Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PT 2nd year > Patho-ch2 > Flashcards

Patho-ch2 Flashcards

1
Q

devoted to the study of the structural, chemical, and functional changes in cells, tissues, and organs that underlie disease

A

Pathology

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

concerned with the common reactions of cells and tissues to injurious stimuli

A

General pathology

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

Examines alterations and underlying mechanisms in organ specific diseases such as ischemic heart disease

A

Systemic pathology

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

Four aspects of a disease process: give their definition.

A
  • Etiology- cause
  • Pathogenesis- biochemical and molecular mechanisms of its development
  • Morphologic changes- structural alterations induced in the cells and organs of the body
  • Clinical manifestations - functional consequences of these changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Two classes of etiology

A

Genetic - inherited

Acquired - e.g., infectious, nutritional, chemical, physical

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

Symptoms and signs of disease

A

Clinical manifestations

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

Clinical course and outcome of disease

A

Progress

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

Cell’steady state

A

Homeostasis

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

reversible functional and structural responses to changes in physiologic state

A

Adaptations

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

NIS: Altered physiologic stimuli; some nonlethal injurious stimuli
CR:?

A

Cellular adaptations

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

NIS: Increased demand, increased stimulation (e.g., by growth factors, hormones)
CR: ?

A

Hypertrophy/ hyperplasia

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

NIS: Decreased nutrients, decreased stimulation
CR: ?

A

Atrophy

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

NIS: Chronic irritation (physical or chemical), reversible change in which one differentiated cell type (epithelial or mesenchymal) is replaced by another cell type
CR: ?

A

Metaplasia

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

NIS: Reduced oxygen supply; chemical injury; microbial infection
CR: ?

A

Cell injury

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

NIS: Acute and transient
CR: ?

A

Acute reversible injury, cellular swelling fatty change

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

NIS: Progressive and severe (including DNA damage)
CR: ?

A

Irreversible injury- cell death. Necrosis apoptosis

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

NIS: Metabolic alterations, genetic or acquired; chronic injury
CR: ?

A

Intracellular accumulations, calcification

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

NIS: Cumulative sublethal injury over long life span
CR: ?

A

Cellular aging

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

Nutrient deprivation triggers an adaptive cellular response called_______ and may also culminate in cell death.

A

Autophagy

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

This is stimulated by estrogenic hormones acting on smooth muscle through estrogen receptors, eventually resulting in increased synthesis of smooth muscle proteins and an increase in cell size.

A

Uterine hypertrophy

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

associated with increased atrial natriuretic factor gene expression

A

Cardiac hypertrophy

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

peptide hormone that causes salt secretion by the kidney, decreases blood volume and pressure, and therefore serves to reduce hemodynamic load.

A

Atrial natriuretic factor (ANF)

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

Occurs when there is a need to increase functional capacity of hormone sensitive organs; when there is need for compensatory increase after damage or resection

A

Physiologic hyperplasia

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

caused by excessive or inappropriate actions of hormones or growth factors acting on target cells.

A

Pathologic hyperplasia

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

Type of atrophy common during normal development

A

Physiologic atrophy

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

Type of atrophy, has several causes and it can be local or generalized

A

Pathologic atrophy

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

Enumerate the common causes of pathologic atrophy.

A
  • Decreased workload (atrophy of disuse)
  • Loss of innervation ( deneevation atrophy )
  • Decreased blood supply
  • Inadequate nutrition
  • Loss of endocrine stimulation
  • Pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

AKA Profound protein-calorie malnutrition

A

Marasmus

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

brain and sometimes the heart may undergo progressive atrophy, mainly because of reduced blood supply as a result of atherosclerosis called_______

A

Senile atrophy

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

The most common epithelial metaplasia

A

Columnar to squamous

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

formation of cartilage, bone, or adipose tissue (mesenchymal tissues) in tissues that normally do not contain these elements

A

Connective tissue metaplasia

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

A direct link between transcription factor dysregulation and metaplasia is seen with _____________ deficiency or excess, both of which may cause metaplasia

A

vitamin A (retinoic acid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Hallmarks of reversible injury

A

reduced oxidative phosphorylation with resultant depletion of energy stores (ATP), cellular swelling caused by changes in ion concentrations and water influx, intracellular organelles, such as mitochondria and the cytoskeleton, may show alterations.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

a form of cell death that is characterized by nuclear dissolution, fragmentation of the cell without complete loss of membrane integrity, and rapid removal of the cellular debris AKA “programmed cell death”.

