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NURS 1650 - Here We Go Again > Intro To Patho > Flashcards

Intro To Patho Flashcards

1
Q

Physiology

A

Study of functions of the body

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2
Q

Pathology

A

Study of structural/functional changes

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3
Q

Pathophysiology

A

Changes that occur with injury/disease

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4
Q

Disease

A

Interruption or disorder of body system(s)/organ structure(s)
- s/sx
- etiologic agents

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5
Q

Disorder

A

Abnormality of structure or function that has not been classified a “disease”
- commonly used interchangeably with “disease”
- applied to mental health conditions

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6
Q

Etiology

A

How a disease process is initiated or provoked
Ex: smoking is a cause of lung cancer

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7
Q

Idiopathic Etiology

A

Etiology is unknown

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8
Q

Iatrogenic Etiology

A

Unintentionally caused by a health care provider or institution
- medications, surgeries, other tx

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9
Q

Pathogenesis

A

The sequence of cellular/tissue/organs events that take place throughout the disease process
- evolve to show clinical manifestation

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10
Q

Clinical Manifestations

A

Evidences of disease
- Related to primary problem
OR
- The body’s attempt to compensate

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11
Q

Sign vs. Symptom

A

Sign
- Objective, observable; local vs. systemic

Symptom
- Subjective; complaints/concerns
- Comes from the patient

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12
Q

What are some examples of signs? (Clinical Manifestations)

A
  • High HR upon auscultation
  • ECG showing ST segment elevation
  • Low BP
  • Low BG level
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13
Q

What are some examples of symptoms? (Clinical Manifestations)

A
  • Patient says they feel chest pain
  • Patient feels their rapid heart rhythm and says “ I have palpitations”
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14
Q

Clinical Course

A

Evolution of the disease over time
- Acute vs. Chronic
- Exacerbation vs. Remission
- Prognosis —> likely outcome

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15
Q

Prognosis

A

Likely outcome of a disease
- part of its clinical course

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16
Q

Complication vs. Sequela(e)

A

Complication:
- disease or injury from the treatment of a preexisting disease/injury

Sequela(e):
- abnormal condition resulting from a disease or injury; neg consequence of a disease or injury

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17
Q

What are some examples of complications?

A
  • Pt. develops a C.diff infection after being hospitalized for a r hip fx
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18
Q

What are some examples of sequela(e)?

A
  • Patient w R hip fx develops a limp
  • Diabetic pt develops CKD and neuropathy
  • Diabetic pt has an episode of hypoglycemia
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19
Q

Epidemiology

A

Study of disease occurrence in populations

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20
Q

Incidence of a disease

A

Number of NEW cases in a population during a period of time

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21
Q

Prevalece

A

Measure of ALL the existing disease cases at a point in time

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22
Q

Morbidity

A

Diseased state

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23
Q

Mortality

A

Death

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24
Q

Homeostasis

A

Physiologic steady state; stable internal environment

Ideal set point —> pH, body temp

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25
Q

Allostasis

A

Dynamic process that maintains or re-establishes homeostasis or balance in response to stressors and changes in the environment

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26
Q

What does it mean that allostasis is an “adaptive process”?

A

The body’s original homeostatic set point may not always be possible achieve again, so the body sets a new homeostatic state
- example: COPD

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27
Q

What is a compensatory mechanism?

A

Physiologic changes initiated when the body is under stress

An attempt to maintain homeostasis

28
Q

What happens if a compensatory mechanism remains chronically “turned on”?

A

May turn into a vulnerability
- Can kill you
Meant to be SHORT-TERM RESPONSES to a disturbance (crucial for trauma/acute illnesses)

29
Q

Stress

A

Real or perceived threat to the balance of homeostasis
- biological vs. psychological
- acute vs. chronic

30
Q

What two systems are involved in the body’s neurohormonal response to stress?

A
  1. Sympathetic Nervous System (epinephrine, norepinephrine)
  2. Hypothalamic-Pituitary-Adrenal (HPA) Axis (cortisol)
31
Q

Why is an increase in blood glucose important during a significant stressor or trauma?

