General Pathology Exam 3

Front 1

What are some kinds of labile cells?

Back 1

Hematopoietic, lymphoid, mucosal, epithelial, and epidermal cells

Front 2

What are some kinds of stable cells?

Back 2

Parenchymal, glandular, mesenchymal, and

endothelial cells

Front 3

What are some kinds of permanent cells?

Back 3

Neurons, cardiac muscle, and skeletal muscle

Front 4

What are some factors that assist with

regulation of the size of cell populations?

Back 4

-Rate of proliferation

-Rate of differentation

-Rate of cell death (apoptosis)

-Stem cells (embryonic or adult)

---tissue, hematopoietic, BM stromal, or

multipotent progenitor cells

Front 5

What are growth factors?

Back 5

Soluble peptides secreted by mature cells

Front 6

Growth factors have roles in which processes?

Back 6

-Embryonal and fetal development

-Adaptive growth responses

-Tissue repair (regeneration, fibrosis)

-Neoplasia

Front 7

Growth factors generally act locally or

systemically?

Back 7

Locally

Front 8

Growth factors have specific receptors on what?

Back 8

Target cells

Front 9

What is the most important factor that regulates how big a tissue or organ gets?

Back 9

The rate of cell death (apoptosis)

Front 10

Do many tissues have stem cells in them?

Back 10

Yep. That helps them to turnover. They go from stem cells to some degree of differentiation then continue to proliferate and turnover and can

further differentiate.

Front 11

______ stem cells are pluripotential cells

Back 11

Embryonic

Front 12

What are 4 different categories of adult stem cells?

Back 12

-Tissue (remain in each organ for turnover)

-Hematopoietic

-Bone marrow stromal (become fibroblasts, chondroblasts, osteoblasts, etc.)

-Multipotent progenitor

Front 13

Which family of growth factors also has
inhibitory effects on proliferation of cells?

Back 13

Transforming growth factor-beta

Front 14

Do growth factors influence differentiation of cells?

Back 14

Yep.

Front 15

What do proto-oncogenes encode for?

Back 15

Growth factors, growth factor receptors, or

signal transduction proteins or enzymes

Front 16

Oncogenes are genes involved in what?

Back 16

Neoplasia

Front 17

What are two major points for cell cycle

regulation that are key points for cyclins, CdKs, CdK inhibitors, and surveillance mechanisms to sense DNA damage

Back 17

-G1/S checkpoint (check for DNA damage)

-G2/M checkpoint (check for damaged or

unduplicated DNA)

They just want to check that everything is

"hunky dory" at these points

Front 18

What are some other factors affecting cell

proliferation?

Back 18

-Chalones

-Cytokines

-Nervous and endocrine input

-Extracellular matrix

-Certain viruses or toxins

Front 19

What is cell differentiation?

Back 19

Genetic "commitment" to specialized functions

Front 20

What do cyclins influence?

Back 20

Cyclin-dependent kinases (CdKs)

Front 21

What are some things that help with regulation of cell differentiation?

Back 21

-Growth factors

-Extracellular matrix

-Nervous and endocrine influences

-Injury associated factors (inflammatory

cytokines, viruses, toxins)

Front 22

What are some examples of different

developmental defects?

Back 22

Agenesis, aplasia, hypoplasia, dysplasia

Front 23

What are chalones?

Back 23

Inhibitory peptides that are analogous to growth factors and are inhibitory to the protein that makes them

Front 24

What are some cytokines that affect cell

proliferation?

Back 24

IL-6, TNF

Front 25

How do the nervous and endocrine systems

affect cell proliferation?

Back 25

They have nutritive effects on their target cells

Front 26

How can the ECM affect cell proliferation?

Back 26

It is the medium that holds soluble growth

factors (chalones, cytokines) and provides a scaffold for cellular migration

Front 27

What are some adaptive growth responses?

Back 27

Atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia

Front 28

Do the same factors impact cell differentiation as those that impact cell proliferation?

Back 28

Yep, they're the same

Front 29

What does congenital mean?

Back 29

Present at birth

Front 30

What is teratology?

Back 30

The study of congenital malformations or

developmental defects

Front 31

What are genetic/intrinsic factors?

Is it a cause of developmental defects?

Back 31

-Spontaneous (somatic) mutation--the zygote has already formed but during development, something went wrong so that individual is born with a defect

-Inherited defect (germ cell mutation)--either the sperm or ovum is defected and that can affect more than one animal

Yes.

Front 32

What is neoplasia?

Back 32

A non-adaptive proliferation of cells

Front 33

What are environmental/extrinsic factors?

Is it a cause of developmental defects?

