Cell Injury / Adaptive Response - exam 1

Question 1

Syndrome

Answer 1

cluster of related symptoms and/or signs typically due to a single cause in a patient

Question 2

Pathogenesis

Answer 2

sequence of events by which the disease develops

Question 3

Pathognomonic

Answer 3

a particular abnormality found only in one condition (“classic” for particular disease)

Question 4

Forme fruste

Answer 4

very mild variant of a more serious disease

Question 5

Incidence

Answer 5

number of new cases per unit of type (cases per 100,000 people per year)

Question 6

Prevalence

Answer 6

number of cases at any one time (cases per 100,000 people)

Question 7

What hurts a cell?

Answer 7

• hypoxia: #1 cause
• poor nutrition
• infections agents
• immune injury
• chemical agents
• physical agents

Question 8

Hypoxia

Answer 8

• 3 mechanisms: ischemia, hypoexmia, failure of oxidative phosphorylation
• Ischemia and hypoxemia can be fixed clinically
• can’t fix failure of oxidative phosphorylation as we can’t make cells use O2

Question 9

Ischemia

Answer 9

• also called ischemic hypoxia
• lack of arterial blood flow (occlusions)
• pump failure

Question 10

Hypoxemia

Answer 10

-also called hypoxic hypoxia
-low O2 in the blood
-failure to ventilate or perfuse lungs
-failure of lungs to oxygenate blood
-inadequate RBC mass
Inability of hemoglobin to carry/release O2
-pumps are vessels are fine, but the blood does not carry O2 properly

Question 11

Failure of oxidative phosphorylation

Answer 11

• also called histotonix hypoxia
• cells are not using O2 properly
• ex: cyanide, carbon monoxide, dinitrophenol

Question 12

Hypoxic injury

Answer 12

1. lack of O2 stops oxidative phosphorylation and electron transport chain; Na+/K+ ATPase fails causing Na+ to stay inside the cell
2. anaerobic metabolism leads to lactic acid accumulation and pH drop (due to Na+ staying inside the cell); proteins denatures; leakage of intercellular proteins
3. Ca+2 ATPase fails: Ca+2 enters cytoplasm from ECF and ER; irreversible at this point
4. Ca+2 entry is key step leading to cell death

Question 13

Free radical injury

Answer 13

• common mechanism of cell injury
• radicals are unpaired electrons in outer orbital
• damage cell membranes and causes DNA mutations when trying to pair unpaired electrons
• WBC use free radicals to kill invaders, but also hurts normal tissue
• There is limited ability to depose of free radicals

Question 14

Chemical injury

Answer 14

• depends on nature of poison: acid/alkalis destroy membranes, formaldehyde crosslinks proteins and DNA
• other poisons: cyanide (blocks electron transport chain); chemotherapy (damages DNA); carbon monoxide (replaces O2 on hemoglobin and blocks electron transport chain)

Question 15

Cellular accumulations and deposits

Answer 15

• can be indicative of cell injury or systemic disease

- 5 main types: triglycerides, glycogen, complex lipids or carbohydrates, pigments, calcium

Question 16

Triglyceride accumulation

Answer 16

• fatty change, steatosis
• involves liver or heart
• not injurious to cells, but marker for injury
• closely linked to heavy drinking, obesity/metabolic syndrome, malnutrition, outdated tetracycline, ileal bypass surgery
• is reversible if you abstain for a period of time

Question 17

Glycogen accumulation

Answer 17

• infusion of glucose (dextrose)

- glycogen storage disease (inborn errors of metabolism)

Question 18

Complex lipids or carbohydrate accumulation

Answer 18

• storage disease (inborn errors of metabolism)

- ex: Gaucher’s, Tay-Sachs’

Question 19

Pigment accumulation

Answer 19

• Carbon: smoke & soot, enguled by macrophages
• lipofuscin: remnants of interceullar membranes damaged by free radicals (never go away); indicator of oxidative stress; seen in hard working organs
• melanin: produced by melanocytes; two different forms (eumelanin and pheomelanin); hyperpigmentation
• Bilirubin: yellow-orange; product of hemoglobin breakdown; conjugated by liver and excreted in bile
• jaundice: too many red cells being broken down; liver can’t conjugate bilirubin fast enough; biliary obstruction

