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Histopathology Lecture > Prelims > Flashcards

Prelims Flashcards

1
Q

Salmonella incubation time

A

2 days

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2
Q

Chicken Pox incubation time

A

2-3 weeks after exposure

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3
Q

Intermediate stage between the incubation and illness

A

Prodromal

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4
Q

Hepatitis B incubation time

A

2-3 months

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5
Q

It is when a person is highly contagious and experiencing fulminant symptoms and evident signs

A

Illness

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5
Q

Is characterized as a stage on which some of the early symptoms starts to appear before the appearance of specific diagnostic-related symptoms

A

Prodrome

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5
Q

Increased size and functional capacity of cells

Increased tissue size via enlargement of cells (due to an increase in organelles and structural proteins)

A

Hypertrophy

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6
Q

The final stage of infection which is typical for the recovery stage

A

Convalescent

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6
Q

Decrease in size and function of the cell

Cells shut down its metabolic processes to conserve energy

A

Atrophy

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6
Q

Reduction in cell number

Degradation of cytoskeletal proteins occurs via the
ubiquitin-proteasome pathway

Electron microscopy shows the presence of autophagosomes

A

Numerical Atrophy

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6
Q

Enlargement of a tissue or organ owing to an increase in the number of cells

Increased number as a consequence of cell division

A

Hyperplasia

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6
Q

Trophy or Plasia

Change in ssize

A

Trophy

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7
Q

Trophy or Plasia

Change in number

A

Plasia

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8
Q

Type of Atrophy

such as loss of motor innervation in our skeletal muscles

A

Innervation

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9
Q

Type of Atrophy

Organs are temporarily enlarged and then undergo degradation via atrophic processes

A

Involution

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10
Q

Type of Atrophy

Physiological aging of cells that affects all organs; includes formation of “lipofuscin deposits”

A

Senile aging

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11
Q

These are yellow-brown, granular pigments found in organs such as heart, lung, colon, kidney, liver, and eye

Formed by the peroxidation of polyunsaturated lipids of subcellular membranes

A

Lipofuscin deposits

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12
Q

Overgrowth of cells with enlarged, dark, irregular nuclei

“increased cell division, incomplete maturation of cells”

Reversible and non-malignant

A

Dysplasia

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13
Q

Increased proliferation of “abnormal cells”

A

Neoplasia

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14
Q

Reversible change of one cell type into another

Cells adapt to a change in the environment by altering their morphological appearance

A

Metaplasia

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14
Q

Metaplasia of “corneal squamous cells”

A

Bitot spots

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15
Q

Keratinizing squamous metaplasia of the “bladder”

A

Pearl-like plaques

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15
Q

Smoking can cause ciliated pseudostratified columnar epithelium of the bronchi to?

A

Stratified squamous epithelium

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15
Q

Anaplasia is also known as?

A

Differentiation

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15
Q

Marked regressive change in adult cells towards a more primitive or embryonic cell type

Cellular alterations resemble dysplasia, although more marked, more disorganized, and irreversible

A

Anaplasia

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15
Q

Replacement of cell losses by identical cells to maintain tissue or organ size

A

Regeneration

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16
Q

Tissue loss is both homogeneously functionally and structurally replaced

A

Complete regeneration

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17
Q

Tissue loss is replaced by tissue of an inferior quality

A

Incomplete regeneration

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18
Q

Characterized by reversible cellular swelling and fatty change

A

Hydropic degeneration (Early Stage)

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18
Q

This occurs when the cells cannot adapt to their new environment

A

Cellular injury

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19
Q

Decreased oxygen results in decreased production of ATP

A

Tissue Hypoxia

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20
Q

A molecule with unpaired electrons in the outer orbit.

AKA “reactive oxygen species” (ROS)

A

Free radicals

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21
Q

Hydrogen Peroxide (H2O2) and Superoxide (OH-)4 are examples of?

A

Free Radicals

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22
Q

Superoxide (OH-)4 is broken down by what enzyme?

A

Superoxide dismutase

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23
Q

Hydrogen Peroxide (H2O2) is broken down by what enzyme?

