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Diseases and Diagnosis > Block 1 > Flashcards

Block 1 Flashcards

1
Q

What is a morphological diagnosis?

A

Describes the affected structure, process, distribution, severity, time course. Long names

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2
Q

What is the etiological diagnosis?

A

Diagnosis that names causative agent

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3
Q

What is the disease diagnosis?

A

States name of disease

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4
Q

What is a lesion localized to a single area

A

Focal

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5
Q

What is a lesion in multiple areas on the same tissue/organ?

A

Multifocal

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6
Q

What is a lesion in multiple areas with overlapping regions?

A

Multifocal to coalescing

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7
Q

What is a lesion fulling spread throughout a tissue/organ?

A

Diffuse

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8
Q

What is a lesion localized to one portion of an organ/tissue?

A

Locally extensive

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9
Q

What are the 4 categories of duration?

A

Acute
Subacute
Chronic
Chronic-active

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10
Q

What is the last part of a word that means inflammation?

A

“-itis”

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11
Q

What does purulent mean?

A

Puss

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12
Q

What are the two anti-inflammatory and immunosuppressive cytokines?

A

IL-10 and TGF-B

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13
Q

What is the subset CD4 T cells that help suppress the immune response via physical contact?

A

T regs

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14
Q

What do T regs express on their cell surface?

A

CD4+ and CD25+

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15
Q

What transcription factor do T regs express?

A

FOXP3

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16
Q

What are the macrophages that suppress inflammation?

A

M2 macrophages

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17
Q

What cytokines do M2 macrophages release to suppress inflammation?

A

IL-10 and TGF-B

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18
Q

What does PD-1 do on T cells?

A

PD-1 is a cell surface suppressor which shuts down T cell activation

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19
Q

What does cancer do to PD-1 on T cells?

A

PD-1 (programmed cell death) is upregulated which shuts down most all T cell activation therefore stopping the activation of the suppressive cells (stopping the cells that kill the cancerous cells)

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20
Q

What is tolerance in immunilogical terms?

A

Tolerance is when the immune system fails to mount an immune response toward a specific antigen

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21
Q

What does a failure of self-tolerance lead to?

A

Auto-immune disease

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22
Q

What are the 2 mechanisms of tolerance in the immune system?

A

Central tolerance and peripheral tolerance

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23
Q

What is a cryptic antigen?

A

Self-antigens that are revealed secondary to inflammation

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24
Q

What are the 3 ways that peripheral tolerance addresses auto reactive imune cells?

A

Peripheral deletion
Anergy
Regulatory T cells

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25
Q

What is peripheral deletion?

A

T and B cells recognize self antigens in the lymph nodes

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26
Q

What is anergy?

A

Shut down of self reactive T and B cells due to lack of all 3 signals

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27
Q

What causes anergy?

A

Removal of either co-stimulation or cytokines (1 or 2 of the 3 signals required for activation)

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28
Q

What induces differentiation into T regs?

A

Presence of IL-10 or TGF-B

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29
Q

What blood do you use in a biochem panel?

A

Red top, serum

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30
Q

What “top tube” do you use for CBC? Biochem profile?

A

Purple top
Red top

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31
Q

What percent of healthy animals will have at least 1 abnormal result?

A

60%

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32
Q

What is the one type of result that is significant if it falls slightly outside of the reference interval?

A

Electrolytes

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33
Q

What type of error is most common in laboratory results?

A

Preanalytical

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34
Q

What is in a routine serum biochem profile?

A

Electrolytes, minerals, proteins, enzymes, lipids, and glucose

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35
Q

What are the 4 aspects to disease?

A

Etiology, pathogenesis, morphological change, functional consequences

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36
Q

What are the 2 subsets of etiology?

A

Intrinsic and extrinsic

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37
Q

What are the 2 subsets in intrinsic etiology?

A

Primary and secondary

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38
Q

What is a primary intrinsic etiology?

