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Veterinary Pathology I > Midterm I > Flashcards

Midterm I Flashcards

1
Q

What is the fundamental cause of necrotic cell death?

A

Depletion of ATP below 10%

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2
Q

What are the ways in which cells can be injured?

A
  1. Mitochondrial damage
  2. Depletion of ATP
  3. Influx of Ca+ and loss of Ca+ hemostasis
  4. Accumulation of free radicals
  5. Defects in membrane permeability
  6. Damage to DNA and proteins
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3
Q

What are the characteristics of irreversible cell injury?

A
  1. Inability to reverse mitochondrial dysfunction

2. Profound damage to membrane function

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4
Q

What are coagulation factors, where do they come from and what is their purpose?

A

Plasma proteins made by the liver which function to form fibrin

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5
Q

Hemostasis

A

The arrest of bleeding; mechanism to stop bleeding when a vessel is damaged

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6
Q

What does PT measure?

A

Stands for prothrombin time and measures the extrinsic and common coagulation pathway with fibrin being most important part of clot formation

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7
Q

What does PTT measure?

A

Stands for partial prothromboplastin time and measures the intrinsic and common coagulation pathway with results indicating there is a deficiency of a coagulation factor like in hemophila

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8
Q

Which coagulation factors are part of the extrinsic pathway and how is it activated?

A

7 and Tissue factor

Endothelial injury and release of TF

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9
Q

Which coagulation factors are part of the intrinsic pathway and how is it activated?

A

12, 11, 9, and 8

Platelets contacting the basement membran..aka collagen..during vasoconstriction

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10
Q

What are D-Dimers and what does this measurement tell us?

A

Cross-linked polymers produced as a result of accelerated hemostasis and breakdown of fibrin in a clot. If too high, indicate that there are too many clots being produced in body aka disseminated intravascular coagulation

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11
Q

What does prothrombin do and which coagulation pathway is it part of?

A

It activated thrombin within the common coagulation pathway..activated by factor 10

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12
Q

How is fibrin in a clot created?

A

Factor 10 stimulates prothrombin to activate thrombin which activated fibrinogen to make fibrin

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13
Q

What substance breaks down fibrin in a clot? How is it activated?

A

Plasmin

Plasminogen activated plasmin

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14
Q

What is disseminated intravascular coagulation?

A

A condition in which abnormal clots form inside vessels using up clotting factor which makes them unavailable in a part of the body that needs a clot to stop bleeding. Leads to clots everywhere and massive bleeding. Has many causes.

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15
Q

What is the buccal mucosal bleeding time and what do results tell us?

A

It is a measure of primary hemostasis and defeciency in von Willebrand factor. If this is normal, it means platelets are functioning normally with adequate von Willebrand’s factor needed for platelet plug to stick to wall

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16
Q

How do you perform a BMCT test?

A
  1. Lateral recumbency and lift upper lip with a gauze muzzle
  2. Using a lancet choose area free of blood vessels
  3. Depress into mucosa and remove
  4. Allow blood to bleed onto filter paper until it stops, count time..don’t directly touch incision.
  5. Make sure dog can’t taste blood and try to lick
  6. Normal is 1.5 to 4 min for dogs and 1.5 to 2.5 for cats
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17
Q

What is phytonadione and why would it be given if you suspect there is an issue with coagulation factors?

A

Vitamin K
It is needed to produce the factors involved in the intrinsic, extrinsic, and common coagulation pathways…2, 7, 9, 10. (I’m 27 and will die when i am 90)

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18
Q

If the animal was deficient in vitamin K, which tests would be affected?

A

PT and PTT

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19
Q

What three factors work together during hemostasis?

A
  1. The vessel wall with endothelial cells
  2. Platelets
  3. Coagulation System
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20
Q

What are some important antithrombotic mediators?

A
  1. Prostacyclin (PGI2)
  2. Nitric Oxide (NO)
  3. Heparin like molecules
  4. Thrombomodulin
  5. Tissue plasminogen activator (t-PA)
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21
Q

What are some important prothrombotic mediators?

