Nycc Pathophys Lab Final

Front 1

Neoplasia

Back 1

new growth
ie. tumor

Front 2

Benign neoplasm

Back 2

-do not invade, do not metastasize
- localized overgrowth of cells
-well differentiated
-look and act normal
-well circumscribed/encapsulated
-clear borders

Front 3

Malignant neoplasm

Back 3

-INVADE & METASTASIZE (or have potential for metastasis)
-no clear boundaries
-loss of at least some aspect of differentiations

Front 4

Well differentiated

Back 4

=normal/benign tissue

Front 5

Poorly differentiated

Back 5

=lack of resemblance to cell type of origin
=malignant

Front 6

Metastasis

Back 6

leaving tissue or origin and moving elsewhere in the body via: Hematogenous, Lymph, or Direct Seating

Front 7

Hematogenous Spread

Back 7

Metastasis via the blood

Front 8

Lymphatic Spread

Back 8

Metastasis via the lymph

Front 9

Direct Seating

Back 9

Metastasis via attaching directly onto another organ/tissue (nearby)

Front 10

Most common benign neoplasm of the breast

Back 10

Fibroadenoma

Front 11

Most common MALIGNANT neoplasm of breast

Back 11

Invasive ductal carcinoma (Scirrhous adenocarcinoma)

Front 12

What neoplastic cell(s) are involved in fibroadenoma?

Back 12

Stroma and Epithelium

Front 13

What is the neoplastic cell involved in invasive ductal carcinoma?

Back 13

TDLU
terminal ducts lubular unit

Front 14

Characteristics of fibroadenoma and invasive ductal carcinoma (compared to normal breast)

Back 14

highly pleomorphic
hyperchromatic
large compared to cytoplasm

Front 15

Invasion (Infiltration)

Back 15

Spread within the primary site/organ

Front 16

Carcinoma

Back 16

malignant growth of epithelial origin

Front 17

Pleomorphism

Back 17

vary large and bizarre cells= Tumor Giant Cells

Front 18

Hyperchromatism

Back 18

large dark staining nuclei

Front 19

Tumor Giant Cell

Back 19

Pleomorphic (large and bizarre shapes), may be multinucleated

Front 20

What condition commonly leads to hepatoma (carcinoma of the liver)?

Back 20

Cirrhosis

Front 21

carcinoma

Back 21

malignant- of epithelial origin

Front 22

hematuria

Back 22

blood in urine

Front 23

nephrectomy

Back 23

removal of a kidney

Front 24

What is the single most common presenting sign of renal cell carcinoma

Back 24

hematuria

Front 25

What is the most common lifestyle risk factor associated with Renal Cell Carcinoma

Back 25

Smoking (Tobacco Use)

Front 26

What is the most common sites of metastasis associated with Renal Cell Carcinoma

Back 26

Lung
Bone

Front 27

What are the recommendations (of the American Cancer Society) for mammography for women?

Back 27

Women over the age of 40; or if at high risk: 10 years prior to when relative was diagnosed.

Front 28

What is the purpose of a baseline mammogram?

Back 28

comparison

Front 29

What is a tumor Marker

Back 29

Substances that are produced by cancer or by other cells of the body in response to cancer or certain benign (noncancerous) conditions. Most tumor markers are made by normal cells as well as by cancer cells; however, they are produced at much higher levels in cancerous conditions.
Most are proteins

Front 30

2 Types of Tumor Markers

Back 30

1. Ectopic Proteins
2. Normal cell products synthesized in excess by tumor cells (i.e. PSA)

Front 31

What are the current American Cancer Society recommendations for PSA testing?

Back 31

50yo (if life expectence >10 years)

Front 32

#1 cause of death in the US

Back 32

Heart Disease

Front 33

Between 1991-2007 we have been more successful in treating which... Heart Disease or Cancer

Back 33

Heart Disease (even though both have been increasingly successful)

Front 34

#1 cause of cancer men?

Back 34

Prostate

Front 35

#1 cause of cancer women?

Back 35

Breast

Front 36

#1 cause of cancer deaths in the US?

