Weeks 1 - 3 Flashcards

1
Q

Give an example of physiologic atrophy:
(3)

A
  • Thymus decreased in size during childhood.
  • Uterus decreases in size after child birth.
  • Tonsils shrink in adolescents.
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2
Q

Causes of pathological atrophy:
(3/6)

A
  • Decrease in workload
  • Decrease in use, pressure, blood supply
  • Decrease in hormonal stimulation or nutrition.
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3
Q

Give an example of pathologic atrophy:
(1)

A

Disuse atrophy: skeletal muscle after removal of a cast.

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4
Q

What is hypertrophy:

A

Increase in cell size

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5
Q

Give an example of physiologic hypertrophy:

A

Hypertrophy of myocardial cells (myocytes) as a result of endurance training.

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6
Q

Give an example of pathological hypertrophy:

A

HTN / heart valve dysfunction (chronic hemodynamic overload).
Prolonged hypertrophy = contractile dysfunction = heart failure.

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7
Q

What’s the difference between physiologic hypertrophy and pathologic hypertrophy regarding heart muscle:

A

• physiologic hypertrophy: cellular matrix is preserved.
• pathological hypertrophy: increased interstitial fibrosis, cell death, abnormal cardiac function.

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8
Q

What’s the difference between physiologic hypertrophy and pathologic hypertrophy regarding heart muscle:

A

• physiologic hypertrophy: cellular matrix is preserved.
• pathological hypertrophy: increased interstitial fibrosis, cell death, abnormal cardiac function.

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9
Q

What is hyperplasia?

A

Increased cellular division rate which increases NUMBER of cells

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10
Q

What is the process of hyperplasia?

A

• Injury = severe / prolonged damage = cell death.
• Production of hormone / growth factors = remaining cells synthesize cell components = mitosis (cell division).

• Increased output from tissue stem cells.

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11
Q

Give an example of pathological hyperplasia:

A

Benign prostatic hyperplasia (BPH)

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12
Q

Mature cells have a differing capacity for hyperplastic or ____________ growth.

A

Mitotic

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13
Q

What is metaplasia?

A

REPLACEMENT if cells

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14
Q

Give an example of metaplasia:

A

“Smokers Lungs” - reversible
Normal columnar violated epithelial cells of the bronchial lining have been replaced with stratified squamous epithelial cells.

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15
Q

6 major players of fluid balance:

A

• Hydrostatic pressure (water OUT of capillaries into surrounding tissue)
• Oncotic pressure (water INTO capillaries from surrounding tissue)
• Renin angiotensin-aldosterone system (RAAS)
• Aldosterone (think sodium)
• Antidiuretic Hormone (ADH) (think water)
• Natriuretic peptides (RAAS antagonist)

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16
Q

How Hydrostatic Pressure function?

A

Fluid moves from intravascular space to interstitial space via capillaries because capillary hydrostatic pressure (blood pressure) is higher than oncotic pressure.

Water moves from capillaries to interstitial space via blood pressure.

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17
Q

How does Oncotic Pressure function?

A

Influenced by plasma proteins (albumin).

Low plasma albumin = edema = decrease in Oncotic pressure = pulls fluid INTO capillary.

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18
Q

How does the Renin Angiotensin-Aldosterone System (RAAS) function?

A

• Renin is an enzyme secreted by juxtaglomerular cells in the kidney.

• Sympathetic nerve stimulation and decreased perfusion of the renal vascular = low blood volume / pressure = renin release = cascade of antiotensins = vasoconstriction.

• Opposes natriuretic peptides

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19
Q

How does Aldosterone function?

A

• Regulates sodium and potassium

• Increased sodium and water decreased potassium.

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20
Q

Hyperaldosteronism causes:

A

• Hypokalemia
• Hypernatremia

• Increased fluid volume

21
Q

Hypoaldosteronism causes:

A

• Hyperkalemia
• Hyponatremia

• Decreased fluid volume

22
Q

How does Antidiuretic hormone function:

A

• Decreased plasma volume = increase in serum sodium = decreased blood pressure = decreased perfusion.

23
Q

What percentage of total body weight is fluid in infants?

A

75% to 80%

24
Q

Why are infants vulnerable to fluid imbalances?

(3)

A

• Fluid is 75% to 80% TBW
• High metabolic rate
• Immature kidneys can’t counter fluid losses

25
Q

Why are older adults at risk for fluid imbalance?

A

They have a diminished thirst sensation

26
Q

How do natriuretic peptides function?

A

Decrease blood pressure and increase sodium and water excretion.

