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VetMed Year 4- Term 1 > 1-Jul-14 > Flashcards

1-Jul-14 Flashcards

1
Q

Where do platelets come from?

A

Myeloid stem cells - CFU-Meg -> Platelet. Also erythrocyte, neutrophil and monocyte come from myeloid

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2
Q

When spun down which part of the PCV tube contains the leukocytes

A

Buffy coat

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3
Q

Why does stress cause a leukophillia?

A

Leucocytes washed off wall of BV

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4
Q

How to distinguish a plasma cell?

A

Eccentric nucleus. Abundant cytoplasm.

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5
Q

Normal ratio of circulating pool to marginated neutrophil pool?

A

Normally 1: 1 but in cats can be 1: 3 i.e. 3 x as many marginated cells as circulating

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6
Q

Half life of neutrophil

A

5 to 10 hours (very short)

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7
Q

What is a degenerative left shift?

A

Left shift= more immature neutrophils (i.e. more bands than segmented). Degenerate: Already left blood, fighting with bacteria therefore neutropenia and bands > segmented

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8
Q

what would a regenerative left shift be?

A

Left shift: but neutrophillia i.e. immune system is keeping up

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9
Q

What type of left shift is normal in cows/horses

A

Cows/Horses tend to start infections with neutropenia and bands > segmented therefore DEG LEFT SHIFT but this is because they don’t have a storage pool. Give antibio until regen

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10
Q

Why is a degen left shift more serious in dogs?

A

In dogs a degen left shift implies the immune system is behind as the storage pool has been used up and bands > segmented with a neutropenia. Give ANTIBIO

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11
Q

Right shift

A

Hypersegmentation

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12
Q

How to differentiate toxic change from degen left shift

A

Toxic change is ‘faulty’ neutrophils caused by accelerated production NO NEED FOR TOXINS

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13
Q

What species are neutrophils NORMALLY low?

A

Greyhounds NORMAL leukocyte levels are much lower i.e. 2 x 109 instead of 3 x 109

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14
Q

When neutrophils are below what amount are prophalactic antibiotics indicated?

A

<2x 10 e9/ L

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15
Q

How does the degree of differentiation help determine cause of neutrophillia?

A

Well differentiated–>look for underlying infec Poorly differentiated–> myeloid leukememai

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16
Q

Why does steroid induced neutrophillia have more highly segmented neutrophils?

A

Longer in circulation therefore more segmented

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17
Q

Normal nucleus of lymphocyte should be same size as …

A

Normal nucleus of lymphocyte should be same size of RBC.

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18
Q

How does longevitiy differ between t cells and b cells

A

can’t differentiate on microscopy but t cells long lived and b cells mostly short lived.

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19
Q

Endothelial cells are pro or anticoagulant?

A

Flattened endothelial cells are both pro and anti coagulant. Normally anticoagulant and inhibit platelet aggregation. Barrier to prevent subendothelial collagen (which is procoagu)

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20
Q

Where are Von Willebrand factors produced? Circulates bound to factor ____

A

Endotelial and formed in Weibel Palade. Also produced by platelets and MEGAKAROCYTES. Responsible for platelet adhesion to collagen. Circulates bound to factor 8

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21
Q

How long do platelets circulate for

A

5-9 days in most species.

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22
Q

Platelets are derived from cytoplasm of

A

Megakarocytes from bone marrow mediated by thrombopoeitin. Pale basophilic`

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23
Q

Why do we look at platelet and neutrophil numbers before erythrocytes whn suspecting bone marrow problem

A

Platelets produced from megakaryocytes in bone marrow. Circulate for 5-9 days c.f,. neutrophil half life 5-10 hours. RBC = 60-100 days therefore longer to notice change.