A

Genomic related
-Family/breed
-Mutation

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39
Q

What is a secondary intrinsic etiology?

A

Physical Abnormalities
-Age, sex, species

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40
Q

What are the 2 subsets of extrinsic etiology?

A

animate and inanimate

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41
Q

What is an animate extrinsic etiology?

A

Pathogens

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42
Q

What is an inanimate extrinsic etiology?

A

Energy, xenobiotics, surgical

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43
Q

***What is the flow of pathogenesis?

A

Biochemical change>Functional alterations>Morphological lesions >Clinical signs

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44
Q

What is idiosyncratic?

A

A patient specific disease

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45
Q

What are lesions?

A

Visible manifestation of disease

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46
Q

What are the different levels, in order, of visualizing lesions?

A

Gross pathology > Histopathology > Ultrastructural pathology

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47
Q

What is pathognomic?

A

A lesion so distinctive and unique that it can only be caused by one etiology

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48
Q

What is the prognosis?

A

Prediction of future outcomes
Usually worded (excellent, good, fair, guarded, poor)

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49
Q

What are disturbances in electrolytes normally caused by?

A

Vomiting, diarrhea, and kidney disease

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50
Q

What are the major cations?

A

Na+ (largest), Ca, Mg, K

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51
Q

What are the major anions?

A

Cl, PO4, HCO3, A (proteins)

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52
Q

What level is sodium when animal is dehydrates?

A

Higher

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53
Q

What balances the cation, Na?

A

Cl and HCO3

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54
Q

What disease is usually indicated from high potassium (hyperkalemia)?

A

Addison’s
Low aldosterone = high levels of potassium

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55
Q

What hormone removes potassium from the blood?

A

Aldosterone

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56
Q

What does chloride usually follow?

A

Sodium (NaCl)

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57
Q

What is bicarbonate an indicator of?

A

Acid/base status

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58
Q

What is low bicarbonate indicative of?

A

Metabolic acidosis
A high bicarbonate is metabolic alkalosis

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59
Q

What different things can you check on a biochemical profile for the liver?

A

Hepatocellular injury
Cholestasis
Synthetic injury

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60
Q

What are the indicators for livers on a chem profile?

A

ALT, AST, ALP, cholesterol, CK, biliruben

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61
Q

What increases with hepatocellular injury?

A

ALT and AST

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62
Q

What increases with cholestasis?

A

ALP and bilirubin

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63
Q

Why is ALT increased during hepatocellular injury?

A

ALT is found in hepatocytes so when it is increased, that means there is damage to the hepatocytes

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64
Q

Why is an increase in AST nonspecific?

A

AST is found in liver, muscle, and blood

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65
Q

When is an increase in AST notable for hepatocellular damage?

A

When it is marketed (more than 3x)

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66
Q

What enzyme is measured most for muscle injury?

A

CK (creatinine kinase)

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67
Q

What liver biomarkers are used to assess synthetic function?

A

Cholesterol, albumin, glucose, and BUN

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68
Q

When should measuring cholesterol occue?

A

After fasting (or may be higher)

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69
Q

What are the steps of bilirubin metabolism?

A

Bilirubin in blood goes through liver
Liver conjugates bilirubin
Bilirubin enters intestine where it is either excreted in urine or stool

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70
Q

What is biliruben excreted in unrine called?

A

urobilinogen

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71
Q

What is biliruben excreted in stool called?

A

Stercobilinogen

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72
Q

Where is conjugated bile secreted?

A

Into bile

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73
Q

What is cholestasis?

A

Slowing or stopping of bile through the biliary system

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74
Q

Increased bilirubin can mean what 3 things?

A

Pre-hepatic icterus
Hepatic icterus
Post-hepatic icterus

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75
Q

What is total protein made up of?

A

Albumin and globulin

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76
Q

What does increased total protein mean?

A

Anything that increases immunoglobulins
Neoplasm, inflammation, dehydration

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77
Q

What does decreased total protein mean?

