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Physiology Final > physiology final > Flashcards

physiology final Flashcards

2
Q

What is the job of the kidneys?

A

maintain the constancy of the body’s internal environment

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3
Q

How do they accomplish this?

A

By regulating the volume and composition of extracellular fluids

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4
Q

What do they use to excrete metabolic end products?

A

Nephrons

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5
Q

What else are the kidneys involved with?

A

regulation of the total amount of many important substances in the extracellular matrix.

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6
Q

What are the 7 main functions of the kidneys?

A

1- regulation of the concentration of numerous ions. 2- excretion of organic compounds. 3- fluid balance. 4- acid-base balance. 5- blood pressure regulation. 6- erythrocyte volume regulation. 7- Vitamin D activation

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7
Q

How do the kidneys accomplish #1? (from previous ?)

A

excretion or preservation of Na, Cl, K, Ca, PO4 - balance their intake, production or excretion through other routes

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8
Q

How is #2 accomplished?

A

1) elimination of substances like urea and creatinine in amounts equaling their production rates. 2)elimination of drugs, FO, and toxins

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9
Q

3?

A

1)regulate water. 2) regulate osmotic pressure of EC fluids. 3) produce urine

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10
Q

4?

A

excretion of H+ or HCO2 as needed

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11
Q

5

A

renin-angiotensin system and renal-body fluid balance system

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12
Q

6>

A

through formation and release of erythropoetin

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13
Q

7?

A

vitamin D hydroxylation to render it useful.

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14
Q

How much more salt than water do humans typically consume each day?

A

20-25%

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15
Q

How is that excess salt/water disposed of?

A

Urine

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16
Q

What sensors determine how much is to be excreted?

A

water volume sensors, salt sensors, osmolality sensors,

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17
Q

How do these sensors instruct the kidneys on what to do?

A

via hormones.

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18
Q

Where does all the action in the kidney take place?

A

Nephrons

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19
Q

What is a nephron encased in?

A

a maze of peritubular capillaries

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20
Q

What are the components of a nephron?

A

1) Glomerular capsule, 2) PCT, 3) loop of Henle, 4) DCT, 5) collecting duct

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21
Q

What are the components of the vasculature of a nephron?

A

1) intralobular artery. 2) afferent arteriole 3) glomerulus 4) efferent arteriole 5) peritubular capillaries 6) venule and intralobular vein

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22
Q

What are the 3 versions of a nephron?

A

1) superficial. 2) mid-cortical. 3) juxtamedullary

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23
Q

What 3 activities do kidneys engage in?

A

1) filtration 2) reabsorption 3) secretion

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24
Q

Where is the bulk of the work done?

A

in glomeruli and PCTs

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25
Q

What remains in the final end of the tubules?

A

urine

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26
Q

How does blood enter the kidney and nephron?

A

through Renal artery

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27
Q

What does the blood return to circulation through?

A

renal vein

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28
Q

The nephron is said to “clear” what?

A

the blood of unwanted substances - removes unwanted agents from the plasma

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29
Q

What is clearance?

A

the amount of plasma cleared of a given substance

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30
Q

How can glomerular filtration rate be measured?

A

by looking at the clearance of something that is freely filtered and not reabsorbed at all.

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31
Q

How can you measure cortical perfusion?

A

by looking at the clearance of something that is secreted from the peritubular capillaries into the nephric tubules

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32
Q

What establishes a natural filtration and absorption process?

A

normal blood pressure and osmotic drives

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33
Q

How does blood pressure move water?

A

creates a hydraulic “push”

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34
Q

How does osmotic drive move water?

A

osmotically active solutions “draw” water toward them.

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35
Q

What happens to pressure through the nephron?

A

steadily falls

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36
Q

What are two critical locations for pressure ?

A

1) Glomerular capillaries. 2) peritubular capillaries

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37
Q

What happens in glomerular capillaries?

A

High BP like arteriole end of a system capillary

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38
Q

What happens in the peritubular capillaries?

A

Low BP like venule end of systemic capillary

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39
Q

What do high pressure beds create?

A

net outward flow (loss)

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40
Q

What do low pressure beds create?

A

net inward flow (gain)

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41
Q

What order does fluid flow through PCT and Peritubular cap beds?

A

PCT first, then into peritubular.

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42
Q

How does osmolality and glomerulus set up return of water?

A

glomerulus loses fluid but keeps cells and proteins, peritubular caps are very osmotically active - draws fluid back from nephric tubules.

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43
Q

Does water resorption become easy or difficult?

A

Increasingly difficult.

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44
Q

What is glomerulonephritis?

