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Part I Boards Review > General Pathology Material > Flashcards

General Pathology Material Flashcards

1
Q

4 cellular adaptations to stress:

A

hypertrophy, hyperplasia, metaplasia and atrophy

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2
Q

the ability for a cell to adapt may be exceeded. this leads to either ___ or ___ cell injury

A

reversible; irreversible

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3
Q

term that refers to the build up of fat within a damaged cell:

A

steatosis

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4
Q

The cellular adaptation characterized by an increase in size of the cells/organs. no new cells are created.

A

hypertrophy

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5
Q

what is hypertrophy the result of?

A

overloading or an increase in growth factors

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6
Q

the cellular adaptation characterized by an increase in the number of cells and an increase in growth factor

A

hyperplasia

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7
Q

the cellular adaptation characterized by a reduction in cell size and reduced function

A

atrophy

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8
Q

during atrophy, cells decrease in size which results in a ____ in protein synthesis and ____ in protein breakdown

A

decrease; increase

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9
Q

when cerebral tissue atrophies, what happens to the gyri and sulci

A

the gyri narrow and the sulci widen

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10
Q

the cellular adaptation that is characterized by the reversible replacement of one mature cell type with another

A

metaplasia

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11
Q

when does metaplasia occur?

A

it is an adaptation to prolonged stressors

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12
Q

what is the risk of metaplasia?

A

malignant transformation

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13
Q

the type of cellular injuryis transient and mild. It results in cellular swelling, steatosis, and there is no damage to the membranes or nucleus.

A

reversible cellular injury

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14
Q

This type of cellular injury is prolonged and severe. It results in mitochondrial dysfunction or disturbed membranes.

A

irreversible cellular injury

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15
Q

What two things can happen to a cell that has undergone an irreversible cellular injury?

A

apoptosis or necrosis

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16
Q

This type of cellular death is always pathological and inflammatory. It can be caused by trauma, toxin, or ischemia.

A

necrosis

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17
Q

This type of cellular death is physiological/pathological and non-inflammatory. It can be caused by a decrease in growth factors or damage to DNA/proteins.

A

apoptosis

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18
Q

What are the morphologic patterns of tissue necrosis?

A
  • Coagulative (gangrenous)
  • Liquefactive
  • Caseous
  • Fat
  • Fibrinoid
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19
Q

This type of necrosis is due to vascular occlusion, which results in the death of tissue and solid organ infarction. The tissue structure is preserved, firm.

A

Coagulative necrosis (ischemic necrosis)

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20
Q

This is a type of coagulative necrosis found in an extremity. It can be caused by peripheral vascular disease in people who have diabetes or atherosclerosis.

A

Gangrenous necrosis (dry, wet, gas)

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21
Q

This is a type of necrosis where dead cells are completely digested and a liquid viscous mass forms. It can be caused by infections or hypoxia in the CNS.

A

Liquefactive necrosis

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22
Q

This type of necrosis has a “cheese-like” appearance. It is enclosed within a distinctive border and is typical of tuberculosis infections.

A

Caseous necrosis

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23
Q

This is a walled-off accumulation of macrophages.

A

granuloma

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24
Q

This type of necrosis is characterized by the local destruction of fat. Its gross morphology is chalky white.

A

fat necrosis

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25
Q

This type of necrosis is due to autoimmune reactions and requires light microscopy to identify. Immune complexes and fibrin are deposited into the arterial walls, which weakens them and increases the risk of aneurysm.

A

fibrinoid necrosis

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26
Q

What are some conditions that may result in fibrinoid necrosis?

A

-Polyarteritis nodosa (affects the coronary artery)
-Systemic lupus erythematosus (affects the renal vessels)
-Malignant hypertension (high blood pressure)
Transplant rejections

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27
Q

This term is used to describe programmed/regulated cellular death. It occurs in unneeded or irreparable cells and involves enzymatic breakdown of DNA and cytoplasmic proteins. Inflammation does not occur in this process.

A

apoptosis

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28
Q

This type of apoptosis occurs with embryonies (gill slits, webs), endometrium, breasts, immune cells, and normal cell populations.

A

Physiologic apoptosis

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29
Q

This type of apoptosis occurs in DNA damaged cells, misfolded proteins, and viral infections. It may accompany atrophy.

A

Pathologic apoptosis

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30
Q

During apoptosis, what does the activation of caspases lead to?

A

cellular fragmentation

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31
Q

This apoptotic pathway involves the decrease of GF, DNA damage, misfolded proteins, and an increase in mitochondrial membrane permeability.

A

mitochondrial (intrinsic) pathway

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32
Q

Which caspase is activated in the mitochondrial (intrinsic) pathway?

A

caspase 9

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33
Q

This apoptotic pathway involves the binding of surface molecules to “death receptors”. This pathway eliminates self-reactive lymphocytes or virus infected cells.

A

death receptor (extrinsic) pathway

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34
Q

Which caspase is activated in the death receptor (extrinsic) pathway?

A

caspase 8

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35
Q

Myocardial infarction and cerebral infarct are conditions that result from what type of cellular injury?

