Haemolymphatic, Oncology & Immunology Flashcards by Tori Brown

Lymphatic system

Shadow circulatory system that drains fluid from the interstitial space and tissues processing it in the lymph nodes and then returning it to venous circulation

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Erythropoeisis

The genesis of RBC that begins in the bone marrow
Dependent on EPO (hb synthesis, stimulated by renal hypoxia, stimulates reticulocyte release)

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Purpose of blood

To transport oxygen, platelets, WBC, and products of cellular metabolism
Also regulates body temperature, pH and depends against phagocytosis from WBC, also provisions clotting factors and platelet activation

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Genesis and removal of RBC

EPO release from kidneys in response to renal hypoxia > bone marrow makes and releases reticulocytes from erythroid progenitor cells > RBC circulate and live approx. 68 days in cats and 110 days in dogs before being phagocytosis by macrophages and either recycled or destroyed via extra vascular haemolysis

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Neutrophil

Most abundant circulating WBC
Phagocytic and target microorganisms and tissue debris via chemotaxis
Band neutrophils; unsegmented immature WBC that are in high numbers due to an inflammatory response ‘left shift’

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Eosinophils

Red/pink granules within the cytoplasm - anti-inflammatory substances
Make up about 5% of circulating WBC but higher numbers in response to anaphylaxis and some GI parasites
Flagged by basophils to site
Quickly migrate to tissues after they are released

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Basophils

B for blue granules - histamine and heparin; flags eosinophils for phagocytosis; local anticoagulation
Rarest WBC seen; inflammation and hypersensitivity reactions

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Monocytes

Largest of WBC, mature fast
Become macrophages once enter tissues
Vacuolisation in a moderate cytoplasm
Clean up debris from infection and inflammation
Presence generally indicates chronic infection due to their long life span
5-6% of WBC population

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Lymphocytes

T cell; thymus > about 80% of lymphocytes
B cell; lymph node > produce Ig’s
NK; don’t require activation and lyse abnormal cells/tumour cells

No phagocytic ability
Round to oval nucleus, slightly bigger than RBC

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Platelets

Formed from mekaryocytes in the bone marrow
Major player in haemostasis

Normal 200,000-800,000
Haemorrhage <30,000

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A regenerative anaemia

Macrocytic, hypochromic, anicytosis, polychromasia, nRBC
Appropriate response of the bone marrow to blood loss/haemolysis/destruction
Takes 2-3 days in cats and 4-5 days in dogs

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Non-regenerative anaemia

Bone marrow doesn’t respond appropriately
Normochromic, normocytic > hypochromasia (central pallor - Fe deficiency) and microcytic
Aplastic = bone marrow fault
Low to no reticulocytes/nRBC

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Polycythemia

Inappropriate elevation of RBC >50-60% and increase Hb that increases blood viscosity decreasing effective microcirculation
Primary/Vera = myeloid stem cells from EPO are increasing RBC
Secondary = increased RBC production I.e. PDA, renal amyloidosis, infection, inflammation

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IMHA

premature RBC destruction due to a type II hypersensitivity reaction with some predisposition to middle-aged female spaniels, poodles and collies. Can be a primary or secondary disease.

Autoantibodies IgM, IgG and IgA target patients own membrane antigens and activate the complement and membrane attack complex which causes haemolysis and release of pro-inflammatory mediators putting the patient at risk of thromboembolism.
Extravascular haemolysis (liver, spleen) - HBC cleared via bilirubin pathway and thought to be less severe
Intravascular haemolysis - RBC surface damage > influx ECF fluid > cell rupture > free Hb > AKI etc (more severe)

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Other causes of haemolytic anaemia (not immune mediated)

Pyruvate kinase deficiency
Phosphofructokinase deficiency
Hypophosphotaemia
Refeeding syndrome
DKA
Zinc toxicity
Onion and garlic
Acetaminophen

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Microangiopathy

Vessel occlusion, abnormal vascular morphology, fibrin shearing > RBC fragmentation (schistocytes)
DIC, vasculitis, liver disease, neoplasia, heartworm, IV catheterisation

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Signs of immune mediated haemolytic anaemia

Lethargy, weakness, pallor tachycardia, hepatosplenomegaly, systolic murmur (turbulent flow and reduced viscosity), icterus, fever, GI signs, anicystosis, spherocytosis, polychromasia, positive agglutination, +- positive Coombs test

Rouleaux formation

Normal stacking of RBC not to be mistaken for agglutination

Treatment of IMHA

First line; glucocorticoids (prednisolone 1-2mg/kg PO q12 or dex if can’t tolerate pred)
Recognise and address underlying cause
Antiemetics and gastroprotectants
Blood transfusions
IVIG (refractory to therapy - bind complements, reduce antibody production, inhibit monocytes cytokines, modulate B&T clone)
Melatonin (immunomodulatory)
Spelenectomy
+- TPE/Apheresis

