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Pathophysiology > Unit 1: Cellular Injury & Adaptive Responses > Flashcards

Unit 1: Cellular Injury & Adaptive Responses Flashcards

1
Q

Define pathognomonic

A

a particular abnormality is found only in one condition

Ex: bullseye rash is pathognomonic for lyme although it does not have to be present for lyme to exist

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2
Q

Define forme fruste

A

very mild variant of a serious disease

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3
Q

What is the prototype for cell injury?

A

Hypoxia

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4
Q

What is ischemia (ischemic hypoxia)?

A

lack of arterial blood flow (arterial occlusion, venous occlusion), heart failure

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5
Q

What is hypoxemia (hypoxic hypoxia)?

A
  • refers to oxygen content of the blood itself
  • failure to ventilate or perfuse the lungs
  • lack of oxygenated blood
  • inadequate HGB
  • HGB dysfunction
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6
Q

What is histotoxic hypoxia?

A
  • oxidative phosphorylation
  • from cyanide or dinirophenol that inhibits ETC
  • CO poisoning due to high affinity to HGB, decreasing the # of HGB to accept O2
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7
Q

What is the pathway for hypoxic injury?

A

Lack of O2 –> no cellular respiration –> NA+/K+ pump fails (no NA pumped out) –> as a result, H2O follows Na –> edema

Lack of O2 –> pyruvate becomes lactic acid –> decreases pH –> denatures protein –> Ca2+ ATPase FAILS –> build up of CA2+ into cell

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8
Q

What is the relationship between calcium build up and cell death?

A

Calcium build up as a result of hypoxic injury is the key step leading to cell death

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9
Q

What does the activation of phospholipases (from Ca buildup) do?

A

damages cell membranes

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10
Q

What does the activation of proteases (from Ca buildup) do?

A

cleaves intracellular proteins

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11
Q

What does the activation of endonucleases (from Ca buildup) do?

A

cleaves intracellular proteins

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12
Q

What happens to the mitochondrial membrane when Ca is built up?

A
  1. Shuts down oxidative phosphorylation
  2. Releases free radicals
  3. Releases caspases that induce apoptosis
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13
Q

What is the roll of caspase in cell death?

A

Apoptosis

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14
Q

What condition can Ca2+ lead to?

A

Rigor mortis due to induced sarcomere shortening

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15
Q

What produces free radicals?

A

radiation, poisons, normal metabolism

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16
Q

Why are free radicals dangerous?

A

unpaired electron in valence shell, making the atom very reactive, induce reactions in cell membranes, causing adjacent phospholipids to lock together, stiffening the membrane

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17
Q

What is the stable form of free radicals?

A

O2, OH, H2O2

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18
Q

What are 2 ways to dispose of free radicals?

A

Enzymes: superoxide dismutase & catalase
Antioxidants: donates electrons via vitamin E, C

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19
Q

How does cyanide damage cells?

A

blocks ETC

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20
Q

How do mushrooms (toadstools) damage cells?

A

destroys ribosomes, unable to synthesize proteins, thus unable to synthesize enzymes needed for processes

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21
Q

How does chemotherapy damage cells?

A

damages DNA

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22
Q

How does strychnine damage cells?

A

damages motor neuron synapses, spasming of muscles

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23
Q

How does carbon monoxide damage cells?

A

binds to HGB instead of O2, blocking ETC

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24
Q

What does fatty changes indicate?

A

cellulary injury or systemic disease

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25
Q

How does fatty changes occur? (6)

A
  1. heavy alcohol use
  2. Obesity
  3. Metabolic syndrome
  4. Malnutrition/hyperalimentation
  5. Outdated tetracycline
  6. Ileal bypass for weight reduction
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26
Q

What are the mechanisms of fatty changes (steatosis)?

A
  1. too much free fat coming to the liver
  2. too much fatty acid oxidation by the liver
  3. Excess esterification of fatty acid to triglycerides by the liver
  4. Too little apoprotein synthesis by the liver (not enough enzymes to digest fat)
  5. Failure of lipoprotein secretion by the liver (not enough transport protein to transport fat out of cell)
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27
Q

Is alcoholic steatohepatitis reversible?

