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DWT exam 1 > clin path 2 > Flashcards

clin path 2 Flashcards

1
Q

microchromic microcytic in anemia pattern

A

external chronic hemorrhage
iron deficiency

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2
Q

where can bilirubin be conjugated in the dog?

A

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

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3
Q

hemolytic anemia bilirubin metabolism

A
  1. macrophages on overdrive killing RBCs
  2. hepatocytes cannot keep up and conjugate all the bilirubin
  3. causes increase in unconjugated bilirubin in blood
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4
Q

fasting hyperbilirubinemia

A

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

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5
Q

functional cholestasis

A

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

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6
Q

obstructional cholestasis

A

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

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7
Q

intravascular hemolysis

A

Site of RBC destruction: Blood vessels

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

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8
Q

extravascular hemolysis

A

Site of RBC destruction: Macrophages (sinusoidal capillaries)

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

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9
Q

ghost cells

A

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

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10
Q

spherocytes

A

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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11
Q

hemoglobinemia

A

free hemoglobin in blood
can be from ruptured RBCs

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12
Q

causes of hemolytic anemia

A

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

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13
Q

immune mediated hemolytic anemia

A

antibodies target self RBCs

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14
Q

how do antibodies to self RBCs form in IMHA?

A

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

Alloimmune

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15
Q

primary (nonassociative) IMHA clinical signs

A

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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16
Q

IMHA mechanism

A
  1. antibodies (IgG) against RBCs
  2. opsonization and agglutination
  3. complete or partial phagocytosis of RBCs
  4. aggregates of RBCs
  5. biliruben, hemoglobin degredation products (AAs, biliruben, iron,), spherocytes, ghost cells
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17
Q

IMHA blood smear

A

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

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18
Q

infectious hemolytic anemia (associative)

A

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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19
Q

diagnosing infectious hemolytic anemia

A

blood smear!!
check for parasites on RBCs

20
Q

diagnosing infectious hemolytic anemia

A

blood smear!!
check for parasites on RBCs

21
Q

oxidative hemolytic anemia (associative)

A

Pathogenesis
* Toxin ingestion, drug administration
* Oxidative RBC injury

Signalment
* Dogs, cats, horses, sheep

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

22
Q

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

A

methemoglobinemia
blood is brown

23
Q

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

A

heinz bodies

24
Q

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

A

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

25
Q

fragmentation hemolysis

A

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

26
Q

blood smear of fragmentation hemolysis

A

acanthocytes, keratocytes, schistocytes

27
Q

oxidative hemolytic anemia blood smear

A

ecentrocytes, heinz bodies

28
Q

bicytopenia

A

at least 2 cells from bone marrow are decreased

29
Q

pancytopenia

A

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

30
Q

myelosuppression

A

suppressed marrow production of cells
decreased hematopoetic precursors

31
Q

myelotoxin

A

damages bone marrow/precursors

32
Q

myelophthisis

A

marrow is replaced with something else
generalized marrow hypoplasia

33
Q

non regenerative anemia criteria

A

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

34
Q

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

A

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

35
Q

myelosuppressive agents/toxins

A

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

36
Q

non regenerative vs regenerative IMHA

A

non regenerative: precursor immune related anemia (PIMA)

37
Q

polycythemia

A

too many cells = erythrocytosis

38
Q

relative hemoconcentration erythrocytosis

A

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)

39
Q

relative redistribution erythrocytosis

A

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

40
Q

Primary absolute erythrocytosis

A

polycythemia vera
RBC neoplasia

41
Q

secondary absolute erythrocytosis

A

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

inappropiate
* EPO secreting tumor

42
Q

Fibrinogen

A

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

43
Q

4 stages of hemostasis

A
  1. vasoconstriction
  2. primary hemostasis = platelets, von Willebrand factor (vWF)
  3. secondary hemostasis= coagulation cascade (Tissue factor, converts fibrinogen to fibrin)
  4. thrombus and antithrombotic events (shut off coagulation)
44
Q

edothelial cells of blood vessel

A

have all the maincomponents of hemostasis

45
Q

PP:Fib ratio in normal animal
horse and ruminant

plasma protein: fibronogen

A

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

46
Q

dehydration PP:Fib ratio
horse and ruminant

A

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

47
Q

inflammation PP:Fib ratio
horse and ruminant

A

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

DWT exam 1 (13 decks)

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