Back 36

Lung (and Bronchus)

Front 37

Which cancer rate has declined the most in men? 1930-2007

Back 37

Stomach

Front 38

Which cancer rate has increased the most in females? 1930-2007

Back 38

Lung/Bronchus

Front 39

What ethnic group in the U.S. has the highest death rate due to cancer?

Back 39

African American (males and females)

Front 40

Adenoma

Back 40

benign neoplastic growth of glandular epithelium

Front 41

_______ tumors are more likely to take up radioactive iodine than ______ tumors

Back 41

Benign
Malignant

Front 42

Differentiation

Back 42

resemblence to the mature normal cell of the tissue of origin

Front 43

"-oma"

Back 43

implies benign growth

Front 44

"-carcinoma"

Back 44

implies malignant growth; of epithelial origin

Front 45

"-sarcoma"

Back 45

implies malignant growth of mesenchymal origin

Front 46

"adeno-"

Back 46

neoplastic growth of glandular epithelium
adenoma= benign
adenocarcinoma= malignant

Front 47

anaplasia

Back 47

cellular atypia; lack of differentiation (usually associated with metastasis or en route)

Front 48

Histologic evidence of malignant tumors (6)

Back 48

Invasion (most impt!!)
Anaplasia
Pleomorphism
Hyperchromatism
Loss of architecture
Increases mitotic activity

Front 49

Invasion

Back 49

spread within the primary site tissue/organ of origin

Front 50

How does hematogenous metastatic spread occur?

Back 50

malignant cells invade arteries/veins
(i.e. Thyroid)

Front 51

How does lymphatic metastatic spread occur?

Back 51

malignant cells invade nearby lymph vessels and into LNs where they proliferate
(i.e. aorta)

Front 52

How does direct seeding metastatic spread occur?

Back 52

(direct seeding=direct extension)
metastatic cells invade through Connective Tissues into adjacent organ/tissues OR 'float' through closed body cavities to organs/tissues within I.e. Ovarian cancer cells --> small bowel

Front 53

2 components of tumors

Back 53

1. parenchyma (proliferating cells)
2. stromal components (blood vessels and CT)-- angiogenesis

Front 54

What pattern of inflammation is illicited via malignancies?

Back 54

Chronic inflammation

Front 55

Which WBCs aid in tumor immunity?

Back 55

****CD8+ T-Cells (recognize TSAs)
Macrophages
B-lymphocytes
Natural Killer Cells

Front 56

Organ tropism

Back 56

homing of malignant cells to specific organs for no understandable reason
I.e. Renal/Prostate Cancers-->Bone
GI cancers --------------> Liver
Lung cancers ---------->Brain

Front 57

What is involved in the GRADING of cancer?

Back 57

Assessing the level of differentiation; to predict the clinical aggressiveness.
Can only be completed via biopsy and microscope

Front 58

What is involved in STAGING cancer?

Back 58

assessing the extent of spread of cancer; provides a Prognosis*
TMN scale

Front 59

Tumor Immunosurveillance

Back 59

recognizing and destroying of cancer cells by the immune system

Front 60

Desmoplasia

Back 60

formation of abundant dense CT stroma
(I.e. 'schirrous' carcinoma of the breast= hardened, desmoplastic response that makes breast feel hard and 'stony')

Front 61

MC primary bone tumor

Back 61

Osteosarcoma/Osteogenic Sarcoma

Front 62

Traits of Osteosarcoma (4)

Back 62

1. Bimodal age expression-- most common in adolescents (boys>girls), and elderly
2. Long bones of extremities; in the metaphysis
3. Mutations of Rb and p53 genes (Tumor supressor genes)
4. Mets to LUNG via hematogenous spread, other bones, pleura and heart

Front 63

Osteosarcoma most often metastasizes to the _________ via which type of spread??

Back 63

to the LUNG
via HEMATOGENOUS spread

Front 64

2nd MC Primary Bone Tumor

Back 64

Chondrosarcoma

Front 65

Characteristics of Chondrosarcoma (3)

Back 65

1. MC in 30-60yo
2. in flat bones (ribs, pelvis, scal, sternum)
3. Mets to LUNG (hematogenous)

Front 66

Marked dysplastic epithelial changes, still confined to the basement membrane (pre-invasive)

Back 66

Carcinoma in situ

Front 67

Why do we grade cancers?