Question 20

Calcium accumulation

Answer 20

• calcium phosphate, calcium hydroxide
• dystrophic calcification (wrong place) - can create masses
• normal calcification: pineal glands, airway cartilages, mitral valve annulus, aortic valve sinuses
• abnormal calcification: breast cancer, caseous necrosis of TB, surgical scars, pancreatic necrosis, retained abortions
• metastatic calcification: occur in abnormal places

Question 21

Cell death

Answer 21

-types: coagulation, liquefactive, caseous, apoptosis

Question 22

Coagulation necrosis

Answer 22

• usually due to ischemic hypoxia or free radical injury (exception in the brain)
• death of groups of cells
• DNA gets destroyed, but the cell itself stays intact
• dead cells produce acute inflammatory response
• may be replaced by scar, destroyed, walled-off, infected, or even healed

Question 23

Liquefaction necrosis

Answer 23

• usually due to bacterial infections, poisons, or ischemic hypoxia in CNS
• death of groups of cells
• results from hydrolysis via lysosomal or WBC enzymes “pus”
• cells are completely gone or just a gross gelatinous mass
• no inflammatory process

Question 24

Caseous necrosis

Answer 24

• also called saponificaiton
• usually due to immune injury in response to certain infections (TB, fungus)
• death of groups of cells
• is less common depending on the pt population
• crumbled, gross-pale, cheesy
• cells are interrupted and nucleus disappears, but they are not completely gone

Question 25

Apoptosis

Answer 25

- programmed cell death - two main triggers: mitochondrial damage, death receptors - usually due to immune response or in response to cellular damage - single cell death - cell membrane remain intact - no inflammatory response - remains are phagocytized by macrophages

Question 26

Gross necrosis

Answer 26

- large area cell death - Dry gangrene: coagulation necrosis; usually no infection - Wet gangrene: liquefactive necrosis; foul-smelling and infected

Question 27

Living cell adaptions

Answer 27

- changed in response to stress, injury, or lack of normal stimulation - these are our responses that try to mitigate our injury - 5 types: atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia

Question 28

Atrophy

Answer 28

- response to cell stress or lack of stress - decrease in cell size not cell number - generally reversible if stress is taken away (or added) - ex: loss of breast tissue after menopause, loss of muscle mass inside a cast - misnomer: involved in cell loss rather than decreased size

Question 29

Atrophy causes

Answer 29

- loss of motor innervation - decreased blood supply - loss of hormonal stimulation - malnutrition

Question 30

Hypertrophy

Answer 30

- increase in cell size not increase in number | - ex: skeletal muscle of strength athlete, breast size during pregnancy

Question 31

Hyperplasia

Answer 31

- increase in cell number - may be physiologic or pathologic - ex: female breast at puberty, t-cell response to infection - generally reversible with removal of stimulatory agent

Question 32

Hyperplasia causes

Answer 32

- compensatory: growing back - hormonal stimulation - genetic mutations: risk for cancer

Question 33

Metaplasia

Answer 33

- adaptive substitution of one cell type for another - theoretically reversible - often involves epithelium in response to a stimulus - ex:stratified squamous to columnar epithelium in esophagus of people with chronic reflux

Question 34

Dysplasia

Answer 34

- also called atypia or atypical hyperplasia - uses in reference to epithelium - loss of cell uniformity or orientation - resembles cancer cells, but not invasive yet - results from genetic mutations to create a growth advantage - precancerous - benign: will not invade or spread (usually)

Question 35

Anaplasia

Answer 35

- confided to an epithelium (dysplasia) or invading (cancer) - when bizarre cells obtain blood supply a mass is formed - malignant

Question 36

Gaucher's

Answer 36

glucocerebroside

Question 37

Tay-Sachs'

Answer 37

ganglioside