A

Glutathione
Catalase

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24
Q

If formed, enzymatic process phagocytize free radicals

A

Antioxidants

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25
Q

Irreversible Cellular Injury

“Loss of Basophilia”

A

Nuclear karyolysis

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26
Q

Irreversible Cellular Injury

“Shrinkage of nucleus”

A

Pyknosis

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26
Q

Irreversible Cellular Injury

“Fragmentation of nucleus”

A

Karyorrhexis

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26
Q

Uncontrolled breakdown of cells in response to injurious stimuli

A

Necrois

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27
Q

2 main types of necrosis

A

Liquefactive Necrosis
Coagulative Necrosis

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28
Q

Types of Necrosis

“Protein denaturation” is more prominent than enzymatic breakdown

Cell architecture is maintained

A

Coagulative Necrosis

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29
Q

Types of Necrosis

Occurs in situation which “enzymatic breakdown” is more prominent than protein denaturation

These occur in organs that lack a substantial protein-rich matrix (brain)

A

Liquefactive Necrosis

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30
Q

Types of Necrosis

“Massive death” of tissue caused by the obstruction to the blood flow

A

Gangrenous Necrosis

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31
Q

2 types of Gangrenous Necrosi

A

Dry Gangrene
Wet Gangrene/Gas Gangrene

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32
Q

Gangrene caused by Diabetes Mellitus

A

Dry Gangrene

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32
Q

Gangrene when there is “increased” bacterial infection

A

Odor Gangrene

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33
Q

Gangrene strongly associated with bacterial infections

A

Wet Gangrene/Gas Gangrene

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34
Q

Types of Necrosis

“Cheesy-looking necrosis” associated with “tuberculosis” infection and other granulomatous disease processes

A

Caseous Gangrene

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34
Q

A form of chronic inflammation due to some infections (mycobacterial), foreign bodies, and other chronic stimuli

A

Granuloma

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35
Q

Types of Necrosis

A term applied to change in adipose tissue due to trauma or release of enzymes from adjacent organs

A

Fat Necrosis

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36
Q

Fat Necrosis combines with “calcium” to form?

A

Chalky deposits

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37
Q

Types of Necrosis

A special form of necrosis that usually occurs in “immune reactions” in which complexes of antigens and antibodies are deposited in the walls of blood vessels but may also occur in severe hypertension

A

Fibrinoid Necrosis

37
Q

Enzyme necessary for apoptosis

A

Caspases

38
Q

Phases of Apoptosis

Action of caspases cause death of cell

A

Execution

38
Q

Phases of Apoptosis

Caspases (cysteine aspartic acid proteases) become catalytically active

A

Initiation phase

39
Q

It is called the “wear-and-tear pigment”

A

Lipofuscin

39
Q

Phases of Apoptosis

Phagocytosis occurs

A

Disposal

40
Q

Mechanism of Apoptosis

Mitochondria releases cytochrome-C, which combines with Apaf-1 (apoptosis activating factor-1) to activate caspases

A

Initiation of Intracellular Pathway

41
Q

Mechanism of Apoptosis

Fas-Fas ligand binding

Fas ligan binds to a membrane of the tumor necrosis factor family known as the “Fas receptor”

The activated Fas receptor activates FADD (Fas-associated death domain)

FADD activates caspases

A

Initiation of Extracellular Pathway

42
Q

Mechanism of Apoptosis

Apoptotic cells and their fragments entice phagocytes by producing “eat-me” signals

A

Clearance of Apoptotic Cells

43
Q

Cell death initiated by engagement of TNF receptors as well as other poorly defined triggers

Receptor-interacting protein (RIP) kinase

A

Necroptosis

43
Q

Cell death associated with activation of cytosolic danger-sensing protein complex called “inflammasome”

Activation of caspases that induce the production of cytokines that induce inflammation, often manifested by “Fever”

A

Pyroptosis

44
Q

Mainly due to kidney problems and accumulations often involve “intermediate filaments”

A

Protein Accumulations

44
Q

Glycogen accumulates as part of glycogen storage disorders

Most common organs affected are “liver” and “skeletal muscle”

Ex. McArdle Syndrome

A

Glycogen Accumulations

44
Q

Type V Glycogen Storage Disease (GSD V)

It is a rare inherited condition in which the body is not able to break down glycogen

Gene problem in the enzyme “muscle glycogen phosphorylase”

A

McArdle Syndrome

45
Q

Protein accumulation in the liver seen in alcohol cirrhosis

A

Mallory hyaline (streaks)

45
Q

Protein accumulation seen in Alzheimer’s Disease

A

Neurofibrillary tangles

46
Q
A
46
Q

2 Forms of Iron Accumulation

A

Hemosiderosis
Hemochromatosis

46
Q

What gene code of telomeres protects the ends of t he chromosome and they shorten with cell divisions?

