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4th Year Exams > LR&H > Flashcards

LR&H Flashcards

1
Q

With low PCV - what is the first question you always want to ask?

A

Is this anemia regenerative or non-regenerative?

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2
Q

If suspected IMHA, what are the best diagnostic tests to confirm?

A

In Saline Agglutination test - will agglutinate due to antibodies on RBC surfaces
Coomb’s test

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3
Q

What is the difference between pyrexia and hyperthermia?

A

Pyrexia - body’s increase in hypothalamic set point as a response to a pathological state carried out by pyrogens (cytokines)
Hyperthermia - sudden, uncontrolled increase in body temperature due to a failure of the body’s thermoregulation - body unable to lose enough heat in relation to the production (heat stroke, exercise)

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4
Q

What are the first tests to do when anemia is suspected?

A

PCV/TP

Blood smear

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5
Q

What will be seen on a blood smear with regenerative anemia?

A 
Polychromasia - bluer RBCs = immature 
Aniscytosis - different RBC cell sizes 
Spherocytes - dents in RBCs - extravascular hemolysis 
Ghost cells - intravascular hemolysis
Reticulocytes/polychromatophils
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6
Q

How to differentiate between 1º and 2º IMHA?

A

Trigger factors - infectious, UTI, drugs, toxins, neoplasia
Abdominal/thoracic radiographs
If negative without abnormalities - 1º

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7
Q

Treatment for 1º IMHA

A

Blood type and blood transfusion
Prednisolone to stop immune-mediated destruction
Clopidogrel - decrease risk of thromboembolic disease
Add a second immuno suppressant (chlorambucil in cats and azathioprene in dogs) to taper down corticosteroid
Consider using a gastroprotectant (omeprazole)

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8
Q

Reasons for pyrexia with IMHA

A

Immune mediated diseases cause recurrent pyrexia

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9
Q

What will be seen on a blood smear with iron-deficient anemia?

A

Microcytosis
Hypochromasia - RBCs very pale
- Usually due to chronic intestinal loss of iron

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10
Q

What are the canine blood types?

A

DEA 1, 3, 4, 5, and 7 - positive or negative
Generally, test for DEA 1 because there are anti-DEA 1 antibodies that will form if you give DEA 1 positive blood to a DEA negative dog
* Naturally occurring ABs are uncommon for all other DEAs*

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11
Q

What are the feline blood types?

A

A, B, or AB

* Cats have naturally occurring alloantibodies to A or B antigens (unless AB type) – ALWAYS BLOOD TYPE CATS!

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12
Q

With severe thrombocytopenia, what are the major diagnoses?

A
  • Could be artefactual (on CBC measurement)
  • Immune-mediated thrombocytopenia
    1º - just occur, idiopathic
    2º - underlying disease process, neoplasm, infection, drug treatment
  • BM disease (fibrosis, neoplasia)- kicking out platelets
  • DIC - disseminated intravascular coagulation - coagulopathy forming clots in body using platelets - usually not severe thrombocytopenia ** ALWAYS SECONDARY PROCESS TO NEOPLASIA/Pancreatitis/etc.*
  • Drug therapy - phenobarbitone
  • Infectious disease - lepto
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13
Q

What is the ddx in a dog with signs of shock with harsh lung sounds, bilateral SCLERAL hemorrhage (no trauma), and thrombocytopenia?

A

Angiostrongylus vasorum

Dx with Angiosnap, Baermann

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14
Q

DDX for 2º hemostasis disorders

A

Hepatic failure - has to be severe - produces coagulation factors, albumin
Rodenticide intoxication
Inherited coagulopathies - hemophilia (affect one clotting factor)
Heparin administration

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15
Q

When looking at blood smear - what are the three components to look at?

A

Red Blood cells
White blood cells
Platelets

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16
Q

How to recognize left shift toxicity on blood smear?

A

You will see band neutrophils with parallel walls of the nucleus and FOAMY cytoplasm and basophilia of cytoplasm where it looks BLUE
Toxicity - accelerated production meaning that cells are produced too fast - do not look normal

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17
Q

What is the most common cause of thrombocytopenia?

