SAM.HI4: Non-Malignant Splenic Dz

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Last updated 12:28 AM on 5/25/26
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73 Terms

1
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Changes in RBCs seen w/ splenic dz (5)

Anemia.

Schistocytes.

Acanthocytes.

Spherocytes

nRBCs.

<p>Anemia.</p><p>Schistocytes.</p><p>Acanthocytes.</p><p>Spherocytes</p><p>nRBCs.</p>
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Schistocytes are highly suggestive of

Neoplastic splenic dz

<p>Neoplastic splenic dz</p>
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nRBC can be seen w/

benign conditions such as EMH (spleen is not able to prevent release of immature cells when stimulated)

<p>benign conditions such as EMH (spleen is not able to prevent release of immature cells when stimulated)</p>
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Leukoerythroblastic response

Increased nRBC and immature WBCs that can be seen w/ splenic dz.

<p>Increased nRBC and immature WBCs that can be seen w/ splenic dz.</p>
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Rads in Dx of splenic dz

size and position of the spleen.

evidence of effusion.

<p>size and position of the spleen.</p><p>evidence of effusion.</p>
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Generalized or focal splenomegaly on rads

may result in a mass effect in the mid-abdomen w/ displacement of other abdominal organs.

<p>may result in a mass effect in the mid-abdomen w/ displacement of other abdominal organs.</p>
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Rads w/ splenic torsion or hemorrhage (2)

decreased detail +/- effusion

torsion - abnormal placement of the spleen.

<p>decreased detail +/- effusion</p><p>torsion - abnormal placement of the spleen.</p>
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FNA is useful in the dx of dzs that cause

diffuse splenomegaly and some focal lesions

<p>diffuse splenomegaly and some focal lesions</p>
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Which lesions have low yield w/ FNA

cavitated masses - not reco due to hemorrhage risk

<p>cavitated masses - not reco due to hemorrhage risk</p>
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Which method is often performed for cavitated lesions/hemorrhage

Splenectomy > splenic biopsy

<p>Splenectomy &gt; splenic biopsy</p>
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Removal of the spleen may predispose animals to developing certain infections (3)

Mycoplasma spp.

E. canis.

Babesia canis.

12
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Nodular Hyperplasia occurs as a result of

proliferation of normal cells of the spleen.

<p>proliferation of normal cells of the spleen.</p>
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4 types of Nodular Hyperplasia.

Lymphoid.

Splenic stromal.

Hematopoietic.

Complex.

<p>Lymphoid.</p><p>Splenic stromal.</p><p>Hematopoietic.</p><p>Complex.</p>
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Which splenic pathology is a form of MH

Splenic myelolipoma.

<p>Splenic myelolipoma.</p>
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Lesions of nodular hyplerplasia

focal, but there may be multiple.

<p>focal, but there may be multiple.</p>
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Nodular hypoplasia on US

hypoechoic

<p>hypoechoic</p>
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How can nodular hyperplasia lead to hematoma in the dog?

distortion of the splenic vasculature by hyperplasia

<p>distortion of the splenic vasculature by hyperplasia</p>
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Why is it suspected that cats are less likely to have splenic hematomas?

different anatomy of the spleen and orientation of the vasculature.

<p>different anatomy of the spleen and orientation of the vasculature.</p>
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Splenic hematomas are more common in

large breeds - GSD and standard poodles.

<p>large breeds - GSD and standard poodles.</p>
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Hematomas may occur

alone or be associated w/ MH, neoplasia, trauma, or idiopathic.

<p>alone or be associated w/ MH, neoplasia, trauma, or idiopathic.</p>
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Clinical manifestation of dogs w/ hematomas

healthy

hemoabdomen

<p>healthy</p><p>hemoabdomen</p>
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EMH occurs as the

workload of the spleen increases

<p>workload of the spleen increases</p>
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Workload of the spleen increasing can be due to increased (4)

removal of normal cells.

activity of the mononuclear-phagocytic system.

activity of the lymphoid tissues.

blood cell production.