A

Ischemia-reperfusion injury

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36
Q

This type of calcification occurs through cellular injury/aging and most often occurs in necrotic cells.

A

Dystrophic calcification

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37
Q

This is an autosomal dominant mutation that is characterized by dysfunctional soft tissue repair and trauma to a tissue resulting in heterotopic ossification.

A

Fibrodysplasia ossificans progressiva

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38
Q

This type of calcification is characterized by the accumulation of Ca in normal tissues. It most often occurs in vessels, kidnys, lungs, and G.I. mucosa.

A

metastatic calcification

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39
Q

These conditions are characterized by an accelerated aging process.

A
  • Progeria (mortality around teens)

- Werner syndrome

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40
Q

What are some examples of leukocytes?

A
  • Lymphocytes
  • Monocytes
  • Neutrophils
  • Eosinophils
  • Basophils
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41
Q

What is the difference between granulocytes and agranulocytes?

A

Granulocytes: acute inflammatory cells, fast acting, and contain granules
Agranulocytes: slow acting, but last a long time. Do not contain granules

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42
Q

What types of cells detect injury or infection?

A

Macrophages, dendritic cells, and mast cells

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43
Q

When an injury or infection is detected what do immune cells typically do?

A

Secrete cytokines and attract plasma proteins, which induces/regulates inflammation

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44
Q

What are the five steps of inflammation?

A
  • Recognize the injury/microbe
  • Recruit leukocytes
  • Remove agent (phagocytosis)
  • Regulate (control) response
  • Resolution and tissue repair
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45
Q

What are some stimuli of acute inflammation?

A

Infection, trauma, ischemia, necrosis, foreign bodies, and hypersensitivity reactions.

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46
Q

What are the components of acute inflammation?

A
  • Vascular changes

- Leukocyte recruitment and activation

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47
Q

This pattern recognition receptor of acute inflammation recognizes all types of infectious pathogens and is located in the plasma membrane.

A

toll-like receptors

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48
Q

This pattern recognition receptor of acute inflammation recognizes products of dead cells (uric acid, ATP) and crystals. It is located in the cytoplasm.

A

Inflammasome

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49
Q

What are some of the vascular changes associated with acute inflammation?

A
  1. Immediate vasoconstriction (few seconds)
  2. Vasodilation
  3. Increased permeability of fluid leading to increased viscosity and diapedesis
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50
Q

What are the mechanisms of increased permeability during acute inflammation?

A
  • Endothelial contraction
  • Endothelial necrosis
  • Leakage from angiogenesis
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51
Q

Which associated with inflammation, exudate or transudate?

A

exudate

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52
Q

What are the steps of leukocyte recruitment?

A
  1. Margination and rolling (selectins)
  2. Firm adhesion to endothelium (integrins)
  3. Transmigration between endothelial cells
  4. Chemotaxis toward target tissue
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53
Q

Which leukocytes predominates acute inflammation?

A

For the first 48 hours neutrophils dominate

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54
Q

This is an immunoglobulin G (IgG) and is a component of phagocytosis. They target/label a cell for destruction and enhance macrophage binding and breakdown.

A

Opsonins

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55
Q

What is the process of targeting/ labeling a cell for destruction?

A

Opsonization

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56
Q

What are the four types of inflammation?

A

Serous, fibrinous, suppurative (purulent), and ulcerative

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57
Q

This type of inflammation is characterized by serum accumulating within or below the epidermis. It usually produces a blister.

A

serous

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58
Q

This type of inflammation is caused by a severe injury and is characterized by a large amount of vessel permeability, which allows large molecules out of circulation and the formation of fibrin-rich exudate and scars. Primarily occurs in the pericardial sac, peritoneum, and pleural cavity.

A

fibrinous

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59
Q

This type of inflammation is characterized by a localized infection of pus-forming organisms (Staph. aureus). A pus-filled abcess usually forms.

A

suppurative (purulent)

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60
Q

This type of inflammation usually occurs near an organ or tissue surface and characterized by a shedding of necrotic tissue. Peptic ulcers and aphthous ulcers are good examples.

A

ulcerative

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61
Q

These cell-derived mediators of inflammation increase white blood cell production, adhesion, and migration. They are produced by mast cells, endothelial cells, and macrophages.

A

cytokines

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62
Q

These cell-derived mediators of inflammation are primarily produced by neutrophils and macrophages. They are used to kill and degrade microbes and a prime example is nitric oxide, which is used in vasodilation and microbial killing.

A

reactive oxygen species

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63
Q

This plasma protein-derived mediator of inflammation is involved with opsonization and the membrane attack complex. They vasodilate and increase permeability.

A

complement proteins

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64
Q

What three things characterize chronic inflammation?

A
  • Mononuclear leukocyte cells
  • Tissue destruction and fibrosis
  • Vessel production and repair
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65
Q

These are the dominant cells at the site of chronic inflammation. They eliminate microbes/dead cells, initiate angiogenesis/fibrosis, and are activated by endotoxins, cytokines, and foreign bodies.