A

Immune-mediated thrombocytopenia

ABs produced against platelet antigens

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18
Q

Summarize the 3 stages of hemostasis

A

1º - formation of the platelet plug - damage to endothelium –> release of vWF –> platelet adhesion to exposed collagen –> platelet shape change and aggregate –> degranulate and release pro-coagulants
2º - coagulation cascade and generation of the insoluble fibrin to stabilize the plug
3º - enzyme breakdown of fibrin by plasmin - fibrinolysis

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19
Q

What are some tests utilized to evaluate platelets?

A

Automated platelet concentration counts with machine - can be inaccurate if blood clotted/clumps
Estimated platelet count from blood smear
Buccal mucosal bleeding time

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20
Q

What are some causes of thrombocytosis?

A
  • Physiological - epinephrine –> splenic contraction releasing more into circulation
  • Reaction - inflammation, hemorrhage, iron deficiency
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21
Q

What are some laboratory evaluations of coagulation?

A
  • Activated clotting time (ACT) - draw blood, incubate, see how long it takes a clot to form
  • Partial thromboplastin time (PTT) - test for intrinsic and common pathways of coagulation
    If Prolongation of PTT alone - defects of intrinsic pathway like Hemophilia A or B
  • Prothrombin time (PT) - test for extrinsic and common pathways of coagulation
    If prolongation of PT alone - consider early vitamin K deficiency, liver disease, early DIC, F7 deficiency
    IF BOTH PROLONGED - Vitamin K deficiency, DIC, liver failure
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22
Q

Which portion of the spleen is NOT fixed?

A

The tail end - it is relatively mobile

HEAD END fixed in the abdomen by the gastrosplenic ligament

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23
Q

What are common differential diagnoses for splenomegaly?

A

Localized: hematoma, abscess, hemangiosarcoma, lipoma, leiomyoma/sarcoma

Diffuse:
Splenic torsion/trauma, Splenic Hyperplasia, lymphoma, leukemia, Infection, IMTP

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24
Q

What virus is mostly associated with feline lymphoma?

A

FeLV
Once the virus integrates itself into the host genome - it can integrate into a proto-oncogene causing neoplastic transformation
Usually causes thymic/mediastinal lymphoma

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25
Q

What is the most common site of lymphoma in a cat?

A

GASTROINTESTINAL LYMPHOMA

*low grade GI lymphoma usually T cell

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26
Q

What is the most common type of lymphoma in a dog?

A

Multicentric lymphoma

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27
Q

What are the common diagnostic approaches to lymphomas?

A
  • FNA
  • Biopsy and hitopathology
  • US! Especially when it is suspected GI lymphoma
  • Endoscopic biopsies - when difficult to tell on US
  • ExLap
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28
Q

What is the best treatment protocol for feline lymphoma?

A

High grade - COP protocol - cyclophosphamide, oncovin (vincristine), prednisolone (COAP for renal/CNS lymphoma)
Low grade GI lymphoma - Chlorambucil and Prednisolone

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29
Q

What cells do myelomas form in?

A

PLASMA CELLS

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30
Q

What are we trying to differentiate between when looking at a lymph node cytology? And what are the differences?

A

Hyperplasia, inflammation, neoplasia, metastasis
NORMAL - will be dominated by small lymphocytes ~ 90%
Hyperplastic - Increased number of medium to large lymphocytes but LESS THAN 50%
Lymphadenitis - Increased inflammatory cells - neutrophils, macrophages, eosinophils
Lymphoid neoplasia - >50% immature medium to large lymphocytes/monotonous! - few small ones seen
Metastasis - foreign cells present
* when sampling submandibular LN - ensure you are not sampling the salivary glands

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31
Q

What is the main symptom seen with paraneoplastic syndrome and what are the clinical signs seen with this?

A

HYPERCALCEMIA

PD/PU, dehydration, depression, weakness, anorexia, vomiting, constipation, dysrhthymias, muscle tremor

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32
Q

What are the clinical stages for lymphoma? What are the substages?

A 
Stage 1-5
1- single LN enlarged (RARE)
2- multiple LNs in one area enlarged
3- generalized lymphadenomegaly 
4- stage 3 + spleen and liver involved
5 - stage 4 + BM involvement

Substage
a - WITHOUT clinical signs
b - WITH clinical signs

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33
Q

How would you differentiate between stage 3 and stage 4 lymphoma?

