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Pathophysiology > Chapter 1/2 > Flashcards

Chapter 1/2 Flashcards

1
Q

Plasma membrane function

A

semi-permeable membrane. Barrier bw external and internal cell environment. Fluid movement across membrane (cell edema + dehydration)

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2
Q

Sodium potassium pump function

A

electrochemical gradient of the cell.
- 3NA+ out of cell, 2K+ into the cell.
- Active transport (ATP)
- resting membrane potential
- maintains fluid volume

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3
Q

Implication of Na/K pump

A

drugs can alter pump activity
- cardiac glycosides

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4
Q

Mitochondria

A

energy production.
- Aerobic resp : convert organic molecules into ATP
- active tissue has more mitochondria. (muscle)
- maternal DNA
- issues lead to neurological disease (ALS)

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5
Q

Lysosome

A

clean up cellular debris
- digestive/ ingestive enzymes
- lack of lysosomes can lead to Tay-Sachs bc debris isn’t destroyed

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6
Q

What is autolysis?

A

cell death
- lysosomes release enzymes to destroy cell

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7
Q

What is herterolysis?

A

Digest foreign material

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8
Q

Proteasomes

A

degrade proteins and polypeptide chains.
- increased activty linked to cachexia (starvation mode)

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9
Q

Peroxisomes

A

break down free radicals and long chain fatty acids
- adrenoleukodystrophy : disfunctional peroxisomes

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10
Q

Endoplasmic reticulum

A

transport system
- smooth ER: lipids (corticosteroids)
- rough ER: proteins
ER stress: cancer, obesity, and diabetes bc protein cant travel. (causes are lack of sleep, anxiety, etc)

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11
Q

Ribosomes

A

protein synthesis “factories)
- rRNA
- targeted by antibiotics

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12
Q

golgi apparatus

A

package, process and secrete proteins
- receive protein from ER
- stores proteins in vesicles for release (ACTH, insulin)

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13
Q

Secretory vesicles

A

carry and release cell secretions
- formed from ER-golgi system

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14
Q

Microtubules/ microfilaments

A
  • hollow, help w/ cell division (intracellular transport)
  • solid and flexible, cell movement (muscle cells)
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15
Q

Nucleus

A

contains genetic material
- DNA: nucleotides purines (A+T) and pyrimidines (C+T)

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16
Q

centrioles

A

-involved in cell division
- pathway for transporting secretory vesicles to the cell’s perimeter

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17
Q

What types of substances can pass more easily across a cell membrane

A
  • O2 and CO2
  • steroid hormones (testosterone, estrogen, and cortisol : cholesterol)
  • Fatty acids
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18
Q

how does cell communication occur?

A
  • Receptors act like locks and keys.
  • Things that act with these receptors are hormones, medications, and neurotransmitters.

-Protein channels let things in and let things out.

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19
Q

What happens in oxidation (aerobic metabolism)

A
  • requires O2, loses e-
  • glucose to pyruvate, which enters krebs cycle
  • high yield of energy (ATP)
20
Q

Anaerobic metabolism

A
  • O2 not available (hypoxia)
  • glucose to pyruvate to lactic acid
21
Q

What is the difference between transcription and translation

A

transcription: occurs in nucleus, copies DNA to mRNA
translation: occurs in ribosome, reads mRNA and converts it to amino acid chain (tRNA)

22
Q

What is difference between passive and active transport?

A

Active transport: utilizes ATP, moves against pump (low -high)
Passive transport: no energy required, moves with gradient (high-low). Osmosis, diffusion

23
Q

What is an example of active transport

A

Sodium/potassium pump
- sodium out and potassium in
- essential for nerve and muscle function

24
Q

8 types of cell adaptation

A

Atrophy: cell shrink
Hypertrophy: cell increase (physiological vs patho)
Hyperplasia: increase in cells
Metaplasia: genetic reprogramming, one cell into another
Dysplasia: abnormal cell growth
neoplasia: benign or malignant, new growth thats disorganized and uncontrolled

