Midterm I Flashcards
(269 cards)
1
Q
In pathology, the origin of disease is specifically referred to as: (the “why”)
A
Etiology
2
Q
In pathology, the development of disease is specifically referred to as: (the “how”)
A
Pathogenesis
3
Q
T/F Clinical signs and symptoms usually occur fairly quickly after the origin of injury
A
False; they are several steps removed
4
Q
Please arrange the following terms in the general order of timing:
- cell response
- disease treatment
- cell injury
- etiologic agent
- disease state
A
Etiologic agent -> Cell injury -> Cell Response -> Disease State -> Disease Treatment
5
Q
What are commons categories of etiological agents/causes of cell injury?
A
Hypoxia, Infectious agents, Physical injury, Chemicals/drugs, Immune Response, Genetic abnormalities, and Nutritional Imbalance
6
Q
What type of necrosis do Aspirin burns (drug/chemical injury) cause?
A
Coagulative Necrosis
7
Q
Ischemia induces cell injury by reducing the amount of ATP production. Which of the following are NOT potential consequences of reduced ATP production?
- Influx of Ca, water, and NA that causes cell swelling
- Increased anaerobic glycolysis that increases acidity
- Increased protein synthesis from increased attachment of ribosomes
A
Increased protein synthesis from increased attachment of ribosomes
(it actually decreases because of detachment)
8
Q
The Fenton Reaction involves production of ROS using what divalent cation?
A
Iron/Fe++
9
Q
Disulfide linkage, Lipid per oxidation, and protein strand excisions disrupt cell membranes. What are the consequences of these dysfunctions?
A
Increased Permeability
Loss of proper Ca++ regulation
10
Q
ROS cause (SS or DS?) DNA breaks.
A
Single stranded
11
Q
What are 2 major sites (purines and pyrimidines) of ROS single strand DNA breaks?
A
thymidine and guanine
12
Q
Without intact cell membranes, Ca++ regulation is lost. Is there an increase or decrease in cytoplasmic Ca++? What happens in the cell after this change in concentration?
A
Increased cytoplasmic Ca++. The excess Ca++ helps activate intracellular enzymes that can decrease ATP, decrease phospholipid, cause protein disruption, and DNA damage
13
Q
Cell injury may cause ______, ______, or ______.
A
reversible injury, cell adaptation, or cell death
14
Q
Reversible cell injury is:
- acute or chronic
- short or long duration
- low or high intensity
- shrunken or swollen cell
A
acute, short duration, low intensity, and swollen cell
15
Q
T/F One mechanism is known for the conversion of reversible cell injury to change to irreversible.
A
False; no signature event
16
Q
When cells switch from reversible to irreversible injury, a sequential change in function and morphology occur. Please arrange the following:
- light microscopic changes
- ultrastructural changes
- gross morphological changes
- cell death
A
Cell death, ultrastructural changes, light microscopic changes, then final gross morphological changes
17
Q
What are the 4 types of necrosis? Which one is the most common?
A
coagulative (most common!), liquefactive, caseous, and enzymatic (fat)
18
Q
During coagulative necrosis, which of the following cell features retains its original histological appearance?
- Nucleus
- Cytoplasm
- Cell outline
A
Cell outline; cells become anucleated cells with pink (acidic) cytoplasm
19
Q
An abscess is an example of what type of necrosis?
A
liquefactive
20
Q
Tuberculosis causes what type of necrosis?
A
caseous
21
Q
What happens to fat cells during fat/enzymatic necrosis?
A
become anucleated saponification of fat cells
22
Q
T/F Apoptosis is a maintainer of homeostasis
A
True
23
Q
Which of the following are examples of excessive apoptosis? inhibition of apoptosis?
- AIDS
- Cancer
- Neurodegenerative disease
- Myelodysplasis
- Autoimmune disease
- Viral diseases
A
Excessive: AIDS, neurodegenerative disease, and myelopdysplasia (can’t form blood cells in marrow)
Inhibition: cancer, autoimmune disease, and viral diseases
24
Q
Which are associated with apoptosis?
- single cell or multiple cells
- cell shrinkage or cell swelling
- chromatin condensation or cell lysis
- inflammation or no inflammation
A
single cell
shrinkage
chromatin condensation
no inflammation
25
What receptor/ligand pair is responsible for the extrinsic pathway of apoptosis? Is this pathway specific or non-specific?
Fas and TNF receptor
| Specific
26
What cell injury is responsible for the intrinsic pathway of apoptosis? Is this pathway specific or non-specific?
GF withdrawal, DNA damage, or protein misfiling
| Non-specific
27
Is chronic cell injury typically higher or lower strength of insult?
Lower strength/intensity for longer time
28
Decrease in cell size and function is what cellular adaptation?
Atrophy
29
What are some causes of atrophy?
decreased workload (mm.), loss of IN, decreased blood supply (kidney), poor nutrition (wasting), decreased hormones (breast post menopause), and aging (brain)
30
Increase in cell size and function is what cellular adaptation?