A

disorder of renal glomeruli - collection of diseases that effect the glomerular membrane.

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45
Q

What is the most common subtype?

A

inflammatory processes - diffuse proliferative form

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46
Q

What is the most common cause?

A

Post-streptococcal glomerulonephritis

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47
Q

What are the clinical features?

A

Oliguria (decreased urine output. Edema. HTN. Foamy urine. Brown urine

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48
Q

Lab findings?

A

Glomerular caps appear damaged. Hematuria. Proteinuria. Immunofluorescence shows granular deposits.

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49
Q

What does chronic form lead to?

A

renal failure - steady loss of glomeruli

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50
Q

What does renal function begin with?

A

production of glomerular filtrate

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51
Q

What is the overall strategy in the urinary system?

A

filter huge amounts of blood and recover nearly all of the good stuff.

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52
Q

How much renal blood flow is there?

A

1000 - 1200 ml/min to kidneys

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53
Q

How much cardiac output does this equal?

A

20-25%

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54
Q

What is this known as?

A

The renal fraction

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55
Q

What is glomerular filtrate?

A

the amount of plasma “lost” from blood volume when delivered to glomeruli

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56
Q

how much is produced from glomeruli filtation?

A

160 - 180 l/day (2x ones body weight)

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57
Q

How much is recovered after glomeruli filtration?

A

1 -2 l/day leaves as urine. = recovery rate of 99%

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58
Q

What type of membrane is on glomeruli?

A

consists of type 2 capillaries and a visceral bowmans capsule covering of podocytes`

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59
Q

describe the permeability of glomeruli capillary beds?

A

several hundred times more permeable than the typical type 1 kind

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60
Q

What does this allow for?

A

Substantial filtering

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61
Q

What determines what passes through?

A

size, molecular shape and charge.

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62
Q

what does the endothelium block?

A

formed elements fenestrations much smaller than platelets

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63
Q

What does the basement membrane block?

A

proteins negatively charges basement membrane materials repel negatively charged plasma proteins

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64
Q

what are slit pores?

A

space between pedicels that allows the remains to flow through.

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65
Q

What is glomerular filtration a function of?

A

pressure across the glomerular membrane.

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66
Q

what is the capillary blood pressure?

A

60 mmHg = outward force

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67
Q

What is the colloidal osmotic pressure?

A

32 mmHg = inward force

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68
Q

What is the capsular pressure of filtrate?

A

18 mmHg = inward, backward force

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69
Q

is capillary force higher or lower than systemic capillary blood pressure?

A

very high

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70
Q

When does colloidal osmotic pressure rise?

A

as filtration continues

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71
Q

What is the net driving force?

A

adding up forces 60 + (-)32 + (-)18 = 10 mmHg OUT

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72
Q

what is total filtration?

A

NDF x Kf (filtration coefficient) = GFR

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73
Q

what is the GFR

A

glomerular filtration rate

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74
Q

What would the GFR be for the above info?

A

12.5 ml/min/mmHg X 10 mmHg = 125 ml/min

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75
Q

What would the GFR be for an entire day?

A

125 ml/min X 60 min X 24 hr = 180 liters/day

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76
Q

What would affect this total?

A

increased or decreased glomerular pressure.

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77
Q

How do fluctuations in BP alter GFR?

A

They probably don’t alter it much. (unless it’s an extremely dramatic change)

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78
Q

What is the autoregulation range?

A

when MAP is between 80 and 180 mmHg

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79
Q

What kind of innervation is significant to the kidneys?

A

Sympathetic

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80
Q

Is it more extensive to afferent or efferent?

A

afferent

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81
Q

What substances can cause renal arterial vasoconstriction?

A

Angiotensin 1. vasopressin/ADH, epi, norepi, thromboxane A2, endothelin

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82
Q

which cause vasodilation?

A

Acetylcholine, ANP, dopamine, histamine, nitric oxide, some prostaglandins

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83
Q

What does an increase or decrease in plasma colloidal osmotic pressure cause?

A

in hypoproteinemia it causes edema in systemic capillaries

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84
Q

What happens with an increase of decrease in bowmans capsule pressure?

A

tubule obstructions or severe kidney stones will cause fluid to back up and increase pressure

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85
Q

what happens with an increase or decrease in glomerular capillary permeability?

A

thickening or plugging of membrane pores

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86
Q

What happens with an increase or decrease in glomerular capillary total surface area?

A

glomerular destruction will decrease available membranes for GFR. (seen with nephric disease that remove functional tissue.

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87
Q

What is final Glomerular filtrate normally similar to?

A

Plasma minus its proteins.

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88
Q

What is glomerulonephritis?

