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Pathology 1 > Introduction to Pathology > Flashcards

Introduction to Pathology Flashcards

0
Q

4 Aspects of Disease Process (4 Components of the study of Pathology)

A
  1. Etiology= Cause, target for therapeutics
  2. Development= Pathogenesis, steps for disease to occur
  3. Lesions= Molecular and morphologic changes
  4. Clinical Manifestations= Functional Components, Why does this matter?
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1
Q

Pathology

A

The study of disease (NOT the study of lesions)

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2
Q

3 Etiologic Components

A
  1. Genetic
  2. Acquired
  3. Multifactorial (Mostly)
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3
Q

Pathogenesis Examples

A

Molecular Revolution- Looking at details on molecular level (not always practical)
Mutant Genes

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4
Q

Lesion Components

A

Visible footprints of disease
Structural alterations=gross changes
Molecular analysis= molecular changes

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5
Q

Homeostasis Adaptations

A

Homeostasis= normal environment
Adaptations in response to a stimulus to achieve homeostasis are variable and reversible
1. Hypertrophy= increase cell size
2. Hyperplasia= increase cell number (+/- size)
3. Atrophy= shrink in size (ex. unable to use a limb-> muscle waste)
4. Metaplasia= changing of one tissue into another, usually in response to chronic irritation (usually epithelial to stratified squamous or connective tissue to bone); makes sensitive tissue more resistant

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6
Q

Cell Injury Outcomes

A
  1. Adaptation: Adapt to injury, not severe injuries
  2. Reversible Injury: Not severe injuries
  3. Cell Death: Necrosis, Apoptosis
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7
Q

Necrosis

A

Unplanned Death

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8
Q

Apoptosis

A

Programmed cell death (moderates immune system and embryologic development)

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9
Q

Intracellular Accumulation

A

Results of cell injuries:

Protein, lipids, carbohydrates, calcification

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10
Q

Hypertrophy

A

Increase Size
Can coexist with hyperplasia
For muscle- the stimulus is increased workload
Increases strength, work ability- cell still has normal proteins but have increased in number due to growing cell size
Some limited ability for cellular proliferation
Can result in cardiac failure in heart (adaptation leads to cell injury-> hypertrophic cardiac myopathy)
Mechanisms (Can be physiologic or pathologic):
-Increased production of cellular proteins (how cells grow), mechanical sensors, vasoactive agents, alteration of gene expression to more fetal types
-Physiologic- related to phosphoinositide 3 kinase/Akt
-Pathologic- related to G-protein-coupled receptors

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11
Q

Hyperplasia

A

Increase in number of cells
Can Occur with Hypertrophy (and usually does)
Occurs in response to a stimulus
Physiologic: hormonal-increases capacity of tissue (ex. lactation in response to prolactin) or compensatory- increases mass after
damage/partial resection (ex. liver regeneration= hypertrophic response)
Pathologic: Excess of hormones, process remains controlled (feedback mechanism in place-stimulus driven), distinct from neoplasia, some infectious agents (papilloma viruses), can provide environment for carcinogenesis (when controlled
process gets out of control)
Mechanisms: Factor driven proliferation (needs stimulus->maintains control); growth factors, hormones

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12
Q

Atrophy

A

Reduced size of an organ or tissue

Decrease in cell size and number

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13
Q

Physiologic Atrophy

A

Important in embryologic development (need things to develop fully)
Ex. Notocord (spinal cord), thyroglossal duct, uterine involution

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14
Q

Pathologic Atrophy

A
  1. Decreased workload (skeletal muscle)- can lead to apoptosis and irreversible loss
  2. Loss of innervation (skeletal muscle)- neurologic diseases (skeletal muscle depends on nerve stimulation)
  3. Diminished blood supply (senile brains, senile testes)-changes in arterial walls
  4. Inadequate nutrition (cachexia=muscle wasting)-waste fat stores first, then our protein (muscle)-> late stages of starvation
  5. Loss of Endocrine stimulation (castrated animals)-secondary sex glands diminished
  6. Pressure (from benign neoplasms)- expand and grow, compresses neighboring tissue (different from hyperplasia b/c still under control from neighboring tissue so no atrophy)
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15
Q

Cascade of Events of Atrophy

A
  1. Decrease in cell size
  2. Decrease in cells needs
  3. Decrease in organelles (to reduce metabolic needs)
  4. Decreases function for survival
  5. Potentially leads to apoptosis (cell gives up)
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16
Q

Mechanisms of Atrophy (Can lead to atrophy)

A
  1. Decreased protein synthesis (not enough put in)
  2. Increased protein degradation (take to much out at end)- proteasomes via ubiquitin-proteasome path
  3. Increase autophagy (autophagocytic vacuoles)- cell essentially feeding on itself, leads to product called lipofuscin granules, leading to brown atrophy/pigmentation
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17
Q

Metaplasia

A

Change one thing into another
Reversible change (one differentiated cell replaced by another differentiated cell type)
Ex. Columnar epithelium to stratified squamous; chronic inflammation fibrous tissue to bone
If persistent can lead to malignant transformation due to chronic stimulation (long term damage- run risk of some cells going out of control)
Reprogramming of stem cells

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18
Q

Reversible Cell Injury

A

If you remove the damaging stimulus you can reverse the injury
Reduced oxidative phosphorylation
Depletion of energy stores
Cell swelling-result of decreased ox phos and decreased energy, Na/K pump stops working so pressure inside results in swelling (vs hypertrophy where cells still have normal ion concentrations)
Changes in ion concentrations leads to water influx

19
Q

Cell Death

A

Irreversible damage to cell
2 Types: Necrosis and Apoptosis
*Be able to explain differences on exam

