Pathology I

Question 1

The tendency of the body to seek and maintain a condition of balance or equilibrium within its internal environment, even when faced with external changes

Answer 1

Homeostasis

Question 2

Refers to the mechanisms of development and progression of disease, which account for the cellular and molecular changes that give rise to the specific functional and structural abnormalities that characterize any particular disease

Answer 2

Pathogenesis

Question 3

Refers to why a disease arrises

Answer 3

Etiology

Question 4

Describes how a disease develops

Answer 4

Pathogenesis

Question 5

Metabolism, differentiation and specialization, neighboring cells, availability of substrates are all?

Answer 5

Constraints on a cell

Question 6

Reversible functional and structural responses to changes in physiologic and some pathologic stimuli to maintain homeostasis

Answer 6

Adaptations

Question 7

If the limits of adaptive response are exceeded, we see

Answer 7

Reversible injury, irreversible injury, and cell death

Question 8

New cells from proliferating mature cells & stem cells

Answer 8

Hyperplasia

Question 9

Non-dividing permanent cells (muscle, nerve) get bigger

Answer 9

Hypertrophy

Question 10

What is an example of

1. ) Physiologic hypertrophy?
2. ) Pathologic hypertrophy?

Answer 10

1. ) Skeletal muscle

2. ) Cardiac muscle

Question 11

Endometrial & prostatic hyperplasia is an example of

Answer 11

Pathologic hyperplasia

Question 12

An increase in the size of cells => increase in size of

Answer 12

Organ

Question 13

Occurs in tissue whose cells have a limited capacity to divide

Answer 13

Hypertrophy

Question 14

Turn on signal transduction pathways => induction of genes => protein synthesis

Answer 14

Mechanical and trophic triggers of hypertrophy

Question 15

The normal adult prostate gland shows compound tubulo-acinar glands lined by pseudostratified columnar and/or cuboidal epithelium and separated by a supporting

Answer 15

Stroma

Question 16

The supporting stroma consisting of bundles of smooth muscle cells separated by bands of

Answer 16

Fibrous tissue

Question 17

An extremely common condition seen in men over the age of 50 years

Answer 17

Benign Prostatic Hyperplasia

Question 18

The histologic hallmark of BPH is the

Answer 18

Expansile Nodule

Question 19

The cause of BHP is most likely related to excess stimulation of the prostate gland by

Answer 19

Testosterone or DHT

Question 20

A proliferation of cells in organs whose cells can replicate

Answer 20

Hyperplasia

Question 21

Hyperplasia is controlled: remove stimulus and proliferation

Answer 21

Ceases

Question 22

Decrease in stress or trophic factors => decrease in organ size

Answer 22

Atrophy

Question 23

Atrophy can be caused by an increased degredation due to

Answer 23

Ubiquitin-proteosome degradation

Question 24

A reversible change whereby one adult cell type is replaced by another one

Answer 24

Metaplasia

Question 25

A cell type vulnerable to a particular stress is replaced by one that is less vulnerable in

Answer 25

Metaplasia

Question 26

The drawbacks of metaplasia is the loss of

Answer 26

Specialized function, and growth deregulation

Question 27

Change in metaplasia results from altering the maturation program of

Answer 27

Stem cells

Question 28

In a smoker’s bronchi, ciliated columnar cells => tougher squamous cells. This is an example of -But protective mucus secretion and ciliary clearance is lost

Answer 28

Metaplasia

Question 29

As the stress continues to affect the metaplastic epithelium, we may see

Answer 29

Malignant transformation

Question 30

Characterized by generalized swelling of the cell and its organelles; blebbing of the plasma membrane; detachment of ribosomes from the endoplasmic reticulum; and clumping of nuclear chromatin

Answer 30

Reversible injury

Question 31

Characterized by increasing swelling of the cell; swelling and disruption of lysosomes; presence of large amorphous densities in swollen mitochondria; disruption of cellular membranes; and profound nuclear changes

Answer 31

Irreversible injury

Question 32

Nuclear condensation (pyknosis), followed by fragmentation (karyorrhexis) and dissolution of the nucleus (karyolysis) is an example of

Answer 32

Irreversible injury

Question 33

Laminated structures (myelin figures) derived from damaged membranes of organelles and the plasma membrane first appear during the

Answer 33

Reversible stage

Question 34

Can cause direct membrane damage

Answer 34

Ischemia

Question 35

What are the earliest, i.e. reversible changes seen in cell injury?

