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3MED FB Robbins > I - Cell Injury, Cell Death and Adaptations > Flashcards

I - Cell Injury, Cell Death and Adaptations Flashcards

1
Q

Increase in size of cells resulting in increased size of organ.

A

Hypertrophy(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 34

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2
Q

Increase in number of cells.

A

Hyperplasia(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.35

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3
Q

Hypertrophy or hyperplasia?Uterus during pregnancy

A

Both Estrogen stimulated SM hyperthrophy and hyperplasia (TOPNOTCH)Robbins Basic Pathology, 9th ed. p.34

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4
Q

Hypertrophy or hyperplasia?Wound healing

A

Hyperplasia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.4

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5
Q

Hypertrophy or hyperplasia?
Female breast at puberty

A

Both. (TOPNOTCH) Robbins Basic Pathology 9th ed., p 36

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6
Q

Cellular adaptation of non-dividing cells such as myocardial fibers.

A

Hypertrophy (TOPNOTCH)

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7
Q

A 50 y/o male has untreated hypertension for several years. What cellular alteration will be most likely seen in the myocardium?

A

Hypertrophy (TOPNOTCH)

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8
Q

A 40 y/o male underwent partial hepatectomy. What cellular adaptation will the liver most likely undergo?

A

Hyperplasia(TOPNOTCH)

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9
Q

The most common stimulus for hypertrophy of muscle

A

Increased workload (TOPNOTCH) Robbins Basic Pathology, 9th ed., p.34

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10
Q

A 65 y/o male presents with 3-month history of weak stream, straining, and hesitancy. There is no history of prostate cancer. Prostate was severely enlarged without nodules. PSA level is 3 mcg. What cellular adaptation does the prostate most likely undergo?

A

Hyperplasia(Case of BPH) (TOPNOTCH)

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11
Q

Stimulus for hyperplasia in BPH

A

Hormonal stimulation by androgens. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 36

BPH (Benign Prostatic Hyperplasia) is a condition where the prostate gland grows in size, and it is commonly seen in older men. The stimulus for hyperplasia in BPH is primarily related to hormonal imbalances. Specifically, it is related to an increase in the levels of dihydrotestosterone (DHT), which is a metabolite of testosterone.

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12
Q

Cellular adaptation in papilloma virus infection

A

Hyperplasia (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 36

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13
Q

Reduction in the size of an organ or tissue due to decrease in cell size and number

A

Atrophy(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 35

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14
Q

A 60 y/o female has been experiencing hot flushes and irritability. Her uterine epithelium will most likely reveal what type of cellular adaptation?

A

Atrophy(in menopause)(TOPNOTCH)

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15
Q

Chronic production of this cytokine is thought to be responsible for appetite suppression and lipid depletion, culminating in muscle atrophy and marked muscle wasting (cachexia)

A

Tumor necrosis factor (TNF)(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 35

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16
Q

A reversible change in which one differentiated cell type is replaced by another cell type.

A

Metaplasia (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 37

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17
Q

A 49 y/o female had a chronic history of heartburn. Biopsy done showed glandular changes in the distal epithelium of the esophagus. What cellular adaptation is present?

A

Metaplasia. This is a case of Barret’s esophagus (squamous to glandular epithelium) (TOPNOTCH)

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18
Q

The basal cell changes seen in reflux esophagitis is an example of this adaptive change

A

Metaplasia (TOPNOTCH)

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19
Q

Most common epithelial metaplasia

A

Columnar to squamous(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 37

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20
Q

Type of metaplasia in trachea and bronchi in habitual cigarette smoking

A

Columnar to squamous(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 37

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21
Q

Its hallmarks are reduced oxidative phosphorylation with resultant depletion of energy stores in the form of ATP and cellular swelling

A

Reversible injury(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 38

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22
Q

Type of cell death characterized by nuclear dissolution, without complete loss of membrane integrity.