Back 67

an attempt to predict the clinical behavior of a malignancy and to establish criteria for therapy/treatment

Front 68

Explain the: Gleason Grading System

Back 68

based on 5 histologic patterns of tumor formation and infiltration. 2 scores given based on 2 biopsies. Each graded 1-5 and then added together. Lower scores=well-differentiated and High scores=poor differentiation

Front 69

MC grading system

Back 69

PAP Smears
-screen for cervical dysplasia/cancer
-uses 3 grades

Front 70

CIN grading system

Back 70

CIN=Cervical intraepithelial neoplasia
-based on increased nucleus:cytoplasm ratio
CIN I: mild dysplasia
CIN II: moderate
CIN III: severe dysplasia/carcinoma in situ

Front 71

Staging assesses for...

Back 71

cancer spread

Front 72

We stage cancers to...

Back 72

aid in prognosis, treatment/therapy options

Front 73

TMN system

Back 73

T: Size of primary tumor (T1-T4)
N: Regional LN spread (N0-N3)
M: presence of metastasis (M0-M1)

Front 74

T0N0M0

Back 74

Carcinoma in situ

Front 75

chondrosarcoma

Back 75

malignant bone cancer

Front 76

Chondrosarcoma preferentially metastasizes to...

Back 76

LUNGS
(bone --> lungs)

Front 77

Who is most prone to chondrosarcoma?

Back 77

MC in 30-60yo
(seen in flat bones)

Front 78

Key risk factor associated with Squamous Cell Carcinoma of the Larynx

Back 78

Smoking
(and male)

Front 79

Most common presenting symptom with squamous cell carcinoma of the larynx

Back 79

Hoarseness

Front 80

What may present clinically in a patient that suffers from Pancreatic Cancer involving the head of the pancreas?

Back 80

Jaundice
-present in ~50% of these cases
(otherwise an asymptomatic cancer so this is very important!)

Front 81

Pancreatic cancer preferentially metastasizes to the??

Back 81

Liver, Lungs, +/- periosteum

(bc it is in the periosteum, sits on the liver, goes to the lungs)

Front 82

2 Staging systems used in Osteosarcoma

Back 82

1. Surgical Staging
2. AJCC (we use)

Front 83

What portion of osteosarcomas are diagnosed when localized?

Back 83

4/5
(1/5 are diagnosed when it has already become metastatic)

Front 84

What route of metastasis does osteosarcoma typical spread by?

Back 84

Hematogenous Metastatic Spread (to the Lungs!)

Front 85

What specific areas of bone are typically involved in the metastatic spread of prostate cancer?

Back 85

Vertebral column
Ribs
Pancreas

Front 86

Vaccine for Prostate Cancer

Back 86

sipuleucel-T

Front 87

sipuleucel-T targets what type of cells?

Back 87

Dendritic Cells (it acts as an antigen-presenting cell; helps to strengthen the immune system)

Front 88

What specific lymphocyte can recognize TSAs and destroy/lyse antigen producing cancer cells?

Back 88

CD8+ T Lymphocytes

Front 89

3 factors considered in STAGING

Back 89

1. Tumor size
2. Presence of LN mets
3. Presence of distant mets

Front 90

Paraneoplastic conditions

Back 90

Remote effects (produced by cancer) that are not attributable to tumor invasion or to metastasis. Rarely lethal but dominate the clinical course and therefore important to recognize to treat early!

Front 91

PBH

Back 91

Benign Prostatic Hyperplasia

Front 92

Most prevalent cancer in US men

Back 92

Adenocarcinoma of the Prostate

Front 93

Characteristics of adenocarcinoma of the prostate

Back 93

Small malignant glands iwth enlarged nuclei
Prominent nuclei
Dark cytoplasm

Front 94

Prostate cancer preferentially metastasizes to the seminal vesicles via....

