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DWT > DWT Exam 1 > Flashcards

DWT Exam 1 Flashcards

1
Q

Reticulocytes in cat

A

Aggregate and punctate

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2
Q

Increased nucleated RBCs is called

A

Metarubricytosis

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3
Q

Normal regenerative Reticulocytes numbers <dog></dog>

A

Dog >800000
Cat >600000
Horse none

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4
Q

Appropriate metarubricytosis

A

Is when there is also Reticulocytosis regeneration so bone marrow releases both

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5
Q

Inappropriate metarubricytosis -bone marrow and spleen

A

Bone marrow cant hold nRBC and usually nRBCs removed by the spleen

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6
Q

Mean corpuscular volume

A

The size change in of the cell - micro or macrocytosis

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7
Q

What do you use to determine anemia

A

Hct or PCV

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8
Q

What increases bilirubin in circulation/ blood?

A

Hemolysis
Fasting hyperbilirubinemia
Functional Cholestasis
Obstruction Cholestatis

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9
Q

Enzootic or endemic

A

Continuous transmission -disease presence in location multiple times
En=on going

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10
Q

Epizoonotic

A

Peaks in baseline (endemic damage); high damage here

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11
Q

World wide epidemic

A

Pandemic

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12
Q

Isatrogenic and Nosocomical infections are similar because

A

They happen under care of veterinarians

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13
Q

Recrudescence defined

A

Is when the latent virus flares up with stress

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14
Q

Vertical transmission

A

Virus embedded in genome and passed through the germ line- this happens with retrovirus which wont shed

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15
Q

Susceptible vs permissive

A

Susceptible = able to be infected
Permissive = able to create viral progeny

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16
Q

What determines the host range for a pathogen?

A

The glycoproteins on the host

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17
Q

The process of viral infection :

A

1 attachment is no energy
2 penetration
3 uncoated to release genome into cytoplasm
4 mRNA translation
5 dna/rna replication
6 Maturation and assembly [intracellular, at PM, or at nuclear membrane]

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18
Q

Disease is in __
Cytopathic Effect is in ___
Define CPE

A

Disease in Vivo
CPE in vitro (synctia, inclusion bodies [think nuclear inclusion bodies in herpes], lysis, rounding

CPE is the morphological changes that happen to virus infected cell

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19
Q

There are 3 mechanisms by which virus spread to organs (systemic spread)
Name the most efficient

A

Viremia (hematogenous spread ) most efficient
Lymphatic spread
Neural spread- cns

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20
Q

Saprophyte

A

Lives on decaying organic matter and can sometimes cause disease (parasite but not usually a pathogen)

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21
Q

Parasite

A

A general term that is an organism that lives on or with another which it gets sustenance from
Have the potential to be a pathogen

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22
Q

Susceptibility vs permissive -virus
Pathogenicity vs virulence -bacteria
Infectivity

A

Susceptible= ability to enter and infect host
Permissive = ability to make new viral progeny in the cell
Pathogenicity = ability of bacteria to cause disease
Virulence = the variation in the ability; how much disease caused by bacteria
Infectivity = bacterias ability to enter tissue and multiple and infect

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23
Q

Define and which is more common: obligate pathogens and opportunistic pathogens
saprophytes are which?

A

Opportunistic pathogens- bacteria that is normal flora and cause disease when something changes in host

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24
Q

What is the most common reason the host lets in less virulent pathogen?

A

Bc of tissue damage and lower host innate defense mechanisms

NOT immunocompromised

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25
Q

High or low virulent bacteria: which are opportunistic pathogens?

A

Note: they are also commonly isolated from infection= highly virulent
Need less host tissue compromise and less numbers of bacteria

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26
Q

When biofilm act as organism

A

Quorum sensing

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27
Q

Name host predisposing factors: 3 of them

A

1 innate factors (age species sex)
2 Internal factors - Internal damage
3 External factors -nutrition environment

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28
Q

Define fomite

A

A source of bacteria
It is an inanimate object that has bacteria residing on it

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29
Q

The process of bacterial infection

A

Attachment
Penetrate
Evade host mechanism
Ability to multiply and cause damage to host= virulence factors

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30
Q

Highly virulent bacteria :

A

S. Aureus, E. Coli, Streptococci

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31
Q

Low virulent bacteria:

A

S. Epidermidis, Norcordia spp.

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32
Q

Hypertrophy

A

When the size increases but the number of cells does not increase

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33
Q

Hyperplasia

A

Increase in the number of cells that results
Still increase size of tissue

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34
Q

Difference between hyperplasia and neoplasia

A

Hyperplasia is controlled and neoplasia is uncontrolled by stimulus

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35
Q

Atrophy

A

When tissue fully developed
Had all these cells originally but now they have gone away
Hypoplasia - is when the tissue is not fully developed from immunological standpoint but there is fewer cells

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36
Q

Mechanisms of cell injury (different from causes)

A

Atp depletion
Gene destruction
Membrane disruption
Metabolic disturbance

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37
Q

Etiologic

A

The cause of the disease

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38
Q

Causes of cell injury

A

Oxygen loss [hypoxia, ischemia]
Physical destruction
Genetic damage
Workload imbalance [like w hypertrophy- just making cells bigger]
Nutrition
Age
Immune disfunction
Toxins

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39
Q

Connect infarction, hypoxia, and ischemia

A

Ischemia means there is less blood flow to a tissue
Which results in hypoxia where the tissue is not oxygenated enough
If it gets really bad then it becomes an infarction where the tissue becomes necrotic

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40
Q

Reversible cell injury

A

Hydropic degeneration leads to sodium and water in cell which causes cytoplasmic vacuoles

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41
Q

Ischemia -reperfusion injury

A

This is when there is low blood flow then there is blood flow and oxygen which leads to ROS production which furthers tissue damage

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42
Q

Pyknosis

A

Necrotic cell is shunk, round, dark

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43
Q

Karyorrhexis

A

Nuclear fragmentation

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44
Q

Karyolysis

A

Nuclear dissolution ; pale nucleus

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45
Q

Heinz bodies

A

Aggregates of hemoglobin due to oxidative injury

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46
Q

Different types of hemolytic anemia

A

Immune mediated hemolytic anemia ; bilirubin [extravascular], sphereocytes [extravascular], ghost cell [intracellular membrane attack complex], agglutinations
Infectious hemolytic anemia
Oxidative hemolytic anemia - chocolate blood; iron loss= methemoglobinemia, globin loss= heinz bodies, membrane destroyed= eccentrocytes
Fragmentation hemolytic anemia

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47
Q

Oxidative hemolytic anemia clinical signs:

A

Toxin ingestion

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48
Q

Empirical therapy:

A

administration of therapy based on previous experience

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49
Q

Aetiological diagnosis or definitive diagnosis

A

Specific identification of bacteria causing disease

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50
Q

Identify the bacteria definitively by…

A

Collecting a sterile sample and culturing
Finding antibody
Finding antigen
DNA detection of the bacteria

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51
Q

Site with normal flora need to see:

A

Pathogens that are not a part of the normal flora of that region that can cause disease
OR an increased amount of the normal flora that can cause disease

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52
Q

Bacterial infection determination

A
  1. Is it bacteria- pathognomic evidence?
  2. Presumptive [empirical therapy] or definitive analysis
  3. Which test [collect sample, antibody, antigen, genetic]
  4. Where to collect sample
  5. Time to collect sample [disease shed, antibiotics,
  6. Specific location localized
  7. Is this a sterile site
  8. are strict anaerobes involved?
  9. How to collect bacteria
  10. Sampling site
  11. Evaluate collected sample
  12. Stable transport to lab
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53
Q

Is a draining tract the site of infection?

A

NO

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54
Q

Where does the fat go

A

Bone marrow
Heart
Around kidney
Mesentery
Subcutaneous

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55
Q

What are the 5 gross patterns of necrosis

A

Coagulation necrosis where blood is cut off
Casseous necrosis- leukocytes [leuk its cheese]
Liquificaitive necrosis
Gangrenous necrosis- localized
Fat necrosis - sopinification of fat

56
Q

Compare contrast necrosis and apoptosis

A

Necrosis the cell expands and there is inflammatory response ->pyknosis, karyorrhexis, karyolysis.
Apoptosis. The cell shrinks -> apoptotic bodies that macrophages eat
- no inflammatory response

57
Q

What activates the caspase cascade

A

Apoptosis signals:
Intrinsic -mitochondrial membrane damage which leads to proapoptosis chemical cytochrome C release
Extrinsic - which is the FAS receptor TNF receptor family