<p>removal of normal cells.</p><p>activity of the mononuclear-phagocytic system.</p><p>activity of the lymphoid tissues.</p><p>blood cell production.</p>
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EMH on U/S (2)

Dogs - Diffuse splenomegaly that is hypoechoic.

Cats - diffuse nodular.

<p>Dogs - Diffuse splenomegaly that is hypoechoic.</p><p>Cats - diffuse nodular.</p>
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Aspirate results for EMH (2)

increased number of medium to large lymphocytes and plasma cells (hyperplasia).

increased number of blood cell precursors on splenic aspirates nRBCs peripherally may be seen.

<p>increased number of medium to large lymphocytes and plasma cells (hyperplasia).</p><p>increased number of blood cell precursors on splenic aspirates nRBCs peripherally may be seen.</p>
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Splenic congestion can be seen w/ (2)

acepromazine.

barbiturates.

Portal HT.

Venous HT - R sided HF and CaVC occlusion.

<p>acepromazine.</p><p>barbiturates.</p><p>Portal HT.</p><p>Venous HT - R sided HF and CaVC occlusion.</p>
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Splenic congestion on U/S

normal echotexture, but may have distended vasculature.

<p>normal echotexture, but may have distended vasculature.</p>
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Splenic torsion spp trend

rare overall, but more common in dogs

<p>rare overall, but more common in dogs</p>
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CS of dogs w/ splenic torsion (4)

shock.

anorexia.

V.

Abdominal pain.

<p>shock.</p><p>anorexia.</p><p>V.</p><p>Abdominal pain.</p>
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Torsion can rarely be

chronic and intermittent.

<p>chronic and intermittent.</p>
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Rad findings of splenic torsion

decrease detail in the abdomen secondary to abdominal effusion.

<p>decrease detail in the abdomen secondary to abdominal effusion.</p>
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U/S findings of splenic torsion (2)

Abnormal location.

Diffuse enlargement.

<p>Abnormal location.</p><p>Diffuse enlargement.</p>
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Tx for splenic torsion

Stabilization then Sx.

<p>Stabilization then Sx.</p>
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Splenitis def

Inflammation of the spleen.

<p>Inflammation of the spleen.</p>
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Splenitis may result in

diffuse splenomegaly

<p>diffuse splenomegaly</p>
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What is formed during each phase of hemostasis (2)

Primary - platelet plug.

Secondary - Stable clot via fibrin.

<p>Primary - platelet plug.</p><p>Secondary - Stable clot via fibrin.</p>
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Primary hemostasis CS (3)

Petechia and ecchymoses.

Blood from mm (can be either).

Bleeding immediately after venipuncture.

<p><strong>Petechia and ecchymoses.</strong></p><p>Blood from mm (can be either).</p><p>Bleeding immediately after venipuncture.</p>
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Secondary hemostasis CS (3)

RARE petechia and ecchymoses.

Bleeds into cavities.

Delayed bleeding after venipuncture.

<p>RARE petechia and ecchymoses.</p><p><strong>Bleeds into cavities</strong>.</p><p>Delayed bleeding after venipuncture.</p>
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Primary hemostasic disorders (3)

Thromboyctopenia.

Thrombocytopathia.

vWD.

<p>Thromboyctopenia.</p><p>Thrombocytopathia.</p><p>vWD.</p>
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Thrombocytopenia Etiologies- non-path (2)

Breeds - Cavaliers and Sight hounds.

Artifact.

<p>Breeds - Cavaliers and Sight hounds.</p><p>Artifact.</p>
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Manual count of platelets (2)

Feathered edge.

Normal = 10-20/hpf.

<p>Feathered edge.</p><p>Normal = 10-20/hpf.</p>
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BMBT tests for

thrombocytopathia (platelet function) or vWD - need to have a normal platelet number

<p>thrombocytopathia (platelet function) or vWD - need to have a normal platelet number</p>
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Process for BMBT (4)

Lateral recumbency.

Lancing device.

Catch excess while not disturbing site.

2-4m.