A

TTAGGG

46
Q

Accumulation of iron in “organs”

Without resultant side effects

This iron pigment is frequently within macrophages

A

Hemosiderosis

47
Q

Fat Accumulation is also called as?

A

Steatosis

47
Q

Term used for aggregates of “ferritin micelles”

A

Hemosiderin

47
Q

Hemosiderin stains positive(+) in what stain?

A

Prussian Blue

48
Q
A
48
Q

Accumulation of iron in “parenchymal cells” resulting in side effects

Including Congestive Heart Failure, Diabetes Mellitus, and Cirrhosis

Can be acquired or heridetary

A

Hemochromatosis

48
Q

A disease where there is manifestation of premature aging and a defective DNA Helicase

A

WERNER Syndrome

49
Q

Type of Opsonin

“Recognized by Fc receptors on WBC”

A

IgG

50
Q

Type of Opsonin

“Recognized by CR 1,2,3 on leukocytes”

A

C3b

51
Q

Type of Opsonin

“Recognized by C1q on leukocytes”

A

Collectins

52
Q

Uses 2 oxygen molecules to produce superoxide radical (O2)

Superoxide radical converts to hydrogen peroxide (H2O2) which degrades foreign substances

A

NADPH Oxidase

53
Q

Converts hydrogen peroxide and halogen (CI) to HOCl

Then causes halogenation or lipid protein peroxidation

A

Myeloperoxidase

54
Q

Protein-rich fluid with specific gravity of more than 1.020

A

Exudate

55
Q

Protein-poor fluid with
specific gravity of less than 1.012

A

Transudate

56
Q

The main tissue is an outpouring of fluid with a low plasma protein and cell content

Appearance: Relatively clear, watery fluid

A

Serous Inflammation

57
Q

Acute inflammatory exudates has a high plasma protein content

Appearance: finely particulate, thick fluid

A

Fibrinoid Inflammation

58
Q

Acute inflammatory exudates is particularly rich in neutrophil leukocytes

Pus-thick, creamy fluid composed of large numbers of living and necrotic PMNs and necrotic tissue debris

A

Suppurative (Purulent) Inflammation

59
Q

Collection of semi-liquid pus within tissues

A

Abscess

59
Q

S. pneumoniae, E. coli, N. meningococci, and N. gonococci are bacteria that produce purulent inflammation

These are called?

A

Pyogenic bacteria

60
Q

Mediator in Repair

Stimulates granulation tissue formation

A

Epidermal Growth Factor (EGF)

61
Q

Mediator in Repair

Induces blood vessel formation

A

Vascular Endothelial Growth Factor (VEGF)

62
Q

An active process resulting from arteriolar dilation and increased blood inflow, as occurs at sites of inflammation or in exercising skeletal muscle

A

Hyperemia

62
Q

Mediator in Repair

Stimulates blood vessel formation and wound repair through macrophages, fibroblasts, and endothelial cell migration

A

Fibroblast Growth Factor (FGF)

62
Q

Mediator in Repair

Promotes migration and proliferation of fibroblasts, smooth muscle cells, and monocytes

A

Platelet-Derived Growth Factor (PDGF)

63
Q

Mediator in Repair

Act as growth inhibitor for epithelium

A

Transforming Growth Factor-B (TGF-B)

63
Q

A passive process resulting from impaired outflow of venous blood from a tissue

It can occur systemically as in cardiac failure, or locally because of an isolated venous obstruction

A

Congestion

64
Q

Effusion of the peritoneal cavity is called?

A

Hydroperitoneum or Ascites

64
Q

Is severe, generalized edema marked by profound swelling of subcutaneous tissue and accumulation of fluid in body cavities.