A

Apoptosis(TOPNOTCHRobbins Basic Pathology, 8th ed. p.7

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23
Q

Type of cell death which is energy-dependent, tightly regulated, and associated with normal cellular functions.

A

Apoptosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.7

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24
Q

Type of cell death which results from a pathologic cell injury.

A

Necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.9

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25
Q

Type of cell death associated with inflammation.

A

Necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10

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26
Q

It is the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis. It is characterized by nuclear shrinkage and increased basophilia.

A

Pyknosis(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.42

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27
Q

It is the destructive fragmentation of the nucleus of a dying cell.

A

Karyorrhexis (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10

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28
Q

It is the complete dissolution of the chromatin of a dying cell.

A

Karyolysis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10

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29
Q

This is the first manifestation of almost all forms of injury to cells.

A

Cellular swelling(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.8

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30
Q

Small clear vacuoles within the cytoplasm, representing pinched-off segments of the endoplasmic reticulum.

A

Hydropic change or Vacuolar degeneration (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.23

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31
Q

Appearance of lipid vacuoles in the cytoplasm.

A

Fatty Change(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.23

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32
Q

Surface blebs, increased eosinophilia of the cytoplasm, cellular swelling.

A

Reversible/ Early Ischemic Injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18

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33
Q

Cell injury with loss of nuclei, cellular fragmentation and leakage of cellular contents.

A

Irreversible/ Necrotic cellular injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18

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34
Q

Cell injury with loss of microvilli, blunting, appearance of smal amorphous densities, ER dilation and disaggregation of granular and fibrillar elements.

A

Reversible/ Early Ischemic Injury(TOPNOTCH)Robbins Basic Pathology, 9th ed., p.41

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35
Q

A form of tissue necrosis in which the component cells are dead but the basic tissue architecture is preserved. The affected tissues take on a firm texture.

A

Coagulative necrosis(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.43

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36
Q

Characterized by digestion of dead cells, resulting in transformation of the tissue into a liquid viscous mass.

A

Liquefactive necrosis(TOPNOTCH)Robbins Basic Pathology , 9th ed. p.43

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37
Q

Refers to focal areas of fat destruction, typically resulting from release of activated pancreatic lipases into the substance of the pancreas and the peritoneal cavity. The foci of necrosis contain shadowy outlines of necrotic fat cells with basophilic calcium deposits, surrounded by an inflammatory reaction.

A

Fat necrosis (TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 44

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38
Q

A special form of necrosis usually seen in immune reactions involving blood vessels. Deposits of immune complexes, together with fibrin that has leaked out of vessels, result in a bright pink and amorphous appearance in H&E stains, called “fibrinoid” (fibrin-like) by pathologists.

A

Fibrinoid necrosis (TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 44

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39
Q

Seen in focal bacterial or, occasionally, fungal infections, because microbes stimulate the accumulation of inflammatory cells and the enzymes of leukocytes digest the tissue.

A

Liquefactive necrosis (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10

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40
Q

This term is usually applied to a limb, generally the lower leg, that has lost its blood supply and has undergone coagulative necrosis involving multiple tissue layers.

A

Gangrenous necrosis(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.43

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41
Q

Friable, white appearance of necoris. It appears as a structureless collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border.

A

Caseous necrosis(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.43

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42
Q

Obstruction of the blood supply would lead to which type of pathologic process in the brain parenchyma?

A

Liquefactive necrosis (TOPNOTCH)

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43
Q

The type of necrosis seen in tissue injury associated with acute pancreatitis

A

Enzymatic fat necrosis. (TOPNOTCH)

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44
Q

A 32 y/o male complains of chronic cough and weight loss. CXR showed an ill-defined mass along the apex of the right lobe. Sputum AFB was positive. Biopsy of the lung will most likely reveal what kind of necrosis?

A

Caseation necrosis (TOPNOTCH)

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45
Q

These are chemical species with a single unpaired electron in the outer orbital.

A

Free radicals(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18

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46
Q

They block free radical formation or inactivate free radicals. Examples of these are the lipid-soluble vitamins E, A, and C, and glutathione in the cytosol.