A

US to look at spleen and liver

FNA 2 organs to ensure involvement

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34
Q

What are the treatment protocols for B cell lymphoma vs. T cell lymphoma in dogs?

A
  • B cell - COP or CHOP - Cyclophosphamide, Oncovin (Vincristine), Prednisolone
    H = DOXORUBICIN (CHOP slightly better than COP)
  • T cell - LOPP - Lomustin, Oncovin (Vincristine), Procarbazine, Prednisolone
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35
Q

Are mediastinal lymphomas usually associated with T cells or B cells?

A

T CELLS BITCH!!!!! FOCUS!!!!

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36
Q

Once exposed to FeLV, what are the 3 primary outcome stages?

A
  1. Abortive - effective immune response (test negative) so have antibodies
  2. Regressive - ineffective immune response but will not shed virus and eventually become asymptomatic (test positive and then negative)- left with LATENT infection
  3. Progressive - ineffective immune response, continue to shed virus throughout life and have a decreased life expectancy (test positive)
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37
Q

What is the core protein as the basis for FeLV diagnostic tests?

A

Core protein p27!! (gag protein) antigen detection by ELISA

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38
Q

How is FeLV mainly transmitted?

A

Saliva, nasal secretions, feces, urine, milk (and blood transfusions)- usually spread via prolonged contact - shared food and water, mutual grooming

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39
Q

What is the main route of transmission for FIV?

A

Bite wounds - large amount of virus in the saliva/blood

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40
Q

What are the stages of FIV pathogenesis?

A

Acute (high amounts of replication- in T cells, B cells, macrophages) –> asymptomatic carrier –> general lymphadenopathy –> terminal (AIDS) - not many cats (~10%) get to terminal stage

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41
Q

What type of cells does FIP infect?

A

MACROPHAGES! Duh

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42
Q

What is the cause of feline infectious anemia?

A

Mycoplasma hemofelis - attach to RBCs leading to immune-mediated destruction

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43
Q

What is the main form of treatment for FIA?

A

Doxycycline
Flea control!
Blood transfusion if necessary
May need immunosuppressive therapy if know IMHA but waiting for mycoplasma results

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44
Q

What is the main diagnostic test for EIA?

A

Plasma lactate concentration and PvO2 levels
Testing PCV is useless
COGGINS TEST or ELISA

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45
Q

What is the best blood product to use with coagulopathies?

A

FRESH (frozen) PLASMA

high in all the clotting factors

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46
Q

What is cryoprecipitate mostly used for?

A

Patients with vWF disease as it is enriched with factor 8, vWF and fibrinogen

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47
Q

What are some common differentials for non-regenerative anemia?

A

Renal disease - decreased EPO
Endocrine disease - hypothyroid, hypoadrenocorticism
FeLV - depressed erythropoiesis, dysplastic production of RBCs
Non-regenerative BM
- Neoplasia crowding out
- Fibrosis

Iron deficiency anemia can become non-regenerative in long term

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48
Q

Bleeding patients: what is the clinical approach?

A

1) Trauma (hemorrhage) or impaired homeostasis?
- If platelets around 100 x 10^9/L then hemorrhage is more likely.
- If platelets < 25 x 10^9 then consider immune mediated thrombocytopenia
- If platelets within range but dog is bleeding -> consider vWD or platelet function defect
2) Impaired homeostasis due to platelet defect (thrombocytopenia or functional issue) or coagulation?
- Buccal mucosal bleeding time-> if increased then the dog has platelet deficiency. If normal -> coagulation defect
- Presence of petechiae/ecchymoses -> the dog has platelet defect
- Presence of internal bleeding/large hematoma -> coagulation defect more likely

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49
Q

Platelet numbers <10 x 10^9/ L, what are the differentials?

A

1) IMMUNE MEDIATED
- Primary
- Secondary to SLE, drugs, vaccines, neoplasia
2) DIC
- If PT and PTT are also prolonged

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50
Q

An otherwise well CKCS presents with thrombocytopenia on an automated CBC count, is that an issue?

A

Not really, they have giant platelets that get counted as erythrocytes. Look at smear to be sure
Also ALWAYS look at smear platelets in cats, sheep, goat

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51
Q

At what level of vWF antibodies (ELISA) is the dog likely to suffer clinical signs?
At what level is the dog likely to transmit the disease to offspring?

