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My RUSVM Path 1 > deck_4797640 > Flashcards

deck_4797640 Flashcards

1
Q

What is miasma theory?

A

One of the first theories re: pathology, prevalent in medieval Europe, India and China. “Bad air” causes diseases such as cholera, chlamydia and black death.

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2
Q

What is the significance of Koch’s postulates?

A

Identifies the specific causative agents of tuberculosis, cholera and anthrax. Gave experimental support for the concept of infectious disease.

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3
Q

Definition of etiology

A
  1. the study or theory of the factors that cause disease and the method of their introduction to the host2. the causes or origin of a disease or disorder
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4
Q

What are the 2 major classes of factors causing disease?

A
  1. Genetic- inherited mutations and disease-associated gene variants or polymorphisms. More and more idiopathic diseases are being discovered to be genetic. 2. Acquired- infectious, nutritional, chemical, physical
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5
Q

What does an asymmetrical brain lesion indicate?

A

It is not systemic, didn’t come through the blood stream

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6
Q

Leuko- vs. polio-

A

White matter vs Grey matter

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7
Q

Encephalo- vs. myelo-

A

head vs spinal cord

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8
Q

Pathognomic lesion definition

A

A lesion that is typical for a certain agent

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9
Q

How many words does an etiological diagnosis have?

A

Two words. e.g. Cryptococcal encephalitis, traumatic fractures, etc.

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10
Q

What is a classical infectious disease and some examples

A

Infectious disease with one etiological agent and one disease (e.g. anthrax caused by bacillus anthracis, rabies caused by rabies virus)

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11
Q

Classical genetic disease definition and examples

A

Single gene disorder –> one inherited diseasePKD 1 gene –> polycystic kidney disease, osteogenesis imperfecta, spider lamb chondrodysplasia)

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12
Q

What is the difference between primary and secondary vitamin deficiency?

A

Primary vitamin deficiency- animal isn’t ingesting itSecondary vitamin deficiency- Anything else that prevents the vitamin from getting to the tissues and having effect, e.g. animal is ingesting it but there is some factor antagonizing its actions or there is malabsorption of the vitamin or the disease isn’t being processed correctly.

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13
Q

What is an example of One etiological agent –> Multiple diseases

A

Vitamin E deficiency (and excess intakes of polyunsaturated fatty acids, because these antagonize Vitamin E) can cause tons of different diseases any many different species.

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14
Q

EDx and MDx of this lesion? How would this happen?

A

EDx: Traumatic fractureMDx: Ventral fracturesFractured skull of a horse and fractured scapula of a horse.This can happen if they fall back and hit their head on a wall. Bleeding within the cranial cavity results in more severe and quicker changes because of space available

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15
Q

Description of lesionEtiology and method of diagnosisEDx

A

Description: Cavitational lesions, bilateral asymmetrical (pathognomonic lesion for EDx). Thalamus, cerebellum and mesencephalon of a cat shown intransverse sections.Etiology and method of diagnosis: Cryptococcus neoformans found by histopathEDx: Cryptococcal encephalitis

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16
Q

What is malasia?

A

Necrotic brain tissue

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17
Q

Lesion description:Dx:Etiology:

A

Lesion description: Spine of suffolk lamb, longitudinal section. Multiple disorganized ossification centered resulting in variation of the size, shape and orientation of the vertebrae.Dx: Spider lamb chondrodysplasiaEtiology: Single base change in the tyrosine kinase II domain of FGFR3

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18
Q

Lesion description:MDx:Dx:Etiology:

A

Description: Grossly diffuse, non-homogeneous- pink, red, black and greyish color. Histopath- central and mid-zonal areas are hemorrhagic and the hepatocytes that are being replaced are necrosing. The border cells are the functioning ones. Not a true hepatitis bc there is not an excessive amount of inflammatory cells on histopath.MDx: Diffuse hepatocellular necrosis and hemorrhageDx: Hepatosis dietetica (nutritional hepatic necrosis)Etiology: Deficiency of Vitamin E and/or Selenium

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19
Q

Description of lesion:Dx:Causes:

A

Description of lesion: Focal gastric ulcer with some hemorrhage in the stratified squamous epithelium is surrounding the cardia (pars esophagea) of the stomach of a pig.Dx: Gastric ulcer (pars esophagea), aka ulcerative/necrotizing gastritisCauses: Ingestion of finely ground grain or pelleted feed (possibly deficient in vitamin E). Fermentation of sugars in the feed (increases acidity). Stress of confinement rearing (common bc pigs lower in hierarchy are stressed). Helicobacter pylori overgrowth. Common in growing pigs.

