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Fall 17 - Gen Path > Midterm I > Flashcards

Midterm I Flashcards

1
Q

In pathology, the origin of disease is specifically referred to as: (the “why”)

A

Etiology

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2
Q

In pathology, the development of disease is specifically referred to as: (the “how”)

A

Pathogenesis

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3
Q

T/F Clinical signs and symptoms usually occur fairly quickly after the origin of injury

A

False; they are several steps removed

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4
Q

Please arrange the following terms in the general order of timing:

  • cell response
  • disease treatment
  • cell injury
  • etiologic agent
  • disease state
A

Etiologic agent -> Cell injury -> Cell Response -> Disease State -> Disease Treatment

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5
Q

What are commons categories of etiological agents/causes of cell injury?

A

Hypoxia, Infectious agents, Physical injury, Chemicals/drugs, Immune Response, Genetic abnormalities, and Nutritional Imbalance

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6
Q

What type of necrosis do Aspirin burns (drug/chemical injury) cause?

A

Coagulative Necrosis

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7
Q

Ischemia induces cell injury by reducing the amount of ATP production. Which of the following are NOT potential consequences of reduced ATP production?

  • Influx of Ca, water, and NA that causes cell swelling
  • Increased anaerobic glycolysis that increases acidity
  • Increased protein synthesis from increased attachment of ribosomes
A

Increased protein synthesis from increased attachment of ribosomes
(it actually decreases because of detachment)

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8
Q

The Fenton Reaction involves production of ROS using what divalent cation?

A

Iron/Fe++

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9
Q

Disulfide linkage, Lipid per oxidation, and protein strand excisions disrupt cell membranes. What are the consequences of these dysfunctions?

A

Increased Permeability

Loss of proper Ca++ regulation

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10
Q

ROS cause (SS or DS?) DNA breaks.

A

Single stranded

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11
Q

What are 2 major sites (purines and pyrimidines) of ROS single strand DNA breaks?

A

thymidine and guanine

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12
Q

Without intact cell membranes, Ca++ regulation is lost. Is there an increase or decrease in cytoplasmic Ca++? What happens in the cell after this change in concentration?

A

Increased cytoplasmic Ca++. The excess Ca++ helps activate intracellular enzymes that can decrease ATP, decrease phospholipid, cause protein disruption, and DNA damage

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13
Q

Cell injury may cause ______, ______, or ______.

A

reversible injury, cell adaptation, or cell death

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14
Q

Reversible cell injury is:

  • acute or chronic
  • short or long duration
  • low or high intensity
  • shrunken or swollen cell
A

acute, short duration, low intensity, and swollen cell

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15
Q

T/F One mechanism is known for the conversion of reversible cell injury to change to irreversible.

A

False; no signature event

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16
Q

When cells switch from reversible to irreversible injury, a sequential change in function and morphology occur. Please arrange the following:

  • light microscopic changes
  • ultrastructural changes
  • gross morphological changes
  • cell death
A

Cell death, ultrastructural changes, light microscopic changes, then final gross morphological changes

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17
Q

What are the 4 types of necrosis? Which one is the most common?

A

coagulative (most common!), liquefactive, caseous, and enzymatic (fat)

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18
Q

During coagulative necrosis, which of the following cell features retains its original histological appearance?

  • Nucleus
  • Cytoplasm
  • Cell outline
A

Cell outline; cells become anucleated cells with pink (acidic) cytoplasm

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19
Q

An abscess is an example of what type of necrosis?

A

liquefactive

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20
Q

Tuberculosis causes what type of necrosis?

A

caseous

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21
Q

What happens to fat cells during fat/enzymatic necrosis?

A

become anucleated saponification of fat cells

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22
Q

T/F Apoptosis is a maintainer of homeostasis

A

True

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23
Q

Which of the following are examples of excessive apoptosis? inhibition of apoptosis?

  • AIDS
  • Cancer
  • Neurodegenerative disease
  • Myelodysplasis
  • Autoimmune disease
  • Viral diseases
A

Excessive: AIDS, neurodegenerative disease, and myelopdysplasia (can’t form blood cells in marrow)

Inhibition: cancer, autoimmune disease, and viral diseases

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24
Q

Which are associated with apoptosis?

  • single cell or multiple cells
  • cell shrinkage or cell swelling
  • chromatin condensation or cell lysis
  • inflammation or no inflammation
A

single cell
shrinkage
chromatin condensation
no inflammation

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25
Q

What receptor/ligand pair is responsible for the extrinsic pathway of apoptosis? Is this pathway specific or non-specific?

A

Fas and TNF receptor

Specific

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26
Q

What cell injury is responsible for the intrinsic pathway of apoptosis? Is this pathway specific or non-specific?

A

GF withdrawal, DNA damage, or protein misfiling

Non-specific

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27
Q

Is chronic cell injury typically higher or lower strength of insult?

A

Lower strength/intensity for longer time

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28
Q

Decrease in cell size and function is what cellular adaptation?

A

Atrophy

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29
Q

What are some causes of atrophy?

A

decreased workload (mm.), loss of IN, decreased blood supply (kidney), poor nutrition (wasting), decreased hormones (breast post menopause), and aging (brain)

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30
Q

Increase in cell size and function is what cellular adaptation?

A

Hypertrophy

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31
Q

What are some causes of hypertrophy?