A

macrophages

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66
Q

These cells are involved with innate and adaptive immunity. They sustain chronic inflammation.

A

lymphocytes

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67
Q

This is an increase in blood leukocyte count (15-20 k/uL) and very common with bacterial infections.

A

Leukocytosis

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68
Q

This is an extremely large increase in blood leukocyte count (40-100 k/uL), mimics leukemia, and is involved with chronic inflammation.

A

Leukemoid reactions

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69
Q

This is a decrease in blood leukocyte count

A

Leukopenia

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70
Q

These are regulators of the cell cycle.

A

cyclins

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71
Q

These cells that have an intrinsic proliferative capacity are continuously dividing and are typically found in epithelia and hematopoietic cells.

A

labile

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72
Q

These cells that have an intrinsic proliferative capacity are typically in a quiescent state (G0), have limited replication, and are typically found in solid organs (kidney, liver, pancreas).

A

stable

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73
Q

These cells that have an intrinsic proliferative capacity are terminally differentiated, injury is irreversible, and are typically classified as neurons, skeletal, and cardiac muscles.

A

permanent

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74
Q

What types of cells produce growth factors?

A
  • Macrophages and lymphocytes at the site of inflammation

- Stromal or parenchymal cells in response to injury

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75
Q

What are the general functions of growth factors?

A

Stimulate:

  • cellular proliferation/repair
  • cellular migration
  • cellular differentiation
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76
Q

What are growth factor signaling mechanisms?

A

Autocrine: acts on secreting cells
Paracrine: acts on adjacent cells
Endocrine: systemic, via the circulatory system

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77
Q

What are the steps of scar formation?

A
  • Angiogenesis
  • Fibroblast migration and proliferation
  • Collagen deposition (scar)
  • Remodeling (lifetime)
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78
Q

What are the steps of angiogenesis?

A
  • Vasodilation
  • Pericyte separation
  • Endothelial migration and proliferation
  • Capillary remodeling
  • Development and maturation of: pericytes, smooth muscles, and basement membrane
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79
Q

These enzymes breakdown collagen, require zinc ions as a cofactor, and are produced by fibroblasts, macrophages, etc.

A

Matrix metalloproteinase (MMPs)

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80
Q

What are the phases associated with the healing of a skin wound?

A
  • Inflammation
  • Granulation tissue
  • ECM deposition and remodeling
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81
Q

After sutures are removed from an injury what is the strength of that wound compared to normal tissue? After the 1st month? After 3 months?

A

10%; 70%; 80%

-injured tissue never reaches its previous strength after healing.

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82
Q

This is the active process of increasing blood volume within tissues. It is done by arteriolar dilation, causes tissue erythema (redness), and results from inflammation or exercise.

A

Hyperemia

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83
Q

This is the passive process of increasing blood volume within tissues. It is done by decreasing venous outflow, causes tissue cyanosis (blue), and results from venous obstruction.

A

Congestion (congestive heart failure, DVT (deep vein thrombosis), testicular torsion)

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84
Q

This this type of congestion is characterized by alveolar capillary engorgement, edema, and hemorrhage.

A

Acute pulmonary congestion (Acute respiratory distress syndrome (ARDS))

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85
Q

This type of congestion is characterized by the alveolar septa becoming fibrotic and the presence of alveolar macrophages and hemosiderin (“heart failure cells”)

A

Chronic pulmonary congestion (congestive heart failure (CHF))

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86
Q

This type of congestion is characterized by a “nutmeg liver”, steatosis, fibrosis (cirrhosis), hemorrhage, and necrosis.

A

Congestive hepatophy (hepatic congestion (CHF)

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87
Q

An increase in this type of pressure is characterized by an increased intravascular pressure most likely caused by impaired venous return.

A

hydrostatic pressure

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88
Q

This type of edema is characterized by transudate (protein-poor) fluid and no osmosis.

A

pitting edema

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89
Q

This type of edema is characterized by exudate (protein-rich) fluid and osmosis.

A

non-pitting edema

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90
Q

This type of hemorrhage often starts off with a reddish/blue color due to the presence of hemoglobin, transitions to a greenish color as hemoglobin is broken down into bilirubin, and then a yellowish color as bilirubin is broken down into hemosiderin. The areas are typically 1-2 cm large.

A

Ecchymosis

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91
Q

What three factors compose virchow’s triad?

A

Endothelial injury, abnormal blood flow, and hypercoagulability

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92
Q

These types of thrombi occur at the site of stasis and grow in the direction blood flow. They can result in congestion, tenderness, and pitting edema.

A

venous thrombi

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93
Q

What are some inherited mutations that result in coagulation disorders?

A
  • Factor V (decreases antithrombotic)

- Prothrombin (increases thrombotic)

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94
Q

What are some examples of solid, liquid, and gaseous emboli?

A

Solid: fat (marrow), plaque debris, tumor fragment
Liquid: amniotic fluid (labor)
Gaseous: nitrogen (decompression/caisson disease), air (needle)

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95
Q

Systemic thromboemboli are within what system? Arterial or Venous?

A

arterial system

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96
Q

80% of systemic thromboemboli arise from what type of thrombi?