A

a disorder of renal glomeruli usually due to inflammatory processes, most commonly as a diffuse proliferative form

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89
Q

What does post-streptococcal glomerulonephritis result in?

A

deposition of circulating immune complexes that further attract neutrophils

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90
Q

What happens to the G membrane?

A

becomes clogged and inflammatory reaction make it worse

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91
Q

What are the clinical features?

A

oligouria due to loss of filtration. Edema and HTN due to fluid accumulation

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92
Q

What are the lab findings?

A

G capillaries appear damaged -> hematuria. Foaming of urine from proteinuria. Thickening of G membrane

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93
Q

Is there treatment?

A

yes. Mild can heal on own. Eliminate HTN. dialysis

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94
Q

What is Fanconi’s syndrome?

A

a collection of very uncommon diseases that involve the kidneys

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95
Q

What do all forms affect?

A

The behavior of the nephron, especially PCT

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96
Q

What does this result in?

A

deficient renal tubular excretion

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97
Q

What are common sources of this problem?

A

alteration in transporters. Disturbances in cellular energy metabolism. Changes in permeability

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98
Q

Clinical signs?

A

in children: polydipsia, malnutrition, infection. Adults: pain in weight bearing joints, dehydration

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99
Q

Lab findings?

A

aminoaciduria, cystinuria, glycosuria, phosphaturia. Hypokalemia, metabolic acidosis, hypercalciuria

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100
Q

What is the principle activity in the nephric tubules?

A

recovery of most filtrate.

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101
Q

What is the primary function of the rest of the nephron?

A

reabsorption of glomerular filtrate

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102
Q

What are the 4 mechanisms of tubule exchange?

A

1) some substances actively resorbed. 2) some actively secreted. 3) some passively resorbed 4) some passively secreted

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103
Q

What is the flow rate of G filtrate suggestive of?

A

where most of the work is done.

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104
Q

Where is flow rate highest?

A

PCT

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105
Q

2nd highest?

A

Loop of Henle

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106
Q

3rd highest?

A

DCT

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107
Q

4th highest?

A

collecting duct

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108
Q

What does flow rate begin and end at within the PCT?

A

125 ml/min and falls to 45 ml/min

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109
Q

What does flow rate fall to at end of DCT?

A

15 ml/min

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110
Q

What does flow rate fall to at end of CD?

A

0.7 ml/min

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111
Q

How much urine does this work result in each day?

A

1 l/day. (0.7 X 60 X 24)

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112
Q

How much nephric flow takes place in PCT?

A

2/3 of all flow. (70% of water resorption)

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113
Q

What 3 kinds of basic solutes does the kidney process in the tubules?

A

1) Nutritionally important substances. 2) ions/electrolytes 3) metabolic end-products

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114
Q

What does the recovery of specific filtered solutes reveal?

A

reveals what part of the nephron does what.

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115
Q

How are nutritionally important solutes absorbed?

A

to completion

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116
Q

What kind of transport is the basic mechanism of glucose?

A

secondary active transport

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117
Q

What is co-transport of Na+ and GLU made possible by?

A

Na+/K+ exchange pump (requires ATP)

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118
Q

How does GLU moves across the basal side into the ECM?

A

facilitated diffusion. (with GLUT2 protein)

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119
Q

What does GLU transportation require?

A

Energy

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120
Q

What is total GLU absorption a function of?

A

The number of transporters. (which is a function of surface area)

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121
Q

How much is normally absorbed?

A

All of it. Absorbed to completion

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122
Q

What is TMG?

A

total glucose that can be absorbed… tubular transport max

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123
Q

What does this represent?

A

The number of funtioning nephrons.

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124
Q

What is the estimated amount?

A

350 mg/min

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125
Q

What is this AKA?

A

tubular absorption capacity.

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126
Q

What does this mean?

A

tubules can reabsorb 350 mg of glucose every minutes

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127
Q

Where is it done?

A

PCT

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128
Q

What is the renal threshold of glucose?

A

where glucose might appear in urine

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129
Q

How can renal threshold be calculated?

A

by using TMG (375..round up from 350?). a GFR of 125. and plasma glucose concentration of 100 mg/100ml = (375/1)x(1min/125ml)x(100/100) = 300mg/100ml of plasma.

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130
Q

Is this quantity higher or lower than normal plasma glucose levels?

A

higher.

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131
Q

What does that mean?

A

no glucose should be in the urine.

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132
Q

What does this say about the kidneys?

A

That they are not meant to control the concentration of blood glucose.

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133
Q

What happens to the amount of GLU resorbed compared to filtered load?