A

A rise in BG prepares the body to have enough energy to respond to the stressor or trauma

32
Q

What is allostatic overload?

A

Widespread, multi-system effects of chronic stress

33
Q

Hypertrophy

A

INCREASE in cell SIZE
- Triggered by mechanical and/or tropic signals

34
Q

Atrophy

A

DECREASE in cell SIZE
- associated w damage or disuse

35
Q

Hyperplasia

A

INCREASE in cell NUMBER
- incr. rate of cell division

36
Q

Metaplasia

A

Replacement of a well-differentiated, mature cell with another well-differentiated cell type
- new type usually able to withstand the stressor better

37
Q

Dysplasia

A

Deranged/disorderly cellular growth, with variations in size, shape and arrangements
- cells usually poorly differentiated
- may lead to cancer

38
Q

Example of metaplasia: Lung epithelium in smokers

A

Cell type changes from columnar cells to squamous cells that can better tolerate the repeated stress of the cigarette smoke

Eventually, though, cells may become dysplastic

39
Q

Ischemia and Infarction - cell injury

A

Decrease in ATP | Multiple downstream effects
- cell swelling, death
- inability to power key functions (NA/K pump)

40
Q

Direct chemical or radiation damage to DNA

A

Leakage of pro-apostolic proteins
- Decreased ATP
- cell death

41
Q

Increased calcium entry into cells - cell injury

A

Entry of Ca2+
- Increase mitochondrial permeability
- Activation of multiple cellular enzymes
- Enzymes degrade cell membranes, proteins, DNA
- Accumulation of intracelular Ca++ will cause cell death

42
Q

Generation of ROS (reactive oxygen species) - cell injury

A

Increase ROS
- Damage to lipids, proteins, DNA
- ROS are extremely damaging to cells

43
Q

Direct injury to cell membranes, lack of membrane integrity due to loss of ATP - cell injury

A

Damage to plasma membrane
- loss of cellular components
Damage to lysosomal membrane
- enzymatic digestion of cellular components
We can measure incr cellular components in pt.’s serum levels
- cells burst and release their contents into the bloodstream

44
Q

Injury from radiation, chemicals, toxins, pH changes, ROS - cell injury

A

Protein misfolding, DNA damage
- activation of pro-apoptosis proteins
- cell death
- misfolded proteins cannot carry out their functions

45
Q

Inflammation - cell injury

A

Critically important response to injury
Very common response
When chronic, can cause significant cellular/tissue injury
- fibrosis, scarring
- generation of ROS
- infiltration by WBCs, constant cell signaling leading to more inflammation

46
Q

Ischemia

A

Interruption of blood flow
- blood clot blocking a vessel
- blood vessel compression
Ischemia cell death most commonly affects the heart (myocardial infarction) or brain (stroke)
- can also occur in the periphery, kidneys, liver, gut, and other tissues

47
Q

What deficits lead to the manifestations of ischemia?

A

Hypoxia (lack of tissue oxygen)
- compromises ATP production
- leads profound energy deficit for cell functions
Lack of blood flow
- buildup of waste products that are not removed
- loss of constant energy supply to tissues in the form of glucose and other metabolic substrates

48
Q

What is the major downstream effect of ischemia?

A

Decreased ATP production
- leads to dysfunction of Na/K pump (disrupts ionic homeostasis and cell integrity)
- increases anaerobic glycolysis
- causes detachment of ribosomes from the endoplasmic reticulum

49
Q

How do pressure ulcers lead to ischemia?

A

Sustained pressure over a bony prominence leads to compression of blood vessels, ischemia, and ultimately tissue necrosis (death)
- immobile pts at higher risk of dev pressure ulcer
- also can be due to medical devices being left in place for an extended period of time

50
Q

What is infarction?

A

The permanent (irreversible) loss (death) of cells caused by an extended period of ischemia

51
Q

What are ROS - reactive oxygen species?

A
  • Radicals like hydroxyl radical (OH most reactive ROS of all)
    • contain an atom that has an unpaired electron in its outermost shell. Highly unstable configuration
  • Molecules Ike hydrogen peroxide H2O2
  • Ions like hypochlorite ion OCI-
  • Molecules which are both ion and radical like superoxide anion O2-
52
Q

What is Glutathione (GSH) and what does it do?