Back 33

-Teratogens

-Certain nutritional deficiencies (ex. vitamin A deficiency)

Yes.

Front 34

Is congenital a "cause"?

Back 34

Nope, it just means "present at birth"

Front 35

What are some modes of elimination or deletion of certain cell populations?

Back 35

-Apoptosis

-Degeneration

-Necrosis

Front 36

Do most developmental defects have a

genetic mutation associated with it?

Back 36

Yes, many are spontaneous mutations in a

single animal (somatic)

Front 37

What are the 3 main groups of teratogens?

Back 37

-Viruses

-Toxins

-Drugs

Bacteria are generally not teratogens--they often lead to mummification, embryonic death, or abortions.

Front 38

Do developmental defects always involve the killing of cells to cause the defect?

Back 38

No

Front 39

What are the different mechanisms for

developmental defects?

Back 39

-Elimination or deletion of certain cell

populations

-Influences on migration, proliferation, and/or

differentiation of cells during development

-Teratogens usually have their influence at

specific times in gestation

Front 40

What does agenesis mean?

Back 40

Complete failure of a tissue or organ to develop

Front 41

What is aplasia?

Back 41

Failure of a tissue or organ to develop, but a

rudimentary structure exists (there is often a connective tissue remnant)

There's a little "marker" telling you where the

organ or tissue should have been

Front 42

What is hypoplasia?

Back 42

Failure of a tissue or organ to attain full size (i.e. underdeveloped)

There is functional tissue there but it's small

Front 43

What is dysplasia?

Back 43

Most commonly, it refers to abnormal structural development of a tissue or organ

It's just kind of a messed up structure. It doesn't look like an abnormal volume of the organ, but it's abnormally organized.

Front 44

Is atrophy or hypoplasia an adaptive response?

Back 44

Atrophy

Hypoplasia is just underdeveloped, it never got to normal size

Front 45

What is excessive accumulation of CSF?

Back 45

Hydrocephalus

A developmental defect, means "water on the brain"

Front 46

What is the term for an underdeveloped (small) cerebellum?

Back 46

Cerebellar hypoplasia

It's a congenital defect, present at birth

Front 47

What is the least likely infective cause for

agenesis or aplasia of an organ during

development?

Back 47

Bacterial infection

Front 48

If an organ is totally absent from birth, what do we call it?

Back 48

Agenesis

Front 49

If an organ is abnormal from birth, what do we call it?

Back 49

Dysplasia

Front 50

What is the term for CSF filling the spinal cord?

Back 50

Hydromyelia

Front 51

What is the term for cyclopia?

Back 51

Synopthalmos

Front 52

What is the term for a cleft palate?

Back 52

Palatoschisis

These neonates often die of aspiration

pneumonia

Front 53

What is spina bifida?

Back 53

A condition where the bones of the spine don't form entirely around the spinal cord

Front 54

What is a bubble of meningeal tissue filled with fluid called?

Back 54

Meningocoele

Front 55

What is myelodyaplasia?

Back 55

Abnormally formed spinal cord

Front 56

What do you call it when there's two pieces of the abnormally formed spinal cord?

Back 56

Diplomyelia

Front 57

What is fluid in the spinal cord called?

Back 57

Hydromyelia

Front 58

What is the term for the incomplete ventral

fusion of the lateral body wall folds?

Back 58

Schistosomas reflexus

Front 59

What is atrophy?

Back 59

Decrease in cell size and/or decrease in cell number

Front 60

What are causes/mechanisms of atrophy? (4)

Back 60

-Decreased work load

-Decreased nutrient supply (decreased blood flow, specific nutrient deficiency, or with chronic disease)

-Decreased nervous stimulation

-Decreased hormonal stimulation

Front 61

Physiologic atrophy is synonymous with what?

Back 61

Apoptosis

(ex. thymic atrophy)

Front 62

What is the mechanism of disuse atrophy?

Back 62

Decreased workload

Front 63

What is the mechanism of denervation atrophy?

Back 63

Decreased nervous stimulation

Front 64

What is the mechanism of endocrine atrophy?

Back 64

Decreased hormonal stimulation

Front 65

What is the mechanism for pressure atrophy?

Back 65

Decreased nutrient supply or physical harm to cells

Front 66

What is a treatment for prostatic hyperplasia?

Back 66

Neuter it

Front 67

Alzheimer's disease-afflicted brain is

exemplative of which kind of atrophy?

Could see in a dog with cognitive dysfunction

Back 67

Senile atrophy

Front 68

What is a medical term for emaciation?

Back 68

Cachexia

Skeletal muscle mass decrease

Front 69

What is the mechanism of cachexia atrophy?