A
  • Clinical signs if <35% (0% in Type III)

- Transmission if <50%

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52
Q

What is Evans Syndrome

A

immune mediated anemia + thrombocytopenia

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53
Q

Infectious causes of thrombocytopenia

A

FeLV, Ehrlichia, Leishmania

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54
Q

A dog with type 1 vWF disease needs surgery, what can you administer to prevent excessive bleeding?

A

Desmopressin

55
Q

Bleeding patient, prolonged PT and PTT, jaundice, increased FDP: what are the main differentials and how do you distinguish them?

A

Both Vit K deficiency and Liver disease can cause these, need to look at other liver parameters.
ALSO Vit K is fat soluble vitamin, needs Bile to be absorbed. If Bile duct blocked-> Vit K deficiency.

56
Q

Bone marrow shuts down, in what order do cells decrease?

A

Neutrophils first, then platelets, then erythrocytes

57
Q

How to differentiate between Extravascular vs Intravascular Hemolysis

A

Extravascular -> macrophages bite into RBC in liver/spleen, if cell not destroyed will try to repair membrane so get spherocytes, icteric plasma
Intravascular -> Complement pokes holes in RBC, Hb leaks out and left with ghost cells, pink/red plasma

58
Q

Differentiate causes of hemolysis based on blood smear findings

A

Spherocytes + ghost cells -> IMHA or possibly infectious (Mycoplasma, babesia…)
Heinz bodies/ eccentrocytes -> oxidative damage
Schistocytes/keratocytes -> shear injury from vasculature (DIC, hemangiosarcoma, fibrin, severe hepatitis, vasculitis, heart worm, heat stroke)
Acanthocytes -> associated with splenic disease (ex. hemangiosarcoma)

59
Q

How does FeLV cause anemia?

A

it’s a myeloproliferative disease (bone marrow suppression from viral infection of hematopoietic stem cells) -> non-regenerative, see both normocytic and macrocytic RBC

60
Q

Where do you store a blood smear?

A

Room temp (NOT in the fridge)

61
Q

Is PCV or HCT more reliable?

A

PCV. HCT is an automated count

62
Q

Where are RBC produced?

A

Foetus -> Liver and Spleen
Neonate -> Bone marrow
Growing animal -> BM of all bones but spleen remains an important site of hemopoiesis in diseases that shut down the BM (myelofibrosis). In this case can see hyperplastic splenic nodules

63
Q

Normal PCV in dog and cat

A

Dog = 45%, cat= 35%

64
Q

Macrocytic RBC on smear with NO polychromatophils. Differentials?

A

FeLV, myelodysplasia or normal in some poodles

65
Q

Polychromatophil vs Reticulocyte

A

Retics -> new methylene blue stain
Polych -> Diff-Quick/Giemsa stain
They are the same shit

66
Q

Causes of erythrocytosis

A

Dehydration
Epinephrine release-> splenic contraction (temporary)
Response to low O2 (appropriate, secondary)
EPO secreting tumor (inappropriate, secondary)
Myeloproliferative disorder (primary)

67
Q

Toxins/drugs that can cause oxidative damage to RBC

A

onions, paracetamol (cats), propylene glycol, garlic, zinc, copper, red maple (horses)

68
Q

Major differential of anemia in farm animals

A

PARASITES!!!!
GIT parasites especially (haemonchus, strongyles, nematodirus)
Get really suspicious if they are only worming with one product (like ivermectin) and if they are overstocking.
Best way to diagnose -> PM. otherwise can do FEC

69
Q

Cocker or English Springer with acute hemolytic episode. What is one likely differential for these breeds?

A

Phosphofructokinase Deficiency

70
Q

Sites for BM sampling

A

Iliac crest or proximal humerus

71
Q

Why can anemia develop after starting insulin treatment in a DKA patient?

A

due to hypophosphatemia. P is transported inside cells with glucose, so there is none left for RBC synthesis (P is an important membrane component)

72
Q

How do you diagnose Failure of Passive Transfer in foals?