A

Decreased production via liver
Loss from GI or kidney

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78
Q

What causes hypoalbuminemia?

A

Decreased production by hepatocytes (liver disease)
Loss from renal or GI loss

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79
Q

Do younger animals have decreased globulins?

A

YES

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80
Q

How do you determine globulin from albumin and TP?

A

TP-albumin = globulin

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81
Q

What does decreased globulin indicate?

A

Liver disease, synthetic function

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82
Q

Will cats have hyperglycemia at vet?

A

YES, EXCITED

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83
Q

What is another name for persistent hyperglycemia?

A

Diabetes mellitus

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84
Q

What is DIC?

A

Disseminated intracellular coagulation (Death is coming)

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85
Q

What are the 4 mechanisms of cellular injuries?

A

Membrane injury
Nuclear damage
ATP depletion
disturbances in cellular metabolism

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86
Q

What are the 3 cell responses to injury/stress?

A

Adaptation
Degeneration
Cell death

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87
Q

What is adaptation related to cell injury/stress?

A

React to stress so that a new homeostatic state is established

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88
Q

What is Degeneration related to cell injury/death?

A

Reversible cell injury from which a cell can adapt and recover. Either intracellular or extracellular components

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89
Q

What is Death related to cell injury/death?

A

Irreversible cell injury results in cell death

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90
Q

What are the 2 reversible cell responses?

A

Adaptation
Degeneration

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91
Q

What are the 2 irreversible cell responses?

A

Necrosis
Autolysis

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92
Q

What are the 4 types of cell adaptation?

A

Hyperplasia
Metaplasia
Hypertrophy
Atrophy

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93
Q

What is atrophy?

A

Reduction of cell size

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94
Q

What is hypertrophy?

A

Increased cell size

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95
Q

What is hyperplasia?

A

More cells

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96
Q

What is metaplasia?

A

Replacement of cell type

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97
Q

What type of adaptation does a portosystemic shunt cause to the liver?

A

Atrophy of hepatocytes
Due to decreased blood flow

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98
Q

What type of cell adaptation would a chronic smokers mucosal lining undergo?

A

Metaplasia

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99
Q

What are the 4 types of reversible degeneration that a cell can undergo?

A

Hyropic (acute cell swelling)
Fatty change
Glycogen accumulation
Myxomatous

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100
Q

What causes degeneration of cells?

A

Sublethal injury

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101
Q

What is hydropic degeneration?

A

Swelling due to water accumulation

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102
Q

What happens to ATP when hydropic injury occurs?

A

ATP is decreased where water moves into cell

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103
Q

What is the cell degeneration, fatty change?

A

Fatty vacuole accumulation in non-adipose cells

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104
Q

What are causes of fatty change?

A

Hypoxia, anemia, starvation

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105
Q

Where does fatty change usually occur?

A

Liver, kidney, and muscle

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106
Q

What gross things can you appreciate on cellular degeneration?

A

Softer tissue
Light tissue
Larger organs

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107
Q

What is hepatic lipidosis in cats?

A

Accumulation lipoproteins in liver leading to fat storage

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108
Q

What stains can be used to see adipose cells?

A

Oil Red O
Suden Black

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109
Q

Where does glycogen accumulation begin?

A

Centrilobular regions due to lower oxygen content

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110
Q

What is myxomatous?

A

Accumulation of mucin-like material

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111
Q

What does myxomatous cause?

A

Conversion of mature proteins to embryonic forms

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112
Q

What types of tissue does myxomatous occur in?

A

Connective tissue and adipose tissue

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113
Q

When does myxomatous most often occur?

A

During cachexia (muscle loss) and starvation

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114
Q

What is microcirculation?

A

Exchange of nutrients and waste between blood and extravascular tissue

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115
Q

What is the space between cells and the microcirculation?

A

Interstitium

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116
Q

Edema is the accumulation of abnormal quantities of fluid in the interstium

A
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117
Q

What controls the balance of fluid between the arteriole and the interstitial space?