A
  1. Von Willebrand’s factor
  2. Tissue Factor
  3. Plasminogen activator inhibitor-1
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22
Q

Which two mediators in hemostasis do you want to be present at all times? Why?

A
  1. Tissue plasminogen activator (t-PA): promotes fibrinolysis which breaks down fibrin, helps to accerlate the breakdown of clots
  2. Plasminogen activator inhibitor-1 (PAI-1): inhibits t-PA therby preventing fibrinolysis
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23
Q

What are the three reactions platelets go through during hemostasis?

A
  1. Adhesion and shape change
  2. Secretion
  3. Aggregation
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24
Q

What do platelets secrete after they have attached to the collagen of the subepithelium and sent pseudopods across the defect forming a plug?

A
  1. ADP: mediator of platelet aggregation
  2. Thromboxane A2: platelet aggregator and vasoconstrictor
  3. Fibrinogen: glue that sticks platelets together
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25
Q

Which part of hemostasis is reversible?

A

Primary

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26
Q

What is the term for when there are reduced platelets causing spontaneous bleeding throughout body ( but below 20,000 per L)

A

Thrombocytopenia

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27
Q

According to new research is it believe that __________ pathway of coagulation starts first and the __________ pathway amplyfies the reaction.

A

Extrinsic

Instrinsic

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28
Q

Which are coagulation factors affected by Vitamin K antagonists like warfarin?

A

2 (prothrombin), 7, 9 and 10

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29
Q

How does the coagulation cascade remain localized?

A

Antithrombin factors like Antithrombin III, protein C and S, and plasmin

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30
Q

Which measurement a is mainly concerned with primary hemostasis? Secondary?`

A

Buccal mucosal Bleeding time

PT and PTT

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31
Q

An animal appears to be bleeding from larger vessels (ecchymoses) and is hemorrhaging into body cavities. Or on the other side of spectrum, the animal has an increased risk of thrombus formation due to the hypercoagulative state from excessive production of thrombin. Which phase of hemostasis is likely malfunctioning?

A

Secondary

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32
Q

If there is a defect in primary hemostasis, what are we most likey to see clinically?

A

Hemorrhage from small blood vessels (petechiae) or overactive platelets/ increased von wilderbrand factor puts animal at higher risk for thrombus formation

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33
Q

What is another term for hemorrhage?

A

Extravasation

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34
Q

Hematoma

A

focal accumulation of blood in tissue

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35
Q

Hemarthrosis

A

blood in joint space

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36
Q

Hymobema

A

bleeding into eye

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37
Q

Hemopericardium

A

blood in the pericardial sac

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38
Q

Eptaxis

A

bleeding from the nose

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39
Q

Hemoptysis

A

coughing up blood from the respiratory tract

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40
Q

Melena

A

blood in stool that has been digested

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41
Q

Petechial hemorrhages or petechiae

A

small, pinpoint foci of hemorrhage up to 1-2mm usually seen on conjunctive, gums, and non-haired areas

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42
Q

Ecchymotic hemorrhages or ecchymoses

A

large hemorrhages up to 2-3 cm

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43
Q

Purpura

A

a lesion that includes petechiae, ecchymoses or both

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44
Q

How much blood can you lose before you go into hypovolemic shock or circulatory failure?

A

20-40%

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45
Q

If a small amount of blood is chronically lost, what occurs with the bone marrow and rest of body?

A

Bone marrow will not continue to respond with making more red blood cells which can lead to iron deficient anemia

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46
Q

What parts of a clot can be reabsorbed and what can’t?

A

The plasma can be reabsorbed but nothing else can be, must be broken down and recycled

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47
Q

How is a hematoma broken down?

A

Fibroblasts and endothelial cells invade a clot and create new vascular networks that bring macrophages, enzymes, plasmin, and other factors in to break down clot leaving hemosiderin from the macrophages.

48
Q

What are the causes of hemorrhage?

A
  1. Trauma: most common
  2. Damage to endothelial cells via viremia, septicemia, or toxemia through cytokines
  3. Disorders of coagulation
49
Q

How does sweet clover toxicity cause hemorrhage in cows?