Back 94

Direct Seeding/Extension

Front 95

MC benign neoplasm of the breast

Back 95

Fibroadenoma

Front 96

MC histological type of breast cancer

Back 96

Invasive Ductal Carcinoma
-irregular white, firm mass surrounded by fatty tissue
-invasive ductal carcinoma cells invading stroma

Front 97

Type of staining that can show evidence of HER2 in breast cancer cells

Back 97

Cytochemical Staining

Front 98

HER2

Back 98

-Human epidermal growth factor receptor
-signals cell growth in response to estrogen
-oncogene (also ERB2)
-marker for Breast Cancer

Front 99

Protooncogenes

Back 99

normal genes which promote normal cell growth

Front 100

Oncogenes

Back 100

altered versions of normal protooncogenes which promote autonomous growth in cancer cells; promote cell growth in the absence of normal mitogenic signals (I.e erb, ret,myc, ras, sis)

Front 101

Tumor Suppressor Genes

Back 101

aka Anti-oncogenes
-produce proteins which apply breaks to cellular proliferation
-mutations of these genes allow for excessive cellular proliferation
-p53, Rb, BRCA1/2, APC)

Front 102

Apoptotic Genes

Back 102

genes that regulate apoptosis, normal apoptotic balance is achieved by balance of anti-apoptotic and pro-apoptotis genes

Front 103

Some malignancies express overexpression of _________Bcl-2 or deletions of ____________bax

Back 103

Anti-apoptotic Bcl-2
Pro-apoptotic bax

Front 104

how does a primary lung cancer present?

Back 104

One large main tumor invades the parenchyma

Front 105

4 Histological Subtypes of Lung Carcinomas

Back 105

1. Well-differentiated squamous cell carcinoma
2. Gland-forming adenocarcinoma
3. Small cell carcinoma
4. Large cell carcinoma

Front 106

Which types of lung cancers are associated with cigarette smoking?

Back 106

Squamous Cell and Small Cell Carcinomas

Front 107

MC lung cancer among women and non-smokers

Back 107

Adenocarcinoma

Front 108

Metastatic lung cancer is ____ prevalent than primary lung cancer

Back 108

MORE- because many cancers metastasize to the lungs.
~1/3 of all cancer deaths show metastasis to the lungs

Front 109

Most prevalent skin cancer

Back 109

Basal Cell Carcinoma
(particularly in fair-skinned people)
-not highly metastatic

Front 110

2nd most prevalent skin cancer

Back 110

Squamous Cell Carcinoma
-not very metastatic

Front 111

3rd most prevalent skin cancer

Back 111

Malignant melanoma
-increasing in incidence at the fastest rate of the skin cancers therefore high metastatic potential

Front 112

what skin cancer has the higheset metastatic potential?

Back 112

Malignant Melanoma

Front 113

What is the growth pattern of Malignant Melanoma?

Back 113

1. Inital Radial Growth (good prognosis)
2. Vertical Growth phase- into dermis (poor prognosis)

Front 114

Leukemia

Back 114

Neoplastic disorders of uncontrolled proliferation of hematopoietic stem cells, originates in bone marrow, malignant cells spill into peripheral circulation.

Front 115

Leukemias are classified based on what 2 things?

Back 115

malignant cell maturity and cell type

Front 116

Describe Acute Leukemias?

Back 116

involve more blast, immature cells, more poorly differentiated

Front 117

Describe Chronic Leukemias?

Back 117

more mature cells involved, better differentiated

Front 118

Describe Lymphocytic Leukemias?

Back 118

from lymphocytic lines (T and B Lymphocytes)

Front 119

Describe Myelogenous Leukemias?

Back 119

from myeloid lines (granulocytes, monocytes)

Front 120

ALL

Back 120

Acute Lymphocytic Leukemia

Front 121

AML

Back 121

Acute Myelogenous Leukemia

Front 122

CLL

Back 122

Chronic Lymphocytic Leukemia

Front 123

CML

Back 123

Chronic Myelogenous Leukemia

Front 124

Lymphoma

Back 124

malignant neoplasms of cells native to lymphoid tissue, mostly LNs, most involve B Lymphocytes

Front 125

2 Classifications of Lymphoma

Back 125

1. Hodgkin's Lymphoma
2. Non-Hodgkin's Lymphoma

Front 126

What is the malignant cell in Hodgkin's Lymphoma?