A

Cardiac mural (wall) thrombi

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97
Q

This term is used to describe emboli which cross from the venous system to the arterial system.

A

Paradoxical embolism

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98
Q

What are some origins of paradoxical emboli? What can they cause?

A

Origins:

  • Originates as a deep vein thrombosis
  • Crosses to the arterial system through Atrial or ventricular septal defect

Results in stroke

99
Q

These cells produce platelets.

A

Megakaryocytes

100
Q

What is the traditional definition of shock?

A

Peripheral vasoconstriction

101
Q

Both cardiogenic and hypovolemic shock cause traditional signs and symptoms of shock, which are…

A
  • Cyanosis
  • Decreased urine output
  • Increased respiratory rate
  • Decreased level of conciousness
  • Hypotension
  • Release of aldosterone
  • Constriction of splanchnic vessels
102
Q

What demographic is the most likely to develop autoimmune conditions?

A

Childbearing aged females

103
Q

This autoimmune condition is characterized by a failed self-tolerance leading to massive antibody formation (anti-nuclear antibodies (ANA), IgG). It is extremely variable, has an insidious onset, and can occur in any organ.

A

Systemic lupus erythematosus (lupus)

104
Q

What types of hypersensitivities are involved in lupus?

A

Type III (immune complex deposition) and Type II (autoantibodies against various cells)

105
Q

This is a systemic autoimmune disease characterized by exocrine gland (lacrimal and salivary) destruction and enlargement. It is also positive for ANA and a type IV hypersensitivity.

A

Sjogren syndome (SS)

106
Q

This condition is a part of Sjogren syndrome and characterized by dry eyes.

A

Keratoconjunctivitis sicca

107
Q

This condition is a part of Sjogren syndrome and characterized by dry mouth.

A

Xerostomia

108
Q

If Sjogren syndrome is affecting the body alone, what is called?

A

Sicca syndrome

109
Q

Which other autoimmune conditions are patients with Sjogren syndrome most likely to have?

A

Rheumatoid arthritis, lupus, or systemic sclerosis

110
Q

This systemic autoimmune disease is characterized by extensive fibrosis in multiple tissues and vascular destruction in small arteries. It most commonly occurs in the skin.

A

Systemic sclerosis (scleroderma)

111
Q

What are some common features of systemic sclerosis?

A
  • Raynaud phenomenon
  • Malabsorption
  • Dysphagia
  • Renovascular hypertension
  • Renal failure
  • Pulmonary hypertension
  • Dyspnea
  • Myalgia
  • Arthritis
112
Q

This type of systemic sclerosis has mild skin involvement (fingers, face, late visceral involvement) and is also called CREST syndrome.

A

Limited systemic sclerosis

113
Q

What is CREST syndrome?

A
  • Calcinosis
  • Raynaud phenomenon
  • Esophageal dysmotility (fibrosis of the lower 2/3)
  • Sclerodactyly (hard/ eroded skin)
  • Telangiectasia (spider veins)
114
Q

This type of systemic sclerosis has rapid/widespread skin involvement, early visceral involvement, and is aggressive.

A

Diffuse systemic sclerosis

115
Q

This primary immune deficiency disorders has an onset of 6 months and often occurs in males. It is caused by failed B cell maturation resulting in the inability to produce antibodies. It is treated by a good prognosis and IgG infusions.

A

X-linked agammaglobulinemia (Bruton disease)

116
Q

This primary immune deficiency disorder is due to a decreased antibody response to infection. Individuals have normal B cells but no plasma cells. This results in an increase in autoimmunity.

A

Common variable immunodeficiency

117
Q

This primary immune deficiency disorder is due to a decreased IgA production. Most cases are asymptomatic or very mild and characterized by upper GI and respiratory infections.

A

Isolated IgA deficiency (most common)

118
Q

This primary immune deficiency disorder is due to an increase in IgM and decrease in IgG, IgA, and IgE. Most are X-linked mutations and are characterized by recurrent pyogenic bacterial infections.

A

Hyper-IgM syndrome

119
Q

This primary immune deficiency disorder is known as the “bubble boy” disorder and is characterized by lymphopenia (no T or B cells) and lymphoid atrophy.

A

Severe combined immunodeficiency (SCID)

120
Q

This primary immune deficiency disorder is due to a defective TH17 resultin in chronic mucocutaneous fungal infections.

A

Defects in lymphocyte activation

121
Q

This primary immune deficiency disorder is characterized by defective complements, phagocytes, TLRs, and can result in multiple infections.

A

Defects in innate immunity

122
Q

What types of tests can be used to screen for HIV?

A
  • ELISA test (gp120)

- Western blot

123
Q

This stage of AIDS occurs after 3-6 weeks after infection and is characterized by pyrexia, pharyngitis, myalgia, and viremia.

A

acute phase

124
Q

This stage of AIDS occurs 2-10 years after infection and is characterized by generalized lymphadenopathy, a steady decrease of CD4+ cells, and gradually increase viremia. Other features may include a reemergence of shingles, extended pyrexia, fatigue, and candidiasis.