A

Antioxidants(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 48

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47
Q

Most common cause of cell injury in clinical medicine.

A

Ischemia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18

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48
Q

Patient presented with heaviness in the chest, nausea, and diaphoresis. Troponin I and CKMB were noted to be elevated. What is the mechanism of the elevation of cardiac enzyme?

A

Leakage of intracellular proteins through the damaged cell membrane reflecting irreversible injury and cell death in the tissues. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 50

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49
Q

Composed of membrane-bound vesicles of cytosol and organelles seen in programmed-cell death.

A

Apoptotic Bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.19

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50
Q

Characterized by cell shrinkage, chromatic condensation, formation of cytoplasmic blebs and apoptotic bodies, and phagocytosis by macrophages.

A

ApoptosisTOPNOTCH) Robbins Basic Pathology, 9th ed., p. 53

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51
Q

Type of cell death in embryogenesis

A

ApoptosisTOPNOTCH) Robbins Basic Pathology, 9th ed., p. 52

52
Q

Type of cell death in menopause

A

ApoptosisTOPNOTCH) Robbins Basic Pathology, 9th ed., p. 52

The type of cell death that occurs in this context is apoptosis, which is a programmed cell death that occurs in response to changes in hormone levels or other physiological factors.

53
Q

Restoration of blood flow to ischemic but otherwise viable tissue paradoxically results in exacerbated and accelerated injury.

A

Ischemia-Reperfusion Injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18

54
Q

Pathway of apoptosis trigerred by loss of survival signals, DNA damage and accumulation of misfolded proteins. Inhibited by Anti-apoptotic members of the Bcl family.

A

Mitochondrial / Intrinsic Pathway(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.22

55
Q

Pathway of apoptosis responsible for elimination of self-reactive lymphocytes and damage by cytotoxic T lymphocytes. Initiated by TNF receptors.

A

Death Receptor / Extrinsic Pathway(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.22

56
Q

It involves sequestration of cellular organelles into cytoplasmic autophagic vacuoles that fuse with lysosomes and digest enclosed material.

A

Autophagy(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 61

57
Q

Refers to any abnormal accumulation of triglycerides within parenchymal cells. Most often seen in the liver but can also occur in the heart, sk m., and kidneys.

A

Fatty change/Steatosis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 62

58
Q

Other name for macrophages in contact with lipid debris of necrotic cells or abnormal forms of lipoproteins. Filled with minute, membrane-bound vacuoles of lipid, imparting a foamy appearance to their cytoplasm.

A

Foam cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.24

59
Q

Presence of cholesterol-filled macrophages in subepithelial connective tissue of skin or tendons.

A

Xanthomas(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.24

60
Q

Hypertrophy or hyperplasia?Cardiomegaly due to hypertension

A

Hypertrophy due to increased workload(TOPNOTCH)

61
Q

Most common exogenous pigment?

A

Carbon(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26

62
Q

“Wear and Tear pigment”?

A

Lipofuschin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26

63
Q

Pigment produced by tyrosinase-catalyzed oxidation of tyrosine to dihydroxyphenylalanine.

A

Melanin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26

64
Q

Hemoglobin-derived granular pigment that is golden-yellow to brown in color. Accumulates in excess of iron.

A

Hemosiderin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26

65
Q

Histochemical reaction used to identify hemosiderin.

A

Prussian blue test(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26

66
Q

Abnormal calcium deposition occuring in the absence of calcium metabolic derangements.

A

Dystrophic calcification.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26

67
Q

Calcium deposition in normal tissues occuring in the presence of hypercalcemia.

A

Metastatic calcification (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26

La calcificación distrófica es el depósito de sales de calcio en tejidos dañados o muertos, pero en presencia de niveles normales de calcio en suero. La calcificación distrófica se produce en tejidos que están dañados por enfermedades, traumatismos, inflamación crónica, ateroesclerosis, necrosis tumoral, entre otros.

