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PSL301 > Term Test 2 > Flashcards

Term Test 2 Flashcards

1
Q

What are physiological risk factors for cardiovascular disease?

A
  • High levels of LDL’s
  • diabetes mellitus

-> astherosclerosis

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2
Q

What are controllable risk factors for CVD?

A
  • smoking
  • obesity
  • sedentary lifestyle
  • hypertension
  • cholesterol
  • stress
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3
Q

What are the four functions of the respiratory system?

A
  1. Breathing
  2. Protect against pathogens
  3. Vocalization
  4. Regulate body pH
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4
Q

How do the airways condition air?

A

a) warm temperature to 37 C
b) Humidify 100%
c) Filter air

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5
Q

How does the respiratory system filter pathogens?

A
  • mucus traps pathogens, cilia push mucus to pharynx which pushes to esophagus for digestion in GI tract
  • immune cells secrete antibodies and disable pathogens
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6
Q

What is the purpose of the bifurcations in the airways?

A

Distribute air to large surface area of alveoli and lower air velocity so gas exchange has enough time

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7
Q

1st bifurcation

A

right and left main bronchi

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8
Q

2nd-4th bifurcation

A

Lobar Bronchi (has cartilage to maintain shape

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9
Q

5-11th bifurcation

A

Segmental Bronchi

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10
Q

12-16th bifurcation

A

Terminal bronchioles (stabilized by SM bronchiolar muscles)

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11
Q

how does alveolar gas exchange occure?

A

passive diffusion

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12
Q

How is blood transported to and from the lungs?

A

[deoxygenated blood] right ventricle of heart -> pulmonary trunk -> pulmonary arteries -> pulmonary arterioles -> capillaries [gas exchange at lungs -> oxygenated blood] -> pulmonary venules-> pulmonary veins -> left atrium of heart

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13
Q

What is the blood volume and pressure of the lung?

A

Volume = 10% of cardiac output
Pressure = 25/8mmHg, low because proximal to heart

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14
Q

How does pulmonary congestion cause heart failure?

A
  1. left ventricle not working -> right ventricle hypertrophy to overcompensate -> lower compliance of heart, working harder -> fluid buildup in heart and lungs -> heart failure
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15
Q

How is the respiratory system protected from pathogens?

A
  1. Filtering action of nose hairs
  2. Mucous and action of cilia lining airways
  3. Antibodies secreted into respiratory surface
  4. Macrophages in respiratory tract and alveoli
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16
Q

Vt

A

Tidal volume: Amount of air exhaled or inhaled during a normal breath

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17
Q

IRV

A

inspiratory reserve volume: the maximal volume of air that can be forcibly inhaled beyond the tidal volume (after a normal breath)

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18
Q

ERV

A

expiratory reserve volume: the maximal amount of air that can be forcefully exhaled beyond the tidal volume (after a normal breath)

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19
Q

RV

A

residual volume: the amount of air still in the lungs after a forced exhalation

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20
Q

IC

A

inspiratory capacity: the maximal volume of air that can be inhaled after a normal expiration (Vt + IRV)

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21
Q

FRC

A

functional respiratory capacity: volume in the lungs after a normal exhalation (Vt + ERV)

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22
Q

VC

A

vital capacity: the greatest volume of air that can be exhaled after taking the deepest possible breath in (IRV + ERV + VT)

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23
Q

Total Lung capacity

A

total lung capacity: maximum amount of air your lungs can hold (IRV + ERV + VT + RV)

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24
Q

How does obstructive lung disease impact lung volumes and capacities?

A

OLD (ex. asthma) -> more airway resistance via bronchoconstriction
- reduced IRV
- increased RV
- increased TLC

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25
Q

How does inspiratory restrictive lung disease impact lung volumes and capacities?

A

IRLD (ex. pulmonary fibrosis) -> less compliant lung due to damage or scar tissue
- reduced TV
- reduced IRV
- greatly reduced TLC

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26
Q

How does expiratory restrictive lung disease impact lung volumes and capacities?

