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POM Final > Principles Of Pathology > Flashcards

Principles Of Pathology Flashcards

1
Q

Major definitions of pathology (3)

A
  1. The science that studies the structural, molecular, and functional manifestations of a disease, and the mechanisms that cause disease. 2. The structural and functional manifestations of a disease. 3. A disease.
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2
Q

What are the targets for prevention and treatment of a disease?

A

Etiology (Cause) and Pathogenesis (Mechanisms of disease)

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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

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4
Q

What is a diagnosis?

A

The name of a disease

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5
Q

What is an etiology?

A

The cause of a disease

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6
Q

Etiology Mnemonic

A

VINDICATE: Vascular Inflammatory Neoplastic Drug/toxin Infectious Congenital/genetic Autoimmune/immune Traumatic/physical Endocrine/metabolic/nutritional

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7
Q

What is pathogenesis?

A

The sequence of events that leads from the etiology to the manifestations of disease

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8
Q

What is a symptom?

A

Disease manifestation perceived and reported by the patient

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9
Q

What is a sign?

A

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

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10
Q

What is a differential diagnosis?

A

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

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11
Q

Subcellular changes in reversibly injured cells

A
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12
Q

What is hypertrophy?

A

Increased size of cells

Example: cardiomyocytes

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13
Q

What is Hyperplasia?

Example: epidermis (normal/psoriasis)

A

Non-neoplastic increase in number of cells (in organ or tissue)

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14
Q

What is Atrophy?

Example: frontal lobe; thinned gyri, widened sulci

A

Reduced size of cells or organs

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15
Q

Etiologies of Atrophy (7)

A
  • Reduced Functional Demand (e.g. skeletal muscle atrophy caused by denervation)
  • Inadequate Oxygen Supply (e.g. kidney atrophy caused by renal artery stenosis)
  • Insufficient Nutrients (e.g. skeletal muscle and fat atrophy caused by starvation)
  • Interrupted Trophic Signals (e.g. endometrial atrophy after menopause)
  • Persistent Cell Injury (e.g. gastric mucosal atrophy caused by chronic gastritis)
  • Increased Pressure (e.g. localized skin atrophy caused by prolonged bed rest)
  • Chronic Disease (e.g. cachexia caused by chronic disease)
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16
Q

What is Metaplasia?

A

Conversion of one differentialed cell type to another

Example: endocervix; squamous metaplasia/normal colomnar epithelium

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17
Q

What is Dysplasia?

A

Disordered growth and maturation of the cellular components of a tissue; may be a precursor to malignant neoplasia

example: dysplastic epithelium of uterine cervix; lacks normal polarity & large hyperchormatic nuclei (normal left, dysplastic right)

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18
Q

What is Neoplasia?

A

The autonomous growth of cells that have escaped normal regulation of cell proliferation.

Localized = benign

Metastasize/capable of = malignant

Examples: benign = thyroid follicular adenoma; malignant = colonic adenocarcinoma, metastatic to liver

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19
Q

Uterus with multiple leiomyomas

A
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20
Q

Hydropic degeneration

A

abnormal swelling because of increased water within organelles

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21
Q

Adrenal Neoplasia

A

Benign adrenal adenoma

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22
Q

What are the two major pathways to cell death?

A

Apoptosis: cell death caused by activation of internal molecular pathways leading to cell death

AND

Necrosis: cell death caused by pathological lethal injury that often originates outside the cell

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23
Q

Histological nuclear changes demonstrated by cell death (3)

A

Pyknosis: The nucleus becomes smaller and stains deeply basophilic because of chromatin clumping.

Karyorrhexis: The pyknotic nucleus breaks up into many smaller fragments.

Karyolysis: The nucleus may be extruded from the cell or have progressive loss of chromatin staining resulting in the disappearance of the nucleus.

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24
Q

Coagulative Necrosis

A

Nuclei disappear (karyolysis) and cytoplasm becomes more homogeneous (and often more acidophilic) resulting in residual ghosts of cells with no nuclei

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25
Q

Gross vs. Histological features with MI

A
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26
Q

Liquifactive Necrosis

A

Rapid dissolution of cells that liquefies necrotic tissue.