A

It contains dicumarol which is a vitamin K antagonist> coagulation factors prothrombin, 7, 9 and 10 are not created.

50
Q

What is a thrombus?

A

The pathological counterpart of a blood clot formed under abnormal conditions.

51
Q

Whar are the causes of a thrombus?

A
  1. Endothelial injury (most important)
  2. Alterations to blood flow; either stasis or turbulence
  3. Hypercoagulability via platelet coagulation factors
52
Q

Whar are some problems associated with a thrombus?

A
  1. Ischemia

2. Embolism

53
Q

What is the difference between a thrombus and a clot?

A

A thrombus is more friable and attached to the endothelium while a clot is free and is more rubbery and smooth

54
Q

What differentiates an arterial thrombus from a venous thrombus besides the location?

A

Arterial is formed under high blood flow rate conditions doesnt occlude vessel right away, and contains mainly fibrin and platelets as the red blood cells are swept away leaving it white/gray and friable.
Venous is formed under slow blood flow rate conditions and accumulate all the elements of a blood clot, not as well attached but will occlude and more likely to become an embolism.

55
Q

What are examples of good fates of a thrombus?

A
  1. Dissolution via the fibrinolytic system
  2. Recanalization of an organized thrombus where macrophages and endothelial cells break up fibrin forming a new opening for blood flow
56
Q

What are examples of bad fates of a thrombus?

A
  1. Propagation where it enlarges in direction of heart until an embolism or occlusion occurs
  2. Embolization where a piece breaks off and moves downstream to a smaller vessel where is occludes and causes ischemia
57
Q

If tests in a patient abnormal levels of D-Dimers and FDPs, thrombocytopenia and prolonged coagulation, what disease process is most likely occuring?

A

Disseminated Intravascular Coagulation (DIC)

58
Q

How would you want to treat DIC?

A

Treat the underlying problem, but in the meantime:
If there is severe bleeding: Replacement platelet concentration, cryoprecipitate, and fresh frozen plasma
If it is slowly evolving: Heparin to initiate fibrinolysis and make clots smaller

59
Q

Embolism

A

detached intravascular mass carried by blood from original site to distant site

60
Q

What is it called when an embolism attaches to a wall and occuledes flow?

A

Thromboemboli

61
Q

What are the types of emboli we may encounter?

A
  1. Catheters
  2. Fat
  3. Bone marrow
  4. Neoplastic cells
  5. Clumps of bacteria or fungi
  6. Parasites
  7. Amniotic fluid
  8. Thrombus
62
Q

Which species suffers from saddle thrombus most and what caused it?

A

Cats
Left atrial thrombi traveled to the iliac bifurcation causing lameness, pain, cool temp, and no femoral pulse in pelvic limbs=bad prognosis

63
Q

Infarction

A

Focal area of ischemic necrosis in tissue/organ caused by occlusion

64
Q

If there is venous occlusion in loose tissue such as the spleen or liver or tissue with double circulation, what type of infarct is most likely?

A

Red/hemorrhagic because blood pools in the organs

65
Q

If there is a white/anemic infarct in a tissue, what probably caused it?

A

Arterial occlusion in a solid organ like the kidney or heart because blood is not getting to the area.

66
Q

What does an infarct usually look like beside the white/pale or red/hemorrhagic appearance?

A
  1. Wedge-shaped with apex pointing toward occluded vessel
  2. Coagulation necrosis
  3. Well defined margins within 24 hours
  4. Hyperemia/inflammation at margins
  5. Scar tissue replaces after a long time
67
Q

Hyperemia and Congestion

A

Increased volume of blood in tissue with blood still in vessels

68
Q

Active Hyperemia

A

Active, arteriole or arteriole mediated process where dilated vessels bring increased blood flow to area

69
Q

What are the two types of active hyperemia?

A

Physiologic: increased blood flow to muscles during exercise, face when blushing, or at necropsy when blood pools on lower side of body
Pathological: Inflammation

70
Q

What are the different types of passive congestion?