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20
Q

Definition of ulcer

A

An ulcer is a deep necrotizing lesion in a tubular organ. When more superficial, it is called erosion.

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21
Q

What causes of death lead to fulminating pulmonary edema in animals? Why?

A

Sepsis, Toxemia, Aspiration of gastric contents, PancreatitisAll –> hyperreactive macrophages –> directly or idirectly generate overwhelming amounts of cytokines –> some cytokines prime neutrophils stationed in the lung capillaries –> release of enzymes and free radicals –> diffuse endothelial and alveolar damage –> pulmonary edemaSyndrome analogous to ARDS/ shock lung (acute/adult respiratory distress syndrome) in humans

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22
Q

What are some examples of autoimmune diseases that are caused bymultifactorial diseases?

A

Systemic lupus erythematosusType III hypersensitivity

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23
Q

What is the difference between having multiple etiologies and multiple factors? Give anexamples of each.

A

Multiple etiologies: Bovine respiratory disease complex. Can be caused by pneumonic mannheirniosis (Mannheimia haemolytica), respiratory histophilosis (Histophilus somni), etc.Can also have multiple steps (first stage primary agents and second stage opportunistic bacteria)Multiple factors: Pneumonias of pigs. Factors include host, infectious agents, environmental determinants, mgmt practices, etc.

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24
Q

What are the 5 main types of pathological processes?

A
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25
Q

What are the 8 main types of etiologies?

A
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26
Q

Description of lesion:Dx:

A

Description of lesion: Squamous metaplasia of the esophagus of a parrot. The raised white plaques are keratin.Dx: Avitaminosis A (a type of disease of adaptation, degeneration and cell death)

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27
Q

Dx if inflammatory cells are found on histology:Etiology:

A

Dx: Embolic nephritis (kidney of horse) (a type of disease of inflammation and repair)(Embolic means a descending type of infection coming from the blood stream. Initially goes in the cortex)Etiology: Caused by Actinobacillus equuli

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28
Q

MDx:Etiology:

A

MDx: Congenital porphyria of cow bone (a type of tissue deposit/pigmentation)Etiology: Defect in heme synthesis caused by a deficiency in uroporphyrinogen III cosynthetase

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29
Q

Dx:Causes:

A

Dx: Chronic passive congestion (nutmeg liver) of liver of a cow (a type of circulatory disorder)Causes: right sided heart failure, ingestion of hepatotoxin (i.e. Wedelia glauca, etc.)

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30
Q

Dx:Etiology:

A

Dx: Globoid cell leukodystrophy of a dog (a type of Lysosomal storage disease, type of genetic disorder)Etiology: Defect in an enzyme (galactosylceraminidase)

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31
Q

MDx:Etiology:

A

MDx: Acute allergic rhinitis with secondary plant foreign body (disease of immunity, lupus is also an example of this)Etiology: Type I hypersensitivity reaction- plant allergen

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32
Q

Dx:Etiology:

A

Dx: Bovine abomasal lymphoma (type of neoplasia)Etiology: Bovine leukemia virus

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33
Q

Dx:Etiology:

A

Dx: Epithelial plaques, papular stomatitis of the hard palate mucosa of a calf (type of microbial infection)Etiology: Parapoxvirus

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34
Q

What is the DAMNIT-V scheme?

A
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35
Q

What are idiopathic diseases? Name some examples.

A

Diseases of unknown cause or spontaneous originEpilepsy, hypertrophic cardiomyopathy, renal amyloidosis, canine polyarteritis, pulmonary fibrosis, laryngeal hemiplasia

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36
Q

Define cell adaptation and give examples.