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24
Q

Platelet has what two receptos

A

1 for Von Willebrand factor 1 for Fibrinogen Both can have deficiencies

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25
Q

Primary haemostasis steps

A
  1. Damage to endothelium causes exposure of subendothelial collage 2. Von Willebrands factor is released from damaged endotelim 3. Platelet adhesion occurs 4. Platelets bind to collagen via 2 receptors
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26
Q

When referring to coagulation we are referring to ____

A

Secondary haemostasis Involving Tissue Factor and final step is Fibrinogen–>Fibrin

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27
Q

Extrinsic factor involves

A

Factor VII and Tissue Factor = Factor 10

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28
Q

Factor___ converts prothrombin to thrombin

A

Factor 5 converts prothrombin to thrombin which allows fibrinogen to be converted to fibrin.

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29
Q

Fibrinolysis is enzymatic breakdown of fibrin by ___

A

Plasmin which is derived from plasminogen in the plasma membrane of platelets.

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30
Q

Platelet count can be done on blood collected into EDTA tube. Which species is this unreliable?

A

Cats, sheep and goat and overlap between rbc/platelets. Cats= platelet clumping also very common. Do manual count

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31
Q

Which breed of dog should manuel platelet counts be done in?

A

Cavalier King Charles. INHERITED DISODER = LARGER PLATELETS therefore counted as rbc’s Appear thrombocytopenic as don’t need as many as larger.

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32
Q

< what reference interval = thrombocytopenia

A

t normally cause a decrease past this

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33
Q

Worry about spontaneous bleeding when platelet conc is <

A

< ~25 x 10 9/L

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34
Q

Buccal mucosal bleeding time =

A

Measures length of time for platelet plug to form, Evaluates primary haemostasis / platelet function. Blot blood until stops

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35
Q

What will happen to buccal mucosal time for coagulopathies

A

Coagulopathies = secondary haemostasis = fibrinogen therefore will not affect buccal mucosal time (only tests primary haemostasis/ primary function test)

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36
Q

Does the buccal mucosal test for thrombocytopenia

A

Does require some platelets but more a platelet FUNCTION test

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37
Q

Mechanisms of thrombocytopenia

A

Increased platelet destruction: IM (most common), Haemorrhage , DIC, Sequestrum (e.g. spleen) OR DECREASED PRODUCTION/ INFECTIOUS

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38
Q

Evans Syndrome

A

Concurrent immune mediated thrombocytioenia and anaemia. Thrombocyt= bleeding and have deficient blood cells as well!

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39
Q

During haemorage, numbers of platelet should not drop below

A

Should not be below 100 x 10 9 Difficult to distinguish between bleeding causing thrombocytopenia or thrombocytopenia causing bleeding

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40
Q

If platelet count is >100 x 10 9 but still low then likely cause is

A

If >100 x 10 9 platelets then bleeding/haemorrhage is likely causing the thrombocytopenia. If <100 x 10 9 then likely something else e.g,. DIC, Immune-mediated

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41
Q

4 infectious organisms that cause thrombocytopenia

A
  1. FeLV 2. BVD 3. Ehrilichia 4. Leismania 5. Babesia
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42
Q

Which breed of cows are predisposed to thrombocytopenia

A

Simmetals predisposed to bleeding

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43
Q

Causes of thrombocytosis

A

Physiological: epinephrine induced splenic contraction Reactive (most common) due to increased thrombopoeitin or IL6 (inflamm, haemorrhage, iron deficiency)

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44
Q

Why does Iron Deficiency cause thrombocytosis

A

Anaemia for a week duration = thrombocytosis. Due to cross link when getting more rbc’s from bone marrow also increases platelets.

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45
Q

Essential thrombocythermia

A

Myeloproliferative disorder - bone marrow problem / neoplasia

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46
Q

Von Willebrand factor exists in what 3 forms

A

Small, medium and large form. Where large form is the most efficient. Circulates bound to factor 8.