A

ERLD (ex. obesity) -> organs push diaphragm up
- reduced ERV
- reduced TLC

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27
Q

What is the relationship b/w FEV and FVC, and what does it tell you?

A

After maximal inhalation:
FEV: forced exhalation after 1 second
FVC: forced exhaled air (vital capacity)

ratio = how much air is exhaled in first second (normal = 80%)

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28
Q

FEV and FVC in obstructive lung disease?

A

Very low FEV: air has trouble escaping lung, esp at high velocities
Low FVC: problem with all air escaping at all points

ratio is around < 80%

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29
Q

FEV and FVC in restrictive lung disease?

A

Low FEV: lung damage
Low FVC: low lung compliance

ratio is > 80% -> inability to retain air -> lung transplant potentially

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30
Q

How do the muscles of inspiration increase lung volume when breathing?

A

Muscles:
- sternum
- scalene (first two ribs)
- external intercostals
- diaphragm

ribs + sternum move up in a bucket handle fashion -> increased volume

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31
Q

what are the muscles of expiration, and when are they active?

A

internal intercostals, abdominal muscles

inactive at rest during regular breathing, active when breathing frequency is high

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32
Q

What role does interpleural pressure play in breathing?

A

Pleural fluid/interpleural space maintains a negative pressure. Since pressure goes from high to low, this causes the volume to increase when the alveolar pressure is increased form breathing, sucking lungs into thoracic cavity.

negative pressure created from tug of war between ribcage moving outward, and lung moving inward.

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33
Q

What is pneumothorax, and how is it treated?

A

Collapsed lung.

  • apply wet dressing to reestablish pleural fluid
  • add positive pressure to mouth by inflating lungs
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34
Q

Relationship between thoracic and alveolar pressures?

A

Thoracic pressure changes faster than alveolar pressure

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35
Q

How is lung compliance defined?

A

How much lung volume changes when interpleural pressure changes.

How much will the lung move when pressure changes? See graphs in slides (W2)

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36
Q

How are compliance and elasticity related?

A

Inversely related:
- more elastic means more rigid/returns to original form -> less compliant (bendable to your will) and vice versa

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37
Q

What influences lung compliance?

A
  • Elastin fiber network
  • surface tension in alveoli
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38
Q

How is lung compliance measured?

A

Cl = V/P

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39
Q

How does surface tension influence compliance?

A

Greater surface tension-> lower volume of alveoli -> greater pressure -> less compliant -> more elastic

Surfactant reduces surface tension

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40
Q

How can pressure be measured in relation to surface area?

A

P =2T/r

r = radius
T = surface tension

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41
Q

How do surfactants influence surface tension?

A

Reduce surface tension

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42
Q

what are the 3 kinds of air flow, and how where are they seen?

A

Laminar: trachea
Turbulent: alveoli
Intermediate: bronchus

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43
Q

how is resistance measured?

A

L = length(viscosity)/radius^4

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44
Q

how can bronchiole resistance be altered?

A

Bronchoconstriction (histamine with allergies)
- increases resistance

Bronchodilation (CO2, epinepherine bind B2 receptors)
- with increased exhalation

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45
Q

Dead and fresh air explanation!

A

review diagram at the end of lecture for explanation!

Basically, when you inspire, you inhale 500mL of fresh air. The 150mL of air that was in the dead space moves into the alveoli, so only 350mL of fresh air enters the alveoli, and the remaining 150mL of fresh air goes into the dead space. When you expire 500mL, the first 150mL comes out of the dead space, so only 350mL leaves the alveoli, leaving 150mL, which becomes stale air that goes into the alveoli. We start the process over again from the beginning.

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46
Q

PB

A

Atmospheric pressure, 760 mmHg

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47
Q

PB humidified air

A

760mmHg - 47mmHg

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48
Q

PO2, PCO2, FO2, FCO2

A

PO2 = PB x FO2
PCO2 = PB x FCO2

FO2 = 21%
FCO2 = 0.04%

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49
Q

what determines the amount of gas in solution?

