Introduction to Pathology Flashcards

1
Q

What is a disease?

A

Molecular, cellular, tissue, organ, and organismic damage caused by an etiology and dealt through pathologic mechanisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is etiology?

A

Etiology is the cause of a disease (infection, injury, genetic, chemical)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is pathogenesis?

A

The mechanisms through which a disease damages the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a symptom?

A

Something your patient has recognized and tells you “I have a dry throat”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is a sign?

A

A quantitative result of physical or laboratory testing “The patient has a temperature of 102 F and a low white blood cell count”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Is all cell damage irreversible?

A

No! If cells are minimally hurt they can bounce back by eliminating toxins and sloughing off excess cellular material.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are hallmarks of cell damage?

A

Plasma membrane blebs (loss of circular shape).
Ribosomes detached from rough ER
Mitochondrial swelling.
Aggregated centrioles and microtubules.
Increased intracellular volume (maybe to dilute toxins?)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is hypertrophy? Where does it often occur?

A

Increase in cell size (not number). This often occurs when cells swell in response to antigens. Another great example is exercise. As you exercise, your muscles grow larger, not more numerous.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is hyperplasia? Where does it often occur?

A

Increase in cell number. Hyperplasia is intentional or organized cell proliferation. Non-invasive, non-cancerous, but just an increase in cell number. This can often happen around glands.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is metaplasia?

A

Change in cell type! This can happen as a response to toxins in the environment (the columnar cells of the airway become squamous when exposed to cigarette smoke, and the esophageal lining changes drastically under chronic exposure to gastric reflux).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is dysplasia?

A

Unorganized, but noninvasive, growth of cells in a tissue. Dysplasia is hindered by the confines of the tissue. It is often a precursor to neoplasia (cancerous growth)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is neoplasia?

A

Uncontrolled, invasive growth. The growth can be benign or malignant.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is atrophy? What are common causes of atrophy?

A

Decrease in cell size.

  1. Decreased “load” (you work a muscle less, or change the weight load on your bones and they will change shape)
  2. Decreased nutrition (no nutrients, cell will shrink to a sustainable size)
  3. Inhibition of molecules signaling growth “trophic signaling”
  4. Chronic injury (pancreatitis?)
  5. Lack of oxygen (cell is starved, can’t survive)
  6. Increased pressure (bed rest can kill/weaken muscle groups)
  7. Chronic disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do hypertrophic cells show up in microscopic stains?

A

They’re always larger, can have lots of fluid or fat built up (this would show as clear or very light pink in the stain), and can have enlarged nuclei.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does hyperplasia show up in microscopic stains?

A

Increased thickness of tissue (with a semi-conserved shape). Increased number of cells of one type. They will still appear organized.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What would metaplasia look like in a microscope slide?

A

Epithelial metaplasia would show up as a disruption in a nice consistent wall of epithelial columnar cells (or could be another type) by a clump of clearly divergent cell types. Would be localized. Metaplasia is more common in tissues that can be exposed to irritants and toxins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What would dysplasia look like in a microscope slide?

A

You’d have a mass of cells that were not polarized (aren’t maturing normally from the basal membrane to the apical lumen-facing cells. normally apical cells will have more cytosol, maybe even not have their nuclei anymore. Basal cells will be dense and seem directed towards apex). Dysplasia would have a mass of cells that looked like they should maybe be basal cells going all the way throughout. The cells wouldn’t be facing a given direction or anything but would just be filling space where possible. But dysplasia is NONINVASIVE so it would be localized changes in structure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What would neoplasia look like in a microscope slide?

A

Invasive, unorganized growth of cells into underlying tissue. Often you’ll see scar-tissue developing as a response, neutrophils also invading the area.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How would you tell the difference between benign and malignant neoplasia in a microscope slide?

A

Benign seem like they have something of a pattern. Malignant look ugly! They spread out in any direction possible, are a lot more stringy, and have nuclei with very odd shapes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What phase is used to describe a benign growth?

A

“___oma”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What phrase is used to describe a malignant growth?

A

“carcinoma” “sarcoma”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How would hyperplasia or hypertrophy appear different than neoplasia in an organ?

A

Neoplasia will have a “growth”, something that sticks out and is clearly different in structure. The cells are not differentiated throughout the growth. Hyperplasia or hypertrophy would lead to an increased organ size or thickness, but for the most part structure is conserved. You could have localized increased size, but looking “swollen” versus looking like an extra blob

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is apoptosis?

A

Mediated/intentional cell death. Usually caused by internal signals (cytochrome c release from mitochondria) but can come from external signals (TNF).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is necrosis?

A

Cell death via damage. Not intentional, always caused not-on-purpose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How does an apoptotic cell look different than a normal cell?