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47
Q

Von Willebrand disease clinical signs

A

mucosal bleeding, GI epistaxis, haematuria. Bleeding may be absent NO PETICHAIE Prolonged mucosal bleeding time without thrombocytopenia

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48
Q

Type 1 Von Willebrand disease

A

Most common (90% of cases) All 3 multimers present (small, medium, large) but in decreased concentration Seen in Dobermans Autosomal inhertiance so male/female affected equally

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49
Q

Type II Von Willebrand disease

A

Large multimers disproportionally decreased . Severe and uncommon. German shorthaired pointers. Autosomall

50
Q

Type III Von Willebrand disease

A

Absence of all multimers. Die quickly Seen as puppy dogs

51
Q

Tests for Von Willbrand disease collected into what tubes?

A

Collect blood into citrate or EDTA tube. If collected into citrate tube needs to be dilated 1:9 with blood. Seperate plasma immediately and ship with ice,

52
Q

How will a) clotting and b) lipemia affect the Von Willebrand factor test

A

Citrate 1:9 ratio., Clot will decrease number of factors= false positive Lipaemia doesn;t affect.

53
Q

50-70% vWF:Ag =

A

Carrier status likely to transmit to offspring. 70% = normal

54
Q

Doberman in for elective ovariohysterctomy. Suspect vWd what preventative treatment can be given for type 1 vWd

A

Type 1: small, med, large multimers present in lower conc. Desmopressin can increase release of vWF from endothelial cells and be a prophalaysis during surgery. Intranasal prep

55
Q

Important when testing blood for vWF

A

Minimise trauma when extracting due to activating platelets etc. 1:9 ratio citrate to blood. Centrifuge and remove plasma within 1 hour freeze if to be transported Analyse within 4 hours or freeze plasma

56
Q

How to measure activated clotting time (ACT)

A

Tests intrinsic and common pathway 2ml whole blood into ACT tube containing diatomaceous earth. Incubate for 60 seconds at 37 degrees. Time to initial clot formation is ACT time. Will be prolonged by thrombocytopenia Less sensitive than PTT

57
Q

Partial thromboplastin time (PTT) tests for…

A

Intrinsic and Common pathway of coagulation Incubate citrated plasma with excess phospholipid / contact activator and Calcium DON’T NEED PLATELETS LIKE YOU DO FOR ACT Measure time for formation of a clot

58
Q

Difference between activated clotting time and partial thromboplastin time

A

ACT = less specific than PTT but ACT can be done NEXT TO PATIENT. PTT= Lab test and everything is provided in excess ACT relies of platelets and will be prolonged by thrombocytopenia.

59
Q

Long PTT indicates

A

Problem in factors or intrinsic (XII, XI, IX, VIII) or common pathway (X,V, II) Requires a <30 % in a factor for a prolonged PTT. Not affected by thrombocytopenia (as providing the factors)

60
Q

Test for EXTRINSIC and common pathway

A

Prothrombin time Incubate citrated plasma with tissue thromboplastin (=tissue factor) and citrate. Measure time for clot formation

61
Q

Why will liver failure cause prolonged Prothrombin time

A

Liver produces clotting factors. Vit K deficinecy and factor VII deficiency will also cause increased prothrombin time Prothrombin time tests extrinsic and common pathway. Test citrted plasma with tissue thromboplastin (tissue factor) and citrate.

62
Q

How to remember ACT, PTT,PT

A
63
Q

A prolonged PTT but a normal PT would be indicitive of a problem where?

A

SEE TRIANGLE TO WORK OUT

Intrinsic pathway fault

64
Q

Prolonged PT but normal PTT would be indicitive of problem where

A

Extrinsic pathway problem

65
Q

Abnormal PTT and PT would indicate a problem where?

A

Common pathway

or Problem is intrinsic AND extrinsic pathway

OR Vit

66
Q

FDP test is…

Use ____

A

Fibrin degration products. Use Serum

Latex agglutination test.

Useful test for DIC

67
Q

Most common cause of vitamin K deficiency in a) dogs b) cattle

A

a) dogs: rodenticide toxicity
b) cattle: sweet clover ingestion

Vit K factors: 2, 7, 9, 10

all produced in liver

68
Q

Which are the vit K dependent factors

A

II, VII, IX, X

69
Q

Which vit K dependent factor has the shortest half life

A

Factor VII therefore rodenticide/ sweet clover poisoning will notice this decrease first.

