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Patho Exam #1 > Patho Exam #1 > Flashcards

Patho Exam #1 Flashcards

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1
Q

Ischemia-Reperfusion Injury

A

Restoration of blood flow to ischemic but viable tissues results in increased cell injury and necrosis (myocardial and cerebral ischemia).
Increased ROS production during deoxygenation can exacerbate damage. Influx of calcium may cause injury.
Inflammation induced by ischemic injury increases with repercussion bc of increased influx and activation of leukocytes.

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2
Q

Hypertrophy

A

Enlargement of cells that = increase in size of organ. Caused by increased functional demand or growth factor or hormonal stimulation. Can progress to cell injury if the stress is not relieved or exceeds adaptive capacity of the tissue.

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3
Q

Hyperplasia

A

Increase in # of cells that stems from increased proliferation which = larger organ. Hyperplasia ceases when signals that initiate it stop, which is different from cancer.

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4
Q

Atrophy

A

Reduced organ or tissue size caused by reduction in size and number of cells. Causes are decreased workload, diminished blood supply, inadequate nutrition, aging. Results from combination of decreased protein synthesis and increased protein degradation. May be accompanied by autophagy which is where starved cell eats its own organelles to survive.

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5
Q

Metaplasia

A

When one adult cell type is replaced by another cell type that is better suited to withstand the adverse environment. If persistent may lead to malignant transformation.

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6
Q

Oxidative stress (ROS)

A

Oxidative stress is cellular damage induced by accumulation of ROS a free radical. Causes can be infections, toxins, radiation, inflammation, ischemia reperfusion injury. Normally produced in redox reactions during energy generation or in phagocytic leukocytes (neutrophils). Main ones involved in cell injury are Superoxide (O₂⁻), Hydrogen peroxide (H₂O₂), Hydroxyl radical (OH*). Antioxidants neutralize them before they cause damage.

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7
Q

Coagulative Necrosis

A

Preserves tissue architecture for several days after injury. Firm texture. Characteristic of infarcts/ishemia in all solid organs except the brain.

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8
Q

Liquefactive Necrosis

A

Seen with bacterial or fungal infections bc enzymes of leukocytes digest (liquefy) the tissue. ie. Pus or abscess.

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9
Q

Gangrenous Necrosis

A

Limb that has lost blood supply and undergone coagulative necrosis. Wet gangrene is when bacterial infection is superimposed.

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10
Q

Caseous Necrosis

A

Often in Tuberculous infection. “Cheese-like”. Tissue architecture is obliterated. Often surrounded by collection of macrophages and inflammatory cells, characteristic of granuloma.

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11
Q

Fat Necrosis

A

Focal areas of fat destruction due to abdominal trauma or acute pancreatitis. Released fatty acts combine with calcium to produce chalky white lesions.

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12
Q

Fibrinoid Necrosis

A

Can only be detected on microscopic examination. Deposited immune complexes and plasma proteins have leaked into the walls of injured vessels and produce a bright pink appearance. Most seen in vasculitis.

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13
Q

Excessive Scarring

A

Excessive formation of the components of the repair process can lead to hypertrophic scars and keloids. Hypertrophic scars are usually from thermal or traumatic injury to deep dermis but regresses over months. Keloids grow beyond boundaries and don’t regress.

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14
Q

Angiogenesis

A

process by which new blood vessels form from pre-existing vessels.
-To heal wounds
-During growth and development
-In response to tissue damage or low oxygen
-It also occurs abnormally in conditions like cancer, where tumors need new blood vessels to grow.
Key players:
VEGF (Vascular Endothelial Growth Factor) – main signal that tells the body to grow new vessels
Endothelial cells – line the blood vessels and are the ones that multiply and migrate to form new vessels

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15
Q

Histamine

A

Major vasoactive amine found in mast cells, basophils and platelets. Causes dilation of arterioles and increases permeability of venues by binding to histamine receptors H1 on endothelial cells. Common antihistamine drugs block that receptor.

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16
Q

Serotonin

A

vasoactive mediator in platelets and neuroendocrine cells such as GI tract. Is vasoconstrictor.

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17
Q

What triggers a foreign body granuloma?

A

Inert materials (e.g., talc, sutures) that elicit a response without strong T-cell activation.

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18
Q

What triggers an immune granuloma?

