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A&P lecture 2 > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Excess NaCl intake

A

Avg 2-3x more than what we need
Too much increases plasma osmolarity and causes cells to shrink
Handled via mass balance

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2
Q

2 part response to salt intake

A

Cardiovascular (fast)
Renal (slow)
Vasopressin and thirst response change ECF volume, BP, & osmolarity

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3
Q

Reabsorption vs. secretion regulation

A

ONLY regulate reabsorption
Can’t increase secretion of salt

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4
Q

Aldosterone

A

Steroid hormone from adrenal cortex
Increases Na reabsorption and K secretion in distal nephron

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5
Q

Slow Aldosterone response

A

Production of new channels via transcription/translation

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6
Q

Fast aldosterone response

A

Increase activity of the channels present

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7
Q

Ion transporters targeted by aldosterone

A

Na/K pump
ENaC (Epithelial Na Channel)
ROMK (Renal Outer Medulla K channel)
SEE DIAGRAM Slide 31

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8
Q

Primary stimuli for aldosterone release

A

Increased Extracellular K+ (detected by adrenal cortex, protection against hyperkalemia)
Low blood pressure (Triggers RAAS)

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9
Q

RAAS

A

Renin Angiotensin Aldosterone System
GO OVER PATHWAY/DIAGRAM slide 34

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10
Q

6 possible effects of ANG II

A

Constrict arterioles
CVCC (SNS) to increase Cardiac response
Hypothalamus to increase vasopressin and thirst
Adrenal cortex to release aldosterone
Proximal tubule to increase Na reabsorption
All lead to increased BP and/or Increased volume and maintained osmolarity

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11
Q

ACE-inhibitors

A

Lower BP by preventing conversion of ANG I to ANG II
Increases vasodilation

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12
Q

Angiotensin receptor blockers (ARB)

A

Competitive binding of AT1 receptors prevents intracellular response to ANG II

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13
Q

Renin Inhibitors

A

Reduce Renin activity
Can’t be used in combo with other RAAS drugs

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14
Q

Natriuresis

A

Losing sodium in urine

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15
Q

Natriuretic peptides

A

Oppose RAAS system
Decrease BP

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16
Q

Atrial natriuretic Peptide (ANP)

A

Produced in cardiac atria
Myocardial stretch (Increase BP) triggers release
Enhances Na and water excretion, multiple effects

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17
Q

Brain Natriuretic peptide (BNP)

A

Produced in some neurons and ventricular myocardium
Marker to estimate heart failure

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18
Q

Hypokalemia

A

Low IF K+
Increases K+ gradient
Resting membrane potential becomes more negative, so harder to excite cells
Muscle weakness, feeling tired

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19
Q

Hyperkalemia

A

Excess IF K+
Decreases gradient
Resting membrane potential becomes less negative so it’s easier to fire AP
Cardiac arrythmias, fast HR
Less excitable over time

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20
Q

Common disturbances of K+ levels

A

Kidney disease, ED, K+ loss in diarrhea, certain diuretics

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21
Q

What response when K+ too high

A

Aldosterone increase K+ excretion via increase activity/expression of Na/K pump

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22
Q

Thirst reflex

A

Osmoreceptors in hypothalamus
Receptors in mouth/pharynx respond to cold water to reduce thirst and vasopressin

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23
Q

Salt appetite

A

Crave salt when Na lost; linked to aldosterone and angiotensin
Hypothalamic response - osmoreceptors monitor plasma

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24
Q

Fluid loss

A

Excess sweating, vomit, diarrhea, hemorrhage

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25
Q

Fluid gain

A

Excess water consumption dilutes ECF; hyponatremia, hypokalemia
Amateur athletes over hydration

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26
Q

Severe dehydration

A

5-10% water loss, goal is to restore BP, ECF volume, and osmolarity
Lose way more H2O than ions in sweat

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27
Q

3 Major mechanisms to oppose dehydration

A
  1. Conserve fluid and prevent further loss
  2. Trigger CV to increase BP
  3. Stimulate thirst to establish normal volume and osmolarity
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28
Q

4 systems involved to respond to dehydration

A

CV
RAAS
Renal
Hypothalamic
GO OVER FLOW CHART SLIDE 49

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29
Q

pH

A

Measure of H+ concentration
7.38-7.42 in the body
Change in 1 log unit is a 10 fold difference in ion s

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30
Q

Why is pH homeostasis critical for life

A

Acidic pH denatures proteins
Acidosis reduces neuron excitability and depresses ventilation
Alkalosis enhances neurons excitability

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31
Q

Primary sources of acid

A

Diet and metabolism

32
Q

Primary elimination of acid

A

Ventilation and Renal

33
Q

Three main mechanisms to cope with pH change

A

Chemical buggers (1st line of defense)
Ventilation (2nd line of defense)
Renal (last line, slower, control excretion/reabsorption of H+ and HCO3-)

34
Q

Chemical buffer Mechanism

A

Buffer moderates but does not prevent pH change (temporary)
Most combine with H+

35
Q

Intracellular buffers

A

Proteins
Phosphate ions (HPO42-)
Hemoglobin

36
Q

Extracellular buffers

A

Bicarbonate
600,000x more concentrated than H+

37
Q

Ventilation buffer mechanisms

A

Respiratory compensation (increase CO2 production increases ventilation)
Nearly instant response

38
Q

Hypoventilation

A

Decrease rate and depth
Increases CO2
More acidic so increase vent to overcome

39
Q

Hyperventilation

A

Decreases CO2
More basic pH so decrease ventilation

40
Q

Renal buffer mechanisms

A

Alters pH directly by excreting or reabsorbing H+ OR indirectly by changing the rate that HCO3- is excreted or reabsorbed