A
  1. Acute, local
  2. Chronic, local
  3. Chronic, generalized
71
Q

Passive congestion

A

Occurs when there is impaired venous drainage

72
Q

What occurs during right-sided heart failure in the context of passive congestion of blood?

A

It is a chronic, generalized type, Usually, there is either pulmonic stenosis or tricuspid insufficiency which causes blood to back up into vena cava and into the liver. This dilates the central veins, causes hypoxia, atrophy, and loss of hepatocytes with dilation of sinusoids =nutmeg liver

73
Q

If a dog is suffering from a chronic, generalized passive congestion problem affecting the lungs, what is likely going on?

A

Left-sided heart failure either due to aortic stenosis or mitral valve insufficiency.The blood backs up into the left atrium and pulmonary veins where it increases the hydrostatic pressure in lungs. This causes them to become wet and edematous which causes capillaries to rupture and the RBCs release to be phagocytized by macrophages creating heart failure cells

74
Q

What are some examples of chronic, local passive congestions?

A
  1. Tumors/abscess compressing veins
  2. Cirrhosis of liver compressing hepatic vein
  3. Thrombus occluding vein slowly
75
Q

What are some examples of acute, local passive congestions?

A

Equine colic where intestine has torsed causing strangulation from venous pressure.
Any time a vein is obstructed in a tissue

76
Q

Anasarca

A

Generalized, severe, subcutaneous edema

77
Q

What conditions could cause a globoid heart shape on a radiograph?

A
  1. Hydropericardium

2. Hemopericardium

78
Q

What are the four main causes of edema?

A
  1. Increased hydrostatic pressure due to increased volume of blood in vessels
  2. Reduced plasma oncotic pressure due to hypoproteinemia (albumin)
  3. Decreased lymphatic drainage
  4. Increased permeability of vessels from endothelial cells separating from each other
79
Q

In what ways could hydrostatic pressure in vessels increase?

A
  1. Increased IV overload
  2. Congestive heart failure
  3. Venous thrombosis
  4. Sodium retention
80
Q

In what ways could plasma oncotic pressure decrease?

A
  1. Chronic blood loss (loss of proteins) via parasitism
  2. Nephrotic syndrome-loss of albumin from glomerular damage in kidneys
  3. Protein loss from intestinal neoplasia or inflammation-diarrhea and weight loss
  4. Poor diet low in protein
  5. Poor absorption of protein in GI tract
  6. Severe liver damage causing low production of albumin
81
Q

What does edema look like grossly?

A

Swollen, pitted when pressed, cool temp, and can ooze heavy clear or yellow fluid

82
Q

What does edema look like histologically?

A

Pale/eosinophilic fluid causing separation of tissue

83
Q

What are the four types of shock?

A
  1. Hypovolemic
  2. Septic
  3. Cardiogenic
  4. Neurogenic
84
Q

If wild animals are extremely stressed while being captured, what type of shock would they most likely suffer from?

A

Neurogenic

85
Q

What are some examples of cardiogenic shock?

A
  1. Myocardial infarction
  2. Pulmonary embolism
  3. Heart rupture
  4. Cardiac tamponade
86
Q

What types of bacteria usually cause septic shock?

A

Gram negative from releasing endotoxins

Gram positive from releasing exotoxins

87
Q

What is the first thing you do if a patient is going into hypovolemic shock?

A

Place an IV and give fluids to increase blood volume and blood pressure. If you can’t get it in vein , go intra-osseus or intra-abdominal.

88
Q

Shock

A

Peripheral circulatory failure with inadequate perfusion of tissues

89
Q

What are the clinical signs of shock?

A
  1. Increased HR and RR
  2. Weak pulse
  3. Cool skin
  4. Pale mucous membranes
  5. Increased capillary refill time
  6. Mental confusion to unresponsivness
90
Q

Which organs are most likely to be affected by hypoxia during shock?

A
  1. Brain
  2. Heart
  3. Lungs
  4. GI tract
  5. Adrenal glands
  6. Kidneys
91
Q

What induces secondary renal hyperparathyroidism and hypercalcemia with parathyroid hypertrophy? What condition can this cause?