A

chronic (latent) phase

125
Q

This stage of AIDS occurs when you have 1 month), weight loss and CNS defects.

A

crisis phase

126
Q

This condition is due to misfolded proteins being produced and accumulating in a variety of tissues. This can result in damage to tissues and a disruption of function.

A

Amyloidosis

127
Q

This type of amyloid protein is associated with amyloid precursor protein leading to the production of cerebral plaques (Alzheimer’s disease). They are also associated with Down syndrome.

A

Beta-Amyloid

128
Q

What is the most common tissue affected by amyloidosis?

A

kidneys

129
Q

What are the two structural components of a tumor?

A

Parenchyma and stroma

130
Q

This component of a tumor is composed of transformed cells that are neoplastic and clonal. This components also determines the biological nature (aggressiveness) of the cancer.

A

parenchyma

131
Q

This component of a tumor is composed of supportive tissue and is non-neoplastic. This component is involved in long-term tumor survival.

A

stroma

132
Q

These are benign epithelial neoplasms which have finger-like fronds.

A

papilloma

133
Q

These are benign tumors of capillary endothelial cells.

A

Hemangioma

134
Q

These are benign tumors of smooth muscle (“fibroid”).

A

Leiomyoma

135
Q

These types of malignant tumors are formed from mesenchyme (mesoderm) and can develop at any age. Examples include bone, muscle, vasculature.

A

sarcomas

136
Q

These types of malignant tumors are formed from epithelia (ectoderm, endoderm) and most commonly occur in mid to late adulthood. Examples include lung, breast, and colon.

A

carcinomas

137
Q

This is the most common benign tumor of the female breast. It contains two tissue types and is only fibrous neoplasia.

A

fibroadenoma

138
Q

This is a benign tumor of tissue native to a particular site. It is well-differentiated.

A

hamartoma

139
Q

This is a mass that projects from a mucosal surface.

A

polyp

140
Q

This is the first phase of carcinoma progression and is characterized by disorderly proliferation, cells are irregular, and non-neoplastic.

A

dysplasia

141
Q

This is the second phase of carcinoma progression and is characterized by dysplasia throughout the epithelia. It is well-localized and has no penetration of the basement membrane.

A

carcinoma in situ: early neoplasm

142
Q

This is the third phase of carcinoma and involves local destruction of cells, penetration of the basement membrane, and the most likely to metastasize.

A

invasive carcinoma: more aggressive

143
Q

What are the four characteristics of neoplasia?

A
  • Differentiation and anaplasia
  • Rate of growth
  • Local invasiveness
  • Metastasis
144
Q

This characteristic of neoplasia is used to describe how closely cells resemble their precursors both structurally and functionally.

A

differentiation

145
Q

This characteristic of neoplasia is used to describe a loss of differentiation.

A

anaplasia

146
Q

What is the rate of growth of a benign tumor? Malignant?

A

Benign: slow and controlled
Malignant: fast and uncontrolled

147
Q

In terms of local invasion, how would benign and malignant tumors be described?

A

Benign: well-localized, isolated, non-invasive, and likely to be encapsulated
Malignancy: is destructive, has progressive invasion (local and distant), and is less likely to be encapsulated

148
Q

This characteristic of neoplasia is used to describe secondary implantation into remote tissue and is the most reliable indicator of malignancy.

A

Metastasis (mets)

149
Q

This method of metastasis is the most common mode of cacinoma metastasis and is determined by site and tumor parenchyma.

A

Lymphatic spread

150
Q

In lymphatic spread of cancer, what is typically the first area to be affected by?

A

Sentinel lymph node

151
Q

This method of metastasis is very rapid and is the most common mode of sarcoma metastasis.

A

Hematogeneous spread

152
Q

In hematogeneous spread of cancer, what is typically the first area to be affected?

A

capillary beds

153
Q

What are the three categories of hereditary cancer?

A
  • Autosomal dominant cancer syndromes
  • Autosomal recessive syndrome
  • Familial cancer of uncertain inheritance
154
Q

This type of hereditary cancer is due to a single gene mutation that is inherited. It is usually named by its marker phenotype (BRCA1).

A

Autosomal dominant cancer syndromes

155
Q

This type of hereditary cancer is due to two altered alleles leading to genomic instability. Defective DNA repair enzymes are present and the best example of this is Xeroderma pigmentosa (sensitivity to UV light).

A

Autosomal recessive syndrome

156
Q

This type of hereditary cancer is the most sporadic cancer and has some familial association. There is no marker phenotype and has multifactorial inheritance.

A

Familial cancer of uncertain inheritance

157
Q

What are the four types of regulatory genes that could be involved in carcinogenesis?

A
  • Proto-oncogenes
  • Tumor suppressor genes (TSGs)
  • Apoptosis genes
  • DNA repair genes
158
Q

This term is used to describe an abnormal number of chromosomes.

A

Aneuploidy

159
Q

What are the three types of structural abnormalities?

A
  • Balanced translocations
  • Deletions
  • Gene amplification
160
Q

These are non-coding RNA molecules that function to inhibit gene expression. They also suppress translation.