<p>Lateral recumbency.</p><p>Lancing device.</p><p>Catch excess while not disturbing site.</p><p>2-4m.</p>
44
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Platelet fxn analyzer is used for dx of

congenital thrombocytopathia

<p>congenital thrombocytopathia</p>
45
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vonWillebrand factor deficiency breeds

Doberman - up to 70% carry, type 1

Shetland sheepdog

Scottish terrier

German shorthair

Chesapeake bay

Golden

Bernese

Welsh corgi

GSD

Basset

<p>Doberman - up to 70% carry, type 1</p><p>Shetland sheepdog</p><p>Scottish terrier</p><p>German shorthair</p><p>Chesapeake bay</p><p>Golden</p><p>Bernese</p><p>Welsh corgi</p><p>GSD</p><p>Basset </p>
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vWD Type 1 (3)

Most common form.

Low quantity of factor.

Live normal lives.

<p>Most common form.</p><p>Low quantity of factor.</p><p>Live normal lives.</p>
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vWD Type 2 (2)

More severe form.

Malformed factor, but has normal quantity.

<p>More severe form.</p><p>Malformed factor, but has normal quantity.</p>
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vWD Type 3 (2)

Most severe form.

No factor produced.

<p>Most severe form.</p><p>No factor produced.</p>
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CS of vWD (3)

Petechia and ecchymoses.

Epistaxis.

Peri-op bleeding.

(Hematuria, Hematemesis, and Melena)

<p>Petechia and ecchymoses.</p><p>Epistaxis.</p><p>Peri-op bleeding.</p><p>(Hematuria, Hematemesis, and Melena)</p>
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Dx of vWD (2)

BMBT

Measure factor - detects Type 1 and 3.

Qualitative assay - detects Type 2 (measures binding vWF to collagen).

<p>BMBT</p><p>Measure factor - detects Type 1 and 3.</p><p>Qualitative assay - detects Type 2 (measures binding vWF to collagen).</p>
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Tx for vWD - general concept based on type

Type 1 - may not bleed.

Type 2 and 3 - Tx.

<p>Type 1 - may not bleed.</p><p>Type 2 and 3 - Tx.</p>
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Tx for vWD (3)

Desmopressin acetate.

Cryoprecipitate.

FFP.

<p>Desmopressin acetate.</p><p>Cryoprecipitate.</p><p>FFP.</p>
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Desmopressin acetate in tx of vWD

Type 1 and 2 given SC 30m prior to procedures.

<p>Type 1 and 2 given SC 30m prior to procedures.</p>
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Cryoprecipitate in tx of vWD

Has more vWF at lower volume. Given q8-12h.

<p>Has more vWF at lower volume. Given q8-12h.</p>
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Platelet dysfxn can be

congenital or acquired.

<p>congenital or acquired.</p>
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Dx of platelet dyfxn (4)

Bleeding w/ prolonged BMBT.

Normal vWF, platelet numbers, clotting times.

Abnormal platelet aggregation.

DNA tests.

<p>Bleeding w/ prolonged BMBT.</p><p>Normal vWF, platelet numbers, clotting times.</p><p>Abnormal platelet aggregation.</p><p>DNA tests.</p>
57
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Disorders of secondary hemostasis includes (4)

Vit K deficiency.

Hemophilia A or B.

Factor 12 deficiency.

DIC.

<p>Vit K deficiency.</p><p>Hemophilia A or B.</p><p>Factor 12 deficiency.</p><p>DIC.</p>
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Etiologies of Vitamin K deficiency (4)

Rodenticide.

Inhibited Vit K production by intestinal microflora.

Liver dz - cholestasis.

Severe fat malabsorption (EPI, Biliary duct obstruction, Lymphangiectasia).

<p>Rodenticide.</p><p>Inhibited Vit K production by intestinal microflora.</p><p>Liver dz - cholestasis.</p><p>Severe fat malabsorption (EPI, Biliary duct obstruction, Lymphangiectasia).</p>
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Pathogenesis of Rodenticide

Inhibits Vitamin K epoxide reductase resulting in loss of factor 2, 7, 9, and 10.

<p>Inhibits Vitamin K epoxide reductase resulting in loss of factor 2, 7, 9, and 10.</p>
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Dx of Vit K deficiency (3)

Exposure to rodenticide.