A

they match up…. to a point

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134
Q

When will excretion happen?

A

When the TMG is reached.

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135
Q

What is the actual renal threshold for glucose?

A

180 - 200 mg/dl

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136
Q

What is this number due to?

A

splay or bending in the theoretical curve.

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137
Q

What does splay represent?

A

nephron variability

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138
Q

What is there a specific transporter for?

A

each kind of sugar and for each kind of facilitated diffusion on the basal surface

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139
Q

Where are larger carbohydrates broken down?

A

PCT

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140
Q

What enzyme does this?

A

surface amylase. (and maltase)

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141
Q

What are they broken down to?

A

simple sugars

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142
Q

How are some large carbohydrates brought across the tubule wall, and what is their fate?

A

Pinocytosis.. lysosomal destruction

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143
Q

How are amino acids moved across?

A

similar to simple sugars (and glucose). By secondary active transport.

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144
Q

Where are larger peptides broken down?

A

PCT.

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145
Q

What breaks them down?

A

surface peptidases

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146
Q

What are they broken down to?

A

to amino acids.

147
Q

What are all the previous substances considered to be?

A

nutritionally important.

148
Q

Where have all of the previous substances been reabsorbed, and to what extent?

A

in the PCT and to completion

149
Q

When do the rest of the tubules become important?

A

When processing substances that the PCT did not complete

150
Q

What is the average intake of salt per day?

A

8-15 g/day

151
Q

What is the most common cation of the ECM?

A

Na+

152
Q

Why are there multiple methods for Na+?

A

because it is linked to the cotransport of many solutes.

153
Q

Wherre does the Na+/K+ exchange pump move Na+ to?

A

exterior of the cell on the basal surface.

154
Q

Why does Cl- generally follow Na+?

A

for electrogenic reasons.

155
Q

How much Na+ and Cl- are resorbed in the PCT?

A

65 percent

156
Q

Where else, and how much, are they resorbed?

A

25% in asc. Limb of loop of henle. 5% in DCT. 5% in CD.

157
Q

What does the amount of resorption equal?

A

the amount of salt intake (until there is excess)

158
Q

How can reabsorption be INDIRECTLY controlled?

A

by body osmolality

159
Q

What hormone controls this?

A

aldosterone

160
Q

What does aldosterone work through to achieve this?

A

BP regulatory scheme.

161
Q

What does increase aldosterone lead to?

A

increased Na+ resorption

162
Q

What does decreased aldosterone lead to?

A

decreased Na+ resorption

163
Q

How does aldosterone work?

A

it works on DCTs by altering the number of Na+/K+ exchange pumps and their activity

164
Q

What kind of regulation is this?

A

Distal nephron function

165
Q

What else does Na+ (and Cl-) effect?

A

the macula densa

166
Q

When does it effect the macula densa?

A

as filtrate passes through the DCT (the densa cells communicate with JG cells)

167
Q

What does increased Na+ do to JG cells?

A

stimulates them to decrease secretion of renin (and angiotensin) and decrease aldosterone

168
Q

What does decreased Na+ do to JG cells?

A

stimulates them to increase secretion of renin (and angiotensin) and increase aldosterone

169
Q

What does changing Na+ intake do? (big picture)

A

alter water retention, lead to changes in BP, and CV changes that will lead to altering Na+ retention

170
Q

What are the kidneys the prime regulators of?

A

body sodium (and chloride) content

171
Q

What is ANF?

A

atrial natriuretic factor (or peptide… ANP)

172
Q

What does it do?

A

its a hormone from the right atrium and has a potent effect on kidneys. Acts as a diuretic.

173
Q

When is it released?

A

with atrial stretch.

174
Q

What does a release of ANF cause?

A

increased production of urine and thereby decrease blood volume

175
Q

What else does this hormone cause?

A

decreased renin release. Decreased aldosterone secretion

176
Q

What is potassium?

A

a potentially dangerous cation

177
Q

Where is K+ processed?

A

It is variably processed by nephric tubules.

178
Q

What much match K+ intake?

A

urinary excretion

179
Q

Where is 98% of K+ found?

A

inside cells (internal K+ balance)

180
Q

What factors effect K+ balance within cells?

A

many factors: notably, stimulants and acid/base chemistry of the ECF

181
Q

What factors increase K+ levels in the ECF? And what do they lead to?

A

hyperosmolarity, cell lysis, exercise, acidosis. They lead to Hyperkalemia

182
Q

What factors decrease K+ levels in the ECF? What does this lead to?

A

Hypo-osmolarity, insulin, alkalosis. Leads to Hypokalemia

183
Q

What are two kinds of alpha and beta adrenergic agonists?