A
  1. partial pressures of gas in solution
  2. solubility of gas
  3. temperature of solution
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50
Q

What is the relationship b/w pressure and solubility of O2 and CO2 in water?

A

At equilibrium, the partial pressures are the same, but more CO2 dissolves in water than oxygen does at the same pressure.

CO2 is more water soluble

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51
Q

What is Fick’s Law Of Diffusion

A

gas transfer = constant x partial pressure gradient x surface area / wall thickness

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52
Q

which respiratory diseases lower the PO2?

A
  1. Emphysema (misshapen alveoli -> reduced SA)
  2. Fibrotic lung disease -> wall thickness
  3. Pulmonary edema -> increased diffusion distance
  4. Asthma -> bronchoconstriction -> less O2 in
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53
Q

What are the consequences of low arterial PO2?

A
  1. low blood O2 concentration
  2. small gradient between blood and tissues
  3. low O2 delivery to tissues
  4. poor tissue function and disease
54
Q

How do PO2 and PCO2 change through the blood?

A

alveolar and arterial (100 and 40)
tissues and venous (40 and 46)
atmospheric (160 and 0.3)

see diagram.

55
Q

what percent of oxygen is transported in the blood vs dissolved in plasma?

A

98% vs 2%

56
Q

How much oxygen is released at the tissues during rest?

A

25%

55^ during excercise

57
Q

How do pH, temperature, and PCO2 impact Hemoglobin saturation of oxygen?

A
  • lower pH -> lower saturation (acidic environment)
  • higher temperature -> less saturation (denaturation)
  • higher PCO2 -> lower O2 saturation
  • 2,3-DPG -> lower saturation
58
Q

What is the relationship between fetal and maternal hemoglobin?

A

fetal hemoglobin has 2 alpha and 2 gamma chains -> more affinity for oxygen than maternal (2 alpha, 2 beta) -> increased fetal survival

59
Q

how is carbon dioxide transported in the blood?

A

7% dissolved in venous blood
23% bound to hemoglobin
70% formed H2CO3 via CA (carbonic anhydrase) -> HCO3(-) in plasma
- Cl comes in for HCO3 to go out
CA also -> H+, buffered by hemoglobin

60
Q

how is carbon dioxide released at the lungs?

A
  • dissolved CO2 diffuses into alveoli
  • Hb-CO2 dissociates, releasing CO2 into alveoli
  • HCO3 enters RBC (Cl out) -> H2 + CO2 via CA -> CO2 release
  • Hb-H dissociates to form H2 above
61
Q

What is the Haldane effect?

A

As PO2 increases, amount of CO2 carried decreases.

High PO2 -> oxygenated blood -> more CO2 offloaded at lungs
When PO2 low -> venous blood carries more CO2

62
Q

what do central and peripheral chemoreceptors respond to?

A

Central: increased [H+] in CSF
Peripheral: increased [H+] in blood; sensitive when PO2 low

63
Q

How do chemoreceptors influence ventilation?

A

Central chemoreceptors:
H+ -> medullary chemoreceptors -> medulla oblongata and pons stimulated -> somatic motor neurons (insp/exp) -> muscle movement

Peripheral chemoreceptors:
Low O2 + H+ -> carotid and aortic chemoreceptors -> afferent sensory neurons -> medulla oblongata and pons stimulated -> somatic motor neurons (insp/exp) -> muscle movement

64
Q

how do the central chemoreceptors respond to PCO2 to increase ventilation?

A

Increased PCO2 -> Increased H2CO3 -> increased H+ in CSF -> bind central chemoreceptor -> stimulate respiratory control centers -> increased ventilation -> reduced CO2

65
Q

how do the peripheral chemoreceptors respond to PO2 to increase ventilation?