PT prolonged (36-72h) followed by PTT.

CBC suggesting hemorrhage.

<p>Exposure to rodenticide.</p><p>PT prolonged (36-72h) followed by PTT.</p><p>CBC suggesting hemorrhage.</p>
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Tx for Vit K deficiency - Early exposure w/ no bleeding (2)

Decontamination w/ emesis and charcoal.

Check PT at 36-48h post-exposure +/- Vitamin K.

<p>Decontamination w/ emesis and charcoal.</p><p>Check PT at 36-48h post-exposure +/- Vitamin K.</p>
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Tx for Vit K deficiency w/ bleeding (3)

Plasma w/ red cells PRN.

SC or PO vitamin K x 2-4wks.

Measure PT 36-48 after completion

<p>Plasma w/ red cells PRN.</p><p>SC or PO vitamin K x 2-4wks.</p><p>Measure PT 36-48 after completion</p>
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Hemophilia A and B inheritance

Autosomal X-lined recessive - males are affected

<p>Autosomal X-lined recessive - males are affected</p>
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Dx of Hemophilia A and B (2)

Normal PT and prolonged PTT.

Measure factors.

<p>Normal PT and prolonged PTT.</p><p>Measure factors.</p>
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Tx for Hemophilia A and B (2)

FFP for factors.

Red cells PRN.

(Can develop Ab's to transfused factors)

<p>FFP for factors.</p><p>Red cells PRN.</p><p>(Can develop Ab's to transfused factors)</p>
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Factor XII deficiency is a common

intrinsic pathway deficiency in cats

<p>intrinsic pathway deficiency in cats</p>
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Dx for Factor XII deficiency (3)

Normal PT and prolonged PTT.

Normal fibrinogen.

No clinical bleeding b/c clot does not depend on 12 (may have prolonged bleeding w/ hemorrhage).

<p>Normal PT and prolonged PTT.</p><p>Normal fibrinogen.</p><p>No clinical bleeding b/c clot does not depend on 12 (may have prolonged bleeding w/ hemorrhage).</p>
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IMT etiology general (2)

Idiopathic - more severe.

Associated or secondary.

<p>Idiopathic - more severe.</p><p>Associated or secondary.</p>
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IMT etiologies - Secondary (5)

HS - drugs and anaphylaxis.

ABX - sulfa.

Infection.

Neoplasia.

Systemic inflammatory.

<p>HS - drugs and anaphylaxis.</p><p>ABX - sulfa.</p><p>Infection.</p><p>Neoplasia.</p><p>Systemic inflammatory.</p>
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IMT - infectious etiologies (5)

Anaplasma.

Neorickettsiae.

Babesia.

Erlichia.

Leshmania.

<p>Anaplasma.</p><p>Neorickettsiae.</p><p>Babesia.</p><p>Erlichia.</p><p>Leshmania.</p>
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Dx for IMT (4)

Platelets <20k.

MPV may be increased.

Immune mediated or blood loss anemia.

Platelet Ab - intermittently available and does not differentiate primary v. secondary.

<p>Platelets &lt;20k.</p><p>MPV may be increased.</p><p>Immune mediated or blood loss anemia.</p><p>Platelet Ab - intermittently available and does not differentiate primary v. secondary.</p>
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Tx for IMT - options (4)

RBC transfusion if anemic.

Glucocorticoids + adjunct.

Vincristine - premature platelet release (helpful in actively bleeding, unstable P).

Romiplastin - thrombopoietin receptor agonist.

<p>RBC transfusion if anemic.</p><p>Glucocorticoids + adjunct.</p><p>Vincristine - premature platelet release (helpful in actively bleeding, unstable P).</p><p>Romiplastin - thrombopoietin receptor agonist.</p>
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Tapering for IMT (2)

GC: Taper q2wks w/ normal platelets by 25%

Adjunct: stop or taper once off pred.

<p>GC: Taper q2wks w/ normal platelets by 25%</p><p>Adjunct: stop or taper once off pred.</p>