A

Apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

“accidental” and unregulated form of cell death resulting from damage to cell membranes and loss of ion homeostasis

A

Necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

deficiency of oxygen, which causes cell injury by reducing aerobic oxidative respiration

A

Hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Enumerate the causes of cell injury

A
  • Oxygen deprivation
  • Physical agents
  • Chemical agents and drugs
  • infectious agents
  • immunologic reactions
  • genetic derangements
  • nutritional imbalances
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the two features of reversible injury recognized under light microscope?

A

Cellular swelling and fatty change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

cells are incapable of maintaining ionic and fluid homeostasis, result of failure of energy-dependent ion pumps in the plasma membrane

A

Cellular swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Occurs in hypoxic injury and various forms of toxic or metabolic injury and manifested by the appearance of lipid vacuoles in the cytoplasm.

A

Fatty change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

first manifestation of almost all forms of injury to cells

A

Cellular swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Ultrastructural changes of reversible injury

A
  • Plasma membrane alterations
  • mitochondrial changes
  • dilation of ER
  • nuclear alterations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

form of necrosis in which the architecture of dead tissues is preserved for a span of at least some days; firm texture

A

Coagulative necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

localized area of coagulative necrosis

A

Infarct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

characterized by digestion of the dead cells, resulting in transformation of the tissue into a liquid viscous mass

A

Liquefactive necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

A necrotic material that is frequently creamy yellow because of the presence of dead leukocytes

A

Pus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Not a specific pattern of cell death, usually involves lower leg that has lost its blood supply

A

Gangrenous necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Superimposed bacterial infexn, more liquefactive because of the action of degradative enzymes and leukocytes

A

Wet gangrene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

most often in foci of tuberculous infection; “cheeselike” and is derived from the friable white appearance of the area of necrosis

A

Caseous necrosis

50
Q

Appearance of structureless collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border; is characteristic of a focus of inflammation called_____

A

Granuloma

51
Q

focal areas of fat destruction resulting from release of activated pancreatic lipases into the substance of the pancreas and peritoneal cavity called____________. Occurs in abdominal emergency known as________

A

Fat necrosis, Acute pancreatitis

52
Q

Seen in immune reactions involving blood vessels, occurs when complexes of antigens and antibodies are deposited in the walls of arteries, these deposits together with fibrin result in a bright pink and amorphous appearance in H&E stains

A

Fibrinoid necrosis

53
Q

Large whorled phospholipid masses that replaces dead cells

A

Myelin figures

54
Q

Enumerate the 3 patterns of appearance during nuclear changes in necrosis. Describe each.

A
  • Karyolysis- basophilia of chromatin fades, loss of DNA
  • Pyknosis- nuclear shrinkage, increased basophilia, chromatin condenses
  • Karyorrhexis- pyknotic nucleus undergoes fragmentation
55
Q

Necrotic cells and cellular debris that are not destroyed or absorbed that allows deposition of calcium salts and minerals and calcified

A

Dystrophic calcification

56
Q

Fundamental cause of necrotic cell death

A

Reduction/ Depletion of ATP

57
Q

Enumerate: Cellular enzymes activated after increased cytosolic Ca2+ and their roles

A
  • Phospholipases - causes membrane damage
  • proteases - membrane and cytoskeletal protein damage
  • endonuclease - nuclear damage (dna and chromatin fragmentation)
  • ATPase - depetion of ATP
58
Q

Chemical species that have a single unpaired electron in an outer orbit.

A

Free radicals

59
Q

Type of oxygen derived free radical whose role is well established in cell injury.