A

norepi and epi.

184
Q

How do norepi and epi have variable effects on cells?

A

they enhance or inhibit the Na+/K+ exchange pump.

185
Q

What do some alpha antagonists cause?

A

decrease in plasma K+ levels

186
Q

What do some beta antagonists cause?

A

increase in plasma K+ levels (propanolol)

187
Q

How is processing of K+ accomplished?

A

By way of active pumps and simple channels.

188
Q

How much resorption of K+ is done in PCT?

A

70 percent

189
Q

Where else is it resorbed and how much?

A

20% in loops of henle, and 10% in DCT (and upper CD)

190
Q

What mechanism for K+ resorption is used in PCT?

A

passive. With NaCl and water

191
Q

Where does the critical action of resorption of K+ take place?

A

DCT

192
Q

What does the primary mechanism for K+ resorption depend on?

A

the DCT cell sub-type.

193
Q

What are the two sub-types?

A

Alpha-intercalated and principle.

194
Q

What determines which sub-type is used?

A

body needs. And electrochemical gradient that drives K+

195
Q

which sub-type is used with decreased K+ intake?

A

Resorption = alpha-intercalated cells

196
Q

which sub-type is used with increased K+ intake?

A

Secretion = principle cells

197
Q

Which is the main action?

A

principle cells

198
Q

What factors affect the principle cells?

A

Dietary K+, Aldosterone, Acid-base, flow rate, luminal anions

199
Q

What does this insure?

A

that K+ levels do not rise too high in the blood

200
Q

What does increase aldosterone cause with K+? and how?

A

decrease K+. by minimizing secretions in DCT

201
Q

What is the prime regulator of the body’s K+ content?

A

the kidneys, duh

202
Q

How much more H2O does the average human consume than is needed?

A

20-25%

203
Q

What is the average intake of H2O per day?

A

2.5 Liters

204
Q

Which is tougher to manage -> H2O disposal, or H2O retentions?

A

Retention

205
Q

How much H2O is resorbed in the PCT?

A

70%

206
Q

Where else is H2O resorbed?

A

15% in loops, 5% in DCT, 10% in CD

207
Q

How does the nephron adjust body water levels?

A

By producing either a dilute or concentrated urine

208
Q

What kind of urine does excess body water lead to?

A

dilute urine… increased urine volume

209
Q

What kind of urine does lack of body water lead to?

A

concentrated urine… decreased urine volume.

210
Q

What is osmolality?

A

measure of the tendency of a solution to induce osmosis.

211
Q

What is the average body fluid osmolality?

A

300 mOsm… body/blood osmolality

212
Q

Which portion of the tubules is relatively impermeable to water?

A

CD

213
Q

What is the average osmolality in the PCT?

A

300 mOsm

214
Q

What is the average osmolality in the DCT?

A

100 mOsm

215
Q

What about in the CD?

A

can fall to 50 mOsm (very dilute, but not 0 because of regular waste)

216
Q

What does this mean?

A

Whatever is left in the DCT will probably flow out with urine

217
Q

What has to happen to the CDs to maintain renal concentration?

A

they need to become more permeable to give water a reason to want to leave.

218
Q

Where does the bulk of water recovery happen?

A

in the PCT and into peritubular capillaries.

219
Q

What do the medullar peritubular capillaries recover?

A

The resorbed water from the CD

220
Q

How many nephrons are JM?

A

15%

221
Q

Do animals with high urine concentration ability have more or less JM nephrons?

A

much higher…. i.e. hopping mouse has 85% JM

222
Q

What is related to renal concentration ability in animals?

A

loop number and length.

223
Q

What are counter-current systems?

A

pipes that double back on itself. - they have special properties.

224
Q

What do counter-current systems involve?

A

allowing a tubule to communicate with itself.

225
Q

How is this communication accomplished?

A

through the loops of henle!

226
Q

In kidneys, instead of heat (his analogy for CC systems) what is magnified?

A

osmolality

227
Q

What about loops of henle make this possible? (specific feature)

A

thick ascending segments and counter-current flow

228
Q

What is possible through the thick ascending loops?

A

actively pumping NaCl into the interstitium

229
Q

Step 1:

A

filtrate goes through thick ascending loops and pumps NaCl out to interstitium (CC multiplier)

230
Q

Step 2:

A

after increase in NaCl , new filtrate enters descending limb - H2O leaves to saline interstitium = further concentrates tubule

231
Q

Step 3:

A

Subsequent filtrate reach thick asc loops, NaCl pumping out still, Solute REENTERS desc limb = further concentrating it

232
Q

Step 4:

A

Subsequent filtrate in thin limb has vigorous H2O removal (hypertonicity). = Thin limbs equilibrate with interstitium

233
Q

Step 5

A

Dilute tubular fluid passes to distal nephron. Exposed to hypertonic medullary interstitium. = Powerful osmotic drive for H2O to leave.