A

Increased fxnal demand (heart), increased or imbalanced nutrition (big gut), increased hormonal stimulation (preg uterus)

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32
Q

Increase in cell number is what cellular adaptation?

A

Hyperplasia

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33
Q

Is hyperplasia typically irreversible?

A

No, take away stimulus and it goes away

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34
Q

Alteration in cell differentiation is what cellular adaptation?

A

Metaplasia

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35
Q

Squamous metaplasia of the bronchus is typically of what etiology? What are the consequences of the cellular change from columnar to squamous?

A

Smokers

Tougher tissue but less efficient at removing debris

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36
Q

Intestinal metaplasia of esophagus is typically of what etiology? What are the consequences of the cellular change?

A

Chronic reflux disease

Turns to mucous producing to protect tissues

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37
Q

What are the 4 mechanisms of intracellular accumulations?

A

Lack of enzyme, abnormal metabolism, defect in protein folding, ingestion of indigestible material (AKA carbon particles)

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38
Q

Cholesterol accumulations in vessels can lead to ______ or ______.

A

Atherosclerosis (narrowing arteries) or cholesterol thrombus

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39
Q

Alzheimer’s disease and Mallory bodies are what type of cellular accumulation?

A

Protein

Alzheimers is plaques in neurons while Mallory bodies is intermediate filaments in hepatocytes

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40
Q

Carbohydrates glycogen storage disease is most characterized by what activity?

A

DECREASE in glucose 6 phosphatase activity (usually fatal)

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41
Q

What is an example of an exogenous pigment accumulation that we may induce in dentistry?

A

Amalgam tattooing of soft tissue

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42
Q

What are the classic signs of inflammation?

A

Redness, swelling, heat, and pain

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43
Q

Pick the following characteristics that go with acute inflammation:

  • vasoconstriction or vasodilation
  • increased or decreased vascular permeability
A

vasodilation and increased vascular permeability

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44
Q

What cytokines mediate vasodilation?

A

NO, PGs, and Histamine

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45
Q

T/F During normal vascular flow, some fluid leaks out of vessels

A

True; the fluid leaks and is picked up by resident lymphatic cells

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46
Q

Which happens first during inflammation? vasodilation or arrival of neutrophils

A

Vasodilation

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47
Q

Which fluid accumulation in inflammation is characterized by:

  • Low protein content, low specific gravity
  • Non-inflammatory - intact endothelium
  • Inflammatory - early endothelial contraction
A

Transudate

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48
Q

In order to allow fluid accumulation, what happens to the local hydrostatic pressure and colloid osmotic pressure?

A

Hydrostatic pressure INCREASES

Colloid osmotic pressure DECREASES

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49
Q

Which fluid accumulation in inflammation is characterized by:

  • High protein content, high specific gravity
  • Inflammatory response
A

Exudate

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50
Q

Rank the order of types of exudate in order of increasing severity: purulent, sanguineous, and fibrinous

A

Fibrinous (high protein, few cells)
Purulent (high protein, many cells)
Sanguineous (high protein, blood, great deal of destruction)

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51
Q

Endothelial cell contraction is mediated by which cytokines?

A

PAF, histamine, bradykinin, leukotrienes

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52
Q

Endothelial cell retraction is mediated by which cytokines?

A

IL-1, TNF, IFN

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53
Q

After an injury, reversible endothelial contraction occurs first and lasts ____ hours, then endothelial retraction follows after _____ hours and can lasts up to ____ hours.

A

Contractions lasts 0-1 hours

Retraction follows after 4-6 hours and can last 24+ hours

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54
Q

What cytokines, released during inflammation, cause pain?

A

PGE and Bradykinin

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55
Q

What cytokines, released during inflammation, cause fever?

A

IL-1, TNF, PGE

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56
Q

List the leukocyte order of events after endothelial cell activation during inflammation.

A
  • Margination - physical slowing forces
  • Rolling - leukocyte attracted to E- and P- selectin
  • Adhesion - leukocyte attach to interns VCAM and ICAM
  • Emigration or transmigration - leukocyte binds to PECAM and moves through endothelial cells
  • Chemotaxis - act on microbes and produce chemotaxis cytokines to attract other leukocytes
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57
Q

T/F Neutrophils clean up areas of infection or necrosis

A

False, they lead to apoptosis that then gets cleaned up by macrophages

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58
Q

How quickly can monocytes reach sites of infection? How long do they live in tissues as macrophages?

A

emigrate within 48 hours

Live up to MONTHS in tissues (only 1-2 days in circulation)

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59
Q

Besides neutrophils and monocytes (early responders), what other inflammatory cells can participate in response?

A 
lymphocytes (immune functions - T and B cells)
eosinophils (allergic response & parasites)
mast cells (histamine/allergic reaction)
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60
Q

Define Cellulitis.

A

Diffuse tissue infiltration by PMNs with edema

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61
Q

Define Abscess.

A

Localized collection of PMNs or liquefactive necrosis

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62
Q

Define Ulcer.

A

Erosion of an epithelial surface exposing underlying connective tissue

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63
Q

Chronic or acute inflammation?

  • Duration days-weeks
  • Localized
  • No immune response
  • Often reversible
  • Contains PMNs
A

Acute inflammation

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64
Q

Chronic or acute inflammation?

  • Duration days-years
  • Systemic
  • Adaptive immune response
  • Maybe reversible
  • Contains macrophages and lymphocytes
A

Chronic inflammation

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65
Q

T/F Tissue destruction from chronic inflammation leading to fibrosis (scarring) is common

A

True (longer duration = more likely)

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66
Q

What are the 2 types of chronic inflammation and which one is more common?

A

Non-specific (most common)

Granulomatous

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67
Q

There are many different degrees of capacity of proliferation during wound healing. Which is characteristic of continuously dividing cells that can be repaired easily? and what is a site where this occurs?

A

Labile capacity

surface epithelium in mouth

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68
Q

There are many different degrees of capacity of proliferation during wound healing. Which is characteristic of some replicative activity that can produce scars if replaced? and what is a site where this occurs?

A

Stable capacity

SM cells and fibroblasts

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69
Q

There are many different degrees of capacity of proliferation during wound healing. Which is characteristic of nonproliferative cells? and what is a site where this occurs?

A

Permanent capacity

Neurons and cardiac m.

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70
Q

What factors affect wound healing? and which is the primary cause of delayed healing?

A

Infection (primary cause)

Poor nutrition, steroid therapy, mechanical factor, and poor tissue perfusion

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71
Q

Healing by first intention (stitches) produces:

  • very little scar or larger, less functional scar
  • reduced or increased chance of infection
  • heals quicker or slower
A

Very little scar
Reduced chance of infection
Heals quickly

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72
Q

What is edema?

A

Increases fluid within interstitial tissues

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73
Q

Edema is characterized by _______ hydrostatic pressure and _______ venous return.

A

Increased hydrostatic

Decreased venous return

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74
Q

Which of the following does NOT describe an edema (increased fluid)?

  • reduced plasma osmotic pressure
  • lymphatic obstruction
  • sodium and water loss
  • inflammation
A

Sodium and water loss (both are actually retained)

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75
Q

What are two other terms for edema?

A

Anasarca and hydroplane

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76
Q

What is effusion?

A

Collection of fluid in body cavity or space

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77
Q

During hyperemia, tissue blood volume (increases or decreases) secondary to neurogenic mechanisms or inflammation.
Is this active or passive?
What color does it appear?

A

Increased tissue blood volume
Active
Red from increased RBC

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78
Q

During hyperemia, tissue blood volume (increases or decreases) secondary to impaired venous return.
Is this active or passive?
What color does it appear?

A

Increases
Passive
Blue because RBC slow down/build up

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79
Q

Hemorrhage is the loss of blood from injury or physical disruption.
Internally, it is defined by size. The largest mass of blood is called:

A

Hematoma

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80
Q

Hemorrhage is the loss of blood from injury or physical disruption.
Internally, it is defined by size. A bruise greater than 1 cm but not quite a hematoma is called:

A

Ecchymosis

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81
Q

Hemorrhage is the loss of blood from injury or physical disruption.
Internally, it is defined by size. When it falls between 0.3-0.9cm it is called:

A

Purpura

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82
Q

Hemorrhage is the loss of blood from injury or physical disruption.
Internally, it is defined by size. The smallest amount, 1-2mm in size is referred to as:

This can present in patients with what condition?

A

Petechia(e)

Mononucleosis

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83
Q

What 3 major components help promote hemostasis after injury?

A

Endothelium, Platelets, and Coagulation Cascade

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84
Q

T/F Endothelium can be both procoagulant and anticoagulant

A

True

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85
Q

What promotes platelet adhesion to collagen?

A

von Willebrand factor

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86
Q

Which (Intrinsic or extrinsic?) system initiates coagulation cascade using what factor?

A

Extrinsic using tissue factor

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87
Q

Which (Intrinsic or extrinsic?) system finishes coagulation cascade using what factor?

A

Intrinsic using Factor XII (Hageman)

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88
Q

What is the end product of the coagulation cascade? What is the products function?

A

Thrombin cleaves fibrinogen to form fibrin (holds platelets together)

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89
Q

T/F Coagulation cascade can occur without the presence of platelets

A

False, platelets are necessary

Enzyme activity occurs at surface phospholipid complex of platelets

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90
Q

Platelet adhesion, secretion, and aggregation are apart of (primary or secondary?) hemostasis.

A

Primary

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91
Q

What event is known as secondary hemostasis?

A

Coagulation cascade

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92
Q

PGI2 helps promote or slow hemostasis.

A

Slow, it is a counter regulator of hemostasis

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93
Q

All of the following are counter regulators of hemostasis EXCEPT:

  • ADP
  • Antithrombin III
  • Protein S
  • Protein C
  • Thrombomodulin
A

ADP promotes hemostasis

ADPase is a counter regulator

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94
Q

During hemostasis, thrombin cleaves fibrinogen to form fibrin. What 2 molecules are produces to participate in fibrinolysis to help trim/clip fibrin net?

A

tPA (tissue plasminogen activator) and plasmin

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95
Q

T/F Coagulation cascade repairs endothelium after injury

A

False, simply stops bleeding

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96
Q

T/F Thrombin’s only role in body is to cleave fibrinogen during hemostasis.

A

False; thrombin also has many other functions including immune response

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97
Q

What are the 3 components of Virchow’s Triad (3 things that can lead to thrombosis)?

A

Endothelial injury, alterations in blood flow, and hypercoagulability

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98
Q

T/F Endothelial injury will lead to increased prothrombotic activity

A

True

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99
Q

During normal blood flow, the flow is ____. (turbulent or laminar)

A

laminar

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100
Q

What 2 alterations in blood flow can happen to induce thrombosis?

A

Turbulence and stasis

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101
Q

What are 3 inherited conditions for hyper coagulability?

A
  • Factor V Leiden (cannot cleave Va and continue prothrombotic activity)
  • Prothrombin mutation (excess transcription)
  • AT III deficiency
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102
Q

What are some acquired conditions for hyper coagulability?

A
  • Prolonged bed rest
  • Cancer
  • Extensive tissue injury
  • Pregnancy
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103
Q

What is the color appearance of arterial thrombosis? venous thrombosis?

A

Arterial - white

Venous - red

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104
Q

Distinct lines of Zahn are characteristic of thrombosis in what types of vessels? Indistinct lines?

A

Distinct - Arterial

Indistinct - Venous

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105
Q

What are the 4 common fates of thrombi?

A
  • dissolution/resolution
  • embolization
  • propagation
  • organization/recanalization
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106
Q

What is DIC?

A
  • disseminated intravascular coagulation

- widespread/systemic activation of the coagulation cascade and fibrinolytic systems

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107
Q

T/F DIC (disseminated intravascular coagulation) can produce both micro thrombi and hemorrhage

A

True; elevates coag cascade and fibrolytic

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108
Q

With acute DIC, what is most critical? With chronic DIC, what is most critical?

A

acute is hemorrhage - don’t want to bleed too much

chronic is thrombi - need to allow effective passage of blood

109
Q

What are some causes of DIC?

A

infection (G- bacteria), obstetric complications (placental abruption or retained dead fetus), neoplasm, shock, and massive tissue injury

110
Q

What is an embolus? What is the majority/most common?

A
  • an intravascular solid, liquid, or gaseous mass carried by the blood to a site distant from its point of origin
  • majority is dislodged thrombus, likely from deep vein
111
Q

What is pulmonary thromboembolism?

A

Embolus (formed from a thrombus) that has been carried to lungs

112
Q

What are the range of clinical consequence for a pulmonary thromboembolism?

A

No clinical manifestation, pulmonary hypertension, pulmonary hemorrhage, pulmonary infarction, up to sudden death (Saddle embolus) from blockage of major trunk to lungs

113
Q

What are the places of origin for systemic embolism?

A

left atrium, left ventricle, atherosclerotic plaque

114
Q

What is infarction? What are the 2 types of infarction?

A

Area of ischemic necrosis from blockage of blood supply

Red (hemorrhagic) and white (pale)

115
Q

The following are characteristic of what type of infarction (red or white)?:

  • venous occlusion
  • loose tissue
  • dual blood supply
  • previous congestion
A

Red

116
Q

The following are characteristic of what type of infarction (red or white)?:

  • arterial occlusion in solid organ
  • NOT loose tissue
A

White

117
Q

What is shock?

A

Systemic hypoperfusion (loss of blood flow)

118
Q

What are the 5 pathophysiologic categories of shock?

A 
Cardiogenic
Hypovolemix
Septic
Anaphylactic
Neurogenic
119
Q

What is the #1 cause of death in ICUs? (200,000 annually)

A

Septic Shock

120
Q

What causes septic shock? What molecule is associated with it?

A

gram-positive or gram-negative bacteria

pathogen-associated molecular patterns (or PAMPs)

121
Q

During nonprogressive shock, compensatory mechanisms (CAN or CANNOT) maintain perfusion

A

CAN

122
Q

Which of the following does NOT happen progressive shock?

  • maintained perfusion by compensatory mechanisms
  • anaerobic metabolism from decreased O2 in tissues
  • lactic acidosis from increased lactate
  • DIC
A

Maintained perfusion by compensatory mechanisms does NOT happen, perfusion is inadequate

123
Q

T/F Irreversible shock leads to multiple organ failure and death

A

True

124
Q

What are some clinical manifestations of shock?

A
  • tachycardia, tachypnea, hypetension, cool clammy skin (EXCEPT SEPTIC SHOCK)
  • confusion, cyanosis, low urine output, acidosis, high lactic acid
125
Q

What two components are necessary to develop a neoplasm?

A

Parenchyma (neoplastic cells) and stroma (supporting CT and BV)

126
Q

What is a benign gland-forming epithelial tumor or tumor derived from glandular tissue?

A

Adenoma

127
Q

What is a benign surface epithelial tumor characterized by numerous finger-like projections

A

Papilloma

128
Q

What is the proliferation of tissue normally found at that site?

A

Hamartoma

129
Q

What is the collection of tissue not normally found in that anatomic site?

A

Choristoma

130
Q

What is a neoplasm derived from more than one germ layer?

A

Teratoma

131
Q

Mesenchymal malignancies are called..?

A

Sarcoma

132
Q

Epithelial malignancies are called..?

A

Carcinoma

133
Q

Malignancy of lymphoid tissue?

A

Lymphoma

134
Q

Malignancy of melanocytes?

A

Melanoma

135
Q

Pleural malignancy?

A

Mesothelioma

136
Q

Testicular malignancy?

A

Seminoma

137
Q

Benign tumors are:

  • small or large
  • poorly or well demarcated
  • slow or fast growing
  • poorly or well differentiated
  • locally invasive?
  • typically metastasized?
A 
Small
Well demarcated
Slow growing
Well differentiated
Not locally invasive
Not metastasized
138
Q

Malignant tumors are:

  • small or large
  • poorly or well demarcated-slow or fast growing
  • poorly or well differentiated
  • locally invasive?
  • typically metastasized?
A 
Large
Poorly demarcated
Fast growing
Poorly differentiated
Locally invasive
Often metastasized
139
Q

What differentiation is the most extreme disturbance in cell growth and differentiation?

A

Anaplasia

140
Q

What are features of anaplasia?

A

Pleomorphism, nuclear hyperchromatism, variation in nuclear size and shape, numerous and atypical mitoses (the tripole mitosis)

141
Q

What differentiation is disorderly, but non-neoplastic growth or proliferation? Also referred to as epithelial process of maturation?

A

Dysplasia

142
Q

T/F Although dysplasia is non-neoplastic, it has the potential to become invasive carcinoma

A

True

143
Q

Mild, moderate, and severe dysplasia are usually distinguished by..?

A

Extent of abnormal cells through the epithelial layer
Mild - basal only
Moderate - into parabasal (1/2 way though)
Severe - up to superficial cells

144
Q

If tumors outgrow their blood supply, this results in …

A

ischemic necrosis

145
Q

What is the MOST RELIABLE feature to distinguish malignant from benign tumors?

A

local invasiveness

146
Q

T/F Benign tumors are never fatal

A

False, although they do not typically invade, their location can make them extremely dangerous and lead to death

147
Q

What type of tumors have a fibrous capsule?

A

Benign

148
Q

What percent of newly diagnosed patients with solid tumors will already have obvious metastases? What percent have hidden metastases?

A

30% obvious

20% hidden

149
Q

What is considered the hallmark of malignancy?

A

Metastasis

150
Q

What are the 3 pathways for metastasis?

A
  1. Seeding within body cavities
  2. Lymphatic spread
  3. Hematogenous spread
151
Q

Which pathways (hematogenous and lymphatic) are associated with which types of malignancies (Carcinoma and sarcoma)?

A

hematogenous - sarcoma (liver and lungs)

lymphatic - carcinoma (lymph nodes)

152
Q

What proportion of cancer risk is attributable to environmental sources?

A

roughly 2/3 (65%)

153
Q

T/F Stomach cancer in Japan is 7 times more frequent than in the US

A

True

Breast and prostate 4-5X less common in Japan

154
Q

What percentage of deaths in children <15 years of age is due to cancer?

A

10%

155
Q

Cancer occurs in 1 of every _ people.

A

1 of 5

156
Q

What are 3 categories of genetic predisposition to cancer?

A
  1. Inherited cancer syndromes
  2. Familial cancers
  3. Defective DNA repair
157
Q

Inherited cancer syndromes are usually (single or multiple) gene mutation and generally autosomal (recessive or dominant) transmission

A

Single gene mutation

Autosomal Dominant

158
Q

Retinoblastoma, adenomatous polyposis, and multiple endocrine neoplasia are examples of what category of genetic predisposition to cancer?

A

Inherited cancer syndromes (single gene and autosomal dominant)

159
Q

Early age onset, tumors arising in 2 or more close relatives, and multiple or bilateral tumors are associated with what category of genetic predisposition to cancer?

A

familial cancers

160
Q

Colon, breast, ovary, and brain malignancies have been reported to occur in ____ patterns

A

familial patterns

161
Q

Defective DNA repair is usually autosomal (recessive or dominant) transmission

A

autosomal recessive

162
Q

T/F Acquired Preneoplastic Disorders is a type of genetic predisposition to cancer

A

False, it develops over time and you are not born with it

163
Q

Persistent regenerative cell replication, villous adenomas of the colon, and leukoplakia of oral or genital mucosa are examples of …?

A

acquired preneoplastic disorders

164
Q 
White plaque on oral mucosa that:
-has sharp margin.borders
-is thin/exhibits fissures
-cannot be rubbed off or Id'ed as anything else
is referred to as:
A

leukoplakia

165
Q

Nonlethal genetic damage that is central to all cancers is referred to as:

A

carcinogenesis

166
Q

What 3 classes of normal regulatory genes are affected by carcinogens?

A
  1. proto-oncogenes (growth promoting)
  2. cancer suppresor genes (growth inhibiting)
  3. apoptosis genes
167
Q

T/F Carcinogenesis is a single step process at the genetic level

A

False it is multi step at both the phenotypic and genetic levels

168
Q

Oncogenes encode proteins called _____ that lack normal controls and regulation

A

Oncoproteins

169
Q

What 2 mechanisms turn proto-oncogenes into oncogenes?

A
  1. Structural mutation of the gene, resulting in abnormal product
  2. Altered regulation of gene expression, resulting in increased production of a normal growth-promoting protein
170
Q

What gene is most commonly affected for transcription factors?

A

MYC

171
Q

MYC gene dysregulation leads to activation of ____ causing cells to divide

A

Cyclin-dependent kinase (CDK)

172
Q

What is Knudson’s hypothesis regarding tumor suppressor genes?

A 
Two mutations ("hits") in genome of cell required to induce retinoblastoma
Families who pass on one mutation in allele only have 1 allele to mutates to induce RB
173
Q

What gene is the single most common target for genetic alteration in human tumors?

A

tp53

174
Q

What is TP53’s role in normal cell cycle? after mutation?

A

normal: inhibits cell cycle progression to allow time for DNA repair
mutation: doesn’t stop cell cycle and therefore DNA cannot be repaired, eventually leads to uncontrolled cell division

175
Q

What is Lo-Fraumeni syndrome?

A

inherited defect of one TP53 allele (means 25x increase risk for malignancy before 50)

176
Q

What is the prototypic anti-apoptosis gene?

A

BCL2

177
Q

Overexpressed BCL2 leads to :
A. Steady decrease in number of cells
B. Increased cell division
C. Cell protection for apoptosis

A

C. Cell protection for apoptosis

often seen in “low-grade” lymphomas

178
Q

Tumors cannot grow larger than _____ in diameter unless they are vascularized

A

1-2mm

179
Q

What are the 2 major phases of metastasis?

A

Invasion of ECM and vascular dissemination with adhesion of tumor cells

180
Q

Hereditary nonpolyposis colon cancer is a condition with unstable DNA. What defect is associated with this condition?

A

mismatch repair defect (MSI)

181
Q

Xeroderma pigmentosum is a condition with unstable DNA. What defect is associated with this condition?

A

Inability to repair UV damage, leads to increased skin cancers

182
Q

Bloom syndrom and familial breast cancer (BRCA1 and 2) are conditions with unstable DNA. What defect is associated with these conditions?

A

fragile DNA disease

183
Q

What are types of karyotypic changes in tumors? (3 answers)

A

balanced translocations, deletions, and gene amplification

184
Q

T/F Chemical carcinogens are only from naturally occurring chemicals

A

False, can also be synthetic

185
Q

Chemical carcinogens can be both direct and indirect carcinogens. What is the difference between the two?

A

Direct requires no chemical transformation while indirect become active only after metabolic conversion

186
Q

Chemical carcinogens are highly reactive ______ affecting DNA, RNA, and cell proteins

A

electrophils

187
Q

Radiation carcinogens include UV, Xrays, gamma, and radionuclides and typically have a (short or long) latency for cancer

A

long

188
Q

T/F Viral oncogenes are a type of carcinogen

A

True

189
Q

What is an example of an RNA oncogenic virus?

A

Human T-Cell Leukemia Virus Type 1

190
Q

What are some examples of DNA oncogenic viruses?

A

HPV- cervical cancer
EBV- Burkitt Lymphoma
HepB- hepatocellular carcinoma
HHV8- Kaposi sarcoma

191
Q

What are the human body’s tumor immunity cells?

A

tumor antigens, cytotoxic Tcells (CD8), NK cells, macrophages, and humoral factors

192
Q

What are 3 types of biochemical assays to diagnose cancer?

A

prostate-specific antigen (PSA), carcinoembryonic antigen (CEA), and alpha-fetoprotein

193
Q

What are 3 types of molecular diagnosis of cancer?

A

ISH, FISH, and PCR

194
Q

T/F Medial calcific sclerosis (Monckesberg’s) typically presents as hypertension in patients

A

False, it is usually clinically insignificant

195
Q

What are the 2 types of arteriolosclerosis? Which is more common

A

Hyalin (more common) and hyperplastic

196
Q

T/F Atherosclerosis typically affects artioles

A

False; affects larger arteries

197
Q

Fatty streaks appear in most children and may or may not progress to ____

A

atheromas

198
Q

Advanced plaque in artherosclerosis in the pre-clinical phase can lead to what 3 different things in the clinical phase?

A
  • aneurysm and rupture
  • occlusion by thrombosis
  • stenosis
199
Q

Vulnerable plaque has a (thin or think) fibrous cap between lipid core and endothelium

A

Thin - more vulnerability to exposure lipid core

200
Q

What are 5 complications of atherosclerosis?

A

gangrene, MI, cerebral infarction (stroke), renal a. stenosis, and aortic aneurysm

201
Q

Sever hypertension is defined by BP greater than

A

160/106mmHg

202
Q

Hypertension affects approximately _% of the population

A

25%

203
Q

T/F Most hypertensions have no symptoms

A

True, especially in low/moderate

204
Q

Left ventricular concentric hypertrophy in order to provide normal cardiac output is referred to as

A

compensated

205
Q

hypertrophy no longer adequate enough to provide normal cardiac output due to decrease myocardial contraction leads to _____ which results in left ventricle dilation and eventually leads to _____

A

decompensation

CHF

206
Q

Accelerated (Malignant) Hypertension is:

  • rapid or slow onset
  • rare or common
  • independent or superimposed on previous hypertension
  • high or low systolic and diastolic pressures
A

rapid onset
rare
superimposed on previous hypertension
high systolic and diastolic pressures

207
Q

What disease is the failure to pump an adequate amount of blood to supply the metabolic requirement of the organs?

A

congestive heart failure

208
Q

How many people in US are affected annually by CHF?

A

5 million

209
Q

How many people die annually from CHF?

A

300,000

210
Q

What are 3 compensatory mechanisms during heart disease?

A

Activation of neurohumoral system
Frank-Starling mechanisms
Myocardial hypertrophy

211
Q

Which compensatory mechanism is associated with the release of norepinephrine with increased heart rate and contractility as well as the activation of renin-angiotension sys with water/salt retention?

A

Activation of neurohumoral system

212
Q

Which compensatory mechanism is associated with the increased end-diastolic filling volume stretching cardiac muscle fibers?

A

Frank-Starling mechanisms

213
Q

Which compensatory mechanism is associated with the increase in muscle fiber size, resulting in increased thickness of ventricular wall but without increase in size of lumen?

A

myocardial hypertrophy

214
Q

Which sided heart failure usually precedes the other?

A

left side usually comes first and leads to right side

215
Q

Which sided heart failure is caused by pulmonary hypertension?

A

right-sided heart failure

216
Q

Which side ventricular failure manifests clinically as pulmonary edema, chronic cough, and orthopnea?

A

left ventricular failure

217
Q

Which side ventricular failure manifests clinically as congestion of liver (nutmeg liver) and edema of subcutaneous tissues, especially lower extremities?

A

Right ventricular failure

218
Q

Congenital heart disease occurs in __ out of every 1,000 live births

A

6-8

219
Q

There are both cyanotic and noncyanotic forms of congenital heart disease. What are the 3 forms of noncyanotic? Which is most common

A

VSD (ventricular septal defect) is most common 4/1,000
ASD (atrial septal defect) is 2nd most common 1/1,000
PDA (patent ductus arteriosus)

220
Q

There are both cyanotic and noncyanotic forms of congenital heart disease. What are the 2 forms of cyanotic?

A

Tetrology of Fallot

Transposition of great arteries

221
Q

What are the 4 anomalies in tetrology of fallot?

A

VSD, Narrowed RV outflow, Override VSD by aorta, RV hypertrophy

222
Q

What refers to a group of related disorders that are all characterized by imbalances between myocardial blood supply and myocardial oxygen demand?

A

ischemic heart disease (IHD)

223
Q

What is the leading cause of death in the US (at 500,000 annually)

A

IHD

224
Q

What are the 4 clinical types of IHD?

A

angina pectoris
MI
Chronic IHD with CHF
Sudden cardiac death

225
Q

What is referred to as intermittent chest pain caused by transient, reversible, myocardial ischemia?

A

angina pectoris

226
Q

Stable angina may present as referred pain along ______. It is relieved by rest or _______.

A

left arm or jaw (why it’s relevant to us)

relieved by sublingual nitroglycerin

227
Q

Unstable angina is increasing frequency of chest pain without exertion. Typically lasts _____ than stable angina. Often precedes more serious ____.

A

longer than stable angina

precedes more serious ischemia

228
Q

What is necrosis of cardiac muscle caused by ischemia?

A

acute myocardial infarction (MI) or heart attack

229
Q

How many MI’s annually in US? What proportion are fatal?

A

1.5 million

1/3 fatal

230
Q

Sever ischemia lasting longer than ______ will cause irreversible myocyte injury and cell death

A

20-40 minutes

231
Q

Myocardial ischemia also contributes to ____ probably because ischemic region cause electrical instability

A

arrhythmias

232
Q

What are clinical manifestations of MI?

A

chest pain, shortness of breath, nausea/vomiting, diaphoresis/sweating, low grade fever

233
Q

What protein is a good indicator of MI and should show up in blood within 5 hours of chest pain

A

isoform of creatine kinase (CK-MB)

234
Q

During autopsy, MIs less than ____ old are not apparent but begin to turn reddish-blue after ______

A

12 hours

12-24 hours

235
Q

What is the most common cause of sudden heart disease? (80-90%)

A

IHD

236
Q

Primary cardiomyopathy (disease of heart mm.) is defined by:

A

is it solely confined to heart muscle

237
Q

Secondary cardiomyopathy is defined by:

A

involved disease of heart m. as a part of systemic disorder

238
Q

What are the 3 functional patterns of cardiomyopathy?

A

dilated (most common)
hypertrophic
restrictive

239
Q

Dilated cardiomyopathy shows dilation of _____ and therefore issues with (systolic or diastolic)

A

all 4 heart chambers

systolic (ejecting blood from heart)

240
Q

Hypertrophic cardiomyopathy is a (primary or secondary) and (genetic or acquired) cardiomyopathy

A

primary

genetic

241
Q

Hypertrophic cardiomyopathy is autosomal ____ and has issues with (systolic or diastolic)

A 
dominant
diastolic (problems filling bc stiff ventricles)
242
Q

Required cardiomyopathy is a (primary or secondary) cardiomyopathy and has issues with (systolic or diastolic)

A

secondary

diastolic

243
Q

Myocarditis is most commonly caused by what pathogen?

A

viruses (coxsackie A and B)

244
Q

Mitral valve stenosis is a result of ______ and typically affects (children or adults)
The bacteria is typically tested for during what common illness?

A

acute rheumatic fever (ARF)
children and only 20% of adults
Strep testing because Streptococcal pharyngitis

245
Q

What are the 3 forms of rheumatic carditis?

A

pericarditis
endocarditis
myocarditis

246
Q

__carditis is characterized microscopically by ______ which are collections of mononuclear inflammatory cells and fibroblasts (granulomatous inflammation)

A

Myocarditis

Aschoff bodies

247
Q

What refers to a valve that fails to close completely, allowing backflow of blood.