A

Reactive oxygen species (ROS)

60
Q

Increased production or decreased scavenging of ROS leading to increased free radicals is called _______

A

Oxidative stress

61
Q

Enumerate ways of generetaion of free radicals

A
  • reduction-oxidation process during normal metabolic processes
  • absorption of radiant energy
  • rapid bursts of ROS produced in activated leukocytes during inflammation
  • enzymatic metabolism of exogeneous chemicals/ drugs
  • transition metals
  • nitric oxide
62
Q

Enumerate the enzymes that act as free radical-scavenging systems

A
  • Catalase
  • Superoxidase dimutases
  • glutathione peroxidase
63
Q

Autocatalytic chain reactions

A

Propagation

64
Q

Pathologic effects of ROS

A
  • Lipid peroxidation inf membranes
  • Oxidative modification of proteins
  • Lesions in DNA
65
Q

Biochemical mechanisms that may contribute to membrane damage

A
  • Reactive oxygen species(lipid peroxidation)
  • decreased phospholipid synthesis
  • increased phospholipid breakdown
  • cytoskeletal abnormalities
66
Q

Most important sites of membrane damage

A
  • mitochondrial membrane
  • plasma membrane
  • lysosomal membrane
67
Q

Two phenomenas attributed to irreversible cell injury:

A

Mitochondrial dysfunction, membrane damage

68
Q

Enumerate the mechanisms of cell injury

A

ATP depletion, mitochondrial damage, influx of calcium, increased permeability of cellular membrane, accumulation of reactive oxygen species (ROS), accumulation of damaged DNA and misfolded proteins

69
Q

A protective response to deal with hypoxic stress, which promotes new blood vessel formation, stimulates cell survival pathways, and enhances anaerobic glycolysis.

A

Hypoxia-inducible factor-1

70
Q

reperfused tissues may sustain loss of cells in addition to the cells that are irreversibly damaged at the end of ischemia.

A

Ischemia-reperfusion injury

71
Q

Two general mechanisms that chemicals induce cell injury

A

Direct toxicity, conversion to toxic metabolites

72
Q

Fragmented apoptotic cells is called_____

A

Apoptotic bodies

73
Q

AKA “falling off”

A

Apoptosis

74
Q

Genetically programmed necrosis by distinct type of genes

A

Necroptosis

75
Q

Apoptosis in physiologic situations

A
  • destruxn of cells during embryogenesis
  • involution of hormone-dependent tissues upon hormone withdrawal
  • cell loss in proliferating populations
  • elimination of potentially harmful lymphocytes
  • death of host cells that have served their usefull purpose
76
Q

Pathologic apoptotic conditions

A
  • DNA damage
  • Accumulation of misfolded proteins
  • cell death in certain infections
  • pathologic atrophy in parenchymal organs after duct obstruxn
77
Q

Morphologic and biochemical changes in apoptosis

A
  • Cell shrinkage
  • chromatin condensation
  • formation of cytoplasmic blebs and apoptotic bodies
  • phagocytosis of apoptotic cells / bodies by macrophages
78
Q

Apoptosis results from activation of what enzymes

A

Caspases

79
Q

Caspases become catalytically active

A

Initiation phase

80
Q

Other caspases trigger the degradation of critical cellular components

A

Execution phase

81
Q

Major mechanism of apoptosis in all mammalian cells

A

Intrinsic (mitochondrial) pathway

82
Q

Anti-apoptotic proteins; posess _____ BH domains called_____

A

BCL2 , BCL-XL, MCL-1; 4; BH1-4

83
Q

Apoptotic proteins; posses ___ BH domains

A

BAX and BAK; 4

84
Q

Sensor proteins; posses _______ BH domain called______

A

BAD,BIM,BID,Puma,Noxa; 1; BH3-only proteins

85
Q

Cytochrome C binds into a protein called______

A

APAF-1(Apostosis-activating factor-1)

86
Q

Wheel-like hexamer

A

Apoptosome

87
Q

initiated by engagement of plasma membrane death receptors on a variety of cells

A

Extrinsic (Death receptor-initiated) pathway

88
Q

Cytoplasmic domain involed in protein-protein interactions

A

Death domain

89
Q

Best known death receptor____; related protein_____

A

Type 1 TNF receptor (TNFR1); Fas (CD95)