Opposes RAAS system

27
Q

What are 3 kinds of natriuretic peptides?

A

Includes:
• Atrial natriuretic peptide (ANP)
Produced by myocardial atria
• Brain natriuretic peptide (BNP)
Produced by myocardial ventricles
• Urodilatin
Produced by kidneys

28
Q

What are 5 functions of sodium:

A

• Regulator of fluids
• Nerve impulse conduction
• Acid-base balance
• Cellular chemical reactions
• Transport of substances across cellular membrane

29
Q

What are some causes of hyponatremia?
(4)

A

• Hypoaldosteronism
• Loss of sodium
• Inadequate intake
• Medications

30
Q

Physiological (cellular) effects of hyponatremia:
(3)

A

• Hypoosmolality
• Cellular swelling (water INTO cells)
• Altered cellular function

31
Q

What causes clinical manifestations of hyponatremia:

A

Altered action potential in neurons and muscles = impaired nerve conduction and neurological changes.

32
Q

What are clinical manifestations of hyponatremia?

A

Mild:
• Nausea
• Vomiting
Severe:
• Lethargy
• Seizures
• Coma
*Older patients = major cause of morbidity

33
Q

What are clinical manifestations of hypernatremia?

A

• Central nervous system (severe)
• Coma
• Seizures

34
Q

What are some functions of potassium?
(2)

A

(K+(ICF) : (K+(ECF) = Major determinant of the resting membrane potential necessary for transmission of nerve impulses.

• Aids in acid-base balance.

35
Q

K+ affects resting membrane potential by:
(3)

A

• Maintenance of cardiac rhythms
• Skeletal muscle contraction
• Smooth muscle contraction

36
Q

K+ affects resting membrane potential by:
(3)

A

• Maintenance of cardiac rhythms
• Skeletal muscle contraction
• Smooth muscle contraction

37
Q

How does potassium help maintain acid-base balance?

A

Acidosis (excess H+ ions) forces H+ (acid) INTO cells pushing K+ (base) OUT of cells to neutralize acidity.

38
Q

What are some causes of hyperkalemia?
(6)

A

• Renal disease
• Massive trauma
• Insulin deficiency
• Addison’s Disease
• Excessive potassium ingestion
• Metabolic acidosis

39
Q

What are some causes of hypokalemia?
(6)

A

• Anorexia - malnutrition
• Renal tubular failure
• K+ losing diuretics
• Hyperaldosteronism
• Vomiting
• Diarrhea

40
Q

What is the result of potassium shifting from ECF to ICF?

A

Hypokalemia:
• Cardiac irregularities
• V fib
• Decreased tendon reflexes

41
Q

How does insulin affect potassium?

A

Insulin causes potassium to move from ECF to ICF

42
Q

What are some causes of Respiratory Acidosis:
(5)

A

• Chronic respiratory disease (COPD)
• Barbiturate / sedative overdose
• Severe pneumonia
• Respiratory muscle weakness
• Pulmonary edema

43
Q

What is the pathophysiology of respiratory acidosis?
(4)

A

• Increased CO2 (hypoventilation)
• Compensatory response: kidneys increase retention of bicarbonate (HCO3-)
• Kidneys secrete hydrogen (H+)
• Bicarbonate is regenerated by the kidneys

44
Q

What are some causes of respiratory alkalosis?
(3)

A

• Hyperventilation
• Increased loss of CO2
• Stimulated respiratory center

45
Q

What is the pathophysiology of respiratory alkalosis?

A

Increased bicarbonate (HCO3-) excretion by kidneys.

46
Q

What are some causes of metabolic acidosis?

A

Increased H+ ions and anion gap will KILU.
• Ketoacidosis
• Ingestions (ethylene, salicylates)
• Lactic acidosis (shock)
• Uremia

Bicarbonate loss (Normal anion)
• Diarrhea
• Renal Failure

47
Q

What are some causes of metabolic acidosis?

A

Increased H+ ions and anion gap will KILU.
• Ketoacidosis
• Ingestions (ethylene, salicylates)
• Lactic acidosis (shock)
• Uremia

Bicarbonate loss (Normal anion)
• Diarrhea
• Renal Failure

48
Q

What are some clinical manifestations of metabolic acidosis?

A

Kidneys in trouble - lungs try to help.
Kussmaul respirations are a compensatory response to blow off CO2 (hyperventilation)

Vomiting to rid acid

49
Q

What are some causes of metabolic alkalosis?

A

Vomiting
Hypokalemia
Any condition raising aldosterone or mineralocorticoids
NG suctioning
Diuretic therapy