41
Q

Apical Na+H+ exchanger

A

NHE
Active transporter brings Na+ into cell to move H+ against its gradient

42
Q

Basolateral Na+-HCO3- symporter

A

Moves Na+ and HCO3- out of epithelial cell into interstitial fluid

43
Q

H+K+ ATPase

A

Moves H+ into urine in exchange for reabsorbed K+
Can lead to K+ imbalance

44
Q

Na+NH4+ antiporter

A

Moves NH4+ from cell to nephron lumen in exchange for Na+

45
Q

Bicarbonate Reabsorption

A

Filter 1lb of HCO3- per day
PT reabsorbs by converting it into CO2 then back into HCO3-
OR metabolism of glutamine which leads to net reabsorption of Na+ and HCO3- (by product of glut. metab)

46
Q

Bicarb reabsorption Diagram

A

Go over diagram
Draw it out
Know transporters

47
Q

Acid Excretion

A

Distal nephron
Intercalated cells contain CA
Type A and Type B cells

48
Q

Type A cells

A

Intercalated cells secrete H+ and reabsorb HCO3-
Used in acidosis

49
Q

Type B Cells

A

Intercalated cells that secrete HCO3- and reabsorb H+
Used in Alkalosis

50
Q

Intercalated Cells Acid base balance

A

DIAGRAM
Transporters

51
Q

Acid base disturbances categorized by 2 things

A

Direction of pH change (Acidosis/alkalosis)
Source of disturbance (metabolic or respiratory)

52
Q

Respiratory Acidosis

A

Hypoventilation and CO2 retention
Elevates PCO2
Decreased pH with elevated HCO3-
Renal compensation is the only method (Type A cells)

53
Q

Causes of Respiratory acidosis

A

Drugs that depress ventilation
Increased airway resistance
Impaired gas exchange
Muscle weakness
COPD

54
Q

Metabolic acidosis

A

H+ input exceeds excretion
Lactic acid production (lactic acidosis)
Ketone production (Ketoacidosis)
Loss of HCO3- due to diarrhea
Ventilation and renal compensation (type A)

55
Q

Respiratory alkalois

A

Results from hyperventilation (too much CO2 exhaled)
Alveolar ventilation increases but not metabolic CO2 production
Only compensation is renal HCO3- secretion (Type B) and H+ reabsorption

56
Q

Metabolic alkalosis

A

Excessive vomiting of stomach acid or excessive ingestion of bicarbonate
Reduces H+ and increases HCO3-
Plasma CO2 decrease
Ventilation (Hypovent to retain CO2) and renal compensation (Type B, secrete HCO3- reabsorb H+)

57
Q

Challenges exercise presents to homeostasis

A

Increase BP, vent, temp, HR, ATP demand, water loss
Decrease pH (More acidic)

58
Q

Systems integrated in exercise response

A

CV, renal, respiratory, nervous

59
Q

Energy forms in skeletal muscle

A

ATP stores
Phosphocreatine (PCr)

60
Q

Phosphocreatine (PCr)

A

Transfers phosphates to ADP to make ATP via creatine Kinase
Only provides energy for ~15s of intense contraction (sprinting, weightlifting)

61
Q

Pathway of energy for muscles

A

Recreate diagram!
3 main pathways: Anaerobic (glycolyis, lactase), Aerobic (CAC, ETC), PCr

62
Q

Where does glucose come from

A

Liver glycogen or dietary intake

63
Q

Where can fatty acids be used

A

Only in aerobic metabolism

64
Q

Anaerobic metabolism

A

No need for O2
Advantage is speed of ATP production
Disadvantage is quantity of ATP ~2 and contributes to metabolic acidosis via lactic acid

65
Q

Aerobic metabolism

A

Uses O2
Advantage is high yield ~32 ATP
Disadvantage is generation of ATP is much slower
Much longer sustained contraction

66
Q

What process produces ATP fastest

A

PCr
But lowest muscle endurance

67
Q

Fat glucose usage in exercise

A

At lower intensities, fat is primarily used but as intensity increases glucose takes over
See graph

68
Q

Oxygen consumption (VO2)

A

O2 combines with H to make H2O in mitochondria
Determines intensity (L/min)

69
Q

VO2 Max

A

Indicator of ability to perform endurance exercises
Greater number = greater ability to do work

70
Q

Why does ventilation increase so quickly when exercise begins

A

Anticipation of oxygen demand (feedforward control)
Stretch receptors in muscles trigger increase in vent.

71
Q

How come PO2 and PCo2 stay constant during exercise

A

Exercise hyperventilation keep them equal

72
Q

Cardiovascular response to exercise

A

Mechano-sensory info from muscles –> motor cortex
Descending pathways activate CVCC –> sympathetic output increases CO and constrict most peripheral arterioles

73
Q

Prime factor of exercise tolerance

A

O2 delivery
CO = HR* SV

74
Q

Blood flow during exercise

A

Vasoconstriction of non exercising tissue and dilation of exercising tissue pushes blood to muscles

75
Q

Why does the BP increase during exercise not trigger homeostatic compensation

A

Motor cortex signals “reset” baroreceptor threshold
Baroreceptors afferents are blocked (central inhibition)
Sensory input (H+) and muscle mechanoreceptors override the baroreceptors

76
Q

What causes activation of CVCC at the onset of exercise

A

Muscle mechanoreceptors

A&P lecture 2 (4 decks)

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