A

Occurs when the cell homeostasis is distorted by stresses or pathologic stimuli. The cell is not dead, just morphologically different from the normal cell. Can return to normal morphology and homeostasis when the stress is removed.Cells preserve viability and function.Reversible change!Principles responses of adaptation are: atrophy, hypertrophy, hyperplasia, metaplasia

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37
Q

Define homeostasis

A

Tendency to stabilize the normal body states of the organism;it is the ability to maintain internal equilibrium by adjusting its physiological processes

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38
Q

Define and give causes and examples of atrophy

A

Decrease in size and/or number of the cells and their metabolic activity after normal growth has been reached. Remember, cells are not dead. They are still functioning, just smaller.Decreases protein synthesis and increases protein degradationCauses: decreased workload, denervation (e.g. recurrent laryngeal nerve denervation –>laryngeal atrophy), decreased blood supply or oxygen, inadequate nutrition, loss of endocrine stimulation, agingExamples: muscle disuse of limb in cast, sedentary atrophy, adrenal cortex atrophy by reduction of ACTH stimulation (steroid therapy), atrophy in tissues adjacent to a tumor due to pressure and compromised blood supply, physiologic atrophy (e.g. non-lactating mammary gland atrophy), serous atrophy of heart or bone marrow(lack of fat, dilated lymphatics)

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39
Q

What type of cell adaptation is caused by panleukopenia?

A

Hydrocephalus with compression atrophy of a cat can be caused by intrauterine infection of panleukopenia.

40
Q

Define hypertrophy.What type of cells get this?

A

Hypertrophy is increased size of cells and their functions. Synthesis of more organelles and structural proteins–> bigger cells.More common in cell with little or no replication, stable or permanent cells such as cardiomyocytes and neurons.

41
Q

Examples of physiologichypertrophy

A

Hypertrophic pregnant uterusWeightlifter with hypertrophic muscle cells

42
Q

Most important exampleand etiologies of pathologic hypertrophy

A

Cardiac hypertrophy beyond the limit that it can keep up with the burdencan lead to regressive changes (lysis and loss of contractile elements)and ultimately cell death and cardiac failure in extreme cases. This is an example of how adaptation to stress can progress to functionally significant cell injury if the stress is not relieved. Concentric when walls grow inward (reduction of chamber size), eccentric when they grow outward. Haphazardly arranged cells on histopath, can even have fat or fiber replace muscle cells in extreme cases.Etiologies of cardiac hypertrophy:Aortic valve disease, hypertension, Genetic mutation (e.g. Main Coon cat)

43
Q

Define hyperplasia. What type of cells does this occur in?

A

Increase in number of cells of an organ. An enlarged organ can be differentiated as hyperplastic or hypertrophic by histology.Occurs in cells capable of replication, e.g. lymph tissue, skin, etc.Hyperplastic nodules are usually irreversible and have no proper function.

44
Q

What are some examples or physiologic and pathogenic hyperplasia?

A

Physiologic hyperplasia- Hormonal (breast growth during pregnancy) or compensatory (post-hepatectomy liver growth)Pathologic hyperplasia- most commonly caused by excessive hormonal or growth factor stimulation, e.g. epidermal thickening (repeated irritation) or respiratory mucosa (in viral infections), fibrous hyperplasia (MDx) of gingiva

45
Q

Define metaplasia

A

Change in phenotype of a differentiated cell. Response to chronic irritation –> cell withstand stress. May result in decreased functions or increased propensity for malignant transformation (neoplasia). Reversible if cause is removed! Most often in epithelial cells.

46
Q

Examples of metaplasia

A

Chronic irritation in lungs (smokers)Vitamin A deficiencyEstrogen toxicityMammary tumors

47
Q

Define dysplasia

A

Refers to abnormal development, mostly of epithelial cells. Term is mostly used in neoplastic processes, near-synonym but not as advanced as”carcinoma in situ.” It is in between metaplasia and neoplasia.

