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Pathophysiology > Homeostasis, Stress Response, & Alterations in Cellular Function > Flashcards

Homeostasis, Stress Response, & Alterations in Cellular Function Flashcards

1
Q

Which of the following is correct regarding the “Normal” Distribution?
A. Most of the time, a normal distribution is “skewed” to either the left or the right

B. 95% of the time, the correct measured value will fall somewhere between + / - 2 standard deviations of the mean

The mean and the median are never the same

The smaller the population you are studying (n value), the more likely the results will be normally distributed

A

B

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2
Q

Which of the Following is the best example of secondary prevention?
A. Measles vaccination

B. Reducing the amount of dietary salt in a hypertensive patient

C. Administering IV fluids in the ER

D. Wearing a cast following a wrist fracture

A

B

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3
Q

The incidence of Disease is basically defined as?
A. The total number of existing cases of disease X in a specific population

B. The percentage of patients in a specific population that have disease X

C. The number of new cases of disease X in a specific population

D. The likelihood an individual with a positive test result has disease X

A

B

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4
Q

Which of the following is incorrect?
A: Oxygen is one of the most destructive substances in the body

B: Exotoxins are more virulent than endotoxins

C: During the coordinated stress response, vasoconstriction and vasodilation are occurring simultaneously

D: It is impossible for any cells to make ATP without a constant supply of oxygen

A

D

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5
Q

Which of the following choices would be consistent with the stress response?
A. Vasodilation in the renal vascular beds

B. Vasoconstriction in the skeletal muscles

C. Bronchoconstriction

D. Pupillary Dilation

A

D

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6
Q

Which one of the following is not a stress hormone?
A. Cortisol

B. Norepinephrine

C. Acetylcholine

D. Epinephrine

A

C

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7
Q

Which of the following would not be consistent with the stress response?
A. Increased Blood Pressure

B. Increased blood flow to the mesentery

C. Increased systemic vascular resistance

D. Sodium retention in the kidneys

A

B

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8
Q

Which of the following is the best example of Coagulative necrosis?
A. Reperfusion injury following a myocardial infarct

B. Pancreatitis

C. Tuberculosis infection

D. An MRSA soft tissue infection

A

A

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9
Q

Which one of the following vitamins is likely to be affected in a person with severe fat malabsorption?
A. B12

B. D

C. C

D. B6

A

B

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10
Q

Which one of the following statements is correct?
A. Vitamin excess is probably a more common problem than vitamin deficiency is

B. Vitamins do not serve as anti-oxidants

C. British sailors were called “limeys” because they sucked on limes in an attempt to replace depleted vitamin D levels

D. A Vitamin K-depleted individual would be prone to bleeding

A

D

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11
Q

Etiology

A

WHY does disease occur?

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12
Q

Pathogenesis

A

HOW does disease occur?

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13
Q

Clinical manifestations

A

WHAT does the disease look like?

signs and symptoms

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14
Q

Treatment implacations

A

HOW does the treatment impact it?

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15
Q

validity

A

accuracy- the degree to which the measured value represents the actual value

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16
Q

reliability

A

precision- the ability of a test to render the same results in repeated measurements

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17
Q

incidence

A

number of new cases

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18
Q

prevalence

A

number of existing cases

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19
Q

sensitivity

A

probability a test will be positive in a person with the disease

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20
Q

specificity

A

probability a test will be negative in a person without the disease

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21
Q

positive predictive value

A

likelihood a person with a positive test has the disease

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22
Q

negative predictive values

A

likelihood a person with a negative test does not have the disease

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23
Q

epidemiological variables

A 
age
gender
lifestyle
socio-economic status
geographic location
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24
Q

primary level of prevention

A

preventing a disease from occurring in the first place

immunizations

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25
Q

secondary level of prevention

A

preventing complications of the disease

screenings like PAP smears and mammograms

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26
Q

tertiary level of prevention

A

treating the disease

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27
Q

sympathoadrenal system: adrenal cortex

A

Cortex => production of glucocorticoids (cortisol- think sugar metabolism) and mineralocorticoids (aldosterone- think pulling salt back to get water retention)

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28
Q

sympathoadrenal system: adrenal medulla

A

Medulla => production of catecholamines (epinephrine and norepinephrine)

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29
Q

what effect does cortisol have?

A

Catabolism by breaking down fat and muscles into fatty acids and AAs which can be turned into glucose

30
Q

what effect does aldosterone have?