A

Physical barriers (arteriole wall)
Differences in pressure
Concentration of substance

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118
Q

What are the driving forces of fluid exchange?

A

Arteriole blood pressure (ABP)
Colloid osmotic pressure (COP)
Interstitial fluid pressure (IFP)

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119
Q

What is the active driving force of fluid exchange?

A

Arteriole blood pressure

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120
Q

What is the passive driving force of fluid exchange?

A

Colloid osmotic pressure
Interstitial fluid pressure

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121
Q

When do we get edema?

A

When this balance between the fluid exchange is off

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122
Q

What tube is used to run a chem profile?

A

Red top

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123
Q

What type of blood is used in a red top?

A

Serum

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124
Q

What does a purple top tube have that a red top doest? (In terms of the blood)

A

A buffy coat (fibrinogen)

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125
Q

What percent of error is pre-analytical? (Our fault)

126
Q

What percent of healthy animals will have at least 1 “abnormal” value?

127
Q

What are the tests most commonly used to determine kidney function tests (GFR)?

A

BUN, Creatinine, and Phosphorus

128
Q

What is urea?

A

A by-product of protein breakdown produced in the liver

129
Q

What is creatinine?

A

A by-product of muscle metabolism

130
Q

What is an increase in BUN and Cr called?

131
Q

What are the 3 different potential reasons for azotemia?

A

Pre-renal: dehydration (vomiting/diarrhea)

Renal: Acute or chronic kidney disease

Post-renal: ruptured bladder or urethral blockage

132
Q

What are the minerals ran on a routine chem panel?

A

Mineral
Phosphorus

133
Q

CALCIUM IS REPORTED AS TOTAL (NOT IONIZED) ON CHEM PANEL

134
Q

What does high phosphorus indicate?

A

Kidneys are main route of phosphorus excretion so high phosphorus may indicate pre-renal, renal, or post-renal disease

135
Q

What does low phosphorus indicate?

A

Possibly kidney disease

136
Q

What is the most common cause of hypercalcemia in dogs?

137
Q

What is a cause of hypocalcemia?

A

Low albumin (decreased protein-bound fraction)

138
Q

Describe autolysis

A

Dead animal
Diffuse
No tissue reaction

139
Q

Describe necrosis

A

Alive animal
Focal to multifocal
Induces local tissue reaction

140
Q

How does autolysis occur?

A

Progressive tissue anoxia via microbes eating tissue, mostly from gut microflora

141
Q

What type of animals will autolyse faster?

A

Large, obese, thick-coated, and herbivores (due to GI microflora)

142
Q

What general idea causes quicker autolysis?

A

Anything that increases heat

143
Q

What is livor mortis

A

Blue/purple color due to congestion of blood in external tissues

144
Q

What is dessication?

A

Poikilotherms (cold blooded) may dry out instead of autolysis

145
Q

What is putrefecation?

A

Bubble formation on internal tissues due to bacterial fermentation. Tissue also turns pale

146
Q

What is imbibition?

A

Internal: Tissue discoloration
Hemoglobin imbibition: red stain
Pseudomelanosis: blue-black discoloration
Bile imbibition: Green-brown

147
Q

What is chicken fat?

A

Clotted serum chunks in autolysis

148
Q

What is currant jelly?

A

Clotted erythrocytes in autolysis

149
Q

Where do blood clots settle in autolysis during microscopy?

A

Down due to gravity

150
Q

How are thrombi in post mortem different from thrombi in ante mortem?

A

Post: unattached to walls, shiny/wet
Ante: thrombi attached to wall, dry/dull, tail extends downstream

151
Q

What are organisms that grow on dead tissue?

A

Saprophytes

152
Q

How do you know saprophytes are invaders?

A

Gram (+) anaerobic rods
No inflammatory response

153
Q

Do autolytic borders have sharp or rigid borders?