48
Q

MDx:

A

Nephrolith (xanthinuria) with hydronephrosis, cortical and medullary atrophy and medullary fibrosis, diffuse

49
Q

MDx: (right and left are different)Dx:

A

MDx: Skin, hyperplasia on the right, dysplasia on the leftDx: Squamous cell carcinoma in situ of a female DSH cat

50
Q

MDx:Etiology:

A

MDx: Gastric hypertrophy of a snake. (histology needed to differentiate it from hyperplasia)Etiology: Cryptosporidium

51
Q

Lesion description:MDx:

A

Lesion description:whitish, multifocal nodular areasof a feline stomachMDx: Gastric lymphoid hyperplasia

52
Q

MDx:

A

MDx: Hepatocellular carcinoma with nodular hyperplasia, dog

53
Q

MDx 1:MDx 2:Etiology

A

MDx 1: Hydronephrosis with secondary diffuse cortical atrophyMDx 2: HydroureterEtiology: Ureteral obstruction

54
Q

MDx:Associated cell adaptation:

A

MDx: Cystic renal disease, akaPolycystic kidney diseaseAssociated cell adaptation: atrophy

55
Q

Show how reversible and irreversible cell injuries progress.

A
56
Q

What are some morphological correlates with reversible and irreversible cell injury?

A

Reversible cell injury: cellular swelling, fatty changes (lipidosis)Irreversible cell injury: necrosis, apoptosis, other types of cell death

57
Q

Define acute cell swelling and give some alternate names for it.

A

aka hydropic degeneration, hydropic change, cytotoxic edema (CNS), ballooning degeneration (epidermis)Definition: Early, reversible, sub-lethal manifestation of cell damage, characterized by increased cell size and volume due to water overload. Most common and fundamental expression of cell injury. Mitochondria and ER are the organelles that can dilate to hold extra water and when they can’t hold any more is when it goes from reversible to irreversible.

58
Q

Which types of cells are highly vulnerable to hypoxia and cell swelling? Which ones are not sensitive to hypoxia?

A

Highly vulnerable:Cardiomyocytes, proximal renal tubule epithelium, hepatocytes, endothelium, CNS neurons, oligodendrocytes and astrocytes (cytotoxic edema)Not sensitive: adipose, bone, skeletal muscle, CT

59
Q

What is the etiology of acute cell swelling?

A

Loss of ionic and fluid homeostasis. Loss of water and ion transport across the cell membrane, mainly sodium.Failure of cell energy production, cell membrane damage, injury to enzymes regulating ion channels of membranes.E.g. Mostly from hypoxia and toxic agents! Can also be due to physical mechanical injury, free radicals, viruses, bacteria or immune-mediated injury

60
Q

What is the pathogenesis of acute cell swelling?

A
61
Q

What are some gross characteristics of acute cell swelling?

A

Slightly swollen organ with rounded edgesPallor when compared to normalCut surface: tissue bulges and cannot be easily put in correct positionSlightly heavy (“wetorgan”)

62
Q

What does cellular swelling look like histologically?

A

H2O uptake dilutes the cytoplasm, so cells are enlarged with pale cytoplasm.May show increased cytoplasmic eosinophilia.Nucleus is in normal position with no morphological changes- this is important!It can be difficult to appreciate with the light microscope though.

63
Q

What is this pathognomonic lesion?What is its etiology?What does it look like histologically?

A

Ballooning degeneration of epidermis resulting in vesicle formation (bullae/blister)- it is an extreme variation of hydropic degeneration.Histo is seen in picture on the right. On the left is its avian counterpart.Etiology: vesicular exanthema of swine virus, a calcivirus (vesivirus) on the snout of a pig

64
Q

What are the ultrastructural changes of cellular swelling?

A

All changes start at the outside and move toward the center of the cell.1. Plasma membrane alterations, such as blebbing, blunting and loss of microvilli.2. Mitochondrial changes, including swelling and the appearance of small, amorphous densities3. Dilation of the ER, with detachment of polysomes; intracytoplasmic myelin figures may be present.4. Nuclear alterations, with disaggregation of granular and fibrillar elements.

65
Q

What is the difference in definition of cell swelling and cell enlargement? What are the proper terms for each?

A

Cell swelling- Hydropic change, fatty change. Due to increased uptake of H2O and then to diffuse disintegration of organelles and cytoplasmic proteins.Cell enlargement- Hypertrophy. Caused by increase of normal organelles.

66
Q

What is the prognosis of cellular swelling?

A

It depends on the number of cells affected and importance of cellsGood prognosis if oxygen is restored before the point of no return. Poor prognosis if the hypoxia progresses to irreversible cell injury.

67
Q

What is the discoloration shown in this figure?