As factor VII has the shortest half life, if caught early enough PT time will be increased first

AS FACTOR VII IS EXTRINSIC AND COMMON

then PTT as 2,7,9,10 influence all three pathways

70
Q

Affect on platelet numbers and buccal muscosal bleeding time post rodenticide posioning

A

Rodenticide posioning = vit K deficiency therefore normal buccal mucosal time and platelet numbers (may have thrombocytopenia secondary to haemorrhage but unlikely to influence BMBT)

71
Q

DIC haemostatic abnormalities

A

May be acute or chronic.

Cannot have DIC without thrombocytopenia

Prolonged PT/PTT

Elevated FDP’s

Decreased fibrinogen (as using it up)

Decreased antithrombin III
Want 3 or 4 of these for diag of DIC

72
Q

Treatment of DIC

A

Stop coagulation

Heparin

Transfusion of whole blood/plasma

73
Q

Difference between Echymosis and Petichiae

A

Echymosis >1cm

Petichia <1-2mm

Platelet defect likely i.e. platelet function

GOOD TEST FOR PLATELET FUNCTION = BUCCAL MUCOSAL BLEEDING TIME

74
Q

Function of the FelV retrovirus

A

ssRNA to dsRNA integration into host DNA.

  1. destruction by immune response
  2. infection with virus protection
  3. transformation to neoplasia (LYMPHOMA!)
75
Q

Core FeLV protein that is the basis for most diagnostic tests is

A

p27 - gag protein

May circulate in plasma or excreted in tears/saliva

Snap testing/ ELISA.

Anti p27 not effective as masked in capsid

76
Q

Envelope protein of FeLV

A

P15E- Spike - immunosuppression

gp70 (knob) defines subgroup- A,B,C,

A= Only one cat to cat

B= endogenous

C= mutant form of A

Ab subgroup specific- important for vaccination!

77
Q

Important of FeLV subgroup (how is it determined)

A

gp70 (knob) defines subgroup- A,B,C,

A= Only one cat to cat

B= endogenous

C= mutant form of A

Ab subgroup specific- important for vaccination!

78
Q

Epidemiology of FeLV in UK Cats

A

1-2% in ‘healthy’ cats

20% in symptomatic cats

79
Q

Pathogenesis of FeLV

A

Either effective immune response (p27 negative) can still lead to latent form which leads to latent virus in bone marrow, lymphoid tissue = malignancy

OR INEFFECTIVE IMMUNE RESPONSE = persistant viraemia

80
Q

Define the terms ABORTIVE, REGRESSIVE and PROGRESSIVE with regard to FeLV infection

A

ABORTIVE: Effective immune response- virus cleared and p27 negative

REGRESSIVE: Transient viraemia –> Latent viraemia (bone marrow, lymphoid tissue) non replicating

PROGRESSIVE: Replication in marrow/lymphoid, p27 positive- PROGRESSES to persistant viraemia

81
Q

Survival of FeLV outside body

A

Prodominantly saliva and nasal secretions

Also in milk, faeces and urine.

ONLY SURVIVES FEW HOURS OUTSIDE BODY due to ENVELOPE

sharing food bowls, mutual grooming

IN UTERO SPREAD

82
Q

Clinical signs of FeLV

A

iNAPPETANCE, WEIGHT LOSS/WASTING, Poor coat condition, Lymphadenopathy, persistant fever,

pale mucos membranes, occular disease (FUNDIC EXAMS IMPORTANT= UVEITIS), gingivitis, stomatitis, abortion in queens, infections of skin

83
Q

Pathogenesis of FeLV secondary infections

A

FeLV is IMMUNOSUPPRESSIVE.

bone marrow suppression, viral infection of haemopoeitic stem cells, anaemia- non regenerative, aplstic or regrenerative, thrombocytopenia

84
Q

Why is anaemia common in FelV

A

bone marrow suppression, viral infection of haemopoeitic stem cells, anaemia- non regenerative, aplstic or regrenerative, thrombocytopenia

