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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
Q

Pathogen-Associated Molecular Patterns (PAMPs)

A

molecular patterns associated with pathogens recognized by immune system

26
Q

Efferocytosis

A

Process of dying/dead cell (apoptotic/necrotic) cells removed by phagocytic cells

27
Q

Explain the process of efferocytosis via the mitochondria

A

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
Q

High Burden Efferocytosis

A

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
Q

Defects caused by high-burden efferocytosis

A

Autoimmune disease, chronic lung disease, neurodegenerative disease

30
Q

Coagulative Necrosis

A

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
Q

Liquefactive Necrosis

A

dead cells have acidic pH which activates lysosomal enzymes (causes liquefaction)

32
Q

What happens in liquefaction occurs too quickly?

A

Abscess/ cyst formation

33
Q

Fat Necrosis

A

death of adipose tissue (results from trauma or pancreatitis)

34
Q

Caseous Necrosis

A

Tuberculosis

35
Q

Gangrene

A

cell death involving a large area of tissue regardless of cause

36
Q

Dry Gangrene

A

form of coagulative necrosis characterized by blackened, dry, wrinkled tissue; separate from adjacent healthy tissue

37
Q

Wet Gangrene

A

Liquefactive necrosis (typically in internal organs)

37
Q

What is a disorder that can exhibit secondary liquefaction?

A

Myocardial Infarcts (initially coagulative necrosis)

37
Q

Gaseous Gangrene

A

Gangrene caused by bacterial infection that produces odor

37
Q

Infarction

A

When a large area involved in ischemia and hypoxia

38
Q

White Infarctions (Anemic Infarcts)

A

Affect solid organs; occlusions consist of platelets; organs become white/pale

39
Q

Red Infarctions (Hemorrhagic Infarcts)

A

Occlusions consist of RBCs and fibrin strands (lungs)

40
Q

Occlusion

A

blockage of blood vessel (causes ischemia and tissue damage)

41
Q

Volvulus

A
  • Ischemia induced cell injury
  • Segment of gut twists on its mesentery
  • Entire bowl becomes dilated, gangrenous, hemorrhagic because of complete vascularization of gut
42
Q

What happens if ischemia occurs and cytosolic Ca2+ increases?

A
  1. Protease activation -> Cytoskeletal damage and cell swelling -> Membrane damage
  2. Phospholipase activation -> phospholipid loss and lipid breakdown products -> membrane damage
43
Q

What happens if ischemia occurs and there is a decrease in ATP?

A

Decreased phospholipid reacylation and synthesis

44
Q

What are the risks of reoxygenation of tissue?

A
  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
Q

Proteolysis

A

breakdown of proteins into smaller peptides or amino acids

46
Q

Normal cardiac tissue

A
  • Branching and connected striated cardiocytes (intercalated disks)
  • Creatine Kinase (CK)
47
Q

Myocardial Ischemia

A
  • Occlusion of coronary artery
  • Lack intracellular striations
  • Nucleus pyknotic
  • Lactic dehydrogenase- 1 and creatine kinase MB released from dead cardiocytes in serum
48
Q

Intracellular Striations

A

regularly spaced structures in cell

49
Q

Lactic-Dehydrogenase-1

A

enzyme involved in conversion of lactate to pyruvate

Pathophysiology Exam 2 (8 decks)

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