Answer 35

Decreased ATP and cell swelling

Question 36

What are two signs of irreversible cell injury?

Answer 36

Extensive membrane injury and severe mitochondrial damage

Question 37

On a microscopic scale, reversible injury shows

Answer 37

Swelling and fatty change

Question 38

Lysosome rupture and mitochondrial amorphous densities are signs or

Answer 38

Irreversible damage

Question 39

One of the events that occurs in hypoxic or ischemic injury is

Answer 39

Cellular swelling

Question 40

The decrease of oxygen tension in the cell results in impairment of mitochondrial

Answer 40

Oxidative phosphorylation

Question 41

Since ATP is used to maintain the cellular ion pumps, the lack of ATP leads to an influx of

Answer 41

Sodium and water

Question 42

There is also an efflux of calcium. However, we still see a net increase in

Answer 42

Osmotic load

Question 43

In addition inorganic phosphates, lactate, and purine nucleosides accumulate in the cell and contribute to the

Answer 43

Osmotic load

Question 44

The microvilli (mv) are lost and have been incorporated in apical cytoplasm; blebs have formed and are extruded in the lumen (L). Mitochondria are slightly dilated in a proximal tubule with

Answer 44

Reversible injury

Question 45

Markedly swollen mitochondria containing amorphous densities, disrupted cell membranes, and dense pyknotic nucleus are seen in a proximal tubule with

Answer 45

Irreversible damage

Question 46

Oxygen deprivation such as hypoxia and ischemia are major agents of

Answer 46

Cell injury

Question 47

Anaphylaxis and autoimmune disease are both agents of

Answer 47

Cell injury

Question 48

With cellular injury, ATP levels drop to

Answer 48

5-10% of normal

Question 49

What are the three major causes of the ATP depletion seen in cellular injury?

Answer 49

Decreased O2 nutrients, mitochondrial damage, and toxins (ex: cyanide)

Question 50

ATP depletion, mitochondrial damage, loss of Ca2+ homeostasis, oxidative stress, defects in plasma membrane, and protein/DNA damage are mechanisms of

Answer 50

Cellular injury

Question 51

The loss of Ca2+ homeostasis can be seen by initial release of Ca2+ from intracellular stores. Followed later by influx across the

Answer 51

Plasma membrane

Question 52

Some diseases such as Alzheimer's, Huntington’s, Parkinson’s, and +/- type II diabetes are the result of

Answer 52

Protein/DNA damage

Question 53

Unregulated cell death from damage to cell membranes, loss of ion homeostasis, and denaturation of cellular proteins

Answer 53

Necrosis

Question 54

A passive response to injury, i.e. there is no energy required

Answer 54

Necrosis

Question 55

Necrosis is always

Answer 55

Pathologic

Question 56

There is no individual cell phagocytosis with

Answer 56

Necrosis

Question 57

What are the 5 types of Necrosis?

Answer 57

1. ) Coagulative 2. ) Liquefactive 3. ) Gangrenous 4. ) Caseous 5. ) Fat

Question 58

Underlying tissue architecture is preserved –Characteristic of infarcts (ischemic necrosis)

Answer 58

Coagulative necrosis

Question 59

Focal bacterial/fungal infections –Characteristic of CNS infarcts –Liquid, viscous mass

Answer 59

Liquefactive Necrosis

Question 60

Clinically, an ischemic limb with coagulative necrosis. –Called “wet” if bacterial superinfection => liquefaction

Answer 60

Gangrenous necrosis

Question 61

Tissue architecture & cell outlines obliterated –Surrounded by distinctive inflammation: granuloma

