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Pathophysiology Exam 2 > Lecture 12 > Flashcards

Lecture 12 Flashcards

1
Q

Dystrophic Calcification

A

Deposition of Ca2+ salts in damaged/necrotic tissue (tissue injury or chronic inflammation)

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2
Q

Examples of where dystrophic calcification is seen

A

Chronic renal failure (impaired renal excretion of phosphate), deposits in eyes, heart, blood

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3
Q

Sequelae

A

Condition as consequence of previous disease or injury

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4
Q

Atrophy

A

decreased cell size

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5
Q

Hypertrophy

A

increased cell size

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6
Q

Hyperplasia

A

increased cell number

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7
Q

Metaplasia

A

conversion of one cell type to another

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8
Q

Dysplasia

A

Disorderly growth

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9
Q

Anoxia

A

Complete absence of oxygen in tissues

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10
Q

Ischemia

A

decreased blood flow to tissue

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11
Q

What are the effects of anoxia on ATP synthesis and the ATP-dependent Na+/K+ pump?

A

Anoxia -> decrease ATP production (because of decreased oxidative phosphorylation) -> decrease of Na+ pump -> increased influx of Ca2+, water, Na+ -> increased efflux of K+ -> organelle and cell swelling, loss of microvilli

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12
Q

Looking at specifically mitochondrial swelling because of anoxia, what is a secondary effect?

A

further decreased ATP production -> anaerobic glycolysis -> increased lactic acid production -> more acidic pH -> clumping of nuclear chromatin

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13
Q

Alpha1- Antitrypsin (AAT)

A
  • Inhibitor of proteases normally released from neutrophils at sites of inflammation
  • produced in liver
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14
Q

Alpha1- Antitrypsin (AAT) Deficiency

A
  • Autosomal recessive disorder involving SERPINA1 gene
  • Impairs secretion of AAT from hepatocytes to serum
  • Three alleles (M, S, Z) inherited codominantly: allows for several forms and degrees of deficiency
  • Symptoms: liver disease (cirrhosis), lung disease in adults
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15
Q

Sequelae of AAT Deficiency

A

Emphysema

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16
Q

Emphysema

A
  • Decreased AAT levels = walls of respiratory bronchioles, alveolar ducts, alveoli destroyed by elastases and other proteases
  • Elastase (because AAT cannot inhibit it) causes destruction of elastic fibers
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17
Q

Elastase

A

Proteolytic enzyme that breaks down elastin (produced by neutrophils)

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18
Q

How does cigarette smoking cause emphysema without an AAT deficiency?

A

Induces alveolar macrophages to secrete proteases and chemoattractants to recruit neutrophils (which then release elastase and bombard normal AAT)

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19
Q

Chemoattractants

A

Substrates that attract immune cells to site of inflammation/infection

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20
Q

Necrosis

A

Group of cell death (consequence of injury and inflammation)

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21
Q

Apoptosis

A
  • Single cell death; not always pathologic process, but sometimes needed for development and tissue remodeling
  • Cells must have the suicide gene
22
Q

Capsase

A

Cysteine proteases that play role in apoptosis

23
Q

What begins the process of apoptosis?

A

Capsase activation

24
Q

Pyroptosis

A

inflammatory form of cell death (triggered by microbial infections) that results in release of pathogen-associated molecular patterns (PAMPs)

25
Pathogen-Associated Molecular Patterns (PAMPs)
molecular patterns associated with pathogens recognized by immune system
26
Efferocytosis
Process of dying/dead cell (apoptotic/necrotic) cells removed by phagocytic cells
27
Explain the process of efferocytosis via the mitochondria
Mitochondria in resting macrophage interact with ER -> enables cell to isolate Ca2+ within the two organelles -> encounters dead cell -> mitochondria breaks up into smaller pieces (fission) -> mitochondria and ER no longer intact -> Ca2+ accumulates in fluid of cell -> macrophage degrades dead cell
28
High Burden Efferocytosis
Process by which apoptotic cells are cleared by a single macrophage in a short period of time (prevents tissue from dying and developing inflammation)
29
Defects caused by high-burden efferocytosis
Autoimmune disease, chronic lung disease, neurodegenerative disease
30
Coagulative Necrosis
Ischemic cell injury causes loss of plasma membranes ability to maintain electrochemical gradients -> influx of Ca2+, dysfunction of mitochondria, degradation of plasma membrane and nuclear structures
31
Liquefactive Necrosis
dead cells have acidic pH which activates lysosomal enzymes (causes liquefaction)
32
What happens in liquefaction occurs too quickly?
Abscess/ cyst formation
33
Fat Necrosis
death of adipose tissue (results from trauma or pancreatitis)
34
Caseous Necrosis
Tuberculosis
35
Gangrene
cell death involving a large area of tissue regardless of cause
36
Dry Gangrene
form of coagulative necrosis characterized by blackened, dry, wrinkled tissue; separate from adjacent healthy tissue
37
Wet Gangrene
Liquefactive necrosis (typically in internal organs)
37
What is a disorder that can exhibit secondary liquefaction?
Myocardial Infarcts (initially coagulative necrosis)
37
Gaseous Gangrene
Gangrene caused by bacterial infection that produces odor
37
Infarction
When a large area involved in ischemia and hypoxia
38
White Infarctions (Anemic Infarcts)
Affect solid organs; occlusions consist of platelets; organs become white/pale
39
Red Infarctions (Hemorrhagic Infarcts)
Occlusions consist of RBCs and fibrin strands (lungs)
40
Occlusion
blockage of blood vessel (causes ischemia and tissue damage)
41
Volvulus
- Ischemia induced cell injury - Segment of gut twists on its mesentery - Entire bowl becomes dilated, gangrenous, hemorrhagic because of complete vascularization of gut
42
What happens if ischemia occurs and cytosolic Ca2+ increases?
1. Protease activation -> Cytoskeletal damage and cell swelling -> Membrane damage 2. Phospholipase activation -> phospholipid loss and lipid breakdown products -> membrane damage
43
What happens if ischemia occurs and there is a decrease in ATP?
Decreased phospholipid reacylation and synthesis
44
What are the risks of reoxygenation of tissue?
1. Ischemia -> proteolysis (catabolism of ATP, GTP, nucleic acids) -> abundant purines produced (reperfusion) -> uric acid and activated oxygen radicals 2. Reperfusion -> restoration of blood flow -> toxic oxygen via accumulation of purines oxidized by xanthine oxidase -> uric acid
45
Proteolysis
breakdown of proteins into smaller peptides or amino acids
46
Normal cardiac tissue
- Branching and connected striated cardiocytes (intercalated disks) - Creatine Kinase (CK)
47
Myocardial Ischemia
- Occlusion of coronary artery - Lack intracellular striations - Nucleus pyknotic - Lactic dehydrogenase- 1 and creatine kinase MB released from dead cardiocytes in serum
48
Intracellular Striations
regularly spaced structures in cell
49
Lactic-Dehydrogenase-1
enzyme involved in conversion of lactate to pyruvate

Pathophysiology Exam 2 (8 decks)

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