A 
SNAP ELISA:
< 4 g/L = transfer failure
>8g/L = successful transfer
In between = partial failure
Can give colostrum via nasogastric tube (1 or 2 L, 500mL at a time) or plasma transfer if the foal >12hrs old
73
Q

At what age are foals most susceptible to infectious diseases? Even when PT was successful

A

between 1 to 2 mo. in this period MDA are at their lowest and the foal is just starting to make its own
Foal will be fully immunocompetent @ about 5-10mo

74
Q

A foal < 3d old presents anemic, jaundiced, lethargic/collapsed. Most likely DDX? What do you do?

A

Neonatal isoerythrolysis

DO NOT GIVE MORE COLOSTRUM. Give fluids + RBC only (no plasma) from the mare

75
Q

What drugs can cause BM suppression in horses?

A

Phenylbutazone and chloramphenicol

76
Q

How do you see RBC regeneration in horses?

A

BM aspirate only. they have no retics! Also their RBC normally present Howell-Jolly bodies (which is a sign of responsive anemia in other species)

77
Q

What do you do if a foal starts having an immune reaction during plasma transfusion?

A

Stop -> give Flunixin -> wait 1-2h -> restart v slowly

78
Q

Is congenital immunodeficiency a thing in horses?

A

Yes, but only for Arabian foals. No functional T or B cells -> die around 5mo
Combinational immunodeficiency

79
Q

Why do horses take longer to recover from anemia?

A

Their BM is v slowly responsive and they rely on a huge splenic reserve of RBC

80
Q

Horse is suffering from acute hemorrhage: what do you use to quantify the severity?

A

Blood lactate concentration and PvO2. PCV in acute blood loss will be normal.

81
Q

Mare delivered a foal the day before, now presents colic, pale MM, tachycardia… Most likely DDx?

A

Uterine artery rupture. prognosis v poor, treatment aimed at stabilizing CVS

82
Q

Good colostrum protocol

A

Collect colostrum from a healthy dam (no Johnes, no mastitis…)
Test the colostrum (SG> 1.048, thick)
Store the colostrum (can stay 7d in the fridge)

83
Q

Reasons for cow’s poor quality colostrum

A 
Not collected during her first milking, 
short dry period, 
abortion/premature calf, 
the dam is a heifer, 
dairy cows have shittier colostrum in general
mastitis
84
Q

List possible transfusion adverse reactions

A
  • FNHTR (Febrile non-hemolytic transfusion reaction) -> pyrexia, no hemolysis
  • volume overload
  • anaphylactic shock/allergic rxn
  • sepsis
  • disease transmission
  • acute hemolytic crisis
85
Q

Difference between shock and dehydration

A

Shock -> loss of intravascular volume
Dehydration -> fluid loss from the other spaces (interstitial and intracellular)
Correcting shock is quick (fluid bolus), but it takes longer to correct dehydration

86
Q

List cells in the Neutrophil Prolipherative Pool

A

Myeloblast, granulocyte, myelocyte

87
Q

List 3 pools of mature neutrophils

A 
Storage pool (sits in BM), 
Circulating pool (what you measure on bloods), Marginated pool (what you see on cytology. Cats have 3x more marginated than circulating)
88
Q

Describe a toxic neutrophil

A

Toxic neutrophil=left shift neutrophil IN CIRCULATION (Degenerate when in tissue -> cytology)

  • foamy cytoplasm
  • basophilia of cytoplasm (looks blue)
  • C shaped nucleus
  • larger size
  • toxic granules
  • Dohle bodies
89
Q

Degenerative vs Regenerative Neutrophil Left Shift

A 
Degenerative= neuropenia, bands> segmented = BM not keeping up with demand
Regenerative = neutrophilia, segmented> bands = BM's got this shit
90
Q

Possible causes of neutropenia

A 
- INCREASED DEMAND
endotoxin
inflammatory response (infectious or immune med)
- REDISTRIBUTION
higher number of marginated neutrophils (anaphylaxis, endotoxicity)
- DECREASED PRODUCTION
Infectious agents targeting BM (FeLV, parvo, Ehlrichia)
Chemotherapy
Crowding out of BM (lymphoma)
Myelofibrosis
- INEFFECTIVE PRODUCTION 
myelodysplasia
- CONGENITAL ABNORMALITIES
91
Q

what dog breeds commonly present neutropenic?