90
Q

cytoplasmic death domains form a binding site for an adaptor protein that also contains a death domain and is called_______

A

FADD (Fas-associated death domain)

91
Q

Two initiating pathways converge to a cascade of caspase activation

A

Execution phase

92
Q

Ligand that “flips out” for phagocytosis

A

Phosphatidylserine

93
Q

Happens when unfolded or misfolded proteins accumulate in the ER because of inherited mutations or stresses triggering cellular responses

A

Unfolded protein response

94
Q

Form of programmed cell death accompanied by the release of cytokine IL-1 with biochemical similarities to apoptosis

A

Pyroptosis

95
Q

Process in which cell eats its own contents

A

Autophagy

96
Q

Double-membrane bound vacuole

A

Autophagosome

97
Q

Enumerate the three types of autophagy. Describe each

A
  • chaperone-mediated autophagy - direct translocation of lysosomal membrane by chaperone proteins
  • microautophagy - invagination of lysosomal membrane
  • macroautophagy - sequestration and transportation of cytosol in an autophagosome
98
Q

Autophagy-related genes are called______

A

Atgs

99
Q

Failur to degrade a metabolite due to enzyme deficiencies

A

Storage diseases

100
Q

Abnormal accumulation of triglycerides in parenchymal cells

A

Steatosis / fatty change

101
Q

Clusters of foamy cells found in subepithelial connective tissue of the skin and in tendons producing tumor masses

A

xanthomas

102
Q

smooth muscle cells and macrophages within the intimal layer of the aorta and large arteries are filled with lipid vacuoles, most of which are made up of cholesterol and cholesterol esters

A

Atherosclerosis

103
Q

Focal accumultaions of cholesterol-laden macrophages foun din the lamina propria of gallbladder

A

Cholesterolosis

104
Q

Lysosomal storage disease causing mutations in enzymes for cholesterol trafficking results in accumulations of cholesterol in multiple organs

A

Niemann-pick disease type C

105
Q

ER distention producing Large homogeneous eosinophilic inclusions called_______

A

Russell bodies

106
Q

Alterations within cells or extracellular space giving s homogeneous glassy pink appearance in histologic sections

A

Hyaline / hyaline change

107
Q

Readily available energy source stored in the cytoplasm of healthy cells

A

Glycogen

108
Q

Two kinds of pigments. Describe

A

Endogenous -produced in the body

Exogenous - from the outside of body

109
Q

The most common exogenous pigment

A

Carbon

110
Q

Blackening of tissues of the lungs and involved lymph nodes

A

Anthracosis

111
Q

Serious lung disease caused by aggregates of carbon dust that may induce fibroblastic reaxn or emphysema

A

Coal worker’s pneumoconiosis

112
Q

Form of localized exogenous pigmentation of the skin

A

Tattooing

113
Q

An insoluble pigment; AKA _________ or _________

A

Lipofuscin; lipochrome, wear-and-tear pigment

114
Q

Brown-black pigment formed when the enzyme tyrosinase catalyzes oxidation of tyrosine into dihydroxyphenylalanine

A

Melanin

115
Q

One of major storage forms of iron

A

Hemosiderin

116
Q

Localized hemosiderosis

A

Common bruise

117
Q

Systemic overload of iron

A

Hemosiderosis

118
Q

Increased absorption of dietary iron due to an inborn error of metabolism

A

Hemochromatosis

119
Q

abnormal tissue deposition of calcium salts, together with smaller amounts of iron, magnesium, and other mineral salt

A

Pathologic calcification

120
Q

result of a progressive decline in cellular function and viability caused by genetic abnormalities and the accumulation of cellular and molecular damage due to the effects of exposure to exogenous influences

A

Cellular aging

121
Q

Cells become arrested in terminally nondividing state

A

Replicative senescence

122
Q

Alterations within cells or extracellular space giving s homogeneous glassy pink appearance in histologic sections

A

Hyaline / hyaline change

PT 2nd year (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions