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gen path final Flashcards

1
Q

Continuously dividing cells

A

Skin, oral cavity, vagina, cervix, exocrine ducts, GI tract

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2
Q

Stable

A

Endothelial cells, fibroblasts, smooth muscle, most solid organs (kidney, pancreas, liver)

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3
Q

Permanent

A

Neurons, cardiac muscle, skeletal muscle

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4
Q

HYPERTROPHY

A

Increase in size of cell increase in
size of organ
* Occurs in cells with limited capacity to
divide
* Physiologic
* Uterus enlarging during pregnancy
* Pathologic
* Cardiac enlargement secondary to
hypertension

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5
Q

HYPERPLASIA

A
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6
Q

ATROPHY

A

Decrease in size of cells
* Loss of cell substance by reduced
protein synthesis and increased
protein degradation
* Causes
* Decreased workload
* Diminished blood supply
* Inadequate nutrition
* Loss of endocrine stimulation
* Aging

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7
Q

METAPLASIA

A

one cell type replace another type of cell
May predispose to malignant transformation

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8
Q

DYSPLASIA

A

Disordered cellular growth
* Proliferation of precancerous cells
* May be reversible
* May progress to cancer

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9
Q

APLASIA

A

Failure of cell production during embryogenesis
ex: missing kidney

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10
Q

HYPOPLASIA

A

Decrease in cell production during embryogenesis

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11
Q

HYPOXIA

A

cell injury
oxygen deficiency

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12
Q

ROS

A

Chemically unstable
* Attack nucleic acids, cellular
proteins, and lipids

21

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13
Q

where do ROS come from normally?

A

1- respiration and energy generation
2- neutrophils and macrophages

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14
Q

why do ROS accumulate

A

1- radiation
2- exogenous chemicals
3- inflammation

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15
Q

mechanism to minimize ROS injury

A

1- free radicals scavengers
2- antioxidants

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16
Q

antioxidants

A

Vitamins E, A and C and β-carotene

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17
Q

mechanism of ROS injury

A

1- membrane damage
2- protein crosslinking
3- DNA damage

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18
Q

irreversible cell injury causes

A

Inability to restore mitochondrial
function
* Loss of structure and function of plasma
membrane and intracellular membrane
* Loss of DNA and chromatin structural
integrity

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19
Q

necrosis

A

Cellular membranes fall apart
* Cellular enzymes leak out and digest cell
* Causes inflammatory response

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20
Q

COAGULATIVE NECROSIS
etiology
gross appearance
histological features

A

ETIOLOGY
* Infarct in solid organs
* Does not occur in the brain
GROSS APPEARANCE
* Tissue appears firm
HISTOPATHOLOGIC FEATURES
* Cell outlines preserved
* No nucleus
* Eosinophilic (pink)

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21
Q

LIQUEFACTIVE NECROSIS etiology

A

Bacterial/fungal infections
Hypoxia in CNS

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22
Q

liquefactive necrosis gross appearance

A

Dissolution of tissue into viscous liquid

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23
Q

ID

A

GANGRENOUS NECROSIS
ETIOLOGY
* Ischemia of limb
GROSS APPEARANCE
* Coagulative necrosis resembling
mummified tissue
* Can have superimposed
liquefactive necrosis

33

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24
Q

CASEOUS NECROSIS

A

ETIOLOGY
* Tuberculosis infections
* Body tries to “wall off” infection
GROSS APPEARANCE
* “Cheese like” friable yellow-white
necrotic tissue
HISTOPATHOLOGIC FEATURES
* Caseating granulomas

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25
Q

FAT necrosis etiology

A

Lipase breaks down fat cells
* Calcium accumulates
* Seen in pancreatitis

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26
Q

fat necrosis gross appearance

A

Chalky, white deposits in fat

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27
Q

fat necrosis histological features

A

Outlines of dead fat cells (no nuclei)

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28
Q

FIBRINOID NECROSIS

A

immune mediated condition
hypertension
eosinophilic in walls of blood vessels

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29
Q

APOPTOSIS

A

Does not illicit inflammatory reaction

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30
Q

what are the main cell type in acute inflammation

A

Neutrophils

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31
Q

what are the main cell type in chronic inflammation

A

Lymphocytes and macrophages

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32
Q

inflammatory response (the 5R’s)

A

1.Recognition of injurious agent
2. Recruitment of leukocytes
3. Removal of the agent
4. Regulation of the response
5. Resolution (repair)

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33
Q

RECOGNITION OF INJURIOUS AGENTS
microbes
cell damage
circulating proteins

A

microbes-> TLRS
cell damage -> inflammsome
circulating protiens-> complement system

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34
Q

TOLL-LIKE RECEPTORS (TLRs)
location
cells
function

A

Present in plasma membranes
* Extracellular microbe detection
* Present in endosomes
* Ingested microbe detection
* Expressed by macrophages, dendritic
cells, and other cells
* Recognize pathogen-associated
molecular patterns (PAMPs) in
microbes
* Produce cytokines to trigger an
immune response

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35
Q

INFLAMMASOMES
function

A

All cells have receptors that recognize damage-associated molecular patterns
(DAMPs)
* Examples of DAMPs
* Uric acid – product of DNA breakdown
* ATP – released from damaged mitochondria
* DNA – shouldn’t be in cytoplasm
* Receptors activate a cascade resulting in cytokine (interleukin-1) production

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36
Q

REACTIONS OF BLOOD VESSELS IN ACUTE INFLAMMATION

A

vasodilation and vascular permeability

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37
Q

Rolling/loose attachment mediated by which enzyme

A

selectins

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38
Q

Adhesion. mediated by which enzyme

A

integrins

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39
Q

what is made during the regulation of response to acute inflammation

A

Anti-inflammatory lipoxins made

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40
Q

MEDIATORS OF ACUTE INFLAMMATION

A

Cell-derived
* Arachidonic acid metabolites
* Mast cell products
* Cytokines
* Plasma-protein derived
* Complement

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41
Q

ARACHIDONIC ACID METABOLITES
source
key metabolites
role

A

SOURCE
* Produced from cell membrane phospholipids
KEY METABOLITES
* Prostaglandins
* Cause vasodilation and increase vascular permeability
* Lead to redness and swelling
* Thromboxane A2
* Promote platelet aggregation and vasoconstriction
* Involved in clot formation
* Leukotrienes
* Increase vascular permeability
* Act as chemotactic agents for leukocytes
* Contribute to bronchospasm
ROLE
* Amplify and sustain the inflammatory response

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42
Q

what are the mast cells products

A

histamine
initiate the inflammatory response

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43
Q

cytokines
source
metabolites
role

A

SOURCE
* Macrophages, lymphocytes, endothelial cells, and others
KEY CYTOKINES
* Interleukins (IL-1, IL-6, etc.)
* Endothelial activation
* Promote fever
* Activates leukocytes
* Tumor Necrosis Factor (TNF-⍺)
* Endothelial activation
* Promotes fever
* Activates leukocytes
ROLE
* Regulate intensity and duration of immune response

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44
Q

what are the activation pathways of the complement systems

A

Classical
* Triggered by antibodies binding to pathogens
* Alternative
* Activated directly by pathogen surfaces
* Lectin
* Initiated by mannose-binding lectin attaching to
pathogen surfaces

24

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45
Q

what is the function of the complement system

A

Bridges innate and adaptive immunity, enhancing
the ability to clear microbes and damaged cells

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46
Q

OUTCOMES OF ACUTE INFLAMMATION

A

COMPLETE RESOLUTION
* Damaged parenchymal cells regenerate
* Cellular debris and microbes removed by macrophages
* Edema fluid resorbed by lymphatics

HEALING BY CONNECTIVE TISSUE REPLACEMENT
* Scarring or fibrosis
* 3 scenarios
* Substantial destruction
* Involves tissues that can’t regenerate
* Abundant fibrin exudate can’t be adequately cleared
* Connective tissue grows into area creating a mass of fibrous tissue

PROGRESSION TO CHRONIC INFLAMMATION
* Injurious agent persists or something is interfering with the normal process of healing

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47
Q

CAUSES OF CHRONIC INFLAMMATION

A

Persistent infections
* Hypersensitivity diseases
* Autoimmune diseases
* Allergies
* Prolonged exposure to toxins

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48
Q

MACROPHAGES origin

A

monocytes in blood
macrophages in tissues

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49
Q

MACROPHAGES functions

A

Phagocytosis
* Antigen presentation
* Present antigens to T cells
* Cytokine production
* Tissue repair
* Secrete growth factor

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50
Q

LYMPHOCYTES function

A

1- T cells
* Helper T Cells (CD4+)
* Release cytokines to activate other immune cells
(macrophages)
* Cytotoxic T cells (CD8+)
* Directly kill infected or damaged cells
2- B cells
* Differentiate into plasma cells

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51
Q

plasma cells functions

A

1-Antibody production
2- Formation of immune
complexes

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52
Q

______ associated with allergic
reactions and parasitic infections

A

EOSINOPHILS

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53
Q

EOSINOPHILS functions

A

1-Release cytotoxic granules
2-Produce cytokines and chemokines
3-Release mediators

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54
Q

Chronic inflammation occurring when a material is difficult to
digest/remove
1- presistent t cells response to microbes
2- immune mediated inflammatory response
3- forgien body

A

GRANULOMATOUS INFLAMMATION

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55
Q

GRANULOMATOUS INFLAMMATION histological features

A

large epithelioid
surrounding lymphocytes
giant cells
central necrosis

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56
Q

SYSTEMIC EFFECTS OF INFLAMMATION (ACUTE AND CHRONIC)

A

fever
LYMPHADENOPATHY
LEUKOCYTOSIS
ACUTE-PHASE PROTEINS ( C-reactive protein (CRP), fibrinogen, serum amyloid A
(SAA))

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57
Q

what are the key processes in repair

A

1-Regeneration
* Proliferation of cells that survived injury (or stem
cells)
2- Scar formation
* Deposition of connective tissue (mostly collagen)

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58
Q

_______ play a central role in repair

A

Macrophages

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59
Q

Which of the following tissues has the highest
capacity for regeneration?
a. Cardiac muscle
b. Skeletal muscle
c. Oral mucosa
d. Neurons
e. Liver

A

oral mucosa

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60
Q

types of wound healing

A

1- PRIMARY INTENTION
* Clean, close wound edges
* Surgical incision approximated with sutures
* Sutured periodontal flap
* Paper cut
* Regeneration > scarring
2- SECONDARY INTENTION
* Larger open wounds
* Extraction sites
* Gingival graft donor site
* Burns
* More granulation tissue and scarring

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61
Q

what type of regeneration occur in stable tissues

A

limited
ex) If one kidney is removed the other
undergoes hyperplasia and
hypertrophy
If half the liver is removed, it will
regenerate

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62
Q

in regeneration What cells/tissues are proliferating?

A

1- Injured tissue
* Attempt to restore normal structure
2- Vascular endothelial cells
* Provide nutrients for repair process
3- Fibroblasts
* Source of fibrous tissue for scar

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63
Q

REPAIR SEQUENCE

A

1- Clot forms immediately after injury
2- Day 1: Neutrophils migrate in and
phagocytose foreign substances and necrotic
tissue
3-Day 2: Macrophages enter, granulation tissue
(capillaries and immature fibroblasts) start to
form, protected by a fibrin clot
4- Day 3-6: Lymphocytes and plasma cells enter
5- Day 7: Clot digested, initial repair complete
6-Day 14: Fibroblasts mature, collagen

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64
Q

TGF-β

A

Stimulates production of and inhibits breakdown of ECM proteins

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65
Q

PDGF

A

Migration and proliferation of fibroblasts and smooth muscle cells

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66
Q

FGF

A

Fibroblast migration

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67
Q

Cytokines

A

IL-13 stimulates collagen synthesis and fibroblast migration

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68
Q

FACTORS THAT CAN PREVENT HEALING/REPAIR

A

infection
nutrition
steroid use
poor perfusion
foreign bodies
type and extent of injuy
location of injury
abberation of cell growth

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69
Q

ID

A

KELOIDS
excessive formation of collagen during the repair process

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70
Q

Granulation tissue is primarily composed of which
of the following?

A

Fibroblasts and new blood vessels

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71
Q

Which of the following organs/tissues is correctly matched with its potential adaptive response?
1- Myometrium, metaplasia

2- Heart, hyperplasia

3- Breast, hypertrophy

4- Skeletal muscle, atrophy

A

Skeletal muscle, atrophy

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72
Q

All of the following are present 2-3 days after extraction of a tooth during normal healing, EXCEPT one. Which one is the EXCEPTION?

1- VEGF
2- Fibroblasts
3- Multinucleated giant cells

4- Macrophages

A

3- Multinucleated giant cells

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73
Q

Papillary cystadenoma

A

characterized by adenomatous papillary processes
that extend into cystic spaces, as in
cystadenoma of the ovary.

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74
Q

Oncology

A

the study of neoplasm

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75
Q

what are the 2 anatomic component of neoplasia

A

1- Parenchyma: neoplastic cells , determine how a tumor is named
2- Stroma: supporting ct and vasculature

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76
Q

Well differentiated
Poorly differentiated

A

more resemblance
little resemblance

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77
Q

Anaplasia

A

dedifferentiated or undifferentiated

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78
Q

Dysplasia

A

A microscopic, potentially reversible,
altered growth or maturation pattern.
it is precancerous =may progress
to malignancy, but in bones it doesnt imply a precancerous growth just altered growth.

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79
Q

Carcinoma in-situ

A

Dysplastic changes involving the full-
thickness of the epithelium.
pre cancerous

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80
Q

Papilloma
(Benign Epithelial Tumors)

A

finger-like epithelial
projections overlying cores of vascular fibrous
connective tissue.
Arises from surface epithelium (Squamous-
skin, larynx, tongue. Transitional- bladder,
ureter, renal pelvis)

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81
Q
A
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82
Q

Benign Mesenchymal
1- Fibroma
2- Chondroma
3- Leiomyoma
4- Rhabdomyoma
5- Lipoma
6- osteoma
7- Angioma

A

1-fibrous tissue
2-cartilaginous
3-smooth muscle
4-skeletal muscle
5-fat
6-bone
7- vessels

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83
Q

Benign Mixed tumors

A

pleomorphic adenoma
(salivary), fibroadenoma (breast)- only fibrous
portion is neoplastic

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84
Q

Teratoma

A

neoplasm with cells derived from
more than 1 germ layer, totipotent cells

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85
Q

Hamartoma

A

disorganized tissue native to the
site (non-neoplastic generally)

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86
Q

Choristoma

A

disorganized tissue at unexpected
site (non-neoplastic)

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87
Q

Polyp

A

a mass that projects above a mucosal
surface

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88
Q

Some Notable -oma
Exceptions

A

*Malignancies:
1- Lymphoma
2-Melanoma
3-Mesothelioma
4-Seminoma
5-Glioblastoma
6-Hepatoma (hepatocellular carcinoma)
*Granuloma, hematoma (non-neoplastic)
Malignant Epithelial

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89
Q

Squamous cell carcinoma

A

from squamous epithelium (skin, mouth,
esophagus, vagina) or areas of squamous
metaplasia (bronchi or cervix)
*Marked by production of keratin

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90
Q

Transitional cell carcinoma

A

from urinary tract epithelium

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91
Q

Adenocarcinoma

A

glandular origin
* Includes tumors of GI mucosa,
endometrium and pancreas

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92
Q

sarcoma is bengin or malignant ?

A

malignant

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93
Q

ID

A

CYSTIC

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94
Q

ID

A

PAPILLARY

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95
Q

ID

A

Tubular

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96
Q

ID

A

solid

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97
Q

clinical and gross appearance of benign tumors

A

*clinical
1-Non-cancerous
2- Slow growing
3-Remains localized, does not
spread, may cause local
damage
4-Surgically removable
5-Survivable - good prognosis
*gross
1-Well-differentiated
2-Normal mitoses
3- Encapsulation

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98
Q

clinical and gross appearance of malignant tumors

A
  • clinical
    1-Cancer, latin for “crab”
    2- Rapid growth
    3-Invade and destroy adjacent
    tissues
    4-Metastasis-defining feature of
    malignancy
    5-Can cause death –> poor
    prognosis
    *gross
    1-Well to poorly differentiated
    (or anaplastic)
    2- Atypical mitoses
    3-Non-encapsulated
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99
Q

Metastasis

A

Hallmark of malignancy
30% of newly diagnosed malignant
tumors have clinically evident
metastases

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100
Q

T/F
cancer is a genetic disorder , from acquired random mutation or from environmental exposure.

A

T

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101
Q

T/F
genetic changes are heritable with accumulation of mutation leading to characteristics of cancer

A

True

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102
Q

neoplasm is a multistep process , what are the steps ?

A

1- initiation: genetic damage causes a single cell growth.
2- promotion: additional genetic
damage over time leads to
heterogenous population of cells
(visible clinically)
3- progression: evolution and
selection of more aggressive
tumors capable of metastasis that
are less responsive to treatment

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103
Q

Carcinogens:
1-
2-
3-
May act together to elicit genetic
alterations leading to neoplasia

A

1- chemicals
2- radiant
3- microbial agents ( viruses- HBV, EBV, etc)

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104
Q

What genes are affected that form neoplasms?

A

1-Proto-oncogenes- increase growth
2- tumor supressor genes- stop cell growth/ help with DNA repair
3- Apoptosis regulation genes- determine cell death
4- tumor cell interaction genes- CTL, kill cells with unrepaired genetic damage

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105
Q

The immune system (cell-mediated) helps
prevent tumor formation or progression
what are the evidence ?

A

↑ frequency of cancer in
immunocompromised hosts (congenital,
transplant, AIDS)

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106
Q

Epidemiology

A

the branch of medicine
which deals with the incidence,
distribution, and possible control of
diseases and other factors relating to
health.

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107
Q

risk for bronchogenic CA

A

Smoking induced squamous metaplasia,
dysplasia of bronchial mucosa

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108
Q

risk for endometrial CA

A

Endometrial hyperplasia and dysplasia

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109
Q

risk for squamous cell carcinoma

A

Oral, vulvar and penile leukoplakia

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110
Q

risk for colorectal carcinoma

A

Villous adenoma of colon

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111
Q

Are Benign Tumors
Premalignant?

A

no but a few exceptions (i.e.
adenomas of the colon can
undergo malignant
transformation)

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112
Q

what are the environmental factors associated with increase risk of cancer

A

1- Occupational
2-Chronic sun exposure
3- Cigarette smoking
4-Chronic alcohol consumption
5- Obesity
6- Oncogenic viruses (e.g. HPV)

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113
Q

T/F
statement one: Older individuals are most likely to get cancer (80% are >55yrs old)
statement two: In children (0-15yrs), cancer
accounts for just over 10% of
deaths (leukemia, lymphoma, CNS
tumors, bone/ST sarcomas)

A

True for both statement

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114
Q

what is the tumor effects on the host

A

1-Location is crucial (e.g. pituitary, bile duct)
2-Hormone production – seen in endocrine
gland tumors (pancreas, adrenal cortex)
3- Bleeding and infection
4-Intestinal complications (intussusception
or obstruction)

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115
Q

what are the general features of Paraneoplastic Syndromes?

A

1-Symptoms not related to tumor spread or
hormone production
2-10-15% of cancer patients
3- May indicate underlying neoplasm
4-Can be lethal
5-Can mimic metastatic disease
6-Diverse, associated with many tumors
Cachexia

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116
Q

ID

A

Cachexia
(paraneoplastic syndorme)

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117
Q

what is Cachexia?

A

1- Progressive loss of
body fat and lean body
mass with weakness,
anorexia and anemia
2-High metabolic rate
3- Caused by tumor and
host cytokines (e.g.
TNF- decreases
appetite), not due to
tumor’s nutritional
demand
(Paraneoplastic Syndrome)

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118
Q

grading of tumors

A

Estimates aggressiveness based on cytologic
differentiation
*Grade I, II, III, IV (in order of increasing
anaplasia)

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119
Q

staging of tumors

A

Size of primary tumor and extent of regional and
distant (metastasis) spread
1-TNM system [T= tumor size (1-4), N= regional
nodal involvement (0-3); M= metastasis(0,1)]
2-AJC system (0 to IV scale)

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120
Q

what are the two categories Cytologic Smear (cells on a slide)?

A

1-Direct scraping-good for superficial
fungal and herpes infections
2-Fine-needle aspiration (FNA): for
readily palpable lesions (breast,
thyroid, lymph nodes and salivary
glands)

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121
Q

Immunohistochemistry IHC

A

*Useful to determine the cellular
differentiation of poorly differentiated
tumor cells (e.g. epithelial, mesenchymal)
* Useful in diagnosis of lymphomas to
determine lineage (B or T cell) and
differentiation stage and in treatment of
B-cell lymphomas (i.e. if have cell surface
CD20, can give the CD20 inhibitor
rituximab)

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122
Q

Flow Cytometry

A

Requires fresh tissue (no
formalin) – helps classify
leukemias, lymphomas

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123
Q

Tumor Markers- Serology

A

1-PSA- low sensitivity and low specificity
2-carcinoembryonic antigen (CEA)- cancers
of colon, pancreas, stomach and breast
3-α-fetoprotein- hepatocellular carcinomas,
yolk sac remnants
*PSA, CEA and α-fetoprotein are not good
for early detection but great for detecting
recurrences

124
Q

Molecular Diagnosis

A

*PCR- can detect monoclonality in lymphoid malignancies
*FISH/PCR

translocation
gene amplification

125
Q

omics
clinically

A

DNA easier to work with than RNA
 Current trend is to develop methods to sequence
several hundred key genes to detect mutations
in as few as 5% of tumor cells
 Use DNA arrays to identify changes in DNA copy
number (amplifications, deletions)
 In the future, may use epigenomics to predict
drug efficacy
Future of Cancer Diagnostics
 Paradigm shift to classify tumors based on
mutation and associated therapeutic
targets rather than on morphology or cell
of origin
 Optimal diagnosis and management
combines histopathology with relevant
molecular diagnostic techniques (IHC,
FISH, PCR, flow cytometry, all of the –
omics etc.)

126
Q

t/f
Paradigm shift to classify tumors based on
mutation and associated therapeutic
targets rather than on morphology or cell
of origin

A

T

127
Q

what are the 4 main compartments of the body occupied by WBC

A

1-Bone marrow- production
2-Bloodstream- transport
3-Lymph nodes- immune activation
4-Site of infection or immune stimulation- can be
within any organ or soft tissue- what you see
clinically

128
Q

Leukopenia

A

decreased serum level of leukocytes

129
Q

Leukocytosis

A

elevated serum levels of leukocytes,
mostly neutrophils [normal = 4-10,000/mm3 (or μl)
which elevates to 15-20,000/mm3 ]

130
Q

Neutrophilic

A

bacterial infections or when there is
tissue necrosis (burns, myocardial infarctions)

131
Q

Lymphocytotic

A

chronic infections and some viral
infections

132
Q

Monocytotic

A

chronic infection

133
Q

Eosinophilic

A

allergies (asthma, hay fever), parasitic
infections, drug reactions

134
Q

Lymph node (LN) evaluation- usually small ___ and ________ is considered normal

A

less than 0.5 and non palpable

135
Q

Lymphadenopathy (LAD)- usually firm and enlarged >1 cm
what are the difference between painful and non painful

A

-Painful LAD: usually seen in the
LN that is draining a region of
infection (acute lymphadenitis)

-Non-painful LAD: seen with
chronic inflammation (chronic
lymphadenitis), metastatic cancer
or lymphoma

136
Q

t/f
<2 wks or >1 yr without size change is unlikely to be a neoplasm
Risk for cancer: >6wks and not better by 12 weeks

A

both statements are true

137
Q

LAD symptoms (miami)

A

1-Malignancy: fever, drenching night sweats and
unexplained weight loss of greater than 10% of body weight. supraclavicular LAD adults or children- up to 50% have intraabdominal malignancy
2-Infectious: fever, chills, fatigue, and malaise
3-Autoimmune: arthralgias, muscle weakness, and rash
4-Miscellaneous: other specific findings of each condition
5-Iatrogenic: history of new medications

138
Q

Neutropenia

A

decreased neutrophils in blood

139
Q

Agranulocytosis

A

decreased granulocytes (neutrophils,
basophils and eosinophils) in blood

140
Q

Neutropenia/Agranulocytosis pathogenesis and symptoms

A

pathogenesis :either decreased production in bone marrow or increased destruction in the peripheral blood
symptoms : ulceration (oral, often gingival)- deep, punched out

141
Q

what are the causes of decreased production of neutrophils in bone marrow

A

1- leukemia
2- aplastic anemia
3- chemotx

142
Q

what are the causes of destruction of neutrophils in peripheral cells

A

1- immune mediated injury (drugs)
2- chronic infection
3- splenomegaly

143
Q

Neutropenia/Agranulocytosis treatment

A

1-Remove the offending agent
2-Control infections (antibiotics,
antifungals etc.)
3- Give granulocyte colony-stimulating
factor (G-CSF) to stimulate granulocyte
production

144
Q

WBC Neoplasms Classification is based on morphologic and molecular criteria
Broad categories based on origin and
differentiation include:

A

1-Lymphoid neoplasms
2-Myeloid neoplasms
3-Histiocytic neoplasms

145
Q

Lymphoid neoplasms– Etiology

A

increased risk for translocations and
transformation in B cells because in germinal
centers they undergo1- somatic hypermutation to increase antibody affinity
2- class switching to produce multiple antibody types
(i.e. from IgM to IgG, IgA, IgE) to the same antigen)
*uncommon to occur in T cells because T CELLS are gnomically stable

146
Q

Leukemia

A

involvement of the bone marrow and
peripheral blood

147
Q

Lymphoma

A

Tumor masses in lymph nodes or other
tissues

148
Q

Lymphoid Neoplasms: WHO
classification criteria

A

1-Morphology (H&E appearance)
2-Cell origin (immunophenotyping by IHC and/or
flow cytometry)
3- Clinical features
4-Genotype (karyotype, presence of viral
genomes)

149
Q

Leukemia- General

A

*Group of hematologic malignancies
characterized by tumor cells that originate in the
bone marrow and spill over into the blood
*Diffuse infiltration into lymph nodes, spleen,
liver and gingiva causing general enlargement
*Derived from single transformed cell exhibiting
clonal growth.
*Typically, all of the clonal cell population have
the same surface markers

150
Q

Acute Leukemia: Etiology

A

1- ionizing radiation
2- toxins
3- Antineoplastic chemotherapeutic drugs
4- chromosomal abnormalities

151
Q

What signs and symptoms do you expect a
patient to have who has Acute leukemia?

A
  • myelophthisic anemia: replacement of normal
    hematopoietic cells by neoplastic “blasts” (myeloblasts, erythroblasts, and megakaryocytes) in bone marrow causing:
    1- neutropenia : infections (oral ulcers, herpes, and candida)
    2- Anemia: fatigue and SOB(shortness of breath)
    3- Thrombocytopenia: bleeding
    4- these changes leads tp high WBC count and extramedullary hematopoiesis
152
Q

what are the two types of acute leukemia?

A

1-Acute Lymphoblastic Leukemia
(ALL)
2- Acute Myeloid Leukemia (AML)

153
Q

Acute Lymphoblastic Leukemia
(ALL)

A

1- most common cancer in children
2- Derived from an immature B (pre-
B) or T (pre-T) cells called
lymphoblasts
3- good prognosis

154
Q

Acute Myeloid Leukemia (AML)

A

1- affect older adults
2-Derived from an immature B (pre-
B) or T (pre-T) cells called
lymphoblasts
3- low rate of survival

155
Q

Chronic Leukemia

A

1- Neoplasm of mature circulating lymphocytes (high WBC count)
2- *CML- high WBC- neutrophils
* CLL- high WBC- lymphocytes

156
Q

Chronic lymphocytic leukemia (CLL)

A

1- most common cancer in adults in the western world
2- slow growing tumor
3- increased BCL2 , often asymptomatic
4- if it involves lymph nodes its called SLL
5- Cure only achieved with
hematopoietic stem cell transplant
6- Some tumors transform to more
aggressive diffuse large B-cell
lymphoma (Richter
transformation)–patients die within
a year

157
Q

Chronic myeloid leukemia

A

1- show an increase in granulocyte
2- Philadelphia chromosome: BCR-
ABL t(9:22) translocation causing a
fusion protein
3- Some cases undergo transformation
into an acute leukemia (“Blast
Crisis”)
4- treatment: Tyrosine kinase
inhibitors (e.g. imatinib (Gleevec))
induce sustained remissions and
prevent progression to blast crisis

158
Q

Myelodysplastic syndrome (MDS)

A

bone marrow is replaced by coronal, multipotent stem cells with capacity for differentiation into red
cells (erythroid precursors),
granulocytes and platelets.
high risk for transformation of AML

159
Q

B Cell Lymphomas

A

1-Hodgkin Lymphoma
2- Non-Hodgkin Lymphomas
 Follicular lymphoma
 Marginal zone lymphoma
 Diffuse Large B cell lymphoma
 Burkitt lymphoma
 Plasma cell disorders: multiple myeloma

160
Q

Hodgkin lymphoma

A

1- Typified by the Reed-Sternberg (RS) cell which is germinal center B cell (Some have EBV infection)
2- Adolescents/young adults or patients
>50 yrs
3- Painless LAD: single node spreads to
contiguous nodes (lower cervical,
supraclavicular or mediastinal lymph
nodes)
4- “B symptoms” (fever, weight loss,
night sweats), pruritus and anemia
occur with more advanced disease
5-Treatment: Chemotx, advanced
disease also receives radiotherapy.
Immunotherapy (anti-PD-1
antibodies) for refractory disease
6-prognosis: Five-year survival: >90%

161
Q

Follicular lymphoma

A

1- translocation causes overexpression of BCL2
2->50 YEARS
3- Painless, generalized lymphadenopathy
4- 30-40% progress to diffuse large B-cell
lymphoma

162
Q

ID

A

Extranodal marginal zone lymphoma

163
Q

Extranodal marginal zone lymphoma

A

Arise in mucosa-associated lymphoid tissue
(MALT) associated with epithelium
(stomach, salivary glands etc.) and can cause
swelling
Sustained by chronic inflammation triggered
by autoimmune disorders (Sjogren syndrome
in salivary glands, Hashimoto thyroiditis) or
sites of chronic infection (H. pylori gastritis)
H pylori -specific T cells drive growth and
survival of B cells. If you kill the bug, tumor
shrinks. But, polyclonal B cell growth can
evolve into monoclonal change and spread to
distant sites.
When localized, cured by simple excision
followed by radiotherapy

164
Q

ID

A

Diffuse large B-cell lymphoma

165
Q

Most common type of lymphoma in
adults
 Some have a t(14;18) translocation
of BCL-2 and others have
translocations of MYC (oncogene)
 Often symptomatic, rapidly enlarging
mass either within a lymph node or
extranodal in virtually any organ or
tissue
 Aggressive tumor, requires intensive
combination chemotherapy and anti-
CD20 drugs with 60–80% complete
remission

ID

A

Diffuse large B-cell lymphoma

166
Q

Burkitt lymphoma

A

FASTEST GROWING HUMAN TUMOR
TRANSLOCATION OF MYC AND IGH
CHLIDREN AND YOUNG ADULTS
JAW MASSES ASSOCIATED WITH EBV IN AFRICA
ABDOMINAL MASS IN NORTH AMERICA
STARRY SKY

167
Q

M proteins are large and restricted to plasma
T/F

A

TRUE

168
Q

Condition with Abnormal Igs

A

MULTIPLE MEYLOMA

169
Q

Multiple myeloma

A

A common lymphoid malignancy
 Median age = 70 years
 Primarily involves bone marrow with associated
lytic lesions (often “punched-out”
radiolucencies) throughout the skeleton
(vertebral column, ribs, skull etc.)
 Most frequent M protein is IgG. If kappa or
lambda light chains are produced their small size
allows excretion in the urine (Bence-Jones
proteins)
Defective production of normal B cells→ high risk for bacterial infections
 Renal dysfunction due to
 obstructive proteinaceous casts (Bence-Jones
proteins, complete immunoglobulin, albumin etc.)
 Light chain deposition in the glomerulus or
interstitial
 Hypercalcemia leads to dehydration and renal stones
 Bacterial pyelonephritis due to
hypogammaglobulinemia

170
Q

Multiple myeloma: Clinical

A

PUNCHED OUT RADIOLUCENCIES
Hypercalcemia causes confusion,
weakness, lethargy
RECURRENT BACTERIAL INFECTION
RENAL INSUFFECIENCY
REQUIRES BONE MARROW EXAM

171
Q

Histiocytosis X

A

Langerhans cells: Immature dendritic cells that capture

172
Q

Langerhans Cell Histiocytosis

A

1-Neoplastic cells appear more like tissue
macrophages (histiocytes) rather than
dendritic cells. Eosinophils also present
2-Acute/chronic presentations that affect skin,
viscera and/or bone
3-eosinophilic granuloma of bone
4-Skull, ribs, vertebrae and mandible are
commonly affected (similar locations as
multiple myeloma)
5-Dull pain and tenderness often present
6- ILL DEFINED RADIOLUCIENCIES

173
Q

What is the most common leukemia of adults in the Western world?

A

chronic lymphocytic leukemia

174
Q

Histiocytic neoplasms are proliferations of which of the following cell types?

A

dendritic cell or macrophages

175
Q

multiple “punched-out” radiolucencies throughout the skeleton?

A

multiple myeloma

176
Q

liver functions

A

1- synthesis of bile, serum proteins (albumin, clotting factors, and globulins), lipid.
2- metabolism of fats, cho, amino acids.
3- stores glycogen, iron, b12, folate and vitamin A.
4- produces urea and hepcidin.
5- breaks down circulating estrogens
6- detoxification of blood.

177
Q

biliary system

A

a group of organs and ducts
1- liver produces bile
2- galbladder , stores and release bile to the duodenum when food is eaten
3- bile ducts transport bile from liver to duodenum.

178
Q

whats is bile and what is its function

A

bile is a green/yellowish substance composed of bile acid, bilirubin, salts, cholesterol and other waste products.
1- aids in the digestion of fats
2- serves as the primary pathway for elemination of bilirubin and other toxic substances.

179
Q

what does the hepatic panel test detects ?

A

1- synthesis of liver enzymes
a) albumin
b) albumin + globulins
c) pt and inr- presence and function of coagulation factors
2- bilirubin processing and bile secretion
GGT+ ALP
3- extent of liver damage
AST and ALT

180
Q

ID

A

Jaundice

181
Q

what is Jaundice, etiology, pathogenesis?

A

its a yellow discoloration of the skin and sclerae of the eyes
etiology: elevated level of bilirubin ( its the yellow breakdown of redblood cells which becomes a component of bile)
pathogenesis: depends on where bilirubin metabolism altered

182
Q

what are the Reasons why a person may have elevated bilirubin

A

1- bile isnt being formed
2- breakdown of large amounts of blood
3- obstruction of bile flow out of the liver

183
Q

Normal bilirubin metabolism

A

Bilirubin alone is highly toxic and insoluble and can’t be
excreted; it has to be managed
How is it metabolized?
* RBC’s are consumed by macrophages
* Protoporphyrin (from heme) is converted to biliverdin
then to unconjugated bilirubin (UCB) which binds tightly
to albumin
* Albumin carries UCB to the liver
* Uridine glucuronyl transferase (UGT) in hepatocytes
conjugates bilirubin (making it water-soluble and non-
toxic)
* Conjugated bilirubin (CB) is transferred to bile canaliculi
to form bile, which is stored in the gallbladder
* Bile is released into the small bowel to aid in digestion
* Intestinal flora converts CB to urobilinogen (colorless),
which is oxidized to stercobilin (makes stool brown) and
urobilin (yellow) which are mostly excreted in the feces.
* Some urobilin is reabsorbed into blood and filtered by
kidney, making urine yellow

184
Q

causes of jaundice

A
185
Q

fulminant hepatitis

A

a severe life threatening form of acute hepatitis

186
Q

______ is the only DNA disorder hepatitis, the rest are RNA

A

HBV

187
Q

hepatits viruses table

A
188
Q

dental implication of hepatitis B and C

A
189
Q

alcoholic liver disease types and features

A
  • leading cause of liver disease in the western countries
  • mediated by acetaldehyde
    *types
    1-Steatosis- fat accumulation in hepatocytes.
    Liver is large, soft, yellow, and greasy (“fatty liver”)
    Often asymptomatic or mild RUQ discomfort, fatigue, weight loss
    2-Alcohol hepatitis
    hepatocyte swelling with necrosis and acute inflammation.
    3-Fibrosis- cirrhosis
  • features
    1-painful hepatomegaly and elevated liver enzymes (AST> ALT)
    2- jaundice
    3-Portal hypertension—splenomegaly, ascites
    4-Malnutrition and vitamin deficiencies (thiamine, Vitamin B12)
    b/c alcohol replaces normal diet
    5-Other symptoms: malaise, weight loss, fever, nausea, vomiting
190
Q

Non-Alcoholic Fatty Liver Disease (NAFLD)

A

1- Associated with obesity with insulin resistance, type 2 diabetes mellitus
* most common cause of incidental elevation of serum transaminases
2-Diagnosis of exclusion; ALT > AST

191
Q

Drug-induced Liver Damage

A

liver is the major drug metabolizing and detoxifying organ…so very
susceptible to injury
* Mechanisms
* Direct toxicity
* Hepatic conversion to an active toxin (metabolite)
* Drug or metabolite acts as a hapten that binds to a cellular protein,
making it immunogenic
* Drug reactions can be
* predictable (dose-dependent): Ex: acetaminophen- converted to toxic
metabolite
* idiosyncratic (unpredictable): immediate or delayed (weeks to months)

192
Q

Cirrhosis
etiology
clinical features
treatement
prognosis

A

1- Progressive, diffuse
fibrosis/scarring of the liver
2- Etiology:
* U.S.- HCV, alcoholic liver disease,
NASH
* Developing world: HBV, HCV
3- Clinical features
* The patient may be clinically “silent”
(no symptoms- “compensated”), only
elevated AST, ALT
* If symptomatic (“decompensated”)—
anorexia, weight loss, weakness,
debilitation and eventual signs of liver
failure and portal hypertension
*4-Treatment: none available except
liver transplantation
5-Prognosis
* Fibrosis is irreversible Many patients die from
Progressive liver failure
* Hepatocellular carcinoma (cancer)

193
Q

Potential complications of cirrhosis in the dental chair

A
  • Unpredictable drug metabolism (only occurs with severe disease)
  • Impaired hemostasis and bleeding (thrombocytopenia and low coagulation factors)
  • Increased risk of infection
    *If compensated- treat at ULSD watching for complications
194
Q

Chronic passive congestion

A

Pathogenesis - impeded
venous return from right
heart causes blood stasis in
liver
* Cause – most often COPD or
restrictive pulmonary
disease leading to R. heart
failure
* Gross pathology (nutmeg
liver)

195
Q

Cholelithiasis (Gallstones)
Most often represents __________in
the bile
risk factors ?

A

crystallized cholesterol
obesity
being a female
age

196
Q

t/f
Hepatocellular carcinoma most commonly metastasizes to the lung.

A

True

197
Q

Normal Skin- Epidermis layers

A
  • Stratum germinativum (basal layer) –
    single layer of dividing cells that give rise
    to all epithelial cells
  • Stratum spinosum (squamous layer) –
    layer of keratinocytes that mature and
    acquire keratin as they are pushed toward
    the surface
  • Stratum granulosum (granular layer) –
    thin layer that acquires large basophilic
    granules called keratohyalin
  • Stratum corneum – composed of
    orthokeratin (without nuclei)
  • Rete ridges – epithelial projections that
    anchor epithelium to underlying CT
198
Q

Normal Skin- Dermis layers

A
  • Basement membrane – reticulin fibers that act as
    a scaffold for epidermis
  • Papillary dermis – loose collagen and elastin
    directly below the rete ridges
  • Reticular dermis – dense structural collagen
199
Q

Adnexal Structures (next to/joined with) skin

A
  • Hair follicles – all locations except palms and soles
  • Sebaceous glands – oil glands accompanying each
    hair follicle and in other locations without hair
    (mucosa) – lubricates hair and antibacterial
  • Arrector pili muscles – smooth muscle that
    attaches to hair follicle
  • Eccrine sweat glands – all locations -
    thermoregulators
  • Apocrine sweat glands – under armsAr
200
Q

Normal Skin- Other Cells

A
  • Epidermal melanocytes – clear
    cells living in the basal layer
  • Dermal melanocytes – spindly
    cells living in papillary dermis
  • Langerhans cells – dendritic
    histiocytic antigen processing
    cells living in stratum
    spinosum
  • Merkel cells – receptors for
    light touch - live in the basal
    layer
201
Q

ID

A

flat lesion
macule: a flat, non-palpable change in shape or color that is ≤ 1.0 cm

202
Q

ID

A

flat lesion
Patch- a flat, non-palpable change in shape or color that is > 1.0 cm

203
Q

ID

A

raised lesion
Papule- solid, ≤ 0.5 cm

204
Q

ID

A

raised lesion
Nodule- solid, >0.5 cm (sessile vs. pedunculated)

205
Q

ID

A

raised lesion
Vesicle- fluid-filled elevation ≤ 0.5 cm

206
Q

ID

A

rasied lesion
Bulla- fluid-filled elevation > 0.5 cm

207
Q

Papillary – lesion composed of multiple fronds or projections (may be sessile or pedunculated)

A
208
Q

ID

A

Atrophy- thinning of the mucosa (red)
* Erosion- depressed lesion, incomplete loss of mucosa (red)
* Ulcer- complete loss of mucosa (dark yellowish)
* Scar- result of injury causing mucosal atrophy or hypertrophy

209
Q

Histologic Terms
1- Hyperparakeratosis
2- Hyperorthokeratosis
3- Hypergranulosis
4- Acanthosis
5-Acantholysis
6- Spongiosis
7- Papillomatosis
8- Dyskeratosis
9-Exocytosis

A
  • Hyperparakeratosis – thickened parakeratin
  • Hyperorthokeratosis – thickened orthokeratin
  • Hypergranulosis – thickened granular cell layer (accompanies
    hyperorthokeratosis, never parakeratosis)
  • Acanthosis – thickening or hyperplasia of stratum spinosum
  • Acantholysis – loss of intercellular bridges and cohesion of cells of stratum
    spinosum
  • Spongiosis – edema of stratum spinosum, widened intercellular bridges
  • Papillomatosis – hyperplasia of papillary dermis, resulting in multiple surface
    elevations
  • Dyskeratosis – abnormal formation of keratin below surface
  • Exocytosis – infiltration of epidermis by inflammatory cells
210
Q

Acute Inflammatory Dermatoses

A

1- days to weeks
2- inflammation and edema caused by mononuclear infiltrate instead of nutreophils
3- self limited or become chronic
4- Urticaria (Hives)
Eczema

211
Q

ID
erythematous, edematous, and pruritic
plaques are termed wheals.

A

Urticaria (Hives)

212
Q

Urticaria (Hives)

A

1- TYPE ONE HYPERSENSETIVITY REACTION
2- MAST CELLS DEGRANULATION
3- MAST CELLS CAUSE dermal microvascular
hyperpermeability
4- Localized or generalized, small, pruritic
papules to large erythematous plaques
5-usually develop and fade within hours,
but can persist for days to months
6- Tx: antihistamines, leukotriene
antagonists (block IgE) or steroids

213
Q

Group of conditions showing pruritic,
erythematous papules, and possible
vesicles which ooze and crust and later
coalesce into raised scaly plaques

A

ECZEMA

214
Q

ECZEMA

A

Etiology: allergen (delayed
hypersensitivity), defect in keratinocyte
barrier, drug hypersensitivity, UV light,
physical/chemical irritant
* Example: allergic contact dermatitis
(e.g. poison ivy)
* Environmental agent that reacts with self-
proteins creating neoantigens that
sensitizes T cells.
* On re-exposure, memory CD4+ T cells are
activated and release cytokines that
recruit inflammatory cells and cause
epidermal damage

215
Q

IS Psoriasis ACTUE OR CHRONIC SKIN LESION ?

A

CHRONIC

216
Q

well-demarcated, pink to salmon–colored
plaque covered by loosely adherent silver-
white scale

A

PSORIASIS

217
Q

PSORIASIS

A

VERY COMMON IN THE US
Increased risk for heart attack and stroke
and affects 10% of arthritis pts
IMMUNE MEDIATED , T CELL
TNF
skin of the elbows, knees, scalp etc. (oral
lesions extremely rare)
psoriatic arthritis is a severe complication
of this disease.
TREATMENT: TNF ANTAGONIST
Diagnosis
* Auspitz sign – pinpoint bleeding upon scratching scale
off lesions
* Koebnerization – creation of lesions by scratching

218
Q

Infectious Dermatoses

A

Fungal: superficial dermatophyes
Bacterial: impetigo

219
Q

DEFINE THE FOLLOWING
Tinea capitis:
Tinea barbae
Tinea corporis
Tinea pedi

A

Tinea capitis – head; causes
focal alopecia
* Tinea barbae – beard area of
men
* Tinea corporis – body; caused
by heat and humidity and
exposure to animals
* Ringworm
* Tinea pedis – athlete’s foot
fungus with superimposed
bacterial infection

220
Q

a yeast that infects
intertriginous zones

A

Candida
local causes- intertriginous zones
(areas on skin that stay moist)
* Systemic causes
* Steroids
* Antibiotics
* Diabetes
* Immunosuppression
* HIV
* Chemotherapy/radiation

221
Q

Range from fragile vesicles to flaccid bullae that
rupture and leave an amber to “honey-colored” crust

A

Impetigo

222
Q

Impetigo

A

Superficial skin infection of face or extremities with Streptococcus pyogenes and/or Staphylococcus aureus, entering broken skin
* Common in children, crowded living conditions, poor hygiene, hot/humid climates
May resemble exfoliative cheilitis, recurrent herpes simplex or mimic child abuse
* Treatment
* For isolated lesions- topical mupirocin.
* Bullous or more extensive lesions- 1-week course of a systemic oral antibiotic that is effective against both S. pyogenes and penicillin-resistant S. aureus. * cephalexin, dicloxacillin, Augmentin
* for PCN allergic (clindamycin)

223
Q

Acquired hyperpigmented, hyperkeratotic, velvety skin: axilla,
groin, and back of neck

A

Acanthosis Nigricans (AN)
Types:
* Malignant AN- associated with internal GI malignancy
* Benign AN
* Associated with endocrinopathies (i.e. diabetes, Addison’s DX, hypothyroidism, acromegaly) or syndromes
* Drug ingestion (oral contraceptives or steroids) tissues show insulin resistance
* Oral lesions
* finely papillary lesions (not brown) of lips and tongue
* Often associated with internal malignancy

224
Q

Slow growing, fluctuant/rubbery nodule of the
face or neck often derived from hair follicles
* May have a yellowish to white or normal skin
appearance
* Tx: surgical excision. Good prognosis

A

Epidermoid Cyst

225
Q

“stuck on”, “dirty candle wax”,
“dried mud on brick wall”
appearance
Composed of basal cells that
produce keratin inclusions

A

BENIGN
Seborrheic Keratosis
Very common, skin of face and
trunk, >40yrs
if hundreds appear suddenly (sign
of Leser-Trelat)= paraneoplastic
syndrome- may have internal
malignancy (e.g. GI carcinoma) IMAGE ON LOWER RIGHT

226
Q

Scaly plaque with sandpaper
texture

A

Actinic Keratosis (AK)
*Common on facial skin and
vermilion zone (actinic
cheilosis/cheilitis) of the lips in
fair-skinned persons over 40
years of age
* Hyperkeratosis
* dysplasia
*Solar Elastosis

227
Q

Actinic Keratosis TREATMENT AND Prognosis

A

Treatment
* cryotherapy, surgical excision, laser ablation,
photodynamic therapy
* 5-fluorouracil (Effudex), imiquimod 5%
cream, diclofenac 3% gel

Prognosis
* ~1/4 may regress with reduced sun exposure
* ~8% risk of malignant progression with ~1%
over 2 yrs
* Average time to progression is about 2 yrs
* Monitor patients for progression and new
lesions
Treatment: 5-fluorouracil

228
Q

Clinical: fleshy, firm nodule with a
keratinized, crusty or ulcerated
surface

A

Squamous Cell Carcinoma
Sun-induced cancer usually in
existing actinic keratosis (field
effect- large exposed area causes
transformation of multiple cells
over time
* CURABLE IF NOT IN A LATE STAGE

229
Q

noduloulcerative (most common):
umbilicated papule that may show central
ulceration/hemorrhage, rolled pearly white
border, lack of adnexal skin structures (hair);
May be referred to as a “rodent ulcer”
* sclerosing (morpheaform): mimics scar tissue

A

Basal Cell Carcinoma
Arises from the basal cells of the
epidermis or germ cells in hair follicles
* THE MOST COMON SKIN CANCER
Affected patients are typically over 40
years of age, have a fair complexion and a
history of chronic sun exposure
Most develop in the middle third of the
face
May show some similarity to
ameloblastoma

230
Q

Basal Cell Carcinoma TREATMENT AND PROGNOSIS

A

Treatment
* Excision, electrodessication, curettage; Mohs surgery for planes of fusion
(nasolabial fold, eye)
Prognosis
* Excellent, rare metastasis, >95% of patients cured after first treatment
* Larger, recurrent or tumors in embryonic planes of fusion are more
aggressive and require Mohs surgery
* F/up important: 44% chance of 2nd BCC and 6% chance of SCC w/in 3
yrs

231
Q

Benign Melanocytic Skin
Lesions

A

1- Ephelis/ephelides
2- Actinic Lentigo
3- Melanocytic Nevi

232
Q

Ephelis/ephelides

A

brown macule,
increased pigment with sun
exposure but normal
numbers of melanocytes

233
Q

Actinic Lentigo

A

brown
macule common on dorsal
hand and face- shows a
linear increase of
melanocytes in the basal
layer

234
Q

Melanocytic Nevi

A

Nevus= any congenital skin lesion;
Melanocytic nevus= any benign congenital
or acquired neoplasm of melanocytes
Acquired melanocytic nevi
* Benign neoplasms caused by mutation in
BRAF or RAS (oncogenes).
* Develop early in life (average Caucasian has
about 20); rare intraorally.
* Well defined, < 6mm in diameter.
* Progression: Begin as flat lesions with a
uniform color (dark brown or black) that
elevate and fade with aging.
* Treatment: None, unless in an area of
repeated trauma or a cosmetic concern.
* Prognosis: Excellent, malignant
transformation is extremely rare

235
Q

Dysplastic Nevi

A

Can be sporadic or familial (familial dysplastic
nevus syndrome- strong association with
melanoma)
* RAS or BRAF mutations are common
* Larger than acquired nevi (>5mm) and may
have hundreds
* Sun-exposed and not sun-exposed skin
* >10+ dysplastic nevi= increased risk for
melanoma (marker for melanoma risk)
* Macules or plaques with pebbly surface, often
variable pigmentation and irregular borders

236
Q

Most are cutaneous (>90%); third most
common skin cancer; dramatic increased
incidence in recent decades

A

Melanoma

237
Q

Non-UV melanomas have____ mutations

A

KIT

238
Q

UV-induced melanomas

A

UV light induces RAS/BRAF
mutaƟon→ →p16
inactivation (vertical
growth) →p53 mutaƟon
(metastasis

239
Q

SUN EXPOSURE MELANOMAS TYPES

A

1- Superficial Spreading
2-Lentigo maligna

240
Q

Superficial Spreading

A

Most common type
* BANS: Back, arms, neck, scalp
* months to few years radial phase (plaque)
before vertical phase (nodule forms)

241
Q

Lentigo maligna

A

Malar skin of elderly fair complexioned
people with chronic sun exposure
* Flat brown macule that slowly expands
radially over 10-15 years before entering
vertical growth stage

242
Q

Acral lentiginous

A

Unrelated to sun exposure; main type in
Blacks and Asians
* Very short radial growth phases (months)
before invading; poor prognosis
* Most mucosal melanomas are this type
(including oral)

243
Q

Nodular

A
  • elevated, fast-growing mass
  • Unrelated to sun exposure
  • No radial growth, starts as vertical growth
  • Worst prognosis
244
Q

Melanoma Clinical
Diagnosis

A
  • asymmetry
  • border irregularity
  • color variegation (multiple colors)
  • diameter greater than 6 mm (size of
    a pencil eraser)
  • evolving- lesions that have changed
    over time
245
Q

Prognosis OF MELANOMA

A

Breslow tumor thickness is the single most important prognostic
indicato

246
Q

WHAT ARE SOME OF THE systemic diseases with good to moderate quality evidence supporting the association with periodontal disease
?

A

1-Cardiovascular Disease
2-Diabetes Mellitus
3-Respiratory Disease: aspiration pneumonia, chronic obstructive pulmonary disease
4-Adverse Pregnancy Outcomes
5-Cerebrovascular Disease / Ischemic Stroke
6-Rheumatoid Arthritis
7-Chronic Kidney Disease
8- Cancer: esophageal, breast, lung, pancreatic, prostate,
colorectal, digestive tract, and head & neck cancers

247
Q

The pathologic mechanism for the association between systemic disease and periodontal disease fall into 3 major categories:

A

1-Bacteremia: Periodontal pathogens (bacteria) in deep periodontal pockets can easily penetrate through ulcerations of the inflamed epithelium, enter the bloodstream and can invade other tissues and organs causing damage by direct or indirect (inflammatory, Immunological) mechanisms.
2- Inflammation: Inflammatory mediators (biomarkers) originating in the periodontal microbiome enter the bloodstream and are deposited in tissues and organs causing damage by direct or indirect (inflammatory,
immunological) mechanisms.
3- Immune Response: Antibodies to periodontal pathogens and their toxins found in the periodontium can attack crossreactive antigens found in other tissues and organs.

248
Q

One of strongest bidirectional relationships between periodontal disease (PD) and systemic disease is seen with_______

A

cardiovascular disease (CVD

249
Q

PD (especially extensive and severe PD) is associated with an increased risk of: (CARDIOVASCULAR)

A

coronary atherosclerosis, coronary heart disease
(CHD) and fatal ischemic heart disease (IHD);
– carotid atherosclerosis and ischemic stroke.

250
Q

Chronic ischemic heart disease (IHD) is associated with ____________, leading to an
environment that favors ____________

A

reduced blood flow to the gums
periodontal pathogen proliferation and periodontal tissue destruction.

251
Q

Medications commonly used to treat CVD, such _______ are known to cause ________
which can complicate oral hygiene and exacerbate PD.

A

calcium channel blockers
gingival overgrowth

252
Q

normal hemostasis steps

A
  • Arteriolar vasoconstriction
  • Primary hemostasis (platelet plug)
  • Secondary hemostasis (deposition of fibrin)
  • Clot stabilization and resorption
253
Q

ARTERIOLAR VASOCONSTRICTION
(normal hemostasis first step)

A

*Occurs immediately after injury
* Mediated by endothelin

254
Q

PRIMARY HEMOSTASIS

A

*Formation of platelet plug
*Adhere to ECM through binding of
glycoprotein Ib (GpIb) to vWF , promote platelet adherence
*Activated platelets
* Change shape – increased surface area
* Release secretory granules
* Adenosine diphosphate (ADP)
* Thromboxane A2 (TXA2)
* Platelet recruitment and aggregation
* Activated platelets undergo aggregation

255
Q

SECONDARY HEMOSTASIS

A
  • Tissue factor exposed at site of injury
  • Membrane-bound procoagulant
    glycoprotein
  • Binds and activates factor VII
  • Thrombin generated
  • Cleaves fibrinogen to form fibrin
  • Fibrin meshwork forms
  • Activates more platelets
  • Consolidation of initial platelet plug
256
Q

CLOT STABILIZATION AND RESORPTION

A
  • Tissue plasminogen activator (t-PA)
  • Made by endothelial cells
    *Limits clotting at site of injury
257
Q

_________ are the regulators of hemostasis

A

Endothelial cells

258
Q

INTRINSIC PATHWAY

A
  • Initiated when blood contacts
    negatively charged surfaces
  • Exposed collagen from damaged
    blood vessels
  • Key factors
  • Factor XII
  • Factor XI
  • Factor IX
  • Factor VIII
  • More complex
259
Q

EXTRINSIC PATHWAY

A
  • Initiated by exposure of tissue factor (TF) during injury
  • Key factors
  • Tissue factor (TF)
  • Factor VII
  • More simple
260
Q

COMMON PATHWAY

A
  • Convergence of intrinsic and
    extrinsic pathways
  • Key players
  • Factor X
  • Prothrombin
  • Thrombin
  • Fibrinogen
  • Thrombin
261
Q

LABORATORY TESTING used for extrinsic pathway?

A

PT
INR

262
Q

LABORATORY TESTING used for intrinsic pathway?

A

PTT

263
Q

Periodontal Disease and Cardiovascular Disease can exacerbate each other through shared inflammatory pathways and microbial mechanisms, including:

A

– Systemic Inflammation and Immune Response
– Bacterial Dissemination (Translocation)
– Oxidative Stress
– Hyperlipidemia
– Potential Autoimmune Responses

264
Q

 Systemic Inflammation and Immune Response in pd and cvd disease

A

PD pathogens (e.g., Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Tannerella forsythia) release virulence
factors, including lipopolysaccharides (LPS), that leadto local and systemic inflammatory immune responses.
Pro-inflammatory macrophage/ monocyte-derived
cytokines (IL-1β, IL-6, IL-8, TNF-α) and inflammatory markers such as C-reactive protein (CRP) are elevated in patients with PD and are known to play a role in CVD progression by promoting endothelial cell dysfunction and
atherosclerosis: – Production of these cytokines and CRP exacerbate atheromatous plaque formation in coronary artery
walls, leading to an increased risk of CAD and IHD.
Studies have shown that reduced NO bioavailability
contributes to atherosclerosis and hypertension,
(which are established risk factors for CVD).

265
Q

 Bacterial Dissemination (Translocation):

A

Bacteremias containing PD pathogens (especially
Porphyromonas gingivalis & Tannerella forsythia) may embed within blood vessels and/or be deposited in atheromatous
plaques and:
– induce a pro-coagulant response (increasing the risk
for coronary artery thrombus formation), and/or
– invade, colonize and proliferate in coronary artery
endothelial cells and coronary artery smooth muscle
cells, and:
 exacerbate atheromatous plaque formation, and
 contribute to plaque instability and an increased risk
of CV events like acute MI and stroke.

266
Q

 Oxidative Stress*:

A
  • The immune response to PD pathogens generates
    reactive oxygen species (ROS), which:
    – contribute to tissue destruction in the periodontium;
    – can enter systemic circulation and cause oxidative
    damage in distant tissues, including the vasculature.
  • Similarly, oxidative stress in the CV system can
    exacerbate vascular inflammation and lead to endothelial
    dysfunction, contributing to the progression of CVD.
267
Q

Hyperlipidemia

A

PD can alter blood lipid profiles, with some evidence suggesting that it exacerbates hyperlipidemia and oxidative stress, both of which are known contributors to
CVD:
– LPS and other bacterial products from PD pathogens
can stimulate the liver to produce more lipids resulting
in elevated levels of cholesterol and triglycerides (that
are known contributors to atherosclerosis and CVD).

268
Q

 Potential Autoimmune Responses:

A

Some antibodies generated against PD pathogens can be immunologically cross-reactive with host tissues potentially leading to autoimmune reactions that target vascular tissues.
– This may further accelerate endothelial damage and
promote atherogenesis, complicating both oral and
cardiovascular health.

269
Q

Research suggests that treating PD can lead to a
reduction in systemic markers of inflammation, includingCRP, potentially reducing the risk of cardiovascular events (like acute MI).
t/f

A

True

270
Q

DISORDERS RELATED TO HEMOSTASIS

A

1- BLEEDING DISORDERS
a- Thrombocytopenia
* Immune thrombocytopenic purpura
(ITP)
b-Hemophilia A
c-Hemophilia B
d-Von Willebrand Disease
e-Vitamin K deficiency
2- THROMBOTIC DISORDERS
a- Thrombosis
b-Hypercoagulable state
c-Embolism

271
Q

THROMBOCYTOPENIA

A

Low platelet count
<150,000 platelets/μl
causes
* Decreased production
* Bone marrow dysfunction (aplastic
anemia, cancer)
* Drug-related (alcohol,
chemotherapeutic)
* HIV infection
* Increased destruction
* Autoimmune (immune
thrombocytopenic purpura)
* Nonimmunologic
* Other: hypersplenism, multiple
transfusions

272
Q

ID

A

IMMUNE THROMBOCYTOPENIC PURPURA

273
Q

IMMUNE THROMBOCYTOPENIC PURPURA
category
etiology
demographics
clinical presentation
diagnose
treatment

A

category: immune mediated
etiology : Antibodies against platelet membrane glycoproteins IIb/IIIa or Ib/IX complexes
clinical presentation: * Petechiae (small areas of bleeding under skin/mucosa)
* Easy bruising
* Epistaxis (nose bleed)
* Gingival bleeding
* Hemorrhage after minor trauma
demographics: more common in women
diagnose : Laboratory testing shows thrombocytopenia
treatment : * Immunosuppressive agents
* Splenectomy
* Spleen is the site of anti-platelet antibody
production

274
Q

ID

A

HEMOPHILIA A

275
Q

HEMOPHILIA A
category
etiology
demographics
clinical presentation
diagnose
treatment

A

category: developmental
etiology: * Deficiency of Factor VIII
* X-linked recessive disorde
demographics: more common in male
clinical presentation: * Easy bruising
* Massive hemorrhage after trauma
* Spontaneous bleeding into joints (hemarthrosis
diagnose: PTT
treatment : Factor VIII infusions

276
Q

ID

A

HEMOPHILIA B

277
Q

HEMOPHILIA B
category
etiology
demographics
clinical presentation
diagnose
treatment

A

category: developmental
etiolgy: * Deficiency of Factor IX
* X-linked recessive disorder
demographics: male
clinical presentation: Indistinguishable clinically from hemophilia A’
diagnose: PTT
treatment: Factor IX infusions

278
Q

VON WILLEBRAND DISEASE
category
etiology
demographics
clinical presentation
diagnose
treatment

A

category: developmental
etiolgy: * Autosomal dominant
* Deficiency or dysfunction of von Willebrand
factor (vWF)
demographics: Most common inherited bleeding disorder
clinical presentation: * Can be mild
* Mucosal bleeding
* Easy bruising
diagnose: PTT
treatment: * Desmopressin
* Increases vWF and factor VIII

279
Q

VITAMIN K DEFICIENCY
category
etiology
demographics
clinical presentation
diagnose
treatment

A

category: metabolic
etiolgoy: * Inadequate dietary intake
* Malabsorption
* Inhibition by certain medications (warfarin
demographics: * Newborns
* Long-term antibiotic use
* Malabsorption syndromes
clinical presentation: * Easy bruising
* Prolonged bleeding
* Hemorrhage in severe cases
diagnose: PT
treatment: * Vitamin K supplementation
* Fresh frozen plasma if necessary

280
Q

THROMBOSIS
category
etiology
demographics
clinical presentation
diagnose
treatment

A

category: injury
etiology: * Formation of a blood clot (thrombus) within a
vessel
* Endothelial injury
* Abnormal blood flow
* Hypercoagulability
demographics: More common with increasing age and immobility
clinical presentation: Depends on location of clot
diagnose: * Ultrasound
* CT scan
* Ventilation Perfusion (VQ) Scan
treatment:Anticoagulant

281
Q

HYPERCOAGULABLE STATE CLINICAL PRESENTATION

A

recurrent thrombosis

282
Q

EMBOLISM
category
etiology
demographics
clinical presentation
diagnose
treatment

A

category: injury
etiology:* Blood clot becomes dislodged
* Travels and obstructs vessel
* Can also occur with fat, air, and amniotic fluid
demographics: can occur to anyone
clinical presentation: * Pulmonary embolism: shortness of breath, chest pain,
cough
* Stroke: sudden weakness or numbness on one side,
difficulty speaking
DIAGNOSIS
* CT pulmonary angiography
* MRI or CT scan
* Echocardiography
TREATMENT
* Anticoagulation therapy
* Thrombolytic therapy
* Surgical intervention
36

283
Q

that DM increases the
risk and severity of various oral conditions including:

A

PD, caries, xerostomia, oral candidiasis, and
glossodynia / burning mouth syndrome.

