Cellular Adaption To Stress Flashcards

1
Q

Involves the cause of disease as well as the mechanisms leading to the presentation of signs and symptoms in the patient

A

Pathology

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

Name the 3 types of physiologic cells in the body:

A
  1. Labile cells
  2. Stable cells
  3. Permanent cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

These physiologic cells do not normally regenerate but may do so in certain situations (liver cells after hepatitis or partial liver donation)

A

Stable cells

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

Which type of physiologic cells are normally replaced at different intervals? (Ex: Enterocytes, gastric and squamous epithelium)

A

Labile cells

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

Cardiac muscle cells do not regenerate during a lifetime. These are called ___ cells

A

Permanent

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

The 3 patterns of injury to cells?

A
  1. Reversible injury
  2. Persistent stress
  3. Irreversible (lethal) injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Two types of reversible injury?

A
  1. Hydropic swelling

2. Fatty metamorphosis

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

This type of reversible cell injury is due to accumulation of triacylglycerol in the cell. It is most commonly caused by alcohol intake

A

Fatty metamorphosis

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

Metabolism of alcohol involves what three substrates which contribute to triacylglycerol synthesis?

A
  1. NADH + H+
  2. Acetate
  3. Acetyl CoA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

The result of failure of energy dependent ATP pump in plasma membrane leading to inability to maintain ionic and fluid homeostasis

A

Hydropic swelling

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

An increase in cell size. (Ex: enlarged heart in a well-trained athlete)

A

Hypertrophy

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

The reversible replacement of one cell type by another. (Ex: replacement of urinary transitional epithelium with squamous epithelium due to repeated UTI’s)

A

Metaplasia

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

A decrease in cell size. (Ex: a bodybuilder stops working out, muscles become smaller)

A

Atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

A disorderly proliferation of cells with varying size and shape of nuclei. May become cancer if the irritating stimulus is not removed. (Ex: mucosa of bronchus of a smoker)

A

Dysplasia

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

An increase in cell number. (Ex: endometrial glands during proliferative phase of menstrual cycle)

A

Hyperplasia

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

A decrease in cell number. (Ex: smaller thymus with advancing age)

A

Involution

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

A marker of past injury in cardiomyocytes?

A

Lipofuscin pigment

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

Marker of past injury in hepatocytes?

A

Mallory bodies

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

Neurofibrillary tangles are markers of past injury to what type of cells?

A

Brain cells (neurons)

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

Macrophages that have engulfed lipid debris

A

Foam cells

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

Irreversible cell injury is also known as:

A

Necrosis

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

List the 3 lipid bilayer membranes involved in necrosis

A
  1. Cell plasma membrane
  2. Inner mitochondrial membrane
  3. Lysosomal membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

A group of molecules that injure the lipid bilayer membrane through the process of lipid peroxidation

A

Reactive Oxygen Species (ROS)

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

Oxidative degradation of lipids

A

Peroxidation

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

List the three most common Reactive Oxygen Species (ROS):

A
  1. Superoxide
  2. Hydrogen peroxide
  3. Hydroxyl radical
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

List the three changes to the cell nucleus during necrosis:

A
  1. Pyknosis (shrinkage)
  2. Karyorrhexis (fragmentation)
  3. Karyolysis (dissolution - nucleus no longer visible)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

The final event in lethal cell injury is massive leakage of ____ into the cytosol, which destroys all of the critical parts of the cell

A

Calcium (Ca2+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Individual cell death without an inflammatory reaction

A

Apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

More widespread cell death with an inflammatory process

A

Necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Cell death resulting from a hepatitis infection of liver cells would fall under what category?

A

Apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

The major pathway of cell death in many injuries (trauma, infections, toxins, ischemia)

A

Necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

An inadequate blood supply to an organ or part of the body, especially the heart muscles

A

Ischemia

33
Q

Name the two steps in apoptosis:

A
  1. Intrinsic pathway (mitochondrial)

2. Extrinsic pathway (death receptor)

34
Q

Which step of apoptosis is triggered by the loss of survival signals and DNA damage. Mediated by proteins called caspases

A

Intrinsic

35
Q

Which apoptosis pathway is Tumor Necrosis Factor (TNF) receptor mediated?

A

Extrinsic

36
Q

Most common type of necrosis:

A

Coagulative necrosis (Ex: myocardial infarction…heart attack)

37
Q

This type of necrosis is most commonly caused by ischemia (loss of blood supply) secondary to atherosclerosis (build up of plaque in arterial walls). Component cells die, but basic architecture is preserved

A

Coagulative necrosis

38
Q

In ___ necrosis, dead cells are completely digested resulting in transformation of the tissue into a liquid, thickened, viscous mass. (Ex: brain abscess)

A

Liquefactive

39
Q

___ necrosis results from enzymatic release of activated pancreatic lipases into the pancreas. Fatty acids combine with calcium to form a white area called saponification, OR traumatic injury to fatty tissue

A

Fat

40
Q

A combination of coagulation and liquefactive necrosis forming a granuloma (mass of granulation tissue) Associated w/tuberculosis

A

Casseous necrosis

41
Q

____ necrosis is seen in immune reactions involving small blood vessels. Occurs when antigens and antibodies are deposited in arterial walls together with fibrin that has leaked out of vessels

A

Fibrinoid

42
Q

This type of necrosis is due to disrupted blood supply secondary to bone fracture.