Often caused by intense, localized infiltration of neutrophils at sites of severe acute inflammation

Localized acute inflammation with liquifactive necrosis is called an abscess

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27
Q

Caseous Necrosis

A

Necrosis caused by tuberculosis; marginal zone of aggregated macrophages & central zone of necrosis containing amorphous debris derived from necrotic host/mycobacterial cells.

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28
Q

Granulomas (necrosis)

A

gross nodular lesions

29
Q

Granulomatous Inflammation (necrosis)

A

Dense infiltrates of macrophages

30
Q

Fat necrosis

A

Affects adipose tissue

Most commonly results from pancreatitis or trauma –> release of lipases that free up fatty acids that bind calcium to form calcium soaps (saponification)

31
Q

What is inflammation reacting to?

A

A tissue reacting to a pathogenic insult

32
Q

What is inflammation mediated by, and how?

A

Extracellular molecular signals:

  1. activate humoral and cellular inflammatory pathways
  2. cause the movement of fluid and leukocyes from blood –> extravascular compartment
33
Q

What does inflammation do? (3)

A
  1. localizes/eliminates case of injury
  2. removes injured tissue components
  3. leads to repair
34
Q

Cardinal signs of acute inflammation (5)

A

Rubor (redness), Calor (heat), Tumor (swelling), Dolor (pain), Functio Laesa (loss of function)

35
Q

Acute vs. Chronic Inflammation (cell types)

A

Acute (left): densly packed (polymorphonuclear neutrophils) PMNs with multilobed nuclei

Chronic (right): mononuclear leukocytes (lymphocytes, monocytes, macrophages and plasma cells-arrows)

36
Q

Acute vs Chronic Inflammation (overall response)

A

Acute:

  1. Vasodilation –> increased blood flow causing: redness and transudation of fluid causing edema
  2. Activation of humoral mediators causing: pain, exudation of plasma proteins, transmigration of neutrophils

Chronic:

  1. Influx of mononuclear leukocytes (lymphocytes, monocytes, macrophages, plasma cells)
  2. Increased extracellular matrix (collagen)
37
Q

Response to injury state descriptions (8)

A
38
Q

Outcome of an injury (2)

A

Injury initiates response that either leads to

1) complete resitution of tissue
2) chronic changes (scarring)

39
Q

Early events following hemorrhage

A
  1. Humoral activation: coagulation (stops hemorrhage)
  2. Cellular activation: platelets, mast cells, neutrophils, & endothelial cells
40
Q

Cellular activation against hemorrhage

A
  1. Mast Cells: degranulate
  2. Neutrophils: follow chemotactic gradient to site of injury
  3. Monocytes:
    a) enter site of acute inflammation, releases factors similar to neutrophils
    b) transform into macrophages
  4. Macrophages: phagocytic & secrete cytokines to attract lymphocytes
    5) Lymphocytes, macrophages, fibroblasts, and endothelial cells: produce growth/proliferation factors to mediate repair
    6) Granulation tissue: endothelial proliferation –> new capillaries grow into devitalized tissue, supply O2/nutrients for repair
    7) Scar: result of excess collagen (fibrosis/scar) at site
41
Q

Acute Myocardial Infarction Timeline

A
42
Q

What is thrombosis? When does it occur?

A

The activation of circling platelets and coagulation factors (Thrombin converts fibrinogen –> fibrin)

Occurs when endothelial function is altered, endothelial continuity is lost, or blood flow is reduced.

43
Q

What are ischemic diseases?

A

Disease characterized by reduced blood flow to the heart; Caused by thrombosis that obstructs adequate flow

44
Q

Thrombosis-related Diseases

A

Hemorrhagic: caused by inadequate thrombosis

Ischemic: caused by thrombosis obstruction of flow

Thromboembolic: cause by embolization of thrombosis

45
Q

Lower Extremity Deep Vein Thrombosis (DVT) Possible causes/outcomes

A

Causes: stasis, vascular injury, hypercoagulability, advanced age, sickle cell disease

Outcomes: lysis, propogation, organization, recanalization, embolization

46
Q

What is the partial thromboplastin time (PTT) test and what is it used for?