A

The apoptotic cell has fragments of nuclei blown apart all throughout the cell, each encapsulated by a vacuole. Looks like bubble wrap with drops of dye in it.

Normal cell has one large nucleus, circular, most of the other organelles won’t show up in a stain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

In microscope slides, what organelle do you look to to observe cell damage?

A

The nucleus! It will change structure for both apoptosis and necrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are signs of a necrotic cell?

A

Pyknosis: nucleus becomes smaller and stain gets darker (chromatin clumping)
Karyorrhexis: Pyknotic nucleus blows up
Karyolysis: nucleus is pushed out of the cell or chromatin is degraded, nucleus no longer visible.

28
Q

What are signs of necrosis in a tissue?

A

Fragments of cells everywhere.

29
Q

What are different types of necrosis?

A

Coagulative, liquifactive, caseous, and fat necrosis

30
Q

What is fat necrosis?

A

Pancreatitis or trauma can cause fat tissue to be damaged. Lipases, which degrade lipids, are released and activated earlier than intended. Instead of breaking down food they break down tissue. The freed fatty acids (from tissue degradation) bind with calcium ions to form calcium soaps (saponification). Looks nasty green

31
Q

What is coagulative necrosis?

A

Nuclei disappear, but the “ghosts” of cells remain. You can still see the cell shapes, but it’s starting to deteriorate.

32
Q

What is caseous necrosis?

A

This is seen in tuberculosis. Macrophages aggregate around an injured region of necrotic tissue. The macrophages contain the necrotic region as a dense bright pink-stained clump of cell chunks. The lesions (cell chunk clusters) are called granulomas. The macrophage surroundings are called granulomatous inflammation.

33
Q

What is liquifactive necrosis?

A

Cells are rapidly dissolved by neutrophils. Tissue is liquified. This often leads to the formation of cavities. A liquifactive necrotic region with inflammation is called an abscess.

34
Q

What are common classifications of etiology?

A
VINDICATE:
Vascular
Inflammatory
Neoplastic (cancerous)
Drug/Toxin
Infection
Congenital/genetic
Autoimmune/immune
Trauma
Endocrine/metabolic
35
Q

What is inflammation? What causes inflammation?

A

Inflammation is a movement of fluid and immune cells (and pathogens) to a localized region of the body where they can be dealt with. It is often red, hot, painful, and swollen. Inflammation occurs during an infection, or whenever there is tissue damage. The body uses inflammatory pathways to get rid of damaged cells and transport important molecules to the site of injury/infection.

36
Q

How is inflammation mediated?

A

Extracellular molecular signals activate cellular and humoral pathways to pull fluid and leukocytes (white blood cells) out of the blood. Overexpression of inflammation can lead to secondary disease.

37
Q

What are histologic hallmarks of acute inflammation?

A

polymorphonucleated cells (looks like they have multiple nuclei. these are neutrophils), densely packed. Vasodilation (blood vessels expand/loosen to allow more blood flow through)

38
Q

What are histologic hallmarks of chronic inflammation?

A

Mononuclear white blood cells, plasma cells, less densely packed.

39
Q

What is the common pathway from injury to healing?

A

Injury, acute inflammation, chronic inflammation, formation of granulation tissue, formation of scar tissue or regeneration of cells.

40
Q

What is the difference between acute inflammation and regular tissue?

A

Vasodilation is the big one. Acutely inflammed tissue has massively dilated blood vessels. This causes some of the “redness” associated with swelling. Humoral mediators are activated, which is where the feeling of pain comes from. Plasma and neutrophils are exuded (gotten rid of through pores) from the tissue.

41
Q

What is a major difference between acute and chronic inflammation, histologically?

A

Chronic=mononuclear
acute=looks like polynuclear, but really isn’t
chronic has more collagen/extracellular matrix, won’t seem as dense

42
Q

What are the steps of superficial wound recovery?

A

Injury, erythema(inflammation)/scab formation, further erythema and purulent exudate (removal of plasma/neutrophils/junk), scab changes color as healing continues, granulation tissue is developing, scarring

43
Q

What is primary intention in healing?

A

When a wound is closed it can heal from the bottom up without needing to make new epithelial cells, sort of stitching things together

44
Q

What is secondary intention in healing?

A

When a wound is left open it has to fill a valley instead of a canyon and the granulated tissue has to grow up along the cavity. Leads to more scarring and takes longer to heal.

45
Q

What are the steps to blood clot formation and wound healing?

A

After the wound, endothelial cells recruit platelets to block the hole. Coagulation cascade is triggered (forming blood clot). Mast cells make blood vessel dilate to recruit neutrophils and other clotting agents. Neutrophils follow chemotactic gradient to get to injury. Neutrophils recruit monocytes, which become macrophages. Macrophages recruit lymphocytes. Lymphocytes stimulate endothelial cell proliferation, neovascularization, and stimulate proliferation of fibroblasts/epithelial cells to close up wound

46
Q

What are platelets for?