A

Yes, through abstinence

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28
Q

What causes glycogen, complex lipids and carbohydrates accumulation?

A

errors in metabolism, genetic mutations causing lack of enzyme or enzyme function

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29
Q

What does Gaucher’s disease store?

A

glucocerebroside

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30
Q

What does Tay-Sach’s disease store?

A

ganglioside

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31
Q

What does Niemann-Pick’s disease store?

A

spingomyelin

32
Q

What does Hunter’s & Hurler’s disease store?

A

glycosaminoglycans or mucopolysaccharides

33
Q

What does Fabry’s disease store?

A

trihexoside

34
Q

What is melanin?

A
  • protects epidermal cells from generating free radicals when skin is exposed to UV light
  • generated from tyrosine
  • present in melanocytes and their tumors (melanomas)
35
Q

What are the 2 types of melanin and their function?

A

Eumelanin: protects from UV light
Pheomelanin: generates free radicals on UV exposure (redheads)

36
Q

Who makes no melanin?

A

albinos

37
Q

What hormone causes hyperpigmentation?

A

ACTH from the pituitary gland

38
Q

What causes hyperpigmentation other than ACTH increase?

A

Hemochromatosis: decreased breakdown of melanin

39
Q

What are common areas on the body that have hyperpigmentation?

A

extensor surfaces of elbows, creases of palms and digits, gingiva

40
Q

What does carbon deposits cause?

A
  • engulfed by macrophages
  • anthracosis, black lung disease
  • inert, ugly looking lungs
41
Q

What is lipofuscin?

A

Product of oxidation, causes free radical damage to cellular membrane. Causes wear and tear due to increased activity from accumulation

42
Q

What is bilirubin?

A

product of Hgb breakdown, yellow-orange, excreted in bile. Causes jaundice when accumulated.

43
Q

What causes jaundice? (3)

A
  1. excess breakdown of RBCs via hemolytic processes (sick, cell, thalassemias, pernicious anemia)
  2. Liver can’t conjugate bilirubin fast enough due to liver disease
  3. biliary obstructions: gallstones, pancreatic cancer
44
Q

What are the 4 reasons that liver can’t conjugate bilirubin fast enough?

A
  1. Liver disease
  2. Newborn physiologic jaundice of the newborn
  3. Breast feeding (first few weeks)
  4. Hereditary Defects (Gilbert’s non-disease, Crigler - Najjar)
45
Q

What are the normal instances of calcification? (4)

A
  1. Pineal gland (in brain)
  2. Airway cartilages
  3. Mitral valve annulus
  4. Aortic valve sinuses ( can lead to aortic stenosis, dystrophic calcification of sinuses of valve)
46
Q

What are abnormal instances of calcification? (5)

A
  1. Breast CA
  2. Caseous necrosis of TB
  3. Surgical scars
  4. Pancreatic necrosis (when enzymes do not get to stomach to digest food, it digests itself)
  5. Retained abortions (lithopedion”
47
Q

What occurs with metastatic calcification?

A

Indicator of a calcium or phosphorus metabolism dysfunction

-occurs with high Ca/phosphate level

48
Q

What areas have pH gradients? (3)

A
  1. Small airway walls
  2. Gastric fundus epithelium
  3. Renal tubular walls
49
Q

Define necrosis

A

gross (visible) & microscopic changes that indicate cell death

50
Q

What is coagulation necrosis?

A

Death of a group of cells, gross, soft, pale. Micro loss of nuclei but cytoplasm intact. Dead cells product acute inflammatory response, infiltration of neutrophils. May be replaced by scar, destroyed, walled off, infected or even heal.

51
Q

What is Liquefactive necrosis?

A

Usually due to bacterial infections or poisons, or ischemic hypoxia in CNS. Death of group of cells. Results from hydrolysis via lysosomal or WBC enzymes (pus). Gross- gelatinous mass or nothing.

52
Q

What is caseous or saponification necrosis?