A

Greyhounds and Lurchers

92
Q

Possible causes of Neutrophilia

A 
- INCREASED DEMAND 
Infectious agents
Immune mediated disorders
Inflammation
- NO DEMAND, INCREASED PRODUCTION
Chronic leukemia -> well differentiated neutrophils
Acute leukemia -> poorly differentiated (prognosis v poor)
- INCREASED PERSISTENCE IN CIRCULATION
Steroid effect (see inflamm leukogram)
- REDISTRIBUTION
stress/excitement -> wipes out marginated neutrophils into circulation 
prevented from exiting circulation
93
Q

Causes of Lymphopenia

A 
- INCREASED DEMAND
Chyle loss (enteropathy or chylothorax)
Antigenic stimulation
- REDISTRIBUTION
Steroids (kicks them back into BM or tissue)
- DECREASED PRODUCTION
Destroyed by infection (distemper, FeLV, panleukopenia virus, parvo, FIV)
Chemo drugs 
Congenital (Bassett Hounds)
94
Q

Causes of Lymphocytosis

A 
- INCREASED DEMAND 
Persistent antigenic stimulation (Leishmania)
- NO DEMAND, STILL INCREASED
Chronic leukemia
Acute leukemia 
Stage V lymphoma (a lot more common than leukemia)
- REDISTRIBUTION
Hypoadrenocorticism
95
Q

What interleukin stimulates Eosinophil release?

A

IL-5

This is why you can have eosinophilia in lymphoma and MCT (paraneoplastic)

96
Q

What do you expect to see in a puppy CBC?

A

lower HCT, higher WBC

97
Q

Adrenaline response on CBC

A

neutrophilia

lymphocytosis

98
Q

Leukogram of chronic inflammatory disease

A

Neutrophilia (L shift or not)
Lymphocytosis
Monocytosis

99
Q

Difference between stress leukogram and acute inflammatory leukogram

A

Stress leuko -> only see neutrophilia WITHOUT left shift. Also the neutrophilia is only mild/moderate
Both have lymphopenia, monocytosis and eosinopenia

100
Q

FeLV tests and FIV test: which one tests for antigen and which one for antibody?

A 
FIV= antibody (cannot test kittens before 6mo due to MDA)
FeLV= antigen (can test anytime)
101
Q

What are some common complications of splenic surgery?

A

Increased DIC risk
Increased arrhythmia risk
Hemorrhage (have you seen how many mf vessels there are??)
Infection
Compromised blood supply of stomach and pancreas (dumb bitch ligated the wrong vessel)

102
Q

What is the median survival for splenectomy + chemo in HS patients? What chemo protocol do you use

A
  • 6mo MS

- Doxorubicin protocol

103
Q

Common sequelae of Multiple Myeloma

A
  • Blood hyperviscosity (due to high globulins)
  • Bone lysis
  • Bence Jones proteins deposited in the nephron -> glomerular filtration compromised
  • Cytopenias
104
Q

Difference between lymphoma vs leukemia?

A
  • lymphoma originates from lymphoreticular cells in spleen, LN, or lymphoid tissue anywhere (liver, bone marrow, etc.)
  • leukemia originates from hematopoietic precursor cells in bone marrow/spleen (lmyphoid or myeloid)
105
Q

Would you rather get Acute Leukemia or Stage V Lymphoma?

A

STAGE V LYMPHOMA DUH!!!

  • ALL patients often way sicker
  • ALL cytopenias are more marked
  • Acute leukemias don’t respond well to chemo due to severe cytopenias at onset (Especially Acute Myeloid Leukemia, if you get that you’re actually fucked)
106
Q

How does FeLV affect the bone marrow?

A
  • High risk of developing lymphoma
  • myelodysplasia (BM crowded up by neoplastic cells)
  • bone marrow suppression (infects hemopoietic cell precursors)
107
Q

What FeLV protein is the target for vaccination?

A

gp70

108
Q

What T cell ratio is abnormal with FIV?