Back 126

Reed-Sternberg (RS Cell)

Front 127

Non-Hodgkin's Lymphoma is characterized by which cells?

Back 127

any malignant lymphoid cell/s other than RS

Front 128

CLL
--describe

Back 128

*most common adulthood leukemia, ~55yo
*acquired disorder usually of B-cell lineage with proliferation of mature lymphocytes
*B lymphocytes cannot mature into plasma cells (immune dysregulation with ~1/2 developing hypogammaglobulinemai)
*presence of SMUDGE cells-malignant cells have fragile cell membranes and "smudge" during slide preparation

Front 129

What are the potential clinical consequences of all leukemias

Back 129

interference with all hematopoietic cell production (RBCs, WBCs, and platelets) in bone marrow ---> severe anemia, bleeding disorders, leukopenias

Front 130

Most common malignancy in young adults (MC 10-30yo)

Back 130

Hodgkin's Lymphoma

Front 131

Reed-Sternberg cell is characteristic of what

Back 131

Hodgkin's Lymphoma

Front 132

Characteristics of RS Cells

Back 132

Large, binucleate cell with prominent nucleoli
"Owl-eye" appearance
Origin is unknown
--Hodgkin's lymphoma presents in a single LN or chain of LNs

Front 133

What is a tell-tale sign under the microscope of lung tissue that a person is a smoker?

Back 133

Anthracotic pigment

Front 134

What histological subtype of lung cancer is the MC cause of paraneoplastic hypercalcemia?

Back 134

Small cell carcinoma

Front 135

What is a Pancoast tumor

Back 135

any lung tumor growing in the apex of the lung which may extend to involve the 8th cervical and 1st and 2nd thoracic nerves

Front 136

Pancoast tumors occur MC in which type of cabcer

Back 136

Squamous cell carcinoma of the lung

Front 137

A Pancoast tumor in a patient would present as.....

Back 137

shoulder pain that radiates down the arm with an ULNAR distribution

Front 138

Polyp

Back 138

neoplasm that arises from colonic epithelium; protrude up into the lumen

Front 139

Is FAP (Familial Adenomatous Polyposis) benign or malignant?

Back 139

Benign- glandular growth in the colorectal mucosa (does NOT extend below the mucosa)

Front 140

What is a Tumor Suppressor Gene?

Back 140

=Anti-oncogene
It stops growths/cellular proliferation. Mutations of TSGs allow for excessive cellular proliferation--> potential for malignancies

Front 141

At what age does the American Cancer Society recommend colonoscopy screening to begin for colorectal cancer?

Back 141

50yo

Front 142

3 most prevalent types of skin cancer (list in order of prevalence)

Back 142

1. Basal Cell Carcinoma
2. Squamous Cell Carcinoma
3. Malignant melanoma

Front 143

how does the drug ipilimumab work as a molecularly targeted drug in the treatment of malignant melanoma?

Back 143

specifically targets the protein molecules CTLA-4

Front 144

By which metastatic route does colon cancer usually spread to distant areas of the serosa and peritoneum?

Back 144

Direct seeding

Front 145

MC route of metastatic spread from the Colon to the Liver

Back 145

Hematogenous

Front 146

What immune cell has the greatest impact in defense against cancer by its ability to recognize TSAs on cancer cells and destroy them via cell lysis

Back 146

CD8+ cytotoxic T lymphocytes

Front 147

Congestion

Back 147

impaired exit of venous blood
=increased amnt of deoxygenated blood (congestive heart failure, passive congestion of liver)

Front 148

2 forms of congestion that we saw in lab

Back 148

1. Pulmonary Edema
2. Passive congestion of liver

Front 149

Pulmonary Edema

Back 149

venous congestion
commonly associated with LEFT sided heart failure
causes edema fluid(transudate) to accumulate in alveoli

Front 150

Also known as "Nutmeg Liver"