58
Q

Dystropic calcification vs metastatic calcification

A

Dis trap house - in the trap house that the necrosis happened at - locally at the site is calcium released into mitochondria

Metastatic- calcium in the blood circulation
- renal failure ; Vit D inc; increased parathyroid hormone ; bone destruction

59
Q

Cells getting old leads to…

A

Less oxidative phosphorylation
Less nucleic and protein synthesis
Shorter telomeres - less replication

60
Q

Intracellular accumulation…

A

Abnormal cell metabolism
Lipids
- hepatic lipidosis : too much fat as triglycerides going to liver-> liver overworked OR decreased metabolism of fat [if losing weight then the fat needs to be broken down right]
Glycogen
Pigment - melanin /tattoo ink

61
Q

Enveloped or non enveloped associated with seasonal disease?

A

Enveloped

62
Q

Composition of virus

A

Viral genome -DNA or RNA not both
Viral protein:
Structural protein : the virion (viral attachment protein)
Spike protein
Non-structural- enzymes for replication/ polymerases
[esp in rna virus that replicates in cytoplasm]
Lipid

63
Q

DNA virus is shaped …

A

Icosahedral

64
Q

Viral incubation period >< generation time

A

Incubation period is from the point of getting infection to showing signs
Generation time is point of getting illness to spreading infection
I > G

65
Q

Bovine respiratory disease complex (2 virus) family? Name? Which is more severe?

A

Bovine parainfluenza 3 BI3
Bovine Respiratory Synactia Virus BRSV- more severe

Both not immunogenic and from the paramyxovirus

66
Q

Bovine papular stomatitis vs vesicular stomatitis virus

A

Both affect mucosa of bovines
Bovine papular stomatitis is a dsDNA virus in the pox virus family so it is enveloped with intracytoplasmic inclusion bodies
Bovine Vesicular stomatitis is a ssRNA virus in the Rhabdovirus family that subclinical and endemic

67
Q

Negri body

A

Intracytoplasmic inclusions of the rabies vaccine - part of the rhabdovirus

68
Q

Antigenic shift vs antigenic drift

A

Antigenic shift is the ability to combine segmented DNA to create a new strain via recombination - othomxyoviridae, reovirus, bunyavirus all have segmented genomes

69
Q

Cause of diarrhea in young pigs and calves

A

Bovine Viral Diarrhea Virus [ssRNA] - pestivirus
Bovine coronavirus - coronavirus

Pigs: Transmissible Gastroenteritis coronavirus
and Porcine epidemic diarrhea virus - something else

70
Q

Virulence factors for bacteria

A

Villi for attachment, slime capsule for evading host phagocytosis, survival within cells (facultative intracellular parasite), iron sequestering, survival in protected site, toxin to cause tissue damage

71
Q

Acid fast bacteria

A

Is least affected by detergents and exists within cells
Gram Positive is more affected by detergents than gram negative

72
Q

Microcytic and hypochromic are indicative of

A

Iron deficiency

73
Q

ITAM

A

In t and B cells - are attached to the alpha and beta receptors and help transduce the signal of the antigen binding into the cell
- a continuation of the TCR
- on side of Immunoglobulin with Ig a and Ig b

74
Q

Which t cell helps kill intravescular pathogens? ( different from cell death)

A

CD4 which brings in the macrophages, B cells, ETC after binding to the MHC class 2

75
Q

Erythrocytosis is induced by ___ growth factor

A

Erythropoietin is what is released from the kidneys
which is a growth hormone that drives RBC formation
- decreased erythropoietin leads to selective erythroid hypoplasia due to chronic kidney disease
- increased erythropoietin leads to Absolute secondary erythrocytosis (appropriate or inappropriate)

76
Q

Features of epitopes recognized by B cells

A
77
Q

4 functions of antibody

A

Neutralization _-toxins
Opsinization extra cellular - think going on OPPs is extra
Complement activation leads to lysis and ingestion ‘
Adcc -antibody dependent cellular toxicity when antibody is on target cell it binds Fc gamma and attracts nk (natural killer)

78
Q

Mast cell activation

A

Uses IgE and Fc epsilon to bind to mast cell and real ease histamine granules that lead of allergic response

79
Q

Most abundant immunoglobulin

A

IgA

80
Q

Urticaria

A

Hives

81
Q

Neonatal Isoerythrolysis in Horses

A

Type 2 hypersensitivity have different erythrocyte antigens so the mares colostrum is going to have antibodies that are going to attack the fools erythrocytes and that’s going to cause hemolysis

82
Q

Autoimmune diseases are wit which hypersensitivity?

