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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
Fluid gain
Excess water consumption dilutes ECF; hyponatremia, hypokalemia Amateur athletes over hydration
26
Severe dehydration
5-10% water loss, goal is to restore BP, ECF volume, and osmolarity Lose way more H2O than ions in sweat
27
3 Major mechanisms to oppose dehydration
1. Conserve fluid and prevent further loss 2. Trigger CV to increase BP 3. Stimulate thirst to establish normal volume and osmolarity
28
4 systems involved to respond to dehydration
CV RAAS Renal Hypothalamic GO OVER FLOW CHART SLIDE 49
29
pH
Measure of H+ concentration 7.38-7.42 in the body Change in 1 log unit is a 10 fold difference in ion s
30
Why is pH homeostasis critical for life
Acidic pH denatures proteins Acidosis reduces neuron excitability and depresses ventilation Alkalosis enhances neurons excitability
31
Primary sources of acid
Diet and metabolism
32
Primary elimination of acid
Ventilation and Renal
33
Three main mechanisms to cope with pH change
Chemical buggers (1st line of defense) Ventilation (2nd line of defense) Renal (last line, slower, control excretion/reabsorption of H+ and HCO3-)
34
Chemical buffer Mechanism
Buffer moderates but does not prevent pH change (temporary) Most combine with H+
35
Intracellular buffers
Proteins Phosphate ions (HPO42-) Hemoglobin
36
Extracellular buffers
Bicarbonate 600,000x more concentrated than H+
37
Ventilation buffer mechanisms
Respiratory compensation (increase CO2 production increases ventilation) Nearly instant response
38
Hypoventilation
Decrease rate and depth Increases CO2 More acidic so increase vent to overcome
39
Hyperventilation
Decreases CO2 More basic pH so decrease ventilation
40
Renal buffer mechanisms
Alters pH directly by excreting or reabsorbing H+ OR indirectly by changing the rate that HCO3- is excreted or reabsorbed
41
Apical Na+H+ exchanger
NHE Active transporter brings Na+ into cell to move H+ against its gradient
42
Basolateral Na+-HCO3- symporter
Moves Na+ and HCO3- out of epithelial cell into interstitial fluid
43
H+K+ ATPase
Moves H+ into urine in exchange for reabsorbed K+ Can lead to K+ imbalance
44
Na+NH4+ antiporter
Moves NH4+ from cell to nephron lumen in exchange for Na+
45
Bicarbonate Reabsorption
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
Bicarb reabsorption Diagram
Go over diagram Draw it out Know transporters
47
Acid Excretion
Distal nephron Intercalated cells contain CA Type A and Type B cells
48
Type A cells
Intercalated cells secrete H+ and reabsorb HCO3- Used in acidosis
49
Type B Cells
Intercalated cells that secrete HCO3- and reabsorb H+ Used in Alkalosis
50
Intercalated Cells Acid base balance
DIAGRAM Transporters
51
Acid base disturbances categorized by 2 things
Direction of pH change (Acidosis/alkalosis) Source of disturbance (metabolic or respiratory)
52
Respiratory Acidosis
Hypoventilation and CO2 retention Elevates PCO2 Decreased pH with elevated HCO3- Renal compensation is the only method (Type A cells)
53
Causes of Respiratory acidosis
Drugs that depress ventilation Increased airway resistance Impaired gas exchange Muscle weakness COPD
54
Metabolic acidosis
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
Respiratory alkalois
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
Metabolic alkalosis
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
Challenges exercise presents to homeostasis
Increase BP, vent, temp, HR, ATP demand, water loss Decrease pH (More acidic)
58
Systems integrated in exercise response
CV, renal, respiratory, nervous
59
Energy forms in skeletal muscle
ATP stores Phosphocreatine (PCr)
60
Phosphocreatine (PCr)
Transfers phosphates to ADP to make ATP via creatine Kinase Only provides energy for ~15s of intense contraction (sprinting, weightlifting)
61
Pathway of energy for muscles
Recreate diagram! 3 main pathways: Anaerobic (glycolyis, lactase), Aerobic (CAC, ETC), PCr
62
Where does glucose come from
Liver glycogen or dietary intake
63
Where can fatty acids be used
Only in aerobic metabolism
64
Anaerobic metabolism
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
Aerobic metabolism
Uses O2 Advantage is high yield ~32 ATP Disadvantage is generation of ATP is much slower Much longer sustained contraction
66
What process produces ATP fastest
PCr But lowest muscle endurance
67
Fat glucose usage in exercise
At lower intensities, fat is primarily used but as intensity increases glucose takes over See graph
68
Oxygen consumption (VO2)
O2 combines with H to make H2O in mitochondria Determines intensity (L/min)
69
VO2 Max
Indicator of ability to perform endurance exercises Greater number = greater ability to do work
70
Why does ventilation increase so quickly when exercise begins
Anticipation of oxygen demand (feedforward control) Stretch receptors in muscles trigger increase in vent.
71
How come PO2 and PCo2 stay constant during exercise
Exercise hyperventilation keep them equal
72
Cardiovascular response to exercise
Mechano-sensory info from muscles --> motor cortex Descending pathways activate CVCC --> sympathetic output increases CO and constrict most peripheral arterioles
73
Prime factor of exercise tolerance
O2 delivery CO = HR* SV
74
Blood flow during exercise
Vasoconstriction of non exercising tissue and dilation of exercising tissue pushes blood to muscles
75
Why does the BP increase during exercise not trigger homeostatic compensation
Motor cortex signals "reset" baroreceptor threshold Baroreceptors afferents are blocked (central inhibition) Sensory input (H+) and muscle mechanoreceptors override the baroreceptors
76
What causes activation of CVCC at the onset of exercise
Muscle mechanoreceptors

A&P lecture 2 (4 decks)

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