Back 69

Decreased nutrient supply

Front 70

What is serous atrophy of fat?

Back 70

The fat stores in the body are being broken down to derive energy

Turns gelatinous and translucent

Front 71

Which takes longer, cachexia or serous atrophy of fat?

Back 71

Cachexia

Front 72

What are the main places that you look for serous atrophy of fat?

Back 72

Pericardial and epicardial fat, mesenteric fat, bone marrow, and perirenal fat

Front 73

What is the normal percentage of fat in the bone marrow of an adult animal?

Back 73

60%

This is useful in legal cases where starvation could have occurred

Front 74

What is hypertrophy?

Back 74

Increase in cell size

Front 75

What are the two main causes/mechanisms of hypertrophy?

Back 75

-Increased work load (physiologic or pathologic)

-Increased hormonal stimulation (physiologic or pathologic)

Front 76

What often happens to the heart secondary to aortic valvular stenosis?

Back 76

Myocardial hypertrophy

Front 77

Mammary gland hypertrophy associated with

lactation is what kind of hypertrophy?

Back 77

Physiologic hypertrophy--increased hormonal

stimulation

Front 78

Myocardial hypertrophy secondary to aortic

valvular stenosis is which kind of hypertrophy?

Back 78

Pathologic hypertrophy--increased work load

Front 79

What is hyperplasia?

Back 79

Increase in cell number

Front 80

What are the causes/mechanisms of

hyperplasia?

Back 80

-Chronic irritation (mechanical/physical,

including inflammation or toxic)

-Increased hormonal stimulation (physiologic or pathologic)

-Virus infection (DNA viruses)

-Unknown causes

Front 81

A very large nucleus is indicative of what?

Back 81

High cellular activity, such as with hypertrophy

Front 82

Hyperplasia can only happen with which cell types?

Back 82

Labile or stable cell types

Labile--epithelial cells, bone marrow

Stable--parenchymal, glands, organs

Front 83

What is the difference between hyperplasia and neoplasia?

Back 83

Hyperplasia--cells will be organized in their usual way

Neoplasia--uncontrolled and disorderly, not

regulated by normal processes

Front 84

The mammary gland is composed of which cell type?

Back 84

Stable

Front 85

Which kinds of viral infections can cause

pathologic hyperplasia?

Back 85

Papilloma, pox, or herpesvirus infections

Front 86

What is metaplasia?

Back 86

Substitution of one fully differentiated cell type with another fully differentiated cell type not normally found in that tissue

Front 87

What is the purpose of metaplasia?

Back 87

Replacement of vulnerable cells with cells more resistant to the injurious agent

The trade off is loss of specialization though

Front 88

What are 4 causes/mechanisms of metaplasia?

Back 88

-Chronic irritation (mechanical or inflammatory)

-Certain nutritional deficiencies or excesses

-Excessive hormonal stimulation

-Age-related/unknown causes

Front 89

What is dysplasia in mature animals?

Back 89

Disorderly or atypical hyperplasia, is an adaptive growth response

Front 90

What is dysplasia in young growing animals?

Back 90

Abnormal development or growth

(developmental defect)

Front 91

What is metaplasia that can be seen in the dura mater in older large breed dogs?

Back 91

Osseous metaplasia of the dura mater

It is an incidental finding of no significance

Front 92

What are clinical signs of equine motor neuron disease?

Back 92

Weight loss, hind limb weakness and trembling, muscle atrophy

A degenerative condition that affects the lower motor neuron in older horses

Denervation atrophy--there are clusters of fibers that are smaller than normal

Front 93

What are clinical signs of PPID in horses?

Back 93

Hirsutism, decreased muscle tone, PU/PD

POMC--a metabolite is ACTH so horses with it can have high ACTH

See enlargement of pituitary gland, a benign neoplasm of chromophobe cells of pars

intermedia. Also, adrenal glands have pale, thickened cortices and nodules on surface (they are stable cells, so have hypertrophy and

hyperplasia).

Front 94

ACTH elevation stimulates cortisol from the adrenal gland from what?

Back 94

Zona fasciculata (middle layer)

Front 95

Why is hirsutism associated with PPID in horses?

Back 95

Hypothalamus regulates shedding. PPID mass pushes up on it and inhibits shedding.

Front 96

What makes tears stain red?

Back 96

There is porphyrin there

Front 97

What is chromodacryorrhea? What causes it?

Back 97

The secretion of so-called "bloody tears" from the harderian gland which nearly circumscribes the eye within the bony orbit

Chronic sialodacryoadenitis caused by SDA virus (coronavirus)