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Pathology 1 > chapter 2 > Flashcards

chapter 2 Flashcards

1
Q

Cell injury =
how can they die?
EX:

A

anything that disrupts cell structures/ deprives cell of o2 and nutrients..
reverses
irrevereses if this cells die
ex: ischemia-hypoxia, during MI lack of 02 injures myocard cells

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2
Q

Cell adaption =

A

reversible structural/ functional response to physiologic (normal) and pathologic (adverse) conditions. and still remain in a steady state.

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3
Q

Cell injury/ adaption are the same how?

A

Both are reversible.

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4
Q

Atrophy is?
physiologic(normal) happens?
Pathologic(adverse) happens?
3 FUCKING EXAMPLES

A 
= decrease in size/ work
= happens w. EARLY development.
(THYMUS PUBERTY)
= happens w. DECREASE in workload.
(- UBIQUIT BY MALNUTRITION
- PROTEIN DEGEN IN PROTEASOMS
- PROTEIN SYN DECREASE
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5
Q

Hypertrophy is?
Physiologic(normal) happens?EX?
Pathologic(adverse) happens?EX?

A

= increase in size/ work demand or hormones.
= strength training (PREG HORMONE INDUCED UTERINE, MECH: STRENGTH, TROPIC: GROWTH, VASOACTIVE)
= hemodynamic overloads (HYPERTENSION = HEART DYSFUNCTIONS)

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6
Q

Hyperplasia is?

```
Physiologic(normal) happens?(2
EX:(2))
Pathologic(adverse) happens?
(1)
(EX(1))
~~~

A

= increase in cell #
= 1. Compensatory: allows organs to regenerate normal process.
(EX: LIVER REMOVAL, HYPERPLSIA OF LIVER COMPENSATES FOR LOSS.
- WOUND HEALING INFLAM. PROCESS)
2. Hormonal: replaces lost tissue/ supports new growth.
EX:ENDOMETRIUM;INCREASE ESTRO VS PROGESTRO
= Excessive hormonal/ growth factor stimulation. Produces an abnormal proliferation of normal cells.

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7
Q

Dysplasia is?

PRECURER OF? UNLESS?

A
  • abnormal changes in size, shape, organization of cells
    it’s not a true cell adaptation.
  • AKA atypical hyperplasia (atypical increase in cell number)
    PRECURCES OF CANCER, UNLESS EFFECTS BASEMENT THEN CANCER(NEOPLASM).
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8
Q 
Metaplasia is?
Involved in?
EX: (2)
1. 
2. SOMETHING DAMAGES SOMETHING
A
  • reversible replacement of 1 mature cell type by another less differentiated mature cell.
    involved in: tissue repair, damage, regenerating.
    EX:
    SMOKING; CILLIATED COLUMNAR -> SQUAMOUS.
    GASTRIC REFLUX DAMAGES SQUAMOUS
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9
Q

The conditions that allow cellular adaption to occur?

  • ?
  • 4 types?
A
  • The adaptation may be physiologic (normal) or pathologic (abnormal).
  • Four types:
    atrophy, hypertrophy, hyperplasia, metaplasia.
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10
Q

Ischemia-hypoxia =
Def?
Ex?

A
  • when you have ischemic aka lack of bld flow you have hypoxia aka lack of O2.
  • EX: Ischemia aka low blood flow; atherosclerosis(plaque build up in arteries) and thrombosis(attacks plaque in artery in heat) AKA clot formation, no blood flow aka ischemia
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11
Q

ischemia-reperfusion=

  • Def:
  • ischemia-reperfusion Injury Due To?
  • More?
  • what causes damage where?
  • overload of what?
  • opens what?
  • whats escaping?
  • whats activating?
A
  • Blood flow and o2 restores.
  • More oxidative stress
  • (ROS) that cause membrane damage and mitochondrial Ca+ overload.
  • Opens mitochondrial permeability transition pore with ATP escaping and apoptosis activating,
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12
Q

ischemia-reperfusion is impt but come with?

A

their own injuries.

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13
Q

Ischemia-reperfusion types of injury in?

6

A
  1. myocardial,
  2. hepatic,
  3. intestinal,
  4. cerebral,
  5. renal,
  6. stroke
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14
Q

Free radicals are?

A

SINGLE unpaired electron outer orbits,
making it capable of inducing injury,
initiating chain rxn.

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15
Q

ROS are?

A

chemically reactive molecules formed are :natural oxidant species in enzymes/organelle

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16
Q

ROS largest source is?

A

mitochondrial oxidative phosphorylation..(MITO IS THE LARGEST SOURSE

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17
Q

Explain in detail how ROS’s largest source

A

Mito oxidative phosphorylation:
-o2 reduced to water in oxidative phosphorylation.
- So because of electron leakage.
- o2 creates REGENERATIVE ROS like hydrogen peroxide.
so a bunch of ROS in just regular ass mito.

18
Q

Perioxisomes generate ROS how?

A
  • metabolizes long fatty acids
  • ER stressed
  • lots proteins produced
  • lots of protein folds
  • leads to ROS
19
Q

Enzyme systems that can generate ROS:

A
  1. cyclooxygenase system
  2. cytochrome P450,
  3. nitric oxide synthase systems.
20
Q

Enzyme systems that can generate ROS:

nitric oxide synthase EXPLAINED??