A

Mitral valve regurgitation

248
Q

What valve condition is caused by fibrosis and calcification reducing valve cusp mobility? This can be due to what valve disease?

A

Aortic valve stenosis

chronic rheumatic valve disease

249
Q

What type of aortic valve stenosis usually occurs with advanced age in 70s or 80s? What type has a much younger initial onset?

A

advanced age - degenerative (senile)

much younger - congenital bicuspid

250
Q

What valve disease includes valve cusp destruction (endocarditis), myxomatous degeneration, and dilation of the aortic root?

A

Aortic valve regurgitation

251
Q

What is usually caused by a bacterial infection in a heart valve although it may be caused by fungus or other infection?

A

infective endocarditis

252
Q

What is one easily visible clinical sign of infective endocarditis?

A

splinter hemorrhages in nail bed

253
Q 
What type of endocarditis is this?
-short duration
-virulent organism
(Staphylococcus aureus)
-large friable vegetations
-previously normal valve
-prominent tissue destruction
A

acute endocarditis

254
Q 
What type of endocarditis is this?
-longer duration
-low virulent organism
(Streptococcus viridans)
-small vegetations
-previously abnormal valve
-less tissue destruction
A

subacute endocarditis

255
Q

What valve disease may be caused by infection (usually due to direct spread of an adjacent infection)?

A

Vasculitis

256
Q

What are the 3 classification of vasculitis?

A

Large vessels
Medium vessels
Small vessels

257
Q

Giant cell (temporal) arteritis and takayasu arteritis are examples of:

A

Large vessel vasculitis

258
Q

Polyarteritis nodosa (classic) and Kawasaki syndrome are examples of:

A

Medium vessel vasculitis

259
Q

Microscopic polyarteritis and Wegener’s granulomatosis are examples of:

A

Small vessel vasculitis

260
Q

What are the 4 pathogeneses of immune-mediated vasculitis?

A
  1. immune complex formation
  2. ANCA (antineutrophilic cytoplasmic antibodies)
  3. Anti-endothelial cell antibodies (AECA)
  4. Cell mediated
261
Q

ANCA is most commonly associated with what size vessel vasculitis?

A

Small vessel vasculitis

262
Q 
What is this:
Etiology: Unknown (?T-cell mediated)
Clinical: Rare before 50, Fever, weight loss, headache, visual problems, pain and tenderness over temporal artery, polymyalgia rheumatica. 
Pathology: Granulomatous inflammation
intimal proliferation/fibrosis
A

Giant Cell (Temporal) Arteritis (large vessel)

263
Q

What is this:
Etiology: unknown; similar to temporal arteritis, just in a younger person
Clinical: F&raquo_space; M, age < 40 years, weak arm pulses (“pulseless disease”), visual disturbances, neurologic manifestations
Pathology:
-Involves aortic arch and branches
-Intimal fibrosis
-Granulomatous inflammation with fibrosis

A

Takayasu Arteritis (large vessel)

264
Q 
What is this:
Etiology: unknown (at one time, 30% of patients positive for Hepatitis B, now < 8%)
Clinical: acute-relapsing-chronic, fever, weight loss, hematuria, renal failure, hypertension, abdominal pain, melena
Pathology:
Haphazard, segmental inflammation
Kidney > heart > liver > GI
Fibrinoid necrosis, PMNs
Thrombosis, aneurysms
Heal by fibrosis
A

Polyarteritis Nodosa (medium vessel)

265
Q

What is this:
Etiology: anti-endothelial antibody (?) triggered by viral infection
Clinical: Infants and young children, fever, mucous membrane erythema (eyes/mouth), skin rash, cervical lymphadenopathy; usually self-limited
Pathology:
-Coronary artery vasculitis (accounts for fatalities in 1–2%)

A

Kawasaki disease, also known as mucocutaneous lymph node syndrome (medium vessel)

266
Q

What is this:
Etiology: Ag-Ab complexes/MPO-ANCA
Clinical: skin rash, multiple other organs, fever
Specific disorders: drugs, bacteria, foreign proteins, tumor proteins
Pathology:
-Involves microvasculature
-Fibrinoid necrosis
-Karyorrhexis of PMN’s (leukocytoclastic vasculitis)

A

Microscopic Polyangiitis (small vessel)

267
Q

What is this:
Etiology: neutrophil-related endothelial damage mediated by PR3-ANCA
Clinical: strawberry gingivitis, sinusitis, pneumonitis, renal failure, glomerulonephritis
Pathology:
-Affects upper and lower respiratory tract, kidneys
-Necrotizing granulomas
-Vasculitis with fibrinoid necrosis

A

Wegener Granulomatosis (small vessel)

268
Q

What is this:
Etiology: endothelial injury from substance in cigarette smoke
Clinical: cigarette smoking, < 35 years, pain of extremities, ischemic ulcers, gangrene
Pathology:
Vasculitis with thrombosis

A

Thromboangiitis Obliterans
(Buerger Disease)

269
Q

What is this:
Pathology:
- intimal tear - split between mid & outer third of the media
-media may be normal or have degeneration
Complications:
-rupture – hemorrhage
-branch obstruction
Predisposing conditions: hypertension, connective tissue disorders (Marfan)

A

Dissecting Aortic Hematoma

Fall 17 - Gen Path (2 decks)

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