A

Platelets bind with fibrin to form polymerized fibrin strands that hold the injured region shut (clot formation)

47
Q

What is fibrin for?

A

A clotting factor, holds a pre-thrombus together to stop blood from flowing through a hole.

48
Q

What type of cells are involved in creating new vascularization of tissue?

A

Lymphocytes induce endothelial cell proliferation.

49
Q

What are lymphocytes?

A

Lymphocytes are involved in healing from injury. They stimulate fibroblast/epithelial/endothelial proliferation. Fibroblasts help with healing tissue. Epithelial cells cover up injury. Endothelial cells create new blood vessels.

50
Q

What are mast cells?

A

Mast cells are used to control the localized dilation of blood vessels. In injury response, mast cells cause vasodilation.

51
Q

What is granulation tissue?

A

The stage in healing where new capillaries are being formed. If you ripped the scab off the tissue would appear to have little bumps.

52
Q

How does cell regeneration /injury response change depending on tissue type?

A

Some cell types do not regenerate. If you damage the heart or the brain, all you get is scar tissue. You will not get any new functional cells. The liver and skin are extremely proliferative and can easily recover from injury.

53
Q

What is fibrosis?

A

Fibrosis is a compartmentalization of healthy tissue by regions of scar tissue (fibrin/collagen). The healthy tissue cannot grow back into a whole tissue because the regions of fibrosis blockade the nodes of healthy cells. This is seen in liver regeneration after long term alcoholism.

54
Q

How can you identify fibrosis?

A

Using the masson trichrome staining for collagen (stains collagen blue) you can clearly see the difference between regions of healthy tissue and regions of fibrosis.

55
Q

What is a thrombus?

A

A blood clot! Good when you have an injury, bad when random. Thrombus can develop when blood flow slows or is reduced, endothelial continuity is lost (jagged vessel) or endothelial function is altered (vessel starts recruiting platelets or something). A thrombus that blocks blood flow is said to cause ischemic disease. An inability to form blood clots is called a hemorrhagic disease.

56
Q

What is an embolism?

A

An embolism is a thrombus that has broken away from its site of formation and is traveling the body. The embolism can get stuck in another part of the circulatory system and block blood flow.

57
Q

What is deep vein thrombosis?

A

A blood clot in your legs. It can be caused by vascular injury, sitting/standing around for too long, sickle cell, aging (can’t cause but increases risk), or genetic predisposition to making thrombi.
Once DVT happens, the thrombus can either lyse (break up), embolize (break off), recanalize (have blood vessels pushed through it), propagate (get bigger), or organize (become part of the vessel wall. This happens when endothelial cells grow over the thrombus. Fibroblasts grow into it, collagen coats it. It becomes permanent).

58
Q

What is the partial thrombolastin time test?

A

A blood test to see how quickly you can form blood clots. Important to know before sending a patient in to get surgery. Invented at UNC Chapel Hill!

59
Q

What is aplasia?

A

You’ve got the embryonic/primordial cells that would become the tissue/organ of choice, but the differentiation never occurs. You end up with an absent organ.

60
Q

What is agenesis?

A

Lack of the embryonic priomordial cells that differentiate into the tissue or organ of interest, leading to a complete absence of the tissue/organ.

61
Q

What is hypoplasia?

A

Reduced size of organ/tissue caused by inadequate development.

62
Q

What is dysplasia (in tissues)?

A

Abnormal tissue differentiation. You have the cells for the tissue, but they developed into the wrong thing, or a nonfunctional version of the tissue.

63
Q

What is atresia?

A

Incomplete formation of a lumen (lumen is one of the “holes” in the body)

64
Q

What is ectopia?

A

A normally formed, healthy organ that’s in the wrong place in the body.

65
Q

What is a teratogen? What is an example of a teratogen-induced condition?

A

A teratogen is an environmental factor that causes malformation of an embryo. The zika virus, passed by mosquitoes, causes microcephaly, or inadequate neurogenesis.

66
Q

What is the issue in cystic fibrosis?

A

Cystic fibrosis transductance receptor is defunct. You can’t pass chloride through the cells. Without passing chloride you can’t pass water. Mucus becomes very thick because it’s not hydrated. Bacteria is able to hide safely and grow in the mucus. The mucus doesn’t move very easily (in the lungs or the pancreas or the intestines) so things get stuck. In the pancreas some zymogens can get stuck and cause pancreatitis. In the lungs bacteria will get stuck and cause infection. In the intestines sometimes excrement gets stuck.