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AFN Pathophysiology > Lesson 1.2 General concepts of pathophysiology > Flashcards

Lesson 1.2 General concepts of pathophysiology Flashcards

1
Q

Natural history

A

The progression from the initial change associated with the disease to recovery or death

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2
Q
  1. Lesion
  2. Sign
  3. Symptom
  4. Sequelae
  5. Complication
  6. Resolution
A
  1. Tissue abnormality caused by disease or trauma
  2. Objective finding, can be documented (provider can verify it)
  3. Subjective feeling or complaint (what the patient says happened)
  4. Conditions resulting from disease or trauma
  5. New problem resulting from the presence of a disease
  6. The disappearance of a disease and return to health
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3
Q

Inherited (familial)

A

Mutations result in abnormal protein production (cystic fibrosis)

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4
Q

Congenital

A

Prenatal (in utero) and neonatal (1st two months) disorders of development (atrial-septal defect)

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5
Q

Metabolic

A

Inherited or acquired deficiencies or abnormalities of metabolic systems or processes (phenylketonuria, diabetes)

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6
Q

Degenerative

A

Gradual breakdown of tissue and loss of function (osteoarthritis)

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7
Q

Neoplastic

A

Loss of growth control (cancer)

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8
Q

Immunologic

A

Caused by an over- or under-responsive immune system, against self antigens (rheumatoid arthritis) or environmental antigens (allergy)

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9
Q

Infectious

A

Microorganisms, parasites, or toxins they produce, resulting in tissue destruction (influenza)

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10
Q

Physical agent-induced

A

Trauma or toxicity (laceration or burn)

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11
Q

Nutritional

A

Deficiency and excess of nutrients (vitamin D deficiency, hypervitaminosis A)

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12
Q

Iatrogenic

A

Caused by the health care system (e.g., errors, therapy, complication, misdiagnosis)

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13
Q

Psychogenic

A

Originating in the mind (e.g., somatoform disorders)

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14
Q

Idiopathic

A

Cause is unknown (e.g., idiopathic scoliosis)

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15
Q

Factors affecting “Normal”

A 
Genetic variations (Gilbert’s syndrome)
Cultural variations (diet, literacy)
Age differences (body composition)
Gender differences (Hct, Hgb)
Environmental differences (altitude-Hct)
Diurnal variations (serum cortisol)
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16
Q

Adaptation helps cells adapt to ________. Injury occurs when cells are unable to ______ to stress
Death is the end stage of ________ cellular injury: Necrosis, Apoptosis, Autophagy

A

Stress
Adapt
irreversible

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17
Q
  1. If injurious agent is removed, cell reverts back to normal state, both morphologically (appearance) and functionally.
  2. Cell will not revert to normal, even when agent of injury is removed. Occurs in persistent or severe injury. Death of cell is inevitable.
A
  1. Reversible injury

2. Irreversible injury

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18
Q

An increase in the size of cells with resulting increase in organ size. Caused by increased production of intracellular components (myofilaments)

A

Hypertrophy

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19
Q

Results from an increased functional demand or specific hormonal stimulation. Enhances the function of the tissue

A

Physiologic hypertrophic

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20
Q

Results from an increased functional demand or specific hormonal stimulation but causes pathology. Generally results in altered function.

A

Pathologic hypertrophic

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21
Q

Reduction in cell (and organ) size by reduction in mass of cell components. Physiologic or pathologic causes. If prolonged, atrophy may progress to cell death by apoptosis or autophagy. Often related to cell trophism → activation of ubiquitin ligase → proteosomal degradation of proteins → prolonged leads to autophagy

A

Cellular adaptation atrophy

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22
Q 
Normal changes in cells and organs, generally related to typical developmental or hormonal changes: 
Embryo development
Decreased workload
Change in degree of endocrine
stimulation (post-menopausal 
vaginal atrophy)
Aging (reduced muscle mass)
A

Physiology atrophy

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23
Q

Changes in cells and organs related to some pathology:

  1. Nerve injury (carpal tunnel syndrome)
  2. Diminished blood supply (vascular dementia or senile atrophy)
  3. Inadequate nutrition (cachexia)
  4. Loss of endocrine stimulation (pituitary pathology)
A