Back 150

Passive Congestion of the Liver

Front 151

Passive Congestion of the Liver
---characteristics

Back 151

venous congestion near central vein
Usually due to RIGHT sided heart failure
Pressure increases so liver sinusoids dilate=atrophy=sinusoids can rupture=hemorrhage

Front 152

Hyperemia

Back 152

increased blood flow (arterial) due to arterial dilation
due to increased function demand (exercise, inflammation)

Front 153

Hemorrhage

Back 153

discharge of blood out of the vascular compartment

Front 154

Petechiae

Back 154

small, pinpoint hemorrhages, typically due to thrombocytopenia, decreased coagulation proteins or increased intravascular pressure ==increased vascular fragility

Front 155

Purpura

Back 155

superficial hemorrhage in the skin, same causes as above for petechiae

Front 156

Ecchymosis

Back 156

larger superficial hemorrhage int he skin, "bruises", usually a result of trauma
Larger than 1cm

Front 157

The clinical significance of hemorrhage is dependent on what (3) factors?

Back 157

1. rate of blood loss
2. site/location
3. volume of blood loss

(i.e. the brain does NOT tolerate hemorrhage well, no room for expansion

Front 158

Thrombus

Back 158

an aggregation of platelets, fibrin, WBCs and RBCs due to an inappropriate activation of coagulation, which is adhered to the vascular endothelium

Front 159

4 main Constituents of a Thrombus

Back 159

1. Platelets
2. WBCs
3. RBCs
4. Fibrin

Front 160

Virchow's Triad

Back 160

the 3 main predisposing factors of THROMBUS formation
1. damage to endothelium (most impt!!)
2. alterations in blood flow: arterial system will have increased turbulence while the venous system is in stasis
3. Increases coagulability of the blood (increased pro or decreased anti-coagulant proteins

Front 161

3 main predisposing factors of thrombus formation

Back 161

Virchow's Triad
1. damage to endothelium (most impt!!)
2. alterations in blood flow: arterial system will have increased turbulence while the venous system is in stasis
3. Increases coagulability of the blood (increased pro or decreased anti-coagulant proteins

Front 162

Clinical consequence of Arterial Thrombosis

Back 162

blockage of oxygen, ischemia
=Thromboembolism
***accounts for the major cause of morbidity and mortaility in the US

Front 163

#1 cause of mortality in the US

Back 163

heart disease- heart attack- MI

Front 164

#3 cause of mortality in the US

Back 164

stroke (cerebral infarction)
#1 cause of morbidity

Front 165

Venous Thrombosis clinical consequence

Back 165

Congestion +/- Edema

Front 166

4 possible fates of Thrombosis

Back 166

1. lysis/dissolution
2. organization and recanalization
3. propagation
4. embolization (thrombus breaks free and moves freely)

Front 167

Embolism

Back 167

any detached intravascular mass, usually a piece of a thrombus= THROMBOEMBOLISM
(less common: fat/air/amniotic/cholesterol embolism

Front 168

Pulmonary Emboli

Back 168

90% originate from thrombosis in deep veins of the lower extremities at risk: surgical patients, prolonged bed rest, obestity

Front 169

Saddle Embolism

Back 169

a thromboembolism lodges at a bifurcation in the vasculature forming a saddle appearance

Front 170

Infarct

Back 170

an area of ischemic necrosis within a tissue or organ, usually caused by occlusion of arterial supply

Front 171

Cerebral Infarct=----------------

Back 171

Stroke

Front 172

2 types of Cerebral Infarcts

Back 172

1. Ischemic (~80%)
2. Hemorrhagic (~20%)

Front 173

Ischemic (Cerebral) Infarct

Back 173

usually due to local thrombosis (slow progression) or embolization
Anti-coagulation therapy may help in initial treatment

Front 174

Hemorrhagic (Cerebral) Infarct

Back 174

Involves rupture/leakage of blood vessel
Hypertension
May involve embolization

Front 175

Transudate edema occurs due to:

Back 175

osmotic or hydrostatic changes (non-inflammatory)