Leukopaenia

Reduced WBC and usually due to reduced neutrophil count
Bone marrow suppression; increased destruction; sequestration from spleen

Leukocytosis

Increased WBC usually in response to infection or inflammation
Left shift = increased immature neutrophils (regenerative = mature neutrophils and immature neutrophils; nonregenerative = more immature neutrophils but not many mature)

Effect of corticosteroids on neutrophils

Increase demargination from bone marrow 4-8h after administration which normalises after 1-3 days of treatment

ITP

Increased platelet destruction mediated by the immune system (Type II hypersensitivity)
Primary or secondary
Signs; Petechiae, ecchymoses, haematuria, HGE, retinal haemorrhage, epistaxis etc

ITP Treatment

Immunosuppressive (glucocorticoids and work within 7 days)
PPI’s and antiemetic
Vincristine (increases PLT from megakaryocytes, reduces platelet consumption, increases platelet count quickly)
IVIG
Splenecotmy
Transfusions (fWB, cryo’s)

Mild allergic reactions

Usually just cutaneous signs - urticaria - pruritis - facial oedema - fever erythema Respond well to antihistamine

Anaphylaxis

Type I hypersensitivity Hypovolaemic and distributive shock Vasodilation GI signs Respiratory signs Hepatic congestion Histamine release Mast cell degranulation

Very basic/brief pathophysiology of sepsis

Invader > macrophages to microbes > PAMPS, DAMPS > phagocytosis > pro and anti inflammatory cytokines (TNFa, IL6, IL1), chemokines and NO production/release > leukocyte activation > either controlled or ramping in of pro-inflammation > pro inflammatory response exhausted > CARS > immunoparalysis > healthy tissue damage > ischaemia, cellular damage, apoptosis, DIC, MODS > death

Tumor lysis syndrome

Suspected in any patient receiving chemotherapy Rapid death of tumor cells > release of tumor DNA, K, Phosphate, xanthine > AKI, urate nephropathy and tubular damage (CaP deposition) > Oliguria renal failure Treatment: Rasburicase ( give as prophy), dextrose, allopurinol (prevents conversion to xanthine), 0.9% NaCl, calcitonin, furosemide

Paraneoplastic syndrome

Systemic illness resulting from neoplasia but are not related to the primary disease Usually lead to endocrine effects I.e. hypercalcaemia and hypoglycaemia Other systemic: anaemia, thrombocytopaenia, neurological signs I.e. lymphoma > increased calcium

DIC

Intravascular activation of coagulation leading to generalised coagulopathy, thrombosis and organ dysfunction Proinflammation > IV fibrin formation > microvascular thrombi > organ dysfunction > thrombocytopaenia > widespread haemorrhage Prolonged coagulation, increased FDP, increased D-dimers, thrombocytopaenia haemolytic anaemia declining antithrombin levels Treatment; FFP and cryoprecipitate therapy

What is the process of blood components creating stable clots and destroying those clots when they are no longer needed called? a. Hematopoiesis b. Hemostasis c. Coagulation d. Thrombopoiesis

Primary polycythemia is referred to as what? a. Erythrocytosis b. Polycythemia vera c. IMHA d. Regenerative anemia

Small red blood cells that appear darker than normal RBCs that are devoid of central pallor are called what? a. Schistocytes b. Acanthocytes c. Echinocytes d. Spherocytes

Stacking of red blood cells when not mediated by antibodies is called what? a. Rouleaux b. Agglutination c. Reticulocytosis d. Passive immunity

The passage of antibodies from one individual to another, such as through the ingestion of colostrum, is what type of immunity? a. Cellular immunity b. Humoral immunity c. Passive immunity d. Acquired immunity

Apoptosis is defined as what? a. Cellular injury b. Disruption of the endothelial glycocalyx c. Thrombosis of the microvasculature d. Programmed cell death

The acute and potentially life-threatening emergency involving the death of tumor cells is called what? a. Apoptosis b. Chemotherapy c. Tumor lysis syndrome d. Radiation therapy

A systemic illness that is induced by neoplasia but that occurs in a separate body system is called what? a. Paraneoplastic syndrome b. Tumor lysis syndrome c. Oncolysis d. Chemosepsis

Calcium is which clotting factor? a. I b. IV c. VI d. X

Activated platelets forming a platelet plug is which step of hemostasis? a. Secondary hemostasis b. Fibrinolysis c. Primary hemostasis d. Thrombolysis

IVIG

Bind to Fc receptors on macrophages to prevent B cell’s which make autoantibodies. Attenuates complement damage and induces anti-inflammatory cytokines Used in immune mediated diseases May cause type I IgE hypersensitivity reaction (human product)