A

microRNAs

161
Q

How do cancer cells express self-sufficiency in growth signals?

A
  • Produce own GFs
  • Stimulate stromal GFs
  • Altered GF receptors
162
Q

These genes encode inhibitory proteins, normally decrease cellular proliferation, and regulates growth (“apply brakes”).

A

tumor suppressor genes

163
Q

This term is used to describe reversible cell cycle arrest (G1). There is minor DNA damage and an increase in repair genes.

A

Quiescence

164
Q

This term is used to describe a permanent cell cycle arrest. There is major DNA damage and has failed repair.

A

Senescence

165
Q

This condition is characterized by a mutation in the TP53 gene and results in multiple tumors.

A

Li-Fraumeni syndrome

166
Q

When angiogenesis occurs in tumor cells, what do the blood vessels typically look like?

A

Poorly organized: leaky, dilated, and tortuous

167
Q

What are the steps involved with invasion of the ECM by cancer cells?

A
  • Loosening of tumor cells
  • Breakdown of ECM
  • Changes in ECM attachment
  • Migration of tumor cells
168
Q

What is the “glue” that holds cells together?

A

E-cadherin

169
Q

What are three DNA repair systems?

A
  • Mismatch repair
  • Nucleotide excision repair
  • Homolgous recombination repair
170
Q

What condition is characterized by a defective nucleotide excision repair system?

A

Xeroderma pigmentosum

171
Q

What is radiation carcinogenesis characterized by?

A

Formation of pyrimidine dimers

172
Q

What is the most common form of cancer in the US?

A

skin cancer

173
Q

What are some examples of oncogenic DNA viruses?

A
  • Human papillomaivrus (HPV)
  • Epstein-Barr virus (EBV)
  • Hepatitis B and C viruses (HBV, HCV)
  • Kaposi sarcoma herpesvirus (KSHV) a.k.a. human herpesvirus-8 (HHV-8)
174
Q

What are some antitumor effector mechanisms?

A
  • Cytotoxic T cells (CD8+ T cells)
  • Natural killer cells
  • Macrophages
175
Q

Cancer is the most common among the immunocompromised. True or False?

A

true

176
Q

Grading (I-IV) and staging of cancers are based on what?

A

The degree of cellular differentiation

177
Q

How many stages of cancer are there and how are they determined?

A
  • Stage 0-IV

- Determined by the size of the primary tumor, lymph node involvement, and presence of metastasis.

178
Q

What substance indicates problems with the prostate gland when found in high amounts?

A

prostate specific antigen

179
Q

These are permanent changes in DNA.

A

Mutations

  • Germ line (hereditary): all cells
  • Somatic (acquired): some cells
180
Q

This term refers to all of the last trimester and one month after.

A

perinatal

181
Q

This term refers to the newborn (first four weeks).

A

neonate

182
Q

This term refers to the child after the first year.

A

infant

183
Q

This term refers to single mutations which may have a variety of phenotypic effects.

A

Pleiotropy

184
Q

This term refers to multiple mutations being expressed as the same trait.

A

Genetic heterogeneity

185
Q

This condition is autosomal dominant and characterized by a fibrillin (structural protein) gene mutation. Some characteristics include arachnodactyly, bilateral lens subluxation, ruptured aorta, and basilar invagination.

A

Marfan syndrome

186
Q

This condition is a group of single-gene disorders (autosomal dominant or recessive) caused by defective collagen synthesis. It is characterized by hyperextensible skin and hypermobile joints.

A

Ehlers-Danlos syndrome

187
Q

This is the most common Mendelian disorder (autosomal dominant). It is caused by a mutated LDLR gene and characterized by impaired LDL transport and catabolism.

A

Familial hypercholesterolemia

188
Q

These are cholesterol deposits on tendons.

A

Xanthomas

189
Q

This condition is autosomal recessive and caused by a mutation in the CFTR gene. This results in decreased chloride ion transport resulting in viscous secretions (lungs and pancreas) and increased salt in sweat.

A

cystic fibrosis

190
Q

This is the most common condition caused of death due to cystic fibrosis?

A

cor pulmonale

191
Q

This condition is autosomal recessive and individuals who have this can’t metabolize phenylalanine into tyrosine. This due to a mutated phenylanalanine hydroxylase.

A

Phenylketonuria (PKU)

192
Q

This condition is autosomal recessive, which results in an abnormal galactose metabolism metabolism (mutated GALT gene). It can lead to CNS, liver, and kidney damage.

A

Galactosemia

193
Q

This is a group of rare autosomal recessive conditions characterized by a lack of lysosomal enzymes and an accumulation of metabolites. It can lead to CNS damage, hepatosplenomegaly, and cellular dysfunction.

A

lysosomal storage disease

194
Q

Tay-Sachs disease, Niemann-Pick disease (Type A, B, C), Gaucher disease, and Mucopolysaccharidosis are examples of what type of disease?