A

Na retention

31
Q

coordinated stress response

A

Stored nutrients are broken down => metabolic fuel to maintain blood sugar
Hemodynamic parameters => raise BP and heart rate
Blood flow => shunted from skin and gut to the muscles, heart, and lungs
Volume expansion => aldosterone retains salt which increases intravascular volume

32
Q

effects of catecholamines

A

Heart- increased rate and contractability
Blood vessels- skin and gut constrict while muscles, heart, and lungs dilate
GI tract- decreased activity
Liver- mobilizes energy stores by gluconeogenesis (making sugar) and glycogenolysis (breakdown of stored sugar)
CNS- arousal, attention, and vigilance

33
Q

disease

A

excessive or inappropriate physiological stress response (CHRONIC)

34
Q

signs and symptoms

A

multiple effects on multiple body systems (ACUTE)

35
Q

atrophy

A

cells shrink with loss of function

36
Q

hypertrophy

A

too much growth with an increase in cell mass and function

37
Q

hyperplasia

A

too many cells

38
Q

metaplasia

A

replacement of one cell type with another

39
Q

dysplasia

A

disorganized appearance of cells where they have abnormal shapes and sizes

40
Q

necrosis

A

pathological cell destruction

41
Q

coagulative necrosis

A

the most common that is essentially ischemia where the loss of cell membrane causes calcium ion influx and mitochondrial dysfunction that causes lytic enzyme activation and cell destruction

Heart muscle injury

42
Q

liquifactive necrosis

A

lysosomal enzymes dissolve tissue- bacterial infection can cause WBCs to activate which causes cells to be digested with degradative enzymes which leave liquified cellular debris which can be pus in an abscess or cyst

43
Q

fat necrosis

A

death of adipose tissue commonly associated with trauma- pancreatitis where there are high levels of pancreatic enzymes which causes fat cells to be digested and triglycerides to be released leads to hydrolysis into FFAs by pancreatic lipase to be saponified and shows chalky white tissue

44
Q

caseous necrosis

A

clumpy cheese appearance where cellular debris is walled off

TB and granulomatous diseases

45
Q

apoptosis

A

programmed cell death

46
Q

gangrene

A

death of a large area of tissue usually due to ischemia

Dry => coagulative necrosis common on extremities
Wet => visceral organs
GAS gangrene => clostridium infection

47
Q

mechanisms of tissue ischemia and hypoxia

A

Lower mitochondrial dysfunction due to low ATP

Sodium-potassium pump fails due to hydropic swelling of cells

Reperfusion injury

Calcium influx causes the activation of degradative enzymes

Oxygen influx causes the formation of reactive radicals and oxidative injuries

Lactic acidosis= pyruvate (end product of glycolysis) that is caused by the lack of ATP production during hypoxia when the metabolism becomes anaerobic (Pyruvate -> lactate -> low pH -> acidosis)

48
Q

fat-soluble vitamins

A

A D E K

49
Q

water soluble vitamins

A

B C Niacin Folate Pantothenic acid Biotin

50
Q

vitamin A

A

vision and healthy skin

deficit- visual

51
Q

vitamin D

A

calcium metabolism

deficit- rickets and osteomalacia

52
Q

vitamin E

A

important antioxidant

deficit- neurological impairment

53
Q

vitamin K

A

important cofactor in the clotting cascade

deficit- bleeding

54
Q

vitamin B

A

cofactor in metabolic reactions

deficit- (B12) pernicious anemia

55
Q

vitamin C

A

cofactor in redox reactions

56
Q

folate

A

DNA synthesis and pre-natal importance

deficit- anemia and neural tube defects

57
Q

vitamin A deficit

A

visual

58
Q

niacin

A

NAD

deficit- pellagra (dementia/dermatitis/diarrhea)

59
Q

radiation cell injuries

A

Ionization releases free radicals and causes cell destruction and genetic damage

60
Q

hypothermia cell injury

A

Causes blood vessel constriction

61
Q

electrical cell injury

A

Disruption and neural/cardiac impulses

Hyperthermic destruction of tissues

62
Q

hyperthermia cell injury

A

Microvascular coagulation and accelerated metabolic processes

63
Q

idiopathic etiology

A

cause is known

64
Q

iatrogenic etiology

A

cause is the result of unintended or unwanted medical treatment

65
Q

bell curve of diagnostic variables

A

A standard deviation of 2 means 95% of the population falls within that normal range

66
Q

homeostasis

A

maintaining internal conditions in a stable state by keeping parameters relatively the same

67
Q

allostasis

A

the body’s response and adaptive changes to achieve homeostasis

68
Q

general adaptation syndrome

A

alarm reaction- fight or flight

stage of resistance- allostasis

stage of exhaustion- no longer able to effect a return to homeostasis after prolonged exposure

69
Q

allostatic load

A

wear and tear on the body and brain from the stress responses

70
Q

hydropic swelling (oncsosis)

A

the accumulation of water which is the first manifestation of most reversible cell death injuries

  • Due to a malfunction with the sodium-potassium pumps that are dependent on ATP
  • Characterized by a large, pale cytoplasm with a dilated ER and swollen mitochondria
  • Severe is when the ER ruptures and forms water-filled vacuoles
71
Q

autophagy

A

where lysosomes that fuse with intracellular structures leading to the hydrolytic degradation

72
Q

reperfusion injury

A

most of the cellular damage occurs after the blood supply has been restored to the tissues

Three components:

  • Calcium overload
  • Can trigger apoptosis or activate enzymes that degrade membrane lipids
  • Formation of reactive oxygen molecules (free radicals)
  • Subsequent inflammation

Pathophysiology (2 decks)

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