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POM Test 2 > Pathology > Flashcards

Pathology Flashcards

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1
Q

Definitions of pathology

A

1) Science that studies the structural, molecular and functional manifestations of disease and the mechanisms that cause disease 2) The structural and functional manifestations of disease 3) A disease (structural molecular and functional, just structural and functional, disease)

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2
Q

Things that pathologists do…

A

evaluate surgical, cytologic, hematologic and autosy specimens microbiology, immunology, coagulation and biochemical testing blood transfusion, apheresis, stem cell and donor services genetic testing and tissue typing

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3
Q

What is a disease?

A

Molecular, cellular, tissue, organ and organismic damage caused by an etiology and mediated by pathogenic mechanisms (disease = damage, of what? cell, tissue, organ caused? etiology, what else: pathogenic mechanisms)

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4
Q

How to name disease

A

caused by, then what happens ex. bacterial pneumonia (inflammatory process in lung) can also have molecular characterization ex. ER/PR/HER2 - invasive ductal carcinoma

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5
Q

Cause of a disease

A

Etiology (VINDICATE)

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6
Q

Mechanism of a disease

A

Pathogenesis

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7
Q

Etiology Mnemonic

A

Vascular Inflammatory Neoplastic Drug/toxin Infectious Congenital/genetic Autoimmune/immune Trauma/physical Endocrine/metabolic/nutritional

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8
Q

Diagnosis

A

name of disease

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9
Q

Pathogenesis

A

sequence of events that leads from the etiology to the manifestations of disease (sequence, etiology –> disease manifestations)

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10
Q

Symptom

A

Disease manifestation perceived and reported by pt

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11
Q

Sign

A

Manifestation of disease that can be identified by physical examination, lab tests, imaging studies and other methods

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12
Q

DD

A

A ranked list of the most likely diagnoses based on the signs and symptoms of disease in a given pt.

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13
Q

Reversible or not reversible subcellular changes? cellular swelling disaggregated ribosomes dialated vesicular ER aggregated cytoskeletal elements mitochondria swelling

A

Reversible

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14
Q

What are some cellular response to injury?

A

1) Hypertrophy 2) Hyperplasia 3) Atrophy 4) Metaplasia 5) Dysplasia 6) Neoplasia

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15
Q

Hypertrophy

A

increased SIZE in cells

note: results in increased organ or tissue size, cells are larger so nucleus is also larger

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16
Q

Hyperplasia

A

increased NUMBER in cells

Note: maturation is normal (see in picture the top of the cells still no nuclei), this picture has squamous epithelial cells

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17
Q

Atrophy

Causes of atropy

A

reduced size of cells or organs (opposite of hypertrophy)

Causes:

  • reduced functional demand
  • inadequate oxygen supply
  • insufficient nutrients
  • interrupted trophic signals
  • persistent cell injury
  • increased pressure
  • chronic disease
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18
Q

Metaplasia

A

conversion of one differentiated cell type to another (that conversion was META!)

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19
Q

Dysplasia

A

disordered growth and maturation of the cellular components of a tissue (Dysplasia = DYSordered growth)

Dysplasia may be a precursor to malignant neoplasia.

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20
Q

Neoplasia

A

autonomous growth of cells that have escaped normal regulation of cell proliferation (neoplasia = NEO regulation yes proliferation)

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21
Q

Neoplasia - benign

A

neoplasmas that remain localized

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22
Q

Neoplasia - malignant

A

neoplasmas that spread to distant sites (cancer)

malignant neoplasms have less well differentiated cells that have larger nuclei that are pleomorphic, atypical, hyperchromatic and more often undergoing mitosis