Hypertrophy
31
What are some causes of hypertrophy?
Increased fxnal demand (heart), increased or imbalanced nutrition (big gut), increased hormonal stimulation (preg uterus)
32
Increase in cell number is what cellular adaptation?
Hyperplasia
33
Is hyperplasia typically irreversible?
No, take away stimulus and it goes away
34
Alteration in cell differentiation is what cellular adaptation?
Metaplasia
35
Squamous metaplasia of the bronchus is typically of what etiology? What are the consequences of the cellular change from columnar to squamous?
Smokers
| Tougher tissue but less efficient at removing debris
36
Intestinal metaplasia of esophagus is typically of what etiology? What are the consequences of the cellular change?
Chronic reflux disease
| Turns to mucous producing to protect tissues
37
What are the 4 mechanisms of intracellular accumulations?
Lack of enzyme, abnormal metabolism, defect in protein folding, ingestion of indigestible material (AKA carbon particles)
38
Cholesterol accumulations in vessels can lead to ______ or ______.
Atherosclerosis (narrowing arteries) or cholesterol thrombus
39
Alzheimer's disease and Mallory bodies are what type of cellular accumulation?
Protein
| Alzheimers is plaques in neurons while Mallory bodies is intermediate filaments in hepatocytes
40
Carbohydrates glycogen storage disease is most characterized by what activity?
DECREASE in glucose 6 phosphatase activity (usually fatal)
41
What is an example of an exogenous pigment accumulation that we may induce in dentistry?
Amalgam tattooing of soft tissue
42
What are the classic signs of inflammation?
Redness, swelling, heat, and pain
43
Pick the following characteristics that go with acute inflammation:
- vasoconstriction or vasodilation
- increased or decreased vascular permeability
vasodilation and increased vascular permeability
44
What cytokines mediate vasodilation?
NO, PGs, and Histamine
45
T/F During normal vascular flow, some fluid leaks out of vessels
True; the fluid leaks and is picked up by resident lymphatic cells
46
Which happens first during inflammation? vasodilation or arrival of neutrophils
Vasodilation
47
Which fluid accumulation in inflammation is characterized by:
- Low protein content, low specific gravity
- Non-inflammatory - intact endothelium
- Inflammatory - early endothelial contraction
Transudate
48
In order to allow fluid accumulation, what happens to the local hydrostatic pressure and colloid osmotic pressure?
Hydrostatic pressure INCREASES
| Colloid osmotic pressure DECREASES
49
Which fluid accumulation in inflammation is characterized by:
- High protein content, high specific gravity
- Inflammatory response
Exudate
50
Rank the order of types of exudate in order of increasing severity: purulent, sanguineous, and fibrinous
Fibrinous (high protein, few cells)
Purulent (high protein, many cells)
Sanguineous (high protein, blood, great deal of destruction)
51
Endothelial cell contraction is mediated by which cytokines?
PAF, histamine, bradykinin, leukotrienes
52
Endothelial cell retraction is mediated by which cytokines?
IL-1, TNF, IFN
53
After an injury, reversible endothelial contraction occurs first and lasts ____ hours, then endothelial retraction follows after _____ hours and can lasts up to ____ hours.
Contractions lasts 0-1 hours
| Retraction follows after 4-6 hours and can last 24+ hours
54
What cytokines, released during inflammation, cause pain?
PGE and Bradykinin
55
What cytokines, released during inflammation, cause fever?
IL-1, TNF, PGE
56
List the leukocyte order of events after endothelial cell activation during inflammation.
- Margination - physical slowing forces
- Rolling - leukocyte attracted to E- and P- selectin
- Adhesion - leukocyte attach to interns VCAM and ICAM
- Emigration or transmigration - leukocyte binds to PECAM and moves through endothelial cells
- Chemotaxis - act on microbes and produce chemotaxis cytokines to attract other leukocytes
57
T/F Neutrophils clean up areas of infection or necrosis
False, they lead to apoptosis that then gets cleaned up by macrophages
58
How quickly can monocytes reach sites of infection? How long do they live in tissues as macrophages?
emigrate within 48 hours
| Live up to MONTHS in tissues (only 1-2 days in circulation)
59
Besides neutrophils and monocytes (early responders), what other inflammatory cells can participate in response?
```
lymphocytes (immune functions - T and B cells)
eosinophils (allergic response & parasites)
mast cells (histamine/allergic reaction)
```
60
Define Cellulitis.
Diffuse tissue infiltration by PMNs with edema
61
Define Abscess.
Localized collection of PMNs or liquefactive necrosis
62
Define Ulcer.
Erosion of an epithelial surface exposing underlying connective tissue
63
Chronic or acute inflammation?