20
Q

Necrosis

A 
Unplanned, externally driven (cell membrane damage)
Damage to membrane results in lysosomes escape
ALWAYS PATHOLOGIC (never physiologic)
21
Q

Apoptosis

A

Planned, internally driven (triggered by something fragmenting DNA)
Secondary to DNA damage
Nuclear dissolution (nuceli dissappear)
Often PHYSIOLOGIC

22
Q

Hypoxia

A

Not enough oxygen (ex. being buried)
Can be atmospheric or due to ischemia
*Know difference between hypoxia and ischemia for test

23
Q

Ischemia

A

Reduced blood flow

Leads to local hypoxia (ex. strangling=ischemia 1st, then leads to hypoxia)

24
Q

Physical Cause of Hypoxia

A

Trauma, temperature, radiation, electric shock

25
Q

Chemical Agents/Drugs That Causes Hypoxia

A

Poisons (ex. poisonous plants)

Environmental pollutants

26
Q

Infectious Agents/Causes of Hypoxia

A

Virus, bacteria, fungi, protozoa, metazoan parasites
Classes are Important and leave different footprints (ex. virus does something different than bacteria and will leave a different patterned lesion to help us get to a proper diagnosis)

27
Q

Causes of Hypoxia

A

Physical agents, chemical agents/drugs, infectious agents, immunologic reactions (ex. autoimmune), genetic derangements, nutritional imbalances

28
Q

Hypoxia Cause- Genetic Derangements

A

Variation in genomes leading to differing responses to other agents
Ex. some get sick and some die with the same stimulus, resistance in some populations

29
Q

Morphology of Cell Injury

A 
Slower than histochemical change
Swelling of cell (cell is unable to maintain osmotic pressure)
Blebbing of plasma membrane (external change, small outpocket formed)
Detachment of ribosomes from endoplasmic reticulum (metabolic machinery)
Clumping of nuclear chromatin
Decreased ATP formation (all changes lead to decreased ATP)
Loss of membrane integrity
Defects in protein synthesis
Cytoskeletal damage (ex. microtubules)
DNA Damage
"Point of no return"- nebulous (cell is unable to keep going at some point)
Cell death (started externally so necrotic even though there is DNA damage)
30
Q

Reversible Injury Changes

A

Two Major Changes

  1. Cellular swelling from failure of energy- dependent ion pumps
  2. Fatty change lipid vacuoles in cytoplasm (usually liver, heart)
31
Q

Necrosis

A 
Unplanned cell death
Morphologic Hints
Increased Eosinophilia (cells stain red)
Myelin figures
Karyolysis- lyse nuclei
Pyknosis- condensation of nuclear material, turns basophilic (black)
Karyorrhexis- dissolution of nucleus
32
Q

6 Types of Necrosis

A
  1. Coagulative
  2. Liquefactive
  3. Gangrenous
  4. Caseous Necrosis
  5. Fat Necrosis
  6. Fibrinoid Necrosis
33
Q

Coagulative Necrosis

A

Architecture preserved

Leads to dull, firm tissues (dull tissue=necrotic)

34
Q

Liquefactive Necrosis

A

Digestion of dead cells (disappear)
Bacterial, some fungal infections
Inflammatory cell components and debris=pus
Typical of central nervous system because CNS doesn’t have much fibrous support to support dead tissue

35
Q

Gangrenous Necrosis

A

Usually a limb

Bacterial and vascular events

36
Q

Caseous Necrosis

A

Always involves macrophages
“Cheeselike” from macrophages and necrotic cells
Cottage cheese like lesions

37
Q

Fat Necrosis

A

Focal to locally extensive saponification of fat

Looks like a bar of ivory soap (white, opaque)

38
Q

Fibrinoid Necrosis

A

Deposition of antigen-antibody complexes in vessel walls

39
Q

Mechanisms of Cell Injury

A

Response depends on severity
Consequences depend on type, state, availability of cell
Different biochemical mechanisms lead to different consequences depending on which cellular component involved
Any injury can trigger multiple interconnected mechanisms

40
Q

Depletion of ATP (mechanisms)

A

Reduced oxygen
Reduced nutrients
Mitochondrial damage

41
Q

Depletion of ATP (consequences)

A
  1. Leads to decreased activity of sodium pump in plasma membrane
  2. Glycogen depleted/lactic acid builds up (increased acidity)
  3. Failure of calcium pump leads to influx of calcium (failure of metabolism leads to failure of pumps)
  4. Reduced protein synthesis
  5. Proteins misfold/unfold
  6. At some level the mitochondrial and lysosomal membranes fail
  7. Necrosis
42
Q

Mitochondrial Damage

A

Opening of mitochondrial permeability transition pore

Release of proteins that activate apoptotic pathways

43
Q

Influx of Calcium

A

Influx of calcium also opens mitochondrial permeability transition pore
Calcium activates enzymes:
-phospholipases=membranes
-proteases=membranes and cytosol
-endonuclease=nucleic acid breakdown
-ATPases=contribute to decreased energy
Calcium directly activates caspases leading to apoptosis

44
Q

Oxidative (free radical) Stress

A

Forms from: normal metabolism (removed rapidly in normal metabolism), radiant energy, inflammation, enzymatic metabolism of exogenous chemicals/drugs, transition metals (copper, iron), nitric oxide
Free radicals= Unstable

45
Q

Free Radical Removal

A

Antioxidants (iron and copper)

Enzymes- catalaze, superoxide dismutase, glutathione peroxidase

46
Q

Free Radical Damage

A

Leads to a chain reaction of damage
Lipids in membranes
Proteins (enzymes, structure)
Nucleic Acids (mutations)

Pathology 1 (2 decks)

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