234
Q

Step 6:

A

ADH present. H2O leaves to interstitium = concentrated urine in tube. Antidiuresis now makes concentrated urine.

235
Q

What determines the degree of hypertonic medullary interstitium (high osmolality)?

A

the length of the loops

236
Q

What is the saltiest place in the human body?

A

Medullay pyramids.

237
Q

What important structures insure all of this happens?

A

The vasculature in the area.

238
Q

What do vasa recta do?

A

serve to preserve and accentuate the effect. Also recover NaCl from filtrate

240
Q

Step 1:

A

blood descends in medullary interstitium. H2O leaves and NaCl enters = Increase in osmolality of vasa recta blood.

241
Q

Step 2:

A

Blood returns from deeper medulla is high concentrated and loses its NaCl to the upper interstitium and H2O enters.

242
Q

What do ascending vasa recta do?

A

Serve to capture resorbed H2O from CDs

243
Q

Where do they send this?

A

to the body

244
Q

Why is ADH critical?

A

changes the permeability of the CDs.

245
Q

What does an increase in ADH cause?

A

water recovery ? increased urine

246
Q

What does decreased ADH cause?

A

water loss ? decreased urine

247
Q

Where is ADH synthesized?

A

in neuro-secretory cells of the paraventricular nuclei and supraoptic nuclei of the hypothalamus

248
Q

Where do they project axons to?

A

posterior pituitary

249
Q

Where does ADH land on the kidneys?

A

receptors (V2) of the CD

250
Q

What does this cause?

A

insertion of reserve pools of cytoplasmic aquaporin-2 proteins.

251
Q

What is increased when this happens?

A

increases permeability of these cells. Also increases synthesis of aquaporins

252
Q

What do the membranes of epithelial cells lack in tubules that are relatively impermeable to water?

A

aquaporins.

253
Q

What is diabetes insipidus?

A

failure of ADH

254
Q

What does it cause?

A

excessive excretion of large amounts of dilute urine. Excessive thirst.

255
Q

What are the causes of diabetes insipidus?

A

insufficient secretion of ADH, inheritance of mutated gene for ADH V2 r/c, inheritance of mutated gene for aquaporin-2

256
Q

How much filtrate could be lost each day with DI?

A

20 liters

257
Q

What is pyelonephritis?

A

an infection of the kidneys; more common in adult females.

258
Q

What causes pyelonephritis?

A

bacteria condition of the renal medullary pyramids originating from reflux in urine from bladder.

259
Q

What are the acute symptoms of pyelonephritis?

A

fever. Burning urine. Aching ab pain.

260
Q

What kind of urine do you find in pyelonephritis?

A

dilute urine…

261
Q

Why?

A

Invasion of bacteria in the medullary pyramids lessen their ability to produce hypertonic osmolality.

262
Q

What is urine concentration and diuresis determined by?

A

changes in body chemistry

263
Q

What is water diuresis?

A

common experience involving increased urine output due to water causing the posterior pituitary to lessen the amount of secreted ADH.

264
Q

What is water intoxication?

A

When water intake exceeds the bodies ability to expel it

265
Q

What is the normal max diuresis?

A

About 16 ml/min.

266
Q

What is considered too much intake of water?

A

when intake exceeds a sustained rate of 1 l/hour.

267
Q

What can happen at this point?

A

brain edema ? convulsions, death

268
Q

What kind of urine is produced with diabetes mellitus?

A

sweet urine!

269
Q

Why is it sweet?

A

because the Tmg of the PCTs is exceeded.

270
Q

How much urine is produced in diabetes mellitus?

A

a large amount due to osmotic load on the nephrons. (known as osmotic diuresis)

271
Q

What is hydrogen disposed as?

A

as an acid

272
Q

What 3 mechanisms manage hydrogen concentration?

A

Blood plasma buffers. Respiratory ventilation. Renal excretion of an acid or alkaline urine.

273
Q

How does blood plasma buffers manage H concentration?

A

rapidly- taking seconds to accomplish , with minimal gain due to temporary binding of hydrogen

274
Q

How does respiratory ventilation manage [H]?

A

Slower taking minutes to an hour with higher gain due to change in plasma chemistry (as HCO3)

275
Q

How does renal excretion of an acid or alkaline urine manage [H]?