- Duration days-weeks
- Localized
- No immune response
- Often reversible
- Contains PMNs
Acute inflammation
64
Chronic or acute inflammation?
- Duration days-years
- Systemic
- Adaptive immune response
- Maybe reversible
- Contains macrophages and lymphocytes
Chronic inflammation
65
T/F Tissue destruction from chronic inflammation leading to fibrosis (scarring) is common
True (longer duration = more likely)
66
What are the 2 types of chronic inflammation and which one is more common?
Non-specific (most common)
| Granulomatous
67
There are many different degrees of capacity of proliferation during wound healing. Which is characteristic of continuously dividing cells that can be repaired easily? and what is a site where this occurs?
Labile capacity
| surface epithelium in mouth
68
There are many different degrees of capacity of proliferation during wound healing. Which is characteristic of some replicative activity that can produce scars if replaced? and what is a site where this occurs?
Stable capacity
| SM cells and fibroblasts
69
There are many different degrees of capacity of proliferation during wound healing. Which is characteristic of nonproliferative cells? and what is a site where this occurs?
Permanent capacity
| Neurons and cardiac m.
70
What factors affect wound healing? and which is the primary cause of delayed healing?
Infection (primary cause)
| Poor nutrition, steroid therapy, mechanical factor, and poor tissue perfusion
71
Healing by first intention (stitches) produces:
- very little scar or larger, less functional scar
- reduced or increased chance of infection
- heals quicker or slower
Very little scar
Reduced chance of infection
Heals quickly
72
What is edema?
Increases fluid within interstitial tissues
73
Edema is characterized by _______ hydrostatic pressure and _______ venous return.
Increased hydrostatic
| Decreased venous return
74
Which of the following does NOT describe an edema (increased fluid)?
- reduced plasma osmotic pressure
- lymphatic obstruction
- sodium and water loss
- inflammation
Sodium and water loss (both are actually retained)
75
What are two other terms for edema?
Anasarca and hydroplane
76
What is effusion?
Collection of fluid in body cavity or space
77
During hyperemia, tissue blood volume (increases or decreases) secondary to neurogenic mechanisms or inflammation.
Is this active or passive?
What color does it appear?
Increased tissue blood volume
Active
Red from increased RBC
78
During hyperemia, tissue blood volume (increases or decreases) secondary to impaired venous return.
Is this active or passive?
What color does it appear?
Increases
Passive
Blue because RBC slow down/build up
79
Hemorrhage is the loss of blood from injury or physical disruption.
Internally, it is defined by size. The largest mass of blood is called:
Hematoma
80
Hemorrhage is the loss of blood from injury or physical disruption.
Internally, it is defined by size. A bruise greater than 1 cm but not quite a hematoma is called:
Ecchymosis
81
Hemorrhage is the loss of blood from injury or physical disruption.
Internally, it is defined by size. When it falls between 0.3-0.9cm it is called:
Purpura
82
Hemorrhage is the loss of blood from injury or physical disruption.
Internally, it is defined by size. The smallest amount, 1-2mm in size is referred to as:
This can present in patients with what condition?
Petechia(e)
| Mononucleosis
83
What 3 major components help promote hemostasis after injury?
Endothelium, Platelets, and Coagulation Cascade
84
T/F Endothelium can be both procoagulant and anticoagulant
True
85
What promotes platelet adhesion to collagen?
von Willebrand factor
86
Which (Intrinsic or extrinsic?) system initiates coagulation cascade using what factor?
Extrinsic using tissue factor
87
Which (Intrinsic or extrinsic?) system finishes coagulation cascade using what factor?
Intrinsic using Factor XII (Hageman)
88
What is the end product of the coagulation cascade? What is the products function?
Thrombin cleaves fibrinogen to form fibrin (holds platelets together)
89
T/F Coagulation cascade can occur without the presence of platelets
False, platelets are necessary
| Enzyme activity occurs at surface phospholipid complex of platelets
90
Platelet adhesion, secretion, and aggregation are apart of (primary or secondary?) hemostasis.
Primary
91
What event is known as secondary hemostasis?
Coagulation cascade
92
PGI2 helps promote or slow hemostasis.
Slow, it is a counter regulator of hemostasis
93
All of the following are counter regulators of hemostasis EXCEPT:
- ADP
- Antithrombin III
- Protein S
- Protein C
- Thrombomodulin
ADP promotes hemostasis
| ADPase is a counter regulator
94
During hemostasis, thrombin cleaves fibrinogen to form fibrin. What 2 molecules are produces to participate in fibrinolysis to help trim/clip fibrin net?
tPA (tissue plasminogen activator) and plasmin
95
T/F Coagulation cascade repairs endothelium after injury
False, simply stops bleeding
96
T/F Thrombin's only role in body is to cleave fibrinogen during hemostasis.
False; thrombin also has many other functions including immune response
97
What are the 3 components of Virchow's Triad (3 things that can lead to thrombosis)?