25
Q

Atrophy and hypertrophy example

A

Atrophy: paralysis = shrinkage of muscle

Hypertrophy:
- Physiological - cell increase w/ supporting tissues (strength training).
- pathological - cell increase w no support ( enlargement of heart from hypertension)

26
Q

Hyperplasia example

A
  • estrogen stimulates growth of breast cells in pregnancy for milk
  • maladaptive: too much can cause keloid formation
27
Q

Metaplasia example

A

GERD
- reflux of stomach acid
- prolonged changes cell structure and type
- new maladaptation can be precancerous (barrets esophagus)

28
Q

Dysplasia example

A

chronic inflammation or precancerous condition
- Pap smear (precancerous)

29
Q

Neoplasia example

A

Benign: look and act like normal cells, well differentiated/borders. don’t metastasize
Malignant: poorly differentiated/no border, invade surrounding tissue

30
Q

Hypoxic cellular injury

A

O2 deprivation= anaerobic resp
- low energy and altered biochem activity
(Myocardial ischemia)

31
Q

Free radical injury

A
  • small reactive O2 molecule formed during aerobic metabolism, disrupting cell membrane
    (cardiac muscle ischemia)
32
Q

Physical agents of injury

A

mechanical trauma, temp extremes, sunburn, etc. Direct trauma to cells
(lacerations, burns, electrical shock)

33
Q

Chemical injury

A

can be caused by endogenous biological /exogenous synthetic substances that injure plasma membrane
(endo: elevated ions; diabetes)
(exo: drugs, pollutants

34
Q

infectious agent injury

A

microorganisms cause injury (bacteria, virus, parasites)
(H-Pylori)

35
Q

Injurious immunological rxns (cell injury)

A

immune system attacks healthy cells
(Rheumatoid arthritis)

36
Q

Genetic defects (cell injury)

A

genetic disorders can damage and mutate DNA = abnormal proteins
(Down syndrome)

37
Q

Nutritional imbalances (cell injury)

A

under/over malnutrition can affect cell function
(starvation: marasmus)

38
Q

Review Basic concepts of cell injury chart slide 48

A
39
Q

What is intracellular accumulations and list some examples

A

accumulation of excessive amounts of substances, (cellular constituents, environmentally acquired substances, or cell breakdown products) bc of abnormal metabolic function, exposure to high amounts of environmental material, or aging

Ex: fatty liver, Xanthelasma - high cholesterol
- Anthracosis: coal miner’s lung and black lung
- Jaundice : caused by bilirubin, in liver disease

40
Q

Explain how genetic damage affects DNA. What are genes that trigger cancer cell mutations? what is a common cause of this cancer gene mutation?

A
  • Codons of mutations on a gene from a specific allele
  • Happens during Transcription and Translation maybe from radiation or another outside environmental like smoking Has 1st hit then 2nd
41
Q

What happens in the cell when theres hypoxic injury

A
  • diminished O2 to cells
  • most common
  • Ischemia (diminished circulation); atherosclerotic plaque and clot formation
  • Anemia, lacks sufficient hemoglobin thus O2
  • pulmonary issues (embolism)
  • Hypoxia causes the cell to enter anaerobic metabolism (lactic acid)
42
Q

Whats a free radical and what can protect against them?

A

Contain unpaired e- which interact w and disrupt plasma membrane

  • superoxide dismutases and antioxidants
43
Q

How are antioxidants helpful? what vitamins are known as antioxidants?

A

counteract free radical injury through consumption of antioxidants such as vitamins A, E, and C, and beta-carotene

44
Q

Whats the difference bw necrosis, apoptosis, and gangrene

A

Necrosis: cell death due to injury; irreversible; lack of O2; skin disintegrates, lysosomal activation and autolysis
Apoptosis: programmed cell death; no adverse rxns
Gangrene: prolonged ischemia, infarction, and necrosis

45
Q

What are examples of ionizing radiation

A

X-rays, Radiation treatment, chemo

Pathophysiology (4 decks)

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