Por otro lado, la calcificación metastásica se produce en tejidos normales debido a un aumento de los niveles de calcio en suero, lo que resulta en una sobrecarga de calcio. Esto puede ocurrir en enfermedades como hiperparatiroidismo, hipervitaminosis D o enfermedad renal crónica. Los tejidos más comúnmente afectados por la calcificación metastásica son los riñones, los pulmones y las arterias.

En resumen, la principal diferencia entre calcificación distrófica y metastásica es que la primera ocurre en tejidos dañados o muertos y en presencia de niveles normales de calcio en suero, mientras que la segunda ocurre en tejidos normales debido a un aumento de los niveles de calcio en suero.

68
Q

Grossly seen as fine white granules or clumps, often felt as gritty deposits. Histologically, intra/extracellular basophilic deposits.

A

Calcium salts(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.27

69
Q

A result of a progressive decline in the proliferative capacity and lifespan of cells.

A

Cellular aging(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.29

70
Q

Appears as round or oval masses with intensely eosinophilic cytoplasm, nuclei with various stages of chromatin condensation and aggregation, karyorrhexis.

A

Apoptotic cell(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.20

71
Q

Membrane bound vesicles of cytosol and organelles quickly extruded and phagocytosed without eliciting inflammatory response.

A

Apoptotic bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.20

72
Q

Clear vacuoles within parenchymal cells, displacing the nucleus to the cell periphery.

A

Fatty change (TOPNOTCHRobbins Basic Pathology, 8th ed. p.24

73
Q

Focal, intracellular fat deposits creating alternating bands of yellowed myocardium with alternating bands of darker red-brown uninvolved heart or “tigered effect”.

A

Fatty change of the heart(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.24

74
Q

Rounded, eosinophilic accumulation of newly synthesized immunoglobulins in the rough ER of plasma cells.

A

Russel bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.25

75
Q

Eosinophilic cytoplasmic inclusion in liver cells composed of aggregated intermediate filaments which resist degradation. Seen in patients woth alcoholic liver disease.

A

Mallory body / “alcoholic hyalin”(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.25

76
Q

Aggregated protein inclusions that contain microtubule-associated proteins and neurofilaments, reflecting disrupted neuronal cytoskeleton.

A

Neurofibrillary tangles in Alzheimer’s disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26

77
Q

An insoluble brownish-yellow granular intracellular material that accumulates as a function of age and atrophy. Appears as perinuclear electron-dense granules on electron microscopy.

A

Lipofuschin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26

78
Q

What substance accumulates in the cytoplasm of liver cells in steatosis?

A

Triglyceride (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 62

Esteatosis es la acumulación anormal de lípidos (principalmente triglicéridos) en células parenquimatosas, como las células hepáticas. También se conoce como “hígado graso” y puede ser un signo de daño hepático o enfermedades metabólicas como la obesidad y la diabetes. La esteatosis hepática puede ser reversible si se trata la causa subyacente, pero si no se controla, puede llevar a una inflamación crónica del hígado y daño irreversible.

79
Q

Mechanism of triglyceride accumulation in malnutrition

A

Defective transport (TOPNOTCH)

80
Q

A 70 y/o woman was brought to the clinic because of a 3 year history of progressive memory impairment, difficulty finding words, and irritability. What is the pathogenesis of this condition?

A

Abnormal folding of AB peptides causing aggregation within neurons and apoptosis (Case of Alzheimer Disease) (TOPNOTCH)

81
Q

Pathogenesis: abnormal folding of PrPSC causing neuronal death (affected prion protein)

A

Creutzfeldt-Jacob disease (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 58

The given pathogenesis describes the mechanism of Prion diseases such as Creutzfeldt-Jakob disease, where abnormal folding of PrPSC (an abnormal form of a normal cellular protein called prion protein) leads to the accumulation of the misfolded protein in the brain, causing neuronal death and neurological symptoms.