Endothelial injury, alterations in blood flow, and hypercoagulability
98
T/F Endothelial injury will lead to increased prothrombotic activity
True
99
During normal blood flow, the flow is ____. (turbulent or laminar)
laminar
100
What 2 alterations in blood flow can happen to induce thrombosis?
Turbulence and stasis
101
What are 3 inherited conditions for hyper coagulability?
- Factor V Leiden (cannot cleave Va and continue prothrombotic activity)
- Prothrombin mutation (excess transcription)
- AT III deficiency
102
What are some acquired conditions for hyper coagulability?
- Prolonged bed rest
- Cancer
- Extensive tissue injury
- Pregnancy
103
What is the color appearance of arterial thrombosis? venous thrombosis?
Arterial - white
| Venous - red
104
Distinct lines of Zahn are characteristic of thrombosis in what types of vessels? Indistinct lines?
Distinct - Arterial
| Indistinct - Venous
105
What are the 4 common fates of thrombi?
- dissolution/resolution
- embolization
- propagation
- organization/recanalization
106
What is DIC?
- disseminated intravascular coagulation
| - widespread/systemic activation of the coagulation cascade and fibrinolytic systems
107
T/F DIC (disseminated intravascular coagulation) can produce both micro thrombi and hemorrhage
True; elevates coag cascade and fibrolytic
108
With acute DIC, what is most critical? With chronic DIC, what is most critical?
acute is hemorrhage - don't want to bleed too much
| chronic is thrombi - need to allow effective passage of blood
109
What are some causes of DIC?
infection (G- bacteria), obstetric complications (placental abruption or retained dead fetus), neoplasm, shock, and massive tissue injury
110
What is an embolus? What is the majority/most common?
- an intravascular solid, liquid, or gaseous mass carried by the blood to a site distant from its point of origin
- majority is dislodged thrombus, likely from deep vein
111
What is pulmonary thromboembolism?
Embolus (formed from a thrombus) that has been carried to lungs
112
What are the range of clinical consequence for a pulmonary thromboembolism?
No clinical manifestation, pulmonary hypertension, pulmonary hemorrhage, pulmonary infarction, up to sudden death (Saddle embolus) from blockage of major trunk to lungs
113
What are the places of origin for systemic embolism?
left atrium, left ventricle, atherosclerotic plaque
114
What is infarction? What are the 2 types of infarction?
Area of ischemic necrosis from blockage of blood supply
| Red (hemorrhagic) and white (pale)
115
The following are characteristic of what type of infarction (red or white)?:
- venous occlusion
- loose tissue
- dual blood supply
- previous congestion
Red
116
The following are characteristic of what type of infarction (red or white)?:
- arterial occlusion in solid organ
- NOT loose tissue
White
117
What is shock?
Systemic hypoperfusion (loss of blood flow)
118
What are the 5 pathophysiologic categories of shock?
```
Cardiogenic
Hypovolemix
Septic
Anaphylactic
Neurogenic
```
119
What is the #1 cause of death in ICUs? (200,000 annually)
Septic Shock
120
What causes septic shock? What molecule is associated with it?
gram-positive or gram-negative bacteria
| pathogen-associated molecular patterns (or PAMPs)
121
During nonprogressive shock, compensatory mechanisms (CAN or CANNOT) maintain perfusion
CAN
122
Which of the following does NOT happen progressive shock?
- maintained perfusion by compensatory mechanisms
- anaerobic metabolism from decreased O2 in tissues
- lactic acidosis from increased lactate
- DIC
Maintained perfusion by compensatory mechanisms does NOT happen, perfusion is inadequate
123
T/F Irreversible shock leads to multiple organ failure and death
True
124
What are some clinical manifestations of shock?
- tachycardia, tachypnea, hypetension, cool clammy skin (EXCEPT SEPTIC SHOCK)
- confusion, cyanosis, low urine output, acidosis, high lactic acid
125
What two components are necessary to develop a neoplasm?
Parenchyma (neoplastic cells) and stroma (supporting CT and BV)
126
What is a benign gland-forming epithelial tumor or tumor derived from glandular tissue?
Adenoma
127
What is a benign surface epithelial tumor characterized by numerous finger-like projections
Papilloma
128
What is the proliferation of tissue normally found at that site?
Hamartoma
129
What is the collection of tissue not normally found in that anatomic site?
Choristoma
130
What is a neoplasm derived from more than one germ layer?
Teratoma
131
Mesenchymal malignancies are called..?
Sarcoma
132
Epithelial malignancies are called..?
Carcinoma
133
Malignancy of lymphoid tissue?
Lymphoma
134
Malignancy of melanocytes?
Melanoma
135
Pleural malignancy?
Mesothelioma
136
Testicular malignancy?
Seminoma
137
Benign tumors are:
- small or large
- poorly or well demarcated
- slow or fast growing
- poorly or well differentiated
- locally invasive?