A

slow, taking hours to days with the highest gain since it results in true elimination from body.

276
Q

How do the kidneys regulate [H+]?

A

by increasing or decreasing [HCO3]

277
Q

Where is filtered bicarbonate primarily resorbed?

A

in the PCT

278
Q

Where is resorption of bicarbonate finished?

A

in the distal nephron

279
Q

Where is the final acidity completed?

A

in the distal tubules. Therefore it is the most important determinant in the final pH of the urine.

280
Q

What actively secretes H+?

A

the nephron

281
Q

How is H+ ultimately lost?

A

as H2O in urine

282
Q

Is urine normal acidic or basic? And why?

A

slightly acidic because all the HCO3- is resorbed, leaving the urine with a lower pH

283
Q

What is the normal pH of urine?

A

6.5 - 7 can vary

284
Q

What is the range of pH urine could be within?

A

4.5 - 8.5

285
Q

Why won’t it fall below 4.5?

A

That is the level when active secretion is exceeded.

286
Q

What are acids and acidifying salts as diuretics?

A

some of these supply nephrons with a filtered acid load that counteracts the ability to secrete H+

287
Q

What does this lead to?

A

ability to exchange Na+ is somewhat compromised (also, with increased Na+ comes increased H2O loss)

288
Q

What is acidosis?

A

increase in H+ (decreased pH)

289
Q

What does this cause?

A

as H+ rises it exceeds available HCO3- to titrate against ? acid urine

290
Q

What is alkalosis?

A

increasesd HCO3-

291
Q

What does it lead to?

A

as HCO3- rises it exceeds available H+ secretions ? alkaline urine

292
Q

What 2 chemical systems handle the buffering of H+ in distal nephron?

A

phosphate buffer. Ammonium buffer.

293
Q

What is the phosphate buffer?

A

HPO4-2 + H+ ? H2PO4-

294
Q

What is the ammonium buffer?

A

NH3 + H+ ? NH4+

295
Q

Where is ammonia produced?

A

from glutamine in the nephron

296
Q

Why does urine sometimes smell like ammonia?

A

ammonia ion being converted back to ammonia when exposed to air (has to sit in open air for a long time)

297
Q

What is urea?

A

a common waste molecule from the end-stage of protein catabolism.

298
Q

Why does urea use the aquaporin channel?

A

To diffuse in the collecting ducts.

299
Q

How quickly does urea move through the tubule cells?

A

much slower than water…. so it tends to just pass out with urine.

300
Q

What is BUN?

A

Blood-urea-nitrogen. Measure of urea in blood. (higher than normal shows abnormal renal function)

301
Q

Where is calcium found?

A

extracellular

302
Q

Where is phosphate found?

A

intracellular fluid

303
Q

How is calcium balanced?

A

With net loss from body.

304
Q

What normally regulates calcium?

A

parathormone in the parathyroid gland.

305
Q

What does calcitonin make the kidneys do?

A

excrete Ca2+

306
Q

What do the kidneys have a natural tendency to do with calcium and phosphate?

A

keep (reabsorb) PO4-2 and excrete Ca+2

307
Q

What is this modified by?

A

parathormone in the parathyroid gland.

308
Q

What does regular PTH secretion lead to?

A

kidney keeps Ca2+ and lets PO4-2 go

309
Q

What is the net effect of this?

A

increase serum Ca2+

310
Q

What do all forms of Fanconi’s syndrome affect?

A

the normal behavior of the nephron

311
Q

Which portion of the nephron is mostly affected?

A

PCT

312
Q

What do the diseases that produce this result in?

A

abnormal renal tubular excretion (as electrolytes and nutrients spill into the urine)

313
Q

What are the clinical signs and symptoms of Fanconis in children?

A

children: polydipsia, malnutrition, susceptibility to infection.

314
Q

What are the clinical signs and symptoms of Fanconis in adults?

A

pain on weight-bearing joints, dehydration, polyuria.

315
Q

If left untreated what might this lead to?

A

Muscle-wasting and death

316
Q

What does pyelonephritis do to the medulla?

A

fould the ability of the ascending loops to do their job.

317
Q

What is the result?

A

failure of the renal concentration mechanism. ? large volume dilute urine.

318
Q

What does hemostatic maintenance of the ICF involve?

A

stabilized with appropriate nutrient delivery, waste removal, and ionic/osmotic balance.

319
Q

What surrounds this compartment?

A

ECM, which also has to be maintained.

320
Q

What maintains the ECF?

A

The blood

321
Q

What is the average percent of body fluid in adults?

A

60%

322
Q

What is it in infants?

A

80%

323
Q

What about in the elderly?