82
Q

Pathogenesis: absence of enzymatic activity in lungs causing destruction of elastic tissue

A

Alpha-1-antitrypsin deficiency (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 58

83
Q

Fundamental cause of necrotic cell death

A

Reduction in ATP levels(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 45

84
Q

Other term for fatty change

A

Steatosis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 62

85
Q

Most common causes of significant fatty change in the liver

A

Alcohol abuse and non-alcoholic fatty liver disease(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 62

86
Q

Alteration within the cells or in the extracellular space that gives a homogeneous, glassy, pink appearnce in H&E histologic section

A

Hyaline change(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 61

87
Q

In this disease, glycogen can be seen in renal tubular epithelial cells, liver cells, B cells of islets of Langerhans, and heart muscle cells.

A

Diabetes mellitus(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 64

88
Q

A condition when there is systemic overload of iron, hemosiderin may be deposited in many organs and tissues.

A

Hemosiderosis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 65

89
Q

An inherited disease characterized by extreme accumulation of iron, associated with liver, heart, and pancreatic damage, and resulting in liver fibrosis, heart failure, and diabetes mellitus.

A

Hemochromatosis. (TOPNOTCH)

90
Q

A rare metabolic disease causing black pigment deposition in the skin, connective tissue, and cartilage.

A

Alkaptonuria(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 64

91
Q

Foci of dystrophic calcification which appears as lamellated configurations because of their resemblance to grains of sand. Seen in some types of papillary cancer.

A

Psammoma bodies (TOPNOTCH)

92
Q

Jaundice (ictericia) is due to accumulation of what pigment?

A

Bilirubin. (TOPNOTCH)

93
Q

What type of necrosis is most characteristic of ischemia involving the heart or kidney?

A

Coagulative necrosis (TOPNOTCH)

94
Q

What type of necrosis is most often caused by sudden ischemia from vascular occlusion?

A

Coagulative necrosis (TOPNOTCH)

95
Q

A 56 y/o man died after 24-hour hospitalization for severe crushing chest pain. The type of necrosis of myocardium will most likely reveal:

A

Coagulative necrosis (TOPNOTCH)

96
Q

The kidney in nephrocalcinosis is an example of what type of calcification? Dystrophic or metastatic?

A

Metastatic calcification (TOPNOTCH)

La calcificación distrófica es el depósito de sales de calcio en tejidos dañados o muertos, pero en presencia de niveles normales de calcio en suero. La calcificación distrófica se produce en tejidos que están dañados por enfermedades, traumatismos, inflamación crónica, ateroesclerosis, necrosis tumoral, entre otros.

Por otro lado, la calcificación metastásica se produce en tejidos normales debido a un aumento de los niveles de calcio en suero, lo que resulta en una sobrecarga de calcio. Esto puede ocurrir en enfermedades como hiperparatiroidismo, hipervitaminosis D o enfermedad renal crónica. Los tejidos más comúnmente afectados por la calcificación metastásica son los riñones, los pulmones y las arterias.

En resumen, la principal diferencia entre calcificación distrófica y metastásica es que la primera ocurre en tejidos dañados o muertos y en presencia de niveles normales de calcio en suero, mientras que la segunda ocurre en tejidos normales debido a un aumento de los niveles de calcio en suero.

97
Q

Dystrophic or metastatic calcification? Calcific aortic stenosis

A

Dystrophic calcification(TOPNOTCH)

La calcificación distrófica es el depósito de sales de calcio en tejidos dañados o muertos, pero en presencia de niveles normales de calcio en suero. La calcificación distrófica se produce en tejidos que están dañados por enfermedades, traumatismos, inflamación crónica, ateroesclerosis, necrosis tumoral, entre otros.

Por otro lado, la calcificación metastásica se produce en tejidos normales debido a un aumento de los niveles de calcio en suero, lo que resulta en una sobrecarga de calcio. Esto puede ocurrir en enfermedades como hiperparatiroidismo, hipervitaminosis D o enfermedad renal crónica. Los tejidos más comúnmente afectados por la calcificación metastásica son los riñones, los pulmones y las arterias.