- typically metastasized?
```
Small
Well demarcated
Slow growing
Well differentiated
Not locally invasive
Not metastasized
```
138
Malignant tumors are:
- small or large
- poorly or well demarcated-slow or fast growing
- poorly or well differentiated
- locally invasive?
- typically metastasized?
```
Large
Poorly demarcated
Fast growing
Poorly differentiated
Locally invasive
Often metastasized
```
139
What differentiation is the most extreme disturbance in cell growth and differentiation?
Anaplasia
140
What are features of anaplasia?
Pleomorphism, nuclear hyperchromatism, variation in nuclear size and shape, numerous and atypical mitoses (the tripole mitosis)
141
What differentiation is disorderly, but non-neoplastic growth or proliferation? Also referred to as epithelial process of maturation?
Dysplasia
142
T/F Although dysplasia is non-neoplastic, it has the potential to become invasive carcinoma
True
143
Mild, moderate, and severe dysplasia are usually distinguished by..?
Extent of abnormal cells through the epithelial layer
Mild - basal only
Moderate - into parabasal (1/2 way though)
Severe - up to superficial cells
144
If tumors outgrow their blood supply, this results in ...
ischemic necrosis
145
What is the MOST RELIABLE feature to distinguish malignant from benign tumors?
local invasiveness
146
T/F Benign tumors are never fatal
False, although they do not typically invade, their location can make them extremely dangerous and lead to death
147
What type of tumors have a fibrous capsule?
Benign
148
What percent of newly diagnosed patients with solid tumors will already have obvious metastases? What percent have hidden metastases?
30% obvious
| 20% hidden
149
What is considered the hallmark of malignancy?
Metastasis
150
What are the 3 pathways for metastasis?
1. Seeding within body cavities
2. Lymphatic spread
3. Hematogenous spread
151
Which pathways (hematogenous and lymphatic) are associated with which types of malignancies (Carcinoma and sarcoma)?
hematogenous - sarcoma (liver and lungs)
| lymphatic - carcinoma (lymph nodes)
152
What proportion of cancer risk is attributable to environmental sources?
roughly 2/3 (65%)
153
T/F Stomach cancer in Japan is 7 times more frequent than in the US
True
| Breast and prostate 4-5X less common in Japan
154
What percentage of deaths in children <15 years of age is due to cancer?
10%
155
Cancer occurs in 1 of every _ people.
1 of 5
156
What are 3 categories of genetic predisposition to cancer?
1. Inherited cancer syndromes
2. Familial cancers
3. Defective DNA repair
157
Inherited cancer syndromes are usually (single or multiple) gene mutation and generally autosomal (recessive or dominant) transmission
Single gene mutation
| Autosomal Dominant
158
Retinoblastoma, adenomatous polyposis, and multiple endocrine neoplasia are examples of what category of genetic predisposition to cancer?
Inherited cancer syndromes (single gene and autosomal dominant)
159
Early age onset, tumors arising in 2 or more close relatives, and multiple or bilateral tumors are associated with what category of genetic predisposition to cancer?
familial cancers
160
Colon, breast, ovary, and brain malignancies have been reported to occur in ____ patterns
familial patterns
161
Defective DNA repair is usually autosomal (recessive or dominant) transmission
autosomal recessive
162
T/F Acquired Preneoplastic Disorders is a type of genetic predisposition to cancer
False, it develops over time and you are not born with it
163
Persistent regenerative cell replication, villous adenomas of the colon, and leukoplakia of oral or genital mucosa are examples of ...?
acquired preneoplastic disorders
164
```
White plaque on oral mucosa that:
-has sharp margin.borders
-is thin/exhibits fissures
-cannot be rubbed off or Id'ed as anything else
is referred to as:
```
leukoplakia
165
Nonlethal genetic damage that is central to all cancers is referred to as:
carcinogenesis
166
What 3 classes of normal regulatory genes are affected by carcinogens?
1. proto-oncogenes (growth promoting)
2. cancer suppresor genes (growth inhibiting)
3. apoptosis genes
167
T/F Carcinogenesis is a single step process at the genetic level
False it is multi step at both the phenotypic and genetic levels
168
Oncogenes encode proteins called _____ that lack normal controls and regulation
Oncoproteins
169
What 2 mechanisms turn proto-oncogenes into oncogenes?
1. Structural mutation of the gene, resulting in abnormal product
2. Altered regulation of gene expression, resulting in increased production of a normal growth-promoting protein
170
What gene is most commonly affected for transcription factors?
MYC
171
MYC gene dysregulation leads to activation of ____ causing cells to divide
Cyclin-dependent kinase (CDK)
172
What is Knudson's hypothesis regarding tumor suppressor genes?