A

A blood test that measures the time it takes for blood to clot. It is used to:

  1. find cause of abnormal bleeding/bruising
  2. check for low levels of clotting factors that can cause bleeding disorders
  3. check for conditions that cause excess clotting problems, thrombophilia
  4. check if it’s safe to do a procedure/surgery
  5. check liver function
47
Q

Genetic abnormal morphogensis (example)

A

Autosomal dominant polycystic kidney disease (ADPKD)

Incidence of 1:500 live births, causes ~10% of end-stage kidney disease in the USA. Caused by mutations in genes for proteins involved in primary cilium function, cell cycle regulation and intracellular calcium transport in epithelial cells.

48
Q

Abnormal Morphogensis: Agenesis

A

Complete absence of an organ or component of an organ (e.g. renal agenesis)

49
Q

Abnormal Morphogensis: Aplasia

A

persistence of an undeveloped organ anlage without the mature organ (e.g. renal aplasia)

50
Q

Abnormal Morphogensis: Hypoplasia

A

reduced size caused by incomplete development (e.g. microcephaly)

51
Q

Abnormal Morphogensis: Atresia

A

incomplete formation of a lumen (e.g. esophageal atresia)

52
Q

Abnormal Morphogensis: Dysplasia

A

abnormal tissue differentiation during development (distinct from dysplasia developing in a previously normally developed tissue) (e.g. renal dysplasia)

53
Q

Abnormal Morphogensis: Ectopia

A

normally formed organ that is outside its normal anatomic location (e.g. ectopic kidney)

54
Q

Teratogenic Abnormal Morphogenesis (example)

A

Microcephaly induced by maternal Zika virus infection

Zika virus infection of fetal neural stem cells causes inhibition of the Akt-mTOR pathway, leading to defective neurogenesis

55
Q

What is a teratogen?

A

a factor that causes malformation of an embryo

56
Q

What is Cystic Fibrosis? What is the etiology? Characterization?

A

Most common lethal autosomal recessive disorder in whites

Results from defective chloride channel: the cystic fibrosis transmembrane conductance regulator (CFTR)

Characterized by: chronic pulmonary disease, deficident exocrine pancreatic function, complications of inspissated/thick mucus in other organs (small intestine, liver and reproductive tract)

57
Q

Tissue sample:

A

Normal Breast

58
Q

Tissue sample:

A

Lactating adenoma

Increase in size of globular (ducts)

Lots of nuclei, not atypical

More glandular cells - HYPERPLASIA - NORMAL

59
Q

Tissue Sample:

A

Normal Bronchus; pseudostratified ciliated columnar

60
Q

Tissue sample

A

Metaplastic (stratified squamous epithelium) bronchus

61
Q

Tissue Sample:

A

Normal Lung

62
Q

Tissue Sample:

A

Bronchogenic squamous cell carcinoma

invasive atypical cell groups with stromal desmoplasia

63
Q

Tissue Sample:

A

Debrided wound tissue

developing capillaries, fibroblasts, and residual chronic inflammatory cells

64
Q

Tissue Sample:

A

Cirrhotic Liver, H&E stain

Regenerating hepatocytes + Fibrosis

65
Q

Tissue Sample:

A

Cirrhotic liver, trichrome stain

Regenerating hepatocytes + Fibrosis

66
Q

Tissue Sample:

A

Lung: Cystic Fibrosis

Obvious neutrophilic inflammation exudate; Areas of consolidation with a mixed hemorrhagic and inflammatory component

67
Q

Tissue Sample:

A

Bronchiole, CF

Neutrophilic exudate

68
Q

Tissue Sample:

A

Pancreas, CF

Acini show marked necrosis, Ducts are distended with viscid secretions, Fibrotic bands (characteristic of chronic pancreatic injury) encase damaged exocrine elements

POM Final (5 decks)

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