A

Lipofuscin- aka wear and tear pigmentEvidence of a previous injury (e.g. neuron)

68
Q

What is the definition of a fatty change?

A

Sub-lethal cell damage characterized by intracytoplasmic fatty vacuolation. It may be preceded or accompanied by cell swelling (difficult to differentiate the 2 by microscopy).All major classes of lipids can accumulate in cells (e.g. triglycerides, cholesterol (esters), phospholipids, abnormal lipid-carb complexes (lysosomal storage disease), etc.

69
Q

What is lipidosis?What type of cells does it occur in?What is its prototype and its clinical manifestations?

A

Accumulation of triglycerides and other lipid metabolites (neutral fats and cholesterol) within parenchymal cells (e.g. liver, heart muscle, skeletal muscle, kidney)Hepatic lipidosis- prototype. Clinical manifestations are usually alterations in function (elevated liver enzymes, icterus) bc liver is central to lipid metabolism.

70
Q

What is the etiology of a fatty change?

A

Main causes: chronic hypoxia (e.g. clot, pneumonia, high altitude, anemia, chronic heart failure), toxicity, metabolic disordersSeen in abnormalities of synthesis, utilization and/or mobilization of fat

71
Q

What is the pathogenesis of fatty change?

A

Impaired metabolism of fatty acids –> accumulation of triglycerides –> formation of intracytoplasmic fat vacuoles

72
Q

Describe the gross appearance of fatty change, specifically to the liver.

A

Hepatic lipidosis is aka fatty liver, fatty change, hepatic steatosisDiffuse yellow if all cells affected.Enhanced reticular pattern if only some cells affected.Edges are rounded and will bulge on section.Tissue is soft, often friable, greasy and cuts easily. Some sections may float in liquid if disease is severe.

73
Q

When does physiologic hepatic lipidosis occur?

A

In late pregnancy (pregnancy toxemia) and heavy early lactation (ketosis) in ruminants

74
Q

What are some pathologic etiologies of hepatic lipidosis?

A

Nutritional disorders- obesity, protein-calorie malnutrition (impaired apolipoprotein synthesis), starvation (increased mobilization of triglycerides)Endocrine diseases- diabetes mellitus (increased mobilization of triglycerides), feline fatty liver syndrome, fat cow syndrome (unknown cause)Neimann Pick disease (phospholipid sphingomyelin)- a lysosomal storage disease)

75
Q

Describe the histological appearance of fatty change.

A

Well delineated, lipid-filled vacuoles in cytoplasm. Vacuoles vary in quantity or size and may displace the nucleus to the periphery of the cell.

76
Q

What is the prognosis of fatty change, hepatic lipidosis specifically?

A

Initially reversible, but can lead to irreversible hepatocyte death.ID and tx of predisposing diseases and aggressive nutritional support is required for therapy of hepatic lipidosis. Oral appetite stimulants can be given but are usually inadequate alone. Mortality is high without treatment.Most often seen in cats secondary to anorexia, can also be seen in mini horses, ruminants and camelids.

77
Q

What are some indicators of irreversible injury by fatty change?

A

Severe swelling of mitochondriaExtensive damage to plasma membranes (gives rise to myelin figures)Excessive swelling of lysosomes and vacuolesHappens to myocardium 30-40 mins after ischemia. Cell death mainly occurs by necrosis, but sometimes apoptosis.Necrotic change is seen ultrastructurally in less than 6 hours, histologically in 6-12 hours and grossly in 24-48 hours.

78
Q

What are the similarities anddifferences between karyolysis, pyknosis and karyorrhexis?

A
79
Q

What is the gross appearance of necrosis?

A

Pale, soft, friable and sharply demarcated from viable tissue by a zone of inflammation.

80
Q

(Turkey)MDx:Etiology:Dx:

A

(Turkey)MDx: Hepatitis, multifocal to coalescing, subacute, severe necrosis. Reddish in center (non-functional, blood vessel dies resulting in leakage on the inside of the circles) and whitish around borders (functional and spreading)Etiology: Histomonas meleagridisDx: Blackhead disease

81
Q

What are some light microscopy changes of necrotic cells in cytoplasm (cause and effect)?