154
Q

Is necrosis and oncotic necrosis the same?

155
Q

What are causative agents for cell death (necrosis)

A

Oxidative stress
ATP decrease
Loss of Ca homeostasis
Mitochondria damage

156
Q

2 main causes of necrosis?

A

Failure of mitochondrial function
Breach of cell membranes

157
Q

What is the pathogenesis of cell death?

A

Cell injury
Influx of Ca2+
Ca2+ activates degradative enzymes
Further mitochondrial/membrane breakdown

158
Q

Describe free radicals

A

Molecule with unpaired electron. Normally controlled by antioxidants but if overwhelmed, the mitochondria will be further depleted

159
Q

What are common gross morphological changes of necrotic tissue?

A

Irregular contours
Sharp demarcations
Paler
Colored rim: red or white

160
Q

What are microscopic changes in necrotic cells?

A

Loss of internal cell detail
Hypereosinophilia of the cytoplasm
A visual gradient
Nuclear changes

161
Q

What is karyolysis?

A

Nuclear fading

162
Q

What is pyknosis?

A

Nuclear shrinkage

163
Q

What is karyorrhexis?

A

Nuclear fragmentation

164
Q

What are the functional molecules involved in apoptosis?

165
Q

What is the execution caspase for apoptosis?

166
Q

What are the 4 types of necrosis?

A

Coagulative
Liquifactive
Caseous
Gangerenous

167
Q

What is coagulative necrosis?

A

Cell outline remains
common in kidney, liver, muscle

168
Q

What causes coagulative necrosis?

A

Heat, decreased blood flow, toxins

169
Q

What are the subtypes of coagulative necrosis?

A

Fat necrosis
Zenker’s necrosis

170
Q

What is fat necrosis?

A

Coagulative necrosis of adipose tissue

171
Q

What is Zenker;s necrosis?

A

Coagulative loss of striated muscle (cardiac and skeletal muscle)

172
Q

Describe saponification

A

Release of Ca an dK after adipose breakdown causing formation of soaps on pancreas surface

173
Q

What is liquefactive necrosis?

A

Enzyme breakdown of tissues resulting in dissolving or liquefying

174
Q

What is the term for liquefactive necrosis of the CNS

175
Q

What type of necrosis is an abcess?

A

Liquefactive necrosis! Bacterial enzymes consuming tissue

176
Q

What does a thiamin deficiency cause?

A

Polioencephalomalacia

177
Q

What is caseous necrosis?

A

Cheese-like
Granular and friable

178
Q

What does a caseous necrosis typically form?

A

A granuloma

179
Q

What is a granuloma?

A

Cell debris and inflammatory cells surrounded by connective tissue capsule

180
Q

What is gangrenous necrosis?

A

Coagulative necrosis that turns into gangrenous

181
Q

What are the 3 types of gangrenous necrosis?

182
Q

What is wet gangrenous necrosis?

A

Coagulative + liquefactive + saprophytic bacteria

183
Q

What is dry gangrenous necrosis?

A

coagulative + infarction
On distal limbs due to vasoconstriction

184
Q

What is gas gangrenous necrosis?

A

coagulative + anaerobic bacteria producing a toxin

185
Q

What happens if a quantity of dead tissue is too large to be removed from the body?

A

A sequestrum is formed

186
Q

What is a sequestrum?

A

A persistent fragment of necrotic bone

187
Q

What is immune regulation?

A

The ability for the body to balance clearing a pathogen while not harming self

188
Q

What is contraction?

A

Massive reduction in CD8 and plasma cells

189
Q

What remains after contraction?

A

Memory cells

190
Q

What are the 2 immunoregulatory cytokines?

A

IL-10 and TGF-B

191
Q

What does a Treg express?

A

CD4+, CD25+, and FOXP

192
Q

What do M2 macrophages produce?

A

IL-10 and TGF-B

193
Q

What does PD-1 do?

