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PBD I Exam I > Robbins Chapter 1 - Cell Responses > Flashcards

Robbins Chapter 1 - Cell Responses Flashcards

1
Q

What is hypertrophy?

A

Increase in the size of cells leading to an increase in the size of the organ

Note: Cells with the ability to divide may concurrently undergo hyperplasia

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2
Q

What are the mechanisms of stimulating hypertrophy (3)? Which processes seem to be physiologic and which seem to be pathologic?

A

Stimulate mechanical receptors, signaling of growth factors, or vasoactive amines

Mechanical sensors appear to be physiologic. Growth factors and vasoactive amines tend to be pathologic.

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3
Q

What are the biochemical pathways of hypertrophy and their nature (pathologic or physiologic)?

A

PI3K/Akt (Protein Kinase B) is related to physiologic hypertrophy

GPCR are associated with growth factors and therefore are associated with pathologic processes

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4
Q

Provide an example where hypertrophy is associated with the switch to a neonatal/fetal protein

A

Switch from alpha myosin heavy chain to beta myosin heavy chain in muscle hypertrophy

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5
Q

Provide an example of developmental genes being re-expressed in hypertrophy

A

Re-expression of ANF in cardiac hypertrophy

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6
Q

Give an example of orgenellar hypertrophy

A

Barbituates can cause hypertrophy of the sER in hepatocytes due to increased demand for cytochrome P450.

May result in decreased effectiveness of barbituates and alcohol. Also may observe increased production of ROS.

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7
Q

What is hyperplasia? What are two types of hyperplasia?

A

Increased number of cells in an organ or tissue.

Hormonal and Compensatory.

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8
Q

What is a specific feature of hyperplastic smooth muscle cells?

A

Hypertrophic vascular smooth muscle cells may exhibit polyploidy

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9
Q

What is atrophy?

A

Reduced size or number of cells

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10
Q

Give an example of physiologic atrophy

A

Regression of thyroglossal duct in embryonic development

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11
Q

What are the types of pathologic atrophy (6) and relevant examples?

A

Disuse - can result in osteoporosis if prolonged
Denervation
Diminished blood supply - Progressive artherosclerosis can result in brain and heart atrophy
Inadequate nutrition. Murasmus - protein-calorie malnutrition causing skeletal muscle to be consumed as energy. Kwashiorkor - Deficient in proteins; child still has fat and presents with systemic edema due to loss of oncotic pressure.
Loss of endocrine stimulation - menstruation as a result of loss of estrogen stimulation
Compression - Orbstruction of the ureter can cause hydronephritis and compression on the kidney

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12
Q

What is cachexia? What is the theorized mediator?

A

Marked muscle wasting. TNF due to it’s mobilization of nutritional sources and suppression of appetite

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13
Q

What is the general biochemical process responsible for atrophy?

A

Increased protein degradation and decreased protein production due to the ubiquitin-protease pathway.

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14
Q

What is brown atrophy?

A

Indicative of autophagy leading to lipofuschin granules. This is also referred to as aging pigment.

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15
Q

What is metaplasia and give 3 examples?

A

Reversible change in which one differentiated cell type is replaced with another. Result of extracellular signals altering the stem cells which give rise to the tissue.

Chronic irritation of the respiratory tract can cause the switch from columnar epithelium to stratified squamous. Results in decreased mucous production and loss of ciliary action.

Chronic irritation of endocervix will lead to squamous metaplasia.

Barrett Esophagus.

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16
Q

What are the general causes of cell injury (7)?

A

Oxygen deprivation, physical agents chemical agents, infectious agents, immunologic reactions, genetic derrangements, and nutritional imbalances.

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17
Q

What are the morphological changes witnessed in reversible cell injury (6)?

A

Cellular swelling, fatty changes, plasma membrane blebbing, mitochondrial swelling, ER swelling and detachment of proteosomes, nuclear alterations

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18
Q

What are the morphologic changes in necrosis (3)?

A

Increased eosinophilia - due to loss of cytoplasmic RNA (basophilic) and denaturation of cytoplasmic proteins (eosinophilic).

Myelin Figures - formed by the insertion of water between the lipid bilayer. Eventually phagocytosed or degraded, which is associated with saponification and calcification.

Nuclear Changes

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19
Q

What are the 3 types of nuclear changes?