A

Retention of phosphates in the kidney
Osteodystrophy and Ca deposits in the GI mucosa, kidney, and alveolar septa ( places where acid/base transitions occur and pleural surfaces)..metestatic calcification

92
Q

Enterolith

A

Mineral concentration or calculus formed around a foreign object in the GI system.

93
Q

If an animal ingested a carcinogenic plant or cholecalciferol ( stuff in rodenticide), what type of mineralization would we see?

A

Metastatic

94
Q

Who is a badass?

A

YOU are a badass!

95
Q

A geriatric cow has mineral deposits with degeneration of the extracellular matrix, what type of deposition is this?

A

Dystrophic

96
Q

What type of mineralization is caused by Vitamin D toxicosis?

A

Metastatic

97
Q

What are common sites of dystrophic mineralization?

A
  1. Myocardium
  2. Skeletal muscle
  3. Granulomas
  4. Dead parasites
98
Q

What is going on during splenic capsular siderocalcinosis?

A

The spleen will be black, it looks like shit, but apparantly it isn’t hurting the animal. It is an example of dystrophic calcification where iron salts get crazy and hemosiderin and sometimes hematoidin hangs out. Thought ot be caused by age and minor hemmorhage.

99
Q

After an animal dies, what will you see first to last as minutes turn into hours in the context of cell injury?

A

Biochemical alterations-Ultrastructural changes-Light microscope changes-Gross morphological changes

100
Q

When a cell is injured and swelling occurs, what is the best way to tell histologically if the cell is filling with water or lipids?

A

Lipid vacuoles will be well-demarcated and water vacuoles will not be.

101
Q

When we see water swelling in a cell, what is likely the main dysfunction causing it to occur?

A

Energy dependent ion pumps in the cell membrane have failed causing ionic fluid imbalances

102
Q

When we see lipid swelling in a cell, what is likely the main dysfunction causing it to occur?

A

Toxic or metabolic injury

103
Q

Oncosis

A

Cell injury with swelling (acute)

104
Q

What are the four main changes at the ultrastructural level that occur during cell swelling?

A
  1. Plasma membrane alteration
  2. Mitochondrial changes
  3. Dilation of ER
  4. Chromatin alterations
105
Q

During oncotic necrosis, which two tests can help us detect if there is liver damage or skeletal injury? Will these tests help with apoptosis (atrophy of cells)?

A

ALT=liver damage
Creatine Kinase
No, because plasma membrane still intact

106
Q

Karyolysis

A

Nucleus will lyse and disappear and occurs mainly in oncotic necrosis

107
Q

Pyknosis

A

Nucleus shrinks and condenses becoming very basophilic and occurs mainly in oncotic necrosis

108
Q

Karyorrhexis

A

Nucleus is broken into fragments and occurs mainly during apoptosis

109
Q

At the end of oncotic necrosis, what is left in place of the cell?

A

Myelin bodies that may calcify (dystrophic) or become degraded/phagocytized

110
Q

If you are asked to give the etiology, what will you say?

A

You will talk about the precise agent/insult that is causing whatever problem you are seeing. Ex. Equine herpes virus 1

111
Q

If you are asked to give the etiological diagnosis, what will you give?

A

You will talk about the precise agent/insult that is causing the problem and what process is going on to cause the problem. Ex. bacterial hepatitis

112
Q

As far as giving a gross morphological description to an organ, when would we call something chronic?

A

Longer than 7-10 days with evidence of fibrosis and/or granulomatous inflammation and/or hypertorphy or atrophy

113
Q

What are some markers for acute disease when looking at gross specimens?

A

Suppurative inflammation (pus) and hemmorhage

114
Q

What is the main difference between calling a lesion diffuse or disseminated?

A

A diffuse lesion will be affecting the WHOLE organ while disseminated means the whole organ is affected EXCEPT FOR the parenchyma.

115
Q

What would you call an inflamed cecum?

A

Typhlitis

Veterinary Pathology I (3 decks)

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