A

An important antioxidant and free radical scavenger
- converts hydrogen peroxide to 2 molecules of water
- Certain disease states may result from insufficient glutathione

53
Q

How are ROS neutralized?

A

Under normal, healthy conditions, ROS produced by mitochondria are neutralized by enzymes and peptides that convert them to non-toxic molecules
Example: Glutathione (GSH)

54
Q

Which organelles are more likely to initiate apoptosis?

A

Rough ER

Mitochondria

55
Q

REVIEW: Rough ER

A
  • Protein Synthesis
  • Quality control: misfolding detected —> STOP transcription and translation, incr production of chaperone proteins to fix problem
  • Can initiate apoptosis if unfolded proteins accumulate and cause excessive ER stress
56
Q

REVIEW: Smooth ER

A
  • Maintains homeostasis
  • Metabolic enzymes synthesize hormones and lipids, degrade drugs and other biochemicals
  • The ER membrane calcium ATPase maintains normal low levels of intracelular calcium
57
Q

REVIEW: Mitochondria

A
  • ATP production
  • Calcium storage (similar to smooth ER)
  • When damaged, causes outer mitochondrial membrane leak, proteins such as cytochrome C enter cytoplasm and signal for apoptotic pathway of cell death
58
Q

Cell injury that damages mitochondria or disrupts rough ER synthesis results in….

A

Cell apoptosis

59
Q

Apoptosis Purposes

A

Tightly regulated cell “death program” - normal process for the most part
- Balances cell division (otherwise the tissue would grow or shrink)
- Destroys damaged or infected cells (immune system)
- Protects against dev of cancer (cancer cells can evade apoptosis)

60
Q

Extrinsic signs for apoptosis

A

Coming from outside the cell
- absence of a “survival” signal from neighboring cells or ECM
- presence of a “death” signal involving activation of “death receptors” (TNF receptors)

61
Q

Intrinsic signs for apoptosis

A

Coming from inside the cells; initiated by mitochondrial or ER stress
- Cell injury
- Growth factor withdrawal
- DNA damage (by radiation, toxins, free radicals)
- Proteins misfolding (ER stress)

62
Q

How do intrinsic and extrinsic signals cause apoptosis?

A
  1. Activate enzymes called capases that begin a cascade
  2. Cell shrinks and condenses, cytoskeleton collapses, nuclear envelope disassembles, nuclear DNA breaks up into fragments
  3. Apoptotic bodies form
  4. Cell surface is changed, exposing molecules that cause dying cell to be rapidly phagocytosed (by a neighboring r macrophage cell, before leakage of cellular contents occurs)
63
Q

Necrosis results in:

A
  • Induces inflammation (w associated pain, swelling) that perpetuates tissue damage
  • May damage neighboring tissue
  • Membrane swelling, rupture, and cellular dissolution; with leakage of cellular contents
  • Messy, disorganized process
64
Q

Feature of necrosis and apoptosis

*Cell size

*Nucleus

*Cellular contents

*Adjacent information

*Physiologic or pathological role

A

On slide 81

Cell size
- Swell vs. shrink

Nucleus
- disrupted vs. intact

Cellular contents
- leak into blood stream vs. released in apoptotic bodies, phagocytosed

Adjacent information
- frequent (leading to swelling + pain) vs. none

Physiologic or pathological role
- invariably pathological vs. often physiologic

65
Q

Autophagy Purposes

A

“Self-eating” primarily through lysosomal mechanism - also tightly regulated process
- Removes and/or recycles protein aggregated and damaged organelles
-promotes cell survival and tissue homeostasis

Possibly triggered by cellular nutrient depletion/deprivation —> increases during fasting

Also seen in degenerative diseases

66
Q

What key substances cannot be produced by mitochondria in regions of ischemia or infarcted tissue?

A

ATP

Answer after lecture

67
Q

What key cellular functions are disrupted when ATP cannot be produced?

A

Na/K pump —> ionic imbalance
Build up of waste products
Increase in blood glucose

NURS 1650 - Here We Go Again (20 decks)

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