A

Low PO2 -> close K+ channels -> depolarize cell -> open Ca channels -> exocytosis of dopamine containing vesicles -> action potential -> signal to medullary centers to increase ventilation

66
Q

how is the chemoreflex modulated by negative feedback loops

A

central response -> increased PO2, which inhibits stimulation of low pO2 on peripheral chemoreceptors in carotid and aortic bodies

central response -> low PCO2, which inhibits increased PCO2 response on central and peripheral chemoreceptors

67
Q

How is [CO2] vs [HCO3] modulated?

A

[CO2] by respiration, so faster (5-10 minutes)
[HCO3] by renal and other systems, so slower (8-12 hours)

68
Q

How does acidosis (inc H+) impact respiratory and metabolic pH regulation?

A

Respiratory:
reduced CO2 excretion (lung disease, overdose of sedatives)

Metabolic:
gain of H+, loss of HCO3 (ketoacidosis, diarrhea)

69
Q

How does alkalosis (dec H+) impact respiratory and metabolic pH regulation?

A

Respiratory:
excessive Co2 excretion (hyperventilation)

Metabolic:
loss of H+, gain of HCO3

70
Q

How does the body compensate for acidosis?

A

Chemoreceptors activated
1. breakdown bicarbonate stores to produced HCO3
2. bicarbonate binds H+ -> carbonic acid
3. carbonic acid goes to lungs -> CO2 and H20 release

H+ secreted by kidneys as NH4+. Other buffer systems absorb H+ -> reduced H+

71
Q

How does the body compensate for alkalosis?

A

Chemoreceptors inactivated
1. H2CO3 from lungs -> H+
2. H2CO3 form lungs -> HCO3 -> sodium bicarbonate in bicarbonate reserve
3. H2CO3 from kidneys -> H+ + HCO3
4. buffer systems release H+

72
Q

How do brain areas control respiratory rhythm?

A
  • Higher brain centers in the medulla oblongata -> pontine respiratory groups (PRG) -> input to VRG and DRG

Key point:
pre-motor neurons in the VRG and DRG activate the respiratory motor neurons in the spinal chord.

  • Nucleus tractus solitarius (NTS) contains dorsal respiratory group (DRG) -> phrenic nerves (cervical spinal chord C3-5) -> diaphragm
    - DRG -> intercostal nerves (thoracic spinal chord, T1-12) -> intercostal muscles (DRG goes to inspiratory muscles)
  • Ventral respiratory group (VRG) -> Pre-Botzinger complex (pacemaker)
  • VRG -> expiratory, some inspiratory, pharynx, larynx, and tongue muscles
73
Q

Which brain centers fire during inspiration?

A

pre-Botzinger, rostral VRG, phrenic nerve, a little bit of hypoglossal nerve, but fires more during expiration
- when isolated, pre-Botzinger in-vitro follows in vivo breathing patters

Botzinger complex does not fire.

Coordination between two systems

74
Q

What 8 factors influence rhythmic breathing?

A
  1. Voluntary control (speech) from motor cortex
  2. chemoreceptors -> chemical control of breathing
  3. reflexes like sneezing and coughing
  4. posture affects intercostal and abdominal muscles
  5. startling events
  6. emotions like fear, anxiety, sorrow
  7. exercise
  8. pain increases breathing
75
Q

What is the general organization of factors that affect breathing?

A

See image on slide (W5)

cough + voluntary control (motor cortex) + posture (cerebellum) + rhythm generator (medulla) -> respiratory motor neurons ^
|

emotions + limbic -> reticular formation <- sensory stimuli

76
Q

what is the feedback pathway that regulates breathing?

A

see slide W5

77
Q

where are stretch receptors found?

A

trachea to bronchioles, send info via vagus nerve

78
Q

what are the main functions of the stretch receptors?

A
  1. control breathing patterns: tidal volume and frequency
  2. respond to dyspnea (shortness of breath): mismatch b/w stretch receptors and chemoreceptors
79
Q

how does the hering breuer reflex prevent overstretching of the lungs?