Front 176

Causes of Transudate Edema

Back 176

1. Heart failure (causes pitting)
2. Renal failure (fluid/electrolyte imbalances; often with diabetes)
3. Lymphatic blockage/obstruction

Front 177

Hemodynamic disorders

Back 177

affect vasculature and blood flow

Front 178

Hemorrhage

Back 178

discharge of blood out of the vascular compartment. Can cause:
Hematoma, Petechiae, Purpura, Ecchymosis

Front 179

Arteriosclerosis

Back 179

thickening and loss of elasticity of SMALL arteries/arterioles
(athero- is med/large arteries)

Front 180

Common underlying cause of arteriosclerosis?

Back 180

Chronic hypertension

Front 181

5 habits that will help prevent ISCHEMIC stroke
(also prevent HBP and diabetes)

Back 181

1. walk everyday
2. maintain a healthy weight
3. avoid cigarette smoke
4. enjoy alcohol in moderation
5. eat as nutritiously as possible

Front 182

Which sex has higher prevalence of stroke?

Back 182

Females

Front 183

Atherosclerosis

Back 183

endothelial damage makes vessel wall more permeable to lipids--> chronic inflammation (narrows vessels)
Occurs in med/large arteries
Smooth m. proliferation into T. Intina
Intimal thickening, extends into luman
Presence of "foam" cells
Over time dystrophic calcification occurs

Front 184

Foam Cells

Back 184

macrophages and smooth muscle cells which ingest lipids ("foarmy", cytoplasmic appearance)

Front 185

2 components of Atherosclerotic Plaque

Back 185

1. Superficial fibrous cap (contacts lumen, fibrosis, chronic inflam. cells, foam cells)
2. Deeper necrotic core
cholesterol deposition (cholesterol clefts), necrotic cellular debris, chronic inflammatory cells, foam cells

Front 186

3 Complications of Atherosclerosis

Back 186

1. Stenosis (continued growth of plaque, or continued narrowing of lumen)
2. Thrombosis- occlusion (potential for embolization)
3. Aneurysm- weakening of the tunica media causing a dilation and thinning of the artery wall (could rupture)

Front 187

Progression of lesions of atherosclerosis (3)

Back 187

1. Fatty streak (5-10yo)
2. Atheromatous plaque (fibrofatty plaque, fully formed)
3. Complicated Atherosclerotic Lesion

Front 188

Aneurysm

Back 188

weakening of the T. Media
causes dilation and thinning of artery wall (potential for rupture)

Front 189

MC site of aneurysm formation

Back 189

Abdomina Aorta (AAA) near bifurcation of Iliac and Renal aa

Front 190

Aneurysms form due to...

Back 190

complications of atherosclerosis

Front 191

Dissecting aneurysm

Back 191

Blood enters vessel wall (hematoma), separates the layers of the wall as it dissects a path along the length of the blood vessel
Ie. Marfan's, hypertension, aging

Front 192

Cystic Medial Necrosis

Back 192

focal loss of elastic and muscle fiber is t. media lead to cystic pools of matrix collected between cells and tissues

Front 193

Varicose Veins

Back 193

abnormally dilated tortuous veins
produced by increased intraluminal pressure and loss of support

Front 194

Predisposing factors of Varicose Veins

Back 194

Familial tendency, long periods of standing, obesity, pregnancy, aging
Ie. Superficial leg vv, hemorrhoids, esophageal varices, varicocele (scrotum)

Front 195

Vasculitis

Back 195

inflammation/necrosis of the walls of blood vessels

Front 196

Etiology of Vasculitits

Back 196

Infectious agents, immune mechanisms, truama, radiation

Front 197

Temporal Arteritis is also known as

Back 197

= Giant Cell Arteritis
= Granulomatous Arteritis

Front 198

MC form of systemic vasculitis in adults

Back 198

Temporal Arteritis

Front 199

Characteristics of Temporal Arteritis

Back 199

-chronic granulomatous inflammation of intima and media
-most often affects the temporal arteries: headaches +/- visual symptoms

Front 200

Predisposing factors of vericose veins

Back 200

Genetics
Standing for long periods of time