A

lysosomal storage diseases

195
Q

This condition is characterized by an inability to metabolize Gm2 gangliosides due to a mutated hexosaminidase A enzyme. It can result in destruction of CNS, PNS, and ANS tissue leading to mental retardation, blindness, and motor weakness.

A

Tay-Sachs disease (Gm2 gangliosidosis)

196
Q

What feature is characteristic of Tay-Sachs disease?

A

A cherry-red central macula (retina)

197
Q

This condition in general is characterized by an accumulation of sphingomyelin due to a deficiency in acid sphingomyelinase

A

Niemann-Pick disease

198
Q

This type of Niemann-Pick disease is the most severe and results in visceromegaly and neurological damage. It is lethal by age 3.

A

type A

199
Q

This type of Niemann-Pick disease results in visceromegaly and no neurological damage. It is most commonly limited to hepatosplenomegaly.

A

type B

200
Q

This is the most common type of Niemann-Pick disease. It is a non-enzymatic deficiency characterized by defective lipid transport (mutated NPC1 or NPC2) and results in ataxia, dystonia, dysarthria, or psychomotor regression.

A

type C

201
Q

This condition is due to a mutated glucocerebrosidase gene resulting in the accumulation of glucocerebroside, which results in enlarged phagocytes, severe hepatosplenomegaly, osteolysis, osteonecrosis, and pancytopenia.

A

Gaucher disease

202
Q

How many types of Gaucher disease are there?

A

Type I: Most common, less severe, and occurs in Ashkenazi Jews

Type II and III: more severe and have neurological disturbances

203
Q

Gaucher disease creates what type of unique deformity?

A

Erlenmeyer flask deformity (bones)

204
Q

This condition is characterized by a deficiency in ECM breakdown enzymes. Some common features include skeletal deformation (“Gargoylism”), clouding of the cornea, arterial deposits, mental retardation, joint stiffness, heart valve disease, and hepatosplenomegaly.

A

Mucopolysaccharidosis (MPS)

205
Q

This type of mucopolysaccharidosis is an autosomal recessive condition, which results in α-L-iduronidase deficiency. Characteristics include corneal clouding, skeletal abnormalities, and mental retardation. It is severe and lethal by 6-10 years.

A

Hurler syndrome (MPS Type I)

206
Q

This type of mucopolysaccharidosis is an X-linked condition, which results in an L-iduronate sulfatase deficiency. It has no corneal clouding and is slowly progressive.

A

Hunter syndrome (MPS Type II)

207
Q

Hurler (MPS Type I) and Hunter (MPS Type II) syndromes both accumulate what two substances?

A

Heparan sulfate and dermatan sulfate

208
Q

These are a group of inherited enzymatic deficiencies (most commonly autosomal recessive) characterized by impaired glycogen metabolism leading to glycogen accumulation in the liver, skeletal muscles, and heart

A

Glycogen storage diseases

209
Q

This glycogen storage disease is characterized by a deficiency in glucose-6-phosphatase and decreased liver glycolysis leading to hepatomegaly and hypoglycemia.

A

von Gierke disease (hepatic type)

210
Q

This glycogen storage disease is characterized by a deficiency in muscle phosphorylase deficiency and decreased muscle glycolysis leading to weakness/cramps.

A

McArdle disease (myopathic type)

211
Q

This glycogen storage disease is characterized by a deficiency in lysosomal acid maltase deficiency and affects every organ, particularly the heart (cardiomegaly).

A

Pompe disease (Type II glycogenosis)

212
Q

These disorders are characterized by altered chromosomes (numeric/structural).

A

Cytogenetic disorders

213
Q

What are the common names for these autosomal cytogenic disorders? Trisomy 21, Trisomy 18, Trisomy 13, and fragmented 5th chromosome.

A

Trisomy 21=Down syndrome
Trisomy 18=Edwards syndrome
Trisomy 13=Patau syndrome
Fragmented 5th chromosome= Cri du chat syndrome

214
Q

This condition is due to a deletion in chromosome 22, long arm (q), band 11. It results in facial dysmorphism, cardiac defects, cleft palate, cognitive delays, and hypoplasia in the thymus and/or parathyroid gland.

A

22q11.2 deletion syndrome

215
Q

This manifestation of 22q11.2 deletion syndrome is characterized by thymic hypoplasia (decreased T cell immunity) and parathyroid hypoplasia (hypocalcemia (tetany)).

A

DiGeorge syndrome

216
Q

This manifestation of 22q11.2 deletion syndrome is characterized by pronounced structural defects, both facial and cardiac, and mild immunodeficiency.

A

Velocardiofacial syndrome

217
Q

These conditions have the allosome (chromosome 23) involved, are less severe and, more compatible with life. Those affected, may be phenotypically normal.

A

Allsomal cytogenic disorders

218
Q

This term refers to X-inactivation and is typically present in allosomal cytogenetic disorders.

A

Lyonization (1 female X chromosome is inactivated and becomes a Barr body)

219
Q

This allosomal cytogenic disorder is most commonly 47, XXY (nondisjunction during meiosis). It is the most common cause of male hypogonadism and sterility and is characterized by testicular atrophy, gynecomastia, and eunuchoid habitus.