```
Two mutations ("hits") in genome of cell required to induce retinoblastoma
Families who pass on one mutation in allele only have 1 allele to mutates to induce RB
```
173
What gene is the single most common target for genetic alteration in human tumors?
tp53
174
What is TP53's role in normal cell cycle? after mutation?
normal: inhibits cell cycle progression to allow time for DNA repair
mutation: doesn't stop cell cycle and therefore DNA cannot be repaired, eventually leads to uncontrolled cell division
175
What is Lo-Fraumeni syndrome?
inherited defect of one TP53 allele (means 25x increase risk for malignancy before 50)
176
What is the prototypic anti-apoptosis gene?
BCL2
177
Overexpressed BCL2 leads to :
A. Steady decrease in number of cells
B. Increased cell division
C. Cell protection for apoptosis
C. Cell protection for apoptosis
| often seen in "low-grade" lymphomas
178
Tumors cannot grow larger than _____ in diameter unless they are vascularized
1-2mm
179
What are the 2 major phases of metastasis?
Invasion of ECM and vascular dissemination with adhesion of tumor cells
180
Hereditary nonpolyposis colon cancer is a condition with unstable DNA. What defect is associated with this condition?
mismatch repair defect (MSI)
181
Xeroderma pigmentosum is a condition with unstable DNA. What defect is associated with this condition?
Inability to repair UV damage, leads to increased skin cancers
182
Bloom syndrom and familial breast cancer (BRCA1 and 2) are conditions with unstable DNA. What defect is associated with these conditions?
fragile DNA disease
183
What are types of karyotypic changes in tumors? (3 answers)
balanced translocations, deletions, and gene amplification
184
T/F Chemical carcinogens are only from naturally occurring chemicals
False, can also be synthetic
185
Chemical carcinogens can be both direct and indirect carcinogens. What is the difference between the two?
Direct requires no chemical transformation while indirect become active only after metabolic conversion
186
Chemical carcinogens are highly reactive ______ affecting DNA, RNA, and cell proteins
electrophils
187
Radiation carcinogens include UV, Xrays, gamma, and radionuclides and typically have a (short or long) latency for cancer
long
188
T/F Viral oncogenes are a type of carcinogen
True
189
What is an example of an RNA oncogenic virus?
Human T-Cell Leukemia Virus Type 1
190
What are some examples of DNA oncogenic viruses?
HPV- cervical cancer
EBV- Burkitt Lymphoma
HepB- hepatocellular carcinoma
HHV8- Kaposi sarcoma
191
What are the human body's tumor immunity cells?
tumor antigens, cytotoxic Tcells (CD8), NK cells, macrophages, and humoral factors
192
What are 3 types of biochemical assays to diagnose cancer?
prostate-specific antigen (PSA), carcinoembryonic antigen (CEA), and alpha-fetoprotein
193
What are 3 types of molecular diagnosis of cancer?
ISH, FISH, and PCR
194
T/F Medial calcific sclerosis (Monckesberg's) typically presents as hypertension in patients
False, it is usually clinically insignificant
195
What are the 2 types of arteriolosclerosis? Which is more common
Hyalin (more common) and hyperplastic
196
T/F Atherosclerosis typically affects artioles
False; affects larger arteries
197
Fatty streaks appear in most children and may or may not progress to ____
atheromas
198
Advanced plaque in artherosclerosis in the pre-clinical phase can lead to what 3 different things in the clinical phase?
- aneurysm and rupture
- occlusion by thrombosis
- stenosis
199
Vulnerable plaque has a (thin or think) fibrous cap between lipid core and endothelium
Thin - more vulnerability to exposure lipid core
200
What are 5 complications of atherosclerosis?
gangrene, MI, cerebral infarction (stroke), renal a. stenosis, and aortic aneurysm
201
Sever hypertension is defined by BP greater than
160/106mmHg
202
Hypertension affects approximately _% of the population
25%
203
T/F Most hypertensions have no symptoms
True, especially in low/moderate
204
Left ventricular concentric hypertrophy in order to provide normal cardiac output is referred to as
compensated
205
hypertrophy no longer adequate enough to provide normal cardiac output due to decrease myocardial contraction leads to _____ which results in left ventricle dilation and eventually leads to _____
decompensation
| CHF
206
Accelerated (Malignant) Hypertension is:
- rapid or slow onset
- rare or common
- independent or superimposed on previous hypertension
- high or low systolic and diastolic pressures
rapid onset
rare
superimposed on previous hypertension
high systolic and diastolic pressures
207
What disease is the failure to pump an adequate amount of blood to supply the metabolic requirement of the organs?
congestive heart failure
208
How many people in US are affected annually by CHF?
5 million
209
How many people die annually from CHF?
300,000
210
What are 3 compensatory mechanisms during heart disease?
Activation of neurohumoral system
Frank-Starling mechanisms
Myocardial hypertrophy
211
Which compensatory mechanism is associated with the release of norepinephrine with increased heart rate and contractility as well as the activation of renin-angiotension sys with water/salt retention?