A

CD4+ : CD8+

FIV destroys CD4+, which usually are more abundant

109
Q

Common clinical signs in FIV patients generally seen once reach final stage of infection

A
  • gingivostomatitis (recommended to extract all molars and premolars if very painful)
  • anemia/cytopenias
  • opportunistic infections (mycoplasma, toxoplasma, herpes..)
  • neoplasia (lymphoma)
  • ocular signs (uveitis, chorioretinitis)
  • CKD
110
Q

Outcomes of FCoV infection

A

60-70% -> clear infection
10-15% -> chronic shedders and infected
5%-> develop FIP (FCoV develops mutation of S spike protein to invade macrophages)

111
Q

What kind of immune response leads to the different kinds of FIP?

A
  • partial response = DRY (some cell mediated response present, cytokine overproduction–>neutrophils–>granulomas)
  • poor response = WET (only antibody production–>immune complexes, no cell mediated response)
112
Q

Classical clinical signs + labs of wet FIP

A
  • pyrexia/general unwellness
  • diarrhea
  • dehydration
  • jaundice (with hyperbilirubinemia but normal liver parameters)
  • effusions (pleural and abdominal)
  • uveitis/chorioretinitis
  • mild NR anemia, may have neutrophilia/lymphopenia
  • hyperglobulinemia (polyclonal increase in gamma globulins) *Alb:Glob ratio usually low <0.8
113
Q

Characteristics of wet FIP effusion tap

A
  • high protein >35
  • low cellularity
  • straw color
114
Q

Confirmatory tests for wet and dry FIP

A
  • Rivalta test for wet

- Immunohistochemistry of several tissue samples for dry (you look for FCoV presence within macrophages)

115
Q

How long does FIP persist in the environment

A

7 w

116
Q

Does Mycoplasma hemofelis tx achieve cure?

A

Nooope

Can recover from acute infection but the parasites can become latent and can flare up in times of stress

117
Q

What kind of damage does Mycoplasma hemofelis cause?

A

IMHA with extravascular hemolysis (in the spleen, which will look enlarged)

118
Q

Mycoplasma hemofelis treatment

A

Doxicycline and pred

Must remember to keep on flea control (flea is a vector for transmission)

119
Q

What can happen to the spleen during GDV?

A

short gastric arteries can get ripped away and head of spleen can become necrotic

120
Q

Why does the risk of blood-borne infection go up with splenectomy?

A

White pulp of spleen crucial for producing antibody response to antigens presented in blood

121
Q

What causes polyclonal gammopathy?

A

infectious diseases (Leishmania, Ehrlichia), chronic inflammatory conditions, or immune-mediated conditions

122
Q

What causes monoclonal gammopathy?

A

Neoplastic disease (ex. myeloma or B-cell lymphoma)

123
Q

How does Leishmania cause proteinuria?

A

Glomerulonephritis

124
Q

Grades of lymphomas cats vs. dogs:

A

Dogs usually intermediate or high

Cats can be low or high

125
Q

What would you expect to see on the leukogram of a patient with Addison’s?

A

Opposite of stress leukogram!
Neutrophils and monocytes WNL
Lymphocytosis
Eosinophilia

126
Q

If a cat is infected with FeLV younger than 2 months old, they will always develop which type of infection?

A

Progressive!!!!!!!

127
Q

What are the clinical signs of a progressive FeLV infection?

A

Immunosuppression
Neoplasia (lymphoma obviously)
Bone marrow disorders (it’s a leukemia virus)

128
Q

Someone brings in a tom cat who has been in a fight a week ago with another cat and you test him for FIV but the result is negative. What do you recommend to the owner?

A

Could truly be negative but probably safest to re-test in 60 days because could be infected but has not yet seroconverted

129
Q

Why are automatic platelet counts not accurate for cats, goats, and sheep?

A

Overlap between RBC size and platelet size (mistakes RBC for platelets)
Platelet clumping also very common in cats

130
Q

When would you need to use PCR to test for FeLV?

A

Suspicious of cat presenting with bone marrow disorders but testing negative on antigen test. This looks for FeLV provirus or RNA in bone marrow- detects latent (regressive) infection and can be confirmatory test in progressive infection

131
Q

A cat with known exposure to FeLV tests negative. What do you recommend to the owner?

A

If recent exposure, safest to re-test in 30 days

132
Q

When might you test an adult cat for FeLV?

A

struggling to treat an infection or they keep recurring

133
Q

Mild anemia is common in animals with which kinds of disorders?

A

Endocrine, also longstanding disease

4th Year Exams (8 decks)

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