A

Karyolysis - fading of basophilia of chromatin due to degradation by cellular endonucleases
Note: Nuclei will not be visualized

Pynknosis - condensation and shrinkage of the chromatin

Karyorrhexis - fragmentation of a pyknotic cell

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20
Q

Describe coagulative necrosis and gangrenous necrosis

A

Architecture of dead tissue is preserved and exhibits a firm texture. Commonly seen in ischemic injury, except in the brain.

Gangrenous necrosis is coagulative necrosis of the limb

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21
Q

Describe liquefactive necrosis and wet gangrene

A

Liquefactive necrosis presents with a liquid viscous mass of digested and dead cell. This manifestation is due to the infiltration of leukocytes. Typically seen in ischemic injury of the CNS and focal bacterial/fungal infections.

Wet gangrenes is coagulative necrosis of a limb with a superimposed bacterial infection.

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22
Q

Describe caseous necrosis

A

Foci of white, friable necrosis

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23
Q

Describe fat necrosis and a clinical example

A

Focal areas of fat destruction associated with fat saponification. In acute pancreatities lipase will leak into the abdominal cavity resulting in calcifications

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24
Q

Describe fibrinoid necrosis

A

Aggregation of immune complexes and fibrin within the walls of blood vessels

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25
Q

In what infections would gaseous gangrene occur?

A

Infection of coagulative necrosis with Clostridium welchi or perfinges

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26
Q

Describe depletion of ATP as a mechanism of cell injury

A

Inactivation of the Na-K ATPase will cause cellular swelling.
Anearobic processes will be activated, increasing lactic acid and inactivating enzymes due to low pH.
Failure of calcium pump and subsequent increase in intracellular calcium having widespread effects.
Detachment of ribosomes from the ER and misfolded proteins causing an unfolded protein response.

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27
Q

Describe mitochondrial damage as a mechanism of cell injury

A

Injurious stimuli for mitochondrial damage include ROS, increased Ca, and hypoxia. Damage causes formation of the mitochondrial permeability pore, which causes a loss of membrane permeability and also oxidative phosphorylation. Aditionally, cytochrome C is able to activate pro-apoptotic pathways in the cytosol.

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28
Q

What is the action of cyclosproine?

A

Binds cyclophillin D to inhibit formation of the mitochondrial permeability pore

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29
Q

Describe increased calcium influx as a mechanism of cell injury

A

Release of calcium from intracellular stores is casued by hypoxia. It will build up in the mitochondria and cause activation of cytosolic enzymes: proteinases, phospholipases, endonucleases, ATPases, and caspases

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30
Q

Describe accumulation of ROS as a mechanism of cell injury

A

Results in autocatalysis of lipid peroxidation leading to membrane damage. ds and ss DNA breaks. Damage to protein structure.

31
Q

What are the common radicals (3)?

A

Superoxide, hydrogen peroxide, hydroxyl ions

32
Q

How do transition metals participate in production of ROS?

A

Metals are able to donate and accept electrons. The fenton reaction describes the exchange of electrons from ferrous iron to hydrogen peroxide to form ferrric iron and hydroxyl ions. Iron must be reduced to take part in fenton reaction. Reduction is mediated by the free radical superoxide.

33
Q

What are mechanisms of ROS removal and related examples?

A

Antioxidants - vitamin A, vitamin E, ascorbic acid, and glutathione

Transition metal binding proteins

Enzymatic scavenging - superoxide dismutase, catalase, and glutathione

34
Q

Describe the functions of catalase, superoxide dismutase, and glutathione

A

catalase - decomposes hydrogen peroxide in peroxisomes

Superoxide dismutase - converts superoxide to hydrogen peroxide. Manganese SOD is found in mitochondria. Copper-Zinc SOD is found in the cytoplasm.

Glutathione - breaks down hydroxyl and hydrogen peroxide free radicals through interaction with NADP

35
Q

Describe the difference between hypoxia and ischemia?

A

Ischemia is the lack of blood supply to an area leading to depletion of oxygen along with important metabolic substrates. Hypoxia is the restriction of oxygen being supplied to an area. Ischemia tends to have a more rapid effect and severe effect on cells

36
Q

Describe the mechanism of HIF-1 in reducing ischemia

A

HIF-1 is a transcription factor induced by hypoxia. It increases the expression of VEGF, promotes anaerobic glycolysis, and activates survival pathways.