A

When you take a slow deep breath,
- RAR afferent activity decreases
- SAR more activated
- Inc BP activates barroreceptors
- heart rate only lowers slightly, by 3 BP exhalation vs 8 BP inhalation

longer rhythmn doesn’t make huge difference in pressure, only a 5mmHg change -> no overstretching to compensate

80
Q

what are irritant receptors and what do they do?

A

found in airway and lung -> breathing and bronchoconstriction -> several reflexes.

laryngeal and tracheal receptors -> cough reflex via vagus nerve

epipharyngeal receptors -> aspiration reflex via glossopharyngeal nerve

nasal receptor -> sneeze reflex via trigeminal nerve

juxta-pulmonary nerve -> breathing via vagus nerve

81
Q

What factors impact TBW?

A

Sex:
men > women because men have more muscle and women have more fat

Age:
TBW decreases with age because you lose muscle and gain fat

Chronic illness:
Lose muscle mass reducing TBW

82
Q

What is the distribution of fluids in the body?

A

60% of weight is TBW
- 2/3 (40%) is intracellular
- 1/3 (20%) is extracellular

Extracellular division
- 75-80% interstitial
- 20-25% plasma

83
Q

How do solute concentrations vary in different compartments?

A

Na high in ECF, K high intracellular

Nah get out, K come in!

Osmolality is the same b/w compartments

84
Q

What does the NaK ATPase work, and what inhibits it?

A

Pumps out 2 Na, brings in 2K.

Uses ATP hydrolysis for energy

Ouabain and digoxin inhibit it:
- steroid derivative and steroid glycoside respectively

85
Q

What happens to ICF and ECF volumes if your drink water alone with no solutes?

A

ECF [Na] decreases -> osmolality decreases, pushing water from ECF to ICF -> increased cell size (hypotonic)

ECF and ICF volume increase

86
Q

What happens to ICF and ECF volumes if we eat salt (NaCl)?

A

ECF [Na] increases -> osmolality increased, pushing water from ICF to ECF -> hypertonic cells (cells shrink)

ECF volume increases, ICF volume decreases

87
Q

What determines the movement of fluids between interstitial and capillaries?

A

Starling forces:
Hydrostatic pressure gradient established by heart
- move fluid to ECF from caps
Oncotic pressure gradient from blood albumin
- move fluid to caps from ECF
Leaky capillaries -> fluid movement between pores

Fluid flux = permeability (hydrostatic - oncotic)

88
Q

how much of cardiac output is renal blood flow?

A

1/5

CO = 5L/min, RBF = 1L/min

89
Q

how do starling forces and blood flow impact ultrafiltration?

A

Starling forces are what produce ultrafiltration.

Pt (hydrostatic force) -> increased GFR
pi (oncotic pressure) -> decrease GFR
leaky capillary -> increased GFR
Q (plasma flow) -> increased GFR

90
Q

how is single nephron GFR (SNGFR) calculated?

A

SNGFR = Kf (delta P - delta pi)

deltaP = Pt(GC) - Pt(tubular)

deltapi = pi(GC) - pi(t)

91
Q

what is the glomerular filtration rate?

A

100-125mL/min or 150-180L per day

92
Q

what is the most important determinant of GFR?

A

renal blood flow, which is determined by blood flow and vascular resistance

93
Q

how does autoregulation of renal blood flow and GFR work?

A

renal blood flow is consistent across mean arterial pressures (70-150mmHg)
myogenic reflex in afferent arteriole impacts BP -> GFR
- BP falls -> vasodilation in afferent arteriole -> increase blood flow -> increased renal capillary pressure -> increased GFR
- BP rises -> vasoconstriction in afferent arteriole -> increased resistance -> less blood flow -> reduced renal capillary pressure -> reduced GFR

94
Q

what is the tubular-glomerular feedback (TGF)?