A

Type 3 immunocomplex

83
Q

Arthus reaction
(Cutaneous vasculitis)

A

IgG binds the antigen and makes a immunocomplex
this immunocomplex attracts complement
Then binds to FC receptors in leukocytes and mast cells and creates permeability and a local inflammatory response

84
Q

Immune mediated glomerulonephrititis

A

Type 3 hypersensitivity where the filtration is compromised because of immunocomplex is that happened there

85
Q

Contact dermatitis happens with which type of hypersensitivity

A

Contact dermatitis happens with hypersensitivity four because it’s going to be the one that happens delayed for example with poison ivy where TH1 release is IS gamma and results in a localized skin bump and redness

86
Q

Hypersensitivity versus auto immunity

A

They are both inappropriate immune responses
Hypersensitivity is against an allergen or antigen an auto immunity is against self

87
Q

Interferons type 1

A

Antiviral and promote inflammation and stop the virus from replicating
Recruits macrophages and T cells
Bad in diabetes type 1 where it’s autoimmune and targeting pancreaTic beta cells

88
Q

Diabetes type l mechanism

A

PRR activated which induces type l interferon which attracts macrophages and t cells to the pancreatic bata cell, it also increases the mhc1 class on the cell which makes the CD8 t cell kill it
The broken down beta cell pieces will be presented by APC to CD4 T cells and macrophages too
T cell will make cytokines the that will be picked up by nearby beta cell
Increase inflammation w MHC class one antigen presenting cells PRR T cells macrophages MHC2

89
Q

Systemic lupus enythematus

A

Nets bind nuclei acid and nuclei acid binds autoantibody → complexactivates dendrite cell →interferon type l→ increases TH2 which increases the bee cells and TH 17 which increases NETs

90
Q

Celiac’s disease

A

The auto immune disease might be type one or type four
Uses T cells and macrophages it attacks the villi of the gastrointestinal tract and reduces absorption

91
Q

True or false a robust normal response to self is good

A

F should have a deficient response to self otherwise it is auto immunity

92
Q

Central tolerance

A

When B cells and T cells are removed from the thymus or bone marrow before they are sent to peripheral organs if they are auto immune

93
Q

Peripheral tolerance

A

When T and B cells that recognize cells are removed from peripheral organs like the spleen So depletion after it’s already gone to peripheral Oregon

94
Q

True or false too much TH 17 will result in auto immunity

A

True- we want self tolerance not inflammation

95
Q

Primary hemostasis

A
96
Q

Positive acute phase protein

A

Increases with inflammation -hepcin and fibrinogen

97
Q

Prednisone and prednisolone : which is the prodrug?

A

PREDNISONE IS PRODRUG
Converted to prednisolone
Glucocorticoids

98
Q

Hepatomegaly and splenomegaly can happen with hemolytic anemia

A

The macrophages are eating the RBC in the spleen and there will be lymphocytes too contributing to it- the liver and the spleen will be enlarged

99
Q

Ghost cells argue for___hemolysis

A

Intervascular hemolytic anemia

100
Q

IMHA

A

PRIMARY
SECONDARY- associative process: hemoparasites
- Carprofen can lead to secondary IMHA

101
Q

Hienz body, pkycnocytie, eccentrocytes are pathognumonic

A

Oxidative hemolytic anemia

102
Q

Prions are have a long or short incubation period

A

Long incubation period
-a normal glycoprotein misfolded so they are not immunogenic
-vacoulation of neurons and neurophils

103
Q

Discuss TSE= BSE and Scarpie, Chronic wasting disease

A

Scrapie is in sheep- no inflammation just vacoulation
It jumped to BSE because of eating the brains and spinal cord of sheep
CWD is the TSE in deer and elk
Scrapie and CWD spread via pasture

104
Q

Which viruses have no proofreading ability and have ran dependent DNA polymerase

A

Retroviruses which include Feline leukemia and Bovine leukemia

105
Q

What are the two components in corticosteroids

A

Glucocorticoids and Mineralocorticoids

106
Q

What do glucocorticosteroids do (2 things)

A

Transactivation of anti inflammatory response and trans repression of pro inflammatory response

107
Q

Acetate and acetonide esters

A

are insoluble GLUCOCORTICOIDS and are given IM, SQ, IA.
act w time

108
Q

Succinate and phosphate esters

A

soluble GLUCOCORTICOIDS given IV

109
Q

Cox 1 and Cox 2 function
Which one is a coagulant?