En resumen, la principal diferencia entre calcificación distrófica y metastásica es que la primera ocurre en tejidos dañados o muertos y en presencia de niveles normales de calcio en suero, mientras que la segunda ocurre en tejidos normales debido a un aumento de los niveles de calcio en suero.

98
Q

Dystrophic or metastatic calcification?Left anterior descending coronary artery with atheromatous plaques

A

Dystrophic calcification(TOPNOTCH)

99
Q

Dystrophic or metastatic calcification? Sarcoidosis

A

Metastatic calcification (TOPNOTCH)

100
Q

Dystrophic or metastatic calcification? Paget disease

A

Metastatic calcification (TOPNOTCH)

101
Q

After a tibial fracture in a 19 year old football player, the leg is immobilized to permit healing. The leg muscles decrease in size due to: (A) decrease in cell size, (B) decrease in cell number, (C) inadequate nutrition, (D) loss of hormonal stimulation

A

decrease in cell size (atrophy) (TOPNOTCH) Robbins Basic Pathology, 8th ed. P. 4

102
Q

A 30 year old thalassemic male has been receiving multiple blood transfusions throughout his life. What is the expected intracellular accumulation in the parenchymal cells of his liver, heart, and endocrine organs?

A

Hemosiderin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26

La hemosiderina es un pigmento de hierro que se encuentra en el cuerpo humano. Es producido cuando el hierro es liberado de la hemoglobina en los glóbulos rojos y se deposita en los tejidos, especialmente en el hígado y el bazo. La hemosiderina es visible en las células como gránulos de color marrón-amarillento y su acumulación en exceso puede ser un signo de ciertas enfermedades, como la hemocromatosis y la anemia hemolítica crónica.

La talasemia es un trastorno genético de la sangre que se caracteriza por una producción insuficiente de hemoglobina, la proteína que transporta el oxígeno en los glóbulos rojos. Esto puede dar lugar a anemia, ictericia, agrandamiento del bazo y otros problemas de salud. La talasemia se puede clasificar en diferentes tipos según los genes involucrados y la gravedad de la enfermedad.

103
Q

An 80 year old female is found to have calcified aortic valves. Which of the following is the likely cause? (A) renal failure with secondary hyperparathyrodism, (B) accumulation of calcium in damaged valves despite absence of calcium derangements, (C) parathyroid-related protein production from an underlying malignancy, (D) hypercalcemia from multiple myeloma

A

Accumulation of calcium despite absence of calcium derangements (dystrophic calcification) (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp26-27.

104
Q

In industrialized nations, what are the most common causes of fatty change in the liver?

A

Alcohol abuse and diabetes (TOPNOTCH) Robbins Basic Pathology, 8th ed. P 23.

105
Q

A 22 year old female is on the first day of her menses. Which of the following characterizes the events in her endometrial cells: (A) endometrial cells show shrinkage and nuclear condensation, (B) neutrophils accumulate around the cells, (C) severe mitochondrial swelling and plasma membrane destruction, (D) accumulation of amorphous pink material

A

Option (A) - endometrial cells show shrinkage and nuclear condensation - characterizes the events in the endometrial cells during the first day of menstruation. (Apoptosis) (TOPNOTCH) Robbins Basic Pathology 8th ed., pp 19-20

106
Q

Cuales son las hiperplasias fisiológicas?

A
  • Hormonal
  • Compensadora (regeneración del hígado)
107
Q

Cuando la hiperplasia es patológica?

A
  • Est. hormonal excesiva
  • Infecciones víricas
108
Q

Que es la hipertrófia fisiológica?

A

Aumento del útero en el embarazo, por ejemplo
Lactancia
Fisiculturismo

109
Q

Ejemplo de hipertrofia patológica

A
  • Hipertrofia del ventrículo izquierdo
110
Q

Que es atrofia?