Activation of neurohumoral system
212
Which compensatory mechanism is associated with the increased end-diastolic filling volume stretching cardiac muscle fibers?
Frank-Starling mechanisms
213
Which compensatory mechanism is associated with the increase in muscle fiber size, resulting in increased thickness of ventricular wall but without increase in size of lumen?
myocardial hypertrophy
214
Which sided heart failure usually precedes the other?
left side usually comes first and leads to right side
215
Which sided heart failure is caused by pulmonary hypertension?
right-sided heart failure
216
Which side ventricular failure manifests clinically as pulmonary edema, chronic cough, and orthopnea?
left ventricular failure
217
Which side ventricular failure manifests clinically as congestion of liver (nutmeg liver) and edema of subcutaneous tissues, especially lower extremities?
Right ventricular failure
218
Congenital heart disease occurs in __ out of every 1,000 live births
6-8
219
There are both cyanotic and noncyanotic forms of congenital heart disease. What are the 3 forms of noncyanotic? Which is most common
VSD (ventricular septal defect) is most common 4/1,000
ASD (atrial septal defect) is 2nd most common 1/1,000
PDA (patent ductus arteriosus)
220
There are both cyanotic and noncyanotic forms of congenital heart disease. What are the 2 forms of cyanotic?
Tetrology of Fallot
| Transposition of great arteries
221
What are the 4 anomalies in tetrology of fallot?
VSD, Narrowed RV outflow, Override VSD by aorta, RV hypertrophy
222
What refers to a group of related disorders that are all characterized by imbalances between myocardial blood supply and myocardial oxygen demand?
ischemic heart disease (IHD)
223
What is the leading cause of death in the US (at 500,000 annually)
IHD
224
What are the 4 clinical types of IHD?
angina pectoris
MI
Chronic IHD with CHF
Sudden cardiac death
225
What is referred to as intermittent chest pain caused by transient, reversible, myocardial ischemia?
angina pectoris
226
Stable angina may present as referred pain along ______. It is relieved by rest or _______.
left arm or jaw (why it's relevant to us)
| relieved by sublingual nitroglycerin
227
Unstable angina is increasing frequency of chest pain without exertion. Typically lasts _____ than stable angina. Often precedes more serious ____.
longer than stable angina
| precedes more serious ischemia
228
What is necrosis of cardiac muscle caused by ischemia?
acute myocardial infarction (MI) or heart attack
229
How many MI's annually in US? What proportion are fatal?
1.5 million
| 1/3 fatal
230
Sever ischemia lasting longer than ______ will cause irreversible myocyte injury and cell death
20-40 minutes
231
Myocardial ischemia also contributes to ____ probably because ischemic region cause electrical instability
arrhythmias
232
What are clinical manifestations of MI?
chest pain, shortness of breath, nausea/vomiting, diaphoresis/sweating, low grade fever
233
What protein is a good indicator of MI and should show up in blood within 5 hours of chest pain
isoform of creatine kinase (CK-MB)
234
During autopsy, MIs less than ____ old are not apparent but begin to turn reddish-blue after ______
12 hours
| 12-24 hours
235
What is the most common cause of sudden heart disease? (80-90%)
IHD
236
Primary cardiomyopathy (disease of heart mm.) is defined by:
is it solely confined to heart muscle
237
Secondary cardiomyopathy is defined by:
involved disease of heart m. as a part of systemic disorder
238
What are the 3 functional patterns of cardiomyopathy?
dilated (most common)
hypertrophic
restrictive
239
Dilated cardiomyopathy shows dilation of _____ and therefore issues with (systolic or diastolic)
all 4 heart chambers
| systolic (ejecting blood from heart)
240
Hypertrophic cardiomyopathy is a (primary or secondary) and (genetic or acquired) cardiomyopathy
primary
| genetic
241
Hypertrophic cardiomyopathy is autosomal ____ and has issues with (systolic or diastolic)
```
dominant
diastolic (problems filling bc stiff ventricles)
```
242
Required cardiomyopathy is a (primary or secondary) cardiomyopathy and has issues with (systolic or diastolic)
secondary
| diastolic
243
Myocarditis is most commonly caused by what pathogen?
viruses (coxsackie A and B)
244
Mitral valve stenosis is a result of ______ and typically affects (children or adults)
The bacteria is typically tested for during what common illness?
acute rheumatic fever (ARF)
children and only 20% of adults
Strep testing because Streptococcal pharyngitis
245
What are the 3 forms of rheumatic carditis?
pericarditis
endocarditis
myocarditis
246
__carditis is characterized microscopically by ______ which are collections of mononuclear inflammatory cells and fibroblasts (granulomatous inflammation)
Myocarditis
| Aschoff bodies
247
What refers to a valve that fails to close completely, allowing backflow of blood.
Mitral valve regurgitation
248
What valve condition is caused by fibrosis and calcification reducing valve cusp mobility? This can be due to what valve disease?