A

Cox 1 - GI tract cytoprotective - decrease acid and increase mucus ; coagulation
Cox 2- Inflammatory response with fever and heat and pain [if there are 2 cox then its gonna be more painful] ;anti coagulation
- help with healing and in kidney

110
Q

Natural Prostaglandins
PGI1
TXA2
PGE2
PGF2a

A

PGI1 : Platelet gets it - antiplatelet vasodilation
TXA2: Ticket X accepted : pro platelet vasoconstriction
PGE2: please get eradicated: pro inflammatory
PGF2a: no inflammatory response

111
Q

T/F cox 2 specific NSAID induce thrombosis

A

True because they are naturally anticoagulation factors

112
Q

NSAID effects

A

Analgesia for pain and Antipyresis [antifever], can also be given for endotoxins, they can be anticoagulant [COX2 blocked thrombosis], Immune suppression, Kidney issues, GI ulcers, hemorrhage, IMHA and pancytopenia [ bone marrow failure], clostridium myositis

113
Q

Which drug causes laminitis in horses

A

Glucocorticoids

114
Q

Solutions go in
Aqueous suspensions go in

A

IV or IM
IM or SQ

115
Q

Determinant etiological factor

A

Directly related to the cause of the disease
Intrinsic would be genetic changes
Extrinsic would be Biological- bacteria/virus, Physical- Mechanical, and Chemical - toxin

116
Q

Cells that go through…
Hypertrophy

A

Skeletal muscle, cardiac muscle

117
Q

Cells that go through…
Hyperplasia

A

Epithelial, bone marrow [ie. lactation mammary gland gets more cells]
CANT: cardiac muscle, neurons

118
Q

Metaplasia is _cell differentiation or cell replacement__

A

REPLACEMENT

119
Q

Microaerophile

A

low amount of o2 needed and come co2

120
Q

T/F bacteria in sterile site transitorily do not cause inflammation because they are cleared out

A

True - host defense mechanisms

121
Q

If highly virulent pathogen and little host tissue compromise what to treat bacteria or host?

A

treat bacteria

122
Q

Are virulence factors of bacteria expressed constitutively?

A

No they are expressed as needed

123
Q

Endogenous vs exogenous bacterial infection

A

Endogenous infection comes from the bacteria on the skin/mucous membrane and as commensals
Exogenous is from environment

124
Q

How to sample uterus for bitch

A

guarded swab

125
Q

Sample mare uterus

A

Guarded swab

126
Q

Horse: sterile caudal to the larynx

A

True ; includes trachea which is sterile

127
Q

First thing to see with bacterial culture

A

Inflammation
Followed by any pathogen, and if its a mixed infection

128
Q

4 components of a virus

A

Viral genome
Structural and non structural proteins
Spike protein
Lipids

129
Q

4 Point rule for sterile site

A

Is there inflammation on the isolate
Is it collected from the proper site
Is there bacteria in the sample
Will the bacteria cause disease

130
Q

All DNA viruses replicate in nucleus except

A

Poxvirus

131
Q

All RNA virus replicate in cytoplasm except

A

Coronavirus (Alphacprona- FIP, canine corona, TGE/ Porcine epidemic diarrhea virus Gammacoronavirus- Bovine coronavirus), orthomyxovirus (influenza), retrovirus (FeLV, BLV)

132
Q

All RNA virus replicate in cytoplasm except

A

Coronavirus (Alphacprona- FIP, canine corona, TGE; Gammacoronavirus- Bovine coronavirus), orthomyxovirus (influenza), retrovirus (FeLV, BLV)

133
Q

Effect of virus on cell metabolism

A

Inhibit
Cellular transcription
RNA processing pathways
Cell translation
DNA synthesis

Basically when virus invades it hijacks the genome

134
Q

CPE of virus

A

syncytia, cell lysis. cell rounding, inclusion bodies

135
Q

Where is herpes latent?

A

trigeminal ganglia

DWT (5 decks)

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