A

In between coagulation and liquefactive. Usually due to immune injury in response to certain infections (TB, fungus). Death of group of cells. Crumbled, friable debris. Gross, pale, cheesy

53
Q

What is apoptosis?

A

Programmed cell death, usually due to immune response. Death of a single cell. Cell membrane remains intact, no leakage of cell contents. No inflammatory response. Remains phagocytized by macrophages.

54
Q

Examples of apoptosis (5)

A
  1. Embryologic remodeling of hands
  2. Breast shrinkage after lactation period
  3. Cells in outer layers of epidermis
  4. Neurons that don’t synapse
  5. Killing of virally infected cells
55
Q

What is gangrene?

A

Advanced and grossly visible necrosis.

56
Q

What is dry gangrene?

A

mostly coagulation necrosis, usually no infection

57
Q

What is wet gangrene?

A

mostly liquefactive, purulent appearing, foul-smelling and caused by infection

58
Q

What are the living cell adaptations?

A

How cells adapt to stresses, metabolic or lack of normal stimulation, mitigate injurious agent if effective. If ineffective, cell death. Triggered by reversible alterations in gene activity.

59
Q

Define atrophy

A

-Decrease in cell size, may result in decreased organ size. Typically reversible. Fewer organelles & decreased function, some may die.

60
Q

What causes atrophy? (4)

A
  1. Loss of motor innervation
  2. Decreased blood supply (low level ischemia)
  3. Loss of hormonal stimulation
  4. Malnutrition
61
Q

What are the 2 misnomers of atrophy?

A

Involve cell loss rather than decrease in size.

  1. Brains of heavy drinkers
  2. Shrinkage of testes due to steroid use.
62
Q

Define hypertrophy

A

Increases in cell size, thus may increase organ size. Cells have increased protein synthesis, increased organelles.

63
Q

What causes hypertrophy?

A

Increased workload or increased hormonal stimulation. Can by physiologic or pathologic

64
Q

What are examples of hypertrophy?

A
  1. Skeletal muscle of strength athlete
  2. Heart of obese person (athletes can also experience this but it is due to being an efficient pump, lower resting HR).
  3. Heart of HTN pt
  4. Smooth muscle of uterus in pregnancy
65
Q

What are misnomers of hypertrophy?

A
  1. Benign prostatic hypertrophy (due hyperplasia)

2. Calluses (due to hyperplasia)

66
Q

Define hyperplasia

A

Increase in cell number, may result in increased organ size. May be pathologic or physiologic. Generally reversible with removal of stimulatory agent except if caused by genetic mutations.

67
Q

What causes hyperplasia?

A
  1. Compensatory “growing back”
  2. Hormonal stimulation
  3. Genetic mutation : risk for cancer
68
Q

Define metaplasia

A

Change in growth. It is an adaptive substitution of one cell. Theoretically reversible. Often involves epithelium in response to a stimulus. If due to genetic mutation, not reversible.

69
Q

Examples of metaplasia

A
  1. Columnar to stratified squamous epithelium in gallbladder with stones
  2. Columnar to stratified squamous epithelium in cervix of women with HPV
  3. Stratified squamous to columnar epithelium in esophagus of people with chronic reflux (Barrett’s)
70
Q

What is Barrett’s disease?

A

When stratified squamous cells convert to columnar epithelium cells in the esophagus of people with GERD. Pre-malignant state.

71
Q

Define dysplasia?

A

Loss of cell uniformity and orientation. Resembles CA cells but not invasive. Results from genetic mutations that create a growth advantage.

72
Q

Define anaplasia

A

Advanced stage of dysplasia. Nuclear changes. Irreversible. Confined to an epithelium. Becomes malignant if neoplasm exhibits anaplasia.

73
Q

Define neoplasia

A

New growth. When bizarre cells obtain blood supply that forms a mass.

74
Q

Proto oncogenes

A

normal growth and differentiation genes

75
Q

Oncogenes

A

mutated proto oncogenes with potential to become cancerous.

Pathophysiology (5 decks)

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