A

Klinefelter syndrome

220
Q

This allosomal cytogenic disorder is due to the absence of 1 X chromosome (45, X). This is characterized by short stature, amenorrhea (streak ovaries), a decrease in secondary sex characteristics, webbed neck, aortic coarctation, cubitus valgus, and widely spaced nipples (shield chest).

A

Turner syndrome

221
Q

This condition is a triple-repeat mutation that is the most common cause of familial mental retardation. Some characteristics include macroorchidism, long face, large mandible, etc.

A

Fragile X syndrome (FMR1 mutation)

222
Q

This disease of genomic imprinting is due to paternal imprinting and maternal deletion of 15q12. It results in mental retardation, seizures, ataxia, and inappropriate laughing (“happy puppet syndrome”).

A

Angelman syndrome

223
Q

This disease of genomic imprinting is due to maternal imprinting and paternal deletion of 15q12. It results in mental retardation, short stature, hypotonia, obesity (hyperphagia), small hands/feet, and hypogonadism.

A

Prader-Willi syndrome

224
Q

What does TORCH stand for and what condition is it involved with?

A 
T: Toxoplasma 
O: other: syphilis, HIV, hepatitis B virus, tuberculosis, malaria 
R: rubella 
C: CMV (cytomegalo virus) 
H: HSV (herpes simplex virus)

-It is involved with transplacental perinatal infections

225
Q

This congenital condition is due to a decrease in surfactant production, which results in difficulty in inflating alveoli. It is also known as “Hyaline membrane disease”.

A

Respiratory distress syndrome

226
Q

This congenital condition occurs in premature babies, they require enteral feeding, and is characterized by necrosis, ulcerations, congestion, distended, and friable appearance of the intestines.

A

Necrotizing enterocolitis (NEC)

227
Q

This condition is due to the accumulation of edema, during gestation. It is caused by fetal anemia leading to hypoxia, cardiac failure, and pooling

A

Fetal hydrops

  • Hydrops fetalis (generalized, lethal)
  • Cystic hygroma (local, may not be lethal)
228
Q

What are the two clinical manifestations of fetal hydrops?

A
  • Immune hydrops: antibody-induced hemolysis

- Nonimmune: chromosomal abnormalities

229
Q

What is the 1st and 2nd most common cause of death from 4-14 years.

A

1st accidents, 2nd cancer

230
Q

What are the three benign pediatric tumors?

A
  • Hemangiomas (capillaries)
  • Lymphangiomas (lymphatics)
  • Sacrococcygeal teratomas
231
Q

What tissues are the most commonly affected in pediatric malignant tumors.

A

Hematopoietic, neuronal, and soft tissues

232
Q

What are three unique pediatric cancers?

A
  • Neuroblastoma
  • Retinoblastoma
  • Wilms tumor
233
Q

This is a pediatric malignancy of neural crest-derived cells and have tumor cells that surround a neutrophil in a rosette pattern (Home-Wright pseudo-rosette), which have the potential (90%) to secrete catecholamines. The younger you are when diagnosed the more favorable of a prognosis.

A

neuroblastoma

234
Q

This is a pediatric malignancy of the posterior retina. It most commonly occurs at the age of 2 and has two types (genetic and sporadic). It is commonly characterized by flexner-wintersteiner rosettes.

A

Retinoblastoma

235
Q

This type of retinoblastoma is characterized by multiple and bilateral tumors in the retina.

A

Genetic retinoblastoma

236
Q

This type of retinoblastoma is characterized by isolated and unilateral tumors in the retina.

A

Sporadic retinoblastoma

237
Q

This feature is described as cuboidal cells surrounding an empty lumen and is a hallmark feature of retinoblastoma.

A

Flexner-Wintersteiner rosettes

238
Q

This is a pediatric malignancy of the kidney. It most commonly occurs between the ages of 2-5 years and presents as a palpable mass with abdominal pain, fever, and hematuria.

A

Wilms tumor (nephroblastoma)

239
Q

What three syndromes are associated with Wilms tumor?

A
  • WAGR syndrome (Wilms tumor, Aniridia, Genitourinary, and mental Retardation)
  • Denys-Drash syndrome (DDS)
  • Beckwith-Wiedemann syndrome (BWS)
240
Q

What are the four most common metallic environmental pollutants?

A

Lead, mercury, arsenic, and cadmium

241
Q

This condition may result from toxic exposure to mercury and can result in ataxia, numbness, deafness, blindness, or cerebral palsy.

A

Minamata disease

242
Q

This condition is a result of toxic exposure to cadmium and can result in bone loss and renal failure.

A

Itai-Itai disease

243
Q

This syndrome is a result of chronic alcoholism. It is characterized by thiamine (vitamin B1) deficiency, varying forms of amnesia, and confabulation (creation of fake memories).

A

Korsakoff syndrome

244
Q

What are some of the major health concerns of a thermal injury?

A
  • Hypovolemic shock: >20% of surface is affected

- Sepsis, which leads to organ failure (most common is Pseudomonas aeruginosa)

Part I Boards Review (19 decks)

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