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23
Q

Hydropic Degeneration

A

Irreversible change due to cell swelling

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24
Q
A
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25
Apoptosis
Cell death caused by activation of internal molecular pathways leading to cell death (physiological tissue remodeling during embryonic development, renewal of epithelial layers) Can be physiological (epithelial sloughing before renewal) or pathological (hep virus-induced hepatocyte loss) Mitosis increases and apoptosis decreases.
26
Necrosis
Cell death caused by pathological lethal injury that often originates outside the cell (injury by hypoxia, inflammation, molecular toxin, burn etc)
27
Example of Apoptosis
Cell death caused by activation of internal molecular pathways * tissue remodeling during embryonic development * renewal of epithelial layers * Pathway with TNFR receptor that Tumor necrosis factor binds and then triggers a molecular pathway that activates varioius caspaces Picture: single weird cells amoung normal cells
28
How to determine cell death histologically?
Nuclear changes
29
Pyknosis
The nucleus becomes smaller and stains deeply basophilic because of chromatin clumping (it is like an osis in there with all that staining and chromatin clumping)
30
Karyorrhexis
The pyknotic nucleus breaks up into many smaller fragments (the nucleus breaks up into hexagons)
31
Karyolysis
The nucleus may be extruded from the cell or have progressive loss of chromatin staining resulting in the disappearance of the nucleus (the nucleus is lysed)
32
Coagulative necrosis
Nuclei disappear (karyolysis) and cytoplasm becomes more homogeneous (and often more acidophilic) resulting in residual ghosts of cells with no nuclei. (necrosis = cell death that originates outside cell, coagulative = cytoplasm homogenous, ghost cells!)
33
MI Gross feature and histologic features
Gross features: localized discoloration Histologic features: ischemic coagulative necrosis
34
Liquifactive Necrosis
Rapid dissolution of cells that liquifies the necrotic tissue. Most often caused by neutrophils at sites of severe acute inflammation. Localized acute inflammation with liquifactive necrosis is called an abscess. * liquifies * abscess * neutrophils
35
Caseous Necrosis
Necrosis caused by tuberculosis * zone of aggregated macrophages * central zone of necrosis containing amorphous debris * gross lesions called granulomas * granulomatous inflammation
36
Fat necrosis
Affects adipose tissue and results from pancreatitis or trauma * release of lipases that free up fatty acids * fatty acids bind to calcium and form soaps (saponification)
37
Inflammation
Reaction of tissue to pathogenic insult
38
What is inflammation mediated by?
Extracellular molecular signals
39
What do the extracellular molecular signals do in inflammation?
Activate humoral and cellular inflammatory pathways and cause movement of fluid and leukocytes from blood into extravascular compartment * activate pathway * movement of fluid and leukocytes from blood
40
What are the three things that inflammation does?
1. Localizes or eliminates the cause of injury 2. Removes injured tissue components 3. Leads to repair
41
What are features of classic inflammatory response?
42
What type of cells characterize acute inflammation?
Polymorphonuclear neutrophils (PMN)
43
What type of cell characterizes chronic inflammation?
Mononuclear leukocytes (lymphocytes, monocytes, macrophages, plasma cells)
44
What are the steps in acute inflammatory response?
1. Vasodialation 1. Increased permeability of dialated vessels which causes increaed blood flow (redness) 2. Transudation 1. flow of fluid out of the tissue 2. if fluid has protein content this is called exudation 3. Activation and recruitment of neutrophils (vasodialation, transudation/exudation, neutrophils, vascular response)
45
Chronic Inflammation
Neutrophils stimulate mononuclear leukocytes. These will stimulate a repair process which results in increased extracellular matrix. (mononuclear leukocytes and extracellular matrix, cellular mediated response)
46
What are mononuclear leukocytes
1. Lymphocytes 2. Monocytes 3. Macrophages 4. Plasma cells
47
Response to injury steps What happens and who is involved?