A

Persistent microbes or antigens that activate T-cells, leading to macrophage activation via cytokines (especially IFN-γ).

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19
Q

What cytokine is most important in immune granuloma formation?

A

Interferon-gamma (IFN-γ) from TH1 cells.

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20
Q

What are epithelioid cells?

A

Activated macrophages that resemble epithelial cells; they form the core of granulomas.

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21
Q

What kind of necrosis is found in TB granulomas?

A

Caseating necrosis (cheese-like appearance).

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22
Q

Which granulomatous disease typically has non-caseating granulomas?

A

Sarcoidosis

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23
Q

What type of inflammation is Crohn’s disease associated with?

A

Non-caseating granulomatous inflammation

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24
Q

What are multinucleated giant cells?

A

Fused macrophages found in granulomas, especially around foreign materials or chronic infections.

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25
What’s the function of TNF-α in granulomatous inflammation?
Helps maintain the granuloma’s structure by promoting inflammation and cell recruitment.
26
Why does the body form granulomas?
To isolate and contain difficult-to-eradicate pathogens or foreign materials.
27
What is the primary role of macrophages in chronic inflammation?
phagocytosis cytokine secretion orchestrating tissue repair or destruction.
28
Where do macrophages originate from?
From hematopoietic stem cells in bone marrow → become monocytes in blood → migrate to tissues and differentiate into macrophages.
29
How are macrophages activated in chronic inflammation?
Activated by: Microbial products (via Toll-like receptors) Cytokines, especially IFN-γ from TH1 cells Other signals from damaged tissues
30
What are the two major macrophage activation pathways?
Classical (M1): induced by microbial products + IFN-γ → promotes inflammation, kills microbes Alternative (M2): induced by IL-4, IL-13 → promotes tissue repair and fibrosis
31
What are the functions of M1 macrophages?
-Produce ROS, NO, and lysosomal enzymes -Promote inflammation -Kill microbes
32
What are the functions of M2 macrophages?
-Secrete growth factors for angiogenesis and fibroblast activation -Involved in tissue repair and fibrosis
33
What key cytokines do macrophages secrete in chronic inflammation?
TNF, IL-1, IL-6, IL-12, and chemokines
34
How do macrophages influence chronic inflammation progression?
-Recruit other immune cells (e.g., lymphocytes) -Induce tissue damage if activation is prolonged -Promote healing or fibrosis, depending on signals
35
Leukotrine receptor antagonists
block leukotriene receptors (zafirlukast). used to treat ALLERGIC ASTHMA AND ALLERGIC RHINITIS
36
Costicosteroids
broad-spectrum antinflammatory agents that reduce the transcription encoding COX-2, phospholipase A2, proinfammatory cytokines and iNOS
37
Lipooxygenase inhibitors
5-lipoxygenase is not affected by NSAIDS. agents that inhibits leukotriene production (zileuton) is useful in ASTHMA treatment
38
Cyclooxygenase inhibitors
inhibit COX-1 and COX-2 thus inhibiting prostaglandin synthesis. ASPIRIN AND NSAIDS. COX-2 inhibitors (celecoxib) may increase cardiovascular events
39
What is leukocyte recruitment?
The process by which white blood cells are attracted and guided from the bloodstream to the site of tissue injury or infection.
40
What are the four key steps of leukocyte recruitment?
-Margination -Rolling -Adhesion -Transmigration (diapedesis)
41
What mediates leukocyte rolling along the endothelium?
Selectins (E-selectin, P-selectin on endothelium; L-selectin on leukocytes)
42
What molecules mediate firm adhesion of leukocytes to endothelium?
Integrins on leukocytes binding to ICAM-1 and VCAM-1 on endothelial cells
43
What cytokines increase expression of adhesion molecules on endothelium?
TNF and IL-1
44
What is transmigration (diapedesis) and where does it occur?
Movement of leukocytes through the endothelium, mainly in post-capillary venules
45
What molecule is key in mediating diapedesis?
PECAM-1 (CD31), expressed on both leukocytes and endothelial cells
46
After exiting blood vessels, how do leukocytes find the exact site of injury?
Via chemotaxis, following a gradient of chemotactic agents
47