A

Cell surface receptor on T cells that deactivates T cells (cancer cells use this to deactivate T cells)

194
Q

What is tolerance?

A

Lack of an immune response towards something (like self)

195
Q

FAILURE OF SELF-TOLERANCE IS AN AUTO-IMMUNE DISEASE

196
Q

What are cryptic antigens?

A

Antigens only revealed secondary to inflammation

197
Q

What are the 3 methods of peripheral tolerance?

A

Peripheral deletion
Anergy
Regulatory T cells

198
Q

What is peripheral deletion?

A

Apoptosis in lymph nodes of self reactive cells

199
Q

What is anergy?

A

APC dont express all 3 signals required so self reactive T or B cell shuts down

200
Q

How is pregnancy possible with 1/2 paternal?

A

Up regulation of Tregs and Tregs with IL-10 and TGF-B in placenta

201
Q

What bovine disease causes abortions?

202
Q

What is cytopathic BVD?

A

Infection is lytic, causing cell death (cytolytic)

203
Q

What is non-cytopathic BVD?

A

Infection results in replication but not kill the cell

204
Q

What type of BVD occurs in utero?

A

non-cytolytic BVD

205
Q

When must exposure to BVDV occur in utero?

A

80-120 days
Prior to or during negative selection

206
Q

Calves infected in utero become PI calves (persistently infected)

207
Q

How is BVD tested for?

A

Ear notching shows brown/orange cirus

208
Q

What are symptoms of BVD in non-pregnant cows?

A

Oral ulcerations
Diarrhea
Pneumonia

209
Q

What is mucosal disease associated with BVD?

A

Disease that occurs in PI animals with infection of cytopathic strain of BVD

210
Q

What is primary autoimmunity?

A

Genetic susceptibility with no obvious trigger

211
Q

What is secondary autoimmunity?

A

A result of some trigger

212
Q

What are superantigens?

A

Antigens produced by bacteria that activate massive numbers of T cells through bridging the MHCII

213
Q

What are cryptic epitopes?

A

Self tissue released as antigen to T cells

214
Q

What causes agglutination with IMHA?

A

Antibodies can bind 2 RBCs which causes agglutination of cells

215
Q

What does a Coombs test detect?

A

Presence of erythrocyte-directed auto-antibodies

216
Q

What is targeted in myasthenia gravis?

A

Acetylcholine receptors in neuronal junctions

217
Q

How do you test for myasthenia gravis?

A

Tensilon test

218
Q

What are the 2 phases of type 1 hypersensitivity?

A

Sensitization phase: first encounter
Effector phase: re-encounter

219
Q

What is the primary cell in type 1 hypersensitivities?

A

Mast cells (IgE and histamines)
NOT eosinophils

220
Q

How do infections result from atopic dermatitis?

A

Scratching from pruritus causes trauma and moisture

221
Q

Which is the drug that actually treats the “itch”

A

Lokivetmab (cytopoint)

222
Q

How does cytopoint work?

A

Anti IL-31 antibodies

223
Q

What is hyperemia?

A

Too much blood flow in (erythema)

224
Q

What is congestion?

A

Not enough blood flow out (cyanosis)

225
Q

What is the nutmeg appearance?

A

Right sided heart failure in dogs due to hypoxia (cyanosis due to congestion)

226
Q

What are the heart failure cells?

A

Hemosiderosis

227
Q

What is melena?

A

Digested blood in feces

228
Q

What is hematochezia?

A

Undigested blood in feces

229
Q

What is rhexis?

A

Hemorrhage via physical disruption of the vascular wall

230
Q

What is diapedesis?

A

Hemorrhage via a leakage through intact vascular wall

231
Q

What is petechia?

A

Pinpoint hemorrhage

232
Q

What is ecchymoses?

A

Blotchy hemorrhage

233
Q

What is suffusive?

A

Paintbrush-like hemorrage streaks

234
Q

What is hyphema?

A

Bleeding into anterior chamber of eye

235
Q

What is hemoptysis?