A

Avascular necrosis

43
Q

____ necrosis is a variant of casseous necrosis typically seen in tertiary syphilis.

A

Gummatous

44
Q

Coagulative necrosis involving multiple tissue layers, often refers to the skin and subcutaneous tissue

A

Gangrene

45
Q

Fluid accumulation in tissue outside the vascular system is known as:

A

Edema

46
Q

Fluid accumulation in a confined anatomic space (joint, pleural or peritoneal cavity, pericardial sac)

A

Effusion

47
Q

Fluid with a low protein content is known as ___, high protein content known as ___

A

Transudate, exudate

48
Q

The 5 clinical signs of inflammation?

A
  1. Redness
  2. Heat
  3. Swelling
  4. Pain
  5. Loss of function
49
Q

Most common cause of acute inflammation?

A

Staphylococcal or streptococcal infection

50
Q

Superficial skin infections are known as:

A

Impetigo, folliculitis

51
Q

A deeper infection that has invaded the lymph nodes is known as:

A

Erysipelas

52
Q

A deep infection of the subcutaneous tissue is called:

A

Cellulitis

53
Q

Where is the site of cellular and most fluid transfer into the surrounding tissue?

A

Post capillary venules

54
Q

Leukocyte accumulation at the margin of vessels is called ____ (inflammatory response)

A

Margination

55
Q

When WBC’s fall and tumble on the endothelial surface of the blood vessel it is called ___

A

Rolling

56
Q

The most common leukocytes to migrate to the area of injury? These begin arriving in the first 24 hours.

A

Neutrophils

57
Q

After neutrophils have arrived at the site of injury during the first 24 hours, ___ and ___ (of leukocytes) begin arriving in the next 24 hours

A

Monocytes, macrophages

58
Q

Name the 5 stages of the cellular response to injury

A
  1. Margination
  2. Adhesion
  3. Transmigration (emigration)
  4. Chemotaxis
  5. Phagocytosis
59
Q

During cell adhesion, ___ on the leukocyte cell surface interact with ___ on endothelial cells

A

Integrins, ligands

60
Q

___ are secreted by many cells at the site of inflammation causing the firm adhesion of leukocytes to their appropriate ligands

A

Chemokines

61
Q

After adhesion, the activated leukocytes squeeze through the endothelial cells (called diapedesis) to enter the area of injury. This step is called ____

A

Transmigration (emigration)

62
Q

Once transmigration occurs, directed movement of the cells along an increasing concentration gradient to the area of injury occurs. This step is called ___

A

Chemotaxis

63
Q

C5a complement, leukotriene B4 (LTB4), and fragments of collagen and fibrin are examples of ___ agents

A

Chemotactic

64
Q

List the three steps in phagocytosis:

A
  1. Recognition and attachment
  2. Engulfment
  3. Killing and degradation
65
Q

When NADPH oxidase (enzyme) is not present for phagocytosis, it is known as:

A

Chronic granulomatous disease of childhood

66
Q

A genetic defect in gene coding for the fusion of the phagocyte with the lysosome is known as ____ syndrome

A

Chediak-Higashi

67
Q

The mediators of inflammation can be broken into three groups, they are:

A
  1. Cell derived
  2. Arachidonic acid derived
  3. Plasma derived
68
Q

___ cells release histamine, which causes vasodilation

A

Mast

69
Q

____ release serotonin, which causes vasoconstriction

A

Platelets

70
Q

The arachidonic acid derived mediators of inflammation have two pathways. Name them

A
  1. Cyclooxygenase pathway (blocked by NSAIDS)

2. Lipooxygenase pathway (blocked by Steroids-both pathways are blocked by steroids)

71
Q

Complement proteins are part of which mediators of inflammation category?

A

Plasma-derived

72
Q

In reference to the arachidonic acid derived mediators, ___ causes vasodilation and therefore edema

A

Prostaglandins

73
Q

In reference to the arachidonic acid derived mediators of inflammation, ____ causes vasoconstriction

A

Thromboxane

74
Q

In reference to the arachidonic acid derived mediators of inflammation, ____ causes small muscle contractions

A

Leukotriene

75
Q

The three pathways that makeup the classical blood coagulation pathway are:

A
  1. Intrinsic
  2. Extrinsic
  3. Common
76
Q

The two major pathways of the complement system are:

A
  1. Classical

2. Alternative

77
Q

The ___ pathway is activated by antigen-antibody complexes. Operates in acquired immunity

A

Classical

78
Q

The ___ pathway is directly activated by the presence of bacteria or other microorganisms. Operates in innate or natural immunity

A

Alternative