A

Disminución del tamaño de un órgano o tejido con disminución de función

111
Q

Como se dá la sustitución de células en una metaplasia?

A

epitelio por epitelio
mesénquima por mesénquima

112
Q

Cual es el epitélio más fuerte que tenemos?

A

El escamoso

113
Q

Como se llama la metaplasia de epitelio escamoso a columnar en el esófago?

A

Esófago de Barret

114
Q

Si las influencias a producir Metaplasia persisten se puede desarrollar…

A

cancer

115
Q

Que es Agenesia, Aplasia, Disgenesia y Atresia?

A

Agenesia: falta de formación de un órgano o estructura.
Aplasia: ausencia de una estructura por falta de desarrollo.
Disgenesia: desarrollo anormal de un órgano o estructura.
Atresia: ausencia o cierre anormal de una abertura natural en el cuerpo.

116
Q

La necrosis es patológica o fisiológica?

A

Patológica

Necrosis: accidental y no regulada, causada por afectación las membranas celulares y perdida de la homeostasis. Genera inflamación. El contenido no sale de la celula (ej: el nucleo permanece). Es patológico.
Ej: isquemia, exposición a toxinas, infecciones y traumas

117
Q

La apoptosis es fisiológica o patológica?

A

Puede ser los 2

Apoptosis: el ADN o las proteínas estan dañadas, sin reparación, la propia celula se mata. Se caracteriza por disolución nuclear, fragmentación de la celula. No hay inflamación. Es fisiológico y patológico.

118
Q

Cuales son los cambios morfologicos en una necrosis y en una apoptosis?

A
119
Q

Ejemplo de cambio de una lesión

A

Normal / reversible y irreversible

120
Q

Tipo de necrosis

A

Necrosis coagulativa: la estructura permanece preservada, textura firme (solido), las células perden sus nucleos.

  • Micro: células eosinofilas anucleada
  • Ej: isquemia secundaria a obstrucción de un vaso (infarto)
  • Ocurre en todos los órganos, excepto en encéfalo.
121
Q

Tipo de necrosis

A

Necrosis licuefactiva: digestión de células muertas

  • Macro: masa viscosa liquida, pus amarillento (linfocitos muertos) y consistencia pastosa.
  • Ej: isquemia en encéfalo (hipoxia), infección bacteriana focales, infecciones fúngicas.
122
Q

Tipo de necrosis

A

Necrosis caseosa: se produce en focos de infección tuberculosa.

  • Macro: material blanquecino y friable, parece un queso.
  • Micro: acumulación de células
    fragmentadas y residuos granulares amorfos englobados por un borde inflamatorio.
  • Aspecto característico “granuloma”
123
Q

Tipo de necrosis

A

Necrosis grasa: no es un patrón espeficico de muerte, áreas de destrucción de grasa, con liberación de lipasas pancreáticas hacia el peritoneo.

  • Macro: saponificación
  • Micro: limites de adipocitos
    necróticos en sombra con depósitos de calcio basolfilos rodeados por inflamación
  • Ej: pancreatitis aguda
    *urgencia medica
124
Q

Tipo de necrosis

A

Necrosis gangrenosa: no sigue un patrón especifico de muerte celular. Se aplica a las extremidades, principalmente en las inferiores, que perderan la irrigación y se necroso (coagulativa), entonces es una necrosis gangrenosa seca.
*si es una infección bacteriana es licuefactiva, o sea necrosis gangrenosa humeda

125
Q

Tipo necrosis

A

Necrosis fibrinoide: se encuentra en reacciones inmunes que ocurren en los vasos sanguíneos, registra cuando se depositan complejos Ag-Ac en las paredes vasculares. Los depósitos de estos inmunocomplejos junto con la fibrina (vasos), condiciona un aspecto amorfo y rosa brillante en la tinción H-E.

126
Q

Para un diabético, como se llaman las necrosis?

A

Gangrenosa seca, cuando es coagulativa
Gangrenos úmeda, cuando es licuefativa

3MED FB Robbins (36 decks)

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