A

Coughing up blood

236
Q

What is Hematemesis

A

Vomiting up blood

237
Q

What is hemorrhagic diathesis?

A

Systemic bleeding caused by a deficit of clotting factors

238
Q

What is coagulopathy?

A

Hemostasis defect

239
Q

Where does thrombosis normally occur?

A

Veins
more serious in arteries tho

240
Q

What is released during endothelial damage and exposure of subendothelial release?

A

Platelet-activating factor (PAF)

241
Q

What are the 3 corners of Virchow’s Triad?

A

Endothelial damage
Abnormal flow rate
Hypercoagulability

242
Q

What are the 6 types of thrombi?

A

Mural
Obterating
Occlusive
Saddle
Septic
Vegetative

243
Q

What are the different characteristics between a venous thrombi and an arterial thrombi?

A

Venous: RBC, non-infarction, more common, embolize
Arterial: WBC, infarctious, more deadly, cause alternating layers

244
Q

What does embolize mean?

A

Pieces breaking off a thrombi

245
Q

What are alternating layers in arterial thrombi called?

A

Lines of Zahn

246
Q

What are the 4 resolutions to a thrombi?

A

No scar
Inelastic scar
New channel formed
DIC

247
Q

What are the possible outcomes of an embolism?

A

Either ischemia or infarction

248
Q

What is an infarct?

A

A local area of ischemia necrosis from a blockage/occlusion

249
Q

What color is an arterial infarction?

A

White
blood cant enter

250
Q

What color is a venous infarction?

A

Red-black
blood cant leave

251
Q

What happens in DIC?

A

Endothelial damage
Multiple thrombus form
consumes all clotting factors
widespread petechia and ecchymoses

252
Q

What are Russell Bodies?

A

Hyaline bodies present in cytoplasm

253
Q

What are Mott Cells?

A

Plasma cells that contain russell bodies (immunoglobulins)

254
Q

What is hyaline

A

Abnormal accumulation of protein

255
Q

How is hyaline found in cells?

A

Glomerular damage causes proteinurea, causing protein being taken up by tubular cells (intracellular hyaline droplets)

256
Q

What are crystalline protein inclusion bodies?

A

“Brick inclusions”
Normal in hepatocytes and renal cells

257
Q

What are viral inclusion bodies

A

Accumulation of viral proteins

258
Q

What are amyloid fibrils?

A

Abnormally folded proteins into Beta sheets

259
Q

What is the precursor for reactive systemic amyloid associated (AA)?

260
Q

What is the precursor for primary amyloid amyloid light-chain (AL)?

261
Q

How does amyloid occur?

A

Circulating SAA
Misfolding (neoplasia or infection)
Enter cells
Mutated SAA aggregate together

262
Q

What do you use to stain for amyliod in live tissue?

A

Fresh tissue - Lugol’s iodine

263
Q

What stain do you use for amyloid in histo?

A

Congo red stain

264
Q

What stain do you use for amyloid in polarized light?

A

Congo red positive apple green fluorescence

265
Q

What is the main consequence of amyloidosis?

A

Organ failure (liver and kidney)

266
Q

Does gout occur in dogs, cats, cows, etc

267
Q

What dont other animals get gout?

A

They have an enzyme called uricase

268
Q

What is gout?

A

Deposition of sodium urate crystals on tissues

269
Q

What causes gout?

A

Dehydration, kidney failure, high protein diets

270
Q

What are the 2 types of gout?

A

Articular
Visceral (pericardium and renal)

271
Q

What are the 2 types of calcification?

A

Dystrophic
Metastatic

272
Q

What is dystrophic calcification?

A

Calcification of necrotic or diseased tissue

273
Q

What is metastatic calcification?

A

Calcification of normal tissue
Hypercalcemia

274
Q

What are 4 ways that hypercalcemia happens resultin gin metastatic calcification?