A

Catalyzes the synthesis of nitric oxide FROM l-arginine

-Its a powerful vasodilator increasing blood flow to organs in process called flow-mediated vasodilation

21
Q

Main Roles of ROS in Cell Injury?

A
  1. CAN produce in that reperfusion injury.
  2. Free radicals can be removed
  3. accumulate in cells either because of insufficient removal or excess production and lead to cellular injuries
22
Q

Identify Cellular accumulations of cellular injury?( things that can go wrong in cell that can cause cell injury)
(8) list and describe

A
  1. water accum =
    Loss of ATP production/ Na+/K+ pump = swell.
2. Lipid accum =
fatty liver (alcoholism, obesity, type2 diabetic)
  1. Glycogen (carbs)accum =
    a lot of vacuoles form in cytoplasm/ Glycogen storage diseases (RARE)
  2. Proteins accum = renal convoluted tubule of the nephron and in the antibody-forming-> B lymphocytes.
  3. Pigments: Melanin, hemoproteins (iron overload), bilirubin (jaundice)
  4. Ca+: calcium salts clump/ harden, interfering with normal cell structure/ function
  5. Urate: too much uric acid = gout.
23
Q

Identify SYSTEMIC accumulations of cellular injury?( how injuries effect systems)
(8)

A
  1. Fatigue/ malaise
  2. Fever
  3. Loss of well-being
  4. Appetite changes
  5. Increase heart rate
  6. increase wbc
  7. Pain
  8. Cell enzymes in extracellular fluid:
    LDH, CK, others elevated in blood = biochem markers of cellular injury.
24
Q

Coagulative necrosis
in?
does?
stuc change =

A
  • In: kidneys, heart, adrenal glands.
  • Does: Protein denaturation they’re unfolding losing 3d shape losing function.
    (So Changes protein albumin from gelatinous and transparent to firm and opaque)
  • Structural change = functional change.
25
Q

Liquefactive necrosis:
in?
Does?

A

In: Neurons, glial cells in brain
Does: Hydrolytic enzymes form liquid-filled cyst or form pus.

26
Q

Caseous necrosis:
what type of infection?
combination of?

A

is: Tuberculosis pulmonary infection

Combination of coagulative liquefactive necrosis, cheese looking substance that is walled off.

27
Q

Fat necrosis:
In?
What?

A

In: breast, pancreas, other ab structures
What: breaking apart fat is going to be done by lipase enzyme action.

28
Q

Gangrenous necrosis:
IS:?
Types:?
Severity level?

A

is: SEVERE arteriosclerosis in lower leg,
Types of:
Dry gangrene (usually coagulative),
Wet gangrene (liquefactive)
Gas gangrene (caused by bacterial infection causing bubble of gas to form)
- BAD, can lead to amputation

29
Q

Necrosis

A
  • Destruction of cell memb leaking content.
  • Autolysis, autodigestion
  • inflammation changes
30
Q

Apoptosis
def?
Types (2)?

A
  • Cellular fragmentation, fragments get cleaned up by phago. Engulfing and cleans up whole mess.
    -Types:
    Type 1- programmed cell death,
    Type 2- autophagic cell death
  • NO inflammatory changes
31
Q

Life span=
def?
years?

A

Human life span birth->death, max 80-100 yrs.

32
Q

Life expectancy =

A

average # yrs. of life remaining

33
Q

Extracellular aging =

  1. bind/link too?
  2. structural alterations?
  3. disease/stress associated with it?
A
  1. Collagen binding(reduce elasticity) / cross linking, Increase free radicals effects on cells.
  2. Structural alterations of fasica, tendons, ligaments, bones, joints.
  3. Peripheral vascular disease, vascular oxidative stress.
34
Q

Cellular aging

whats mainly happening (3)

A
  1. Atrophy-decrease functioning, loss of cells
  2. Capacity of DNA repair = reduced (increase risk for neoplasia)
  3. Cumulative damage of mito DNA, show in Diabetes, cancer, and heart failure.
35
Q

Tissue systemic aging

  • whats happening affecting what systems?
  • types of diseases?
A
  1. Progressive stiffness and rigidity in arterial, pulmonary, and musculoskeletal systems.
  2. Sarcopenia, osteopenia(low bone mass age), arthritis
36
Q

Frailty:
is?
Involves?
(7)

A

=Complex clinical syndrome

  1. Involves:
    - oxidative stress
    - dysregulation of inflammatory cytokines and hormones
    - malnutrition
    - physical inactivity
    - dynapenia
    - falls
    - disability.
37
Q

dynapenia which is loss of strength, this happens a lot faster then

A

loss of related bone mass

38
Q

Dynamic process/ something that can change. This happen in which Age related issue?

A

Frailty, because it depends on the old person and how well they rehabilitate

39
Q

Old person who falls increases?

A

Fragility( being easily broken)

40
Q

old person who doesn’t increase their balance or increase frailty this can lead to?

A

lose their function independence/ have to depend on people to care for them.

41
Q

SOMATIC DEATH=

  • is?
  • doesn’t involve
  • postmortem changes involved are? (5)
A

= death of ENTIRE person

  • death not from inflammation
    1. Cessation or resp/circulation
    2. Algor mortis: Reduced temp
    3. Livor mortis: Purple skin, due to gravity and pulling of blood in random regions of blood.
    4. Rigor mortis: Muscle stiffening
    5. Postmortem autolysis: Putrefactive(decay) changes associated with release of enzymes and lytic dissolutions

Pathology 1 (2 decks)

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