85
Q

What type of neoplasm are FeLV (p27+VE) cats more likely to develop

A

LYMPHOMA (most often thymic and multicentric)

Expect it within 2 years

86
Q

Tests for FeLV

A

Snap test ELISA for p27 protein is screening test for FeLV then qPCR for confirmation

87
Q

A negative test snap test result indicates

(6 things)

A
  1. unexposed
  2. elimination of previous infeciton
  3. early infection (re test 9-12 weeks)
  4. latent infection
  5. localised infection
  6. false negative
88
Q
A
89
Q

Treatment of FeLV

A

Prevent secondary infections

Neuter if entire

Confine indoors?!

IF sick, treat secondary illness

90
Q

Policy of FeLV vaccination

A

Test before vaccinate. If already p27 positive no point vaccinating.

If indoors cat little point

91
Q

Prevalence of FIV in UK

A

Also retrovirus

Normal UK 3-5% (more than FeLV)

Sick 18%

MAINLY TRANSMITTED BY BITING

92
Q

Difference in transmission of FeLV and FIV

A

FeLV: Mutual grooming

FIV: Aggressive (needs to be innoculated- saliva)

Some vertical transmission likely

93
Q

5 phases of FIV

A
  1. Acute- transient mild illness days to weeks
  2. Asymptomatic carrier: can last up to 10 years.
  3. persistant lymphadenopathy: can persist for months

Mononuclear cells- neutropenia/lymphopenia

terminal phase

94
Q

Which has a higher risk of lymphoma FIV or FeLV

A

FIV: 5 times more likely for LYMHOMA and SCC

FeLV: 60 times more likely (thymic/mediastinal)

95
Q

Antibody test for FIV

A

P24 (c.f. FeLV = p27 gag protein!)

Interference with vaccination/ MDA

Most cats develop antibodies within 60 days

96
Q

Test kittens from __ months of age onwards for antibodies for FIV

A

6 months.

Takes time to sero convert.

Cat takes 60 days to develop antibodies against p24 protein.

MDA can interfere with test.

IFA now recommended test

97
Q

FIP causative agent

A

feline coronavirus infection is common, clinical disease is uncommon

FIP is a fatal disease of domestic and non-domestic cats

98
Q

Feline coronavirus survival in environment

A

short lived (24 hr at room temp) but can survive 7 weeks if protected from heat, light and chemicals.

Replicate in cytoplasm

Occurs envelope from ER or Golgi

99
Q

Majority of oro-nasal Feline Coronarvirus infection results in

A

Presence in normal cats

70% transient infection.

10% Persistant infection

5% FIP

100
Q

FIP pathogenesis

A

Feline infectious peritonitis. Mutation of feline coronavirus,

Immune complex disease

  • vasculitis, complement activation, excessive cytokine production

Endothelial cell retraction, increased vascular permeability (protein rich exudate)

101
Q

How does the type of cell-mediated immune response influence the outcome of infection with feline cornoavirus

A

Strong response: protection

Partial response: Non-effusive disease (granulomatous disease- dry form)

Poor response: Effusive disease (wet form- protein rich exudate)

102
Q

75% of FIP cases are the ____form characterised by __

A

75% FIP are effusive form characterised by protein rich exudate causing ascites, pleural effusion (= dyspnoea), and more rarely pericardial effusion.

103
Q

Predelection sites for non-effusive FIP?

A

Eye (may present with uvevitis, brain/cns, kidney, liver and localised region of intestine)

104
Q

What is the use of IFA and ELISA tests for cats infected with FCoV or FIPV

A

Positive titre indicates prior exposure to FCoV not necessarily presence of FIP. High titre may indicate granulomatous form

105
Q

Vaccination for FIP

A

Intranasal

Wants strong cell-mediated immune response without strong antibody response

=Primusil

106
Q

Only way to clinically diagnosis FIP

A

Histopath only way to diagnose FIP.