Name 4 major chemotactic agents for leukocytes.
-Bacterial products (e.g., N-formyl peptides) -C5a (complement) -IL-8 (chemokine) -LTB4 (leukotriene B4)
48
Which leukocytes are recruited early vs. late during inflammation?
-Early (6–24 hrs): Neutrophils -Later (24–48+ hrs): Monocytes/macrophages
49
What is the difference between cancer grading and staging?
-Grading = based on histologic appearance (differentiation and mitotic activity) -Staging = based on extent of spread (tumor size, lymph node involvement, metastasis)
50
What does cancer grade describe?
How much tumor cells resemble normal cells — their degree of differentiation
51
What are typical cancer grade levels?
-Grade I: Well-differentiated -Grade II: Moderately differentiated -Grade III: Poorly differentiated -Grade IV: Undifferentiated/anaplastic
52
What does cancer stage describe?
The extent of tumor spread in the body (based on clinical, radiologic, and surgical data)
53
What is the most widely used cancer staging system?
TNM system (developed by AJCC)
54
What does the TNM system stand for?
T = Tumor size and local invasion N = Regional lymph node involvement M = Presence or absence of distant metastasis
55
In the TNM system, what do T1–T4 indicate?
Increasing size and/or local extent of the primary tumor
56
In the TNM system, what do N0–N3 indicate?
Increasing involvement of regional lymph nodes
57
In the TNM system, what does M0 vs. M1 mean?
M0 = No distant metastasis M1 = Distant metastasis present
58
Why is staging more important than grading in clinical practice?
Staging correlates more closely with prognosis and guides treatment decisions
59
What is human papillomavirus (HPV)?
A non-enveloped DNA virus from the papillomavirus family that infects epithelial cells, causing benign and malignant lesions.
60
How is HPV transmitted?
Through direct contact, usually sexual, but also through skin-to-skin or vertical transmission (mother to baby).
61
What types of HPV are considered high-risk for cancer?
HPV-16 and HPV-18
62
What types of HPV cause benign warts (condyloma acuminatum)?
HPV-6 and HPV-11
63
What oncogenic proteins are produced by high-risk HPV types?
E6 – degrades p53 tumor suppressor E7 – inactivates RB tumor suppressor
64
How does HPV contribute to carcinogenesis?
By producing E6 and E7, which disable tumor suppressor genes and promote uncontrolled cell growth.
65
What test is used to screen for HPV-related cervical changes?
Pap smear (Papanicolaou test)
66
What vaccine protects against HPV infection?
The HPV vaccine (e.g., Gardasil) – covers high-risk types (16, 18) and low-risk types (6, 11)
67
What is differentiation in the context of neoplasia?
The extent to which tumor cells resemble their normal cell counterparts in structure and function.
68
What does a well-differentiated tumor mean?
The tumor closely resembles normal tissue, often retains some functional capacity (e.g., hormone production).
69
What does a poorly differentiated or undifferentiated tumor indicate?
The tumor looks very different from the normal tissue and usually shows more aggressive behavior.
70
What is anaplasia?
Lack of differentiation; hallmark of malignancy, with primitive, abnormal-appearing cells.
71
What are morphologic features of anaplasia?
-Pleomorphism (variation in size/shape) -Hyperchromatic nuclei -Increased nuclear-to-cytoplasmic ratio -Abundant, abnormal mitoses -Loss of polarity -Giant tumor cells
72
Is anaplasia reversible?
No — anaplasia is irreversible and reflects a high-grade malignant tumor.
73
What is pleomorphism?
Variation in size and shape of cells and nuclei — a common feature of anaplasia.
74
What does increased nuclear-to-cytoplasmic ratio suggest?
A shift toward larger nuclei and less cytoplasm, typical in malignant (anaplastic) cells.
75
What do abnormal mitotic figures in a tumor indicate?
Rapid and disorganized cell division, a marker of high-grade malignancy.
76
What are tumor markers?
Substances (usually proteins) produced by tumor cells or host tissues in response to tumors; found in blood, urine, or tissue.
77
What tumor is associated with PSA (Prostate-Specific Antigen)?
Prostate cancer (Note: also elevated in benign prostatic hyperplasia and prostatitis)
78
What tumor is associated with CEA (Carcinoembryonic Antigen)?
Colorectal cancer Also seen in pancreatic, gastric, and breast cancers (Note: not specific)
79
What tumor is associated with AFP (Alpha-Fetoprotein)?
-Hepatocellular carcinoma -Yolk sac tumors (testes or ovary) -Also elevated in some GI tumors