Pathologic atrophy

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24
Q

Cellular adaptation hyperplasia

A

An increase in the number of cells in an organ or tissue, possibly resulting in increased volume.
Requires DNA synthesis, only occurs in cells capable of proliferating. Stimulated by growth factors, some cytokines and hormones. Physiologic or pathologic

25
Q

Physiologic hyperplasia

A

Often caused by hormonal effects (endometrial hyperplasia during the menstrual cycle)
Compensatory (wound healing)

26
Q

Pathologic hyperplasia

A

Increase in cellularity of tissues due to dysregulation of growth (benign prostatic hyperplasia)
May predispose to neoplasia

27
Q

Metaplasia

A

A reversible change in which one adult cell type is replaced by another adult cell type in order to function under stress or other pathologic stimulus . Usually caused by chronic irritation and inflammation.
May predispose to neoplasia

28
Q

Cellular adaptation Metaplasia

A

Metaplastic transformation of esophageal stratified squamous epithelium (left) to mature columnar epithelium (Barrett’s metaplasia).

29
Q

Deranged cell growth within a tissue, with cells of varied shape, size, appearance.
Loss of normal morphology → loss of normal function . Associated with genetic mutations. Metaplastic cells may become dysplastic with continued exposure to offending agent. Related to chronic irritation, inflammation, other pathologic stimuli (human papilloma virus). Considered premalignant

A

Chronic adaptation dysplasia

30
Q

cellular adaptation: Intracellular accumulations

A

Inadequate removalof a normal substance secondary to defects in packaging and transport (liver steatosis, atheroma, cholesterolosis)

31
Q

Cellular adaptation: Intracellular accumulations

A

Accumulation of an endogenous substance as a result of genetic or acquireddefects in its folding, packaging, transport, or secretion (ofα1-antitrypsin, kidney disease, Alzheimer’s, amyloidosis, hyalinosis)

32
Q

Cellular adaptation: Intracellular accumulations

A

Deposition and accumulation of anabnormal exogenous substancewhen the cell has neither the enzymatic machinery to degrade the substance nor the ability to transport it to other sites (lipofusin, pneumoconiosis, hemosiderosis)

33
Q

Cellular adaptation: Intracellular accumulations

A

Failure to degradea metabolite due to inherited enzyme deficiencies, typically lysosomal enzymes (lysosomal storage diseases)

34
Q

Cellular adaptation: Abnormal calcification of tissues due to

A

Dystrophyic calcification and Metastatic calcification

35
Q

Metastatic calcification

A

Deposition of calcium in otherwise normal tissue; almost always coincides with abnormal calcium levels

36
Q

Cause of metastatic calcification (four causes)

A
  1. Increased secretion of parathyroid hormone (PTH)
  2. Resorption of bone tissue,secondary to primary tumors of bone marrow (multiple myeloma, leukemia)
  3. Vitamin D–related disorders, including vitamin D intoxication, sarcoidosis
  4. Renal Failure
37
Q

Subsequent bone resorption (hyperparathyroidism due to parathyroid tumors and ectopic secretion of PTH-related protein by malignant tumors)

A

Increased secretion of parathyroid hormone (Metastatic calcification)

38
Q

Secondary to primary tumors of bone marrow (multiple myeloma, leukemia) or diffuse skeletal metastasis (breast cancer), accelerated bone turnover (Paget disease), or immobilization

A

Resorption bone tissue

39
Q

Vitamin D intoxication, sarcoidosis (macrophages activate a vitamin D precursor), and idiopathic hypercalcemia of infancy (Williams syndrome - abnormal sensitivity to vitamin D)

A

Vitamin D related disorders (Metastatic calcification)

40
Q

Causes retention of phosphate, leading to secondary hyperparathyroidism

A

Renal Failure (metastatic calcification)

41
Q

Deposition of calcium locally in dying/necrotic tissue with normal calcium levels and normal calcium homeostasis (seen in aging/damaged tissues, atheromas)

A

Dystrophic calcification

42
Q

Morphologic changes (reflect initial membrane damage)

A
  1. Cell swelling (water influx)
  2. Mitochondrial and ER swelling (water influx and protein accumulation)
  3. Nuclear and chromosomal changes (decreased pH, enzyme activation)
  4. Detachment of ribosomes from endoplasmic reticulum (ATP depletion, reduced protein synthesis)
  5. Cytoplasmic blebs (cytoskeleton disruption)
43
Q

What is the difference between “sign” and “symptom

A

Sign is an objective finding, can be documented (provider can verify it)
Symptom is a subjective feeling or complaint (what the patient says happened)

44
Q

What is the difference between “degenerative” disease and “neoplastic” disease?