284
Q

active
PD in patients with DM can lead to:

A

a significant increase in insulin resistance and
mean blood glucose levels, and
– contribute to worsening glycemic control that will exacerbate DM over time.

285
Q

Systemic Inflammation ( Periodontal Disease and Diabetes)

A
  • The inflammatory mediators originating from PD including
    CRP, cytokines (especially TNF-α and IL-6), and LPS
    from P. gingivalis can interact systemically with lipids, free
    fatty acids and advanced glycation end-products (AGES),
    all of which are play a role in the pathophysiology of DM.
  • This interaction induces or perpetuates activation of the
    intracellular inflammatory pathways (all of which are
    associated with insulin resistance).
  • The activation of these intracellular inflammatory pathways
    (in monocytes, macrophages, endothelial cells, adipocytes,
    hepatocytes and muscle cells) promotes and contributes to
    an increase in the overall insulin resistance, which may
    worsen glycemic control in patients with type 2 DM and PD.
286
Q

Benefits of controlling PD in patients with DM:

A

Multiple controlled clinical studies indicate that following
nonsurgical treatment of PD, patients with type 2 DM may
experience a significant reduction in HbA1c between 0.27%
to 0.48% within 3 to 6 months following treatment.
* For comparison, treatment of type 2 DM with metformin
results in a mean 1.0% reduction in HbA1c.

287
Q

Periodontal Disease and Aspiration Pneumonia

A

Dental plaque and oral biofilms can act as a reservoir for
pathogens such as Staph. aureus, Bacteroides, Prevotella
Fusobacterium, Peptostreptococcus, and can be an important risk factor for the initiation and progression of various respiratory infections.
 Bacteria from dental plaque and
oral biofilms may be aspirated
into the respiratory tract and
cause aspiration pneumonia.

288
Q

The stages oral biofilm
maturation are:

A
  1. Attachment
  2. Initial colonization
  3. Secondary colonization
  4. Maturation
289
Q

Periodontal Disease and COPD
:Possible Pathophysiologic Mechanisms

A

1- Systemic Inflammation
2-Bacterial Dissemination (Translocation)

290
Q

Periodontal Disease and COPD
 Systemic Inflammation:

A

The link between COPD and PD is largely attributed to
shared inflammatory mechanisms:
– Both conditions are associated with an increase in
systemic levels of pro-inflammatory cytokines
(especially TNF-α and IL-6), and CRP.
* Patients with PD have increased levels of these
cytokines in their gingival crevicular fluid (GCF), which
can spill over into the systemic circulation and contribute
to and exacerbate chronic inflammation associated with
COPD.

291
Q

Periodontal Disease and COPD
Bacterial Dissemination (Translocation):

A

– Inducing Airway Inflammation: The PD pathogens and
cytokines increase airway inflammation, leading to a worsening
of COPD symptoms.
– Reducing Immune Response in the Lungs: Chronic
inflammation from PD pathogens may weaken the lung’s
ability to clear other pathogens, increasing susceptibility to
respiratory infections.
– Contributing to Lung Remodeling: The ongoing inflammation
can contribute to undesirable structural changes in the lung
tissue, worsening airflow obstruction and progression of COPD.

292
Q

Treating PD in patients with COPD may reduce systemic
inflammation and improve respiratory outcomes:

A

– reduced exacerbation frequency and a slower lung
function decline rate, and
– lower hospitalization rates and reduced all-cause
mortality.

293
Q

Periodontal Disease and Adverse Pregnancy Outcomes

A

The occurrence of pregnancy gingivitis is extremely common,
occurring in 30 – 100% of all pregnant women. The condition is
characterized by gingival erythema, edema, hyperplasia, and
increased bleeding.
 Pregnancy involves immunologic adaptations to tolerate the fetus,
including a shift from a pro-inflammatory T-helper 1 (Th1) response
to a more anti-inflammatory T-helper 2 (Th2) response:
* While this immunologic shift is crucial for preventing fetal
rejection, it can compromise the host’s immune response to PD
pathogens, allowing PD to progress more aggressively in
pregnant women.

294
Q

correlated poor maternal
periodontal health with:

A

LBW
PTB

295
Q

Periodontal Disease and Adverse Pregnancy Outcomes
Systemic Inflammation:

A

PD pathogens release toxins
(including LPS) and stimulate a local immune inflammatory
response leading to the release of prostaglandins, proinflammatory cytokines (IL-1β, IL-6, TNF-a) and CRP that
can enter the bloodstream and reach the uterus and
placenta contributing to PTB:
* Increased levels of LPS are linked with pre-term labor
induction, and studies show that LPS from PD
pathogens can cross the placental barrier, leading to fetal
inflammation causing an increased risk of PTB.
* Women with PD tend to have higher systemic levels of
prostaglandins, CRP and cytokines associated with
labor and can increase the risk of PTB.

296
Q

Periodontal Disease and Adverse Pregnancy Outcomes
Oxidative stress

A

resulting from PD can impair placental
function, resulting in restricted nutrient and oxygen delivery
to the fetus, leading to LBW:
* Studies indicate that PD pathogens increase oxidative
stress markers which correlates with an elevated risk of
LBW.

297
Q

Periodontal Disease and Adverse Pregnancy Outcomes
Bacterial Dissemination (Translocation):

A

Bacteremias
containing PD pathogens (especially P. gingivalis and
Fusobacterium nucleatum) may seed and colonize
placental tissue and the uterus directly inducing an
inflammatory responses that may lead to pre-term labor
and PTB.

298
Q

ENDOTHELIAL CELLS FUNCTION

A
  • Maintain permeable barrier
  • Nutrients, electrolytes, and oxygen
    can pass
  • Balance coagulation and
    anticoagulation
  • Balance vasoconstriction and
    vasodilation
  • Regulate inflammation and
    immunity
  • Regulate cell growth
299
Q

ENDOTHELIAL DYSFUNCTION

A
  • Caused by high levels of
    activating stimuli for sustained
    periods
  • Impaired endothelium-
    dependent vasodilation
  • Hypercoagulable states
  • Increased free radical
  • Increased risk of:
  • Thrombosis
  • Atherosclerosis
  • Hypertension
  • Diabetes
300
Q

BLOOD PRESSURE REGULATION

A
301
Q

RENIN IS SECRETED IN RESPONSE TO WHAT?

A
  • Low blood pressure
  • Elevated circulating catecholamines
  • Low sodium levels in kidney
302
Q

HOW DOES Angiotensin II RAISES BP ?

A
  • Induces vascular smooth muscle
    contraction
  • Stimulates aldosterone secretion
  • Increases tubular sodium resorption
303
Q

Aldosterone MADE BY THE ADRENAL GLAND TO RAISE BLOOD PRESSURE BY DOING THE FOLLOWING:

A

Increases sodium resorption (and
water) in kidney
* Drives potassium excretion in urine

304
Q

HYPERTENSION
CATEGORY
ETIOLOGY
DEMOGRAPHICS
CLINICAL PRESENTATION
DIAGNOSE
TREATMENT

A

CATEGORY
* Injury
ETIOLOGY
* Primary/essential hypertension
* 90-95% of cases
* Reduced renal sodium excretion
* Increased vascular resistance
* Environmental factors (stress, obesity, smoking, physical
inactivity, high dietary sodium)
* Secondary hypertension
* Primary renal disease
* Renal artery narrowing
* Adrenal disorders
DEMOGRAPHICS
* Over 25% of the population
CLINICAL PRESENTATION
* Often asymptomatic
HYPERTENSION
| 16
DIAGNOSIS
* Normal: <120/80 mm Hg
* Elevated: 120-129/<80 mm Hg
* Stage 1: 130-139/80-89 mm Hg
* Stage 2: ≥140/ ≥90 mm Hg
* Based on more than 2 readings on more than 2 occasions
TREATMENT
* Antihypertensive medication
* Weight loss
* Sodium restriction
* Increased physical activity
* Limited alcohol
* Dietary changes

305
Q

GUIDELINES FOR TREATING PATIENTS WITH HYPERTENSION , DENTAL SETTING

A
306
Q

CONSEQUENCES OF HYPERTENSION

A
  • Arteriosclerosis
  • Can lead to nephrosclerosis, an
    ischemic kidney disease
  • Accelerated atherosclerosis
  • Weakened vessel walls
  • Dissecting aneurysms
  • Cerebral hemorrhage
  • Left ventricular overload
  • Cardiac hypertrophy
  • Heart failure

gen path final (2 decks)

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