A

increased Na @ juxta-glomerular junction -> adenosine release -> VSMC (vascular smooth muscle cell) constriction in afferent arteriole -> increased resistance -> reduced plasma flow -> reduced GFR

95
Q

How does the efferent arteriole increase GFR?

A

angiotensin release -> efferent arteriole constriction -> increase capillary pressure -> increased GFR

96
Q

what is convection?

A

Movement of small solutes with bulk flow of water.

97
Q

what is perm selectivity

A

the idea that proteins increasing in size are less permeable to glomerular capillary membrane

98
Q

what size and charge of a molecule increases its perm selectivity?

A

< 15 kDa -> freely filtered
Positive charge

99
Q

how much albumin does a healthy person excrete?

A

10mg/day

100
Q

How does creatinine measure GFR?

A

produced by muscles, freely filtered and not absorbed. what goes in comes out.

measure creatinine clearance = (urine flow rate) x urine creatinine / plasma creatinine = 90-120mL/min

GFR best indicator of kidney health

101
Q

how is perm-selectivity measured in humans?

A

total protein : 0.15mg/day
albumin: 30mg/day in urine

102
Q

how is water filtered in the glomerulus?

A

plasma flow (500mL/min) reaches afferent arteriole, 20% filters into nephron, >19% reabsorbs

103
Q

How do polarized kidney epithelial cells reabsorb Na?

A

a) sodium hydrogen exchanger (NHE) on luminal membrane brings Na into cell while pumping H out
b) sodium co-transporters: Na transported with gluc, phosphate, etc. (SGLTs, NaP)
c) epithelial sodium channel (ENaC) brings sodium in

Na/K ATPase on basolateral membrane pushes Na into blood/interstitium for reabsorption

104
Q

Proximal tubule

A

“Power House - bulk reabsorption”
2/3 reabsorption of Na, Cl, K, water, bicarbonate

Luminal sodium transport protein:
NHE3

Glucose, phosphate, amino acid co-transporters only found here

bicarbonate reabsorption

very leaky

105
Q

Thick ascending limb of loop of henle

A

20-30% of filtered sodium

Luminal transport protein:
Na-K-2Cl (NKC22) inhibited by furosemide

water impermeable; fluid leaving is else concentrated than plasma (hypotonic)

salt added to instersitium without water -> concentrates urine

106
Q

Distal convoluted tubule

A

reabsorbs 5-10% filtered Na and water

Luminal sodium transport:
sodium chloride co-transporter
inhibited by thiazides (less potent than furosemide)

urinary dilation

107
Q

collecting duct

A

reabsorbs 1-3% filtered Na

Luminal sodium transport:
ENaC (epithelial sodium channel)

aldosterone -> more sodium reabsorption (more channels)

vasopressin (ADH) -> water reabsorption via aquaporin-2

less permeable to chloride. negative charge of lumen -> K secretion (+ charge)

108
Q

relationship between glucose filtration and plasma concentration

A

Linear until you reach transport maximum (300mg/mL) @ 375mg/min

glucose not excreted until maximum is reached

109
Q

how is glucose transported from the kidney lumen to ECF

A
  1. Na-Gluc symporter brings glucose into epithelial cell with Na (low affinity, high capaccity)
  2. GLUT transporter brings gluc to ECF via facilitated diffusion (high affinity, low capacity)
110
Q

How much sodium does the kidney glomerulus filter each day?

A

22,500 mmoles liters

111
Q

How do you lose sodium?

A
  • sweating
  • diarrhea
  • vomiting
  • hyperglycemia

Diuretics (increased production of urine)
- blood loss
- decreased intake

112
Q

how do you gain sodium

A

Diet: processed food, fast food

113
Q

how much sodium is excreted

A

150 mmoles, from 21,000 mmoles filtered, so < 1%

114
Q

What sensors sense a loss of BP in the plasma?