A

Tumor causing increased PTH
Bone destruction from neoplasia
Vitamin D too high from intake
Renal disease causing retention

275
Q

What is von Kossa stain used for?

A

Staining calcium black for metastatic calcification

276
Q

Where do cats often get reactive amyloidosis?

A

Pancreatic islets of Langerhans

277
Q

Why should you control the amount of vitamin D an alpaca gets?

A

Highly sensitive to it and may cause calcification

278
Q

What causes cyanosis in cat foot pads?

A

Secondary to a saddle thrombosis

279
Q

What are the borders like between autolytic and normal tissue?

A

SHARP borders

280
Q

What is oncotic necrosis?

A

swelling of cells leading to eventual burst

281
Q

What is karyolysis?

A

Nuclear fading

282
Q

Unlike autolysis’ clear line, what does necrosis have?

A

A visual gradient

283
Q

What is karyorrhexis?

A

Nuclear fragmentation

284
Q

What is pyknosis?

A

Nuclear shrinkage

285
Q

What are the 4 electrolytes on a panel?

A

Chloride
Sodium
Potassium
Bicarb

286
Q

What is sodium balanced by?

A

Chloride and bicarb

287
Q

What disease does hyperkalemia indicate?

A

Addison’s (hypoadreno)

288
Q

What does transfusion plasma have in it?

A

albumin, antibodies, clotting factors

289
Q

What transfusion cannot be used for dogs with von Willebrand?

A

Stored plasma (4 year shelf life)

290
Q

What is cryoprececipitate?

A

Precipitate that forms when frozen fresh plasma (FFP) is thawed slowly
Used for von Willebrand disease

291
Q

What are the different types of blood component therapies?

A

Whole blood
Packed RBCs
Fresh Plasma
Frozen fresh plasma
Stored plasma
Cryoprecipitate
Cryosupernate

292
Q

Why are greyhounds good dogs for blood donor?

A

High DEA 1.1 negative
Higher PCV than other breeds
Docile
Good veins

293
Q

What are 5 signs of inflammation?

A

Heat
Pain
Soreness
Loss of function
Swelling

294
Q

What are the 4 main stages of leukocyte adhesion cascade?

A

Margination
Rolling
Activation/adhesion
Transmigration

295
Q

What is the ligand that leukocytes bind to during endothelial transmigration?

A

PECAM-1 with CD31

296
Q

What are the classifications of inflammations?

A

Serous
Fibrinous
Catarhhal
Hemorrhagic
Purulent
Eosinophilic

297
Q

What is serous inflammation?

298
Q

What is fibrinous inflammation?

A

fluid and fibrin protein

299
Q

What is catarrhal inflammation?

A

fluid, fibrin, and mucoid

300
Q

What is hemorrhagic inflammation?

A

erythrocytes, protein, fluid

301
Q

What is purulent/supprutative inflammation?

A

neutrophils and everything else

302
Q

What is eosinophilic inflammation?

A

eosinophils

303
Q

What are the 3 forms of chronic inflammation?

A

Supporutive
Nonsuppurative
Granulomatous

304
Q

What are hallmark signs of suppurative chronic inflammation?

A

Abscess and/or cellulitis

305
Q

What things normally cause nonsuppurative chronic inflammation?

306
Q

What are the 2 hallmarks of granulomatous chronic inflammation?

A

Macrophages +/- multinucleated giant cells

307
Q

What are the 2 types of MNGC and what is their appearance?

A

Foreign body: In middle of cell scattered
Langhan’s: Semi-circle

308
Q

Draw out the granuloma architecture. What cells does it contain?

A

Fibroblasts
Macrophages
Multinucleated giant cell
Epithelioid cell
kymphocyte

309
Q

What are the 4 outcomes of acute inflammation?

A

Resolution
Healing by fibrosis
Abscess formation
Chronic inflammation

310
Q

What is the initiating response to injury?

A

Direct Endothelial Damage

Diseases and Diagnosis (25 decks)

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