80
What tumor is associated with CA-125?
Ovarian cancer (Note: used to monitor treatment/recurrence, not good for screening)
81
What tumor is associated with CA 19-9?
Pancreatic cancer (Also seen in GI cancers)
82
What tumor is associated with hCG (Human Chorionic Gonadotropin)?
-Choriocarcinoma -Testicular germ cell tumors -Also elevated in some trophoblastic tumors
83
What tumor is associated with Calcitonin?
Medullary thyroid carcinoma
84
What tumor is associated with S-100 protein?
-Melanoma -Also in neural tumors and Langerhans cell histiocytosis
85
What tumor is associated with Immunoglobulins (M-protein spike)?
Multiple myeloma and other plasma cell dyscrasias
86
What is metastasis?
The spread of cancer cells from the primary site to non-contiguous distant sites, forming secondary tumors.
87
What is a euploid?
A cell with a chromosome number that is a multiple of the haploid number (23)—e.g., 46 (diploid), 69 (triploid), or 92 (tetraploid).
88
What is polyploidy?
A condition where cells have more than two full sets of chromosomes, such as triploidy (69) or tetraploidy (92).
89
What is aneuploidy?
A chromosomal abnormality in which a cell has a number of chromosomes that is not a multiple of 23, due to gain or loss of one or more chromosomes.
90
What causes aneuploidy?
Usually caused by nondisjunction during meiosis or mitosis.
91
What is mosaicism?
A condition where an individual has two or more cell populations with different genotypes, all originating from one zygote.
92
What is translocation?
Transfer of a part of one chromosome to another chromosome
93
What is a Robertsonian translocation?
A chromosomal abnormality where the long arms of two acrocentric chromosomes fuse, forming one chromosome, and the short arms are lost.
94
What is deletion?
Involves loss of a portion of a chromosome
95
3 features to distinguish between benign and malignant
differentiation and anaplasia local invasion metastasis
96
benign tumor
localized end in oma
97
malignant
locally invasive and has capacity to spread are referred to as cancers
98
hallmarks of cancer
self sufficiency in growth signals insensitivity to growth inhibitor signals altered cellular metabolism evasion of apoptosis limitless replicative potential sustained angiogenesis invasion and metastasis evasion of immune surveilance
99
oncogenes
mutated or over expressed versions of normal cellular genes called proton-oncogenes. trigger pro-growth signaling pathways and enhance cell survival
100
tumor suppressor genes
normally prevent uncontrolled cell growth but when mutated allow transformed phenotype to develop, usually both normal alleles of tumor suppressor genes must be damaged for transformation to occur
101
how do malignant neoplasms spread
seeding within body cavities lymphatic spread hematogenous spread
102
leukemias and lymphomas
always assumed to be malignant
103
klinefelter syndrome
characterized by male hypogonadism in individuals with at least two X chromosomes and one or more Y chromosomes, most affected have a 47, XXX karyotype resulting from nondisjunction of sex chromosomes during meiosis
104
characteristics of klienfelter syndrome
hypogonadism elongated body reduced hair gynecosmastia
105
Turner syndrome
characterized by hypogonadism in phenotypic females resulting from partial or complete monosomy of the short arm of the X chromosome such as 45, X
106
characteristics of Turner syndrome
growth retardation, short stature, webbing of neck, low posterior hairline, shield like chest with wide spaced nipples, lymphedema of hands and feet, and cardiovascular abnormalities
107
trisomy 21
most common chromosomal disorder characterized by an extra copy of chromosome 21 resulting in chromosome count of 47
108
most common cause of trisomy 21
meiotic nondisjunction occurring in ovum
109
features of trisomy 21
flat facial profile oblique palpebral features epicanthic folds
110
leading cause of severe intellectual disability
down syndrome
111
disorders of autosomal dominant inhertance
manifested by heterozygous state, so at least one parent is affected. both males and females are affected and both sexes can transmit the condition ex. Huntington disease
112
amyloidosis
condition associated with a number of disorders where extracellular deposits of fibrillar proteins are responsible for tissue damage and dysfunction
113

Patho Exam #1 (2 decks)

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