Non-effusive harder to diagnose

Other IFA/ elisa only tells you infection with feline coronavirus

107
Q

Feline infectious anaemia treatment

A

Doxycycline i.e. a tetracycline susceptible. (NO CELL WALL)

Mycoplasma haemofelis = LARGE FORM, Candidatus Maycokplasma haemomuntum= SMALL FORM, Candidatus Mycoplasma turicensis.

ECTOPARASITE CONTROL!!

108
Q

Pathogenesis of reoccurance of Mycoplasma

A

Mycoplasma caused IM haemolytic anaemia. Concurrent disease due to immunosuppresion; if recover from infection = chronic infection for long period of time

Reactivation and Recurrance possible.

109
Q

Mycoplasma haemofelis is gram ___

A

Gram negative

Routes of transmission: Fleas, blood transfusion, female cats to neonates (in utero, nursing), fighting,

More common in young entire males, often latent hidden in spleen

110
Q

Relavance of FeLV in pathogenesis of Mycoplasma

A

Disease more common in young male cats, concurrent illness (i.e. FeLV = acute disease, recovered cat may relapse with stress.

111
Q

Changes in PCV for Mycoplasma

A

Rapid decrease in PCV as organisms in blood go to spleen.

PCV rises again as organisms disappear.

Some cats PCV continues to fall due to RBC destruction.

112
Q

Test for Mycoplasma hemifelis

A

Positive Coombes test. Extravascular haemolysis by MACROPHAGES in liver, spleen, lungs and bone marrow.

113
Q

Clinical signs of M. haemofelis.

A

ACUTE: lethargy, inappetence/anorexia, fever (39degrees-41), anaemia, splenomegaly and icterus (pre-hepatic)

CHRONIC: Normal or sub norm temp. icterus/splenomegaly less likely.

114
Q

Type of anaemia for Mycoplasma haemofelis

A

regenerative anaemia, reticulocytosis.

Polychromasia

If v. acute may be pre regenerative (takes 2-3 days)

115
Q

What is important to remember when giving Doxacycline

A

Doxacline is a tetracycline used for the treatment of Mycoplasma haemofelis (no cell wall)

It can cause gastric effects (muscosal irritation), abdo discomfort, vomiting, inappertence and oesophagitis and potential stricture formation THEREFORE MUST BE GIVEN WITH FOOD OR WATER

same for clindamycin (for cats)

116
Q

Cats with type b blood will die if given

A

cats with type B blood will die if given blood transfusion with type A blood.

Cats with type A given Type B won’t die but will have tranfusion reaction. NOT EVEN ONCE!!!

Dogs can normally be given tranfusion once without problem.

117
Q

Why might prednisalone be given to treat mycoplasma haemofelis

A

Along with doxacycline, immunosuppressive therapy (prednisalone) may inhibit erythrophagnocytosis (IMMUNE MEDIATED anaemia!)

118
Q

With liver disease would expect an increase in ____ test first because…

A

With liver disease would see prolonged PT test first (same as rodenticide poisoning)

Factor 2,7,9 and 10 all activated by liver therefore affects common, instrinsic and extrinsic pathways.

Factor VII = shortest half life therefore PT first affected.

119
Q

Mechanism by which Factors 2,7,9 and 10 are vit K dependent

A

Factors 2,7,9 and 10 are produced by liver.

Need to be activated by vit K depedent carboxylase which requires decreased VitK (via Vit K reductase)

This vit K reductase is inhibited by Coumarin like rodenticides

120
Q

In event of rodenticide poisoning, Vit K needs to be supplemented. How is this given

A

NOT IV= ANAPHALAXIS

NOT IM= HAEMATOMA

GIVE ORALLY OR PARENTERALLY

121
Q

Test for Fibrolysis

A

Latex aggluination test

Measure Fibrin Degration Products.

TESTS ON SERUM (c.f. PT, PTT, ACT= citrated plasma)

DIC = +++ FDPs but also with liver disease

Jugular vein thrombosis, liver disease, haemorrhage

122
Q
A

VetMed Year 4- Term 1 (12 decks)

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