A

Anasarca

65
Q

Originate from deep venous thromboses and are responsible for the most common form of thromboembolic disease

A

Pulmonary emboli

66
Q

It is a state in which diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion and leads to cellular hypoxia

A

Shock

66
Q

It is an area of ischemic necrosis caused by occlusion of the vascular supply to the affected tissue

A

Infarct

67
Q

It is an autoimmune disease involving multiple organs, characterized by a vast array of autoantibodies, particularly “Antinuclear Antibodies (ANAs)”, in which injury is caused mainly by deposition of immune complexes and binding of antibodies to various cells and tissues

A

Systemic Lupus Erythematosus (SLE)

68
Q

Chronic disease characterized by “Dry eyes” and “Dry mouth” resulting from immunologically mediated destruction of lacrimal and salivary glands

A

Sjogren Syndrome

69
Q

In Sjogrens, what is the term used for “Dry eyes”

A

Keratoconjunctivitis sicca

69
Q

In Sjogrens, what is the term used for “Dry mouth”

A

Xerostomia

70
Q

Other name of Systemic Sclerosis

A

Scleroderma

70
Q

Identify the Abnormal Protein in the Autosomal Dominant Inheritance Diseases

  1. Marfan Syndrome
A

Fibrillin

71
Q

An immunologic disorder characterized by excessive fibrosis in multiple tissues, obliterative vascular disease, and evidence of autoimmunity, mainly in the production of multiple antibodies

A

Systemic Sclerosis (Scleroderma)

72
Q

Identify the Abnormal Protein in the Autosomal Dominant Inheritance Diseases

  1. Ehler-Danlos Syndrome
A

Collagen

72
Q

Belongs to a group of disorders characterized by necrotizing inflammation of the walls and blood vessels that show strong evidence of an immunologic basis

A

Polyarteritis Nodosa

72
Q

The disease is characterized serologically by high titers of antibodies to U1 ribonucleoprotein.

A

Mixed Connective Tissue Disease

72
Q

Identify the Abnormal Protein in the Autosomal Dominant Inheritance Diseases

  1. Hereditary Spherocytosis
A

Spectrin
Ankyrin
Protein 4.1

72
Q

Identify the Abnormal Protein in the Autosomal Dominant Inheritance Diseases

  1. Familial Hypercholesterolemia
A

LDL Receptor

73
Q

Identify the Abnormal Protein in the Autosomal Dominant Inheritance Diseases

  1. Neurofibromatosis, Type 1
A

Neurofibromin-I (NF-I)

73
Q

Identify the Abnormal Protein in the Autosomal Recessive Inheritance Diseases

  1. Cystic Fibrosis
A

Cystic Fibrosis Transmembrane Regulator

73
Q

Identify the Abnormal Protein in the Autosomal Dominant Inheritance Diseases

  1. Adult Polycystic Kidney Disease
A

Polycystin-I (PKD-I)

74
Q

Identify the Abnormal Protein in the Autosomal Recessive Inheritance Diseases

  1. Phenylketonuria
A

Phenylalanine Hydroxylase

75
Q

Identify the Abnormal Protein in the Autosomal Recessive Inheritance Diseases

  1. Severe Combined Immunodeficiency (SCID)
A

Adenosine Deaminase (ADA)

75
Q

Identify the Abnormal Protein in the Autosomal Recessive Inheritance Diseases

  1. Tay-Sachs Disease
A

Hexosaminidase

76
Q

Identify the Abnormal Protein in the Autosomal Recessive Inheritance Diseases

  1. alpha and beta-thalassemia
  2. Sickle Cell Anemia
A

Hemoglobin

77
Q

Identify the Abnormal Protein in the X-Linked Recessive Inheritance

  1. Hemophilia A
A

Factor VIII

77
Q

Identify the Abnormal Protein in the X-Linked Recessive Inheritance

  1. Duchenne/Becker Muscular Dystrophy
A

Dystrophin

77
Q

Identify the Abnormal Protein in the X-Linked Recessive Inheritance

  1. Fragile X Syndrome
A

FMRP (Fragile X Mental Retardation Protein)

78
Q

A transmission pattern characterized by expression in heterozygous state

Affects both males and females equally

Both sexes can transmit the disorder

Often involve “dysfunctional receptors and structural proteins”

A

Autosomal Dominant

79
Q

A transmission pattern that occur when “both copies” of a gene are mutated and frequently involve “enzymes”

Males and females are affected equally

A

Autosomal recessive

80
Q

A transmission pattern that is transmitted by heterozygous females to their sons, who manifest the disease

Females only become “carriers”

A

X-Linked

81
Q

Gold standard for Covid-19 Tests

A

PCR

81
Q

If asymptomatic, but exposed to COVID-19, wait at least __ days after exposure before taking a test

A

5 days

81
Q

To be sure, FDA recommends __ negative antigen tests for individuals with symptoms or __ antigen tests for those without symptoms, performed 48 hours apart

A

2 negative tests for those with symptoms
3 tests for those without symptoms

Histopathology Lecture (2 decks)

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