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Pathophysiology > Cell Injury / Adaptive Response - exam 1 > Flashcards

Cell Injury / Adaptive Response - exam 1 Flashcards

1
Q

Syndrome

A

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

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2
Q

Pathogenesis

A

sequence of events by which the disease develops

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3
Q

Pathognomonic

A

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

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4
Q

Forme fruste

A

very mild variant of a more serious disease

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5
Q

Incidence

A

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

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6
Q

Prevalence

A

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

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7
Q

What hurts a cell?

A
  • hypoxia: #1 cause
  • poor nutrition
  • infections agents
  • immune injury
  • chemical agents
  • physical agents
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8
Q

Hypoxia

A
  • 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
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9
Q

Ischemia

A
  • also called ischemic hypoxia
  • lack of arterial blood flow (occlusions)
  • pump failure
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10
Q

Hypoxemia

A

-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

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11
Q

Failure of oxidative phosphorylation

A
  • also called histotonix hypoxia
  • cells are not using O2 properly
  • ex: cyanide, carbon monoxide, dinitrophenol
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12
Q

Hypoxic injury

A
  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
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13
Q

Free radical injury

A
  • 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
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14
Q

Chemical injury

A
  • 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)
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15
Q

Cellular accumulations and deposits

A
  • can be indicative of cell injury or systemic disease

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

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16
Q

Triglyceride accumulation

A
  • 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
17
Q

Glycogen accumulation

A
  • infusion of glucose (dextrose)

- glycogen storage disease (inborn errors of metabolism)

18
Q

Complex lipids or carbohydrate accumulation

A
  • storage disease (inborn errors of metabolism)

- ex: Gaucher’s, Tay-Sachs’

19
Q

Pigment accumulation

A
  • 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
20
Q

Calcium accumulation

A
  • 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
21
Q

Cell death

A

-types: coagulation, liquefactive, caseous, apoptosis

22
Q

Coagulation necrosis

A
  • 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
23
Q

Liquefaction necrosis

A
  • 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
24
Q

Caseous necrosis

A
  • 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
25
Q

Apoptosis

A
  • 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
26
Q

Gross necrosis

A
  • large area cell death
  • Dry gangrene: coagulation necrosis; usually no infection
  • Wet gangrene: liquefactive necrosis; foul-smelling and infected
27
Q

Living cell adaptions

A
  • 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
28
Q

Atrophy

A
  • 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
29
Q

Atrophy causes

A
  • loss of motor innervation
  • decreased blood supply
  • loss of hormonal stimulation
  • malnutrition
30
Q

Hypertrophy

A
  • increase in cell size not increase in number

- ex: skeletal muscle of strength athlete, breast size during pregnancy

31
Q

Hyperplasia

A
  • 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
32
Q

Hyperplasia causes

A
  • compensatory: growing back
  • hormonal stimulation
  • genetic mutations: risk for cancer
33
Q

Metaplasia

A
  • 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
34
Q

Dysplasia

A
  • 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)
35
Q

Anaplasia

A
  • confided to an epithelium (dysplasia) or invading (cancer)
  • when bizarre cells obtain blood supply a mass is formed
  • malignant
36
Q

Gaucher’s

A

glucocerebroside

37
Q

Tay-Sachs’

A

ganglioside

Pathophysiology (5 decks)

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