A

40-50%

324
Q

Which compartment decreases with age?

A

interstitial compartment

325
Q

Which compartments remain fairly stable throughout life?

A

Plasma, and intercellular compartments.

326
Q

Why do women have less water than males in their body?

A

Because they have more fat which is low in water.

327
Q

Where does our water intake come from? And how much from each?

A

Drink = 50%, food = 35%, oxidation = 15%

328
Q

How does water exit our body? And how much from each?

A

Urine = 60%, sweat & ventilation = 35%, stool/feces = 5%

329
Q

What do the kidneys do in response to diarrhea?

A

conserve fluid as to balance the body.

330
Q

what kind of urine would the distilled water group produce?

A

large volume dilute

331
Q

What kind of urine would the isotonic solution group produce?

A

balanced isotonic urine

332
Q

What kind of urine would the 10% salt water group produce?

A

decreased volume, concentrated urine.

333
Q

What does the body do when the osmolality of blood rises or falls?

A

manages concentrations of salt and water to correct the change

334
Q

What hemostatic mechanisms are activated when osmolality of blood rises?

A

Secretion of ADH. Thirst. Lesser players

335
Q

What are the lesser players?

A

decrease renin ? decrease aldosterone ? decrease Na+ reabsorption; and decrease ANF ? decrease renal flow.

336
Q

How is ADH released?

A

neurons from the supra optic nuclei emanate from hypothalamus to post. Pituitary

337
Q

What are these neuronal cell bodies sensitive to?

A

osmolality of blood.

338
Q

What happens to these neurons when osmolality of blood rises?

A

secrete ADH. ADH enters blood. Goes to renal CDs. Lands on V2 r/c. Cells add aquaporin. ? promotes H2O reabsorption into vasa recta.

339
Q

What happens to the osmolality of urine when the above takes place?

A

it goes up.

340
Q

what happens to the osmolality of the blood at this point?

A

Returns to normal.

341
Q

What else do these neurons stimulate?

A

the thirst center

342
Q

What is the blood volume and systemic BP like when osmolality of blood is rising?

A

both are low.

343
Q

THUS ?

A

increase osmolality ? increase ADH secretion ? water retention (anti-diuresis)

344
Q

the opposite is also true ?

A

decrease osmolality ? decrease ADH ? water loss (diuresis)

345
Q

What can a water deficit be caused by?

A

excessive sweating or osmotic diuresis.

346
Q

What might this result in?

A

fluid shifting from intracellular to extracellular compartment

347
Q

What can water excess be caused by?

A

Excessive drinking, excessive ADH

348
Q

What might this result in?

A

fluid shifting from extracellular to intracellular compartment.

349
Q

What homeostatic mechanisms are activated when blood volume falls?

A

secrete ADH, secrete renin angiotensin and aldosterone, decrease ANF ? decrease renal flow.

350
Q

What else will a fall in blood volume cause?

A

fall in BP

351
Q

What 2 things will a rise in renin cause?

A

increase angiotensin 1&2 ? systemic constriction ? increase BP. AND increase aldosterone ? increae Na+ reabsorption in distal nephron ? decrease fluid loss

352
Q

THUS ?

A

decrease blood volume ? increase renin/angiotensin & aldosterone ? increae BP and decrease water loss

353
Q

Salt deficit from vomiting, diarrhea, excessive sweating results in what?

A

fluid shifting from extracellular to intracellular compartment.

354
Q

Salt excess from excessive intake can result in?

A

fluid shifting from intracellular to extracellular compartment

355
Q

What is incontinence?

A

The failure to store urine when desired

356
Q

What is incontinence a disorder of?

A

involving a lack of control of the urinary bladder

357
Q

When does renal function end?

A

when there is an accumulation of urine in the bladder. (after having left the renal calyces, pelvis, and ureters.

358
Q

What kind of reflex is micturation?

A

autonomic spinal cord reflex though it can be inhibited.

359
Q

What happens to pressure as urine accumulates in the bladder?

A

internal pressure rises

360
Q

When do ramp signals begin in the bladder?

A

When fluid reaches 30-50 ml. - rises rapidly when over 300-400 ml

361
Q

When does active signaling begin?

A

100 ml, but very strong by 300 ml

362
Q

What is the secondary nerve associated with micturation?

A

pudendal n

363
Q

What does the pudendal do during micturation?

A

inhibits internal urethral sphincter.

364
Q

What neurophysiological or anatomical factors can cause incontinence?

A

destruction of sensory fibers to CNS. Crush injury to sacral region of spinal cord. Injury to region above sacral region.

Physiology Final (2 decks)

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