37
Q

How is transient induction of hypothermia successful in reducing ischemic injury?

A

Decreases the metabolic demands of cells causing reduced swelling, decreased production of ROS, and inhibition of the inflammatory response.

38
Q

Describe ischemic reperfusion injury

A

Reperfusion introduces a new supply of oxygen, lymphocytes, and immunoglobulins to enter an ischemic area. Oxygen can cause the further production of ROS. Lymphocytes can cause inflammatory injury. IgM tends to deposit on ischemic tissue leading to the activation of the complement cascade.

Note: Overall the effect is beneficial, but damage will be furthered

39
Q

Describe mercuric chloride poisoning

A

Mercury binds to sulfhydryl groups of membrane proteins causing increased permeability and inhibition of ion transport.

Note: most greatly effects the GI tract and the kidneys

40
Q

Describe damage caused by CCl4

A

Chemical used in dry cleaning which is converted to a toxic product by cytochrome P450. Blocks protein synthesis through damage to rER. Blocks synthesis of apoproteins in the liver leading to steatosis. Causes membrane permeability due to lipid peroxidation

41
Q

What are the morphologic changes of apoptosis?

A

Cell shrinkage, apoptotic bodies, and chromatin condensation at the periphery of the cell

42
Q

Describe caspases. Initiators and executioners.

A

Caspases are pro-enzyme which, when enzymatically cleaved, can activate the apoptotic pathway. Initiator caspases include -8 and -9. Executioner caspases include -3 and -6.

43
Q

Describe the difference in apoptosis and necrosis upon electrophoresis of DNA.

A

Apoptotic DNA breakdown is organized and will give a “DNA ladder” appearance. Necrosis is random degradation of DNA with a smeared appearance.

44
Q

What alteration in the plasma membrane occurs in order to increase recognition by phagocytic cells?

A

Phosphatidylserine will flip from inside the cell to outside

45
Q

Describe the intrinsic (mitochondrial) pathway of apoptosis

A

Permeability of the mitochondrial membrane is inhibited by anti-apoptotic proteins such as Bcl-2, Bcl-x, and Mcl-1. When stress occurs there is increased production of BH3 only proteins (bim, bid, and bad) which inhibit Bcl proteins and activate Bax and bak. Bax and bak will insert into the mitochondrial membrane causing the release of the cytochrome C. Cytochrome C will bind apaf-1 causing the formation of the apoptosome and activation of caspase-9.

46
Q

What is the action of DIABLO?

A

binds and inactivates inhibitors of apoptosis (IAPs)

47
Q

Describe the extrinsic pathway of apoptosis

A

When Fas binds to FasL it causes the aggregation of three Fas proteins which will attract FADD. FADD facilitates the aggregation and auto-activation of caspase-8.

Note: Fas can also activate Bid in some cells, connecting the two pathways

48
Q

What is the action of FLIP?

A

FLIP binds to pro-caspase-8 preventing its cleavage and subsequent activation. Viruses and healthy cells can utilize FLIP.

49
Q

What is the role of p53 in apoptosis?

A

p53 accumulates in cells which have undergone DNA damage. It causes cell cycle arrest and production of BH3-only proteins –> apoptosis.

Note: this is the most common mutation in cancer

50
Q

What is the unfolded protein response?

A

Accumulation of unfolded proteins causes the upregulation of chaperone proteins, decreased translation, and enhanced proteosomal degradation.

51
Q

Describe steatosis and some possible causes (4).

A

Steatosis is the accumulation of triglycerides within parenchymal cells of the liver. Can also occur in the heart, muscles, and kidneys.

Caused by alcohol, CCL4, hypoxia, or starvation

52
Q

What morphologic changes would be observed in steatosis?

A

Clear vacoules within parenchymal cells. Fat will appear red with sudan IV or oil red-o stains.

53
Q

What causes the tigered effect in myocardium?

A

Fat deposition in response to prolonged mild hypoxia.

54
Q

What is cholesterolosis?

A

Focal accumulations of cholesterool laden macrophages within the lamina propria of the gall bladder

55
Q

What is a xanthoma?

A

cluster of foamy cells within the subepithelial connective tissue

56
Q

What is atherosclerosis?