A

Arterial baroreceptors (carotid body and aortic arch), afferent arteriole
- signal to brainstem via nerves IX (carotid) and vagus (X)
- sense wall tension

atrial stretch receptors

115
Q

how do arterial baroreceptors sense low blood pressure and modulate SNS output?

A

sense wall tension from high pressure and high volume -> increased nerve traffic -> decreased SNS output

less traffic -> increased SNS output “balloon too empty”

sensory nerve fibers -> baroreceptors in internal carotid artery walls + carotid body chemoreceptors + baroreceptors in aorta

parasympathetic nerve fibers -> SA node

sympathetic nerve -> heart

116
Q

how does SNS activation impact the renin-angiotensin system?

A

renin converts angiotensinogen to angiotensin I -> angiotensin II via ACE

117
Q

How does the afferent arteriole impact the renin-angiotensin system?

A

low pressure -> afferent arteriole -> renin -> renin converts angiotensinogen to angiotensin I -> angiotensin II via ACE

118
Q

how is renin stimulated?

A

baroreceptors in aorta, carotid body, afferent arteriole, low Na intake

119
Q

how does angiotensin II increase Na reabsorption by the kidney?

A

Proximal tubule:
increase activity of NaH antiporter

Distal convoluted tubule:
increase activity of NCC

increased resistance -> decreased hydrostatic pressure + increased oncotic pressure in peritubular capillaries -> net reabsorption in peritubular capillaries

Collecting duct:
angiotensin II -> aldosterone -> transcription -> open Na channels + more Na channels + more Na/K ATPases

120
Q

What happens when you eat too much sodium or sit in a hot-tub?

A

Water increases in ECF -> excrete more sodium (?)

121
Q

how do atrial myocytes modulate sodium levels?

A

in response to increased atrial vascular stretch (high volume) -> ANP hormone -> aldosterone + vasodilation -> increased GFR -> reduced Na reabsorption in collecting duct (CD)

122
Q

how does ANP alter CD reabsorption of Na?

A

binds receptor NPR-A on lumen -> cGMP -> inhibition of ENaC, NaK ATPase + TPR2

inhibits Na reabsorption

123
Q

How accurately does the kidney maintain ECF volume?

A

when having excess Na consumption, takes time for ECF volume to increase to 300 mMol.

after a few days new steady state is made for Na where intake == excretion

124
Q

where is water reabsorbed in the kidney

A

PT: 70%
Loop: 15%
DCT + CT: 15%

125
Q

what is the normal volume of excreted water in the kidneys? abnormal?

A

Normal: 1.5L/day (<1%)
Dehydrated: 0.5L (<0.3%)
Over-hydrated: 3.0L (<2%)

126
Q

How are water levels sensed in the body?

A

hypothalamic osmoreceptors located in anterior hypothalamus OVLT via stretch inhibited channels
- osmoreceptor cells shrink with low water -> channels open -> depolarize cell -> action potential -> increased AVP + thirst

127
Q

how does the loop of henle concentrate urine?

A

countercurrent multiplication

from cortex to medulla, you have a concentration gradient going from less to more concentrated -> water pushed out of descending tubule. ascending water impermeable -> no water movement, but Na move out of tubule.

128
Q

how does vasopressin (ADH) respond to decreased cell size (hypertonic)

A

vasopressin binds receptor -> cAMP activation -> inserts AQP2 into apical (luminal) membrane -> water from CD lumen to blood

129
Q

how do you make concentrated urine generally? (desert)

A

> 300mosmol/kg
- hypertonic medullary intersitium
- NaCl added from ascending limb into urine, and urea from MCD
- countercurrent arrangement of vessels -> maintain solutes
- vasopressin opens water channels
- water from lumen to interstitium

130
Q

how do you make dilute urine? (chug chug chug)

A

<300mosmol/kg
- no ADH -> collecting duct water impermeable
- NaCl reabsorbed by DCT, CCD, MCD -> dilute urine
- minimum urine osmolality (50mosmol/kg)

PSL301 (2 decks)

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