RBC look like spherocytes)
hemoglobinemia
free hemoglobin in blood
can be from ruptured RBCs
causes of hemolytic anemia
immune mediated hemolytic anemia(IMHA)
infectious hemolytic anemia
oxidative hemolytic anemia
fragmentation hemolysis
immune mediated hemolytic anemia
antibodies target self RBCs
how do antibodies to self RBCs form in IMHA?
Autoimmune:
Primary (nonassociative or Idiopathic) or
Secondary (associative)
* Infection
* Neoplasms
* Drugs
Alloimmune
primary (nonassociative) IMHA clinical signs
Dogs»_space; Cats
Young to middle aged
Predisposed breeds
History & Physical Examination:
-megaly
* Lymphadenomegaly
* Splenomegaly
* Hepatomegaly
Vomiting & diarrhea (V/D)
Polyuria & polydipsia (PU/PD)
Fever
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
IMHA blood smear
agglutination of RBCs, clumps
not rouleaux (chains of RBC, normal in horses)
infectious hemolytic anemia (associative)
Pathogenesis
* Direct RBC lysis
* Innocent bystander
* Expose hidden antigens > IMHA
Signalment
* Cat, Cattle»_space;> Dog, Horse
* Variable
History & Physical Examination
* Similar to idiopathic IMHA
* -megaly
* Lymphadenomegaly
* Splenomegaly
* Hepatomegaly
Vomiting & diarrhea (V/D)
Polyuria & polydipsia (PU/PD)
Fever
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
- vasoconstriction
- primary hemostasis = platelets, von Willebrand factor (vWF)
- secondary hemostasis= coagulation cascade (Tissue factor, converts fibrinogen to fibrin)
- 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
