Cell Injury Adaptive Response Flashcards

1
Q

Symptoms

A

patient’s subjective observations/descriptions, usually not quantifiable

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2
Q

Signs

A

abnormalities on physical exam, usually quantifiable; what you detect on physical exam

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3
Q

Syndrome

A

cluster of related symptoms &/or signs typically due to a single cause in an individual patient

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4
Q

Etiology

A

the “cause” of a disease; overly simplistic to think that a disease can have one single cause;
example: measles-> several causes such as lack of immunizations, poverty, the disease itself, etc.

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5
Q

Pathogenesis

A

sequence of events by which the disease develops

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6
Q

Pathognomonic

A

a particular sign/abnormality is found only in one condition or disease; example: forme fruste- very mild variant of a more serious disease
Example: Gilbert’s disease

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7
Q

Incidence

A

number of new cases per unit time; usually expressed as “new cases per 100,000 people per year“

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8
Q

Prevalence

A

number of cases at any one time; usually expressed as “cases per 100,000 people”

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9
Q

Risk

A

how much your particular situation increases your chance of getting a disease compared with everyone else

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10
Q

Diagnosis

A

name given to the particular disease once identified

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11
Q

Prognosis

A

expected outcome for a particular case of a disease;

Influenced by diagnosis, the age & general health of the patient, available treatments.

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12
Q

Hypoxia- #1, prototype for cell injury

A

-Poor nutrition (lack of nutritious substrates); Cells respond in different ways
-Infectious agents: several mechanisms depending on agent; viruses multiple in host cell and cause cell to explode
-Immune injury (overly responds)
4-5 types, antibody- or T cell-mediated
-Chemical agents (poisons, toxins, too much water, too much salt); Noxious stuff or too much good stuff
-Physical agents: trauma, radiation, etc.

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13
Q

Ischemia (ischemic hypoxia)

A

Involves lack of arterial blood flow (arterial occlusion, venous occlusion); Pump failure
*Lack of oxygen due to a clot or blockage; shunts

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14
Q

Hypoxemia (hypoxic hypoxia)

A

Low oxygen in the blood

  • Failure to ventilate or perfuse the lungs
  • Failure of lungs to oxygenate blood
  • Inadequate RBC mass
  • Inability of hemoglobin to carry or release oxygen
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15
Q

Histotoxic hypoxia

A

the inability of cells to take up or use oxygen from the bloodstream, despite physiologically normal delivery of oxygen to such cells and tissues.
Examples: cyanide, carbon monoxide, and dinitrophenol

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16
Q

Different cells tolerate hypoxia differently. Which lasts longer between the brain and a leg?

A

A leg can last longer than the brain

17
Q

Lack of ___ stops oxidative phosphorylation/ETC, which results in the ____ failing.

A

O2, which results in the Na+/K+ ATPase failing

18
Q

What is an early sign of cell injury?

A
  • Na+ & H2O enter cell, causing acute cellular edema
  • cellular leakage
  • example: if liver enzymes are high after/during a vigorous workout, it can damage skeletal muscle cells
19
Q

Anaerobic metabolism leads to _______ & ______, which denatures proteins.

A

lactic acid accumulation and pH drop

20
Q

If the Ca+2 ATPase fails, then what occurs?

A
  • Ca+2 enters the cytoplasm from ECF and ER

- transition from reversible to irreversible injury

21
Q

Ca+2 entry is key step leading to ____ ____.

A

cell death

22
Q

What transpires after Ca+2 entry?

A

-Activates enzymes that damage membranes, proteins, and DNA.
-Opens pores in outer mitochondrial membrane (shuts down oxidative phosphorylation,
mitochondria release free radicals, and mitochondria release caspases that induce apoptosis)
-Rigor mortis due to Ca+2 -induced sarcomere shortening of muscle

23
Q

____ is the key link between depolarization and muscle contraction.

A

Calcium

24
Q

Free radical injury

A
  • Common mechanism of cell injury (radiation, poisons, normal metabolism)
  • Unpaired electron in outer (valence) orbital, typically O2 derivatives. Examples: Superoxide (O2-), hydroxyl (.OH), hydrogen peroxide (H2O2)
  • Having an unpaired electron can damage other molecules that try to pair to he lonely electron
  • Damage cell membranes, cause DNA mutations, aging?
  • Limited ability to dispose of free radicals (Superoxide dismutase & catalase; antioxidants-vitamin E, vitamin C)
25
Q

Examples of chemical injury

A

-Depends on nature of poison (acids/alkalis destroy membranes, formaldehyde crosslinks proteins & DNA)

Other poisons:

  • Cyanide-blocks ETC
  • Mushrooms (toadstools)-destroy ribosomes
  • Chemotherapy-damages DNA to disrupt cell replication (cancer cells)
  • Strychnine-motor neuron synapses
  • Carbon monoxide-replaces O2 on hemoglobin, blocks ETC
26
Q

What cell accumulations and deposits indicate cellular injury
or systemic disease?

A
  • Triglycerides (fatty change, steatosis)
  • Glycogen
  • Complex lipids or carbohydrates
  • Pigments
  • Calcium