* coagulation * cellular activation * platelet, mast cell, neutrophil and endothelial
48
Response to injury steps What happens and who is involved?
* Neutrophils follow chemotactic grandients to sites of in jury
49
Response to injury Step 3 What happens and who is involved?
* Monocytes (a type of mononuclear leukocyte) enter sites of acute inflammation and initially released facters similar to neutrophils
50
Response to injury after monocytes come
* Monocytes transform into macrophages that are phagocytic and secrete cytokines that attract lymphocytes * (Macrophages, lymphocytes)
51
Response to injury after macrocytes and lymphocytes come
* Macrocytes and lymphocytes produce growth/proliferation factors * Fibroblasts * proliferation * produce collagen to "repair" * Epithelial * proliferation that covers wound and extra collagen "repair"
52
Response to Injury after lymphocytes and macrophages produces growth/proliferation factors and fibroblasts and endithelial cells mediate repair
* Endothelial proliferation * new capilaries grow into tissue to supply oxygen and nutrients for repair
53
Response to injury what happens after endothelial proliferation and capillary growth
* new capillaries in granulation tissue * young fibrous tissue * there is also increased collagen and activated fibroblasts
54
Response to injury after granulation tissue
more collagen (fibrosis scar)
55
Purulent exudate
* pus * can indicate secondary infection
56
Acute response to injury in MI
* Coagulative necrosis * Acute inflammation
57
Repair in MI
* Granulation tissue * Fibrous Tissue
58
What is cirrhosis an example of?
* Fibrosis scarring * regernating heptatocytes * Ends up looking like nodules * caused by Hep C or drinking
59
Thrombosis When does it occur? What is involved? What does it cause?
* When does it occur? * endothelial injury * What is involved? * platelets and coagulation factors * What does it cause? * hemorrhagic diseases * if inadequate and you cannot plug holes in vasculature * ischemic diseases * too much thrombosis, heart attack * thromboembolic diseases * thrombus is formed and piece breaks off and blocks blood flow
60
DVT (Deep Vein Thrombosis)
* when you have hypercoaguability and get thrombus in veins of legs * cause? * stasis, vascular injury, hypercoagulability, age, sickle cell disease * outcomes * lysis -dissolves on its own * propagation - gets bigger * organization - endothelial cells grow over * recanalization - new vessles formed * embolization - pieces break off
61
PTT test What is it? What is it used for?
* blood test measures time it takes for blood to clot * used for * abnormal bleeding/bruising * hemophilila * thrombophilia * safe for surgery * liver
62
Agenesis
Complete absence of an organ or component of an organ (agenesis = no genesis)
63
Aplasia
Underdeveloped organ
64
Hypoplasia
Reduced size (ex microcephaly)
65
Atresia
incomplete formation of lumen
66
Dysplasia (tissue)
Abnormal tissue differntation during development
67
Ectopia
Normally formed organ that is outside its normal anatomic location
68
A factor that causes malformation of an embryo
Teratogen Zika virus is an example of a teratogen
69
Most common lethal autosomal recessive disorder in whites
CF
70
What causes CF?
Defective chloride channel called the transmembrane conductance regulator (CFTR)
71
Symptoms of CF
* chronic pulmonary disease * deficient exocrine pancreatic function * thick mucus
72
73
What is the purple in this picture?
glands
74
What are the white parts in this picture?
cells filled with fat (lactating breast)
75
If this is the bronchiol what process has taken place?
metaplasia
76
carcinoma
cancer arising in the epithelial tissue
77
Where are the neoplastic epithelial cells in this picture?
Dark regions and the lighter regions are fibrous tissue (this makes the carcinoma firm- results from desmoplasia) This is the lung.
78
What process does this show? What are the cells that are making up the blood vessels?
healing endothelial cells
79
What is this picture?
can see fibrosis and regenerating hepatocytes
80
What is this picture?
CF lung
81
What is this a picture of?
Bronchiol filled with cells from CF
82
What are letters A, B and C in this picture?
A- necrosis B- deucts with secretions C - fibrotic bands this is the pancreas
83

POM Test 2 (8 decks)

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