A

Denatured proteins –> increased binding of eosin (pink)Loss of RNA –> Loss of basophiliaLoss of glycogen particles –> Glassy homogeneousEnzyme-digested cytoplasm organelles –> Vacuolation and moth-eaten appearanceCalcification can be seen

82
Q

What is the significance of patterns of tissue necrosis?

A

May provide clues about the underlying causeDo not reflect underlying mechanisms but are used by pathologists and clinicians.

83
Q

Define and show gross characteristics of coagulative necrosis.What causes this and what tissues does it occur in?

A

e.g. infarcts, nutritional myopathyCommon cause: ISCHEMIA (reduced blood perfusion)in all solid organs except the brainArchitecture of dead tissue is preserved up to several days.Ultimately necrotic cells are removed by phagocytosis by WBCs and by digestion by lysosomal enzymes of WBCs.Infarcts shown in pictures. They are usually caused by obstruction or obliteration of blood vessel. Turn red, then white. Wedge/triangle shaped. Often acute necrosis.

84
Q

What does coagulation necrosis look like on cytology?

A
85
Q

What type of necrosis is associated with Vitamin E/ selenium deficiency?What does this look like grossly and on cytology?

A

Vitamin E/ selenium (antioxidant)deficiency causes Nutritional myopathy aka white muscle disease.Grossly, heart in picture has locally extensive nutritional muscular degeneration and (coagulative) necrosis. White streaks alternating with muscle color. Loses muscle striation, becomes large and fragmented.Cytologically, skeletal muscle shows degeneration and (coagulative)necrosis. The area in the highlighted circle has blood supply cut off so will appear white grossly.

86
Q

How is liquefactive necrosis characterized?What types of tissues does this usually occur in?

A

Necrotic architecture is liquefied. Dead cells are digested –> transformation of the tissue into a liquid viscous mass.Typically in CNS!Abscess is in this categorybc under cytology, tissue is unrecognizable, you only see inflammatory cells, bacteria, etc.Occurs in: tissue with high neutrophil recruitment and enzymatic release with digestion of tissue, tissues with high lipid content, focal bacteria and occasionally fungal infections. Microbes stimulate the accumulation of WBCs (including neutrophils) and the liberation enzymes from these cells.Neutrophils cause collateral damage bc just attackwhatever’s there.

87
Q

(Sheep, brain stem)MDx:

A

Bilateral symmetrical encephalomalaciaAreas with arrows are affected. Matter is missing so necrosis. Necrosis in CNS is always called malacia, which is a type of liquefactive necrosis.

88
Q

(Horse)MDx:Etiology:EDx:

A

MDx: Multifocal necrohemorrhagic leukomyelitisEtiology: Sarcocystic neuronaEDx: Sarcocystic leukomyelitis

89
Q

(Horse)MDx:EDx:DDx:

A

(Horse)MDx: Multifocal hemorrhagic poliomyelitisEDx: Viral poliomyelitisDDx: Equine herpesvirus 1Rabies (Lyssavirus)West Nile virus (Flavivirus)

90
Q

(Sheep)Dx:Causes:

A

(Sheep)Dx: Polioencephalomalacia

91
Q

GoatDx:Type of necrosis:

A

GoatDx: Pituitary gland abscessLiquefactive necrosis (usually abscesses are surrounded by a CT membrane, but not in brain because brain doesn’t have CT)

92
Q

Define AbscessWhat are the 2 types of Abscess?

A
93
Q

Describe and show histology of liquefactive necrosis.

A
94
Q

Define gangrenous necrosis.What type of tissue does it occur on?2 types?

A

Gangrenous necrosis is not a specific pattern of cell death but begins mostly as coagulative necrosis (likely due to ischemia).Usually used in reference to distal extremities (toes, udder, ear, pinna) and involves multiple planed of tissue.Dry gangrene- no bacterial superinfection, appears dry.Wet gangrene- bacterial superinfection has occurred, tissue appears liquefactive by actions of degradative enzymes in the bacteria and attracted WBCs.

95
Q

Define caseous necrosis.Name some possible causes.

A

(Cottage) cheese-like.Friable (crumble) white. Necrotic debris represents dead WBCs.Possible causes include myco-, coryne-, fuso- bacterium and fungal infections.

96
Q

What type of necrosis is shown here?

A

Caseous necrosis

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