A

Degenerative is the gradual breakdown of tissue and loss of function (osteoarthritis) vs
Neoplastic is the loss of growth control (cancer)

45
Q

List etiological factors of disease that affect the normal function of tissue

A

Inherited, congenital, metabolic, degenerative, neoplastic, immunologic, infectious, physical agent, nutritional, Iatrogenic, psychogenic, and idiopathic

46
Q

List 3 mechanisms of cellular death as a result of injurious stimuli

A

Necrosis
Apoptosis
autophagy

47
Q

Differentiate between “hypertrophy” and “hyperplasia”

A

Hypertrophy is an increase in the size of cells with resulting increase in organ size
caused by increased production of intracellular components (myofilaments).

Hyperplasia is an increase in the number of cells in an organ or tissue, possibly resulting in increased volume. Requires DNA synthesis, only occurs in cells capable of proliferating.

48
Q

What mechanism of cellular adaptation and injury is a result of a collection of iron within cells of the liver due to hemochromatosis?

A

Intracellular accumulations

49
Q

Name the response of the cell to injury that depends on 3 factors

A
  1. Length of time of exposure to the injurious agent
  2. Dose of injurious agent
  3. Type of cell and its ability to adapt: Determined by metabolic and mitotic status as well as where the tissue is located (ex: neurons less able to adapt to hypoxia than cardiomyocytes)
50
Q

__________Changes start immediately upon injury → morphologic changes occur after ________derangements

A

Biochemical

Biochemical

51
Q

Name the 2 phenomena characterize irreversibility of injury

A

Inability to reverse mitochondrial damage

Profound disturbance in membrane function

52
Q

Cell Injury cause by biochemical changes occur

A
  • -Mitochondria
  • -Calcium homeostasis
  • -Membranes: Endoplasmic Reticulum and Nucleus – DNA
53
Q

Cell injury in mitochondria

A

Injury via reduced O2 or increased [Ca]i and Reactive Oxygen species (ROS)
Results in: ATP depletion and loss of ATP-dependent cellular processes . Increased anaerobic glycolysis, generating lactic acid. ROS generation. Leakage of content from within the mitochondria. Reduced intracellular pH, causing denaturing of proteins and lipids. Injury may be significant enough to cause necrosis or apoptosis

54
Q

Free radicals produced by a single unpaired valence electrons on oxygen. Normal product of Ox-Phos and degraded by cells → excess leads to oxidative stress implicated in most pathologic process (cytotoxicity, cancer, aging, degenerative disease…)

A

Reactive Oxygen species (ROS)

55
Q

Injurious agents interfere with membrane-bound calcium ATPase → calcium enters and accumulate in cytosol and organelles. Calcium activates intracellular enzymes. Results in biochemical changes, water influx, organelle and cell swelling and loss of function, cell death

A

Cell injury Calcium homeostasis

56
Q
  1. ____________destroys membrane phospholipids
  2. ____________destroys cell proteins, e.g., cytoskeleton
  3. _____________results in ATP depletion
  4. _____________degrades nuclear DNA
A

(calcium activates intracellular enzymes)

  1. Phospholipases
  2. Proteases
  3. ATPases
  4. Endonucleases
57
Q

Cell injury membrane changes occurs via

A
  • Ischemia → ATP depletion → Ca influx → phospholipase activation
  • Direct damage by bacterial/viral toxins, lytic complement components, physical/chemical damage
58
Q

Leakage of intracellular proteins into the circulation ___________of cell injury/necrosis

A

specific marker

AFN Pathophysiology (3 decks)

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