Aortic valve stenosis
| chronic rheumatic valve disease
249
What type of aortic valve stenosis usually occurs with advanced age in 70s or 80s? What type has a much younger initial onset?
advanced age - degenerative (senile)
| much younger - congenital bicuspid
250
What valve disease includes valve cusp destruction (endocarditis), myxomatous degeneration, and dilation of the aortic root?
Aortic valve regurgitation
251
What is usually caused by a bacterial infection in a heart valve although it may be caused by fungus or other infection?
infective endocarditis
252
What is one easily visible clinical sign of infective endocarditis?
splinter hemorrhages in nail bed
253
```
What type of endocarditis is this?
-short duration
-virulent organism
(Staphylococcus aureus)
-large friable vegetations
-previously normal valve
-prominent tissue destruction
```
acute endocarditis
254
```
What type of endocarditis is this?
-longer duration
-low virulent organism
(Streptococcus viridans)
-small vegetations
-previously abnormal valve
-less tissue destruction
```
subacute endocarditis
255
What valve disease may be caused by infection (usually due to direct spread of an adjacent infection)?
Vasculitis
256
What are the 3 classification of vasculitis?
Large vessels
Medium vessels
Small vessels
257
Giant cell (temporal) arteritis and takayasu arteritis are examples of:
Large vessel vasculitis
258
Polyarteritis nodosa (classic) and Kawasaki syndrome are examples of:
Medium vessel vasculitis
259
Microscopic polyarteritis and Wegener’s granulomatosis are examples of:
Small vessel vasculitis
260
What are the 4 pathogeneses of immune-mediated vasculitis?
1. immune complex formation
2. ANCA (antineutrophilic cytoplasmic antibodies)
3. Anti-endothelial cell antibodies (AECA)
4. Cell mediated
261
ANCA is most commonly associated with what size vessel vasculitis?
Small vessel vasculitis
262
```
What is this:
Etiology: Unknown (?T-cell mediated)
Clinical: Rare before 50, Fever, weight loss, headache, visual problems, pain and tenderness over temporal artery, polymyalgia rheumatica.
Pathology: Granulomatous inflammation
intimal proliferation/fibrosis
```
Giant Cell (Temporal) Arteritis (large vessel)
263
What is this:
Etiology: unknown; similar to temporal arteritis, just in a younger person
Clinical: F >> M, age < 40 years, weak arm pulses (“pulseless disease”), visual disturbances, neurologic manifestations
Pathology:
-Involves aortic arch and branches
-Intimal fibrosis
-Granulomatous inflammation with fibrosis
Takayasu Arteritis (large vessel)
264
```
What is this:
Etiology: unknown (at one time, 30% of patients positive for Hepatitis B, now < 8%)
Clinical: acute-relapsing-chronic, fever, weight loss, hematuria, renal failure, hypertension, abdominal pain, melena
Pathology:
Haphazard, segmental inflammation
Kidney > heart > liver > GI
Fibrinoid necrosis, PMNs
Thrombosis, aneurysms
Heal by fibrosis
```
Polyarteritis Nodosa (medium vessel)
265
What is this:
Etiology: anti-endothelial antibody (?) triggered by viral infection
Clinical: Infants and young children, fever, mucous membrane erythema (eyes/mouth), skin rash, cervical lymphadenopathy; usually self-limited
Pathology:
-Coronary artery vasculitis (accounts for fatalities in 1–2%)
Kawasaki disease, also known as mucocutaneous lymph node syndrome (medium vessel)
266
What is this:
Etiology: Ag-Ab complexes/MPO-ANCA
Clinical: skin rash, multiple other organs, fever
Specific disorders: drugs, bacteria, foreign proteins, tumor proteins
Pathology:
-Involves microvasculature
-Fibrinoid necrosis
-Karyorrhexis of PMN’s (leukocytoclastic vasculitis)
Microscopic Polyangiitis (small vessel)
267
What is this:
Etiology: neutrophil-related endothelial damage mediated by PR3-ANCA
Clinical: strawberry gingivitis, sinusitis, pneumonitis, renal failure, glomerulonephritis
Pathology:
-Affects upper and lower respiratory tract, kidneys
-Necrotizing granulomas
-Vasculitis with fibrinoid necrosis
Wegener Granulomatosis (small vessel)
268
What is this:
Etiology: endothelial injury from substance in cigarette smoke
Clinical: cigarette smoking, < 35 years, pain of extremities, ischemic ulcers, gangrene
Pathology:
Vasculitis with thrombosis
Thromboangiitis Obliterans
(Buerger Disease)
269
What is this:
Pathology:
- intimal tear - split between mid & outer third of the media
-media may be normal or have degeneration
Complications:
-rupture – hemorrhage
-branch obstruction
Predisposing conditions: hypertension, connective tissue disorders (Marfan)
Dissecting Aortic Hematoma