A

Foam cells formed from macrophages and smooth muscle cells in vascular intima becoming burdened with cholesterol

57
Q

What are reabsorption protein droplet caused by?

A

Increased protein leakage at the glomerular membrane leading to reaborption into vesicles at the proximal tubule. These are called hyaline droplets.

Note: will disappear if proteinuria is addressed.

58
Q

Describe alpha1- antitrypsin mutations.

A

The defective mutation of antitrypsin has the genotype zz and the protein is referred to as antitrypsin-z. This causes accumulation of the misfolded protein in hepatocytes leading to hepatic fibrosis due to necrosis of cells. The effective protein is no longer circulating in the blood where it inhibits the action of elastase –> emphysema.

59
Q

What is hyaline change and what is alcoholic hyaline?

A

An accummulation of a substance within cells or extracellularly which appears glassy and pink upon H&E. Alcholic hyaline occurs in hepatocytes and is associated with keratin filaments. Extracellular hyaline can occur through the extravasation of plasma proteins in hypertension or diabetes mellitus

60
Q

Which two stains are used to detect glycogen and what color presents?

A

PAS and carmine stains will give a red to violet color.

61
Q

Describe the manifestations of coal worker’s pneumoconosis.

A

Inhaled carbon particles are absorbed by lung macrophages. This leads to blackening of the lungs and the tracheobronchial lymph nodes.

62
Q

What is lipofuscin? What process is it a sign of? What is the color of the pigment? In what situations doe it typically present?

A

Lipofuscin is an insoluble pigment composed of lipids and phospholipids complexed with proteins.
This is a sign of ROS production due to lipid peroxidation.
The pigment of lipofuscin is brown-yellow and granular.
Appears in the liver and heart of aging patients. Also in severely malnourished patients and cancer cachexia.

63
Q

What are the two black pigments that present in the body? Describe ochronosis?

A

Melanin and hemogentistic acid are both responsible for black pigments. Melanin is the only one relevant for testing. Hemogentistic acid occurs in alkaptonuria. Ochronosis is the deposition of melanin in skin, cartilage, and connective tissue.

64
Q

What is hemosiderin? What stain is used to detect it? Where can this commonly be found?

A

Hemosiderin is a golden, yellow-brown pigment indicating the presence of ferritin, a complex of apoferritin and iron. This can be detected with prussian blue stain. Can be found in location of RBC breakdown: hemorrhage, liver, spleen, and bone marrow.

65
Q

What is hemosiderosis? What are it’s general causes (3)? Does it cause damage to parenchymal cells?

A

Systemic overload of iron and it’s deposition. Can be caused by hemolytic anemia or increased iron intake, including repeated blood transfusions. It does not typically cause damage to parenchymal cells.

66
Q

What sequellae result from hemochromatosis (3)?

A

Liver fibrosis, heart failure, and diabetes mellitus

67
Q

What is dystrophic calcification?

A

calcification of necrotic tissues which appears as fine white clumps

68
Q

How does calcium appear on an H&E stain?

A

basophillic (purple/dark-pink)

69
Q

What is heterotopic bone and what are psammoma bodies?

A

Heterotopic bone can form at the center of calcifications. Once these calcification acquire layers they become psammoma bodies.

Note: psammoma bodies are common in papillary cancers (thyroid)

70
Q

Describe the mechanism behind continues calcium deposition in necrosis.

A

Membrane damage causes the sequestration of calcium in vesicles. Calcium ions then bind to the phosphate groups of the membrane lipids. Phosphatases will also expose phosphate groups which can interact with calcium ions. The net effect is the creation of a mineral matrix to which further deposition can occur.

71
Q

What is metastatic caclfication?

A

Deposition of calcium in normal tissues

72
Q

Metastatic calcification is typically a result of hypercalcemia. What are four general causes of hypercalcemia?

A

Increased secretion of PTH
Destruction of bone marrow - Due to a primary (myelome) or secondary (breast) tumor of the bone marrow, increased turnover (Paget), or immobilization
Vitamin D disorder
Renal failure causing retention of phosphates and secondary hyperparathyroidism

73
Q

Where does metastatic calcification typically occur?

A

Predominately in the gastric mucosa, kidneys, lungs, systemic arteries and pulmonary veins. This is because these tissues present alkaline environments by secreting acids.

PBD I Exam I (3 decks)

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