Answer 61

Caseous necrosis

Question 62

Caseous necrosis is mainly due to

Answer 62

Tuberculosis

Question 63

Shows vague outlines of necrotic fat cells

Answer 63

Fat necrosis

Question 64

Typically from release of activated pancreatic lipases in acute pancreatitis

Answer 64

Fat necrosis

Question 65

Since the etiology of coagulative necrosis is often ischemia, the infarct occurs in a vascular distribution that is wedge-shaped with a base at the

Answer 65

Organ capsule

Question 66

Outline of the myocardial cells are preserved, but the fibers have a “smudgy” appearance with increased eosinophilia and decreased numbers of nuclei

Answer 66

Coagulative necrosis due to MI

Question 67

In coagulative necrosis the necrotic process is due mainly to

Answer 67

Protein denaturation

Question 68

When hypoxic injury leads to cell death, it often results in coagulative necrosis except in the

Answer 68

Brain (where we see liquefactive necrosis)

Question 69

Usually the result of a bacterial or fungal infection, because these processes evoke a massive influx of inflammatory cells, which release various degradative enzymes

Answer 69

Liquefactive necrosis

Question 70

For unclear reasons, a hypoxic insult to the brain (as opposed to most other organs) results in

Answer 70

Liquefactive necrosis

Question 71

As this infarct in the brain becomes organized and resolved, the liquefactive necrosis leads to resolution with

Answer 71

Cystic spaces

Question 72

Often the result of mycobacterial or fungal infection

Answer 72

Caseous necrosis

Question 73

Characterized by acellular pink areas of necrosis

Answer 73

Caseous necrois

Question 74

Necrosis of the acinar cells of the pancreas releases lipase and proteases that in turn lead to injury and death of

Answer 74

Adipose cells

Question 75

If fat necrosis is extensive, sufficient calcium may be deposited to result in hypocalcemia and in some cases even

Answer 75

Tetany

Question 76

Programmed cell death -a rational way of getting rid of cells

Answer 76

Apoptosis

Question 77

In apoptosis, activation of caspase cascade => catabolism of

Answer 77

Proteins and DNA

Question 78

Results in: chromatin condensation, cytoplasmic blebs/apoptotic bodies, phagocytosis

Answer 78

Activation of caspase cascade

Question 79

What are the two pathways for apoptosis?

Answer 79

Intrinsic and extrinsic

Question 80

In the intrinsic pathway, cell injury leads to 1. ) Activation of? 2. ) Inhibiton of?

Answer 80

1. ) Bax and Bak | 2. ) Bcl-2

Question 81

This causes mitochondrial membrane channels to release

Answer 81

Cytochrome c

Question 82

Cytochrome c release into the cytoplasm leads to activation of

Answer 82

Caspase cascade

Question 83

Cell surface death receptors (Type I TNF receptor, Fas) bind their ligands => activate caspase cascade in

Answer 83

Extrinsis Apoptosis

Question 84

Most apoptosis is actually

Answer 84

Physiologic

Question 85

However, DNA damage, misfolded protein response, and certain infections are three types of

Answer 85

Pathologic apoptosis

Question 86

Proteolytic enzymes that are important in the chain of intracellular events that lead to apoptosis

Answer 86

Caspases

Question 87

The extrinsic pathway functions through the

Answer 87

Death receptor

Question 88

The death receptor binds

Answer 88

Fas and TNF

Question 89

Members of the TNF receptor family

Answer 89

Death receptors

Question 90

The death domains bind to the

Answer 90

Adapter proteins

Question 91

Too little apoptosis leads to increased cell survival which can cause

Answer 91

Cancer and autoimmune diseases

Question 92

Mutated cells survive without apoptosing in

Answer 92

Cancer

Question 93

Increased apoptosis leads to excessive cell death. This can result in

Answer 93

Neurodegenerative diseases, ischemic injury, and death of virus infected cells

Question 94

Failure to eliminate self-reactive lymphocytes –failure to eliminate dead cells, a source of self-antigens

Answer 94

Autoimmune diseases